Not a typo.
Not April Fool’s Day.
Not a spontaneous and mystical possession by the spirit of George McGovern.
Not even a social experiment to see how many people I can get to unsubscribe from this blog in the span of a day (PLEASE STAY, I LOVE YOU).
Maybe a little bit of this, though:
Oh, Homer!
Over a year ago, I gave a presentation at the Ancestral Health Symposium called “Lessons From the Vegans: What the Paleo Movement Can Learn From the Success of Plant-Based Diets.” In retrospect, I probably should’ve called it “Lessons from the Low-Fatters: What the Paleo Movement Can Learn from the Success of People Who Eat Ridiculous Amounts of Carbs and Don’t Keel Over,” but that was too long for the conference brochure. And for my verbally dyslexic mouth. And also, I didn’t know it was really going to be about fat until I fell down an extended PubMed rabbit hole and, upon regaining consciousness two days later, realized I had found the Nerd Project to end all Nerd Projects.
In truth, though, this post started brewing long before my talk. Having witnessed some pretty impressive healing when I noshed among the low-fat raw vegans (and, after a decade of self-experimenting, concluding I do best on a lower fat diet myself), I just can’t get on board with the categorical “Fat rules, carbs drool!” trend infiltrating both mainstream and alternative nutrition. There are too many exceptions to the rule, too many gaps in the theory, and too many skinny fruitarians frolicking in the sun-dappled fig orchards.
But even beyond that, this post is born of a belief I hold dearly—one that guides my approach to research and underlies the very mission of this blog:
We can’t ignore evidence in order to preserve an ideology.
At least not under the guise of “science.”
When confronted with something that challenges our belief system, the worst possible thing we can do is clamp our hands over our eyes and say, “You do not fit into my understanding of reality; therefore, you do not exist. BE GONE, NON-EXISTING ANOMALY.” Yet that’s what so many of us do—often without even realizing it—when faced with outcomes our chosen philosophy can’t explain. On the flip side of cherry picking, we cherry-throw-out: selectively deleting data that threatens our version of the truth, nipping any cognitive dissonance in the bud before it has a chance to rattle our worldview. It’s easy to be “right” when we’ve shoved all competing evidence into the wood chipper!
For a long time in the nutrition world, our thrown-out cherries were the ones challenging the low fat ideology. We discarded the high fat Inuit cherries and the milky, bloody Masai cherries; the coconut-filled cherries of the Tokelau; the cherries of the traditional reindeer-herding Sami; even the smothered-in-butter French cherries—just to name a few.* It didn’t make sense that these populations could exist and be healthy with their fat-gorging ways, so we slapped them with a “paradox” sticker and deemed them weird exceptions to the Dietary Laws that govern the rest of us.
* For the record, all these examples come with some major caveats, and I don’t think they should be used as evidence to support the kind of high-fat diets many people are eating today (though they don’t necessarily stand as counter-evidence either). More on that in an upcoming post!
Only in more recent years have those cherries been rescued from the compost bin and plopped back into the world’s collective fruit bowl (please wash before consumption). Bestselling books like “Good Calories, Bad Calories” and “The Big Fat Surprise” carved new histories in which fat was an innocent bystander, dragged into the mud by bad science and even badder scientists. The phrase “healthy fat” moved from oxymoron status to popular catchphrase. People whir 80 grams of butter into their coffee and call it breakfast. Apparently Bob Dylan had it right in all but plurality: Time, it is a-changin’!
As awesome as the pro-fat movement has been for challenging outdated beliefs and reviving some truly nutritious foods, there’s been a dark side to the process as well. All of a sudden, the same rhetoric once leveled against high-fat diets is being slung against low-fat ones. Not only is low fat (and by consequence, high carb) not the dietary angel we once thought, the new story goes, but it’s actually the source of all edible evil: the driving force behind our obesity epidemic, a major contributor to heart disease, the puppet master pulling those blood-sugary strings of insulin resistance and diabetes. If only the USDA had recommended 6 to 11 servings of bacon instead of 6 to 11 servings of grains, we wouldn’t be in this mess!
See the problem here?
In the process of redeeming fat, we traded one form of oversimplified blame for another. And it’s led to a brand new wave of cherry genocide. We now dismiss (or paradox-sticker) high-carb populations in the same way we justified ignoring the high-fat ones. We snub decades of clinical success involving fat reduction (to the point where you might think such evidence doesn’t even exist—in which case, you’re in for a surprise with this post!). We deny the potential for low-fat diets to be anything other than a metabolic train wreck, ending in a smoking heap of shrapnel and insulin injections. “Surely those low-fatters are starving all the time,” we proclaim. “Surely they’re making themselves diabetic! They might feel okay right now, but won’t those carby diets go all Cujo on them as the years progress, eating their souls and whatnot?”
Let me be frank here.
If we’re really after the truth, we can’t keep throwing away perfectly good cherries. Seriously. It’s gotta stop. When we censor data we don’t like instead of revising our theories accordingly, we perpetuate the same problems we’ve been battling for decades: partial truths treated as gospel; public policies that do more harm than good; baffled consumers who can’t figure out if it’s the omelet that’s killing them or the OJ they wash it down with.
Do we really want to keep heading down that road? It probably goes somewhere awful! Like Stockton. (Sorry, Stockton.)
Hence why we’re gathered here today, around this massive compilation of pixels, delving into a decidedly hot topic. This post is my attempt to rescue some discarded cherries and return them to the Fruit Bowl of Our Lives. Which, if nothing else, will one day make a fantastic soap opera.
I do want to make one thing abundantly clear before we continue, though. The title “In Defense of Low Fat” doesn’t imply its inverse, “In Attack of High Fat.” Quite the opposite! My goal here is to create a space where two very different dietary approaches can sit down for tea, respectfully coexist, and interact without any subsequent homicide investigations. In fact, I’ll be arguing for a more panoramic view of nutrition where the success of both high-fat and low-fat diets are compatible, and maybe even make sense. It just requires zooming out farther than we’re used to looking, and acknowledging that our ever-rivaling communities could actually learn a lot from each other.
For the sake of reading ease, this sucker is divvied up into two parts: this one, which discusses the crazy-huge body of research behind truly low-fat diets (especially the really obscure stuff!), and the upcoming Part 2, which ties everything together with science, and whatnot. And because this post is long even by my standards, I’ve created a clickable Table of Contents to help you navigate the labyrinth. Good luck! (You’ll need it…)
TABLE OF CONTENTS
1. Carbosis: The Magic of Truly Low-Fat Diets
2. The Low-Fat History You Probably Haven’t Heard
- Walter Kempner: Rice and sugar and diabetes reversal, oh my
- Roy Swank: Kickin’ some Multiple Sclerosis butt… by nixing saturated fat
- Lester Morrison: ???
- Nathan Pritikin: Heart-unbreaker extraordinaire
- Ancel Who?
4. Modern Diet Doctor Squad: An update and apology for jumping the gun
5. Up Next…
Note: a lot of the papers discussed in this post are trapped behind paywalls. I have copies of the full text for all of the ones I discuss in depth, though, so shoot me an email if you’d like to read any!
1. Carbosis: The Magic of Truly Low Fat Diets
Let’s cut to the chase. My thesis, if all this can be boiled down into one, is that two unique metabolic states exist on either extreme of the fat-intake spectrum. One ends around 10% fat and the other begins around 65%. Both zones have their own benefits, and can elicit surprisingly similar effects.
This is a PowerPoint slide I made representing what seems to be going on.
Image rejected from the Lancet due to insufficient sparkles.
In sum:
- Something special happens at very high levels of fat intake (and very low levels of carbohydrate intake). That thing’s called ketosis. It’s where your body creates ketones to use when glucose is scarce, and where fat metabolism is optimized.
- Something equally special happens at very low levels of fat intake (and very high levels of carbohydrate intake). I’m not aware of a formal name for this, so I’m dubbing it carbosis until further notice. It’s a state where insulin sensitivity dramatically improves, and where carbohydrate metabolism is optimized.
- Between those two extremes, especially towards the very middle, is what I’m calling the Macronutrient Swampland. It’s not necessarily a bad place to be if you’re eating a high quality, non-energy-surplus diet and are at a healthy weight (or getting there!), but it’s hard to see the therapeutic effects of reducing fat intake while you’re in this zone. And it tends to be the most potent area for food reward, making it easy for people to overeat here. Any health improvements seen in the Swampland will typically be from losing weight, eating more protein (which has its own special metabolic effects), or boosting food quality (i.e., switching to less processed, “low reward,” nutrient-denser fare), rather than from moving laterally across the macronutrient spectrum.
Here’s the kicker: the Macronutrient Swampland is where our standard definition of “low fat” squarely lands—30% of calories. When we conduct those “low fat” studies with sucky results, they’re almost always using a fat intake of 30% of calories. When the USDA tells us to eat low fat, they mean 30% of calories. When the American Heart Association tells us to eat low fat, they mean 30% of calories. This number has been parroted far and wide across the Western world, drilled into our noggins, and slapped with a skull and crossbones in the “LOW FAT SCREWED UP AMERICA” narrative.
The only problem? It’s not actually low fat.
It’s not low fat relative to the many populations that eat (or ate) their traditional starchy diets: the Okinawans (12% of calories as fat), the Tarahumara Indians (12% of calories as fat), the pre-industrialized Thai (8.9% of calories as fat), the traditional Hawaiian (10% of calories as fat), the traditional Taiwanese (16% of calories as fat), the African Bantu (14 – 17% of calories fat), the traditional Pima (8 – 12% of calories as fat), and the highlanders of Papua New Guinea (3% of calories as fat), just to name a few. It’s not low fat relative to the carby diets that really do have clinical track records for treating modern diseases (which, as we’ll see in this post, hover almost universally at that 10% mark). And perhaps most importantly, it’s not low fat relative to what Americans already eat—which is about 34% of our calories these days, per the most recent available data.
That last point is what utterly handicaps our modern “low fat” research. Nudging 34% fat down to 30% in studies and then claiming nope didn’t work is absolutely face-palm worthy. It’d be like dismissing low-carbohydrate diets because switching from 50% carbohydrate to 46% doesn’t have a profound clinical affect. We’d unleash the hounds on a logical blunder like that, right?
This is a problem that tends to get the plant-based diet community a bit hot under the collar, and I have to agree with them. One of our biggest scientific bloopers was choosing a Swamplandy 30% of total calories as the benchmark for “low fat.” It’s resulted in a slew of unimpressive studies that make us think low-fatting is categorically worthless. I’ll probably never live this down, but I mostly agree with an article T. Colin Campbell wrote about the “low fat mythology” addressing this very topic. (Though in case you’re wondering, I stand by my criticisms of the China Study and Campbell’s rat studies. Nothing in this post supports the idea that animal protein is uniquely harmful, and acknowledging when some parts of the plant-based movement are legit doesn’t give a free pass to the ones that aren’t!)
And that’s just the tip of the iceberg lettuce. On top of our wonky definition of where “low fat” starts and ends, we’ve erroneously conflated “low fat” with the corn-syrup-injected, processed-up-the-wazoo, won’t-rot-for-200-years-because-woah-preservatives menu that emerged when the food industry found a new market to tap. As soon as the USDA released the Food Guide Pyramid in 1992, food manufacturers were all “Let’s low-fat ALL OF THE THINGS,” and accomplished that very feat. So now we hear “low fat” and remember the era of Fig Newtons and rice cakes and sadness, so much sadness. And also Susan Powter.
Once upon a time, though, low fat meant something different. Something hopeful. Something positive. Something that didn’t taste like regurgitated cardboard turd pellets. And the research that emerged from this era was a thing of great beauty! There were low-fat diet studies that actually studied low fat diets (imagine that!), and the notion that 30% fat was equivalent to 10% fat was just a twinkle in a future USDA employee’s eye. Even though our understanding of nutrition’s nitty gritty was less sophisticated back then, research designs were often better, testing “high fat” with things like fresh cream instead of the confounder-riddled carrot cake and milkshakes used in more recent trials.
Hence, much of this post will be a blast to the pre-low-fat-craze past—a romp through the research that artfully dodged the Macronutrient Swampland, and an introduction to the thought-leaders that have all but vanished from scientific memory. After that, in the next post, we’ll explore the mechanisms that tie it all together.
LET US BEGIN.
The Low-Fat History You Probably Never Heard
The popular version of events goes something like this:
America was happily eating its buttery, meaty, cholesteroley fare until Ancel Keys came along with the idea that fat causes heart disease. He cherry-picked data to make it seem like his theory was true, narrowed the culprit down to saturated fat, manipulated the Powers That Be into believing him, and then bull-horned the message far and wide until we all bought his myth. Low fat started with him!
Unfortunately, that’s a big, pre-chewed wad of baloney.
Here’s the deal. People were already whipping out low-fat diets to treat diabetes, multiple sclerosis, high blood pressure, kidney failure, heart disease, and obesity when Keys was a mere young’un shoveling bat poop in Arizona. Heck, the ancient Egyptians prescribed a near-fat-free diet of wheat, grapes, honey, and berries for what was almost certainly diabetes (“too great emptying of urine”). And contrary to popular belief, the early-1900s evidence supporting low fat didn’t come exclusively from rabbits and test tube experiments and correlative scatterplots: it came from actual human people eating actual food with their actual mouths.
If anything, our pal Keys was a latecomer to the idea that fat could play a role in chronic disease. The notion that he single-handedly criminalized fat is complete and utter fiction. He might’ve been the loudest and most unflappably confident voice in the choir, but he certainly wasn’t singing solo.
Here’s a more realistic timeline of the past century, albeit still very incomplete. (Click to make ‘er big!)
Without further ado, let me introduce you to some of these disembodied heads.
Walter Kempner: Rice and sugar and diabetes reversal, oh my
Here’s one for the Paradox Files.
In the 1930s, a man by the name of Walter Kempner fled an increasingly Jew-hostile Germany and landed square in the halls of Duke University… where he proceeded to totally blow the medical community’s mind. His mission: treat kidney disease. His solution: put renal-failing folks on a special diet low in sodium, protein, and fat—a menu devised from in vitro experiments he’d done on kidney tissue.
At the time, very few researchers believed that food could have any effect on kidney disease. Or high blood pressure. Or diabetes. Or heart disease. Or most other chronically wrong-going things in the body. As with Ancel Keys, who was pretty much laughed out of the WHO conference where he presented his “fat causes heart disease” idea, Kempner spent the first chunk of his career swimming upstream in a river of skepticism.
But his colleagues’ dubiousness didn’t last long. After placing patient after so-called-hopeless patient on his unique regimen, it became clear that Kempner’s diet worked. Really ridiculously well. And it became equally clear that the kidney wasn’t the only body part made happy by the new cuisine. Obesity, diabetes, high blood pressure, heart failure, coronary artery disease, psoriasis, and arthritis often saw major improvement or total reversal as a result of the diet. During the course of his career, Kempner treated over 18,000 patients with the above conditions—all by changing what went on the stabby end of their forks.
So what was in this mystical diet of his? Brace yourself!
- White rice
- Fruit
- Fruit juice
- Refined table sugar
- In some cases, vitamin supplements (A, D, thiamine, riboflavin, and niacin)
…And not a darned thing else. Kempner summed up the details himself in a 1974 article, readable here:
A patient takes an average of 250 to 350 gm. of rice (dry weight) daily; any kind of rice may be used provided no sodium, chloride, milk, etc. has been added during its processing. … All fruit juices and fruits are allowed, with the exception of nuts, dates, avocados and any dried or canned fruit or fruit derivatives to which substances other than white sugar have been added. Not more than one banana a day should be taken. White sugar and dextrose may be used ad libitum; on an average a patient takes about 100 grams daily, but, if necessary, as much as 500 grams daily should be used. Tomato and vegetable juices are not allowed.
In other words, it was the CARBPOCALYPSE. Along with feasting on impressive amounts of white rice, people were averaging 100 grams of pure sugar a day, and some ate over a pound of it. That’s up to 2,000 calories from refined sugar alone—the same amount deliciously packed into 25 Cadbury Creme Eggs.
(Wisely, Kempner knew his diet was at no risk of being crowned Dietary Homecoming Queen. He apparently described it as a “monotonous and tasteless diet which would never become popular,” and whose only saving grace was the fact that it worked. And as I mentioned in my AHS presentation, he apparently whipped some of his patients in order to help them comply, as—in his words—”the risk to their life was so great that it warranted harshness.” Ouch!)
Here’s a breakdown of how the diet panned out, macronutrient-wise. Image from Duke University files; red graffiti my own doing, to indicate percent of total calories:
What’s really noteworthy is that the diet wasn’t automatically calorie restricted. In fact, some patients had to increase their energy intake to help them gain weight, or to stabilize their weight if they were losing too much. That’s important, because it means we can’t write this off as a diet that improved biomarkers solely by inducing weight loss (Twinkie Diet, I bow in your general direction). It also means that many people spontaneously ate less than they needed when stuffing their faces with unlimited amounts of starch and sugar… as long as fat intake was super low.
If this seems totally baffling and Twilight-Zoney, that’s because it is. According to my calculations, there is an 84% chance that you are now Googling “rice diet Snopes” or contacting my mother to inquire about my recent psychotic break (joke’s on you; she thinks I’m great!). I urge you to keep reading, though, because we’re about to get to the ooey, gooey data at the center of this carb-filled Tootsie Pop.
Let’s start with something weighty: an obesity paper published in 1975 in the Archives of Internal Medicine, which should be of particular interest to anyone convinced refined carbs are inherently fattening:
Here, Kempner compiled data from 106 slimmed-down patients—a mere slice of the thousands he treated over the years—who all dropped at least 100 pounds on his program and achieved a normal weight. (The average loss amongst them was 140 pounds, and one man melted away over 300). These particular losers ranged from 16 to 65 years old, and featured a mix of women and men.
When it came to blasting obesity, Kempner employed what he called a “rice-reduction diet”—the same protocol he’d designed for renal failure and hypertension, but with lower calories:
In the unmodified initial diet, 90% to 95% of the caloric intake is carbohydrate, taken as rice and fruit. As in the original rice diet, salt intake is exceedingly low (less than 60 mg of sodium per day) and fluid intake is thus markedly reduced to prevent water intoxication. Thus, the initial diet is low-calorie, low-salt, low-protein, low-fat, and essentially free of cholesterol.
After getting into that sugary, starchy groove for a month, the dieters could start eating veggies again (which were initially nixed due to their sodium content—kept low, in part, to help tame high blood pressure and “reduce the stimulatory effect of salt on food intake”). A bit later on, lean meats could also make a triumphant gustatory return.
Thanks to Kempner’s hawkish monitoring and dietary tweaking, obedient dieters were greeted with a steady (and often plateau-free) slide towards a healthy weight, like so:
And since we’re all such visual creatures, here are some photos demonstrating the rice diet in action, first published in Kempner’s aforementioned obesity paper. This young woman lost 123 pounds in just shy of a year:
And here we have 278 pounds obliterated in a bit over a year, doing the same. His fasting triglycerides dropped from 187 mg/dL to 85 mg/dL:
And this lovely lady lost 115 pounds in 33 weeks. Her fasting blood sugar dropped from 315 mg/dL to 100 mg/dL, and her triglycerides plummeted from 516 mg/dL to a peachy keen 79 mg/dL—after eating a diet literally made of refined sugar and starch.
Looking at these sugar-fueled Incredible Shrinking People brings an important point to mind. If we assume weight loss is just a matter of calories in versus calories out, the rice diet isn’t any more remarkable than other low-calorie bootcamps: folks ate less and lost weight. Dur. But if you’ve hung around the internet for very long, you might’ve seen the theory—popular within some corners of the low-carb world—that successful weight-loss diets are invariably low carbohydrate diets (or at least low refined sugar and starch diets), regardless of what other rationale those diets masquerade under (low fat, high fiber, low calorie, food combining, eating only on Tuesdays in the presence of an ovulating jackalope, etc.).
How? Because folks inevitably slash their carb intake when they eat less food overall, the theory goes. This rests on the premise that insulin is the wizard behind the curtain of obesity, and that quelling its wrathful swings—triggered by carbohydrates and refined carbohydrates in particular—is necessary for losing weight. Gary Taubes explained this concept in detail in a 2010 blog post:
Simply put, anyone who tries to diet by any of the more accepted methods (i.e., Weight Watchers), and anyone who decides to “eat healthy” as its currently defined, will remove the carbohydrates from the diet that may be — if the carbohydrate/insulin hypothesis is correct — the most fattening. And if they’re trying to cut calories, they’ll be removing some number of total carbohydrates as well. And if these people lose fat on these diets, this is a very likely reason why.
The rice diet might be the most compelling hole-poker we have for that theory. While most carby programs—say, Pritikin or McDougall or Ornish—eschew refined grains and sugar (and thus could fit snugly into the insulin-centric concept above), Kempner’s program sure didn’t. He fed folks almost nothing but the “most fattening” carbohydrates and still managed to slim them down. Does your brain hurt yet?
Of course, losing weight is a far different beast than maintaining a 100-pounds-lighter frame after the losing’s been done—leading us to the question: what happened to these folks in the long run? Did they maintain their weight loss? Gain it all back? Develop a crippling phobia of small, white, oblong granules, requiring years of psychotherapy and Riki Lake guest appearances to overcome?
Alas, Kempner noted that long-term results were “not yet available for the patients analyzed in this report,” and I’ve yet to find any follow-up papers revealing their fate. The only clue I’ve seen comes from the first page of the “Rice Diet Renewal” book, which states that 43% of rice dieters had maintained their weight loss (or lost even more) six years after their stint in the program. (For comparison’s sake, an Annual Review of Nutrition paper estimates that on average, about 20% of folks who’ve lost significant weight are able to maintain that loss for at least a year.)
All that said, the rice diet was about far more than impressively svelte before-and-after shots. As alluded to earlier, it also had the uncanny side effect of improving diabetes and insulin resistance—even when weight loss wasn’t part of the equation. I warned you this was gonna get weird! Kempner published a whole paper on the topic in 1958, which you wouldn’t know by looking at its hauntingly empty PubMed entry:
(Email me if you want the full text!)
For starters, Kempner was just as perplexed as us modern-day health enthusiasts might be when it comes to the effect his diet had on diabetics. As he penned in the paper you cannot see:
We have for the past 15 years treated numerous diabetic patients with the rice diet. Since more than 90 percent of the calories in this diet are derived from carbohydrates, it was anticipated that increased amounts of insulin would be necessary to keep the blood sugar at its previous level. However, the opposite proved to be true. … Not only is the rice diet well tolerated but in many instances the blood sugar and the insulin requirements decrease.
In this report, Kempner analyzed 100 diabetics who’d entered the rice diet program between 1944 and 1955. All of them strictly followed the diet for at least three months (often much longer), and they were observed an average of nearly two years—with some folks monitored for up to eleven years after they’d first embarked on the carby cuisine.
The findings? Ladies and gents, place your bets…
More than half of those 100 diabetic ricers—63%—actually saw their fasting blood sugar drop by at least 20 mg/dL during the diet. Only 15% had their blood sugar go up significantly. The remaining 22 saw little to no change.
To get a visual sense of those numbers, here’s an aptly named pie graph (don’t worry; it’s fat and carb free!). “Increased” or “decreased” is defined as a change of at least 20 mg/dL:
Let’s repeat that: eating almost nothing but starch and sugar and fruit, the majority of diabetic patients lowered their blood sugar levels. In fact, when everyone’s results were pooled together, the average blood sugar change was a drop of 47 points.
‘Twas a similar story in Insulin Land. Of the study’s participants, 68 entered the scene already dependent on insulin. As the carbs raged on, 21 of those insulin-injecters didn’t have to change their dosage; nine needed an increase (including four people who initially weren’t on any insulin at all); and—again comes the cruel, cruel defiance of prediction—42 slashed their usage significantly. In fact, 18 folks were able to discontinue their insulin entirely. Feasting on white rice. And sugar. And fruit juice.
Here’s another delicious graph of pie, calculated for the 72 patients who needed insulin at some point during the study:
Once again: eating virtually nothing but this…
…the majority of diabetics ended up with better glucose control and insulin sensitivity, and in some cases freed themselves from diabetes entirely.
Let that sink in for a minute.
Or two, if you need to grab a glass of water and ward off the vapours.
Just to be clear, the point here isn’t that the rice diet is the Best Thing Ever for diabetics and everyone should trade their insulin pumps for a metric ton of Skittles (nobody needs to taste that many rainbows). After all, 15% of the rice-dieting diabetics actually got worse, many of the improvers still had above-normal blood sugar (despite huge drops from baseline), and we could probably hack Kempner’s protocol to make it more nutritionally sound without ruining its therapeutic effects. Clearly, it ain’t perfect. All I’m saying is that these results totally fly in the face of what most of us consider possible. Sugar and white rice improving diabetes? Blasphemy!
All that said, an important critical-thinky question remains: was this all just a byproduct of weight loss? We know that restricting calories and dropping pounds can definitely boost insulin sensitivity and glucose control, regardless of whether the diet used is particularly healthy. It’s one thing to not be diabetic because you’re eating kale and grass-fed buffalo whose ancestors were blessed by Sacagawea, and another to not be diabetic because you’re living on napkins and crack. Can we at least say that the successful diabetics were the ones who lost weight throughout the program, spontaneously eating less, unamused by a diet that had exactly one-and-a-half flavors?
NOPE. As Kempner pointed out, any obese patients were indeed encouraged to lose weight—but the improvements in blood sugar levels and insulin requirements occurred “both in patients who lost weight and in those who did not have a significant weight change” (his words). Kempner’s data, both in this paper and in the massive collection of his work filed away at Duke University, showed that the diet could benefit diabetics even when their weight and energy intake didn’t budge.
And it didn’t end there. The rice diet also proved helpful for heart failure. It rapidly healed psoriasis. It excelled at its original goal of treating high blood pressure. The “good for” list stretched on nearly as far as those endless bowls of rice! As early as 1949, Kempner had observed that the rice diet was healing more than 70% of his seriously ill, not-responding-to-other-treatments patients from a wide spectrum of disease backgrounds. That figure stayed pretty stable as the decades rolled on.
Psoriasis obliteration on the rice diet.
Just last year, the Journal of Electrocardiology published something of a Rice Diet Resurrection, dredging up Kempner’s key findings and blasting open his oft-forgotten legacy: “An archaeologic dig: A rice-fruit diet reverses ECG changes in hypertension.” In it, the authors pointed out something pretty important regarding the ultimate success of the diet. A band-aid treatment it was not; the rice diet actually seemed to permanently reverse the conditions it set out to treat, at least for many adherents:
A poorly known but important observation was that patients who were able to follow the regime, and who were slowly guided through a gradual modification of the diet over many months, were able to transition into a very tolerable low fat, largely vegetarian diet, while leading a normal, active life, without medications, indicating that the disease state had been permanently modified.
“Permanently modified” probably needs a qualifier, since those folks couldn’t make a total return to their former gustatory ways. But over time, they could start eating a more diverse diet with (lean) animal foods, all manner of vegetables, a moderate level of salt, and the magnificent return of tastiness. Not too shabby, considering many of those folks were initially riding a bullet train towards death. (In another very recent article, “Who and what drove Walter Kempner?“, the authors noted that in Kempner’s day, life expectancy for anyone with malignant hypertension—one of Kempner’s main patient demographics—was only six months. The fact that he gave most of them decades of recouped earth time was pretty fantastic.)
So whatever became of the rice diet? Like most things in life, it lost out to stuff that was newer, prettier, shinier, and easier to squeeze inside an FDA-approved pill. Kempner relinquished the Rice Diet throne in 1992 (and in case you’re wondering, died of a heart attack five years later, at the age of 94—though it’s unclear what his own diet and lifestyle actually were). After his departure, the rice diet predictably loosened up: the program later allowed “a wider selection of largely vegetarian food choices,” though still with low sodium and protein intake (and ostensibly less whipping).
In his 1983 article “Kempner Revisited,” Eugene Stead—who’d worked at Duke alongside the Rice Man himself—summed up Kempner’s unorthodox legacy in a way that captures my own thoughts:
Who in his right mind would have ever thought that rice and fruit could modify vascular disease appreciably? Who would have fed a protein-deficient patient, losing large quantities of protein in his urine, a protein-poor diet? Who would have dared to give a more than 90% carbohydrate diet to a diabetic? Every expert knew that cholesterol levels were not influenced by diet. Nevertheless, all these leads have paid off richly.
Kempner walkin’ the talk. From Duke University files.
Ultimately, I find Kempner’s work both important and wildly uncomfortable.
Important, because it exposes some cracks in our current view of carbohydrates and sugar—areas where our thinking has room to grow and our assumptions have room to crumble.
Uncomfortable, because it demolishes my long-held rationale for why low fat, veganish diets can be successful: that they work because they involve switching to whole foods (Kempner’s sure didn’t!); that they work because they reduce refined sugar and starch intake (the very lifeblood of the rice diet!); that they work because they increase disease-fighting plant compounds (nary a vegetable to be seen under Kempner’s strictest watch). Let me go on record here: I TOTALLY stand corrected!
Perhaps the only areas of overlap with an ancestral framework are that all that rice would’ve provided a decent source of resistant starch, gluten was nowhere to be seen, and the uber-lean diet would’ve smashed polyunsaturated fat (PUFA) intake to smithereens. (If you haven’t caught wind of the PUFA-hatin’ yet, these fats are garnering quite a bad rap due to their unstable, oxidation-prone structure—especially omega-6 PUFAs, the pro-inflammatory Evil Cousins of omega-3s. But even PUFAs as a whole have taken a clobbering in some spheres (hello Ray Peat!), and higher-than-trivial intakes have been indicted as a cause of many terrible things.)
Indeed, after my AHS talk, a few people contacted me suggesting it may be the PUFA reduction that improved sugar metabolism and other aspects of health, thus allowing rice dieters to thrive on an otherwise nonsensical diet. And more broadly, that rock-bottom PUFA intake might be the biggest reason low fat, plant-based diets have any positive effect on chronic diseases to begin with. That would leave saturated and monounsaturated fat in the clear, needlessly nixed in the quest for better health.
I might be inclined to guess the same thing, if not for one human-sized monkey wrench by the name of Roy Swank.
Roy Swank: Kickin’ some multiple sclerosis butt… by nixing saturated fat
You might be familiar with our current diet-wielding, multiple-sclerosis-blasting warrior Terry Wahls, but less known is the fellow who preceded her by over half a century: Roy Swank. And what a story he had!
Swank exited the womb practically destined for greatness. Along with growing up near my beloved home city of Portland, young Swank was musically gifted, athletically inclined, and devastatingly suave. He spent his formative years wooing his future wife, Eulalia, in his dad’s mortuary hearse (chicks dig that stuff), and started driving a local doctor around town to see patients when he was just 13. It was then that his interest in medicine roared to life! By the time he was 26, Swank had racked up a Bachelor of Science, a PhD, a medical degree, and a fitting destiny for his surname.
But our relevant saga began in 1948, when Swank got invited to Montreal to research multiple sclerosis (MS)—a devastating autoimmune disease affecting the brain and spinal chord. He soon discovered a peculiar trend: across the globe, MS was rare in areas where saturated fat intake was low, but much more common where meat and dairy were a mainstay. And as he scoured disease patterns from the previous two decades, Swank noticed that World War II heralded a drop in MS rates wherever meat and dairy were rationed. The clincher came with a Norwegian survey he helped conduct, which showed MS was clustering around the country’s rural, mountainous, dairy-noshing farming regions, while coastal fishing communities—whose fat intake was lower and mostly polyunsaturated—were pretty much spared.
And you might get a kick out of this: when plotting MS prevalence against national intake of animal fat, Swank arrived at a perfect upward curve that was nearly indistinguishable from the one we vilified Ancel Keys for. Here’s Keys’ six-country graph overlaid with Swank’s MS data. Eerie, no?
From page 13 of “The Multiple Sclerosis Diet Book” by Roy Swank.
We can (and should!) fly our “correlation isn’t causation” flag here, but keep in mind that MS research was in its infancy back then. Population trends were the only thing researchers had to work with. So, armed with the scant clues of his time, Swank put his thinking cap on and devised the first-ever dietary experiment for multiple sclerosis. And it went a little somethin’ like this:
- Low total fat
- Very low saturated fat (10 – 15 grams per day, maximum)
- Small amounts of polyunsaturated vegetable oils and fish oil (10 – 40 grams per day)
- Grains
- Vegetables
- Fruit
- Skim milk
- Fish and other seafood
- Extremely lean land-animal products (skinless chicken and turkey; egg whites; trimmed meats)
- 60 to 90 grams of protein daily, mostly from fat-free animal foods
To put his hopeful menu to the test, Swank rounded up 150 MS patients—70 men and 80 women—to guinea-pig his diet in real life. And we’re not just talking a breezy month or two of experimenting; starting in 1948, he meticulously followed these folks for 50 years and beyond, keeping track of what each person ate and how much their disease progressed after they entered the study. One of his most detailed papers, “Multiple sclerosis: fat-oil relationship,” documented the 34-year results of that massive undertaking.
As Swank explained in his paper, the patients had to keep detailed food logs of their daily gustatory adventures. They also trekked to a Montreal clinic once every two weeks to get their MS assessed and endure a pop quiz about their eating habits. (Due to humans being sucky remember-ers (and notorious “historical revisionists” of our own mistakes), dietary recalls are often unreliable—but Swank collected so many of them, over such a vast span of years, that he could paint a pretty accurate picture for each patient.) Once their new, Swank-approved eating habits had stabilized, those patients were weaned onto less frequent clinic checkups and did much of their reporting by snail mail.
To gauge how each person’s disease changed throughout the study, Swank used a neurological grading system ranging from 0 to 6, abridged here for reading ease:
0. Remission, more or less
1. Some neurological symptoms, with fatigue and periodic exhaustion
2. Mild physical impairments
3. Severe physical impairments
4. Wheelchair-bound, with memory impairment
5. Confined to bed and chair
6. Dead
From the get-go, the goal was to slash participants’ animal fat intake down from an average of 125 grams per day (pre-Swankification) to a maximum of 10 to 15 grams per day (post-Swankification). Starting in 1951, they could also add 5 grams of cod liver oil and eat between 10 and 40 grams of “fluid vegetable oils” daily, though saturated fat was supposed to stay as low as possible.
Of course, we humans are wont to err, and not all of the patients colored within the low-fat lines. Swank noted that some people “doubled or even tripled the amount of [saturated] fat* recommended,” and that in lieu of a control group, those variations made it possible to see how different fat intakes correlated with MS progression over the decades. Yay math!
* A Swanky disclaimer: although I’m employing more familiar terminology for the sake of this blog post, note that Swank uses the words “fat” and “oil” a bit differently in his papers. “Fat” in his work refers only to saturated fat, while “oil” refers only to unsaturated fats. So if you take a gander at any of his publications (which I recommend you do!), just keep in mind that his “fat” translates to our definition of “saturated fat” rather than “total fat.”
By the 34-year mark, a bit over half of the original group—81 people—had passed away. That’s actually pretty promising: Swank noted that when he first started studying MS, most patients were expected to end up bedridden or wheelchair-bound within a decade or two, and the assumption was that “all would be dead within 35 years.”
But where it gets really interesting is when the Swankers were divided up based on their average saturated fat intake. Of those who didn’t exceed 20 grams per day (70 people), only 31% died over the course of the study (20% specifically from MS). But of those who ate more than 20 grams of saturated fat per day (74 people), a whoppin’ 80% perished in that same time frame (62% specifically from MS). Voila:
And when we break it down a bit further, something even more interesting emerges: the saturated fat/mortality trend wasn’t linear. Like, at all. Folks eating between 20.1 and 30 grams per day had ridiculously similar mortality rates to those eating 30.1 to 50 grams and beyond. Basically, once people crossed the 20-grams-per-day threshold, it didn’t seem to matter how much saturated fat they were eating: mortality rates rapidly maxed out and then stayed relatively constant. It’s like a saturated-fatty version of the Macronutrient Swampland, where everything outside the “magic” zone is super samey!
FYI: average saturated fat intake for the lowest bracket was 17 grams per day; for the middle bracket, 25 grams per day; and for the highest bracket, 42 grams per day.
(In case you’re wondering, it didn’t seem to be a matter of having a longer but more miserable, enfeebled life for the low-fat adherents. As Swank noted, “Patients on our low-fat diet have been remarkably free of bacterial and viral infections, ‘colds and flu’ occur rarely, and recovering from urinary and other bacterial infections has been rapid when appropriately treated.” Indeed, quite a few measures of their health improved.)
The Swankers’ disease progression—as tracked by that neurological scale mentioned earlier—followed a similar trend. For the folks eating 20 or fewer grams of saturated fat per day, the disease remained relatively stable, with just over half a grade of progression (worsening) on average. But for the subset of folks eating between 20.1 and 30 grams per day, the disease progressed an average of 2.6 grades. And for those chowing down on more than 30 grams per day, the disease worsened by an average of 3.0 grades. (To help conceptualize that, a three-grade change is the equivalent of going from “mild physical impairments” to “confined to bed and chair.”)
Here are more Smurf-colored bars for the visually inclined:
And because I love me some graphs, here’s another one straight from Swank’s paper, showing the dramatic drop in exacerbation (flare-up) rates before and after folks got all Swanky:
Pretty impressive, no?
In addition to all this fun stuff, Swank commented (again, in his 1991 paper “Multiple sclerosis: fat-oil relationship“), that some patients needed an even steeper slash in their saturated fat intake—down to 10 grams per day, maximum—in order to “gain an improvement in energy and freedom from severe fluctuations of disease.” Swank wrote:
In recent years, this experience induced us to eliminate all meats and other sources of fat from the diet of many patients when first seen. We estimate that saturated animal fat was reduced to ~5 g/day plus the fractional or trace amounts of fat contained in many foods. It is our impression that these patients improved faster than others in whom this was not done.
In the vein of Devil’s Advocation, though, we should give our critical-thinking wheels a whirl and see if there are any alternative explanations for these findings. Could there be some suspicious lifestyle confounders like we see in studies today? Were saturated fats lumped in with hydrogenated ones and mutually given the boot, while only the latter was a true health-harmer? Was the supplementation of cod liver oil, chock full of omega-3 and vitamin-A-rich goodness, enough to explain the mortality patterns? Was the culprit saturated fat itself, or was it just guilty by association—maybe serving as a proxy for generalized I-Don’t-Give-A-Hoot-About-My-Health-itis, as the rebels who ignored Swank’s “eat less saturated fat!” message were more likely to ignore the “sugar is bad” or “vegetables are good” or “don’t run with scissors while chewing arsenic candy” messages as well?
As much as I love wailing my confounder alarms, I don’t think the usual suspects apply in this case. Here’s why!
- Hydrogenated fats were indeed banned from the menu, but not until 1951—two or three years after folks started the diet, at which point they’d already seen profound improvements.
- Likewise, cod liver oil (and other omega-3-rich fluid oils) weren’t allowed during the first couple years of the diet, and again, folks saw an 80% decrease in their MS flare-up rates during that time.
- As for potential bad-guy carbs skewing the results? Remember, Swank developed his diet in the late 1940s—decades before refined grains and sugar joined the Dietary Villain ranks and were widely considered harmful. In fact, his diet didn’t restrict refined grains or sugar to begin with, so it wouldn’t make sense that a “screw it all” mentality would result in folks rebelliously downing processed carbs. (Heck, in Swank’s Multiple Sclerosis Diet book, there are plenty of recipes calling for white flour and sugar, and no indication that his patients—at least during the first few decades—were told to stick to whole-food sources of carbohydrate.)
And lest we wonder if the folks eating more saturated fat were also eating more of those gnarly, high-PUFA vegetable oils we so love to hate (thus obscuring the real relationship between saturated fat and MS progression): no dice! Swank’s data showed pretty clearly that the more saturated fat people ate, the less vegetable oil they were eating—an inverse correlation of -0.62 by the study’s 22nd year. Likewise, as Swank explained in the paper we’ve been discussing, higher unsaturated oil intake went hand-in-hand with better outcomes in terms of disability and mortality. The inclusion of vegetable oils “seemed to make patients feel better, increased their energy, and improved the condition of hair and skin,” even though Swank maintained they weren’t necessary for treating MS itself (since his patients took a fantastic turn for the better before those oils were added back to the diet).
Hence why I called Swank a “monkey wrench” a bit earlier on. In contrast to the theory that rock-bottom PUFA levels are the real reason very low fat diets work (while saturated fat would be an innocent, needlessly reduced bystander), Swank found the opposite to be true—that saturated fat had the strongest relationship with MS progression and mortality, while polyunsaturated fat levels could be scaled up or down without negatively impacting health. At least within that 10 to 40 gram range. And at least for multiple sclerosis (although mortality from other chronic diseases dropped during Swank’s diet as well).
That said, there is another possibility that could maybe, maybe, MAYBE be obscuring the saturated fat trend: Neu5Gc. This is a little sialic acid molecule that humans, rather uniquely, can’t synthesize. We produce a similar molecule called Neu5Ac, but lost the ability to make Neu5Gc after splitting from our last common ancestor with the great apes. Because gene mutations ‘n stuff. Other primates (and almost all mammals) can still synthesize Neu5Gc just fine!
Here’s why it matters: even though we can’t make Neu5Gc on our own, we can incorporate it into our tissues when we ingest it from food. And the prime sources of Neu5Gc happen to be red meat and dairy, the same food-vehicles that deliver most of our saturated fat. Because Neu5Gc looks like a foreign substance to our paranoid human innards, we’re capable of producing antibodies against it (although levels of those antibodies vary widely from person to person), which, in turn, can stir up all sorts of trouble. So far, we’ve got theories about a potential role for anti-Neu5Gc’s antibodies in systemic inflammation, cancer, heart disease, hypothyroidism, and also… WAIT FOR IT… multiple sclerosis. (See: “Why does multiple sclerosis only affect human primates?” and “Missing links in multiple sclerosis etiology. A working connecting hypothesis.“)
From “Quantitative analysis of sialic acids in Chinese conventional foods by HPLC-FLD,” 2014.
I waffled over whether to even include this speculation here, since Neu5Gc research is just a wobbly-kneed babe in the woods right now, and we’d need a lot more data before we could definitively link it to any disease. But, considering that 1) humans are the only primate that develops multiple sclerosis, 2) humans are the only mammal that can’t make Neu5Gc (and that produce antibodies against it), 3) multiple sclerosis tends to cluster around areas with a higher intake of Neu5Gc-containing foods (land meat and dairy), and 4) there’s a plausible mechanism linking Neu5Gc with the development of multiple sclerosis (through the effects of antibodies on the blood-brain barrier and axon-myelin unit)… well, all I’m sayin’ is it seems quite intriguing!
That said, Swank actually had some compelling, research-backed ideas about why saturated fat per se could trigger MS, which we’ll discuss in Part 2 of this post. It’s worth noting that he didn’t believe saturated fat causes multiple sclerosis, just that it “precipitates or accelerates it in susceptible individuals,” as he wrote in 1954. It’s not outside the realm of possibility that Neu5Gc somehow plays the role in the development of MS, while saturated fat, under specific conditions, aggravates it. So, even if this Neu5Gc stuff pans out, it doesn’t necessarily pardon saturated fat!
At any rate, we’re not quite at the end of Swank’s research rope. In 2003, he published the 50-year results of his never-ending study: “Review of MS patient survival on a Swank low saturated fat diet.” By that time, after 16 years of letting them do their own thang, he’d managed to track down 15 of his surviving participants and pull them in for interviews and in-person visits. They were all between 72 and 84 years old. (Swank himself was 94, and in case you’re wondering, was still goin’ strong until he passed away in 2008 at the age of 99). Amazingly, only two survivors needed help walking and had any sign of their disease; as for the others, Swank described it thusly:
The remaining 13 patients were remarkably well. They were very active, could care for themselves, could walk as necessary, and were normal mentally. … [They] stood and were active and unusually youthful looking, with very smooth facial skin devoid of wrinkles due to good subcutaneous circulation. They were all in friendly, good spirits, had joyful laughter, and generally quite youthful behavior. This study also indicated that patients with MS, if they rigorously follow the extremely low-fat diet proposed by Swank, which contains no more than 10 to 15 g/d of saturated fat, can expect to survive and be ambulant and otherwise normal to an advanced age.
Take note of that “good subcutaneous circulation” comment, because it’s at the crux of Swank’s theory about why saturated fat is harmful for MS patients (hint: it has to do with blood cell aggregation and oxygenation). More on that in the next blog-post installment! We’ll be coming back to some of Swank’s research and ideas when we discuss the science behind why low-fatting works, because he’s just that awesome.
In the meantime, we’re hardly done with our historical saga. Next up is another obscure figure from the dusty, carb-encrusted pages of science’s past: Lester Morrison.
Lester Morrison is a man of mystery. A mystery, in part, because he was using low-fat diets to treat heart disease years before Ancel Keys supposedly introduced the idea to the world. A mystery also because for a guy who did some neat stuff, he’s totally not Google-stalkable. Nary a pixel of his face could be found in my sleuthing efforts, and the only bio-esque document seems to be his obituary.
Here’s what we do know. A rather precocious and multitalented individual (along with being a physician, he was an accomplished violinist, historian, symphony concertmaster, novelist, and maybe also Spiderman, and won his first research award when he was a sweet 16), Morrison plunged into the research field with an initial focus on gastroenterology. His first taste of Fat Suspiciousness came in the 1940s, after noticing heart disease and stroke mortality dropped hand-in-hand with wartime food rationing—which curbed, among other things, dietary fat. As he explained in his 1955 article, “A nutritional program for prolongation of life in coronary atherosclerosis,” World War I saw the first parallel dance between food rationing and heart disease, with the British blockade of Germany; World War II was fat-jà-vu all over again:
During World War II … the various Scandinavian governments supplied the information that, when fat in the diets of the population had to be reduced to a minimum because of the scarcity of dietary fats, the death and sickness rate from atherosclerosis was likewise reduced to a minimum. As soon as the war ended and dietary fat once again became plentiful, the mortality rate and morbidity rates from coronary and cerebrovascular disease promptly soared to prewar levels and even began to surpass them.
If you’ve read my critique of Forks Over Knives—a documentary that cited the same wartime stats as evidence for low-fat-plant-based superiority—then you already know I have some bones to pick with those correlations. As I explained in my critique, the rationing-induced changges involved far more than tanking total dietary fat: during World War II, seafood consumption doubled; sugar intake halved; vitamin K2 intake rose; trans-fat-containing-margarines all but exited the table. Not to mention, any situation of food restriction tends to boost vascular health, at least initially.
Nonetheless, the link between war rationing and mortality seemed to catch a lot of eyes, and Morrison’s were two of ’em. Cardiovascular disease had slayed a hefty portion of family (including his mom and dad), so the issue was quite near to his heart (literally!). Thus, he was inspired to investigate the matter in a more controlled setting.
In 1946—years, again, before Keys was hot on fat’s trail—Morrison launched a dietary study involving 100 people who’d recently survived a heart attack. For 50 patients, he left their menu as-is: fairly high in fat (80 – 160 grams per day) and high in cholesterol (200 – 1800 mg per day). For the other 50, he prescribed a war-rationing-inspired diet limited to 20 – 25 grams of fat per day—with continual supervision for both the patients and their families to ensure they stuck with it (and the boot given to anyone who couldn’t promise total compliance). He then followed everyone for eight years to see how many folks perished from each group.
In his papers “Arteriosclerosis: Recent advances in the dietary and medicinal treatment” (1951) and “A nutritional program for prolongation of life in coronary atherosclerosis” (1955), Morrison gave a detailed outline of his experimental diet, which was designed specifically to lower folks’ cholesterol. (Worth noting: the diet didn’t limit sugar or other sweeteners, and didn’t reduce animal protein intake, as a variety of lean meats and dairy were allowed. In fact, it prescribed 60 – 100 grams of mostly animal-based protein per day, and folks ended up eating closer to 120 grams on average—well above the 5% threshold deemed toxic by T. Colin Campbell. Just sayin’!)
The encouraged edibles:
And the no-nos: 
(Patients were also encouraged to take a multivitamin containing vitamin A.)
The results? You can probably guess where this is headed! As intended, the diet tanked people’s total cholesterol—by an average of almost 100 mg/dL, in fact. But that’s just the beginning. At the three year mark, 15 people from the control group had died of heart disease, compared to only seven from the low-fat group. (That’s a difference of 70% versus 84% survival.) By the eight year mark, the survival rates had whittled down to 24% of the control group versus 56% of the low-fat group (again, most deaths being from heart disease). And by the study’s 12th year? A whoppin’ nobody was alive from the control group, whereas 34% of the low-fat group was still roaming this lovely green earth.
12-year data taken from Morrison’s “Diet in Coronary Atherosclerosis,” JAMA, June 25, 1960.
(Along with the whole “dying less” thing, Morrison noted that his fat-restricted patients frequently reported “a sense of optimism, well-being, and good spirits” after adopting the diet—a sentiment Swank echoed as well, though without either of their studies being blinded, it’s hard to say how much was just a placebo effect.)
As with the other old research we’re resurrecting in this post, the beauty of Morrison’s study is that it gracefully dodged some confounders that muck up science today. Back when he conducted his fat-slashing experiment, nobody was telling the public that sugar and refined carbs were bad along with fat. No one had an inbox full of Meat’s gonna kill ya news headlines. No one had nutrition labels on their food, or a reason to fear egg yolks, or retinas permanently emblazoned with the image of the Food Pyramid. Heck, even smoking wasn’t widely considered a health hazard yet (the Surgeon General didn’t officially declare a causal link between smoking and lung cancer until 1957). Americans’ minds were clean slates, and prescribing a shiny new dietary change (like reducing fat) didn’t invoke the same confounder cascade we see today. How grand!
All that said, in Morrison’s case, there were two potential caveats we should take note of. One, the low-fat group saw some initial weight loss—an average of 21 pounds for men and 17 for women during the first three years, but with no additional changes during the rest of the study—whereas the control group remained weight-stable the whole time. And two, the low-fatters appeared to spontaneously increase their protein intake, making it hard to know what macronutrient change—the uppage of protein or downage of fat—was really driving the results. Could these be the true wizards behind the better-survival curtain?
It’s certainly possible, though I’m hesitant to say they could fully account for 12 years of dramatically lower death rates. Protein doesn’t seem uniquely beneficial for heart disease patients, and there’s a dearth of research looking at intentional weight loss on post-heart-attack survival—so we really have no way of knowing how big a factor that was for Morrison’s patients. (Oddly enough, population studies show that being overweight rather than normal-weight actually predicts better long-term survival for people who have heart disease—and what’s more, losing weight after having a heart attack is counter-intuitively associated with higher mortality rates. Researchers call this the “obesity paradox“: carrying extra weight tends to increase people’s risk of getting heart disease, but for folks who already have the disease, it seems to prolong life. Of course, there could be quite a few alternative explanations for that trend, which are thoroughly discussed here. Interesting, nonetheless!)
At any rate, Morrison was excited (but wisely cautious) about his study’s results, and ended up penning a book called “The Low-Fat Way to Health and Longer Life,” which he published in 1958—the same year Ancel Keys launched the Seven Countries Study. But, refreshingly non-gun-jumping scientist that he was, he also called for “similar surveys utilizing larger numbers of cases for statistical evaluation” in order to deepen and replicate his findings.
And as luck would have it, those surveys eventually came from one of his very own patients: Nathan Pritikin!
Nathan Pritikin: heart un-breaker extraordinaire
(NOTE: unless otherwise referenced, the background info in this section comes from the memoir, “Pritikin: The Man Who Healed America’s Heart,” which is actually one of the most interesting biographies I’ve ever read!)
Small world gettin’ smaller, eh?
Nathan Pritikin is probably best known for two things: 1) promoting an uber-low-fat diet (and running a longevity center dedicated to such); and 2) being downright chummy with George McGovern—the senator in charge of the 1977 Dietary Goals for the United States. (As I detailed in “Death by Food Pyramid,” McGovern ate a quasi-Pritikin diet for many years, delivered Pritikin’s eulogy, and drew a fair bit of inspiration from the man while crafting America’s new low-fat food recs.)
Pritikin’s dietary saga started with the same World War II trends that inspired so many of his fat-slashing contemporaries. Thanks to some work he’d done on bombsights for the Air Force (he was a prolific inventor and engineer by trade), Pritikin had free-for-all access to classified military documents—including the mortality data being churned out for civilians and prisoners. His puzzle-loving mind was intrigued that heart disease rates were dropping in areas plagued by intense stress and low food availability, when most health authorities expected the opposite to occur.
In 1955, an increasingly health-interested Pritikin made a trek to visit Mystery Man Morrison. The two nerded out about heart disease theories, and at the good doctor’s urging, Pritikin had his cholesterol tested for the first time—revealing a borderline-high level of 280 mg/dL. Although he started making some minor dietary tweaks after that, it wasn’t until an official heart disease diagnosis in 1958 that Pritikin kicked his nightly-pint-of-ice-cream habit and got serious about healing himself.
And we’re talking serious serious. For the next ten years, Pritikin guinea-pigged his body with every dietary permutation imaginable. He’d go for weeks eating almost nothing but lentils, or brown rice, or brown rice plus beef; he’d make slight or dramatic adjustments to his vegetable-grain-meat ratios; he’d experiment with eating ten dates after dinner (fruit, not women; this was before Tinder). And in true scientist fashion, he got his blood tested after each new food stint—meticulously documenting changes in his cholesterol levels, triglycerides, fasting and non-fasting glucose, red blood cell count, white blood cell count, hemoglobin, platelets, carbon dioxide, electrolytes, free thyroxine, and pretty much everything else he could cajole his docs into measuring. Be still, my nerd heart!
Although he managed to whittle his cholesterol down to 155 mg/dL with a lowish-fat menu (including a daily helping of nuts, tiny amounts of oil, and some fish and meat), his next EKG didn’t show a lick of improvement. But the man was not deterred! Pritikin low-fatted harder. He nixed the nuts and oil and meat. He pounded his total cholesterol down to 120 mg/dL. And at his next EKG six months later, the report was music to his ears (and a shock to his diet-skeptical doctors): “Definite improvement since the [last] tracing … Normal electrocardiogram.”
Ensuing stress tests over the next few years confirmed that his once-diseased ticker was, for all intents and purposes, healed.
By the 1970s, Pritikin had not only dialed in his own diet to his strict standards of perfection; he’d also amassed hundreds of low-fat devotees—family, friends, friends of friends, and eventually word-of-mouthers—whom he counseled over the phone for free. And in 1976, the real fun began: Pritikin opened the doors of his first Longevity Center in California. Riiiiight here:
The Casa Del Mar building, later transformed into Pritikin’s healing grounds. From Santa Monica Library Archive.
It was in this magical palace, wringing patients through a 26-day diet overhaul and hawkishly watching their food intake, that Pritikin could document the effects of his program on a large-scale basis.
And document he did! Although his reputation was that of a heart-healer, Pritikin’s diet did far more than assuage troubled arteries. Just as Kempner saw, the uber-fatlessness had the fortunate side effect of rapidly—and often permanently—healing diabetes. The earliest PubMed-able record of Pritikin’s success with diabetics came in 1976, with this little gem:
(FYI: Pritikin’s name isn’t on this paper, but it darn well should be. Scandalous tidbit alert! In 1974, Pritikin divulged the details of his diet to a Dr. James W. Anderson—an internationally acclaimed diabetes researcher at the time—and proposed an official study to test the uber-low-fatness on diabetics. Pritikin designed every detail of the study, drummed up $10,000 to fund it, created meal plans, and then received a grand total of zero credit for any of his contributions once the study was completed and published. In fact, Anderson proceeded to repackage Pritikin’s diet under a different name (the “HFC Diet,” standing for the “High Fiber, High Carbohydrate Diet”) and claimed it as his own invention—conducting a number of additional studies so successful that, in 1979, the American Diabetes Association was inspired to downsize its recommended fat intake. Despite years of haranguing Pritikin for more funding money (and thanking him profusely in their private correspondences), Anderson never publicly mentioned his collaboration with Pritikin or credited him for originating the diet. Buuuurn.)
So what was this study all about? For one week, 13 diabetic men—all who needed either insulin or oral drugs to control their blood sugar—ate the standard American Diabetes Association diet of the time: 34% fat and 43% carbohydrate, the rest made up of protein and wishful thinking. After that, they spent at least two weeks in Carbsville, eating a diet of only 9% fat and 75% carbohydrate. (The two diets were isocaloric, meaning they had the same number of calories, and were designed to help folks maintain their weight rather than lose or gain any.)
Surely that carb palooza sent their blood sugar into a frenzy! …Except it didn’t. After switching from the ADA diet to Pritikin-hijacked-by-Anderson one, nine patients had their insulin and oral drugs completely discontinued—at which point their fasting blood sugar was actually lower than it had been when they were still on medication. (The cutoff for drug discontinuation was a fasting blood sugar of 120 mg/dL.) It only took nine days of low-fatting to make that happen! Another patient’s insulin needs dropped from 28 to 15 units per day. As a further head-scratcher, fasting triglycerides, contrary to what we might expect, dropped significantly for ten men. The only folks who didn’t see any benefit from the 9% fat diet were the three who had the most advanced diabetes at the study’s onset—needing 40 to 55 units of insulin per day.
A tabular and graph-ular representation of changes in fasting blood sugar, in case you’re curious:
Even more intriguing, those results weren’t just a result of weight loss. Only five patients dropped more than three pounds, and there was no difference in fasting blood sugar and triglyceride levels between them and the weight-stable folk. And most importantly, the results seemed to stick: after the study, the nine most successful patients were weaned onto more flexible diets—60 to 65% carbohydrate instead of 75%. And after at least four months of followup, the researchers noted their blood markers hadn’t changed and the “control of the diabetes has been satisfactory without any drug therapy.” Pretty neat, huh?
Okay, okay: this study was tiny and used only men and we could find plenty of things to complain about (more womenfolk! Longer time frame! More Instagram pictures of the researchers’ feet overlooking exotic and envy-inducing locales!). Those are fair criticisms, to be sure. But this study does offer something we hardly ever see: a direct comparison between a Swampland menu (34% fat) and a Carbosis menu (9%), with the subsequent revelation that Oh hey, they actually have totally different results!
Again, as I’m trying to hammer home in this post, most of our “low fat” studies are actually only comparing different shades of Swamplandness—without ever hitting that fantastical 10% that brings a dramatic metabolic shift. And that makes us think that low fat is just a sham that does nothing except make our food taste like rabbit chow. So finding a study-gem like this, where fat intake actually does dip into the magic zone, and where the impressive results challenge our “low fat is bunk” narrative, is a rare and valuable find—even if it could be better designed.
That said, we’re in luck because Pritikin actually published some of his own studies on diabetics, and they were bigger and longer. Two of those papers came out in 1982 and 1983, respectively:
- Response of non-insulin-dependent diabetic patients to an intensive program of diet and exercise.
- Long-term use of a high-complex-carbohydrate, high-fiber, low-fat diet and exercise in the treatment of NIDDM patients.
The first paper looks at how 60 diabetics fared during the 26-day program; the second paper looks at how they did once released back into the scary, high-fat-food-filled ‘real world.’ In the latter, Pritikin described the in-house program as such:
During the 26-day session, the patients were served and taught to prepare the Pritikin high-complex-carbohydrate, high-fiber, low-fat diet. The diet consisted of unprocessed natural food with no supplements, e.g. guar. Less than 10% of the total calories were obtained from fat, … 13% from protein, and the remainder from carbohydrate (90% complex—whole wheat grain, rice and bread, beans, peas and other vegetables, and fresh fruit). … Protein was derived primarily from vegetable sources, except for nonfat milk, which was served daily, and small amounts of fish or fowl, of which 85 g/wk were provided.
Right off the bat, we can see the study wasn’t free from animal protein, as folks were allowed to drink a fair amount of skim milk, chock full of that awful casein vilified in The China Study. It also contained very small (but not irrelevant) amounts of poultry and fish—about this much per week:
Image from HealthFinders Collaborative.
On top of that, the Pritikinites who started out overweight had their calories restricted, but everyone else could eat as much as they wanted (ad libitum). And all the participants were encouraged to go on short walks each day.
So what happened? At the end of their 26-day bootcamp, their pancreases exploded! Just kidding. They did super well. Of the 23 patients who’d entered the program needing to take oral hypoglycemic drugs, all but two had ditched them by the end of the program:
And of the 17 folks who’d been taking insulin (with dosages ranging from 14 to 75 units per day), all but four were released from its needly shackles:
(After crunching the numbers, it turned out people’s reduction in fasting blood sugar was not correlated with weight loss, or with the amount of walking they did, or other changes that we might suspect played a role. Dietary adherence reigned supreme!)
Okay, I know what you’re thinking. Those results are nice and all, but 26 days is nothing in the span of a person’s disease history. Heck, I’ve had hold-sessions with Comcast last longer than that! What happened afterwards? Did Carbjo cometh?
Luckily, Pritikin wanted to know the answer to those questions too. Between two and three years after their romp at the Longevity Center, the patients got a phone call quizzing them on how well they’d stuck with the diet, how much they were exercising, and whether their medical status had changed. They also had to answer dietary recall surveys and food-frequency questionnaires, and got a fasting blood-sample kit in the mail, which is kind of weird but probably a lot more exciting than bills and MasterCard offers.
The results? Compared to when they were freshly released from their low-fat boot camp, seven more people were taking oral hypoglycemic drugs, and four more people were taking insulin. Does that mean the diet failed?! Can we sling a big, fat “I told you so!” to the low-fat warlords and reassure ourselves that the diet is bogus? Actually:
… the main difference between those patients who went back on medication at follow-up compared with those remaining off medication was the percent of calories derived from fat.
Basically, those who stuck with the diet kept reaping the initial rewards, but those who gallivanted back into the Swampland paid dearly!
Of course, all that’s a mere smidgen of the data that got churned out from the Longevity Center over the years. R. James Barnard, who’s served as Research Director at the Pritikin Center (among quite a few other professional feats), published over 100 studies on the Pritikin Program, looking at everything from cancer to diabetes to heart disease.
Hi, James!
And while part of me would love to sit here and write about EVERY SINGLE ONE of those studies in attempt to explode the internet with Literally the Longest Blog Post Ever, another part of me—the part that realizes even the most patient of my readers have sanity limits and day jobs—has vetoed that plan in favor of a briefer sampling. Behold!
ESCAPE HATCH FOR THE FATIGUED OF BRAIN: what follows is a pretty long and sciency scroll of scientific scienceness. I know this blog post is big. I know your brain is turning into soup. CLICK HERE if you want to bypass the study summaries and get back to Pritikin’s life narrative!
Note: the Pritikin Program involves both the Pritikin diet and an hour of daily walking. Although we could definitely consider exercise a confounder (since it can independently improve metabolic and hormonal markers), studies of walking alone haven’t demonstrated anything nearly as dramatic as what’s been achieved with the Pritikin Program. At best, we could wager that walking probably boosts the results of the program, but only contributes to a fraction of its overall effects.
Another note! Unless otherwise mentioned, all the studies below allowed an ad libitum (non-calorie-restricted) energy intake. The participants could eat as much as their hearts desired out of any Pritikin-friendly item except for fish and poultry, which were capped at three servings per week (combined).
Prostate Cancer Protection
- Long-term adherence to the Pritikin Program was a major boon for squashing out insulin resistance and reducing prostate cancer risk. Folks who followed the diet between 1 and 28 years reduced fasting insulin by 52%, fasting glucose by 20%, HOMA IR (a measure of insulin resistance) by 62%, and fasting triglycerides by 45%. And in a group of overweight men, even a quick jaunt on the program (two weeks) reduced fasting insulin by 30%, fasting glucose by 14%, HOMA IR by 40%, and fasting triglycerides by 33%. Not impressed yet? Blood from the Pritikin-fed fellows (both two-week and long-term) drastically slowed the growth of prostate epithelial cells, suggesting benefit for the prevention of prostate cancer.
From “Effect of diet and exercise intervention on the growth of prostate epithelial cells.” Barnard, 2008.
- In a similar study of both short-term (11 days) and long-term (average 14.2 years) Pritikin followers, more evidence of prostate cancer protection emerged. The short-termers saw a 20% drop in insulin-like growth factor 1 (IGF-1) levels and a 53% rise (that’s a good thing!) in insulin-like growth factor binding protein 1 (IGFBP-1); the long-termers saw a solid 55% drop in IGF-1 and 150% rise in IGFBP-1. (IGF-1 has been strongly associated with cancer due to its role in regulating cell growth and death, and and IGFBPs are proteins that bind insulin-like growth factors and neutralize some of their unsavory activities.) Likewise, the short-term group saw a 25% drop in fasting insulin levels and the long-term group saw a 68% drop. As with the previous study, both groups’ Pritikin-ified blood was particularly awesome at fighting cancer: the serum from the short-termers caused a 30% decrease in the growth of LNCaP cells (a line of human prostate cancer cells) and serum from the long-termers caused a 44% decrease, compared to baseline. Both groups’ blood also increased the rate of death for those cancer cells.
- Yet another study of Pritikin dieters (27 obese men) showed the program may be an excellent defense against the disease: the men saw a 28% increase of sex hormone-binding globulin (which binds androgens and appears to help protect against prostate cancer) and a 43% drop in fasting insulin; for three men who started out with slightly elevated PSA (prostate-specific antigen) levels, the diet also reduced that. According to the researchers, “The increase in SHBG would result in more testosterone being bound and, therefore, less of the androgen available to act on the prostate. The decrease in insulin might also decrease mitogenic activity in the prostate.”
- One more on the prostate front! An analysis of post-Pritikin-Program blood shed light on the mechanisms behind the aforementioned anti-cancer effects: apparently, the Pritikin Program reduced tumor cell inflammation and resulted in lower NFκB activation in LNCaP cells. (NFκB, or “nuclear factor kappa-light-chain-enhancer of activated B cells” if you want to be fancy about it, is a protein complex involved in DNA transcription, cell death, and cytokine production.) The program’s results also seemed to hinge on reducing IGF-1 levels, because when the researchers added back IGF-1 back to the participants’ squeaky clean, post-Pritikin-Program serum, the results were completely reversed:
From “Analyzing serum-stimulated prostate cancer cell lines after low-fat, high-fiber diet and exercise intervention.” Barnard, et al., 2011.
Reduced LDL Oxidation and Spiffed-Up HDL
- Three weeks on the Pritikin Program resulted in LDL particles that, even by paleo- and low-carb-advocate standards, were much less likely to oxidize and promote heart disease. In a group of 80 Pritikinning men and women, average LDL particle size increased (with larger LDL considered less atherogenic), and 27% of the folks who’d started out with LDL pattern B switched to LDL pattern A (again, considered less atherogenic). In vitro, the participants’ LDL also became more resistant to copper-induced oxidation—with a 21% drop in initial oxidation, 13% increase in lag time (the delay before oxidation happens, as the LDL’s antioxidants become depleted), a 20% reduction in peak diene formation (a way to measure oxidation), and a 17% reduction in maximal rate of diene formation. All of that jargon basically means the LDL had become far more resistant to oxidation—at least based on this particular assay (there’s always some uncertainty about how well in vitro (outside the body) studies translate to in vivo (inside the body)).
From “Effects of diet and exercise on qualitative and quantitative measures of LDL and its susceptibility to oxidation.” Barnard, 1996.
- Similarly, a study in postmenopausal women found that the Pritikin Program led to more oxidation-resistant LDL particles.
- Even though the Pritikin Program often reduces HDL (the so-called “good cholesterol” lipoprotein), it makes the existing HDL that much awesomer. A study of obese men found that after three weeks in Pritikin Land, the HDL inflammatory index (AKA the ability of HDL to prevent LDL from oxidizing) changed from “pro-inflammatory” to “anti-inflammatory.” The activity of platelet activating factor acetylhydrolase also increased, LDL decreased by 26%, and triglycerides decreased by 29%. Basically, even though HDL was lower than at baseline, its function was mucho improved—”suggesting increased turnover of proinflammatory HDL,” according to the researchers.
From “Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors.” Barnard, et al., 2006.
Breast Cancer Protection
- In postmenopausal women, the Pritikin Program fantastically improved the major metabolic and hormonal risk factors for breast cancer: on average, insulin dropped 29%, insulin-like growth factor 1 (IGF-1) dropped 19%, insulin-like growth factor binding protein 1 (IGFBP-1) increased 32%, estradiol (among women who were on hormone therapy) dropped 34%, and estradiol (among women who weren’t on hormone therapy) dropped 37%. In vitro, serum from those Pritikinettes dramatically slowed the growth (and induced apoptosis, or programmed cell death) in three breast cancer cell lines (MCF-7, T-47D and ZR-75-1) compared to blood from the same ladies before they’d started the diet.
- In a study of pre-menopausal women, two months of the Pritikin diet led to some fun breast-cancer-protective hormonal changes: serum estrone and estradiol (types of estrogens) fell during the women’s early folicular and late luteal phases (with decreases ranging from 18% to 26%), with no negative impact on ovulation. (Exposure to ovarian hormones, especially estrogen, appears to increase breast cancer risk, so these changes could be expected to reduce it.)
From “Effects of a very low fat, high fiber diet on serum hormones and menstrual function. Implications for breast cancer prevention.” Barnard, et al., 1995.
Colon Cancer Protection
- In women, a 26-day Pritikin diet improved some risk factors of colon cancer by reducing fecal secondary bile acids (which are linked to the promotion of colon cancer).
Heart Disease, and Related Adventures
- Here’s a goodie called, “Effects of an intensive exercise and nutrition program on patients with coronary heart disease: Five-year follow-up.” (There’s no link because for some awfully frustrating reason, this paper is nonexistent online, and I was only able to track it down via the library. Email me if you want a PDF copy!) This study followed the progress of 64 Pritikin adherents with coronary heart disease, five years after they left the sheltered, intensive clutches of the residential program. Prior to entering the program, 59% of the patients had experienced a heart attack and 80% had angina (chest pain). During that five-year follow-up, four people died (one of cancer, two of a heart attack, and one of heart failure during a mitral valve replacement), and two additional folks had non-fatal heart attacks. Reports of angina dropped from the initial 80% to only 32%. Fascinatingly, despite the fact that this was a highly diseased group with the odds stacked against them in terms of morbidity and mortality, their annual death rates ended up being close to that of the “regular” population after they Pritikinized their lives! (At the time the paper was written, post-heart-attack mortality was around 10 to 15% for the first year following the event, and as high as 50% by the third year.)
From “Effects of an intensive exercise and nutrition program on patients with coronary heart disease: Five-year follow-up.” Barnard et al. J Cardiac Rehab 1983;3:183-190.
- In 31 obese men, the Pritikin Program brought awesome improvements in a huge range of risk factors for heart disease—including blood lipids, oxidative stress, inflammation, and cell adhesion. After just three weeks, there were significant drops in LDL (25% lower), triglycerides (28% lower), fasting glucose (12% lower), insulin (30% lower), HOMA IR (33% lower), C-reactive protein (39% lower), soluble cell adhesion molecules, inflammatory cytokines, and monocyte adhesion. And to sweeten the deal, nine out of the 15 men who entered the program with an official diagnosis of metabolic syndrome no longer met diagnostic criteria by the time their three weeks of low-fatting was up.
- In 15 hyperlipidemic men, two weeks of the Pritikin bootcamp improved a number of risk factors for heart disease: it lowered the men’s blood pressure, slashed triglycerides, reduced the aggregation velocity and maximum aggregation of platelets, and reduced the formation of thromboxane (which is made by platelets and promotes blood clotting and constriction of blood vessels).
- Combined with daily aerobic exercise, the Pritikin diet facilitated major improvements in myocardial blood flow. After six weeks, resting blood flow decreased by 12%, and hyperemic blood flow increased by 9%—leading to an improved myocardial flow. (It’s impossible to know how much diet versus exercise played a role in these results, though!)
- In postmenopausal women on hormone replacement therapy, the Pritikin Program heralded some promising changes on the heart-disease-protection front. After just two weeks, 20 women saw significant drops in their BMI, glucose levels, insulin levels, all serum lipids, and HOMA IR. The researchers conclude that these “rapid improvements may reduce the risk of acute myocardial infarction (MI), and if sustained, these changes may mitigate the risk for atherosclerosis progression and its clinical consequences.” Not too shabby.
- In a small study of 11 men, the Pritikin Program appeared to be uber protective against atherosclerosis progression. In the span of 21 days, the program dropped LDL by 23%, triglycerides by 41%, fasting insulin by 46%, and fasting blood sugar by 7%. Serum 8-iso-PGF 2 alpha (a product of lipid perodixation) also sank, whereas nitric oxide availability rose. In Barnard, et al.’s words: “The present study is the first to show that unrestricted consumption of a low-fat, high-fiber diet and daily exercise can mitigate oxidative stress, improve NO availability, and normalize BP in obese men within 3 weeks.”
From “Effect of diet and exercise intervention on blood pressure, insulin, oxidative stress, and nitric oxide availability.” Barnard, et al. 2002.
From “Effect of diet and exercise intervention on blood pressure, insulin, oxidative stress, and nitric oxide availability.” Barnard, et al. 2002.
Diabetes Damage Control!
- For 70 diabetics, a 26-day jaunt in the world of Pritikin led to all sorts of disease-blasting perks: fasting blood sugar fell by 24%, blood pressure dropped by 10%—and even better, 71% of the folks who’d been taking oral hypoglycemic drugs pre-Pritikin were able to ditch their prescription (ditto for 44% of the folks taking insulin and 61% of the folks who’d been taking blood pressure medication)! Also, VO2max (“functional maximum oxygen uptake) improved by 41%.
- In diabetic men, a three-week Pritikin Program reduced heart-disease risk factors associated with diabetes: the program whipped down fasting glucose by 20%, dropped fasting insulin by 30%, and totally clobbered markers of oxidative stress, inflammation, and monocyte-endothelial interaction (a major part of the heart disease process). Boom!
- Among 652 non-insulin-dependent diabetics, three weeks of the Pritikin Program significantly improved their condition: fasting glucose dropped by 16%, and 71% of folks taking oral hypoglycemics (and 39% of the folks taking insulin) were able to discontinue those medications. Triglycerides and blood pressure also fell to delightful new lows.
- In diabetics, the Pritikin Program reduced fasting insulin in diabetics by an average of 33% in just three weeks, and restored normal fasting insulin levels in 59% of insulin-resistant folks in the same time frame. (Triglycerides also dropped across the board!)
In the Elderly
- Among 70 folks aged 70 and older (average age of the group being 78.7), 26 days of the Pritikin Program totally spiffed up their health: they lost an average of five pounds, total cholesterol and triglycerides fell significantly, their treadmill performance increased by 49%, the type II diabetics of the group reduced their fasting blood sugar by 27%, and half of the patients taking blood pressure medication were able to discontinue it.
But What About the Children?!
- In overweight and normal-weight children, two weeks of the Pritikin Program yanked down multiple cardiometabolic risk factors: insulin levels fell (by 28.1% in overweight kiddos and 52.5% in normal-weight kiddos, respectively), HOMA-IR fell (28.4% and 53.1%, respectively), leptin levels fell (44.1% and 69.3%, respectively), and a variety of proinflammatory cytokines were reduced (molecules that increase inflammation in the body). LDL went down by 24.5% and 29.4%, while HDL hardly budged. Those changes didn’t correlate with weight loss, either!
Effect of Pritikin Program on inflammatory cytokines. From “Effects of an intensive short-term diet and exercise intervention: comparison between normal-weight and obese children.” Barnard, 2013.
- Also in children, two weeks on the Pritikin Program (for 19 overweight kiddos) massively improved factors associated with heart disease: the program tanked LDL by 25.3% and triglycerides by 39.5% (HDL didn’t significantly change); 8-isoprostaglandin F2 alpha (a marker of lipid peroxidation) fell by 81%, CRP fell by 41%, and MMP-9 (a measure of plaque stability and progression) fell by 49%. Markers of endothelial cell activation (ICAM-1 and sE-selectin) also went kerplunk! As the researchers summed it up:
“The primary findings of this study provide evidence that even a short-term lifestyle modification program may (1) improve the lipid profile; (2) decrease production of the reactive oxygen species superoxide and hydrogen peroxide and increase NO production; (3) decrease endothelial cell activation and adhesion; (4) decrease inflammation; (5) decrease monocyte chemoattraction; and (6) decrease MMP-9, a marker of plaque destabilization, all of which may contribute to a reduction in atherosclerosis progression.”
From “Effect of a short-term diet and exercise intervention in youth on atherosclerotic risk factors.” Barnard, et al., 2007.
- WE’RE NOT DONE WITH YOU YET CHILDRUNS. Yet another study on overweight youth found, again, a massive drop in insulin (33%), HOMA-IR (29%), triglycerides (40%), systolic blood pressure (10%), diastolic blood pressure (10%), and LDL (27%), with no change in HDL. All seven of the kiddos who were classified with metabolic syndrome at the start of the study had reversed their diagnosis by the end of it!
And that’s just a freakin’ handful of the research out there. Seriously. A handful. If you want to venture into the full-on Pritikin Research Safari, I recommend bringing snacks and water, ’cause you’ll be gone awhile!
Just to be clear, I’m not trying to say that the Pritikin Program is wildly successful for everyone who jumps aboard, or that it’s unequivocally the best treatment for the diseases it’s been used for. The point I want to make is more conceptual than anything. Contrary to the belief that low-fat, high-carb diets raise insulin levels, muck up glucose control, encourage obesity, and promote inflammation, the overwhelming majority of studies published on the Pritikin diet have shown the polar opposite. That doesn’t mean there isn’t a range of outcomes within each study; indeed, some participants do well, some do really well, and some don’t do well at all, even when the collective effect is positive. But seriously, the Pritikin Program yields impressive results, and it’d take a whole lotta’ somersaults of logic to conclude otherwise.
I know your brain is probably maxed out on scienceness now, so let’s resume our narrative of Mr. Pritikin’s life! First up, an interesting parallel between his way of thinking and that of the modern Paleo community.
In the early ’70s, Pritikin wrote a three-volume opus compiling his theories—dotted with hundreds of scientific references—about every major condition of the time: atherosclerosis, angina, high blood pressure, gout, arthritis, gallstones, kidney stones, diabetes, lung cancer, colon cancer, prostate cancer, breast cancer, as well as hearing and vision diseases. He was convinced they were all, essentially, manifestations of a huge mistake called “What Americans Typically Eat.” In fact, Pritikin had a fascinatingly ‘ancestral’ approach to nutrition (back at a time when linking diet to chronic disease period was considered cuckoo for Cocoa Puffs), which he discussed in the introduction to his three-volume work:
Such a postulation linking diet and the scourge of degenerative diseases may seem far-fetched, until one reflects upon some basic biological facts. All animals, man included, have a diet that emerged from the long-term experience of the species in nature over many thousands of years. Now, man no longer eats foods his body was designed to eat, but has created a synthetic diet—the penalty of which is to endure the adverse effects of short-term experience. The more man’s diet departs from foods to which he is biologically suited, the more the adverse effects.
Whereas the modern incarnation of Paleo has drawn heavily from higher-fat-eating societies (the Inuit and Masaai are particularly cherished), Pritikin found dietary consistency among the starch-based populations: the Tarahumara Indians, the Bantu, and the natives of New Guinea, whose traditional low fat intake and virtual freedom from heart disease fed into his overarching philosophy about food. Just keep that in mind if you find the idea of low-fat eating to be ancestrally preposterous!
For what it’s worth, Pritikin certainly walked his talk. Before his mortal departure, he’d requested an autopsy be performed so the world could have an honest look at his once-diseased heart. The results were published in a New England Journal of Medicine article called “Nathan Pritikin’s heart,” where the state of his ticker blew the pathologist away:
The epicardium was smooth, and no scars were visible. The endocardium and all valves were normal. … The coronary arteries were soft and pliable … there were no raised plaques and no compromise of the lumens. No clots were present. … No infarcts of any size, or other finding referable to vascular disease, were present in any organ.
The report concluded, “In a man 69 years old, the near absence of atherosclerosis and the complete absence of its effects are remarkable.”
Important note on Pritikin’s death: Critics of Pritikin (Priticritics?) often point to his departure from the world—death by suicide, amidst a painful battle with leukemia—as evidence that his low-fat diet either pulverized his mental health (suicide) or gave him cancer (leukemia). Those are both pretty bold claims, so let’s take a moment to assess them.
In the 1950s, Pritikin went through a series of high-dose radiation treatments for a skin condition, pruritus ani, that was stubbornly resisting all the pills and ointments he tried. Over the course of two months, he got blasted with a total of 220 rads (“radiation absorbed doses”) of unfiltered x-rays—the equivalent of getting 3700 chest x-rays or 22 million dental x-rays. Not surprisingly, it wreaked havoc: he soon ended up with a blood condition he’d battle for the rest of his life, later diagnosed as a rare form of leukemia. That all happened before he embarked on a low-fat diet.
Pritikin actually managed to keep his disease in remission for almost three decades, but in late 1984, saw an unfortunate resurgence of symptoms—including leg swelling so severe that he had to stop going on his beloved daily runs. His docs ushered him onto some experimental chemotherapy, telling him it was the only way he could ever resume jogging. Not only did the chemo not help, it also left Pritikin with crippling anemia, kidney failure, diabetes, all-consuming pain, and 30 pounds stripped off his already slender body. In February of 1985, he flew out to New York for a second opinion, was told his case was hopeless and he would certainly die within the next six months, and proceeded to take his own life in a hospital bed in Albany.
As George McGovern reflected, “He was always in charge of his life. It rather followed he’d want to be in charge of his death.”
With all that in mind, can we implicate Pritikin’s diet in his sad demise? With enough mental gymnastics and anti-low-fat bias, sure—but I don’t think it’s particularly logical or fair. Did his diet shorten his life, or lengthen what was originally a grim prognosis? And if we make an automatic diet-death jump, should we do the same for the recent passings we’ve seen in the high-fat community (low-carb guru Barry Groves, saturated-fat-redeemer Mary Enig, or “Carbohydrates Can Kill” author Robert Su)?
As drawn as our human brains are to stories and anecdotes, I think it’s wiser to look at bigger, statistically stable data instead of case studies. Everyone has to die of something, and food isn’t the only tool of the grim reaper.
Oh hey! Remember this guy?
The one who allegedly pulled the low-fat theory out of thin air, manipulated the American Heart Association into believing it, and took the world by storm with his Machiavellian wiles?
The one who cherry-picked his way into a groundless theory?
The one whose very countenance makes us tremble with rage, as we thrust our butter-encrusted fists in the air in defiance?
Yeah… him.
Let’s get real here for a minute. When it comes to evidence supporting low-fat recommendations, Keys was more like the ending caboose than the engineer driving the train. He was far from the first person to think that fat could play a role in chronic disease. We didn’t need his suspiciously curvilinear six-countries graph, we didn’t need his Seven Countries Study, and we didn’t need his can’t-prove-causation epidemiological utterings to form our “low fat movement.” Those things certainly played a role in pushing low-fat theory into the realm of public policy, but holy massive research pile Batman, there was plenty of evidence already there before he made his own contributions! Heck, Keys was clearly aware of his low-fat predecessors by the time he hit the scene: he even referenced the Rice Diet in his now-infamous 1953 paper “Atherosclerosis: A Problem in Newer Public Health” (PDF), where his six-country graph made its grand debut.
Even if you exit this blog post still believing “low fat” is an awful sham, we can’t keep spreading the myth that Keys was its originator. Every time we place the low-fat movement squarely on his shoulders, a kitten gets ejected from a machine gun and blasts a hole through the ozone. Do you really want to destroy the planet? Do you? I didn’t think so! Let’s just agree right now to put this whole myth to rest, and fill our alotted “hatin’ on Keys” time with more important matters, such as how to invent prosthetic goosebumps for people who cannot feel fear and/or coldness.
Modern Diet Doctor Squad: An update and apology for jumping the gun
Although this post isn’t diving into research by the modern “Plant-Based Diet Doctor Squad” (Caldwell Esselstyn, John McDougall, Dean Ornish, Neal Barnard, and by some definitions Joel Fuhrman), I do want to comment on the first gentleman in that lineup—the heart-disease-bustin’ Esselstyn of the renowned Cleveland Clinic.
If you aren’t already familiar with him, Esselstyn is a super cool cat who I want to adopt as my grandpa, and who’s been treating death-bed-borderline heart disease patients for decades. In my Forks Over Knives critique, I criticized his fat-shunning program on account of the high triglycerides and low HDL it produced in some of his patients, while also pointing out the inconclusiveness of his published work due to its tiny sample size. Allow me to awkwardly quote my self of four years ago:
Holy triglycerides, Batman! Although Esselstyn’s diet helped lower most of his patients’ triglycerides, a couple still have values in the major danger zone (362?). Some of those HDL numbers are looking pretty sorry as well.
All in all, Esselstyn’s study shows that a whole-foods, plant-based diet is probably infinitely better for cardiovascular health than the junky cuisine many folks eat. But it’s far from conclusive evidence that this diet is the best we can do for reversing heart disease, or that it would generally be effective in a population beyond his 11 self-selected subjects. A diet that reduces triglycerides and increases HDL more than his did, for instance, might have an even better outcome.
I’ve written a lot of things in my life. Some of those things have been wrong. This is one of them.
While I still suspect Esselstyn’s diet could be unveganized without harming its therapeutic effect (perhaps through the addition of gelatin, seafood, and whole-grain unicorn flour), I’m no longer convinced that low HDL and high(ish) triglycerides are bad in the context of unprocessed low-fat diets. I’ll explain why that’s the case in Part 2! But in a sneak-peek nutshell, it has to do with the improved quality of HDL (which we saw with one of the Pritikin Program papers) and the fact that higher trigs are typically a marker for insulin resistance, and when that’s absent, a heftier number probably isn’t pathological (which you can read more about in this paper yonder). We also have plenty examples of non-Western cultures that remain virtually free from heart disease, despite having triglycerides we’d consider too high and HDL we’d consider too low (hellooooo there Kitavans!)
As for the issue of Esselstyn’s statistically wobbly sample size (only 11 people who stuck with the diet through its 10-year follow-up): it was a fair criticism at the time, and one that’s been echoed by plenty of others. But it’s time to put that quibble to bed, preferably with enough sleeping pills so that it never again rouses. Why? It just so happens that in July of 2014, Esselstyn published a bigger, badder, bodacious-er study of 198 people instead of his original handful. The prescribed diet was the same oil-free, animal-food-free, whole foods regimen he’d been using for decades—with no confounding elements from exercise, meditation, psychosocial support, or yoga to be had. And the results were just as impressive—if not more so—than the ones he achieved in his earlier work:
- Among the 177 folks who stuck with the diet (for an average length of 3.7 years), there was only one cardiovascular event related to disease progression: a stroke. That’s a recurrent event rate of 0.6%.
- Among the 21 folks who strayed from the program, 13 had cardiac events. That’s a recurrent event rate of 62%.
- (The five other deaths in the adherent group included three cancers, one pulmonary embolus, and one case of pneumonia.)
Image from “A way to reverse CAD?” Esselstyn, 2014.
Image from “A way to reverse CAD?” Esselstyn, 2014.
For sure, there’s still plenty of stuff we could nitpick about this study (and his previous ones): there was no control group; the patients were abnormally motivated and self-selected (rather than reflective of the general heart-disease population, who might not be so inclined to give up steak forever); the study wasn’t randomized; and some level of self-fulfilling prophecy could’ve been at play, since the patients were told initially how awesome the diet was and how stupendously it was going to scrub out their arteries.
But even with those shortcomings, I’ll say it loud ‘n clear: I’m impressed. The study documents true heart disease arrest, and actual reversal for some. We don’t yet have any published studies of that sort on ketogenic, low-carb, or paleolithic diets (as far as I’ve seen!). And in my old age, I’ve come to appreciate the fact that real-world outcomes (i.e., whether or not someone keels over and dies) are more valuable than intermediate risk markers (like specific blood lipid ratios). It doesn’t matter that your health looked good on paper if you still end up in the ER!
And now, for an apology.
For the past few years (five? six? seven ate nine?), I’ve asserted that the success of plant-based diets is due to their whole-foodsness (eliminating processed junk, refined sugar, and refined flour), their low PUFA intake regardless of total fat (with the implication that higher non-PUFA fat consumption would be hunky dory), and the increase in other health-promoting behaviors that come with making a big change in the foods you eat (more exercise, less drinking and smoking, less couch-potatoism, etc.). I still think those things are relevant. But I now believe I dismissed the role of low total fat intake before I gave the data a fair and thorough analysis. This is a breach of the standards I hold myself to as a science blogger, which involve impartially examining all evidence before drawing conclusions.
So, I’d like to take this opportunity to say, HEY GUYS: I’m sorry.
To the aforementioned doctors: I’m sorry for jumping the gun with your research and being snarky when I reference you. I don’t always agree with the way you interpret your own work; I’m often unsettled by your debate tactics; I worry that the co-mingling of animal rights activism and nutritional research is toxic for remaining scientifically objective. But good heavens, I sure dismissed y’alls results before digging as deep as I should have—and in the process, missed out on some amazing opportunities to broaden my understanding of diet (and communicate those findings to my readers). Thanks for being on this planet and helping broken people heal.
To my readers: You guy are the best, seriously. Somehow you put up with these sporadic and unreasonably long blog posts and say nice things to me and wish me a happy birthday, sometimes with the inclusion of cat pictures, which is very wonderful. I don’t take your readership, your trust, or my quasi-position in the public eye lightly. And while I can’t guarantee that every word I write in this blog will be totally accurate, or that the ideas I present now and in the future will stand the test of time, I can promise that I strive to question my own biases just as rigorously as I question others’. That process of questioning will result in errors coming to light, which I see as a very good thing indeed: science (and its interpretation) should be self-correcting! Thanks for hanging in there with me. I’m honored for your readership.
Hopefully by now, some things have become clear:
- We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.
- We probably can’t even blame refined sugar for that stuff (at least not in isolation). Oh, the pain of shattering assumptions!
- We can’t ascribe the effects of low-fat, plant-based diets to their lack of animal products. Quite a few of the uber-low-fat studies here still allowed a fairly high animal protein intake, and still managed to whip people into diseaseless shape. Sorry, vegans!
- Ancel Keys did not invent low-fat.
- Ancel Keys did not invent low-fat.
- Once more, with feeling! Ancel Keys did not invent low-fat.
- I need to employ the “delete” button a little more rigorously. (Can you imagine how computer-crashy this blog post would be if I hadn’t split it into two parts?)
Admittedly, I’ve gone pretty easy on some studies in this post and—had I decided to devil’s-advocate from the other side—could’ve critiqued certain ones far more aggressively. But there’s a reason I didn’t go into BAD SCIENCE INCINERATOR MODE, and it’s not because I got bought off by the garbanzo bean industry (they’re gonna have to try a lot harder than 43 cents). For one, the sheer volume and consistency of the research here points to something very real, something totally non-under-the-rug-sweepable—and analyzing each individual study in search of holes and inadequacies wouldn’t change that fact. And secondly, there’s a whole universe of scientific mechanisms explaining why the diets discussed here work: the ability of dietary fat to reduce insulin sensitivity, the effect of different fats on tissue oxygenation and blood flow, the little-known ways that saturated fat can make LDL more likely to get incorporated into plaque, and all sorts of other fun stuff. That’s what the next post is about, so stay tuned!
In sum, there comes a point where it’s more of an intellectual stretch to rationalize something away than to accept that it may have merit. My friends, we’ve reached this point on the issue of low-fat diets. Let’s face it: they can actually do some good. And it’ll make a whole lot more sense why after you read Part 2!
Guess what? You made it to the end! Please remove of your pixel-dizzy eyes from the computer screen and get some fresh air. You freakin’ earned it!
ONE LAST THING. I want to give the stickiest, gooiest hug and eardrum-shattering shout-out to the amazing folks who donated to this blog over the course of the last year. You guys single-handedly made this post (and the one that’s coming next!) possible to finish, and your support allowed everything in here to reach a much wider audience than just the inanimate objects in my office-room. Thank you, thank you, thank you. If we meet in person, I’ve got a hug with your name on it; if we don’t, here’s a whole tray of Internet Bonus Biscuits! Mwah!
I fear that a picture of actual biscuits may be offensive to some readers, so I’ve chosen a picture of a cat “making biscuits,” which is the next best thing.
This is an excellent review of importance of fats, protein and carbohydrates on the prevention, treatment and reversal of major chronic diseases in the United States.
I highly recommend this post to traditional and integrative physicians, as well as their patients.
I just yesterday returned from a (Dr. John) “mcDougal 3-day weekend” that included Drs. Colin Campbell, Caldwell Esselstyn ( your grandpa wanna be, Denise), Michael Greger (author of How Not To Die), John McDougal, and several other like minded souls. Denise, these folks all follow a whole grain, plant based diet that you describe in your blog about Dr. Esselstyn and they are all strict vegans. Surely you know this so can you make the leap that yeah, there are more roads to Dublin, and a whole food plant based (WFPB) diet is one of them? Even if your analysis, for arguments sake, of The China Study is correct, Colin Campbell’s conclusion is to eat a WFPB diet, in his case a strict vegan diet. Can you declare that while his study had many faults yet his diet is in fact one road to Dublin?
Ps you should come to one of Dr. McDougals events, with a disguise, maybe, but an open mind, which your discussion in this blog in general, and about Dr. Esselstyn in particular, convince me you have in spades. I love to read your blog, even if I come from the dark side (vegan), because I want to read both sides of this issue, health.
Denise does not need a disguise as she has given her apology. She should come as she is. I applaud Denise for this superb article. There is a Turkish proverb that reads: “No matter how far you have gone on the wrong road, turn back.” Denise has done that and I give her kudos to admit some of the earlier faults and now become more of the writer she has become.
There is something in all of this. Of course not everyone does well on high fat, low carb, high carb or low fat. We are all unique individuals. For people with metabolic syndrome who fail to lose weight on any diet, the scientific evidence seems to report better results with low carb high fat. But I am sure there are exceptions to this. Only the individual person can decide what diet is best for them. I had metabolic syndrome and the very low carb high fat diet did wonders for me, I am now a normal sized person, my diabetes has improved immensely. But I cannot digest fat very well, no gallbladder. I have since moved to eating lots of fruit and very little animal products and am continuing to lose weight without any negative impact on my blood sugars. So there are two extremes and they both had a purpose for me, but at different times, and they both worked well. There is no reason to think that one philosophy of eating is the only way to eat forever. We change. I believe as long as your diet is not full of processed foods, the unhealthy fats, and sugars – either low fat or high fat could be appropriate.
OMG, I love that you wrote this post. I can’t wait to delve into this. But I first wanted to say how much I appreciate that you are on the scene. Finally, something that ties together the success of super low-fat plant-based diets and LCHF diets. Thank you Denise!!!!
You are missing one key point. Not all fats are bad. In fact, essential fats are essential for cell homeostasis and cannot be made by your body. They are called essential fatty acids. Your low fat diet will starve your body for these essential fats causing a host of symptoms and facilitate over 60 chronic diseases according to the National Academy of Science. Your program is sound for trans, saturated and monounsaturated fat. It is dangerous for ignoring the need for essential fat which can easily be verified.
And how much of these “essential fatty acids” does one need to get these alleged benefits? Nowhere have I seen it to be more than a couple of grams per day, which can covered by only a couple of eggs.
I wish the answer to your question was simple. But it isn’t because each person responds to nutritional inputs differently for a number of reasons. For example, genetics is a huge wild card in fatty acid metabolism. That is why the “one size fits all” numbers you quote are incorrect and dangerous for some people.
Thankfully there is a simple affordable pin prick serum mail-in test that will generate a comprehensive 3 page report of your complete fatty acid profile. Based on gas chromatography, it provides research-level accuracy that is certainly appropriate for consumer use. You can read about the technology here:
https://en.wikipedia.org/wiki/Gas_chromatography%E2%80%93mass_spectrometry
You obviously haven’t heard that there is no such thing as an essential fatty acid. Once again, scientific fact becomes scientific false. Maybe Denise will do a blog post on this.
I refer you to:
The National Academy of Sciences which links 60 chronic diseases to Omega 3 essential fatty acid deficiency.
The National Lipid Association that states the deficient Omega 3/6 ratio of the general public impacting all chronic diseases.
https://www.lipid.org/communications/reachmd/3942
The International Society for the Study of Fatty Acids and Lipids position papers
http://www.issfal.org/statements/pufa-recommendations
Behind each statement are hundreds of studies supporting essential fatty acids.
Please cites your studies that conclude “there is no such thing as essential fatty acids”.
https://pranarupa.wordpress.com/2012/12/25/pufa-because-this-wouldnt-be-a-ray-peat-themed-blog-without-at-least-one-post-on-pufa/
In 1938, a biochemist William Brown volunteered to go six months eating an extremely low-fat diet. He consumed a diet of defatted milk and cottage cheese, sucrose, potato starch, orange juice and some vitamin and mineral supplements. His blood lipids became more saturated and their concentrations of linoleic and arachidonic acids were cut in half. He experienced an absence of fatigue, his high blood pressure returned to normal, and migraines he had suffered from since childhood vanished, his metabolic rate increased and he lost weight, his respiratory quotient increased suggesting greater carbohydrate oxidation, lower respiratory quotients are associated with diabetes. The diet produced no deficiency, and likely corrected a PUFA excess. Six months on a specially prepared laboratory diet, no deficiency, if these fats are essential they’re essential in such tiny amounts that its almost meaningless to call them essential.
http://jn.nutrition.org/content/16/6/511.full.pdf
EFFECTS OF PROLONGED USE OF EXTREMELY LOW-FAT DIET ON AN ADULT HUMAN SUBJECT
Our bodies can store a full winter’s worth of vitamin D in fatty tissues. Storage of six months worth of essential fatty acids would not be surprising.
1 day’s supply of Vitamin D3 is ~125ug. ∴180 days’ supply of Vitamin D3 is ~22.5mg.
1 day’s supply of EFAs is ~2g. ∴180 days’ supply of EFAs is ~360g. That’s a lot to store!
Hi, Certain conditions, related to fat assimilation, prevent vitamin D storage, as Dr Trevor Marshall discusses in one or more videos on YouTube.
Your cited review references classic studies and is very interesting in that, even though it dates to 1938, nothing in it is directly contradicted by the voluminous contemporary science I’ve read to date. But the INTERPRETATION of study results has changed greatly from yours. And there are some curious anomalies.
For starters, the title includes the phrase “prolonged use” of the extremely low fat diet and yet the study is only over a few months and the conclusions specifically warn, “it cannot be assumed that the human subject could subsist indefinitely on a diet completely devoid of the unsaturated fatty acids”.
All the observed good results you cite are due to reducing saturated fat in the subject diet, which is a really good thing on which we can all agree. But your interpretation that, “The diet produced no deficiency, and likely corrected a PUFA excess.” is dead wrong in light of new findings.
Here is what is happening. Some of the stored fats in the human body are the essential ones which it draws on when the subject does not consume them. That is why immediate deficiency symptoms did not occur. Yet your study reports serum level of essential fats dropped by almost HALF. So the subject was in significant deficiency of essential fats and his body made up for it by drawing down on stores it had accumulated.
A further complication is that the stored essential fat is mostly omega 6 because there is a huge amount of it in the modern diet. But a quicker major deficiency of omega 3 fat is inevitable. Since both level and ratio of these fats are deemed to play a role, reducing the excess omega 6 in fat stores is probably good as you claim. But the major problem is a GROSS DEFICIENCY of omega 3s. This is why the ISSFAL recommendation I cite posts no safe limit on omega 3 fat intake but a likely limit to omega 6 fat.
The easy solution for consumers is to do the simple serum test which embraces contemporary science to determine their essential fatty acid status and then be guided by test results.
,
I’m not discounting the deficiency in EFAs, as I’ve read about a rare case of it, but I just wonder how one, living a modern lifestyle would be unfortunate enough to develop such a deficiency. EFAs in all their forms are either added to our foods or naturally occur in fish and some plants. Even on an intentionally low PUFA diet like Peat’s it’s nearly impossible to go under 4g without compromising calories and nutrient density.
And by the way, out of pure ignorance, what would constitute a deficiency? I’m not sure if the FDA/ AMA has made recommendations regarding the minimum daily value. Would such a deficiency stem from intentional avoidance or a genetic/ physiological malfunction?
I also think the term “essential” is loaded with meaning. The public would understand essential as “necessary (for health) when in the original scientific terminology essential described fatty acids that, unlike cholesterol, cannot be produced by the body.
I think Ray Peat’s argument (and his proponents) raise the question: If our body cannot produce them on its own, we must be able to survive without them? (The human body is often programmed to be able to sustain itself.) I’m not settled on this since I can’t see a logical reason to avoid fatty (and tasty) things like avocados, fish and olive oil. But I don’t know… I’m trying it out!
Forsythia, salbers12 is right, omegas 6 and 3 ARE essential. Check out Susan Allport’s book “The Queen of Fats” for a great case example of someone suffering from too little Omega-3
It is actually very difficult to avoid “essential fats”. You can go without nuts and seeds and olives and avocado, but all fruit and vegetables have some pufa!
Your ignorance is dangerous. All pufa are not essential. It’s almost impossible to avoid the w6 essential fatty acid, linoleic acid found in seed oils, but the w3 essential fatty acids – linolenic acid or the elongated versions EPA and DHA – are simply not found in the diets of 25% of Americans according to William Lands. Since the same enzymes process both families and the prostaglandin progeny of w6 fatty acids are overwhelmingly inflammatory, while the prostaglandins derived from w3 fatty acids are anti-inflammatory, we are more or less likely to suffer chronic inflammation according to the w6/w3 ratio of our diets. Japan wins, we lose. “The potential attributable burden of disease ranged from 20.8% (all-cause mortality in men) to 99.9% (bipolar disorder)” https://www.ncbi.nlm.nih.gov/pubmed/16841858. Read and salve your ignorance.
That paper assumes that differences in dietary percentages of “essential” fatty acids are responsible for mortality differences between Japan and the US!
It also assumes that the ratio of n6 to n3 should be at lower.
It then makes recommendations based on those assumptions.
The best advice from that paper is to consume fewer n6 fats.
http://www.bmj.com/content/346/bmj.e8707 is an RCT which found raising w6 increased both all cause mortality and heart death quite dramatically
https://circ.ahajournals.org/content/99/6/779.full.pdf is an RCT which showed that raising w3 halved heart deaths – I believe this is the most successful dietary intervention ever studied
An excellent citation that agrees with my extensive reading. I’m not entirely clear on several statements that may be worth exploring. The National Academy of Science now links over 60 chronic diseases to omega 3 deficiency. So it seems a pretty safe correlation whether it is justified by this paper or not. The the optimal cellular-level target appears to be equal amounts of LC omega 3 & 6 FA. How best to achieve this is the question? Two serum measurements that bear on this are the LEVEL of LC omega 3 and the RATIO of LC omega 3s to 6s. Both need to be addressed. For example, if the ideal ratio of 1 to 1 is achieved but the level of omega 3s is too low, there is not enough present for optimal cellular function. Additionally, if the optimum level of LC omega 3s is present but the ratio is too high the the omega 6s swamp cell receptors so that the 3s are not absorbed. The best plan is a personal blood test and be guided accordingly.
I think you’ve nailed it!
I have begun sprinkling flax seeds and chia seeds, both excellent sources of 3’s, on one or two of my meals each day. I’ve cut out all animal products so have reduced my 6’s. Wanna make sure you actually use the stuff and don’t leave it in a container in the fridge? Go to the store ( I found it at Bed Bath and Beyond) little containers that you put the seeds in and are really easy to access and pour. Makes a big difference in how readily you use the stuff. I do it every day without thinking now. Experiment with different containers until you find the easiest. I did.
The root source of DHA is algae: fish eat the algae and the DHA climbs up the food chain. The ALA that is in plants CAN be converted to DHA, but some people do it better than others. Seems to have to do with your genetics … people who lived inland have better ability to convert plant omega-3’s into the longer ones that people need. Anyway, if one does not want to eat fish for whatever reason, the next-best source is algae. supplements.
“By now, everyone has heard that omega 3s are good for your brain. However, omega 3 is a generic name for a family of fats. Docosahexaenoic acid (DHA), a specific type of omega 3 found in fish, krill and algae, is what your brain is made from. While humans have the ability to convert the type of omega 3 in walnuts and seeds into DHA, new research has shown that the degree to which these omega 3s are converted is dictated by your genes.”
http://thatnutritiongirl.com/tag/omega-3-2/
I think this is particularly important for vegan women that are planning to have children. The development of the brain is very much dependent on the amount of DHA in the mother … if the mother is not genetically able to convert flax seeds to DHA, the baby will suffer.
Um, Jonathan, YOU need to learn what you’re talking about before you start shooting off your arrogant piehole. First, learn what “essential” means in the context of nutrition. An essential nutrient is a nutrient required for normal human body function that the bod either can’t synthesize at all, or not enough for good health. The 18C omega fats linoleic acid and alpha-linolenic acid ARE indeed essential–we have to ingest them. As far as longer-chains, EPA and DHA, we can make them from ALA, but conversion rates are low enough (~8–21% to EPA, 0–9% to DHA) as to make them conditionally essential. You are correct that we can easily obtain w6 from our diet, but we don’t really know the minimum levels for w3. Nor the ideal 6:3 ratios: 2:1? 4:1? Read that “Queen of Fats” book and you’ll see a test case that went for years without any w3 before starting to suffer overt systems. Some people eating ancestral diets, e.g. the Pima Indians in Arizona and their Tarahumara cousins in Chihuahua State, were plenty healthy before Euro intervention even though these inland desert and arid land dwellers ate diets rich in beans and corn and got far less EPA and DHA than the Japanese, Inuit, and other peoples living near cold-water seas rich in high-w3 marine life. Leafy greens do include small levels of ALA because they need that w3 in the thylakoids for photosynthesis so Richiebogie is at least partially correct when he says “… vegetables have some pufa.” As far as that PubMed study you tout, that’s just one more of the zillions of meta-studies out there, completely correlative, nothing clinical about it, confirming nothing at all. The study leads even make that clear, putting “estimations” in the title. Correlation does not imply causation. Get off your high horse.
Umm, feelings run high! Every word you say is true. I chose Lands’s pdf because it was to hand and because it gives a good overview. However …
http://www.bmj.com/content/346/bmj.e8707 is an RCT which found raising w6 increased both all cause mortality and heart death quite dramatically
https://circ.ahajournals.org/content/99/6/779.full.pdf is an RCT which showed that raising w3 halved heart deaths – I believe this is the most successful dietary intervention ever studied
This one cut all-cause mortality too. So we have RCTs in which more w6 increased all-cause mortality, and more w3 reduced all-cause mortality. Yes, they’re secondary prevention trials, and, yes, Sydney probably ate more trans fats but this is the best data I can find to justify my dietary choices. My coronary artery calcium score is zero after 15 years of lowcarb (because I’m Type I, not because of dietary convictions), taking fish oil and avoiding seed oils.
Had I been lulled into complacency by advice like richiebogie’s “It is actually very difficult to avoid “essential fats””, I think it likely I’d now have rampant atherosclerosis. Which is why I say it’s dangerous bollocks.
Jonathon, is it this from richiebogie you reacted to?:
“It is actually very difficult to avoid “essential fats”. You can go without nuts and seeds and olives and avocado, but all fruit and vegetables have some pufa!”
If so, I think you may have read too much into his comments. I don’t see him advocating using seed oils or other w6 bombs.
btw, I interpret this as him saying you get pufa in a great many foods. Do you think he’s wrong?
In any event, you should have sought clarification from him before you adopted your high and arrogant tone. Just saying.
He said its very difficult to avoid “essential fats”, no explanation, no references – seemed pretty arrogant to me – perhaps he can clarify that?
All I know is that doctors have been selling me variations on the theme for 15 years and I’m hale and hearty while one of them retired prematurely with Parkinson’s, and a second died with dementia blind from ARMD, all conditions for which lchf has been found to help. Had I taken their advice, I’d probably be with them now.
When people come on cocksure with what I know to be untrue, then I feel I must oppose them since this may help people who find themselves in the position I found myself in 15 years ago, fighting the conventional medical wisdom – which is turning out to be more and more wrong.
If I come off as arrogant, then maybe it’s because I’ve got something to be arrogant about, like being alive
Jonathan, again, what *exactly* did Richiebogie you took such issue with? Please quote it, thanks.
He wrote: “It is actually very difficult to avoid ‘essential fats'”. It’s not true. Why do you ask?
Jonathan, I do mainly what you’re doing, only I don’t get pufa (or anything else) through supps, just through food (mainly canned salmon and sardines). I try to keep ALL pufas low because pufa is the most oxidizable of the fats, esp w3, I init did the spreadsheet work on those to make sure I was getting enough w3 (Mary Enig of “Know Your Fats” gives 3–4g/day), and obviously no seed/nut oils and limit fatty grain-fed meats.
About the RCTs. The first one you cite, the Sydney Diet Heart Study, doesn’t test w3 at all, merely subs w6 with SFA. The Lyon Diet Heart Study does look at w6/w3 balances, but where’s the sample rate? Can’t seem to find it, maybe just overlooking it.
Finally, your CA calcium score, Vit A/Vit D/Vit K balances can also greatly affect that. Those fat-solubles work together to transport serum ca to bone.
Yes! I think your strategy has the best chance of lengthening healthspan.
“Saturated fat protected the livers of rats given alcohol, but replacing the saturated fat with corn oil resulted in oxidative stress and severe liver damage (Ronis 2004). Moreover, there’s a robust inverse association between saturated fat intake and ischemic stroke in both American (Gillman 1997) and Japanese men (Yamagishi 2010) – the more saturated fat eaten, the less the likelihood of a stroke” from an essay I wrote.
Ramsden’s meta-analysis concludes “Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death” http://www.ncbi.nlm.nih.gov/pubmed/21118617
I take the fish oil because I tested low in cell-wall w3’s, thought to be a diabetic trait where w3’s are burned for energy preferentially over glucose when insulin is high, causing insulin resistance. I do take K2, but I started after I got the zero calcium score.
As you point out, the RCT evidence is woefully inadequate but what the hell we’ve got to eat something!
Therese Dolacek found among about 6,000 middle-aged men with lousy risk factors for heart disease in the MRFIT Usual Care group that 20% of them reported zero intake of conditionally-essential w3 fatty acids. She went on to say “Analysis of the combined fatty acids predominantly found in fish … demonstrated significant inverse associations with CHD, CVD, and all cause mortality groups but not for cancers … The benefit … [at] 664 mg/day … [was] … 40, 41, and 24% lower [incidence respectively when compared to zero intake]” http://tinyurl.com/p7jt9fh
So I’d amend your gnomic utterance to: “It’s actually very difficult to avoid eating the pattern of ‘essential fats’ associated with heart health and less death if you eat fish”
Pardon me for being a little insane on this topic, it’s the legacy of my 30-year fight against the conventional medical wisdom that diabetics should eat lfhc and avoid saturated fat. The way you put it implies you can’t help getting your “essential fats”, don’t worry about them – dangerously misguided advice IMO
This is the medical wisdom my conventional MD handed me in 2007 when I was diagnosed Type 2 diabetic. It is anything but “lfhc and avoid saturated fat”.
https://www.novomedlink.com/content/dam/novonordisk/novomedlink/resources/generaldocuments/CountingCarbandMeal_EG.pdf
After two weeks of following this protocol my fasting blood glucose dropped from 200 to 100 without any other medication.
Any doctor that would recommend lfhc to treat diabetes with lfhc is insane, certainly not conventional by 2007 Illinois standards.
Wow! They advocate more than 50% carb calories, what were you eating before?? Dr Richard Bernstein suggests 6% as an upper limit of carb calories. Allick 2004 points out that such a low carb intake depletes liver glycogen by about half which prevents the liver from raising the blood sugar via glycogenolysis, allowing the diabetic to have normal fasting blood sugar http://www.ncbi.nlm.nih.gov/pubmed/15579777. Being Type I, I have to keep to that level to prevent high fasting blood sugars – you must have beta cells producing enough insulin to get away with such a high carb intake
There’s no advocacy of carbs at any level (you don’t have to use the sample meals), and you could construct it VLC if you so desired. It’s biased against high glycemic carbs, and set up so typical SAD dieters will use it.
My problems were overeating high glycemic carbs and fats and being sedentary. Specifically I was eating huge amounts of frosted mini wheats and raisin bran. I suppose that my carbs were 70% of total calories diabetic at 2500 total calories per day and no exercise, dropped to 40% of total calories at 1500 total calories per day and 350 calories per day exercise with the carb exchange system. After I’d controlled blood sugar and lost 25 lbs, I increased the exercise to 700 calories per day, the food to 1800 calories per day and started putting the high glycemics back in. I was able to maintain a 2 lb/week weight loss rate for 6 months doing this, stopping it after 50 lbs lost. Since then I’ve continued to increase the exercise. I aim for Cordain’s 1000 calorie per day historic Paleo exercise by walking and biking. I eat to maintain weight, typically 2300-2500 calories per day, on ca 50% carb, 35% fat, 15% protein, and have stayed at target weight for 8 years.
VLC Paleos have called me asymptomatic in the past. However, I couldn’t eat this way without all the exercise or if I hadn’t lost the weight. I’m certain that I stopped what I was doing, my trigs would go from 35 back well above 100, my blood sugar would go from under 100 back to 200 fasting, my CRP from below 6 back to 8, and my HDL down from 70 to 30.
thhq, what is the “non-inflammatory” range for your CRP measure? 1–3?
My Dr. wanted it under 6.
Sent from my iPhone
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My Dr. recommended getting CRP below 6, and the test shows a healthy range 4.8%-5.6%, so I don’t think this is the high sensitivity test. I started at 8.2% in 2/07, and by 8/07 was below 6% (after 6 months of the carb counting and 50 lbs weight loss). I’ve been at that level until the last test in 2/14. I moved in 2014 and my current Dr. doesn’t run it.
Wow, that’s impressive! Congratulations!
Thhq, I agree with Jonathan here. If I stayed on this high-carb diet that Novo Nordisk proposes, I’d be injecting insulin by now. And I ask you the same question as Jonathan: What percent carb diet did you eat before?
Bear in mind your BG levels don’t tell the whole story. With such a diet, you may have near-normal BGs but chronically high serum insulin levels, esp if you have insulin resistance. Chronically high serum insulin may also harm you in various ways, e.g. promote growth of amyloid plaque in the brain that lays the groundwork for Alzheimer’s. E.g. the same enzyme that dismantles insulin also dismantles the amyloid plaque, but works on insulin first. So chronically high insulin may mean never enough enzyme left over to break down the plaque. You can get an inkling of your insulin levels with the C-peptide test, but to really put a fine point on it, you need the euglycemic clamp, and expensive and involved test not regularly done.
This proposes another mechanism for how chronically high insulin levels promotes brain plaque development:
http://www.medicaldaily.com/alzheimers-may-be-late-stage-type-2-diabetes-relationship-between-insulin-amyloid-plaques-and-enzyme
Wow, just WOW. Talk about cherry picking, dismissing anything that can, god forbid, brake the fabric of the little pattern we are trying to build, and leap frog from diet to MS with several other subjects in between to overcome reading sharpness with a totum revolutum devoid of unbiasedness.
The agglutination of causalities without a minimal effort to look beyond the obvious first impression is flabbergasting, The dismissal with the wave of a hand of historical data is insulting.
I will be honest, I did not read the very few last paragraph, cause though you write very well, your style is, simply put, chaotic, you are very capable of giving a headache to an aspirin.
But with that said, the article is pseudo science, yes it is. It’s obvious that you don’t have a scientific background, you don’t challenge the methodology, you don’t provide articles where the testing hypothesis has being duplicated following the same program, and I don’t mean 10 or 15, but hundredths, that is how peer review works. You do make a half hearted attempt to play Devil´s Advocate, but excuse me if I am not overly convinced or satisfied by it.
But let me address the first shortcoming. The P. diet, is a diet which is first and foremost high in fiber, then high in carbo and almost lacking fat and animal protein. It requires strict adherence to it for life, AND relies heavily on exercise. Of course you gonna get the improved body, of course you gonna get rid of type 2 diabetes, you are exercising. You just barely brushed aside the whole core of the diet like if it were an innocent passer jaywalking onto your fine article. Then you don’t address the number of maladies caused by a diet deprived of fat or with very low fat intakes, liver cancer, brain malfunction, cell membrane integrity, hormonal imbalance, etc. All of that without going into the trivial detail that not all fats are created equal, and the same goes for carbohydrates.
You also take as example people from indigenous tribes, as role models for the diet benefits, since they don’t have heart disease, well yeah, but they suffered from severe malnutrition, anemia, are susceptible to viral infection and have a high incidence of certain types of tumors associated with low fat and animal protein intakes. The bantus don’t have that diet by choice, they have it by geography, and by the way, their infant mortality is enormous, cuz somewhat carbos are not sufficient to provide synthesis of mother’s milk.
So stop pandering your neo sophism, reading nutrition books and science papers is not a magic wand to turn you into a scientist, or an expert on the matter. I read many books in quantum physics and relativistic theory, it does make me a physics expert either, because although I have the math background to understand the theory, I don’t have enough of it to propose hypothesis using a few cherry picked articles.
Regards
Hilarious. The high carb cheerleaders sounded exactly like you when the China Study article was released here!
3 paragraphs on how she’s not a “scientist” (even though she never claims to be one) and then more condescending babble about nothing.
Get a life, dude.
Please do more research into efa’s. Especially R. Peat’s. They are NOT essential. I feel making a statement like that without really researching will harm and may kill a lot of people.
At last- -!! But I’m not going to read this tonight- – I shall waken in the morning but stay in bed and read and digest until I’ve ‘got it’. I’ve been wondering when it was going to appear, ever since you prematurely hit the ‘Publish’ button some months ago. Good night, from the South of Africa
1. Thank you / this is great / you’re awesome.
2. I have absolutely no idea what to ever eat anymore…..like, ever.
3. Do you happen to have some sort of magical machine that gives you more time in the day than the rest of us?!?!?!?
4. Thank you!
Eric
Eric, my reaction exactly (and I’ve written a diet book!). Thanks, Denise!
Brian
P.S. I would add a 3b: I wish I also had a time machine to do a few N=1 trials, repeated with washout periods, of high-fat, low-fat (really low-fat), and a couple variants of in-the-middle-fat diets.
I was a Registered Dietitian working in Marin County, California, at a very large cardiology group when low fat diets were popular. I am still an advocate of low fat eating and controlled, careful fat eating–I have not fallen for the “high fat, high protein” way of eating. (I see too many impaired renal function patients and colon/breast/prostate cancer patients to feel excess protein and fat are good for people.)
What I find “hilarious” about the movement to blame “carbs for the obesity epidemic and the explosion of Type 2 diabetes” is that for that statement to be true, EVERYONE in the population would have needed to be eating a very low fat, very high carbohydrate diet–all the time for that to happen (if it was even true.) The truth was (and is) that it was very difficult for people to eat a very low fat diet–AND VERY FEW PEOPLE ACTUALLY DID IT–even those who were cardiac patients. It has always struck me as ironic that no one ever really checked to see if people were really eating low fat and high carbohydrate diets before they were blamed for the health disasters. The association was too “theoretical” without sufficient data to back it up. People self-identified with a low fat diet and would say they ate that way–but that did not mean they ate that way all the time.
Keep up the good work–you are a brave soul. I envy your dedication.
One of the good responses. Thanks for your story.
Like Denise was saying, the still are whole populations who eat very high fat and have very little cardiovascular disease – the Maasai, the Eskimo, some populations in China, etc. An idea is that it probably has to do with other factors, too – like level of physical activity and place of living (the Eskimo live in very cold weather most of the time, so fat is probably necessary for them anyways). The thing is, nobody even thinks of the fact that air is a nutrient too – so maybe, if you breath clean air, you can eat more fat and still not get sick – or something of the sort. Since most of the diseases are plurifactorial, fat cannot be the only one causing – or curing – heart disease…
Not only that, but there is still no proof that dietary fat even causes heart disease in the first place- (or the corollary, that low fat “cures” heart disease). If any of these diets DO cure heart disease, then it could likely be due to any number of factors, not the low fat element. Based on all I’ve read, it still seems a bit unclear exactly what causes heart problems. There are a lot of theories out there, but nothing has been scientifically proven. And there are so many “paradoxes” as well……
Ditto.
Denise, YOU ARE MY HERO!!! #thatisall
Chapeau!
Very detailed post, must have been a lot of work! I know it might seem mysterious or surprising to some why low fat vegan works so well. Our bodies are natural starchivores (low fat plant based), just Google ‘omnivore vs frugivore’ and look at the chart – from teeth, to stomach, intestines, etc. Even Denise does a low fat diet. So it makes perfect sense when we eat our natural human diet why our bodies would perform so well, reverse heart disease, etc. But humans are uniquely able to adapt to lack of carbs by going into ketosis – an emergency state during starvation or illness. When no glucose is available (emergency state) our body switches to using fat to survive. Not something we want to do on a regular basis in a healthy state. We avoid all the nutrients, fiber and phytochemicals that plants have to offer. It’s fairly simple to understand.
I know people here probably don’t accept the china study links between protein and cancer, so here are 5 other ways meat causes cancer that you may not have heard about https://www.youtube.com/watch?v=PlhJU57KUd for example estrogen, IGF-1, hydrogen sulfide, Neu5Gc. Sure we can scavenge some meat for calories and survival but it’s not going to help us thrive and live to 100+. People jumped all over your china study critique because they like to hear good things about their bad habits.
The success of LCHF is usually based on short term weight loss (assuming caloric deficit and includes loss from glycogen stores and associated water depletion) which creates associated reductions in say blood pressure, but it’s not able to reverse heart disease such as with Dr. Esselstyn’s studies. They have bad breath, constipation and revert to caffeine or laxatives to stimulate the bowels. Check out the longest living populations in Okinawa and 7th day adventists they blow away the masai and eskimos (why we use small isolated tribal populations who didn’t live as long and were shown to have atherosclerosis is a question for another day). 🙂
Keep up the great work!
That’s peculiar since my bowel works much better when I stop eating fiber and eat only meat.
My system also runs much more smoothly when I reduce my fiber intake. In fact, I can’t do a high carb diet anymore, since I am intolerant to so many of the foods; there would be nothing left for me to eat.
And- in response to Will- I eat LCHF, but I am underweight, and therefore am not even trying to lose weight. But I’ve seen massive improvements in my health since I started eating this way about 4 years ago. I had pretty massive health issues when I ate a plant based, low fat diet; (I also went through a phase of eating a very low fat diet, of exactly the kind that Denise describes). So my first point is that the benefits of LCHF- for many of us, anyway- are NOT solely due to “temporary weight loss”. My second point is that no one particular diet is the “absolute correct one” for all people.
I lost 150+ pounds on LCHF, so I’ll assure it was not water weight alone. I have excellent bowel function. I think you miss her point, BOTH diets seem to work. Some people do well on one or the other, if vegan suits you great, go for it, but stop spreading the lie that LCHF doesn’t work for people like me, it’s simply not true.
Exactly. I’m pretty sure Denise is not on a diet with less than 10% of calories from fat, either.
Exactly
Vegan nonsense at its finest. Posting that in the comment section of a blog that clearly states how BOTH diets are perfectly fine show how narrow-minded you guys are. Shaking head really
Then there is the notion that neither diet is ideal. And that swampland is only swampland when carbs and fats are combined in the one meal.
My bet is Denise will have something to say in terms of following both diets, but not a mix of the two.
We will see…
If you cannot have roast potatoes with your roast then please kill me now!
“They have bad breath, constipation and revert to caffeine or laxatives to stimulate the bowels.”
Is that so? I don’t know any LCHF eaters who have had bowel problems. I assume you must have access to a large database to make this assertion with such confidence.
Many low-carbers who convert from the SAD find they actually consume more vegetables than before. Often their fiber intake increases substantially.
I’m unaware of studies showing that LCHF is incapable of reversing heart disease. There are certainly studies that shows it reverses metabolic markers “associated” with heart disease, but these are questionable indicators. LCHF hasn’t been studied in depth, and in most cases the LCHF diets that have been trialed are in the “swampland” Denise has described.
I think Denise is presenting objective analysis. And she didn’t prove anything regarding the superiority of low-fat diets (or try to), She is pointing out there is “magic” at both ends of the spectrum.
And I might add that the “magic zone” at the LCHF end is far, far larger.
I disagree. I run a Facebook group with LCHFers and that is a huge complaint, either they have very loose stools, or constipation. Either way, it is a common complaint. I have myself had extremely loose and often stools on LCHF. I eat higher carb, and the problem instantly disappears. In both diets, I am eating a lot of veggies/starches. The only difference is the amount of sugar and fat.
Will . whey you aré in Ketosis you do not avoid all the nutrients because you can still eat as much as vegetables you want with all the micronutrients and phitochemicals
Will, you simply fail to offer rigorous evidence for the claims you make. Nor can you. And your vid link is broken.
What do you consider “short term”? I’ve lost 65 pounds in the last six months (30 pounds disappeared in the first 30 days) eating LCHF. I am no longer pre-diabetic, my LDL is down, my VLDL is way down, my HDL is up, etc, etc…. Oh, and I’m not friggen hungry all the time, which for a weight loss diet is VERY important to insure compliance. To drive that last point home, I even fast two days a week. That’s how “not hungry” this diet makes me feel. BTW, I had never been on a diet before more than two or three days in my entire life, and I had put off doing this diet on my doctors advice, as I didn’t want to have the severe hunger pains I had on my three day diet stint in high school 33 years ago.
If your doing LCHF and have constipation, then your not doing the diet correctly (hint, your eating too much protein, and not enough low starch vegetables & fiber). The most common mistake people make on this diet is thinking that it is high fat AND high protein diet (it’s not). It is a high fat, very low carbohydrate, & MODERATE protein diet. Too much protein and two things happen. First you stop loosing weight, because your body tries to turn the excess protein into sugar. The other thing that happens, and yet another reason you stop losing weight, is that ya can’t poop anymore 8^].
I DO think that the author may be onto something though, when speaking about the “magic” that happens on the extremes of fat & carbohydrate dietary intake levels, and the macro-nutrient swamp that is the Standard American Diet.
I watched a Horizon (BBC’s version of NOVA) episode on weight loss and diets a few months ago, where they had taken two identical twins who were about the same weight, and fed them different diets. One was high fat & protein, almost no carbs. While the other was almost all Carbs, lowerish fat, minimum protein. What was interesting were the results. Both gained a little bit of weight, because neither was following a truly LCHF or VLF diet (too much processed foods, etc). Here’s the interesting part… Although allowed to eat as much as they wanted, both tended to eat about the same amount of calories. Hmmmm…..
Near the end of the program, another scientist shared the results of a feeding study he did on 3 sets of rats. The 1st set of rats he fed a high carb very low fat diet. The 2nd set he fed a high fat very low carb diet. Neither of those two sets of rats gained any significant amount of weight, or had any significant disease problems. The 3rd set of rats gained weight like crazy, and were having various health problems, and way higher mortality rates… He fed the 3rd set of rats “cheesecake” exclusively. The cheesecake would be akin to a Standard American Diet (SAD). The scientist’s theory of why this was, is because the 3rd set of rats ate WAY more calories than the other two sets of rats.
His example of why goes like this: Take a bowl of heavy cream, a spoon, and start eating. You’ll soon quit, as it won’t take much to have your fill. Now (sometime later), do the same thing, but this time with a bowl of sugar. Again, it won’t take long for you to stop eating spoonfuls of sugar. NOW (again, sometime later), pour the bowl of sugar into the bowl of heavy cream, mix them, and get out your spoon again. This time you’ll most likely consume the entire bowl… Why? Because when you add sugar and fat together at a certain ratio (something not found often in nature), it kind of turns off your brain’s satiety switch, and hence causes you to over eat. BTW, sugar+cream+cold=ice cream…. At a certain ratio of sweetness to fat, we can’t help but want to have more.
They tested this hypothesis by giving out free donuts to random strangers. Of the 3 types of donuts they gave out (glazed, chocolate frosting, & powdered sugar), one type was consistently chosen the most. It was the glazed doughnut, as it has the same sugar to fat ratio as ice cream does.
Now that’s food for thought ;-).
The thing that’s missing in this whole discussion is protein. Of the ways we get calories, there’s pretty good evidence that protein is a better plan than either fat or carbohydrates. Indeed, one could argue that the success of low-carb diets is largely due to the fact that they are high-protein diets: Atkins’s own argument was that the fat was in the diet to make you less hungry, not because it was inherently good for you. Weightlifters and other health types have been advocating high-protein diets for years, and having generally good health with them.
I think you are doing a disservice to your readers if you paint the diet question as “high fat vs. high carbs.” The most credible evidence I’ve seen favors diets featuring lots of protein, plenty of fruits and vegetables, enough fat to reduce food cravings, small amounts of sugar and simple carbohydrates, and less total food intake. I’m guessing you wouldn’t find any of that controversial?
PO8:
Sorry but a high (animal) protein diet is a disaster for someone like me who has high uric acid levels. I eat way less meat than most people and I can bring on a gout attack at will simply by upping my protein intake from fish, beef, poultry and pork. Through trial and error I do best on low fat. Vegetable protein doesn’t seem to have any effect on my uric acid/gout nor does dairy and eggs (as demonstrated in studies).
The human liver simply cannot process enough protein to meet our energy needs. For that reason, we need to get more than half of our calories from some combination of carbohydrate and fat. This article suggests it should be one or the other, but not both.
People keep saying the low carbohydrate diet is high protein. A properly formulated low carbohydrate diet supposed to be moderate protein, high fat and very low carb. This is like Atkins and what the other low carb gurus out there say it should be moderate protein.
So basically if you had listened to me you’d have been right all along.
lol
Fascinating! Excellent work. I’ve been checking your website for months looking for updates. I can only imagine the amount of research and work that went into writing this. Can’t wait for part 2 and wondering if genetics will help make sense of it all.
I will be at the Anaheim conference in November. Looking forward to meeting you there.
Am I really the first commenter or has it been so long in reading that a page refresh would show a different truth?
Anyway, it’s post like this that show why I read your work and trust you. I don’t have a lot of time left over in life to read about nutrition science. Thank goodness for you thorough review and overall entertaining presentation. Can’t wait until part 2!
Wonderful and amazing article. What I wonder is what you ate yesterday.
“… we could nitpick about [Esselstyn’s studies]: … the patients were abnormally motivated and self-selected (rather than reflective of the general heart-disease population, who might not be so inclined to give up steak forever)”
These issues may be relevant to the prospects for widespread adoption of the dietary regimen, but they do not confound the results of the studies.
One of the largest impediments to widespread adoption is the conviction of medical professionals that it’s impossible for almost all patients to change the way they eat.
Michael Greger (nutritionfacts.org) analogizes thus, mimicking a hypothetical M.D. saying, several decades ago something like, “I’d try harder to get my patients to quit smoking, but I know how they love it so!”
but it is so much fun running with scissors while chewing arsenic candy!
Wow! It is an incredibly good read, so far only read until the end of the Walter Kempner – Rice diet part, its great results was definitely what made me question the low carb ideologies. Now I think its effectiveness is due to its ability to increase the metabolic rate, by completely eliminating PUFA and fats, along with amino acids like tryptophan which supports Ray Peat’s work as you mentioned aswell.
Have to go to bed to get some sleep gains, (living in EU) but can’t wait to wake up tomorrow and finish the rest of it, thank you so much for this Denise!
Tremendous! Thank you! I have not read part two yet so am at this point a confused but open-minded paleo adherent. Always looking to optimize the program based on new information.
You are awesome.
“We can’t ignore evidence in order to preserve an ideology.”
So fucking awesome to read this. Thank you.
Brilliant!
Harold Himsworth never used a word where a paragraph would do, you fall asleep reading him – but he noticed in 1935 that giving carbohydrates increased insulin sensitivity in rabbits, which is to say that more carbohydrates can be tolerated on a high-carbohydrate diet, and confirmed the effect in humans http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1394223/pdf/jphysiol01610-0047.pdf
Perhaps the first low-fatter?
I LOVEEE how you put science behind everything you say!!
Excellent post: shows once again one size does not fit all. Hard to understand how Pritikin had some heart issue, yet clean coronary arteries. And yes, genetics do count. Many tout Jack LaLanne, and yet I believe he had a brother who was not health oriented who lived in to his 90’s.
Many on a very low fat diet will have their LDL size shrink and an increase in Ldl_P and yet not be insulin resistent ( much to the chagrin of the paleo crowd) which appears to be contrary to the data you cite in your piece. Krauss and others say that 1/2 the population will experience it and perhaps those on the very low fat diet who did not have a positive outcome might fit in to this profile.
Hi Steve,
Thanks for your comments! As for your point here —
“Many on a very low fat diet will have their LDL size shrink and an increase in Ldl_P and yet not be insulin resistent ( much to the chagrin of the paleo crowd) which appears to be contrary to the data you cite in your piece. Krauss and others say that 1/2 the population will experience it and perhaps those on the very low fat diet who did not have a positive outcome might fit in to this profile.”
Indeed, there’s generally (but not always, as we saw in this post) a decrease in LDL size on very high-carb diets. I’m no longer convinced LDL particle size is as significant as some health figures are claiming. Large, fluffy, supposedly ‘protective’ LDL predominates in people with familial hypercholesterolemia, who develop atherosclerosis as early as their 20s and 30s (or even earlier for homozygotes!); likewise, low-fat doctors like Ornish have reversed heart disease in patients even when their LDL particles are small. I suspect in Western populations, LDL particle size is part of a cluster of hallmark elements for metabolic syndrome rather something inherently harmful, and that its association with heart disease diminishes in the context of non-SAD diets. I’ll be going into more detail about that in either the next blog post or the one after it!
Denise, looking forward to your LDL post and how it relates to the consumption of saturated fats and dairy.
thanks.
Tim Steele’s “Potato Diet” is what shifted my belief in the powers of a near-zero fat diet! If anyone who is having a hard time losing weight on low carb wants to see dramatic results, just eat nothing but potatoes for a week! You’ll see. Read about it here:
http://www.vegetablepharm.blogspot.com/p/the-potato-diet_14.html
This post made me think of Tim’s potato diet too! I’m glad Denise mentioned the RS content of the rice diet, because I was curious about that.
Denise, this was such an awesome read! Reading things you write is always an enjoyable experience, and makes me feel like I’m getting a brain massage. I’m also a sucker for myth-busting and paradigm-destruction, so that made it even more fun to read. I can’t even imagine how long this must’ve taken you to research and write.
Now that you point it out, it is funny how so little attention is paid to some of the extremely high-carb/low-fat ancestral diets. And when attention is paid, it’s to defend “safe starch,” with little discussion of the accompanying low fat intake.
I’m also glad you mentioned Ray Peat, because the rice/sugar diet made me think of him. I’ve been meaning to make myself understand his dietary recommendations for ages, and just haven’t gotten around to it. I’m super excited to read part 2!
Revisiting cherished theories? Admitting that you were wrong? What a rare thing to find in the diet world. My hat goes off to you. Keep up the good work.
You are brave, girl! It took guts and grace to do this piece–somewhere between a call-out to Thomas Kuhn and a confession to Pope Francis – :).
I’ve followed your writings from the China Study on, agreeing and disagreeing here and there, but admiring your stamina, civility, smarts, good humor, inventiveness, insight and analytical prowess.
I’ve followed even longer Pritikin (since his first book); Ornish (since before his publication of his study showing that a low-fat/et al ‘program’ can reverse heart disease); McDougall (since his first book) and Roy Swank via my first exposure to McDougall. Both McDougall and Pritikin have written about Kempner’s work & I read numerous of his earliest research studies on the Rice Diet website (not sure they’re still available at this site.)
McDougall was/is one of Swank’s biggest fans and was instrumental in funding and designing a Swank-ish MS study in collaboration with OSHU about which one can read here: https://www.drmcdougall.com/2014/07/31/results-of-the-diet-multiple-sclerosis-study/
One has to wonder if the patients in the McDougall ‘arm’ might have done a bit better with a bit more PUFA, as per Swank…but that arm did get randomly assigned the sickest patients in the study. Love McDougall for his helping SO MANY PEOPLE but he’s not the first person I recommend to someone suffering from heart disease (or any of the other diseases that appear to improve, as you so ably demonstrate in your review of the low-fat research, in a significant majority of folks who stick to these low-fat diets). He’s dogmatic to a fault…and his recent coloring book for children borders on the offensive in so many ways (and I am a semi-vegan–for health and environmental reasons) that it makes it really difficult for me to send those in need to his website.
Love Esselstyn too despite the similarities he shares with McDougall. He’s a kinder, gentler, more avuncular McDougall–and his latest study keeps adding to his cred.
But my biggest thanks are for the intro to Lester Morrison! Must have read about him in one of Pritikin’s books but it’s been at least thirty years and it was really fun and educational to be re-informed and enlightened if in fact I had already been exposed to his work and then forgotten about it.
I’m looking forward to part 2. And to the good news on HFLC diets.
I’m sure you’ve seen the recent study by Kevin Hall et al purporting (by others…and Hall) to disprove the carbohydrate-insulin hypothesis in a head to head study of a low carb vs a very low fat diet- http://www.cell.com/cell-metabolism/abstract/S1550-4131(15)00350-2
“Highlights
•19 adults with obesity were confined to a metabolic ward for two 2-week periods
•Cutting carbohydrates increased net fat oxidation, but cutting fat by equal calories had no effect
•Cutting fat resulted in more body fat loss as measured by metabolic balance
•Mathematical model simulations predicted small long-term differences in body fat”
Stephen Guyenet has two nice takes on this study: http://wholehealthsource.blogspot.com/2015/08/a-new-human-trial-seriously-undermines.html
http://wholehealthsource.blogspot.com/2015/08/more-thoughts-on-recent-low-fat-vs-low.html
Both Hall and Guyenet ‘guess’ that an even lower carb diet might show more positive results.
Here’s Hall’s response to the Taubes and Teicholz-like critics: http://www.weightymatters.ca/2015/08/guest-post-dr-kevin-hall-asks-is.html
Hall notes that he’s already finished a study that responds to the many complaints his team has received from the low-carb groups re the first study: https://clinicaltrials.gov/ct2/show/NCT01967563
He’s hinting…but the results haven’t been published yet. Love the suspense!
I am sure I am one of many who truly appreciate the enormous amount of time you have spent on your newest endeavor….and I am really looking forward to whatever comes next: paradox, spoiler, or whatever! Sock it to us! 🙂
Just for people who look at the magic of the rice diet, this extreme part of the program was not long term – just like atkins 20g/day thing was not long term. The rice diet contained extremely low levels of protein, and largely rice protein. Rice protein is great and all, but low in many amino acids, especially lysine, and even more so once you adjust for actual available lysine rather than just total. This is not a diet that is to be consumed for a long time.
The diet was followed for as long as the patient needed to follow it. That might be 6 months in certain cases!
Accomodation is not your friend.
Well, haven’t read all 1.2 million words of Part ! yet…, but I did catch a great mixed metaphor possibility:
BACON-SCENTED rainbow farts from flying, floating, or even incorporeal unicorns, as catechism may demand.
Interesting read. But is there any practical application? Who is going to eat less than 10% fat as a lifestyle? Would be more useful to see an analysis of food combinations for realistic living. If you have a meal high in carbs, that is ok, just ensure its low in fat, etc. These are entertaining post and kudos on your dope writing style… but clinicians are left with the job of actually guiding patients to make realistic changes, which 65% fat or 10% fat are neither for most people.
There are a ton of people already eating this way. Anyone following McDougall, Pritikin, Ornish, Barnard (forgetting any), and possibly Fuhrman are all eating a whole foods plant-based (i.e. vegan) diet. They also feed it at True North Health, the fasting center in northern CA, but it is inspired largely by McDougall as well.
The ATOZ study showed that while Ornish says to eat less than 10% of calories from fat, people who follow (or think they are following) Ornish actually eat about 20-30% of calories from fat – too much for the benefits cited in this article.
There’s also a ton of people eating at the other extreme: moderate animal source foods, low carb, high fat, who are doing very well indeed. Check out Mark’s Daily Apple, for multiple examples. Some people do well as vegans, others – with different biochemistries – don’t. Success on any diet depends far more on factors like the enzymes that our bodies are able to produce than adherence to ideology, at any position on the continuum. For every triumphant vegan story, there’s an equally triumphant ex-vegan story, just as there are people who trumpet their success on their paleo diet and others, once staunch disciples, who now call it the fail-eo diet.
There never was any single ancestral diet, and humans don’t even have a clear ancestral line! More and more DNA work shows that early Homo sapiens interbred (in different times and in different places) with Neanderthals, Denisovans, and a species so far called Species X that some researchers think may prove to Homo erectus. Adding to the excitement, Neanderthals and Denisovans may have interbred. I look forward to the day when babies are food-typed at the same time and as routinely as they’re blood-typed.
…unless also Esselstyn and Campbell, et al
Thanks for your comments! My hope is that by understanding the mechanisms behind macronutrient interaction, we’ll be able to apply the relevant concepts to less rigid diets and create something sustainable. That said, there really are plenty of people out there eating less than 10% fat — folks following the McDougall program, etc. — so it’s not impossible. My own diet falls around 15% fat on many days, and I find it both easy and enjoyable.
“My hope is that by understanding the mechanisms behind macronutrient interaction, we’ll be able to apply the relevant concepts to less rigid diets and create something sustainable.”
+1, though I’m totally down with obtaining 90% calories from maple syrup.
I’m very curious to hear what your research suggests on the topic of potential mechanisms. Your post above seems to foreshadow greater attention paid to the cellular environment, e.g. in your references to quality of blood flow and the levels of O/CO2 available to individual cells. A related theme concerns how the very low fat diets (VLFDs) above may affect electrolyte balance. Do you have any pet theories about the role that cellular metabolism plays in human health? Or whether or not VLFDs provide an “optimal” environment for cellular metabolism?
Yours is my favorite nutrition blog. I’m staying tuned.
Denise
Have you seen these studies that use low fat high carbohydrate macrobiotic diets to reverse diabetes?
http://www.medscape.com/viewarticle/832732
The Effect of the Macrobiotic Ma-Pi 2 Diet vs. the Recommended Diet in the Management of Type 2 Diabetes
The Randomized Controlled MADIAB Trial
http://www.hoajonline.com/internalmedicine/2052-6954/2/3
Ma-Pi 2 macrobiotic diet intervention during 21 days in adults with type 2 diabetes mellitus, Ghana 2011
http://onlinelibrary.wiley.com/doi/10.1002/dmrr.2519/pdf
Ma-Pi 2 macrobiotic diet and type 2 diabetes mellitus: pooled analysis of short-term intervention studies
http://medrewes.eu/wp-content/uploads/2014/08/Hindawi_MaPi2_2012.pdf
Medium- and Short-Term Interventions with Ma-Pi 2 Macrobiotic Diet in Type 2 Diabetic Adults of Bauta, Havana
http://www.wjgnet.com/1948-9358/full/v6/i3/403.htm
Gut microbiota and Ma-Pi 2 macrobiotic diet in the treatment of type 2 diabetes
http://medicc.org/mediccreview/articles/mr_119.pdf
Ma-Pi 2 Macrobiotic Diet Intervention in Adults with Type 2 Diabetes Mellitus
With regard to Dr Morrison
http://circres.ahajournals.org/content/19/2/358.full.pdf
Prevention of Atherosclerosis in Sub-Human Primates by Chondroitin Sulfate A
By Lester M. Morrison, M.D., Katsumi Murata, M.D., Ph.D., J. Joseph Quilligan, Jr., M.D., O. Arne Schjeide, Ph.D., and Leon Freeman, Ph.D.
https://www.dropbox.com/s/17vsix1d1qbctft/morrison1973.pdf?dl=0
CORONARY HEART DISEASE: REDUCTION OF DEATHRATE BY CHONDROITIN SULFATE ALESTER M. MORRISON, M.D., F.A.C.A., AND NORBERT L. ENRICK, PH.D
AMAZING. Please post part II soon!!!
Fascinating! Those of us who’ve been around quite a spell (I’m 66) already know that reality is far more complex than our dearly-held beliefs would have it, but we so effortlessly forget that, as we slip into dietary dogma (and political dogma, etc., ad infinitum). I’ve just been thinking deeply about just this issue in regard to feeding the cats. Of all the dozen or two cats, and seven or eight dogs, I’ve had in my time, Tibey is the first one I had to take to the vet (UTI). Brought him home today, $6,000 in the hole. We have a first-rate vet who gave excellent medical care, but she gave a bag of kibble labeled Urinary Health. Ingredients? Chicken, corn, corn gluten, soybean oil, and on and on to pukedom. I’ve fed him and his brother a species-appropriate diet, based upon Kymythy Schultze’s recommendations, for about six years, since weaning. I also have Dr. Becker’s book, and, in rereading it I noticed that she says the diet of wild felines includes only 7% fat! So I’ve been giving them too much (they are lean, sleek, incredibly athletic, and, of course, lovable) I assumed that the negative effects of excess dietary fat would result partly from the displacement of other essential nutrients, but the studies you’ve discussed sound largely like starvation, junk food diets, so what gives? Food for a great deal more thought, a great deal. Thank you so much for this fine piece of work. It is good for us to shatter our myths from time to time-keeps us properly humble.
my husband lived in taiwan from ’63 to ’97. yes, he was very thin on a traditional, low-fat, mostly rice diet in taiwan before the economic boom hit in his middle school years. he was thin because he was poor and went to bed hungry every night. he does have beautiful teeth, though. when i lived in taiwan off and on for 7 years i got a lot thinner, but my body i believe canabalized my muscle. i had been very athletic before the move to taiwan. living in taiwan i only walked a lot of exercise. when i got home and took a hike in the woods with a friend, my fingers swelled up i believe because my heart wasn’t pumping the way it should have been. i was only 24 at the time.
So “eat anything in moderation” is out then!
Well, technically, ‘paleo’ can encompass high carb diets as well as low carb ones while still maintaining its’ core tenants. I wonder if I should try a high carb diet? It sounds pretty insufferable though…
Dear Denise:
Thank you very much for writing this. I really appreciate that you are willing to publicly change your mind and admit you were wrong about something. I really appreciate how you mostly refrained in this article for advocating for a new replacement theory to explain everything and allowed yourself instead to dwell on evidence against a current theory. And I really appreciate that you forced your attention onto uncomfortable evidence, and that in doing so you forced me to do likewise. I do indeed find these results surprising and discomforting, and I’m glad to be forced to think about them.
I do have two objections, but before I launch into them I want to emphasize that these objections do not give my weary brain an “out” and let me shove this uncomfortable evidence out of sight and forget about it.
The first objection is that these results are all from an earlier era, not randomized, and so it’s hard for me to know how this kind of treatment would compare to alternative treatments tested under better-controlled, randomized conditions. I did a quick bit of googling and hit upon this updated, randomized trial from McDougall:
https://www.drmcdougall.com/2014/07/31/results-of-the-diet-multiple-sclerosis-study/
Apparently the results were so disappointing that it didn’t get written up into a paper but was instead merely a poster: http://www.neurology.org/content/82/10_Supplement/P6.152 . The actual results aren’t all there (it says “Click to enlarge” but it doesn’t enlarge for me). The excuse from McDougall at the end of that web page about randomization resulting in too many more-sick patients going into the test group doesn’t make any sense. They could still have reported improvement in those patients, if they had improved, or if their rate of decline had been lower than expected.
So my first objection is that as far as I know (which isn’t far), these phenomenal results have failed to replicate when attempted under better-controlled conditions.
My second objection is this: “We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.”
No, that’s wrong. Earlier in your post you argued that reducing fat from 34% to 30%, and finding no improvement, shouldn’t be used as an argument that reducing fat to 10% wouldn’t be beneficial. That’s a good argument! And for the exact same reason, the fact that increasing carbohydrate to 90% was beneficial (in these non-randomized experiments) should not be used as an argument that increasing carb from 48% to 54% is not a chief cause of our current health crises.
Sincerely,
Zooko
i think the takeaway lesson from this is that this writer is not, and should not be regarded as, a health authority. you’re doing the right thing in doing your own research; she has no credentials, she simply reads a lot about nutrition. as do i, and as you do as well, i take it.
Dear Denise: if you could delete this comment, which is a slightly earlier version of my comment below, that would be cool. I don’t see a way to delete it myself.
Hey Zooko,
Thanks for the great comments! Those are some excellent points. In response —
1) The lack of robust study design is definitely the biggest problem with studies from that era. Ideally, I would LOVE to see a “true” low fat diet and a “true” low carb or keto diet go head-to-head with a great study design, relatively large sample size, and sufficient follow-up period. Maybe one day the Funding Gods will descend and grant such a thing. Until then, I appreciate the older studies because, despite weaker designs, they’re free from other notorious forms of confounding plaguing research today (especially healthy user’s bias).
That said, I’m very familiar with that McDougall study and will talk about it a bit in the next post. What I find fascinating is that the biggest difference between the two men’s studies is that McDougall used a strict vegan diet for his, and Swank allowed a wide variety of animal products (and considerably higher protein intake), so long as they were lean (trimmed meats, skim milk, egg whites, plenty of seafood). That raises the possibility that the vegan component was actually harmful (or less beneficial), that something in the lean animal products in the absence of saturated fat was also helpful, or any other of a variety of options; the mens’ diet were similar in fat intake but not identical elsewise. Relapse rates had already dramatically improved for the Swankers by one year, so I’m hesitant to suggest McDougall’s study just wasn’t long enough for the results to start manifesting, but I suppose that’s a possibility as well (seeing as Swank’s 50-year monitoring of some patients allowed a much fuller view of their disease progression than one year for the McDougall study).
It also raises the intriguing possibilities about MS symptoms improving independently of improvements in brain lesions/MRI scans. Swank didn’t use MRIs in his study or measure brain lesions; he only went by objective changes in the patients’ physical capabilities and their number of relapses over the years. So we can’t even say for sure that his study improved MS on the basis of lesions. McDougall’s study does show a trend of improvement in FSS score and MFIS score between 0 and 12 months, especially a pretty dramatic jump when they first started the diet from baseline — so the patients WERE improving in some measure. Why did they improve without concurrent improvements in MRI scans? Could it be possible that the diet alleviates MS symptoms in a different way and sheds light on a different element of MS etiology? I find it fascinating as a possibility, though certainly inconclusive, and I’m not as well versed in MS as I’d need to be to know if that theory could even hold water.
Anyway, Swank’s results (and rationale) will make a lot more sense after Part 2. He conducted (and drew from) a lot of additional research on both animal models and humans, showing some very specific changes in blood and tissue oxygenation from dairy fat (meals of nothing but pure cream — and in the 1940s, before dairy was largely crap). Anyway, stay tuned for that, as it does add more credence to Swank’s findings.
2) “”“We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.”
No, that’s wrong. Earlier in your post you argued that reducing fat from 34% to 30%, and finding no improvement, shouldn’t be used as an argument that reducing fat to 10% wouldn’t be beneficial. That’s a good argument! And for the exact same reason, the fact that increasing carbohydrate to 90% was beneficial (in these non-randomized experiments) should not be used as an argument that increasing carb from 48% to 54% is not a chief cause of our current health crises.”
Ah, I disagree. We can’t blame low-fat, high-carb diets for heart disease and diabetes and obesity because the nations (America, etc.) suffering from these conditions have NEVER eaten low-fat, high carb diets. We’ve eaten moderate-fat, moderate-carb diets, which may be the worst of the worst. 🙂
It would make sense that the well balanced proteins from lean meat, which tend not to be allergenic, would be much better with respect to an autoimmune disease like MS than plant proteins, which tend to induce immune system reactions.
I think it’s ridiculous to assert that a 15% fat 80% carb diet isn’t “low fat, high carb”. 20% carb, 60% fat diets – typical strict paleo – are always referred to as low carb, high fat, after all. People who go below 10% carbs are usually referred to as being on “very low carb”, “ketogenic”, or in some cases, for those on 0% carbs, “zero carb”. Similar wording should be used for the other end of the spectrum.
Heart disease has been with us for a while, but we can absolutely blame low fat, high carb for the obesity epidemic. What we can’t blame is VLF (very low fat) or no-fat diets.
”We’ve eaten moderate-fat, moderate-carb diets, which may be the worst of the worst.”
Even worse yet, Denise.
We have eaten mostly a moderate (SFAs, refined PUFAs, and trans-fat) fat, and moderate (sugar and refined carb) diets. That’s the SAD. Lots of meat, refined carbs, and junk. No wonder we’re in the state we’re in. Anyone blaming the low-fat diet for our current health state is not being honest. As you have shown, lots of population ate successfully a truly low-fat, high unrefined carbs diet with excellent health.
Thanks for your article.
” We’ve eaten moderate-fat, moderate-carb diets, which may be the worst of the worst. :)”
What about Ancel Keys Med Diet? It lies in the middle of Swampland, yet it allows the eating of all foods…in moderation. As a result it is the best of the worst, at a minimum.
Pushing macronutrient extremes in search of a perfect health diet is an interesting game to play. But it takes extreme motivation, a flexible schedule and an open wallet. Most people can’t sustain these diets for more than a few months, so their usefulness is confined to emergencies like weight loss, celiac, and IBS.
Dear Denise:
Thank you very much for writing this. I really appreciate that you are willing to publicly change your mind and admit you were wrong about something. I really appreciate how you mostly refrained in this article for advocating for a new replacement theory to explain everything and allowed yourself instead to dwell on evidence against a current theory. And I really appreciate that you forced your attention onto uncomfortable evidence, and that in doing so you forced me to do likewise. I do indeed find these results surprising and discomforting, and I’m glad to be forced to think about them.
I do have two objections, but before I launch into them I want to emphasize that these objections do not give my weary brain an “out” and let me shove this uncomfortable evidence out of sight and forget about it.
The first objection is that these results are all from an earlier era, when randomization was not practiced, and so it’s hard for me to know how this kind of treatment would compare to alternative treatments under better-controlled, randomized conditions. I did a quick bit of googling and hit upon this updated, randomized trial from McDougall:
https://www.drmcdougall.com/2014/07/31/results-of-the-diet-multiple-sclerosis-study/
Apparently the results were disappointing — no improvement in brain imaging or in disease burden for the low-fat diet arm. So disappointing, apparently, that they didn’t get written up into a paper but instead merely a poster: http://www.neurology.org/content/82/10_Supplement/P6.152 . The actual results aren’t all there (it says “Click to enlarge” but it doesn’t enlarge for me). The excuse from McDougall at the end of that web page about randomization resulting in too many more-sick patients going into the test group doesn’t make any sense. They could still have reported improvement in those patients, if they had improved, or if their rate of decline had been lower than expected.
So my first objection is that as far as I know (which isn’t far), these phenomenal results have failed to replicate when attempted under better-controlled conditions.
My second objection is this: “We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.”
No, that’s wrong. Earlier in your post you argued that reducing fat from 34% to 30%, and finding no improvement, shouldn’t be used as an argument that reducing fat to 10% wouldn’t be beneficial. That’s a good argument! And for the same reason, the fact that increasing carbohydrate to 90% was beneficial (in these non-randomized experiments) should not be used as an argument that increasing carb from 48% to 54% is not a chief cause of our current health crises.
Sincerely,
Zooko
Two follow-ups to my own comment:
1. I realized that I didn’t find that McDougall trial through Google — I found it by reading admgm’s comment. Sorry to have forgotten that, admgm.
2. There’s another way that trials from this era are unreliable, and that’s selection effects by the experimenter after the beginning of the experiment. For each subject who did well under their care, the experimenter would take credit for it, and for each subject who did badly, the experimenter would investigate and find some way that the subject was not following the protocol and blame the subject for it. Then they would write up a report showing that their treatment had a nearly perfect track record. To prevent such shenanigans is why nowadays we require Intention To Treat analysis.
Some of the parts of your post about just counting the results in adherers reminded me of this, and so did the part about whipping the patients, because those experimenters who blamed patients for their failure would also tend to be the ones who bullied patients.
(As an aside, I think that *both* Intention To Treat *and* adherer analysis should be standard instead of just ITT, but that’s a topic for another day.)
Denise – beyond this post being, honestly, the most interesting thing I’ve read in the health-o-sphere this year, it’s inspiring.
It takes big stones to backtrack on your beliefs and admit they were short/wrong/misguided/whatever – something that so few in this biz are willing to do (or are even capable of doing).
Well done. Way to set the bar high. Looking forward to part 2.
My thoughts exactly!
I respect how Denise is slowly and politely Denise is removing herself from the wacko paleo community she found herself involved with. Just have a look at the first few AHS talks she did. They must be pretty embarrassing to watch, especially considering the type of people she found her associated with. Leaving the Raw food wacko’s and jumping into the wacko paleo camp was probably a pretty big move for her.
Finding out that the paleo sect that she jumped into is just as wacko or even worse than the raw food cult she left was involved in must of been pretty brutal.
Actually what the article is saying is that it’s the wackos at both ends that have it right, and the people who preach moderation that are wrong.
Courageous angel!
Personally I’ve tried both ends of the dietary spectrum. Both require an adjustment period. And while both may be magical in their own way, intuitively I’ve leaned toward the high carb pole.
This diet war has raged for a good while now, but a clear and rational evaluation such as this represents a major push forward for the high carb camp.
Essential fats and carbs don’t mix well. One option is to cut the fat, the other to cut the carbs. Cutting fat is evidently a health inducing option, whereas high fat has its issues longer term.
Essential fats and carbs mix very well indeed, and have for millenia. The problem for millenia has been finding enough fat, at a price that the average person can afford. It’s only recently that people have had a problem with being in the middle of the swamp. That’s where I live, and eat my daily 1000 calories carb, 1000 calories high fat, 400 calories protein, and maintain healthy weight. You cannot overeat for what you do, and I get the 1000 calories a day Cordain recommends for a minimal level of Paleo exercise. Ditch the car/subway/bus, ditch the chair, and walk bike or run to the nearest bakery for the donut you need to get your needed calories for the day. They’re not empty calories if you metabolize them.
Believe me the middle of the swamp is the sweet spot. Not an Atkins/Taubes/Eades/Jimmy Moore CVD risk-land, nor a Jobs/Pritikin wrecked liver-land. Every food every day, within reason.
Wow, this was an amazing read, thank you for pulling this all together. It’s left me confused not really knowing if there is a way forward. I do wonder at the effect of all these extremes on the gut biome, and wonder that the restricted nature of some of these diets actually promote healing and remission by improving the gut health. I got diagnosed with Hashimotos this February, prior to the blood tests (out of desperation with ballooning weight), I went on the HCG diet which is virtually no fat. My symptoms improved amazingly (mainly the pain and fatigue), even though I didn’t loose as much weight as I hoped. It wasn’t until I started taking thyroid medication that the weight slipped away. I follow a restricted paleo diet. I look forward to reading part 2, is there going to be any help with a way forward?
I appreciate your hard work in pursuing the truth, I lost 50Kgs and got rid of diabetes through low fat diet only to afterwards change my mind and admit publicly that a high fat diet is superior so I can definitely appreciate your humility and your science based rather than ego based approach. But I do have five comments/questions here –
1) To get below the magic number of 10% fat – one has to reduce consumption of animal products and with that to reduce the consumption of DHA, EPA, B12, Iron, Zinc, Iodine, Glycine, etc, etc. What is the impact of such a diet on the *brain’s health*? What is the impact on our hormones? On our sex drive? On Homocysteine levels? On the activation of so many genes in our body. I am aware that you said that many of these low fat diets do allow some consumption of animal products – but the question is how much and whether that is enough. Health is not only about cardio vascular health and cancer prevention. I would love it if your part 2 (or part 3) will take that into consideration. Let’s see the whole picture.
2) I wasn’t aware that we humans can’t synthesize Neu5GC and that actually we have antibodies against this thing. I was under the ancestral approach impression that whatever we were evolutionary accustomed to eat – was good for us – this is why we survived so far and so based on this understanding if really there was a problem with the Neu5GC then we would all become vegans by natural selection process. We know that this is not true because never ever has there been a vegan society lasting more than several generations.
3) How easy it is to live one’s life on the low fat diet? I think you have to be quite the masochist to adhere to such a regime. So yea, suppose that after you answer points (1) and (2) above and indeed low fat diet is even a bit better than high fat diet – which diet should one pursue? How much can a person sustain such a harsh low fat diet and convince himself that he feels great? I would choose the easier diet, the one that I can pursue for the rest of my life.
4) Why is it that you are focusing only on the extreme diets? Either very low fat or very high fat? Doesn’t it make sense that humans, throughout the last 2.5 million years ate a diet that is somewhere in the middle?
5) Does this blog post mean that you now moved from advocating high fat to low fat? Or is it that you merely indicate that there’s a viable low fat diet option?
Hi Aviel,
Thanks for the great questions! I’ll address them as best I can, in order:
“1) To get below the magic number of 10% fat – one has to reduce consumption of animal products and with that to reduce the consumption of DHA, EPA, B12, Iron, Zinc, Iodine, Glycine, etc, etc. What is the impact of such a diet on the *brain’s health*? What is the impact on our hormones? On our sex drive? On Homocysteine levels? On the activation of so many genes in our body.”
— I’d say, first of all, that 10% of calories as fat is an average and not necessarily the goal of every single meal of every single day. I’ll be covering this in Part 2, but for folks who aren’t trying to reverse their diabetes or advanced heart disease, occasional (2 – 3 times per week) higher fat meals with nutrient-dense animal foods is unlikely to ruin the carbosis benefits and will make for a more nutritionally complete diet.
That said, a low-fat diet doesn’t necessarily reduce intake of those micronutrients, apart from DHA and EPA. Liver (rich in vitamins A, D, E, K, B12, iron, copper, etc.) is only 25% fat, and can easily be integrated into a low-fat diet without pushing the macro averages above 10%. Clams are only 9% fat and also very high in B12; other shellfish like oysters supply a lot of animal-based nutrients as well and are relatively low in fat. Bone broth is low fat and rich in glycine. Insects are mostly protein, for those daring to go there! 😉
As for DHA and EPA, the need isn’t particularly high if omega-6 intake is low, so small amounts of seafood will probably be sufficient here. Interestingly, it seems fat restriction actually increases omega-3 status — see http://jn.nutrition.org/content/131/2/231.full: “Consumption of a low fat diet alters fatty acid patterns in a manner similar to that observed with feeding of (n-3) long-chain fatty acids. This change is likely related to decreased competition for the enzymes of elongation and desaturation, with reduced total intake of 18:2(n-6) favoring elongation and desaturation of available (n-3) fatty acids.”
As for the impact of very low-fat on brain health, sex hormones, etc., I’d love to see more research delving into that using non-vegan diets. Considering that many populations have successfully subsisted and reproduced on diets in the 10 – 15% fat range, I doubt it harms reproductive functions as long as energy intake and micronutrient content is sufficient. Neurological health deserves more attention, and my guess is that there will be a range of response due to individual variation and ApoE status. Homocysteine is unlikely to be a problem as long as folate and B12 status are good.
“2) I wasn’t aware that we humans can’t synthesize Neu5GC and that actually we have antibodies against this thing. I was under the ancestral approach impression that whatever we were evolutionary accustomed to eat – was good for us – this is why we survived so far and so based on this understanding if really there was a problem with the Neu5GC then we would all become vegans by natural selection process. We know that this is not true because never ever has there been a vegan society lasting more than several generations.”
— Per evolutionary theory, we only need to survive until reproductive years in order to keep our DNA in the gene pool. The problems associated with Neu5GC (in theory, anyway) wouldn’t show up until later in life, after reproduction; and historically, the biggest killers were immediate things like acute infections, traumatic injury, etc. before chronic disease had a chance to take hold. Also, if Neu5GC really is an issue (still highly speculative!), it involves interaction with bacteria that may be a more neolithic phenomenon.
“3) How easy it is to live one’s life on the low fat diet? I think you have to be quite the masochist to adhere to such a regime. So yea, suppose that after you answer points (1) and (2) above and indeed low fat diet is even a bit better than high fat diet – which diet should one pursue? How much can a person sustain such a harsh low fat diet and convince himself that he feels great? I would choose the easier diet, the one that I can pursue for the rest of my life.”
— I disagree here! I actually very much prefer a low-fat diet to a high-fat one (although my only experience with low carb, high-fat on a personal level was only a 6-week experiment a few years ago — I experienced no detectable advantages and had a few problems worsen). There are thousands (? I’m guessing) of followers of the McDougall program, Ornish, Pritikin, etc. who appear very content with their diet. Apart from my six-week experiment, my diet has been pretty low fat for the past 10 years and I actually prefer it taste-wise and texture-wise to higher-fat eating plans. If you’re interested, Angelo Coppola has a “Plant Paleo” diet plan that fits into the low-fat bracket but is very nutritionally replete and looks delicious: http://www.humansarenotbroken.com/about/plant-paleo/
“4) Why is it that you are focusing only on the extreme diets? Either very low fat or very high fat? Doesn’t it make sense that humans, throughout the last 2.5 million years ate a diet that is somewhere in the middle?”
— I’m focusing on the extreme diets as a way to explore macronutrient interaction and its impact on human health. I’ll explain more in Part 2 why I think we can isolate some of the effects from these extreme diets and apply them to more flexible eating plans. To get there though, we have to study what exactly is happening on a biological level — which is why these studies (and the more mechanistic research I’ll go through in Part 2) are valuable!
I’d say it’s historically much more likely that we swung between macronutrient extremes than ate a diet in the middle: warmer seasons would feature abundant fruit and plant foods (high carb), winter would have lower high-energy plant food ability but perhaps more large game; and even in the shorter term, times of gathering (plant foods, small lower-fat/higher-protein mammals and insects and reptiles) would be punctuated by sporadic successful kills, in which case gorging on meat was likely. Even geographically, tropical areas tend to produce more sugary and starchy foods (fruits, tubers/roots) and polar regions are lower carb with more animal-derived nutrition.
“5) Does this blog post mean that you now moved from advocating high fat to low fat? Or is it that you merely indicate that there’s a viable low fat diet option?”
I’ve never advocated high fat (or any specific diet, for that matter), so I guess the technical answer is no. I’ve defended high fat when the science used to discredit it is bad, and I’ll continue to do so when the occasions arise — as well as recommend it when it seems the best choice for someone’s specific situation. But I’d be quite a hypocrite to advocate a high-fat diet when my own experience with it was unimpressive and I’ve been eating a low-fat diet for the last decade! 🙂
We need to keep in mind that the body fat composition of the wild game, even the hooved mammals, that our Paleo ancestors ate was a far cry from that of today’s typical feedlot-fattened, selectively bred cattle and grain-fed poultry. Outdoor Life lists the fat content for various types of wild game commonly hunted today, and many of these animals have less than 10% fat in their meat. These include mule deer, elk, antelope and several others. So even during seasons when our ancestors consumed a fair quantity of red meat, it probably wasn’t hard for them to keep their intake in the 10-15% fat range. History buffs have probably encountered the term “rabbit starvation” in the diaries of early explorers, a situation where a person’s body fared poorly because the meat he was consuming was so lean.
Wild game is about 10% fat by weight. That comes to about 50% fat by calories – more after accounting for bones and such. Our livers cannot handle more than about 40% of calories from protein – thus rabbit starvation – so at those times we ate meat, we were getting most of our calories from fat.
I don’t think it’s a coincidence that the whole body body fat percentage of wild game is very similar to the fat percentage to which steaks are typically trimmed. Most of the extra fat on feedlot animals is trimmed and discarded.
No. As a scientist, organic foodie, and math nerd, I DO know the pitfall of comparing calories on a weight vs. calorie basis. The Outdoor Life analysis was based on calorie percentages, NOT on weight. For example, 3.5 oz. of elk meat at 0.9 g fat, total 137 calories. See http://www.outdoorlife.com/photos/gallery/hunting/2013/02/wild-game-nutrition-guide-organic-meat/?image=3
Wild game is very different from “trimmed steaks” from grain-fed beef, and one reason people complain of elk as being too “dry”. Most of the fat on beef cuts in grocery stores is NOT trimmed. Even when I buy grass-fed beef, I end up trimming a huge amount of fat from it. At certain seasons, yes, the fat in wild game is higher. The protein handling problem is likely just what was causing a problem for the folks suffering from rabbit starvation. And please remember that fat and protein are only two of the macronutrients — our Paleo ancestors ate a lot of carbs — root veggies and tubers and fruit and such. Despite what some bacon-addicted “modern Paleos” will tell you.
That Outdoor Life analysis does not reflect the whole animal. It reflects a trimmed 3.5 oz serving. And most of the fat absolutely is trimmed off of beef cuts in grocery stores. To see what a steak from a feedlot animal looks like if it really isn’t trimmed, have a gander at the picture here:
http://cavemanforum.com/diet-and-nutrition/how-to-get-more-healthy-tasty-affordable-animal-fat-in-my-diet/msg67510/#msg67510
Yes, that’s more than half an inch of fat most of the way around the steak.
Now, wild animals do not have that much fat, which in domestic cattle can be up to 40% of total carcass weight. However, even wild ungulates do have substantial amounts of fat in deposits in the belly and in the rump at the base of the tail, amounting typically to around 10% of the total carcass weight. That’s more than half of the total carcass caloric value. Paleolithic humans would have had no problem getting fat to eat.
Yes….and I was under the impression also that early humans, and many modern hunter-gatherers, ate plenty of fat. Animals with fat were sought after; and though some wild animals are lower in fat, there are plenty that have fat on them. Early humans used to eat brain marrow, also high in fat, and Inuit and other native people ate fatty fish and sea mammals. Many hunter-gatherers processed the fat of certain animals, to be used later- (ever heard of oolichan grease? Not sure if I spelled it right….And then of course there’s pemmican….) So, yes; I agree with Psychohist.
yes. Plus Paleolithic and Paleolithic-style cultures also selectively hunted the older animals late in the season who had really good stores of fat on them. Modern day “theorists” don’t ever consider these sorts of details.
The idea that they selectively hunted old fat animals is also a theory and quite the generalization.
No it has been observed in Paleolithic style cultures.
There is no such thing as a paleolithic style culture. There are hunter gatherer style cultures but even then, little to none that do not also utilize some sort of agriculture or animal husbandry. Gathering data from these cultures no not in any way validate any theory of our paleolithic ancestors. And please don’t mention Inuit cultures, they are a very young culture and are about as far removed from any ancestors that have any influence on 99.99% of modern humans.
Zach: I believe you are talking about modern day hunter-gatherers. However, many of these observations were made in the 1800’s and early 1900’s, the time of the explorers. Back then, there were not only more hunter-gatherer cultures in existence, but they were also living a more “pure” hunter-gatherer lifestyle. Since you don’t want anyone to mention the Inuit, I won’t, but let me give another example: the Sioux Indian (as well as other Plains Indians). The Sioux lived mainly from buffalo meat, and it was noted that when they hunted, they did indeed choose the fatter animals.
Generally, since hunting expends a lot of calories, it has been noted by observers that hunting cultures tend to try to seek out the most nutrient dense foods; in other words, preferring to kill a bigger animal over a smaller one, or choosing the animals with the most fat on them- (at least they did this whenever possible. I may also hasten to add that modern day hunter-gatherers have fewer choices, due to encroachment, being pushed off their lands and into more marginal territory, etc.) It is theorized that Paleolithic people probably behaved in a similar manner, though I guess we don’t know this for sure. But it makes sense, seeing as we somehow survived through the ice age.
I’m not saying that all hunter-gatherers *have* to eat lots of fat.Those that have access to more plant foods and other carbohydrates could probably get by with less fat. But the “low carb” hunter-gatherers- and there were quite a few- would have had to have eaten adequate fat.
I spent some time on this site. That area had a rich history dating back centuries. There are links to a diary of white explorers living off of game, who reported eating currents they found made them sick, but they mentioned there was nothing really wrong with the currents. Perhaps due to a change in gut bacteria(my theory ). It may have been on this site that I read certain berries were added to the meat and fat to preserve them.
http://www.history.alberta.ca/headsmashedin/default.aspx
This book was at one time available to read free online.
http://www.aupress.ca/index.php/books/120137
I have never tried a diet of just meat and fat.
Zach, what you say makes no sense. People can argue the semantics of “paleo,” now a highly co-opted and abused word. But the fact that a society following an ancestral lifestyle, like the Hadza, even if they also practice agriculture and/or animal husbandry, doesn’t necessarily alter how they pursue their hunting and gathering, nor does it necessarily make it different from dedicated hunter-gatherers past or present. As far as “validating any theory” not sure what you mean by that either. It’s unlikely we’ll ever know in detail what pre-agricultural societies ate. We need to use the evidence at our disposal. This includes what direct evidence we do find (e.g. bones showing cut marks), analyses of bone and dentition, and, yes, examining the lifestyles and foodways of modern day hunter-gatherers. And absolutely we need to include Inuit cultures who migrate to the NA Arctic in ~900AD, and who come from the same common ancestors as nearly all of us only 40,000 yo. That’s only 2000 generations ago–time for a handful of successful SNPs to survive, like lactase persistence–but not for the very many conditions that are are determined multifactorially, such as Type 2 diabetes, driven by MNPs locvated on at least six genome sites.
Good points, wbryanh. And I’ll repeat one of the comments I made earlier above, that there is very good evidence that early humans broke open the brains of the animals they killed and sucked on the brain marrow. (Very high in fat). Some even theorize that this is what made our brains become bigger.
Excellent overview, thank you Denise!
For me, the problem with all of these studies is that they focus on the same type of person. Either they’re all overweight or they all suffer from some kind of disease. It would be very helpful if, at the very least, studies were designed that tested how overweight people and those with normal weight, or how sick and healthy people react to the same type of diet.
My point is, there are basically two different kinds of people who, for simplicity’s sake, can be put in one of two categories – heat sensitive or cold sensitive. It’s actually a bit more complicated than that and environmental factors are tied to this as well, but in general these groups’ reaction to the different types of food is inherently different and they develop altogether different types of diseases when they eat the wrong diet for their type. Simply put – their bodies are unable to maintain a certain elemental balance and diseases develop because of that.
Thus, when the same type of diet is tested on people from both groups, the results might be markedly different. While one group may do well on a certain diet, the other might actually develop all kinds of problems. To find out which diet is good for a person, one has to find out to which group the person belongs, without ignoring environmental factors and other individual differences in the person’s lifestyle, all of which have an effect on their metabolism and ultimately their health. For example, it makes a huge difference if a person does primarily physical or primarily mental exercise.
Yes, I think that is the point. Denise is showing that there is not just one kind of diet that can help people. Frankly if you live long enough and have tried a great number of diets yourself for various purposes and at various times in your life and spoken with a number of other people who have done the same, you don’t need elaborate research or studies begin to understand that ( beyond eating real, well produced and fresh food) there is not one best way of eating. We need to better understand why some diets work best for specific conditions and specific people. The point is to get beyond trying to win the LCHF/HFLC wars and to collaborate on trying to discern how to target diets for individuals, healthy ones and sick ones. My bet is that there will be numerous variations.
Hello,
I think you have a typo. Search for “changges” which I think should be “changes” with only one ‘g’ letter.
V/r,
Bryan
The sooner people lose their obsession with macronutrient ratios, the better. Carbs, fats & proteins can be obtained from:-
1. Minimally-processed animal & vegetable produce.
2. Over-processed crap-in-a-bag/box/bottle.
We should be basing our diets on 1.
The Food Product industry wants us to base our diets on 2 and uses every marketing trick in the book to “make it so”.
Did you miss the part where the successful very low fat diets had milled rice and refined sugar as major elements?
No. In what way does your comment contradict the fact that we should be basing our diets on 1.?
Just because it’s possible to be healthy on a diet of milled rice and refined sugar for *one* *year* doesn’t mean that it’s the optimum diet for *life*.
Do you have any evidence that 1. isn’t a better choice over a lifetime? Kempner’s trial only lasted for one year, so there would have been no long-term health problems caused by micronutrients missing from his diet.
The actual evidence Denise presents is that 1. doesn’t matter if you are on a very low fat diet.
There is also evidence that whole grains are worse from an autoimmune perspective than refined white flour. In general, for nonpaleo foods, processed versions seem if anything healthier than unprocessed versions.
Whole grains contain oils in the outer coat that can go rancid. Consuming rancid oils from stale whole grains is definitely not good for optimum health. Refining grains removes these oils, which is a good thing. However…
Refined grains are lower in certain minerals (copper & manganese, for example). If this is compensated for by eating other foods that are high in those minerals, it’s not a problem. A diet comprising milled rice, refined sugar & fruit juice will be lacking in the above minerals.
A very low fat diet comprising veggies, root veggies & tubers, legumes, whole grains and whole fruits will be high in the above minerals.
Please provide evidence showing that fresh whole grains are worse from an autoimmune perspective than refined white flour.
“Please provide evidence showing that fresh whole grains are worse from an autoimmune perspective than refined white flour.”
It’s because whole grains have more toxins like gluten and wheat germ agglutinin. These toxins lead to more leaky gut and then trigger autoimmune responses due to molecular mimicry.
As someone with an autoimmune disease, I’m perfectly happy avoiding both whole and refined grains. Doesn’t hurt anything, and I’ve got both bases covered.
“It’s because whole grains have more toxins like gluten and wheat germ agglutinin. These toxins lead to more leaky gut and then trigger autoimmune responses due to molecular mimicry.”
You’ve got it the wrong way round. Whole grains have an outer husk which *doesn’t* contain gluten, so the relative gluten content of whole grains is lower than for refined white flour. Also, despite thorough chewing, whole grains have a much smaller surface area than refined white flour, reducing absorption through the gut wall.
As you have gut permeability issues & AI disease, you’re better-off sticking to meat & veg!
The opposite is the case. There is much more missing in refined grains than just copper and manganese (althouth those trace minerals are crucial for phase II enzymes). We always have to be wary of the fallacy of reductionism when evaluating the health effects of a complex, natural food. There are many more differences between whole and refined grains, all being at least as significant as the content of micronutrients:
1) Fiber, of course, but the term “fiber” is as much an overgeneralized umbrella term as the term “fat”. Both comprise a huge variety of compounds with very different health effects. While in contrast to fatty acids, all known types of fiber seem to have beneficial effects (well, except a well known side-effect from large doses), some excert their effects simply by increasing the mass of the intestinal lumen, some have probiotic effects, and some excert potent physiological effects even beyond acting as a prebiotic. Whole grains – particularly oats and barley, but also wheat and rye – contain large amounts of β-glucans in the bran – a type of fiber that is also found in fungi but fruits an vegetables are generally devoid of – that is partially absorbed and partially metabolized by gut bacteria. It excerts powerful immune-regulating effects, not only on the intestine (which we now know to be crucial on a systemic level) but also systemically through intestinal absorption of the β-glucans and their bacterial metabolites. Here is a comprehensive review on β-glucans done by a hobby researcher.
2) An abundance of seconary plant metabolites concentrated in the bran, phenolic compounds such as simple phenolic acids and tannins, compounds related to B-vitamins such as PABA, and – probably most importantly – significant amounts of inositol hexaphosphate or phytic acid. The very compound that paleo lore has painted as a villain of whole grains may in fact have highly beneficial effects in well nourished Westerners, as it has a high binding affinity to iron and does chelate iron not only in the intestinal lumen but is also absorbed through passive diffusion and acts as an chelator of free iron in the blood stream, as testified by many people who suscessfully lowered their iron overload by taking supplemental IP6. Ironically, Paleo dieters who avoid phytic acid like the plague would probably derive the most benefit from it, given the high heme iron and saturated fat load of such dietary patterns and their well-known inflammatory effects.
3) Last but not least: structure. Whole grains ain’t whole grains. The aspect that usually gets lost first when engaging in reductionist methodology of nutritional science is the three-dimensional, cellular structure in which nutrients are delivered within a whole food matrix. Usually it accounted for only as a factor in bioavailablity (e.g. carotenoids), but it may have effects far beyond this aspcect. By legal definition, whole grain products are all products made out of unrefined grains. However, the literal meaning would be a grain that is not milled to flour but still intact or coarsely cracked. Bread baked from grist instead of flour has a significantly lower glycemic and caloric load, because much of the starch that remains tightly contained within the cellular structure is indigestible and thus acts as a prebiotic fiber in the large intestine similar to resistant starch, further improving gut health.
Of course, eating some refined grain know and then won’t hurt – it’s simply a wasted opportunity to eat something much more healthy. I’m the first to admit, though, that I sometimes happily waste this opportunity in exchange for a delicious, crispy croissant. 😉
1. & 2. If someone’s diet consists entirely of grains, then what you say would have a significant effect. Who eats a diet of rice and nothing else whatsoever?
3. I totally agree. See http://nigeepoo.blogspot.co.uk/2010/02/problem-with-whole-grain-cereals.html
I don’t like orthorexia a.k.a. “clean” eating. As long as the diet is *based* on whole, minimally-refined animal & vegetable produce, there’s some wiggle-room for refined foods. 😀
Actually a huge number of people around the world DO live off mostly grains, sometimes for their entire lives. With very little in the way of vegetables. That is why the IIRC developed “golden rice” … to save the sight and lives of millions of children.
Oddly though, some of those grain-eaters are actually surprisingly healthy. Like this guy:
He’s from a culture that eats mainly sorghum, 3 meals a day. Other places in Africa eat mainly millet, or their own version of corn, or yams. Or peanuts or milk. One of the first questions one asks when meeting a stranger is, “What is your staple?” … I guess they define the culture by the main food. When you see the pictures though, the people are typically tall, with straight teeth and wide smiles … even when they are living at a barely subsistence level.
I haven’t yet seen a culture with healthy people living mainly off wheat or barley though. Even in the ancient Egyptian and Roman days … skeletons of the rich and the poor were both pretty bad. Even Oetzi, with all his exercise. The French are healthier than Americans, but not nearly as robust as your average Japanese mountain villager who lives off yams.
Well, in chapter 3 of Dr. Price’s “Nutrition and Physical Degeneration” he found the Swiss in perfect health eating mainly whole rye.
Major-General Sir Robert McCarrison’s “Studies in Deficiency and Disease” he found the Hunza eating mainly whole wheat, barley, maize, apricots and milk. He describes them as “unsurpassed in perfection of physique and in freedom from disease in general, whose sole food consists to this day of grains, vegetables, and fruits, with a certain amount of milk and butter, and goat’s meat only on feast days.” His findings are documented in Guy Wrench’s “Wheel of Health.”
Egyptians and Otzi had the unfortunate dental abscesses from millstone grit and sand which destroyed their teeth and their health. Difficult to know how they would have done without that issue.
Rice is so low in protein that I think of it as a “filler”, rather than a staple. Eating beans with rice improves the AA profile a lot. Tubers are good.
In the 1st world, the problem is over-consumption. For nearly 100 years, the 1st world masses have been manipulated to over-consume, as it keeps them happy & docile and it’s good for the economy.
Have you seen http://www.dailymotion.com/video/x2d29tf_the-century-of-the-self-part-1-of-4-happiness-machines_school ?
I agree, white rice is totally nutrition-less. Which is what makes the Kempner studies so amazing. Even more amazing to me is that the Chinese railway workers were noted as being MORE healthy on a diet of mainly rice and vegetables and dried octopus, than the Irish beef and potatoes guys. OK, the Chinese boiled their water and did less whisky! But still … they worked 10-11 hour days at hard labor on mainly rice, lived in hard conditions, and were noted for being “healthy”.
Billions of people live off mainly rice. They DO get nutrition problems if they don’t also get some vegies and protein too. But given that, they do fine and tend to be healthier than the people getting the Western diet.
I think the idea that scarcity protected people is mostly a myth. Comparisons have been done calorie-for-calorie with Westerners, for the same exercise levels. The Chinese often eat MORE calories for the same exercise level, and yet tend to be skinnier and healthier. Your average Japanese doesn’t go to bed hungry either, and is likely more healthy than the average American.
However, the Chinese have *less* tolerance for “The Western Diet”, whatever that is .. and get diabetes with less weight gain. It seems to have something to do with the actual food choices.
Asians appear to have limited Sub-cutaneous Adipose Tissue (SAT) hyperplasia, which limits fat storage capacity below the skin. As a result, Visceral Adipose Tissue (VAT) stores are filled prematurely, leading to the Metabolic Syndrome, as VAT deposits are much more metabolically-active than SAT deposits. This is a.k.a. “Skinny-fat”.
See http://nigeepoo.blogspot.co.uk/2012/06/adipocyte-hyperplasia-good-or-bad.html
The SAD/SED combination of refined carbs + fats results in fats being stored, as carbs are burned preferentially. A high-carb, low-fat diet suits Asians much better!
Having re-read what I wrote about Adipocyte Hyperplasia and the comments from June 2012, the following thought processes occurred:-
Adipocyte Hyperplasia occurs mostly during childhood, as that’s when rapid hyperplasia of other cells occurs a.k.a. growth.
A slim child which becomes a slim adult has few SAT adipocytes, predisposing said adult to get excess VAT rather than SAT if chronic over-eating occurs during adulthood.
A fat child which becomes a fat adult has lots of SAT adipocytes, allowing said adult to get rolls of SAT rather than VAT if chronic over-eating occurs during adulthood.
heathertwist said: “I haven’t yet seen a culture with healthy people living mainly off wheat or barley though. Even in the ancient Egyptian and Roman days … skeletons of the rich and the poor were both pretty bad. Even Oetzi, with all his exercise.”
Indeed there were healthy grain eating cultures that were observed in the early 1900s when various of prominent doctors were researching nutrition, at the time. The idea that grains are not a good food for humans comes from the “porotic hyperostosis” study of ancient skeletons. The bones of early farmers were found to have lesions which were thought to be due to iron deficiency as a consequence of eating grains instead of meat.
However, it only became clear a few years ago (2009) that the lesions were not due to iron deficiency, making the original hypothesis flawed.
The causes of porotic hyperostosis and cribra orbitalia: a reappraisal of the iron-deficiency-anemia hypothesis (2009)
So, the original hypothesis is obsolete—yet it is still used to claim that grains are problematic. The skeletal lesions were perhaps due to episodes of starvation or something else. We don’t really know. But, I’m not sure why grains would be assumed to be the only culprit of causing such lesions and skeletal issues. Now that the original hypothesis has been deemed obsolete, another explanation is needed.
Keep in mind that societies became larger, infections were more rampant, and food was scarce at times. Societies were adapting and there was a lot of turmoil. Mass starvation was also said to have happened as early farming practices depleted the soils to oblivion. Some say this turmoil and social stress is evident at archaeological sites like Göbekli Tepe and Caynou, where mass death, genocides or sacrifices appear may have happened.
Also the high levels of cavities in early Neolithic skeletons has been attributed to the wearing down of teeth from poor milling standards. Attrition broke the enamel, which led to dental abscesses and promoted cavities.
See: Teeth and Bread in Ancient Egypt (1972)
This is very different from the sugar-promoted cavities we have today. (Honey was their main sugar, but honey is believed to be protective of dental caries). Arteriosclerosis has been linked to dental infections. If we wanted to, we could probably link all of their health issues to poor dental health and starvation, but that too would be highly speculative. Incidentally even Paleolithic teeth have also been found to have significant wear and tear.
The point being is that it’s very easy to create a narrative both vilifying and defending grains by using ambiguous archaeology.
“Indeed there were healthy grain eating cultures that were observed in the early 1900s when various of prominent doctors were researching nutrition, at the time. ”
I would really like to see such a study! I’ve been looking. There are loads of healthy skeletons of “grain eaters” in general, just not wheat-eaters. Hard bran and everything, their teeth might wear down, but they didn’t have the soft enamel that has become common now. If you combine the soft enamel with sugar, it causes cavities. But most cultures don’t have soft enamel: just a few do, and those ones also have significant skeletal changes (crooked teeth, narrow mouth etc) which one associates with vitamin malabsorption.
It’s also not clear what the “prominent doctors” considered “healthy”. Price was rather specific: he counted cavities and took pictures of the dental arches! But the cultures he considered “healthy” were oat-eaters. And the Swiss, who ate barley bread. The Swiss also drank a lot of raw milk though, and it turns out that raw milk interferes with one of the factors in wheat that is a problem. Also, it turns out that the Swiss had gone through a big problem with goiter not long before Price studied them. The Swiss government started trucking in iodized salt because so many of the recruits failed their physicals because of goiter.
He did notice that English poor folk got healthier when supplemented with whole wheat bread, raw milk, and cod-liver oil. Which may show that whole wheat is better than white wheat, or that raw milk really does help, or that the vitamin involved happens to be in cod-liver oil. Anyway, the Chinese did fine on white rice and vegies and fish, for the most part, without extra raw milk or cod-liver oil.
The main reason I got curious about this was my daughter. Until she was 6, she ate a normal US diet, and her tooth enamel was really soft. “Sticky” as the dentist put it. She got cavities constantly. Then we switched from wheat to rice, and her next visit … no sticky teeth. Didn’t get any more cavities from that point, even though she ate (and eats) plenty of sugar.
So for some people, at least, it turns out that wheat messes with vitamin absorption and also with the gut biota, which is where Vit K is produced. I don’t know if it’s Vit K or Vit D or what else, but I think something is going on that interferes with skeletons and teeth.
It could well be that this happens a whole lot less with whole boiled or parched grains … those digest slower and feed bacteria less. The whole grains … of any type … also interfere with iron absorption but in general I think that’s a good thing (as was some level of hookworm!).
Anyway, sure, one can skew history, and skew statistics. But it’s a weak argument. Anyway, I’ve never made the argument that “grains” caused anything bad: just one or two particular grains which have weird effects on humans.
heathertwist said: “I would really like to see such a study! I’ve been looking.”
Are you not familiar with McCarrison’s observations on the Hunza? They ate a lot of whole wheat and milk and a few other foods, of course (even the bible says one cannot live on bread alone). McCarrison also did experiments on rats where he gave one set of rats a British diet (white flour, margarine, etc) and another set of rats the Hunza diet of whole wheat and milk. The rats eating a Hunza diet had no discernable disease. His study was done to prove that the success of the Hunza diet had nothing to do with genes.
Sir McCarrison presented his findings before the Royal College of Surgeons and his observations are summarized in the 1938 book, “The Wheel of Health,” by Dr. Guy Wrench. (Free on Google Books).
In his lectures, McCarrison remarked:
He was their doctor for 7 years and described them as one of the finest and physically fit races he had ever seen. The Hunza are no longer healthy now eating a modern diet.
heathertwist said: “There are loads of healthy skeletons of “grain eaters” in general, just not wheat-eaters.”
Well, if you dig into the history books, you’ll see that wheat was considered the healthiest and most revered of all foods. The word cereal comes from the name for the ancient Roman goddess, Ceres—the goddess of grains and agriculture. Ceres was said to have discovered wheat, and given the gift of agriculture to humankind.
Hippocrates not only recommended wheat bread, but experimented heavily with different preparations.
If wheat was so deleterious, you’d think that Hippocrates would have noticed it and warned against its consumption instead of recommending it for the prevention of disease.
Avicenna recommended bread as a key staple of the diet. Paracelsus believed that wheat had mystical properties, and Aristotle thought foods made from wheat suits our bodies best. A 19th century encyclopedia says that wheat is the most nutritious and most important edible plant in the entire vegetable kingdom. Surely if wheat was so terrible, we would see evidence in the history books.
Over 250 years ago, Swedish biologist Carl von Linné, the father of modern taxonomy and modern ecology, wrote two texts—Ceres noverca arctoum and De pane diaetetico—that were wholly devoted to bread and bread-making. Citing his own observations as well as those of the greatest medical authorities of antiquity, he wrote.
Von Linné also provided examples of how bread could prevent or cure specific diseases. Although rye was popular in his home country of Sweden, von Linné considered wheat bread to be “the most excellent of all.”
In the 19th century, Thomas Hodgkin, the prominent English physician and first to observe Hodgkin’s disease, wrote:
heathertwist said: “Price was rather specific: he counted cavities and took pictures of the dental arches! But the cultures he considered “healthy” were oat-eaters. And the Swiss, who ate barley bread.”
Actually, Price said the Swiss ate whole rye bread and milk. Price wrote:
“Anyway, sure, one can skew history, and skew statistics. But it’s a weak argument.”
I’m mainly pointing out that people often use the Neolithic skeletons to demonize grains when in fact nobody actually knows what actually caused the bad skeletons. If wheat were so problematic, you’d think somebody would have noticed this before white flour triggered the dyspepsia epidemic in the 19th century. Yet, everyone who wrote about wheat seemed to think it was the best thing since, well, sliced bread.
OK, some people say the Hunzas are awesome. I don’t see a lot of evidence for that … unlike the Okinawans, Sardinians, Japanese mountain people, Masai … where are the studies? One visitor did write a book about them and noted:
“As their diet is deficient in oils and vitamin D, all Hunzas have soft teeth, and fully half of them have the barrel chests and rheumatic knees of sub-clinical rickets.”
As paleoedge noted:
“But there is a problem with this climate theory; why did the Inuits maintain their darker tone? The reason is theorized to be because northern Europeans switched vitamin D rich meat for low-fat vitamin D deficient grain, while the Inuit maintained a vitamin D rich meat based diet without grains. It turns out, Dr. Cordain found out that wheat contains an anti-nutrient called WGA, a lectin that binds to cellular glycoproteins. Once in the gut, WGA binds to a cell receptor, and then a nuclear pore found in every cell in the body that blocks the transport and absorption of vitamin D. According to Dr. Cordain, WGA has a half-life of four hours, which means if you are sunbathing while consuming wheat, the vitamin D is most likely being blocked from the sun. Whoa!”
However, my grandmother grew up in Germany, and lived to be 96. Her diet included wheat, but really not that much … like the Hunza, there were a lot of other vegetables, lots of dairy, and limited meat. The grains tended to be mainly oats. They rarely got wheat growing up (it was for rich people) and it was a lower-quality wheat at that.
http://paleoedge.com/how-much-meat-plants-and-dairy-did-farmers-consume/
Actually there is a theory that white skin actually developed in the Middle East, as an adaptation to eating wheat. The white skin people eventually moved North, and I guess the people that live there now are better adapted (or just sickly: what are the caries rates in the Middle East?).
http://news.sciencemag.org/archaeology/2015/04/how-europeans-evolved-white-skin
“Then, the first farmers from the Near East arrived in Europe; they carried both genes for light skin. As they interbred with the indigenous hunter-gatherers, one of their light-skin genes swept through Europe, so that central and southern Europeans also began to have lighter skin. The other gene variant, SLC45A2, was at low levels until about 5800 years ago when it swept up to high frequency.”
Interestingly, Sardinia, which was one of the wheat-exceptions, appears to be no longer:
http://paleoedge.com/how-much-meat-plants-and-dairy-did-farmers-consume/
“According to Sarah Wilson who visited Sardinia with National Geographic, “the longevity phenomena seems to have come to an abrupt halt, even reversed. It’s almost like as soon as money came to the island (which it did about 50 years ago) the locals went from famine to feast, taking on the health consequences that come with abundance. Young Sardinians are incredibly overweight. And Sardinia has one of the highest incidences of celiac disease, I’m guessing from eating so much bread and pasta where the gluten content has shifted due to the more processed wheat strains available today.”
heathertwist, Duck Dodgers: I have also read that the health of the Hunza was not all that awesome, though it was better than most people’s health today. Like most native cultures, they did have an absence of diabetes, cancer and heart disease; however, compared to other native groups, they did have goiter, and a reasonable number of cavities.
heathertwist, I believe in another post you mentioned that you are a celiac? Me too! “Welcome to the club”. In researching celiac disease years ago, I remember reading that most of those cultures that did eat wheat traditionally also ate many more other grains, mostly gluten free, like millet or teff, buckwheat, etc. In other words, they varied their grains. It was stated that we as a culture today eat far more wheat than most cultures of the past, because we eat almost exclusively wheat. (For instance, I’m pretty sure I’ve read that the Hunza also eat buckwheat and millet). Some of these other types of grains have become obsolete, and few people in the West even know about them. (Apparently, wheat is more convenient to grow and transport). And my guess is that if the Swiss were eating lots of rye bread, it was most likely fermented sourdough; this would remove some of the anti-nutrients and make it more digestible- (I don’t know: Weston Price didn’t mention that they fermented it. However, wheat was traditionally fermented, so maybe he didn’t feel the need to mention it?) It could also be possible that drinking full fat milk, and/or eating meat (or cod liver oil) helps mitigate some of the harmful effects of wheat by replacing nutrients. So in other words, eating wheat in a traditional culture would be different from eating lots of wheat and sugar with low fat milk in a modern day culture.
In any case, wheat bread of the past was very different from modern wheat bread. Not only was the wheat different- (it was lower in gluten; the bread would have been flat, dense, and not “fluffy”)- it might have been fermented, and, nowadays, there are many shortcuts to bread making. Rather than relying on a long process of letting the dough rise, there are many additives that are used today to speed up the process. Not only are some of these additives questionable for human health, but also, in not using a slow, traditional process, it might make the wheat more deleterious.
Finally, I don’t think we can have a discussion about wheat without mentioning that which interests me the most: the opioid effects! Duck Dodgers, I wonder if many of these historical figures praised the benefits of wheat because it makes people “feel good”? It is definitely, absolutely addictive, like sugar; I see many people who are addicted to it, all around me. (I was addicted to it even while it was killing me). Some have even suggested that the widespread shift from hunting and gathering to farming may have had something to do with opiates and addiction. I find that theory very interesting……
“heathertwist, I believe in another post you mentioned that you are a celiac? Me too! “Welcome to the club”. In researching celiac disease years ago, I remember reading that most of those cultures that did eat wheat traditionally also ate many more other grains, mostly gluten free, like millet or teff, buckwheat, etc”
Well thanks! An interesting time to be part of that club … !
There is something interesting going on with the heritage wheat too. One of the aid organizations sent some wheat berries to a town that traditionally ate mainly wheat. But the kids developed celiac symptoms from the American wheat. It probably shouldn’t be toooo surprising … heritage corn and beans are sure different from the modern ones. But the heritage wheat didn’t seem to help the Egyptians or Romans, so it’s hard to say.
“And my guess is that if the Swiss were eating lots of rye bread, it was most likely fermented sourdough; this would remove some of the anti-nutrients and make it more digestible- (I don’t know: Weston Price didn’t mention that they fermented it. However, wheat was traditionally fermented, so maybe he didn’t feel the need to mention it?)”
I haven’t seen that rye and barley are anywhere near as harmful as wheat though. It is true that celiacs cross-react to rye and barley, but would a culture that ONLY ate rye and barley have the same issues? Celiac is a very specific kind of auto-immunity, but there doesn’t seem to be a similar kind of illness that is triggered by, say, millet or quinoa.
The “healthy Swiss” weren’t all that healthy either. They had a super-high rate of goiter until the Swiss government started trucking in iodized salt circa 1920.
http://www.iccidd.org/newsletter/idd_aug13_growth_and_iq.pdf
Now, my grandma grew up in a German village and she did live to a grand old age (96) with no heart disease, high blood pressure, tooth loss, etc. She didn’t get white wheat much as a kid (they got a slice per week as a treat) but she certainly ate it a lot, esp. cookies, when she came to America. But further, she was somewhat sun-phobic and kept the shades drawn, and covered herself from head to toe with long sleeves, high necklines, thick stockings, hat … which was traditional for her growing up. So I always wondered why she never got rickets? Or goiter, for that matter.
The answer appears to be that in her day, one of the favorite foods were fish. Pickled herring was big, and river eel, and even salmon. Another favorite food was mushrooms, which they gathered themselves in the local forests. Mushrooms dry and keep very well, and guess what? They are an incredible source of Vit D, esp. if they are sun-dried, and actually high in protein too. Cheap food for anyone who wants to gather them. Otzi was found with a string of dried mushrooms!
“Placing regular mushrooms in direct sunlight for an hour (winter) will generate your daily needs of vitamin D in a serve (100g or three button mushrooms – See more at: http://www.powerofmushrooms.com.au/health-nutrition/health-nutrition/vitamin-d/#sthash.SLdZIjq4.dpuf”
Price used cod liver oil as a magic cure of sorts, which would provide Vit D and Vit A (the two that tend to be problematic), and, I think, iodine?
So maybe that is part of the reason the Egyptians had more issues with wheat … it was too hot and dry there to have a lot of mushrooms!
” It is definitely, absolutely addictive, like sugar; I see many people who are addicted to it, all around me. (I was addicted to it even while it was killing me).”
Amen to that! I think this is one reason that there is such a strong reaction to the “anti-gluten” people. I mean, in our culture, we have people who won’t drink milk, won’t eat sugar, won’t eat meat, won’t eat chocolate unless it’s fair trade … I’ve gone on my share of food experiments. But the “no wheat” food experiment had people talking to me like I’d joined an evil cult and they got seriously angry.
Also though when kids stayed overnight at our house, they would start going bonkers at the end of day 2. Got headaches and had anger fits. One, her Mom reported, started screaming on the drive home “I have to have spaghetti!” so they stopped for food. There was not spaghetti so the girl had a meltdown. Mind you we DO have spaghetti and bread, and these kids were too young to understand that our spaghetti was missing the gluten part. But they definitely were going through withdrawals.
heathertwist- I had a look at the link you posted about the Swiss. They mention that some “alpine villages” had problems with goiter, but there was no mention of the specific valley that Weston Price visited, where the people were so healthy: the Loetschental Valley. It was a very remote part of Switzerland where the people still ate only traditional, natural food, whereas in most other parts of Switzerland the people ate very differently. As I recall, he made the distinction that the people in this valley were much healthier than the average Swiss elsewhere. So I’m still not sure about that; unless there is a link somewhere that states specifically that those people had goiter?- (but even if they did, it may be hard to find the evidence). So, who knows?
That was very interesting what you wrote about people getting sick when their heritage wheat was replaced by American wheat!
There is also the theory that in some African countries, where the people are starving and are fed government rations of wheat, some of those children who still look emaciated may be suffering form celiac disease rather than actual starvation. I think there was no proof of this, just speculation, but I hope someone is looking into this possibility. When people suddenly eat lots of wheat when it’s not part of their traditional diet, celiac is likely to occur.
Also, I guess that was a good point about rye and barley. Although they both have gluten, they are most likely not harmful in the way that wheat can be. I guess it’s possible that a culture eating just rye and/or barley may not have the same problems as wheat eating cultures.
Last thing about wheat: Denise Minger, in her “China Study” rebuttal, noticed there seemed to be a correlation between wheat eating groups of Chinese and heart disease.
The bit I read about the wheat berries in food aide was an actual report, not just an anecdote. But it was years and years ago!
Yes, Denise did an amazing job of analyzing The China Study in terms of wheat, rather than meat. It is the case worldwide that the places that grow wheat tend to also be the places that have cows or goats … they are the inland people! The coastal people can get food more easily by eating fish, and rice grows better in warm or wet places (wheat gets moldy easily). Inland people have other confounding issues too, notably lack of iodine and lack of fish. The more fish people eat, the statistically more intelligent they tend to be.
Cordain is saying that the WGA in wheat is what blocks the Vit D … not the “gluten” (gluten is a total misnomer, but the term has stuck!). WGA stands for “Wheat Germ Agglutinin” Barley and Rye have something similar, but I don’t know that it is the same thing. Try baking bread from barley or rye and you get the idea … they are really different.
I also don’t know to what degree raw milk blocks the process. Apparently it DOES block a lot of it, which might be one reason why raw milk got suck kudos as a health food. Drinking raw milk with your wheat might be the magic bullet-dodger!
“On another note, not only does wheat contain gliadin, which upregulates zonulin, which increases intestinal permeability, it also contains an obscure compound (thaumatin like proteins) which also increase intestinal permeability. Hence wheat represents a triple time bomb (gliadin, WGA and thaumatin like proteins) which maintain physical and physiological characteristics that almost certainly impair gut function, interact with our immune systems to produce low level inflammation, and impair vitamin D metabolism (not a vitamin at all, but a hormone having receptors in virtually every cell in the body).” (Cordain)
http://thepaleodiet.com/wheat-the-triple-time-bomb/#.VldSl3arTME
Interesting link! There’s a lot about wheat there.
I have also read about wheat and vitamin D, in other sources. (As well as the idea that white skin might be a recent adaptation to grain eating). It’s all very interesting.
There’s also some evidence that wheat eating might interfere with magnesium absorption.
Oh yeah, and I forgot to mention, that was totally fascinating about the children going through wheat withdrawal! Yes, I can believe it too. I’ve seen this kind of thing; (with sugar too). As wheat and sugar often appear together in foods, that’s a double whammy.
heathertwist said: “Dr. Cordain found out that wheat contains an anti-nutrient called WGA, a lectin that binds to cellular glycoproteins.”
Matt LaLonde, and many others, have questioned Dr. Cordain’s overlooking the fact that people do not eat raw wheat…
Even Dr. Ayers, an actual glycobiologist, says that cooked lectins are fine (see his user comments, below the post, where he discusses WGA).
heathertwist said: “On another note, not only does wheat contain gliadin, which upregulates zonulin,”
Actually, certain ancient types of tetraploid wheat (e.g.; Graziella Ra, Khorasan wheat/Kamut) have even greater amounts of total gliadin than modern accessions. Interestingly, during the 1800s, gluten (and gliadin) were considered to be the most nutritious vegetable compound. This may explain why cultures preferred wheat varieties with higher levels of gluten. For instance, Einkhorn was the least reactive wheat, and more reactive wheats were preferred by cultures, even during the Neolithic.
In the 19th century, doctors recommended gluten bread for diabetics. 6th century Chinese actually added wheat gluten to their foods as a protein source. It’s only been since about 1950 that people began to have problems with gluten. Of course, everyone blames “modern wheat varieties” but few seem to notice that wheat is now heavily processed (fumigated, reconstituted and sometimes bromated). Also, the protective oils often removed to improve shelf life. It’s a bit like adulterating, fumigating and removing the Vitamin E from a mongongo nut and wondering why someone eating those heavily processed nuts would have health issues.
heathertwist said: “which upregulates zonulin which increases intestinal permeability, it also contains an obscure compound (thaumatin like proteins) which also increase intestinal permeability. Hence wheat represents a triple time bomb (gliadin, WGA and thaumatin like proteins) which maintain physical and physiological characteristics that almost certainly impair gut function,”
Those who make this insinuation—that a temporary upregulation of zonulin promotes health issues—are often the same people who recommend using liberal amounts of coconut oil for cooking and eating. Ironically, these individuals don’t seem to realize that lauric acid, found concentrated in coconut oil, is known to upregulate zonulin and causes the same intestinal permeability that gluten does.
There’s little evidence that a temporary upregulation of zonulin is problematic in a healthy individual. For all we know, it may plat a role in oral tolerance.
Even celiac researcher Alessio Fasano explains that it’s no big deal for healthy people:
He goes on to explain that people with celiac secrete too much zonulin and their tight junctions stay open longer than it should.
Anyhow, it’s probably unhelpful wise to scare healthy people into fearing these normal processes, particularly when other popular foods, like coconut oil, have the same likely normal effect.
Uh oh….I do eat raw peanuts from time to time. But I don’t notice myself having issues with them at all. In fact, I’m normally quite sensitive to foods; I have trouble digesting most other legumes, even if they are soaked and cooked. Could it be that it’s personal, and our bodies react differently to lectins and other anti-nutrients?
Yeah, some groups have spent thousands of years adapting to wheat (and to milk!) and some groups have not. And some people don’t think they have any much reaction at all. There is just this amazing coincidence that the healthiest cultures are the ones with the least wheat, and that a lot of people drop wheat and suddenly feel a whole lot better. And things like the China Study. My prediction is it will be like say, “Sugar of Lead” … the rich Romans added it to their wine and no one could see any problem with it. Except rich people kept going crazy.
Anyway, lectins are not always destroyed by heat. Gluten for sure isn’t … the whole point of gluten is to get bread to rise. WGA maybe could be destroyed by cooking it enough, but apparently it is not:
“.whilst variable amounts of agglutinin were found in wholemeal pasta probably as a consequence of thermal inactivation during food processing..”
http://www.sciencedirect.com/science/article/pii/S095671350300104X
“The concentration of WGA in white flour is about 3 to 4 milligrams per 100 grams, whereas in whole wheat it’s 10 times that, it’s an order of magnitude higher. But at physiologic levels, we’re only talking nanogram concentrations in bloodstreams. We know from tissue studies, these in vitro studies, that cells respond at nanogram concentrations, so nanogram concentrations can easily be achieved by consuming 4 to 7 milligrams per 100 grams.”
http://www.meandmydiabetes.com/2011/11/30/loren-cordain-autoimmune-disease-and-food-triggers/
So they are working with WGA as a drug-delivery system and it works it seems in really tiny amounts. There aren’t many lectins in canned beans, but there are some left in homemade beans, and it’s fairly common for people to get sick (and even die) from home-cooked kidney beans. Cooked bread has “variable amounts” of WGA in it, and some of it is inactivated by other foods with it. Or not. So the effect likely has to do with how it’s cooked, what you eat with it, and what your genes are. Hardly a glowing recommendation for a highly wheat-based diet.
Fasano is Italian, and hardly a health-food person. He’ll probably live a normal Italian life and get arthritis and heart disease at the usual age, like all the other Italians, who are in fact the most wheat-adapted. He likely takes Vit D pills or eats Vit D enriched foods too, and has his cavities filled like everyone else. He’ll get osteoporosis as expected as he gets older and likely a few root canals. So he’ll live longer than a celiac would who was eating wheat, and won’t live with a constant stomach-ache … and he’ll be able to eat Big Macs and pizzas, which is important to him. But will not live as long or be as healthy as the average Japanese mountain villager.
But what would his life be like if his Big Macs did NOT have wheat in them? (or added iron, for that matter). That is the question. The experimenters who are trying it out … the no wheat lifestyle … are beginning to answer that question. Maybe it’s just another odd dietary fad. Or maybe the non-wheat people will end up being quite a bit healthier. Right now we have these massively parallel food experiments going on with fat, sugar, meat, GMO, fish, and grains. I say the more the merrier … try something out, see how it works for you, and share with the rest of us.
“Could it be that it’s personal, and our bodies react differently to lectins and other anti-nutrients?”
It’s definitely personal, but our flora are likely responsible for much of our adaptations.
We find indigenous cultures take steps to minimize wild plant toxins, but wild plant toxins often make our domesticated foods look quite tame (domestication is a kind of toxin reduction). Their gut flora adapts to their diet.
This is a key point to understand because while on the surface we often don’t have the ability to digest certain foods, like dairy, seaweed, or grain toxins, our gut flora can quickly adapt to break down those foods. For instance, most Masai are lactose intolerant, but their flora adapts to their high dairy diet. Japanese individuals possess the genes for the consumption of the algal polysaccharide porphyran in their microbiomes, which are rarely found in North American and European individuals. We cannot digest phytate, but our flora can.
Plus most lectins and antinutrients are also known to have beneficial properties:
The dreaded kidney bean lectins have anti-fungal and anti-viral activities and lectins in general have anti-cancer properties too. Phytates have anti-cancer functions and therapeutic properties against diabetes mellitus, atherosclerosis, coronary heart disease and reduces kidney stone formation. Toxic glycoalkaloids, found in potatoes and nightshades, have been shown to offer antiallergic, antipyretic, anti-cancer and anti-inflammatory effects; blood sugar-lowering effects, and anti-pathogenic effects against viruses, protozoa, and fungi. Cyanogenic glycosides have anti-cancer properties. Phytosterols, polyphenols, flavonoids and tannins, alkaloids, phytates all have anticancer, antioxidant or endocrine normalization properties as well.
Notice a pattern? Antinutrients are not so black and white after all. They aren’t always bad. In the context of adapted gut flora, I suspect they help maintain homeostasis (i.e. a proper balance of what we might consider “good” or “bad”… yin/yang).
Duck Dodgers- thanks for the clarification about lectins (and other anti-nutrients. Actually, I had read that about phytates before, but I didn’t know it applied to the others). This explains why I feel fine with peanuts (though I eat them in moderation), as well as nightshade vegetables, of which I eat a lot of! Not only do I digest them well, but they don’t seem to be causing me any harm and I feel very healthy when I eat them. However, I’m not sure about the “adaptation” theory; though I had exposure to foods like wheat and soy for a good part of my life, I never “adapted” to them. I think it probably has to do with more than just damaged gut flora- (if anything, I think those foods might have caused damaged gut flora, in my case). And there are so many vegetables and fruits that most people think of as being benign and even healthy, that I can’t digest at all! Basically, I just go by how I feel, and screw all those conventional “recommendations”.
“There is just this amazing coincidence that the healthiest cultures are the ones with the least wheat”
Yes, an amazing coincidence that those who eat the most white flour are unhealthy. Like most anti-wheat sentiments, this statement conflates the difference between white flour eating cultures and traditional whole wheat. It should be obvious that any refined food is problematic, and wheat is the king of refined grains in the modern world.
The problem with that conflation is that it ignores the cultures that thrived on, revered and worshiped wheat. Prescribed by Hippocrates, Paracelsus, Avicenna, Aristotle, favored by the Spartans, the Greeks and the Romans, and observed by countless scholars who wrote about its health effects. In every single instance, throughout Western history, wheat was unanimously considered to be the healthiest of all foods by the most prominent medical authorities—and this sentiment existed until the industrial revolution.
Furthermore, gluten was discovered in 1742 and even through the 19th century was believed to be the most nutritious plant compound. Not only did most cultures prefer higher gluten wheats, but it’s only since the 1950s that many people began to have trouble with gluten.
Anyhow, the “amazing coincidence” would be like condemning all meats without recognizing that processed meats are completely different from eating whole animals. It’s misleading. If you’ve never seen how modern flour is made, it’s extremely processed.
Let’s not pretend that modern wheat milling is indicative of traditional wheat consumption. It’s common knowledge that bread is broken.
Good points. Qualitative, mostly-opinion statements like “the healthiest populations eat the least wheat” are problematic for many reasons: their qualitative nature; their failure to define what “healthiest” is; their failure to present any quantitative analysis; their dependence on apparent correlations, rather than establishing causative relationships; their failure to deal with confounding factors; and many others. Of course, the statements in support of wheat suffer the same shortcomings. And many of the assertions are made without any backup from the historical record. For example, sea vegetables are not a food that only the Japanese began to eat in quantity, and then only in recent times. Coastal peoples throughout the world have used them for many centuries.
Annie, yup. You wrote what I was thinking. So much assertion of unknowable things.
Qualitative? In terms of say, the Hunzas … there isn’t much data. But in terms of the China Study … it is much more studied. Also the Japanese mountain people. They exist NOW and aren’t hard to find or hard to study.
In terms of ancient peoples … we are getting good data now too. The plaque off Neanderthal’s teeth, or the contents of Oetzi’s stomach … yeah, we are understanding exactly what they were eating. The Romans kept records of what they fed their slaves, and we have the bones of the slaves to compare to. And of the nobles (a lot of them are full of lead!). The railroads in the 1800’s have exactly what they fed to their workers too, and loads of data about illnesses.
It’s basically an exciting time, I think. A lot of research is finally coming to a kind of “universal field theorem” of human nutrition. I’m not sure anyone knows where it will lead. Like Denise, I’ve gone down a lot of tracks in studying this, and I’m certainly not going to say “Hey, but THIS TIME I’m right!”. We should share though, because that’s how we get to the next step.
Absolutely, the statement I flagged as qualitative is exactly that. There are reams of data on many populations, but that does not make the statement. “the healthiest populations eat the least wheat” any less qualitative. Healthiest in terms of what criteria? Which populations were evaluated and by what criteria? Is there a positive correlation between quantity of wheat consumed and “healthiness”? If so, is it statistically significant? Is there a tabular or graphic illustration of the correlation? If such a correlation exists, what confounding factors may have influenced it? The statement as it was made is a classic illustration of a qualitative statement on the subject of diet and health.
“Is there a positive correlation between quantity of wheat consumed and “healthiness”? If so, is it statistically significant? Is there a tabular or graphic illustration of the correlation? If such a correlation exists, what confounding factors may have influenced it?”
And the problem is that the discussion around the qualitative statement usually goes like this:
Person A: Studies and published observations show that whole grains are considerably healthier than refined grains and refined grains tend to promote degenerative diseases.
Person B: There is evidence that wheat promotes chronic disease.
Person A: No, you found evidence that refined white flour promotes chronic disease. But we already knew that.
Repeat ad nauseam.
“Which populations were evaluated and by what criteria? Is there a positive correlation between quantity of wheat consumed and “healthiness”? If so, is it statistically significant?”
I’m basically pointing you to Denise’s excellent (and detailed) analysis of the China Study. There are books and studies that say more or less the same thing, though yes, most of them are not so detailed. The China Study though was of a large population, eating largely homegrown foods, in towns where the population typically ate the same kinds of foods day in and day out. Denise crunched the numbers. She does have the results.
“Wowza! By the way, wheat flour also correlates significantly with hypertensive heart disease and stroke, but I’m mainly going to look at coronary heart disease in this post. (And although wheat looks like it could have a nonlinear relationship with heart disease, with the highest wheat eaters having disproportionately steeper rates than non-wheat eaters, I’m going to treat it as linear for the sake of this analysis. That way, the worst that’ll happen is we’ll underestimate the potential effect of wheat, which—for now—is better than overestimating it.)”
http://rawfoodsos.com/2010/09/02/the-china-study-wheat-and-heart-disease-oh-my/
http://rawfoodsos.com/the-china-study/
I expect there will be a lot more hard data in the next decade or so, esp. as so many people are doing their various “diet experiments”. All those n=1 experiments do add up eventually. There have been some interesting studies though, done on correlations between, say, anti-gliadin IgA and the prevalence of certain diseases. Or the percentage of people whose symptoms get better on a non-wheat diet even though they are not celiac. Anyway, they are detailed and there are dozens of them.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4015193/
https://med.virginia.edu/ginutrition/wp-content/uploads/sites/199/2014/06/Parrish-June-15-2.pdf
Duck, you say to Heathertwist: “…One could easily create any narrative they wanted to with such vague clues. I’ve often wondered if the whole point of Paleo™ is to base a particular diet on extremely ambiguous data.” This to sum up your words on Oetzi, how there are many factors, not just diet, that affected his health…”
We can say the same about early grains! Even early grains may well have been much less healthy for us than a hunter-gatherer diet.
In an earlier post, you say: “…cultures that thrived on, revered and worshiped wheat…” Duck, we don’t need to fact-check your comment to know that the “thrived on” assertion is unknowable at best. And certainly suspect.
No question, the Ag Rev allowed humans to civilize. Our planet’s population explored 2500x since then. But because calories became much easier and more reliably available doesn’t mean they made us *healthier.* We have evidence for the opposite:
http://www.ncbi.nlm.nih.gov/pubmed/21507735
“…empirical studies of societies shifting subsistence from foraging to primary food production have found evidence for deteriorating health from an increase in infectious and dental disease and a rise in nutritional deficiencies…”
And this from Pulitzer-Prize winning anthropologist Jared Diamond (http://www.ditext.com/diamond/mistake.html):
“…The farmers gained cheap calories at the cost of poor nutrition, (today just three high-carbohydrate plants — wheat, rice, and corn — provide the bulk of the calories consumed by the human species, yet each one is deficient in certain vitamins or amino acids essential to life.)…”
Duck, about this you say:
“… Prescribed by Hippocrates, Paracelsus, Avicenna, Aristotle, favored by the Spartans, the Greeks and the Romans, and observed by countless scholars who wrote about its health effects. In every single instance, throughout Western history, wheat was unanimously considered to be the healthiest of all foods by the most prominent medical authorities—and this sentiment existed until the industrial revolution…”
Even if fact-checking bore out your high-flown assertions, should anyone be surprised if early prominents did extol wheat’s virtues? If you had a choice to eat nutritionally inferior food or to starve to death, which would you choose? That quickly became the option in many places after the Ag Rev when human population started exploding and developing large permanent communities, creating an absolute need for the most abundant reliable easiest-to-obtain calories. No government could possibly recommend against wheat–even to the current day. And of course the medical authorities from Hippocrates on up to the 1970s when the McGovern Committee developed the US’s disastrous dietary guidelines, they all lacked sufficient data on wheat to make properly informed pronouncements on it. Back in the day, they lacked blood serum tests to measure inflammation biomarkers, they lacked sophisticated IT to do large epidemiological studies, they lacked the basic nutritional biochem we know today. People usually didn’t live long enough for chronic disease to clearly manifest–until the past century. I submit to you that, over the 10–12k years from the Ag Rev, only now are we able to begin to properly assess wheat’s true health effects–even apart from all the processing such as fortification–which you so correctly point out.
heathertwist said: “or the contents of Oetzi’s stomach … yeah, we are understanding exactly what they were eating”
I think the problem is concluding skeleton/health conditions based on mainly diet when other factors are known to have a significant, or even greater, effect on bone and joint health. Many ancient civilizations and cultures had to deal with famines and plagues, and dental attrition which promoted abscesses and infections, and poor growth, etc. all of which may have had a significant effect on their skeletal remains and health. To link those problems to mainly diet alone can be more than a little misleading.
Case in point, it’s been insinuated that Otzi’s poor health and skeletal remains may have been due to his diet. However, Otzi was known to have dental attrition, was genetically pre-disposed to heart disease, and a rather serious infection (possibly the oldest known case of Lyme disease) that may be linked to poor skeletal and joint status. His diet was the least of his problems. He was a very sick individual.
One could easily create any narrative they wanted to with such vague clues. I’ve often wondered if the whole point of Paleo™ is to base a particular diet on extremely ambiguous data.
“We can say the same about early grains!”
Of course. I only pointed out the historical and written evidence to show that the anti-grain evidence is inconclusive at best, and misleading at worst. Nobody can ever really prove anything one way or the other. Though, I doubt it helps anyone to only have an anti-grain sentiment given the extremely vague data we are dealing with.
“Even if fact-checking bore out your high-flown assertions”
Please. I’ve already given the sources here.
Do note the references showing that bread, and specifically wheat, was considered to be the healthiest of all foods right up until the mid-19th century when plenty of other foods were available. The idea that grains are an ideal food is not just an ancient belief. The belief lasted right up until the industrial revolution when prominent scientists like Carl von Linné (1757) and Thomas Hodgkin (1841) documented the well known health promoting effects of (wheat) bread. It hardly seems like something we should easily dismiss—we’re talking about actual written opinions based on actual observations, all spanning thousands of years.
“People usually didn’t live long enough for chronic disease to clearly manifest–until the past century”
Let’s not conflate life expectancy at birth with life span. Hippocrates lived to between 83 and 90 years of age. Aristotle lived to 62. Von Linné lived to 70. Medieval scholars had an average lifespan of 59–84.3 years in the Middle East and 69–75 in Islamic Spain. New England colonists had lifespans of 62-65 years. Is that not long enough for chronic disease to clearly manifest? Spoiler alert. Eventually we all die. 🙂
Duck, very interesting observations on wheat, thanks for your comments. A few questions if you have some time.
1. Do you think that white flour is a problem and whole wheat is ok, or it doesn’t matter, any wheat flour is ok? Perhaps the milling process is what makes the difference?
2. I’m curious, do you have any theory on why americans are getting fatter and fatter and more and more people world wide are having Diabetes? If it’s not wheat, then what? Do you blame sugar or simply too much calories? and if it’s increased caloric intake, why did it happen?
Thanks.
It should be painfully obvious by now that unsaturated oils are the driving factor in the obesity AND disease epidemic. Secondary would be added food fillers such as fortification, lecithins, gums, dyes, etc.
Bottom line, if you eat real food and real food ingredients, life will be ok.
Zach, what is real food? is sugar real food? is flour real food? Is broccoli real? And if whole grains that are milled are real food, then why oil extraction from grains is not real food?
Hi Anna. I surfed through the forum (yet again) this time to revisit your other comments, including your exchange with Neisy. So I’m smiling in the possibility you include rhetorical elements in your questions to Duck’n’Zach 🙂
In any case, why don’t I take a crack at your Qs?
About your Zach Qs, it’s hard to know exactly what he means when he says “unsaturated” oil. Does he include the monounsaturates which, after all, qualify as “unsaturated?” Including that Mediterranean Diet darling, olive oil? From my reading and tracking my food and health numbers for the past nine years, I’m quite disposed to the idea that an overabundance of omega-6s polys you usu find in the SAD (Standard American Diet) could be raising systemic inflammation and setting the table for chronic disease. Legume/nut/seed oils (e.g. from soybean, peanut, corn, and sunflower seed) are exceptionally high in omega-6 (w6) and these are products most people consumed till researchers devised cost-effective ways to extract these oils in the late19th c and turn of the last century. Before then, people mainly used lard and suet (tallow). In this sense, what Zach may mean by “real food” is a food that has not undergo novel refinements, such as those hexane-processed high w6 oils which he may consider to not be “real foods.” But of course Zach should answer for himself. Back to olive oil, it has a long history and it is relatively low in w6. I used it almost every day. I get extensive blood panels every three months and check my blood sugars throughout the day, and all my number remain quietly in the normal zone, and I’m now 55. Many of my numbers were well out of whack when I was 46 and was diag’ed T2D. These have since steadily improved, most of all my BGs, which are now normal (mostly 75–95 mg/dL), and my C-Reactive Protein, a popular biomarker for systemic chronic inflammation, which steadily dropped over 3 years from from 4.6 (inflammatory) to 0.6 (anti-inflammatory). In fact, all my blood panel numbers are now normal.
As for your Duck Qs, my take is that we should regard warily *all* wheat flour. White flour, for the very fast carbs/gluten/lectins and loss of nutrients replaced by fortification plus chemicals introduced in its processing, the potential downsides of which Duck amply covers through the forum (search on “fortification”) Whole wheat includes the bran and comes with its own concerns, e.g. phytic acid that, in your GI, can steal essential minerals from your food. Though some will argue that, in the case of iron which we too often get too much of, phytic acid could be a *good* thing. You can find detailed explorations of this here: http://www.marksdailyapple.com/why-grains-are-unhealthy/ and of course in Wheat Belly and Grain Brain. For my part, I quit grains early on (2007) simply because grains are high in carbs–long before I faced the additional health questions of gluten, hemoagglutenating lectins, and phytic acid. I wrote a spreadsheet to track my meals, keyed detailed nutrient data into it from the USDA Nutrient Database (a tremendous resource if you get a chance to play with with it: http://ndb.nal.usda.gov/ndb/foods), and found I could easily get all my micronutrients (vits + mins) without eating a single grain. Again Anna this is just my n=1. Please get as many health checks as you can, as often as you can. I can make specific suggestion for you on that if you want.
Finally your Q on why Americans are getting fatter and fatter and more and more people around the world are developing diabetes. I suspect this is very multifactorial, going way behind wheat and the threadbare “too-much-food/too-little-exercise” trope. We live in an unprecedented bewildering era of change. America was already well on its way to becoming sedentary in the 1950s/60s, and still much slimmer then. HFCS arrived to the US in 1975, and we kept upsizing sugar water esp since HFCS was so cheap. Chemical companies also keep creating new compounds, many of which are estrogenic and so promote metabolic syndrome–I can give you the proposed mechanistic chain for that for you if you want. Then there’s widespread use of antibiotics which can profoundly disrupt our microbiome, more and more violation of our circadian rhythms through working night shifts, and many many many other factors. Mark’s Daily Apple does an excellent job discussing these elements, http://www.marksdailyapple.com. And of course, I look forward to Zach and Duck’s answers, should they decide to respond to your questions.
Hi, Anna. To respond, I suppose real food would constitute foods that we can consume and get a net positive in terms of nutrition and also that are unadulterated with man made substances, i.e. they came from nature and required little to no preperation to eat. I would say that use of fire for cooking, rocks for pulverizing, water for soaking, etc is probably as far as one should go for prep.
So to answer your questions, no I don’t think that refined sugar or refined grains should be considered food, yes they are edible and give us calories but in terms of health, they are a net negative. Natural sources of sugar however (honey, cane, maple, etc) are probably healthy, same for whole grains which require little more than a rock, water and heat to eat.
Oils are anempty calorie and net negative. Before the industrial age, oil was hardly ever consumed and rendered fats were the norm. Of course it’s not completely black and white and not all oils are created equal. I would take an expeller pressed oil from a whole real food (coconut, olive) over a machine and chemical solvent extracted oil from a non edible food any day. (Cotton seed, rape seed, canola, etc)
Zach, your definition of real foods is very subjective and biased.
I think if one would eat a lot of honey and maple syrup, it will have a similar effect of eating a lot of table sugar. Btw, one can make sugar with water, flame and rocks.
it’s highly debatable what “net positive” is in terms of nutrition. We can’t possibly know how to calculate this.
Most of the veggies we eat are modified and bread by humans and required much more then water flame and rocks.
You can have expeller pressed canola oil, would it make it healthy? It has lots of omega-3s and some people consider it healthier then olive oil:
http://www.rd.com/health/the-great-olive-oil-misconception-dr-ornish-responds/
Whatevers clever, you can worry and fret, I’ll eat the grains and sugars and be lean, energetic and happy.
Done with this blog till the next post, love the carb love!
Zach, all the best to you. Too bad you avoided the discussion.
Bryan, thanks for your reply 🙂
To your point about fats, Zach doesn’t seem to like detailed discussions and precise definitions. It’s easier to debate this way.
You can see my view of why the world is getting fatter and fatter in my reply to Duck. It’s somewhat similar to yours. I’m not convinced about antibiotics because I’ve met many people who basically eat them for food, yet are very thin.
Thanks for sharing your health history, my experience was very similar, although I didn’t have diabetes or major health issues. I certainly feel healthier and more energized eating LC, even compared to whole soaked sprouted grains/nuts and freshly milled oats ala dr. Price. And I have objective markers to back it up. My fasting insulin is 1.8, triglycerides are 40, down from 135, CRP is 0.4. So high fat diet hasn’t increased my inflammation markers.
What other tests or health checks do you routinely do? Have you ever tested your leptin level?
As you’ve seen from my previous posts, thanks for reading btw, I’m leaning towards thinking that
CR and protein restriction matters more then the type of nutrients for the most part and if one has a metabolism that’s not damaged. But subjectively I enjoy LCHF diet more then HCLF (I prefer bacon to beans) and it’s easier for me to maintain it. For me LCHF is naturally CR and hunger is very rarely present compared to HC, when I felt the need to snack all the time.
How many carbs do you eat normally? And what do you think about ketosis long term?
Thanks!
Hi Anna, you’re very welcome. I like your style 🙂
About Zach, if you search for my handle in this forum, you’ll see the exchanges I had with him earlier and then finally put an end to, concluding it was a sheer waste of time. I find it’s pointless to argue with anyone who’s long on religious fervor and testosterone and short on science. Zach doesn’t want an genuine discussion and sharing of ideas that don’t jibe with his own. He just wants to beat into you how great HCLF is and how everyone should do it.
About what you say: “I’m not convinced about antibiotics because I’ve met many people who basically eat them for food,…” When you get a chance maybe clarify that? At the moment I’m picturing waifs honking down handfuls of Cipro caps 🙂
Once I left grains (July 2007) I left them totally, not even trying things like fermented teff which seems to work well for Ethiopians. That’s not because I harbor an anti-grain dogma–I don’t–as I’ve explained in posts to Duck and others. It’s only because I’ve never felt a compelling need to seek out fermented heirloom grains. My grain-free LCHF foodway, mainly organic and pasture-raised locally produced foods, satisfies me utterly. But I’m certainly open to trying fermented heirloom grains and see how I fare with them. I completely agree that CR transcends the HCLF/LCHF debates–esp for people who are not yet deep into metabolic syndrome.
About my carb intake, I usu eat ~40–80g per day. Some days it’s zero (fasting), Occasionally up to 100-120 grams during the summer when the high-sugar fruits ripen. In the latter case, I just put up with my higher BGs (110–135 post-prandrial)
About ketosis long-term, I simply haven’t seen a compelling argument against it.The only reason to eat carbs is for the glucose, and our bods make plenty for our needs, esp from excess protein. ~ 75% of the excess protein we eat, our liver makes glucose out of it. The only exception is when doing extended resistance training, like free weights at the gym, working out regularly to fail, trying to put on muscle mass. In that case I found I needed to chow a high-fast-carb meal within 45m after the workout in order to continue to grow muscle mass. In those cases, my post-meal BGs would often be in the 60s, even after a 100+ g carb meal! But this post-resistance recovery meal is the ONLY exception I’ve found for me for eating carbs.
Most of all, Anna, I’m very glad you get plenty of health tests. I truly feel that’s our best shot to learn what actually works for us. There’s so little true science out there, and of course it can’t account for individual metabolic diffs. I’m still eager to read research papers and listen to people steeped in the field, be they formerly credentialed folks or autodidacts. But ultimately it is for the ideas, for things to investigate further and to try. You also find plenty of caveats and shortcoming in the tests, but you learn to cross-ref your results, not to read too much into any one result. In this fashion we straggle and crawl toward something that might resemble the truth 🙂
For my tests, at home I check weight/BF%/BP/HR in the morning, and test BGs 4x/day, including at peak post-meal times. For blood panels, beyond the usual CBC, lipid panel, liver and kidney enzymes, etc. lineup, I get these:
– C Reactive Protein. Which you get. Congrats on your anti-inflamm 0.4!
– Hemoglobin A1c. Avg blood sugar over 60–90 days. Useful because you can have a normal FBG and still too-high post-prandrial BGs. Ideally <5.0%
– C Peptide. Proxy for basal serum insulin. S/b <1 ng/L adj
– Iron panel (TIBC, Transferrin, etc), since systemic iron overload *is* a common prob, and I eat meat and cook in cast iron
– T3 and T4 for Thyroid. TSH can give a false reading.
– Mercury. Get one to check, then repeat IF you eat a lot of fish high up on the thophic scale, e.g. tuna, king mackerel.
– Consider for other heavy metals too, e.g. lead, cadmium, selenium. If you eat lots of shellfish and esp if you eat lots of Brazil Nuts, you may want to check selenium.
About Lipid testing: the current standard is woefully inadequate and uninformative. It measures just total trigs and c'stol, and gives no idea of the number of size of the lipoproteins these lipids travel in though serum. Many researchers consider certain of the lipoproteins–not their lipid cargos–to be the actual atherogenic elements coursing through our blood. Esp older, smaller more highly oxidized LDL and–yes–HDL–lipos. The current direct-lipo measure tests like VAP and NMR may still not be ready for prime-time. Mark Sisson discusses them here: http://www.marksdailyapple.com/how-to-interpret-advanced-cholesterol-test-results His post is already a few years old, but it's a good starting point.
Finally about leptin. I haven’t been able to wheedle this out of my doc, but I admit I haven’t pressed that hard either. I fast frequently (18h–3d) and almost never feel an acute desire to eat. At this point I can go pretty much as long as I want without eating, and feel fine, though I don’t see a point to go beyond three days. –Bryan
Bottom line bro is that you feel the need to writ short story sized posts that I bet are directly inverse to how healthy you are. I have great health and don’t feel the need to argue or post a mountain of studies yo get my point across.
I have read mountains of information and none of it makes a hill of beans compared to achieving true health. True health comes from being able to utilize carbohydrates, plain and simple. One can never be truly healthy restricting calories or carbs. Sorry but that’s the plain truth. You guys and girls restricting macros, fasting, searching out heirloom fermented teff (lol) will never experience true health until you get to the root issue of being under carbed.
Sure Zach. How you feel, etc.
Zach, my carb deprived brain can’t handle your comments full of assumptions, vague statements and lack of coherent thought process or quality references. May be my brain doesn’t have enough glucose to truly understand your point. So I hope you forgive me that I will not reply any further to your comments. Let’s agree to disagree.
Bryan, thanks for Zach warning 🙂
To clarify my antibiotic point, it was a gross exaggeration on my part. I meant to say that they take antibiotics so often, it’s almost like food. I think the gut flora influence on our health is grossly exaggerated as well. It’s a new FAD. I’m not saying it doesn’t matter, I’m saying it doesn’t matter as much for the vast majority of people compared with other abuses they take, especially metabolic syndrome.
My concern about ketosis is the lack of test subjects, so to speak. Inuits being a strange genetic exception, no population has subsisted in a constant ketosis for a prolonged amount of time, so we simply don’t know. That’s why I try to stay on the edge of it, coming out of it periodically with protein and carb binges, which are fun anyway.
I’ve noticed similar results to yours after my resistance training, although I’ve never had BG in the 60th!
I used to test my BG often, I’ve kind of relaxed and stopped it now for the most part and test occasionally after a carb binge to see it around 135-145.
I did ferritin testing as well, love cooking in cast iron! and had to do a few blood donations to bring it down to 80 from 140. I’ve heard lots of bad thing about iron, so trying to keep it at a lower range point.
I eat lots of sardines, salmon, shrimp, so not much large fish at all, thanks.
Also, how do you check for selenium? do you mean too much of it? I don’t eat much nuts, but take selenium 1xweek.
I agree on cholesterol testing, I don’t put much faith in it at all.
Thanks!
Hi Anna. Glad to save you some time and frustration 🙂
About antibiotics, those are one of the very many novel inputs in our lives that came along post WWII. Starting ~ decade ago, researchers started showing great interest in it as shown here: http://hmpdacc.org/ Michael Pollan wrote a compelling piece on it too:
http://www.nytimes.com/2013/05/19/magazine/say-hello-to-the-100-trillion-bacteria-that-make-up-your-microbiome.html
There’s some though that gut microbes help mediate insulin response and blood sugars though it’s mostly correlative at this point, such as what you read here:
http://www.the-scientist.com/?articles.view/articleNo/41033/title/Sugar-Substitutes–Gut-Bacteria–and-Glucose-Intolerance/
Mechanistically flora mediating BGs and insulin response is a plausible idea because so much of proper blood sugar regulation is about proper *signaling.* You can have plenty of insulin output and even decent insulin sensitivity, and still have BG issues.
You can think of our bods as a large corporation and those trillions of microbes as little temps workers which our bod gives room and board and “hires” and “fires” at will depending on the specific and ever-changing tasks it needs done.
About persistent ketosis, you’re right we haven’t seen much of it in the Ag Age starting ~12k years ago. We have many questions, many of which research may never be able to answer. E.g. can we all still thrive in persistent ketosis? If not, did some of permanently lose the ability to thrive in persistent ketosis since the dawn of Ag, e.g. through one or several SNP mutations? Or can those Ketosis intolerant people become tolerant once their gut microbiome adjusts. As for the Inuit’s genetic exception, I hope people don’t read too much into that. The Inuit may be much closer to us than some believe. Just because the Inuit have SNP variants that *may* (and I emphasize *may* since we have not directly tested this) preferentially direct dietary fat to skeletal muscle and brown adipose tissue doesn’t means the rest of the world will fare poorly on a high fat diet. E.g. it could be we have evolved more robust ways to vet dietary fat in the GI and send the excess to the exit, i.e. not bring it systemic. Bottom line, again, keep observing your own experience. I’ve been in steady ketosis almost nine years. I still regularly get as many tests as I can and monitor myself, and have been doing and feeling terrific.
About my low post-resistance-training BGs, they may have been a combo of keen insulin sensitivity brought on by my intense 90–120 minute workouts and my unstable sugar control due to my early and mild diabetes. It’s not uncommon for early diabetics to get slight hypos even without taking meds. Again, that could be due in part to bad signaling, possibly from unbalanced gut biome. Fortunately, I never get the “feak and weebles” unless my BG dropped below ~44 mg/dL, which happened only a handful of times. When I stopped taking supps, including chromium picolinate, I stopped getting those super low BGs.
About the fish you eat, excellent! Funny how many fish low on the food chain are also high in Omega-3, like the salmon and sardines you eat, herring, smelt, and other cold-water species. I eat shrimp too when I can find it (and afford it) wild. I totally avoid farmed raised shrimp as those ponds are often polluted, sometimes with heavy metal laden effluent from factories, esp in China. See Taras Grescoe’s book “Bottomfeeder” for scary details on that.
About serum selenium, I don’t check for it because I stopped taking all supplements in 2009–I could fill a book with the reasons why I stopped supps!–and I limit the only food source that’s outrageously high in selenium, which are Brazil Nuts. Selenium’s one of the easier minerals to overdose on, and supp makers occasionally flub up the formulations with tragic results:
https://www.lawyersandsettlements.com/legal-news-articles/case/total-body/ –Bryan
Regardless of how you interpret their SNPs it would be at least worth pointing out that the Inuit have never been observed to be in ketosis.[1][2][3][4]
The one exception was Heinbecker showed in his follow-up experiments (in 1931 and 1932) that even (non-Pregnant/lactating) Eskimos who regularly ate carbohydrates had difficulty making ketones.*
Before their unique genetics were discovered, it was stated by the researchers that they were not in ketosis due to a high protein diet. However, the genetic evidence on CPT1a now explains why they had difficulty producing ketones and why Inuit children have difficulty fasting. (aka “hypoketotic hypoglycemia”).
Anyhow, I think it’s worth pointing out to Anna that the Inuit are not an example of a population in perpetual ketosis. They clearly metabolize fats differently than we do and they do not exhibit ketosis as we do.
* Pregnant/lactating women have exaggerated ketone production and the pregnant/lactating Eskimos in Heinbecker’s experiments made more ketones, while fasting, but were still well below what we would expect from pregnant/lactating women.
Hi Duck. What you say here: “I think it’s worth pointing out … the Inuit are not an example of a population in perpetual ketosis.” So far I’m left with a much different impression. That 1972 paper suggests the test subject Inuit *are* indeed ketotic.
It’s important to note someone could be in ketosis *at relatively low serum ketone levels.* Just like certain lucky folks can be in glycolysis and still enjoy low blood glucose levels. It’s possible that, due to his/her genetic variants and/or other adaptations and conditions, an Inuk may well be in ketosis even when serum ketone levels appear relatively low–low enough to show negative on test strips.
For the record, here’s a couple of ketosis defs: WebMD defines it as “…a normal metabolic process… your body … burns fat instead [of carbs]…”
http://www.webmd.com/diabetes/type-1-diabetes-guide/what-is-ketosis. The Wiki (http://en.wikipedia.org/wiki/Ketosis) says: “Ketosis is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood…”
OK, back to that 1972 paper. It has the most recent research of your links. http://ajcn.nutrition.org/content/25/8/737.full.pdf I started with it with the idea that study results are the most accurate due to ongoing improvements in medical testing and diagnostics.
Duck, the paper never mentions “ketosis” or “glycolysis.” But the authors sure do imply ketosis. They say “…[The negative ketone body test result] does not preclude an increase in ketone body production during this time…” and “…the Eskimos had high serum FFA and low glucose levels (approximately 65 mg/100 ml) indicated that free fatty acids played a major role in body energy production…” Reading this, given their high level of serum FFAs, the subjects sure don’t seem glycolytic. What else could they be then except ketotic? –Bryan
Bryan, I’m well aware that they burn a lot of FFAs in other areas of their bodies. And I’m aware of ketoadaptions. But the genetics clearly explain how they could not burn much FFAs in their livers like we do—they literally have a deficiency of the liver enzymes to do this—hence their known tendency for hypoketotic hypoglycemia.
wbryanh said: “Reading this, given their high level of serum FFAs, the subjects sure don’t seem glycolytic. What else could they be then except ketotic?”
No one denies that they burn a lot of fat for heat. But the point being that their livers appear to be protected (or at least spared) from metabolizing a lot of FFAs due to their CPT1a mutations. They just don’t do ketosis like we do. And the studies show this as well. They evolved differently than we did, due to their harsh climate.
Duck, let’s be clear. Your evidence, however interesting, in NO WAY indicts persistent ketosis. Your assertions “the Inuit have never been observed to be in ketosis…” and “…the Inuit are not an example of a population in perpetual ketosis.” are misleading at best, and most likely wrong. Inuit on VLC foodways most likely *are* in persistent ketosis. You even lean toward that in places. E.g. in your previous post you appear to contradict yourself by saying: “…[The Inuit] just don’t do ketosis like we do.”
Persistent ketosis may well remain a terrific option for Inuit and non-Inuit alike. Here’s why:
In their 1972 report–by far the most relevant of the five links you supply–fully describes ketosis, however “hypoketotic” it may be. http://ajcn.nutrition.org/content/25/8/737.long
Ho et al observed in the serum of those 168 Inuit “high FFAs” [free fatty acids], and “low BGs.” Sorry, Duck, but that’s ketosis. The only other energy-burning option is glycolysis, and given the high serum FFAs in these healthy test subjects, it sure isn’t glycolysis. Even the authors allow their results “do not preclude an increase in ketone body production during this time. Again, Duck, someone can be in ketosis even *at relatively low serum ketone levels* so long as glucose is not their primary fuel at that time.
What you say here: “…their livers appear to be protected (or at least spared) from metabolizing a lot of FFAs due to their CPT1a mutations…” You imply that that CPT1a mutation somehow evolved with the aim to prevent overloading and burdening the liver with FFAs. Please remember Duck this implication reflects your opinion. *It is not fact*. Even for folks lacking the CPT1a variant, you’ll find little evidence that a ketotic diet, even long term, burdens and harms their livers. There’s plenty of evidence to suggest a long-term ketotic diet does not harm the liver at all: e.g. here: http://www.hopkinschildrens.org/high-fat-ketogenic-diet-to-control-seizures-is-safe-over-long-term.aspx Duck if you can present strong evidence to the contrary, I’ll gladly stand corrected. The Inuit CPT1a variant may have evolved for reason having nothing to do with purported liver sparing. Many ancestrally-living Inuit lived on subsistence VLC foodways in intensely cold environments requiring huge amounts of calories just to generate enough thermal energy to survive. It’s quite plausible that CPT1a may have stuck in order to direct more FFAs to the skeletal muscle and brown adipose tissue. We simply can’t say for sure what specific selection pressures drove the spread of this variant in the Inuit.
Bottom line (again!): Whatever foodway–HCLF, HFLC, “Swampland,” whatever–get regularly tested and see how you are doing. If anyone happens to have any qualms about persistent ketosis, please regularly test your liver enzymes and your blood for FFAs and ketone bodies. Get a ketone testing meter or ketone test strips. Easy enough to do. You absolutely shouldn’t let these Inuit studies dissuade you from exploring any foodway, including VLC. The still meager, poorly understood, and caveat-filled results we see from the Inuit studies–many from 70 or more years ago–no way confirms or even strongly suggests any danger of persistent ketosis for us. –Bryan
Relax, Bryan.. Nowhere in my comment did I ever say that the Inuit didn’t burn FFAs. And nowhere in my comment did I ever say this proves anything good or bad about ketosis. I could care less.
All I said is that they don’t do ketosis like Westerners do.
Do you deny that most Inuit have CPT1a deficiencies? Do you deny that a CPT1a deficiency tends to cause hypoketotic hypoglycemia?
That’s just what the research says about the Inuit. That’s all I’m pointing out. They do ketosis differently from the way we do. That’s all.
Duck why do you ask me these two questions?:
“Do you deny that most Inuit have CPT1a deficiencies? Do you deny that a CPT1a deficiency tends to cause hypoketotic hypoglycemia?”
If you had read my post carefully, you’d know I don’t deny either one.
What is your point? How are these relevant to the main message. That we should feel free and safe to experiment with persistent ketosis?
Bryan said: “Duck why do you ask me these two questions? If you had read my post carefully, you’d know I don’t deny either one.”
Ok.. just wasn’t sure if you were acknowledging it or not. Understood.
Bryan said: “What is your point? How are these relevant to the main message. That we should feel free and safe to experiment with persistent ketosis?”
Yes, people should feel free to experiment, if they wish. They just shouldn’t be doing it under the pretense that they will be burning fats like the Inuit do. The Inuit are not an example of what happens in Western metabolisms.
…Also, many studies point out that the Inuit also ate considerable quantities of protein, and apparently have enlarged livers (which happens to be a symptom of CPT1a) with increased capacity for gluconeogenesis, which is originally why the old researchers did not believe they were in ketosis, despite burning lots of FFAs throughout their bodies. As multiple studies have pointed out, the ratios of fatty-acid to glucose were observed to be well below the generally accepted level of ketogenesis. [1][2][3][4]
But, I agree, people should experiment if they want to. They should just understand that they are going to burn FFAs differently from the Inuit. That doesn’t make ketosis good or bad, of course.
Maybe many/most non-Inuit can handle a persistent ketogenic diet *better* than the Inuit. As ironic as that sounds, given the ancestral Inuit’s VLC foodway.
There’s little evidence to show that ketosis burdens the livers of people in the Western developed world. Even though we generally lack the CPT1a variant that appears to be more common in the Inuit.
Bryan said: “Maybe many/most non-Inuit can handle a persistent ketogenic diet *better* than the Inuit. As ironic as that sounds, given the ancestral Inuit’s VLC foodway.”
lol.. That’s certainly a perspective I’ve never heard before. 🙂
Bryan said: “There’s little evidence to show that ketosis burdens the livers of people in the Western developed world.”
I wouldn’t know. Has it really been that well studied? I do remember Tolstoi in 1936 tested Stef and Andersen’s glucose response after their year-long Bellevue experiment and found they had a “false diagnosis of diabetes” that tends to happen after a long fast (i.e. very poor glucose control and/or physiological insulin resistance). That seems to be a temporary and normal response to fasting/ketosis as far as I know.
Perhaps it’s no big deal and soon reverses after some time on a varied diet. But, I’m not sure anyone really knows the long term consequences of it. Probably something people should at least be aware of.
I just (superficially) tried to find a link about this, but couldn’t find anything off hand- (it takes time, which I just don’t have right at this moment). However, I do know that Dr.’s Phinney and Volek have done some long term testing with low carb diets, and found no harm. They write about some of this in their book “The Art and Science of Low Carbohydrate Living”. In addition, there are several doctors who have been in long term ketosis; I know Dr. Phinney himself, and I believe Dr. Volek also. And, Dr. Eric Westman has been on a long term ketogenic diet- (he mentions it in his debate with Dr. Colin Campbell, which is on You Tube). These people seem to be in pretty good health, and they are doctors, so they must be aware of their health markers. There is also a book called “Ketopia” (which I haven’t read, though it sounds interesting). This is also about ketogenic diets, all the health benefits, and long term effects I believe.
Having said all that, I will admit that constant ketosis may not be the best thing for everyone. Children can generally make metabolic adaptations pretty quickly, but some adults may have difficulty if it’s not what they’re used to. However, it does appear that many people thrive on a ketogenic diet.
The modern evidence we have for ketogenic diets are clinical studies which are overwhelmingly either positive or neutral on them. We don’t have epidemiological studies on them, but not sure how much that even matters. Epidemiological studies have debatable value given their inherently correlative nature and issues of self-reporting.
Most people who want to try a persistent ketosis foodway should have no compunctions whatsoever! Go for it!
Duck, right? That’d be funny if we (assuming you are not Inuit) *did* handle ketosis better than those far Northern peoples. But the more we discuss and analyze this issue, the more I’m thinking it’s plausible. We may have the advantages, e.g. adequate persistent ketone levels, with no apparent downsides, at least none broadly documented. I can’t speak to the 1936 Stef and Andersen experience, but I can speak about my own in 2015. I am in persistent ketosis and even then, my BGs can start to float stubbornly higher, likely due in part to my marginal insulin output. In such a case I fast anywhere from 18h to three days, however long it takes to push me back onto the “right side of the metabolic divide.” Fasting always corrected my BGs, and it appears to be getting more effective. When I first started fasting in 2009, for a few years I used to have to occasionally do 2- and 3-day fasts to get the desired effect. But since ~2012, 18h fasts has been reliably doing the trick, and even these I need to do less and less. –Bryan
Duck,
I know the whole Inuit/ketosis thing has been in the spotlight and is very controversial, so I’m not putting all my stakes on them being in ketosis.
Having said that, it’s their protein that they metabolize differently, that I find interesting. They have so much brown fat and are able to decouple lots of ATPs as free heat, so they could eat much more protein then us and still be in ketosis.
And if ketosis defined simplistically as burning and using mostly fat for fuel, they certainly were in ketosis. Their mutations may just affect how they get in and out of ketosis, not how they “do it” or stay in it.
I’d say there are more similarities then differences between how we and inuit burn FFA, after all we both evolved and have mitochondrion that can burn only carbs or fat for fuel. We burn most of the fat not in the liver anyway, so I think it’s very similar how we and inuit burn fat.
Morgana,
thanks for reminding me about Dr. Phinney, I meant to read his stuff and forgot.
Bryan,
what is the longest modern study of people in ketosis have you seen? preferably not epileptic kids, because their disease will screw the results anyway.
Anna said: “And if ketosis defined simplistically as burning and using mostly fat for fuel, they certainly were in ketosis. Their mutations may just affect how they get in and out of ketosis, not how they “do it” or stay in it.”
Well, according to Wikipedia, “Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood.”
Wikipedia also defines “ketone bodies” are defined as, “Ketone bodies are three water-soluble molecules that are produced by the liver from fatty acids during periods of low food intake (fasting) or carbohydrate restriction”
The article goes on to say, “Ketone bodies are produced from acetyl-CoA (see ketogenesis) mainly in the mitochondrial matrix of hepatocytes (liver tissue) when carbohydrates are so scarce that energy must be obtained from breaking down fatty acids”
So, no, I don’t believe that’s the actual definition of ketosis. The Inuit don’t do it like that.
Duck, technically you are correct, “Ketosis is a metabolic state where *most* of the body’s energy supply comes from ketone bodies”. Although I’m sure it’s debatable how “most” it is.
But ketone bodies are made mostly from FFA, some call ketones a byproduct of FFA metabolism. So in ketosis state our mitochondria uses ketones (made from FFA) and FFA (directly), so as I was saying in general terms, mitochondria is “using mostly fat for fuel”.
So I’m not sure what’s the argument here.
Anyway, if most of ketones are made in the liver, may be that’s why inuits’ liver is so enlarged? To produce more ketones? Idk.
But I still fail to see how they “do it” differently? both, us and them, burn ketones and FFA for energy while in ketosis. They may be able to get in and out easier, meaning their liver is more adapt at producing them, for example, or they have some other mechanism for additional ketone production, possibly.
But on a deep mitochondrial level we are exactly the same while in ketosis – we burn the same ketones and the same FFA to live.
“Anyway, if most of ketones are made in the liver, may be that’s why inuits’ liver is so enlarged? To produce more ketones? Idk.”
No. They do not produce more ketones. They struggle to produce ketones. As the research on CPT1a explains, the Inuit have difficulty producing ketones and this is why the Inuit can have difficulty fasting—particularly their children who tend to die of SIDS without regular breastfeeding around the clock. We don’t have difficulty fasting like that.
The mutation promotes “hypoketotic hypoglycemia” (low ketones, low blood sugar).
Anna said: “But I still fail to see how they “do it” differently? both, us and them, burn ketones and FFA for energy while in ketosis. .”
No.. the difference is that we burn “mostly” ketone bodies (acetoacetate and β-hydroxybutyrate) while they are known to have “extremely low levels of ketones”.
Anna,
I think Bryan had a rather accurate way of looking at it… Westerners appear to be “better” at ketosis than the Inuit.
It seems paradoxical, but I think Bryan is technically correct. The Inuit aren’t very good at producing ketones. But Westerners are quite good at it.
Duck, Anna–Anna I saw your recent comment and was thinking along your lines–this does seem like a distracting semantical snarl on “ketosis.” What does “ketosis” truly mean anyway? Duck, you pulled the def from the Wiki–not an unimpeachable source. But can I blame you? We can’t even find agreement on the def in the medical dictionaries. Many of those sources still imply it’s something pathological. Even doctors still confuse “ketosis” with “ketoacidosis.” We need to get past the surprisingly vague names of these metabolic states, which we use sloppily anyway. We often say “ketotic” to distinguish from the absence of the primacy of glycolysis. Maybe instead we should say “glycolysis” and “aglycolysis?”
In ant event, all that takes us away from the main question that triggered all the Inuit diet discussions. In search of what many of us want to know: Can we thrive on persistent LCHF? Even VLC?
The Inuit appear to do just that (with certain restrictions like freq child feeding) on VLC. Great. That’s a perfectly valid starting point for rest of us. Fellow humans being who diverged from us not so many thousands of years ago are up there in the Wild Blue North making VLC work. The Inuit are not from Mars. Genetically speaking we are still very very very very closely related. The fundamental mechanisms of energy production remain just the same. Our mitochondria oxidize glucose and beta-oxidize fats in just the same ways. It doesn’t at all mean we can’t take meaningful macronutrient lessons from the Inuit that we can effectively apply to our own lives. Their SNP variants appear to merely tweak the ketone body/FFA balance likely due to the Inuits’ special environment. So what if then that *may* make the Inuit not strictly “ketotic?”–whatever that means. So what if those with the CPT1a deficiency variant derive a greater proportion of their energy directly from the free fatty acids than non-variant VLCers? Our plasma albumin tows FFAs directly to the many types of cells that need the energy. Bypass the liver! Collect 200 ATPs!
Finally, let’s remember the idea that the Inuit with the CPT1a deficiency variant are “hypoketotic” Not “aketotic.” They are obviously producing *some* ketones. Plus that Wiki says the liver is the main but not the *sole* source of ketone bodies.
If anything, my recent discussions with you Duck makes me think that those of without the SNP variant may actually fare *better* on VLC than the Inuit. We have very little evidence that persistent VLC overloads and injures the liver. My little n=1 redux, I’ve been doing VLC it for over eight years. My extensive blood work has consistently improved in that time. Liver enzyme levels (AST, ALT, ALP) are always normal. –Bryan
What I haven’t heard here is any discussion of gluconeogenesis. Discover has a nice article about a lot of the issues with the Inuit:
http://discovermagazine.com/2004/oct/inuit-paradox
At one point I was in a group where a researcher with a zoo chimed in. She was saying that true carnivores are NOT “in ketosis” at all … they convert protein to glucose. Which isn’t efficient, but it works. If a lion or bobcat in a zoo is throwing ketones … it is ill and needs treatment.
She said the same is true for the Inuit. You maybe could find some other researcher and see if they agree. It may well be true that Europeans don’t have that ability so much, but the low-carb hunters probably would. Same as a lion.
Heathertwist said: “What I haven’t heard here is any discussion of gluconeogenesis”
Yes, exactly (actually I did mention it briefly). As I had mentioned in an earlier comment, all of the researchers who actually studied the Inuit firsthand (not talking about those who just wrote about them) believed that they were relying too heavily on gluconeogenesis to be in “ketosis”. They were eating far too much protein.
Their enlarged livers were believed to assist in gluconeogenesis beyond what Westerners can do. And their significant excretion of urea was also seen as evidence of this.
Actually there was a paper that was just published this past September that summarized all of the available Inuit research, and it too explained how they were a high protein culture that relied heavily on gluconeogenesis.
As you can see, they handle their food differently than we do. When white Arctic explorers lived with the Inuit, the white men had to eat a lot of fat and limit their protein to stay in ketosis. However, the Inuit were known to eat enormous quantities of meat, preferably dipped in fat. The point being that the Inuit did not limit their protein intake—they ate it constantly throughout the day to avoid fasting.
Interestingly, Stefannson never claimed that the Inuit ate 80% fat. In fact, his Inuit recipe for pemmican (when based on caribou rather than bison and the standard recepie was 2/3 lean caribou meat to only 1/3 melted fat) was relatively lean. LCHF Magasinet not only explained the Inuit/ketosis myth but they calculated the fat content of the Inuit pemmican would be less than 60%. You might get into mild ketosis if the fat content exeeds about 2/3 of calories, but but 60% wouldn’t achieve it even if the inuits ate 100% pemmican year around.
So, again, all of the evidence points to a high protein diet in the Inuit. They just weren’t eating enough fat to be in “ketosis”.
Duck, just curious, where’s the actual clinical proof that supports what you say about the Inuits’ “…enlarged livers…” and “…their significant excretion of urea…”?
I’ve been googling “Inuit liver autopsies” and “Inuit urine output” which so far turns up nothing except those comments from Harold Draper in Discover Mag and replicated elsewhere “recalling his 1970s studies.” Trouble is, I can’t find links to Draper’s actual studies. I’m not saying they don’t exist. Just saying I haven’t so far been able to find them.
Duck if you have links that prove what you assert, it’d be great if you post them here for us.
In the meantime, Duck, that new paper from Hardy et al is very interesting! Ever since I read Wrangham’s excellent little book “Catching Fire,” I’ve been following the research on the role starchy roots/tubers may have played in our pre Ag Rev evolution. Looking forward to digging into Hardy’s work. It’ll be a while till I have much to say on it. Most of the refs therein are books or stuck behind paywalls. At the moment, I’m ordering what cited pubs I can. Thanks –Bryan
Well, the Hardy paper references Kaleta, et al. 2012. But Harold Draper mentions increased urea in his 1977 paper. Both should be freely accessible.
I don’t know if Draper ever saw an Eskimo liver, but in his paper he just talks about urea clearance and high water intake with high protein.
CPT1a deficiency is known to cause enlarged livers, so I don’t doubt that they have them.
Of course, at the time, Draper didn’t know about their CPT1a mutations, but I’m sure he would have found that fascinating.
Draper mentions lack of fiber, but actually glycans in (raw?) animal tissue can be broken down by some bacteria (how meat is tenderized, for instance), so I imagine they had biomes similar to a carnivore might. They also ate rotting meats, a traditional delicacy which was claimed to offer health benefits.
???
Duck these don’t answer the question at all!
In the Draper paper, he says *nothing* about enlarged Inuit livers. Draper does say this about urea: “…their high-protein diet imposed on Eskimos a need to dispose of an unusually large metabolic load of urea…” But he doesn’t give a shred of evidence on how he determined that. It’s a completely unsupported comment.
In the Kaleta, et al. 2012 paper, I searched on “liver” and “urea” and came up with -nada-. Where are the relevant passages?
Again Duck… Where’s the actual clinical proof that supports what you say about the Inuits’ “…enlarged livers…” and “…their significant excretion of urea…”?
So far you’ve shown -NADA-
You made that assertion. It is reasonable for us to ask you to list the specific text that backs up your assertion. Duck, it is not asking too much of you. –Bryan
Bryan,
I specifically said that Draper never explained the evidence, beyond the very high urea excretion. See this quote from Discover Magazine, who interviewed Draper:
“Bigger livers”. At any rate, the high urea excretion is the byproduct of high protein intake.
I too could not find where Draper actually saw the bigger livers, but that’s what Draper appears to have told Discover when they interviewed him. Or perhaps Discover was getting their sources elsewhere. They are generally considered to be a reputable source, however.
Regardless, CPT1a deficiency is known to cause enlarged livers:
So, according to the NIH, enlarged livers is a common symptom of CPT1a deficiency.
So Duck, we’ve established you totally lack clinical evidence for Inuit having bigger livers. Or having to pee excessively. That your statement saying “Their enlarged livers … And their significant excretion of urea …” may well be complete nonsense. OK.
You cite an NIH paper that says “…People with CPT I deficiency can also have an enlarged liver…” We can chuck this out too. It’s only a general discussion that applies to all peoples with the deficiency, e.g. Hutterites as well as Inuit. It includes no evidence about enlarged Inuit livers. Duck if we buy your argument that “The Inuit are different from us” shouldn’t we then avoid to assume their livers will respond like ours to that deficiency?
Actually this is fascinating discussion. For years I’ve heard these “Inuit enlarged liver, Inuit pee a lot” factoids, you being the latest purveyor of them. I never questioned them till now. Now I find out we have no true evidence for them after all! I can regard this as the latest stool of med-anthro bullsh*t to scoop away till someone does real actual observations on the Inuit and their livers and urinary patterns. Thanks for this. –Bryan
Bryan, I found it!
It seems Draper was just referring to the well known observations of enlarged livers commonly observed in Eskimos:
So there you go. It was just an observation referenced in the literature. And there is plenty of evidence of high urinary nitrogen excretion in the Eskimo literature. They were well known to have a high protein diet.
Ya know… there’s no need to scream “nada” every time you think there’s a gotcha. We can both easily look into this stuff. No need for me to do all the work here!
Duck, I posted my last frustrated note to you before I got this evidence from you. I’ve reviewing it now. I’m sorry if I showed some frustration here, but it’s what happens when someone’s trying to snow us, when trying to back up their statements with really flimsy evidence as has been the case on this topic till now. If you had said “I know there’s real evidence, please give me time to find it” or somesuch, that be great! Will be back soon –Bryan
But what you say Duck, “We can both easily look into this stuff. No need for me to do all the work here!” I respectfully disagree. You make the assertion, you do the work to back it up. Down to the actual text to support what you’re asserting. We all should be doing that and I try to do AMAP. Otherwise we could be tossing out there all kinds of assertions without being sure what we’re talking about and letting “others sort it out.” We are dealing with fascinating but enormously complex material than directly affects our lives. We need to be as rigorous with ourselves as possible. Don’t mean to lecture Duck, but you have to admit, you haven’t been consistently great about that 🙂 –Bryan
Bryan,
This is not some flimsy assertion. I have yet to find a single paper or study—referencing actual measurements on actual Eskimos—that did not conclude that the Eskimos were eating a high protein diet. For example, the following researchers all concluded that the Eskimo diet was a high protein diet and were not in ketosis:
Krogh & Krogh 1914 (Nobel Prize winner)
Lusk 1914
Joslin 1917 (first doctor to ever specialize in diabetes in the US)
Schaffer 1921
Heinbecker 1928, 1931, 1932
Tolstoi 1929
McClellan & DuBois 1930 (Stefansson’s own doctors)
Rabinowitch 1936
Rabinowitch & Corcoran 1936
Rabinowitch & Smith 1936
Kaare Rodahl 1952
Sinclair 1953 (A detailed review of the literature)
Ho 1972
Hui 1975
Bang, Dyerberg & Hjorne 1976
Draper 1977
Bang, Dyerberg & Sinclair 1980
VanItallie & Nufert 2003
Leonard & Snodgrass 2005
Hardy 2005
They all say the Inuit ate high protein, because they did. So, the scientific literature says—without a doubt—that the Inuit were high protein. Therefore, I believe it is you who needs to show otherwise.
Bryan said: “You make the assertion, you do the work to back it up.”
Sorry, but it’s not my assertion. It’s just what the literature says. All of the literature says high protein and no ketosis. If you disagree, it’s you who will have to show otherwise.
Cheers.
Duck, to be clear, I wasn’t questioning you about the Inuit protein intake. I’m not ready yet to do that. Like I said earlier, I can’t yet get near enough data from the Hardy paper. Thanks for all the links. Most of them you’ve already posted and I’ve reviewed them to varying degrees. But you’ve included a few new ones; thank you for those. Looks like I’ll have to learn Danish 😉
What I did question: The enlarged liver/freq peeing thing. Most of the comments addressing that presumed issue point back to that Discover mag article. That site quality is mostly OK–I’ve worked for large consumer tech and general interest pubs for over 20 years and ex-colleagues went on to edit and write at Discover, Popular Science, etc. But that article’s simply a reporting job and doesn’t cite any studies, at least not for our topic here. One of the things I’ve learned in the biz is how the internet can propagate and replicate CW till it gets to the point that even a lie told enough times looks like the truth.
About assertion, Duck indeed you were asserting: “Their enlarged livers … their significant excretion of urea …” Sorry, but that is the case. It’s right there in your post. It’s up to you to supply solid credible evidence to back that up. If I disagree with your assertion, yes, it is up to me to find credible rebuttals. But if you fail to provide strong and relevant evidence to back it up, I’m well within my rights to ask you for it. I am sometimes willing to do your work. But you shouldn’t *expect* me to do your work.
Duck what you say here: “All of the literature says … no ketosis.” Of course that’s false. You yourself quoted literature saying “hypoketotic…” “Hypoketotic” is not “aketotic.” We know the Inuit *do* in fact produce ketones, if not to our level. Only how much? I’ve yet to see serum ketone measurement actually listed in mmol/L (millimolar) or in any other concentration units. Maybe they are there in one of those linked you posted, and I haven’t seen it yet. But Duck, the larger issue has to do with the fact that “ketosis” is a surprisingly nebulous and ill-defined term. Someone can assert that if an Inuk has 0.000001 mmol/L of serum ketones, he is in “ketosis.” Who are we to say he’s wrong? What is the minimum mmol/L of serum ketones to declare someone “ketotic?” You don’t know. No-one else knows either. –Bryan
Sounds good, Bryan. If ketosis is a surprisingly nebulous and ill-defined term, then I don’t even know what to say about it. 🙂 At this point the literature says what the literature says. There’s not much more to say!
About decided the term “ketosis” is nigh near meaningless, it’s funny to arrive at that point isn’t it Duck? After all the keyboard sturm und drang about Nanook and his ketones.
As for what you say “At this point the literature says what the literature says…” that’s right. And much of the literature saying quite different things!
So Duck, what definition of “ketosis” will you stick with? –Bryan
“what definition of “ketosis” will you stick with?”
Probably the classical definition mentioned by Sinclair 1953 and others. It seems like there is a recent movement to redefine what ketosis is—and that’s fine—but I’ll leave that to others to sort out.
OK, once again I posted to you before seeing your answer.
That 1953 Sinclair paper is behind a paywall. If you wouldn’t mind posting his ketosis def here …
Thanks –Bry
“…If ketosis is a surprisingly nebulous and ill-defined term, then I don’t even know what to say about it. 🙂 …”
Duck, why don’t we start with that Wiki def you cited earlier: https://en.wikipedia.org/wiki/Ketosis
“Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood.”
Using that def, are the Inuit in “ketosis” or not? Do we know? How many calories do they derive from serum ketones? Serum glucose? Serum FFAs? BTW, when the liver breaks down excess protein, not *all* of it become glucose. About a quarter of it becomes fat.
Who’s actually measured these things in our far northern friends? Do you know?
And Duck, most important, if insulin levels remain low, low enough to continue to allow release of fats from adipose tissue, *does it all really matter?*
Is it like arguing how many angels can dance on the head of a pin? –Bry
I hear you Bryan. It’s impossible to define the diet. I get it. Nevertheless, they are known to be a high protein culture. There’s really nothing left to say. I’m getting on a plane in the morning and have to head to bed. It’s been fun. Be well and take care.
OK Duck. Sleep well, and have a good trip. See you back here. –Bry
To be clear, Duck, you *do* furnish a lot of links. It’s only that the quality of the evidence you cite can really vary. But you have a lot of great ideas. Given the state of most “science” out there, I’ll take the ideas! –Bryan
Hi Duck. Sorry. But if you are trying to imply that enlarged Inuit livers were somehow “unhealthy” you’re still batting zero.
What you said: “…It seems Draper was just referring to the well known observations of enlarged livers commonly observed in Eskimos…” Draper offers three refs for these “well known observations” as you call them. They are “Brown, 1955; Hildes, 1958; and Schaefer, 1971.”
Once again these texts prove elusive. However, thanks to our Jonathan Christie here, we have Dr Schaefer’s 1959 glowing report on exceptionally robust Inuit health. In it Schaefer refs Brown and Hildes works for the same years that Draper cites:
“…Many seal-eating Eskimos *though perfectly healthy*, have a relatively large liver. This hepatomegaly was first described by Brown and confirmed by Hildes….” You can see his report here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1831365/pdf/canmedaj00812-0101.pdf
Duck, this strongly suggests that Schaefer found nothing in the earlier Brown and Hildes works that suggests these Inuits’ livers were pathologically enlarged. Nothing from Brown and Hildes to suggest their livers were in any way “unhealthy.”
And Duck, about what you said “…And there is plenty of evidence of high urinary nitrogen excretion in the Eskimo literature…” Even now, you persist to fail to show even one shred of real evidence to back up your claim.
Finally Duck what you say here “…[the Inuit] were well known to have a high protein diet…”
So what? Where’s the evidence that the Inuits’ protein intake, whatever percent of the diet that was, harmed their health in any persistent way?
As you requested Duck, I’m rating your work on this topic to date a quieter all-lower-case “nada.”
It still means “nada.” –Bryan
“Hi Duck. Sorry. But if you are trying to imply that enlarged Inuit livers were somehow “unhealthy” you’re still batting zero.”
Thanks for the straw man argument, but no that’s not what I was saying. The scientists I cited believed that their enlarged livers were due to their high protein diet. Of course, I explained that already, but you’re having trouble following that point for some reason.
“Once again these texts prove elusive. However, thanks to our Jonathan Christie here, we have Dr Schaefer’s 1959 glowing report on exceptionally robust Inuit health.”
Wonderful. And guess what? Schaefer beleived their glowing health was due to their, high protein diet.
That’s what I’ve been trying to tell you all this time. They don’t even eat like you do.
“And Duck, about what you said “…And there is plenty of evidence of high urinary nitrogen excretion in the Eskimo literature…” Even now, you persist to fail to show even one shred of real evidence to back up your claim.”
Enough with the lies. I already gave you links to all of the literature. Krogh & Krogh 1914 showed high nitrogen from high protein. As did Rodahl 1952 and others.
“Finally Duck what you say here “…[the Inuit] were well known to have a high protein diet…” So what? Where’s the evidence that the Inuits’ protein intake, whatever percent of the diet that was, harmed their health in any persistent way?”
It’s all documented in the links I’ve provided earlier. ALL of the research says they were high protein—even Schaefer. Even the LCHF Magasinet Swedes understand what you are having trouble seeing.
But once again you’ve missed the point. The point is not whether they were healthy or not. We really don’t know since even Inuit mummies are well known to have had significant arterioclerosis (possibly from inhaling soot from their lamps). That’s not the point.
The point is that the Inuit were eating so much protein that all of the researchers who looked into their enlarged livers believed they were relying heavily on gluconeogensis for much of their energy. And a grand total of ZERO believed that they were relying heavily on ketones.
Is that how you eat, Bryan? Do you eat a high amount of protein and reserve most of your fat for burning lamp fuel for heat? If you are able to eat a high protein diet and can stay in ketosis, then I agree with Peter on this one, who says:
Peter sums it up nicely. Why on Earth would you want to use this extreme culture with unique genes and a high protein diet as the poster boys for a ketogenic diet anyhow? Makes zero sense.
“As you requested Duck, I’m rating your work on this topic to date a quieter all-lower-case “nada.” It still means “nada.”
And once again you’ve resorted to argument from fallacy.
I really have no interest in debating your fallacies any further, Bryan. If you want to know my opinion, then you should read all of the links I provided which actually observed real Eskimos. The literature stands on its own. The literature says they were not in ketosis (the original definition, which you are now trying to change) and that they ate a high protein diet. All of those references I provided refer to the Inuit’s observed high protein diet, which the researchers believed furnished their carbohydrate via gluconeogenesis.
And if you yourself eat a raw, high protein diet, then you can feel proud that you eat like an Inuit and are super healthy. However, if you are into protein restriction, then I have no idea what you are doing looking into a culture that doesn’t even eat like you do. It’s mind boggling.
There’s really nothing else left to say.
Duck, about the Inuit Paradox, to remind you why so many of us care and what we really want to know:
– Can the Inuit Paradox inform our decision–us non-Inuit folks–to try a persistent VLC foodway?
– Does the Inuit Paradox offer real evidence to consider to optimize dietary omega 6/omega 3 balance to lower our systemic inflammation?
The Inuit Paradox keeps offering tremendously exciting and relevant evidence to suggest the above approaches may indeed work to greatly improve our health. Duck, to date, no amount of “evidency-ness” you’ve shoveled onto this forum, when we closely or often even merely cursorily examine your sources, even begins to discredit the Inuit Paradox. Your slew of links have never–and I mean *never*–delivered rigorous evidence to discredit that Paradox. Your vague implied warnings against adopting lessons from the ancestral Inuit foodway: “…they are not like us,” “they burn fatty acids very differently,” “they do not exhibit ketosis as we do” and so forth, are simply that–vague and wholly unsupported warnings. Nothing you said and shown should even remotely dissuade anyone from experimenting with VLC. Ancestrally-living Inuit can and routinely DID thrive on VLC, even a near no-carb diet. By nearly all measures, many ancestrally-living Inuit enjoyed all-around robust health. Here’s a summary of the info that recently surfaced that we bat around here:
– the Inuit have one or a few genetic SNP variants (And so? In re: VLC, why should we care?)
– they “eat a high-protein diet” (So what? Why should we care? What’s “high?” anyway?)
– they “may or may not be in ketosis” (So what? Why should we care?)
– the conflicting accounts/non-accounts of CVD in ancestrally-living Inuit like those found in the 1940 Bertelsen report (I finally have this report. **Bertelsen utterly fails to say what the people who referenced it–including Ottawa Heart’s Dr Fodor–have been saying or implying it says.** Stay tuned for details.)
These points above are either wrong or fail to relate to our goals to find an optimum foodway to preserve and enhance our health.
So Duck, with your impressive ark of non-evidence, can I blame you for trotting out your tired litany of distractions? You recycle your irrelevant points accented with argumenta ad hominem: “…The scientists I cited believed that their enlarged livers were due to their high protein diet…Of course, I explained that already, but you’re having trouble following that point for some reason…That’s what I’ve been trying to tell you all this time. They don’t even eat like you do…” Meanwhile Duck you pose a silly rhetorical question, with a side of unsupportable assumption (the lamp fat thing), for which you already know the answers: “…Is that how you eat, Bryan? Do you eat a high amount of protein and reserve most of your fat for burning lamp fuel for heat?…” Again Duck, of course I don’t eat high protein and you know it. The point is that the diet is VLC–remember? I’ve made clear here I eat 15% protein and mostly fat. There’s plenty of evidence to suggest even the Inuit prefer fat. Maktaaq (Muktuk) is blubber that’s well over 90% fat by calores: http://ndb.nal.usda.gov/ndb/foods/show/8354 In that 2004 Discover Mag link you’ve cited before Duck, http://discovermagazine.com/2004/oct/inuit-paradox , raw muktuk… to many [Inuit], it’s a mainstay.” Canadian Arctic explorer and ethnologist Vilhjalmur Stefansson spent a great deal of time researching the Inuit. His observations and his own experiences and further experiments with a very high meat diet led Stefansson in his book “Fat of the Land.” to propose a diet that is mostly fat. Ho et al in 1972, http://ajcn.nutrition.org/content/25/8/737.full.pdf , says “…Approx 50% of the calories were derived from fat and 30 to 35% from protein.”
Then Duck we see this old saw from you–“I’ve Posted The Links…” You say: “…It’s all documented in the links I’ve provided earlier. ALL of the research says they were high protein—even Schaefer. Even the LCHF Magasinet Swedes understand what you are having trouble seeing…” complete with yet more ad hominem, accusing me of “…having trouble seeing…” something which I’ve never denied to begin with. Sure it’s perfectly plausible, even likely, the Inuit ate a higher percentage of protein than many others following their ancestral foodways. Duck, so what? I’ve seen zero evidence to suggest a higher protein has in any way impacted Inuit health, except possibly episodically and temporarily when sparse food availability forced them to eat ultra high protein.
Duck what you say here, in your one bolded comment in your post: “…the Inuit were eating so much protein that all of the researchers who looked into their enlarged livers believed they were relying heavily on gluconeogenesis for much of their energy…” Duck, I give that a big bolded “So What?” See my protein/fat discussion above. How much are their livers “enlarged?” Marginally bigger,like 5%? Who’s actually measured it? Does it even matter? You’ve yet to show even one researcher to determine this was an unhealthy adaptation. Indeed Schaefer said in 1959 “…Many seal-eating Eskimos *though perfectly healthy*, have a relatively large liver…” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1831365/pdf/canmedaj00812-0101.pdf
Also your phrase “relying heavily on gluconeogenesis” is meaningless. “Heavily” as compared to what? Just ketosis? What about lipolysis? In that Ho report linked above, we read this: “The fact that the Eskimos had high serum FFA and low glucose levels (approximately 65 mg/100 ml) indicated that free fatty acids played a major role in body energy production…”
Here Duck you quote an irrelevant passage from Hyperlipid’s Peter:
http://high-fat-nutrition.blogspot.com/2014/11/the-p479l-gene-for-cpt-1a-and-fatty.html
and yet completely ignore his main message: You quote from Peter: “I have some level of discomfort with using the Inuit as poster people for a ketogenic diet. That’s fine. They may well have eaten what would be a ketogenic diet for many of us, but they certainly did not develop high levels of ketones when they carried the P479L gene.”
Duck what you conveniently leave out: Peter actually ardently *supports* VLC and ketosis. He writes further down in that same blog post:
“I’m always amazed by the concept that a ketogenic diet might be temporarily therapeutic but must be discontinued because it eventually becomes Bad For You… point-scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health…”
Finally Duck, you emerging fave distraction: Your spurious charges of “argument of fallacy.” You say “I really have no interest in debating your fallacies any further…” Duck, sure, that’s easy to say when you conveniently leave out specifics and examples to support your charges, or even show proof I’ve made even one argument to you “from fallacy.” Whatever. We’re used to that from you. Duck, if it makes you feel better to believe all that–whatever all that’s even supposed to be or to mean–then please be my guest. It won’t change the fact that I and very very many other folks derived health-saving and even life-saving lessons from the Inuit Paradox.
Duck, I’ll conclude with Peter’s conclusion out of his same post you cited:
“…point-scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health. Destroying a circular argument about Inuit diets may may the destructor feel good. Destroying the feet, eyes and kidneys of a person with type 2 diabetes, who need a ketogenic diet, as a spin off from that victory must be difficult to live with. I don’t know how anyone can do this.”
Amen.
–Bryan
Bryan said: “Can the Inuit Paradox inform our decision–us non-Inuit folks–to try a persistent VLC foodway?”
No it cannot. Because they do not eat anything like Western VLC dieters do. To imply otherwise is dishonest.
Bryan said: “Does the Inuit Paradox offer real evidence to consider to optimize dietary omega 6/omega 3 balance to lower our systemic inflammation?”
Unknown. They possess unique genetic adaptions to apparently metabolize fats differently than we do. Incidentally, Hugh Sinclair once attempted to consume a high n-3 PUFA diet and it caused him to have difficulty with clotting and hemorrhages.
Bryan said: “Nothing you said and shown should even remotely dissuade anyone from experimenting with VLC.”
This is a straw man argument (which seems to be your expertise). I am not trying to dissuade anyone from experimenting with VLC. I am pointing out that the whole of the scientific literature says that the Inuit diet is not a proxy Western VLC diets.
Bryan said: “Ancestrally-living Inuit can and routinely DID thrive on VLC, even a near no-carb diet.”
Wonderful. And they did it by eating excessive levels of protein. The exact opposite of what Western VLC diets promote. They were converting enormous amounts of protein into carbohydrates via gluconeogensis. gluconeogensis = production of glucose. Glucose inhibits ketosis.
Bryan said: “the Inuit have one or a few genetic SNP variants (And so? In re: VLC, why should we care?)”
Because Westerners don’t have those SNPs and we don’t know if they are necessary for thriving on a VLC diet. That should be an obvious variable to consider.
Bryan said: they “eat a high-protein diet” (So what? Why should we care? What’s “high?” anyway?)”
Because protein is restricted in Western VLC diets. Protein knocks people out of ketosis. You should know this of course. And if you have difficulty understanding this, then I will point you to Peter’s article on the subject.
Peter writes:
Read that again. (See my next post for documented Inuit protein consumption).
The Inuit eat an excessive amount of protein, they do not restrict it. Therefore, they cannot be used as a proxy for a Western VLC or ketogenic diet.
Bryan said: “I’ve seen zero evidence to suggest a higher protein has in any way impacted Inuit health”
Another straw man argument. I never said their high protein intake was deleterious. Rather, my point is that their high protein diet is the exact opposite of the protein restriction advocated by Western VLC dieters. Please do your best to understand that point. You should never imply that the Inuit diet is a proxy for Western VLC. Peter’s post on protein and ketosis proves this. And yes, I’m aware that Peter promotes Western VLC diets. That’s why he’s uncomfortable with using them for “poster boys” of ketogenic diets.
Bryan said: “Canadian Arctic explorer and ethnologist Vilhjalmur Stefansson spent a great deal of time researching the Inuit. His observations and his own experiences and further experiments with a very high meat diet led Stefansson in his book “Fat of the Land.” to propose a diet that is mostly fat.”
Yes, his “own experiences” are the key there. Stefansson was advocating a Western version of the Eskimo VLC diet. However, Stefansson was a white man who claimed to have gotten sick when he tried to eat a high protein diet. The only way Stefansson could survive in the Arctic was to restrict protein and eat high fat. You’ve just proven my point. White people cannot eat the high protein diet that the Inuit consume. Stefansson’s experience proved it and his own doctors admitted that he was unable to consume the observed high protein intake in an Eskimo’s traditional diet .
Bryan said: “Ho et al in 1972, says “…Approx 50% of the calories were derived from fat and 30 to 35% from protein.”
Yes. Ho is getting figures from Krogh & Krogh 1914. Krogh & Krogh observed excessive protein intakes. Again, you are proving my point. Western VLC dieters do not consume that much protein, particularly if they want to remain in ketosis.
Bryan said: “How much are their livers “enlarged?” Marginally bigger,like 5%? Who’s actually measured it? Does it even matter? You’ve yet to show even one researcher to determine this was an unhealthy adaptation.”
Straw man. I never said it was an unhealthy adaptation. The point is that they are relying protein to produce a lot of glucose, which inhibits ketosis. This glucose production is why no scientist ever claimed they were in ketosis. A Western VLC dieter restricts protein to stay on a VLC diet. That’s my point.
Bryan said: “your impressive ark of non-evidence”
I don’t see how presenting you with a century of scientific evidence is “non-evidence.” See my next post if you aren’t going to bother reading it.
Bryan said: “It won’t change the fact that I and very very many other folks derived health-saving and even life-saving lessons from the Inuit Paradox.”
I do not deny that a ketogenic diet can be therapeutic for some. However, since the Inuit were not in ketosis, whatever “life-savings lessons” you think are derived from the Inuit Paradox are based on a misunderstanding of what the Inuit actually consumed (in reality a high protein diet).
Bryan said “Duck, I’ll conclude with Peter’s conclusion… “…point-scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health. Destroying a circular argument about Inuit diets may may the destructor feel good. Destroying the feet, eyes and kidneys of a person with type 2 diabetes, who need a ketogenic diet, as a spin off from that victory must be difficult to live with. I don’t know how anyone can do this.”
Lol. I agree with Peter. And his statement would be relevant if someone here was trying to use the Inuit’s non-ketosis to dissuade others from trying a trying a VLC diet. But no one here is doing that, so again… it’s a straw man (once again).
It makes no difference if the Inuit were healthy or not because their diet has nothing to do with a Western VLC diet. As you like to say… “Nada”.
We agree that they burn a lot of FFAs, but they also produce a lot of endogenous glucose from their excessive protein intake (see my next post). How is that like a Western VLC diet? It’s not.
Cheers.
Duck, the Inuit Paradox absolutely can and *should* inform non-Inuit who contemplate a persistent VLC foodway, esp them who fear it because “no one’s ever done it before.” I never suggested we should eat all the same things as the Inuit. It’s the nutrient lessons we learn from them. I’m not going to start eating muktuk. But I’m making sure to eat salmon with the skin and bones. Both have high long-chain w3 and plenty of other nutrients. Nothing “dishonest” about that Duck. That’s very valuable to know and act on.
About Hugh Sinclair’s tissues with clotting on high w3, again you fail to read my comment correctly. I said “*optimize* dietary omega 6/omega 3 balance.” I had a similar clotting issue till I dialed back down my w6/w3 ratio from 1:1 to 3–4:1. I was fine afterwards and still kept getting lower CRPs.
Duck if “Nothing you said and shown should even remotely dissuade anyone from experimenting with VLC.” is a straw man argument as you claim, then why do you keep flogging the ill-defined idea that “the Inuit diet is not a proxy [for] Western VLC diets?” Do you do this out of a burning academic interest? People here want to learn how to get and remain healthier. If they need reassurance that they can safely achieve that on LCHF, the Inuit experience can help them hugely. Does that mean we have to eat 50% fat/35% protein like the Inuit do? Of course not. I eat 80% fat/15% protein. Point is Duck, it’s to reassure people they may well do very well on *persistent low-carb* and should not be the least bit afraid to experiment with it.
About what you say here: “Wonderful. And the [Inuit] did it by eating excessive levels of protein. The exact opposite of what Western VLC diets promote. They were converting enormous amounts of protein into carbohydrates via gluconeogensis. gluconeogensis = production of glucose. Glucose inhibits ketosis.” Duck, where to start with this flabby mess you spilled here? Again, your view that it’s “excessive” protein has never been proven. That’s simply your opinion. About it being “opposite to Western VLC” of course that’s wrong. Both are low carb. It’s a matter of setting the fat/protein balance that works best. About gluconeogenesis you have no idea how much of this ancestrally-living Inuit generate. Ditto for “enormous amounts of protein”–“enormous” is simply your personal feeling. Duck, obviously you’re welcome to all your opinions on all this. Just please understand they are not supported by the actual science. None in that “century of scientific evidence” you stuck up here.
Duck you say “Because Westerners don’t have those [Inuit] SNPs and we don’t know if they are necessary for thriving on a VLC diet…” *Sigh* Been there, done that already Duck. If anything, westerners are *better* at producing ketones. In any event, I’ve always suggested that people going on VLC get blood tests if only to assuage any concerns they may have.
About my comment: “Bryan said: they “eat a high-protein diet” (So what? Why should we care? What’s “high?” anyway?)” and your answer: “Because protein is restricted in Western VLC diets…” Duck yes you persist to misunderstand me. Where have I ever said we should eat a high-protein diet? Take a look round. You won’t find me saying that anywhere. And of course you’ve never answered what you think what constitutes “excessive.” Not holding my breath for that.
What you say here “The Inuit eat an excessive amount of protein…” Duck, you think if say this enough times maybe one day it’ll come true? Just wondering.
Oh but wait, then we get this from you! “I never said [the Inuit’s] high protein intake was deleterious.” Oh really? Duck, sure, you didn’t *say* their “high” protein intake doesn’t harm them. But do you believe it does? If not, then Duck why do you just say “The Inuit eat an excessive amount of protein…”? Pray reconcile these two statements for us.
About what you say. “You should never imply that the Inuit diet is a proxy for Western VLC.” Gee Duck. Maybe if you say it enough times, that’ll become true too. Maybe Bryan blog comments exhorting folks to chow unseemly amounts of protein will start spontaneously popping up all round the webosphere 🙂
Duck, you say: “… You’ve just proven my point. White people cannot eat the high protein diet that the Inuit consume. Stefansson’s experience proved it and his own doctors admitted that he was unable to consume the observed high protein intake in an Eskimo’s traditional diet…” Yes Duck. If you want to take Stefansson n=1 as “proof” that “white people” can’t eat the high protein diet the Inuit consume, sure, be my guest. Whatever. I’ve never advocated a high-protein foodway anyway. You know. Just in case I haven’t told you that before. And Duck, a news flash: You’ll find other kinds of non-Inuit folks out there besides “white people.”
Our exchange here: Bryan says: “Ho et al in 1972, says “…Approx 50% of the calories were derived from fat and 30 to 35% from protein.” Duck says: ”Ho is getting figures from Krogh & Krogh 1914. Krogh & Krogh observed excessive protein intakes…” Sure Duck. I’ suppose you’ll actually bother to back up that assertion of “excessive protein intakes” with actual K & K text? I’ve learned not to hold my breath for actual proof from you. If that text evidence actually exists and you actually post it, please remember this is nutrition science from over a hundred years ago around the time we were discovering “vital amines.” Duck, if this becomes yet another assertion you fail to support, I won’t mind.
About this: “I never said [high protein intake] it was an unhealthy adaptation.” Hmm. You’ve gone on about “enlarged livers” and “…their significant excretion of urea…” OK Duck whatever you say.
About this mess: “The point is that they are relying protein to produce a lot of glucose, which inhibits ketosis. This glucose production is why no scientist ever claimed they were in ketosis. A Western VLC dieter restricts protein to stay on a VLC diet. That’s my point.” Oh really Duck? “Glucose inhibits ketones” is your point? Gee, all this time I thought it was the Inuit “hypoketotic hypoglycemic” state you kept going on about. You know, yielding those raging 65mg/dL serum glucose levels ready to put the boots to any ketones with enough temerity to try to leave the liver. And I was thinking all this due to that CPT1a deficiency variant gene you kept going on about–you know, the deficiency that inhibits ketone production. Silly me Duck. Please enlighten us: What mg/dL of serum glucose do you need to start inhibiting ketosis? Enquiring minds want to know.
You say: “I do not deny that a ketogenic diet can be therapeutic for some. However, since the Inuit were not in ketosis, whatever “life-savings lessons” you think are derived from the Inuit Paradox are based on a misunderstanding of what the Inuit actually consumed (in reality a high protein diet).” Yes Duck, been around this block with you too a few times. What’s up with your amnesia? Mon pauvre, try to remember. Hint Q: Compared to Inuit, how well might non-Inuit handle “ketosis?”
And finally this Duck–good job putting words in my mouth: Duck says:“I agree with Peter. And his statement would be relevant if someone here was trying to use the Inuit’s non-ketosis to dissuade others from trying a trying a VLC diet. But no one here is doing that…” Well, Duck, that’s wrong too. You can sure find folks here inveighing against VLC. But Duck, please consider this: You’ve come up with one argument after the next to drive home the idea that the Inuit–the world’s top success story of ancestral VLC–are so “different” from us that their experience can serve little or no use to us. You efforts have the effect to cast doubt on what is perhaps the most inspiring example of low-carb success our planet offers. You upbraid people including me for imagined arguments of fallacy, meanwhile doggedly perpetuating the fallacy of insisting that people who suggest we take lessons from the Inuit are advocating “their high-protein diet” and even that we should eat their foods. Your insistence in this matter borders on an odd obsession. Your stubbornly refuse to see that VLC advocates, in the main, are *not* advocating a high-protein. Why do you do this? Your verbal contortions would be risible except this is very important stuff we’re discussing. Our diet decisions directly impact our health and lives. Duck, I’m not saying you shouldn’t spin your academic arguments regarding the Inuit. That stuff’s great fun and, most of all, we should feel free to voice our views here. But I say again to you, in this important matter, I *will* call bullsh*t when I see it. Most of all, people–especially people with high blood sugar issues–need to know they should feel absolutely free and SAFE to try VLC and even consider it as a lifetime choice, not just a “therapy.” The evidence suggests a low-carb moderate-protein very-high-healthy-fat foodway is perfectly safe. –Bryan
Bryan,
You’ve accused me of not presenting evidence, despite that I provided links to over 100 years of scientific observations on the Eskimos. Since you won’t take the time to read any of it, here’s what the scientists who observed the Eskimos found with their protein consumption (and nitrogen production) from high protein and high gluconeogenesis production.
Krogh & Krogh put a handful of Eskimos individually into a respiration chamber for 4 days at a time and fed them lots of Seal meat. They wrote:
This was the first of many observations of high nitrogen excretion—a sign of significant glucose production from gluconeogenesis and not ketosis.
The Kroghs explained in their highly detailed report that the Eskimos would not enter the chamber unless they were promised various quantities of bread (and sugar for their coffee) during the experiment. The Kroghs agreed and gave them lots of bread/sugar some days and only a little bread/sugar on the VLC days. On VLC days, the Kroghs found that roughly half of their 54g of carbs came from bread/sugar and more than half came from glycogen in the meats. According to Rink 1855, Inuit were known to source bread and sugar since white man appeared in the 1800s, so we don’t know if these modern carbs craved by the Eskimos replaced other traditional carbs in their diet (Angelica, for instance) or if they were new additions to their diets.
In 1931, Heinbecker wrote:
Again, See Peter’s post on the importance of protein restriction in Western VLC diets.
In a review of all the available literature by 1953, Hugh Sinclair wrote:
4 kg of meat daily? Half the fat of what would be needed to reach ketosis? Hmm… And Peter says steaks aren’t ketogenic. So, Western VLCers do not eat this way, of course. Unlike the Eskimos, Western VLC dieters restrict protein. That’s been my point all along. You cannot use the Eskimo diet as a proxy for a Western VLC diet.
Not only did Rodahl observe high protein, but observed even higher protein intake during the Winter:
Bryan, do any Western VLC dieters regularly consume 300gm of protein per day? Is it advocated as part of a VLC lifestlye? No, of course not. Because doing so would result in a metabolism that relied too heavily on gluconeogenesis (i.e. glucose) for energy.
Therefore, you cannot use the Inuit as a proxy for the health of a Western ketogenic diet. They don’t eat anything like Western VLCers do. Nor do any of us have their genes or metabolisms that allow them to eat this way.
My overarching point is that the Inuit cannot be a proxy for Western VLC or ketosis. To imply otherwise is dishonest when we see that all of the scientific literature shows otherwise.
This is not to say that a Western VLC diet is unhealthy—I have no idea if it is or is not. It may very well be that VLC is the best diet in the world! Who knows? All I’m saying is that you cannot use the Inuit as an example of Western VLC. That should be obvious given what was actually observed about the Eskimo diet.
Feel free to dig into the Inuit all you like. And feel free to advocate a ketogenic diet to those who may need it. Just be aware that at 300gm of protein per day, the Eskimos are not eating anything like a Western VLC diet.
Peter is wise to distance himself from the Inuit. You should follow his lead.
Cheers.
Duck, thank you for this very interesting material. Really, I do visit your links or had been. But it does get discouraging when so many you’ve posted go to material that’s stuck behind paywalls or in books or doesn’t address the issue.
Like I made clear in my last mail, you don’t need to sell me on the idea that the Inuit can eat a lot of protein. I never disputed it. I’m not convinced all Inuit around the north ate whopping amounts of protein all the time. There’s plenty of evidence to suggest they eat more fat when given the choice. They land a big bowhead whale, and they’re literally savoring the maqtaak for days. Since most Inuit live near the sea and hunt blubber-rich marine mammals, they often get a chance to eat a lot of fat, and can give the excess protein to their dogs. Nonetheless, I can imagine they need to eat high protein often enough that they’d have to adapt to it.
And how do they adapt? Duck I had to laugh when you asked me: “Bryan, do any Western VLC dieters regularly consume 300gm of protein per day?“ That was *me* from July–October 2007! During those four months I was averaging 300g protein per day. That was 40–50% of my calories. I know this because, during that time, I carefully weighed everything I ate down to the gram and entered all that into my spreadsheet. During that high-protein time, this “white boy” actually felt fine as I recall. At that time I walked 8–10 miles per day, and had plenty of strength to do that. The two main downsides: people told me I had ammonia breath and I had to get up several times per night to pee. Reading this about the Inuit makes me more curious about high protein. Who knows how my bod would have adapted if I carried it beyond those four months? But starting in October, I start systematically dialing up the fat percent till I got to my current level (80%) in spring 2008. I much preferred to eat the fat–the “flavor carrier”–over the protein.
This is also interesting: “Inuit were known to source bread and sugar since white man appeared in the 1800s” Reading through Bertelsen’s report in 1940, I was a little surprised to learn many of his Inuit patients had already adopted a lot of western-style food and habits, especially smoking and drinking alcohol. More on that later.
I want to spend more time looking at what you posted, and especially to crunch a few of their numbers. I’m going to bed now and will come back to this tomorrow. –Bryan
Bryan, you probably didn’t notice, but I had already provided the Krogh & Krogh many days ago (remember, you thought you’d “have to learn Danish,” but all you had to do was scroll past the Danish introduction). Due note the high levels of gluconeogenesis as shown by their high nitrogen excretion, which shows the Inuit rely heavily on glucose production. Those enlarged livers appear to be a (healthy?) symptom of that glucose production—I never said it was deleterious. If we can agree on that, then we’re in good shape here.
None of what I presented here was intended to prove that the Inuit were unhealthy. It was only done to show that they were not in ketosis and therefore cannot be used as an example of a “healthy” ketogenic culture (as has often been done by LCHF advocates).
It’s simply erroneous to use the Inuit as “poster boys” for a ketogenic diet or somehow to prove the safety of a ketogenic diet. You can’t do that given what the scientific literature says about their high protein diet and their unique genetic adaptations for fat burning. I say it’s dishonest to use them as poster boys, but even if you disagree with me, relying on the Inuit to prove the safety of a ketogenic diet so is to commit the fallacy of affirming the consequent—a logical fallacy of inferring the converse from the original statement.
An example of this fallacy would be:
“All cats are animals. Ginger is an animal. Therefore, Ginger is a cat.”
I think anyone can see the problem with that logical fallacy. One can easily commit this exact same fallacy by saying:
“The Inuit VLC diet is healthy. A ketogenic diet is VLC. Therefore, a ketogenic diet is healthy.”
I’m trying to get you to understand that this logical fallacy illustrates why the Inuit cannot be used as “poster boys” for a ketogenic diet.
If you want to argue it’s possible that a culture can exist and thrive on VLC, then that’s fine. But that’s an entirely different statement and you’d need to clarify that they did not eat a Western ketogenic diet.
But arguing that Ginger is a cat is unacceptable and fallacious.
Cheers
I’ve been reading this back-and-forth about the Inuit for awhile, but haven’t commented until now. A few things come to mind: first off, who exactly are *the Inuit*? Aren’t they a series of different tribes in the Arctic region? Couldn’t they conceivably be eating slightly different diets? If we monitored the glucose reaction and ketone production of 4 Americans, could we come to any conclusions about the American diet and the health of all Americans?
I was under the impression that at least some of the Inuit ate pretty high fat diets. If you watch the documentary “My Big Fat Diet”- (you can google it on You Tube), those Inuit traditionally used a liberal amount of oolichan grease (not sure if I spelled that right). They dipped their fish in it, synonymous with dipping lobster in butter. Some Inuit ate mostly seal meat, which is pretty high in fat. Many groups rendered fat which they used to make pemmican. And I had read that berries preserved in seal fat was a delicacy which many of them ate in the winter. So I believe some of the tribes could have been eating a ketogenic diet; at least, I’m not convinced you can rule it out entirely.
About the protein issue: protein turns into glucose *only* if you eat more protein than what is needed for body processes, like tissue and cell regeneration. So it only turns into glucose if you eat an excess of what the body requires. This means that that amount will be different for each person. Some can eat a higher amount of protein and still be in ketosis- (I believe I may be one of those people). It could be that, living in a cold climate, exercising as they do, and eating zero to minimal carbohydrate might mean that they require more protein. Some of the papers you gave links to simply claimed “they couldn’t be in ketosis because they ate too much protein”, but I’m not convinced that’s true. Again, I’m not sure you can rule it out. In western, very low carb diets the protein recommendation may be on the low side in order to ensure that the majority get into ketosis, as that varies from person to person.
If they used urine ketones to measure whether or not they were in ketosis- (I’m pretty sure blood ketone meters are a more recent thing)- that method is notoriously inaccurate, as when people are keto-adapted they often utilize the ketones rather than excrete them.
I’m not saying they definitely were in ketosis all the time; I don’t know this one way or the other. And, as I said, this may have varied between different groups of Inuit; it may have even varied between the seasons. These are just a few thoughts I had.
Morgana, The Inuit are a group of culturally similar indigenous peoples inhabiting the Arctic regions of Greenland, Canada, and Alaska. They used to be called “Eskimos” but that was considered to be offensive since it supposedly translated to “raw meat eaters”. Of course, their tendency of eating raw meat is yet another reason why they do not eat like Westerners do. I don’t see too many Western VLCers eating lots of raw meat.
Morgana said: “I’m not convinced that’s true”
As it has been explained by Peter, and others, the majority of Inuit have CPT1a mutations that while they burn FFAs, they struggle to produce ketones. As Peter wrote,
Even if you could prove that high protein is ketogenic, they cannot be used as an example of a “ketogenic” culture because of their highly prevalent CPT1a mutation. Everyone produces some ketones, including me, but we wouldn’t consider me to be “ketogenic” just because I produce some ketones.
Interestingly, the Inuit deficiency of CPT1a appears to force FA oxidation to brown fat. See the main graphic here, in this paper:
Adipose Fatty Acid Oxidation Is Required for Thermogenesis and Potentiates Oxidative Stress-Induced Inflammation
Since we don’t have CPT1a deficiencies, this suggests that we are burning fat in different cells than they do (mainly brown fat). They need to produce heat, after all. They were known to be warm to the touch, even on the coldest days.
Anyhow, the high protein diet is just another reason on top of their unique deficiency in CPT1a why they were not considered to be ketogenic.
It seems like people now suddenly want to redefine what “ketogenic” is, however the classic therapeutic ketogenic diet contained a specific ratio by weight of fat to combined protein and carbohydrate. (This is the “customary convention” of ketosis that Sinclair 1953 referred to). We should all be able to agree that the Inuit did not satisfy the classic “customary convention” of ketosis. Certainly the children did not as they have been known to die when their bodies attempt to rely on ketones for survival. If there is a brand new definition of what “ketogenic” is, that would be news to me.
Now, if you want to redefine what a “ketogenic” diet is, then you ought to institute a name change since the Inuit obviously do not produce many ketones. Otherwise we are conflating the medically recognized definitions.
Morgana said: “Some can eat a higher amount of protein and still be in ketosis”
If you have evidence showing a lowering of the ketogenic dietary fat requirement for people who are not using one of the three known changes in fat sourcing and protein demand (weight-loss, athletic demand or MCT oils), you’ll have to provide evidence. That would be groundbreaking (you should publish it!) and it would be great to have a citable reference for that. I have yet to find any evidence to change the ketogenic/anti-ketogenic macro-nutrients ratio for situations outside of those three known changes.
Of course, the Inuit were not trying to lose weight and they are known to have difficulty fasting after hours of strenuous work—they require snacks to avoid hypoketotic hypoglycemia.
This is not to say that the adult Inuit could never be in a mild ketosis. I’m sure some did enter ketosis in some situations, like starvation. Nevertheless, as Bryan has pointed out, they don’t do ketosis as well as Westerners do. And they don’t satisfy the customary convention of a ketogenic diet and they burn fats very differently than we do.
So, again, I have no idea why anyone would think they are a proxy for a Western customary ketogenic diet. A VLC diet? Yes, albeit a very unique one (very high n-3 PUFA with extremely rare PUFA-burning genes).
As you can see, there was a reason why Peter distanced himself from the Inuit. And he wasn’t alone. This debate first happened in Sweden and prominent Swedish LCHF advocates Andreas Eenfeldt[1][2] and Annika Dahlquist[3] quickly distanced themselves from the Inuit after they reviewed the evidence.
Those are the words of one of the most prominent LCHF doctors in Sweden. So, I don’t see what the fuss is here.
Obviously this revelation does not detract from the efficacy of a ketogenic diet. It just means that the Inuit are not a proxy for such a diet. The Swedes, and Peter, seem to understand this quite well. I’m surprised others here aren’t able to reach the same conclusion.
Duck Dodgers- I think you misunderstood much of what I was trying to say, and, although you supplied several links, you didn’t really supply many answers. My main point was that there are different groups of people who are called “Inuit”, and it’s unclear to me how many of them have actually been studied, how many of them really eat a high protein diet- (I know at least some Inuit eat a higher fat diet), how many of them really have this genetic mutation- (according to the link you posted some, but not all)- and if we can make a generalization about all Inuit based on- (at least, the link I looked at)- 4 people. It doesn’t matter to me what Andreas Eenfeldt believes about the situation, I like to see evidence and come to my own conclusion. By the way, I’m not saying you’re wrong, it’s just that the links you’ve posted have raised more questions for me than answers.
But first: about raw meat: yes, I do eat raw meat, and I’m sure that at least some low carbers do too. I eat raw herring this time of year, and occasionally raw salmon. I eat salted, hung dried ham in the form of Parma ham or Serrano ham. I also eat a venison salami sometimes; I like carpaccio of all sorts, and many people eat steak tartare, so yes, some of us do eat raw meat. I’m not sure what the point is, it might be neither “here nor there”, but I just thought I’d mention that I do eat it.
Also, I don’t think I was “changing the definition of ketosis”. Ketosis is normally defined by a blood ketone reading of at least .5 Mm to about 3.0- (this is the optimal range). The classic ketogenic diet used to treat epilepsy in the past is neither here not there; it is not necessary to use that diet to go into ketosis, and actually, nowadays they’ve discovered that the less restrictive Atkins diet works just as well for people with epilepsy. The ability to get into ketosis varies from person to person; there is no “one size fits all” in terms of a certain macronutrient profile. According to Dr. Seyfried, women often can get into ketosis easier than men; and according to Dr. Jeff Volek, thin people and athletes also generally have an easier time getting into ketosis. (I won’t supply links, sorry, it’s too late here and I’m getting ready for bed. These were 2 interviews I saw on You Tube. Unfortunately they are long, and I don’t know at exactly what mark they said these things). In any case, what that means is that some people are able to eat more carbohydrate than others and still be in ketosis, i.e., the blood meter range; this goes for protein as well. Of course, obviously eating a huge amount of protein will keep one out of ketosis, it’s just that I’m not totally convinced that *all* Inuit ate a huge amount of protein, though it looks like some did.
Not sure if you’ve bowed out of this discussion or not, but I thought I’d clarify those few points.
Morgana, to chime in about the raw meat (and fermented meat since Inuit do that too), more non-Inuit folks eat it than we may realize. Many eat raw oysters. Sashimi is quite popular in Japan and in many metro areas in North America. Some sauces, like true fish sauce and Worcestershire sauce has fermented anchovies in it. About the herring, I get that in our season for it (this month and next) and pickle them, except I eat the milt and roe sashimi-style (raw) as is common in Japanese cuisine. Same with uni (sea urchin) when I can find it in the store. I gently split the uni open clamshell-style with a cleaver, squeeze some Meyer lemon juice on the orange-y egg sacs and down the hatch yum. Tastes like the sea. Also, like you, I make tartare, from meat and salmon. You find cultures all over the world fermenting fish: https://en.wikipedia.org/wiki/Fermented_fish
Swedes ferment herring (surströmming) and the Icelanders ferment shark (Hákarl). Granted those two ferments are acquired tastes to be sure! But few people think the Swedes and Icelanders are fundamentally “different from us” because they eat raw meats. –Bryan
Why would eating raw meat make anyone think the eaters are “fundamentally different”? Many European nations, as well as Asian ones, have their raw meat dishes: carpaccio, ceviche, etc. In the early 1900s, when forensic medicine was in its infancy, German immigrants in large cities contracted trichinosis by eating raw pork — they did it in the motherland, and had no problem there because they didn’t feed their hogs garbage as we did in the US (As an aside, the fascinating, and, I fear, now out-of-print, book, “Eleven Blue Men” has some fascinating stories of early medical forensics, including how the trichina problem was identified). It seems only in the second half of the 20th Century that Americans got turned off on the idea of raw flesh. Perhaps that was a a good thing, with the mass production of beef.
Annie what you ask: “Why would eating raw meat make anyone think the eaters are ‘fundamentally different’?” This traces back to what Duck wrote to Morgana a couple of days ago (the 13th):
“Of course, their [the Inuit] tendency of eating raw meat is yet another reason why they do not eat like Westerners do…”
This is part of Duck’s persistent efforts to categorically portray “the Inuit” and “the Inuit diet” as profoundly different from “us” and “our diet.” As though “the Inuit” are some monolithic block of people who all share the same special adaptive genes and eat just the same type of diet at all times, however far-flung they may be around the circum-Arctic. Duck categorically asserts things like “…the Inuit diet is not a proxy Western VLC diets”, that “ [the Inuit] …evolved differently than we did,” and “The Inuit are not an example of what happens in Western metabolisms.” He even suggests “the Inuit diet” is somehow unsuitable and even harmful, saying things like: “…they [stayed in gluconeogenesis] by eating excessive levels of protein…” and “…Krogh & Krogh observed excessive protein intakes…” and “…they …produce a lot of endogenous glucose from their excessive protein intake…”
All this to imply that “the Inuit” are so different from us that the rest of the world can derive no lifeway or foodway lessons from them. As Morgana, I, and some others here have been suggesting, the picture is much more complex and nuanced. I maintain that the Yupik-Inuit ancestral foodways are likely much healthier than how Duck portrays them and that they can serve as a tremendous inspiration and guide for the many millions of metabolically sick people who are considering VLC but viscerally fear it due to life-long massive pro-carb anti-fat acculturation. However much I may have misunderstood certain details of it at the time I learned about it in 2007, the Inuit experience critically aided my journey back to health. –Bryan
Hi Morgana. Good question “who exactly are *the Inuit*? The nomenclature’s a WIP. I attended high school in Canada with lots of First Peoples including Inuit from Quebec and Iqaluit in the part of former NWT now called Nunavut. My Inuit classmates were already eating loads of SAD of course, but still hunted (on snowmobiles, in power boats) and did seem partial to maktaaq (muktuk = blubber = 90+% fat). This was back when Canada started moving to call them Inuit. We slid into referring to all the closely related circumpolar peoples “Inuit” even though the Yupik of far eastern Siberia and Alaska don’t call themselves that. Many sources still collectively refer to all of them as “Eskimo” though some promote “Inuit-Yupik.” These two links offer more detail on them and somewhat complement Wikis and US/Canada gov’t sources:
http://www.britannica.com/topic/Eskimo-people
http://www.inuulitsivik.ca/northern-life-and-inuit-culture/who-are-the-inuits
Ancestrally, Inuit-Yupik typically didn’t live so much in “tribes” as in very small single- or several-family units. Most live near the sea and traditionally derive most of their calories from large very blubber-rich marine life, like seals and the bowhead whale. Morgana you said “I was under the impression that at least some of the Inuit ate pretty high fat diets.” and all I’ve learned agrees with that: Fat was the Inuit-Yupik’s main calorie source. At least for the coastal peoples, and most Inuit-Yupik are coastal dwellers. Morgana, you ask “Couldn’t they conceivably be eating slightly different diets?” yes they do, depending on where they live and the season. Veg-wise at one end of the spectrum, some ancestrally-living Siberian Yupik (at least in Chukotka) most consistently included veg, even using root cellars. Alaskan Inuit and Yupik Some regularly ate sea veg, other not so much. At the other end of the spectrum are the far Northern Greenland Inuit, like those around Qaanaaq, who ate virtually no veg because it was rarely available. The inland Inuit, like the reindeer Yupik in Siberia and caribou hunters in Alaska, had a harder time getting iodine, so ate the thyroid glands of these big ungulates, esp during the typical times to conceive children.
For the ancestral foodway stuff I expect you’ll want my sources and I’m busy trying to find them! This is from my research 5–7 years ago, early on in my LCHF journey. Please bear with me while I find them. Meanwhile you can find some of it in Susan Allport’s book “The Queen of Fats.”
Finally Morgana about what you say: “… I believe some of the tribes could have been eating a ketogenic diet…” The more I delve into this matter with Duck and others, the more the Inuit experience raises a fascinating question. What conditions define their energy metabolic state(s)? Indeed what conditions define the energy metabolic states of any of us?
For example, let’s look at one of the most recent direct measures we have on this matter. In their 1972 report, Ho et al say:
“…Each Eskimo’s serum was tested for the presence of ketone bodies … and all serums were negative. This does not preclude an increase in ketone body production during this time… The fact that the Eskimos had high serum FFA and low glucose levels (~65 mg/dL) indicated that free fatty acids played a major role in body energy production…”
Picking this apart, I began to realize that terms like “ketosis” and “glycolysis” sorely lack comprehensive definition. No-one can give us a broadly accepted def for those two terms. We foodway-focused folks typically–perhaps sloppily–default to the term “ketosis” as a default state in which *all* fat-derived energy–ketones and FFAs–predominate over glucose derived energy (glycolysis). Maybe we need a more precise term to encompass all fat-derived energy. How about “keto-lipolysis?” How does that sound to everyone?
Let’s go with keto-lipolysis for the moment. Morgana, we still don’t know how to determine which energy-metabolic state predominates–glycolysis or keto-lypolysis. Do we go by sheer millimolars of glucose and fats+ketones in serum at any given moment–whichever has the greatest concentration wins? Or rather is it by calories delivered to our tissues at any given moment–the one that delivers the most calories at any one time wins? Or rather is it whether or not the metabolic conditions at any given moment trip the insulin switch to start/stop mobilizing fats from adipose tissue? Is it some combo of these three conditions? Again, we have no broadly accepted defs. Indeed I find remarkably few *proposed* defs. However, when you look at what Ho et al found–very low serum glucose (65mg/dL) and highly mobilize FFAs, keto-lipolysis wins hands-down by all three defs.
By the FFA-excluding definition of ketosis that Duck promotes, these Inuit are most likely not in ketosis. But for those of us looking at LCHF, that is a moot point, esp since non-Inuit appear to be much better at ketosis anyway. For us seeking to optimize our health through diet, Duck’s strict def of ketosis is utterly irrelevant. Much more important: are these Inuit in glycolysis? Regardless of how much gluconeogenesis they may or may not be doing? By the above defs, these Inuit are definitely not in glycolysis. For us seeking to optimize our health through diet, that’s what we care about. For us, to dwell solely on how much gluconeogenesis the Inuit or anyone else are doing is an utter waste of time. What we care about is whether or not we are in keto-lipolysis or glycolysis. By as many relevant measures of these states as possible –Bryan
Bryan said: “Duck’s strict def of ketosis is utterly irrelevant”
lol. You’ve got to be kidding me. This is yet another fallacy—moving the goalposts.
As if I invented the actual definition of ketosis. Give me a break. What universe do we live in where you get to redefine ketosis as being something that isn’t ketosis?
Do yourself a favor and look up the word “ketosis” in any medical dictionary and textbook. You’ll find that it says that ketosis is a “raised levels of ketone bodies in the body tissues.” The Inuit do not fit that definition.
But feel free to reinvent the definition if you like. lol
Duck, maybe you’ve been missing the message.
For people looking to improve their health with LCHF, looking at ketosis in isolation DOESN’T WORK.
Just wondering Duck. What part of that don’t you understand?
Also, you utterly fail to produce a broadly accepted comprehensive definition for ketosis. We’ve been around this block before. You didn’t do it in your last post. You’ve never done it in any previous posts. You won’t in the future until when and even if the global establishment agrees it. To simply say “raised levels of ketone bodies in the body tissues” doesn’t even begin to cut it. Raised from what level? To what level? Is fat mobilized from adipose tissue or not? What are the serum glucose levels? All those considerations matter greatly for our overall health.
Duck, you can’t even keep your own various defs of “ketosis” straight. On December 3rd, you posted this: “Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood.” Guess what Duck? “Raised” levels of ketones do not necessarily mean “most of the body’s energy supply comes from ketone bodies.” And the def you gave on the 3rd says “ketone bodies in the *blood*” But the def you give today says “ketone bodies in the *body tissues*” So which is it Duck? “blood” or “body tissues?”
Duck, if you want, keep flogging your “Inuit are different” “low ketosis,” “high gluconeogenesis” stuff in your craftily crafting way. Just please don’t expect me to stop calling you on the bullsh*t I find in it. –Bryan
Bryan said: “So which is it Duck? “blood” or “body tissues?”
lol. It makes no difference since the Inuit cannot manage to produce many ketones either way!
And with that, I’m afraid our time is done here, Bryan. As I mentioned earlier, the Inuit debate already happened in Sweden last year and it was decided by LCHF advocates that the Inuit have no business being compared to a ketogenic diet. Peter obviously agrees. As do I. So, there’s nothing left to say. That debate ended a year ago. Let it go.
Take care, Bryan. I’m out.
Take care Duck. Bye bye. –Bryan
wbryanh- My question “who are the Inuit” was basically a rhetorical question. The point I was trying to make to Duck Dodgers is that- since “the Inuit” consists of many groups of people- it’s not clear to me at all that every single one of them eats a high protein diet, has enlarged livers, and has trouble producing ketone bodies, though I see by the research that at least some do. According to the link that Duck Dodgers posted, in the groups where this mutation appears, approximately 68% of them have this genetic mutation. Although that is a high number, what can we say about the others who don’t have it? (Apparently, according to that same link, the native peoples of inland Alaska don’t have that mutation at all). It is thought that this mutation used to confer a metabolic advantage in the past, but has become detrimental in the present day. In the link below, it is mentioned that this mutation might have ensured that they didn’t over-produce ketone bodies, due to their unique living situation and diet. (This is all conjecture of course, but the article does mention “high fat diets” and “ketosis”, implying that at least some Inuit are, or were, in ketosis):
http://www.sciencedirect.com/science/article/pii/S0002929714004224
By the way wbryanh, you don’t need to supply any links or “proof” for me that the Inuit ate a high fat diet; I’ve read many times that they did, and it was mentioned in the documentary that I wrote about in my post to Duck Dodgers. The “high fat” aspect was even mentioned in the link that Duck Dodgers posted, as it is in the link above. I hadn’t read in the past that they ate huge amounts of protein- (I didn’t realize it was even possible to eat that much protein, as I thought it made people sick). It’s possible I guess that some did and some didn’t. In any case, I’m not saying that all that was said about the Inuit was all wrong, it’s just that- natural skeptic that I am- some of the evidence seemed a bit conflicting to me, and raised a few questions.
Oh OK Morgana. Thanks. That (probably missense) CPT1a variant does intrigue me. My thought is that it compels more FFAs to go straight to thermogenic tissue, e.g. brown adipose tissue. But who knows? I can’t warm to the idea thought that it’s some “liver-sparing” thing. My sense is that our GIs are too good at vetting trigs in the duodenum to allow a whopping load of long-chain polys to go systemic. –Bryan
I said … “to allow a whopping load of long-chain polys to go systemic.” That is, Morgana, except to let them in to burn right away, e.g for thermal energy. –Bryan
Morgana, rereading your post, I’m absorbing more good points you made. 68% of northern indigenous peoples in far eastern Siberia with the variant means almost *a third* of them have the normal CPT1a gene per that link you gave, making them “less different than us:”
http://www.sciencedirect.com/science/article/pii/S0002929714004224
That gene variant rate could be greater or less for the Yupik-Inuit in Alaska, Canada, and Greenland.
To dilute the message and muddy the waters still further, the researchers tested Chukchi and Koryaks as well as “Eskimo” (I assume here they mean Yupik, the only Eskimo people I know of in Siberia). I couldn’t find anywhere it says how many of each group they tested. Was it an even mix of the three groups? Or weighted toward one or two of those groups? It’s likely the “Eskimos” were a minority in this little cohort.
The Koryak are especially interesting because they live south of the Yupik and Chukchi and appear to eat more plant-sourced food. This Koryak Wiki, https://en.wikipedia.org/wiki/Koryaks, says:
“… Salmon and other freshwater fish as well as berries and roots played a major part in the diet…”
The last point on that CPT1a gene variant: How much weight can we put in a sample rate of only 25 people?
Morgana, about the article quote you cited: “…mutation could be protective against overproduction of ketone bodies…” Yes, interesting that this piece also points to a high fat diet with the Yupik and other indigenes. And like you say the risk of “overproduction of ketones” is conjecture. I’ve heard of plenty of accounts of people on high-fat diets testing negative for ketones, and that was my experience too. When I went 80% fat 15% protein 5% digestible carb in early 2008, I tested my ketones for several months and it always came up negative on the strip. That makes sense. Our bods have at least several ways to regulate our ketone body levels. Our very neuron-rich GI constantly communicates with our brain regarding energy needs, and is able to vet to a great degree the dietary fats in the duodenum, deciding whether the body needs them (for structure and energy) or not, letting the excess wend down to the exit. Even if some excess fat goes systemic we may have ways besides CPT1a variants to gate conversion to ketone bodies, like storing the fat in adipose tissue. Finally, we can easily purge unused ketone bodies that exist at physiological levels. β-hydroxybutyrate and acetoacetate spontaneously break down into acetone, a volatile compound we eliminate through our pores and breath. –Bryan
wbryanh- yes, good point about the ketones. Ketosis isn’t “dangerous”, like some people seem to think, and the body has ways to regulate it. In any case, it’s curious why and how that mutation came about. I wonder how prevalent it was in their ancestral past- (before the introduction of modern foods into their diet?) I think it was mentioned somewhere that most of the people who were tested were already eating at least some non-traditional foods, though I don’t know if that has any relevance at all. In any case, I’d like to study this further….(not tonight though, I just got back from a long day of work). I’ll let you know if I find anything.
Morgana, yes, I’m curious to know too. More and more, I wonder what life factors select for it. Duck posted something recently about how the CPT1a deficiency variant is common among the Hutterites. It’s also common in the Koryaks even though they have more consistent access to veg than the Yupik and Chukchi. Anyway the research is there waiting for you when you get rested up. 🙂 –Bryan
wbryanh- Been looking for information about this mutation. It’s hard to find what I’m looking for- (maybe not much is known about it)- but most of the medical literature looks at it as a “deficiency disease”- (it’s the cause of a high infant mortality rate). Since it’s relatively prevalent in certain Arctic communities, it’s suspected that it served an advantage at one time, though no one seems to be in agreement as to what this advantage might have been. I thought this was an interesting link- it states once again that not all Inuit have this mutation (they give some specific information about the percentages). They also mention that the Inuit ate a high fat diet, not necessarily a high protein diet (although I guess one doesn’t preclude the other): http://pediatrics.aappublications.org/content/130/5/e1162.full
It has been mentioned that this mutation seems to protect against diabetes (though I don’t understand the mechanism). I’ve been trying to discover exactly when in time this mutation became prevalent, and if it was before or after the introduction of “Western” foods- (which I guess many of them have been eating for quite awhile). Could be interesting…..
Like always, there’s a bit of conflicting information. I’ll keep looking though.
Hi Morgana. About CPT1a deficiency, I’m into a house repair right now, but the Pediatrics piece you posted is very interesting and I’ll come back to read it more closely. I’m wondering if it has more to do with lots of long-chain w3 in the diet, regardless of calories burned and extreme cold? The highest verified rate of the deficiency I know of are for those 25 indigenes in Siberia that got their genomes sequenced, and they were a mix of Eskimo (Yupik), Chukchi and Koryak, the latter who lived further south, and that 68% or roughly 2:1 for having the homozygote. (Btw, I don’t know of any such sequencing studies for Alaska, Canada, and Greenland Yupik-Inuit.) But all these people are coastal and eat sea life. Then in that Pediatrics piece you posted, on page e1166, you see 1:4 for the coastal BC indigenes on Vancouver Island, where the weather is very mild, and usually don’t have to spend so much energy hunting for food and warding off cold. The ratio drops down dramatically as you move inland away from big w3 sources. The Hutterites in NA are 1:16, but many lived in coastal Europe (Amsterdam, Leeuwarden, Danzig (i.e. Gdansk) before coming to NA, so maybe lots of herring? Anyway, these are my quick thoughts on it.
About the Inuit eating a high fat diet, it makes sense to me. I don’t doubt they eat very high protein at times when they have to. But from just about all I’ve read and heard, the Inuit favor fat. About what level “excessive” protein may be, I found this Wiki that suggests actual numbers:
https://en.wikipedia.org/wiki/Rabbit_starvation
which has this: ” …It has been observed that the human liver cannot safely metabolise much more than 221–301 g of protein per day (for an 80 kg/176 pound person)…” Ducks posted studies of Inuit eating up to that much, 280–300g. I don’t recall any going beyond that, but quite possibly overlooked them. I even have personal experience with a high protein diet. I spent a month in 2007 dialing up to 300g/day protein, and kept it there from Aug–Nov 2007 (not July–Oct like I said earlier) and felt fine except for ammonia breath and peeing 3–4x/night. Fact is, no-one commits to any figure that constitutes “excessive.” That Wiki continues:
“…given the lack of scientific data on the effects of high-protein diets, and the observed ability of the liver to compensate over a few days for a shift in protein intake, the US Food and Nutrition Board does not set a tolerable upper intake level nor upper acceptable macronutrient distribution range for protein.”
Per this anyway, our livers adjust very quickly to a high-protein diet.
OK Morgana back to carpet-laying. Lots to follow up on! –Bryan
wbryanh- okay, in looking further, it seems that this mutation appeared thousands of years ago; though it’s hard to know how widespread it was, or exactly when it became so prevalent. What about life before this mutation developed: were the Inuit in ketosis? It is a recessive gene, and apparently both parents need to carry the gene in order for it to appear- (I can re-find the links if you need). It’s considered a “deficiency disease”, so researchers have wondered why it’s so prevalent in these Arctic groups. It can cause problems (as we know), like hypoglycemia and high infant mortality, which wouldn’t bode well for the people. It’s been called a “paradox”. Researchers theorize that it probably incurred some kind of benefit in the past, when they were on their traditional diets. One of the common theories is that it “protected them from their high fat diet”; (that is, of course, assuming that high fat diets are “dangerous” and that we need “protection” from them). I haven’t figured out what the mechanism would be that would “protect” them, nor has that been explained. In addition, there are several other theories as to why this mutation might be advantageous (for instance, it keeps them warm, which makes more sense to me).
But looking at it from another angle: what is the “cure” for hypoglycemia? A low carb, or even a ketogenic diet. It was bandied about in the comment section of an article about the Inuit on the blog of Dr. Eades (“Protein Power”) that possibly this mutation appeared in the gene pool, but since they were fat burners (possibly even ketogenic)- the gene just “stuck around”, not doing any damage, whereas in other populations who eat higher carbohydrate diets it would have been selected out. This might explain why it’s far more prevalent in certain populations (the coastal), as you mentioned. Do the inland Inuit eat more carbohydrates? (I believe you said they did). In any case, that’s another possibility, the way I see it; that rather than incurring an evolutionary advantage- (some liken it to sickle cell anemia)- maybe it simply wasn’t causing too many problems on their native diet, but now it is problematic on their modern diets. I’m not saying this is definitely the case; I just believe it could be plausible.
Below is a link explaining how breastfed infants (when they are exclusively breast fed) are in a state of ketosis. I believe the Inuit, like most hunter gatherer cultures, breastfed their babies for a pretty long time. And I guess Duck mentioned that the babies with this gene mutation had to be fed very often- (at least, the ones who had been exposed to modern foods, or formula). It’s kind of hard to ascertain how things were on their native diet, as the Inuit have been exposed to modern foods for quite awhile now. (So, as you mentioned before, maybe they are burning fatty acids, but do “ketosis differently” than we do?)
http://www.ketotic.org/2014/01/babies-thrive-under-ketogenic-metabolism.html
Morgana, what you say here: “…the gene just “stuck around”, not doing any damage…” I definitely want to explore more that option. The longer the fat chain, the less polar it is, thus the less of it travels directly from the duodenum through the hepatic portal because long-chain fats simply don’t travel well in serum. Rather the vast majority of these very long chain w3 fats (20-C and 22-C long) have to take the long roundabout “milk-run” (fat-run?) on chylomicron “buses.” Our GIs load these long-chain fats onto chylomicrons and send them into our lymph system where they travel all the way up to our left subclavian vein where they finally enter serum. (Here’s a Wiki with details on it: https://en.wikipedia.org/wiki/Chylomicron ) I suspect for Yupik-Inuit and related circum-Arctic folks who adapted to such a rugged and intensely cold place, their bods suck up loads of these fats into thermogenic tissue, like brown adipose tissue, long before they ever have a chance to make it down to the liver. So maybe it’s that, despite a diet hugely high in these w3s, remarkably few of these Inuit lipos ever make it to the liver, and so CPT1a fell into disuse. As for evol selective pressures, maybe the need to generate the max thermal energy simply to not freeze to death trumps the problem of need to frequently feed Inuit infants. Of course on all this hard tellin’ not havin’ the actual isotope-tracer tests to show us. But this is one of the ideas I’m noodling around. –Bryan
Expanding on my last comment Morgana, could be the relatively high rates of the CPT1a deficiency homozygote in coastal BC indigenes, like those on Vancouver Island, may be vestigial? At least in part? Left over from when the original First Peoples crossed the Bering Land Bridge 15–20k years ago? We have evidence the homozygote is quite common in current day Siberians from those 25 gene sequences showing the 68% presence for the deficiency in Yupik/Chukchi/Koryak. Could be CPT1a deficiency traveled across the Land Bridge in these original First Peoples, stayed prevalent in the Yupik-Inuit and others in the far north due to enviro pressures, and had time over the relatively few millennia to go only partially heterozygotic. Esp for their relatives such as the coastal indigenes who migrated south and who still eat a high w3 fish diet so less enviro pressure to go heterozygotic. Meanwhile those who migrated inland like the BC interior, away from high w3 and possibly more carbs, experienced more evol pressure to go heterozygotic but even so they still retain vestigially the deficiency. Again all this from reasoning, no proof. –Bryan
Morgana, you bring up other points I’d like to address, but have to stay on the hateful toxic task of laying wall-to-wall. I hope to come back this evening, early morning your time. BTW, It’s Duck who’s been saying the Inuit “…do ketosis differently from the way we do.” I’m not sure what Duck fully and exactly means when he says that. But I’m willing to consider the idea it includes fewer ketones. Which brings up an interesting question: Why do Yupik-Inuit infants need to eat frequently, but the adults can fast? What life-time adaptations allow the adults to do that? I may be overlooking simple answers here, but have my mind on the carpet task. OK Morgana, to be continued. –Bryan
Looking forward to it!
wbryanh- below is a link explaining how glycogen is converted to lactic acid after the animal is killed. One of the points made is that if the animal is stressed, or exercising- (like if it is being hunted?) the glycogen goes into the bloodstream and basically gets used up. Of course, they are talking about muscle meats here, so I don’t know how that applies to liver or to sea animals and their skin:
http://www.fao.org/docrep/t0562e/t0562e02.htm
Generally, there are small amounts of carbohydrate in meat (more in liver), but usually it is considered minimal, and therefore not included in macronutrient ratios. (Well, in the meat that *we* eat anyway). There are also small amounts of carbohydrates in eggs; (the eggs of sea birds were also eaten quite a lot by the Inuit).
Morgana, thanks for the FAO link. I’ve been meaning to look more into glycogen depletion during animal stress like during hunts. The Yupik-Inuit going on often protracted hunts and taking sometimes hours, like in the case of whales, to chase and make the kill. So it’s easy to imagine these creatures convert at least some (most? all?) of their glycogen to lactic acid.
Shellfish–at least bivalves–have a lot of glycogen. I wonder how much the bivalve feels stress and drives its glycogen to lactic acid? –Bryan
wbryanh- below is a link about the carbohydrate content of shellfish after death. (There is a table as well). You will note that although shellfish does contain carbohydrate, it’s still pretty minimal (at least the ones listed). By the way, I don’t agree with everything he writes in this article (mainly his opinion on cheese). But I thought the information about shellfish might interest you:
http://thepaleodiet.com/believe-shellfish-contains-carbohydrate/#.VnMcLVJl9DU
Hi Morgana. Thanks for Cordain’s shellfish carb missive. I hadn’t read anything by him for ages. Shellfish carb loads aren’t negligible and in my early days of taking control of my metabolic health (2007–2009), eating a bowlful of mussels definitely popped my blood glucose levels, though as usual I can’t discount other possible drivers. But even the most carb-filled shellfish (cooked whelks) at 15g/100g are still less carb dense than starchy tubers like boiled potato at 19g/100g of active carbs (http://ndb.nal.usda.gov/ndb/foods/show/3093). and not all that much more than some legumes like lentils at 11.5g/100g of active carbs. (http://ndb.nal.usda.gov/ndb/foods/show/4989) Lentils are on a par with carby shellfish runners-up mussels and abalone. Plus, shellfish comes with a big load of vitamins and minerals which may help offset the BG-popping effect of the carbs.
Interesting, I don’t remember Cordain him being interested in food acid-base issues. I haven’t yet found much research to lead me to put much stock in dietary pH regimens. For healthy people anyway. Our bods offer plenty of ways to balance serum pH. About cheese, some people feel it sits in an ancestral murky zone. But I’ve never had much trouble with it. The path to cheese seems built on completely natural processes. Ruminants like sheep have rennet in their rumen which begins to curdle mother’s milk right in the rumen so the lamb can more easily and completely digest the dairy. –Bryan
Bryan: One note on blood glucose and shellfish. At one point I looked into the whole issue after a long conversation with an insulin-dependent diabetic. He very carefully tracked his sugar intake and blood glucose and dosed with insulin as needed, and had been quite successful at keeping his blood sugar steady.
But what surprised and confused me was that “carbs” were not the main issue. His BG would spike when he ate proteins too, but especially *certain* foods, not protein in general. Gluconeogenesis can be used by the body to produce glucose, but it takes time, and one dish of oysters wouldn’t do it.
What does spike BG quickly is anything that causes the body to release stored glycogen. And this is where one protein meal can have way more effect than another protein meal. Some of the factors have to do with how much assimilatable iron is in the meal, which is also affected by the Vit. C content, and probably polysaccharides and fat, and things like lactoferrin. Shellfish are super-high in minerals, including iron. So is liver, of course. Not so much in fat or “white meat”.
This doesn’t have much to do with the argument about “are Inuit in ketosis” of course, but it does affect the average low-carber who is looking at their BG. There is an excellent full-text article on the subject:
http://diabetes.diabetesjournals.org/content/51/8/2348.full
“Reciprocally, iron influences insulin action. Iron interferes with insulin inhibition of glucose production by the liver. Hepatic extraction and metabolism of insulin is reduced with increasing iron stores, leading to peripheral hyperinsulinemia (48). In fact, the initial and most common abnormality seen in iron overload conditions is liver insulin resistance (49). There is some evidence that iron overload also affects skeletal muscle (50), the main effector of insulin action.”
Anyway, I just think it’s another factor to consider. When I hear from people who are trying to “stay in ketosis” (as measured by ketostix) they often say that “eating too much protein” is an issue, and that they need to just eat mostly fat. But I don’t think “protein” is the only issue with the high-protein foods … the high mineral content has an effect too.
Hi Heather, thanks for the link on iron and T2D. Before I continue on that topic, let me address what you say here:
“Gluconeogenesis can be used by the body to produce glucose, but it takes time, and one dish of oysters wouldn’t do it…”
To be clear Heather, *dietary* glycogen, like what we find in shellfish, doesn’t need to pass through our livers. Our GIs’ α-amylases set upon this “animal starch” like they do on plant-sourced starches we eat like amylose and amylopectin.
https://en.wikipedia.org/wiki/Alpha-amylase
Starch digestion starts with salivary amylases in our mouths and continues in our duodena. So yes, the glycogen in shellfish may well be responsible for popping fragile BGs. I certainly saw that effect in the early days of my efforts to recover what I could of my broken glucose metabolism.
I can’t discount other possible factors like you point out. E.g. shellfish with its abundance of vits and mins, and esp of certain proteins like tropomyosin which can be quite allergenic for many people, causing an immune response, which is an inflammatory event that can pop fragile BGs.
http://cdn.intechopen.com/pdfs/31774/InTech-Characterization_of_seafood_proteins_causing_allergic_diseases.pdf
That said, though the years I saw my carb tolerance generally improved regardless of my carb sources, e.g. shellfish, fruits, etc. So I do lean toward the idea that glycogen was largely responsible for those early effects.
Back to iron, that’s truly one of the big takeaways for me in our forum here. Of many takeaways; we’ve had so many excellent exchanges. I do think iron it could be a big issue that Duck and other people here have discussed. When I carefully tracked my meal nutrients in the spreadsheet (2008–2010), iron was one of those that routinely exceeded the RDI. Because of that, I started getting Iron/TIBC panels in 2009, and found my iron levels ride at the very high end of the normal ranges. I donate blood to lower them, but that effect doesn’t seem to last long. I need to keep digging into this. –Bryan
Yes, I agree the starches get into one’s system very quickly, esp. the dextrose starches. I had not thought about the carb content of seafood much until it came up here. But I do eat a lot of “Asian” style seafood, and shellfish are big on the menu! What is interesting is that a lot of them are just naturally and obviously sweet. I think some of them might even get sweeter as they dry. There might be some reaction that happens … like what happens with mushrooms, when dried in the sun the Vit D content gets very high.
But another weirdness in the Inuit diet may be that it would be high in taurine. There is a lot of taurine in seafood anyway, but it tends to get destroyed by cooking. Populations that tend to eat raw fish … like the Japanese and Inuit … get higher dosages of it. The more taurine, the better the heart-health markers.
So this could affect the Inuit in a few ways that aren’t related to genetics or carb content:
1. Taurine protects against heart disease, regardless of the other factors in the diet.
http://www.ncbi.nlm.nih.gov/pubmed/19239132
2. Taurine helps with fat digestion. It’s used to make bile.
http://www.livestrong.com/article/458271-taurine-and-bloating/
3. Taurine affects ketone production in the liver (in rats anyway: makes the liver more prone to produce ketones).
http://www.ncbi.nlm.nih.gov/pubmed/10629440
4. Taurine is key to glucose transport.
http://www.sciencedirect.com/science/article/pii/S0041008X11004455
In theory human beings can synthesize taurine, but it appears that getting more from your diet has really good health effects.
http://www.lifeextension.com/magazine/2013/6/The-Forgotten-Longevity-Benefits-of-Taurine/Page-01
————-
My body tends to hoard iron also, and after donating blood my hemoglobin just shoots right back up. I’m guessing that’s an adaptation to constant parasites in past ages. But it could also be an adaptation to thousands of years of eating whole grains. My ancestors lived mainly off oatmeal, and whole oatmeal is a big iron-blocker.
heathertwist- thanks for that information on taurine; I didn’t know that before.
Morgana: You are welcome! I learn so much here.
So far it appears that all the “healthy” diets are in fact high-taurine diets (and most of them are also wheat-free, except the French). The Inuit have raw fish and meat. The Japanese and Okinawans, of course, have their raw fish, plus octopus which is super-high in taurine. The French have raw milk cheese, and maybe stuff like pickled herring (which is not cooked). The Maasai and Swiss have raw dairy. The Maasai also have (or used to have) raw blood.
There is a nice PDF here of the world-wide study:
https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=5&cad=rja&uact=8&ved=0ahUKEwiQ4a3ijvDJAhVY2GMKHTCYBNMQFgg9MAQ&url=http%3A%2F%2Fwww.springer.com%2Fcda%2Fcontent%2Fdocument%2Fcda_downloaddocument%2F9780387756806-c2.pdf%3FSGWID%3D0-0-45-722329-p173764225&usg=AFQjCNHKTYjeVqom7LwE6ofYBk6spOeOEA&sig2=zkS5SWOq0WssgmOAoxUFKw
Has a nice graph of mortality rates vs. taurine excretion. Oddly, Finland and Sweden are low on the Taurine excretion graph.
The outliers to this theory are the healthier vegans: the Rice diet and the Japanese mountain people especially. Vegans though, often have *more* heart diseases than average, which is thought to be either the lack of B12 or the lack of “sulfated amino acids”. Also vegans in the US are low on taurine excretion: http://www.ncbi.nlm.nih.gov/pubmed/3354491
So how do some vegans stay healthy? I’m kind of wondering if the vegans that are super-healthy are also the ones that appear to have a high-sulfur diet (and some other source of B12). The Japanese mountain people live near a volcano and eat mainly roots which happen to be high in sulfur … maybe those roots happen to make it easier for the body to synthesize taurine. High-sulfur vegies might do the same thing: broccoli, cabbage etc., which are the backbone of many low-meat diets. Garlic of course, is high sulfur and noted for being “healthy”. Some water supplies are high in sulfur, and some are not.
It really would be ironic if the common feature of “healthy human diets” ends up being the secret of Pottinger’s cats …
Hi Heather, sorry to not write sooner. I was delving into your taurine links. Esp on its sulphur (S) content. Very interesting–thanks for these!
What surprises me a little, I rarely see discussion about vegans getting enough S. It’s so easy to get enough S on a non-vegan diet that those folks don’t have to think about it. But conceivably could be an issue for vegans who don’t eat enough brassicas like broc and cabbage and alliums (allia?) like garlic and onions. Here’s a WAP piece on it:
http://www.westonaprice.org/health-topics/heart-of-the-matter-sulfur-deficits-in-plant-based-diets/
After the “Organic Four” (C,H,O,N) and phosphorus (P) and calcium (Ca), S is one of the most common elements in our bods. We need it for all kinds of critical processes, including to make amino acids and to shuttle electrons in cells in addition to the reasons you gave Heather:
https://en.wikipedia.org/wiki/CHON
https://en.wikipedia.org/wiki/Composition_of_the_human_body
https://en.wikipedia.org/wiki/Sulfur#Biological_role
About our bods making enough of their own taurine from raw S from raw meat, cooked meat, S-rich veg etc. I eat raw meat/shellfish and love it, but could it be we can do fine on dairy/eggs/cooked meat/S-rich veg? I’m still trying to put a finer point on it. Here’s the links that Life Extension supp comp author gave us for it if you guys want to have pokes at it:
6) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994408/ (full)
7) http://www.ncbi.nlm.nih.gov/pubmed/2496406 (abstract)
8) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3501277/ (full)
9) http://www.altmedrev.com/publications/3/2/128.pdf (full)
10) http://www.ncbi.nlm.nih.gov/pubmed/9437654 (abstract)
11) http://www.ncbi.nlm.nih.gov/pubmed/12514918 (abstract)
12) http://www.ncbi.nlm.nih.gov/pubmed/1811446 (abstract)
13) http://www.ncbi.nlm.nih.gov/pubmed/18305447 (abstract)
–Bryan
Heather btw, on endogenous vs supp taurine, I didn’t yet check the quality of the citation-containing journals. That’s a biggie cuz we’ve seen an explosion of bogus pay-for-print research journals the past decade. Even if you see an impressive ref in PubMed, all rich and science-y full of big words and graphs, you still could be getting a low-worth or even worthless report. You can go here to vet journals:
http://scholarlyoa.com/
Any journal I don’t immediately recognize (Lancet, BMJ, etc) I go to that site to check it. Free full texts more often come from bogus journals that the paywalled stuff. But you can find plenty of paywalled junk too.
Also, some of these links call taurine and “amino acid.” Some argue that’s wrong cuz taurine lacks the carboxyl group (-COOH). Anyway FYI: https://en.wikipedia.org/wiki/Amino_acid and of course Wiki’s not an unimpeachable source. –Bryan
Yeah, there are a lot of bogus studies out there now! On taurine though there is SO MUCH study and it mostly seems in agreement. Taurine was one of the first nutrition issues studied … Pottinger’s cats! What amazes me is that I haven’t heard about it much til now. Probably because I assumed that us meat eaters get plenty of it.
The surprising thing though is that it is not the case that a meat-eating diet automatically has enough taurine. When taurine *excretion* is measured, countries like Finland and England come out LOW in taurine. Clearly something else is going on. Likely how much the food is cooked is one big issue. And some foods compete with it. And some people seem to synthesize it better than others. There is so much to still be studied!
http://www.ncbi.nlm.nih.gov/pubmed/11510759
The French come out higher than Finland … maybe all that nice raw cheese. The variation in taurine excretion is kind of odd, given that it is supposedly easy to produce in the body.
I could see how some vegans get more sulfur than others, just based on the types of vegies they eat. Some of the popular vegan diets do stress eating lots of sulfur-vegies. But the rice diet seemed like an anomaly. And then it hit me: in the descriptions of the Rice diet, it was specified that fresh or dried fruit could be used! Given this is in the days when refrigerators were rarer, I’d guess there was a fair bit of dried fruit. And guess what? Dried fruit is often treated with sulfur!
Good set of links, thanks. I’ll peruse them.
And yeah, a lot of places call taurine an amino acid or a “conditionally essential amino acid”. It’s kind of a weird chemical in any case. It doesn’t actually get “used” all that much.
Heather, interesting! About what you say “…The surprising thing though is that it is not the case that a meat-eating diet automatically has enough taurine…” I’ll retract what I said “It’s so easy to get enough S on a non-vegan diet…” till we know more.
And great catch on the hidden sulphur in Kempner’s Rice Diet!
About Pottenger’s cats, first I heard of them, and have to laugh, makes me think of Schrödinger’s cat 🙂 But seriously the raw protein vs cooked animal-protein sources are interesting. Pottenger’s cats cough up confounderballs of course. First they are cats not people (as much as some beg to differ), we’ve had up to nearly two million years (per Richard Wrangham and others) of cooking our food, so we may have evolved adaptations to get/make/conserve taurine, and the results of Pottenger’s work, we can view them only correlatively. But those caveats said, it’s still exciting! About measuring taurine excretion, how to interpret the results? Can we simply say that greater taurine passing comes from greater taurine consumption and/or endogenous production? Or can it mean the excretor is more ably absorbing the available taurine than those who pass more of it, leaving less to go into urine? Or something else? So many variables.
About what you say here Heather, “…a lot of places call taurine an amino acid or a ‘conditionally essential amino acid’…” I agree there’s a lot of confusion about it out there in the web-o-sphere. I think most folks, when they hear “amino acid” they think “protein building block” which taurine almost certainly isn’t. I couldn’t find a single example of a protein that incorporates taurine into its AA chain. And don’t see how it could; its sulfonyl hydroxide sits right where the carboxyl group needs to be in order to link AAs together. See on page 9:
http://www2.fiu.edu/~herriott/ch18-carboxylic%20acids.pdf
All that said, Heather, seems little doubt that our little oddball taurine is important! The relevant section out of this: http://jn.nutrition.org/content/136/6/1636S.long
“…Taurine is the most abundant free amino acid in animal tissues…In addition to its role in the synthesis of the bile salt taurocholate, taurine has been proposed…to act as an antioxidant, an intracellular osmolyte, a membrane stabilizer, and a neurotransmitter. …Taurine is found in mother’s milk, may be conditionally essential for human infants…recent work has begun to reveal taurine’s action in the retina. It appears that taurine, via an effect on a glycine receptor, promotes the generation of rod photoreceptor cells from retinal progenitor cells…”
BTW, another important S-containing compound is the vaunted antioxidant α-lipoic acid, which sports a disulfide bond.
https://en.wikipedia.org/wiki/Lipoic_acid
http://www.ncbi.nlm.nih.gov/pubmed/19998523
I took ALA (cheapo TJ’s racemic mix because I couldn’t afford ALA-R) as part of my gaggle of supps in 2008–2009. –Bryan
Bryan:
“About measuring taurine excretion, how to interpret the results? Can we simply say that greater taurine passing comes from greater taurine consumption and/or endogenous production? Or can it mean the excretor is more ably absorbing the available taurine than those who pass more of it, leaving less to go into urine? Or something else? So many variables.”
My daughter made an analogy I found interesting. She said maybe taurine is like oil in a watch. It just SITS there and doesn’t really “do anything” … but if the oil isn’t there the watch stops.
The people doing the Esselstyn protocol wouldn’t be ingesting any taurine to speak of. Since they are alive and actually healthy you can figure they are making as much taurine as they need. The studies seem to show that vegans do excrete taurine, so they create a little more than what they need? So they would be excreting the extra? And left to ones own devices, one creates more taurine than one actually currently needs? But the vegans do seem to excrete a lot less than non-vegans. And it seems pretty clear that the more taurine you excrete, the healthier you are and the longer you live? So again, where do the Esselstyn and Pritkin vegans fit in here?
So … which would be better: eating very little taurine, plenty of sulfur vegies, and very little fat … or eating lots of taurine with a generally healthy diet? What happens if you heat a high-fat vegan diet anyway?
I don’t know either. Doesn’t seem like it would be a difficult thing to study though.
Yes on the middens! It’s amazing, just how BIG some of those are. Well, if I had the choice of chasing a gazelle or picking through tide pools, I’d vote for the tide pool! Chimps sometimes kill mammals and eat them, but it takes them a lot of time to chew them. Bonobos pick food out of swamps, including shellfish and snails. The bonobos get more Omega 3’s.
Yet another interesting link:
http://www.ketotic.org/2012/08/if-you-eat-excess-protein-does-it-turn.html
Morgana, about excess dietary protein forcing (nor not) gluconeogenesis (GNG), thanks for that ketotic.org link. I’ve wondered about it too, though I admit I generally assumed more GNG till now. With your link I’ll delve more into this. Even before we discuss other possible GNG gating factors, I’d like to point out that a quarter or more–maybe way more–of the protein could be converted to ketones/fats, depending on protein’s amino acid mix. Of the 20 AAs, 13 are obligate glycogenic, 2 are obligate ketogenic (lipogenic?), and the remaining 5 swing either way depending on the bod’s conditions/needs.
https://en.wikipedia.org/wiki/Glucogenic_amino_acid
https://en.wikipedia.org/wiki/Ketogenic_amino_acid
Also Morgana even if we *do* see increased GNG, people with exquisite insulin sensitivity may do such a bang-up job rapaciously sucking glucose into their cells the moment it hits serum that these people keep enjoying very low mg/dL of blood glucose–low enough to still allow fat mobilization. Aren’t low BGs what really matter? Whatever the mix of energy metabolic states we’ve batted around ad naseum–glycolysis, ketosis, lipolysis–what may matter most is whether or not we trip the insulin switch which decides whether we keep fats stuck in adipose or mobilize fat into serum. IOW, it appears the *sustained* concentration* of glucose in serum is what matters, not how glucose is hitting serum at any one time. For ancestrally-living Inuit, all the direct measure evidence fits the bill–low serum glucose, lots of mobilized FFAs.
For the Yupik-Inuit, besides their subsistence foodways, steady hard work and frequent warding off of cold, they appear to have a unique advantage–exceptionally permeable cell membranes. w6 and w3 are our only “essential” fats, meaning we have to get them from diet, and they also appear to populate our cell membranes in proportion to how we get them in our diet. I.e. the less w6 and the more w3, the more w3 in relation to w6 we find in our cell membranes. w3 is slightly more flexible than w6, so a higher w3/w6 cell membrane ratio results in more permeable cells. The ancestrally living Inuit eat the highest w3/w6 ratio foodway of anyone on Earth, so possibly enjoy the most permeable cell membranes. This increased cell membrane porosity may maximize nutrient ingress including glucose and its closely related downstream metabolite, Vitamin C. This may help explain why the Yupik-Inuit seem to do so well on quite low glucose and Vitamin C. We need to look at the effects of high w3/w6 ratio cell membranes on the GLUT1 transporters: https://en.wikipedia.org/wiki/GLUT1 –Bryan
Thanks for that information on amino acids! Wow, I did not know that before. I feel like I’m learning a lot from this thread.
Happy New Year Morgana! Hope your holidays were peaceful and relaxing and healthful. OK, at least two of those three.
I finally returned to your ketotic.com link–via some intriguing stuff on fat-driven gluconeogenesis. Chris Masterjohn looks at the mounting evidence to suggest that our bods can make pyruvate/glucose from…ketone bodies! Specifically, from acetone:
http://blog.cholesterol-and-health.com/2012/01/we-really-can-make-glucose-from-fatty.html
That’s what circled me back to your link which suggests GNG output–even in the presence of excess AAs–remains more or less constant. Until now, I couldn’t picture what else could happen to excess (glucogenic) AAs except to go off to GNG, thus “necessarily forcing BGs higher.” I now consider other GNG processes might be going on at the same time, which the bod dials down as AA-driven GNG ramps up, all to maintain the same net output. Those other GNG sources include glucose from glycerol, the backbone compound for triglycerides. And now, apparently, glucose from acetone. Another candidate example of how we remain the robustly exquisitely homeostatic beings we are (or should be). –Bry
Thanks wbryanh, Happy New Year to you too! Also, thanks for that link, it was interesting. I especially thought that all those ketogenic diet “debunkers”- you know, the people who say the ketogenic diet is “unhealthy” and “unnatural” and is going to kill us- need to have access to this information!
Good timing on your post Morgana. I just made my first post at Chris’ site. I’m afraid I’m a little effusive about the his acetone → pyruvate discussion (thanks to a pair of gin and sodas). But maybe you’ll want to check it out anyway.
http://blog.cholesterol-and-health.com/2012/01/we-really-can-make-glucose-from-fatty.html?showComment=1452118854632#c3355989122137031760
I included that ketotic.com link you posted showing stable net GNG under varying inputs. –Bryan
Just noticed that this my first post on Masterjohn’s site (blog.cholesterol-and-health.com)–yesterday at 2:20pm–it calls me “Unknown.” My followup post calls me WBryanH as expected. –Bryan
The post I looked at (yesterday) called you just “Bryan”. This new link you sent me doesn’t seem to take me to the same article on ketones; there were things about cod liver oil and other stuff. In any case, it was clear yesterday which comment was yours, so no worries.
I’ve been thinking more about this theme. First off, it debunks the idea on “Perfect Health Diet” that there is a such thing as “glucose deficiency”- (I never believed in it in the first place, since I couldn’t find anything to back it up scientifically. I think Jaminet might have just made it up; although, generally, in regards to other matters I do respect much of what he says).
Also, I’m wondering if it might be harder for people who are not yet keto-adapted and used to eating high carb diets to make this conversion? I remember reading on Peter Attia’s blog that when he first started experimenting with the ketogenic diet, it was harder for him to generate enough energy in the beginning, whereas later on his body adapted and it became much easier. I noticed something similar when I first tried a low carb, keto-type diet- (though granted, I was also recovering from chemotherapy and a lot of other horrible treatments, so who knows how much that might have played a part). Eventually though, I noticed I had far more energy, and on a much more “even keel”, than when I was high carb.
In any case, it brings up a lot of questions. Hopefully Chris Masterjohn will do a follow up post.
Morgana, yes, I remember the “low-carb flu” in the first half of August 2007. I noticed it mainly in the first week. I’ve never heard that it lasts more than a few weeks. But evidently even that short time is enough to thwart many people. The only longer-term symptom I experienced was when I smelled baking bread and other baking wheat-based foods. Made it momentarily a little hard to walk past bakeries, doughnut shops and pizza parlors. Took ~ nine months for the fragrance to stop triggering me. Then one day, it magically stopped. I still love the smell of baking grain-based foods. I just don’t think about eating them.
About glucose deficiency–or more like carb deficiency to make clear we’re talking about *exogenous* and not our “home-grown” glucose from glycogen, GNG, etc. I’ve concluded it’s simply impossible for us to quantitatively determine such a problem can ever exist in healthy people. No-one can do this. Not the Jaminets. Nor anyone else.
Even keto champions like Mark Sisson, Emily Deans, etc, keep telling us “some brain cells need glucose.” But, again, no-one seems to have any proof of this.
Our *only* cells I’ve been able to confirm that absolutely positively require glucose at all times are our red blood cells. This because, afaik, our RBCs are our ONLY cells out of our 200+ cell types that *completely lack mitochondria.* Thus, our RBCs–which are essentially hollowed-out hemoglobin “tote sacks”–need to lacto-ferment glucose to generate enough energy for their very modest energy needs. E.g. to keep active nutrient (and maybe ion?) gradients across the cell membrane. Yes, Morgana, I said “lacto-ferment.* Just like we lacto-ferment sauerkraut and kimchi. Our RBCs are little fermenters! Amazing eh? BUT, no-one seems to have any idea how much glucose these cells require. Again, their energy needs are quite modest. They have little else to do besides passively course through our blood to deliver oxygen to cells and cart away the carbon dioxide. But as low as our RBCs’ energy needs are, that constant need may explain why we have to maintain some minimal level of blood glucose at all times. For BG to always be around to serve as little on-the-fly Gluco Happy Meals for the RBCs’ endless trips around our bods.
Here’s the only argument I’ve seen that even begins to make the case for some level of glucose dependency in non-RBC cells:
Biochemical, Physiological, and Molecular Aspects of Human Nutrition
By Martha H. Stipanuk, Marie A. Caudill. Page 211, near top of first column.
“…Other specialized cells are also primarily glycolytic because of a relative lack of mitochondria or limited blood or oxygen supply relative to their rates of metabolism; these include leukocytes, white muscle fibers, cells of the testis, the renal medulla, and some cells of the cornea, lens, and retina of the eye…”
But even here, Morgana, who’s actually *measured* any of this? E.g. who actually measured respiration in our eyes’ lenticular cells? Even for these “remote” cells, how do we know ketones can’t deliver all the energy goods? Those little ketone bodies diffuse through blood and tissue pretty fast and effectively. Esp acetone.
Could it be our RBCs are the *only* reason our bods need to produce glucose at all? At least for energy purposes?
It’s all such a massive load of “WE DON’T KNOW.” –Bryan
There are obligate glucose-requiring cells of the nervous system and/or brain – as a Type I diabetic on a very low-carb diet, I’m not affected by hypoglycemia until my blood sugar has been <60mg% for a long time. Then, I notice purple patches in my visual field, I feel the cold (even if it's not very cold), my thinking slows and I'm prone to errors of judgement. Ketosis protects against the hypoglycemic symptoms we want to avoid – seizures, coma, death – but hypoglycemia still leaves the brain sucking wind https://ketogenicdiabeticathlete.wordpress.com/2015/12/18/hypoglycemia-can-ketones-help-fuel-the-brain/
Jonathan, remember I said “it’s …impossible for us to quantitatively determine such a problem can ever exist *in healthy people.*” E.g. people who can rely on appropriate levels of endogenous insulin and don’t have to inject insulin. Injecting insulin can overwhelm the bod’s “home-grown” glucose, disposing too much of in into cells, driving BGs dangerously low. When we bring med interventions into the picture, all bets are off.
In such a case, your symptoms may come from under-fed RBCs that begin to fail to deliver enough oxygen to your cells. How do you know that’s not the case? We simply have no direct measurement of what’s really going on. We can propose and infer pathways, mechanisms and causes & effects all we want. But it’s very hard hard to prove any of them till we actually measure them. That’s what I’ve been talking about. –Bryan
Emily Deans reckons “Some cells in our brain are actually too small (or have tendrils that are too small) to accommodate mitochondria (the power plants). In those places, we must use glucose itself (via glycolysis) to create ATP” – seems more plausible
http://evolutionarypsychiatry.blogspot.com/2010/08/your-brain-on-ketones.html
Jonathan, I also read Emily Deans’ post where she makes that startling assertion. She doesn’t source it. She doesn’t tell us what we call those cells. She doesn’t even tell us if they are neuronal or glial cells.
Frankly, her claim makes no sense to me.
Our brains have two main classes of cells: neuronal and glial:
https://en.wikipedia.org/wiki/Brain#Cellular_structure
Some of the smallest neurons in the brain are Cerebellar granule cells
https://en.wikipedia.org/wiki/Cerebellum_granule_cell
and they come with mitochondria:
http://www.ncbi.nlm.nih.gov/pubmed/8931459
The smallest glial cells are the microglia:
http://vanat.cvm.umn.edu/NeuroLectPDFs/NeurohistologyLectI.pdf
and they too contain mitochondria:
http://www.ncbi.nlm.nih.gov/pubmed/23815397
In fact, astrocytes, our brains’ most abundant glial cells, not only sport mitos but even appear to make their own ketone bodies!
https://en.wikipedia.org/wiki/Astrocyte
http://www.ncbi.nlm.nih.gov/pubmed/14769487
Looking at this another way, the smallest mitos are 0.5 um in diam while the smallest cells are ten times bigger, 4–5 um. So plenty of room for mitos to fit inside even the smallest cells. RBCs (~ 5um) ditched their mitos. But that’s likely because they didn’t need them since they are basically hemoglobin cargo vessels. RBCs even lack nuclei.
Jonathan, that brain cells have mitos only makes sense. You expect these cells to be extremely active metabolically, which requires lots of energy. Without mitochondria (and thus without a place to perform the Krebs Cycle) the only way cells can produce energy is through anaerobic fermentation, a very inefficient and low-energy-yield process.
I wanted to ask Emily about her comment. But that appears to be a non-starter. I couldn’t post my question to her blog post because she closed the comments. Her FAQ makes it clear “…my email volume is incredible, and I simply do not have the time to respond…”
Jonathan, I do question if Emily’s statement is correct. And even if these mysterious mito-less brain cells do indeed exist, how abundant can they be? If we have just a small number of them, they’d require a vanishingly small amount of glucose to power them. But again, I’m far from convinced they even exist. In my research, time and again, the only cells I read about that completely lack mitochondria are red blood cells. If you find evidence that these mito-less brain cells do indeed exist, I’d love to see it and will gladly stand corrected. –Bryan
Jonathan, thanks for sending me down a glial tendril. Found some interesting stuff that brings up more questions than answers.
Here’s an Emily Deans piece that describes more her suggestion that tendrils rely on glucose: https://www.psychologytoday.com/blog/evolutionary-psychiatry/201109/brain-energy
In it she gives a smidge more detail: “…Certain long nerve tendrils are too spindly to carry mitochondria. Those spindly bits need to run on pure glucose. Glucose becomes ATP… directly via glycolysis…”
At least we now know Emily’s talking about mito-less tendrils, not the brain cell cores the tendrils emanate from. But she gives no idea how many such “certain long nerve (glucose-dependent) tendrils” we find in a “typical” brain. What portion of the brain’s energy do these sop up?
And do these tendrils run on locally made glucose? Of the brain cells, astrocyte glial cells seem to have an exceptionally high number of very thin tendrils. Astrocytes are also the one brain cell type that produces ketones. Chris Masterjohn gave evidence of multiple pathways from acetone (a ketone body) to glucose. So did astrocytes evolve the ability to produce ketones to generate fuel for their own tendrils? Via a pathway to glucose?
I can’t find what a “spindly tendril” is composed of. Or what its energy needs are. Or where the glycolysis takes place to feed the tendril.
On another note, this link tells us brain cells are not wild for free fatty acid fuel, even though FFAs can easily cross the blood-brain barrier: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3790936/ So for brain fuel, looks like it’s mainly ketones and glucose.
Just my random findings and thoughts on the matter before I head to bed. Good night –Bryan
Anyway Jonathan, your statement:
“…In those [brain’s] places, we must use glucose itself (via glycolysis) to create ATP” – seems more plausible.”
the “seems more plausible” part may not at all relate to your symptoms and your low BGs. IF you were also cranking out plenty of ketones at the time.
Sure, glial (and/or neuronal?) cell “spindly tendrils” may indeed need glucose for their ATPs. And so? Maybe your spindly tendrils were getting all the glucose they needed from one or more of the (acetone→glucose) pathways Chris Masterjohn spells out here:
http://blog.cholesterol-and-health.com/2012/01/we-really-can-make-glucose-from-fatty.html
Pathways fed by acetones streaming from your liver and/or your astrocytes.
So, to sum up Jonathan, what caused your brain fog and other symptoms? Did they result from:
1) low BGs underfeeding your brain cells, as you suggest? Or,
2) under-glucosed faltering RBCs failing to deliver enough oxygen to your brain and to clear enough carbon dioxide from your brain? Or,
3) both? Or something else?
I couldn’t even venture a guess which scenario “seems most plausible.”
We’ve often heard the human brain is bioscience’s final frontier. Still, I’m amazed how little we know about it. –Bryan
It’s uncontested that by some mechanism hypoglycemia is less severe in the insulin-dependent if they are keto-adapted, by whatever mechanism – yet the dolts at the American Diabetes Association do not acknowledge even this observation – so IMO there’s no point in waiting for the Catholic church to look through the proverbial telescope before taking action …
Jonathan, if I listened to my Kaiser doc/ADA/mainstream, I’d be injecting insulin now. Instead of enjoying the totally med-free life I currently have.
But I’ll never forget one visit in 2007, when I put my doc on the spot about the macros I should eat. I asked him, in essence: “The higher carbs will surely kill me faster. We can eat only so much protein. That leaves dietary fat. What do you recommend?”
He looked very uncomfortable and anxiously looked around his office like the walls had ears.
He then leaned over toward me and–I kid you not–he *whispered* to me:
( “I’d eat a high-fat diet” )
The he looked around anxiously again, and quickly added:
“Make sure you come in often for your lipid panel!!”
HAHHH!!!
Hilarious, isn’t it! But such an awful human tragedy, all that pain, all those lives snuffed out …
Jonathan, to make clearer.
You assert: “There are obligate glucose-requiring cells of the nervous system and/or brain…”
To back up your assertion, you give your symptoms:
“…I’m not affected by hypoglycemia until my blood sugar has been <60mg% for a long time. Then, I notice purple patches in my visual field, I feel the cold (even if it's not very cold), my thinking slows and I'm prone to errors of judgement…"
All I’m saying: Your symptomatic evidence fails to prove your assertion that the brain has obligate glucovore cells. Why? Could be your symptoms *don't* stem from a glucose shortfall. Instead, it could be your under-glucosed RBCs fail to deliver enough O2 to your brain cells. And maybe those same underfed RBCs fail to remove enough CO2 from your brain cells.
Too little O2 and accumulating CO2 can definitely slow your thinking and cause other troubles!
Jonathan, just trying to make clear your evidence in no way proves or disproves any obligate glucovory in the brain. We aerobically respire fatty acids as well and glucose. That is to say, both energy-producing processes–originated either from fatty acids or from glucose–require sufficient oxygen to work. Perhaps a shortfall of oxygen–not glucose–helped cause your symptoms. Perhaps CO2 buildup helped cause your symptoms. We can't say for sure. But we can’t discount those possible causes. Bottom line: WE DON’T KNOW. –Bryan
Well, as some people say- (Tim Noakes, among others)- there is no such thing as “essential carbohydrates”. We need protein and we need fat, but we don’t need to eat carbohydrate, as our bodies can make them from protein, and even from fat.
And I agree, we probably don’t really know to what extent some of our cells need glucose. Some people (like Jaminet again) claim that ketogenic diets cause dry eyes, or dry mucous membranes in other tissues (like the intestine?) I’ve never noticed this at all in my case. Oh sure, I do seem to have less mucous and post nasal drip on a low carb diet (I assumed that was a good thing?) I don’t notice any problem with eyes, and my digestion is much better on low carb, so I’m assuming that’s another myth.
A propos the smell of fresh bread baking: to this day, the smell of wheat bread fills me with longing. As a celiac, I experienced bread (gluten) addiction; in people with leaky gut, the opiates in gluten can go into the bloodstream and cause something like a “high”; a.k.a. addiction. My whole wheat bread addiction was one of the main things that clued me in to the fact that I was a celiac. But even though the smell is tempting, I know that gluten makes me very, very ill, so that’s enough to stop me eating bread! I guess other people are not so “lucky”, and I can understand how it must be difficult not to give into cravings. When I first found out I was a celiac, and had to go on a gluten free diet- (I was still high carb for years, even though gluten free)- I would smell people’s bread, bagels, pizza crust, etc., just to get the vicarious pleasure!
Going low carb was relatively easy for me, in terms of cravings. Those gluten free breads and carbs taste pretty grim, so I never really missed those foods at all. Sugar was a little more tricky; however, once I stopped for a time, I’ve now come to the point that I actually dislike sugar. I’m highly sensitive to cloyingly sweet foods. Many fruits just taste too sweet for me now. Eating out in restaurants can be hard, as the food is sometimes too sweet, to suit “normal people’s” palates. I feel sometimes like I’m an anomaly in a world of sugar loving people!
Morgana, about sugar, “cloying” is a terrific word for it. Definitely you and I are still exceptions. Every once in awhile I’ll taste something that has a lot of added sugar, and it’s too much and unpleasant. To look at this another way, foods that never tasted sweet to me before now taste quite sweet, e.g. broccoli and *esp* cabbage. When I first started my VLC journey in late July 2007, I went a year without cabbage. When I finally returned to it, I couldn’t believe how sweet it tasted. I googled to see if Big Food was sugaring up cabbage like they did corn! When I was a kid (60s/70s) corn was very starchy. You had to cook it to eat it. But by the 90s, you could eat it raw off the cob and it tasted very sweet.
If there’s one thing that’s come home to me during my journey, it’s that we know *so d*mn little.* So much stubbornly remains beyond our ability to measure. Even something so seemingly basic like: How many cells actually compose us? I was like: “How can we NOT know that?!” And yet our cell-count estimates span almost *two magnitudes:*
http://phenomena.nationalgeographic.com/2013/10/23/how-many-cells-are-in-your-body/
Carl Zimmer, posted Wed 10/23/2013
“…estimates sprawled over a huge range, from 5 billion [I’m guessing CZ meant 5 trillion –B] to 200 million trillion cells…If scientists can’t count all the cells in a human body, how can they estimate it? The mean weight of a cell is 1 nanogram. For an adult man weighing 70 kilograms, simple arithmetic would lead us to conclude that that man has 70 trillion cells. On the other hand, it’s also possible to do this calculation based on the volume of cells. The mean volume of a mammal cell is estimated to be 4 billionths of a cubic centimeter…Based on an adult man’s typical volume, you might conclude that the human body contains 15 trillion cells…”
Much as I try to quantify and ferret out robust evidence, at a certain point Morgana, I had to go with my gut (haha ba dum tss) and choose *some* foodway. Of course Tim Noakes et al can’t *prove* that carbs are wholly optional calories. We have few if any direct measures. Nor can we reasonably expect to see such measures over a long term with a sufficiently large sample rate to let us say “Yes, for sure, that’s the way to go alright!” People reasonably ask: Where are the broad long-term studies for VLC-VHF? I don’t know of any.
That said Morgana, my eight + years living VLC-VHF have been exceptionally and uniformly positive. It may well be the single best thing I’ve ever done for myself. Since I embarked on VLC in 2007 at age 46, EVERYTHING improved by all observed measures I’ve done to date. Without exception. Like you noticed with lowered mucus production and still properly moist eyes, my symptoms cleared up and all else that was well stayed well. Even my springtime allergies nearly totally cleared up. I’m far from the only one who’s experienced frankly wondrous improvements. I’ve heard and read endless accounts about people who radically improved when they went grain-free VLC. Whatever their various mitigating factors may be.
Even mainstream biochem grudgingly mumbles and tilts toward inherent superiority of keto. Oxygen is a necessary evil. It’s key to aerobic respiration, which we humans have to do. But oxygen is… oxidizing! It attacks unstable fats like w3 and causes them to quickly rancidify. It helps create oxidized species like free radicals that rampage through our systems, that appear to wreak havoc and accelerate aging. Well guess what? When we respire fatty acids, kcal-to-kcal, we generate way less O–*6+x* less O–than when we respire glucose. That’s way less O that hangs around the cytosol to attack hapless cellular byfloaters. It’s easy to do the math. Glucose yields only 4 kcal/g and sports a whopping six Os per molecule. A long-chain fat (e.g 18C stearic acid) yields 9+ kcal/g and carries only two Os. Way less O means way less damage to our sensitive mitochondrial tissue and other organelles that bobble around in the cytoplasm and can stray in the path of bully oxygen which rapaciously steals electrons from anything within reach.
Morgana, If you accept the current biochem, it suggests that, at the deepest cellular level, keto lets us work BETTER. In the short term and esp in the long term.
But because we have a surprising paucity of direct empirical evidence, I have to rely on the circumstantial evidence I can find in all the relevant disciplines, which include paleoanthropology, paleoethnography, paleofornesics, organic chemistry, biochemistry, genetics, and nutrition science. I continually review anecdotal evidence, meanwhile always look at its depth, breadth and quality. I collect all the the clinical measures I can coax out of my doc. I often simply stop and ask myself: How do I feel? Even with all that evidence, I feel like pioneer forging (foraging?) into the old known/new unknown. I am my own Grand Experiment, though I meet a growing number of fellow-travelers. At this point, I have to say, I feel great and pretty great about it! To this point, even now, it astounds me that VLC it appears to have only numerous upsides and zero downsides in my regular daily life. I know of no other life change I’ve made that rewarded me with such strong and unalloyed positive results. –Bryan
Cloying is the perfect word for too much sweetness, and is the word I’ve used for decades. A couple of times, when I’ve accidentally sipped iced tea that someone “presweetened”, it’s literally made me gag. The thought of sweetened coffee is gruesome, especially if black without the cream to tone down the sugar. Needless to say, I don’t waste money on those cloying synthetic coffee drinks that are so popular. Fruit is fine usually, but some overripe types, even with no sweetener added, are awful. People think it’s weird that I can’t understand why anyone would add sugar to berries (or even grapefruit). Maybe some of us are different from the general public in the lack of a “sweet tooth”. I’ll have to research to see if there is any indication of a genetic factor. But, even as a child, I preferred dark, dark chocolate to milk chocolate, and literally gagged on things like pineapple upside down cake. The very thought of it makes my throat tighten. When my Mom would make it, I’d beg off on dessert.
annielaurie- I guess there could be a genetic component, though in my own case I highly doubt it, as I come from a family of sugar addicted people. In fact, as a child, I myself was a sugar-o-holic! I know many people say we are “hard wired” to like sugar, but I’m not sure that it’s that simple. (I agree that we are probably hard wired to like the very subtle sweetness of natural fruits and vegetables, the rest I’m not sure about…..) Basically, our taste for sweetness is cultivated. Usually babies and very young children are fed sugar and fast carbs, first thing, while weaning. Actually, it might even start in the womb- (my mother definitely ate lots of sweet foods! Especially chocolate). At one time I loved sugar so much I never imagined I could possibly give it up, but low and behold, after a few weeks on a ketogenic diet, not eating sugar, I grew to dislike the taste. (Though I still like the sweetness of vegetables and some fruits, and of course very dark chocolate; nothing below 85%). Because of my experience with sugar, I am a firm believer that the taste for sugar- (in it’s “cloying” form)- is largely cultivated- (though there may be other aspects at play here too, like genetics, possibly certain deficiencies, etc.)
wbryanh- I know what you mean about corn! I loved corn as a child, but somewhere along the line- (even before I went low carb)- I just decided I didn’t really feel like eating it anymore. It used to have a certain “nutty” taste, which it doesn’t have now. Funny enough, my brother (independently) came to the same conclusion; we talked about it years later. And I know what you mean about the sweetness of vegetables. For me, this is a huge benefit of eating low carb; all my food tastes so much better now! I hadn’t realized how much sugar dulls the taste buds. (Actually, not just sugar. Before I even gave up sugar, I stopped eating all grains, and when I did, other food tasted so much better! So I think something about eating high carb- for me, at least- affected my taste buds). I enjoy the flavors of food so much now. This is one of the things that has kept me wanting to eat low carb, and it also keeps me from wanting to cheat.
Of course, I’ve also experienced a whole slew of health benefits. Too many to mention here…..
Morgana on one level it seems self-evident that if we cut out added sugar that we’ll get more sensitized to what we still eat, that smaller amounts will taste sweet, right? But still, in the months after I went LC, my sense of taste returned so dramatically I wondered, how could that be? Finally this idea hit me: My incipient neuropathy had gone away. My nerve endings everywhere were healing–and beginning to sense more and feel more.
In late 2006/early 2007–the months preceding my T2D diag–I had tingling in my fingers and toes at night. After the diag (29 Mar 2007), I started to restrict cals and exercise like mad, meanwhile kept following the gov’t guidelines (50% carb, “wholehealthygrains,” etc). For a while my RC and all-day walks brought my BGs down from the troposphere, but then they started going up again, till they peaked of 245 on 29 Jul 2007. And this was after a 30 mile hike during which I ate nothing but a Clif Bar every 2–3 hours!
That was it. I went LC that day. That’s how I’ve been rolling ever since.
Constant keto really does seem too good to be true. I keep half expecting some bombshell to drop, that we’ve just discovered some horrible consequence of following LCHF long-term. Doesn’t everything have downsides? Yet the more I follow it and read the latest research on it, the better it looks. For me, there just don’t seem to be any trade-offs. –Bryan
I may have experienced a downside to keto – after 15 years, I got GERD from Helicobacter – fixed with two antibiotics, but then chronic diarrhea which lasted for three years, nothing made much difference – SCD, FODMAPs, food sensitivity testing, Elixa probiotics – I had Candida and high levels of a couple of commensal bacteria (“possible pathogens”) and C. diff so was treated with Nystatin, Cipro and Flagyl with little result. I read Richard Nikoley on potato starch, I’d done psyllium husks and Acacia senegal without improvement but I thought what the hell – and mirabile dictu it’s working! It’s plausible (to me at least) that my low carb diet starved out some desirable bacteria like the bifidos that make sfca’s – I tested low in 2ndary bile acids http://www.upi.com/Health_News/2016/01/06/Antibiotics-promote-C-diff-infection-by-killing-gut-bacteria/1281452107192/ which inhibit C. diff – so I’m convinced (in spite of n=1, many possible confounders, perhaps coincidence) it’s prudent to add prebiotics to the keto diet, especially potato starch since neither psyllium husks nor Acacia senegal made much of a difference …
Jonathan, I’m sorry you had to suffer all that! Ugh!
Did you ever find a proposed mechanism for how long-term keto may have led to your GERD? Besides possibly low bifidos? What I’ve read up to now, eg this:
http://chriskresser.com/more-evidence-to-support-the-theory-that-gerd-is-caused-by-bacterial-overgrowth/
links H Pylori more to carbs, in particular malabsorbed carbs in the GI which start to ferment. Which surprises me, at first glance, that potato starch seemed to clear up the problem that may involve SIBO! Btw, I had one excellent experience with PS, and then nothing after that, neither good nor bad. You can search this forum for my discussion on that.
I’d love to see a site where people doing long-term keto record their experiences and symptoms. To follow LCHF long-term is to ultimately go into the unknown, since relatively few people these days do it. For me, to this point (8.5 years) I’ve had absolutely no negative experience with it. But that’s only a little over half the years you’ve spent in keto. And it could be problems may in fact crop up even after such a long time. I ate HC for my first 46 years, but didn’t get hints of a problem till I was maybe 40. Of course, I wasn’t so focused on the matter either! I’m sure then I missed symptoms that now would look as big as barns.
I have to leave for an appt so will look at your bifido link when I get back. –Bryan
wbryanh, Jonathan Christie- First off, thanks for that Chris Kresser link….that was very interesting! I’ve read lots of his stuff, but not that one.
In any case, my own reason for going low carb in the first place was mainly to help my digestive issues- (though I did not have GERD; that was about the only thing I didn’t have, ha ha). I am a celiac, so I was already gluten free, but I seem to also have issues with fructose and high FODMAP foods in general. Going low carb helped my digestive issues immensely- (among other things), but it still wasn’t perfect. Then last Spring I decided to go on a low FODMAP diet, which I did for about 2 months, and then slowly added back the foods one at a time to see what I was sensitive to. This helped me immensely, as I discovered that even some low carb vegetables cause me problems. And, luckily, I’m not sensitive to all high FODMAP foods, so I can still eat some things like asparagus and shiitake mushrooms; I even discovered, through the diet, that I can eat some fruits- (when I originally went low carb I didn’t eat any, thinking fruits didn’t agree with me at all). I stopped eating grains completely because I notice I feel better when I don’t eat them- (apparently this is true of many celiacs). Luckily for me, the low carb diet- as well as knowing which FODMAP foods I can and can’t eat- totally cured all my digestive problems.
However, as some say, there are times in our lives when one thing works, and then it can happen that things in the body change, and we need to make little tweaks in our diets. My theory is that in this day and age, it’s particularly difficult to eat the very varied diet of our ancestors- as well as the fact that so many foods today just aren’t of the same quality as they used to be. It could be that a particular way-of-eating can work for awhile, but eventually some problems may occur, possibly due to nutrient deficiencies, or changes in gut bacteria. This is why we need to always be vigilant and continue to tweak the diet when we find something has changed. It looks like you’ve done that, Jonathan Christie, by adding in potato starch. I am also aware of the fact that if something ceases to work for me, I need to re-evaluate, and find answers. You’re right, wbryanh, that so little is known about long terms effects of ketogenic diets! (Though there seem to be plenty of people online who have done fine long term. One good example is Dr. Phinney, who looks quite healthy at his age).
Also, since we all have such different microbiomes, I’m convinced that there’s no one-size-fits-all…..just like Denise always points out! In the Chris Kresser link, he talks about stomach acid (or lack thereof) as being a major issue with GERD. I used to be mostly vegan, and I think that that diet caused low stomach acid for me. I was also unwittingly eating a lot of foods that I was intolerant to, causing yet more problems. In my own case, low carb seems to have greatly improved my stomach acid (as well as bile, another thing that was insufficient in my case). All of these digestive enzymes and hormones work together, so if one is off, it can affect all the others. I also think that for some of us, after years on a low fat diet, it can be difficult to suddenly digest high fat foods; the body isn’t used to it, so there may be malabsorption. This is my theory (one of them) as to why some people have problems on a ketogenic diet. If you can’t properly digest the food you’re eating- (my case on a vegan diet)- you won’t be able to absorb the nutrients you need and imbalances will occur.
In any case, this way-of-eating works for me now; but I am aware of the fact that if that ever changes, I need to be flexible.
Morgana, @Jonathan Christie, so much in your latests, wow. Where to start?
Please I hope you’ll bear with me as I speak generally in this post, and address your specifics in the next. When I read your posts I think again about how we live in a world of accelerating complexity–remember Toffler’s remarkably prescient book Future Shock? Our world filled with many thousands of novel substances (esp hormone disruptors like the organo-chlorides and -phosphates, eg BPAs, phthalates, PBDEs) and treatments, (eg antibiotic courses, infant formula and C-sections that deprive neonates of critical immune signatures, inside work and sunscreens that deprive us of healthy uV exposures) and behaviors (eg we face constant low-level stress as we do things ever more by the clock, we often sleep during nonstandard times, which violates circadian rhythms). All these Brave New World things that ramped up in the wake of the Second World War.
Of course we don’t pay attention to any of this when we’re young. We “feel fine” meaning we often stay clueless to subtle developing symptoms because we’re so preoccupied with family and kids and careers and our goals. Meanwhile, these chronic exposures and treatments and behaviors steadily damage us in our early decades, which leaves us, increasingly symptomatic in our middle/later years, to face the daunting task to sort out the myriad causes and effects. So much is by guess and by golly because of the enormously complex and interrelated nature in how our many thousands of bod processes work. We humans are the pinnacle of four billion years of evolution of life on Earth. The exquisite inner harmony and robustness how we are made, it embodies an almost unfathomable intelligence that accumulated over those eons. We are still in kindergarten when it comes to sorting it all out, and when I say “we” I mean even our research community that more and more of us deeply question, and rightly so. As well-meaning as they are, and/or as driven by corporate money as they are, researchers often do a terrible job sorting this stuff out, and we can’t depend on them. Consider those researchers who contributed to the nutrition advice the US started to promulgate in 1980 and which profoundly and even hopelessly lacks granularity, eg, for fats distinguishing only “saturated” and “unsaturated” and not examine the vast diffs of the fats within each of those two much-too-overly-broad categories. Increasingly, in that ancient Aristotelian balance of the Expert vs the Crowd Wisdom, I find the counterbalance of the increasingly engaged and IT-enabled Crowd to be more important than ever.
I want to acknowledge what a super tough job we have and how I admire that we try to sort out and unwind the accumulated damages we incurred in our first 35–50 years and to *understand* what makes us healthy and unhealthy. Maybe you feel I’m silly to say this seemingly self-evident thing, but I know so many people who simply give up and just accept whatever consequences come their way, to not try to sort out why their health slowly comes off the rails, which by the way I am not convinced is entirely a given as we age. Sure, even ancestrals tended to develop *some* CVD as they aged. But what tended to kill them were opportunistic infections that snuck past reduced immune systems (our thymus glands seem inexorably to shrink as we age and so lose immune signatures) and the fallout from from osteoarthritis, like after they fell and broke bones and became immobilized. Those two conditions of aging seem common among ancestrals and us modern-world people.
So what is the answer then? For me it’s, “Less is More.” All the interventions we do, from supps to elim diets to potato starch, I hope we keep in mind these are interventions, that they are temporary and we should limit their terms AMAP, that we should be working to restore our bods to their original balanced health that we are deeply designed to enjoy. I took supplements from 2007-2009, and tapered them off by that last year, as my BGs stabilized. My BGs did rise for a bit after I stopped the supps but then started getting lower and stabler again, which showed me we should be patient and take the long view when we trim out an intervention. Of course I know our health states differ, and that my chronic disease may be milder than others and so gave me less dysfunction to unravel. Still, I hope we can, AMAP, work to *reduce* inputs in our lives. Eg to eat AMAP organic/pesticide-free grass-fed locally-produced minimally-selectively-bred ancestral foods (esp no grains), use older kitchenware–glass, cast-iron, and stainless steel, to replace with hardwood floors those toxic chemical smorgasbords we call wall-to-wall carpets, reduce AMAP the body and hair products we use which are chock full of novel chemistry, regularly intermittent fast, transition to minimal-footware (even barefoot) running so we can benefit from that wonderful exercise without chronic impact on and repetitive injury to our knees and spines.
Often our best body “hacks” are the thing we *remove* from them. Perhaps the best of them of all: intermittent fasting.
Morgana, you say, “…there are times in our lives when one thing works, and then it can happen that things in the body change…” I hope that, with each condition we remediate and then immediately taper off, ultimately with each step we take to *eliminate* novel inputs, we will less and less face the prospect of “things that change in the body” because our bods become ever better to stay homeostatic and healthy and more resistant to the frayings and unravelings of aging. I hope for us to remediate as quickly as possible and then get out of the way to let our bods take care of themselves. –Bryan
I’m not so sure! Vitamin C for example – Pauling reckoned you can’t get enough from diet, your collagen will deteriorate and you’ll wrinkle – there’s a striking difference between my wife and I (who take C) and many of our contemporaries, we’re less wrinkly. I think Cs a keeper, as is magnesium which is woefully underavailable. Same with ALA and ALC, selenium and NAC … substances under-supplied in today’s food because of changes in agriculture, and much-needed because of the increase in xenobiotics. As an overarching philosophical principle it has merit, but there is a grave danger of throwing the baby out with the bath water …
Jonathan Christie- One of the reasons people may need “more” vitamin C nowadays could be that our diets have become so much higher in sugar- (by “our diets” I mean culturally speaking, not individually speaking). Sugar competes with the uptake of vitamin C in the body, so people who eat high sugar and refined flour diets are probably lacking in vitamin C. (Although foods high in carbohydrate also turn to sugar in the body, interestingly enough, natural carbohydrates in the form of fruits and vegetables are generally high in vitamin C). There does seem to be evidence that people who eat low carb require less vitamin C.
In my own case, I don’t take supplements because they make me feel awful for some reason. I tried taking magnesium awhile back, since I kept reading that we are “all probably magnesium deficient”; however, I got really bloated and felt absolutely terrible. And I took this very popular American one (the name eludes me now), the one everyone recommends and says it’s so “easy to absorb without causing symptoms”…..hmmmmm…..I think my body just doesn’t like supplements. I try getting what I need from food.
Interesting stuff! As an insulin-dependent diabetic obligate low-carber I don’t think I have a glucose vs. C uptake issue, but I do believe most every diabetic and citizen with a fasting bg>100 is likely scorbutic. I’m a believer in C because both our calcium scores are zero (as Pauling predicted) after decades of hi-C supplementation – quite unusual in a post-menopausal woman, absolutely unheard of in a 35-year 70-year-old diabetic. Magnesium sends me to the bathroom so I do Epsom sat baths. The other stuff I take doesn’t make me feel one way or the other, they’re a leap-of-faith investment in my future health but I’d drop them in a heartbeat if they made me feel bad!
Jonathan, when did you get your first calcium score? When did you go low-carb? –Bryan
diagnosed with diabetes 1 in1983, started vitamin C ~1985, CT scan ~2004 Ca=0, EBCT scan ~2011 Ca=0
Thanks Jonathan. And LC diet? Do you remember when you got going on that in earnest? –Bryan
1998, the year Dr Richard K. Bernstein published The Diabetes Solution – I was an instant convert, having failed the alternatives!
Jonathan, Dr Bernstein’s Diabetes Solution was my (first) pivotal read! I don’t agree with it all (in that edition anyway) but it was a key read for me.
Dr B’s a terrific living example of what he preaches! Still sharp as a tack even up to a month ago when he made this vid:
I laugh when I think back to the summer of 2007 when I sat in a local coffee shop blurting out “AHA!” “AHA!” as I read his book and people looked over at me. :-)))
I hope I meet him before one of us goes 🙂 –Bryan
Jonathan, here’s what I see: You started Vit C in 1985 with no idea your starting coronary calcium level. Then 13 years later, in 1998, you go low-carb. Then, six years after that, in 2004, you get your first coronary calcium test.
My question: how can you confidently attribute your low CC all to your Vitamin C supp? You had already six years of LC before your first coronary calcium scan. Maybe the low-carb diet played a big role? Maybe even the main role? You certainly gave it plenty of time to work its salubrious magic. And what about the improving quality of your food? If you’re like most of us after diag, you not only go low-carb you steadily ditch whatever SAD junk you ate and move more fully to high quality food, eg locally grown organic/pesticide-free produce, grass-fed meats, and high w3 cold-water fish like salmon that’s lower down on the trophic scale. And who knows what other changes you made since your T1D diag in 1983? You could have made near countless changes in the 21 years leading to your first coronary calcium test. How do you know which change played what role in your improving health? That’s all I’m asking. –Bryan
If you research calcium scores in diabetics, there simply aren’t any reports of zero scores in diabetic men over 60. No black swans. Add to that my wife is also 70 years of age, post-menopausal – Ca scores of zero are very rare in her demographic also. Yes we eat mostly organic and avoid sugar and grains, but any number of people do that. The only thing we have done different is we’ve taken 5 g per day of vit C for 3 decades, and it’s had the effect on us that Linus Pauling predicted, many years before he predicted it: your collagen will resist calcium infiltration i.e. atherosclerotic plaque. And it has. What are the chances? We’re genetically protected, er, by some magic never elucidated by science? I doubt that – but possibly it has to do with vit C functioning as Pauling predicted and protecting against atherosclerosis by strengthening the collagen in our arteries. Honestly, I don’t give a rat’s ass, and that said I’m not going to give up taking vit C to see if I develop a calcium score to satisfy the curiosity of the peanut gallery …
Jonathan, who suggested you should quit your Vitamin C? Right. NO-ONE.
Note I never suggested people should categorically drop their supps or any other intervention. I made this clear in my Dec 4th post to you.
Here, all I did was look at your timeline and asked how you “knew” it was your long-term Vit C therapy that was (largely? wholly?) responsible for your zero coronary calcium score. You said why you believe you should attribute this effect to Vitamin C. Fine. Thank you for your opinion.
As for how rare Ca=0 scores are in your cohorts, I couldn’t say. This study:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC515311/
says “…a 60-year-old non-smoking non-diabetic women with hypertension and high cholesterol would have a 47% chance of having a CAC score of zero…” IOW, almost *half* the women in this senior cohort get Ca=0 results. Does this Ca=0 rate slope off to near zero over the next decade of age, to your wife’s current age? I don’t know.
As for what you say “We’re genetically protected, er, by some magic never elucidated by science?” Yeah, well Jonathan, there *are* plenty of people who appear to be genetically advantaged to cardiovascular protection. I’m surprised you don’t seem to know about any of them. Here’s a recent one:
http://www.ncbi.nlm.nih.gov/pubmedhealth/behindtheheadlines/news/2015-10-22-genetic-variation-reduces-risk-of-heart-disease-in-women/
Jonathan, next time, if you will can the ‘tude, the gratuitous “rat’s-*ss” and “peanut gallery” stuff, that’d be appreciated. I’m very glad you and your wife have zero CC scores. –Bryan
The great majority of diabetics have a calcium score which goes up with age and is associated with a greatly increased heart risk http://www.medscape.com/viewarticle/503651 The ADA points out that *At least* 68% of diabetics 65 years and older die of heart disease so my CAC of zero at 70 years of age is remarkable – but not to you apparently, since 47% of women aged 60 have a CAC of zero (relevance??) and in any case would be easily explainable by genetics. Diabetics are dying left and right of heart disease, so the influence of any genetic protection is miniscule. I’ve fought long and hard to get where I am, don’t expect me to roll over for your trivialization of my rationales for my freedom from heart disease.
Well that’s just it Jonathan. You fought long and hard and made many changes. No-one’s trying to take that away from you. Really, I applaud you! I also ask: Please get over yourself!!
Jonathan, if you don’t want to keep an open mind, if you don’t want to hear challenges to you dearly held beliefs, if you’re here only to flog the wonders of supplemental Vitamin C, then fine. We don’t have to discuss the matter further and I don’t have to pay any more attention to what you have to say on it. Go ahead and believe whatever you want. No-one’s stopping you.
All I’m trying to point out, is that because you worked hard and long and made *many* changes, please don’t expect me to believe you really *know* what therapy primarily affected which of your conditions. Far as I’m concerned, based on what you told us here, you *can’t* know those things.
Case in point: You went low carb six years before your first Ca test. At a time not many people ate low-carb. How can you say *that* didn’t play a major role in your exceptionally good coronary calcium scores? You vastly reduced the inflammatory events in your bod. Reduced BGs meaning less glycation of proteins in your arterial endothelial lining, thus laying fewer seeds to grow arterial plaque. If this meant you reduced the amounts of your injected insulin, that also lowers inflammation with similar and added salubrious effects on your arterial linings.
And what about Vits D and K2? Did you increase those as well? Those fat-soluble vitamins are key to move calcium out of blood and into bone. Less blood Ca means less building material for arterial plaque.
Jonathan, maybe massive amounts of Vit C really is the wonder therapy here. Maybe it isn’t. Who truly knows? Whatever. If it fits your narrative and agenda to keep flogging it, if that’s what gives you the self-validation you seem to need, then please be my guest and we’ll just leave the matter here. I’m not here to listen to folks drone on about their pet beliefs that they can’t sufficiently support with solid evidence. Indeed who try to support them wholly or mainly on mere correlation. –Bryan
Morgana, @Jonathan Christie, I love this convo! JC, about Vitamin C and smooth skin, I think of the clear unblemished skin the ancestral Inuit have and the touted smooth skin of clear of the elderly people who live in the Japanese mountain town of Yuzurihara, and you know other factors are at play. These Inuit got a mere 15mg/day Vit C from food, and these elderly Japanese set the stage for their long healthy lives long before vitamin tabs went mainstream, plus why do they apparently fare so much better than the rest of the Japanese who surely take Vit tabs too? Again, other factors are at play, esp our chronically higher blood sugar levels as you so correctly alluded to Morgana. Glucose outcompetes its downstream metabolite Vitamin C for the GLUT channels that port these nutrients from our blood into our cells. These ancestral Inuit ate very few carbs and ran low BGs, 65 mg/dL, this lower glucose means less Vitamin C can still make it into the cells and do its wonderful collagen upkeep catalysis.
So see what I mean? This may very well illustrate the idea of pursuing *less* — in this case reduce and even remove the carbs. To let our bods make the glucose that it judges it needs. Again, glucose is vital to us. That’s why it makes sense we’ve evolved multiple ways to make it from non-carb nutrients like proteins and fats. And for you Morgana, to stop eating the SAD with all of its novel ingredient and skewed nutrient balances and bioavailabilities. You *removed* and replaced with foods your bod evolved to properly deal with.
And reduce our carbs by how much? This ties back to Masterjohn’s 2012 post showing we make glucose from fat as well as protein, and by multiple pathways. Maybe carbs *are* a truly optional nutrient. For some of us anyway. Maybe most of us?
Jonathan, you say “…there is a grave danger of throwing the baby out with the bath water…” I totally agree! The trick is to identify the “baby.” We do tremendous damage to ourselves with the SAD and our other daily environmental exposures I’ve mentioned before. So we absolutely need to take interventions. Another trick is to know when to get out of our bods’ way as they correct themselves.
Btw, I don’t discount the possibility that we can take interventions to extend our healthy lives beyond what we would normally live in the ancestral environment even spared the acute events of those days (wars, sabertooth tiger attacks, etc). I’m glad people like Ray Kurzweil pioneer this and we may learn valuable things from their experiences:
http://www.vice.com/read/100-pills-a-day-to-live-to-150
It’s just that we really know so little about the enormously involved and complex interactions in our bods that we could do more damage than good, eg to take so much supps Vits C and E that we shut down our bods’ endogenous anti-ox production, the latter which give us the added bennie to increase insulin sensitivity. See here:
http://well.blogs.nytimes.com/2014/11/26/why-antioxidants-dont-belong-in-your-workout/
This is a similar idea to how the testicles can atrophy on ‘roided up athletes (please pardon the rough language in this article):
http://www.esquire.com/lifestyle/health/a4350/steroids-0408/
Again, I wonder if we are very often best off, once we correct imbalances through interventions, to reduce and remove AMAP to let our bods make the nutrients they need. To not force them to deal with nutrients level beyond what they need. –Bryan
The people of Yuzurihara are a super-interesting case to me. I do have a couple of thoughts. One is about cooking methodologies. In Yuzurihara, and in some other “healthy people” places, the common cooking method is to put things in a pot of water and boil them a little. What this does, in practice, is to save all the good stuff that leaches out with other cooking methods. It also makes sure the meat or vegies never get above 190 degrees. So if you eat a lot of tubers, cooked in water … you likely get a fair amount of Vit C. Esp, when greens are added to the water and they are fresh-picked.
The other has to do with fish. It is sort of a rule in Japan that you have a little bowl of soup with each meal. That soup is generally made with dried bonito flakes and kelp. So the “good stuff” from the bonito flakes goes into the water, and so does the “stuff” from the kelp … which gives a nice shot of iodine and taurine with every meal.
I’m not sure how the Yuzuriharans make their broths, but if they follow the traditions of much of Japan, Korea, and China, they use dried fish. In Y. they have a salmonish fish in their rivers, and I could see them saving the guts or bones or whole little fish to use for making broth.
Greens aren’t mentioned much in the writups about Y., but taro and sweet potatoes (two of their main crops) also are very good for greens.
As for the Inuit … they have a diet that is mega-high in taurine, which is also very good for your skin. Taurine also helps regulate magnesium handling … maybe one of the reasons everyone seems to have magnesium issues these days is that we have very low taurine levels.
http://www.healthcentral.com/rheumatoid-arthritis/c/798984/116673/ta/
Hey Heather, Top o’ the Year–
The Yuzuriharans, I also looked into their cooking patterns. Not just how they prep their food but what is their cookware? For example, cast-iron was (still is?) a big part of traditional Japanese cookware, which challenges the ideas here that high iron per se is necessarily bad for us. Esp if, as you suggest, they eat a lot of soups, consume all the broth nutrients which could include iron uptake from the pot. About preserving Vit C, do I read this study right, it appears that you can denature it at 30–60C but preserve it when cook at a *higher* temp band, 70–90C? Today is first time I heard of that, but here check it out:
http://www.ncbi.nlm.nih.gov/pubmed/20546391
Anyway this study seems to align with what you say, to cook at 190F.
I’ll guess the Yuzus get most of their Vit C from the greens. Fresh greens are loaded with it but their starchy tubers don’t have much:
http://printarchive.epochtimes.com/a1/en/au/nnn/2011/04-Apr/Edition%20288/Edition%20288_p12.pdf
“…The diet consists mainly of starchy tubers – satsumaimo, a type of sweet potato; taro, a sticky white root; konnyaku ( = konjac root = shiritaki noodles), a gelatinous root vegetable; and tamaji, a small sweet potato…”
http://ndb.nal.usda.gov/ndb/foods/show/3207 11507, Sweet potato, raw, unprepared: 2.4 mg/100g
http://ndb.nal.usda.gov/ndb/foods/show/3214 11518, Taro, raw: 4.5/mg/100g
http://nutritiondata.self.com/facts/custom/659612/2?print=true konnyaku noodles, negligible Vitamin C
The first two are for the raw tubers, so may get even less Vit C after you cook them. You’d have to eat at least 2kg (4.4lb) of them raw each day to hit the USDA’s RDI of 90mg of C per day. With the greens, they get possibly 200–250mg/day. Well over the RDI, but way below typical supp amounts. Do these oldsters all supp now? Another Q to answer.
But Heather maybe the Yuzu diet carbs are lower than many of us assume? One of those fave foods of theirs, konnyaku, has almost *no* digestible carbs. I regularly eat konnyaku in the form of shiritaki noodles. For that very near no-carb reason. It’s got a great noodle texture but doesn’t budge my BGs. So depending on the balance of these root veg/tubers.
I’d also like to learn how much fish the Yuzus eat. All that Epoch Times link says is that they eat fish, but doesn’t give how much. Could be just the dried flakes like you sugg. Or maybe it works out to several oz of fish per day. I haven’t been able to find the details on it.
What about eggs? None of the sources mention it, but the Japanese eat lots more eggs (tamago) than North Americans. And often raw or near-raw, preserving CLA and other delicate nutrients:
http://www.japantimes.co.jp/life/2014/09/16/food/raw-appeal-eggs/
Bottom line: the Yuzu diet may be much further from a vegan diet that some assume.
That EP link plus this ABC Connie Chung vid from four (or more) years ago:
discusses if hyaluronic acid (HA) might be the “miracle anti-aging ingredient.”
To listen to Connie Chung, the foods definitely have an acquired taste, to put it gently. So could also be the Yuzu diet is low on food reward, a concept Stephan Guyenet often discusses.
And of course, that ABC clip includes that the longevity could be more than diet (cue to 9:00), including exercise and low stress.
And then there’s the blend of their bucolic rural life with the big city (Tokyo) just two hours east, offering options/conveniences.
And what’s in their water anyway? 🙂 –Bryan
Cast iron can leach a fair bit of iron, but it’s hard to say how much is actually absorbed. Iron is rather odd that way. If a meal has heme iron in it, the non-organic iron is more highly absorbed. Also vegies tend to block iron. Our bodies are actually pretty good at blocking iron usually. There is something about the American diet that makes us absorb too much of it. But I’m pretty sure the Yuzus aren’t getting too much iron because they just don’t have a lot of age spots.
Age spots are lipofuscin, which is iron encapsulated in fat to sequester it from the body. If you shine an ultraviolet on your skin in a dark room, the iron deposits show up as black … they sit there and absorb UV. Probably another reason the Yuzus have nice skin. Not much lipofuscin!
Measuring iron absorption is really difficult, which is why it’s easier to just measure ferritin levels. But even ferritin levels aren’t accurate, because so much iron is sequestered in the liver and spleen, skin and brain. What I have noticed though, is that those “healthy centenarians” you see (and my grandma, who was healthy to 96) don’t tend to have many age spots, and their skin is healthy too. So the skin might be a good quick gauge of iron overload.
Thinking about the konnyaku though … I take it daily, though not the “set” version you get in noodles. If you get the “raw” version it has this nice habit of tamping down yeasts and h. pylori and other baddies, while feeding the good bacteria.
Which does make me wonder. The reason cows can manage eating a diet of mainly cellulose, is that they have these nice bacteria that eat the cellulose. The cows (and gorillas) “eat” the dead bacteria, which can be thought of as animal matter? Bacteria at minimum produce butyrate, which is the main fuel for gut cells. But what else are they producing? Vit K maybe, B vitamins. Maybe other vitamins? Other proteins?
At which points all bets are off. You can’t measure the nutrients a person *gets* from just what they *eat*. For all we know these cloistered populations have some symbiotic bacteria that just works really well for them.
For Vit C, there is the issue of how it is measured. It’s really variable depending on cooking methods etc. And there is the issue of how it is used up, which is also really variable. But I dunno either. What does seem to be the case is: whatever they are doing, works. I’m guessing they do eat a lot of greens: most of the Asian cuisines feature plenty of greens.
Eggs: I noticed that too. It’s very odd that they would NOT eat eggs. Maybe chickens don’t do well there? Eggs are very much a “whole food” and people (and rats) can survive on a “nothing but eggs” diet apparently fine.
Carbs: I don’t think their “carbs” are low at all. By simple deduction: they aren’t eating much protein or fat. All the rest is “carb”. How you define “carb” … that is a question! It’s been a big question I’ve had ever since the “low carb” movement got invented. A lot of carbs are semi-digestible, or it depends on the person. I don’t digest fructose well, so probably some bacteria I have does the honors. And probably produces “something” but I don’t know what. There’s a whole slew of “carbs” that have complicated digestion patterns. Xylitol, sorbitol for starters. Xylitol happens to be found in plums and apricots, and kills h. pylori (and others). Glucomannan … polysaccharide in konyakku and aloe, and also in yeast shells, oddly. Fructans … lots of them in sunchokes, which really do set off a lot of people’s guts (“Fartichokes”!). Cellulose … which is thought to be totally not digestible by humans (but is by some bacteria).
The thing about the Yuzus though: the writups talk about them eating a high hyalauronic-acid diet. Yams just don’t seem to have that much HA.
“Starchy vegetables are said to stimulate the production of hyaluronic acid, and may be consumed in the form of white or sweet potatoes, green peas, and carrots.”
http://www.wisegeek.com/what-are-hyaluronic-acid-sources.htm
Mostly what I read is that the best sources of HLA are things like chicken feet. Or eat high-magnesium sources so your body can produce it.
“Although there are no known herbs containing Hyaluronic acid nor specific foods that contain hyaluronic acid, some starchy root vegetables, including Satsumaimo (a type of sweet potato), Konyaku (a type of gletanious root), Satoima (a type of sticky potato), have a greater impact on stimulating the body’s natural production of HA. Like most whole fruits and vegetables, these starchy root vegetables help the body to retain moisture and assist the body in its own lubrication. ”
http://www.primev.com/hyaluronic-acid-ha/secrets-of-herbs-containing-hyaluronic-acid.aspx
So somewhere along the line, the article about the Yuzus missed that point?
heathertwist- I believe that green and black tea both block iron as well? And I’m assuming the Japanese drink quite a lot of green tea? That’s my method, and I hope it’s working…..though I haven’t checked my ferritin in awhile. (I’ll have to do that next time).
I was also under the impression that Japanese people eat a lot of duck eggs- (though maybe not in that part of Japan that you’re writing about). I don’t think they eat many chicken eggs. I wish I could get duck eggs here in North Germany; they just don’t seem to be popular here. I absolutely love duck eggs; I find them far superior to chicken eggs!
Right, both green and black tea block iron. What is interesting to me is that tea is often made in an iron pot. Now, the iron reacts with the tannins I think … the tea in an iron pot doesn’t taste at all like iron to me, but the iron does mellow the tea maybe. Our well water had dissolved iron in it and it sure tasted horrid, so I can’t imagine that the iron-tea-pot iron would be desirable. Complicated reactions!
Drinks though, esp. acidic ones, cause iron to be more absorbed. So drinking a glass of orange juice with a meal (or taking a Vit C tablet) is a good way to get too much iron in your system. Which is exactly what I WAS doing before I got iron overloaded … 😦 . 20/20 hindsight!
Tomatoes do much the same thing as Vit C. Chili though, is an iron blocker.
I drink lots of tea these days too!
Duck eggs are popular in Japan and China, but they eat plenty of chicken eggs. Ducks don’t lay as many eggs as chickens in any case. Most of the recipes seem to be for chicken eggs though. If you watch Maangchi’s videos or read some Japanese recipes or watch movies, it seems most meals call for an egg. When you send your kid to school with lunch, a common thing to do is have a bowl of rice and a whole egg, raw, for the kid to crack over the rice.
Chickens are a really interesting bird. They pretty much spread over most continents. The Polynesians brought chickens with them in their canoes, and hence to South America. Chickens loose around your house (or often, IN the house!) gets rid of the spiders and ticks etc. and fertilizes your plants, and is the world’s greatest garbage disposal.
I do like duck eggs and kept ducks at one point … I stopped because they are just plain messy. But I think both have excellent nutrition! One of the reasons store-bought chicken eggs aren’t so good is that they feed the chickens a lousy diet and they don’t get enough exercise. Mine have super-rich eggs and deep orange yolks … definitely more like a duck egg than like a store-bought egg.
It may be though that the developed eggs have more nutrition, although eating them is a bit gross to Westerners. The ones with embryos are called Balut, and the people I know who eat them swear by them for added energy. Like, if you know you are going to do an overnighter at work, you stop for Balut first.
What is interesting to me about this is that when we’ve had chickens or a goose nest on eggs, the predators left the nest alone for the whole 25 days or so that the mother was sitting. But just before the eggs were ready to hatch … the predator attacked the nest and ate all the eggs (the mother was ok). It is true that the eggs get a certain smell at that point, and I’m guessing that this signals some kind of added nutritional something.
Heather, @Morgana, I’ll quickly add I drink green tea all day long (Yamashiro uji-cha, loose-leaf) and I still have iron retention issues, though they remain (barely) within the normal range. Just to remind, there can be other issues.
BTW, I brew the tea at relatively low temp (155F/68C) and steep it for a short time (1 min for first steep, 2 min for 2nd etc). This way it supposedly preserves the polyphenols, if you believe in the reputed bennies of those phytochems. But I love it because this prep lets the tea give a wonderful floral flavor. Not at all astringent. Along with this tea’s other great features, like terrific appetite dampening. –Bryan
Hey Heather, thanks for all this. A lot to absorb (haha urm). Now that you mention, I did read that non-heme iron is harder to absorb. I tend to retain iron for whatever reason and I like to fry my Spanish eggs in a cast-iron pan. So I need to pay attention to this stuff and I give blood, too, for however much that helps. (At least it helps others!) About lipofuscin spots, those *may* be what I see in a few places on the top of my forearms and in one or two places on the back of one hands. Is there a way to tell a lipofuscin spot from a brown spot of some other etiology? Anyway, I’ll delve into this.
About konnyaku, I need to check into the diffs between the set and raw versions. I do better with the Hosoda Bros noodles (Temaki Shirataki 2P, whatever Temaki and 2P signify) than on the cheapo JFC stuff. Not entirely surprised by this.
For our gut flora, Duck had some interesting idea on this elsewhere in this forum. Including the idea that we should limit the # the species we introduce, since these species in turn foster other species, so better for us to intro a few of the right “foundation” species and let them dictate the rest of the pop. If there’s an arena we know very little about, it’s our gut flora and how they interact with each other and with our bods to supply the nutrients we need and enable the metabolic processes we need. What are there other ferment products besides SCFAs? (eg the butyrate you mentioned) I google this every now and again, and don’t get much.
On Vit C and eggs, we’re good there…On carbs, yes, I’m not suggesting they are low–they do eat starchy tubers after all. Just maybe not as high as we might assume, because the Yuzus eat konnyaku which essentially has zero active (ie enzymatically digestible) carbs. You’re right it seems they don’t eat much fat or protein, though we need to put a finer point on their fish intake, and to learn if they eat eggs after all. It could be they eat a naturally calorie-restricted diet, due in part to that seem to get remarkably little food reward. I’d love for some researchers to get in there and do actual counts: grams of fats, proteins, carbs, total cals, so we know much better what we’re talking about.
Also we need to remember the healthy oldsters, they in the their 80s, 90s, older–they were born before WWII and so confronted few novel chemicals and coped with much lower food availability. Their environment tended to be cleaner and the less developed (and wartime) Japanese econ forced them to adapt to a CR diet. For such folks who never get anywhere near metabolic syndrome, they may do as well on HCLF as LFHC since in either case it’s RC. Plus with the Yuzus, with all their (lightly cooked?) tubers and fresh raw or lightly cooked greens, they could be getting a non-trivial number of calories from fermenting fiber aka mainly non-or-minimally enzymatically digestible carbs (eg resistant starch) which yields 1–2 net kcals/g mainly as SCFAs. A “fat” diet, hah. 🙂 Anyway, I read everything I can find on our latest gut flora discoveries, esp that by Carl Zimmer whom I find writes super well on it in the NYT and other pubs.
About HLA, very interesting they get it from chicken combs. Wonder if you can find also in chicken feet, a very popular item in our local Asian supermarkets and which are great to toss into soups. About your last comment Heather: “…the article about the Yuzus missed that point?” I’ve no doubt they might have. The press so often does. I can say that as a member of that club 😦 –Bryan
Konjac
Several times you’ve referred to the lack of calories in konjac, that it isn’t digested? I’ve heard other people say that too, and being able to see the unchewed noodles (yech). That isn’t my understanding or experience though. My understanding is that konjac does get digested by the bacteria in the colon, basically feeding the butyrate-producers. Maybe it depends on what kind of bacteria one has? It would seem very odd to me that anyone would spend the time and land space to grow a tuber with zero caloric value. Growing and processing konjac is a lot of work! (I have some in my garden).
“Results of the in vitro digestion confirm that KGM and konnyaku are resistant to degradation by digestive enzymes. Gas production in fermentation vessels containing konnyaku and KGM was lower than for inulin from 8 to 24 hours. Both samples produced SCFA concentrations similar to guar gum, which favored acetate and propionate over butyrate production.”
http://www.ncbi.nlm.nih.gov/pubmed/22149628
When I buy konjac powder, it dissolves in water, making a nice thickener that is heat-stable. When that mix has another chemical added to it … pickling lime or baking powder … then it becomes the “noodle” state where it is a solid and very stable. I expect that changes the digestibility? I dunno, but the powder form seems to work better for me. The “raw” form sticks to the gut, and since I appear to get issues with ulcers, it would probably coat the ulcer and help heal it? Also it’s more sticky and makes fructose digest more slowly?
I don’t know what form the Yuzus eat konjac in though. If they just dig up the root and cook it … it’s the raw form I think, not the noodle form.
High-Fat Gorillas
LOL! And an excellent point. I wonder what would happen if you tested the colon contents of the Yuzus. Or the Inuits. I do believe that some folks that are eating huge amounts of fat aren’t actually digesting all of it … fat is one of the few items one can eat that the body can decide to just not process. Some of the undigested fat probably produces butyrate? Sugars though, if unabsorbed, tend to produce dysbiosis which is an issue.
Iron
I tend to absorb too much too. Plus I was snarfing down molasses beer and beef in most meals AND our well water was full of iron. But my aunt had the same issue, so probably it’s genetic. Donating blood is an excellent solution I think. IP6 works rather well too. Tea should work to prevent absorption during a meal, but I don’t know if it affects blood levels.
Ferritin levels are really important in diabetes. There is pretty good evidence that iron might be a major player in causing diabetes. Sure, the older folks may have gotten less food, but a really important thing is that they were not raised on high-iron foods. Most kids got stuff like oatmeal and eggs and milk for breakfast. Bread and cheese and milk for lunch. Maybe one chicken a week, or a pot roast if you had money. Food was largely starches and vegies, and the starches weren’t fortified. Milk, eggs, and beans were the main protein sources. “meat” was largely in the form of sausage or bacon … no fridges. So overall, people had low iron levels.
If you can get hold of a good UV light, shine it on your face and hands while you are in a dark room. The iron deposits show up in black. “Age spots” will be some of them, but a lot of them have no pigment.
Bacterial species
I guess I don’t worry about it much. I figure the mix varies depending on what you are currently eating. I work in the garden a fair bit, so I get dirt bacteria, plus I’m with the chickens. I do take Sacch. Boulardii when I have to take antibiotics though. That is a yeast, not a bacteria, and it’s amazing for handling candida.
It is interesting though. The Japanese seem to have a bacteria for digesting seaweed. Maybe the Yuzus have a bacteria for digesting konjac!
http://www.wired.com/2010/04/sushi-guts/
“The gene that codes for the enzyme has been found in one other place: the genome of Bacteroides plebeius, a microbe found in human intestines. However, not all B. plebeius strains produce the algae-crunching enzyme. It has only been found in Japanese people.”
Calorie Restriction
Since forever we’ve been hearing about how the main issue is that our predecessors … or the “other country” people … are healthier because they are on CR most of the time. I kind of think that is hogwash. Lately there have been actual studies, pairing Chinese businessmen with their American counterparts, for activity levels. The Chinese ate MORE calories. The book “What I Eat” does an even better job, with pictures! The calorie levels and the exercise levels and the fat levels just sooooo do not fit.
I keep looking for patterns, and I have found a couple.
HLA
Most of the sources are the “gooey” pieces, like yes, chicken combs! And yes, chicken feet! Also skin, collagen. I can’t get a good fix on whether tubers actually CONTAIN HLA or if they just promote the body producing it. If “starches” in general stimulate the body to produce HLA, then your rice-eaters in general would have higher levels of HLA.
However, there are also interesting things about antibodies that destroy connective tissue. Turns out that fish oil blocks them? And why are their antibodies eating our connective tissue anyway?
“When the cartilage breakdown due to age it is called osteoarthritis. At times, the immune system of the body can attack its own tissues. This immune attack an affect the synovium or the fluid which provides lubrication and nourishment to the joints. Inflammation is one of the body’s natural reactions to any kind of injury caused to the tissues”
http://www.naturalarthritistreatments.net/arthritis-in-general/fish-oil-for-arthritis
So your Yuzus may make more connective tissue … or, they just don’t destroy it so much. Same with Taurine. Maybe some people eat more of it. Maybe some people don’t use it up so fast.
heathertwist, wbryanh- what ferittin level is considered too high? I’ve seen conflicting opinions. The last 2 times I tested, I was in the “normal” range (by conventional standards) but some Paleo advocates seem to think the higher end of those ranges are too high. So I’m quite confused about that. Also, is it difficult to donate blood- (do you feel faint, or sick afterwards?)
heathertwist- that was very interesting about the Chinese eating more calories. I’ve read that many groups of people, including people from bygone eras, ate more calories than typical Americans do now. I don’t think our problems are so much the amount of calories eaten, rather the composition of the diet.
Diabetes & Ferritin
IIRC the risk for diabetes goes up after a ferritin level of 116 or something. Which is far lower than the cutoff for “high iron levels”. Oddly enough the association has been known for years, but no one ever seems to talk about it.
http://aje.oxfordjournals.org/content/165/9/1047.full
Full study too. So that is from 2006!
Bloodletting
I started donating blood originally because I was afraid of needles. Seriously, if you want to get over being afraid of needles, this is the way to do it! The Dr office is already scary and you are afraid of having whatever XYZ you have, plus the nurse might not be good at finding a vein. But at a donation center, they are REALLY GOOD at finding veins and treat you nicely! My only gripe is there aren’t many GF snacks. Bring your own snack, I recommend. The OJ and coffee is good though.
Donating CAN make you dizzy, so you need to sit down after and drink some liquids. The only time I had problems though was when I walked around a lot after in 90 degree heat.
Bloodletting is known to help diabetes:
http://diabetes.diabetesjournals.org/content/51/4/1000.full
Again, the docs never seem to bother telling people! Bloodletting is very safe. The donation centers always test your blood first, to make sure you aren’t anemic. They also test the blood you donated for stuff like STDs and hepatitis … which appeals to the geek in me. You lose a fair number of calories too (650?).
As they say: “Donate blood. The life you save may be your own.”
IP6
If you can’t donate blood (there are lots of exclusion criteria) then taking IP6 is said to work too.
Amount of food per day
Interestingly, on the Lewis and Clark expedition, the meat ration per man was 9 lbs of meat per day. So if there is an average of 1000 calories per lb, that is like 9000 calories a day! And that’s just the MEAT part. Granted they were working pretty hard, although a lot of the time they were also just sitting around camp. But your average athlete today works out pretty hard too. OTOH, in the book “What I eat”, one of the lowest calorie counts was a gymnast, who spent hours each day balanced on one hand.
Good MornEve Heather and @Morgana:
Heather, you’re right, konjac does yield some calories. I’ve been using a strict def of “digestion”–mainly following that convention of my research materials–to include only those calories we digest with our enzymes and which go system-wide in our bods. I.e. all that “-ase” stuff we do in our duodena and others place in our small intestines. This, as opposed to the calories we get when our colons’ gut flora ferment fiber carbs. Those SCFAs we get from that, I understood to now they feed our colons’ endothelial cells but who knows–maybe we discover they too go systemic. If the Silverbacks get up to half their kcals from hindgut fermentation, you’d think at least some of that goes systemic.
But yes to your point, konjac does yield energy. Maybe we need a term to collectively refer to both processes? Eg “digestiferment?” The yield from ferments appears to be 1–2kcal/g of fermentable fiber. Of course that’d vary by which fiber you eat. Again, another area we have so little info.
Heather. what you say here: “ …fat is one of the few items one can eat that the body can decide to just not process..” YES. That is a huge point! 4–5 years ago I found sources that discuss this very thing and have been trying to find them since to post here for us.
I recall that to import fat is an expensive process. Lipases first have to split the TAGs into FFAs, then the GI has to decide which FFAs get remade into TAGs to bundle onto large chylomicrons then import into our systems for the long and winding trip through our lymph before they even get to blood. Thus our GIs–which btw have millions of neurons for rich info exchange–evolved ways to vet dietary fats in the duodenum, to communicate with the system (via vagus nerve, maybe others) for the bod’s fat needs. Furthermore, high carb levels can invoke enzymes that can hobble this fat-vet process. Evidently in the presence of high carb, we import more dietary fat than we would without the carbs. It’s fascinating stuff and I am trying to find it for us. All this helps explain the idea that “carbs make us fat, but dietary fat makes us thin.”
On iron, here’s what Kaiser sets for ranges:
Total Iron Binding Capacity (TIBC), Total: 236-404 ug/dL
Iron: 41-196 ug/dL
TIBC, Unsaturated (UIBC): 100-315 ug/dL
Transferrin % Saturation: 15–60%
I need to look deeper into this as you and Duck and others made many good points how we may well be overexposed to iron on its heme forms and in novel formulations. One thing we know, iron can feed bacteria. People who survive plagues in the bad old days, they often had anemia and so too little iron to feed the bacteria. Thanks for the uV light idea, I’ll definitely try it.
On calorie restriction, I definitely don’t think it’s “hogwash!” But let’s be clear on terms. I include subsistence diets as “CR” diets, because even in the pre-SAD days, people often seemed to want to eat somewhat more than just what they needed for subsistence. CR is apparently enshrined in some philosophical practices, eg.
https://en.wikipedia.org/wiki/Hara_hachi_bun_me
to eat until you are “80% full.” But in earlier days one often didn’t even need to follow a teaching–life forced it on them. If we go back even a few generations, more people did more physical work and food cost more. Even my American grandparents who worked on farms and did a lot of physical labor, they got enough to eat to match the calories burned, but they didn’t overeat. Even when I first started paying attention to my Dad’s parents’ eating habits when they in their early-mid 60s, it struck me how small the meals they ate. I’m not surprised the Chinese businessmen eat a lot, and I don’t think it’s necessarily healthy. China’s entered a period of unparalleled prosperity and we see the excesses and indulgences that go along with that and obesity there is increasing fast. You can already find “fat farms” in China for their little obese “emperors” and “empresses.”
http://www.reuters.com/article/us-china-obesity-idUSTRE77P4N420110826
Fat camp shows China battling the bulge
About HLA, connective tissue, and immune attacks on it (my step-Mom has terrible rheumatoid arthritis.) all very interesting. So many rabbit holes to dive into! We are still so very near the beginning of our knowledge of these things.
Morgana, maybe there are more fun things to do that the process of giving blood, but the people who collect it, they are always so nice and grateful and do everything they can to make you comfortable.The needle is a little bigger that what you see at the blood draw lab, but I feel a small pinch and that’s it. The actual donation typically takes ~15 mins. You can read, listen to whatever’s on your pocket device, yak with your fellow donators. If you feel faint–and it’s usu psychological, not from actual blood drawdown which is surprisingly little–just tell them and they will monitor you and stop the donation if needed. At the end I always feel fine and great for doing the good deed! –Bryan
wbryanh, heathertwist- thanks for the information about blood donating! Last time I checked, my ferritin level was somewhere in the 70’s. (Can’t remember the exact number). According to some people this is okay, but others claim it’s too high. I was given iron tablets when in the hospital about 6 years ago; I hated taking them, but they basically forced me to. Since then, I’ve read that synthetic iron in the form of supplements is the worst kind, and can hang around in the tissues- (sort of like what Duck Dodgers was talking about). So sometimes I think it may be a good idea to donate. In addition to that, when I was very ill, at one point I needed a blood transfusion myself, so sometimes I think it may be good for me to “give back” to the Universe. I do worry a bit though, since I am underweight (don’t know if that makes a difference?) and have low blood pressure- (which makes me worry about being prone to faintness. Though since I’ve gone low carb, I have far fewer episodes of faintness and dizziness, so maybe it’s nothing to worry about). When they test your blood before you donate, can you get a copy of the results? It might be good for me to see how everything is doing. Since my illness, I’ve been kind of avoiding doctors as much as I can, so I haven’t checked my blood markers in awhile. Is high cholesterol an issue? (I.e., can you still donate blood if you have high cholesterol, and do they even check it?)
Another thing: not only does “bloodletting” help diabetes, but I’ve also read that high iron levels can be an issue with heart disease, and possibly even cancer.
In the study I linked to, it mentioned “High ferritin diabetes”. You really don’t seem to fit that category. Donating blood is, I think, a very good thing … but you might want to wait until you aren’t underweight? Having had undiagnosed celiac for some time (as I think you mentioned earlier?) it’s unlikely you have way too much iron. Celiac involves internal bleeding much of the time, and the inability to absorb food. Getting your OWN nutrient status up is the important thing in that case.
Celiac can also damage the pancreas, according to one endocrinologist that was at a conference I went to. In which case again, the only cure is to get generally healthier?
heathertwist- I had undiagnosed celiac disease for much of my life, yes; however, I have been gluten free for about 11 years now, which is a long time. (I was anemic off and on when I was a child, and I had to take iron tablets). Then when I was in the hospital about 6 years ago, I was given iron tablets for about 6 weeks; which I hated, they gave me digestive problems. At some point after my recovery, I switched to a low carb, Paleo style diet, which means I was suddenly eating red meat- (I had been pretty much vegan before. When I discovered it wasn’t the perfectly healthy diet it was cracked up to be, I started eating meat again). At one point, a few years after I got out of the hospital, when I had my ferritin tested it was all the way up to 100! My doctor felt this was normal, but I had read that that was a little high. After that I started drinking more green tea, and eating red meat and liver in the morning (with tea), and fish or poultry or cheese with dinner (with wine. I’ve read that wine actually aids absorption of iron). Next time I tested it was around 85- (I was wrong in my last post, it wasn’t in the 70’s, but in the 80’s). I hope that’s okay.
As for my weight, I don’t think I can bring it up; I keep trying, but I just stay skinny for some reason. It couldn’t have anything to do with celiac disease anymore, I don’t think. My job requires constant exercise, however. So I might just be like one of those skinny railway workers you write about! Oh, interestingly enough, what kept my weight up and made me “look healthier” was sugar. I stopped eating sugar years ago, and though I feel healthier- I’m sure it is better, in the long run- I look very skinny. It’s a shame; I think I looked better before.
I also have no idea what my blood nutrient status is, as I haven’t tested in awhile. I feel pretty healthy though. Maybe I’ll just wait until my next doctor’s appointment (around late Spring), then check my ferritin level again and decide if I should give blood.
Well, if you give blood and feel ok, then it’s probably ok. You are right: some people are just naturally skinny. Blood cells get replaced regularly anyway, and the blood center will test you for anemia before donating.
The issue with “weight” is an interesting one. I mean, your “weight” consists of your bones and organs, muscles, fat, and water. If you “gain weight” from sugar it’s likely mostly fat and water … which may look nice on a woman (and women need a bit more body fat anyway, to be fertile at least). But as for muscle … unless you have muscle wasting, there isn’t really a guarantee that “more muscle” makes you stronger or anything else. Those railway workers, some of them, were rather skinny by modern standards. Bruce Lee too … he was ripped, but he didn’t have those huge muscles the action heros have these days.
Calories from the colon
Yes. What ruminants do is amazing … but it probably evolved from a lesser version of the same thing? And yeah, bacteria are the Swiss Army Knife of gut adaptation! We do know that the Japanese have their own species of bacteria for digesting seaweed. There is also a bacteria for digesting oxalates, which prevents kidney stones in people who eat lots of high-oxalate foods. We’ve “trained” bacteria to produce all kinds of stuff these days in the lab.
The article mentioned 6%-10%, but also mentioned the amount might be higher in people who ate more fiber. And I’m guessing it depends on the type of fiber. Most people these days don’t get a lot of the “gooey” semi-solid fibers, but there are scads of those in the Yuzu diet! I don’t know if you’ve tried eating those yams, but wow, they are GOOEY. If they didn’t get digested, then your poop would be one big mass of goop, I think. When I eat psyllium, it increases my stool size by quite a bit … I don’t think it gets digested much. But the konjac (gooey style) doesn’t do that at all.
Anyway, we know humans can turn carbs into fat. So if the super-low-fat people are eating carbs, they aren’t spending taurine on digesting fat, and are producing their own fat and proteins from the digesting food. Given that humans have some ability to produce taurine (which is probably genetically determined, plus how much sulfur is available in the diet) then the person should be nicely healthy on a diet of yams (esp. yams grown in volcanic soil).
Goo and yeasts
Another important thing about the “goo” might be that it doesn’t feed yeasts. In fact it tamps them down, esp. konjac. That is another thing that has been mentioned in this conversation … glucose-based starches that have been gelatinized, digest slowly (the “resistant starch” idea). This is really important for farm ruminants, because the yeast and acidophilus overgrowth will kill the animal if they eat too much grain. Turning the grain into something like spaghetti will allow say, a racehorse, to eat more oats without getting ill.
You can test this by putting various types of starch in a jar, then adding some water and yeast. If you do that with sugar, you get instant overgrowth. If you do it with flour, same thing. Do it with rice … yeast will grow, but slowly.
Body Fat and Calorie Restriction
Well, in your family perhaps you ran around a lot, but that sure wasn’t the case in ours. Anyway, it HAS been studied a fair bit and the link between exercise and fat is tenuous. You have some nice fat athletes — Babe Ruth comes to mind. And the farmers around here, a lot of them are quite obese. But hardly couch potatoes. Farming is hard! Look at the Sumo wrestlers in What I Eat. They work out for hours a day! Yes, they eat a lot and gain weight on purpose, but they regard the choice of foods to be a big part of their ability to gain weight. Sumos on the traditional Japanese diet don’t get so fat. They would be more like the railroad workers … eating lots of calories and using lots of calories and staying skinny.
Also, yes, the folks in our grandparents and great-grandparents age were even skinnier. More like the Japanese: short and thin. But why would we assume they were starving? The guys building the railroad certainly weren’t, and not all of them were heavy laborers. The menus of the time were written out, including the allotment for slaves and servants. In an upper-class household, at any rate, everyone had plenty to eat. Even the pampered ladies who didn’t go outside without their parasols and considered breaking a sweat to be very low class. Some of them got a little chunky … most didn’t get obese. With a few exceptions that are worth noting, like Henry 8 and Queen Victoria.
So you have examples of people eating high-calorie high-exercise diets … railway workers, Lewis and Clark soldiers (9 lbs of meat a day!) and staying skinny. We also have examples of high-exercise people that get fat (Henry 8, some farmers, Babe Ruth, sumos, other wrestlers and weight lifters). My take is that there is a trigger for “storing fat” … probably triggering a gene for hibernation. Or a bacteria!
Hi Morgana and @heathertwist. I’m fighting a very rare cold here so been a little out the pic. But still checking in and reading your posts.
Morgana, about the blood donation info, you’re welcome! About getting your blood tested, this likely varies from one country, even one district, to the next. You should check locally where you live. You can also tell them about your weight and BP levels and see if they have concerns. In my experience, the people who assist in your blood donation really want you to have the best experience possible and take very good care of you. Just express your concerns and they will monitor you. If you feel faint, they’ll let you stay on the recliner until you feel better and help you to slowly get up in case you feel any hypotension.
For ferritin levels here’s from the Mayo Clinic:
http://www.mayoclinic.org/tests-procedures/ferritin-test/basics/results/prc-20014449
As far as iron–well you know my wariness on supps! Women lose a bit of iron through their menstrual periods, though I’ve never seen this quantified. I’m sure that loss varies, but it’s hard to imagine in most cases they can’t make it up through dietary iron. As has been discussed here a lot, the problem’s usu too much iron, esp in “fortified” foods. –Bryan
@Morgana, @WBryanH: On the supps: What I’ve read is that people need about 1mg of iron a day. I.e. not much! Unless they are losing blood. Women lose a little normally. People with parasites or internal bleeding can lose a lot!
Ray Peat has a very good article on the subject:
http://raypeat.com/articles/articles/iron-dangers.shtml
“Q: Don’t you need iron supplements if you are anemic?
In general, no.
Many doctors think of anemia as necessarily indicating an iron deficiency, but that isn’t correct. 100 years ago, it was customary to prescribe arsenic for anemia, and it worked to stimulate the formation of more red blood cells. The fact that arsenic, or iron, or other toxic material stimulates the formation of red blood cells doesn’t indicate a “deficiency” of the toxin, but simply indicates that the body responds to a variety of harmful factors by speeding its production of blood cells. Even radiation can have this kind of stimulating effect, because growth is a natural reaction to injury. Between 1920 and 1950, it was common to think of “nutritional growth factors” as being the same as vitamins, but since then it has become common to use known toxins to stimulate the growth of farm animals, and as a result, it has been more difficult to define the essential nutrients. The optimal nutritional intake is now more often considered in terms of resistance to disease, longevity or rate of aging, and even mental ability.”
Calories from the colon
Yes, we are just beginning to understand all this! It does seem that when people are starving, they have a lot less excess calories in their poop. We normally waste a lot of calories. Since a lot of that bulk is just dead bacteria … one would think that over the years of starvation there would be a mechanism to extract more calories from the bacterial mix?
Anyway, it looks like there is some research on it:
“SCFAs absorbed in the colon contribute 6%–10% of the entire energy requirements in humans, and their contribution likely increases in humans who ingest more dietary fiber.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601187/
The Japanese have species of bacteria that digest seaweed … likely they are good at digesting konjac too. But bacteria also produce vitamins, and probably some amino acids too? Your gut CAN absorb all kinds of stuff, which is kind of the point of suppositories.
Interestingly one of the SCFAs that is produced is acetate … aka the stuff in vinegar. Acetate has interesting effects in people, including help regulate blood sugar and causing fat loss.
Fat and starvation
The reason I don’t buy the “everyone was starving” logic that is common these days, is partly because of the 60’s. Back in the day, we weren’t starving. In fact Mom kept bowls of candy out all the time, for snacking. She made huge meals, and we’d raid the fridge as needed. Also we had cases of soda pop in the closet. But she … and everyone else I knew … was thin. There was exactly one “fat kid” in school, who was of course teased a lot. It is true portions were smaller sometimes, but no one I knew restricted themselves on purpose. We ate til we were full. We lazed around reading comic books mostly.
Then suddenly in the ’70s, everyone got fat. And fatter and fatter. Even while we work harder and harder at getting healthy. This is not because we suddenly changed or got richer. “Something” changed, yes. I don’t think anyone knows what it is though. Lots of guesses, but none seem to hold up in court.
Also, body builders. A lot of them eat a high-calorie diet. They work out some, yes. But their point is that if you eat only specific foods, the fact you are eating a lot of calories doesn’t count. We did this at work once. We lost an average of 35 lbs each. We DID track calories, but it wasn’t a low amount of calories. We quit because it got boring I guess. But it worked like a charm.
For a given person though, eating the same usual foods, eating less of the food can cause weight loss, sure. Most people doing CR eat more or less the same foods they ate before, just less of them.
The Chinese and Japanese though, are jumping from their traditional foods to Western foods, and they quickly get ill. I’ve seen the differences in the Asian stores … the Western influence is all over the place, even in the traditional foods. More weird oils, more dry packaged foods (chips!), more beef (beef was scarce for most of history).
Part of the deal on Western foods though, is that they *make* you eat more. I mean, that is the point, isn’t it? The more you eat, the more money I make selling you the food. Traditional food was made to be filling, because well, you want to be thrifty. So I design my chips such that you can eat a whole bag easily and crave more. While the traditional noodle soup … you’d eat one bowl and be full. Try eating 5 hard-boiled eggs, vs. one slice of pizza (more or less same amount of calories).
Iron and bacteria
Yes, iron feeds lots of bacteria. Usually not the ones we want. The cells in the gut absorb some iron and sequester it. Then release it into the blood if needed. Unless that process gets sidestepped, which seems to be what is going on recently.
Babies aren’t supposed to get much iron, and their guts are designed to let mama milk almost directly into the blood. But when you add iron to the formula, the babies get adult bacteria growing there instead of baby bacteria, which is probably not a good thing.
Like I’ve said before, I think part of the deal with the Rice Diet was that it was very low iron. Also low salt. So that likely had a huge effect on sugar handling and kidney function.
“SCFAs absorbed in the colon contribute 6%–10% of the entire energy requirements in humans…”
Heather, I didn’t realize it was normally as high as that. I’d done the calcs on it during my high-fiber days, chowing up to 100–120g fiber per day. If we assume *all* of that ferments and yields 1–2kcal/g, then the range is 100–240 kcals. That top end does come to 10% of the diet, but most people eat less fiber. If you take the 2002 US RDI for it:
http://www8.nationalacademies.org/onpinews/newsitem.aspx?RecordID=10490
38g for men, then the max ferment range comes to 38–76 kcals, a few percent of the daily energy. And again we can’t ferment all fiber. Anyway I need to look closer at the math in that NCBI link you posted.
I wonder if a person can slowly ramp up her fiber to give her hindgut time to adjust, how high could she get it? What percent of total kcals? 20%? 30%?
About what our microbiota can do, wow, we just scratch the surface. Our environments constantly change, so our little bugs must too. Remember how shocked geneticists were to discover human DNA contained only 30,000 genes? They’d assumed up to 10x that much. But makes sense when you think on it. We let the microbiota take care of so much. Our repro cycles (and so our mutation/natural selection cycles) are so long (~25y), our bods proper can’t keep up with the constantly shifting demands without storing a whopping load of DNA, and then you get management probs. Instead why not let our little bugs manage AMAP? Some of them have almost as many genes as we do! And we can “hire” and “fire” them at will, depending on the changing demands our environments pose. Heather what you say: “But bacteria also produce vitamins, and probably some amino acids too?” Here’s a link that talks about the AA production side:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144392/
“…emerging evidence indicates that gut microbes can impact nitrogen balance by de novo synthesis of amino acids and intestinal urea recycling. These contributions are most pronounced in ruminant animals that, amazingly, can live on a protein-free diet because their microbiota is capable of synthesizing most or all amino acids required for survival.”
That last sentence intrigues me because even plants have AAs, so never though ruminants lived on a “protein-free” diet esp since they graze all day and eat lots. So need to look into this more.
About poop, when I fast, I go from daily to as long as almost a week between movements. Yet it’s always fine, no constipation, usu not much volume. To me, that lends weight to the idea we continue to extract nutrients from our colon contents when our bods need it. Again our GI has a whopping load of neurons, often called the “second brain:”
http://www.scientificamerican.com/article/gut-feelings-the-second-brain-in-our-gastrointestinal-systems-excerpt/
And Richard Wrangham in “Catching Fire” spells out his zero-sum gain theory of neurons in our bods, that we grew bigger brains due to the GI shifting neurons to them because we made the GI’s job easier by starting to cook food! Not sure that’s true, but who knows? Also not sure the colon is as neuron-rich as the small intestine. But still. We have evidence that our GIs are enormously and nimbly responsive to emerging conditions.
On acetic acid, that’s the smallest fatty acid, only two Cs on the backbone. Funny that’s what’s in our bottles of Bragg’s! I’ve heard lots of things about vinegar’s healthful effects and I use it every day. I’ve vaguely wondered if any AA goes extra-efficiently into Krebs Cycle since it’s almost already an acetyl from the get-go.
Body Fat and Calorie Restriction
I grew up in the same years as you Heather, and it’s true few of us kids were overweight then, and we already had plenty to eat. We tended to be out and running around, often not wanting to interrupt what we were doing to come to table. I do think we stayed thin in large part because our food was not nearly as engineered then, it didn’t as much press our buttons to “crave” it. Even so, I remember seeing lots of middle-aged folks with growing middles. When I look at my grandparents photos, I don’t see many overweight folks of *any* age. All of them were young during the Depression which indelibly impacted them. I saw them count pennies for everything including food, even though they didn’t have to. They didn’t starve, but for much of their early lives they really did have to pay attention to food costs. When I stayed with them, they always admonished me, they told me “not to bolt my food.” Later I wondered if slowly chewing their food was a way for them to extract more energy from what we might think was a limited amount of food.
And yes like you say, as we rolled into the 70s and 80s, more and younger people got fat. This may be due to a confluence of many factors. Under Nixon, Earl Butz blew away lots of New Deal Ag progs in the name of agri super efficiency, and food costs did drop a lot because of it. Michael Pollan talks about this a lot in Real Food. We started to include HFCS in food in 1975. McGovern et al out out the govt’s disastrous nutrition recommendations in 1987–1980. The chem companies steadily cranked out thousands more new hormone-disrupting chems in that time. PBDE-based flame retardant started to show up in furniture. The list goes on.The main point: accelerating tech since WWII led to a blizzard of changes, many of them we now learn are bad for our metabolisms. And absolutely, the new food is not by accident. It’s like you say, the food industry designs it to press all our evolutionary hot-buttons and buy more of it. Again Pollan writes very well about this, either in Real Food or Omnivore’s Dilemma. –Bryan
Heather, thinking more on the idea that a high-fiber diet is a high-fat diet (due to SCFA ferment products). Several years ago, I broke down the diet of Mountain Gorillas, who eat 40–50 pounds of roughage every day. These gorillas have big hindguts (they look like beer bellies) so they can handle all that fermentation. Anyway, I calc’ed (plus got supporting evidence from somewhere?) that these gorillas got up to their cals from these SCFAs. Thus they “eat” a 50% fat diet–like some or many of the Yupik-Inuit! Hah! –Bryan
“This ties back to Masterjohn’s 2012 post showing we make glucose from fat …” If this pathway produced copious amounts of glucose, I would never have had an insulin reaction – it’s clearly bottlenecked, perhaps to the point of irrelevance. Gluconeogenesis is also too slow to prevent insulin reactions. In healthy starving humans, muscle is lost as well as fat, so it may not be of much help there either.
Dr. Alex Zhavoronkov’s experiment isn’t very likely to bear fruit (or kill him) in time to give us much guidance.
“Dr. Goran would advise “against the use of high-dosages of concentrated antioxidant supplements” however my experience on 5 g of C and 400 mg of Unique E was that I put on muscle easily at the gym, if anything easier than my first go-around at the gym when I got injured quite frequently – so my n=1 experience is that the vitamins protected me from injury and did not prevent me from gaining muscle.
IMO, there’s a scary lot of bollocks out there amongst the good advice, many of them tiny no doubt. I think we all throw the dice with whatever dietary strategy we choose as soon as we realize we’re digging our graves with our teeth, but so long as we achieve a low insulin level we’ll probably have a long healthspan:
“The fact that an age-related clinical event developed in approximately 1 out of 3 healthy individuals in the upper tertile of insulin resistance at baseline, followed for an average of 6 yr, whereas no clinical events were observed in the most insulin-sensitive tertile, should serve as a strong stimulus to further efforts to define the role of insulin resistance in the genesis of age-related diseases” http://www.ncbi.nlm.nih.gov/pubmed/11502781
First Jonathan, I have to agree about insulin resistance and add to that chronically high blood insulin levels. These high levels may bring as much, maybe more, pathology as high BGs. For example, the enzyme (insulin-degrading enzyme or IDE) that dismantles insulin after it spends an average of 71 minutes in our blood, that enzyme also appears to play a role to break down beta-amyloid deposits in the brain. Those which otherwise accumulate and set the stage for Alzheimer’s Disease:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1559921/
If we suffer chronically high insulin levels, we may fail to keep up with breaking down the beta-amyloid because IDEs are always preoccupied breaking down insulin.
We really should be testing blood insulin levels and IRs so can often catch metabolic syndrome at an early point where we can meaningfully reverse it. Too bad the euglycemic clamp takes so much time, costs so much, and takes so much labor. For blood insulin the C-Peptide proxy marker is better than nothing. But not sure how much we can rely on it.
About what you say here: “…If this pathway produced copious amounts of glucose, I would never have had an insulin reaction – it’s clearly bottlenecked, perhaps to the point of irrelevance…”
Actually Jonathan it appears not to work that way. Our bods (except the pancreas) see insulin, not BGs, as the metabolic switch. The pancreas senses BG levels and tells the beta cells to respond accordingly. The liver and the rest of the bod, all they see are blood insulin levels. If they see high insulin levels they assume BGs levels are *already high.* Thus they shut off all endo-pyruvate/glucose production, which includes glycogenolysis and GNG from AAs. Jonathan, remember, your bod doesn’t know the diff between endo and exo insulin. It sees only “insulin.” It thinks high insulin means high BGs.
About what you say here: “…in healthy starving humans, muscle is lost as well as fat…” this depends on the fast length, activity during the fast, and how keto-adapted you are to start with. My experience in 300+ IFs which last as long as 3-⅔ days (88 hours), I lose little to no muscle mass. During these fasts I do bursty resistance training lasting only a few minutes each session. This keeps me out of glyco, but keeps me up-regulated so that my bod conserves more AAs. I weigh myself regularly during my fasts, and lose up to two points in body fat by the end.
About Kurzweil, Zhavoronkov, etc, I’m happy to let them be the pigeons. My main point is that, while we have interrelated processes of almost uncalculable complexity, I can’t categorically say we can’t hack our way to a longer life- and health-span. I’d never do what they do. But I’m happy to sit back and watch them. Who knows? We may learn something. –Bryan
wbryanh, Jonathan Christie- First off, wbryanh, thanks for the dense, and very interesting post! I thought I’d mention that my experience has been quite different to what you’ve written though. In my own case, I’ve felt bad for as long as I can remember…..stemming from when I was a child. Such is the nature of undiagnosed celiac disease. I complained constantly of feeling sick- (but since I wasn’t visibly sick and throwing up, people attributed my problems to “stress”). I sometimes had such intense intestinal pain that I would be doubled over, and couldn’t do anything. I also had pretty bad gynecological issues as a teenager- (whether that has to do with the proximity to the intestine or some other factor- sugar?- who knows). This is not a “sob story”, I’m just making clear that the SAD was obviously very, very bad for me right from day 1. But at some point, I assumed that everyone probably felt as bad as I did; I thought maybe I was weak or something. Since we are raised on this diet, and as a child you don’t know any better, it’s hard to do something different, or even imagine a different reality of any kind. So I tried to remain strong and just deal with my problems.
I totally agree, wbryanh, that the USDA recommended diet is horrible for many people! It obviously made me very ill. Now that I eat a diet that would make the conventional advisers cringe (more meat, more fat, no grains, low carbohydrate) as well as- horrors!- animal fat- I feel way healthier in my 50’s than I ever have in my entire life. Not only am I pain free, but I don’t have those horrible issues dragging me down, making my body feel like a dead weight. I’m sure very few people can say that they feel better in middle age, but there you go…..I just needed to find the right diet for me. I am strongly against “one-size-fits-all” advice. I wouldn’t even think of telling people they have to eat like me, since I’m pretty sure it doesn’t work for everyone.
And what I meant by “things change in the body”: I was talking about how our needs may change at different times in our lives. As a for instance, a growing child may need a different diet from a middle aged man- (another reason why I detest one-size-fits-all advice; just look at the situation with cholesterol!) Here is another example: when I was recovering from all my devastating cancer treatments and operations (at a time when I was very ill), I didn’t have much appetite, but I had very strong desires for fresh squeezed orange juice made with blood oranges. Even though I could barely walk, I hobbled to the fresh produce market every day to buy fresh blood oranges. What would get me out of bed in the morning was the thought of this fresh orange juice, and when I finished my daily glass, I would actually feel depressed, since the moment of joy was gone. Dr. Lustig would have a cow if he heard about that, ha ha, but I’m convinced that that helped to heal me and that I really needed it at the time! (Jonathan Christie would possibly say that it was due to the high vitamin C content, which is a great healer). Now that I’m well again, the thought of fresh squeezed blood orange juice doesn’t really appeal to me. Although I like half a blood orange in a salad every now and then, the thought of a whole juice makes me a little queasy, as all that sugar doesn’t feel good in my stomach normally. But at the time, it felt great and very easy to digest. I’m convinced that it was something I needed at the time, but no longer need. I think there are many examples of these kinds of situations, and we have to be aware of the effect that food has on our body, what seems to “hit the spot”, etc. I think these things are telling us what we need, and those needs may change from time to time.
Morgana, I keep rereading CM’s post:
http://blog.cholesterol-and-health.com/2012/01/we-really-can-make-glucose-from-fatty.html
And wonder all the more why–four years later–so few people/orgs have reacted to it!
We know we have multiple pathways to convert fatty acids/triglycerides to glucose. Not just glycerol to pyruvate which we’ve known for yonks. But even the acetone → pyruvate/glucose pathways, we’ve known those for several decades.
Yet even mainstream scholastic biochem texts kept routinely misleading us–at best. And they still do!
Why is Masterjohn the ONLY guy of any authority to point this out? Why is he still the lone voice out there?? I really don’t get why the near non-response to this intriguing info.
Per this Wiki discussion, Metzler and Metzler appear even to contradict themselves on the matter:
https://en.wikipedia.org/wiki/Talk%3AGluconeogenesis#Um.3F
Scroll down to read about it in “Michaplot”’s long-ish comment.
Lehninger’s Principles of Biochemistry was my main course book way back when in my pre-med days. Amazon lists it as a top seller. The 6th ed (2013) appears to be the latest. I just ordered it. We’ll soon see what’s in there. –Bryan
“I’ve been reading this back-and-forth about the Inuit for awhile, but haven’t commented until now. A few things come to mind: first off, who exactly are *the Inuit*? Aren’t they a series of different tribes in the Arctic region? Couldn’t they conceivably be eating slightly different diets? If we monitored the glucose reaction and ketone production of 4 Americans, could we come to any conclusions about the American diet and the health of all Americans?”
I thought this was very interesting, maybe it’s been quoted here before:
http://www.jbc.org/content/80/2/461.full.pdf
They did rather good observations and tested glucose tolerance on Inuit back in 1928. Also he talks some about the differences in diet in different parts of the North. He tested for ketones using a check for acetone in breath.
1. The Inuit had good glucose tolerance
2. They exhibited mild ketoses after 2 days of fasting.
3. They were not normally in ketosis even though eating very few carbs.
He made an interesting note that some obese white subjects didn’t exhibit ketosis after fasting — his take was that maybe some people have the ability to burn fat without using carbs (or ketones?) to do it. He commented that the ability to do this varies in all humans … children normally require more carbs to burn fat than adults do.
“In relation to the problem of accounting for the slightness of the
ketosis found in the Eskimo subjects, it is therefore apparent that
they, like the obese subjects referred to above, require less carbohydrate
to burn their fat than normal white subjects. Children
on the other hand, as shown by Wilson et al. (S) require a larger
proportion of carbohydrate to permit the complete combustion of
fat. All these data are consistent with the hypothesis that there
are two mechanisms possessed by the animal organism for the
combustion of fat, one of which involves the coincident combustion
of carbohydrate. The varying ketogenic-antiketogenic ratio
might then be a function of the relative effectiveness of these two
biological mechanisms, with the further possibility that adaptation
can be brought about to a low carbohydrate diet by an increase
in the effectiveness of the direct mechanism for the burning of fat. “
Heathertwist, what you quote ” … two mechanisms possessed by the animal organism for the
combustion of fat, one of which involves the coincident combustion of carbohydrate…” Is he suggesting we need a *minimum* level of serum glucose to burn serum fat? If so, I’ve never read this idea in recent research. Indeed, we seem have to drive our blood glucose *below* a certain level to allow fat to mobilize from adipose tissue and into the blood so we can burn it.
Bear in mind Peter Heinbecker observed low ketones in Inuit in 1928, decades before we learned about the CPT1a variant gene that seems to suppress ketone production in many (most?) Inuit. IOW, it’s likely serum glucose levels do not cause the primary effect on low serum ketone levels. –Bryan
heathertwist- Yes, I did see that link earlier. The thing is, they tested 4 subjects, so I’m not sure we can make a generalization about all the Inuit based on this! Though it is fascinating nevertheless.
Well there is that. Although it jibes with everything else I’ve read about testing on the Inuit.
I kind of wonder though, if it really has to do with “high protein diets” and maybe more about certain elements in the diet, esp. the sulfur-containing ones. It seems that the best diets for cardiovascular health are the ones with high levels of taurine … which does not survive cooking, and is found primarily in seafood and organ meats. A number of aboriginal diets did feature either raw or fermented fish or meat.
http://www.ncbi.nlm.nih.gov/pubmed/20804626
Duck you say: “Peter is wise to distance himself from the Inuit. You should follow his lead.”
About following Peter’s lead, good advice. Thanks!
Here’s how Peter conclude that post you refer to:
“Confirming that the Inuit are not poster boys for ketosis is a “so what?” moment for me…It’s a massive dis-service to any one of the many, many people out there who are eating their way in to metabolic syndrome to suggest that a ketogenic diet is a Bad Thing…I’m always amazed by the concept that a ketogenic diet might be temporarily therapeutic but must be discontinued because it eventually becomes Bad For You. It reminds me so much of the converse concept that low fat diets, which might worsen every marker of health which people may care to look at, will deliver major benefits at some mythical future date.
Ultimately, point scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health. Destroying a circular argument about Inuit diets may may the destructor feel good. Destroying the feet, eyes and kidneys of a person with type 2 diabetes, who need a ketogenic diet, as a spin off from that victory must be difficult to live with. I don’t know how anyone can do this.”
Absolutely agree! –Bryan
“Ultimately, point scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health”
We agree. It shouldn’t. But, it’s yet another straw man argument. Explaining to people that the Inuit are not in ketosis does not “destroy people’s chances of health.” Get real.
A ketogenic diet should not require “poster boys” to prove its efficacy. LCHF advocates like Andreas Eenfeldt knows this well and isn’t afraid to explain it to the people he’s trying to help. It shows that he’s above and beyond such storytelling.
I honestly don’t know why anyone would think that exposing a myth is going to “destroy people’s chances of health.” I’m fairly certain that ketogenic diets do not require such myths to help people. If you think such storytelling is necessary, then I don’t know what to say.
Sure Duck. Why not add Hyperlipid’s Peter to your growing list of folks you accuse of slinging “straw-man arguments?”
Let’s look at your comment on Peter’s quote: “…it’s yet another straw man argument. Explaining to people that the Inuit are not in ketosis does not ‘destroy people’s chances of health.’ Get real…”
Well Duck you and I and bunch of other people here know that, at a biochem level, Inuit ketosis may not relate to non-Inuit LCHF states. But there are many others, people new to this, who won’t sort that out right away. Maybe even never. Those people who suffer from diabetes or other metabolic disorders who hear about LCHF but are afraid to try it. They’ve heard all their lives that “they need carbs” and “dietary fat with clog their arteries.” Like most people these nutrition newbies assume “ketosis” means burning ALL fat-derived nutrients. And who can blame them when so many “authorities” present “ketosis” as the default “other” energy metabolic state to glycolysis?
Then these newbies hear about the ancestral Inuit who lived healthy full lives eating almost no carbs. The Yupik-Inuit are the top success story in our world for living ancestrally on low carbs. These newbies get excited thinking “maybe there IS something to LCHF after all. Look how well these far northern people lived on it!”
Then folks like you come along, hell-bent on exploding Inuit myths, asserting “Inuit are not in ketosis,” “Inuit are ‘different’ from us, that “they eat ‘excessive’ amounts of protein (whatever ‘excessive’ is) and finally “we can’t use Inuit as an example.” You ignore the fact that LCHFers can choose any protein/fat balance within LCHF, that what’s most important is to both *lower the amount of carbs* and lower the *effective glycemic index* of endogenously produced glucose–e.g. from gluconeogenesis so as to keep serum glucose low enough to allow full fat mobilization from adipose tissue. From all I’ve see from direct tests of ancestral Inuit, that’s exactly what happens–the ancestral Inuit have lots of mobilized fat and low serum glucose. I have not see one direct measure of ancestral Inuit that doesn’t show full fat mobilization into serum. None of the text sources you’ve copied in here for us has ever shown that.
Duck, so what if you are correct in some of your specific narrow charges? Whether you mean to or not, you risk discouraging those suffering newbies who seek solutions to their metabolic ills, who don’t understand that your attempts to debunk certain Inuit myths has no bearing on their experience with LCHF.
Call Peter’s statement a straw-man argument if you like. I truly don’t care. You strew you “arguments of fallacy” charges around like confetti anyway. What I care about is that the nearly all the Inuit stuff you intone here can grievously mislead those newbies. Duck, you can bet that, as someone who suffered in a state of diabetes, for whom LCHF has put T2D into complete remission and truly gave a new lease on life, I’m going to keep calling this stuff like this out every time I see it. –Bryan
Anna, Duck, here’s a site that goes into a great deal of detail about ketosis. The most extensive treatment on this metabolic state I’ve seen. I’m trying to find how the author, Dr Peter Attia actually defines “ketosis.” I hope he includes it in there somewhere since he goes into such electron-bumping depth.
Also Anna, I scanned that comments and find a lot of reasonably intelligent convo on ketosis.
Anyway guys check it out if you’re so moved:
http://eatingacademy.com/nutrition/ketosis-advantaged-or-misunderstood-state-part-i
–Bryan
Bryan, I’m sure gut micro biome is important, I was just saying what you eat is much more important. How often you exercise too. A high carb meal or a work out is going to affect your insulin response and blood sugar level so much more then your microbes. So people eating RS while on HC diet and not exercising is a bit confusing to me.
Besides, you can change what you eat every meal, you can work out, but you can’t really change your microbes in a meaningful and aware way, it’s not like you can pop a “good bug” pill.
And as for the correlation, how do we know that it’s not the other way around? may be your insulin response affects your microbes?
And what about fasting? my microbes are still there, yet my BG can be 50. It can only be so low during a fast because of ketones, not my bugs.
Our micro biome is very complex, as we all agree, we know and understand is so very little indeed.
Interesting experiment with RS, many people claim good results, I’ve never tried it. It doesn’t really seem natural to eat large concentrated quantities of it in one sitting. As Morgana said, potatoes are relatively new and wasn’t available to many tribes.
I think our bacteria adapts to the type of fiber we eat, every plant we eat has some food for our biome, even meat does! and RS is not a must for our or our biome survival. Plenty of people dr Price observed weren’t eating RS and were healthy.
Also, as Morgana said, if we eat HF diet, we may not need our biome to produce SCFA, or at least not as much.
Oh yes Anna I agree with you in the main. For most people, the more they get right the other elements in life, e.g. doing at least consistent even if modest aerobic exercise with bursts of resistance, organic/pesticide-free whole foods, proper sleep, and proper stress management (that’s a tough one), the more that gut flora corrects on its own. Like you suggest, our systems are very dynamic, no question our system affect gut bug life and vice versa. There are actual “good bug” probiotic pills, but we have very many questions and doubts about those, including how well do they survive the trip through the very hostile stomach environment. However, we have very clear documented evidence that fecal transplant have greatly helped people and even saved their lives. Many health providers, including my HMO Kaiser, now perform fecal transplants.
http://my.clevelandclinic.org/services/digestive_diseases/departments-centers/gastroenterology-hepatology/fecal-transplant
In some cases, the gut flora is so deranged, the “host” needs to do an intervention. In the worst case, like those with stubborn C. difficile, this can mean that fecal transplant mentioned above. Other people less afflicted *may* be able to benefit from a course in resistant starch. But I emphasize *may.* My first dose of potato starch made me feel *wonderfully calm.* No question I derived a benefit. But that was it! I got -nada- from PS and other RS starches after that, least what I could perceive, how I felt and checking BGs.
Bryan,
yes, some people are definitely so sick and their gut flora is so compromised that they need a transplant to help fix it. But that’s a very clear intervention that has clear results, not like eating some probiotic pills, as you were saying that may not even make it through a stomach.
Btw, I wonder if a simple few days fast would have fixed the gut flora issue by simply starving the bad guys?
Brian, how do you know you are in ketosis most of the time? Do you check your ketones level? at 50-80 grams of carbs, depending on your protein intake, I’d expect you to be out of ketosis often after a meal.
Can I ask you why you have stopped all the vitamins? Please share at least some of the reasons that are in your “book” 🙂
Thanks
Hi Anna, sure I can explain it. From 2007–2011, I carefully tracked all the macro- and micronutrients in every meal I ate, using the spreadsheet + USDA Nutrient Database and other measures which I mention elsewhere in this forum. I finally honed my foodway down to a set of foods (still a quite broad list) that works for me and I know the macro counts by heart. I no longer check my ketone levels, but with reasonable cell sensitivity and keto-adaptation, it often tests low/negative anyway. I stopped that but I still check my BG levels, which is a more informative check for me because my native serum insulin is so low (avg 0.6-0.8 ng/L) that even a modest pop out into glycolysis immediately reflects in high BGs. I keep my protein intake modest and very high quality (lots of eggs from pasture-raised chix), so have little or no excess for my bod to turn into glucose/fat. My macro balance is 80% fat, 15% protein, 5% carb.
About vitamins, the main concern is that oversight for this vast $26B market is woefully lacking. It’s truly a Wild West, or Wild East as you’ll soon see. The FDA treats supps as food, and so are in theory subject to the same oversight. In reality the FDA, already terribly understaffed and budget-starved, devotes almost all its monitoring resources to “real” food. This is very troubling when you consider most of the supps ingredients come from China where just about anything goes. Tens of thousands of little Mom & Pop shops produce many of the supp ingredients like glucosamine and condroitin and even in the larger factories which produce vitamins like Vit C, QC can be sorely lacking. E.g. the water they use to process the mins and water soluble vits (like the Bs, and C) could come out a polluted river and be filled with heavy metals like cadmium and mercury. Some years back I spend an hour on the phone with a Solgar manager, who told me the Vitamin C in *all* supps comes from China, because China drove the cost of manuf so far down it put everyone else out of biz. Then there’s actually making the doses to the stated amounts, novel formulations with still unknown bioavailability, possible estrogenic compounds like BPA and phthalates in the gel caps and enteric coatings, and the general concerns of taking pharmacological doses of anything.
Hi Bryan,
thanks for your reply about vitamins and your ketosis/BG tests. I see your concern with contamination, but I guess that for me the benefits of Vitamin C, for example, outweigh the potential dangers of contaminants, which I think our livers are build to handle. Plus vit C helps to detox them anyway. But I think the more “healthy” one is, whatever that means, the less important vitamins are.
Hi Anna–
I totally agree our livers evolved to be able handle a certain level of contaminants. It’s not like pre-ag “paleo” world was a pristine place. Our ancient forebears constantly ran into natural toxins, arsenic, lead, aflatoxins, etc.
My concern is that our modern world bombards us non-stop with novel chemicals, many of which have still undetermined long-term biological effects on us. Their cumulative presence may now be persistently overwhelming our toxin filters. So many of the thousands of humble quotidien products we use are mute monuments to extraordinarily complex engineering, containing up to thousands of compounds, again many of them novel, existing only since 1945. We encounter them everywhere, in our homes, like in carpet and drywall, in our cars, in our kitchenware (plastic, teflon, aluminum), in our workplaces, and yes, in the formulations and coatings of our supps. Once I appreciated this fact, I went into full mitigation mode, to reduce as many potential toxins in my life as possible. I agree with you that Vitamin C benefits us, and that we actually need it to prevent scurvy. That’s one of the reasons I created the “spreadsheet + USDA Nutrient Database”–to assure myself I was getting the RDA on Vitamin C. I am not convinced that pharmacological amount of C or any other micronutrient help us and in fact may even *work against* us, e.g. loads of supp C and E can shut down our own bod’s endogenous anti-ox production and result in greater insulin resistance:
http://well.blogs.nytimes.com/2014/11/26/why-antioxidants-dont-belong-in-your-workout/?_r=0
and above certain levels, supp vits C and E may even become *oxidants*
http://www.theguardian.com/science/blog/2009/nov/03/vitamin-c-pro-oxidant-blood-pressure
And I agree with you than more robust health can reduce our micronutrient needs. Our bods and their microbiomes evolved a tremendous ability to produce, store, and conserve vitamins, to conserve minerals, and to produce their own anti-oxidants. All the more reason to seek our micronutrients through our food. –Bryan
Not at all sure you’re right about that, Bryan. The RDA of C prevents scurvy, but Linus Pauling pointed out that taking more than the RDA engendered more uses for it through induced enzyme formation. His theory of heart disease involves not enough C weakening the collagen of the arterial wall which exposes lysine residues to which lipoprotein(a) attaches as an emergency repair, which becomes plaque.
I had chronic fatigue syndrome in the early ’80s, learned of Dr Cathcart’s bowel tolerance C therapy, took 140 grams per day without so much as a murmur from my guts (!) for three weeks, then rapidly tapered to a normal bowel tolerance of 10 grams per day as my chronic fatigue resolved. I never took less than a gram or two of C from that day to this for fear of a relapse.
The point is that I applied Pauling’s heart disease remedy long before he ever published it, and my coronary artery calcium score is now zero, meaning no atherosclerotic plaque whatsoever – this is a quite remarkable result for a thirty-five year insulin-dependent diabetic, possibly unique.
Just saying.
Hi Jonathan. I don’t question at all your personal experience. The amount of Vitamin C we might benefit from can vary wildly from person to person. You’ve been T1D for many years, so it’s easy to imagine that the common co-morbidities you often find with T1D set up a greater anti-oxidant need. While I generally feel we should regard supps very warily, I’m certainly not saying people with pathologies for which supps might give therapy should avoid them. By all means they should go for it. Indeed, I took supps in 2007–2009 when still early in my T2D remediation. But for people with no frank pathologies, I hope they will consider to seek micros through food where for them the doses are likely to be right-sized, and in the proper formulation and matrix for optimum bioavailability and absorption, plus they avoid the toxins that too often come with supps. About what you say “…not enough C weakening the collagen of the arterial wall which exposes lysine residues to which lipoprotein(a) attaches as an emergency repair, which becomes plaque…” if you can cite specific research that supports it, that’d be great. About your coronary artery calcium score, when did you first start getting that measured and by with method? –Bryan
Abundant refs in Linus Pauling’s How to Live Longer and Feel Better. He and Mathias Rath did the lipoprotein(a) research, find it on PubMed. I had a virtual colonoscopy 10 years ago, then an EBCT scan two years ago, then a CT scan in hospital for my guts. Zero calcium. Pauling pointed out that primates don’t make vitamin C out of glucose like most every other living thing on the planet except guineau pigs and a couple of other creatures. If you scale the amount of C a dog makes to human weight, you get several grams – guineau pig chow contains the human equivalent of 8 grams of C
“Abundant refs in Linus Pauling’s How to Live Longer and Feel Better.” Um. OK.
“an EBCT scan two years ago, then a CT scan in hospital for my guts. Zero calcium…” Jonathon, you started your Vitamin C therapy in the 1980s, right? That’s 30 years before your EBCT scan. While your Vitamin C may well have played a role in abating your coronary artery calcium, that’s quite a long time from the start of the therapy and your scan. We often make countless changes in diets and lives in 30 years. How can you be sure that Vitamin C alone is responsible for these salubrious effects? –Bryan
Quite so. Nevertheless, I’ve been taking grams of C for those 30 years, and the outcome is what Pauling predicted – zero plaque. My doctor said “We think that’s genetic!” so maybe I’m just a fortunate mutant. It’s entirely anecdotal – but anecdotes can be quite convincing when you’re the subject of the anecdote. I generally bow out of debates with folk who have heart disease with: Have you got a better idea?
Just curious, but has anyone else heard that there is risk with Vitamin C supplementation when iron stores are high?
See: Most Free-Radical Injury Is Iron-Related: It Is Promoted by Iron,
Hemin, Holoferritin and Vitamin C, and Inhibited by Desferoxamine
and Apoferritin (1994)
I donate blood, keep to the bottom end of normal. Scary stuff, iron!
Duck, high iron by itself is not really optimal anyway, without vit C, so it’s best to keep it low regardless. So I donate blood.
And if iron was using up all vit C stores, we would get scurvy if iron was high, clearly, not all vit C is used up by iron, so perhaps there is another size to the story, but interesting nonetheless. May be vitamin c actually neutralizes iron by donating electrons?
I know that vit C increases iron absorption.
Duck,
did some more digging about iron and vit C and found some more stuff that seems to debunk the iron/vit C issue that is observed only in vitro, but not really in vivo.
“There is a considerable amount of in vivo research into this vitamin C/Fenton question. Without fail, in vivo research has NEVER been able to demonstrate that vitamin C is dangerous because of Fenton like reactions. Without fail, in vivo research ALWAYS demonstrates a positive effect of vitamin C on oxidative markers and damage in tissues.”
http://vitamincfoundation.org/www.orthomed.com/PDF/BW_iron.pdf
And Bryan,
here is a nice summary of vit C studies that show that vit C is not a pro-oxidant, but instead causes “a reduction in markers of oxidative DNA, lipid, and protein damage”
http://www.fasebj.org/content/13/9/1007.full
Anna, about that FASEB published study on Vit C, does it make clear what kind of C it is? Supplemental or in food? Maybe the report says it somewhere; it just didn’t jump out at me. Also, the authors are affiliated with the Linus Pauling Institute, founded by the man who is likely the single greatest proponent in history for us to take pharmacological amounts of Vitamin C for its purported health bennies. We must consider the bias that may be inherent in this report. Unfortunately the world we live in now compels these concerns. Special interests so often drive “science” these days. We live in a world where revenue-starved gov’ts have had to slash funds for research that once had any hope to be independent. I’m not saying this report concludes wrong info. Just saying we should always questions the sources. –Bryan
Bryan,
I agree, we should question the source, but we should read both sides and see which one makes more sense. To me so far, the Linus Pauling Institute side makes more sense and it’s backed up by my personal experience as well. Besides, they are not making money on vit C as it can’t be patented and is very cheap, so their conflict of interested is much less, although obviously can’t be ruled out. So I’m always looking for the new information about vit C that will make me change my mind.
As for FASEB study, they were looking at multiple studies that used supplemental vit C. Vit c in food is too low to even have 500 mg. Plus, if it were food, it wouldn’t be clear which compound of this food affected the results either.
As for NYT article, I’m not sure about the details, but my suspicion is that they are speculating as it’s hard to measure real anti-oxident production inside a human mitochondria, so I’m not sure how they are claiming that.
And I agree, adding more stuff is not always good. As I’ve said before, I’ve greatly reduces the amount of vitamins I take, but to me vitamin C is a good gamble (as we can’t ever be 100% sure) and I take my chances with it. I’m not striving for just optimal, obviously many people have lived very long lives without supplements, so it’s clearly possible. I’m pushing the envelope in hopes to exact a little more longevity. And if you believe in ROS theory of aging, dealing with ROS is very important and I think vit C helps with that.
And yes, most people should first reduce omega-6 oils, carbs, orange juice, rancid omega-3s pills, antibiotics, Lipitor, coca-cola, etc, before considering sups.
Best, Anna.
“…anecdotes can be quite convincing when you’re the subject of the anecdote…” LOL, Jonathon, so true! –Bryan
Jonathan, very impressive. Out of curiosity, how did you take 140 g of C a day? That’s a lot of pills to swallow. Also, how much C do you take daily now?
thanks
Allergy Research Group Mixed Mineral Ascorbates in water every hour – tastes like chalk! Cured CFS in an aunt and my sister, but not in the daughter of a friend so 75% success in n=4 expt
I was taking 5 grams per day, but then I caught a tummy bug and went down to 2 grams per day since 5 seemed to piss off my guts
Jonathan, cool thanks.
Bryan, most of the studies that test for vit C, use only 500 mg a day, like the study referenced in one of your articles. It’s far too little to make a clinical difference for most people.
Another point, we need vit C not just to prevent scurvy, it’s important for collagen formation, that’s why it’s all the range now in face creams. It’s also heavily used by the immune system, especially when it’s under attack by a virus, for example, bowel tolerance increases dramatically.
It’s also critical for detox (acting as a reducing agent), given that we live in a much more polluted world. Unfortunately, I don’t have any references now to back it up, as I’ve looked into it many years ago. I only have my n=1.
The fact that vitamin C has pro-oxidant as well as anti-oxidant properties is well known and not news. In 1986 Linus Pauling wrote in his book HOW TO LIVE LONGER AND FEEL BETTER in the chapter Vitamins in the Body:
“The ways in which ascorbic acid (Vitamin C) functions in the human body relate first to the fact that it engages on both sides of the universal oxidation-reduction reaction that subtracts or adds hydrogen atoms to a molecule. (Vitamin C) is readily oxidized to dehydroascorbic acid by the surrender, to oxidizing agents, of the two hydrogen atoms… [shown in the figure]
This action is readily reversible, for dehydroascorbic acid acts as a strong oxidizing agent, and by picking up two hydrogen atoms is reduced to ascorbic acid. It is likely that the reducing power of ascorbic acid and the oxidizing power of dehydroascorbic acid are responsible for some of the physiological properties of the substance.” [PAULING, 1986]
from here:
http://www.vitamincfoundation.org/lunec.htm
Hi Anna, you said: “…most of the studies that test for vit C, use only 500 mg a day, like the study referenced in one of your articles. It’s far too little to make a clinical difference for most people…”
What do you think is the minimum daily dose to make a clinical diff for most people? –Bry
Bryan,
To make a difference for really sick people, they need to test vit C close to bowel tolerance levels taking it in divided doses through out the day. And for normal “healthy” people, I’d at least test in grams, not milligrams, again, in divided doses through out the day with 2-3 grams being a minimum tested.
That NYT piece discusses how even 1g (1000mg) per day Vit C can contribute to shut down our bods’ endogenous anti-ox production. Endogenous anti-oxes which appear to give the additional bennie to increase insulin sensitivity. The 2–3 g per day supp Vit C you cite goes well beyond that dose the NYT discusses.
I suspect we’ve learned enough about nutrition to be dangerous to ourselves. Or at least to act against ourselves. However unwittingly.
We are in a unique period in our human existence in which we can, and do, accelerate the “adding” of novel substances to our lives, like supps. Since the end of WWII, we’ve seen and experienced massive novel inputs into our lives, thousands of new organic compounds, antibiotics, etc. Our response to the emerging chronic pathologies from the ’70s onward has been to throw *more* synthetic stuff at them, like supps, in the hopes to mitigate them. Anna, IOW, we keep *adding* stuff with the hope to mitigate the massive amounts of novel inputs we’ve experienced. Where does that endless feedback loop finally stop?
Maybe we should consider to *subtract* stuff from our lives? At least see what happens? –Bryan
Anna, btw, the “Made in USA” label means zip. The manuf can import all the supp ingredients from China, stuff them into caps, and slap a “Made in USA” on the bottle. Perfectly legal 😦
Duck, let’s please not distract from the main point: We can’t say–at all–how healthy or harmful early grains were for people. You often imply that early grains are healthy, or at least not health-harming. E.g. you said: “…the cultures that thrived on…wheat.” The *culture* may have thrived. But we have plenty of evidence to suggest the *individual* did not thrive. The very strong, likely predominant focus in this forum is how we can optimize our *personal* health, no?
You say: “Please. I’ve already given the sources here.” Duck, I wish you’d more carefully read my posts before you answered. You simply confirm what I said. Your most modern source is from 1938. To repeat from my previous post, is long before we have blood marker testing, epidemiology, and biochem understanding to even begin to speak with any authority how healthy or not any wheat is, early or modern. None of your links offer adequate science. The links mainly support beliefs, however widespread these beliefs may be. We all know too well that even a very strong chorus for or against something can, in the end, be proven very wrong. E.g. for 1500+ years the mainstream believed in Ptolemy’s geocentricity–that all celestial bodies revolved around our Earth–until the 17th century. The mainstream believed classical physics until quantum mechanics came along last century.
Indeed Duck you do concede “…Nobody can ever really prove anything one way or the other [regarding how healthy it is to eat early grains]…” But then we move right on to this your graf which starts: “Do note the references showing that bread, and specifically wheat, was considered to be the healthiest of all foods…” You then go on to underscore the reputed wonders of grains, replete with plenty of your italicized words to hammer home your points to us. Duck, can you see how the reader might get the idea you feel early grains were very healthy for us? At the very least, your message is very tendentious toward them.
Finally Duck what you say here is a near total fail: “Let’s not conflate life expectancy at birth with life span. Hippocrates lived to between 83 and 90 years of age. Aristotle lived to 62. Von Linné lived to 70. Medieval scholars had an average lifespan of 59–84.3 years in the Middle East and 69–75 in Islamic Spain. New England colonists had lifespans of 62-65 years.” Really Duck?! Your first three examples are three n=1s? How rookie a logic fail is that? About the scholars, it’s stupid to choose a small and privileged segment of society and imply their average lifespan somehow represents that of the rest of society. Even in a modern Islamic society discussed here: http://bahai-library.com/lapidus_history_islamic_societies the scholars (“ulama”) represented only 20% of society. Your New England colonists stat is most interesting. The link you gave me is broken, but I found this: (http://www.columbia.edu/itc/hs/pubhealth/rosner/g8965/client_edit/readings/week_3/demos_1.pdf). The lifespans table on page 77 aligns with what you say for people 21 and older.
And guess what? The Pilgrim’s main grain food was *corn*–not the glutenous grains like wheat and barley: https://www.plimoth.org/sites/default/files/media/pdf/edmaterials_diet.pdf. Very interesting!
Of course I agree we can’t prove the positive or negative health effects of early grains, glutenous and otherwise. People can keep posting links ad infinitum to support their beliefs, hunches, notions, and predilections. Many of these links are very interesting to read and discuss, but they also can be very misleading. Which is why I’ve been saying here people should ultimately *test themselves* with as many of the health measures they can do at home and coax out of their docs, track them and their lifestyle inputs over as long as term as they can, and learn to interpret their results **in their context and totality**, generally avoid to put a lot of weight on any single measure. We can no more say that ancient grains are health-promoting than we can say they are health-inhibiting.
WBryanH said: “let’s please not distract from the main point”
Well, you and I have different points. While you seem to have an agenda to demonize grains, my main points are that the evidence demonizing grains is circumstantial, at best, and that, right or wrong, Western civilizations believed that wheat was the most nourishing of foods right up until the Industrial Revolution. Perhaps all of our ancestors got it wrong, but it is a simple fact that wheat was once seen as the perfect food.
In fact, the 1857 edition of The New American Encyclopaedia literally states:
This was not a controversial statement at the time. It’s just what people believed (again, right or wrong). The demonizing of grains is based on ignoring other influential factors. I can’t prove that grains are amazing and I won’t say that everybody needs to eat them. I’m simply providing an oposing perspective against all the grain bashing here.
WBryanH said: “Your most modern source is from 1938…The links mainly support beliefs, however widespread these beliefs may be.”
Yep. That’s my point. You do understand. 🙂
WBryanH said: “We all know too well that even a very strong chorus for or against something can, in the end, be proven very wrong.”
Sure. But my first point was that the anti-grain evidence that’s being presented here in these comments is misleading. If you’re going to prove that grains are bad, looking at skeletons and populations that experienced other diseases isn’t going to prove anything.
WBryanH said: “You then go on to underscore the reputed wonders of grains”
Perhaps you misunderstood. I simply pointed out that, right or wrong, our ancestors widely believed that there was no better food than wheat. You can choose to ignore that history if you wish. But, I think it’s worth pointing out.
WBryanH said: “Finally Duck what you say here is a near total fail”
lol. It’s rather funny that you think a fact is a “fail”. Like it or not, those were the average life spans of the time.
So, yeah, you’re one of those individuals who perpetuate shortened life span myths.
WBryanH said: “And guess what? The Pilgrim’s main grain food was *corn*–not the glutenous grains like wheat and barley”
Again, this is misleading as your own source states that they had been “familiar” with English wheat, rye, barley and oats before coming to the New World. I suppose you also think they all had diabetes and were obese in their 70s. lol 😉
WBryanH said: “Many of these links are very interesting to read and discuss, but they also can be very misleading. Which is why I’ve been saying here people should ultimately *test themselves* with as many of the health measures they can do at home and coax out of their docs, track them and their lifestyle inputs over as long as term as they can, and learn to interpret their results **in their context and totality**, generally avoid to put a lot of weight on any single measure. We can no more say that ancient grains are health-promoting than we can say they are health-inhibiting.”
Amen. See, we do agree!
So, let’s end the grain bashing then. None of us know one way or the other.
Duck, it really does seem we’re in alignment on many nutrition issues. Only I need to reject your premise I “demonize” and “bash” grains. I challenge you to find anyway where I categorically assert that people should avoid grains. You won’t find anything remotely like that from me. As far as the fulsome evidence you supply to support your statement that “Western civilizations *believed* that wheat was the most nourishing of foods right up until the Industrial Revolution” sure that is fine. Only Duck, why do you seem to feel the need to supply all this history, since most of us knew it already, or at least have a strong cultural sense of it? Praising grains already was the default till very recently, and it still is in many places. Even the Bible holds grains high. Duck, you really shouldn’t confuse the very appropriate questioning of grains with “demonizing” and “bashing” them.
As far as life spans, you totally miss what I was saying. You say: “…this is misleading as your own source states that they had been “familiar” with English wheat, rye, barley and oats before coming to the New World. I suppose you also think they all had diabetes and were obese in their 70s. lol ;)…” Sure Duck the colonists were “familiar” with these glutenous grains. But in the New World they were eating mainly *corn.* Duck, what part of that don’t you understand?
Duck, I wish you would actually *read* the things you comment on. That’d make things more interesting at least.
Anna said: “Do you think that white flour is a problem and whole wheat is ok, or it doesn’t matter, any wheat flour is ok? Perhaps the milling process is what makes the difference?”
White flour has no nutrition, and therefore it cannot sustain life. White flour is well known to promote degenerative diseases. This was well documented by Dr. Weston Price and Sir Robert McCarrison. In 1931, Sir Robert McCarrison gave a series of lectures, at the Royal College of Surgeons, summarizing his findings, saying:
Dr. Price also observed very healthy Swiss eating mainly whole rye, dairy and very little meat. So, those observations and McCarrison’s studies clearly support the superiority of whole flours over white flours.
However, I think that one can probably get away with eating white rice or white flour if they can find a way to make up for the nutritional losses in other ways. For instance eating white rice or a few slices of baguette with other mineral-rich foods (hemp, cacao, seaweed) may end up being a wash.
European countries seem to do OK on white flours because they do not fortify their flours with enrichments. It’s been known for almost a century that tastebuds can crave B vitamin enrichments that are added to white flours. In most of Europe, there are no enrichments in their white flours so one’s tastebuds automatically craves B vitamins from other sources (i.e. actual food).
So, my feeling is that white flour in the US is particularly problematic due to the enrichments. In Europe, you would naturally gravitate towards getting your nutrition elsewhere. You’d have no choice actually, because if you didn’t get your nutrition elsewhere, you’d become deficient and lose your appetite (a well known symptom of B vitamin deficiency). Therefore, we might say the enrichments added to white flour are something that enables people to eat refined foods as a staple, which they would otherwise be unable to do if the enrichments were not there in the first place. Keep in mind that some countries, like Denmark, actually ban enrichments.
Aside from that, there are likely other issues with modern flours. In France, they have the Pain Décret, which is a law that limits the ingredients of traditional bread to wheat flour, water, yeast, and common salt. In the US, you can add whatever garbage ingredients and enrichments you want to baked goods. Plus, industrial mills fumigate (sometimes bromate) and process the hell out of flours.
Also, industrial whole wheat flours are not ground up wheat berries. What they do is they create white flour using all the processing and then they claim to reconstitute the bran and germ.
This all makes it very difficult to pin down what’s actually wrong with modern flours. My guess is that the processing, adulterations and enrichments are more problematic than wheat itself. However, if someone’s gut is damaged, they will have trouble with wheat no matter how good the wheat is.
Incidentally, the The New York Times recently published an article (see “<a href="“>Bread is Broken“) that claims that industrial mills discard the wheat germ and don’t add it to whole wheat flours—even though they are supposed to by law. It’s a shame because Vitamin E is protective of some of the damaging effects that may be attributed to gluten.
Basically, we don’t eat real wheat anymore. You can grind your own wheat berries or find a baker that grinds its own whole grain flours. Anecdotally, people seem to think that they tolerate real wheat better, and I wouldn’t be surprised.
Anna said: “I’m curious, do you have any theory on why americans are getting fatter and fatter and more and more people world wide are having Diabetes? If it’s not wheat, then what? Do you blame sugar or simply too much calories? and if it’s increased caloric intake, why did it happen?”
Zhou et al. have a relatively new theory that it’s the flour enrichments. They note that developed countries that fortify their flour have significantly more obesity and the timing of mandated enrichment increases mirrors the rise of obesity in those countries. They hypothesize that the enrichments are promoting obesity and possibly stimulating appetites. I think they are on to something.
You can try it yourself. Anecdotally, you may notice that making a recipe (say pizza, for instance) out of enriched flour may stimulate your appetite more than organic unenriched flour. The reseach suggests that the appetite stimulating effect of B vitamins may depend on your B vitamin status however.
Cheers
“White flour has no nutrition, and therefore it cannot sustain life. White flour is well known to promote degenerative diseases. This was well documented by Dr. Weston Price and Sir Robert McCarrison. In 1931, Sir Robert McCarrison gave a series of lectures, at the Royal College of Surgeons, summarizing his findings, saying:”
What I wonder, reading this, is: did you read the blog post we are discussing? White rice is just as nutritionless as white flour, which is exactly the point Denise is making. Actually white rice is WORSE, because it has very little protein. And yet in Kempner’s protocol, people did well on the diet. I do believe iron is a cofounder there. So, IMO, is the fact that rice works differently than wheat. And/or, as Denise theorizes, maybe it has to do with the amount of fat (we are waiting with bated breath for the next post!!!).
As to “we can’t know what happens” … have you even READ Denise’s take on the China Study? I mean that is a long blog post or two and some big number crunching, but you can’t say it doesn’t have many people and it involved home-grown “natural” wheat too. The whole reason I started following rawfoodsos was because of Denise’s brilliant work there. But you are basically trashing the entire basis of her work … she is carefully and mathematically looking at the evidence.
Now if you don’t like the evidence for some technical reason, then sure, talk about the geeky details about why the numbers are wrong. But “It’s too hard to figure out” doesn’t really hack it with geeks; that sounds like the Homer Simpson Defense. And yeah, if you are defending wheat, you should use some of the post-1940 science, which gets down to the chemistry of all this.
Anyway, I get the impression you don’t really understand the science of what you are talking about, and are talking more at an emotional level. As a matter of courtesy though, you should read Denise’s basic article, and also the China Study articles, which are pretty amazing.
Duck, thanks for your reply.
I read dr. Price and he indeed showed that whole grains are better then while flour. I didn’t remember him observing any tribes eating whole wheat though, so thanks for the reference of Hunza indians. Although, it’s hard to draw any conclusion from just one example, especially because they practiced caloric restriction and protein restriction that skews the results:
http://undergroundhealthreporter.com/hunza-diet-health-weight-loss/#axzz3tBUxQwpL
So it’s still not clear to me if whole wheat and whole grains are directly beneficial and life extending or just not as harmful as white flours.
As for the vitamin B flour fortification theory, I didn’t see any evidence of that in Russia, where I’m from. Flour is not enriched in Russia, yet diabetes is on the rise there as well and obesity is becoming more common. Also, my remote relatives in India are vegetarians and have extremely low vit B levels, yet it didn’t affect their hunger, they eat high carb diet, are overweight and pre-diabetic. I don’t know if flour is fortified in india, I doubt that, but they eat a lot of it and have one of the highest per-capita rates of diabetes. So, I don’t think that enrichments of white flour are that consequential.
Why do people overeat if it’s not fortification? because they can! As the world is getting wealthier, the world is getting fatter. So my theory is that overconsumption of food based on availability, access and increased wealth is basically responsible for our obesity epidemic. And diabetes and obesity were always predominately the disease of the rich, who didn’t work much and had access to unlimited food supply.
Pre-industrial revolution agrarian society involved lots of manual labor, walking, etc. to burn/use the carbs they ate. Also, food supply was more limited with practically no snacking on potato chips, chocolate milk, candy, nuts, soda, health bars, etc. People were going hungry much more often. Now the world is getting wealthier and food is getting cheaper because of mass production, subsidies, advancement in agriculture, etc. Combine that cheap food with constant convenient access to it 24/7 and a much less active life style and you will get continuos excess caloric intake that leads to most of the diseases. And this gets worse with every generation because constant insulin spikes or whatever other genome changes in pregnant women, lead to the next generation to be less insulin sensitive and more prone to being overweight.
Even France, with its culture of small portions and no snacking, getting fatter. The French tradition of not opening the refrigerator between meals for a child isn’t as prevalent it once was. Obesity in children is growing at a rate of 17% while obesity in adults is growing at a rate of 6%. The french paradox, ironically could be partly attributed to smoking, as nicotine is an appetite suppressant and lots of french people still smoke. Also, a shot of espresso in the morning, which is very common in France, is appetite suppressing.
I think that carbs need to be tailored to one’s activity level, not precisely, obviously, but if one eats high carb diet that is not calorically restricted, one needs to be active to cycle the glycogen in the muscles to stay insulin sensitive or to practice IF. And while some people can eat high carb and not overeat, for most people constant eating of HC without corresponding physical activity causes increased appetite.
Anna- you’ve been wondering about the obesity/diabetes epidemic. I, too, wonder exactly what the cause is- (though there are many very plausible theories out there). I’m an American living in Germany, and in the 8 or so years I’ve been here, I’ve seen obesity really take off. It does seem to me that in recent years there are far more American-style fast food places here, and more people seem to be eating junk food. I think obesity is pretty well correlated with junk food, and I think, with globalization, this could be the problem worldwide. Some argue that we had fast food back in the 50’s and 60’s, but I think one thing people fail to take into consideration is that many of the ingredients are now different. Along with sugars and high fructose corn syrup- (both of which we’re eating in record proportions, apparently), I wonder if soy and soy oil might not also play a part. (Soy is an endocrine disruptor). In addition to that, there seems to be evidence that some of the additives used in junk food are either addictive, or cause overeating- (similar to what Duck was saying about fortification). For awhile I believed the “high carb” theory, but now I’m not so sure…… well, to be honest, I do notice that generally most people seem to be eating huge amounts of carbohydrate, so it could be that, but that doesn’t really explain how many traditional cultures stayed thin eating relatively high carb diets. Maybe it has something to do with eating processed versus natural carbs, or maybe there were other nutrient dense foods in those populations that were protective? In any case, exactly “what’s causing the obesity epidemic” is a question being asked by many great minds at the moment.
Morgana, thanks for your comments on the obesity epidemic, but may be it’s not some additives or HFCS or junk food, but simply because food is available 24/7 and it’s cheap. It’s easy to eat junk food because it doesn’t require any effort to cook. You can get it any time you want, you don’t need to go home and boil some rice and then wait for it to cook…
Food may be cheap in America; here in Europe it’s not that cheap. In much of the world people don’t have access to good, affordable food. And the thing is, obesity is correlated with poverty, so that doesn’t really explain everything, the way I see it. Although you do have a point, that’s part of it…..but I don’t think it’s the only answer.
Morgana, poverty is relative. Poor in US is not the same as poor in Africa. Junk food is cheap even in Russia. Junk food is cheap relative to income of people in EU. You can’t be obese if you are truly starving. There were no obese people in concentration camps, clearly.
But I’m sure other factors are at play.
For the record, I do think that HFCS and refined linoleic acid oils are also to blame. Interestingly, enriched flour contains a lot of iron which is generally poorly absorbed and is known to promote inflammation in the gut. However, HFCS and linoleic acid are believed to significantly increase iron absorption.
So, it may be eating enriched foods with HFCS and linoleic acid might be particularly bad.
“Only I need to reject your premise I “demonize” and “bash” grains.”
Heh. You literally just wrote a comment warning about the dangers of wheat bran, lectins, and phytic acid while saying “some will argue” that phytic acid is a beneficial. That’s grain bashing. And you’re actively downplaying the research on why antinutrients may be beneficial in those with replete diets.
“As far as life spans, you totally miss what I was saying.”
Life spans have been nearly constant for the past 2,000 years. Furthermore, Americans transitioned to wheat as their principle crop in the 18th century. There’s not much else to say.
Duck, once again, you cite no valid evidence. -Nada-. That’s a recurring problem with you. You do not read thoroughly or carefully.
In essence you’re saying that to question grains is to *bash* and *demonize* them. You’re suggesting that, because I report that my health improved when I left grains, that I’m bashing grains. I’m simply relating my experience.
Duck how does the above NOT underscore your ultimately uncritical grain bias?
Let’s look at what you said:
” …You literally just wrote a comment warning about the dangers of wheat bran, lectins, and phytic acid while saying “some will argue” that phytic acid is a beneficial. *That’s grain bashing*…”
Duck, this refers to comments I wrote to Anna, here:
“my take is that we should regard warily *all* wheat flour. White flour, for the very fast carbs/gluten/lectins and loss of nutrients replaced by fortification plus chemicals introduced in its processing, the potential downsides of which Duck amply covers through the forum (search on “fortification”) Whole wheat includes the bran and comes with its own concerns, e.g. phytic acid that, in your GI, can steal essential minerals from your food. Though some will argue that, in the case of iron which we too often get too much of, phytic acid could be a *good* thing…”
I follow with this:
“I quit grains early on (2007) simply because grains are high in carbs–long before I faced the additional health questions of gluten, hemoagglutenating lectins, and phytic acid.”
I end with this:
“…this is just my n=1. Please get as many health checks as you can, as often as you can…”
What do I actually say here Duck? Do I call grains into question? Absolutely! We all should. Do I “warn about the dangers of wheat bran, lectins, and phytic acid” as you accuse me of doing? No I do not assert they necessarily come with “dangers.” I say only that they pose “health questions.” Do I say everyone should avoid grains? No I don’t. What I AM saying is that people should monitor themselves and see how they do with grains and without grains.
Duck, you really should confront and examine your inherent grain bias.
Wbryanh,
We can agree to disagree. It’s really no big deal. Neither of us are telling people what they have to eat. Question grains all you like. I just think it’s hardly helpful to only question grains without fairly looking at all sides of the story. That’s all. My responses were merely to provide the other side of the story—not to actually prove grains are amazing or whatever.
For the record, I thought heathertwist was the one doing most of the grain “bashing,” referring to Otzi and various skeletons to somehow show that grains were harmful, without considering the other factors affecting the status of those skeletons. It’s a bit more complex than just looking at what was in someone’s stomach at the time of their death.
heathertwist said: “White rice is just as nutritionless as white flour, which is exactly the point Denise is making. Actually white rice is WORSE, because it has very little protein. And yet in Kempner’s protocol, people did well on the diet.”
As I understand it, Kempner’s protocol was not designed for healthy individuals. Rather, it was designed for people to lose weight and regain their health. What isn’t mentioned in the article is that you can achieve the same results with a potato diet (see Chris Voigt) and the success of such a diet is attributed to A) the hypocaloric nature of the diet (you can only cram so many waterlogged carbohydrates into your gut) and B) the significantly increased intake of resistant starch from such a diet (a portion of glycemic starch often passes to the colon as beneficial resistant starch, a kind of fiber). Resistant Starch has been shown in studies to promote much of the health benefits mentioned in this article.
A potato-only diet can be quite therapeutic for weeks or even months. But, a potato-only diet is not really an ideal way to eat long term.
heathertwist said: “have you even READ Denise’s take on the China Study? I mean that is a long blog post or two and some big number crunching, but you can’t say it doesn’t have many people and it involved home-grown “natural” wheat too.”
Yes, I read it awhile back when I myself was anti-grain and low carb. And I don’t recall it ever distinguishing the difference between whole wheat and white flour consumption. Perhaps I missed it. There’s a huge difference between the two, and most anti-grain sentiments miss it.
heathertwist said: “And yeah, if you are defending wheat, you should use some of the post-1940 science, which gets down to the chemistry of all this.”
Ok then.
Wbryanh recommended that one can create a USDA-based spreadsheet and he found he could easily get all his micronutrients (vits + mins) without eating a single grain. However, this approach is rather antiquated and shortsighted (not his fault, it’s just what his anti-grain books told him to do) as it assumes that the health benefits of whole grains are merely due to their basic nutrition profile. Unfortunately, that’s not the case. The health benefits of whole grains are actually believed to come from the phytonutrients that aren’t listed in the USDA database.
For instance, it’s well known that oats are particularly healthy and have anti-diabetic properties. A good deal of the health-promoting effects of oats are believed to largely be from their unique phytochemicals, like avenanthramide and high levels of tocopherols.
Nutritional and functional properties of oats: An update (2014)
Whole grains are not just calories and USDA nutrients. They contain of all sorts of phenolic acids and flavanoids (avenanthramide, ferulic acid, vanillic acid, caffeic acid), carotenoids (leutin, xeazanthin, β-crythoxanthin, β-carotene, and α-carotene), γ-Oryzanol, sterols, stanols, fiber (β-glucan, resistant starch, inulin, oligosaccharides), lignans, and other phytonutrients like amylase and protease inhibitors. [See Table III] A good deal of these health-promoting phytonutrients are removed during the refining process.
So, as much as all these investigations into the known problems with refined grains are very interesting, as far as I can tell (and perhaps I missed it), the anti-grain investigations often ignore the difference between whole grains and refined grains. For instance, I believe the China Study data showed problems with “wheat flour” (not “whole wheat flour”).
Nevertheless, China also has severe iron contamination from antiquated milling equipment made of iron (see Investigation of the wear failure mechanism of a flour milling roller). China also has very high iron in their wheat (see Mineral element concentrations in grains of Chinese wheat cultivars). This may be due to high iron dust from the Gobi Desert, which is known to create enormous iron phytoplankton blooms in the Pacific Ocean. The whole country and its various regions are an ecological and environmental mess. I’m not entirely sure how anyone can easily draw many meaningful conclusions from it without considering those factors.
Finally, the rollermill technology to completely purify white flour has been around since the mid-1800s. Over 90% of the flour consumed in the US is white flour, so it’s hard to say that people are gaining health benefits from giving up whole grains. For all we know, they are just gaining health benefits by giving up (fortified/processed) white flour.
Cheers,
Duck,
Even if properly milled fresh non-fortified whole grains are healthy, don’t you think it’s a moot point because they are simply not available to americans? As you were saying, even whole wheat flour/bread is not really whole wheat, so what’s the point? Nobody is going to mill grains at home… Isn’t it better to avoid it all together then?
Also, your studies claim whole grains as being healthy, but compared to what diets? To white flour/sugar diet or to very low protein starvation diet? Sure, whole grains will be better. I apologize if I missed some links, but have you seen any human studies that compared a whole grain Wheat diet with a diet absent of wheat and refined sugars and not nutrient deficient? How would they compare? How would whole wheat diet compare to a Low carb diet?
I wonder, is there anything in whole grains that a grain-free diet would be missing? or are these “healthy” nutrients in whole grains are only needed to “protect” the body agains the high carb content on these grains?
Thanks.
One of the benefits of eating grains is to not be an orthorexic party pooper. Grains are so incredibly tasty. And yes you can get quality fresh milled grains in america. Also they are mineral dense with a lot of manganese and selenium. Plus they add quality carb calories that displace a lot of inflammatory protein and fat calories in most diets.
Zach, yes I agree with you on one point, the only benefit of eating grains for me is enjoyment, especially freshly baked goods.
Where can I buy bread or other baked goods made form freshly milled grains? I’ve never seen that.
As for selenium and manganese, lots of it is in fish and seafood.
And as for fats/proteins being inflammatory, I’d say carbs, even whole grains, could be just as inflammatory if eaten in access, if not more.
Seafood is so dang contaminated, I’d be hesitant to eat it more than once a week or so.
Can you give me an actual mechanism on how carbs are inflammatory. People love to say that sugar/starch is inflammatory but iv yet to see any proof. Protein and fat on the other hand have many known mechanisms for causing inflammation.
May be seafood once a week is enough for our selenium needs.
You propose whole wheat as an alternative, but you still didn’t answer where an average american can find freshly milled grain products for everyday consumption?
Carbs are inflammatory via insulin resistance and hyperglycemia. Just look at diabetics. Untreated high blood sugar leads to all sorts of complications, it’s common medical knowledge.
And before you say that it’s fat that causes diabetes, not carbs, it doesn’t really matter what causes it, but after you have it, if one keeps eating lots of carbs and calories, diabetes gets worse. So yes, carbs and proteins and fats can be inflammatory if one consumes excess caloric intake. Carbs just make it easier for most people to overeat and LC makes it easier to eat less. Perhaps just like very low fat, I don’t know, I didn’t try it.
A good brand of whole grains is Bobs Red Mill, if you don´t have a store that sells them they can be ordered probably from amazon or go to bobsredmill.com. You can make a heavy bread by soaking 2 cups of whole or cracked grains like buckwheat, rye, wheat – soak overnight then the next day add enough water to blend into a thick paste roughly one cup of water, add a bit of salt, and let it ferment until it rises a little and bubbles a little, one to two days usually. Then bake – not to hot of an oven it makes a heavy loaf and if you don´t bake it enough it will be wettish in the middle. Google how to line a loaf pan with parchment paper and you will get your loaf out of your pan super easy. If you want a thicker loaf use more grain. I suppose you could add yeast or baking powder if you want it to rise a little more.
Rebecca, thanks for the suggestion, but I assume that Bob’s flour is not going to be fresh, probably months old, so oils will be rancid and components oxidized, not exactly freshly milled as people used to eat it…
I was talking about buying whole grains not flours.
Rebecca, sorry, I’ve misunderstood your post. I didn’t realize that you can make bread using only cracked wheat. How does it come out? Does it taste similar to normal whole wheat bread?
thanks!
I have only made this once, I used a mix of whole buckwheat and cracked buckwheat, but the principle applies to wheat and rye either whole or cracked. The taste was good, it will taste like whatever grain you use. But you will not get a big slice like store bought bread, and it will have a heavier, more pound cake like texture.
Cool, thanks.
I work in an organic bakery and we mill organic whole grains. Pretty simple, Google around.
And lol, you’ve never tried a low fat diet and yet you think you have relevant opinions? Fat absolutely causes insulin resistance and diabetes, it’s proven by the fact that billions of cultures eat a high carb diet without suffering from that disease. In that context it is still not carbs that cause inflammation but fat causing inflammation and resistance to insulin.
Go high carb, low fat for a few months and change your life. Seriously.
Zach, you must live somewhere in California or NY if you have access to freshly milled flour goods, good for you. It’s not as common as you think, lol. I googled it, but didn’t find any places. You need to get out from your bubble more often.
I’ve actually tried low fat vegetarian (with fish) diet for a year, so I’m sorry if my opinions offend you. If fat caused diabetes, I’d be dead by now because fat is almost all I eat, lol. Yet, as I type this, it is a clear proof that I’m not dead and my inflammation is almost zero. So may be it’s not fat that causes diabetes, but caloric access or mixing fat with carbs? But once you have it, carbs will make it worse.
Zack, There are countless examples of people reversing diabetes on HF diet, why is it so hard for you to believe?
I believe that some people reversed their diabetes on Low fat diet. The underlying similarity between LF and LC is low caloric intake that leads to weight loss.
Keep an open mind, perhaps your way is not the only way.
I beg to differ that carbs will make your diabetes worse once you have it. I have it, I made my diabetes better doing low carb high fat and have now switched to low fat high carb and my diabetes has improved a bit more. I think the combo of carbs and fat is the culprit it also depends on how damaged your metabolism is. When I started low carb high fat I could not have done low fat high carb, but with the improvements I made I now can do high carb. There are so many things it depends upon. There is no once size fits all.
Rebecca, I agree, one size doesn’t fit all. I meant to say that keeping eating high carb diet while eating fat, basically not changing anything, will keep blood sugar high and your diabetes worse, requiring more and more insulin.
As I’ve said, some people can improve their diabetes on LCHF, some on LFHC, but both seems to reduce their caloric intake and lose weight or reverse insulin resistance.
I live in minnesota…
I feel really sorry for you that you have to eat almost exclusively fat to avoid diabetes. That must suck hard. And no, not a single soul cures themselves of diabetes by not eating at carbs, that is just a band aid for a much bigger issue. For instance, I eat 500g++ a day of carbs but if I eat an extra 200g of fat a day I don’t die of blood sugar poisoning. If you ate your diet and added in 500g of carbs, you might. That’s a big difference. Insulin sensitivity is of utmost importance to health. Eating vlc just means you are very insulin resistant, that is not reversing anything.
Zach, why do you keep jumping to conclusions??? I don’t have diabetes, neve had it either and I love my high fat diet. I love stake, eggs, cheese, butter and bacon, so don’t feel sorry for me now, feel sorry for me when I ate beans, broccoli, sprouted bread and was avoiding rib-eye stake for a year of being a vegetarian.
Btw, What’s that bigger issue that LC diabetes cure causes? Lots of diabetics improved their health on LCHF, it’s well documented, again, why so hard to believe?
I eat mostly LC, but occasionally pig out and eat lots of carbs, not 500, I can’t eat so much and why would I want to? but 100-200 and I’m fine. I’ve had a pizza on occasion and didn’t go into a carb coma. As a matter of fact, just last weekend I probably had 150 gr of carbs for dinner and still alive.
It’s fasting insulin that matters… Mine is 1.8. What’s yours?
No idea on fasting insulin and no need to find out. I’m a glucose storing and burning beast!
But I *have* tried a low fat, high carb diet, and it was the absolute worst thing for me. As Anna said, a low fat, high carb diet can make people- (at least some of us) constantly hungry. This is a sign of possible insulin resistance. In my own case, I had to eat very few calories (which eventually led to anorexia) to keep from gaining weight. So, Zach, I would not recommend your diet willy-nilly to everyone! I personally turned my health around by going low carb high fat. I eat far more calories than I did before, in other words I’m sated, and I’m thin. In addition to that, fat absolutely does not cause insulin resistance (at least not for me). As I said, I’m healthier than I ever was before. and I’m much older now, so that should count for something….. Your way may work for you, but it does not work for everyone.
There are a couple of ways that “carbs” can be inflammatory that I know of:
– Fructans. A whole lot of Northern Europeans don’t digest fructose very well (although we are generally better than most of the world at lactose). So SOME carbs are high in fructans, which is where wheat, onions, sunchokes, fruits, sugar, and a few other items come in. The undigested fructans end up feeding yeast mostly, and that makes for bloating and Candida overgrowth. Rice and many other grains, oddly, do not contain fructose (they are based on glucose). In traditional Japanese recipes, the “sweetener” is usually rice syrup, which is glucose, not sucrose.
— Iron. A lot of carbs in the US have added iron. The iron is quite inflammatory.
— Some whole grains have substances in the husk that don’t get along with everyone. Fermenting does help with that. But some things … like the arsenic in brown rice or the WGA in wheat … don’t ferment out.
— Rancidity and mold. Whole grains esp. can go rancid easily. Unless you store grains carefully, they tend to be pretty rancid and often have a fair bit of mold. The mold has caused some interesting historical times (like witch hunts). Grain mold is a big issue with farm animals and a big cause of birth defects. Most of what you eat is pretty well handled, but there seems to be some amount of mold residue in all grains.
There are similar issues in tubers. Potatoes have solanine. Taro can be toxic if not handled correctly. Tapioca too.
I kind of think some of the logic behind the “rice diet” was just that it avoided the toxic features of some of the other foods. If you were trying to cure kidney issues, you’d want to avoid proteins in general, but also all those toxic things that the kidney filters out.
One thing about eating a “fresh vegetable” diet is that when vegies are moldy or wilty, you’ll notice it! Same with meat … if the meat is old, your nose knows. Fish … wow, old fish is so obvious. But ground flour or meal? How can you tell?
heathertwist said: “Some whole grains have substances in the husk that don’t get along with everyone. Fermenting does help with that. But some things … like the arsenic in brown rice or the WGA in wheat … don’t ferment out.”
I doubt it’s helpful for healthy individuals to worry about cooked WGA. There’s no known evidence of cooked WGA being harmful.
Also, take a look at this:
Sounds like WGA might be rather good for you, don’t you think?
I don’t understand why many here are orthorexic about cooked WGA. It’s like people are trying to find things to worry about without.
To all involved in the “wheat debate”- I thought this post was interesting, as it explains some of the cultural biases of various time periods:
http://www.montignac.com/en/the-history-of-man-s-eating-habits/
If Duck seemed like a grain apologist before, his comment below (at post bottom) removes all doubt.
We very poorly understand the biological behavior of phytochemicals–much less than vitamins and minerals: http://lpi.oregonstate.edu/mic/dietary-factors/phytochemicals
Furthermore Duck cites a link straight out of Big Agra–rife with conflict of interest–to back up his claim. Two of the four leads for that paper he cites, “Whole Grains: Definition, Dietary Recommendations, and Health benefits” work at the General Mills Bell Institute. Gee. How could you expect them to craft their grains message? These people won’t bite the hand that feeds them.
Bottom line, neither Duck nor anyone else can furnish any true science on the effect of phytochems in the human GI tract and serum. No true mechanistic-level studies exist that demonstrate how these very many–estimates range from 1000+ to 5000–and mostly large compounds are supposed to affect our health. The CW on phytos has been that many are anti-oxidants and serve to neutralize oxidants in our bodies. We have no in vivo evidence to show how these compounds actually survive the trip through our GIs, through a powerfully acidic and hostile stomach chamber, and into the small intestine. No-one know what happens to those phytos that survive the trip–many of them quite large, 40 and more carbons long–once they finally arrive to the duodenum, Nutrient Digestion Central. Many phytos are simply too large and too weakly polar to simply enter and travel effectively through our serum. What happens to these phytos in the duodenum? Do we load them onto chylomicrons and send them into our system via the lymph? Do we enzymatically break them down into other components? How much of their vaunted anti-ox properties survive to that point? No-one’s determined this. A more recent hypothesis on phytos suggests they can have a *hormetic* effect–meaning to provide stress stimulus to our bods so our own bods generate their own anti-oxes. Mark Sisson discusses the hormesis idea here: http://www.marksdailyapple.com/hormesis-how-certain-kinds-of-stress-can-actually-be-good-for-you/
The hormesis idea makes sense when you consider the idea that phytochems evolved to help plants repair and defend themselves. Plants can’t get up and hide in a cave to avoid the sun and the creatures that want to eat them. These anti-oxes may well help the plant recover from day-long uV exposure and limit the amount–e.g. by presenting unpleasant-tasting bitter glycosides–that animals graze on it.
All questions above, we’ve eaten plants for millions of years, so I’m quite willing to accept the idea that some phytos help our health. For the moment let’s assume they *do* benefit us. Are grains truly a good source of them? The evidence so far suggests NO. Grains may even be a particularly *poor and narrow source of phytos.* Let’s go back to that Oregon State link: http://lpi.oregonstate.edu/mic/dietary-factors/phytochemicals
There, you find the researchers break out the phytos into a dozen broad categories: carotenoids, chlorophyll/-phyllin, curcumin, fiber, flavonoids, garlic, indole-3-carbinol, isothiocyanates, lignans, phytosterols, resveratrol, and soy isoflavones. For each of the dozen phyto classes, you’ll find a Food Source link. (>Sources>Food).
Of those dozen groups, grains figure prominently and broadly in only ONE of them: fiber. Certain grain products are also high in lignan (in rye) and phytosterols (wheat germ and bran). In those three categories, however, you find plenty of non-grain foods that fare as well or even better than grains.
Phytochems are not new to us. We’ve heard about their purported health bennies since at least the 1980s. When I began my foodway journey in 2007, I naturally looked at them at that time, and have tracking them since. For Duck to suggest I limited my nutrition approach to “USDA Nutrient Database + spreadsheet” is patently ridiculous. It’s yet another case of him assuming something I didn’t say. I created the spreadsheet in 2007 precisely because our authorities relentlessly propagate the pro-grain dogma, telling us we need to eat loads of “wholehealthygrains” for us to stay healthy. I needed to prove to myself that we could in fact, get all our vitamins and minerals from non-grain foods. But of course I didn’t stop there. I’ve always eaten a wide variety of non-grain plant foods. Especially brassicates (e.g. broccoli, brussels sprouts, cabbage, kale), which offer an uncommonly rich and varied assortment of phytos as you can see in that Oregon State site. As far as Duck’s claim that the spreadsheet + USDA Nutrient Database approach is “… what his anti-grain books told him to do…” he extracted that notion out of his derriere. I challenge Duck to find anyone anywhere who recommended that approach. He simply can’t find that. Certainly not in any “anti-grain” book.
Duck writes very well, presents a facade of credibility, and offers interesting ideas to follow up on, esp the questions around fortification. But I’m afraid he’s given so much logic fail and flimsy and even risible evidence to support his claims, I must take what he writes as ideas–occasionally excellent ideas–and nothing more. That’s something at least. But at this point I have to ask: who pays Duck to propagate his pro-grain message?
Here’s that Duck comment: “Wbryanh recommended that one can create a USDA-based spreadsheet and he found he could easily get all his micronutrients (vits + mins) without eating a single grain. However, this approach is rather antiquated and shortsighted (not his fault, it’s just what his anti-grain books told him to do) as it assumes that the health benefits of whole grains are merely due to their basic nutrition profile. Unfortunately, that’s not the case. The health benefits of whole grains are actually believed to come from the phytonutrients that aren’t listed in the USDA database.”
“I’m afraid he’s given so much logic fail and flimsy and even risible evidence to support his claims, I must take what he writes as ideas–occasionally excellent ideas–and nothing more”
wbryanh, I’ll politely ask you to refrain from this kind of argument from fallacy. It seems like in every comment you make an effort to insult my intelligence, simply because you disagree with what I’m saying. Please stop it. We can agree to disagree, but such insults are unnecessary.
Duck, I honestly feel you are an intelligent person. Which is why it surprises me you often offer really quite poor evidence to support your claims. I labored with that disconnect for a while, and finally had to start wondering if you are a paid shill. No other answer jumps to mind at this time.
wbryanh: “Duck, I honestly feel you are an intelligent person. Which is why it surprises me you often offer really quite poor evidence to support your claims.”
Jesus. You just can’t stop with the insulting fallacies. This time it’s Argument from personal incredulity and Argumentum ad lapidem.
How many times do I have to ask you to stop?
wbryanh: “I labored with that disconnect for a while, and finally had to start wondering if you are a paid shill. No other answer jumps to mind at this time.”
Unbelieveable. Now you’re using a genetic fallacy.
I asked you politely to stop and you just hurl fallacies back in my direction. I don’t know what else to say.
For the record I have no conflict of interests. A shill for the grain industry would not be against fortification, which is widely supported by the 13 major grain lobbyists.
I used to be low carb and bought into the anti-grain propaganda after (processed) carbs made me quite sick. At first I felt great, but after almost a year I got even sicker from low carb dieting. It was horrible. Through my own experimentation I regained my health through the Perfect Health Diet and then made even greater health improvements by slowly incorporating real whole grains and legumes back into my diet. It wasn’t the carbs that made me sick, it was the processed and refined carbs that made me sick. You could say I’m post-low carb now.
So, please stop, wbryanh. We can agree to disagree. You don’t have to insult someone just because you have an personal incredulity. That does not give you the right to insult me. I think you don’t even realize you’re doing it.
Duck, do you mind sharing what you mean by “after almost a year I got even sicker from low carb dieting. It was horrible.” What symptoms/issues did you have? I’m honestly interested as I’m always watching out for side effects, as we are all doing our own personal dietary experiments. Thanks.
Anna, I’d be happy to. On my processed SAD diet I was very thin, but had lifelong brain fog, psoriasis, rosacea, dandruff (probably due to candida or some kind of dysbiosis). After going low carb I felt quite good, but I quickly lost 10 pounds that I didn’t need to lose and began to look like a crack addict. Everyone was worried about me. Within a few months panic attacks started and then I lost the ability to fall asleep. My sympathetic nervous system was shot and stress hormones were taking over. I was a mess. My short term memory worsened considerably—I could turn the stove on and forget about it 2 minutes later. It took a lot for me to finally admit that the low carb was the wrong choice for me. My guess is that low carb worsened my candida (I later learned that some candida can thrive on ketones).
And so I began to research the potential benefits of carbohydrates. I learned about resistant starch and began experimenting with increasing fermentable fiber intake. Improved sleep and amazing dreams happened quickly. I began to feel relaxed again (our gut flora create our calming GABA and other neurotransmitters). My memory improved slowly but surely. I solved my candida issue with PHD and other therapies—and for the first time in my life the brain fog lifted and then disappeared over many months. It was incredible.
Over time I learned to incorporate real whole grains and legumes into my diet. Today, I can eat plenty of real whole wheat and my skin stays supple and smooth. If I eat enriched flour, I get a bit of dandruff and rosacea. I didn’t get dandruff or rosacea while eating a good amount of white flour in France—which is how I realized that fortification and flour adulterations might be what was problematic for me. France forbids those impurities in their traditional breads. I began digging into the research and found that indeed fortification may be responsible for some health problems.
Duck, thanks for sharing. Interesting about fortification affecting your health.
Also interesting about your sleep as well. Perhaps it was also a magnesium deficiency and not just a lack of fiber/carbs effect? Greens, beans and grains are very high in magnesium. And magnesium is very important for nervous system as well. It also improves memory and helps panic attacks.
Duck Dodgers- that was interesting about your health journey; now I understand a bit where you are “coming from”- (not that there’s anything wrong with that; I have some relatives who tried eating low carb, had a few similar problems, then tried the Perfect Health Diet, which they say helped them a lot). I, myself, seem to do well on low carb. I would like to respectfully mention that I think the “resistant starch” issue has been over-hyped. I’m not sure that it’s important for everyone. Obviously, your own n=1 tells you it’s good for you. The point is, the study of the microbiome is so new, it’s in it’s “infancy” really; we just don’t enough about it yet. The main reason resistant starch has been touted as being healthy is that we happen to know quite a bit about it. However, there may be other compounds in other foods that we don’t know about yet. Only some gut bacteria have been identified, but there’s a whole world out there that we still know nothing about! Not only that, but the microbiome is a whole ecosystem, so what’s most important is not certain bacteria (at the expense of others), but the right balance of bacteria. This will vary from person to person as well. As some have pointed out, there aren’t that many sources of resistant starch in nature, so some of our hunter gatherer ancestors would have had trouble getting it. (And potatoes are quite new in our diets). I, myself, don’t do well with grains; they actually mess up my digestion horribly, so it’s obviously not helping my microbiome any! I think eating other types of fiber can be just as beneficial. Each person has to find what works best for them, and I think basing it on how you feel can be a pretty good marker.
I agree, Morgana. I don’t think it’s particularly helpful to catalog your microbiome when we barely understand what the various species do (which may indeed be a fad). But there’s of course evidence that the microbiome can effect health in ways we don’t fully understand. There seems to be value in feeding the microbiome something. I don’t think it’s a “fad” to eat fibers. Most indigenous cultures are known to eat considerable quantities of fiber (Hadza for instance). I doubt they do it out of boredom—otherwise it would be a waste of time and resources. Probably makes them feel good.
Duck- I totally agree, the microbiome can affect health in various ways, some of which we are just barely beginning to learn about. And I agree that eating some plant foods and fibers are not a “fad”, but probably good for us. Just for the record, I do eat plant foods- probably more than many- but I stick to the ones I can digest well. Resistant starch is a problem for me, generally, so I probably don’t eat that much of it, and I eat low carb mainly because it’s very good for my digestion. I don’t eat much in the way of potatoes- (occasionally a small amount, that’s all I can tolerate). And as I said, potatoes are a relatively new food. I do eat nuts though, and I think some of them might have resistant starch? (Like cashews: do they have resistant starch? Or almonds? If so, then I do eat some of it).
Duck, Morgana, just wondering. Where does it say we should eat amylose-based resistant starch–like that from potato starch and bananas/plantains–to properly nourish our SCFA-producing gut flora? Where does it say there are no other types of fiber–like those found in leafy greens, colored veggies, fruits, lower-carb root veggies like carrots, and anything else that’s naturally without gluten–that can adequately nourish these SFCA-producing flora? Do grains offer any type of fiber unique to grains that nourish these SFCA-producing flora?
I haven’t been able to find any clear info on any of this. Thanks for your thoughts, ideas and links. –Bryan
wbryanh- I don’t think it *does* say anywhere that we *need* to eat resistant starch! However, a lot of bloggers- (many in the Paleo world, for instance)- started experimenting with resistant starch, then started blogging about it; this is why I called it a “fad” in one of my earlier posts to Duck Dodgers. These are basically “laypeople” who recommend it- (though I respect many of them, for other reasons). Most of the experts who study the microbiome tend to be more cautious, i.e., saying that we need to learn more before we tell people to radically change their diets. But, yes: you basically vocalized my own thought, that other types of fibers may be equally beneficial, and resistant starch may not be necessary. That doesn’t mean that it’s not beneficial for some! My own theory is that how we feel about what we eat probably determines what’s best for us as individuals.
Nowhere does it say we “need” to eat RS. However the research does say that if you wanted to maximize your SCFA production (a big if), you’d almost certainly have to eat RS in order to do it. Many of the non-starchy fibers, like cellulose, just don’t ferment into very much and few very people have the flora to ferment cellulose in the first place. On the other hand, Inulin can be found in dandelion greens, and it is a very powerful fiber. But of course, inulin doesn’t ferment into all SCFAs, so you need a few different fibers to get the full spectrum.
Whether we necessarily need to maximize our SCFA production is another question altogether (I don’t have the answers for that), but suffice to say, many cultures seemed to have had high SCFA production.
A general summary of that research on RS can be found here. I used to supplement with RS and it definitely saved me from the problems I was having. But, I don’t supplement anymore, I just eat real foods now.
Keep in mind a fiber is only fermentable if you have the right flora in place, (why cellulose isn’t considered a MAC), so your mileage may vary depending on which fibers work best for you. For all you know, you may do excellent on dandelion greens and jerusalem artichokes rather than starches. Everyone’s gut is different, and it is possible to modulate your gut over time.
Thanks Duck. Dandie greens seems to work well for me. I’ll forage them from forest duff near my house and make salad with a tin of sardines, fresh garlic, sprouted sunnies, red pepper flakes, a little apple cider vinegar, and juice of a half a Meyer lemon. Oh and some grated pecorino. Delicious and my GI feels good and and BGs usu do really well. So there’s my little n=1.
I’ve been looking for a list of all the diff fibers, what foods you find them in and in what quantities (per 100g), which gut flora they feed, and the fermented products these flora produce. I’ve found putative fiber/food efforts, like this: http://www.webmd.com/diet/compare-dietary-fibers and here:
https://en.wikipedia.org/wiki/Dietary_fiber#Types_and_sources_of_dietary_fiber But nothing that matches the fiber to the flora to the fermented products. If anyone has links for that, that’d be great. –Bryan
Bryan, I’ve seen the different fibers-to-SCFAs before but can’t remember where, offhand. I’ll see what I can find. But, if I remember correctly from the n=1s, the people who did VLC often had poor results from RS. My guess is that due to the lack of starch in their diet, they just didn’t have the biome to process it and they pooped most of it out. Makes sense.
Interestingly, your body will intentionally persorb a finite portion of all fibers into the bloodstream where they may (or may not) have the ability to bind up various free metals or whatever else. Nobody really knows what goes on there, but it’s the same mechanism that brings phenols and antioxidants into the bloodstream as well. All fibers, phenols, antioxidants are just xebobiotic glycans (could be hormetic as you say…nobody knows).
I wouldn’t worry to much about getting the full spectrum of fibers. There are some studies which have found that using just a single fiber can create far more floral diversity than a variety of fibers can.
It’s paradoxical, but makes sense if you think about it. When you have a single fiber, just a few species might grow. But soon species that feed off of the metabolites of the first species (i.e. cross-feeders) begin to flourish from the steady supply of metabolites. And then, perhaps, more species that feed off the metabolites of the second generation of species begin to flourish (cross-cross feeders?) and so on.
It’s sort of like growing a crystal or a snowflake—it gets more complex so long as the foundation is stable.
So, you see, someone who relies on one or two staples (maybe just potatoes like the Irish, or say baobab and a few tubers like the Hadza) likely may have more flora diversity and SCFA production than someone who tries to eat a wide variety of fibers. This might explain why the Kemper protocol worked just fine for those who needed it.
This just goes to the earlier point that there’s so much we don’t know. So, I probably wouldn’t stress about getting all fibers if you’re already doing well with certain fibers. You might be better off sticking to one or two fibers. Nobody really knows.
Thanks for all this Duck, and no rush on those links. I have no GI issues or anything else to resolve at this point, but it remains a big academic interest. About the Microbiome Project, we are at the very beginning of what will likely be an incredibly rich study, like the genome project. Btw that single-fiber idea, with the blooming of gut flora diversity on the potato diet, that’s very interesting. Another example to suggest less can be more and for us to get out of our own bodies’ ways. –Bryan
My pleasure, Bryan.
I found this paper showing SCFA levels from non-starch fibers:
A comparative in vitro evaluation of the fermentation properties of prebiotic oligosaccharides (2001)
Obviously, the results of the comparison only apply to flora that are already in place to ferment these polysaccharides. So, everyone gets different results, which are modulated over time. In other words, if one was a germ-free mouse, they’d obviously get zero SCFAs from taking these fibers.
That paper doesn’t compare with RS, but RS is known to produce a LOT of butyrate. However, again, one typically needs to have a diet high in starch to possess the RS gut bugs for fermentation—otherwise it would just be like eating sand, the RS passing right through you mostly unfermented due to lack of RS-degrading flora. You could change this over time, but it might be best to stick to one or two fibers, preferably from real, whole foods.
Fecal butyrate levels vary widely among individuals but are usually increased by a diet high in resistant starch (2011)
You get the idea. I have seen studies generally comparing the fermentation levels of RS and other non-starch polysaccharides, but I think you can get the idea from this.
Thank you Duck–very much what I’m looking for.
I wonder if some species of flora will ferment multiple types of fiber? Are there species that ferment RS plus fiber from various low-carb foods too? Reason I ask, you say this:
“…one typically needs to have a diet high in starch to possess the RS gut bugs for fermentation…”
Yet when I started the potato starch in ~ 2012, it was already five years being VLC. The very first time I consumed it, my GI, my whole bod felt really really good and calm. And I never experienced GI upset except maybe a little at 4TB/day.
At that time (and now), I eat fiber from various sources, avocado, coconut, various leafy and cruciferous greens, artichokes (including all the leaves), citrus (including the skin)… –Bryan
Bryan, as for which species inulin tend to modulate, this paper may be of help:
Inulin-type fructans modulate intestinal Bifidobacterium species populations and decrease fecal short-chain fatty acids in obese women. (2014)
I really don’t pay much attention to the species though. So, my apologies if this isn’t helpful.
Duck, interesting, thanks again! Btw, I’m not immediately seeing how higher fecal SCFA concentrations somehow suggest higher metabolic risk. Aren’t colonic SCFAs a good thing?
I wonder if there a comprehensive list of the ferments our flora generate? Will keep googling that. –Bryan
Duck, this from you : “…inulin doesn’t ferment into all SCFAs, so you need a few different fibers to get the full spectrum…”
Do you know which flora inulin feeds, and which SCFAs those flora produce?
That’s the kind of info I’ve been looking for for years. Thanks –Bryan
Oh.. and, of course, some modern gut issues, like SIBO, may have issues with some fibers (FODMAPs, RS, etc). So, obviously this is not a blanket recommendation for everyone. Although some people have claimed to have cured their gut issues with fibers—supposedly the fibers may pick up and sweep away bacteria back into colon where they belong. But that’s one of those n=1s that might not work for everyone. Again, YMMV.
For me, I seem to thrive on RS, so it’s now eggs and toast for me in the morning (toasting bread is said to significantly increases RS3 in bread).
Guys FYI: http://lpi.oregonstate.edu/mic/other-nutrients/fiber#introduction
One of the better breakdowns I’ve seen of dietary fiber types and the plants you find them in. Alas, that’s not saying much.
And still no links to the flora these feed and what ferments those flora generate. –Bryan
DIETARY FIBER
Lignin: Lignin is not a carbohydrate; rather, it is a polyphenolic compound with a complex three-dimensional structure that is found in the cell walls of woody plants and seeds (7).
Cellulose: Cellulose is a glucose polymer with β-1,4 glycosidic bonds found in all plant cell walls (see Figure 1 above) (6).
β-Glucans: β-Glucans are glucose polymers with a mixture of β-1,4 glycosidic bonds and β-1,3 glycosidic bonds (see Figure 1 above). Oats and barley are particularly rich in β-glucans (7).
Hemicelluloses: Hemicelluloses are a diverse group of polysaccharides (sugar polymers) containing six-carbon sugars (hexoses) and five-carbon sugars (pentoses) (6). Like cellulose, hemicelluloses are found in plant cell walls.
Pectins: Pectins are viscous polysaccharides that are particularly abundant in fruit and berries (4).
Gums: Gums are viscous polysaccharides often found in seeds (4).
Inulin and oligofructose: Inulin is a mixture of fructose chains that vary in length and often terminate with a glucose molecule (8). Oligofructose is a mixture of shorter fructose chains that may terminate in glucose or fructose. Inulin and oligofructose occur naturally in plants, such as onions and Jerusalem artichokes.
Resistant starch: Naturally occurring resistant starch is sequestered in plant cell walls and is therefore inaccessible to human digestive enzymes (4). Bananas and legumes are sources of naturally occurring resistant starch. Resistant starch may also be formed by food processing or by cooling and reheating.
Guys, my n=1 on resistant starch, I got terrific results in the very beginning, and then quickly sloped off to zero after a few times eating it. I started with Bob’s Red Mill unmodified potato starch (easy, cheap, near-zero carbs), initially 1TB/day and then worked up to 4TB/day. The very first time I tried it, it suffused me and my GI with a wonderful sublime calm. I’ll never forget that. But then that was it. I experienced no dramatic effects after that, either in how I felt and in my BGs.
Morgana, along the lines what you said”…there aren’t that many sources of resistant starch in nature…” after the potato starch stage, I started to experiment with very green banana and raw potato (some feel bananas originated in India). In both cases I could eat ~50g per meal without unduly popping my BGs. I continued to feel no different. It’s almost like a needed a prebiotic “top-off” and then that was it.
And I agree with you Morgana about the complexity of our microflora and how little we understand what they do and especially how they interact. Here Michael Pollan delves into the intrigue, promise, complexity and unknown:
http://www.nytimes.com/2013/05/19/magazine/say-hello-to-the-100-trillion-bacteria-that-make-up-your-microbiome.html?_r=0 –Bryan
wbryanh- Interesting! I never caught on to the “potato starch” bandwagon; I was always skeptical of it, since for me, potato starch just doesn’t seem like a real food, but more like a supplement. (And I assume it’s relatively processed; at least, it resembles a flour, not something I’d want to eat necessarily). But yeah, basically, some of our ancestors might have had access to resistant starch, but certainly not all! (How many cultures had access to bananas? Some, but only a few). Some people had access to plantains, some to manioc…..potatoes are a more recent food…..so, yeah…..I’m just not sure that resistant starch is necessary for all. I suspect that the foods that are “beneficial” probably vary, depending on the rest of the diet the individual is eating. There are some groups that ate very few plant foods- (not just the Inuit; but also the Sioux Indians, I believe also the Mongolians)- and they seemed to thrive. In any case, for me most foods with resistant starch don’t seem to be the foods that I can digest well. (Unless nuts have resistant starch, I think some might). Based on what I’ve read, it sounds like fiber is very important for people who need to live off of a lot of plant foods, as the gut microbes convert the fibers into by-products that in turn “feed” us. But, if you’re eating a more carnivorous diet, this might be less necessary, as the nutrients are readily bio-available in those foods, we don’t need to make the conversion. (I think Dr. Eades writes about this on his blog….or maybe it was Dr. Eric Westman, I might have that confused…..maybe both?).
Hi Morgana. My RS experiment stage, it was a while back when Sisson, Kresser, Nikolay, etc were all glomming onto the wonder “butyrate-spawning-monster” potato starch. So I trying to recall the details of my program, what I did. Honestly, I decided to try RS it because of Sisson. But certainly I had your same processed-product concerns. I decided I’d take PS it just for a very short time, just to see what happens. I did quickly move to the more natural RS sources, but like you say, potatoes at least weren’t paleo/ancestral. My general approach, given our overwhelmingly complex modern world filled with novel products, is that *less is more.* The less done to the food from when it’s conceived to when I get it, the better. The more “heirloom” (meaning less selective breeding) the better. However I started my nutrition and lifestyle journey in 2007 with a quite deranged metabolism, and so accept the idea that selective limited temporary application of non-natural products might help correct me. E.g. I took supplements from 2007 to 2009 before I scaled them down and then stopped all of them. Morgana thank goodness I’ve arrived to a state of health that, for several years now, I haven’t felt I needed any more interventions! –Bryan
Duck, let’s stick to the issue at hand. I’m pointing out where your evidence is poor, and *provide evidence* to support that. In this forum I have done so already many times now. When I question what you say, I *provide evidence* to support what I say. Anyone who cares to search our names in this forum will see I do that. I have always been willing to engage with anyone who questions what I say and the evidence I cite. This is called healthy debate. It’s exactly the kind of thing we should see and engage in here. I am sorry if you feel that when I question you–or when I defend myself again your comments which some people may well interpret as being condescending and insulting to me–that you take that as an insult and a personal affront. Yet I am not entirely surprised. When I questioned grains, you considered that “grain bashing.”
Duck, I am certainly not invalidating your personal experience. I’ve heard a number of success stories with the Jaminets’ Perfect Health Diet. And to remind you, I do feel we align in a number of nutrition areas. I hope I’ve made it clear I feel you offer valuable things here. But I *will* continue to call bullsh*t when I see it.
As will I, wbryanh.
As will I.
Thanks for the interesting and detailed information.
As for dropping grains … well, I do eat them, mainly white rice because I like it. But I will say, if I had to grow all my own food (like the Japanese mountain people) I’d go for tubers! It amazes me that most of the world actually started growing grains at all. I do a fair bit of food-growing, and I did put in some amaranth, sorghum, even wheat at one point. Also I do lots of potatoes and sweet potatoes and taro.
Grains are DIFFICULT.
1. They are quite sensitive to water levels. One drought wipes out the crop. Tubers store their own water.
2. You have to get rid of all the weeds to get the plant to grow. Tubers will usually grow in the middle of a mess of weeds, and kind of take over.
3. You have to harvest them at just the right time or they rot. Tubers you can usually leave in the ground til you are ready to eat them.
4. After you harvest the grain, you have to beat it, de-husk it, grind it, ferment it.
5. Then you have to keep it in a super-dry environment or you get toxic mold.
I can totally understand why hunter-gatherers would gather some grain heads and eat them. But why they started *farming* them is beyond me. I expect some of it is financial. You can store grains in silos for years. Like gold. So you can hoard grains and dole them out during famines. Another answer might be “ethanol”, although you can make decent beer from tubers too, and certainly from fruit.
Our ancestors weren’t really looking at tables about nutrients. It was more like “this tastes good” or “this makes me feel good”. Somehow the grains won out, in much of the world. Like I said, this floors me. I just don’t understand it. The tuber-eaters seem to have done just fine historically, but they swap and do grains if they can.
Heathertwist, you say “But why they started *farming* grains is beyond me. I expect some of it is financial. You can store grains in silos for years.”
Heather I feel what you suggest–selling/bartering of excess, storing for lean times–is a lot of the reason. Grains literally did civilize us by allowing us to engage in widespread food production for the first time, and to do it remaining in one place. We finally could start to develop towns and cities and amass belongings including documents when we developed the first writing systems 5000+ years ago. Jared Diamond discussed the many ramifications in one or more of his books maybe “Guns, Germs, and Steel?”
You say “Somehow the grains won out, in much of the world. Like I said, this floors me. I just don’t understand it. The tuber-eaters seem to have done just fine historically, but they swap and do grains if they can.” Interesting isn’t it? My thoughts: we started growing grains in or near the Fertile Crescent, which stretches roughly from Cairo region in Egypt to modern-day Iraq. Jared Diamond talks about the relatively low natural barriers on the Eurasian continent that allowed wheat and barley to spread far and whole. The runaway most popular tuber, the potato, comes from South America, and explorers brought back to the Old World less than 500 years ago.
About what you say “Our ancestors weren’t really looking at tables about nutrients. It was more like “this tastes good” or “this makes me feel good” we may well find actual chemical properties peculiar to wheat to make us prefer it over other starchy plants. http://www.ncbi.nlm.nih.gov/pubmed/6099562
Dr Davis dwells on the presumed opioid properties of some gluten metabolites in his book “Wheat Belly.” But please don’t rely just on him for info on the topic! –Bryan
Yes, I think there is something to the opioid issue. A lot of foods act like drugs … coffee and chocolate come to mind. They are beginning to find more hard evidence that non-celiacs still have brain changes when they eat gluten.
“95 adults in the U.K. were picked to go gluten-free for three weeks, then go back to normal for another three weeks.When they were gluten free, they got fewer cramps and stomach discomfort, but they also picked up a sharper mental focus because they were less fatigued. The researchers think this is an important breakthrough in the study of how gluten affects us, and our brainpower.
They said: ‘The fact that they were able to start tasks quicker, concentrate better and think clearer during this time, and felt the need to rest less, all point towards the idea that sensitivity to gluten does exist for some individuals who don’t have celiac disease.””
http://www.aol.com/article/2015/12/02/going-gluten-free-could-boost-your-brainpower/21276724/
I’m not sure exactly what factor in wheat causes this though … there is still the FODMAPS thing and the WGA and all the other stuff.
Anyway, for rice I’d think yes, it might be about storage and civilization. Pretty much all the anthropologists agree that “civilization” began with grains of one sort or another. The South Seas Islanders, for instance, didn’t bother with grain, but they also never did large-scale cities or armies etc. But the exceptions are kind of interesting. The Japanese mountain people in Yuzurihara grow only tubers, because the land is too steep for rice. And they are said to be the healthiest of the Japanese.
And interestingly, after living off tubers for a week or three, I still couldn’t give up my rice! The yams and potatoes tasted great, but they don’t have “the thing” … maybe the sheer concentration of calories is what the body is after too.
Anna said: “Even if properly milled fresh non-fortified whole grains are healthy, don’t you think it’s a moot point because they are simply not available to americans? As you were saying, even whole wheat flour/bread is not really whole wheat, so what’s the point? Nobody is going to mill grains at home… Isn’t it better to avoid it all together then?”
Yes, you have a point. I’m not a fan of industrial flours. The French do OK (i.e. good for a Western nation) with their unfortified white flours and strict purity laws (decret pain) and better milling standards.
However, you can find whole wheat berries in any high quality American supermarket—including spelt and farro—for porridges, salads or grinding. In New England it is possible to find gristmill flour—I believe there are still a dozen or so gristmills operating. I believe even Whole Foods sells some gristmill flours in those states. They are excellent. Home grain mills are becoming more popular and are quite good (see them on Amazon). Some people even using coffee grinders to grind their wheat. Anecdotally, I’ve seen some people suggest that the wheat they grind at home is more tolerable than industrial wheat, which does not surprise me. Also, there are plenty of non-wheat whole grains that are available to Americans: Quinoa, Chia, Amaranth, Farro, Kamut, Teff, Sorghum, etc.
Anna said: “have you seen any human studies that compared a whole grain Wheat diet with a diet absent of wheat and refined sugars and not nutrient deficient? How would they compare? How would whole wheat diet compare to a Low carb diet?”
I have not seen such studies. However, one of the known potential problems with low carb diets is that they can be low in MACs (Microbiota accessible carbohydrates) like Resistant Starch, which is well established as being beneficial to health.
https://en.wikipedia.org/wiki/Low-carbohydrate_diet#Resistant_starch
This is one of the major criticisms of a low carb diet. See Tim Steele’s blog for endless details on this. He’s an amazing resource.
Anna said: “I wonder, is there anything in whole grains that a grain-free diet would be missing?”
Well, it would depend on the diet, but a grain free diet might be deficient in resistant starch and other phytochemicals I mentioned in my previous comment. It would depend on what kind of grain free diet one chose. I think the interesting thing about whole grains is they make it really easy to obtain those phytonutrients. (Also, low carb diets can sometimes be deficient in manganese, which is essential for managing iron, but that’s another story and not relevant to your question about a “not nutrient deficient” diet).
Anna said: “or are these “healthy” nutrients in whole grains are only needed to “protect” the body agains the high carb content on these grains?”
I don’t think anyone has the answer to that. My sense, however, is that those phytonutrients help us maintain homeostasis in managing problematic micronutrients like iron. Phytates likely also promote this homeostasis by potentially chelating excess free unbound iron. So, I imagine they are needed, but I suspect no one can say for sure just yet. More research is needed.
Duck,
good point about whole grains for porridges and side dishes. Unfortunately they are not as tasty or convenient as buying bread 🙂 but certainly doable. And making bread at home using home-milled flour is really a time luxury I can’t afford, it’s just not worth it for me as I don’t eat enough carbs to justify the time.
I’ve seen Tim Steele’s blog and had a discussion with him, so I”m not convinced at all on the benefits of RS. I think it’s a FAD. I eat lots of vegetables, so I’m sure my microbes will survive 🙂 or adapt to my diet. I don’t adapt my eating to it, lol.
As for phytochemicals, again, I’m not convinced of their benefits, nonetheless, I eat lots of veggies, coffee, tea and chocolate, just in case 😉
Seafood for manganese and bloodletting for managing iron 🙂
But just in case I’m not missing something, I eat rice, bead or a croissant at least twice a week, I wish I could find it baked from freshly milled flour…
Anna said: “As for the vitamin B flour fortification theory, I didn’t see any evidence of that in Russia, where I’m from.”
Well, I’m still looking into it, but as far as I know, the appetite-stimulating effect of B vitamins doesn’t have to come from fortification. It could feasibly come from anything that has a taste of natural B vitamins (marmite, beer, brewer’s yeast, or yeast extracts, for instance). I assume there is something yeasty in the Russian diet. 🙂 Incidentally, bakers at the turn of the century knew that people preferred the taste of white flour made with brewer’s yeast. Same idea.
Anna said: “Flour is not enriched in Russia, yet diabetes is on the rise there as well and obesity is becoming more common.”
It’s simply a correlation that populations with fortification tend to have more obesity and diabetes. Again, it’s not my finding (it’s Zhou et al‘s)
Anna said: “Also, my remote relatives in India are vegetarians and have extremely low vit B levels, yet it didn’t affect their hunger, they eat high carb diet, are overweight and pre-diabetic.”
I think you are misunderstanding. Low vitamin B status is known to make someone more susceptible to the appetite-stimulating effect of B vitamins. So, anything rich in B vitamins should stimulate their appetite if they have low B vitamin status. If they were truly deficient and not tasting any B vitamins whatsoever, they would likely get beriberi and they would lose their appetites (as what happens with pellagra or the 19th century dyspepsia epidemic). The appetite-stimulating effect of B vitamins has been shown to happen by Osbourne & Mendel, and others, from just a small flavoring of B vitamins—it’s an innate sense we evolved with to choose nutrient-dense foods over nutritionless foods.
Anna said: “I don’t know if flour is fortified in india, I doubt that, but they eat a lot of it and have one of the highest per-capita rates of diabetes. So, I don’t think that enrichments of white flour are that consequential.”
No, fortifications are certainly not the only factor. Again, you’d have to look at the correlations examined by Zhou et al. The correlations are there, but that doesn’t mean they are exclusive. Also, diabetes may be caused by iron overload, or at least by a mismanagement of iron stores—perhaps due to other micronutrient deficiencies. So there are obviously many different ways this can happen. One does not need fortification to become obese or diabetic. Fortification just seems to promote it somehow (perhaps by simply enabling and stimulating people to eat more refined foods as staples).
Keep in mind that in India, diabetes is associated with a large shift from consumption of coarse grains to polished rice and refined wheat as well as sugars. This means that micronutrients like Manganese and copper are literally being refined out of their diets. Both minerals are required for SOD production (like MnSOD), which are our most powerful endogenous antioxidants. Without those minerals and those antioxidants, we lose the ability to manage our iron stores, and this deficiency may be what actually promotes diabetes.
We can’t easily blame carbohydrates alone for diabetes when all of these cultures are becoming more chronically diseased as they refine their carbohydrates. Some researchers believe that the increased fiber and the bitter tannins in whole grains initiate satiation signals that makes it difficult to overeat them. When you refine those satiating compounds away, you will likely eat more than you should. So, it’s obviously multi-factoral (as I’ve previously mentioned).
Duck, I realize that there is correlation between fortification and obesity, but it could be just that, a correlation and not a causation, or at least a very tiny factor. I doubt that if we stop the fortification now, obesity will go away or at least will be reduced significantly.
Also, we agree that a switch from whole grains to refined flours and sugars is party at fault, with increased iron absorption as a by product of reduced anti-nutrietns. So sometimes you clearly want these “anti-nutrients”.
We also agree that we can’t just blame the carbs for obesity epidemic. I blame wealth (and increased food intake that correlates with it) and sedentary life style.
Thanks.
“I work in an organic bakery and we mill organic whole grains. Pretty simple, Google around. ”
Zach is correct. It is pretty simple. There is an organic bakery near me and every morning they throw whole organic grains into the hopper of their mill. They press a button and a short while later later they have freshly milled flour. The mill fits into a large closet.
There are organic bakers all over the country that mill their own flours. You can even find a few in your organic freezer section. Berlin Bakery and Alvarado Street Bakery are two brands that mill their own grains and are sold nationally. (Berlin Bakery only bakes with fresh-ground spelt and they claim it is well tolerated by many who usually have problems with grains). From experience, I can say the Berlin bread definitely doesn’t have an appetite-stimulating effect.. it’s kind of dull tasting, but my kid likes it. 🙂
At any rate, if there are local organic bakers and millers in your area, then I would favor those local options over national brands.
Well, Duck, Idk, I live in South Carolina and before that in FL and there weren’t and aren’t any organic bakeries around. I guess it’s my bad luck. On the other hand, I’m tempted much less : )
Frozen bread just doesn’t have the same apeal as freshly baked, but I’ll try it out .
WBryanH said: “Furthermore Duck cites a link straight out of Big Agra–rife with conflict of interest–to back up his claim.”
Laugh. The references show what the health benefits of grains are believed to be. It’s perfectly legitimate to reference actual cereal scientists for such an opinion on what the health benefits of grains are believed to be. I suppose you’d rather I cite an anti-grain authority. lol 🙂
The point being that grains can be a good source of some phytonutrients (not all), and these phytonutrients are believed to offer grains their health benefits. For instance, γ-oryzanol found in brown rice. Or the significant amount of phenolic compounds found in barley.
Duck, you write: “…It’s perfectly legitimate to reference actual cereal scientists for such an opinion on what the health benefits of grains are believed to be…”
Hmm. You cite opinions from cereal researchers, paid by the cereal industry to write about cereal. And then proceed to imply these are unbiased views.
Um, OK Duck. You’re certainly welcome to feel that way.
Anna said: “I eat lots of vegetables, so I’m sure my microbes will survive 🙂 or adapt to my diet.”
Sure, they’ll “survive,” but low carb vegetables tend to be mainly cellulose (unless you’re eating a good amount of inulin-rich dandelion greens every day). The problem with cellulose is that much of it is not fermented, since most humans lack cellulose-degrading bacteria. You just poop most of it out (good for bulking stool though).
What’s important to understand about fiber is not just consuming it, but also having flora that can ferment it. This is known as Microbiota Accessible Carbohydrates (MAC). Cellulose is not considered to be a MAC because of the lack of cellulose-degrading microbies in humans.
And even if you did have cellulose-degrading flora, cellulose doesn’t really ferment into beneficial SCFAs very well. But hey, as long as you’re aware of the research, do whatever makes you feel good!
Duck, I eat some inulin-rich and other digestible fiber veggies like onions, avocados, apples, cucumbers, carrots, mandarines, sauerkraut, tomatoes, etc. I eat them because I like them. I don’t eat a lot of it, but I eat lots of butter and olive oil, so I’m sure some of it makes to SCFA.
Anyway, my microbiome hasn’t complained so far 🙂
There is no consensus on how to feed or not feed our microbes by the way. We don’t know much at all about it. Many people have lots of problems with veggies. My theory is that a healthy micro-biome adjusts to what we eat. I seriously doubt that our human ancestors were eating lots of vegetable in winter and worried about it. And IF seems to be beneficial as well, while our microbes are totally starving.
Anyway, I don’t claim to know it all, but I feel fine with a small about of veggies.
Mandatory reading for anyone interested in understanding nutritional science and dieting. Looking forward to the next episode.
Very nice work! =)
Denise – This makes perfect intuitive sense. I’m a longtime low-carber myself but I’ve always thought is got to be the modern-day combination of both fat and sugar that is the real problem. Where, in nature is this found? I don’t know. Seems like only man-made food-like substances to me. In real life scenarios, it’s a lot easier to stay in the low carb realm rather than the low fat. Just my opinion,
“I’ve always thought is got to be the modern-day combination of both fat and sugar that is the real problem. Where, in nature is this found?”
JACKPOT!! 🙂
Corn. Follow the trail of corn, from PUFA to tortilla to fatty livestock to HFCS, and you’re on the trail that leads to obesity
Quite so – and let’s not forget the partial hydrogenates in corn oil …
Except not all corn causes obesity. The Pima indians ate nothing but corn and beans, and had no weight issues. Unless they live on the other side of the border and eat American corn. There is some argument about WHY one type of corn causes diabetes and the other does not, but it likely does have to do with how fast the starch breaks down and how the corn is processed.
I bought some “heritage corn” from a Mexican store and worked with it. It was sold in whole grains, which I ground. Even ground though, it works completely different from what you buy as “cornmeal” or “masa” in an American store.
Heathertwist- yes, modern corn has been bred to be far higher in sugar than traditional, native corn. Native Mexican and Indian corn was probably pretty healthy.
Where’s Part 2?
In other words, as far as diet is concerned, extreme is good. I hope that ends the business of pushing for a mushy middle between paleo and vegetarian.
I’m not sure that you can go there from the evidence. Another possibility is that if you wreck your metabolism, you can reset it with an extreme diet.
As a Diplomate of NLA in Lipidology and presently studying for the Obesity boards I swim through the morass of data, personal experience and what works.
All weight reducing diets are restrictive.
To find out if you have a healthy diet you need 3 tests: LDLp, CIMT, CAC
If you have no plaque and your LDLp is <1,000, I think your diet is good for you.
Most obese have Insulin resistance. I think they need LCHF.
Otherwise, eat what you like. God bless.
God I would love to see those test in an experiment of longterm LCHF and HCLF adherants.
Fantastic article, eye opening stuff. Although i think very low fat diets (under 15%) aren’t optimal from a nutrient point of view. I had a look on chronometer to see the lowest amount of fat i could eat and still get enough of everything using only real food. I ended up with 16% as an absolute minimum, although i managed to work it down to 9% using a few “food” supplements and replacements. For example, skim milk and cod liver oil. Can’t wait for the next article.
Also, i cant help but wonder if there is one more golden spot in the swamplands. Matching carb intake with physical activity. Which is pretty much the range 30-40% carbs. Which interestingly tends to be close to the amount modern hunter gatherers tend to eat. http://www.nrjournal.com/article/S0271-5317%2811%2900091-1/abstract “Hunter-gatherer diets were characterized by an identical carbohydrate intake (30%-35% of the total energy)”. They may eat up to 40% due to the glycogen present in fresh meat. Aside from the observation that many hunter gatherers were healthy not much can be drawn from this. I’m unaware of any studies that match carbohydrate intake with exercise. Although the perfect health diet uses similar guidelines and seems to have good results if the testimonials are anything to go by. I would love to see a study comparing low carb, very low fat and intensity matched carb diets.
I also found this, but i cant read past the extract. http://www.ncbi.nlm.nih.gov/pubmed/21679058 . Balanced caloric macronutrient composition downregulates immunological gene expression in human blood cells-adipose tissue diverges. However, i did find an article discussing the paper, here are some interesting quotes. https://www.ntnu.edu/news/feed-your-genes
“what if you could find out how our genes respond to the foods we eat, and what this does to the cellular processes that make us healthy – or not? That’s precisely what biologists at the Norwegian University of Science and Technology (NTNU) have done.
The answer researchers have come up with may surprise you: the best diet, from a gene’s standpoint, is one-third protein, one-third fat and one-third carbohydrates. That’s what the research shows is the best recipe to limit your risk of most lifestyle-related diseases.”
“We have found that a diet with 65 per cent carbohydrates, which often is what the average Norwegian eats in some meals, causes a number of classes of genes to work overtime,” says Berit Johansen, a professor of biology at NTNU. She supervises the project’s doctoral students and has conducted research on gene expression since the 1990s.
“This affects not only the genes that cause inflammation in the body, which was what we originally wanted to study, but also genes associated with development of cardiovascular disease, some cancers, dementia, and type 2 diabetes — all the major lifestyle-related diseases,” she says.
“Both low-carb and high-carb diets are wrong,” says Johansen. “But a low-carb diet is closer to the right diet. A healthy diet shouldn’t be made up of more than one-third carbohydrates (up to 40 per cent of calories) in each meal, otherwise we stimulate our genes to initiate the activity that creates inflammation in the body.”
“Genes that are involved in type 2 diabetes, cardiovascular disease, Alzheimer’s disease and some forms of cancer respond to diet, and are up-regulated, or activated, by a carbohydrate-rich diet,” says Johansen.
Johansen is not a cancer researcher, and is not claiming that it is possible to eliminate your risk of a cancer diagnosis by eating. But she thinks it is worth noting that the genes that we associate with disease risk can be influenced by diet.
“We’re not saying that you can prevent or delay the onset of Alzheimer’s if you eat right, but it seems sensible to reduce the carbohydrates in our diets,” she suggests.
“It was interesting to see the reduction in genetic activity, but we were really happy to see which genes were involved. One set of genes is linked to cardiovascular disease. They were down-regulated in response to a balanced diet, as opposed to a carbohydrate-rich diet,” she says. Another gene that was significantly differently expressed by the diets that were tested was one that is commonly called “the youth gene” in the international research literature.
Perhaps the negative gene changes above 40% carbs become neutral or positive again once fat is lowered enough. Also i am unsure exactly how many diets were tested, i think only two. More diet variations would be interesting.
Great comments! I think the biggest value of the macronutrient extremes (very low fat or very low carb) is for a therapeutic effect once a disease has already initiated; I wonder if some sweet spots in the Swampland can work towards disease prevention via other mechanisms like gene regulation (assuming food quality and lifestyle factors are dialed in). Very interesting…
As for the difficulty in obtaining enough nutrition on very low-fat, I’ll be covering that in the next post — but in the meantime, you might be interested in Angelo Coppola’s “Plant Paleo” diet, which is quite nutritionally sound and very similar to what I’d propose as a low-fat + ancestral combo (vegetables, tubers, legumes, root veggies, fruit, gelatin/cartilage, oysters/other shellfish, weekly organ meats (liver is only 25% fat and fills in many nutritional gaps, especially fat-soluble vitamins), other lean meats and seafood):
http://www.humansarenotbroken.com/about/plant-paleo/
BTW, I think 10 – 15% fat still works fine for that therapeutic effect except for extreme cases of heart disease, diabetes, etc., in which case the stricter level may be needed initially. As someone metabolically healthy, my own diet averages 15 – 20% fat, and I find that to work quite well for me.
neisy,
In the case of Esselstyn’s patients, they continued the VLF diet (no oils, 10% or less fat) even after their heart disease was reversed or improved. It became a lifestyle change. Kempner’s Rice Diet was another story. Much too restrictive for a permanent change but from what I read from your research and from other sources, Kempner’s patient’s problems didn’t appear to resurface.
Where would you say obesity falls on that spectrum? Does it require the same drastic measures such as the rice diet?
I wish there were more focused follow-ups for the studies. If LCHF and HCLF both produce results for the duration of the studies, how would you maintain the results? I’ve come to the conclusion that restriction through diet in my teens has only impaired my health and metabolism. I don’t know how to reconcile this new conclusion with what I feel needs to be done in order to regain my health and weight.
Maybe the real secret is choosing between the two camps, the one that you can live on forever?…
Yes how many times have I wondered what am I supposed to eat. When you have weight issues or health issues I think choosing either extreme as a fine way to go, but that is not necessarily forever, you can always switch to the other extreme as your body and health changes. If you cannot tolerate one extreme for whatever reason try the other one, neither will hurt you in the short term. I personnaly have just done this and my body tells me Yes this is good. And when we are where we need to be – we can relax our dietary guidelines somewhat if we choose too. Listen to your body and how it responds to the changes you make that is the best way to know.
Thanks for the words of encouragement. Did you mean you just did LF and felt better? I’ve done HF for so long that this is terrifying and counter-intuitive, but I’m hopeful. At least I’m letting go of the dogma that one way is healthier.
Do you think a maintenance diet would be somewhere in the middle between the two?
Out of curiosity, what did/ does your diet looks like?
Once upon a time I weighed 205 pounds, I got down to 186 pounds doing low carb high fat and for 13 years no diet worked anymore and I sort of gave up. Then a friend lost a lot of weight doing low carb high fat and I tried again, I had made some other improvements in my health in the meantime and then my body once again responded to LCHF. It was tough going but I got down to 135 pounds over about 5 years time. But I really don´t like all the animal foods all that much except for cheese. I also have type II diabetes and I did not believe I could eat a low fat high carb diet. But I no longer tolerate all that fat in my diet, no gall bladder and getting older ya know. So one day I just started eating tons of fruit, I love fruit, and wonder of wonders with the same medications I took to manage my blood sugar on LCHF my blood sugar stayed the same with the high carb low fat. It is all in the composition of the foods we are putting together in our meals. This is a very recent change for me, and I did not make the change due to anything I had read, I just paid attention to how my body responded and I lost a few more pounds. So what do I eat know, I am not obsessive compulsive about it. I usually eat 3-4 pieces of fruit, whatever I feel like for 2 meals a day, and sometimes all 3 meals. But I do eat vegetables, Ezekial bread and eggs, beef etc… usually once a day, but only if I feel like it. Sometimes I think my body tells me I need some animal protein because I will get a craving to eat some eggs or meat. So then I do. Go figure I never thought in a million years I would get a craving for eggs. What I absolutely believe is that high fat and high carbs is a recipe for disaster for most people, except for the few who are genetically blessed and eat whatever they feel like without any health or weight problems. Most of us fall on one side or the other we do better closer to one extreme or the other. If you thing about all the things we have all been reading, not just this article, somewhere in the middle could be okay if you are a normal weight and have no health problems. If you are worried about being on a high fat diet for so long, try a very low fat diet and see how you respond. But the science clearly shows, at least to my mind, that high carb and high fat are the culprits for many health problems.
HF + HC is the bane of our existence! Probably because it’s so darn tasty. This combination is not found in nature so there’s no danger on overdosing on these when sticking to an ancestral inspired diet like Mark’s or Denise’s.
Wow, your experience sounds just like mine… Only I was always normal weight and grew up either starving (being poor and neglected as a child) or consciously dieting. So, even though I’m supposedly “genetically blessed” I no longer respond to diet and have incurred A LOT of chronic symptoms and obesity at my fairly young age (27). So I’m kind of stuck eating really low-calorie with absolutely no results and a lot of frustration. I idealise Paleo because it worked for me a few years ago and it made me really healthy and happy for a brief time. Of course I wanted bigger, better, faster so I introduced IFing and LC and removed all fruit, got kidney stones and my perfect-health bubble shattered and sent me to a tailspin of binging and depression.
Oops, I’m telling you my life story on a public forum… Sorry about that! Thanks for sharing your experience, it’s at least encouraging. Right now I eat the way you described but it produces no weight-loss for me so I might have to extreme-ise my already extreme diet (by my young peers’ standards. Darn it!)
“this combination is not found in Nature”. I suppose it’s how you define HF/HC, but if a food has both, somewhere in the 50-50 range for each ought to be considered high in both categories, no? Try good old human breast milk. While it can vary over the production cycle as the infant’s age increases, it’s about 52% fat, 42% carbs. For comparison, a cake doughnut is 51% fat, 44% carbs. Coincidence? You decide. Maybe we are genetically programmed to go for this combo.
Check out this video there might be an answer –
This is a great video – explains very simply why some of us our fat – very intersting.
How to Lose Weight Without Losing Your Mind
In nature, the people living on breast milk are supposed to be gaining weight.
And your point is? One commenter stated that the combo does not occur in Nature, not that one could lose or gain weight from it. It does exist in nature, and there is no evidence that our Paleo ancestors (who were probably doing their best to avoid starvation) didn’t eat this combination of nutrients. It seems everyone in the US judges any diet or food by whether it will help them lose weight. Maybe if they didn’t eat junk and sit watching TV 6 hours a day, they could assess foods for their other qualities. And probably enjoy life more.
It’s worth looking at the Asian diets. The traditional Japanese diet, for instance, is quite low fat but a whole lot of Japanese ate that way and were quite healthy. The Japanese mountain people still do, and they do fine on it (lots of active old folks!). Personally it suits me quite well … very good for losing weight and maintaining weight loss, and it doesn’t end up looking too different from neisy’s version of low fat. I think when you concentrate on a “cuisine” you forget about the fat content. The Asian cuisines tend to have more flavor, with a little bit of flavored oil (like sesame oil). I feel about 20 years younger when I eat that way.
However you also get into other issue relating to the source of the macronutrients. I’m beginning to think that to make really tall and muscular humans, you need milk and maybe beef. There is something in dairy that triggers the “grow BIG” gene, and the kids who don’t get dairy when they are growing end up being shorter (albeit as or even more healthy?).
@heathertwist I’ll repaste Ancel Keys’ acerb quote from later on in this thread:
“The team player’s diet is apt to be built on the same philosophy as the old Chinese idea – if you want to be big and strong you eat the muscles of big and strong animals – plus the notions of nutritionists who believe that whatever grows baby rat meat faster is better. So they are stuffed on the biggest (and most expensive, therefore fattest) steaks to be found, they guzzle gallons of milk, and nowadays may be plied with vitamin pills as well.”
He made this comment about feeding the Minnesota Golden Gophers football team early in the 1940’s…and he continues on to how this heavy eating leads to CVD and obesity when they got older and quit working out.
But, yes, it makes those young rats (and humans) grow fast….and it was the basis for the famous paratrooper rations….
Japanese mountain people! This reminds me of children’s stories we used to read to our kids about wise old people, talking badgers and pine forests. There is a nostalgia for that in Japan, transporting people out of their real world of urban stress and soy sauce into their imagined past. All that exercise and fresh air combined with a spartan diet! Autophagy at work producing happy centenarians! Hai!
Yeah, there is a certain amount of mythology about old folks. This town is pretty well studied though.
http://www.livestrong.com/article/312974-yuzurihara-diet/
One of the interesting things is that their skin remains supple and young looking, as do their joints. This is believed to have to do with hyaluronic acid, which is in their favorite yams. So there is more to the topic than just fats!
I’d also comment that these diets have little or no wheat or milk, which are both confounders of a sort because they have a different set of health issues.
Here is another Japanese centenarian. He died recently at 116. His diet was:
According to local media, Kimura ate a three-meal-a-day diet of rice, pumpkins and sweet potatoes.
http://worldnews.nbcnews.com/_news/2013/06/12/18914235-oldest-man-in-recorded-history-dies-at-116-in-japan?lite
So today I started an experiment with eating a yam-based diet. Today I ate 3 purple sweet potatoes, and two bowls of gelatin broth, some konjac root, and a bit of catfish. That diet is close to zero fat.
The thing I noticed today is that I had zero hunger. I stopped at one small (5 oz) sweet potato because I simply couldn’t hold any more. The gelatin may have had something to do with that too, I dunno. But I was running errands and felt no need to stop for a latte or energy bar or anything else. So the question is: if you eat pumpkins and sweet potatoes, does your body synthesize the fats you need? Or would the fats come from “extras” in the Japanese diet, like miso, sesame oil, fish fat? Kimura seems to be in rather good shape for 116.
All plant foods have small amounts of fat. It’s impossible to eat a whole food diet and not get enough of “essential” fat. Everything else can be synthesized.
So my question is: why do SOME people on super-LF diets get dry skin (me, in the past) while some do not? My diet at the time was also whole foods, but a different set of foods, and after a year on that diet I had lost weight but my skin looked 30 years older.
Dehydration comes to mind.
Really there is not much in the way of evidence to suggest omegas have anything to do with skin moisture.
This article concerns our microbiome to our skin, and the problems of dry skin.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279608/
I expect you are right, and that’s more or less what the articles say too. The HA keeps the skin moist and the joints in good shape … without any mention of oils. The yams don’t actually have much HA though, and the mountain people don’t eat meats, which are the usual source of HA.
Also people that for whatever reason don’t get the right fats get eczema, and so do rats. So maybe there is something about the yams, or the miso they eat, that causes people to produce more HA and also to have the right fatty acids.
I looked up satoimo and it’s just taro. The foods these people ate were cheap subsistence. Yams and pumpkins are the exotics, and weren’t common in Japan until 100 years ago. Cheap, easy to grow, nutritious and not overly calorie dense as grown.
We forget that fat and protein were very expensive 100 years ago. When people had no choice but to eat a 90% carb diet, they probably were in a semi-autophagic condition all the time, and on the edge of beriberi. I’m not surprised that your yam diet depressed your appetite. That’s what it should do.
Japanese that live near the ocean traditionally ate a lot of fish, and the fish they eat … like mackerel … is rather oily. Also sea mammals do wash up regularly and they are extremely high in fat. Water birds are also pretty high in fat. So it doesn’t surprise me that they were healthy.
The mountain people don’t live near the ocean, and they grow their own food mostly. Which would make fat very hard to get. Also a diet based on yams doesn’t strike me as balanced? Somehow it seems to work though. There are a couple of other yams that are more “native” to Asia, d. alata and d. opposita. Nice rundown of yams here:
http://www.marksdailyapple.com/difference-yams-sweet-potatoes/#axzz3r7WzOYOH
The “sweet fish” the mountain people eat is maybe Ayu, which is related to salmon, so probably has a fair bit of fat?
http://www.kanoyama.com/fish-facts/
Also if it swims up from the ocean it would provide enough iodine, which is an issue for inland communities.
I used to travel to Japan for business, and ate a lot of salaryman food. Korean barbecue, big bowls of udon, okonomiyaki (a cook it yourself seafood omelet), lots of yakitori sticks, and lots of Kirin beer (sometimes the only liquid on the table). Never a lack of food, but nothing really greasy or fatty. Occasionally our hosts would take us to somewhere expensive, and that’s where the fatty beef appeared, for shabu shabu. Another time it was Chinese, and the centerpiece was a big carp.
I linked this in an earlier section. I’ve always liked it because it contrasts the Japanese and American diet in a unique way.
http://www.theatlantic.com/past/issues/86nov/fallows.htm
I read the Atlantic article and I enjoyed it. He is spot-on … the “exercise” issue I think is mostly a red herring. Or maybe it matters only in the swamp. I live near a lot of farmers, and you really can’t be a farmer without exercising, even if you use a tractor mostly (just CLIMBING on the tractor is work!). But many of the farmers are just huge and very obese, or have major issues with arthritis or whatever. Others are really healthy: they are thin and limber, even in old age. For fun I started asking them about what they eat.
The thin and limber farmers tend to be the chicken farmers, who mainly eat a whole lot of eggs, or the ones who eat a lot of vegetables (many are basically vegetarians or vegans). The less-healthy ones tend to be the beef farmers. But in any case, the “exercise” issue isn’t the main one.
As for being hungry on the “Japanese diet” … the portions really are smaller. But I also wonder if the Americans avoid some of the more nutritious choices. For instance, mackerel is rather high in fat and often served for breakfast. Lunch often includes raw egg yolks. If you have mackerel or a raw egg yolk, it is quite filling! But most Americans would probably avoid both.
Plus of course if you “grew up American” you are just plain BIGGER and so require more calories.
However, my own experience has been that since I’ve switched to a more “Asian” (my version of it) diet, I just eat a whole lot less food. It’s more filling somehow. I do eat all the weirder stuff … the egg yolks and baby whole fish, kimchi, miso, mackerel for breakfast, and now, lots of yams! Since reading this article I’ve doubled down on the low-fat part and am actively avoiding our normal OTHER food (like Indian curry or fried tacos …). Also I am older. My daughter is still growing, and my meals just don’t fill her up at all.
A couple other food anecdotes from Japan. Breakfast often had pieces of dry smoked salmon with white rice. A few times the rice came with a raw egg. The rice is supposed to be hot enough to cook the egg, but usually it ended up raw egg rice glop, which wasn’t too bad. Natto would also show up for breakfast. Snacks on the train – mandarin oranges and smoked chestnuts. The Japanese version of teppanyaki (like Benihana and other US Japanese steakhouse – eating on the grill) was a lot more subtle (no flaming onion ring towers) and used a lot of things you don’t see in the US, like thin sliced grilled winter squash. Finally, snacks at a baseball game: marinated squid or octopus rings. Tasty, but like chewing rubber bands.
Nom! I do love dried squid snacks too. Might be when you get introduced to them. I got them as a kid, and gave them to my kids. They love them. Also some of the other weirder foods. But they can’t stomach McDonalds or most of the other fast food … it tastes “weird” to them.
My only problem with the 15 year Esselstyn study was that ALL of the participants were on statins. In fact Esselstyn said that stains + diet works better than diet alone
There’s a protocol that tries to use carbs based on the amount of resistance excercise: Carb Bacloading by John Kiefer.
Equal macronutrient intake is like the early version of Jonathan Bailor’s diet (Smart Science of Slim), usually used to getting thin. But it doesn’t convert to the same macronutrient at the cellular level where the genes are expressed:
1) If you are getting thin it means you are burning your fat stores – the diet a the cellular level is higher in fat.
2) Fiber and other fermentables can give like 6% of calories for the cells in the form of short chain fatty acids.
Same with very low fat diets – they may be the only human state with a high level of creating fats from carbs by your own cells (that is other than bacterial fermentation). In a “balanced” diets most stored fats comes from the dietary fat.
Some low skin quality is visible in some high-carb vegans. No as bad as drunkard faces, but below normal people of similar age. McDougall himself has bad skin for his age, Durianrider also. But it doesn’t seem to affect Esselstyn, at least as per what’s expected for his age. Perhaps the reason is the first two promote fast-burning starches / fructose respectively, while the latter eats a lot of anti-inflammatory greens and vegetables?
Durian Rider – hmmm
http://anthonycolpo.com/durianrider-66-kilograms-of-obnoxious-unabashed-ignorance/
Interesting link. Interesting also to see there are folks that share my view that some of the more virulent vegan jihadism may have a biochemical basis. Whenever I have broached that subject, the vegan jihadists go into fatwah mode. It would be interesting if someone did a study to examine that possibility. I’ve never encountered any other dietary regime whose followers, at least many of them, display such arrogance and anger. Some that claim they wouldn’t swat a fly also claim that they would gleefully watch an omnivore’s painful death agonies.
Very strange!
Yes, they are. But dietary deficiencies would go far to explain their strangeness, and their rudeness. I’d hate to think that it’s just that only mean-tempered folk become vegan.
Hunger causes high cortisol levels … my family is mostly pretty mellow but when they get hungry, watch out! I’ve gotten in the habit of just making sure they get some food when they get grouchy. The term “fat and happy” has some basis in fact. It might not be so socially acceptable, but fat absorbs toxins in the body too.
But many of the vegans and raw foodists I’ve seen are overly thin IMO, with very little muscle mass. A couple told me they had to change their eating, because they simply couldn’t eat enough calories on their food choices. So I expect that even if they are used to the hunger level, it might in fact be making them grouchy.
Note though that the Japanese mountain people are noted for also being *happy*. They don’t look overly thin either. They aren’t vegans though … they eat a kind of oily fish, though not very much.
Anthony Colpo thinks that refined grain is healthier than whole grain and that dietary cholesterol has no effect body cholesterol. Hmmm. He’d also get smoked by Durian Rider on a bike and Colpo is an avid rider.
Somehow I doubt that
Yagh you guys are nuts. I just finished wood smoking a bunch of ribs and sausage for the winter. Both those guys would smoke me on their bikes but then a 50 lb Schwinn tops out at about 12 mph. No matter what you do.
The best use for bananas is bananas foster.
Here’s a list of alleged good uses for bananas (you can ignore the banana-sicle one)
– Make a face mask
– Tenderize a roast
– Polish silverware and leather shoes
– Brighten up houseplants
– Deter aphids
– Use as fertilizer or mulch
– Add to compost pile
– Attract butterflies and birds
http://www.rd.com/home/banana-uses/
Somehow I doubt you know much.
“Body” cholesterol? I assume you mean serum cholesterol. And, no, unless you have a metabolic disorder, dietary cholesterol doesn’t have an effect on serum cholesterol. Mainstream medicine finally acknowledged this, and it was big news a few months back. It’s even acknowledged by the USDA food mavens, who took it into account in working on their updates to the food “pyramid”, “plate”, “rhombohedron”, or whatever they are going to call it this time.
Zach, never heard of “body cholesterol.” But if you mean “serum cholesterol” there’s no connection between diet and serum cholesterol. The liver both makes cholesterol and breaks it down too depending on the body’s perceived needs for c’stol at that time. Diet has little to nothing to do with it. E.g. I had a vegan godparent who STILL had high c’stol, even though there’s zero c’stol in plant-sourced foods. The FDA is moving toward dropping the dietary c’stol limit, finally getting rid of that idiocy thank God.
Even Ancel Keys knew that dietary cholesterol had no affect on serum cholesterol, because he did the experiments to prove it. It was for this reason that he developed the theory that dietary fat raises cholesterol. (Some of the mainstream government officials who make dietary recommendations got that part wrong, because, you know, they’re not doctors or nutritionists). In any case, it’s been known for a very long time.
Carbohydrates raise triglycerides, so that might have been what Anthony Colpo was talking about when he made that statement about cholesterol.
Guys, “durian rider” is a nobody and a fool. How he ever came to be talked about is beyond me. I advocate 100% fruit diet and imo that guy and everyone associated with him is a joke and are toxic to the perception of the fruit diet. He’s not a serious person, he’s a clown.
Ancel Keys spent a lot of time figuring out how to be healthy in the middle of Swampland (30% fat). His Scientific Diet prescription for weight loss is calorie counting, of both food AND activity (big tables of that), to create large daily calorie deficits. I’ve used that methodology for 8 years to lose 50 lbs and sustain the loss, though I didn’t attribute the method to Keys. I do this living squarely in the middle of Swampland. For lack of a better term, it’s a high carb, high fat diet, with adequate protein.
When I tell people how it works, they are shocked at how much exercise it takes to sustain the weight loss. I walk and bike enough each day to eat 2300-2500 calories and maintain weight. It takes at least 3 hours every day, but it’s broken up through the day. If I ate 1500 I could do this sedentary. But my stomach is a sized for 2500 calories…and my thighs are sized for 1000 calories…my paleolithic ancestors left me with a body optimized for both…
Denise, once again you’ve done truly amazing work and I couldn’t be prouder of you. I wanted to bring up an interesting topic of gut microbiome and what kind of microbes are found in the guts of people on high fat vs high carb diets. It wasn’t until I cut out processed foods, sugars and added more fat and protein into my diet before I saw the result of not getting colds every week (and these weren’t allergies). Remember what I went through for years? Now, being on relatively higher fat with carbs consisting only of fruits and vegetables (no grains), I only get colds maybe twice/3x/year. Your research brings up many good questions and some mighty interesting theories. Great job!!!!
You should have NO CONCERN about your blog being too long. People truly interested in this topic will eagerly devour it … no matter the length. Those less curious can easily skim, scan, skip … and still leave with an incredible amount of useful information.
Thank you very much for your too long to print but too fascinating not to read blogs.
After reading many interesting replies and questions about what does this mean going forward, I see two possible directions. One is we are only safe in the dietary extremes, or quality matters in the middle. The fringes work because they help regulate energy and calorie intake by lowering palatability and creating a primary energy path way, either fatty acids or glucose. Epigenetics shift that optimize usage and feedback as best as possible on that diet regime. The middle ground is mushy because the dual energy pathways can get out of sync. Eating crappy food is gasoline and very dangerous in the middle. The extreme diets ironically allow the toleration of more crappy food. Does that make them better? Maybe not, but just simpler. If the quality is high in the middle, with perhaps some intermittent fasting, you can have both carbs and fat…Ala the French Paradox.
Interesting take, Joe! I tend to agree — my interpretation is that the extremes are best for reversing existing disease (AKA they’re “therapeutic”), but they aren’t necessary for maintaining health in someone who’s already in good shape and has their food quality and lifestyle dialed in.
Mwah and many hugs to you for a yoeman’s job of extracting these compelling findings from forgotten but significant studies and doing it with welcome humor. We love you for doing it!
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From:”Raw Food SOS” Date:Tue, Oct 6, 2015 at 10:21 AM Subject:[New post] In Defense of Low Fat: A Call for Some Evolution of Thought (Part 1)
neisy posted: “Not a typo. Not April Fool’s Day. Not a spontaneous and mystical possession by the spirit of George McGovern. Not even a social experiment to see how many people I can get to unsubscribe from this blog in the span of a day (PLEASE STAY, I LOVE YO”
Fantastic article Denise. The voice of sanity as usual.
I love your honesty!
Great post! I remember watching your AHS talk some time ago in which you speculated on the presence of a metabolic capability to live on a very high carbohydrate low fat as a survival mechanism similar to ketosis, and am glad to see the followup on that. It makes sense for such a mechanism to exist, as starchy tubers are basically the only plant foods readily available in amounts that are capable of supplying one’s daily energy needs.
I look forward to reading your personal views on ‘carbosis’ in part 2 – it seems to me to be like ketosis in that it likely confers specific therapeutic benefits but are probably not a favorable permanent metabolic state.
Personally, I’d think that unless you lived off of chicken breast and egg whites it would be really quite difficult to intake sufficient protein on such an extremely low fat diet.
There are many examples of people experiencing metabolic damage from both too high fat and too high carb. So it’s not all magic at both ends of the spectrum.
The raw foods/fruitarian 801010 diet for example has some horror stories, and the high fat paleo diet seems to see longer term issues also.
The diet being discussed here however is the Kempner/Pritikin/Onish/McDougall/Esselstyn/Barnard diet. This diet would appear sound and supported in terms of its therapeutic benefits.
What do you think are the longer term issues with high fat paleo? I haven’t encountered any in 7 years of the diet, but perhaps that isn’t long enough?
CVD issues, with Atkins himself as the prime example. He was lean and healthy on HFLC in the 1970’s, but by the 1990’s looked jowly and overweight. In the 2000’s he started to exhibit serious CVD problems.
I think that Cordain’s original take on Paleo as a lean meat low carb diet is probably better as a longevity diet. But I don’t know of any examples.
Actually, there is considerable reason to doubt that Atkins had CVD. Atkins got a viral infection, leading to chronic cardiomyopathy, which he freely discussed during his lifetime, including on national television. At the time of his admittance to hospital, he weighed 195lb, not excessive for a muscular man of his height – over 6″. He played tennis weekly. The 258lb commonly cited for his weight was what he weighed when oedema set in as his organs failed. http://usatoday30.usatoday.com/news/health/2004-02-10-atkins-statements_x.htm
As to the jowls, he was 72 years old! This very unflattering photo of him doesn’t indicate that he was overweight, merely that he was showing his age. http://www.cbsnews.com/news/diet-guru-atkins-dead-at-72/.
Hey Andrew,
“it seems to me to be like ketosis in that it likely confers specific therapeutic benefits but are probably not a favorable permanent metabolic state.”
Yes! That’s my interpretation as well.
RE: obtaining protein, it’s actually not too hard if you include gelatin, shellfish, and very lean meats/seafood, and perhaps also legumes. All whole plant foods have some protein, so even nothing but starches, veggies, and fruit will typically wind up yielding 10 – 15% protein (more if you’re heavy on lentils).
Wow, just wow. Thank you for your amazing research and analysis! You are awesome!
Well-timed, Denise. Transitioning from a diet of Primal-inspired magic, I’ve been having a horrible horrible (and I don’t encourage literary redundancy, mind you) time with a Peatish, HCLF eating. It’s been nearly 6 months and except for exacerbating my insomnia, acne and weight nothing has improved.
I even got myself onto the 23andme bandwagon to try and understand my (presumably) shoddy genetic lot in life. The results: supposedly I’m one of the lucky few who respond to any diet and any exercise (my once thin but now obese body was unimpressed, to say the least). Apparently I also have no food sensitivities despite my lifelong suspicions that I do and the inherent tendency to restrict food groups and macro-nutrients (oops…).
To Denise:
Do you think there’s an ancestral/ genetic/ (what-have-you) inclination to do better on one approach over the other?
I also wonder if the perfect median between the two would be a weekly cycle
(a few days of 10-15% F and others of 65% F) or would that just make your body hopelessly confused? (Without MS or Diabetes, obviously.) I find the body does better on consistent (bland) foods.
Hey Lee,
Thanks for sharing your experience! Out of curiosity, does your Peat-inspired diet include a lot of dairy? That seems to be a big issue for some people, especially with acne and weight gain. Along with your 23andme data, you might be interested in getting your gut microbiome analyzed at some point — that seems to be a missing link explaining food sensitivities and variation in response to different diets.
“Do you think there’s an ancestral/ genetic/ (what-have-you) inclination to do better on one approach over the other?”
Quite possibly, but I no longer believe it’s ‘fixed’ in terms of “I have x genetics and therefore my optimal diet is high/low fat”, so much as environmental and lifestyle factors triggering different gene expressions and altering a person’s response to diet in ways that change throughout life.
I actually do believe a cycling between the extremes could work well. I’m writing about that in Part 2! 🙂
Thanks for getting back to me! 😍
I think a Peat diet without dairy is like a Paleo diet without bacon. It could work in theory, it just wouldn’t have the same appeal. 😄 So yeah, dairy is a mainstay of my current diet and I have several SNPs that indicate lactose tolerance into adulthood (though I can’t get high quality dairy and might be better off without it).
I have a nagging fear that my cortisol levels are exacerbated by my sugar intake (from fruit and juice) and thus cause my chronic insomnia, but you and Peat have made me reconsider this phobia. I could just be squared right in the macronutrient swampland and need to revisit my diet.
Circumstances facilitate the reception of new information, and whereas before I would’ve turned my nose and kept to my Paleo-dogma, now I value anything that makes me revisit it. (You can say my self-imposed suffering is an anti-dogma crusade!) So thank you for what you do! 💕
I can’t wait for part 2 and (selfishly) encourage more posts (or an awaited second book!) on making sense of one’s genetics and addressing them with lifestyle. Yeah I’ve read around on this thorny subject, I just don’t think anyone but you can do it justice. 🐰✌
Is there some reason that you switched something “magic” for something “horrible horrible”?
For people who may not be familiar with Peat, here are some of his quotes advocating low fat and/or skim milk: https://goo.gl/zinfaa
I think many people consume too much milk fat, and confuse Peat with the whole milk Weston Price stuff.
I also think many peoples definition of HCLF isn’t really LF.
Finally, something that might explain Freelee’s ability to eat insane amounts of fruit and juice and carbs while staying so enviabily thin! (And my not so enviable results on high fat low carb diets.)
Finally something that might explain the banana’s girls impressive results and ability to maintain such a lean phyisique. I’d searched everywhere for something that could explain this, this post is “everything”, as the kids say these days.
Oddly enough, the original Rice Diet only permitted one banana per day. Was it the potassium? It obviously wasn’t because of the sugar if 100-500g of table sugar was allowed!
Yes because the diet focused on reversing kidney issues and potassium can be problematic.
people, just wanted to say: please, don’t take dietary advice from this writer. i’m not questioning her intentions or her knowledge, but she has no legitimate training or experience in research or clinical work. as you can well see, this post is representative of her transition in terms of knowledge; in her self-education of food and nutrition, she’s making progress and has evolved, in her own terms. she may well continue to evolve until she’s on the same page as those who do have the training, research and clinical experience.
again, not knocking her intentions or her intelligence (although she–like any writer–is in dire, dire, *dire* need of an editor), but she’s no more qualified than any commenter here. whatever side of the so-called “debate” of HC vs. HF you find yourself on, please focus on the peer-reviewed books by trained professionals that has gone through some kind of editorial process.
Yes, let’s all get on statins and PPIs immediately.
I saw no dietary advice here. I saw a very thorough examination of data that says maybe, just maybe, low-carb is not the be-all end-all to dieting.
And why, pray tell me, should one listen to Jonathon Smith. Is he qualified to make such statements?
I wonder, Johnathan, have you read Denise’s blog before or just stumbled across this post? It’s just that she is the least likely blogger to imprart any nutritional advice. I’ve always found her posts enlightening and refreshing becuase even though she’s been taken under the wing of Paleo gurus like Mark Sisson, she was never apologetic about her near-Vegan, low-fat diet. I think the real purpose of her blog is to be a breath of fresh air in a blogosphere of nutritional dogma, and if you notice, those who comment on here come from a variety of dietary walks of life. Don’t worry about us being duped one way or another, we have functioning brains. We just like to read and look at pretty graphs! 😄
She has in no way given advice on what to eat in this article. She is just reviewing some old literature and doing a good job too. As a person with a science background she does a good job dealing with the issues in scientific research. Who cares if she doesn´t have a PhD, or MD behind her name. I have recently made a fairly radical dietary change from LCHF to almost frutarian and have been puzzled over how well my body likes this and that I have even lost a little more weight. She has given me some answers to that, or one of the links that came up in the comments. This is all fascinating stuff, read enjoy, it is a brain puzzle.
I think you need to read all of this again, Denise isn’t offering any dietary advice in there. What she is doing is taking reams of research and presenting it in an accessible format and delving into both sides of the issue. I’m actually not sure what your objection to her is, because it’s not as though she’s trying to present a poorly constructed study that she did herself. On the contrary, she’s taking that ‘peer-reviewed’ research that you’re lauding and explaining it, and referencing the research so that all of us can go and read it ourselves. Most people here have probably learned far more from her than they ever would from the actual studies themselves, due to the way they’re constructed and the original audience they’re intended for.
Jonathon, you miss the point, Denise Minger doesn’t give dietary advice. She does a fantastic job leading us to examine our raging dietary dogmas. I’ve followed a low-carb diet since 2007, it normalized my blood sugars and other blood panel numbers, and have no intention to return to HCLF. Still I find what she writes immensely valuable and informative. Btw Jonathon, if I’d followed the advice of those with “legitimate training and experience in research or clinical work”–including my dear old doc– I’d now be popping oral meds and injecting insulin now instead of controlling it through lifestyle.
-1
Jonathan, you fail to realize two things:
1. Scientific research on nutrition is extremely lacking and not fully understood. Like Sam Harris said:
“I have this feeling that we don’t understand human health and nutrition enough, the fact that there’s any controversy at all about what human beings should eat so as to be healthy, I find to be an incredible scientific embarrassment, the fact that you have debates about carbs and protein and fat consummated by good faith by experts and there is still some uncertainty, is an amazing state of our current situation in science.” – SH
Sam sounds like Ray Peat there:
“Nutrition is one of the most important sciences, and should certainly be as prestigious and well financed as astrophysics and nuclear physics, but while people say “it doesn’t take a brain surgeon to figure that out,” no one says “it doesn’t take a nutritionist to understand that.” Partly, that’s because medicine treated scientific nutrition as an illegitimate step-child, and refused throughout the 20th century to recognize that it is a central part of scientific health care.” – RP
A couple other good Peat quotes, notice the word “hardly:”
“Nutritional research has hardly begun to investigate the optimal ratios of minerals, fats, amino acids, and other things in foods, and how they interact with the natural toxicants, anti-nutrients, and hormone disrupters in many organisms used for food.” – RP
“For fifty years, the mass media have been making the public think about the fats in their diet, filling the culture with clichés about bad saturated animal fats that raise cholesterol, or lately the trans-fats in margarine, and images of arteries clogged by bad fats. The public instruction about the fats we should eat resembles the owner’s manual for a car, that tells you what kind of motor oil and fuel and coolant to use; they are telling us that they know how our body works, and that they know what it needs. But now, even after the human genome has supposedly been partly “decoded,” the biological functions of the fats have hardly begun to be investigated.” – RP
“The amino acids in proteins have been defined as “essential” on the basis of their contribution to growth, ignoring their role in producing long life, good brain development, and good health. The amino acid and protein requirements during aging have hardly been studied, except in rats, whose short life-span makes such studies fairly easy. The few studies that have been done indicate that the requirements for tryptophan and cysteine become very low in adulthood.” – RP
And 2. I don’t need Denise to be a clinical researcher to understand and interpret the studies that she posted that show high starch/carb cultures living very healthfully.
Jonathan said:
“please focus on the peer-reviewed books by trained professionals that has gone through some kind of editorial process.”
Books?
Denise has posted many studies here. I’m not sure why you’re ignoring that. I think it’s clear that you’re angry with something that is not only pro “carb” but pro-the devil sucrose. While you do this you also ignore a key point that Denise wrote above:
“I do want to make one thing abundantly clear before we continue, though. The title “In Defense of Low Fat” doesn’t imply its inverse, “In Attack of High Fat.” Quite the opposite! My goal here is to create a space where two very different dietary approaches can sit down for tea, respectfully coexist, and interact without any subsequent homicide investigations. In fact, I’ll be arguing for a more panoramic view of nutrition where the success of both high-fat and low-fat diets are compatible, and maybe even make sense. It just requires zooming out farther than we’re used to looking, and acknowledging that our ever-rivaling communities could actually learn a lot from each other.” – DM
All you’re doing Jonathan is subtle ad hominem on Denise and you’re not actually refuting anything in her post.
Thanks, Jonathan. Instead I’ll take advice from you. Apparently you never learned to capitalize words properly and write rambling, run-on sentences. Yet you critique Denise’s writing? I’m impressed.
Jonathan Smith: I think Denise is quite welcoming of peer review. A work doesn’t have to be published in a book or journal anymore in order to take part in scientific discourse. You’re free to refute anything that doesn’t sit right to you, but discrediting her entirely due to her lack of “legitimate” (whatever that means) training or research, isn’t helpful or interesting.
jonathan smith, you deserve a seizure for that post.
Thankyou for this. Rather than making people run away, this sort of article will attract the really interested, and I have now subscribed. I have tried vegan, then low-carb paleo, and have recently joined the Peat-clan. I always ran into a roadblock trying to understand why juice-fasting worked (Did this years ago), when it is a very high fructose diet which should instantly kill you according to Paleo-peeps.
If you write, I will read. Thanks. As omnivores, we will make choices. Informed ones are preferable.
Excellent post.
I’d just throw my twopence worth into the mix here.
Many years ago I tried a Pritikin style diet and ended up with problems. Looking back that might have been because I just wasn’t getting enough calories, especially as i was an athlete at the time.
That’s why next time I looked for a diet, I rejected low-fat and went low-carb/paleo. Eventually I ended up with all the symptoms referred to by people like Matt Stone – insomnia, frequent urination, cold extremities. So eventually I had to ditch that as well.
Now, I sort of riff off Peat. Broth, liver, some shellfish, dairy. Lot’s of dairy. I find I do pretty well on it. Some people say they break out with dairy, not me. I break out on PUFAs. I also eat sourdough bread and beef. This diet seems to work for me.
Re. Rice diet for psoriasis
I went gluten free and my psoriasis dissappeared, later went paleo with varrying amounts of carbs and the psooriasis only came (briefly) back when I failed in my diet and ate wheat. In my view it is possible that the prosiasis and arthritis improvements seen on the rice diet are not due to low fat but rather due to avoidance of gluten/wheat
Denise, thank you for a great post! It definitely questions many of the paradigms we thought were settled.
Has anybody seen fasting insulin levels on LFHC diet referenced in any of the mentioned studies? It would be very interesting to look at. Please post if you have.
thanks, Anna.
Neisy, thanks so much for this detailed and highly objective review of the low fat scientific literature dating back to WW I and the earlier years of the 20th century. It is fascinating that so many serious researchers were collecting data on nutrition, disease and weight gain even if their scientific method was lacking sophistication by today’s standards. You have given us an awesome contribution by your analysis of this remarkably complex body of nutrition information. I am eagerly awaiting part 2 and please do not apologize for the length of your blogs as the depth of information is well worth the reading time. Many warm hugs!
Denise, I’m not trying to defend high fat diets. But I wanted to draw your attention to the following fact. There’s enough anecdotical evidence that the original Okinawa diet is anything but low fat. See here for example. http://stan-heretic.blogspot.nl/2009/10/beware-of-okinawa-diet-scam.html I’m not saying that this evidence is 100% true but it intimates that the topic is actually quite complicated.
Also, what about dental health? Aren’t sugar and starch detrimental for our dental health. And on the contrary a high fat diet helps remineralizing teeth? I wonder what would you say.
I’m not trying to defend high fats diets BUT ….
Then you go on to defend high fat diets. lol
You’re joking right. You count that blog post as evidence?
Denise, I’m not trying to defend high fat diets. But I wanted to draw your attention to the following fact. There’s enough anecdotical evidence that the original Okinawa diet is anything but low fat. See here for example. http://stan-heretic.blogspot.nl/2009/10/beware-of-okinawa-diet-scam.html I’m not saying that this evidence is 100% true but it intimates that the topic is actually quite complicated.
Also, what about dental health? Aren’t sugar and starch detrimental for our dental health. And on the contrary a high fat diet helps remineralizing teeth (thanks to fat soluble vitamins)? I wonder what would you say.
Weston Price already covered this that starch and carbs are not detrimental to teeth health, it’s overall nutrition that is.
As for fat soluble vitamins, fat contains very very little vitamins. Most come from organ meats, pro-vitamin consumption and the sun.
I agree that sugar is not detrimental to gum health. Most health issues stem from some sort of vitamin deficiency (for teeth I think K is the main one). You can have great teeth eating both HF or a LF diet.
I think it’s unfair to suggest fat is vitamin deficient because fat rarely occurs in nature without being prepackaged along with protein and a chockfull of vitamins (a slab of tallow, anyone?). Animal protein and dairy are some of the most versatile and complete foods in terms of vitamins. Many plants lack the same spectrum (though tubers come close!). I’m sure there’s a median between the two and I really like the Jaminets for pointing out that nutrient deficiency is a recipe for disaster. This is why I’m so concerned about either HF or LF because in the long run they seem like they would cause some sort of deficiency.
(And I’ve officially hijacked most comments now…! ;D)
In my experience I saw only negative effects from consuming high amounts of fat. Low fat foods such as liver are why higher in most fat solubles than any fatty meat including dairy. Vit d should be synthesized, vit a and k can be produced via pro vitamin forms and vit e is only needed in small amounts when high amounts of pufa aren’t consumed so I see no reason at all to eat high amounts of fat or fatty animal products (egg yolks, cream, tallow) to get your fat solubles
> In my experience I saw only negative effects from consuming high amounts of fat.
You mean, negative effects on your dental health or more generally? Can you elaborate on that?
Well all around but yes on dental health too. Sensitive teeth and a general ache in my molars. I believe it was from being slightly hypo (tsh of 6.0) which I recovered from on a HC diet.
I believe there are far more important things in regards to health than just hitting arbitrary amounts of certain vitamins and minerals. A very healthy and resilient body can achieve greatness on less than ideal diets and a sick body will not always be able to recover even with a copious amount of nutrition. So many variables.
P.S. I was taking a lot of supplements while on low carb as well which may of made things worse. I take zero supplements now and feel no need for them.
Zach… The aching molars, sensitive teeth…to me this indicates sub-clinical hypervitaminosis. The beginnings of what used to be called “Pseudotumor Cerebri” or now known as IIH (idiopathic intracranial hypertension).
It’s been an issue with me for years and any exogenous preformed vitamin A can start the aches again. Along with pressure in the eyes/skull, ascites, bone pain. I think the only safe vitamin A is the one our body makes for us out of beta carotene.
Paleo, and before that, Atkins, I think are exposing people to too much. Fortification with synthetics are doubly bad. Citizens living in first world countries shouldn’t be consuming products fortified with It.
Sorry to have hijacked this thread. When I read about the success of low-fat, mostly vegetarian diets, I can’t help but think it’s somehow due to less iron and a whole lot less preformed vitamin A.
Really interesting stuff, thanks! That could definitely be what was happening. I agree that letting our body produce certain vitamins and other things like cholesterol.
Errr…..I read Weston Price’s book. He absolutely DID say that refined sugar and white flour were bad for teeth, and general health as well.
Refined sugar and white flour is detrimental to teeth because they displace whole food nutrients with empty calories. I said starch and carbs, not empty calories.
It was a little misleading I guess, because refined sugar was used in the rice diet. And someone else in the comment section interpreted the remark about Weston Price as meaning that sugar was not problematic for teeth and gums. I was only trying to clarify the issue. But it is true that Weston Price had nothing against whole, natural starches and sugars, yes. But he was highly critical of refined carbohydrates, white flour and sugar in particular.
Zach you’re wrong. White flour and sugar are detrimental to the teeth because of the direct effect they have in the mouth both on the teeth and in changing the chemistry and pH of the mouth.
No, you’re wrong. There is no possible way to prove direct causation of tooth decay from refined flour and sugar because of the many other factors involved. Anacdotally, millions of people eat plenty of refined flour and sugar with no dental issues.
Zach: who are these people who eat lots of sugar and refined flour, with no tooth decay? I guess you haven’t seen “That Sugar Film”, huh.
In any case, sugar does block the cleansing system of the mouth (the parotid gland). Granted, this is just one theory of dental caries- (though it has been confirmed in rats). Nobody really knows what causes cavities- (hard to believe, ain’t it?!) But, “anecdotally”, sugar and white flour do seem to be problematic, at least for cultures who have just recently turned from their native foods to these foods- (as well as the teenagers in “That Sugar Film”). Also, sugar blocks the body from the uptake of vitamin C, which is important for gum health as well as for the immune system, so I think it can’t exactly be good. In addition, we do have evidence that when early humans changed from hunting and foraging to framing, their teeth and bones suffered greatly.
Oops, I meant to say “farming”, not “framing”.
I think you’re both wrong, the mechanism for tooth decay is that sugar reverses the lymph pump in the pulp of the tooth, preventing the flow of lymph out of the pores of the tooth which allows bacteria to enter the tooth and cause caries http://www.healingteethnaturally.com/dentinal-fluid-transport-steinman-leonora.html Dr Ralph Steinman came up with this – he raised his kids on a sugar-free lacto-ovo diet, they were carie-free – he and his wife both had plentiful caries so this was not a genetic effect
No actually, i was trying to say exactly what you wrote- I just used different words; but, yes, the dentinal fluid transport system, I had forgotten that that was (technically) what it was called. If you look lower down on the link you sent, it is explained that the way this works is via the parotid gland (which controls the hormones involved). Basically, you and I were saying the same thing- (though I probably didn’t explain it well).
Cool!
But how is it that only you and I and 6 other people 1 of whom is dead know this stuff??
Because its fiction. ; )
You’re coming off more and more like a troll Zach
Hi incognito,
Sorry for the late response to this! The Okinawans are an interesting (and probably inconclusive) case because their dietary patterns changed dramatically after WWII. More recent (1970s and beyond) surveys reflect the newer diet; the link in my post tried to gauge the diet circa 1950 (of course, it’s subject to recall flaws and is probably far from perfect!). I would think the pre-WWII diet would be more relevant to any longevity benefit, since it’s what the centenarians from the past few decades grew up eating — but that’s just a hunch at this point.
As for dental health: sugar and starch mostly seem to be a problem in the absence of adequate fat-soluble vitamins. Anecdotally, I developed severe tooth decay (16 cavities!) on a high-fruit vegan diet, but the addition of fat-soluble vitamins from fermented goat dairy (K2, A, some D) and vitamin D supplementation worked wonders even without significantly reducing my fruit sugar intake. Weston Price’s work (not just from his travels, but studies he performed on patients) suggests that vitamins A, D, and K2 are really what dictate the resiliency of teeth against decay.
The prewar Okinawan diet was very heavy in fish, so it was not a very high carb diet. As with all longevity pockets, though, I suspect the key factor was calorie restriction.
Heavy in fish? I wouldn’t expect that over 10% of pre-war Okinawan calories came from meats, and that fatty pork probably was at least equal to fish calorie-wise.
Here is a study that I have quoted to MS clients to debunk the Swank diet and to justify why perhaps it is the eating less processed foods rather than the eating less saturated fat that is the reason why the Swank diet may help… now you are rocking my boat!!!
http://www.ncbi.nlm.nih.gov/pubmed/11117615
Am J Epidemiol. 2000 Dec 1;152(11):1056-64.
Dietary fat in relation to risk of multiple sclerosis among two large cohorts of women.
Zhang SM, Willett WC, Hernán MA, Olek MJ, Ascherio A.
Source
Department of Nutrition, Harvard School of Public Health, Boston, MA 02115, USA. Shumin.Zhang@channing.harvard.edu
Abstract
Ecologic correlations suggest that higher intake of saturated fat and lower intake of polyunsaturated fat might increase the risk of multiple sclerosis (MS), but the results of case-control studies have been inconsistent.
Because no prospective data are available, the authors examined these associations in two large cohorts, the Nurses’ Health Study, which consisted of 92,422 women with 14 years of follow-up (1980-1994) and the Nurses’ Health Study II, which consisted of 95,389 women with 4 years of follow-up (1991-1995). They documented 195 new cases of MS.
The pooled multivariate relative risks comparing women in the highest quintile with those in the lowest were
1.1 (95% confidence interval: 0.7, 1.7) for total fat,
0.7 (95% confidence interval: 0.5, 1.2) for animal fat,
1.2 (95% confidence interval: 0.7, 2.1) for vegetable fat,
0.8 (95% confidence interval: 0.5, 1.3) for saturated fat,
1.1 (95% confidence interval: 0.7, 1.7) for monounsaturated fat,
1.7 (95% confidence interval 1.0, 2.8) for n-6 polyunsaturated fat,
1.3 (95% confidence interval: 0.8, 2.0) for trans unsaturated fat, and
0.7 (95% confidence interval: 0.4, 1.1) for cholesterol.
Omega-3 fatty acids from fish were also unrelated to risk. However, the authors observed a nonsignificantly lower risk of MS for a higher intake of linolenic acid.
Can you shed some light on this??
Thanks
I thought that possibly the high pufa intake could’ve been ameliorating/covering up deficiencies associated with MS by suppressing metabolism?
Hi Patricia,
My first thought with the quoted study is that the range of fat intake probably didn’t encompass low enough levels to detect a correlation between fat intake (especially saturated) and MS. In Swank’s study, anything above 20g/day of saturated fat — whether 21 grams or 60 — had pretty much the same effect on his patients (in terms of exacerbation rates and mortality); the apparent benefits of saturated fat reduction didn’t appear until people were eating in the 10 – 15g/day range.
In the Nurse’s Health Study data, we can see from this table (http://aje.oxfordjournals.org/content/152/11/1056/T1.expansion.html) that women in the lowest quintile for fat intake were still eating 28.7% of their calories as fat, and 11% of their calories as saturated fat. It’s hard to draw a direct comparison between percentages of energy and absolute intake, but 28.7% fat and 11% saturated fat are almost certainly much higher than Swank allowed for his patients. And those were the women in the *bottom* quintile! 80% of the study population ate more fat and saturated fat than they did.
So, it looks like even the “lowest fat” participants in the study were eating well above the levels Swank mandated for his patients. I’d guess that observational studies encompassing a lower saturated fat intake might detect something more significant! 🙂
I do absolutely fantastic on a starch and fruit diet. Got down to my ideal bodyweight of 160 effortlessly from a high on 210 and reversed my beginnings of anklyosing spondylitis, hypothyroidism and IBS issues. Low carb diet completely destroyed my health over the previous 6~ years and took a good 4 to reverse the damage done. Now I am seeing some amazing things happening. I encourage anyone with any health issues to try a low fat, low animal product diet.
Thanks Denise for putting together this massive article. I have read most of the literature from most of these people but finding it in all one place and with all the more obscure stuff is amazing. I don’t know what else you have planned but maybe take it further and cover some of the newer names that you previously mentioned and also the cultures that naturally eat a high carb,low fat diet.
I agree. IMO Low carb masks and exacerbates any underlying metabolic issues. The ‘Different Magic’ at the >65% fat pole is a black magic.
Zach, what about sugar crashes? Do you experience them? After discovering LCHF I realized that my afternoon sluggishness is anything but ‘normal’. It was gone the next day I eliminated sugar and starch. I don’t have weight issues (I switched to LCHF in order to get rid of my sweet tooth), so I’m trying to bring back carbs into my diet. But every time I go beyond a certain point, my afternoon drowsiness return. And I really hate it.
I crashed a lot at first when returning carbs into my diet and it slowly got better the more I pushed the carb limit. Dramatically reducing fat intake and becoming very insulin sensitive helped the most. Now I have zero crash and steady energy. My last meal was literally a 1lb loaf of fresh baked rye bread (organic rye, blackstrap molasses, salt, yeast, water) and quite o bit of blueberry jam and 16oz of apple cider with zero blood sugar issues. I can also fast without issue which some people claim they cannot do on a starch heavy diet.
Thanks for sharing your experience! Yes, so far I was only able to fast easily when I eat mostly meat, liver etc and non-starchy veggies (interestingly enough in my case diary, like cheese, caused food cravings so I had to ditch it). Still I have to experiment and find my sweet spot.
I’m not sure how long you have been eating low carb but I do believe it’s easier to fast and also less energy crashes because a low carb diet usually promotes a sympathetic dominant nervous system, relying on stress hormones to function. By design a low carb diet needs to rely on cortisol and adrenalin to produce glucose. Plus high amounts of meat can be stressful because of the high amount of inflammatory aminos. Also omega 6 will almost always be higher.
Anyway, this can feel great for awhile but in my experience and from lots of interaction on Internet forums, this takes a huge toll on the body. Mainly in the form of low thyroid, auto immune diseases, food intolerances, inflammation, trouble sleeping, insulin resistance and low energy.
I’m sorry, are you talking about LCHF or just LC? You mentioned high amount of meat. I rarely eat more than 80g of protein per day. The excess of protein makes me sluggish, just like carbs.
Also (olive and coconut oil aside) vegetable oils have the highest amount of omega 6, not animal fat: http://authoritynutrition.com/optimize-omega-6-omega-3-ratio/ So I can’t see the reason why I need to dump my butter and lard. Interestingly enough, although I also use coconut oil, I have to be careful, for my body doesn’t tolerate large amounts of coconut oil, while butter and lard is not a problem.
Anyway, I would appreciate if you give me the links on others peoples experience as well as scientific papers describing how LCHF affects cortisol and adrenalin. Because so far I’ve seen only positive feedback: LCHF, keto-, and even zerocarb folks all report a drastic improvement of dental health. Such unanimity makes me suspicious:) Thanks!
One look at Jimmy Moore’s latest labs speaks a lot about a decade on LCHF. Disregulated cortisol, low progesterone, low dhea, prediabetic hba1c, high fasting insulin, etc …. His wife now has hashi’s, “adrenal fatigue” and high fasting insulin. Everyone likes to ignore this living example or attribute the ill health to anything other than the diet.
http://livinlavidalowcarb.com/blog/potpourri-of-health-tests-on-jimmy-moore-in-may-2015/24818
I was wondering about him. He lost so much and looked so good for awhile. The last time I watched him give a talk he was really fat again. I think that happens to everybody if they go back to their old habits, I assumed he was no longer doing low carb. If a person doing low carb started gaining weight again why on earth would anybody keep doing it? I am a successful low carber, have kept the weight off for years and no longer do low carb, but neither did I go back to my original dietary habits either.
If you look back, JM looked the best in 2005 while eating Atkins maintenance (approx 150 gr carbs per day) + doing some exercise. He claims that stopped working for him and he continued to buckle down and low carb harder. Embarking on his nutritional ketosis experiment. His labs are all anyone needs to see how his health is not ideal. Not everyone attributes it to his diet. I’m not sure how you could not attribute it to his diet. A moderately low carb diet isn’t a bad thing especially in the short term but a decade of this hasn’t made him a healthy man. Can’t be a coincidence his wife is right behind him even developing an autoimmune disease which Dr. Schwarbzein discusses in the video talk I posted.
Thanks for the info. I do not understand why people don´t change something that is going wrong. When I stopped eating low and moderate carb and added a lot of fruit to my diet, I could feel my body sucking up the nutrients in fruit and demanding more. That told me it was time to give up the low carb high fat.
Rebecca, out of curiosity, how did you feel that? thanks.
I felt better and better over the years I did low carb high fat, but after awhile I really saw no more improvements. When I switched to a high carb low fat form of eating I feel just as good if not better, I feel lighter. I have plenty of energy, perhaps a bit more than I did with high fat. I still have a few issues I hope to improve. The main one sleeping. I am going to a starch based diet with fruit and veg. It is too soon to tell if it will bring me more benefits, but I believe in experimentation, and am giving it a go.
Oops I didn´t really answer your question. I guess it was just I felt like I could not get enough fruit, I felt like my body was demanding it. But not in the way people get cravings for junk food. I was easily eating at least 8 pieces of fruit a day, and sometimes more. It is really difficult to explain that, it comes from practicing listening to your body and feeling how it responds to everything you put in. It takes time and patience to do this but I think a lot of people do not really listen to their bodies. I learned it from my husband who has an amazing ability to feel how his body is working and how things affect it. He told me you just have to start paying attention and work at it.
Rebecca, thank you for the explanation.
If you`ve got 2 hours. This is a good talk. Dr. Schwarzbein walks through biochemistry and endocrinology to explain why low carb is a stressor. Jimmy`s labs reflect what she`s describing.
https://www.youtube.com/watch?v=6qUSvzUj6jo (part 1)
https://www.youtube.com/watch?v=rm0MG_zYIdQ (part 2)
Thanks! I skimmed her presentation and it looks very intriguing and informative. Totally agree with her that “losing weight” shouldn’t be the starting point of the ideal diet (if such diet exists at all).
I didn’t have weight issues though. But as a long distance runner I developed unhealthy addiction to carbs and sugar foods. But it’s funny. Because she mentions that a LCHF diet can cause insomnia in the long run. For me it’s quite the opposite. The moment I reintroduce substantial amounts of carbs, I immediately get insomnia (not to mention sugar cravings and, paradoxically, the desire to drink more coffee). I wonder why is that.
Trina, I watched the presentation and also checked her book The Schwarzbein Principle. There she says how much carbs you need to eat depending on your activity. Still, she recommends more than 75g of carbs only for very active people. Now, I’m confused: what does she mean by low-carb diet? In other words, how low is low?
Also, in her book and in the presentation she mentions coffee a lot. May be it is the main culprit of high cortisol levels and not low-carb per se. I know a lot of lchf and paleo folks encourage you to drink coffee and even drink the so called bulletproof coffee, and it doesn’t make any sense for me. So Schwarzbein gave me another reason to quit my coffee habit.
She wrote a second book (http://www.amazon.com/The-Schwarzbein-Principle-Transition-Regeneration/dp/1558749640). She wrote that people read the first book and took carb restriction too far. Insulin serves a purpose. The people who seem to suffer ill health are the ones who appear to take low carb to the extreme. If glucose is extremely scarce, you need extreme insulin resistance to conserve it. I’m not condoning her diet, just found that 2 hour talk very interesting from a science stand point.
Just watched this – pretty amazing driving down blood sugars, drives down insulin and drives down nitric oxide. They have known this since 2007. This explains why low carb high fat only works for awhile. Fascinating how she makes the biochemistry understandable. Finally a real reason why carbohydrates are necessary.
I wouldn’t be so fast to state something “finally”. We’ve heard so many final statements already (“meat is murder”, or “fat is your savior”, “you need to run” “actually, jogging is bad for you, go sprining!”), and I’m sure this is not the last one.
Here’s, for example, a totally different opinion: http://www.diagnosisdiet.com/food/carbohydrates/ I wouldn’t go as far as eliminating carbs completely but Dr. Ede is good at questioning our presupposition about healthy diet (like “veggies are good for you” http://www.diagnosisdiet.com/food/vegetables/).
When I said finally, I was using it as an expression meaning – at last I have heard an explaination that makes sense to me. I did not mean it is the final word on the topic – I don´t know why you interpreted it that way.
Dr Ede is a psychiatrist. Not sure what her full understanding of the endocrine system is. She’s also written some posts about wanting to sing to her keto diet so … lol.
I was replying to a link I followed in one of the comments it was to a talk by Dr. Diana Schwarzbein who is an endocrinologist. This is the link to a 2 part talk https://www.youtube.com/watch?v=rm0MG_zYIdQ – this is part 2 it is all about the biochemistry of metabolism. She talks in one part about research that was published back in 2007 where they learned more about insulin metabolism. There is a pathway in the body called P13K that is important in insulin metabolism – basically what happens if you do low carb, or ketotic diets they drive down blood sugar, they drive down insulin, and that drives down NO nitric oxide and you do not want to have this. NO is vital for health. This to me is a very convincing point that doing low carb when your metabolism is already damaged will definately sooner or later make it all worse, and a healthy person could cause theirself metabolic damage eventually eating low carb becasue of how the P13K pathway works. This is published scientific fact about our biochemistry – I think that makes it something we should pay attention too. It could also explain why Dr Atkins died being 60 pounds overweight with severe heart disease, and why Jimmy Moore is now fat again and unhealthy. It still does not tell us what is the best diet to get healthy and stay healthy and vital into old age, but I do believe it is an important piece of the puzzle.
Notice also the effecsk of very high methylglyoxal from long-term low-carbing.
http://freetheanimal.com/2014/11/hormesis-missing-glutathione.html
There are other markers on his labs that should be of big concern (his falling total protein, albumin and globulin levels).
Storage of fat in the wrong places is the underlying cause of atherosclerosis, type 2 diabetes, NASH and so on.
You can’t store fat without dietary fat.
You can’t store fat without dietary carbohydrate.
Which diet is easiest to achieve, most digestible, most appetising, and supplies most of the nutrition you yourself require?
Also, which diet best supports cognition and emotional well-being?
Probably the diet with B12, long-chain PUFAs, and the potential for ketogenesis.
I commenced a very low fat raw food diet four years after puberty, in the context of undiagnosed IBD. It seemed enlivening akin to magic vs the SAD, initially, and remitted the disease. In subsequent years, the main therapeutic value, after depressing insulin(probably), was the ‘control’ of autoimmunity by anergy. This came with deficits: B12, anemia, D, cachexic musulature (despite daily exercise to quell high anxiety), and a general sallow malaise aeons from wellbeing.
In this period I’d noticed a calm reserviour of energy after walking ten kilometers, past the barrier of exhaustion… and this I sought. A diet that facilitates ketogenesis generates this state as default, also resolving the perpetual ‘malabsorbtion’ issues with B12 et. all. It has generated a state less compromised, that has facilitated the reversal of a considerably affecting uveitits, which I did not even know I had such was its constancy.
Yes, ultra low fat whole food diets disarm autoimmunity, especially if tending to underfed, but I’d like to know if there are mechanisms at large beyond the anergic?
Another good source of information is from John McDougal MD. He says the healthiest diet is a starch based diet. As a standard medical Dr. with at least 40 years of experience his website and a book called the Starch Solution are fascinating. Just google him and check it out. I have done vegetarian and vegan in the past looking for that magical solution they promise and nothing happened but made my blood sugars worse. Then I did very low carb and high fat and it worked like magic for awhile. I am now trying the McDougal approach and I like it and my blood sugar tolerates it. We all need different things in our lives at different times and the only way to find what works for you is to experiment with different diets. And what works at one point maynot be good forever, you have to change as things change. And all the chatter about oh it has to be scientificly validated is just crap. Science has told us so many things that are now proved wrong. Give me case studies where I can see the results in real people, if it works for others there is a chance it might work for me. And any diet no matter what kind still needs to be tweaked to meet an individuals needs and tastes. Dr. McDougal has the evidence his approach definately works for his patients. I am fascinated by his concepts of a starch based approach to good health and normal body weight.
Denise,
you have said in your analysis of Swank MS experiment that the diet allowed for “60 to 90 grams of protein daily, mostly from fat-free animal foods”. It’s possible that MS patients used to eat more protein then the above amount and protein reduction was at least somewhat responsible for their improvement?
Hi Anna,
It’s possible that protein reduction played a role for the MS patients, but there’s no way to tell from Swank’s data, as far as I can tell! I’d consider it unlikely that protein intake went down much, because the animal food content of the patients’ diets shifted from items that were higher fat/relatively lower protein to items that were almost pure protein (skim milk, lean meats and fish, etc.). If anything, protein intake may have gone up some. Just speculation, though. I’ll check some of his papers to see if he recorded his patients’ initial protein intake anywhere.
Denise,
I have found an interesting point about the Morrison study from the book below. He was giving his patients additional vitamin C supplements, about 150 mg a day. The author claims that vitamin C was responsible for their improvement, not reduction in fat. I’m not sure if I buy the vitamin C theory, but what if there was some other unknown variable introduced that he didn’t include into the study for some political or other reasons?
https://books.google.com/books?id=4trIQScMS_UC&pg=PA106&lpg=PA106&dq=lester+morrison+diet+low+fat&source=bl&ots=Nlr0Y8PBBH&sig=GhLn8jopjTdppnqw5x1aPVvX6-s&hl=en&sa=X&ved=0CDgQ6AEwBGoVChMIhYT60qq0yAIVypQNCh2ftwG3#v=onepage&q=lester%20morrison%20diet%20low%20fat&f=false
And I found on another blog that he was indeed using a lot of supplements and involved CR:
“Along with a number of vitamins and minerals, Morrison prescribed supplemental wheat germ and brewer’s yeast because of their high B-vitamin content, the latter also containing the important antioxidant mineral selenium. It is now well-recognized that certain B-vitamins lower blood levels of a potentially atherogenic substance known as homocysteine, while a small pilot trial found a marked reduction in mortality among CHD patients taking selenium-rich yeast on a daily basis”
http://microbialinfluence.com/Vegan2/study.html
And high-protein diets can cause appetite suppression.
Even you said that “the low-fat group saw some initial weight loss—an average of 21 pounds for men and 17 for women during the first three years, but with no additional changes during the rest of the study—whereas the control group remained weight-stable the whole time.”
So perhaps the weight loss or CR or supplementation should be credited instead of LF?
Hi Anna,
Interesting finds! Morrison definitely did a lot of work with supplements (most notably chondroitin sulfate), and it’s definitely possible that other factors beyond fat intake influenced his patients’ results. If his low-fat study was the only one of its kind yielding the results it did, I’d be more hesitant to ascribe the therapeutic effect to fat reduction — but the consistency of very-low-fat programs (with or without supplements, whole foods or not) improving cardiovascular disease, combined with the mechanistic studies I’ll be exploring in Part 2, makes me think that fat played a significant role.
I do think weight loss and a reduced calorie intake (even if it happened spontaneously in his patients rather than deliberately) were confounders for his study. Thanks for your comments! 🙂
I’d recommend reading up on Linus Pauling’s theory on heart disease, which ties together effects from both vitamin C and saturated fats. The theory is that in the absence of adequate vitamin C – and “adequate” was several grams a day – to provide the necessary reducing agents to build connective tissue for arteries, saturated fat deposits provided a backup mechanism for reinforcing blood vessel walls. Having neither might eventually result in hemorrhagic stroke.
Psychohist, in the study they were only given 150 mg of vit C, nowhere near a few grams that L Pauling recommends and longer term saturated fat reduction didn’t seem to cause a spike in stokes…
perhaps CR produces/reuses some other antioxidants that can replace vit C/sat fat combo?
Denise, next up Nathan Pritikin diet.
A few points:
1. Again, protein reduction could have had some effect. In fact, cancer and mTor pathway are related.
2. Caloric restriction and/or weight loss could not be ruled out. Just because they were eating “ad libitum”, doesn’t meant that this restricted LF diet doesn’t cause spontaneous CR or activate the same pathways as CR, especially coupled with low protein intake.
Another interesting point is that LF diet leads to a reduction of fasting insulin, similar to LC diet. And a reduction of insulin correlates with various health improvements (according to your posted studies as well as others). So fasting insulin seems to be a good across the board marker of health.
Thanks.
And the same applies to Esselstyn’s study. His diet was most likely naturally very CR diet. “Whole grains, legumes, lentils, other vegetables, and fruit comprised the major portion of the diet.” “Initially the inter- vention avoided all added oils and processed foods that contain oils, fish, meat, fowl, dairy products, avocado, nuts, and excess salt. Pa- tients were also asked to avoid sugary foods (sucrose, fructose, and drinks containing them, refined carbohydrates, fruit juices, syr- ups, and molasses). Subsequently, we also excluded caffeine and fructose.”
http://dresselstyn.com/JFP_06307_Article1.pdf
So, the bottom line for me is that Caloric Restriction is a major possible confounder for most of the studies you’ve mentioned. On top of this, outright protein restriction for many. Falling fasting insulin levels are robust markers of CR, confirming my point.
For me, CR (including protein restriction) comes out as winner. It seems to matter much less LC or LF, whole foods or processed foods, IF + any diet. Instead, CR vs excess calories is where the vast majority of benefits lies.
Thanks again for a great blog post dispelling many misconceptions about carbs.
The first big point made in this blog is that the magic happens on either end of the scale – i.e. the scale of LCHF – LFHC. We have two different metabolisms, one for carbs, and the original one for fat/ketones. Problem comes when trying to run them together – esp eating fats when insulin present (needs proper explanation, bear with!).
If one eat carbs in isolation, the insulin – fat conflict isn’t there, and metabolism is relatively happy – for a bit – at last its not too toxic. I didn’t say it was very nutritious, but the body will survive this situation better than the toxic case of insulin and fat together. So HC diet shows better than a mix….
Paleos didn’t have fridges and corner stores. hey didn’t eat a “balance diet” on each plate. They ate a kill, then went a few days on nuts and berries etc. Food combining stuff.
So in fact we (most of us) can eat both carbs and fats – separately. When I say carbs, I mean real carbs, like veggies. The question how far apart in time – is it lamb for lunch and salad at night? I think the minimum period is enough to get the insulin down after the carbs. Admittedly some carb meals won’t raise insulin substantially.
For my money, LCHF (<25g carbs per day) still best option for most, especially insulin resistant people. I accept you could stay alive and somewhat protected from CHD on HCLF (real food options) but would not be properly fed, perhaps unless suffient DHA ingested.
So for me the Taubes/Teicholz models still completely valid, with the new emphasis of not mixing carbs and fats!!
There are likely other issues to do with gut flora and mixing carbs with fats, it just was't meant to be done this way….
This is a difficult topic for me. I am Asian, I used to be a vegetarian, and I had been basically eating the rice diet (rice, sugar, fruit) most of my life when I got diabetes. The switch to a LCHF diet reversed my symptoms (high blood sugars). Naturally I would like to revert to my previous diet, but my blood sugars will skyrocket.
I am a type II diabetic and did not think I could eat high carb. I did very low carb and high fat for about 5 years, and that helped a lot to control my blood sugars. Then I did a few days of liquid fasting a week for a couple of months and my blood sugars got even better. But then I just was tired of it I don´t even really like meats or poultry or fish. So I started eating lots of fruit, then I found this blog and that led me to an interesting article about a potato diet that goes back to 1849. And another blog led me to the works of John McDougall MD. He advocates an almost no fat starch based diet. He is a standard doctor and he treats patients with diabetes with it. Google him he has a website. And a recent book called the Starch Solution. I am starting to eat like he says and my blood sugar tolerates it with about the same medications I had to use eating lowcarb highfat. I just did not believe in a million years I could eat this way. But when you cut out all the fat and animal proteins your insulin functions differently. And starchy foods, fruits and vegetables all have amino acids and very small amounts of fat. Potatoes have all the essential amino acids. People can live and be healthy on potatoes alone, which has happened in the past. Check out McDougall´s stuff and maybe you will find the answer to let you go back to eating the way you want.
I could try this but I don’t want to go on meds.
I wonder if the rice diet was having a similar effect to an elemental diet, which are basically amino acids and dextrose. fat is added, but they recommend you start very low fat and increase according to tolerance. Elemental diets have been shown to correct sibo better than antibiotics. Correcting a gut microbiosis could possibly have the health benefits you describe. Rice and fruit wouldn’t be a complete protein, but it might be a reasonable whole food version of an elemental diet, with the addition of enough resistant starch to keep big intestinal flora alive during the purge. So, would a diet of similar macrobiotics but different starches be as successful, like, say, bananas with processed fructose? I thought it was interesting that bananas were limited. In other words, is the low fat aspect the crucial one? I remember something lately about a high fat diet not doing good things for leaky gut… but don’t remember the details… And what about fat soluble micronutrients over the long term?
When I had SIBO, IBS and leaky gut, I healed over the course of 2 1/2 years on the GAPS diet. It involved high fat, meats, well cooked vegetables, yet restricted many forms of carbohydrate like all grains, starches, most legumes, unfermented dairy, sugar. Eliminating the starches and sugars and consuming the fat and proteins of GAPS was immensely soothing to my body, mood, and mind. I don’t believe high fat is not good for a leaky gut, unless of course the fat is in the form of PUFAs. I healed on a high fat diet, much to my gratitude and relief.
Generally speaking, Minger is a charlatan.
Evidence to support your insult would be appreciated.
Apparently, generally speaking, Cynthia is a troll
And you are a troll, generally speaking
Name calling is totally inappropriate. This was an opinion piece. And we all have opinions, and a right to form our own opinions.
When calling someone a charlatan, it seems appropriate to furnish grounds unless you’re a troll
My obese, lifetime non-smoker grandfather had a heart attack at age 55. He went on the Kempner rice diet, did great for the next twenty years, and died of a head injury from a bicycle accident at age 75. He ate rice and fruit for breakfast and lunch and meat and vegetables for dinner. My grandmother was distressed that his last meal was “plain rice”. Anecdotal data, but….
Maybe we are over analysizing this. Perhaps our bodies don’t care how we get our calories, just that we get the right amount. Just not too much or not too little. If we get our appropriate nutrients and avoid any serious toxins, our bodies are able to get along just fine. The Rice Diet usually causes initial weight loss then it plateaus. Atkins often the same. Gastric bypass surgery as well. Satiety meets up with healthy calorie intake. Poor diets have low satiety and lead to over eating and eventually energy overload. Insulin resistance beings and the path to chronic degenerative diseases is set. Restore energy balance and IR goes away and disease conditions and risks drop. The middle ground diets can work if we don’t mess up our satiety signals. The French Diet, the Paleo Diet and the Mediterrian Diets do work because they has healthy satiety. Junk food in the Western Diet defeat our energy balance mechanisms. The processed food is designed to defeat normal satiety signals. War ration diets work because scarcity solves the overconsumption problem, willpower is not required.
I read a book years ago where people had benefits from eating nothing but brown rice. People magazine 8/13/79 has an article on the Pritkikin diet
I have gone back and forth with fruitarianism and paleo over the last few years. I have felt amazing on fruit and pretty good on paleo. Then I found out that Arthur DeVany, the grandfather of paleo, just had hip and knee replacements in his early seventies. And Janette and Alan Murray, both low fat raw vegans, ran 366 marathons in 366 days at about the same age. It was a no brainer from then on.
I think what is really important is that healthy diet is either low in fat or low in carbs,
Is there any studies on a 50/50 high fat high carb diet?
Thanks for all the work you put into this. And for your impressive willingness to admit you were wrong. That’s rare. I look forward to the next installment. People’s trollish comments amaze me, especially about your writing. You are a fine writer and I love your sense of humor.
Hi Denise,
I appreciate your research. Do you think some of the differences could be due to genetic differences. I have tried low fat and vegan diets and failed miserably. I switched to a high fat/low carb diet and feel great and look a ton better. I don’t think one size fits all.
Low-carb-high-fat works fine to detox from years of low-fat-high-carb diet.
It is a transition period and gives excellent results in terms of health and weight loss, both are commonly mistaken as the proof that the perfect diet has been found. But once the sugar detox is achieved, a “reasonabe-carb-diet” must be followed.
What low-carbers don’t know is that prolonged periods on a ketogetic diet can effectively cause insulin resistance (yes, the same as high-carb).
Some of us know that perfectly well. However, the insulin resistance is not accompanied by high blood sugar, which is the part of metabolic syndrome that is damaging. Excessive insulin sensitivity can cause hypoglycemia on a low carb diet, so the body adjusts its insulin sensitivity accordingly.
So you’re saying that the Japanese need to detox? You can’t be referring to Americans, who both on a calorie basis and a macro percentage basis, eat one of the highest fat diets on the planet. If lots of fat is what detoxes a person the SAD is doing a bang-up job.
First time reader, and wow that was a long first read! I’ve been doing research on veganism/whole food plant based diets and one of the vegan forums linked to this. One thing I can definitely respect when trying to find the best information is someone who isn’t afraid to correct themself or say they were initially wrong on a certain subject. Anyways, thanks for the words, I’ll be sure to read more.
In a Japanese experiment involving 100 million people, a diet of mostly rice, fish and vegetables yielded the longest life expectancy on the planet.
The japanese love fish rice nad vegetables, but to say its mostly? thats a bit of an exageration. They have wonderful pork, chicken, beef dishes. Deep fried pork in Japan is absolutely fantastic, let alone their tempura style seafood. Rice is typically a side vs a main.
But, most of their food is extremely high quality, fresh, well cared for. Not mass produced garbage – although they have lots of this as well – fantastic selection of candy.
This is my favorite article on thie subject, which I read back in the day. James Fallows describes what happened diet-wise when he and his family moved to Japan for an extended writing assignment.
http://www.theatlantic.com/past/issues/86nov/fallows.htm
Basically they were hungry all the time and had to go to fast food joints to get fat fixes.
What people in the HFLC community don’t get is that the SAD IS a high fat diet. The Japanese eat (or ate) a low fat diet. Not Americans. Ever.
Oh my Denise, you surpass your previous works in sensationalism but you are lacking in examining your own logic I think, on at least this one point. You say that you are:
“Uncomfortable, because it demolishes my long-held rationale for why low fat, veganish diets can be successful: that they work because they involve switching to whole foods (Kempner’s sure didn’t!); that they work because they reduce refined sugar and starch intake (the very lifeblood of the rice diet!); that they work because they increase disease-fighting plant compounds (nary a vegetable to be seen under Kempner’s strictest watch). Let me go on record here: I TOTALLY stand corrected!”
Ha! For the sake of keeping consistency and power in this one article, for the sake of making it more thoroughly convincing you just gave up a perfectly rational and quite healthy stance and declared that you “stand corrected”? Where is your normally solid logic? You are so obviously selling out in order to sound convincing in an article here that really matters minimally toward health.
To wit: ONE SUCCESSFUL DIET DOES NOT DEMOLISH ANOTHER SUCCESSFUL DIET. One successful diet rationale (Kempner’s — successful short term — nothing proven long term, mind you) likewise does not demolish the rationale you had maintained to support a whole food, sugar poor, vitamin/enzyme/polyphenol rich diet. Here I am talking about essentially a typical Blue Zones diet, which unlike Kempner’s diet, has been proven to provide health over a great number of years.
If you wish to stand corrected on something regarding this issue, please consider standing on this correction: success of one plan does not necessitate the failure of another.
I hope when you produce your promised next article on this line, you manage to step aside from the silly notions of percents required for macronutrients. I think your original line of thinking was much more proper, that nutrition depends more on micronutrients than macronutrients, if you want a plan that lasts decades. Obviously you have proven that percentages of macronutrients matter little, just as the other side has proven this to their own satisfaction when they work to minimize carbohydrates.
I hope you can dismiss yourself from going on at length on macronutrients and return to giving advice on how the aspect of veganism that manages to provide bodies with plenty of low calorie carbohydrates is a key to health, whether one is vegan, omnivore, paleo or whatever. I realize the sugar lobby can pour a lot of money into swaying important spokespersons to make statements where the word “sugar” is bandied about as part of a winning strategy. So it becomes even more important, if you wish to retain your respectability, to choose your words and phrases carefully.
You redeem yourself by following with the discussion of Morrison and Pritikin, both of which emphasized a fiber rich diet. Where I think your 10% fat threshold has value is that it allows a maximum of vitamins, minerals, enzymes, and phytonutrients. So I only wish to make the point that so many articles on macronutrients are formulated such that the reader focuses on the percentages of macronutrients, and not on the particular nutrients involved. Vegetable starches are less nutrient dense than greens. They are not something to consider interchangeable within the “carbohydrate” component of a diet. But this important point often, (usually even), is lost in Paleo diet discussions, just as it was lost in Atkins Diet discussions. And of course it is lost in the beginning of this current discussions.
On Roy Swank’s findings, and your go at “alternative explanations”, I’ll add one. Since all participants were allowed oils, which most probably included refined, damaged PUFA, there is the chance that the human body burns saturated fat (and MUFA) in preference to PUFA, and that therefore, the PUFA is more likely to be stored (since so little is actually used by the human body for membranes, etc.) and the stored PUFA is actually what causes the MS, not the saturated fat that forces the storage. I’m thinking Ray Peat might vote for this possibility. I know you pointed out that PUFA consumption was inversely related to the saturated fat, but regardless, if there is an excess of PUFA, over some arbitrary limit, and that limit was reached by all participants, even those with the lowest PUFA intake, then the inverse relationship you spoke of is not of consequence, That is, your “swampland principle” may also apply here, making the percentages of types of fat a moot question if the PUFA just happens to always exceed the limit that causes the MS.
Best of health, and take, in some form or another, some vitamins, and not just with a grain of salt! You need to spend a little more time examining the integrity and substance of your articles, and less time on making them carry a clear, beautiful, though hollow tone.
patronizing
I must have skimmed over this part.
“Uncomfortable, because it demolishes my long-held rationale for why low fat, veganish diets can be successful: that they work because they involve switching to whole foods (Kempner’s sure didn’t!); that they work because they reduce refined sugar and starch intake (the very lifeblood of the rice diet!); that they work because they increase disease-fighting plant compounds (nary a vegetable to be seen under Kempner’s strictest watch). Let me go on record here: I TOTALLY stand corrected!”
This is the crux of the matter. That is, the low fat diet works not because it’s a more wholesome diet overall, but because it removes the fat.
Thanks to Glenn for calling this out!
Hi Glenn,
Thanks for the candid comments! I appreciate the opportunity to clarify some points.
Ah, I may not have communicated my point very well here. I’ll rephrase: I used to assume that low-fat, plant-based diets worked *only* because of the removal of refined sugar and starch, the emphasis on whole foods, the increase in phytochemicals, etc., and that the reduction in fat content was irrelevant — something prescribed unnecessarily by the “plant-based diet doctors.” I still believe all those factors play a major role in making these diets health-promoting (especially long term), but the studies I explored in this post suggest very strongly that fat reduction to about 10% also has powerful, independent effects for specific disease states. The diets described here (especially Kempner, Morrison, and Swank) were still successful even when they included sugar, refined starch, and/or a low micronutrient content. Likewise, Swank and Pritikin found that the primary factor in whether their patients were successful long-term was whether or not their fat intake increased.
I agree! In fact, if you missed it, this is what I wrote elsewhere in the post (emphasis added): “For the past few years (five? six? seven ate nine?), I’ve asserted that the success of plant-based diets is due to their whole-foodsness (eliminating processed junk, refined sugar, and refined flour), their low PUFA intake regardless of total fat (with the implication that higher non-PUFA fat consumption would be hunky dory), and the increase in other health-promoting behaviors that come with making a big change in the foods you eat (more exercise, less drinking and smoking, less couch-potatoism, etc.). I still think those things are relevant. But I now believe I dismissed the role of low total fat intake before I gave the data a fair and thorough analysis.”
Nope! This whole series is about why macronutrients *do* make a difference, but why the effects of macronutrient manipulation only become obvious at the extreme ends of the spectrum. The crux of the discussion isn’t what’s best long-term for the majority of the population; these are therapeutic diets, used to address diseases that are developing or already in place. The next post will offer mechanist explanations for why metabolism changes at very low fat intakes — you may find these more convincing than the studies discussed in Part 1. (I do!)
Interesting theory, but not supported by the data. Please read the Swank section again. His patients achieved dramatic results for several years before high-PUFA oils were allowed back in the diet.
I hope that helps clarify some points! Thanks again for your comments. I do hope you stick around for Part 2, because it may change your mind on the irrelevance of macronutrient changes. 🙂
Thanks for clarifying some things Denise. Yes, I had missed your mentioning that these are only therapeutic diets.
On the issue of whether macronutrients deserve continual emphasis in articles, I’ll step aside for now and wait to read what your next installment brings. I still have strong feelings that without EXTENSIVE disclosures before, during and after any article on macronutrients, the audience, being human, may often go away with distorted perceptions of the importance of having viewed foods by macronutrient category.
Regarding the Swank discussion, I find that I also did not explain my point of view carefully enough for you to understand what I meant, and so, and especially in light of several recent comments on the Swank portion of your essay, I’ll state my point again, but differently:
I had said that “there is the chance that the human body burns saturated fat (and MUFA) in preference to PUFA”. Actually, it is well known that this happens. MUFA and saturated fats (SF) are the preferred forms for creation of energy. Probably because in nature, there never is a great abundance of PUFA in the food supply, outside the consumption of nuts (and yes, in recent history, grains). However, SF is needed continually for building new cell membrane (just as is PUFA). It is also the fat preferred not just to feed heart muscle, but to be stored upon the heart for use in times of stress, as when fats are in short supply as free fatty acids via the blood stream. There are other ways that saturated fats are preferred over the other fats as can be found in this WAPF article which can provide references:
http://webcache.googleusercontent.com/search?q=cache:http://www.health-report.co.uk/saturated_fats_health_benefits.htm
Moving on now, to PUFA.
You had countered my original theory with:
“Interesting theory, but not supported by the data. Please read the Swank section again. His patients achieved dramatic results for several years before high-PUFA oils were allowed back in the diet.”
I didn’t read the article that way. I don’t know what Swank’s actual description of the diet was, but what you said was:
“Very low saturated fat (10 – 15 grams per day, maximum)”
“Small amounts of polyunsaturated vegetable oils and fish oil (10 – 40 grams per day)”
So I am only referring to the PUFA and fish oil that was allowed in the original therapeutic diet. As you can see, there is an allowance for more PUFA via vegetable oils than there is even for SF.
So to make my point more carefully:
Considering what we now know about excess adulterated or oxidized PUFA, especially as manifested in commercial “vegetable oils” and what we know about the rapidity of oxidation of fish oils (studies have shown that up to 80% of fish oil supplements show rancidity in newly opened sample bottles), and what we know about the detrimental effects of these ruined oils on the human body, especially to cellular respiration and circulatory endothelial tissue (Brian Peskin has hundreds of references if you need some), it becomes crucial to not consume any ruined PUFA, and to realize that we also shouldn’t be consuming any significant excess of even pristine PUFA (as from super fresh, relatively unheated veggies, meats or eggs) over what is needed to keep our cellular metabolism healthy. Yet Swank allowed liberal consumption of these oils by his study participants. So how did he improve their conditions? They may have eaten as much PUFA as they had before being inducted into the study. What changed was the consumption of SF. And SF is considered dispensable by most (please see below for my perspective). But when you reduce SF via reduction of *animal products*, you also considerably reduce MUFA consumption. Be patient, I’m almost ready to make a point….
Thus his successful cohort, in spite of being allowed reasonable amounts of PUFA, even unhealthy PUFA as described, made remarkable progress in relieving MS symptoms. Ah, I think I’m ready now to make this point:
All I am pointing out is that since saturated fat has a definite demand in the human body with respect to non-metabolic function, just as does PUFA, when you reduce SF to a certain low level, you are squeezing it’s supply so low (and probably also the MUFA supply) that it no longer can be the preferred source of metabolic calories, but must be almost totally pressed into it’s more essential roles of providing cell/mitochondrial wall structure, etc. But at the same time, an excess of PUFA over what is required for it’s essential functions, must now fill the void to provide fats for cellular metabolism, not just to the heart, but to all cells any time there is a need for energy that glycogen and glucose can’t supply. This situation that Swank has brought about insures that not only will the dangerous, oxidized PUFA that he still allows his subjects to use in almost “normal” quantities not be utilized in cellular and mitochondrial membranes, but that possibly any PUFA they have stored in fat cells that is also already oxidized will be released to be consumed as fuel. We may just have a *PUFA purge* going on here! Thus, in effect, his diet, though emphasized as “low in SF”, is actually a cleanse of the more probable cause of MS. He is possibly getting rid of damaging PUFA by just burning it up.
Don’t take this to be a claim that PUFA directly causes MS. I only want to point out that ridding the body of toxins can help a condition in many ways. In fact, I think the point to be made about the Kempner diet is similar: What is most important is NOT that the diet lacks fat, but that it is essentially a FAST plus enough non-toxic, non-allergenic, non-inflammatory foods to keep a person alive. It is a cleanse. So your point that these diets are therapeutic I *only wish to emphasize*. They are not diets for health maintenance. Their magic is, not so much that they eliminated substantial fat, as that they are so restrictive on many levels that they function as a cleanse.
I hope this helps to clarify why I think the reduction in saturated fats showing success in the Swank protocol is possibly not due to reducing something that is damaging to humans (the saturated fat itself), but due to nutrient/toxin balances thanks to extreme reductions in total fats and a change in the percentages that were allowed within that reduced ration.
An aside: Dr. Terry Wahls pushes nutrient dense, fresh vegetables from the garden as well as the sea. She has refined a method that combats and reverses MS. What she doesn’t emphasize, but promotes regardless, is the consumption of what happens to be reasonable quantities of unspoiled PUFA that are contained in her preferred diet. She has effectively eliminated the ruined PUFA that Swank even still allowed in his diet. So I would say that where Swank HAD TO drop saturated fat very low to protect his cohort from the damage done by the ruined PUFA, Dr. Wahls may be able to accomplish the same effect without limiting intake of such oils as coconut oil. She is providing lots of micronutrients via her fresh, organic diet, and these include only fresh, safe PUFAs. So her diet doesn’t need the reduction in saturated fats. The fact that it is successful somewhat proves that the reduction in fats, especially the saturated fats, is not the key ingredient in whipping MS.
Thanks Glenn, that was very interesting. Enjoyed reading your comments about MS; also, you explained what I tried to- (but you did a much better job than I did)- about why the rice diet may have worked.
But I think you had it right in your comment on the rice diet effectively making the body “think it was fasting”, Morgana. The wartime diet, low in fats, and especially the rice diet, low in so many ultimately necessary nutrients, is so restrictive as to effect some of the same results as a fast. There’s going to be more recycling, and more use of “stores” of nutrients. But there’s probably going to be more disposal of toxins. Needed nutrients are not going to be provided daily and found in circulation. But they must come from somewhere. So especially if weight loss is present, as it is in every fast, recycling is raised to such a degree that while valued minerals and amino acids are preserved, the net effect is to leave unneeded substances (toxins, excess minerals, and even excess hormones – estrogen for example) without a home, and thus they are discarded. So your fasting theory seems sound.
I loved your well thought out comments. I would be curious to hear what people think about . T Colin Campbell, PhD and what he says about research and fats and protein in the following article where he villifies animal protein and not fats.
http://nutritionstudies.org/fallacious-faulty-foolish-discussion-about-saturated-fat/
Glenn, thank you for your well thought out theory and a detailed explanation of the relationship between SF, MS and Swank diet. I do think caloric restriction (of fast, as you call it) could play a much bigger role in alleviating many of the diseases then macronutrients percentages.
But, I have a question to you about the ratio of macronutrients. If I understand you correctly, you don’t think it matters much and doesn’t deserve much discussion. But what about high protein diets activating mTor? Wouldn’t this one macronutrient alone need to be at least somewhat monitored/discussed?
thanks.
Anna, I agree that percentages of macronutrients has a reason to be discussed. I just cringe though, the way it is often discussed, and especially shudder when percentages are laid down as mainstays of entire diet plans.
I don’t want to hijack the thread here, but you pushed me lightly, so I’ll respond a bit now, and I’ll wait for the next article to comment further if prodded, on what I called “the dangers of discussing macro nutrients without EXTENSIVE disclosures before, during and after any article on macronutrients”. Probably Denise will be mentioning a lot of what I have in mind anyway as she is very whole-food, micro-nutrient oriented.
But just for an example, as you brought up proteins. Specifying a blanket limit, or even range for protein without dozens of qualifications is of little use, and with the proper qualifications is a burden to consider, let alone track. As this current article shows, there are times when one can go without levels of fat that are considered healthy, all for therapeutic purposes. The same goes for protein or fasts would not work to one’s benefit. But then there should be disclosures regarding time limits for variations off the recommended range.
There were studies that proved that lowering protein intake below prior limits provided greater longevity. Then followup studies showed that just lowering the amounts of certain amino acids (methionine and tryptophan I believe) gave as much or more boost in longevity as blanket protein reduction.
http://www.ncbi.nlm.nih.gov/pubmed/8001743
Protein requirements vary depending on who’s talking to whom. A body-building blog will have higher levels, while someone talking type-2 diabetes may push for a much lower minimum for protein and even suggest abandoning muscle-building plans because protein utilization often requires more insulin than equal calories of certain carbohydrates. So, two considerations on proteins, but there’s no limit on what might be proper before one sets guidelines.
Better I think is to talk about nutrient density of foods, nutrient characteristics of types of foods (such as carbs). That style of discussion avoids having one reader translate “carb” to mean “Coke”, another “potatoes”, another “spinach”. As you can see, what these foods have in common as “carbs” is far less than their differences. One is essentially a simple sugar, one is a starch but with some significant vitamins and protein, and one is primarily a bunch of micronutrients but with almost decent amounts of protein and fat (if you give credit to it containing some PUFA weighted toward the omega-3), and with SLIM amounts of humanly digestible carbohydrate (relative to the bulk eaten), though there is considerable fiber that will easily take care of a population of colonic bacteria which will likely net out some saturated fat to the host as the fiber is consumed, not to mention more vitamins. These are all “carbs”? Do it still make sense to talk percent of diet to allocate to carbs? Be aware, this is just an opening salvo.
I was under the impression that it was difficult to “overeat” protein, and that people generally- when left to their natural inclinations- will eat a set amount of daily protein, rather consistently. There were some tests done on animals as well as humans, which were mentioned in the Perfect Health Diet book. (Of course, this may not be the case in people who are, for whatever reason, forcing themselves to go against what their body needs/desires). I agree that there are times when people may need more, or less protein; (I’ve noticed my own protein needs changing at times). But this is why carbohydrates or fats tend to be the “changeable” macro-nutrients in diets; lower carb generally means higher fat, or vice versa.
Glen, thanks for your detailed reply. Looking forward to more comments after Part 2.
Hi Glenn,
Thanks for clarifying your comments! I appreciate you taking the time to explain your theory further — it’s certainly very interesting, though I would need to do some research before commenting on its general plausibility.
Unfortunately, I think I also wasn’t clear enough in my reply (and perhaps in my blog post!). The 10 – 40 grams of PUFA weren’t allowed on Swank’s diet for the first two years of the program. Basically, people started enrolling in his program in 1948 – 1949. Until 1951, the diet excluded all vegetable oils and fish oil, along with that sharp reduction in saturated fat. It was only in mid-1951 that Swank allowed his patients to add back those PUFAs. Here’s a direct quote from his “Fat-Oil Relationship” paper:
“From 1949 to mid-1951, (saturated) fat intake, which before entering the study had averaged ~125 g/day … was reduced to 20 – 30 g/day. … In 1951, butter fats and hydrogenated oils were eliminated, and animal fats were limited to 15 g/day. Five grams of cod liver oil, and vegetable oils that remained fluid at room temperature were added and allowed to vary from ~10 to 40 g/day as desired by the patients.”
As you can see in the ‘exacerbation rate’ graph in this post, patients already saw dramatic improvements in the first year of the diet before PUFA-rich oils were added back. The addition of the oils didn’t seem to either help or harm the patients, apart from subjective improvements in their energy and hair and skin.
I hope that clears it up! I’d be happy to send you Swank’s papers if you’d like to read them yourself — just shoot me an email through my contact form. 🙂
Great. Thanks, Denise! The study is clear to me now. Yes, you had implied in your response that PUFA wasn’t allowed, but since you originally published that it was allowed (the 10-40 grams statement), I thought it was allowed from the beginning.
Now though, it seems to me that I am left with the same perspective. Not supported by studies (as you say rightfully would be necessary for better proof), but a perspective that is actually a little clearer and easier to state as a theory:
Cutting out most fats from a diet to cure MS may not be as critical as cutting out all refined PUFA. If that’s what Swank did, that by itself is possibly sufficient to bring remission. If we’re assuming that low saturated fat did the trick, it’s just as easy to assume (and more logical, based on percentages reduced – zero vs 10%) that removing ALL refined PUFA did it. Cutting out all recognizable PUFA from “vegetable oils” is significant in my estimation. PUFA has an essential role as the only source of prostaglandins, and a critical role in cellular metabolism, yet, as Brian Peskin continually writes and refers to studies to back his writings, if one’s cell membranes are substantially occupied by oxidized omega-6 instead of healthy omega-6, the whole function of the linoleic acid is thwarted. Cell walls no longer transport oxygen or other nutrients in and out at optimum rates, and prostaglandins can no longer be supplied in ideal amounts.
http://www.brianpeskin.com/BP.com/reports/CAMB-Fish-Oil-Fallacies-Report.pdf
So assuming the participants in Swank’s study had been consuming adulterated PUFA via “vegetable oils” or foods fried in such oils, and they had had these oxidized PUFAs taking the place of healthy, unoxidized PUFA in their cellular membranes, the elimination of all ruined PUFA from the diet allowed the disposal of the ruined PUFA over time, when cells were replaced. The grains, dairy and even vegetables that still existed on the diet would have provided ample, unoxidized PUFA to be used in new cell generation from the beginning of the study onward, and over time almost all cells would again be functioning normally regarding the dependence on PUFA. This would seem to be a gain for someone in any condition, not just MS. Why? Peskin claims that adulterated, or oxidized PUFA that has been installed into cell membranes actually has NO metabolic function. It is there, but not functional. It is taking the place of a figuratively “living, breathing molecule of PUFA” but is doing nothing. It is a hindrance rather than an aid to cellular respiration. So a person having a lot of ruined PUFA in their cells is actually suffering very severely from a lack of life-supporting mineral interchange, and if each cell that is in this condition can be replaced by a cell that has it’s PUFA dependent abilities restored, there will be a net gain for that individual. This would be the case for Swank’s MS sufferers over time as aged cells were replaced with better functioning cells, including neurons which have a slow replacement cycle.
If this is the effect that occurred in the Swank study, then without even considering saturated fat or it’s reduction, I’m theorizing that the purging of ruined PUFA over time will explain the remission of MS symptoms. Saturated fat may not be involved. Since oxidized omega-6 is already implicated in causing cancer and vascular damage and supported by studies to that effect, it’s not difficult to see it could be causative with respect to MS.
I don’t have studies, but people are starting to suspect:
http://ms.newlifeoutlook.com/swank-diet/2/
http://omegavia.com/omega-6-omega-3-and-oxidized-ldl/
As Peskin pointed out in my first link, as omega-6 intake goes up, presence of omega-6 in cell membranes also goes up. When intake is heavily oxidized oil, that is what you get in your membranes:
http://omegavia.com/oxidized-ldl-cholesterol-lard-less-lipitor/
Glen,
this is a good example of how focusing on macronutrients without paying attention to micronutrients can be confusing.
As you are pointing out, Is the issue total fat restriction, saturated fat or Pufa reduction?
thanks.
When will Part 2 be published?
Thank you.
What would you define a high fat diet to be? I see you say you eat lowish fat, but to your average dieter 45+grams of fat in a day is not low fat. So what exactly is high fat? I’m asking out of genuine curiosity, not criticism. I’ve read so many articles and they refer to either low or high but rarely define what that means. Truly not meaning to sound like an ass! 🙂
Hi roonitune,
This is a great question! And an incredibly difficult one to answer — largely because fat as a percent of total calories and fat in absolute grams will give much different pictures depending on total energy intake. For instance, a 45-gram fat intake will be a larger percent of total energy if someone’s only eating 1000 calories a day versus 2000 calories.
Personally, I define low fat as 10 – 20% of calories on a weight-maintaining energy intake; moderate fat, 20 – 40%, and high fat anything above that. Very low fat, I’d place at 10% of calories and lower on a weight-maintaining energy intake. So the absolute gram amount would have to be calculated based on what each person’s calorie needs are.
I have no scientific rationale for those brackets other than “it seems to fit.” 🙂
It’s like we are waiting for Desperately Seeking Denise Part II
I’ve been really confused for the last few days since reading this post. I ate a bunch of safe-starch and sugar yesterday and today, not because I thought it was a good idea, but because it wasn’t inherently evil anymore. What’s the difference between eating this and a low-moderate carb Paleo meal? I couldn’t find an answer, so I ate them.
Maybe I should just eat what I want, since obviously no one has any idea what the best way to eat is. Carbs are bad, but only with fat… Or… Carbs are best with fat (a la Perfect Health Diet)… Carbs make you fat… Carbs don’t make you fat… Fat makes you fat… Only calories make you fat… Lord help me!
My 78 year old Japanese mother reprimands me harshly for being so anal about food. It’s all in your head!, she says, No matter how many times I scold her for cooking with soybean oil instead of coconut and getting a quick burger and fries at the local Carl’s Junior, she just laughs at me and pirouettes away to her dance classes, her 12 hour days of working in the garden, etc… God, I wish I had her energy, leanness, joie de vivre. The last time I was that lean and felt that good I was partying every night and getting most of my calories from alcohol and street tacos.
Now I read labels obsessively, make every meal at home with the most expensive and esoteric Paleo-approved ingredients. I avoid social settings where food is served, so I don’t have to eat “toxins.” I’m totally isolated and neurotic, but at least I’m eating the healthiest way possible, right? Aargh! Maybe my mom is right.
Denise, if these studies are true, Kempner’s diet sounds way more effective (not to mention cheaper and simpler) than the Paleo diet. We should all be on it!
But… If we’re not doing an ULTRA low fat OR low carb diet, is this article even relevant to us? Do macros matter at all outside of these slim and hard to maintain magic zones?
I think the answers to your questions might be in the following links. I used to do the low carb high fat diets and I did get a lot of health improvements but it stopped working. You can argue either extreme end of the diet spectrum, all backed up with science. I have been doing a starch based diet for less than a week and I am already reducing my blood sugar medication, a clear sign my insulin resistance is improving. I like Dr. McDougal because he is just a regular doctor, not any of the other types that some people call quacks, and he provides all the information necessary for free, yes he does have books and money making things but all the information is free on his web site.
John McDougall MD – No added fats, starch based diet – His web site –
https://www.drmcdougall.com/health/education/newsletter/
Under the programs button there is one that says free McDougal program. Under the connect button there is a discussion board – where people talk about what happens with them, there is an area of success stories… etc.
This is a great video – explains very simply why some of us our fat – very intersting.
How to Lose Weight Without Losing Your Mind
Hi Robin,
I’m sorry to say it, but in many ways, your mom IS right! First of all, I’m sorry for any confusion or destabilized beliefs this post caused. I don’t want to usher otherwise healthy (non-diabetic/non-heart-disease-suffering) people onto unnecessarily extreme diets; this is more an attempt to explore the mechanisms behind macronutrient interaction, with the ultimate goal of applying the relevant findings to less rigid diets (in the form of macronutrient cycling, designing meals to improve insulin sensitivity, etc.). That’s what Part 2 is going to be about.
I will say that stressing out over food is often more harmful than the food itself. Especially if the anxiety about toxins is preventing you from enjoying life and harming relationships (I definitely went there as a raw vegan). The answer probably isn’t alcohol and street tacos, but on the net, health will generally improve if we trade small sacrifices of ‘food perfection’ for a wider range of fulfilling experiences and less self-imposed stress. 🙂
what if it’s really about the microbiome in the gut, and what’s operational in all the different diets is the change of diet which causes a change in the ecosystem of the gut. What matters is to make the change and reduced calories, not the particular macronutrients and their ratios?
Robin, I feel your pain. Your wonderful Mother sounds wise.
oh yey! does that mean I can drink Coca Cola again ?
Nope! check out this video –
This is a great video – explains very simply why some of us our fat – very intersting.
How to Lose Weight Without Losing Your Mind
Rebecca, please stop posting the same video over and over again. For some of us who are following the comments it’s a bit annoying to keep getting the same thing. We all got it and saw it many times over. Here is one just a few lines above your last post.
Thanks.
Sorry, I did not know if it was just going to the person I replied to or if everybody saw it. Thank you for letting me know.
Very interesting post! I read every word- (i.e., it’s just the right length)- and am looking forward to Part 2. Although I seem to do best with LCHF, and had terrible health problems when I tried high carb with very low fat, I totally agree with you that we can’t dismiss the evidence when it seems to contradict what we think we know. So I find this quite fascinating…..and it proves, once again, that different approaches work for different people.
Most interesting for me was the rice/fruit/refined sugar diet- (I just can’t wrap my head around that one!) I’m wondering about fasting, or caloric restriction (as another poster mentioned earlier on). For instance, maybe the reason wartime rationing seemed better for health was due to caloric restriction…..maybe it had nothing to do with a single “element” (fat, sugar)? And maybe, if the body is used to eating lots of fat as well as carbs, reducing one (in this case, fat)- makes the body “think” it’s fasting? (In a similar way to being in ketosis?). In fact, maybe any kind of sudden, extreme dietary change puts a stress on the body, which causes hormesis. (?) Could be a possibility, anyway.
Another thing I wondered about was leptin resistance. Possibly some of the overweight/diabetic people they tested overate because they didn’t feel satiety cues, and when they were put on a diet that heavily reduced fat and salt- 2 of the things that often make people overeat- maybe that helped to regulate their satiety signals? (Probably most people would be less likely to overeat sugar when it comes without fat). It sounds like it was a pretty unpalatable diet, so that may have had something to do with it’s success.
These are only just thoughts, I don’t really know…..therefore, I’m looking forward to hear what you have to say in Part 2.
This video is all about satiety signals and why people are affected differently.
How to Lose Weight Without Losing Your Mind
Attachments area
Preview YouTube video How to Lose Weight Without Losing Your Mind
Thank you for including this.
smokes…
When you said “When it came to blasting obesity, Kempner employed what he called a “rice-reduction diet”—the same protocol he’d designed for renal failure and hypertension, but with lower calories”
and posted the cool pictures, did it look great. Look how much weight they lost. 0.3kg per day… holysmokes.
Finally gotten around to looking at the paper
Lower calories indeed
The initial diet prescribed for most patients (“unmodified rice/reduction diet”) is a low-calorie (400 to 800 kilocalories [kcal]/day, average, estimated)
And then – Always, the prescribed diet is low in calories (less than 1,000 kcal/day)
Under 1000kcal for big fatties… no wonder they lost so much weight.
Craig, it doesn’t matter whether I wallowed in the Swampland or ate <10% fat. If you look closely at the results of these ultra-lowfat diets, average post-study BGs were on average WAY higher that the BGs I now enjoy, and eating infinitely more satisfying foods. Normal fasting BGs are 75–95. I was T2D in 2007, and since *normalized* my BGs with LCHF, averaging 90 mg/dL. Kempner's Rice diet did NOT, in the main, resolve diabetes. The average fasting blood sugar (FBG) for folks after 22 weeks of the Rice Diet was 155 mg/dL! That’s still diabetic! About the Pritikin diet, looking at the study Denise gives, (http://ajcn.nutrition.org/content/29/8/895.full.pdf , Table 2, pg 895), the average post-study FBG was 136–still diabetic! Same thing for a Pritikin 1983 study: post-study FBG average is 133 mg/dL. (http://care.diabetesjournals.org/content/6/3/268.short). If the other ultra lowfat diet studies Denise cited here discussed BGs, she didn't include that discussion in this blog post.
Your experience is interesting to me. To be back at 90 after being type 2 through a high fat diet is. Ot something I’ve come across.
How do you manage to eat such high fat yet low protein? I can’t think of mix of foods that would result in such. And presumably your not concerned re fats and CV disease?
Craig did you get my response to you I posted within the last 12 hours? That details what I eat? I don’t see it here.
Nothing posted
Craig, coulda sworn I posted the answer earlier. Anyway here it’s again, New & Improved etc: The fats I mainly eat are: coconuts, avos, fruit oils (c’nut, olive, red palm, avo). Some nuts/seeds, too, esp low-omega-6 pufa stuff like macadamia nuts, sprouted almonds, and sprouted sunnies. Finally, high omega-3 fish mostly cans of red/pink salmon (w skin and bones) and sardines, less often herring and smelt (whole). For protein (besides the fish), mainly eggs (usu 2x/day), and non-cow cheese. Occas fermented soy, almost always natto.
About dietary fats and CVD, I don’t worry about it in the least. Excess carbs are a MUCH greater risk. Dietary fats are large nearly non-polar molecules–very low-soluble in blood–which our neuron-rich GIs can vet very well in the duodenum. There, our bods bring the needed trigs systemic via chylomicrons and let the excess fats wend down that long and winding intestinal road to the exit. We have less choice with carbs. Carbs quickly break down into the simple sugars (glucose, fructose, galactose), very small highly-polar molecules that easily diffuse across membranes and into our bloodstreams, even in our mouths. To see what I mean, chew on bread for 3–5 min and note the emerging sweetness. Sugars are VERY soluble in blood. Thus they force us to deal with them systemically, and we do so by turning these excess sugars into long chain saturated fat (specifically 16C palmitic acid) which we store in our adipose tissue–and in those intramyocellular layers you discussed earlier. For the past nine years my blood panels have borne out this biochem. My trigs are 45–65 mg/dL and my total c’stol is 200 mg/dL–the low point for all-cause mortality per the NHANES studies.
I’ve got a new doctor who doesn’t believe in blood panels wbryanh….augh….the hypochondriac and former T2 diabetic in me wants those tests for historical record anyway…
My last panel in 2014 was 90 blood glucose, 38 tg, total cholesterol under 200 and HDL of 67. I achieve this with exercise and maintaining my weight slightly over. As far as diet goes, I lean towards Paleo in emphasizing meats and not excluding saturated fats, but I also eat any kind of carbs and end up somewhere around 50-60% carbs, 25-30% fats and 10-20% protein. It’s not much of a shift from what I ate T2 diet-wise, and it’s considerably more calories. The difference is 2-3 hours a day of walking and biking, which appears to metabolize calories of any type (about 1000 calories per day – the typical ancestral Paleo activity level according to Cordain) not very long after they enter the blood stream. There are no bad calories if you’re turning them ALL into CO2. Doesn’t matter whether they come from duck, oysters or poppyseed cake, they all burn up and are gone by the next morning.
Because of the way I do this, I’m probably carrying full glycogen stores all the time. If I were to go low carb for a few days I could probably drop those 5 pounds. But there’s no point, since I am constantly depleting and replenishing those stores by exercising. For the low intensity exercise I do, sugars and starches are the advantaged foods. If I was exercising at higher intensity, fat would have the advantage, but the sugars and starches would still get metabolized.
thhq, no question, we have many problems with the current state of blood panels. First, how relevant are the tests? E.g. measuring lipids measures only the levels of lipids, free, in LDL, in HDL, etc. they don’t measure the actual # of lipoproteins the lipids are carried in. E.g. do you have many smaller more oxidized lipos which are thought to be atherogenic? Or fewer larger “fluffy” newer, less oxidized lipos, considered to be relatively non-atherogenic? No way to tell based on the current default measures. Second, docs and hospitals say or imply that for total c’stol, “lower is better” though if you went to zero you’d be very dead. NHANES suggests that c’stol levels much below 150 mg/dL starts to greatly increase mortality, though from causes other than CVD, eg hemorrhagic stroke and cancer. Various biomarkers coming and going a lot these days, e.g. in the aughts Apolipoprotein (a) was a “for sure” marker of CVD, now dropped at least at my HMO (Kaiser)
All that said thhq, blood panels are better than nearly all the research papers out there, with poor methodologies and highly questionable stats massaging e.g. “p-hacking.” See here:
http://io9.com/i-fooled-millions-into-thinking-chocolate-helps-weight-1707251800
That plus the many agendas of the big money interests that back so much of today’s research, I put almost zero stock in them. One of, if not still THE most downloaded research paper from PLOS of all time is ironically titled: “Why Most Published Research Findings Are False.” You can read it here:
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124
When it comes down to it thhq, it’s nearly impossible to do a study that meaningfully relates chronic health and nutrition. The lag between introduction of causitive factor–nowadays while we’re still in the womb, and onset of symptoms, often decades later, plus that we live in a vastly complex world with hundreds of thousands of novel factors, together makes it impossible to meaningfully associate causes and effects.
About macronutrient balance, thhq, I agree it shouldn’t matter. Kitavans on HCLF, Inuit on near zero carb, etc. After all glucose is essential for a handful of cells, e.g. some brain and adrenal cells are obligate glucovores. We should have at least 40–45mg/dL BG to function properly. Thus we need insulin and insulin sensitivity to dispose of BGs into cells/mitochondria. Carbs were a relative rarity in pre-ag days, so our bods evolved five ways to increase BGs–including our livers make glucose as (perceived) needed–but only one way (insulin) to lower them. We crave carbs because it’s the fastest way to lay in fat–super important back in the bad old days when we routinely went days between meals. More body fat meant more days we could survive without eating.
Thus we need to look beyond the endless HCLF vs LCHC debates and try to learn what’s making so much of our planet carb intolerant? It goes beyond the old “eat less/exercise more” trope. I suspect the huge raft of novel organic compounds–over 100k now–that Big Chem’s been churning out since 1945 and are which on so many of the product we eat and use. Many of these, e.g. BPA and phthalates, are estrogenic, leading to IR –> metab symdrome–> diabetes and other chronic diseases. Also since WWII: routine use of antibiotics that wipe out our gut microbiomes, perhaps permanently disrupting our delicate sugar metabolic dance.
No question exercise a big factor for you thhq. Per what you say, exercise normalized your BGs FOR NOW even though you are back to being basically HC. But do you still suffer high serum insulin levels? If so, your BGs may once again creep back up regardless of your workouts. Get the euglycemic clamp if you can aford it, get the C Peptide test in any event. Basal serum insulin should be low, poss below 1 ng/dL. H-Gs measure out as low as 0.2 ng/dL.
I’ve never had serum insulin tests. My T2 was diagnosed from fasting blood glucose repeats of 190-200, and A1C of 8.2 eight years ago. I just had my annual checkup. My doctor refused doing even routine lipids. He claimed there is too much testing these days, and had the attitude that the tests were only interesting to him and not to me. Fat chance he’d have scheduled insulin. I was ticked because I was fasted and ready for sampling. I might change doc’s next year, but I’ve used up my covered checkup for the year.
I’ve often thought an index of ancestral compliance. Because of my personal experience with exercise, I give active vs sedentary living more weight than diet. Motorized transportation and electronic entertainment carry far greater weight than eating a diet of grass-fed liver, bone marrow and beets IMO. I know that modern factors such as BPA’s etc are important, but secondary to the dietary shift to eating vegetable oils, sugars, and starches far in excess of a person’s metabolic needs. Eating the bag of Cheetos does more damage than the BPA’s in them. They’re the chemical gravy on top of all the fat, salt, cornstarch and fake cheese.
Docs typically don’t do C Peptide unless asked. Took me ~ 3 years to get my doc to sign off on the blood panels I want. It’s a cost vs patient insistence issue, and my pestering started to prevail finally. Now he praises my “awesome BG control–best of all his patients.” Plenty of ppl should be getting A1c along with FBG , but don’t. HMOs etc always trying the rein in costs. For me, exercise is ~ 15% of the matter, diet/non-diet exposures the rest. Heartily disagree that undeclared toxins like BPA and phthalates are necessarily secondary. For some perhaps many, these ubiquitous estrogenics are HUGE. When I first diagnosed I was walking up to and resistance training and BGs still started spiraling out of control. The final day, 29 July 2007, I walked 30 miles eating Clif Bars along the way, 300 cals each one every 2 hours. BGs went from 80 to 245. That day, went LC and gradually started replacing engineered food with whole food. Even now, when I eat foods with BPA–the latest was Thai Kitchen coconut cream in BPA-lined cans–BGs popped from 90 to 130 and stayed elevated for 3 weeks. (BPA is fat-soluble). So back to more expensive but BPA-free Native Forest c’nut cream.
Another example: oxybenzone in Banana Boat sunscreen. One day in 2010, I did a 34-mile hike. Ate only 900 cals that day, mainly avocados. No problem, was fully keto-adapted, felt fine. But BGs rode in the high 90s that day, instead of high 70s/low 80s as had become normal even without the long hike. Next day, eating normal cal load, postprand BGs popped to 120s–130s and pretty much stayed 100+. Like with the BPA in the Thai Kitchen can, took 3 weeks for my BGs to correct. Went to EWG and look up all the ingreds in that sunscreen and oxybenzone sent up big red flags as a big-time endocrine disruptor. That was the first and last time since I started this journey in 2007 that I used sunscreen.
Regarding the craving for foods. I ‘ve always liked Guyenet’s reward explanation better than Taubes’ carb insulin opinions. We crave foods that gratify our taste. I crave a mixture of carbs AND fats. The highly craved chocolate chip cookie gets over half its calories in fat. The same is true of salty snacks like chips. There’s no satiation point eating foods like this because they taste so darn good. Fat and sugar are equal co-factors. Just eating a pure sugar lemon drop, or a pure fat butter stick doesn’t create the same effect.
If you haven’t read Hall’s recent study on the carb insulin theory, here it is. It takes expensive ward studies to test unsubstantiated journalistic theories.
http://wholehealthsource.blogspot.com/2015/08/a-new-human-trial-seriously-undermines.html
I’ve read this post, and take many issues with that study, as I do with virtually ALL of these studies. In this case, small sample rate, 6 days not long enough to get keto-adapted, looks only at normoglycemics not T2Ds, pre-T2Ds, it’s in a metabolic ward cutting out many exposure we get in daily life, etc. In general I find Guyenet has an axe to grind. He’s changed greatly since his Taubes contretemps and that makes me sad. Read his stuff before that Taubes event and Guyenet was refreshingly free of agenda. Now for him it’s all about agenda. All that said, it’s clear carb-only or fat-only brings on less craving than the combo, esp so if they are whole foods.
Guyenet compares the Hall study fat loss rates here:
“Metabolic measures indicated that the low-carbohydrate diet caused a 245 gram (0.5 lbs) loss of body fat over the 6-day diet period, while the low-fat diet led to a 463 gram (1 lb) loss of body fat over the same period.”
Other than reducing insulin secretion, where’s the advantage for rebalancing macronutrients to high fat? That’s about the amount of fat loss I would expect for typical 6 day weight loss dieting using calorie deficits on ANY macronutrient mix. I did that for six months and lost 50 pounds, without being at either low fat or low carb.
Hall goes farther and claims that carbs have a long term metabolic advantage over fats for weight loss, which obviously needs a much longer study.
thhq, again, big emphasis on “needs a much longer study.” And more. The Hall is so rife with issues and possible confounders that it demonstrates not much at all.
thhq- I “hear” what you’re saying about food reward with carbs and fat (my downfall is cashews roasted in coconut oil and salt). However, there are also times when, for “dessert”, I enjoy a nice soft goat cheese drenched in high quality olive oil: fat + fat! In any case, although I do believe we *experience* food reward- otherwise we might not be motivated to get the nutrients we need- I never really thought it was a very good explanation for the obesity epidemic. For one thing, I notice that since I’ve gone low carb, my desire for sugar has dropped way down, so I’m not convinced that our “desire for sugar” is as innate as some people claim. (I still crave moderately sweet foods, like coconut or pumpkin or some fruits; this makes sense, because of the nutrients involved; table sugar is just too cloying for me now). I think that our society’s sugar addiction is probably cultivated. When you think about it, we are weaned onto sugary foods from the time we were babies.
As for the study you posted: I’m not really sure it proved anything. For one thing, both Stephen Guyenet and the study authors mentioned that they reduced the fat in the low fat group more than they reduced the carbs in the low carb group. Also, such a short study doesn’t really prove much. If people have been “sugar burners” all their lives, it takes time- (more time than the study lasted)- to make the metabolic shift for the body to start burning fat efficiently, rather than sugar.
Lastly, I’m not sure the carbohydrate-insulin hypothesis states, specifically, that “all people who eat high carbohydrate diets” will get fat. The implication is that some kind of metabolic damage happens in the body- due possibly to excessive sucrose (or some implicate mainly the fructose part), or maybe something else in our environment, as wbryanh has suggested- which causes insulin resistance. Excess insulin is well documented to put on weight in most of us- (for instance, diabetics who need to take lots of insulin often put on weight). In any case, the people in the study you linked to were all overweight, BUT they were all metabolically healthy. Which could have made another difference in the outcome.
Guyenet SUPPORTS low carb, but he doesn’t like disingenuous techniques. Taubes is sold by the word, and he knows that hubris gets him linage in NYT. Health and scientific accuracy are secondary concerns to selling his books and getting support from the Atkins Foundation.
Carb insulin is very simple: follow the money. Atkins sold millions in books and products, and that’s Taubes is after. As fellow New Yorker Boss Tweed said “I seen my opportunities and I took ’em.”
thhq, you say “Guyenet SUPPORTS low carb.” Just curious, since the Taubes-Guyenet contretemps at the AHS symposium in August 2011, when has Guyenet ever come out “in support of low-carb?” I’d love to see that, as I’m sure others here also would. Thanks in advance for sending us that/those link(s).
I don’t think Taubes’ “Good Calories, Bad Calories” is exactly a book that’s been written for the masses. Usually if your purpose is to make lots of money, you write books in a short amount of time, with simplistic language to appeal to a wide audience. And maybe Atkins made lots of money because there were many people who were desperate for help, as the conventional advice was not working for them?
As I read him, Guyenet supports low carb, but not necessarily high fat. Here’s a passage from 2014:
“I view the low-carbohydrate diet as a tool in the fat loss toolbox, but one that’s most effective as part of a broader overall fat loss strategy. In the Ideal Weight Program, both of our fat loss diets are lower in carbohydrate and high in protein. Our approach is to incorporate multiple diet and lifestyle factors that have been shown to impact food intake and body weight, rather than limiting ourselves to a single-factor intervention.”
http://wholehealthsource.blogspot.com/2014/09/low-carbohydrate-vs-low-fat-diets-for.html
This study he’s reviewing showed an advantage for low carb over low fat for both weight loss and maintenance over a year.
thhq, please think about what you just said. Bear in mind we have only three caloric nutrients: fats, proteins, carbs. Are you seriously suggesting Guyenet is supporting “low carb but not necessarily high fat?” If so, that means you have to go way up on the protein. And you can’t go much more than 30–35% protein due to the risk of nitrogen overload. That’s borne out in anthropological studies. No diet goes above that protein level, including that for the northern Greenland Inuit. They preferred the fat, giving the excess protein to their sled dogs.
Augh. Guyenet is involved in selling a diet plan…so he’s coy with details unless you buy in…
Here’s what I could get for free from Kresser’s 2013 interview:
Stephan Guyenet:
“Sure. Essentially we brought together several researchers including Dan, myself, and a behavioral scientist named Larry Carter, and we put together a program that brought together all of our various expertise to bear on this issue of weight loss. What we designed is an Internet-based, multimedia diet and lifestyle program for natural fat loss and maintenance. It’s a diet and lifestyle modification program that we have based on what we see as the most cutting-edge research to date, and it consists of two basic tracks. Based on a person’s individual goals, they get to select which track they want to go down. There’s track one, which is our most intensive weight loss program, most intensive, most rapid, most effective. This is based around a diet that we designed. It’s called the FLASH Diet. FLASH stands for Fat Loss and Sustainable Health, and this is essentially a high-protein, low-carbohydrate, low-fat diet that’s relatively low in energy density, and this type of diet has been studied extensively in the biomedical literature. It is hands-down the most effective rapid fat-loss procedure that is known, and so that’s what we based track one on. That’s the diet. There’s also a physical activity and a sleep component.”
http://chriskresser.com/what-research-says-about-losing-weight-and-keeping-it-off/
Like the man says, high protein, low carb, low fat – now pay me. The FLASH diet book has a picture of what looks like beef stew and veggies that look like celery on the cover. I can get a recipe for that anywhere. Why does everyone try to resell this as some special plan? I’ll admit that Atkins and Taubes are better at this sort of thing. Or South Park, with their manbearpig. Or Calorie Count, where you can get this all for free.
thhq, when you say “Guyenet supports low carb, but not necessarily high fat,” if it is indeed “low fat” then it can only refer to a temporary diet. This is NOT a foodway someone will follow for the rest of their days.You simply can’t maintain a low-carb high-protein low-fat isocaloric (typ 2000-2500cal/day) diet. That’s too much protein, period.
Guyenet’s diet plan in its broad macronutrient conception is like the Ideal Protein Diet, another popular low-carb-high-protein low-fat diet that’s been making the rounds recently: http://www.idealprotein.com/. Again, their promoters do not intend for you to make this a permanent foodway that you will eat for the rest of your days. Rather they mean you to follow this only as long as it takes to shed the pounds till you arrive at your target weight. My Dad followed the Ideal Protein diet and found it the least onerous of the many weight-loss diet programs he’s tried. Even though it’s near 60% protein, the actual amount of protein is reasonable because total calories is so low, 700-800/day. Go to this Ideal Protein FAQ and scroll down to #22 for the details:
https://www.idealweightandskin.com/Downloadable%20Files/IP/IP%20Frequently_Asked_Questions.pdf
Of course I didn’t read Good Calories Bad Calories!
I lost 50 pounds counting calories before I had ever heard of it.
Taubes says that what I do doesn’t work, from eating 50% dietary carbs to exercising.
But counting calories did work and continues to work. What would I gain by giving my money to someone who calls me out as a moron?
Have you read Eat Well and Stay Well by Ancel Keys? Or Nutrition for Life by Thompson and Manore?
Thanks morgana. I recently found this interesting piece on the body’s mechanisms to protect its weight.
http://www.nytimes.com/2012/01/01/magazine/tara-parker-pope-fat-trap.html?_r=0
It wants its fat back and will resort to dirty tricks to get it….
Another peeve here is that PUBLIC money has been spent to address the carb insulin assertion. The author of the unproven idea calls for those who question the idea to prove it wrong on their dime. So eventually they do. The rebuttal is that they are wrong, their methodology was wrong, ketosis did not take place, etc etc etc.
And who’s going to pay for the next million dollar ward study? How many times do they have to rebut it?
It’s starting to look like professional wrestling matches. Best two out of three falls wins.
What’s been done so far convinces me. High fat diet lowered insulin secretion 22% vs low fat diet. This should have promoted rapid fat loss, and a big immediate advantage over high carb, if the challenged assertion was correct. It didn’t. In fact, it was worse than that, because the fat loss was higher with the high carbs. This is enough to reject the carb insulin assertion IMO. And at the very least, the journalist’s follow-on assertion that high carb diets are ineffective for weight loss should be discarded by EVERYONE.
thhq, your passage: “High fat diet lowered insulin secretion 22% vs low fat diet. This should have promoted rapid fat loss, and a big immediate advantage over high carb, if the challenged assertion was correct. It didn’t. **In fact, it was worse than that, because the fat loss was higher with the high carbs**.”
thhq, my question to you: Where is your evidence to show that “fat loss was higher with the high carbs?” Where’s the study that compares HFLC and HCLF diets and determines the comparative fat loss on both diets?
thhq, your comment: ” [Taubes’] unsubstantiated journalistic theories.” What unsubstantiated theories?!” Do you refer to the GCBC chapter “The Carbohydrate Hypothesis, II: Insulin” starting on page 376? If so, Taubes he makes numerous references to researchers’ comments, e.g Haist and Best in 1966, Wilhelm Falta in 1925, Rosenzweig in 1994, Dole and Gordon in 1956, Yalow and Berson in 1965… Do you need any more?!
I don’t call it a theory. I call it an assertion. The problem with it is not GT’s lack of references. It needs verification, not researcher’s comments. Maybe the GT/Attia $40MM study group will provide the funding to Hall to complete his study. But I’m not holding my breath.
I actually did read the text of GCBC regarding exercise. GT has carefully crafted a series of N=1’s describing people who gained weight exercising. I’m in the process of doing that now, and it’s a good thing. When you’re 62, rebuilding lost muscle mass is key to body integrity (I have broken shoulder tendons to show for loss of musculature in that area). But to hear GT’s assertions, it was as if exercise was the devil and should be avoided, especially by anyone trying to lose weight.
After reading the restrictive high protein diet your father used I remembered Dukan. High protein diets work by starvation, forcing the body to consume its fat reserves rapidly while (hopefully) sparing muscles using the ingested protein. If you keep your total calories down to 500, the total protein calories are not excessive for the body to process. Very likely you will get into ketosis just from the extremely low calories. You will also preferentially metabolize fat (Thompson and Manore’s text is useful to understand why). High protein diets come with strong warnings on reducing exercise.
When GT talks about exercise being useless it makes sense in the context of the restricted calorie ketosis dieters who need to avoid it. GT doesn’t mention this context, and inflates his assertion to include everyone. Since GT’s carb insulin dogma rejects any form of dieting other than ketosis as ineffective it makes sense to avoid exercise. But only for him and his devoted LCHF acolytes. It makes no sense for me, or for HCLF dieters, or for non-obese cultures like Kitavan/Okinawan/French/Japanese, or for almost every pre-1900 culture, or for calorie counters, or for Weight Watchers, or for Cordain-style Paleos.
I’ve read enough of GT’s NYT assertions to get his Atkins-like drift on exercise, salt eating and carb insulin. That’s why I recommend that you read at least one standard nutrition text, if for not other reason than to understand that GCBC dogma is a very narrow view of the world. I don’t like having the pyramid or vegetarianism rammed down my throat, but I now know that a lipid is distinctly different from cholesterol, as well as the functional differences between VLDL, LDL and HDL. I didn’t know that before.
thhq, when you said “Of course I didn’t read Good Calories Bad Calories!” can you see how I somehow got the idea you didn’t read Good Calories Bad Calories? 😉
About Taubes and exercise, I certainly didn’t get your idea that he sees exercise as “the devil and should be avoided, especially by anyone trying to lose weight.” What particular passage(s) of his support your conception of this? Where does GT actually say “Exercise is useless?!” I took him to mean only that you can’t exercise your way out of the wrong diet. That was indeed my case. I was running half-marathons and doing 150-mile/day cycling climbing up to 15,000 feet of mountain passes in a day. Of course I was “carb-loading” according to the conventional wisdom of the day. Despite all this exercise I was still growing love handles and my A1c was creeping up, at 6.2% at the end of this heavy-duty sports stage of my life. Of course I wrote all this off as “bad genes” because after all I was eating “the right diet.” Certainly I feel exercise is important. For me, BG-wise, like I said earlier, it’s 15% of the picture. I do 8–10 minutes of resistance exercises each day and walk 5–10 miles every other day, sometimes run HIIT with 15- to 30-sec sprints. For me this exercise makes the diff between 70s and 110s BGs, but mainly it makes me feel GREAT. About what you say on Dukan, Thompson, Manore, yes, yes, understood all that ages ago. Where you say High protein diets come with strong warnings on reducing exercise.” again thhq please let me remind you NO high-protein super-hypocaloric diet is more than a **temporary fix** lasting only weeks. Please refresh your memory with my previous post on that.
thhq, in general, it strikes me you harbor some sort of animus against Taubes I can’t quite fathom. I honestly don’t recall most or even any of the things you say he said. If you can post actual direct quotes from him, I’ll stand corrected–I’m perfectly fine with that! But really what can I say? His LCHF proposal worked and keeps working splendidly for me. Good Calories Bad Calories literally saved my life or at least, all else being equal, greatly extended it. When you “recommend that I read at least one standard nutrition text,” thhq, I DID read plenty of similar of government-industry dogma and that’s what got me in trouble in the first place! Oh, as far what you say “I now know that a lipid is distinctly different from cholesterol,” thhq where did THAT come from? Cholesterol IS a lipid!
In general blood sugar will go down with exercise, but the opposite does happen with some people. My blood sugar used to go up too much every time I went to the gym, there was even a time I had to take a pill to control my sugar when I exercised. As I have made some improvements in my diabetes this no longer happens. This is one reason yours could have gone up.
Rebecca, you’re right, that was very true for me. And like it did for you, my BGs have gotten a lot better with my recovery through the years. BG spikes had to do with how long I strenuously exercise beyond the aerobic zone which causes us to kick into glycolysis, with our livers kick out glucose to quickly repair rent muscle tissue and otherwise try to make up for anaerobia. My answer it to make only brief forays into the anaerobic zone, leaving it again before my bod decides to go glycolytic. E.g. I do 2–3 minutes of crunches/supermans/pushups 3–4 times/day. And when running, I do full-bore sprints for only 15–30 seconds then spend ample time to recover back into the aerobic zone. Which pretty much describes mild HIIT – High-intensity Interval Training 🙂
If GT hadn’t bashed calorie counting and exercise I wouldn’t have so much fun picking at him. Eades is much worse, and it was one of his vicious ad hominems on Keys that piqued my interest in reading the works of the most important nutritionist rather than spending more time reading blogs of guys selling books and supplements. I worked as a research scientist (pulp & paper) for over 30 years and that affects my attitude too. I’m used to testing assertions fairly and accurately, both by people peddling chemicals and my own strange notions, and usually rejecting them unless they answered real needs (new products, improved performance, higher production, or lower cost). On rare occasions an assertion made it to the level of testing, and on extremely rare occasions one of those tests resulted in a permanent change.
The behavior I saw in the peddlers who failed a test duplicates the HFLC criticisms of Hall’s ward study. There were always immediate claims of unfairness in our testing, and a proliferation of new samples usually appeared to waste more of our time and money. These guys never walked away admitting that their products were dismal failures. Their lives were vested in their assertions, and we were the morons, not them.
Regarding GT and exercise, this passage parallels what I read in GCBC, though it was written earlier and apparently recycled into the book. This is the story of a man who got fatter by exercising:
“It’s difficult to get health authorities to talk about the disconnect between their official recommendations and the scientific evidence that underlies it because they want to encourage us to exercise, even if their primary reason for doing so is highly debatable. Steve Blair, for instance, a University of South Carolina exercise scientist and a co-author of the AHA-ACSM guidelines, says he was “short, fat, and bald” when he started running in his thirties and he is short, fatter, and balder now, at age 68. In the intervening years, he estimates, he has run close to 80,000 miles and gained about 30 pounds.
When I asked Blair whether he thought he might be leaner had he run even more, he had to think about it. “I don’t see how I could have been more active,” he said. “Thirty years ago, I was running 50 miles a week. I had no time to do more. But if I could have gone out over the last couple of decades for two to three hours a day, maybe I would not have gained this weight.” And maybe he would have anyway. If we trust the AHA-ACSM report he co-authored, there is little reason to believe that the amount he runs makes any difference. Nonetheless, Blair personally believes he would be fatter still if he hadn’t been running. Why?”
Read the rest to get the full context.
http://nymag.com/news/sports/38001/index1.html
This was not my experience, nor is the experience of others who have lost weight by exercising. [IMO this man was not counting calories and ate more than he exercised over 30 years. He didn’t take into account the slow loss in metabolic rate with age and kept eating like he was in his 30’s.] You can construct any defense you like for GT, but when I read something that directly contradicts my own experience I’m not inclined to buy that man’s books. I’ve got better things to do with my time and money. But like I said, I’ve got lots of time to quibble about GT. It’s a favorite pastime.
Here’s my short version summary on lipids. A lipid is a blood-soluble structure made of phospholipid, triglyceride and cholesterol, with a protein outer coating. The structure varies according to the function, and density varies with protein content. VLDL’s transfer triglygerides and contain the least protein, LDL’s transfer cholesterol out to the cells and contain the most cholesterol and intermediate protein, HDL’s recycle cholesterol back to the liver from dying cells and contain the most protein. The presence of a lot of HDL means the bloodstream is carrying low overall cholesterol concentration.
thhq, witnessing your growing anti-Taubes rant, forgive me for “fun” not jumping to mind. About GT’s view exercise, again, just can’t see how you feel he’s against it. About calorie-counting, if You have the time and the inclination to do it, then why not? You have time on your hands, as you say. I counted them for a while–even wrote a spreadsheet and plugged meals into it using USDA Nutrient Database data–and learned a lot from it. And it did help confirm I was on the right track. But as a life-long exercise, nope just can’t see doing it! Somehow homo-kind soldiered on for millions of years without counting calories, and my non-cal-counting grandparents and many of their peers lived to ripe old ages, late 80s and early 90s and older. In fact, in America, life expectancies have stalled and even reversed in some cohorts (e.g. middle-aged white men) and health expectancies have been going down for a long time even though we more of us than ever are diligently counting calories. There’s clearly other factors at play here besides failure to add up the grams of fats, carbs and protein we tuck into our maws.
About each camp trotting out the “scientific” research and reams of anecdotal data, yes, agree. I trust just about none of it, including Hall’s recent strange abortive effort and whatever few reports out there that find in favor of LCHF. Please revisit my post for you yesterday on “Why Most Published Research Findings Are False” or go straight here.
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124
The best we can do is sift through the different approaches and try them for ourselves and see which works best and get regularly tests. It’s not easy. It takes time and stick-to-itiveness. It takes careful recording and plenty of reflecting on the data you collect on yourself. The current state of blood biomarker tests is far from perfect. But it offers us the best hope to learn what food- and lifeway truly works for us.
About Taubes’ purportedly dim views of exercise, I read his piece in the New York Mag link you posted. He does abundantly caution the reader to not overestimate its role in weight control. But he also writes: “… [There are] excellent reasons to be physically active…We might just enjoy exercise. We may increase our overall fitness; we may live longer, perhaps by reducing our risk of heart disease or diabetes; we’ll probably feel better about ourselves.” Thhq, reading this, how could you ever construe what GT says to mean “…exercise is the devil and should be avoided”?
Thhq, finally, your statement “A lipid is a blood-soluble structure…” is wrong. You confuse “lipoproteins” with “lipids.” Lipids are *not* blood-soluble. That’s why our bods need to tuck them into lipoproteins which *are* blood-soluble. These large sphere-headed “ferries” then deliver lipids (e.g. fats, sterols) to cells all around our bods via lymph and blood. What you list–VLDL, LDL, HDL–these are all lipoproteins, NOT lipids. Which leads to one of the big failings in the standard lipid blood panel. To repeat from a yesterday post to you: These panels tell us only the levels of lipids, free, in LDL, HDL, etc. They don’t measure the actual number of lipoproteins that carry these lipids. E.g. do you have many smaller more oxidized lipos which are thought to be atherogenic? Or fewer larger “fluffy” newer, less oxidized lipos, considered to be relatively non-atherogenic? No way to tell based on the current default measures.
wbryanh you’ve really skipped over the observation that GT bears a grudge against exercise because it intereferes with Atkins weight loss ketosis. You’re not supposed to do exercise. The preferred metabolism route for fats is staying completely sedentary. This is key to understanding why GT piles up his typical mound of ancient research reports and anecdotes attacking exercise as a valid weight loss technique. My personal experience pretty much matches Ancel Keys 1959 predicted metabolic effect of 70 calories per mile walked at my weight and walking speed. I was sustaining 2 lbs of weight loss per week (on the scale) by walking 10 miles a day and restricting food. You need to track calories daily/weekly/monthly to lose weight this way. Keys called this method of weight loss Scientific Reducing in 1959, it’s called calorie counting now.
I find after 8 years of weight maintenance that I can carry calorie totals in my head (food and exercise), and I mark them down at the end of the day. I total counts using exchanges – units of 70 calories – a methodology I learned when carb counting to control diabetes and very similar to Weight Watchers points. A very simple methodology. When I walk into a Italian restaurant and have an order of pasta with a glass of wine and bread I know exactly what I’m doing to maintain my weight. I prefer this to the technique that you use. I like pasta and bread and I’ll eat your portion for you thankyouverymuch.
You are correct. I meant soluble lipoprotein and said lipid, which is insoluble. Doh. Your original assertion though was that VLDL, LDL and HDL are cholesterols and they are not. HDL for instance is 50% protein, 30% phospholipid, 17% cholesterol and 3% triglyceride according to my text, though other people publish somewhat different compositions. Now a question about what the lipid panels actually test. You say that the measurement is a test of ONLY the lipid associated with each lipoprotein? Not the protein and cholesterol?
Um, I don’t think so. I’ve read Good Calories, Bad Calories- (4 times, in fact!)- and I never remember Gary Taubes saying this about exercise. I think you’ve got that wrong. What he does say is that exercise usually raises appetite, so some people eat more, thereby making it difficult to maintain a reduced calorie, weight loss diet. (Of course, exercise can also make a person more insulin sensitive; which is why I think it works for you, thhq; but we are all metabolically different, and exercise alone doesn’t work for some people; especially possibly very obese people). Gary Taubes talks in his book a lot about how the body adjusts to calories and movement, as it tries to hang on to its fat stores. For instance, if you eat less, you tend to move less (the body is trying to conserve energy); or if you move more, the body feels the need to consume more calories. The book basically explains a lot about the mechanism of hunger, and how that applies to weight loss; which I think is phenomenal, as many books don’t touch on this issue. As far as I know, Gary Taubes doesn’t have anything “against” exercise. And it’s perfectly possible to exercise on a low carb diet. I exercise pretty much constantly- (my job requires it). I find it much easier on a low carb diet; partly because I digest my food better, so I have more energy to move. Also, I’m not distracted by that constant niggling hunger that I had when I ate high carb. I’m not saying everyone will feel the same as I do on this diet- there is no “1 size fits all”- but I just want to dispel the myth about low carb diets and exercise.
What you say Morgana, plus to put another way the insulin-sensitizing effects of exercise, exercise literally “feeds” you. The nutrients–e.g. BGs, lipo-ported fats, etc–are coursing around in your blood, and exercise “opens” the cell doors and lets them in. So often I’ve felt peckish when heading out for a walk or run and lose all appetite and feel great when I’m walking.
Um, NO, thhq, what you say here is dead wrong: “Your [wbryanh’s] original assertion was that VLDL, LDL and HDL are cholesterols…” I said that nowhere. Look again. You won’t find this. I do say “E.g. measuring lipids measures only the levels of lipids, free, *in* LDL, in HDL, etc…”
I am beginning to understand how you can misread and contort what others say.
You ask “You say that the measurement is a test of ONLY the lipid associated with each lipoprotein? The answer: Yes. Fats and sterols are lipids. The lipid panel measures only lipids in lipoproteins. The standard lipid panel looks just at total amounts of triglycerides and cholesterol spread out in some unknown number of lipoproteins. We should directly measure the # and size of lipoproteins themselves so we can better assess atherogenicity. Researchers are developing methods to do just that, including VAP and NMR tests. But last I heard these tests are not yet ready for prime-time.
About Taubes on exercise, you say “…GT bears a grudge against exercise because it interferes with Atkins weight loss ketosis. You’re not supposed to do exercise. The preferred metabolism route for fats is staying completely sedentary…” Thhq, Do you have GT quote(s) that say just those things? Would you mind posting them here? Going forward, it’d really help if you just post actual author quotes instead of giving us only your interpretation of what who-and-who said. And again, GT wrote: “… [There are] excellent reasons to be physically active…We might just enjoy exercise. We may increase our overall fitness; we may live longer, perhaps by reducing our risk of heart disease or diabetes; we’ll probably feel better about ourselves.” Thhq, reading this, I think most people would understand that GT is most definitely NOT anti-exercise. But if you’d rather, just keep ignoring direct quotes like this from Taubes and others and instead keep plopping here what you “think” Taubes and others said. Just don’t be surprised if I stop paying attention. I am glad though your weight-loss method worked for you. Anyone who loses 50 pounds and keeps it off deserves kudos. I know a few people who got fluent in a exchange point system and are very happy with it.
er… change to “not the protein?” The cholesterol goes with the other lipids, as you say. Wish this blog would allow editing.
And in attempting to answer my own question, I found a method used by Johns Hopkins
http://www.cdc.gov/nchs/data/nhanes/nhanes_03_04/l13_c_met_lipids.pdf
I may screw this up, but here’s what it looks like to me:
Total cholesterol, triglycerides and HDL (with the non-HDL cholesterols rendered non-reactive) are measured separately using different series of reactions which release peroxide. The peroxide concentration is measured after treatment with peroxidase to get a color change, of which the intensity is detected by a spectrophotometer (UV?). VLDL is derived by dividing triglycerides by 5, and LDL is derived by subtracting HDL and VLDL from total cholesterol.
So the test is done on the cholesterol in the serum. It measures the cholesterol associated with each lipoprotein, but does not measure the lipoprotein concentration itself.
Thhq, cholesterol and triglycerides have little or no solubility in blood. Maybe testers need first to liberate the lipids from lipoproteins, have them enter serum in the lab before testing them? Anyway, the issue’s really about the atherogenecity of the lipoproteins themselves, not their lipid cargo. Esp as the lipos age, oxidize, get smaller.
http://www.sciencedirect.com/science/article/pii/0891584995021736
Once again wbryanh I stand corrected. I have put the words of my doctor “HDL is good cholesterol, LDL is bad cholesterol” in your mouth, and your version is much more correct than his. This doesn’t get us any further than your proving that I am a moron, but maybe I learned something….if I don’t forget it before my next blood panel…whenever that is…
As far as finding you some choice GT comments on exercise, here’s his summary of the New York magazine article earlier cited, in a chat with Jimmy Moore
“The only real way to test it would be to do a randomized controlled-trial and those are difficult to interpret because as soon as you instruct people to exercise or diet in these kinds of studies you get all kinds of unpredictable psychological and interventional effects. The trials that have been done suggest that exercise has no effect. And as I pointed out in my article in New York Magazine, the world is full of plenty of people who exercise diligently and continue to gain weight from year to year, including several of the world authorities on exercise and weight loss.
If you look at animal studies, it’s pretty clear that animals respond to exercise by eating more and the exercise has no effect on fat accumulation. And while it’s true that part of the job of fattening geese and cattle is immobilizing them, it’s not clear that those examples are relevant to real life. It’s not that I don’t think exercise is good for you because, Lord knows, I do enough of it — as my back and my arthritic knees will attest. I’m just not so sure that the causality goes in the direction that you think it does.”
http://livinlavidalowcarb.com/blog/taubes-is-weight-loss-from-exercising-or-are-you-exercising-because-you-lost-weight/2734
Compared to the straw-man failed weight loss exercisers GT pictures, my personal trial produced steady weight loss, and the causality went exactly where I expected it would at the rate of two pounds a week for six months. This is just the way Ancel Keys predicted that it would go if I used Scientific Reducing. Maybe I’m misreading something (and you’ve seen that I’m prone to that), but it also appears to me that GT does not even accept the idea that sedentary animals that get fat can be compared to humans…
I don’t see a lot of support for exercise in that quote, but I’m sure that you can find some sunshine. I’ll find more quotes if you like, but I might have to go to the library and dredge around in their cc of GCBC, if they still have one.
OK thhq, I reread the exercise sections in GCBG, and GT’s NYMag piece and transcript of Jimmy Moore interview you posted. I see the confusion now. You did not read all of GCBC, but just the sections on exercise. You lack the default context and conditions GT presented to properly understand what he wrote about exercise and weight gain.
To be clear, GT doesn’t deny exercise *per se* burns calories and fat. In GCBC (pg 260) he gives this quote from researcher Russell Wilder: “The patient reasons quite correctly that the more exercise he takes the more fat should be burned and the loss of weight should be in proportion…” Nowhere does GT assert that someone who 1) starts exercising AND 2) eats the same or less caloric load as during his/her pre-exercise days will still gain weight. That’d be silly.
GT most discusses exercise on pp 259-269. In the preceding copy, GT discusses the default conditions in which some people who exercise a lot still gain weight. He assumed we’d bear in mind the default context and conditions he previously and amply laid out. These include: 1) eating very high-carb SAD, 2) not counting calories thus eating *ad libitum*, and 3) doing sustained strenuous workouts. Under those conditions, of course many dedicated exercisers will struggle with weight. Those three conditions give an ideal prescription to keep us mired in full-blown glycolysis, keeping many of us, esp the insulin-resistant and in metab syndrome, in a cycle of madly chowing and madly exercising. Who among us here doesn’t know at least one person who went/is going through that discouraging process? Including me, thhq, as I posted to you about earlier. All my running and cycling, and I still got love handles and T2D.
Thhq, here we see the risk of picking snippets out of his treatise on this complex topic. In GCBC, GT lays out a long buildup, giving context and conditions, to finally present his carbohydrate hypotheses starting only on page 355. If you take time to read GCBC from the beginning, his exercise hypothesis will make sense to you. You’ll see it doesn’t at all refute your own experience. You stick mainly to aerobic–not anaerobic–exercise which preferentially burns fat, You do count your calories and so keep a lid on how much you eat. You do eat whole foods, not the SAD. Taubes default conditions with which he developed his exercise-weight gain hypothesis in no way applies to you.
wbyanh, I’ve given you TWO long passages where Taubes berates exercise as a tool for weight loss. The NY Mag piece predates GCBC, and is recycled into it, and the strategy is the same. The NY Mag piece is written in his awful, disingenuous, ingratiating prose (another reason I can’t read GCBC – I’m used to reading Proust, not hack biographers – 800 pages of this journalist-speak would drive me up the wall), and softens the blow for the general audience. The Jimmy Moore piece, before a friendly audience, cuts to the chase, and GT explains what he was up to when he wrote the NY Mag piece:
-He admits INTENTIONALLY picking N=1 examples of people who gained weight exercising. Where’s Jack LaLanne? Where’s Ancel Keys? Where’s durianrider? Where’s ME? It’s as if all of us who have lost weight exercising don’t exist. There is no counterpoint, just the examples that gained weight. I call this hard evidence that GT IS a cherry picker. [I expect you to ask me again to read all 800 pages of GCBC so I’ll get it. That’s not happening. I ‘ve got all I need right here.]
-He derides the use of controlled studies to test his assertion that exercise is useless for weight loss. Everyone already knows that, studies are expensive and hard to control, it’s like the sun in the sky, and if you don’t believe it…like I said earlier, but now it’s GT actually saying it.
-He talks about exercise as something that damaged his body. He’s cherry-picked himself on this one. I’m sorry it didn’t work out for him like it did for me. Exercise HEALED my body – not just the blood tests, but the weight loss, the higher HDL, the lower blood pressure, etc. GT is calling exercise destructive, not selling it as critical or even useful to lose weight. Right after that he talks about how animal sedentary obesity is not comparable to human sedentary obesity, implying that sedentary behavior is possibly OK (but not coming right out and saying that, just wheedling and insinuating it in his awful way – I’d like to hit him in the head with a copy of Dr. Atkins Diet Revolution at this point…at least Dr Atkins doesn’t beat around the bush about how to get the best results from ketosis dieting).
When I came into my doctor’s office after counting calories for a year, bringing my blood tests into line, and losing 50 pounds, my doctor shook my hand. When I read what GT wrote, and listen to his attitude about what he wrote via Jimmy Moore, I’m not seeing ANY support for what it took me a year to accomplish using exercise. I’m not getting a pat on the back or a handshake from GT for what I did. I’m just another cherry that GT intentionally overlooked when he was carefully picking his tree.
You found the book, used it, it helped you, and that’s great (though you could have saved a lot of painful reading by just using Diet Revolution). If you had lost weight the way I did, you might be more sympathetic with my objections to GT’s assertive “my way or the highway” mentality. As one very healthy vegetarian told me “If GT was right I’d be dead”.
thhq, you completely miss the point in my previous post. Please reread it and try again.
Or thhq maybe don’t bother to reread my post. At this point, you’ve made it so abundantly clear you harbor an animus to this man which goes way beyond “fun” as you earlier called it. You persist to think those few actual GT quotes you bothered to post has him actually say anything categorically bad about exercise regardless of context and conditions in which the exercise is done. You keep irrelevantly discussing things that refer to GT’s style that you find objectionable rather than sticking to facts. Here thhq you say “The NY Mag piece is written in his awful, disingenuous, ingratiating prose (another reason I can’t read GCBC – I’m used to reading Proust, not hack biographers – 800 pages of this journalist-speak would drive me up the wall)” Well thhq, that’s your *opinion.* Full stop. I think you can find many people who feel far differently from you about it. You say “He talks about exercise as something that damaged his body, the closest GT statement I could find that even comes close to what you are talking about is this from that 2008 Jimmy Moore interview: “It’s not that I don’t think exercise is good for you because, Lord knows, I do enough of it — as my back and my arthritic knees will attest..” First, GT actually SAYS he regularly exercises. If he truly felt exercising was useless and even damaging why then would do it? Second, he doesn’t blame exercise *per se* for the damage. He leaves the door open to the possibility that he could be doing them wrong.
Once again thhq you simply refuse to ackowledge the direct GT quotes I’ve posted for you because they don’t suit your pre-conceptions. You pride yourself on rigorous intellectual remove, yet it’s so clear you let your emotions influence and even pervert so much of your thinking. Well then fine. Please just go on irrationally hating on Taubes convincing yourself you’ve somehow supplied real evidence that justifies anything at all, meanwhile wrapping yourself in your intellectual science-y cloak. I won’t stop you! But I will no longer waste my time to continue to post solid information you persist to completely ignore.
I give up wbryanh. You have asked me to read GCBC and I will not do that. I don’t need to. I realize that this book is very special to you, and that GT is very special to you, but you treat this like GCBC is the Bible and GT is Jesus. It’s like you are personally affronted because I do not worship these holy things. Thanks for the discussion and the schooling on lipids anyway.
Sure thhq, you can assume those things or anything you want if it makes you feel better. Far be it from me to try to disabuse you of your high-flown notions. But, bottom line, you have found a system that works for you, at least according to the health measures you have chosen to get to date. You certainly have to work at it but, from all you’ve said, you are enjoy enduring success where many (most?) do not at this time. In all seriousness thhq you deserve all the pride and happiness you feel in that achievement! Please be happy. Take care. –Bryan
And you misunderstand…it was fun to jib-jab on this subject, but I’m tired and need a rest for a while. Back to Thompson and Manore for a reread, or a few more longevity studies.
I’ve read and reread your comments wbryanh. My chief objection is that the NY Mag article has to stand on its own. In rereading it I realized that GCBC predates it, and that it is the GCBC exercise chapter with some modification. It has to stand on its own nevertheless. For every million people that read it in the NY Mag, maybe 1000 bought GCBC, and maybe 100 of them read it from cover to cover. It is not reasonable to say that the people reading the article should be familiar with GCBC in context, and be able to quote chapter and verse to support GT’s assertions. GT has the bully pulpit in NY Mag before the mass audience, and what he says has to be taken at face value.
I don’t see this as an entirely negative approach. GT has challenged CW, and for some people this is the shock treatment they need to deal with their obesity. From what you’ve said it helped you in that way. And there’s no doubt in my mind that HFLC is an effective way to reduce weight.
There is a strong negative effect though. The average reader, who does not go on to buying and reading GCBC, is left with the impression that exercise will cause them to gain weight. They might as well have another stack of pancakes and watch TV for all the good going for a walk would do them.
Four years later there is no reduction in US obesity rates. This despite the best efforts of GT, Oprah, Dr. Oz, Pritikin, Atkins, calorie counters, Weight Watchers, Dukan, South Beach, etc etc etc. That’s the really SAD thing. Despite these wake-up calls from so many concerned people no one is paying attention to their very real health problems.
thhq- do you have a link to this NY Times article, so I can read it? (You may have posted it; if you did, I didn’t see it, and things can get lost so easily in this huge comment section). I seriously don’t remember Gary Taubes saying anything bad about exercise. What he does debunk is the “eat less, move more” mantra, explaining why that doesn’t work for the majority of people. It all fits together with that link that you posted recently (which was interesting, thanks)- about how the body tries to hold on to its fat stores. “Eat less, move more” can work temporarily, but the problem is, either it is too difficult to maintain indefinitely- (people either become hungry again and feel the need to eat a normal amount), or the body conserves energy on a low calorie diet, so people burn less, or even have a hard time exercising.
What might also confuse the issue is that- in terms of pure calories alone- it has been discovered that exercise burns off fewer calories than one might think. There is science to back this up- (if you want a link, I can try to find one). So, exercising alone will not enable the majority of people to lose weight, or at least not much weight. However, It DOES help one maintain weight, i.e., you’re less likely to put on more weight if you exercise. But it can also raise appetite, so that can be problematic for some people, as they would need to keep a calorie deficit if they have lots of weight to lose. (As we’ve already established, exercise *can* also help with insulin sensitivity so some people might actually lose weight through exercise).
Gary Taubes writes a lot about fat versus energy expenditure too. What happens is when people with metabolic syndrome become overweight or obese, they often become low in energy. The body is unable to feed its cells, and unable to mobilize it’s fat stores, so these people often have low energy. In many instances, when they lose the weight, their energy returns and they feel the desire to move around again. The fat, as well as the lack of energy, are not *causes*; rather, they are symptoms of the underlying metabolic problem.
It’s a rather complicated subject, so it’s hard to summarize in a short interview or magazine article (or even in a post in a comment section like I’m trying to do now!) How does one make a complicated subject simple, after all? This may partly explain the misunderstandings and misinterpretations of Taubes’ writings.
Morgana, here you go. Just to make clear, the link thhq gave is from NY Mag, not The NY Times. Here it is, titled “The Scientist and the Stairmaster:”
http://nymag.com/news/sports/38001/
Evidently thhq also confuses the New York Times, with an international circ in the millions, with the much more localized NY Mag. He said “…For every million people that read it in the NY Mag…” Yet per the Wiki, NY Mag has a circ under 409,000.
https://en.wikipedia.org/wiki/New_York_(magazine)
Morgana, this from you: “…’Eat less, move more’ can work temporarily, but the problem is, either it is too difficult to maintain indefinitely- (people either become hungry again and feel the need to eat a normal amount), or the body conserves energy on a low calorie diet, so people burn less, or even have a hard time exercising.”
I agree totally with it, at least when eating HCLF. During my measured cal-counted HCLF period (March–July 2007), I had to ride serious herd on myself to keep from overeating, likely because I was in glycolysis all the time except–as thhq recently discussed–during long sleep nights when we settle into ketosis. This frequent hunger was likely because our bods can store only ~ 2000 cals of carbs at a time (in glycogen aka “animal starch”) which is less than a day’s worth. Thus, when tuned for glycolysis, our bods send out the “fill’er up” signals after just a few hours. Hence “three squares a day.”
When I went full HFLC at the end of July 2007, I was able to circumvent what you describe above. I still cal-counted for a while, but in time I no longer needed to, I began to feel sated at the appropriate times. Once I was regularly in full deep ketosis (~2008-2009), I started doing intermittent fasts, lasting from 18 hours to 3 days. But that time, my bod was used to burning fat, and since we carry around many dozens of thousands of fat cals, the bod feels less urgency to quickly go into conservation mode. I know this for myself by repeatedly measuring my total weight/body fat % over the fast periods, and even for the 3 day fasts, I always steadily lost both total fat AND body fat %, showing that even during fasting, my bod was preferentially burning fat even after three days, NOT cannibalizing muscle for protein. I never fasted beyond 3 days. I’ve fasted many hundreds of times since then, and felt only twice that hunger led me to break the fast. To head off metabolic down-regulation during fasts, I continued to do lots of aerobic exercise and short bursty resistance exercises, making sure to keep them short enough in duration to not kick off glycolysis. Deep ketosis and steady aerobic and light HIIT together worked magic for me. During one 3 day fast, I walked *40 miles* (roughly a third of that each day) and felt an incredible combo of deep calm and great mental sharpness and making fantastic cognitive connections. During my long walks I kept stopping to scribble notes and filled over 20 pages in that time! In each fast, after the initial metab transition period (typ at 15–21h), I never felt hunger until fast-end.
wbryanh- yes, when I was high carb, I, too, felt something similar to what you describe. I got hungry more often and had to eat more often, but oddly enough, I felt both extremes more. Eating lots of carbohydrate would fill me up so much that I actually felt bloated and full, but then a few hours later I would be hungry again. When I first went low carb, I sometimes thought I hadn’t eaten enough, since I didn’t have that really full feeling I got from carbs. It turns out I had; I just had to re-learn what “hungry” and “sated” felt like. I also now do intermittent fasting every day- (between 14 and 16 hours usually), and eat 2 meals, 1 “brunch”, and a dinner. My digestion is much better this way. I am intrigued by your 3 day fasting; I’ve been reading about that, and am interested to try it. According to a Dr. Seyfried, it’s a good way to boost your immune system and “clean out rogue cells”, which can help prevent cancer. I’m a little bit afraid to do a 3 day fast though; partly because I’m already a bit underweight, and don’t want to lose more; mostly because I have naturally low blood pressure, and am a little worried it might get too low, which could be uncomfortable (or maybe even dangerous???) Since I’m pretty sure I already burn fat rather than sugar, I think I could manage it otherwise. If you have any tips or information about it, I’d be interested in hearing it!
Dr Jason Fung treats his patients with fasting. Here is a link to his website.
https://intensivedietarymanagement.com/ There is a lot of information about fasting.
Thank you Rebecca for reminding me to catch up on Jason Fung. I think his writing is very good and approachable, and love how how explains the manifestations and underlying mechanics of fasting and food desire. E.g.:
“…95% of us have never, truly been hungry in the sense of starvation…much of what we perceive as hunger is actually a learned behaviour…hunger starts in the mind…If sweeteners were the answer, we would not have this obesity epidemic, would we? It’s not like people aren’t eating sweeteners. How many people do you know that have tried sweeteners? 95% of everybody? How many people lost significant weight? 2%?…”
Right on!
Hi Morgana. Yes, if you’re underweight and have low BP, I’d certainly take it slow on fasting. When I started fasting, I was well in the BMI range, had just 10–12% body fat, and BP was 90/60. (You can buy scales that measure BF% – I have a Tanita.) Even without fasting, got the occas episode of lightheadedness when I rose quickly, maybe suffered a bit of orthostatic hypotension. Thus, I *eased* into fasting, starting by eating earlier and earlier at evening and breaking fast later and later the next day, that let me sleep for most or a lot of it. So it went, 14hr, 16, 18, 24, etc. till I got up to the three days. For maybe 1–2 years, I frequently felt a “want-to-eat” challenging in the 15–21h stage, but now no longer. Now it’s unchallenging throughout.
Diet-focused folks often abuse the word “cleansing,” but with fasting that may actually be the case! Fasting enhances autophagy, in which our bods, not getting calories from the outside, start to dismantle the molecular flotsam bobbling around in our cells’ cytoplasm (fluid). A less cluttered cytoplasm allows the zillions of metabolic processes that occur within to proceed more smoothly. It’s like cleaning your room–you can get to stuff faster. But even more important, since metabolic processes are often so tightly choreographed.
https://en.wikipedia.org/wiki/Autophagy
wbryanh- thanks for the info! Yes, I would be most interested in fasting for autophagy; I don’t want to lose weight. (I wish there was a way to fast without losing weight). Sometimes I’ve thought maybe I should start with just a 1 day fast first, and see how that goes; however, I’ve done a lot of reading on the subject, and apparently, the first two days are the hardest to get through; after that they say it gets easier, so it seems a shame to stop before the third day. Also, according to Seyfried, you have to fast at least three days to get any benefit. So, yeah….I’ll keep researching the subject, maybe someday I’ll try it. Until then, the daily 14-16 hour fasts seem to be working well too.
Morgana, you’re welcome! If it’s any comfort, even visibly thin people often have enough discretionary fat to last for quite a long time, well beyond three days. But again, bottom line, you need to feel comfortable with it. It took me two years to start to truly fast. What is your body fat %? For women, the healthy range is 15–25% I’d get a reputable scale that gives you your body fat % in addition to your total weight. I bought my Tanita scale at BB&B for $25 and it consistently measures 2% BF above that of the hydrostatic dunk tank. If the DEXA scan is the platinum standard for body fat percent measurement, the dunk tank is the gold standard.
As far as how long it takes to get through the tough part of the fast, it really varies with each person and how deep into ketosis that person is to begin with. For me, the tough stage was ALWAYS in the 15-21h range. After that I was nearly always home free. Now I don’t even suffer any tough stage any more. Btw, I’m not convinced all of us need to fast a minimum of three days. I let my glucometer and how I feel be my guides. If I’m getting readings consistently in the 70s and feel terrific to the point of sublime, I know I’ve fasted enough 🙂
thhq- silly me: in my rather long winded post, I realized I forgot to mention one of the most important bits! And that is, with overweight people who are lacking in energy- (this applies to that paragraph I wrote about energy)- sometimes it’s been advised that they lose the weight first (with a low carb diet), and then exercise later. This is because, as I explained above, once they start losing the weight, the energy often returns naturally. This might be part of the misunderstanding with Taubes’ views on exercising.
Sorry to get them mixed up wbryanh. We could spar over this one too, which was in the NYT.
http://www.nytimes.com/2012/06/03/opinion/sunday/we-only-think-we-know-the-truth-about-salt.html?_r=0
GT gets a lot of high visibility press coverage. Agreed?
@morgana, getting some weight off certainly will give an obese person more ability to exercise. For most people reducing carbs helps, but reducing fats can work just as well. IMO it’s the calories (fat AND carb) that need to be reduced first and foremost to get weight loss started, followed by increasing exercise to keep it going.
I prefer to exercise at low intensity to preferentially metabolize fat over carbs, but it takes a lot of time to get much of an effect. What works even better is sleeping. When you’re as close to idle as you can get, Thompson and Manore state that 90% of metabolism is fat. Unfortunately the metabolic rate is low, approaching RMR, so you have to do a lot of sleeping with very minimal eating to lose weight steadily.
Here, Kevin Hall calls it a theory:
“Journalist Gary Taubes berated nutrition scientists for not understanding the seemingly simple concept of controlling diet variables. He chastised the field for altering multiple diet components at once and said that controlling variables is something that even
“school children are supposed to understand”
The failure of nutrition scientists to understand this basic concept
“has led to what may be another of the great misconceptions in modern nutrition research”
Mr. Taubes then exposes the horrendous misconception:
“carbohydrate-restricted diets are ‘valuable tools’ in the arsenal against overweight and obesity, but they’re just one of the dietary tools.”
Why was such a seemingly reasonable statement proclaimed to be a “great misconception”? Because, in Mr. Taubes’ view, the carbohydrate-insulin theory implies
“that the only meaningful way to lose fat … is by reducing the amount of carbohydrates consumed.” [bold mine KH.]
Doubling down on this claim in his most recent book Why We Get Fat, Mr. Taubes states that
“any diet that succeeds does so because the dieter restricts fattening carbohydrates…Those who lose fat on a diet do so because of what they are not eating – the fattening carbohydrates.”
At the time, I read these proclamations with great interest. I had just begun collecting data from a carefully controlled metabolic ward study which is the first to avoid the confounding nature of changing multiple macronutrients at once. Thankful to have an understanding of clinical trial design equal to an average school child, I also realized that our study would directly test Mr. Taubes’ version of the carbohydrate-insulin theory which has become greatly influential.”
http://www.weightymatters.ca/2015/08/guest-post-dr-kevin-hall-asks-is.html
And this is precisely what launched the Hall ward study we are discussing, which was meant to give the “theory” a fair test.
But you can see how Taubes berates his critics for questioning it. For that reason I call it an assertion. For Taubes, this thing he thought up is like the sun in the sky, gravity, a signed publishing contract, or Biff’s sports almanac. It’s not allowed for anyone to test it or question it. IT’S SIMPLY TRUE AND IF YOU DON’T BELIEVE IT YOU’RE A MORON.
Which is why everyone trained as a researcher instantly questions it.
thhq, did you read Good Calories Bad Calories?
Thhq, no I haven’t read the Keys or Thompson books you mention. But I’m not running on about them either. I don’t trash-talk books I haven’t actually read. That’s why I asked you if you had read it before you started unloading on it. Hall’s study was ambitious. But I repeat, it is RIFE with caveats. He used a small and unusual cohort: obese normoglycemic people. Not T2Ds or pre-T2Ds. The “low-carb” side was definitely not low-carb at 140g carbs/day. Perhaps most egregious, 6 days is almost certainly too short a time to allow for full keto-adaptation. About Taubes’ carbohydrate-insulin hypothesis, I remain quite unconvinced Hall’s study disproves it. Insulin levels dropped for both the low-carb and low-fat groups, more so for the low-carb group. The diff in the LC and LF drops wasn’t much, but then how can we expect there to be? All subjects were insulin-sensitive to begin with, and then they started eating hypocaloric diets with an 800cal/day shortfall, making them even more insulin-sensitive. In short, what does it all prove? Not much I’m afraid! Frankly the whole methodology’s a bit bizarre. If you don’t want to hear these caveats from me, go to Guyenet’s site and read the comments on the Hall study. So many readers took issue with Guyenet’s study he did a followup post five days later. There he tried to address the concerns of his readers and ends up fielding many more concerns. Even Guyenet admits a better study is needed.
So thhq, let’s leave Hall’s ward and re-enter the real world. If carbs are fattening, then why are there lots of people chowing high carb diets who stay thin? Why does that Chinese farmer eat mainly rice yet not get fat? The principal answer likely is that–provided you never entered metabolic syndrome to begin with–the less food you eat and/or the more exercise you do, the less the body cares the source of the calories be they from carbs, fats, or proteins. The closer to subsistence you eat, the hungrier your cells are for the nutrition thus the less insulin you need to dispose the energy, even carb energy, into the cells. Thus your serum insulin level stays low enough not trip the fat-storage switch.
So that’s fine thhq for people in developing countries who do hard physical labor and can afford only a subsistence diet. We live in developed countr(ies) where food and food-like products are cheap and all around us. In such a case I’m not surprised you need to count your calories to stick to your eating plan. Thanks to LCHF, I don’t have to bother with that headache. I enjoy natural satiety and I still lost 62 pounds (230 to 168) and body fat dropped from 26% to 10%, in addition to the other health improvements I list elsewhere in this forum. Most of all *normalized* BGs! I’m not saying LCHF is for everyone. Each of us really should experiment and see what works best. But this foodway lets me live my life AND enjoy great health! Really what more can I say?
I don’t know where this will land wbryanh, but thanks for the dialectic. We’ve achieved the same ends blood-wise by completely different methods.
So now that we’ve arrived at healthiness, what’s the best path to a healthy and long life? I didn’t come into this thread to bicker about GT, though that is one of my favorite pastimes. It was more an interest in the HCLF cultures and persona that attracted me. There’s a lot of modern information on longevity for those cultures (Japanese/Okinawan, eg) and persona (Keys and LaLanne, eg). But there’s very little on LCHF that is contemporary or relevant. Guyenet’s information on traditional Inuits comes from the early 19th century, and shows lifetime in the 30-40 range. What do you know on this subject?
Sure thhq, I’m always happy for constructive convo. It always leads me to think about what I’m doing and better sort it out, and often points to new things to consider. I know you feel you’ve arrived to a healthy place blood-wise, and maybe you’re right, but still I’m curious to learn your C-Peptide and your body-fat percent. I’ve long thought that ancestral cultures span the macronutrient gamut from extreme HCLF to extreme LCHF, so why then is diabetes and other chronic diseases soaring all round the globe? This conundrum led me to research other influences, esp. environmental toxins, esp those in our own homes and everyday products we consume. As far as Guyenet riffing on ancestral-living Inuit living short lives, I assume this is what you’re referring to:
http://wholehealthsource.blogspot.com/2008/07/mortality-and-lifespan-of-inuit.html
First note this is “the ages of death of a traditionally-living Inuit population during the years 1822 to 1836.” Guyenet also includes caveats: “It’s possible that life expectancy would have been higher before contact with the Russians, since they introduced a number of nasty diseases to which the Inuit were not resistant. Keep in mind that the Westerners who were developing cancer alongside them probably had a similar life expectancy at the time.” Thhq, I’m mainly impressed at the fact a few of these Inuit actually made it into their 90s, given their incredibly challenging environment!
Also since WW2, we started adding iron to most carb foods. The idea was to prevent anemia. But iron messes with the gut biome, and also directly causes diabetes. So if you want to make a person more insulin-sensitive, just have them donate blood.
http://diabetes.diabetesjournals.org/content/51/4/1000.full
“In summary, blood letting led simultaneously to decreased blood HbA1c levels and to changes in insulin secretion and insulin resistance ”
Carbs in the US affect iron levels mostly because they are “enriched”. Whole grain carbs are not enriched, plus the bran blocks iron absorption. Pre-WW2 some people used molasses or cast iron pans, or ate a lot of meat, but more people had lower ferritin levels than today, so there was likely less diabetes.
Which makes me wonder. The rice diet was started pre-WW2, so the rice used was probably not enriched. If the same diet was done after WW2, the rice likely would have been enriched, and would it have had the same results? The rice diet was a super-super-low iron diet.
Actually, it’s not just the iron (which is linked to metabolic issues, like diabetes). Rather, it’s the B Vitamins that are known have an affect on appetite.
Although McClain et al. 2015 recently showed that high iron intakes (simulating a high meat diet) are linked to increased appetite, enriched foods themselves have been linked to obesity and increased appetite (Zhou et al. 2014) because of the B vitamins. Thiamin was once known as the “appetite vitamin” (coined by Cowgill) and niacin has been linked to increased appetite, according to Zhou et al. If you do a Google Images search for “ironized yeast” you will find vintage advertisements for pills that were high in B vitamins and iron used to increase appetite and put on pounds. In fact, the discovery of B vitamins happened because it was shown to increase appetites in rats.
Bakers and millers were initially against enrichment before WWII, but right around the time the US Dietary Guidelines were written, grain lobbyists began to become the most vocal proponents of enrichment. The lobbyists pushed the FDA to approve significant enrichment increases during the 1970s, which were finally approved in 1983. It is interesting that Pritikin’s had health issues soon after 1983. To this day, grain lobbyists are the main supporters of food enrichment in the US.
Since 1983, a single slice of bread has as much appetite-stimulating B vitamins as a medium sweet potato, or a cup of beans—and significantly more iron than ever before. The sweet potato is obviously more satisfying due to its mass. Also vitamins can be associated to food tastes, which might provide some advantage to enriched rice consumption (who knows).
More products also became enriched with the new 1980 US Dietary Guidelines (the guidelines were specifically written to encourage enriched grain consumption). When you look at the vitamins that are actually added to the enrichment formula, each one seems to have literature linking it to stimulated appetites. I doubt it’s a coincidence.
At any rate, enriched white rice post-1983 was very different from enriched white rice pre-1983. And the post-1983 diet correlates with increased appetites throughout America.
See Zhou et al.’s series of studies between 2010-2015 linking niacin via enrichment and appetite. Zhou mainly focussed on niacin, but the other B vitamins in the enrichment mix are known to be appetite stimulants as well.
The reason this is all important is because when Osbourne and Mendel discovered B vitamins in the early 1920s, they realized that rats lost their appetites when they were fed nutritionless refined foods. At the time this was considered an innate protective measure to prevent an animal or human from being addicted to nutritionless food. So, if you were manufacturing food, and you wanted people to keep their appetites up, you’d find ways to add those B vitamins to refined food.
And that’s exactly what they did. After 1983, the lobbyists significantly increased the dose of B vitamins (and iron) in refined grains and people had bigger appetites for otherwise nutritionless foods.
Duck, very interesting! Can you supply links for us to follow up on this “Vitamin B drives appetite” stuff? Thank you!
Sure…
http://pmid.us/PMC3932423/
http://pmid.us/PMC2874142/
http://www.nature.com/hr/journal/v34/n12/abs/hr2011133a.html
http://www.biomedcentral.com/1471-2458/10/746
http://dx.doi.org/10.1017/S0007114513001815
I can’t vouch for the effects of niacin on metabolism that they focus on. But, the correlations to B vitamin fortification are striking to my mind—particularly when we match it up to the historical contexts. The amounf of B vitamins in fortified food is very high now. Again, a single slice of enriched bread has about as much B vitamins as a medium sweet potato or a cup of beans. It’s crazy.
High iron intake isn’t doing anyone any favors and could be related to metabolic issues, but we recently found evidence that rats can have organ iron overload (say in the liver) even on a low iron diet. And obese people can be truly iron deficient. That implies that the iron overload in various organs can come from mineral deficiencies—say a deficiency of copper, that would otherwise be protective of such iron mismanagement.
At the moment, we are trying to investigate how quick the effect on appetite is. Anecdotally, we’ve seen some people report that if they make food out of enriched flour, they will eat much more than if they make the same meal with non-enriched flour.
One interesting study on the subject was from 1933:
• “Appetite and Choice of Diet. The Ability of the Vitamin B Deficient Rat to Discriminate between Diets Containing and Lacking the Vitamin,” by Leslie J. Harris, Janet Clay, Florence J. Hargreaves and Alfred Ward (1933)
The scientists ran comparisons between deficient diets and enriched diets (often using Marmite, which is rich in B vitamins) and various flavors to see if the rats associated memories of flavor associations.
Interestingly, sometimes the rats did, in fact, have flavor preferences that mislead the rats when palatability was very high. But, in general, on a real foods diet, the data implies that animals naturally lose their preference for non-nutritious foods as they become deficient and naturally gravitate towards foods that have B vitamins in them. This would likely happen seasonally, of course.
Taken together, you can see why non-fortified countries seem to have an easier time with all this. Their less-nutritious food isn’t laced with the very vitamins that signal safety to our bodies.
Duck, thank you for the links! I will look at them soon –Bryan
Forgot one, Bryan.
Vitamin paradox in obesity: Deficiency or excess?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4549666/
…Also, I thought this paper was interesting.. It reveals the lobbyist group led the charge to increase fortification in the 1983 decision:
The Enrichment Debate (1977)
http://journals.lww.com/nutritiontodayonline/Abstract/1977/07000/The_Enrichment_Dabate.5.aspx
Doctors opposed the increases, but the grain lobbyists eventually pushed it through in 1983.
I’d also point you to this 1933 study:
Appetite and Choice of Diet. The Ability of the Vitamin B Deficient Rat to Discriminate between Diets Containing and Lacking the Vitamin, by Harris et al. (1933)
If you read through that study, you’ll learn that Vitamin B deficient rats crave foods enriched with B vitamins (though they can apparently be fooled under the right circumstances, which is why food education and traditions are obviously a factor).
The fact that rats crave the taste of B vitamins, when they are deficient, is crucial because obese people are known to be deficient in many B vitamins, for various reasons. So, this would explain, among other things, why obese people may be addicted to enriched foods. They are trying to obtain the B vitamins, but their body isn’t absorbing or metabolising them. Inability to metabolize (synthetic) B vitamins can be due to a number of issues, though copper deficiency is known to affect methylation.
One potential link to iron is that B vitamin deficiency is associated with inflammation, and iron fortification is known to promote inflammation in the gut.
Cheers.
@Duck – doesn’t this mechanism, as described in the papers imply that if one wants BOTH vitamin B3 and non-obesity then the way to eat is like this:
1) Divide food into 2 parts: B3 rich part (B3 supplement, meat, enriched flour) and B3-poor part, containing foods low in B3. Assure that you have a sizable B3-poor part, enough to supress appetite.
2) Eat B3 rich foods or supplements first.
3) Wait as long as necessary for the hunger to appear and develop.
4) Eat B3-poor foods – this surpresses hunger.
Thus you end up with both B3 vitamin and no hunger. But this requires giving up on a concept of a meal – a complex mix of everything together – and replace it with precisely timed feedings of separate types of food. That would be difficult culturally and commercially.
GTR. Sorry, no idea. Zhou is mainly focused on niacin (one of the fortificants they significantly increased in 1981). But, Cowgill coined thiamine the “appetite vitamin” and riboflavin is known to have appetitie-stimulating effects as well. The early studies showed that the animals were only stimulated to eat enriched foods when they could taste the vitamins and were deficient in those vitamins—which I would think would be rather common on a poor diet, since most B vitamins come from our gut flora. Obese people have abnormal B vitamin metabolisms as shown by many other studies (and Zhou too) so who knows what’s going on.
Zhou’s overload theories aside, I find it all particularly interesting for the fact that before enrichments were added to foods, people were known to lose their appetites eating nutritionless foods as they slipped into deficiency. Same thing would happen to animals in a laboratory. It’s only when the taste of enrichments (usually as brewer’s yeast in the early days) were added to the foods (and to rat chow) was the nutritionless food able to become a staple. The early studies showed that only a taste or bare adequacy was needed to stimulate appetite. And the brain could learn to crave flavors associated with that stimulation. That’s mainly what I’ve been focused on. The taste of enrichments enable a person or an animal to eat refined foods—otherwise, they would lose their appetite as they became deficient, or be compelled to crave B vitamins elsewhere. When the animals were vitamin B replete, they would be happy eating some nutritionless foods, until they became deficient, and then they would eat foods that tasted like B vitamins. In other words, it’s a protective mechanism. Zhou briefly mentions appetite stimulation, but he seems mainly focused on the abnormal metabolisms of B vitamins in obese subjects.
Those who were obese eating nutritionless foods before fortification seem to have found other ways to stimulate their appetite with the taste of B vitamins (such as with yeasty beer, for instance). And I’d imagine those in unfortified countries would likely have to find a way (multivitamin for instance) to stay replete in B vitamins in order to keep themselves from losing their appetites, if they truly wanted to eat nutritionless foods as staples. A deficiency changes your tastebuds to crave or accept foods with that vitamin or mineral.
Nice bit of history! I was not aware of this about the B vitamins. Also interesting about empty calories. The standard thought is that we overeat empty calories, but I can’t say I’ve ever eaten a lot of plain rice no matter how hungry I am.
It is interesting that Zhou would use iron as a stand-in for meat though. Meat, and protein in general, tends to be an appetite suppressant. Too much meat is toxic of course, as has been mentioned, but it also just makes most people full. Fish and eggs do the same thing, though I think maybe even more so.
Which is another thing about the 1980’s. There WAS a huge push to eat lots of grains … the infamous food pyramid! And to eat less meat. But something else also changed. They tried to scare everyone away from eggs. Egg consumption dropped drastically, while at the same time we were eating more of about everything else.
So when I was a kid, we ate cookies. But they were either homemade, or else looked a lot like homemade. They were made with butter and eggs. You ate ONE cookie or maybe two … there were very filling. Usually with a glass of milk because kids always got milk with everything.
Now like as not the cookies are egg-free. Often low in fat too, and no dairy either. And you can eat the whole package easily. There is no “stop” button on most packaged foods these days. This saves the manufacturer some money, makes the food keep longer, and allows the consumer to ingest way more calories than anyone needs.
Sweet potatoes and beans seem very satiating to me though probably because of the fiber. Fiber fills your tummy, but it also keeps digesting longer and will keep you more satisfied into the next day. The butyrate from the digestion is actually feeding your gut cells. Modern processed foods are also often very low in fiber (even more so in the ’80s) which would encourage one to eat more often.
Zhou didn’t use iron for meat. Zhou is mainly focused on B vitamins and appetite. McClain et al. 2015 used a *very* high poorly absorbed non-heme iron intake to simulate the the highly absorbable heme iron from meat. That seems to be how they simulate iron absorption from meat. The idea was to get ferritin levels up to what is seen in humans on high (cooked) meat diets.
On a side note… My understanding is that there is a ceiling of heme iron you absorb in one meal (~2mg), but cooking meat transforms a good chunk of it to non-heme. And that (and eating meat too often) may be one of the many ways one can get iron overload as there is something called the “meat effect” where meat significantly increases your non-heme iron absorption. Traditional cultures that were high meat tended to eat their meats raw, which may be protective of iron overload due to the heme ceiling. And the microbes are supposedly not bloomed by all the raw heme meat going through the colon due to the antimicrobial porphyrin ring on heme that is otherwise destroyed by cooking. In other words, the iron perhaps becomes more available to pathogens in your colon when you cook meat and destroy the porphyrin ring. Although, eating raw meat can have it’s own issues. 🙂
Ah ok, I got the incorrect researcher.
Interesting that cooking would change the absorption so much. There isn’t much info on humans and non-cooked meat.
The upshot for me though, was that looking into a “Happy Meal” … between the enriched bun, the bit of meat patty, the soft drink, and the fries, the poor little kid gets a major iron overdose.
“between the enriched bun, the bit of meat patty, the soft drink, and the fries, the poor little kid gets a major iron overdose.”
Kids need iron, actually. But the more iron you eat, the more copper you need to utilize that iron—otherwise that iron just promotes inflammation when it’s not utilized properly.
So, iron is just one piece of the puzzle. Most of the fortified iron isn’t absorbed, but what isn’t absorbed causes inflammation, as explained here:
And the more inflamed you are, the less iron you absorb. And during inflammation the body will also keep iron out of the blood, which makes it go into organs and tissues. During chronic inflammation, this is problematic.
Rats deficient in B vitamins will crave the taste of B vitamin enrichments. Inflammation promotes B vitamin deficiencies and methylation issues. Obese people are known to have B vitamin deficiencies and inflammation—mind you this happens on a diet high in enriched foods.
Gut inflammation decreases one’s ability to absorb these micronutrients, but the point is that the B vitamins are craved and so foods fortified with lots of B vitamins are eaten since they are very rich in B vitamins. Because the iron is inflammatory, the fortifications aren’t well absorbed and the cycle of craving, increased appetite, and deficiency continues.
Does B3 vitamins, including niacin, and appetite, especially for carbohydrates, have something to do with NAD+/NADH ratio? Carbohydrate consumption tends to lower NAD+/NADH ratio to quite low levels, to increase it to healthy levels you can either lower calories, do some fasting, takie niacin, nicotinamide, nicotinamide riboside, or oxaloacetate.
So what rats without niacin did might not be a prevention of bad habit, but a simple NAD+ management via lowering calories, while rats with niacin had their NAD+ managed by niacin, thus could afford to eat more without problems at the cellular levels.
…Also if you look at the studies on tastebuds and deficiencies, you’ll find some very interesting findings. For instance, loss of taste (Hypogeusia) is a sign of a micronutrient deficiency (such as copper or zinc). The tastebuds physically change with various deficiencies.
Loss of taste is particularly problematic and common in the elderly, and this can reduce their appetite. Unfortunately, this puts them at even further risk of micronutrient deficiencies.
Heathertwist, very interesting, thank you for this! I haven’t so much explored the iron element (chem joke haha). Yet ANOTHER novel factor introduced to our environment after WWII. I’ll definitely be reading more about what may well be chronic iron overload from wheat-based food “fortification”– To be clear, the Rice Diet did *not*, on average, resolve diabetes, regardless who may be claiming what. Far from it! The average fasting blood sugar (FBG) for folks after 22 weeks of the Rice Diet was 155 mg/dL! That’s still diabetic! Normal fasting BGs are 75–95. If you want to see these results for yourself you can ask Denise to send you the Rice Diet study–she offered to do this for anyone interested in it. You’ll find the table giving those number on page 360. You note that Kempner started the rice diet before WWII. I’m curious to see the results before and after the war. –Bryan
The other is that the levels of blood sugar required to be considered diabetic have been decreasing as medical knowledge advances. What did they consider to be diabetic blood sugar levels when Kemper did the rice diet?
Rebecca, excellent Q! I also wonder that. Kempner & Co also had the problem of much poorer BG measurement. Direct measure of blood glucose didn’t come along until the late 50s, and not in common use until 1981. Before then, urine strips were the best tool, and they didn’t register until BGs hit 180mg/dL, the concentration at which the kidneys started passing sugar into urine.
N=1short term experiment….
Day #1,
Lunch moderately LCHF (some potato salad)
Dinner strict LCHF
Next day fasting blood sugars at 4.8. All good.
Day #2
Lunch HCLF lunch, whole meal bread
Dinner LCHF
Next day fasting blood sugars at 6.1
So day #1 diet wins, just not sure how sustainable it is to remain low carb. Or what percentage carbs represents the sweet spot.
I have tried HCLF for three days in a row to no real effect. Possibly the type of carbs are of importance. Maybe gluten doesn’t help blood sugar levels.
Glad you enjoyed it!
I agree the Rice diet didn’t “cure” diabetes but it did allow some folks to stop using insulin and lowered their blood glucose. Mind you these were folks that needed to inject insulin, not just folks with a bit of high blood sugar. The limits on what is acceptable blood sugar have gotten lower in the past decades.
Diets like Pritikins and McDougall have brought down blood glucose nicely for a lot of people, including some of my relatives. I don’t know that I’d call it a cure though … the person will revert if they go back to their old diet. The thing is, the modern versions of LFHC all ALSO specify “unefined” starches and to avoid “processed foods” … so it’s hard to get any stats on successes from people eating white rice.
The older Asians I’ve seen in the US are typically still thin and active and eating plenty of white rice. However, they also make an issue of the kind of rice they buy, and “American rice” is considered pretty bad. Oddly, the rice headed for the Asian markets around here is grown in California, but is packaged for Korean or Japanese or Chinese markets, and is not enriched.
http://www.dietandfitnesstoday.com/iron-in-white-rice.php
Instant or parboiled rice (the kind more Americans cook) has the highest iron content: 6mg per cup? Which is almost half the recommended daily intake. What is weird to me is that the rice at PF Chang’s also tastes to me to be parboiled … it’s about as far from “rice” in China as it can get.
Anyway, at one point my fasting bg was up to 120. I started donating blood, and also cut down on things like homemade molasses beer and cooking in iron pans, and fewer steaks. I avoid any “enriched” foods, but don’t especially avoid carbs (I’m big on white rice and sushi!). Now my fasting bg is down to 83.
I did have my ferritin and hemoglobin measured and they were on the high side. If you donate blood they will always check you for anemia and tell you if you are low.
Hey wbryanh, just a quick note on the average fasting blood sugar after the Rice Diet and Pritikin: keep in mind the average includes the (small but existent) minority of people who got worse (often MUCH worse), the people whose blood sugar didn’t change, and the people who experienced dramatic improvements. The fasting blood glucose for those who improved was often much lower than the averages reported in the papers, and frequently in non-diabetic ranges, especially with Pritikin’s diet. Reporting averages unfortunately dilutes the full range of change and can give a misleading picture. From what I’ve observed, the people who do well with low fat do *very* well, and the people who do poorly with low fat often do *very* poorly (a number of genetic, environmental, health-context, lifestyle, etc. factors all contribute to which camp a person will fall in). There are definitely people who have returned to non-diabetic levels eating very low fat — the McDougall website has a collection of individual stories here –https://www.drmcdougall.com/health/education/health-science/stars/ — so it certainly is possible!
Neisy, thank you for stepping in! Any change you can post here the post-study BGs on each study subject for the Rice Diets and Pritikin regimes? (I think we can rightly term these “regimes” given the study leads used whips and other stiff coercive methods to ensure compliance for some of the subjects:-) ) It’d be great to be able to see how many, and how great, the outliers are.
But more to the point: Does extreme HCLF *really* work on a par to LCHF for resolving high blood sugars? For the Rice Study, you say:
“More than half of those 100 diabetic ricers—63%—actually saw their fasting blood sugar drop by at least 20 mg/dL during the diet. Only 15% had their blood sugar go up significantly. The remaining 22 saw little to no change.”
But what were the actual starting BGs? And the post-study BGs? That’s what we really need to know to compare efficacy of HCLF to LCHF.
I realize we have a paucity of LCHF studies. Thus must rely on the giant raft of anecdotal data out there. You can find countless accounts of people who actually *normalize* their BGs–as is, get them down to 75–95mg/dL *all the time*–when they go on LFHC. I am one of those many people. My BGs have been normal for nine years, and now I’m 55. An age where my BGs should be getting inexorably worse no matter what stunning physical and dietary gymnastics I perform.
In general, I’m not ready to accept the idea that these very HCLF diets are anywhere near as good as lowering BGs as LCHF. This makes me question the suggestion/implication that the two ends-of-the-fat/carb-macronutrient-spectrum are equally “magic” in their salubrious effects. I need to see more evidence before I can accept that extreme HCLF offers anywhere near as much magic as LCHF. I’d love to see it too, because I find your argument intriguing, but still need more support IMHO to accept the idea we can put HCLF on the same level as LCHF to drive into remission chronic disease–at least for diabetes. Thanks for listening Neisy! Hope to see your answer when you can write back. –Bryan
I think the LCHF or LFHC issues everyone is pondering over depend largely on the individual what kind of results you will get. In the past LCHF did wonders for me. A bit over a month ago I switched to LFHC to see what would happen. I keep my fat under 10% and pretty much eat only whole grains like oats and other whole foods with tiny amounts of bread here and there. Most foods made from flours, and white rice will spike my blood sugar. A big bowl of oats and a banana for breakfast and my blood sugar is fine. To lose weight on a LFHC diet you have to stick with whole foods, cut the fruit to very small amounts, no dried fruit, or nuts, seeds and avocado. So when people say it doesn´t work for weight loss you have to know what they actually do. I am getting down to those last few pounds that are hard to lose, since I started LFHC I have actually lost a few more pounds.
After a month I did my lab work. Total cholesterol 169, tiglycerides 92, VLDL 18, HBa1C 5.2% etc…. everything good. Every individual has to test on themselves what works and what doesn´t work.
If you want to believe one theory or the other fine, test it on yourself and see what happens.
How long did the switchover take? I think there may be an adjustment period in going from one diet to the other. Certainly there is a lot of talk about the ‘low carb flu’ when moving to HFLC diet.
It took no time at all. I never had the so called low carb flu when I started eating that way either.
The reason I ask is because I find the HCLF diet has the opposite result for me. I.e. Send fasting BS levels up. But it may require more persistence.
Hi Rebecca. Were you in a diabetic state before you went HCLF? The Rice Diet most or all the subjects were diabetic going in. Same thing I believe for the Pritikin studies. And did you get your C Peptide tested? Your A1c looks OK (4.6% or lower is ideal), but your reasonable BGs may or may not be at the expense of chronically high insulin output which incurs its own chronic disease risks, Alzheimer’s among them. All that said, whole foods certainly help whether it HCLF or LCHF. Also, I’d consider the C Reactive Protein test, a very good biomarker for chronic systemic inflammation. Mine went WAY down after going whole-food LCHF. It was 4.4 (inflammatory), now 0.6 (anti-inflammatory).
Yes I am diabetic. I take medication but I take the same amount of medication on the LFHC as I did doing Low carb high fat. That to me seemed very strange but if I stick to whole foods it works. I am going to check my c-peptide to see what my insulin is doing. C-reactive protein could be lower but it was only 2 and up to 8 on the lab ranges was considered normal.
wbryanh, heathertwist- Yes, I see a huge amount of bias against red meat in our current culture, and many of these so-called “studies” condemning red meat I think are so wrong! The mentality seems to be “we know that meat is ‘bad’, now we just have to find a way to prove it”. Also, quite a lot of these scientists in some of the recent well-publicized studies were actually vegans, or at least had some kind of conflicts of interests.
In any case, heathertwist, I know what you’re saying- that seafood is very important- but I’m not ready to say that mostly meat diets can’t be healthy too; I’m sure I’ve read that they can be! I wish I could find a link proving what I’ve read about the Sioux Indians. I know I’ve read that they were in excellent health, back in their heyday- (before the time of the white man). I myself am sort of like Peter Attia- (you posted a link about his diet); I tend to eat more poultry and fish too (mostly due to the expense, as well as the fact that I simply often crave fish). But some people I know don’t like fish so much and eat more meat, and they seem to be in very good health.
wbryanh- this is from memory, so may not be totally accurate, but I recall Weston Price visiting parts of Africa where they ate more meat centered diets (though there may have been lakes around too; he didn’t mention it though). Also, parts of Australia that were inland. I’m pretty sure he visited quite a few inland places, and some where they only ate meat without dairy and fish, because at the end of the book he made the comment that those meat diets *only* worked if they ate the offal too. So, even he was aware that just muscle meat wasn’t good. One more thing: the fat of wild animals on their natural diet also contains Omega-3 (was that what you were asking about, regarding fish consumption?)
wbryanh- I’m sure there was another point that you made that I wanted to comment on, but now my mind is a blank; I’ll go have another look and see if I left something out. (It’s been a long day…..)
Morgana, @heathertwist — Guys, about “red” meat, I’d like to emphasize, the studies on it nearly completely lack any granularity. Possibly to the point of meaninglessness. There’s a huge diff in diff sources, types and preps of meat. None of the studies separate out for animal source of meat (lamb, cow, goat, etc), type of meat (low-load muscle meat, eg tri-tip; high-load muscle meat, eg shanks and chuck; and organ meat and their diff types.) and how the source creature was raised, eg grain-fed, grass-fed. Until recently the studies didn’t even distinguish between processed meat (charcuterie) and fresh meat, which was frankly crazy for these researchers to not resolve out. And the studies still don’t distinguish between fresh whole meat like a cut of steak, and *ground* meat, the latter which almost certainly harbors a higher level of microbes like pathological forms of E. coli like the O157:H7 variant.
All that said…I don’t eat much red meat. But not for the purported pathogenic compounds that it allegedly harbors. Rather to focus on what I perceive to be the greater need for the amounts of the nutrients we get in shellfish, finfish, eggs, and non-cow dairy. I simply steer toward the animal flesh of the greatest nutritional value so I can get all my micros without chowing too much protein. The meat I stick to AMAP are organ meats, esp chicken livers and, when they are available, hearts from grass-fed lamb. And, to a lesser degree, lamb shoulder and shanks, and tongue mainly from beef and buffalo, and brain, usu from pork and goat. The actual amounts of these meats are small, and these satisfy me completely and my medical tests come out excellent.
Morgana, what you said: “…One more thing: the fat of wild animals on their natural diet also contains Omega-3…” I more I think about this, the more I realize that ancestrals, no matter where they lived, likely met their relatively modest needs for long-chain w-3 (EPA, DHA) from a variety of sources. There’s of course the animal brain I mentioned earlier, which are likely our most largest and densest source of terrestrial w-3s. Morgana, as you say, the pastured wild creatures will have it, though they generally are lean, low in total fat, but again we don’t need a lot of w-3. Heather (or Morgana?), as you pointed out, very few ancestrals lived far from some water source, fresh or saline. Land mollusks like snails are a source of w-3s. So are insects, which are still a part of most diets around the world:
http://www.sciencedaily.com/releases/2016/01/160111122520.htm
Bottom line: it’s not that I think red meat per se is necessarily bad for us–esp fresh organ meats and high-load whole muscle meats from pasture-raised animals. Rather, it’s that seafood, eggs and non-cow dairy offer nutrients profiles we need without chronic protein overload. –Bryan
I agree there aren’t good studies. Like I said, I’m looking for examples of a culture or even individuals that eat a “mostly meat” diet and are doing well. I think it’s a fair thing to ask. Some have made the point that there has never been a vegan society that did well long term … but in fact we have examples of that (and examples where veganism DIDN’T work so well). Denise gave a good rundown of vegan or near-vegan diets that have done well in studies.
And we have a number of examples of seafood diets that work well in the long run, where the individuals have healthy hearts, good joints, etc. into old age.
But I issue this challenge occasionally and so far no one has actually come up with an example of a mainly-meat-eating culture that’s very healthy. Actually I have the same challenge for wheat-eating cultures … I haven’t seen any culture that eats mainly wheat as a starch that is doing well.
I was thinking of Mongolia, where they do “eat the whole animal” and eat loads of fermented foods. Their lifespan isn’t very good though (it’s gotten way better over the last 40 years), and they have high rates of heart disease and cancer.
http://donmatesz.blogspot.com/2012/09/grass-fed-animal-products-prevent.html
Hi Heather, @morgana —
Heather, looks like to me we tend to meet at the same place on red meat, if maybe from different ideas for why we should make it a relatively modest part of our foodway.
And you’re right, I also can’t think of a high-red-meat eating society that lived exceptionally long lives. Except maybe the Swiss? Average life expectancy there is 81/85 for men/woman at birth:
http://www.bfs.admin.ch/bfs/portal/en/index/themen/01/06/blank/key/04/04.html
They eat a lot of dairy and meat. I don’t hear much about fish in their diet.
https://en.wikipedia.org/wiki/Swiss_cuisine#Foods_and_dishes
I’d definitely be chary to use Mongolia’s life and health stats as any kind of guide for foodways. Many Mongolians were indeed pastoral nomads until the Soviet Union roped the country into its cordon sanitaire 90+ years ago. Since that time, the USSR, through its puppet socialist gov’t in Ulaanbaatar, sought to settle these nomads in cities and towns, and of course this added grain based foods and all kinds of processed foods, largely replacing their pastoral diet. Most urban Mongolians:
http://www.bluepeak.net/mongolia/ulaanbaatar-life.html
are as likely to chow processed Chinese and Russian crap from the local supermarket as mutton off the steppes.
The Soviets also swept through the country and razed nearly all the Buddhist monasteries, destroying a vital anchor of Mongolian life. These severe dislocations and traumas, which sheared away their traditions, plunged many of these proud but now impotent people–once rulers of the largest empire on earth–into existential crisis. This led to an explosion of alcoholism there, aided by the the vodka the Soviets brought in:
http://www.npr.org/templates/story/story.php?storyId=112485545
On top of that, almost half the country’s population lives in UB, which now vies with Delhi, Beijing, and Tehran, for the title of most polluted city on Earth.
http://www.slate.com/articles/health_and_science/medical_examiner/2013/03/worst_air_pollution_in_the_world_beijing_delhi_ahwaz_and_ulaanbaatar.html
The next largest cities, Erdenet and Darhan, are big Soviet-era mining and industrial centers. So you can imagine the toxins that abound in those environments.
For very *many* reasons, Heather, much of Mongolia is quite UNhealthy. Whether or not they eat the high-red-meat pastoral diet.
Heather, about Don Matesz, I’m sorry to say, but I no longer pay much attention to him. I check his site once a year or so and always come away sorely disappointed. I respect his decision to switch from “paleo” (whatever that even means any more) to a plant-based diet. Only so much of what he does is so sloppy and lacks so much rigor he appears to me little more than a shill flogging his newfound foodway.
His post on the Mongolian foodway illustrates that. Matesz kicks it off saying:
“Mongols eat a diet largely composed of milk products, meat, and fat from free-ranging, organic, grass-fed animals. They consume few plant foods because few edible plants grow in the cold continental climate of Mongolia.”
As “evidence” for this, he links us to a Chinese government site–anything but an academic study. First, we should suspect anything that comes from the Chinese government, which till recently told us Beijing’s air was fine to breathe. Next, it’s not even clear if chinaculture.org discusses Mongolians living in Mongolia, or China’s own ethnic minority living in Inner Mongolia.
Even so, Matesz appears not to have closely read his own link! It makes clear it discusses the *traditional* diet and not the modern Mongolian diet that largely replaced it:
“…The Mongolians’ nomadic way of life determined their diet, which traditionally consisted mainly of the meat, milk and other dairy products provided by the livestock which they tended…today, the diet of the Mongolians has been expanded to include vegetables as well as pasta and rice…”
Further down Matesz says: “Most of them eat a WAPF low-carb primal paleo grass-fed animal fat dream diet…” Which for the reasons I supply above, is complete nonsense.
At that point Heather, I–once again–stopped wasting time at Vital Wisdom. –Bryan
I actually know someone who lives in Mongolia and I asked him about that. The guys he knows eat lots and lots of sheep and bread. He has a housekeeper who bought them “a sheep” and promptly processed every piece of it for eating. He is married to a Mongolian. He loves the culture. By all accounts, their diet is still mostly meat and dairy. And grass-fed. Yes: it’s exactly what WAPF would recommend. And what I tried to do here.
Their lifespan has increased in the last 40 years, Russians or no Russians. But the thing is: when you look at the times of Genghis Khan … the Khans had the same set of issues. Whether it is meat or wheat or the combo I don’t know, but shoot, the Pacific Islanders just do not have the same set of issues. Ever.
So whatever Matesz says … he’s pretty accurate in that post according to other sources. I would point out that the Japanese diet is getting replaced even more by the Western diet … but the Japanese are still doing ok. I’m still looking for the specific things that make people “not do ok”.
wbryanh, heathertwist- about red meat: I’m totally frustrated!….I *know* I’ve read about healthy native peoples who ate high animal food diets. I’ve just spent ages trying to find links on the internet, but no go. What I see is mostly very conventional, highly biased information, and frankly, a lot of crap and stupidity based on nothing like science of any kind.
In any case, heathertwist you said that wheat is a confounding factor, and it is. For instance that Otzi character is exactly what the Paleo people use as an example of all the detrimental effects of a grain based diet! There was a definite decline in health when humans switched to agriculture…..so it most probably wasn’t the meat per se. (As I mentioned earlier, I’ve only read about an association between grain- mostly gluten- and arthritis/joint problems, not with meat. Do you have a link for this? If you posted one already, sorry, I must have missed it). It’s difficult for me to see by what mechanism meat could cause joint problems; especially if one is eating the joint meat, and using meat on the bone, and collagen and connective tissue…..I would think this would be healthy, and actually prevent these problems?
The main problem is that most of the healthy Paleo-style meat eating hunter gatherers are cultures of the past. Most modern day meat eating cultures also eat dairy and fish, both high in taurine, so we can’t really compare the effects. However, there are a lot of healthy meat based groups of people around: the French come to mind- (well, traditionally; they’re beginning to succumb to obesity and other problems due to more junk food in the diet). Other healthy groups of meat eaters are the Austrians, and, though many people don’t seem to know this, in some parts of the Mediterranean they eat lots of red meat- (in some parts of Spain and Italy that I’ve visited. Last I checked, the Spanish were healthiest of the Europeans). And wbryanh mentioned the Swiss, also true.
Then the other problem is that modern day cultures who eat meat also eat things like gluten, vegetable oil, processed food, sugar, etc.; all confounders, so there isn’t really much we can prove one way or the other there. I do know personally people who are doing well by eating lots of meat; my father, for one. Though he’s not as old as your mother (heathertwist), he’s in great shape for his 80+ years, looks very young for his age, his brain is sharp and he has no joint problems or arthritis. I also have a cousin who lives mostly on meat and almost no vegetables or fiber, and he’s very healthy; no health problems that I know about.
In any case, the most renowned healthy meat based cultures were hunter gatherers of the past, and unfortunately, I just can’t find the link to prove it. The early explorers wrote about them, but this older information is not readily available on the internet. They were various African tribes, many American Indian tribes (like the Plains Indians, among many others; as I mentioned, there were many centenarians among the Sioux), and the inland dwelling Australian Aborigines. In fact, on observing their excellent health, and seeing they were free from cancer, one of these explorers had the theory that the key to cancer prevention was to eat more fresh meat, like the native people! (It wasn’t Steffanson, who also wrote a book, it was someone else, who’s name eludes me now. I’d love to read that book though).
I’ve also read that the Brazilian gauchos traditionally ate a mostly beef diet, but I can’t find any information online as to what their health status was like. I don’t know much about them….
So, basically, I’m not really convinced that meat eating people are less healthy, because I’ve read so much that states otherwise.
Since I can’t find the perfect link to prove my point- and I’m tired now, I just spent too much time looking around!- I’ll leave you guys with this:
http://www.sarahwilson.com/2012/08/how-to-live-to-100-eat-pork/
Hi Morgana, @heathertwist —
Morgana, thank you for working so hard to track down those healthy ancestrals who eat high animal-sourced diets, (by which you mean high *terrestrial* animal-sourced foods that give red meat right?) I hope you find it–I’m curious!
Your point about being too many confounders to truly suss out the effects of dietary elements–it is for me right on. Not just within the diet, but also so many factors outside the diet, which include pollution, rates of substance abuse, toxic living places and workplaces, and persistent stresses in societies due to poverty, inequality, lack of rule of law, and corrupt governements. I am not sure there’s any group left on Earth we can look to and say “yes, these people enjoy better/worse health than x solely due to the things they do eat/don’t eat.” Again, to look at the Swiss, who eat loads of cheese and sausage and evidently not a lot of seafood, yet enjoy some of the longest average lifespans on Earth. So many factors at play here, which include, for the Swiss, a pristine environment and a very peaceful and ordered and prosperous society.
That leaves us, nutritionally speaking, new pioneers. We study what anthropological, nutritional, biochemical, and genetic evidence we can find, and make ourselves into our own Grand Experiments. And test, test, test. I feel I am very much one of these pioneers because I eat 80% fat, 15% protein, and 5% carb foodway, compelling me into a more or less permanent deep ketosis. This is evidently an uncommon macro balance even among ancestrals, some shoreline Inuit who regularly chow loads of maktaaq being rare examples who eat similar macro balances. So how will this macro balance work for me in the long term? The jury may still be mostly out, but we may already start to see glimmers of the answer. It will make nine years in July I’ve been in deep keto, and I do and feel fabulous at 55. I walk and run as far as I want and as time allow–today just walked eight miles with 40 pounds of groceries and sundries in my pack. And now I sip a seriously fruit-forward malbec, nibble a sharply barnyardy goat tallegio, and write to you! –Bryan
Riffing off of this….
According to my Swiss cookbook, the Swiss were known to use cheese slices as a substitute for bread.
I’ve been drinking a lot of Walla Walla Vintners malbec lately, which is very fruit forward (more than the Argentines or French Cahors) but not at all sweet. I like malbecs for their astringency, so slowly sip them with meals rather than gulp them down. From time to time I take on the even more tannic Madiran and Irouleguy, grown down near the Spanish border. Not many people can stand to drink them, so they’re harder to find.
I’ve also been hitting the Salish seafood a lot. Fresh steelhead, mollusks and crab. It’s saddening to be the only one digging on the beach, then pass lines of cars waiting in the McDonald’s drive thrus on the way home. I don’t have to worry about my favorite spots getting overdug anyway…some of those quahogs must be 40 years old…
Thanks for this thhq. It was nice to read it.
I like Malbecs, and definitely like them fruity and full-bodied but not sweet.
As kids we went to the beach with pails and trowels to dig up loads of steamer clams, steam them in a huge pot, and dunk them in melted butter and fresh mashed garlic. So simple and satisfying. I can’t remember feeling so pleasantly full eating anything else, not at all “drugged.” –Bryan
Another big fan of Malbec here!
“I’ve also been hitting the Salish seafood a lot. Fresh steelhead, mollusks and crab. It’s saddening to be the only one digging on the beach, then pass lines of cars waiting in the McDonald’s drive thrus on the way home. I don’t have to worry about my favorite spots getting overdug anyway…some of those quahogs must be 40 years old…”
Nom! Salish diet!
“The Salish cornucopia includes a great abundance of roots, greens, berries, nuts, apples, seeds, flowers, honey and tree sap, tree bark, fresh plant sprouts, spruce tips, deer, elk, bear, pheasant, ducks, geese, freshwater eel, bullheads, trout, bass, and sea foods including seaweed, crab, seal, whale, sea urchins, mussels and clams, salmon, cod, halibut, and the small fish they call the oolichan. Together these foods and medicines provided a healthy balance of nutrients.”
https://www.culturalsurvival.org/publications/cultural-survival-quarterly/salish-feast-ancient-roots-and-modern-applications
Super-high taurine diet, along with slow carbs and loads of good polysaccharides.
My observation is that the high-taurine foods are more satisfying. Pair a big platter of clams and a good bottle of wine, and you have a feast! Well, that’s what I had for Valentine’s day … the clams were simmered with onions and garlic, probably not too unlike what the Salish would have done with their wild roots.
I also got a book on Japanese Donabe cooking. Their typical broth base (dashi) is made with shaved dried fish (bonito) and kelp, with some roots and greens added, plus some seafood, poultry, or meat. The “carb” level varies, but wow, is it ever satisfying!
http://www.amazon.com/Donabe-Classic-Modern-Japanese-Cooking/dp/1607746999/ref=sr_1_1?ie=UTF8&qid=1456295008&sr=8-1&keywords=donabe+cookbook