In Defense of Low Fat: A Call for Some Evolution of Thought (Part 1)

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:

devils_advocate

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!

fargo-wood-chipper-scene

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’!

time_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?”

carbjo_dog

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

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:

  1. 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.
  2. 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.
  3. 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!)

low_fat_diet_research_timeline

Without further ado, let me introduce you to some of these disembodied heads.


Walter Kempner: Rice and sugar and diabetes reversal, oh my

tree_kempner_2

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:

rice_diet_composition

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:

kempner_weekly_loss

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:

kempner_weight_loss_2

kempner_weight_loss_3

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:

kempner_weight_loss_4

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.

kempner_weight_loss_5

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:

fasting_blood_sugar_rice_diet

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:insulin_usage_rice_diet

Once again: eating virtually nothing but this…

kempner_foods

…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. Even supplements such as Kratom (you can always buy kratom from here) showed no increased benefits in diabetics.

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_rice_diet

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.

nom_nom_kempner

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

roy_swank

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

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:swank_diet_mortality_ms_non_msAnd 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!

swank_diet_34_year_mortality

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:

swank_diet_34_year_deterioration

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:

swank_exacerbation_rates

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

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: ???

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:

foods_permitted_morrison And the no-nos: foods_avoided_morrison(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.

morrison_diet_3_8_12_survival

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

pritikin(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:

pritikin_longevity_center

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:

ADA_vs_Pritikin_fasting_blood_sugar_table

ADA_vs_Pritikin_fasting_blood_sugar_bar_graph

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:

  1. Response of non-insulin-dependent diabetic patients to an intensive program of diet and exercise.
  2. 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:

chicken_3_oz

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:

hypoglycemic_drug_usage_pritikin_dietAnd 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:

insulin_usage_pritikin_diet(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.

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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.
barnard_2008_table

From “Effect of diet and exercise intervention on the growth of prostate epithelial cells.” Barnard, 2008.

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  • 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

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)).
barnard_1996_table

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

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

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

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.)

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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

From “Effect of diet and exercise intervention on blood pressure, insulin, oxidative stress, and nitric oxide availability.” Barnard, et al. 2002.

 From

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

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.”

barnard_2007_2_graph_mmp-9

From “Effect of a short-term diet and exercise intervention in youth on atherosclerotic risk factors.” Barnard, et al., 2007.

barnard_2007_2_graphbarnard_2007_2_graph_crp

  • 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.


Ancel Who?

keysOh 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.


Up Next…

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.

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.

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1,637 comments

  1. IMHO, you seem to be too quick to dismiss the calorie restriction aspect and the eventual weight loss of these diets as the reason for the ‘therapeutic’ benefits. I noticed you mentioned that weight loss doesn’t correlate with the results in multiple places throughout this blog post. Is calorie consumption not a confounding factor in these low fat studies?

    Are you familiar with the Dr. Roy Taylor of Newcastle University diabetes reversal studies? Within a week of a very low calorie diet, hepatic insulin sensitivity and intra-hepatic fat returned normalized while plasma triglycerides halved. In 7 days after just 1.3 kg average weight loss! In obese people, that’s a rounding error. See the link to the study below. I should also mention that despite the diet containing approx 75% sugar, the study participants produced ketones. That’s how compliance was monitored.

    Calorie restriction seems to be a simpler explanation than your ‘Macronutrient Swampland Fat Spectrum’ theory.

    http://link.springer.com/article/10.1007%2Fs00125-011-2204-7

    Here’s a quote from the Kempner Rice Diet in Hypertension study:

    “It is not unusual for the weight to decrease
    more or less markedly during the first
    twenty days. The reason for this weight
    loss may be that the amount of food given
    does not cover the caloric requirements;
    in this case the amount of rice, fruit and
    sugar must be increased unless reduction
    of weight is indicated.”

    This is probably sufficient to reverse liver insulin resistance and alter the hypertensive state.

    Are there not examples of insulin sensitivity improving on a ‘swampland’ diet? How do you explain all the Mediterranean diet studies?

    1. Hi Leonard,

      Thanks for your comments! I generally agree that calorie reduction is a confounder (both for these studies and for low-carbohydrate studies that lead to spontaneously decrease in calories). Weight loss and calorie reduction is probably a big reason anyone on Kempner’s diet saw a drop in triglycerides, for instance, since most studies using high refined carbohydrate/low fiber intake show the opposite, regardless of fat level.

      That said, I’m not sure the confounding is still relevant *years* into the diet, when people’s weight has stabilized (and their energy intake has presumably normalized) but the benefits of the diet remain — as several of the studies in this post demonstrate.

      More importantly though, the reason I’m not ascribing the results to calorie restriction is that we have some pretty convincing, direct evidence that dietary fat increases insulin secretion when eaten with carbohydrate (versus the carbohydrate being eaten alone), especially in diabetics. There are a number of other mechanisms (like postprandial blood lipids) that may also play into the etiology of the diseases discussed here.

      As for your second point, there are absolutely ways to improve insulin sensitivity when you’re still in the Swampland! They just aren’t a result of raising or lowering dietary fat. The crux of this post is that the therapeutic effects of reducing fat (or reducing carbs) aren’t really seen until we hit the extreme ends of the macronutrient spectrum. Things like the Mediterranean diet improve food quality, introduce a higher phenol and antioxidant intake, reduce low-nutrient/heavily process foods, and bring a number of other changes that will reduce disease risk or lessen existing conditions.

      In other words, I’m not saying the only way to improve insulin sensitivity is by eating very low fat or very low carb; just that if we’re going to see a direct effect of macronutrient manipulation, those zones are where it’s gonna happen. 🙂

      1. Denise, just because the weight is stable, doesn’t mean a person is no longer calorically restricted. CR doesn’t mean keep lowering calories and losing weight in perpetuity, does it?

        From wikipedia: “Calorie restriction (CR), or caloric restriction, is a dietary regimen that is based on low calorie intake. “Low” can be defined relative to the subject’s previous intake before intentionally restricting calories, or relative to an average person of similar body type.”

        So yes, they can still be CR years after the initiation of the diet.

        As for “direct evidence that dietary fat increases insulin secretion when eaten with carbohydrate (versus the carbohydrate being eaten alone)”. May be it’s only a problem with repetitive exposure and caloric excess, so the issues could still be caloric excess/restriction and not fat consumption.

        thanks.

      2. Do you have a source for dietary fat being insulinogenic? The data I’ve seen – a long time ago, so I can’t easily provide a source – showed an insulinogenic effect from dietary fat only for women, and not for men.

      3. Hi Denise, Thanks for your reply and really interesting work. Must be exhausting responding to so many comments. Looking forward to your part 2.

        My point was that there could be a much simpler explanation for the results observed. Given that macro-nutrients and calories are dependent variables, how does one determine the underlying cause of the reversal of these diseases? Looking at other studies and seeing common elements I guess.

        I think the problem with this discussion is that it seems to lack a framework or model of disease. Gerald Reaven’s lifetime of work has provided us with such a model. Insulin resistance, and the resulting hyperinsulinemia, most likely is the underlying cause of the diseases studied with the low fat diets mentioned above. From what I can tell this is where the history, biology, epidemiology and clinical data meet. Here’s one example in a study by Reaven mentioned by Stephen Guyenet:

        http://press.endocrine.org/doi/10.1210/jcem.86.8.7763?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

        http://wholehealthsource.blogspot.com/2015/06/insulin-resistance-predicts-variety-of.html

        How do we reverse insulin resistance and so the resulting diseases of hypertension, heart disease and diabetes? And does reversal imply cause?

        Successful studies and examples of reversing or at least decreasing insulin resistance has one thing in common: substantial cut in calories and ensuing weight loss. From the Mediterranean diet, to low fat (vegan or otherwise) to low carb, to intermittent fasting, to juice fasting (ever see the documentary fat, sick and nearly dead), to bariatric surgery, insulin resistance is decreased and when enough weight loss is achieved it is completely reversed. There are even anecdotal evidence of chemotherapy patients reversing diabetes and hypertension from not being able to eat.

        All of this together seems to imply that overnutrition is the cause of insulin resistance. And in susceptible individuals (South asians as a well known example), less overnutrition is required to induce this metabolic abnormality. That’s why BMI and obesity are not perfect predictors of metabolic disease. Some low BMI people are insulin resistant, whereas some obese are not.

        My sense is that food quality is less important than quantity. Usually when “quality” rises, quantity decreases. Mediterranean diet for example. Another confounder?

        An interesting aside to your discussion above (certainly news to me) is that multiple sclerosis might fit in this framework. I wasn’t able to review Swank’s study. It’s much more obvious when it comes to hypertension, heart disease and diabetes (and maybe some cancers) as opposed to autoimmune diseases like MS.

        The ultimate point is that many of today’s well known diet gurus are right in practice, but for the wrong reasons. Reaven plus Roy Taylor seems like a very reasonable model of these diseases.

        More Taylor:

        http://www.ncl.ac.uk/magres/research/diabetes/documents/BantingDiabeticMed.pdf

        http://link.springer.com/article/10.1007%2Fs00125-008-1116-7

        Finally, if you don’t mind, here’s a simple counter-example cherry for your fat spectrum theory:

        Aborigines going back to hunter gatherer lifestyle reversed insulin resistance (cited by Michael Pollan in one of his books). Is it quality or quantity? (See table 1 page 2) Greater than 10% fat consumed on average over the 7 week period, but notice how low calories were. Similar to Kempner’s diet (8 kg loss in a bit over two weeks for C.K. 51 year old male, see Figure 1 on page 2 of “Treatment of Hypertensive Vascular Disease with Rice Diet” by Kempner), weight dropped very quickly.

        http://www.naturaleater.com/Science-articles/traditional-lifestyle-helps-Aborigine-diabetes-.pdf

        Sorry for the long comment. Thanks again.

      4. Neisy, about what you say here “…we have some pretty convincing, direct evidence that dietary fat increases insulin secretion when eaten with carbohydrate (versus the carbohydrate being eaten alone), especially in diabetics.” Did you ever answer psychohist’s question about the source(s) for this direct evidence? You may have, I just couldn’t find it. Anyway I’d really like to see this evidence too when you get a chance. Thanks –Bryan

    2. Leonard, you say:

      “…despite the diet containing approx 75% sugar, the study participants produced ketones.”

      Ketosis on a high-sugar diet seems hard to believe, but in the New England Journal of Medicine I find:

      “Kempner prescribed a diet composed primarily of rice and fruits. It was low in calories, fat, protein, and sodium (<30 mmol per day) and caused ketosis, weight loss, and a decrease in blood pressure.”

      http://www.nejm.org/doi/full/10.1056/nejmsa0903829

      Denise, anyone… What is going on in publications/physiology?

      1. It seems that any time the human body is using fat stores for energy, ketones are produced. It’s not specific to very low carb. So any calorie deficit will produce ketones. Occurs during fasting as well.

    3. Mine did, mostly because I am not sedentary anymore. I’m enjoying being high calorie, high fat AND high carb in the exact center of the swamp.

  2. Hi Denise. Thank you for a fantastic investigation rendering into an extremely good article. I´m from Stockholm area and would like to hand you a Nobel prize but sorry I´m not on the committee and can´t find a suiting prize either; but there should be one bettter than the economy prize.
    You serve an aspect where we can see similar results in many senses with two kind of opposite diets LCHF and LFHC. It could be making sense of why Dr Kelley/Rodriguez could make opposite types of diets to treat cancer and from what I gather getting results. In the western “either or”-type of thinking (dialectical logic) these things usually leads to conclusions like “confusing…so it doesn´t matter how you eat”. In chinese medicine thinking this is more easily understood even though they would have different explanatory models on how to regulate health with diet. I´m looking very much forward to your part 2.
    Peter Torssell (Bach chin med, Jiangxi university)

  3. Denise, Are you familiar with the work of Dr Richard Johnson (U of Colorado, Denver)? He wrote “The Fat Switch” which gives a detailed account of the role of fructose–not glucose–in leading to hypertension and diabetes. Hope you can comment on his findings?

    Sincerely,

    “Have no idea what to think– or eat–anymore”

  4. Truly impressive work done here. But is it low-fat, or is it low-saturated-fat? If I have whole food plant-based low-fat diet and add nuts and seeds to make it like 50/35/15 (carbs/fats/protein), is the magic lost? Should I just experiment, add nuts and seeds, then ditch them and do the blood work? How do I know which is better?

      1. Whether it’s the chicken or the egg (sorry, vegans, that analogy probably sets your hair on end), veganism and self-righteousness go hand in hand. I read an article (on how easy it is to eat vegan) on another blog tonight, wherein the author stated, “But once we accept that veganism is an unavoidable step on the path to an ethical and authentic life, it soon becomes clear that experiences of social awkwardness are trivial compared with the significance that veganism brings.” The author then went on to recommend dumping friends and relatives that didn’t espouse the cult of veganism. I thought that had to be the ultimate in self-absorbed, irony-challenged, self-righteous smugness. But then, I read the comments, wherein one of her friends had written, “Great article. So nice to see an article on veganism that doesn’t bash non-vegans”. Aaaack!!! It’s enough to make one want to go out and eat a 20-ounce piece of prime rib washed down with a fifth of Scotch.

        1. Hahaa! Dunno how I missed this gem of a mini-thread till now. Annie, your idea to “eat 20-ounce piece of prime rib washed down with a fifth of Scotch…” Makes me wonder about the fourth caloric nutrient. Does the acetaldehydic diet cure self-righteousness or make it worse? –Bryan

  5. After the preview of the post title some time ago, I was afraid the post would be full of apologetics for low fat quasiveganism. I’m pleasantly surprised to see the admission that it’s not the feel good things like whole foods and micronutrients that are what’s important, at least in these cases, and that the data suggest that fats have to be not just low, but extremely low, to provide these benefits.

    I myself am a ketogenic paleo proponent, but I have noticed indications over the years that a very low fat diet might work for weight loss, not least because I was extremely thin on such a diet in my own youth. It’s interesting to see some of the older studies on the matter, even if the methodologies aren’t perfect.

    I do have to point out that these results are not actually inconsistent with the carbohydrate insulin hypothesis for obesity.

    I loved Taubes’ “Good Calories, Bad Calories”, but one of the weaknesses in that book is that he never really examines where the fat comes from, that is driven into the fat cells by insulin. He seems to assume that it can come either from dietary fat or from fat produced in the liver from blood sugar, but left unaddressed is the fact that the insulin spike is relatively short lived, while fat production from large amounts of carbohydrates takes longer.

    I would suggest that in fact, obesity requires both sufficient carbohydrates to produce the insulin spike, and sufficient dietary fat to provide a high level of circulating lipids to be driven into the fat cells. On a low carb diet, you don’t store fat because you don’t get the insulin spike; on a very low fat diet, you don’t store fat because there’s no fat to be stored.

  6. Hi Denise,

    Can you please read this, possibly groundbreaking, aritcle: “Iron Fortification, Disease, and Obesity: An Update with Data Refinements,” paying attention to this passage:

    “Links to refined oils

    “Traditionally, many scientists and health gurus have pointed out that refined oils—like those from soy that are high in linoleic acid (LA)—a polyunsaturated omega-6 fatty acid—have been linked to obesity epidemic. We believe this fits perfectly into the exacerbation of micronutrient imbalances found in obesity. We found evidence that a diet high in refined oils might just make you absorb lots of iron, which in excess can promote oxidative stress in organs and tissues. The following chart from this article shows the trend.”

    N.B. That may apply to many high-saturated fat foods as well, but some, such as eggs and cheese, seem to actually reduce iron absorption; tannins and many phenols, etc., do as well.

    … and tell me if you think it’s more than a little plausible that one important benefit of a lower-fat diet (depending, perhaps, on which fatty foods we’re talking about) is a reduction in absorbed iron and therefore inflammation and therefore hypothalamus damage and therefore appetite?

    Further, it occurs to me that because white grains are fairly bland, many (but not all! and this may explain yet another portion of the differential results) people who eat a low-fat, grain, legume, tuber, etc., diet will probably eat whole grains instead of fortified grains—thus dramatically reducing their iron intake while increasing their intake of copper.

    Finally, let me point that Kempner may have had greater success with non-iron-fortified rice than could be obtained in North America now with iron fortified rice.

    1. That link about iron fortification was very interesting! (And I’ve read, though I don’t know if this is true, that high iron levels might be correlated with heart disease as well). This fortification theory might partly explain why some European countries, who also eat moderate fat and carbohydrate- i.e., “mixed diets”- appear to be quite healthy- (there isn’t so much food fortification in Europe). I would also like to point out that soy is an endocrine disruptor as well, aggravating the situation even further.

  7. Hi Denise,

    Can you please read this, possibly groundbreaking, aritcle: “Iron Fortification, Disease, and Obesity: An Update with Data Refinements,” paying attention to this passage:

    “Links to refined oils

    “Traditionally, many scientists and health gurus have pointed out that refined oils—like those from soy that are high in linoleic acid (LA)—a polyunsaturated omega-6 fatty acid—have been linked to obesity epidemic. We believe this fits perfectly into the exacerbation of micronutrient imbalances found in obesity. We found evidence that a diet high in refined oils might just make you absorb lots of iron, which in excess can promote oxidative stress in organs and tissues. The following chart from this article shows the trend.”

    N.B. That may apply to many high-saturated fat foods as well, but some, such as eggs and cheese, seem to actually reduce iron absorption; tannins and many phenols, etc., do as well.

    … and tell me if you think it’s more than a little plausible that one important benefit of a lower-fat diet (depending, perhaps, on which fatty foods we’re talking about) is a reduction in absorbed iron and therefore inflammation and therefore hypothalamus damage and therefore appetite?

    Further, it occurs to me that because white grains are fairly bland, many (but not all! and this may explain yet another portion of the differential results) people who eat a low-fat, grain, legume, tuber, etc., diet will probably eat whole grains instead of fortified grains—thus dramatically reducing their iron intake while increasing their intake of copper.

    Finally, let me point that Kempner may have had greater success with non-iron-fortified rice than could be obtained in North America now with iron-fortified rice.

    1. As I’ve explained in another comment (might be in moderation). It’s not just the iron. The B vitamins added to enriched foods are known to have appetite-stimulating properties. And the levels of the B vitamins (and iron) were significantly increased in 1983 by lobbyists pushing the FDA. High iron diets have also recently been shown to increase appetite as well.

      The entire enrichment formula (particularly after 1983) seems to be designed to increase appetites. See my other comment when it posts.

  8. Swampland is an interesting analogy – a stagnant mix of land and water. Yet the macro-nutrient ratios particular to swampland need not be endured where the mix of each meal is toward one pole or another. For example fruit in the morning, HCLF for at lunch and LCHF for dinner. The body then has 12+ hours to digest and and deal with the fats that don’t mix with the carbs. This woe was promoted with the Fit for Life diet. I call it cycling – as in moving from McDougall to Paleo. Sitting at one end or the other can be a problematic as sitting in the middle/swampland. I don’t know if this cyclical diet has ever been tested. Mixed versus partitioned meals. I mean you don’t find swampland in nature, which I would assume tends toward mono-meals.

    1. “swampland (I assume you mean HF/HC or MF/MC) does not occur in Nature”. But it does. See my note on human breastmilk, at an average of 52% fat, 42% carb. For comparison, as I noted, a cake doughnut is 51% fat, 44% carb. And, while analysis of Paleo trash midden and skeletal remains gives us a good idea what foods our Paleo forebears consumed, we don’t know if the starchy tubers were consumed with the lean red deer, or the fatty sea mammal, or if they were separate meals.

  9. One of the mysteries of Pritikin is, Why didn’t he convince the medical community?

    Bad science seems to have been part of the story.
    Here’s an exerpt from a letter by Pritikin to JAMA, 1984:
    —————
    To the Editor.— Since 1976, JAMA has consistently reported the Pritikin Program unfairly….The so-called Pritikin diet used in the study was neither the Regression diet used at my centers and in all my research since 1974 nor the Maintenance diet described in my books meant for asymptomatic patients….Hutchison’s subjects consumed twice the fat and three times the cholesterol permitted on my more lenient Maintenance diet for well people!
    http://jama.jamanetwork.com/article.aspx?articleid=391685
    —————
    Really, really bad science… dishonest, even.
    Testing something else and calling it the “Pritikin diet” should be beyond unethical.

    1. That depends. If the study is on intention to treat – the only way to control massaging of the data to get the results you want – then it has to take into account people who don’t manage to adhere to the diet. Excluding nonadherers is far worse science.

  10. etc. … and from minger’s recent twitter posting: “if “Eden” = a place free from both vegan AND low-carb dogma, then yes, I would love to go there! ;)”

    hate to say it, but she’s moving away from the low-carb, high-fat nonsense because she’s learning more and more about nutrition …

  11. Denise, I LOVE YOU! Seriously, I wish there were more people so dedicated like you! Thank you for all this work, can’t even imagine how long it took!! Any yay, I’m so glad to FINALLY see confirmed what I had been suspecting all along, that both extremely are actually working…. You’re the first person I know of that actually put together all the research…. We needed this badly! You’re such an enrichment for the nutrition community! Couldn’t be more grateful for this! 😉
    But goddamit I just can’t leave swampland… 😀 (I’m a former vegan as well haha)

    Daniela
    (https://www.facebook.com/Detoxyourlifecoaching)

    PS: Oh and I almost forgot, I love your writing style and sense of humour! Keep going! 🙂

  12. With regard to the Inuit’s high fat diet – it’s all about the genetics

    https://www.ucl.ac.uk/news/news-articles/0915/170915_Inuit_diet
    How the Inuit adapted to Ice Age living and a high-fat diet

    The Inuit diet is an example of how high levels of omega-3 fatty acids can counterbalance the bad health effects of a high-fat diet. Fish oils were thought to be protective as the Inuit have a low incidence of cardiovascular disease, but having discovered their special genetic adaptations to this diet, the researchers from UCL, UC Berkeley and the University of Copenhagen say the benefits of the Inuit diet cannot be extrapolated to other populations.

    http://cteg.berkeley.edu/~nielsen/wordpress/wp-content/uploads/2015/09/Science-2015-Fumagalli-1343-7.pdf
    Greenlandic Inuit show genetic signatures of diet and climate adaptation

    http://www.npr.org/sections/thesalt/2015/09/17/441169188/the-secret-to-the-inuit-high-fat-diet-may-be-good-genes
    The Secret To The Inuit High-Fat Diet May Be Good Genes

    http://www.nytimes.com/2015/09/22/science/inuit-study-adds-twist-to-omega-3-fatty-acids-health-story.html?_r=0
    Inuit Study Adds Twist to Omega-3 Fatty Acids’ Health Story

    http://news.berkeley.edu/2015/09/17/what-the-inuit-can-tell-us-about-omega-3-fats-and-paleo-diets/
    What the Inuit can tell us about omega-3 fats and ‘paleo’ diets

    These genetic mutations in the Inuit have more widespread effects. They lower “bad” LDL cholesterol and fasting insulin levels, presumably protecting against cardiovascular disease and diabetes. They also have a significant effect on height, because growth is in part regulated by a person’s fatty acid profile.

    Nielsen noted that this is some of the clearest evidence to date that human populations are actually adapted to particular diets; that is, they differ in the way they physiologically respond to diets. Just as genome sequencing can lead to personalized medicine tailored to an individual’s specific set of genes, so too may a person’s genome dictate a personalized diet.

    “People ask themselves whether they should be on a Stone Age diet, for example. The response may well depend on their genome,” Nielsen said

    1. Huh…..is this true then of the Masai, the Samburu, the Sioux Indians, Somalian shepherds, the Tokelauans, the French, the Greeks, the Swiss…..I could go on and on……

      1. Morgana, yup, agreed. About the Inuit fat and glucose gene variant studies, a lot of noise signifying … not much. If I had time, I’d research the vested interests behind these studies, or at least those who reported on them. Who rely on uncritical readers to propagate them.

        1. There is no proof, little if any cause and effect diet research out there. There is just a lot of stuff that points us in different directions, and raises interesting scientific questions. I thought the purpose of blogs is to be able to explore issues.

          1. Rebecca, you’re quite right about the lack of proof. The best we can do is try different foodways, track them as carefully as we can, and measure as many health metrics as we can. I was dx’ed T2D in 2007, and after failing on HCLF, I changed to LCHF in July 2007 with intermittent fasts and constant paring down of engineered foods and non-food products. My BGs and health measures have been improving ever since, and it’s a manageable and even very enjoyable lifestyle. Denise’s examination of the extreme LFHC diet is intriguing and Peter over at Hyperlipid proposes some fascinating biochem to explain how it works:

            http://high-fat-nutrition.blogspot.com/2015/10/protons-and-ultra-low-fat-once-more.html

            Thus I find extreme LFHC it a very interesting academic exercise AND a possible fallback foodway if I somehow lost access to high-quality dietary fat. However I’m not yet convinced HCLF can effect permanent metabolic corrections any more than HFLC can so for now still see it as just an alternative therapeutic diet that works for SOME people but far from all, and likely truly normalizes the BGs for just a minority. Plus, there’s other factors besides macronutrients, esp the massive amounts of hormone-disrupting chemicals in very many mainstream products we come in contact with every day.

              1. It just goes to show you can find studies supporting positive results of HCLF and also LCHF for treating disease conditions. Some people will do well on one or the other or maybe even both. I have done well trying both extremes. The point in all of this is, I think, read and decide for yourself if you want to try different dietary regimes. And then pay attention, if it works for you and continutes to work great. If not change. No scientific evidence is going to come out anytime soon detailing a diet for whatever ails us. It is still experimentation time and will be for a long time to come.

                1. Rebecca, I agree. Totally. No study can account for the myriad inputs in our daily lives and our genetic diffs, esp for effects over the long term, over which chronic disease usu develops. Nor will they ever mean much until we greatly refine genetic testing and suss out what the genes actually do, AND if we can convince a meaningful sample of people to agree to live for years in completely and precisely controlled circumstances and submit to around-the-clock observation. Oh, and employ a really smart and completely unbiased research team to develop the methodology and conduct the experiment totally funded by unvested interests. Are you holding your breath for all of that? Neither am I.

                    1. What it strongly suggests is that my LCHF foodway (80% fat, 15% protein, 5% carb) works far better for me than Ma Pi 2 would. See Table 1 here: http://www.researchgate.net/publication/260212681_MA-PI_2_macrobiotic_diet_and_type_2_diabetes_mellitus_pooled_analysis_of_short-term_intervention_studies. Over the same three week time period, for mean glycemia (mmol/L) for Ma Pi 2 study subjects across the four countries, they started out lower than me (9.0 vs my 9.5) and after 21 days finished much higher than me (6.1 vs my 5.0). All my other blood panel numbers normalized too.

                    2. The Ma Pi 2 21-day mean of 6.1 mmol/L is still firmly in the pre-diabetic range. My 5.0 is in the normoglycemic range (4.2–5.3). In three weeks, I dropped from diabetic to normoglycemic.

                1. The book Proteinaholic by Garth Davis MD takes a very intelligent look at the research, and he certainly knows how to evaluate and interpret research studies and makes it clear how he does that.

                    1. Yes he is, but he was not in the past, he used to believe high protein was good. He does not recommend people go vegan or anything like that, he is clear it is up to each person to decide for themselves. He does do a good evaluation of the relevant research out there

                  1. Rebecca, I looked at the doctor’s FB page. It’s very hard not to see him as a strident vegan very much tied to his agenda, however late in life he may have come to it. Even the title of his book gives me pause. We’ve long heard about “sugar-holics” and “carboholics.” But whoever heard of a “proteinoholic?” I googled it, and just about all the top hits relate to this doctor’s book. Not a phrase used in general parlance. Nor have I EVER felt the need to binge on meat the way I often did for baked goods.

                    1. Proteinaholic is a turn of phrase it in no way applies that people are binging on protein. He himself is now a firm vegan, he does not say it is for everyone in his book, but yes he absolutely believes it leads to better health. None of us believe everything we read let alone on blogs. Look at all the reports on research studies by reporters they often get it wrong and are not very often qualified to be able to tell good research from bad. My only point was that if people want to know more about research in these areas the book is very well written in that sense and for those who want to know about both sides of the diet spectrum this is a good one. I read the book.

          2. And yes, meant to say Rebecca, I agree absolutely we should be able to–it’s vital for us to–explore issues! For that I found Denise’s to be one of the best, along with Mark’s Daily Apple, Hyperlipid, and many others. I just take issue with folks who make unsubstantiated assertions using merely correlative evidence. Unfortunately, turning correlation into causation is a huge problem, not just among citizen bloggers but even with the most highly placed professionals.

        2. wbryanh- yes, my problem with the whole thing is that this study was obviously biased from the outset. Basically, the whole tone of the article was “we know that high fat diets are damaging, so let’s try to figure out why it’s not harming the Inuit”. When I see such blatant bias, the whole thing loses credibility for me. This is just not scientific. But, it happens all the time I’m afraid.

          Logically, it does make sense that the Inuit would need a high fat diet, as they need to get enough dietary vitamin D since they have a harder time getting it from the sun. However, this does not necessarily make high fat diets “damaging” for other people, as there are plenty of native groups living in warm countries who also consume a high fat diet and don’t have chronic disease.

          1. Morgana, per your post, I went back and reread the OP’s links. I though it was the OP who wrote “…can counterbalance the bad health effects of a high-fat diet.” But you’re right, he/she copied it from the UCL piece. Another example of how even a solid-rep entity like UCL can be trailing-edge, can mindlessly parrot CW. Even CW like “dietary fat is bad” which a raft of new research seriously challenges.

            The extreme LCHF discussion is very interesting, esp as I start to see emerge biochem mechanistic theories for why it might work (see recent Hyperlipid post). But mainly, I’m wary of the pure macronutrient focus. Human nutrition and health is richly multifactorial. Looking just at one of those factors–here, macronutrients–gives too much potential for confounding factors. Esp these days in our horrendously complex daily environment with 100k novel chemicals since ~ 1945, many of which are estrogenic, are hormone disruptors, which promote chronic cell wall impermeability which helps lay the groundwork for metabolic syndrome, the gateway to much of today’s global scourge of chronic disease. Plus, until recently, food insecurity and subsistence diets were the norm. People had to adapt to what was available, whether LCHF, HCLF, or anywhere in the “swampland.” Viewed through the ancestral lens, a macronutrient “magic-at-the-ends-swampland-in-the-middle” approach, while very interesting, may, in the end, not be relevant. At best it may be something that illustrates proximate causes in a new way, but serves only to confirm and underscore the ultimate causes for our modern nutriment mess. Today’s chronic hypercalorism and chronic environmental toxicity may offer, at bottom, the main explanations for what led us to our current foodway and chronic disease problems. Still, the nerd in me looks forward to Denise’s Part II! –Bryan

            1. I think we should be wary of ascribing too much importance to micronutrients, especially if the data is pointing us to macronutrients as the important factors, as does the data in Denise’s column here.

              1. Psychohist, I agree we should be wary of ascribing too much importance to any “nutritionism” in general, be it macronutrients, micronutrients like vitamins and minerals, phytochemicals, etc. At least at this still early stage of our knowledge of them. I can’t agree though that macronutrients are necessarily the important factors. Completely absent from this discussion: the effect of hidden undeclared toxins present in so much modern food, esp hormone disruptors like BPA and phthalates.

    2. Charles, where in these studies does it actually spell out HOW the genetic variants in Inuit better adapt them to a high PUFA diet? I saw this flurry of announcements about this a month or two back, but none of them explained exactly how the Inuit better utilize PUFAs than the rest of us. In fact, that Berkeley link you give says “…knowledge about the genetic basis of human adaptation to cold climates and lipid-rich diets <>…” the UCL link you give says : “…genetic mutations found in nearly 100 percent of the Inuit are seen in only 2 percent of Europeans and 15 percent of Han Chinese, which means <>…” Charles, first, none of us can synthesize the base PUFAs (linoleic acid, the 18C Omegas 6 and alpha-linoelic acid, the 18C Omega 3). Plus, and more to the point, if the Inuit are already eating loads of EPA and DHA (the longer chain O-3s), then why would they even *need* to synthesize these. To me the reporting on this discovery is exceptionally lacking, even quite poor, and certainly confusing. Any light you can shed on this, I’d appreciate it.

      1. Argg. WP clipped the text between the angle brackets in two places. Replace above with this:

        Charles, where in these studies does it actually spell out HOW the genetic variants in Inuit better adapt them to a high PUFA diet? I saw this flurry of announcements about this a month or two back, but none of them explained exactly how the Inuit better utilize PUFAs than the rest of us. In fact, that Berkeley link you give says “…knowledge about the genetic
        basis of human adaptation to cold climates and lipid-rich diets REMAINS LIMITED…” the UCL link you give says : “…genetic mutations found in nearly 100 percent of the Inuit are seen in only 2 percent of Europeans and 15 percent of Han Chinese, which means they would SYNTHESIZE O-3s DIFFERENTLY FROM THE INUIT…” Charles, first, none of us can synthesize the base PUFAs (linoleic acid aka the 18C Omega 6 and alpha-linolenic acid aka the 18C Omega 3). Plus, and more to the point, if the Inuit are already eating loads of EPA and DHA (the longer chain O-3s), then why would they even *need* to synthesize these. To me the reporting on this discovery is exceptionally lacking, even quite poor, and certainly confusing. Any light you can shed on this, I’d appreciate it.

        1. ??? Charles, I just cited out of that. Here: “…knowledge about the genetic
          basis of human adaptation to cold climates and lipid-rich diets remains limited…”

          If you could stow your snide comments and actually answer the question, I’d appreciate it.

        2. Sure it says “Greenlandic Inuit show genetic signatures of diet and climate adaptation” Big whoop. Doesn’t go into HOW this is supposed to work, AFA I could see. Thus, my original question to you.

        3. Charles, let’s break that Berkeley study down more. Here’s the meat of it with my questions IN FULL CAPS:

          “Previous studies have attempted to understand the genetic basis of human adaptation
          to local environments, including cold climates and a lipid-rich diet (1). A recent
          study found evidence that a coding variant in CPT1A, a gene involved in the regulation of
          long-chain fatty acid –REGULATE HOW?–, has been the target of strong positive selection in native Siberians, possibly driven by adaptation to a cold climate or to a high-fat diet (2). Another study found evidence that adaptation to the traditional hypoglycemic diet of Greenlandic Inuit may have favored a mutation in TBC1D4 that affects glucose uptake –AFFECTS GLUCOSE UPTAKE HOW? AND HOW IS THIS SUPPOSED TO RELATE TO LIPID METAB?– and occurs at high frequency only among the Inuit (3). However, knowledge about the genetic basis of human adaptation to cold climates and lipid-rich diets remains limited…”

          Where’s the takeaway here Charles? In your view? All I see is that researchers found a few gene variants in this Inuit that relate to lipid and glucose metab. In itself, purely correlative. But if these researchers have any idea how the products of these genes are supposed to work mechanistically, they didn’t share it with us. Unless I overlooked it.

        4. Charles, if you can cite the CAUSITIVE evidence in the links you furnished above, then great. Otherwise your claim “With regard to the Inuit’s high fat diet – it’s all about the genetics” is unsubstantiated.

    3. Charles, where in these studies does it actually spell out HOW the genetic variants in Inuit better adapt them to a high PUFA diet? I saw this flurry of announcements about this a month or two back, but none of them explained exactly how the Inuit better utilize PUFAs than the rest of us. In fact, that Berkeley link you give says “…knowledge about the genetic
      basis of human adaptation to cold climates and lipid-rich diets REMAINS LIMITED…” the UCL link you give says : “…genetic mutations found in nearly 100 percent of the Inuit are seen in only 2 percent of Europeans and 15 percent of Han Chinese, which means they would SYNTHESIZE O-3s DIFFERENTLY FROM THE INUIT…” Charles, first, none of us can synthesize the base PUFAs (linoleic acid aka the 18C Omega 6 and alpha-linolenic acid aka the 18C Omega 3). Plus, and more to the point, if the Inuit are already eating loads of EPA and DHA (the longer chain O-3s), then why would they even *need* to synthesize these. To me the reporting on this discovery is exceptionally lacking, even quite poor, and certainly confusing. Any light you can shed on this, I’d appreciate it.

  13. It all comes down to give your body the tools to be healthy. Low fat or high fat, low carbs or high carbs etc., get your minerals and vitamins and fat in the right portions. Miss one take more greens, miss one take more fat, miss one take more carbs etc.

  14. Protein Power had a good discussion on insulin and it also went into the influence of the different macronutrients on insulin and glucagon. This is what the Eades stated in the book:

    large amt of carb and small amt protein elevates insulin the most and quite significantly — they give it a 9

    Carbs by themselves they give a 5

    Carbs plus fat they give a 4

    Protein, Protein and Fat, High protein and low carb they give a 2

    Fat they give a zero. Fat is invisibule to insulin.

    So the most deadly diet is high carb and moderate protein: Burger with fries and a coke comes to mind , rather than white rice and juice.

    1. Burger with fries is a high fat diet, which will leave you dead by mid 70’s. High carb moderate protein would be more like sweet potatoes, rice and fish. Like Okinawans and Japanese ate (traditionally), leaving them dead in their mid 90’s. Both diets are deadly but I’ll take the high carb moderate protein for the extra 15-20 years of life.

  15. I don’t think there is a simple solution to this whole conundrum. This is a universe that insists on having dietary paradoxes.
    Physicists will have developed a grand unifying theory explaining quantum gravity and the origins of belly-button fluff before we come up with a full dietary mechanism for how heart disease develops and the miraculously curings from contradictory diets.

    The only common thread to all successful intervention regimes is the word ‘intervention’. Which makes me think it is not about the macro-nutrients at all, but the fact that someone is actually caring.
    I think we can conclude from the Sydney Diet Heart Study, that high Omega 6 safflower oil is bad, but I have a feeling that if Denise Minger was handing out free kittens to all the people in the intervention group, and smiling at them while taking their blood pressure, the Sydney Diet Heart study results would have been instead certain proof that high PUFA dietary intervention works spectacularly well!
    What the most successful dietary intervention studies seem to show is that good care, strong motivation and convincing pep-talks from an eccentric researcher really work.

    I am aware of a concept called ‘small study’ effect. It is the notably larger effect that is always obtained in smaller studies. As we scale up a study, it is understandable that the special attention the intervention patients get is less. We put this down to ‘bad’ science in the small study, but maybe ‘bad’ science means good medicine?

    Yes, it is just the placebo effect – but it is a drug you cannot have too much of!

    It would be interesting then to run an intervention trial using a traditional witch doctors, kittens* and homeopathy. I am sure that such a trial would produce amazing results providing the patients in the intervention group were getting heaps of attention.

    * the witch doctors and the kittens will be kept separate!

    1. Gordon, thank you very much for these new (to me) things to think about! And I am still totally LOL at this: “… if Denise Minger was handing out free kittens to all the people in the intervention group, and smiling at them while taking their blood pressure…”

    2. Presumably no diet study can ever by placebo controlled (i.e. blinded), and is it possible that when someone changes their diet pretty massively, they get a very strong placebo effect?

  16. I haven’t looked through all the comments, nor all of the text in the post, so please forgive me if this has already been covered in the blog post or comments. I’m thinking about how the patients fare on such low nutrient diets. I understand that an “all-fat diet” such as many low-carbers strive for may lack in magnesium and other necessary stuff, but the rice diets and fruit-rice-sugar diets and such appear to be totally lacking in a lot of nutrients! I’m working really hard to get all the nutrients I need while on a nutrient dense diet with a slightly negative energy balance to lose weight but not lose health. I cannot imagine staying on one of those diets for very long helped anyones levels of anything. How do you think they coped?

    1. “I haven’t looked through all the comments, nor all of the text in the post, so please forgive me if this has already been covered in the blog post or comments.”

      What you’re really saying is: “My question may have been answered in the blog post or the comments but I’m too lazy to read through it all but I want you take the effort and answer my question anyway.”

      No, you’re not forgiven; read the whole post and comments.

    2. They’re weight loss diets, for God’s sake! No one eats like that forever. Atkins is the same thing. You only do HFLC until you accomplish the weight loss then HOPEFULLY go back to a normal diet and maintain.

    3. I have been on diets like that and actually they worked very well for me. Mine were “body builder” diets … uber low fat, with some very lean protein, starch, and vegies. What didn’t work for me eventually was the social aspect (how to eat out?) and I lacked good fats, I think. I seem to need fish oils or my skin gets too dry and I don’t think so clearly. I’m trying it again now with a few tweaks. So far so good. I feel way better … more energetic, stronger.
      The 10% fat isn’t far off from some of the traditional diets. The human body is quite able to synthesize most kinds of fat, but some people don’t digest fats all that well, and I think I’m one of them. I just try to make sure that the 10% is the essential fatty acids, not the stuff my body can easily make or has already stored.
      Now, I’m using white rice as my main starch, and I’m not particularly avoiding fruit or sugar. So how is my blood sugar? Just fine, thank you.
      Long term … I guess I could add more olive oil or ice cream now and then. My diet is more Japanese than Mediterranean though, so maybe it would be more sesame oil. But mostly I’m happy where I’m at. I’m eating loads of my favorite foods, though maybe cooked a bit differently.
      Now as for those Norwegians … back in the day, the Norwegians ate a seafood-centric diet, as did the Japanese. And the Irish and English. And much of Asia. The mammal-wheat/barley diet is new to much of the world, and hasn’t been very successful that I’ve seen. I’m beginning to think though, that the “fat” issue is somehow separate, and with the less than 10% fat, even the mammal/wheat diet is less harmful.

  17. I’m rather content with my current high fat way of eating, having attempted vegan and even fruitarian diets in the past. Campbell’s “China Study” was once my “bible,” but Gary Taubes changed my mind. However, I’m not above experimenting with changes just to see what might happen. I have no need to lose weight, nor any real health problems to fix. However, if I did decide to try “taterism,” I’m worried that my teeth would start to decay again like they did when I was gulping down smoothies made from 10 bananas and assorted fruits for breakfast, lunch, and dinner. With all the glowing results from very low fat diets you’ve posted above, did any of the researchers comment on side effects to oral health?

  18. In years past I’ve tried several diets that worked really well for me. I.e. I ate about what I wanted to eat (not hungry), digested food well, and was skinny. Unfortunately all of the failed after some period of time … either I stopped losing weight, got depressed, or my skin got too dry. I had a very hard time figuring out what the common thing was between these diets, since all were very different philosophically. Nor why they stopped working.
    So now I think I have it … all were (the way I implemented them anyway) very low fat, and as it turned out, yes, low calorie. It’s hard to get high calorie without a lot of fat.
    What messed them up, I think, were 1) Wheat: on one of them, you could start eating wheat again after 8 weeks, which was exactly where the diet “stopped working” for me. 2) Lack of ANY fat: I needed something for my skin at least and 3) Lack of fish oils (fish oils make my brain happy). 4) Dairy. Dairy affects me in weird ways, and when I re-introduced it, the diet also stopped working.
    So I’m trying again, while JUST concentrating on fat calories. It’s not hard for me to keep the fat calories low if I’m eating “basic” foods and not packaged ones. A big bowl of noodles and kimchi with shrimp and broth works fine for me. I add some oily fish and sesame for skin health.
    What I’m finding is that same sense of well-being I had in the old days! What I’m finding is that some of my diets in the old days, although I FELT like I was “eating anything” in fact I tended to eat food I made myself and the actual fat content was lower than I thought it was. For instance: If I make a bowl of rice noodles in a pot of boiling water, and add some frozen shrimp and a cup of frozen peas and some chopped mushrooms and some broth concentrate or Tom Yum mix … it’s a really great huge bowl of noodles. And the fat content is very low. Even adding some salt pork, the fat content is low.
    So a lot of it is about cooking styles and ingredients. That is where the 78-year-old grannies win. My own Mom is 90, and she mostly eats things like … cook some chicken feet. Save the broth. Now boil a bunch of vegies in the broth, eat it with noodles or rice or something. She acts like she eats anything, but if you look at her food, it is in fact low fat. She doesn’t digest fat well at this stage of life, and she has gotten skinnier.
    Anyway, thanks Denise! This has really helped my thinking about all this. The one thing I fear though. The “food combiners” may end up being correct! Maybe one day we need to be low fat, while the next day we need to be low carb. A meat day, and a non-meat day. Sigh.

  19. Well whaddya know….

    Just after I post a similar string on your old Ancel Keys thread, you dug deeper and found his predecessors.

    Now start a string on Eat Well and Stay Well and I will be happy. I’ve just gotten to the part about Scientific Dieting, which was Ancel’s name for what I lost all my weight on (and kept off for 8 years). Calorie counting. Remarkably his counts for walking and bicycling are almost exactly what I use. His taste – and attitude – toward wine are similar to mine.

    I guess that if you do research for a living for 40 years, your mind runs in a similar channel as Ancel’s. The thrill of running an experiment on yourself, then analyzing the results. Paleo brought a lot of things to the table for me, but nothing was along the lines Taubes and Atkins intended. Things like digging clams, picking berries, walking for hours for no apparent reason, reading books about Catalhoyuk and Salish basketmaking. Things a Paleo would DO.

    An actual Paleo needed ketosis like a fish needs a bicycle. It’s the LAST action that saves you when starvation stares you in the face. If you want to live to be 100, Robert Atkins can help you with your obesity, but Ancel Keys is who you want to follow for the long haul. Or Julia Child. Or the Okinawans. Or Lawrence Ferlinghetti. Or Jack LaLanne.

    You’re not a Paleo if you think HFLC is the only way to live a long healthy life.

    You’re a Luddite.

  20. Some say that digesting animal fats and proteins require an acidic medium, while digesting vegetable sources of carbohydrates requires an alkaline medium.

    The theory goes that while we are omnivores, we still need to eat exclusively like a carnivore or a herbivore at each meal, otherwise bad reactions occur in the stomach and intestines. eg. fermentation occurs, and less nutrients are absorbed.

    Therefore we should never eat egg sandwiches, or spaghetti bolognaise, or roast beef and potatoes etc.

    Perhaps that explains the magic of the macronutrient extremes…?

    I am trialling eating fruit in the morning and animal foods like mature cheddar and chicken liver pate in the afternoon to see if I can get the best of both worlds!

    Hopefully I can have my fruit and eat meat too!

    Note they also say that some salad vegetables can digest in either acid or alkaline mediums.

    1. “Some” say and “they” say? I’m not sure where the idea came about that humans evolved eating their carbs separately from their protein and fats. There is no real evidence of that from the archaeological record. Of course, we don’t know for sure in what combinations or in what order they ate the foods whose residues are found in their trash middens and on cave floors. But as difficult as it was during some periods of the Paleolithic to get enough nutrients to survive, such finickiness on the part of opportunistic omnivores does not seem like a good evolutionary strategy. Further, people living the Paleo lifestyle in historical times were extensively documented by European explorers and they never remarked on what would have been to them an extraordinary segregation of foods. You think foragers and gatherers never popped some berries and a juicy grub or two in their mouths at the same time while working? Pemmican and some other traditional foods were a mix of fruit, meat and fat. And some of the primitive Amazonian tribes discovered in the 20th century ate starchy carbs and “Paleo” beer with their feasts that celebrated the hunters’ skill in bringing home a good-sized kill. And what about omnivorous animals that eat the plant materials in their kill’s innards along with the flesh and innards?

  21. As of 2005, Americans were eating about 50% of calories as fat, per the 2008 study by USDA on dietary trends 1970-2005.

    http://www.ers.usda.gov/media/210681/eib33_1_.pdf

    34% came just from fat added to processed foods such as ice cream, chips and pastries. I estimate another 15% from naturally occurring fats in meats, eggs, nuts and fatty vegetables like avocados.

    That puts us squarely on the high fat side of the swamp.

    In 1970, when Atkins launched his attack on the low fat American diet it was a different story. People got his message and disregarded their concern with eating low fat foods (though not the unpleasant part about reducing carbs). The outcome was less than perfect. Carb consumption increased, though not as much as fat consumption. Calorie consumption increased. The internet and e-mail were invented to augment sedentary time. The net result was an epidemic of obesity. We now eat high fat diets but it’s made our health much worse.

    It baffles me that the HFLC community is still focused on defending Atkins’ 1970 tirades. Switching all the fat Americans currently eat from hydrogenated vegetable oil to butter and lard won’t make anyone healthier. HFLC needs to be used as intended: shock treatment for getting obesity under control. But it needs to be applied to current conditions, not some nostalgic Luddite trip back to 1970.

  22. Keys interest in heart health went way beyond population studies. His 1959 book Eat Well and Stay Well is essentially a practicum on how to eat and live in order to reduce CVD risk. He spends 28 pages of the book discussing mortality effects – sex, exercise, salt, fat, stress. He discusses the benefits of unsaturated fats here and there, in particular their effect in stimulating the liver to eliminate cholesterol.

    None of this flows in a highly organized fashion. It’s the result of 20 years working as an academic nutrition researcher, and you get wisdom where you find it. For instance, quoting a section pertaining to heart failure from “Salt and Heart Disease”,

    “Salt restriction is important for the patient with heart failure because it helps control oedema. In heart failure the heart is sluggish in moving blood along the veins to the arteries with the result that a back pressure builds up and fluid tends to accumulate in the body. This waterlogging (oedema) is both distressing and a serious complication. The extra weight of the oedema fluid, which may range from 20 to 60 pounds or more, means that every movement of the body demands excessive work from an already overburdened heart. Fluid in the lungs interferes with respiration and the patient may literally drown from oedema of the lungs.”

    In reading this I immediately thought about Robert Atkins. When I read that he had gained 60 pounds in his last 9 days I couldn’t believe it. Given Atkins serious heart problems, Keys offers a plausible explanation for Atkins death. It is unfortunate that his wife did not permit an autopsy. We would then know whether he had recently suffered a coronary event, or whether he had drowned in oedema fluid.

    1. According to all I’ve heard and read, Atkins had medication-induced edema, and it happened after he was in a coma. (His cause of death was slipping on ice). Medications can sometimes cause drastic effects; I know this, because at the end of my mother’s life she grew to about twice her size, rather quickly, also due to edema from medication. I saw a documentary about Robert Atkins, and they showed him not long before he died; he looked healthy, of normal weight, and energetic. His wife said people were out to get him during his life (I don’t remember her exact words, so this is not a quote)- and she was appalled that the rumors continued after his death. Which may be a reason why she did not want an autopsy. He should be allowed to rest in peace.

      1. I don’t doubt that medication could induce it, but most of the fluids probably came from an IV bottle. The result is the same. The heart can’t move the blood to the liver and kidneys. If the blood can’t move the fluids have to stay in the body.

        I’m trying to be dispassionate about this. As someone who worked as an industrial research scientist for over 30 years, I admire Keys because of what he accomplished as a dispassionate researcher. He was not being sentimental when he developed his high calorie density paratrooper rations, nor was he being sentimental when he created the Med Diet. These were BIG accomplishments that resulted from projects that had highest priority.

        The more humdrum day-to-day stuff of research involves testing small-time theories, most of which are slashed to ribbons and disposed of as quickly as possible. I was called upon to do that a lot. It was usually with eager salesmen trying to sell their product by attacking their competitor. I acted as a first screen to politely propel them back out the door before they could waste the time and money of people in operations. Having done that for years, my outer defense shields go up when I see people like Eades, Taubes and Atkins committing ad hominem attacks on their competitor Keys (Eades called him an old drooler, not a tactic you should resort to after someone has had a stroke at age 98). By unfairly attacking their competitor they set themselves up. They’re too eager to sell their books and products, and their theories unravel under minimal scrutiny. I’ll give Eades credit for piqueing my interest in Keys though…a year ago he wasn’t even on my radar.

        If the HFLC community cannot leave Keys to rest in peace, I have no qualms about leaving Robert Atkins to rest in peace. Keys was interested in CVD mortality. Based on my familial history, so am I. His wife’s paranoia has deprived me of mortality data on THE most important HFLC supporter. In the absence of that I am left with substantial evidence that Atkins died with a weak heart and a history of severe CVD problems. These may or may not have been a result of HFLC, but it is enough for me to kick HFLC out the door as a strategy for long and healthy life. There are several better proven routes which are promising. Keys Med Diet may not be the best but it’s a contender, along with Cordain’s Paleo Diet, Okinawan and Jack LaLanne.

        1. So….what? You’re starting rumors about Atkins just as a sort of revenge, because other low carbers said things you didn’t like about Keys? This is ridiculous, sorry! If someone says something inaccurate about Keys, by all means, feel free to defend him (as I did with Atkins), but there’s no reason to say things that are untrue about his “opponent”. I think we should all be interested in searching for the truth.

          And while we’re speaking of ad hominem attacks against an “opponent”: you do realize that Keys sometimes did this himself, right? Apparently, a Dr. Yudkin had very different theories about heart disease than Keys did (he believed it was caused by sugar)- and apparently, Keys managed to discredit him. The way I heard it, calling someone a “Yudkin” was an insult, back in the day.

          1. Read the next section. Keys was a bit of a blowhard (look at how he blows off ketosis – like waving a red flag in the face of the HFLC advocates), and pretty full of himself when recommending a good bottle of wine. But he had a sense of humor that Taubes, Eades and Atkins lack.

            I just finished up a stint as an executor. I’m not getting any younger, and I’m looking for a best strategy for a long and healthy rest-of-my-life. I don’t see the evidence for HFLC being anything beyond a weight loss strategy to deal with obesity. I don’t see any evidence for raw veganism either. If you know something better than Ancel Keys Med Diet, or Cordain’s Paleo, or the Okinawan sweet potatoes, show me. That’s why I came. Right now I live in the exact center of Denise’s Swampland. I could go for more carbs, or more fat, but I’m not seeing a compelling reason to live out on extremes either way.

            1. thhq- I wasn’t criticizing your diet, I was only irritated by personal remarks about the low carb leaders. I’m personally not convinced that “swampland” is such a bad thing…..at least, many healthy populations seem to be eating both fat and carbohydrates, and doing fine that way.

              And may I also add that low carb does indeed have benefits other than weight loss, at least for some of us! I am actually a thin person, and I’m not looking to lose weight, but I’ve had digestive issues my whole life. I was inspired to go low carb after reading the book “Life Without Bread”; it was written by 2 doctors, and chronicles all the health problems that Dr. Lutz was able to eradicate in his patients while having them eat low carb. The diet really helped me a lot, not just for digestive issues, but for all kinds of other things as well.

              1. Thanks. I really need evidence for a larger HFLC group than just one person. Do you know of any other HFLC groups studied besides the Inuits?

                I have the same feelings about exercise as you do about bread. I worked in Bordeaux, France for 2 years and lost 15 pounds. I was eating ad libitum. Bread, couscous, pizza, fries, pasta, duck (the wonder food), all kinds of seafood, beef occasionally, rich desserts, pastries, and red wine. I was walking an hour each way to work, and constantly wandering around exploring the town. When I moved back to the US I regained all the lost weight and more. 6 years later, when I finally had to lose the weight (obese and diabetic) I started walking again and the weight came off fairly easily. I was able to reduce high blood sugar with carb restriction, but after losing 25 lbs my ability to handle carbs without glucose spikes came back. Because of these experiences I’m not inclined to shift macronutrients to extremes.

                One thing about slipping on ice. I did it a lot living in the Midwest, and hurt my shoulder pretty badly in one fall. Falls become more damaging as you age and I feel for Dr. Atkins in this regard.

                1. thhq: Well, aside from myself, I do read about many other individuals who swear by the LCHF diet, and claim it got their health back in order. As for traditional native cultures: there are the Sioux Indians (and I believe, other Plains Indians). They lived mostly on buffalo meat, ate lots of fat (think: pemmican), and were noted for their exceptionally good health. There were many centenarians, back when they were still eating their traditional, mostly meat diet (sadly, this has changed now). Other examples are the Masai and Samburu cultures, in Africa, who ate mostly meat, milk and blood. They were also very healthy. Then there are other northern cultures like the Mongolians, the Siberians, etc. Also the Sami (native Swedish), who apparently were also very healthy. And it’s probable that our ice-age ancestors ate mostly LCHF, and hey, we survived this long!

                  I don’t mean to imply that you need to change to this diet, especially if your own diet is working for you. But obviously, LCHF works for many people. By the way, I also exercise a lot; I find it very important (and my job requires it). Even still, I think I have some carbohydrate intolerance. Back when I ate high carb, I didn’t measure my blood sugar regularly, but I recognize now that I had symptoms (all gone now that I’ve gone low carb). Even though I’m thin, diabetes and hypoglycemia run in my family.

        2. thhq, you’ve spilled loads of words here, a lot of them around macronutrient balances. Let’s make it simple shall we? Try different diets. See which works. Ancestral foodways range from high carb (e.g. Kitavans) to high fat near near no carbs (e.g. Inuit). In nearly all cases though, the food was organic/pesticide free, non-GMO, fresh, locally produced. Stick to that AMAP. Make sure your food is as pure as possible. Best is the least done to your food between it was raised and when it gets to your kitchen. LFHC works for some. HFLC works for others. For me HFLC works worked wonders. I’m at 80% fat, 15% protein, and 5% carbs. I’m 55, been HFLC for 9 years, feel great, enjoy great blood panels, and feel utterly satisfied. I can’t imagine going back. The whole thing about what food culture figure said what about another food culture figure–it just doesn’t materially contribute to the goal of improving our health.

          1. Thanks. I do have a leaning toward Paleo, though I see it as a lean meat and seafood (especially fresh mollusks like oysters) approach rather than fatty meats. But I strongly believe that there’s a greater benefit comes from activity, rather than macronutrient balances. I like this piece by Cordain.

            http://thepaleodiet.com/wp-content/uploads/2015/08/Exercise-Like-a-Hunter-Gatherer-Organic-Physical-Fitness-Prescription-The-Paleo-Diet.pdf

            Extended exercise turns on my metabolism, and anything available in my bloodstream is used for fuel. I can eat cake or steak and my TG’s and blood sugar are the same. Whether it’s fatty acids, proteins or glucose it all gets turned into carbon dioxide.

  23. An exceptional review by Denise, and she’s not even a biochemist or a physician !
    Thank you for broadening our horizons and shattering private biases and doctrines.
    Waiting for your second part.
    Thank you also for mentioning the Randle cycle on Ben Greenfield’s podcast – certainly opens a new gateway to looking at the relationship between carbosis and ketosis and the plasticity of our physiological adaptations.
    I now regard Terry Whals’ MS ketogenic protocol not as a contradiction to Swank’s work, but rather, complementary.
    Both represent the two extreme ends of the the % fat consumption pseudo-opposites.
    Douze pointe

    1. These series of books are not really rare, and are considered out of date.

      http://www.volumelists.com/detail.php?ser=Life%20Nature%20Library

      However, they do have pictures of how people looked in the environment the lived in and why/how the adaptation helped them to survive. Was the diet optimal? Did the diet or the environment made them that way. Diet was mentioned in the ones I read- The Desert, The mountains, The Forest, and Australia. . One example listed is the Mountain dwellers diet of potatoes, beans in some areas, end ancient grains, and not much meat or fat at all They could not afford to eat their llamas. They were said to have cracked feet, eyes because of lack of fat. They were also hungry and overworked.Chewing the coca leaves at least kept them in a state where they did not feel the hunger or cold as much. But they were addicted. Also in the book the yak butter in Tibet kept those people warm. They at least had enough Yak to eat. Also in those books plants, and many animals are shown as adapting. That what make subspecies. The word epigenetics was not mentioned in those books, but still saying adaptation is enough of an explanation. .

      Dr Weston Price of course noticed the changes in how the nest generation of those people looked, and Price said it was the change in diet, Disease was also mentioned in Price’s book and those Nature series books. The Nature book said if those people left the mountains, they got tuberculosis. but were subject to whopping cough there. Those in Iceland have a long history of putting babies out in the cold, but kept warm to prevent tuberculosis. Studies do seem to indicate sunshine and fresh air will reduce infection.

      So which mountain dweller-Peru, or Tibet was healthier, or did both of them have different problems?. Some in Tibet were eating meat/fat and some wheat, potatoes. Of course, in all those places, the peoples religion played a big part of what was eaten, as much as availability and social status and even if male or female.

  24. “That morning he had advocated lighter lunches and now he ordered nothing but English mutton chop, radishes, peas, deep dish apple pie, a bit of cheese, and a pot of coffee with cream, adding, as he did invariably, ” And uh- Oh, and you might give me an order of French fried potatoes.” When the chop came he vigorously peppered it and salted it. He always peppered and salted his meat, and vigorously, before tasting it.”

    Sinclair Lewis, describing the eating habits of George Babbitt.

    I’ve been thinking about Ancel Keys at the University of Minnesota. He doesn’t write as well as Lewis (or later, Garrison Keillor), but he has the same sharp wit. He taught and researched nutrition in the land of Spam, Betty Crocker and recent Scandinavian immigrants. He discusses the training table of the Golden Gopher football players ca 1940 at length in Eat Well and Stay Well:

    “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.

    This is an indoctrination into adult dietary foolishness. When the rowing blues leave the university and no longer are forced to keep in training they soon turn into heavy business men; not much later the atheromata are in full bloom in their arteries.”

    I think more than a little bit of this high fat animosity creeps into the national diet studies later on. Keys next door neighbor in Italy Marti Karvonen led the Finnish section of the Seven Nations Study. Here’s his description of the Nordic White Diet, which would have been familiar to Keys in Minnesota:

    He remembers Finland in the ‘50s. “In those days, in the winter time, we had bread, potatoes, milk, and pork with layers of fat on it. There was nothing green seen on the table — maybe the table cloth.”

    http://bobbarnetthealth.com/wp-content/uploads/2013/02/AncelKeys.TONICS.pdf

    This is where Keys was coming from. Direct observations of bad diets resulting in bad CVD outcomes.

  25. It would be interesting to see someone do thesis research on the psychopathy of the HFLC community towards Ancel Keys. One could start with Ancel’s summary dismissal of ketosis and build from there:

    “Severe epileptics were once treated with a high fat “ketogenic” diet so as to overwhelm them with fat in their diet (80 per cent of calories) to the point where the fat could only be incompletely “burned” in the body and the “smoke” of this incomplete combustion, the “ketone bodies”, would accumulate in the blood. This is a heroic measure, only justifiable as a last resort in uncontrollable epilepsy. Fortunately, this is practically never used today. The basic physiological unsoundness of the “ketogenic” diet is well recognized. New drugs are available that do a great deal more for the epileptic patient.”

    This was written ten years before Atkins Diet Revolution. Keys hadn’t realized that ketosis could be used to treat another chronic illness – obesity. But Atkins and his later followers wouldn’t let up on Keys. It got sillier and sicker as they fabricated and cherrypicked their ongoing smear.

    Atkins may have first read about ketosis in Keys book for all I know. If he had accepted the “heroic measure” statement maybe we would have been spared Taube’s insulin theories and ad hominem attacks like this one from Eades:

    https://proteinpower.com/drmike/2007/11/04/jack-lalanne-vs-ancel-keys/

    We’ll see who drools last. But first Eades has to make it to 100 on HFLC.

    1. Norm: I think you must mean Durian Ryder? (Yes, he is a loudmouth, ha ha). Personally, I think there is something “not quite right” about him. He may be thin, but he doesn’t look particularly healthy to me; his skin doesn’t look very good. Also, he seems rather hyper and a bit “mental” in my opinion; I’m not sure that he’s the picture of health. I’m not saying all low fat diets are bad, I’m just not sure that Durian Ryder’s particular diet is a good one. I wonder if he has too low cholesterol.

      1. Lol! Durian Rider would put you to shame im Anything athletic. You should keep uninformed opinions to yourself. He and his diet is nothing short of incredible, eating nothing but carbs for 11 years straight and having that level of fitness is amazing. As far as his personality and skin, blaming anything on diet is rediculous because we’ve all seen horrible looking people eating types of diet and the same can be said for mental health.

        1. How the heck do you “know” that Durian Ryder would put me to shame in anything athletic? I am also very fit and athletic, thank you very much! So you should also keep “uninformed opinions” to yourself. It’s fine to disagree with what I say, but criticizing me- when you don’t even know me- is just crude.

        2. Hear, hear, Morgana! Zach’s totally out of line here. You should feel free to give your impressions here. And of course Zach has no idea your fitness level–that’s just meaningless blather. At this link is a guy who shattered the record for the 100-mile Western States run and he professes to eat low-carb:

          http://www.meandmydiabetes.com/2012/08/11/western-states-100-low-carber-wins-ultramarathon-steve-phinney-and-jeff-volek-study/

          For that matter, how do we KNOW Durian Rider eats what he says he eats? Who’s the 24/7 fly on the wall to verify his claims? It’s possible that in the beginning, he actually followed his diet. Then all excited as he is wont to get, DurianRider started wildly flogging his foodway as the panacea and he got his franchise going. Now he’s locked in to his party line, even if he’s quietly discovering that he needs more fat/protein and is eating it. We just don’t know!

          Finally, I’m very suspicious of anyone who claims we should take supplements as a general rule. Here he promotes Vitamin B12 injections: https://www.youtube.com/watch?v=arElYUnWrho

          No thanks! I’ve been LCHF for 8.5 years and it’s been a lifesaver!

          1. Lol! That guy eats high carb when he does his races. Whatsup with low carbers and not doing any background research whatsoever?

            Also yea, no low carb/paleo gurus push supplements. Except omegas, protein powder, stimulants, vit d, magnesium, k2…. I could go on forever. Guarantee the average low carber takes 5x as many supps as vegans.

            1. Sure Zach. DR may chow a lot of carbs for his hard rides. Fast carb recovery meals make sense for heavy resistance training where you’re rending muscle tissue. Mark Sisson makes that clear at Mark’s Daily Apple.

              But what does DR eat at other times? Who’s a fly on the wall watching him? Just sayin. Remember Zach this mouthpiece now has a following and so has pressure to sell a consistent message.

              About supps, Sisson also sells his line of supps, but he very low key about it in his blog, and makes clear that it’s best to get all nutrients through food. I was diag’ed T2D in 2007, been LCHF for 8.5 years, stopped all supps 6.5 years ago, and now have completely normal blood panels including normal BGs.

              About these your sentences: “Whatsup with low carbers and not doing any background research whatsoever?” and “Guarantee the average low carber takes 5x as many supps as vegans.” these are mere words you just pulled out of your backside, the first a mere opinion and the latter with zero substantiation. Zach, maybe you should heed your own admonition?–“You should keep uninformed opinions to yourself.”

              1. Hahaha! Sisson makes his living selling supplements from rubes who are dumb enough to buy overpriced garbage.

                Durian has youtube daily for 6 years or more. He puts on fruit fests with thousands turnout. He talks the talk and walks the walk without a doubt.

                Don’t be jealous you can’t lose those lbs on low carb. It’s just not how our bodies were designed to work. You should follow some of this blog posts advice!

                1. “Don’t be jealous you can’t lose those lbs on low carb.” Zach there you go again, blathering on without a clue of my situation, just like you did with Morgana. I lost 60 pounds on LCHF. Effortlessly.

                  As for “Durian has youtube daily for 6 years or more…” you underscore my point. DR now has a following and so feels a pressure to maintain a consistent message. As far as you saying “He puts on fruit fests with thousands turnout.” so what? That still doesn’t tell us what chows down behind closed doors. Finally Zach you say “He talks the talk and walks the walk without a doubt.” As though your preceding meaningless statements somehow even begin to support this claim.

                  But Zach, please feel free believe what you want to believe. Far be it from me to try to disabuse you of your cherished religious fervor. Just please don’t confuse your beliefs with anything remotely to do with rigorous science and sound nutrition.

                  1. You can say the same for Mark Sisson or anyone else pushing a diet philosophy. What an uncouth thing to say, you are basically slandering someone just because your jealous of them.

                    As for my thoughts on diet, they are based on sound science like this blog post shows. A high carb, very low fat diet is key to health and longevity. Science AND history back this up. Paleo is a silly fantasy fad that is ruining health on a giant scale.

                    1. Let’s compare two vegetarians, Durianrider and Hitler. Both self-righteous, quarrelsome and antagonistic. Avoiding animal foods does not turn someone into some saintly person who respects HUMAN dignity.

                      I won’t dispute that HFLC does exactly the same thing. I spent some time looking for a video of the screaming matches between Atkins and Pritikin, but couldn’t find one. One of the MANY keys to health and longevity is serenity. Living out on polar extremes – dietary, religious, political, etc. – and fighting your “opponents” all the time because they are “wrong” only shortens your own life.

                    2. Zach, your logic fails are legion. First, maybe you should learn what “slander” means before you plop it out here. Look it up hotshot: http://legal-dictionary.thefreedictionary.com/slander

                      “… someone tells one or more persons *an untruth* about another… ”

                      So where am I saying “untruths” about Banana Guy? Right, NOWHERE. I’m simply calling out what we DON’T know about him. And you’re right, we don’t know what any food- and lifeway advocate eats behind closed doors–including Mark Sisson, Robb Wolf, John MacDougall, Dean Ornish, and on. We are then left to sort out and make sense of their messages. To look not just macronutrients and whether the food is plant- or animal-sourced, but also nutritional biochem, genetics, including epigenetics and microbiome genomes, and anthropology including paleo- and cultural anthropology. Most of all, we need to see how a given foodway works on each and every one of us. That includes how well we can tolerate the foodway.

                      Here Zach you sail right off the deep end: “…A high carb, very low fat diet is key to health and longevity. Science AND history back this up. Paleo is a silly fantasy fad that is ruining health on a giant scale.” First, science backs up NOTHING you say. Under clinical observation, few if any people stayed on Kempner’s Rice diet more than a few years. And as far as “resolving diabetes” 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. This Rice Diet is hardly a ringing endorsement for completely resolving diabetes. I was T2D in 2007, and since *normalized* my BGs with LCHF, averaging 90 mg/dL. Zach, Denise will send you Kempner’s report on this if you care to bother to check it for yourself. Swank’s protocol is more interesting, but still the sample rate is small (150 and diminishing) and self-reporting after a short study period. And who independently verified what data Swank & Co entered into the logs? Again, we have to remember that when a researcher gets very invested in a theory and spends his life working on it, all too often the data can start to magically reflect that desired outcome. Same case with Morrison’s post-war study: small sample rate (50 control, 50 on LFHC diet), self-reporting, no independent verification of nutritional data. 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) About the Esselstyn diet results, you can read Denise numerous caveats about this, to which I add that the average study period was under four years and looked just at CVD, not all-cause mortality.

                      The fails just keep on coming. Most people find these diets very difficult to adhere to over the long term. Most include vitamin and mineral supplementation. Maybe funniest of all Zach, none of the studies Denise cites in detail support the vegan lifestyle your beloved DurianRider so stridently touts except that from Esselstyn. Your concluding sentence “Paleo is a silly fantasy fad that is ruining health on a giant scale” could not be more meaningless, ridiculous and even dangerously wrong. For the hundreds of millions of people on Earth who now suffering from serious sugar metabolism dysfunction, based on the “science” I’ve seen the low-fat high-carb diet will hasten their sickness and death compared to the low-carb high-fat foodway.

                    3. Lol, you type up all that just to show your ignorance in your last sentence. FAT is the reason people have issues with sugar. It’s a shame diabetics like yourself don’t know the simple facts that fat, mainly pufa causes diabetes.

                      You can not cure diabetes with a low carb diet, only “manage” it. You can cure it if you rid your tissues of pufa. That is what these people are doing. You should try it!

                      P.S. I never said veganism is the answer, I just find it funny that “banana guy” has more athleticism than any paleo guru out there.

                    4. Zach, please take a moment to reflect on how insane this your comment is: “FAT is the reason people have issues with sugar… ” Zach, I ate HCLF all my life to 46 and *became* diabetic. I went LCHF and my BGs then *normalized.* Are you trying to tell me I imagined my recovery? That my glucometer and my HMO are all telling me the same lie for nine years? You can find countless accounts of other people with the same experience. Please get a grip Zach. The only redeeming shred you said is about PUFAs. We should reduce those as much as reasonable. Esp Omega 6, esp by cutting out veggie/legume oils.

                      Nothing “cures” Type 2 diabetes. Any more than ceasing to drink poison “cures” you from the effects of that poison should you start drinking it again. Zach you will not be able to furnish even a single link to any clinical study that consistent, reliably, irrefutably shows that any diet, LFHC, HFLC, whatever, “cures” T2D across a cohort.

                    5. Gee I wonder why other cultures eating hclf their whole lives don’t developed diabetes? Maybe because they actually eat whole foods and no oils or fortified grains.

                      Fats, mainly pufa absolutely do cause diabetes. Sugar and carbs are only a secondary effect.

                    6. When you were HCLF what did that look like? McDougall and others are extremely low fat, less than 15%. It’s not an very varied or interesting diet as a result, but many swear by it as having turned around any blood sugar issues.
                      So possibly you were in what Denise refers to as swampland. And go out of on the left rather than the right.

                    7. Zach about this from you: “Gee I wonder why other cultures eating hclf their whole lives don’t developed diabetes? Maybe because they actually eat whole foods and no oils or fortified grains.” See my response to your “bubble” comment, where chronic disease is soaring worldwide.

                      About pufa I agree they contribute to the problem. In particular omega 6, and all rancified pufa. We should stop consuming veggie/seed/legume oils. Ditto for fortification, which may contain undeclared toxins acquired during their productions, e.g. heavy metals and estrogenics like BPA and phthalates. Companies in China make most micronutrient supplements. I disagree that sat fats and mono fats “cause diabetes.” These do not oxidize as easily as pufa, esp the sat fats, and so are a very clean fuel. Zach if you eat a lot of fiber you are in effect eating fat. In our colons, our gut flora ferments much of the fiber into short-chain fatty acids which directly nourish the endothelial lining of our colons. When you eat excess carbohydrate–carbs that can’t go to directly build/repair muscle or get made into glycogen–the liver converts that glucose into palmitic acid– a long-chain (16C) saturated fat! That’s why people who chow excess carbs get fat.

                    8. The “fortification with heavy metals” that really makes a huge difference is iron. The reason PUFAs oxidize is largely because iron acts as a catalyst. If the US and some other countries, large amounts of iron are added to white flour, masa, breakfast cereals, and most processed foods. But not to whole grain foods.
                      With saturated fat, the fat is usually attached to red meat, which is high in heme iron, the most absorbable kind. Saturated fat also makes fortified iron in, say, bread, more absorbable.
                      The iron in fruits and vegies isn’t very absorbable at all.
                      So iron messes with insulin levels:

                      http://diabetes.diabetesjournals.org/content/51/8/2348.full

                      To the point where people who are accidentally overdosed with iron and no other changes develop diabetes.

                      I think this point gets ignored in most of this conversation about health. The Maasai may have been drinking blood and having lots of saturated fat, but in fact their diet was super-low in absorbable iron, to the point they were borderline anemic.

                      http://realhealthtalk.com/regulating_iron.html

                      We’re working hard on regulating the amount of fats and sugars … but who is looking into iron levels? Right now half the world is anemic, and the other half is iron-overdosed.

                    9. So maybe the modern increase in the incidence of hemochromatosis is real and caused by our overprocessed food supply, rather than an artifact of better diagnostic tools? Anemia used to be the common problem — I remember my late Mother (born 1913) telling how rural folks used to treat her and other relatives’ anemia with apples or other fruit that had an old iron nail inserted so the fruit’s acidity could transfer the iron into the fruit.

                    10. Yes, it’s pretty hard even to pin down what is “iron overdose”. It used to be believed that no one would overload on iron, because the gut has an intricate mechanism to prevent iron from going directly into the blood until needed. Some people with a weird gene though, circumvented that.

                      However, ANYONE can absorb too much iron if it’s the wrong type. Iron overdose is common when, say, a kid eats iron pills. Or someone makes beer in an iron pot … this is common in Africa and causes iron poisoning. I kind of think that the sailors in the old days ate a LOT of iron, between the iron pots, iron utensils, the molasses rum and beer, and salt beef … which may be why they got scurvy so easily. On the Lewis and Clark expedition, they aimed for 9 lbs of meat per day per person, and also cooked in iron pots. “Bleeding” was, according to Lewis, just exceedingly effective to cure a lot of ailments, and he was really very observant and a good doctor. But probably all of them were also iron overdosed.

                      But no one really knows how much iron a person SHOULD have. Diabetes increases as soon as ferritin goes over something like 116. But less than 300 is considered “normal”. A lot of iron gets sequestered in the liver, spleen, heart or brain, and that can’t be measured without an MRI.

                      I think anemia was a real issue when people routinely had hookworm, roundworm, and tapeworm. Almost everyone did back when. Also some people have internal bleeding. Or a super-low-iron diet. The backwoods folks in the South mostly had hookworm until “shoes” became common (and worm medications).

                      There can also be other issues. If you have a chronic infection, for example, your body can decide to “hide” the iron and make you anemic. I think this happened to my Mom. She IS anemic and her blood levels of iron are low. But her skin is grey … she sequesters the iron by depositing it on her skin, which then gives her skin cancers. She takes iron pills AND eats a lot of meat AND eats iron-enriched foods. Yet she is “anemic”.

                      The reason your body hides the iron is that it feeds the worst kinds of microbes. Lately it’s been found that lowering iron levels is a great way to kill staph. Actually that IS how many antibiotics work. They are basically iron-chelators and thus starve the bacteria.

                    11. 9 pounds of meat a day? Geez. I know folks that run 100-milers and that would last them a good 2 weeks even on a hearty 10-ounce steak a day. I remember reading some time back that depriving harmful microbes of iron would kill them, but, still, even into my 20s, TV commercials were full of warnings about “iron-poor blood” and we were exhorted to eat more liver and take a spoonful of iron tonic every day. Strange how the body handles an element that’s essential to health but can be easily overdosed. My brother developed hemochromatosis at an early age and routine bleeding was one of his treatments. Maybe those old-time barber-surgeons were on to something with their leeches and lancets.

                    12. Yeah, I’m not sure what to make of the 9lbs of meat either. Granted they worked hard … but so do a lot of guys these days too. The only thing I can think is that either it was digested differently, used differently, or they had a high parasite load.

                      Lewis was a careful researcher though and apparently a good doctor. He got 40-odd guys and one gal and baby through the wilderness for 2 years, with only one death (from appendicitis!). He made a lot of notes about edible foods and what the Indians ate, because his mandate was to find if the land was habitable by Europeans. His mother was an herbalist and he was also trained in the doctoring of the day.

                      So his thoughts about all that meat … was likely just pretty “normal” for the day. They didn’t generally have all that much starch. It was easier to hunt buffalo than to find ground tubers (they did trade with the Indians for starches). So likely their bodies were good at turning protein into sugar as needed, but maybe the process isn’t all that efficient.

                      It would be interesting to compare their diet with say, the Chinese railroad workers (who I imagine were also pretty well documented). The Europeans, I’ve heard, got huge rations of beef, along with potatoes. The Chinese:

                      “The workers insisted on eating Chinese food: rice, dried vegetables, dried oysters, dried abalone fish, and some pork and poultry. Much of these foodstuffs came from California sources, such as fresh vegetables. They also drank tea and hot water with occasional wine and opium. The Irish or white workers were fed mainly meat and potatoes along with whiskey. The Chinese diet and especially the use of boiled water reduced the outbreak of dysentery and other diseases.”

                      http://web.stanford.edu/group/chineserailroad/cgi-bin/wordpress/faqs/

                      So these are two groups of very hard workers. One eating mainly rice and seafood and tea, another eating beef and potatoes and whisky. However, they had other habits that make it hard to gauge the diet: the Chinese boiled their water before drinking it (as tea), and also apparently were big on taking baths.

                      BTW in the Asian stores I’ve also noticed the large amounts of dried foods. I’m guessing this is going away as more people have freezers, but there are just huge quantities of dried stuff. Lewis and Clark brought a little “storable” food but it was a newer thing. (L&C salted their meat, and didn’t store vegies much that I could see). The Chinese had it down to an art. Dried food is easy to transport and stores for a long time. Most of the Asian food though is based on rice and vegies, and seafood. The pork and chicken is more of an additive, and very little beef. (Which of course depends on WHERE in Asia we are talking about).

                      Anyway, both groups of workers apparently did a good job at laying track. Probably there are pictures to compare the two groups physical appearance.

                    13. BTW, as to iron overdose … there is an interesting case of the Orkney sheep. These are sheep that happened to eat mainly seaweed for about a hundred years, because that’s where they grazed. Anyway, they adapted. The seaweed chelates copper, turns out. So the sheep now hoard copper. If grazed *without* seaweed, they tend to die from copper overload.

                      I kind of think something like that happened with at least some genotypes of humans. With sheep it only took 120 years or so. There are a number of foods that block iron absorption … notably dairy, tea, chili, whole grains, and yes, seaweed. So it would make sense to me that some people developed the knack for hoarding the mineral, which was rather rare in some diets.

                      Anyway, humans seem to vary more when it comes to handling iron than does say, a mountain goat or a gorilla. But our diets vary more too.

                    14. @zach I wouldn’t be typing this if it wasn’t for someone eating a diet of apples and carrot juice. Carbs, particularly grains, have fuelled human progress. I believe this is due in large part to their portability, which is a problem with fresh foods like oysters, peaches and bananas. But that’s not where I was going with the Hitler comparison…it has a little bit to do with what you call genius…

                      Going to extreme carb dieting appears to produce frenetic activity in some people, both physical and cerebral. In the case of durianrider this has not produced much more than a lot of ranting (I think of Hitler especially here, https://www.youtube.com/watch?v=y2fl-sHUwrc ) and bike tire spinning. Entertaining or irritating depending on how you look at him, but harmless. He hasn’t risen to any great achievement – no iPhones or VW’s – but neither has he come up with V2’s, death camps, amphetamines or blitzkreig.

                    15. As for high meat intake, there is supposedly a limit to how much heme you can absorb in one meal:

                      Heme-Iron Absorption Is Saturable by Heme-Iron Dose in Women (2003)

                      “In our study we found that heme-iron absorption was saturable. Heme-iron absorption after ingestion of physiological doses of hemoglobin and myoglobin is limited; however, the mechanism by which this is produced is not clear. It seems that one of the limiting factors would be the uptake of the heme into the enterocyte, whatever the mechanism. Roberts et al. indirectly demonstrated the presence of a binding protein of heme on the brush border of the rat enterocyte and showed that the capture of heme by the mucosa directly increases the amount of the binding protein on the brush border. They speculated that this binding heme protein may be saturable. If the mechanism of endocytosis proposed by Wyllie and Kaufman is correct, it would be a barrier that limits the intake of heme-iron into the enterocyte.

                      In summary, our results strongly suggested that the absolute maximum amount of iron absorbed from freeze-dried red blood cells containing over 15 mg of iron as heme is 2 mg, showing that heme-iron absorption is saturable. Further investigation is needed to explain the mechanisms underlying this phenomenon in consumption of actual meals and in subjects of varying iron status. The saturability of heme-iron absorption may be a protective factor to avoid iron overload when iron intake is provided primarily by consumption of meats or blood”

                      This kind of makes sense. However, there is the well known meat effect in iron absorption, where eating meat significantly increases your absorption of non-heme iron. When you cook meat, it’s possible to transform ~20% of the heme into non-heme iron. So, you absorb ~2mg of heme and then you absorb more of the cooked non-heme. Taken all together, you would absorb more iron from cooked meat than raw meat. And if you ate the cooked meat with non-heme foods, you’d absorb even more iron on top of what you get from the heme and non-heme in the meat. The point being that a meal of pure raw meat and blood might limit the amount of iron you absorb compared to a Western meal.

                      That might explain why carnivorous cultures always preferred raw meat. Obviously animals too.

                      Colon cancer is associated with heme iron, but there is some recent evidence that it may have something to do with pathogens consuming heme iron and causing issues.

                      Where it gets interesting is that cooking meat destroys the porphyrin ring around heme iron and as it turns out, porphyrins are antimicrobials. So, this implies that eating raw meat perhaps makes the heme iron unavailable to pathogens.

                      Antimicrobial properties of porphyrins (2001)

                      So, this might explain why carnivorous cultures preferred raw meat. Incidentally, the Inuit had anemia with their high (raw) meat intake, but they also had infections and vitamin deficiencies that affect iron absorption.

                    16. wbryanh said: “About pufa I agree they contribute to the problem. In particular omega 6, and all rancified pufa. We should stop consuming veggie/seed/legume oils”

                      It’s possible that linoleic acid is likely only bad for you if you consume it in isolation. If you eat linoleic acid in whole foods, it’s a totally different ballgame.

                      For instance, the !Kung eat significant quantities of Mongongo nuts, which are really high in linoleic acid. If linoleic acid in whole foods were deleterious, we should see it in the !Kung. However, mongongo nuts are extremely rich in Vitamin E (565mg per 100g of Mongongo nuts). All that Vitamin E in the Mongongo nut is protective against the damage from linoleic acid:

                      Protective effect of vitamin E on linoleic acid hydroperoxide-induced injury to human endothelial cells (1991)

                      It seems like perfect luck, but in reality the nut makes all that Vitamin E so that its own linoleic acid won’t go rancid in the Kalahari heat. So, the protective nature of the whole food is for the benefit of the plant/seed/nut/animal, and whatever consumes that whole food just happens to take advantage of that homeostasis. You are what you eat.

                      It’s such a simple concept, but few ever really stop to think about it this way. Whole foods have self-protective mechanisms in place that consumers of those foods get to take advantage of when they eat whole foods.

                      As best as I can tell, the idea that we need to eat more Omega-3 and less Omega-6 (i.e. the fish oil craze) comes from Bang & Dyerberg’s erroneous and now debunked observations that the Inuit were free of heart disease.

                      The Fishy Origins of the Fish Oil Craze

                      And this is even further problematic because even if the Inuit really were quite healthy eating lots of Omega-3, it’s believed that they have very different fat metabolisms than we do. In addition to the CPT1a genes, it was also recently discovered that the Inuit evolved unique genetic adaptations for metabolizing omega-3s and other fatty acids.

                      So, the conventional wisdom on Omega-3:6 ratios may not be all it’s cracked up to be when we look at them in the context of whole foods.

                    17. Duck, I find *lots* of issues with your post. E.g. your claim that Bang and Dyerberg’s work is debunked–far from it. Also, we can draw zero diet conclusions from the Inuit gene-variant studies. More on these in another post. But these don’t take away from your excellent main point:

                      “Whole foods have self-protective mechanisms in place that consumers of those foods get to take advantage of when they eat whole foods.”

                      As much as we learned about nutrition in the last 100 years, we’re still scratching the surface on our bods respond to the complex matrix we get with whole food. Makes me think about the complex interactions between microbes in our gut flora. We’re fast learning who those little players are, but we don’t yet know much about how they play off each other to contribute to our health. Some feel an optimal gut flora balance is very important for optimal sugar metabolism due to proper insulin signaling among other hormone-driven comms.

                      Another example of Mother Nature’s exquisitely honed Grand Plan: The usefulness of Omega 6 (w6) for fattening up for the winter. Nuts, esp in temperate zones, usually have a lot of w6 which contribute to temporarily stiffening our cell membranes, making them slightly less permeable than usual, raising general resistance including insulin resistance, leading to more blood glucose being stored as fat. This way we lay in more fat coming into winter, giving us a little extra insurance during a season when it can be harder to find food. *In general* the closer you move to the equator, the lower the pufa in nuts. Mongongo nuts are an exception, they are quite high in w6 for being in a subtropical climate. Thus high in protective Vitamin E as you pointed out. It doesn’t appear to be uniformly healthy for the !Kung San either. During peaks in the mongongo seasons, San postprandial BGs soar in the 160s. Guyenet hypothesizes this high p-p BG is due to lack of acclimatization when moving from seasonal low carb to (relatively) high carb diets (more mongongo fruit). But because the researchers did not follow up later in that high-carb season, we don’t know if the San metabolism adjusts or not. High w6 remains a possible driver for the Sans’ high p-p BGs. Here’s Guyenet’s post:

                      http://wholehealthsource.blogspot.com/2010/11/glucose-tolerance-in-non-industrial.html

                      And Duck, do you have free link to specific nutrient content of mongongo nuts and fruits? E.g. where you got the “565mg Vit E per 100g” factoid? The link you posted is behind a paywall. Thanks –Bryan

                    18. Duck, on to Bang and Dyerberg’s debunking debunking. You say this: “…Bang & Dyerberg’s erroneous and now debunked observations that the Inuit were free of heart disease…” First the “evidence” you cite is another of the many awful confused science-tripe pieces, topped by click-baity but wrong titles, we too often see in the Webloids which alas includes Slate. Second, in the end, author Elizabeth Preston, even relying on her weak dissenting evidence, doesn’t even claim the B&D results to be necessarily wrong! More research needed!

                      E.g.: “…Bang and Dyerberg were nutritionists, not cardiologists; they didn’t examine anyone’s heart themselves…” First, B&D weren’t cardiologists. So what? That, in itself, doesn’t invalidate their work. They drew the Inuit blood and brought it back to Denmark for analysis by the appropriate experts. And as filled with flaws lipid panels are, certain analyses of them linking serum lipids to heart disease, such as the Total Cholesterol/HDL ratio, are generally considered reliable:

                      http://www.mayoclinic.org/diseases-conditions/high-blood-cholesterol/expert-answers/cholesterol-ratio/faq-20058006

                      Also bear in mind the Inuit that B&D studied ate a mostly or completely an ancestral diet. There was only ONE other comparable study the author cites: “…a report published by a Danish doctor in 1940 also described high rates of heart disease in the Greenland Inuit…” That’s it? What are the details on that report? How clinical was it? Did *this* doctor look directly into the hearts of the Inuit? remember serum tests were much cruder then. The other report she referred to have modern Western diet confounders.

                      Then there’s this garbage: “…What matters most to a disease researcher, Fodor says, is overall mortality: “the number of corpses you count.” A study found that from the late 1960s to early 1980s, Inuit died from all causes at twice the rate of Danes—hardly a lifestyle to aspire to…” Well no kidding! Life was rough up there in the “unforgiving” land as the author earlier noted. From which main causes did these Inuit die from? Infectious diseases. Accidents? Why didn’t the author give us the breakouts?

                      Duck, as flimsy as this reporting is, the author does include this disclaimer: “ [Researcher JoAnn] Manson believes that answer [linking w3 and heart disease] could easily go either way. “The vast majority of researchers who really know this field believe the jury’s still out,” she says. IOW Duck, again, we simply don’t *know* that Bang and Dyerberg arrived at the wrong conclusions.

                      About the fish caps. The reporting can lead us to assume that fish oil caps are, nutritionally speaking, an exact replacement for fresh fish. That is ridiculous. Omega 3 oil rancidifies exceptionally quickly, starting the moment the marine creature dies. It’s already well along in oxidizing by the time you can detect it with your nose–especially when it stuffed in a gelcap that you swallow which previously sat for up to weeks on a shelf at ambient temps. Also, most people take WAY too much w3. Both the main polyunsats–w6 and w3–are very prone to rancidification, w6 somewhat less so. Instead of ramping up our w3 to near pharmacological levels with the caps, we instead should LOWER our w6 to keep a reasonable w6/w3 ratio meanwhile minimizing our total poly fat intake.

                      So what’s a good w6/w3 balance? The ancestral-living Inuit had the lowest ratio, ~0.7. More common ancestral ratios run 1:1 to 6:1. The !Kung San chowing on their w6-rich mongongos may run near the high end of that. Meanwhile, in the SAD, replete with veggie and legume oils, the ratios can run 40:1 to 60:1! Duck, bear in mind the higher the ratio, the stiffer the cell membranes, setting the stage for metabolic syndrome and chronic disease. Above a certain ratio, yes the w6/w3 certainly CAN matter.

                      Duck in your concluding sentence: “…the conventional wisdom on Omega-3:6 ratios may not be all it’s cracked up to be when we look at them in the context of whole foods…” You are right! Because, sticking just to whole foods, it’s almost certain you’ll never go up into a harmful w6/w3 ratio.

                    19. Duck, about the Inuit gene variant discovery, this work is very interesting but concludes nothing about diet and health. I went through this with Charles Grashow elsewhere on this forum. Search on this string:

                      the genetic basis of human adaptation to cold climates and lipid-rich diets REMAINS LIMITED

                      to see my answer to him.

                      I saw the flurry of articles a few months back, but none explain exactly *how* the Inuit are supposed to better utilize PUFAs than the rest of us. That NYT Zimmer link you posted comes closest:

                      “The researchers found several genetic variants at different locations in the genome that were unusually common in the Inuit… several …occurred within a cluster of genes that direct construction of enzymes called fatty acid desaturases [FADS]…”

                      Trouble is Duck, even here, the only logical FAD adaptation here can be for the Inuit to *down-regulate* fatty acid desaturation. This because after all they’re getting all their long-chain (EPA, DHA) w3s from all that blubber they chow. IOW, the Inuit don’t have to *make* as much long-chain w3. This doesn’t at all disprove the fact we all, Inuit and the rest of us, need EPA and DHA and their health bennies, and that you benefit from getting it from diet. We generally aren’t very efficient at making EPA and DHA from the parent 18C w3, namely alpha-linolenic acid (ALA).

                      Finally Zimmer includes but then you get this caveat: “…natural selection might not have favored the FADS variant but a neighboring, as yet unknown piece of DNA that conferred evolutionary advantages…”

                    20. I thought that the Inuit had traditionally minimal- (or even non-existent) heart disease; but in more recent years, they’ve been adding Western foods to their diet, so they now have more health problems (and death) than ever before (?) The problem is that the link about the Inuit and heart disease takes place too late in time, after they were exposed to Western food. Often when a Native culture goes suddenly from their old diet to eating more modern foods- even if only a few of those foods are introduced- they have even more health problems than the rest of the population. So I’m not sure if those studies were accurate of much of their existence. It sounded like a bit of speculation anyway- (i.e., “they probably had heart disease that was not diagnosed, or overlooked”). That doesn’t really prove anything, in my mind, about the Inuit.

                      My personal theory is that people are so convinced about the diet/heart hypothesis (i.e. that saturated fat causes high cholesterol, which causes heart disease)- that every time a paradox crops up (and there are many of these!)- they have to find something to explain it away. Usually, they find some mechanism that is supposedly “protective”. With the French it was red wine, with the Masai it was suspected that they had a genetic mutation (with the Inuit too), with other cultures it was all the anti-oxidants they ate, or the garlic they ate, whatever. So the same with the omega 3 fish oils. Maybe these foods aren’t “magic foods”; instead, maybe the whole hypothesis is wrong?

                      In any case, I’m not quite sure if I “buy into” the whole omega 6/ omega 3 thing. Oh, I agree with wbryanh that seed oils are not good (I stay away from them myself). Mostly because they are highly processed and turn rancid very quickly (and I’ve read that some of them are correlated with cancer). I’m not sure if it’s the omega 6 part that makes them “bad”; (could be, that’s open to debate).

                      In any case, I agree, Duck Dodgers, about omega 6 in whole foods as not being a cause for concern. (I had also read before that the vitamin E is protective). In looking at populations of people who eat nuts, they seem to be very healthy, and nuts seem to possibly even be protective against heart disease- (of course correlation doesn’t equal causation, but at least it’s clear that nut eating people don’t seem to be dying off). At least I’d like to believe this of course, because nuts are one of my favorite foods and I eat them often! My guess is that in terms of whole foods, the O-6, O-3- (if it’s a problem at all) is probably self regulating.

                    21. “Fishing” for the origins of Fodor’s “Eskimos and heart disease” DEBUNKING story.

                      Morgana, right on! You wrote: “I thought that the Inuit had traditionally minimal- (or even non-existent) heart disease; but in more recent years, they’ve been adding Western foods to their diet, so they now have more health problems…”

                      Regarding the “debunking” studies, esp Fodor’s “Fishing” for the origins of the “Eskimos and heart disease story” we may find something rotten. And not in the State of Denmark.

                      Ironically, the debunkers, and an all too credulous and sensation-hungry media, hang their hats on this “seminal” Fodor study, which you can read here: http://ottawa.ctvnews.ca/polopoly_fs/1.1814937!/httpFile/file.pdf

                      Is this a case of “the shark calling the herring black?” We’ll see! What I’ve found so far:

                      Fodor et al provide a list of 60 references. I’ve reviewed to date 35 of those refs. So far Morgana I find an undeniable pattern that is just what you say: Early Inuit and even early non-Inuit native living ancestrally have lower CAD. Later Inuit and non-Inuit natives adopting a more “western” lifestyle have higher rates of CAD.

                      At first blush, this evidence (to date) seems to contradict the authors’ own conclusions! But let’s be clear what the Fodor report does and does NOT say. The authors do not outright *deny* the ancestral high-fish Inuit diet lowers CAD risk. They conclude simply that “ this hypothesis lacked a solid foundation.”

                      I will share later my ideas why the authors would present their findings in such a muddy way.

                      Meanwhile there’s more. In their report I found a decision flowchart that shows the authors narrowed evidence inclusion down to “10 papers related to 10 studies.” Strangely, I can’t find such a list anywhere in their report even though I’ve read it several times. Did Fodor et al accidentally leave out that list out?

                      In the meantime, I’m trying to come up with that 10-paper list, based on that superset of 60 refs. I’m using the filter that Fodor et al included to winnow down to those 10 papers. Here’s that filter:

                      – No relevance to Eskimo population
                      – No direct measurement performed in study population (i.e. metaanalysis, review paper, etc.)
                      – No assessment of CVD or CAD in study population
                      – Full article nonaccessible online

                      Then I read this from the report: Table S1. Evidence regarding low incidence of CAD in Greenland as cited in Bang, Dyerberg et al publications 1971-1980

                      Morgana, this lists seven papers. At least five of them fulfill the inclusion requirements above. Does this mean then that as many as *half* the the 10 papers Fodor et al use to debunk the Inuit diet-low-CAD hypothesis come from the *very same authors* whose research the integrity of which Fodor calls into question?!

                      Fascinating!!

                      Today I emailed the doctor seeking that list of the 10 studies.

                      Stayed tuned!

                    22. wbryanh- yes, keep me posted, I’m curious! But, yes; I have read in many different places, from different sources, that the early Inuit were free from heart disease (and other diseases of civilization). But later on, they had even more problems than most because when native hunter-gatherer type cultures change their diet suddenly, they often become even more sick than the general population because they’re just not well adapted to the modern diet. Many people have unfortunately used their more recent health problems to “debunk” the original observations.

                      Having said that, I’m still not sure that the “protective factor” is the fish- (it might be, as epidemiological studies show that fish eaters are very healthy)- or the omega 3/ omega 6 ratio- (it could be, but I’m not sure there’s enough credible scientific evidence proving that it’s important)- or, and this is my own theory, that maybe the diet-heart hypothesis is wrong, and high (natural) fat diets do not cause heart disease? There seems to be a lot of evidence that refined sugar may be implicated in heart disease. Apparently, this was documented and known about even back in the 70’s, but it’s been covered up….. just like the tobacco industry covered up knowledge about tobacco!

                    23. Morgana, good timing on your response. Just had a lovely 30 minute talk with one of the leads on that study. She couldn’t remember the 10 papers off the top of her head, nor where they are supposed to be listed in the report. She said she’ll reread he report tonight/over the weekend and get back to me. I hope I’ll hear back from Dr Fodor too. He’s retired from Ottawa Heart but Media Relations forwarded my enquiry to the doctor and promised “a very quick response.”

                    24. Hi Morgana! Study second-lead Efythia Helis sent me the list of the 10 papers that she and Fodor et al used in “Fishing” for the origins of the “Eskimos and heart disease story.”

                      This confirms the Fodor meta-study offers nothing conclusive about CAD/CVD in Inuit eating ancestral foodways. The vaunted 1940 Bertelsen paper, though the authors discuss it at length in their Intro, actually *failed* to make their final cut. Very interesting!

                      To refresh your memory, Duck posted a Slate link on Nov 24th as evidence to debunk observations that the Inuit were free of heart disease. Here are the two links to that Slate article and the Fodor study:

                      http://www.slate.com/articles/health_and_science/medical_examiner/2014/08/does_fish_oil_prevent_heart_disease_original_danish_eskimo_diet_study_was.html
                      http://ottawa.ctvnews.ca/polopoly_fs/1.1814937!/httpFile/file.pdf

                      Dr Fodor’s retired to Europe and no longer answering Qs on this meta-study. But the study second-lead Efythia Helis emailed me this morning. From her mail:

                      “…the 10 studies we identified are listed in supplemental tables S3 and S4. Table S3 presents information regarding the only study we identified that used direct measurements on the Eskimo population (Reference # 28). Table S4 lists information from 9 studies that presented data on CVD status in Eskimo/Inuit populations in Canada and the US (references 22,23,29, 30,31,32, 33, 34, 35). In total, 10 studies, listed in two separate tables, which clearly can be confusing. We split them like this, since it was only the study by Jorgensen et al (#28) that used direct measurements on the actual study population…”

                      Morgana, note they include exactly *one* paper that directly measured the Inuit for CAD/CVD, and it’s from 2008! Even Jorgensen et al admit: “The prevalence of markers of CHD was not different from that in Western populations. The Inuit is a population undergoing rapid social and health transitions, with the emergence of cardiovascular risk factors, and there is a need for critical rethinking of cardiovascular epidemiology in this population.”

                      Note the authors do *not* include that 1940 Bertelsen paper in their final cut. They discussed it at length in the Intro, yet the evidence in that Bertelsen paper somehow didn’t rise to the level of evidence to make the cut. Very interesting!

                      You can see those 10 refs starting on page 16 at the CTV link.

                      I’ll finish reviewing the refs and then post my ideas on why these study leads chose to represent this info and highlight certain aspects–like finding flaws in a 1970s Bang and Dyerberg–in the curious way that they did. –Bryan

                    25. I have no clue why the Inuit have any relevance in regards to anyone’s diet, regardless whether they were healthy or not.

                      For one, no one could or would replicate a traditional inuit diet of seal blubber, polar bear organs and fermented fish. Swapping them out for ground beef and a ton of fat is not even in the same ballpark.

                      Also they did not just decide to eat that way because of health reasons. That was a several thousand year adaptation to extreme living conditions. Even if the average low carb enthusiast could replicate an Inuit diet, their physiology is so different that they would probably get real sick real fast.

                      Bottom line, even if they were a healthy culture, which is not proven, that means nothing because the diet and lifestyle cannot be replicated so it has no relevance on a traditional VLC diet. If they were unhealthy eating their traditional diet than that proves very bad for anyone eating a watered down version.

                    26. Morgana, Fodor et al’s “Eskimos and heart disease story” feels more than ever like Fodor’s retirement gift to Big Pharma. No doubt Pfizer, Merck, Astra-Zeneca, and other statin producers love them a tasty dish that casts doubt on the CVD health bennies of a high-fish diet. The less healthy our diet, the more money we fork over for their drugs. In turn, Big Pharma spreads a bit of the wealth to many academic researchers, including Fodor during his active work life.

                      Four author/researchers worked on this study. But I’ll refer just to Fodor. He shaped and had the final word on the study direction and contents: http://ottawa.ctvnews.ca/polopoly_fs/1.1814937!/httpFile/file.pdf

                      Fodor’s stated goal: to determine if there was enough evidence to support the “Eskimo diet and low CVD” hypothesis. In the Intro, Fodor sought to debunk studies Bang and Dyerberg did in the 1970s, studies viewed as seminal to show fish-eating Inuit have lower CVD. Fair enough–those studies do appear to have methodological flaws. And who doesn’t love a juicy debunking story? Especially a largely unquestioning and headline-hungry press?

                      The sad thing is, Fodor fails to discuss a very valuable pattern his sources studies reveal: a whole-foods diet high in actual high omega-3 food may actually lower CVD significantly. In the 10 studies Fodor uses, the trend is abundantly clear: The further back in time you go, the less CVD the fish-eating Inuit had. Why didn’t Fodor call this out? Maybe because it didn’t suit Pfizer et al?

                      In the Intro, Fodor muddies the waters, jumping between fish and fish oil caps. He conflates the two, implying an equivalency even though by publish date (2014) we had plenty of evidence to suggest fish oil caps may not offer the same therapeutic benefits as eating actual fresh fish. Fodor utterly fails to discuss these diffs. He very easily could have. In his list of 60 total refs, if you look at the 50 studies that failed to make the cut, you find many of them for cohorts taking fish oil caps. Overwhelmingly, these suggest that the caps had little or no impact on CVD over the non-cap taking controls/cohorts. Why did Fodor ignore that glaringly obvious pattern?

                      Further down the Intro, Fodor says this: “More recently, a number of studies have confirmed what Bertelsen ascertained more than 70 years ago, i.e. that the prevalence of CAD among Eskimos in Greenland and other Inuit populations in Canada and the US is similar or higher compared to that of non-Eskimo/Caucasian populations.” This statement may be outright wrong. Bang & Dyerberg wrote in 1980: “…Berthelsen (1940), does not even mention [CAD]…” http://link.springer.com/chapter/10.1007%2F978-1-4757-4448-4_1#page-1
                      If true, how could Bertelsen have “ascertained” that those Inuit had western-level CVD rates?

                      Fodor concludes: “We conducted a literature review to assess whether there was sufficient evidence to support the ‘Eskimo diet and low CAD” hypothesis. Our conclusion is that this hypothesis lacked a solid foundation.” Problem is, Fodor doesn’t distinguish between earlier ancestral and more recent Inuit diets that are heavily influenced by western foods. He lumps them together under the vague rubric “Eskimo diet.” We have no direct measures of Inuit CVD before Bang and Dyerberg, whose work Fodor sought to discredit and conveniently drop from the pool of papers he considered for this study. Thus we have *no* studies that give direct measures for Inuit eating a predominantly ancestral diet. That leaves only direct measures of *modern* Inuit who follow an increasingly western diet and lifestyle (e.g. drinking, smoking).

                      We’d be naive to think that Fodor’s many links to Pharma couldn’t influence his research design in subtle, even overt ways. He was Founding President of the Canadian Hypertension Society which gets heavy Big Pharma sponsorship, esp Merck. https://www.hypertension.ca/en/chc. Fodor received honoraria from AstraZeneca, Merck Frosst, Pfizer and Schering for conferences and advisory boards. http://www.totalbodyhs.net/2011/11/08/conflicts-of-interest/ On his CV, he lists major research that’s funded by Big Pharma, e.g. the 2001-2002 AVALON study funded by Pfizer. Should we be surprised then that Fodor came out ardently in favor of Big Pharma’s products? E.g. he says in 2007: “The efficacy and safety of [statins] is outstanding…” http://www.curezone.org/forums/am.asp?i=822300 even though we’d already started to see efficacy and safety concerns emerge about statins since the 1990s. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981 .

                      Fodor published the “Eskimos and heart disease story” study not long before he retired to Europe. I reached out to the retired Dr Fodor and failed. The Institute’s media contact Vincent Lamontagne said he forwarded my questions to Fodor, assuring me “Dr Fodor very quickly responds to questions.” When I heard nothing for 10 days and followed up, Lamontagne then informed me the Doctor would not take questions after all, leaving the unenviable task to the junior leads.

                      Sadly, Fodor’s close ties to large corps is an ever more common pattern we see among academic researchers. In this era of dwindling government and foundation funding, research institutions had to start turning more to Big Biz for funds. http://www.universitybusiness.com/article/big-business-research As Dr. Edwin Gale says: “Money from drug companies is the oxygen on which the academic medical world depends.” http://www.medscape.com/viewarticle/751433 We shoud all be aware of this very troubling dynamic when we review any health and medical research.

                      My thanks to junior lead Efythia Helis for fielding my questions. –Bryan

                    27. wbryanh- Wow, thanks for that long and detailed analysis! That doesn’t surprise me that they’ve been looking at Inuit eating a more modern diet; I had suspected that. I did not know about the ties to the drug companies though. I have also read in a few places- (I think in books, and I can’t remember where, so I can’t send a link unfortunately)- that in epidemiological studies it’s been found that eating whole fish is more effective than fish oil (like you said). It’s suspected that there is a synergistic effect of all the nutrients together in whole fish, which is different from just extracting and isolating the oil. Some have even gone so far as to say that it may not be the omega 3 after all that causes the protective effect, but possibly some other compound that we don’t know about yet. In any case, the Mediterraneans and the Japanese eat quite a lot of fish too, which might partly explain their low risk of heart disease.

                    28. You’re welcome Morgana! I’ve been trying to find the actual 1940 Bertelsen text on Greenland Inuit CVD, I’ve heard such wildly divergent things, from “western-levels of CVD” to “no mentions of CVD.” Morgana, *someone(s) is/are *bullsh*tting us! But who? I’m trying to find the source text to settle the matter once and for all. I emailed Fodor study junior lead Eftyhia Helis about it. She responded with this: “This 1940 report is with Dr. Fodor’s files, which, unfortunately, I have no access to at the moment…I do not think there is a translated version of this…” Next stop–my local library to try to get that volume of “Gronlandsk medicinsk statistik og nosografi.” When I finally find it, I’ll OCR it and run it through Google Translate and see what we get. If it’s short enough, I’ll plop it up here for all of us. –Bryan

                    29. Morgana, about the “Eskimos and Heart Disease” study, one of the junior leads, Effy (Eftyhia Helis), is super nice and helpful. So I invited her to join in here and address whichever points she felt like addressing. That’d be great if she could join in. –Bryan

                    30. Jonathan, that article is excellent, thank you! One of the best pieces I’ve read to describe researcher direct observations on the unusually robust health of ancestrally-living Inuit. Anna, please note at the top of page 386, the discussion on Vitamin C, how these Inuit consumed almost *no* Vitamin C and yet showed no signs of scurvy or other connective-tissue pathologies. Schaefer also reminds us that even in 1959, folks challenged Ancel Keys’ ideas on dietary lipids (page 387). –Bryan

                    31. Anna, yes I was going to write to you about that! That’s another great example of nature’s uber-intelligent plan: Animal-sourced food is very low in both carbs and Vitamin C. So whatever the ancestral dietary “playing field” the competitors are fairly well matched matched.

                      I came across that ~5yo when I first came across the Inuit paradox. Our C RDA is 90mg/day but going on memory, seems like Inuit do fine on ~ 15mg/day, which they get mainly from, I think, muktuk. That blubber is one of the few animal-sourced foods I’ve heard of to have measurable amounts of C. C and glucose are very similar molecules, indeed and I think plants and many (most?) animals make C from glucose. https://en.wikipedia.org/wiki/Vitamin_C . I believe it’s a four-step process, and we lost the ability to do that last step not so many millions of years ago. Anyway, C and glucose complete for the same GLUT1 transmembrane transporters. https://en.wikipedia.org/wiki/GLUT1. Anyway, again going on memory, all cxns welcome.

                      Anna, on a totally diff topic for a moment, was the Indian side of your fam part of the migration to Astrakhan in the 17th cen? I find it a very interesting bit of Russian history few people hear about. Thanks for indulging my curiosity. –Bryan

                    32. Not about carbs, but another thought is that the need for Vit C varies depending on the need for anti-inflammatories.
                      Most of the information about scurvy was obtained on sailing ships in the last few centuries. The sailors at the time lived mostly off salted meat, dark rum, and hardtack. Their cooking pots were mainly cast iron. What you have there is a diet super-high in oxidants and inflammatory factors. Further, the sailors typically lounged around half-clothed in the sun.
                      So the body uses Vitamin C to handle all of the above. A lot of Vit C is used just to handle UV rays on the skin. Vitamin C also reacts with the iron (from iron pots, dark rum, and salt beef). And for some percentage of people at least, wheat is also inflammatory.
                      According to Adv in carbohydrate Chem & biochem page 141, whales are mainly neu5ac, which if true would make them less inflammatory than beef. Fish are mainly neu5ac too.
                      Anyway, your average Inuit wasn’t running around half-clothed or eating beef or swigging rum or cooking in iron pots. So quite possibly their need for Vit C was a lot less.

                    33. Heather,

                      Great point about vitamin C and UV. Thanks.

                      Duck and Bryan,

                      Thank you guys for your patience and dedication in debating the inuits and ketosis, it was very informative. And thank you to everybody else who contributed to the Inuit discussion. I’ve learned a lot.

                    34. Anna thank you and thanks for your questions too. I learned a lot from everybody! Fair to say, a huge amount. I don’t know if this means you’re leaving us now, but if you are then I hope Anna do skorogo! –Bryan

                    35. “Anna, on a totally diff topic for a moment, was the Indian side of your fam part of the migration to Astrakhan in the 17th cen? I find it a very interesting bit of Russian history few people hear about. Thanks for indulging my curiosity. –Bryan”

                      Bryan, the indian side is not blood related, but via marriage very recently.

                    36. Now who’s telling the truth? The truth about the findings of Dr. Bert(h)elsen? The only person before Bang & Dyerberg to extensively observe Greenland Inuit who still lived and ate ancestrally?

                      This matters because many Inuit diet debunkers love to cite this Danish study. A study few of them actually *read* because there doesn’t appear to be an English translation. So who knows where they got their citations from? One such debunker is vegan diet promoter John McDougall, who grandiloquently calls Dr. Bertelsen “…the father of Greenland epidemiology.”

                      https://www.drmcdougall.com/misc/2014nl/feb/grassfed.htm

                      Duck you said: “…As best as I can tell, the idea that we need to eat more Omega-3 and less Omega-6 (i.e. the fish oil craze) comes from Bang & Dyerberg’s erroneous and now debunked observations that the Inuit were free of heart disease. [Debunked by this Fodor study] The Fishy Origins of the Fish Oil Craze…”

                      Should we believe Dr Fodor, the lead on the “seminal” meta-study of meta-studies “debunking” the CW of low IHD in the Inuit? Or should we believe Bang & Dyerberg?

                      In his report Fodor says: “…Bertelsen … described *frequent occurrence of CAD in this Inuit population*…” http://ottawa.ctvnews.ca/polopoly_fs/1.1814937!/httpFile/file.pdf

                      By contrast, Bang & Dyerberg wrote this in 1980: “…Berthelsen (1940), does not even mention [IHD]…” http://link.springer.com/chapter/10.1007%2F978-1-4757-4448-4_1#page-1

                      Please note per the Wiki, CAD = IHD. https://en.wikipedia.org/wiki/Coronary_artery_disease

                    37. wbryanh,

                      The point is that Bang & Dyerberg screwed up, and their errors are what started the fist oil craze:

                      Fish oil and the ‘Eskimo diet’: another medical myth debunked

                      Here is the actual study that finds the problems with Bang & Dyerberg’s research:

                      “Fishing” for the Origins of the “Eskimos and Heart Disease” Story: Facts or Wishful Thinking?

                      Sure, you can explain all this away, but lots of people fell for Bang & Dyerberg inaccuracies. At least admit that they made some big mistakes. The rest may in fact be “wishful thinking”.

                    38. Sorry, Duck. Again, you give -nada-.

                      If you read carefully, I never said B&D was right. What I am saying:

                      **you haven’t shown anything that firmly concludes anything different from what B&D concluded**

                      In that Minnpost link you gave, author Susan Perry gives these studies to support her case. So far, all FAILS.

                      http://www.ncbi.nlm.nih.gov/pubmed/22968891. Study done with supps only. Not the real marine life that real Inuit eat. Huge diffs. As I explained earlier.

                      http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD003177.pub2/abstract. Meta-study from data collected in 2002. Quite possibly most if not nearly all their data comes from Inuit eating SAD. Stuck behind paywall. No details on that data.

                      http://www.sciencedirect.com/science/article/pii/S0828282X14002372. Again, meta-study stuck behind paywall. Used data “…which accumulated on this topic during the past 40 years.” You can be sure most if not nearly all their data comes from Inuit eating SAD. In any event, stuck behind paywall. No details on that data.

                      Duck, you say “…at least admit that [B&D] made some big mistakes…” I don’t know, Duck. Did they? Do you know? Have you actually read their study? Did they conclude things beyond what their methodology would allow them to determine? Some say they do. They can say whatever they want. I’ve seen so many agenda-driven meta-studies with statistical p-factors hacked to a fare-thee-well that AMAP I go right to the primary sources. In this case, I haven’t read the B&D report–that’s behind a paywall too. Abstract’s here:

                      “The plasma-lipid pattern, including quantitative lipoprotein electrophoresis, was examined in 130 Eskimos (69 females, 61 males) — hunters and/or fishermen, and their wives — in the northern part of the west coast of Greenland, and consuming a predominantly meat diet rich in polyunsaturated fatty acids. Most types of lipid were decreased, compared with Danish controls and Eskimos living in Denmark. The most remarkable finding was a much lower level of pre-β-lipoprotein and consequently of plasma-triglycerides in Greenlandic Eskimos than in Danish controls. These findings may explain the very low incidence of ischæmic heart-disease and the complete absence of diabetes mellitus in Greenlandic Eskimos.”

                      BTW, there’s a strong positive correlation between cardiovascular disease (CVD) and diabetes:

                      http://www.heart.org/HEARTORG/Conditions/Diabetes/WhyDiabetesMatters/Cardiovascular-Disease-Diabetes_UCM_313865_Article.jsp/#.VlUiGHarSUk

                      with plenty of mechanistic data to support that correlation. B&D report a “complete absence of diabetes mellitus in Greenlandic Eskimos.” Duck you do not need to peer inside the body to learn this. A simple blood test works fine.

                      Duck, would you start making an effort to provide actual relevant evidence that’s not stuck behind paywalls? This is disappointing and starting to get boring. Thanks for considering.

                      And your final sentence: “The rest may in fact be “wishful thinking”…”

                      Duck, maybe that’s your wishful thinking?

                    39. “The low mortality in Greenland from IHD and the low presence of arteriosclerosis of the aorta and coronary arteries seem well established…” (4)(8)

                      Footnote (8) goes to Inuit autopsy studies. Not mere blood work and other indirect measure. This get right to the heart of the matter (harhar).

                      http://ije.oxfordjournals.org/content/26/6/1182.full.pdf

                      Duck, I’m curious to learn if this wind up in the Fodor meta-study you cited. And how many of those other studies in his meta-study tap into autopsy studies.

                      This evidence is stronger than just about anything I’ve seen so far.

                    40. wbryanh said: “I saw the flurry of articles a few months back, but none explain exactly *how* the Inuit are supposed to better utilize PUFAs than the rest of us”

                      Well, those new genes were just discovered, but the CPT1a gene was discovered awhile ago and that has been documented a bit better. If you take the time to investigate their CPT1a gene, you’ll find that studies have shown that 68% of Eskimos have an autosomal recessive mutation that results in a “CPT1a deficiency,” which is known to cause hypoketotic hypoglycemia (i.e. low ketones and low blood sugar). They prefer to snack constantly because of this—though it’s mainly only dangerous to children (who were traditionally breastfed carby human milk until ages 4-6).

                      It’s been awhile since I looked into this, and don’t really care to look into it again—so I’m only pointing you in the right direction. But, if I remember correctly, the FAs can’t (easily) get into mitochondria in cells that have CPT1a (such as the liver), but it sounds like they CAN get into mitochondria in cells that have CPT1b and CPT1c. CPT1b is prevalent in skeletal muscles, heart and brown adipose cells (good for thermogenesis in a cold environment), while CPT1c is mostly in the brain, though little is known about CPT1c. Again, if I remember correctly, this implies that their livers are protected from burning too many FAs as FAs are preferentially shunted to muscles and other organs. Or something like that. It’s been awhile.

                      Anyhow, the point being is that there is a fair amount of research covering how they burn fatty acids very differently than Westerners do. And therefore, they make a lousy proxy for Western metabolisms who generally do not have their unique genes.

                    41. “…studies have shown that 68% of Eskimos have an autosomal recessive mutation that results in a “CPT1a deficiency…”

                      Duck, this is interesting stuff which I’ll be diving more into. In general, these gene variants–mainly missense mutations?–appear in general to “gate” the ingress of FAs into the cytoplasm–at least for liver cells. Which makes sense for a diet extraordinarily high in extraordinarily oxidizable w3. This presumably spares the sensitive mitochondria from oxidizing events in their midst, minimizing damage. In a sense it’s like insulin gating the ingress of glucose (also oxidizing) to the cytoplasm, with the same goal, to minimize stress on the mitochondria, though obviously by a diff mechanism.

                      That’s my initial take of it anyway. Will dig into it more later.

                      I don’t doubt the Inuit experienced several SNP variances over their thousands of years living in their harsh frigid environment and eating their ultra-low carb high w3 diet. But Duck for you to make the leap that “…they make a lousy proxy for Western metabolisms who generally do not have their unique genes” is a stretch at best. You can’t know it is a “lousy proxy.” None of us know it at this point. You may well be vastly overstating, even erroneously, stating the case. E.g., we don’t know how successfully Non-Inuit and Inuit can up/down-reg when placed in the others’ environment. If you know of any systematic examinations of that, please share. It is wrong to imply that Inuit nutrient metabolism as being so fundamentally different that it can’t offer the rest of us any nutrition lessons. Especially when we include the Inuit experience in a larger examination comparing different ancestral diets.

                      And how do these SNPs even relate to the premise that kicked off this thread? The validity (or lack thereof) of w6/w3 balances?

                      A few posts back you said: “…the conventional wisdom on Omega-3:6 ratios may not be all it’s cracked up to be when we look at them in the context of whole foods…” That’s when you introduced the Inuit w3 topic by saying this: “As best as I can tell, the idea that we need to eat more Omega-3 and less Omega-6 (i.e. the fish oil craze) comes from Bang & Dyerberg’s erroneous and now debunked observations.”

                      Duck, the SNP changes I’ve heard about to date doesn’t *distinguish* between the dietary fats. These Inuit SNPs may preferentially deliver ALL fats to non-liver cells–sats/monos/polys. This doesn’t mean ideal w6/w3 balances aren’t similar across differently groups. Westerners may not be seeing the benefits of fish caps for other reasons besides a presumed irrelevancy of the w6/w3 balance. Esp when we consider the near pharmacological amounts of rancid fish oil in the caps, and people still chowing w6-bomb veggie/legume oils, also all too often rancid.

                      Btw, for the record, per that ADN link it’s “68% of *indigenous people of northern Siberia*…” Not all of Inuit-dom. That matters because the Siberian and NA/Greenland Inuit diverged 15,000 or more years ago.

                      http://www.adn.com/article/20141129/clues-emerging-about-arctic-gene-diet-and-health

                    42. wbryanh,

                      It wasn’t that hard to find a copy of the Fodor study that calls Bang & Dyerberg into question.

                      http://ottawa.ctvnews.ca/polopoly_fs/1.1814937!/httpFile/file.pdf

                      Bang & Dyerberg based their supposition on casual observations that coronary atherosclerosis in Greenlandic Inuit was ‘almost unknown’ and that they consumed large amounts of omega-3 FAs. Except that it was known, as the Fodor paper shows. So yeah, they made a mistake and what’s problematic about it is that their speculation kickstarted the fish oil craze.

                      Anyhow, it makes no difference because even if they were healthy at one time, they don’t metabolize fats the way that we do making them a very poor proxy for Western metabolisms. Here’s two studies on CPT1a that I quickly found that wasn’t behind a paywall. But there are many others besides this one, should you take the time to look.

                      Genetic polymorphisms in carnitine palmitoyltransferase 1A gene are associated with variation in body composition and fasting lipid traits in Yup’ik Eskimos (2011)

                      Polymorphisms in Genes Involved in Fatty Acid β-Oxidation Interact with Dietary Fat Intakes to Modulate the Plasma TG Response to a Fish Oil Supplementation (2014)

                      No, they are not like us.

                    43. “Duck, just checking. This is what you saw, is that right?”

                      I’ve seen that article before. It’s a good summary of the research. Basically the gene is only problematic for babies and young children who can have trouble fasting. The CPT1a mutation is believed to be related to their ability to generate significant body heat from their high PUFA diet. And it’s also believed to be related to their known preference for constantly snacking.

                    44. Like all of the other Eskimo researchers, Otto Schaefer says

                      “The traditional diet of Eskimos contained large amounts of proteins, lesser amounts of fat than generally assumed [29-30] and only small amounts of carbohydrate, mainly in higher complexed form as glycoproteins, and therefore not rapidly absorbable.”

                      pmid.us/PMC1940978

                      Why all the fuss when even Schaefer says they weren’t LCHF? We can’t replicate their high protein diet.

                    45. Thanks Rachel, I’ve wanted to read this study. Only will you point out for us which page on which we’ll find the quote you gave us? You know, the one that starts with “The traditional diet of Eskimos contained large amounts of proteins…” I searched on it in that link came up empty. Thanks for your help Rachel. –Bryan

                    46. Rachel, found it. To make clear, the quote you cite (see below) doesn’t support what you say here:

                      “…even Schaefer says they weren’t LCHF…”

                      The Inuit could still be eating mostly fat, as Ho et al say in their Canadian Inuit report from the same year:

                      “Approximately 50% of the calories were derived from fat and 30 to 35% from protein…”

                      Here’s that quote you cite, from near the top of the second column on page 737:

                      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940978/pdf/canmedaj01654-0029.pdf

                      “…The traditional diet of Eskimos contained large amounts of proteins, lesser amounts of fat than generally assumed (29-30) and only small amounts of carbohydrate…”

                      –Bryan

                  2. Conventional wisdom says that hookworms promote anemia. There are a few problems however…

                    The association makes sense, helminths eat blood, blood contains iron, iron is reduced in blood, therefore helminths promote anemia. However, the helminth load may be determined by the iron available, or the body will withhold iron in tissues to lower iron in the serum in response to helminths. The results may be the same as chronic anemia triggered by bacterial infection.

                    In other words, it could just be that helminths cause anemia of chronic disease. Apparently it takes heavy infestation to cause significant blood loss, and heavy infestation means damage to the gut and poor nutrient absorption, which means the anemia may be just as likely to be due to micronutrient deficiencies as blood loss.

                    The US government was sufficiently convinced of a helminth-anemia link that it carried out a huge program to eradicate helminths.

                    Dietary Iron Content Mediates Hookworm Pathogenesis In Vivo (2006)

                    “… it has also been suggested that hookworm infection modulates iron metabolism in the host, resulting in enhanced reabsorption from the gut as a means of compensating for hookworm-associated blood loss (10, 11). Such a compensatory mechanism was originally put forth to explain the fact that death from overwhelming hookworm anemia is rare, despite calculations that show that iron losses from hookworm infection are likely to far exceed dietary intake in many communities of high endemicity (11, 24).

                    The data presented here offer another potential explanation for this apparent contradiction, namely, that severe iron deficiency may directly influence the ability of hookworms to establish and/or maintain infection. Our findings are supportive of the recent observations that Caenorhabdis elegans and related helminths, including hookworms, lack the ability to synthesize heme and thus depend on exogenously acquired heme as an iron source (26). It is plausible that animals fed a low-iron diet reveal diminished hookworm pathogenicity due to inadequate heme availability for hookworm growth and development.”

                    So helminths metabolize the human-sourced iron and also encourage re-absorption of iron in the human gut, so that enough remains to feed them. Makes sense. It appears to be an efficient, low-waste process.

                    Helminthic anemia impacts women most, especially pregnant women—but again this could be anemia of chronic disease. Even light infection was found to reduce serum iron in pregnant women. Anecdotally, helminths appear to be more of a net benefit, on avg, than a problem, for males. It is indeed complex.

          2. wbryanh: I have a suspicion that “Zach” actually might BE Durian Rider himself! Durian Rider has a habit of lurking around nutrition websites using various pseudonyms. I think this is why he got so emotional when I made a comment about him- (and somewhere else in the comment section, someone posted an Anthony Colpo link about Durian Rider; he got very emotional there too). In any case, both “Zach” and Durian Rider have the same method for promoting their diet: they use Durian Rider’s thinness and “fitness” to claim that it’s the best diet in the world. Durian Rider also likes to make videos where he finds an “opponent”- someone who eats low carb, or maybe just someone who promotes meat eating- and he basically just laughs at that person, saying they are fat. No science, no intelligent conversation, just ad hominem attacks. But doing that on the comment section of a blog over the internet is truly inane, since he has no idea what we look like or how fit we are! If he could see me, he would see how utterly laughable his comments to me were. In any case, I did not answer his last comment about me because I felt that it didn’t warrant an answer- (although what he means by “especially people who hang around fitness blogs”- what he’s trying to imply here (?) it’s totally illogical. This is purely an emotional comment).

            1. Morgana, yes, could be. In the beginning “Zach” seemed a bit more reasonable or at least civil. But seems like now he’s just shrilly issuing empty statements.

                1. Jon, I’m not *quite* ready to write Zach off as a contrarian for contrarian’s sake. He does seem to genuinely believe in HCLF. But that’s just it–belief. If he continues to blurt out dumb stuff unencumbered by rigorous science, then yes I will ignore him. If he gets truly insulting, I expect Denise will ban him. That said, I’m very concerned about the pro-HCLF/anti-LCHF message that some people promote. I feel HCLF can be quite dangerous to hundreds of millions of people. Type 2 diabetes is soaring all round the world. I’ve yet to see a HCLF study that even comes *close* to normalizing blood sugars. At the very least, people serious about this need to get glucometers and give the foodways a fair shake and see how they do. For me, it’s LCHF and has been for nearly nine years.

                  1. WBryanh, how can you say that? The article outlined several studies/dietary programs that cured diabetes. Right? And then there are many more modern studies and clinical results that have underlined these. I’m not aware of any studies where HFLC has cured diabetes as opposed to manage the condition by avoiding carbs. So the exact opposite of what your saying is what’s published.

                    1. Cjarman, as far as “curing” Type 2 diabetes, not only do I see no “cure,” in the main I don’t even see full reversals. It’s there. Take a look.

                    2. Cjarman, dunno how much clearer I can be. Regardless of “who” is claiming “what,” the numbers in those charts that Denise posted say “diabetes!” The limits are in that Mayo Clinic link I posted for you. My own n = 1 tells a similar tale. Before LCHF, my Hemo A1c was 7.0% which equates to an average BG of 170. After starting LCHF, my A1c and quickly dropped, both to 90. It’s nine years later, I’m 55, and my A1c/FBG are *still* 90. That’s a whole lot better that the typical post-study results in any of the studies Denise cites here. I lost 60 pounds, I feel great, I have tons of energy, I sleep better, I *think* better. The so-called “scientific” studies and say and conclude all the things they want. I know what works for me. Like I said above, people should not get caught up in these studies here or most any of the studies–they are full of confouders and mitigating conditions that we’ll be ferreting out and batting around till the cows come home. People should be testing themselves and *see for themselves* which foodway works best for them. Glucometers are cheap, test strips getting cheapers, and it’s an extremely valuable investment in your long-term health. If you do this and follow LFHC and your BGs stay at 75-95 mg/dL all the time and you feel great, then wonderful, why change? But if your BGs are high, you are not at your target weight/BF, you still get the afternoon sleepies, you don’t wake up refreshed, then try LCHF.

                    3. What does HFLC look like in your case? What percentage carbs? I find that if I go HFLC I’m unable to tolerate even a single piece of fruit! Then, when on LFHC, adding in some fats can bring on a yeast bloom.

                      Of late I have tested my blood sugars. What pushes it up is both high fat or high fructose (both result in a reading of 6.1).

                      On high carb I drop back to 4.8, but don’t find that way of eating terribly interesting…

                    4. Craig (Craig right?), I eat 80% fat, 15% protein and 5% carbs. I calc’ed this from pulling the nutrient data from the USDA Nutrient Database and pouring it into a spreadsheet in which I made up menu sheets. The fruits I eat mainly are berries (esp straw-, rasp-, black-), avocados, and olives. About your BGs, how often do you test them and when? Even now, because I continue to be my own Grand Experiment, I test at least 4x/day–at waking, late morning (to check morning effect), 90m after lunch (my first and often only meal of the day) and at ~ 1900. Your 4.8 mmol/L equates to 86mg/dL which is normal. That you get that BG on a high-carb diet (I’m assuming you mean primarily glucose e.g. starch) suggests these invoke a powerful insulin response in you. Which leads to another concern: chronically elevated serum insulin. There’s increasing thought that chronically high serum insulin can be as bad for you (though in diff ways) as chron high BGs. The top test for that is the euglycemic clamp but that’s beyond most people’s resources. But you can get a proxy test for that called C-Peptide. You should aim to have that low, even below 1 ng/mL. Some H-Gs have this as low as 0.2ng/dL. About your higher BG (average right?) of 6.1 mmol/L (= 109mg/dL) on high fat/high fructose, do you mean when eating high fat and high fructose together. Or do you get this same number whether you eat high fat low fructose or low fat high fructose? –Bryan

                    5. Ok – so that is a very low carb diet your on. I’ve typically done about 100-200 grams of carbs when on LCHF. I can feel very much a heavy diet so I typically will skip breakfast and that seems to work ok.
                      With the 6.1 reading, that’s either or. I wouldn’t dare try mixing the two.
                      I used to have a high sugar diet, but have given that up about two years back.
                      It’s all very confusing really. Our traditional diet varies depending upon how far back you look. Presumably we were like other primates and lived primarily on fruits. During the paleo period I can’t see a high carb diet as being feasible in a temperate climate. And with agriculture came the high starch diet…
                      These three I’ve all experimented with, yet remain undecided. And there doesn’t seem to be a happy medium.
                      I’ve more energy on a high carb diet. But more focus and endurance on a high fat diet.
                      My fear is the paleo/HFLC diet will result in insulin resistance or some other metabolic damage, as I’ve witnessed first hand how little carbs I can tolerate when on such a dietary plan.

                    6. cjarman66: I don’t think you need to worry about insulin resistance or metabolic damage on HFLC, or on a Paleo diet. There are anecdotes of modern day aborigines, or Inuit, (among others) who reversed their diabetes and other health problems by going back into the wilderness and eating their native (i.e., “Paleo”) diets. If you feel that you aren’t able to process high amounts of carbs as well on a lower carb diet, it could be that the diet naturally lowers insulin levels; which is a good thing, as too much insulin in the system is also damaging and can cause many health problems. Many people who eat the SAD diet have normal blood glucose levels, but their insulin is above the roof. In this case, it is better for these people to eat fewer carbohydrates, at least for a time. (It’s been labeled “Diabetes in Situ”). If you want more information on this, check out Amy Berger’s website; she has a series of blog posts called “It’s the Insulin, Stupid”. It’s a lot of reading, but I found it quite fascinating. She’s also quite humorous as well.

                    7. My concern is born of the fact that even s piece of fruit will cause a feeling of sugar overload when eating a low carb diet. Possibly it’s too low carb and sets up the insulin resistance as Mark Sisson points out.

                    8. cjarmann66- do you mean that a piece of fruit will cause high blood sugar? Or just a general feeling of eating too much sugar? And does that happen with all carbohydrate foods, or just fruit? The reason I’m asking is that I’ve also read that high blood sugar levels can be caused by foods that you are intolerant to. I don’t know, but if you notice that with certain foods, it could be something to look into. It’s likely that if you don’t eat those foods for awhile, your body becomes more sensitive to the effects- (this is why when people check for food intolerance, they go on elimination diets, then incorporate the foods back in, to see if they notice effects).

                    9. Anything with fructose. Even grated carrot! But anyway I’ve had enough of low carb for now. I determined to find a balance. Skip breakfast, some complex carbs at lunch, fats at dinner and repeat.

                    10. MS writes:
                      14. Go low carb, but not too low carb.

                      Huh? Isn’t low-carb the greatest and most effective path to insulin sensitivity? Partly because it’s often the easiest way to lose weight, low-carb eating can and usually does improve insulin sensitivity. But when you go very low carb, low enough to start relying primarily on ketones and free fatty acids for energy, your peripheral tissues enter an insulin-resistant state to preserve glucose for the parts of the brain that require it. This is normal, and as long as you don’t try to eat a high-fat, high-carb diet, this physiological insulin resistance should pose no harm.

                      Read more: http://www.marksdailyapple.com/25-ways-to-improve-your-insulin-sensitivity/#ixzz3rPqvOgkv

                    11. The exact opposite actually. Since a high fat diet causes insulin resistance, a low carb diet will automatically cause insulin resistance. The fastest way to become insulin sensitive is to go on a very low fat high carb diet. Ridding the tissues of fat and allowing insulin to do its job.

                    12. Hi Zach, yes I’m across this argument. And have gone down the LFHC route and yes I agree that insulin sea usury improves. And it would want to! As all those carbs would be overwhelming otherwise.
                      In my experience however, you need to hit that less than 15% fats level. Otherwise it doesn’t work.
                      It’s as if the cells are fueled by fats or by glucose but just not both at the same time. And that the middle ground is not a balance point, but rather an unholy mix.
                      Less than 15 percent fat I find tolerable for only two or three days. Then something in me starts screaming out for something more substantial.
                      The HFLC route also has its downsides, presumably the lack of glucose for the brain…
                      What seems to work best for me is a period or fasting, followed by a moderate carb load, then the fats, then the fasting period again. Mixing the carbs and fats, or following fats with carbs ain’t great.
                      In their own, both routes, in my experience, have a honeymoon period that lasts only so long.
                      Denise might talk about cycling between the two next up.

                    13. I agree that fat must be kept below 15 and ideally below 10% of calories for it to be most effective. Once pufa is cleared though I have found no issues with going back to a more mixed diet as long as fat is kept mostly saturated.

                      I find a starched base diet to been extremely satisfying though. Stir frys, soups, stews, pasta, etc. They all can be made with little to no added fats but hit all the satiate on signals. Not avoiding sugar also helps feeling satisfied.

                    14. Craig, the Jason Wyrick testimonial, it’s an anecdotal n = 1, with lots of info and context missing. What are the details on his before-change and after-change meals? Could be cutting out all that pasta and moving to leafy greens and legumes, Jason actually *reduced* his carbs along with fat/protein. BTW, eating excess protein is like eating ultra-low-GI carbs. Our bods can’t store excess protein, so must break it down into and our liver turns ~ 3/4 of it to glucose. Cutting down excess protein cuts carbs too. Reducing his overall caloric intake and his subsequent weight loss I’m sure improved his insulin sensitivity. He was able to do that by cutting out highly processed foods, designed to push our evolutionary hot buttons, and replacing them with whole foods. But, again, on his plant-only high-carb diet, we don’t know if he’s generating loads of excess insulin to cover that steady stream of carbs. I’d like to know his C peptide number.

                      https://www.drmcdougall.com/health/education/health-science/stars/stars-written/jason-wyrick/

                    15. He’s not alone. The diet definitely addresses the problem. The theory being that intramyocellar lipids obstruct the action of insulin. Are you aware of this theory? There’s an overview of it here http://youtu.be/OZEXimc9YPs
                      and here http://youtu.be/es4PFR5GZTY

                      So it’s clearly more than an n=1 phenomena.
                      And is it the less carbs and more greens? The rice diet would suggest otherwise.

                    16. Craig, to answer your comment starting that includes: “…Our traditional diet varies depending upon how far back you look. Presumably we were like other primates and lived primarily on fruits…” I agree, and it also depended on where you lived. There are groups following ancestral high-carb foodways like the Kitavans, and they do just fine, or did. The Northern Greenland Inuit who lived ancestrally ate almost NO carbs. We evolved into very opportunistic omnivores, to handle almost any macronutrient mix. It’s just that in our modern times, other novel factors have damaged our ability to properly dispose of serum glucose into our cells/mitochondria. Since the end of WWII 70 years ago, Dupont, Monsanto etc have creating over 100k novel chemicals, some, even many of which, like BPA and phthalates, are estrogenic (i.e. our bods think they are estrogen). Our bods respond to perceived excess estrogen by increasing cell membrane resistance to nutrient/waste ingress/egress. Chronic exposure to estrogenics –. chronic cell wall stiffness –> chronic insulin resistance (IR) –> metabolic syndrome in which IR and insulin keep leapfrogging up. When the beta cells (which make the insulin) cry “uncle” you get Type 2 diabetes.

                    17. Craig, re Jason Wyrick et al, what you say: “diet definitely addresses the problem.” Let’s be clear on what *part* of the diet addresses that prob. Jason went from eating a lot of processed calorie-packed crap to eating whole foods with lots of fiber and micronutrients. That allowed him to *reduce overall calories* and so lose weight, likely the single biggest factor in normalizing his BGs. What if he ate such a diet of whole foods, with the same # of cals, that skewed high fat low carb? Point is, the *quality* of the food is much more important than its macronutrient mix. You see that reflected in the fact that both sides, the HCLF and LCHF folks, can trot out endless numbers of compelling testimonials to support their respective sides. As far as whole foods vs processed foods, Kempner’s Rice diet is a poor defense for processed foods. As I said to Zach: “The average fasting blood sugar (FBG) for folks after 22 weeks of the Rice Diet was 155 mg/dL–still diabetic! Normal fasting BGs are 75–95. This Rice Diet is hardly a ringing endorsement for completely resolving diabetes. I was T2D in 2007, and since *normalized* my BGs with LCHF, averaging 90 mg/dL.”

                      re the Michael Greger vid, here’s the meat (nut?) of what I got from it:

                      1) high insulin response to meat;
                      2) Intramyocellular lipids lead to muscle cell IR, and;
                      3) “preliminary study” from 1927.

                      Let’s first address 1) meat’s high insulin response. Here’s the link to the Holt study MG mentioned, full text is free: http://www.ncbi.nlm.nih.gov/pubmed/9356547 . It makes sense. Meat is protein-rich and cells need insulin to help them take up amino acids, protein’s building blocks. That’s one of the reasons I limit protein to a modest 15% of total cals (remember, I’m 80% fat, 15% protein, 5% carbs)

                      Now 2) intramyocellular lipids. MG merely discussed the IR problem they cause. He fails to definitely show *where* these intramyocellular lipids come from in the first place. At 4:45 MG cites “sat fats as esp lipotoxic and IR promoting Well guess what Craig? If you eat excess carbs, your liver turns these carbs directly into *demon saturated fat* and ships them back out into the blood! Specifically it transforms to palmitic acid (a 16C sat fat).

                      Finally 3) the prelim study from 1927 on a very small cohort to support his claim that a high-fat diet lead to diabetes. Here’s the first page of that study:

                      http://archinte.jamanetwork.com/article.aspx?articleid=535594

                      Alas the rest is behind a paywall. Craig, if you have the full text of it, will you please send it? Thanks. Please understand given the study’s prelim status and the primitive assaying tools we had at that time and the small cohort, I can’t put much stock in this study at this time. Also remember it flies in the face of my own experience. I was diabetic on HCLF, and *normalized* my BGs after going LCHF.

                      re the Jane Esselstyn vid, I started watching it, but I’m sorry Craig, as soon as she asserted (and I quote) “…[glucose is ] … the only thing your brain eats, glucose, that’s it…”, she lost credibility with me and I didn’t want to waste further time on it. Her claim flies in the face of well established fact that the brain also burns ketone bodies. Here’s one of zillions of reputable sources to show that. What’s mystifying is that Jane is an RN and had to learn that: http://watcut.uwaterloo.ca/webnotes/Metabolism/fatKetoneBodyMetabolism.html

                  2. Lol! What kind of bubble do you live in? Billions of people eat a diet of high carb/low fat and have no issues with western disease. It’s only been an issue once western diets high in fat have been inyroduced. Most of the world lives off of a grain of some sort. Rice, corn, wheat, barley, potatoes and other starchs are not just a side dish, they are the bulk of the calories around the world. Every single blue zone culture eats a high carb diet.

                    Did you even read this article? There were people a hundred years ago curing type 2 diabetes with a sugar diet. There are people now like Neil Bernard who cure diabetes on a all carb diet. It’s been established. I honestly have no clue how this is not common knowledge. The paleo/low carb sphere is like this tiny microcosm of people really living in the stone age when it comes to research.

                    1. Zach, good lord, don’t you even think before you hit Enter? “Diabetes, cardiovascular disease, and cancer are among a group of chronic diseases that accounts for most deaths in all regions of the world except South Asia and sub-Saharan Africa.” That’s straight out of this:

                      http://www.prb.org/Publications/Articles/2007/GrowingGlobalChronicDiseaseEpidemic.aspx

                      When you have to live on a subsistence diet, and have to do a lot of physical labor through the day, your bod cares a lot less where that calorie is coming from be it from a carb, or fat, or protein. But then those people often suffer from a lot of nutrient-deficiency conditions like kwashiorkor and iron-deficiency anemia.

                      And Zach when are going to start giving us links to back up your wild claims? Where does it show Neil Barnard or anyone else “cure” Type 2 Diabetes? “Common knowledge” doesn’t cut it pal. About your claim: “There were people a hundred years ago curing type 2 diabetes with a sugar diet.”Let me turn your question back to you Zach: Did YOU even read this article? Maybe you’re thinking of another article? Maybe you conjured this out of thin air? Because I sure didn’t see anything in Denise’s piece to support that wild claim. Kindly point that part out to us OK?

            2. People that frequent health blogs are usually sick and woefully out of shape. Especially ones that eat high fat. Not me though, I’m lean as fu*k, it’s all them carbs.

              Btw I eat dairy so I can’t be durian rider. 😛

              1. Zach great for you that you are “lean as f*ck” as you put it. Btw, how old are you? I mean chonologically? As for your comment “People that frequent health blogs are usually sick and woefully out of shape.” Of course you can’t possibly know that. It would help us all if you stopped yanking stuff out of your derriere.

              2. “Zach”- you eat dairy? Really?!!!! What about all that (gasp) saturated fat? Aren’t you worried about getting diabetes?

                Here’s something to ponder: back in the past, diabetes was actually called “sugar diabetes”. If you look at the words “diabetes mellitus”, the word “mellitus” is from the Latin word for honey. Gee, why did they use words like “sugar” and “honey” to describe diabetes? Could it be that it had something to do with sugar, and nothing whatsoever to do with fat?

                1. Yes because sugar is excreted in the urine. Odd that you know the mean ing of the word but nothing about it. Interestingly doctors over 150 years ago found that by giving their patients butt loads of sugar, they would stop excreting it in urine and effectively curing diabetes

                  Btw I eat low fat dairy.

                  1. “Zach”- yes, it was sugar being excreted in the urine, NOT fat. The copious urinary output is the body’s attempt to rid itself of the sugar in the bloodstream. (And yes, some doctor’s did taste the urine). In 1798, a Dr. John Rollo discovered that carbohydrate diets caused a higher output of sugar in the urine, whereas protein lessened it. Therefore, he put patients on an “animal diet”. This was the standard of treatment for diabetes for many years, until the discovery of insulin.

                    And “Zach”, by the way, you make all these ridiculous claims, but never support them! Who were these people feeding their patients loads of sugar to “cure” diabetes? I even googled it, and found nothing. Oh, but by the way I did find loads of links explaining how people with diabetes type 2 have carbohydrate intolerance, and that they can help themselves by reducing dietary sugars! So, if you want to make a case for something, you’re going to either have to be a little more specific, or post a link, or something. Instead, you resort to ad hominem arguments; (hmmmm, just like Durian Rider).

                    1. Lol, dude you don’t even understand the basic mechanisms behind the “carb intolerance”. Do you think some people just all of a sudden eat too many carbs and become diabetic? If that was the case all of Asia would be dead.

                      Fat blunts insulin effectiveness. Fat causes diabetes, not sugar.

                    2. Lol, there you go again, just being insulting, but not actually saying anything of substance, with no support to back up your claims! If you’re trying to criticize *me* for not “understanding the mechanisms of carbohydrate intolerance”, well, I was writing what doctors and researchers have to say about the subject. So I guess they’re all wrong, huh. (And by the way, I’ll mention one more time that after looking, I did not find any evidence that feeding diabetics sugar will cure them).

                      And I never said that all people eating a high carb diet will “just suddenly get diabetes”, you put those words in my mouth. I only said that fat has nothing to do with it. The traditional Asian diet is a whole foods, non-industrial foods diet, and they did not eat a lot of sugar. And the Masai, the Inuit, the Mongolians, the Siberians, the Sioux Indians (all those high fat people) also did not get diabetes!

                2. They called it “diabetes mellitus¨ because when the urine was sweet tasting, sometimes sugar spills into the urine and before blood tests they probably tasted the urine.

  26. yes, the more I read about nutrition, the more confused I get about what to eat… today I’m kinda sick, and ate gluten free toast with butter, and hot pepper, rice with tomato sauce, low carbing, if I stick with it makes me lose weight, but it is really hard, not eating carbs effects my mood really negatively, I’m allergic to casein and gluten, so that complicates things further, eating rice sounds great..I think if I want to lose the 30 to 35 lbs that I kept on post kids, I just need to eat less, I bought into the theory that it is not the calorie intake that counts, but low and behold, last time I had the same dry cough as today and ate only toast for a week I’ve lost 10 lbs in  a week… but during my 2nd pregancy I  had gestational diabetes which I absolutely kept under control by eating low carb and walking after meals,
    confused to the max though by this blog post, but Denise your writing style is so funny that confusion or not it was worth reading it just for the nerdy entertainment factor, my husband is reading it now, and laughs out loud reading each of your funny  nerdy jokes, thank you for being honest and dig deep into each issue, science in not static, otherwise it stops being science but becomes a dogma

  27. yes, the more I read about nutrition, the more confused I get about what to eat… today I’m kinda sick, and ate gluten free toast with butter, and hot pepper, rice with tomato sauce, low carbing, if I stick with it makes me lose weight, but it is really hard, not eating carbs effects my mood really negatively, I’m allergic to casein and gluten, so that complicates things further, eating rice sounds great..I think if I want to lose the 30 to 35 lbs that I kept on post kids, I just need to eat less, I bought into the theory that it is not the calorie intake that counts, but low and behold, last time I had the same dry cough as today and ate only toast for a week I’ve lost 10 lbs in  a week… but during my 2nd pregancy I  had gestational diabetes which I absolutely kept under control by eating low carb and walking after meals,
    confused to the max though by this blog post, but Denise your writing style is so funny that confusion or not it was worth reading it just for the nerdy entertainment factor, my husband is reading it now, and laughs out loud reading each of your funny  nerdy jokes, thank you for being honest and dig deep into rach issue, science in not static, otherwise it stops being science but becomes a dogma

    1. Hi, just to let you know toast and rice does not sound like low carb, when people do low carb they avoid bread of any kind, all grains and legumes for starters. But sounds like you might do very well with the high carb low fat diet.

  28. When it comes to the subject of carbohydrates in particular, I haven’t found a better study than this one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/ in helping me to choose what, if any, carbohydrates to eat!

    It’s the BEST study, bar none , I’ve ever read on the subject..!! Personally, I heavily base my philosophy of eating on this study, and I’ve read many studies/books on the subject!

    1. I read the article you left the link for and it was interesting. What I find that makes me question it is the fact that the diet studies may have been comparing apples to oranges. There are many so called low carb studies but many have a wide range of what they consider to be low carb, the same is true of low fat studies. A diet comparing a diet of 50 grams of carbs is very different to one using 100 or more grams of carbs. The same for low fat, 25% fat, 30% fat versus 10% fat. You cannot say anything about them in comparison terms unless the are comparing the same amount of fat or carbs. This is an issue that has to be discussed whenever you are comparing different types of diets – something the authors of this paper do not do.

    2. Skyking, thanks for this paper. Makes good sense. My initial read is that, in essence, the cell walls lower carb density and retard carb absorption and even prevent us from absorbing some of those digestible carbs. E.g. carbs that may be tucked inside cells with lots of cellulose in the membrane. Cellulose, we can neither enzymatically digest it nor ferment it, so appears we need highly acidic stomach juices, even physical pulverization of the food, to liberate the carbs contained therein. All this adds up to our GIs powerfully moderating our absorption of what ends up being fewer carbs. All good in my books.

      All that said, Melissa McEwen gives and interesting take on Spreadbury’s paper here, suggesting we created acellular carb foods early on:

      http://huntgatherlove.com/content/acellular-versus-cellular-carbohydrates-and-endotoxins

      She suggests humankind began to high process carby foods earlier than we conventionally think. That we ate highly acellular carbs even well before the Ag Rev. This suggests other factors are at play to promote our modern-day carb intolerance epidemic. AND possibly that we initiated lots more carb intolerance in those very early days. And of course couldn’t know that since we lacked the tools to measure it. –Bryan

  29. Someone mentioned this paper, but I can’t find the comment now to give credit:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402009/

    It’s an amazing paper, and maybe explains a whole lot. The idea is that foods where the plant cells are intact, feed microbes differently than cells that are pulverized. Hence whole steamed rice is very different from ground rice flour. This causes signalling such that eating a ground-grain diet may cause obesity, where eating steamed whole grains does not. Eating a sweet potato is not at all like eating a slice of bread.

    Now another thing that massively affects microbes is *iron*. One thing about white sugar: it doesn’t feed yeast well. This is the principle behind homemade root beer. It’s very sweet, but because there is no nutrient, the yeast die out before the alcohol level gets very high or the bottle explodes. Iron also has a massive effect on insulin levels in the body. Plant-based iron isn’t absorbed easily, but the iron in iron-fortified foods (processed foods) or in meat can be over-absorbed. Mix iron with starches or sugars though, and the microbes go nuts, and your insulin levels go nuts too.

    One thing in common about all these uber-low-fat diets is: they contain whole plant cells and are also very low in fast-absorbing iron. Pritikin allows whole-wheat bread but seems to encourage whole grains. Whole wheat is also an iron-blocker (as is brown rice). Low-carb diets generally don’t have bread or pasta at all. But swampland diets are generally loaded with ground grains and also with high-heme meat.

    1. I’ve been posting the link to this study and commenting on it on various sites, which is where you may have seen it. For some strange reason, strange to me anyways, is that it gets very few responses from readers. Perhaps because it’s too long and most folks didn’t bother reading it, and/or because some well-known blogger/tweeter didn’t post it first…?!

      1. I suspect few people actually read through it or understood it. I’ve sent some papers that were far easier to people I consider smart, but they just couldn’t follow them. This one took some work for me to follow too. It’s worth it though … there are some interesting gems all over in it.

        I guess everyone is too used to the predigested quickie versions. The ground grains of the writing world!

      2. Chris Kresser and others have featured this study in the past, but as I remember, it didn’t generate a huge amount of discussion even back then. Probably you are right, most people don’t want to take the time to read it. The hypothesis makes a lot of sense from an evolutionary perspective.

        But I wish folks would be more rigorous in discussing the consumption of grain among Paleolithic people and historical hunter-gatherer cultures. The archaeological evidence is pretty clear that Paleo people, even the earlier, not-quite-modern-man types, did consume grain. It would have been an amazing coincidence, not to mention a risky survival strategy, if people in several different, widely-separated regions suddenly woke up one morning 10000 years ago and said, “Hey, see that tall grass over there with the seed heads that we’ve never noticed before? Let’s give up gathering and hunting, settle down, and use it as the basis of our diets!” Man has always been the ever-opportunistic omnivore, eating whatever was available, or he would not have survived. That being said, think of how utterly different those wild grains were from our modern ones, and how seldom they were available. Like any wild food, they were eaten in season. They took a lot of energy to gather and process. The “berries” were much smaller than modern versions. And they probably didn’t taste all that great. One theory on the development of agriculture, at least in the Near East, is that Paleo man started storing the wild grain for hard times, discovered that it easily propagates, and the process evolved from there.

        1. The paleo people did consume grain. So did the Medieval Europeans. But hardly anyone actually ground grain into a fine flour. THAT was expensive. If you look into history, you see most people ate “gruel” … which is a kind of long-boiled whole grain mash. Most of it was barley,not wheat (wheat was harder to grow). Also once you grind grain into flour, it goes rancid quickly and molds too.
          So rich people … yeah, they had flour, and bread. And also it was common in certain cultures and places. But rich people were noted for being less healthy in general, so it doesn’t say much.
          Now the history of *bread* … the Egyptians may be the first bread-makers. But they made it in order to make *beer*. When you grind grain and make it into bread, it turns out to be really awesome for making beer. Later people started eating the bread by itself.

          http://ancientegyptonline.co.uk/beer.html

          Well, who knows. But the point is: bread feeds microbes very differently than gruel does.
          So I would challenge anyone here: take a cup of whole grain (any grain except white rice) and boil it until it’s chewable. And eat it.

          Brown rice is the best, but try eating a cup of boiled whole wheat. You CAN do it, and in some times and places people do it. But most Americans won’t. If you do, it will fill you up quickly and you will eat a whole lot less calories than if you ate white bread or whole wheat bread.

          The paleo people ate grain, but it was whole grain boiled or parched. In order to really grind grain you need millstones, which are way too heavy to schlep around. You can grind small quantities on small stones, but it’s not a fine grind. Or it was pre-fermented, as you see with the native Americans. They processed corn with lye before grinding it, which changed the digestion also (and incidentally made it easier to grind and the B vitamins easier to absorb).

          1. In the Bible, it was stated someone in debt, their millstone was not to be taken. There is a lot of work to process grains, and the industrial revolution (machines ) changed how grains were processed-resulting in flours deprived of nutrients, but with a longer shelf life. . A few B vitamins were added.later, but did not make up for was originally in the grain and the fermentation process. The Egyptians also make a lot of cakes-honey and fruits being added.

            http://www.sciencedirect.com/science/article/pii/S0305440383710186

            http://classroom.synonym.com/foods-eaten-during-ancient-egyptian-festivals-9968.html

            “fine flour” was mentioned in the Bible, and Egyptians had a type of fine/white flour, as further milling had to be done.(yes more time consuming and more expensive) Some people today report that they have less problem with white flour,as the brain parts are harder to digest,due to the protein content, or that they do not have the bacteria necessary to digest the fiber. Too much fiber seems to be a problem with some.

            http://www.ancientegyptianfacts.com/ancient-egyptian-diet.html

            In the “Little House” books, the “Long Winter” they faced starvation and had to grind wheat into a flour using a coffee grinder.

            1. Yes, the Egyptians are a super-interesting case! They (and the Mesopotamians) were about the first people ever to eat large amounts of wheat and barley, and to grind it. It was all non-GMO, whole wheat, organic too. And they left lots and lots of mummies so we can judge their health.
              Basically they were in really bad shape, compared to other peoples living at the same time. They had very narrow skeletons, which is likely a sign of lack of Vit D or K … and it certainly wasn’t a lack of sun. One interesting mention in the Bible is that the Egyptian women felt threatened by the Israelites, because the Israelite women could give birth so easily, they would soon outpopulate the Egyptians. Hm. The Israelites were herders more than farmers.
              The richer Egyptians had more meat and plenty of honey. But so did the the nomadic people surrounding them. I think ground grains, esp. wheat/barley, have a unique health risk.
              Rice (according to SkyKing’s article) appears to not always have the same effect. But another thing about wheat is that it is high in fructans, which break down into fructose. Rice breaks down into glucose.
              Also, apparently the Egyptians were mostly vegetarians … they had plenty of fish, but tests on mummies show they didn’t eat fish or meat much.
              https://www.insidescience.org/content/what-did-ancient-egyptians-really-eat/1630

              There are billions of people in the world that eat mainly one starch their whole lives … rice or wheat or yams or millet. The wheat-eaters seem to have the most health problems. Denise’s take on the China Study points that out nicely!

          2. You might find the book “The Leopard’s Tale” by Ian Hodder interesting to read. It’s about the excavation of the early neolithic village Catalhoyuk, and a detailed description of life right on the transition from paleo to neolithic living ca 9000 BC. Cattle (auroch) were not yet domesticated, and required large hunting parties (based on the wall drawings – the inhabitants were prolific painters in their cave-like stack houses). The bones in the middens are mostly smaller animals like sheep and goats. The dwellers were pre-pottery, and cooked on hearths and in tightly woven cooking baskets heated with rocks. Grains were gathered and stored. I had the the impression that they were mostly eaten whole, and probably roasted, since hot rock basket cooking would do little more than soften the grain (not hot enough or long enough to cook the starch and make it digestible).

            Reading this changed my view of Paleo. These people were not eating Bronto burgers and ribs, bombing mammoths with rocks, spearing seals, or chasing buffalo on horses. They were stalking small animals and birds, and stealing their eggs and babies mostly in the springtime, traveling ever longer distances from their dependable water source town to find them. There are shells present, evidence of long distance travel (ca 100 miles) and the beginnings of trade. Some of the animal babies were probably being spared and becoming modern domesticated animals.

            If these people were in ketosis it was not from eating HFLC, but more likely from being on the edge of starvation all the time. They ate anything they could find that they could digest (though it’s apparent that they were headed towards agriculture), and lived in the place most conducive to survival (ie not the Arctic or the high plains). If they were doing heavy lifting and sprints it was as infrequently as possible. Mostly they were walking, gathering more than hunting.

            1. I suspect that grain was probably gathered more to feed animals rather than to eat, since animals can digest the starch beta linkage without needing to have it cooked.

              1. Humans were eating grains long before they had animals to feed. The feeding of grains to animals came with the transition to agriculture. You’d want to have your animals stationary and where you could watch them fatten if you were feeding them grains. Early pastoralists, who might have been the intermediate stage between hunter-gatherers and agriculturalists, took their flocks to pastures to eat grass. They didn’t feed them grains. Even today, grain feeding of cattle comes at the end of their life cycle — they eat range grass until they are brought to feedlots for finishing.

                1. Eating grains is not beneficial to humans unless they are cooked. We cannot gelatinize/rupture the starch cellules to release the starch molecules in our bodies. Ruminants can break down the cellules with enzymes and time, but we can’t. The starch has to be heated above its gel point (ca 50-70C) before we get any food value. As evidence of this, both the caloric value and glycemic index of raw cookie dough are about half that of baked cookies. The uncooked flour in the dough is essentially indigestible particles, of which only a little bit can be digested in the lower GI tract. The same is true of raw potatoes vs cooked potatoes. Without cooking a human might as well eat straw (cellulose – that’s the source of indigestible beta linkages, not starch) as grain.

                  By 9000 BC maybe the people at Catalhoyuk were eating a significant amount of their daily calories as grain, but I doubt it. They did know that to get any calories out of grains they had to be roasted, but they didn’t have even simple technologies (milling and fireproof cooking vessels) we take for granted. On the other hand, animals like cattle, sheep and goats will eat grain in preference to straw. If you were going to tame and fatten animals on a year-round basis grain would be an easy food to collect and store.

                  1. Humans and near humans have been eating grains since there were humans, long before they domesticated any animals, even the dog. The archaeological record is clear on this. When proponents of no-grain diets insist humans did not eat grains until the advent of agriculture, they undermine their credibility because they are ignoring the scientific evidence. Critics of the Paleo diet get a lot of mileage out of the no-grainers’ refusal to acknowledge the scientific evidence. And yes, humans can digest raw grains; perhaps not so well as some animals, and perhaps not without chewing them very well and/or grinding them. They can, and do. I have myself done so, as I am sure many other commenters have. For years, one of my favorite breakfasts was a mixture of raw oats and raw wheat germ, soaked in raw milk with honey. It worked very well for me. I did strength training, ran marathons and weighed about 118 lb on a 5’6″ frame. But I seldom eat grains these days, cooked or otherwise. I agree that grains are not an ideal food for humans, but they are an even more unnatural food for cattle. We are omnivores, cattle are not. Omnivores are opportunistic eaters, and can process just about anything, at least in small quantities. While primitive man ate grains (occasionally and sparingly), wild cattle do not eat grains.

                    1. All I can say is read the book and draw your own conclusions. Mine conclusion is that the technology of grain preparation for human consumption was not very advanced by 9000 BC. 5000 years later, Egyptian and Mesopotamians had moved on. Oxen were being used to move big things, and IMO these animals were primarily grain-fueled. These weren’t goats and lambs skipping around the hills. Millstones, pottery and metal tools had been invented which didn’t exist in 9000 BC. People were still cooking on open hearths or in pits the way they did 400,000 years ago. Only now they were doing it inside. From the soot deposits on their ribs it must have been like living inside a chimney.

                    2. Being an archaeology buff, I am sure I’ll enjoy the book. I’ve requested a hold on it from the local library. However, I fail to see why you feel that the level of technology and food prep at one Neolithic site — Catalhoyuk was a Neolithic, not Paleolithic, site, and by no means even the oldest of the Neolithic sites — determines the use of grains or the effectiveness of cooking methods in other locations around the world in Paleolithic times. These Neolithic villages housed agricultural societies in a temperate climate. Their accomplishments in no way detracts from the performance of humans in earlier, more environmentally challenging conditions. The toolkits and lifeway debris of earlier cultures indicates that they were experts at exploiting their environments. As archaeology advances, our level of knowledge shows that Paleolithic peoples were far more advanced than the images of the grunting caveman that prevailed in the early 20th century. Think of how drastically our image of Neanderthals has changed since that time. And how we’ve come to realize that the ancestors of today’s indigenous Australians had watercraft capable of open-ocean voyages 50,000 years ago. Should we think these people weren’t advanced enough to exploit all the food resources their environment provided? The evidence they left behind says , “not so”.

                    3. Actually, mill stones have been found in much older Neolithic sites than Catalhoyuk. There is a 12,000 year-old site in what was Kurdistan where the excavations have exposed mill stones and troughs for grain processing. And Paleolithic grinding stones (with flour residues) go back a good 30,000 years. Might be helpful to read more than one book….

                    4. What nonsense about cattle not eating grains! What do you think silos are for? Cattle don’t spit out their corn kernals, nor do pigs or chickens. Why do you think the Bible says do not muzzle the ox on the threshing floor? No one was worried about them eating chaff, they didn’t want the oxen to eat the grain. But the cattle have an entitlement to grain for the work they do. That’s the point of the commandment.

                    5. Technology moved in fits and starts. Maybe someone even had a wheel in 9000 BC, and I don’t doubt that some people in other areas were crushing/milling grain to make it more edible. But at that point in human history you had to use what you found locally on habitable sites. That particular village was sited on a lake/swamp, and the evidence is that a lot of animals were eaten, probably attracted to the available water the same as the humans. Other sites might have had an abundance of grains and suitable rocks (Catalhoyuk from what I recall had a lot of clay, which was useful for interior stucco, but not for milling grain). On the coastlines and rivers why bother with any of that stuff if you have infinite fish, water birds, tubers, berries and mollusks.

                    6. And list off some books. I only came across this one while I was researching kilims. My Paleo education comes from books like this and a trip to Lascaux, not from Mark Sisson or even Loren Cordain. I’ll read their blogs but I’ll never spend a dime on their books. Primary sources are better than “a filter of a filter of a filter with random unsubstantiated opinions” thrown in IMO.

            2. The basket weaving techniques and decorations used in central Turkey ca 9000 BC are almost identical those used by North American Indians. Coastal Salish tribes used hot rock cooking baskets well into the 19th century. The Siouxans and Inuits were not Paleo at all, but rather regressed Neolithics who migrated from Asia. Their Neolithic knowledge of agriculture transferred directly into Inca and Aztec culture. In the high latitudes survival required living as what Cordain considered “Paleo”, but is dissimilar from the true Paleo culture of Africa and Asia Minor. Warmer climates produce a much wider range of human foods than buffalo, pemmican and seal blubber.

              1. Who said that domesticated cattle didn’t eat grain? I said it is not a natural food for cattle. Just as doughnuts and sodas are not natural foods for humans, despite the quantity of them we consume.

                1. So when a wild cow (or auroch) eats wild hay it spits out the seeds? Come on. Oats, milo, barley etc all grew wild in the Mideast. Ruminants aren’t picky eaters. That is their NATURAL food.

                  1. Wild hay??? Hay is a manufactured product, consisting of all sorts of green stuff from crop harvesting. Wild cattle eat grasses. Grains are, of course, one type of grass, but the seedhead portion of wild grains is pretty insignificant compared to the grain that is fed to cattle today. Cows have the elaborate digestive systems they do to digest the fibrous, cellulosic portions of the grasses, not the unnatural grain-based diet most of them eat today. Why do you think there is a premium on grass-fed beef?

                    1. If I can’t say “hay”, what should I say? A WILD GRASS PLANT BEARING A SEEDHEAD? OK?

                      There’s a premium on grasslot beef because of the unsustainable land area required, vs the cowschwitz approach. https://en.wikipedia.org/wiki/Harris_Ranch

                      I prefer my beef massaged with beer, with fat marble that melts on the warm plate before cooking. But that’s a notch up from even grasslot and I only eat it on an expense account.

                    2. Oh that is so funny. When I was growing up, “grassfed beef” was the CHEAP stuff, and sales guys would try to talk us into buying the premium corn-fed beef. It costs a LOT to feed a cow corn.
                      As for “unsustainable land use” … growing a cow on grass is about as sustainable as it gets. There are many acres of not-farmable land, which will grow the heritage Longhorn cattle just fine. They are the descendents of the cattle brought over by the Spaniards on their ships. They got loose and were in huge herds, like the buffalo, by the time white people even noticed them. Some people are using the same trick now, to avoid the big brush fires that happen when grass grows unmown.
                      Where I live, farming isn’t very profitable, but grass grows good and it’s been traditional for landowners to pop calves onto the land just to mow the grass. Then a few years later they harvest the beef. But it is very lean beef, not the stuff you buy in the store. To make it fat they may “grain finish” it. But these days they can sell the same cow at a premium as “organic grass fed beef: never fed grain!”

                    3. Grass-feeding is sustainable — it’s how Nature has fed hooved animals for eons. You are reading too much vegan propaganda. It is the raising of vast amounts of grain to feedlot-finish cattle that is unsustainable. Yes, wild cattle may consume incidental amounts of wild grain when grazing. They also consume incidental amounts of insects and soil, but that does not make them bats or earthworms. Concentrated grain feeding of cattle, per the US agribiz model, is evolutionarily unnatural. As for wild hay — perhaps it was eaten by the bovines being stalked by the packs of wild poodles roaming the earth in Paleolithic times.

          3. I’d agree with you on nearly everything. Your elaboration of grain use through the ages will, it is hoped, encourage folks to be more accurate in discussing grains vis-a-vis the Paleo lifestyle. It just weakens the case for the Paleo diet, and leads some people (many of whom need no encouragement) to stereotype and ridicule the Paleo lifestyle when its proponents assert that Paleo peoples “did not eat grain”. Your point about beer making is great. I ‘ve even speculated that maybe the reason people started using grain regularly was due to their experience with fermented grain when some of their stored whole grain got wet. There is archaeological evidence that, even before the Egyptians made beer brewing an art, other peoples were making beer of sorts. Even some isolated and recently-discovered (19th-20th century) peoples make primitive-style beer. Where I would take exception to your comments is the implication that using intact grains is difficult or unpleasant in modern cuisine. In fact, the use teff, farro and such (steamed, boiled or otherwise prepared in intact form) is very trendy among celebrity chefs. And those grains can be as tasty as brown rice. Still, modern peoples are far more dependent on grain than can be justified if taking an evolutionary approach. And I wonder if the grinding process also makes some of the non-grain, “Paleo-friendly” flours less desirable as well? Doesn’t grinding break down their cell walls, too?

            1. Yes, I agree whole grains are trendy right now. Also the use of a whole lot of different kinds of grain, some of which are quite tasty! I actually had a lot of experience with whole wheat though, because I inherited a 50-lb container of it from a previous housemate, and we were poor enough that we loved the free food. NO ONE though, would eat it. We tried cooking it various ways, but there is just something about whole wheat berries that didn’t work for us.
              Nationally, whole wheat berries simply aren’t ingested much, at least not by anyone I’ve met.

              I agree in principle with the idea of a “paleo” diet, in terms of looking to see what our ancestors ate. The issues are as you pointed out … what they ate isn’t what we may THINK they ate. Also there was a wide variety of diets. And not all the cultures were equally healthy. Or thin, or long-lived. It is interesting reading the journals of Lewis and Clark. They were studying the native Americans, and apparently Lewis was getting a reputation as a healer so they came to him with their illnesses. Lewis commented that the natives had a high rate of joint problems (arthritis, sounded like). He also commented on which tribes seemed healthier than others.

        2. I think that the grains were collected mainly to feed and domesticate animals, before efficient cooking methods were developed to allow human consumption. Living in France I saw this attitude towards fresh corn, which is disdained as a food for humans and grown mainly for animal feed.

          1. The poor opinion of corn in many European countries is a relic of the early racist view of the Native Americans that used it as a staple food. Europeans of the 15th-19th century also shunned many other New World foods. Yet, 80% of the world’s current food production is based on New World species.

            1. I don’t think so. Europeans had no problem co-opting tomatoes, squash, potatoes, peppers, etc etc etc. so racism has nothing to do with it. I think in the case of corn they were just copying modern American livestock feeding practices, and didn’t have any French tradition of eating corn-on-the-cob, creamed corn, cornbread, etc. Molasses was similarly hard to get in a French grocery store. They know what it is, but don’t have any use for it, so no one buys it.

              Much of the corn grown in the US is fed to livestock, and so is a lot of the wheat.

              http://corn.osu.edu/newsletters/2011/2011-18/feeding-wheat-to-beef-cattle

              The problem with grain is overfeeding, not a animal’s revulsion to eating it. In the wild, most of the plant (oats, barley, milo, etc.) is roughage with very little weight in the seedhead.

              1. They did no such thing as co-opting those crops, not for a few centuries after they were introduced to them. It took a lot to get them to accept tomatoes and chilis. Tomatoes were thought to be poisonous for a long time, then were avoided because they were thought an aphrodisiac. Molasses (unless made into rum) was also despised as the food of nonwhites (indigenes and slaves). Food preferences today still reflect the attitudes of a less-enlightened past, if we dig into their historical basis.

                1. It didn’t take much time for Europeans to adopt new world beans, chocolate, potatoes and the whole cucurbita family. This year I grew musquee de provence, French pumpkins, instead of the regular jack o’lantern version the squirrels attack. Good eating AND fall ambiance without the rodent damage.

                  And I say co-opting, you say (fill in the blank), let’s call the whole thing off. I’m open to your term, whatever it is. You’ve already said these plants amount to 80% of something in Europe. And let’s not forget Asia, which took almost every Central American exotic fruit and made it their own, along with the tomatoes, peppers and yams. Is this also racist?

                  I think it’s racist to refuse to eat culturally accepted cuisines too. Not in the old days of molasses and corn, but right now. The Paleo that stalks out of an Indian restaurant (or never sets foot inside) because there’s no meat, the food is cooked in PUFA’s, and evil naan bread touched his lips, is a racist. The vegan that refuses reindeer hot pot, or southern fried chicken, or schweinhaxes is a racist. Beyond that, unless it’s due to extenuating circumstances like allergy or religion, it’s rude social behavior. When I lived in France I started drinking wine, because to refuse the wine was an insult to the host.

              2. It is true that in the US, large amounts of corn are fed to cattle. Makes for nice fat steaks! But in order to do that, the cattle have to be fed large amounts of antibiotics, because too much grain will kill a cow. Or a goat. Handfuls of grain may be fed to animals now and then, but until very recently, ruminants got their main food: which is grass and twigs.

                http://www.pbs.org/wgbh/pages/frontline/shows/meat/interviews/pollan.html

                The plaque on Neanderthal teeth clearly shows that they DID eat grain, and probably they ground it too. What I was saying though is that in general it was not in the large amounts we use, nor was the grinding to so fine. If you soak wheat berries and then grind them on a molcajete, you can make them into a nice little flatbread. But it won’t have the same glycemic properties or quick digestion that disrupts the gut microbes (as talked about in SkyKing’s article). For one thing, the grain is whole. For another, it’s often soaked, possibly fermented and partially sprouted. If you are grinding grain by hand, it’s a whole lot easier when it’s soaked plus you don’t get flour dust flying all over your cave. The corn in America was soaked in lye, which also made it digest differently (nixtalamization).

                When “milling” was invented, the paradigm changed. You brought your sack of grain to the miller, who then milled all of it and took part of it in payment. At some point they also learned to remove the husk and make white flour, which doesn’t go rancid so quickly. When that happened it massively changed the digestibility of grains.

                1. Your point about cattle and grain is absolutely correct, as I had noted in responding to another commenter. For human consumption of grain, it would seem that it never was as large a part of the diet for Paleo peoples. It’s logical that hunter-gatherers would treat it like any other seasonal food until late in the Paelolithic era, when they might have begun storing it. Other than finding grinding tools, it is probably hard to tell from DNA, dental residues and such exactly how they processed the grain (soaking, sprouting, etc.) before eating it. It’s interesting that Hodder, in the Leopard’s Tale, points out that, during some phase of the settlement at Catalhoyuk, the human inhabitants consumed raw, whole (unground) grain.

          2. “Living in France I saw this attitude towards fresh corn”

            Well, France actually banned the cultivation of corn back when pellagra was an issue. So, that explains why it’s not popular there.

      3. I just read that paper; it was very interesting! I have always believed this theory, that modern industrial foods are the culprit of obesity, and it is plausible that these foods, over time, cause leptin resistance. It would be interesting to see if soaked and fermented grains have the same effect on the microbiota; traditionally, many native cultures prepared their grains in this way- (and some modern day hunter gatherers do this)- and these people were/are also healthy and not obese. I guess they weren’t able to check that in this particular study. I think they definitely need to do more research, it all sounds very interesting!

        One last thing: I have read that rats and other rodents have a lower tolerance for fat than humans, which may partly explain why fat seems to be less of a factor with humans- (unless it’s combined with lots of refined carbohydrates).

        1. Hyperlipid has point out that lab rodent high-fat diets are so high in trans-fats and sucrose that no conclusions can really be drawn about the effect of a high-fat diet in rodents – the experiments seem designed to fail the LCHF diet. Peter feeds his own rat – Ratty! – a high fat, whole food diet much as the family eats and the last time he mentioned him, he was slim and in good health.

          1. Jonathan Christie- good point. My guess is if they fed them a whole, “real foods” diet, they would be in much better shape. That’s a huge problem, in general, with many of these scientific studies: they are too reductionist. The people involved seem to only be focused on macronutrient content. They don’t seem to take into consideration that feeding them industrial crap that doesn’t resemble real food might have a different effect, and therefore, we can’t really base any conclusions on that.

            1. LCHF diet studies are generally rife with funding and researcher conflicts, so I suspect they mostly do actually know exactly what they’re doing and choose Crisco and sugar to make LCHF look bad – that way, they attract food industry funding and share in that stupendous cash flow which buying corn and selling corn chips generates. Kendrick’s Doctoring Data and Goldacre’s Bad Science have turned me into a conspiracy theorist!

              1. I actually emailed a study researcher. I asked why the high fat used to feed those rats in that study was hydrogenated fat. He wrote me back that rats would only eat hydrogenated fats. Not sure that is true, but that is what he told me.

                1. That’s a crock of BS! Those cheap fats are artificially hydrogenated (saturated), like all the fake margarines and many cooking oils. So we are supposed to believe that rats will only eat fake fats? Rats will eat both saturated and unsaturated fats. They are omnivores, like humans. Try feeding your pet rat a bit of cheese (natural saturated fat). I bet Mikey the rat liked it. Then offer him an almond (unsaturated, i.e.,un-hydrogenated). I bet Mikey the rat liked that, too. Sadly, I think sometimes technicians and scientists will say the most ridiculous stuff to people they think are non-scientists. Medical folks seem to do this as well.

      4. Skyking, I don’t think the paper’s too long. But it’s a tougher read than it needs to be. That’s what’s maybe keeping the readers away. Spreadbury needed to do more editing IMHO.

        E.g. what he says here: “The interindividual variability in ‘Western disease’ incidence in a population eating Western foods is affected by genetic and other factors, but it is mostly these secondary factors that the epidemiology of industrialized populations would be studying if the root causes of metabolic disorders were now present throughout the population.”

        What a mouthful!

        Took me a while to realize Spreadsbury was saying we need to get out of our navel-gazing and compare western cohorts to hunter-gatherer cohorts, not just comparing different western cohorts. That way, we can more clearly see the universal SAD-driven root pathologies that way overshadow any genetic diffs. –Bryan

  30. I hope Peter at Hyperlipid will have something to say about all this. Thanks to Hyperlipid, I tend to look at things from the perspective of the mitochondrion.

  31. Taubes has a way of puffing himself up in the media, which makes him a target, especially of nutrition and physiology academia. His carb insulin assertion fits the circumstances and was for a time undisprovable. Unfortunately he uses that assertion to gain credibility, and starts to say things that are more easily disproved. Things like exercise causing weight gain and the impossibility of weight loss or weight loss maintenance without extreme carb reduction. In my own case these assertions are demonstrably false. Most of the participants in the NWCR (including me) exercise and eat LFHC, which is further disproof of those assertions.

    1. thhq, however may you feel about Taubes personally, however you interpret his behaviors and motives, please remember the concept that insulin stores fat is shared by very many folks in the research community. Simply search on “insulin and fat storage” and you will get many hits for scholarly works. I’m not saying anyone of them are right. But it’s not a radical idea. Furthermore, what Taubes discusses WORKS for me–as best I can tell. I’m been LCHF for nine years, I’m 55 now, and my blood panels and other vitals (HR/BP, weight/body fat%) are great, and most of all I FEEL great! Do I know if some hidden health gremlin lurks in me? Of course not. Same with you. You say HCLF works for you, but how many of your vitals do you regularly measure? We know you have no idea of your fasting insulin level. What about HR/BP/body fat%. Point is thhq, not you nor anyone else has absolute proof that any one food- and lifeway works. In the absence of that, I choose LESS over MORE. No supps, minimize ingredients, stick to iert matierals like glass and stainless steel, for my cooking implements, bare minimum ingreds in soaps, etc.

    2. thhq- has Gary Taubes really said that exercise “causes weight gain”? I find that very hard to believe. What I know he has said is that exercise can raise appetite, which may thwart the weight loss efforts of some people. Basically, the “eat less, move more” mantra doesn’t work for a great majority of the population.

      However, exercise can promote better insulin sensitivity- (maybe not with everyone); I suspect this may be the reason why exercise works so well for you. However, this does not disprove the carbohydrate-insulin theory of obesity: in my opinion, it actually helps confirm it.

      1. Yes he has said that exercise causes weight gain in the NY Mag article (which is a slightly modified form of what he published in GCBC), has carefully selected N=1 examples to make his case, and confirmed that this was his intent in an interview with Jimmy Moore. It’s all discussed on the previous page, and that’s where the links are.

        I don’t think my weight loss should be used to confirm GT’s carb insulin assertion. That needs a ward study, not another N=1. If I had gained instead of losing weight by exercising I would have confirmed his weight gain assertion though…at least as an N=1. If you want to see population results on the benefits of exercise for weight loss and maintenance start with Rena Wing’s NWCR.

        I’ve been thinking a lot about why GT is so hard for me to read. I think a lot of it is because he doesn’t start with an abstract. In 30 years of writing research reports it took me 10 years to learn how to do this. In front of a very familiar audience you can get away with not having an abstract sometimes, but with a mixed audience no one knows where you’re coming from. If you summarize right up front, then use your work to back up your assertions everyone is on the same page. If you do it well, you can skip lots of graphs and the obligatory literature dump, and be done with a new action plan everyone agrees on in time for lunch.

        If Gary had prefaced the NY Mag article with something like “The HFLC ketosis diet is very effective for weight loss. The best efficiency for fat burning in ketosis actually results from reducing exercise, which may surprise you”, and then launched into examples which show this, we would all have been on the same page. But instead he starts right off with N=1 examples of exercise-fail and the literature dump.

        Because he isn’t right up front on ketosis benefitting from reducing exercise, he ends up saying that exercise is something that causes everyone to gain weight. Even though I know where he’s coming from, and that he’s fighting the obesity crisis, I’m rankled that he’s ignored millions of us who have lost and maintained weight by exercising outside of ketosis. Despite what he may believe Weight Watchers, calorie counting, Jenny Craig, LFHC and other non-ketosis dieters increase their weight loss rates when they exercise.

        What’s worse is the effect this discouragement has on someone who quits exercising after reading the article, and who will start to gain weight as a result unless they change something else. A good abstract that lays out ketosis right at the beginning would prevent the misunderstanding.

        1. Journalists don’t write the way scientists do. Narrative writing engages the audience by building drama, and ends with the conclusion. In contrast, a well written research report starts with the conclusion stated as clearly as possible. That’s what the audience expects, because they usually need to discuss it and act on it, then move on.

          When you write a research report you’re not trying to tease your audience with plot twists and turns. They won’t sit still for 200 pages waiting for the fat lady to sing.

          1. thhq- huh….maybe it’s just me, but I really liked his writing style in Good Calories, Bad Calories. What he did was he wrote about the whole history of weight loss research, so it was a slow revealing, and a lot of the “meat’ came at the end. I guess I also prefer that he doesn’t “tell you what to think”, by writing out his hypothesis; rather, he gives you all the different evidence- (on both sides, not just the research that fits with his opinion)- so you can make up your own mind. One of his main points was that before World War 2, there was a lot of very high quality research coming out of Germany. Unfortunately, after the war, we just broke with that history, so a lot of the initial research has been forgotten. Which of course has slowed down the attempts recently to get to the bottom of the obesity epidemic. Franky, I notice this a lot in nutrition science! It’s like everything that was researched before has been forgotten, so how can we advance if it’s like starting anew each time? (Or, sometimes “nutrition science” doesn’t fit with what we know about anthropological data….that sort of thing). People seem to be too reductionist, or one-sided….In other words, Gary Taubes’ writing is less like a scientific study, and more like a history lesson that connects all that went before, but has been lost.

            In any case, I still haven’t seen anything that Gary Taubes supposedly said that was anti-exercise- (not even on the link you sent, are you sure you sent the right one? I found something about salt, which I had already read before). I might try to re-read the exercise chapter in GCBC again, just to be sure. I’ve also never heard anyone say that exercise disrupts fat burning during ketosis (?) Not Atkins, Gary Taubes or anybody…..I’m not saying they never said it, just, it’s a new concept to me. On the contrary, I find I have to sometimes kick myself out of ketosis while doing strenuous exercise, otherwise I just get too skinny! I don’t feel like I *have* to do this though; I do it purely for aesthetic reasons.

            Don’t know if Gary Taubes ever said “everyone gains weight” with exercise- (I still haven’t seen this in writing)- but if he did, then I would disagree with that statement. I do agree with his theory that people get hungrier when they exercise- (I sure do!)- but I don’t gain weight. I actually tend to lose with too much exercise, even if I’m eating more than when I’m sedentary. But this also fits with his general theory, that it’s less about “calories” per se, and more about hormones, metabolism, etc.

            1. Morgana, thank you for saying so much that I failed to. And phrasing much of it so well. I too feel Taubes’ approach is one of a reporter, examining all sides, presenting evidence from all sides, never dogmatically. It’s so true what you say here:

              “…It’s like everything that was researched before has been forgotten, so how can we advance if it’s like starting anew each time?…”

              For me this is a genuine mystery. E.g. how could we forget the success William Banting and his many low-carb followers enjoyed in the 19th cen Victorian England?

              https://en.wikipedia.org/wiki/William_Banting

              As well as the success that Joslin doctors enjoyed with LCHF diets at the turn of the last century and now Joslin appears to be turning back to, if still not near enough:

              http://blog.joslin.org/2015/02/nutrition-revolution-the-end-of-the-high-carbohydrates-era-for-type-2-diabetes-prevention-and-management/

              Even near the end of GCBC, Taubes terms his conclusions merely by the modest term “hypotheses.” What does “hypothesis” mean anyway? Per the google def, it’s merely “…a supposition or proposed explanation made on the basis of limited evidence as a starting point for further investigation.” You can see it here:

              https://www.google.com/webhp?sourceid=chrome-instant&ion=1&espv=2&ie=UTF-8#q=hypothesis

              The main place I fault GT is that his prose can be dense, be a slog. I could do justice to only 10 pages of it a day on average. Maybe in future if we could team up GT with Michael Pollan and MP’s awesome lyrical talent?

              One final point. I’ve been a journalist for thirty years, and understand the problems and pitfalls with reporting in periodicals versus books. Given how these pubs must abridge the info to fit into a short writeup–often simplifying to the point of being wrong–and an edit cycle that’s often out of the hands of the interviewee, we should put a great deal less weight on what Taubes said in periodicals than what he says in his books.

            2. Morgana, rereading your post, this is esp jumping out at me:

              “Gary Taubes’ writing is less like a scientific study, and more like a history lesson that connects all that went before, but has been lost.”

              1. Perhaps I missed something, but doesn’t Gary Taubes use selective history though? If carbs caused everyone to gain weight, then how does he explain that Americans were once thin eating a high carb diet?

                As far as I can tell, Americans consumed roughly 56% carbs / 12% Protein / 32% Fat in 1909, and consumed even more carbohydrates during the 19th century.

                http://ajcn.nutrition.org/content/14/3/169.full.pdf
                http://ajcn.nutrition.org/content/20/8/907.full.pdf

                As you can see from Figure 1 in the first paper, American’s total carbohydrate consumption fell ~30% between 1889 to 1961. And the papers show calories decreased too.

                Unless I missed something (entirely possible) Taubes seems to have skipped right over that part of American history. This ignored historical data implies that there is something else causing significant weight gain in Americans.

                1. Duck, iirc, Taubes does go back to before 1920, before sugar was cheap and readily available. Before WWI, people used mainly molasses as a sweetener, and even that was pricey and used sparingly. Also, we started refining flour in ~ 1920, making those carbs faster to get into our systems meanwhile stripping out its nutrients.

                  About you saying “As far as I can tell, Americans consumed roughly 56% carbs / 12% Protein / 32% Fat in 1909, and consumed even more carbohydrates during the 19th century.” do you have a source for that high carb chowing in the 19th century? This source here:

                  http://onlinestatbook.com/2/case_studies/sugar.html

                  shows a more or less linear increase in sugar consumption from ~ 5lbs/yr/person in 1802 to *100* lbs/yr/person in 2000.

                  About the two papers you link to, the studies go only to the mid-60s, at least a decade before we introduced ultra-cheap high-fructose corn syrup that quickly ended up in everything, and 12–15 years before McGovern et al established official dietary policy across the land.

                  1. “we started refining flour in ~ 1920”

                    Sorry, I don’t understand that. We started refining flour well before that, in the 19th century.

                    The Flour of the Future, by Erastus Wiman (1892)

                    The demand has been made for white bread; fashion calls for it; the millers have complied. Mechanical skill has come to their assistance, and every part of the wheat which would tend to darken the flour is being removed with a precision and thoroughness which are simply wonderful. But does this tend to make the bread better? Does it give the workingman a greater return for his hard-earned loaf? Does this refined milling process give to the convalescing invalid, to the growing child, more strength and nutriment than did the old-fashioned dark bread? The answer to the fore going questions is decidedly in the negative. Indeed, on the other hand, it is impossible to estimate the injury done by the elimination of the most valuable constituents of the grain…What we need is a reversal of the opinion which demands a white, starchy flour.

                    The high demand for white flours during the 19th century were said to be responsible for the dyspepsia epidemic.

                    “Before WWI, people used mainly molasses as a sweetener”

                    Yes. Honey too.

                    “do you have a source for that high carb chowing in the 19th century”

                    Yes. Figure 1 of the first source I listed goes back to 1899. It shows a 30% reduction in carbs to 1961. The whole point of the Dietary Guidelines was to reverse that trend. Americans came to see bread as fattening, and they were eating less flour than ever before. The source is clear that Americans ate mainly complex carbs at the turn of the century, but as you can see, total carb consumption plummeted by ~30%.

                    I thought one of the biggest criticisms of Taubes is that he didn’t do a very good job of distinguishing the difference between complex and simple carbohydrates. Of course, there is a difference.

                    Anyhow, Stephan Guyenet showed what carbohydrate consumption did during the 20th century (see his chart at the bottom of this article):

                    The Carbohydrate Hypothesis of Obesity: a Critical Examination

                    As you can see, Guyenet’s calculations match up with the sources I’ve referenced. Carb consumption only increased by ~25% after the Dietary Guidelines. So, we never got back up to the level of carbohydrates that America had in 1889.

                    I’m not sure why it would be surprising that Americans were high carb in the 19th century. There were no factory farms and grains/porridges were a big part of early American life, going back to the American Revolution. By the 1960s, America had one of the lowest levels of flour consumption of any Western country. Again, this is why the Dietary Guidelines were written—to reverse that trend and to re-align American carb consumption with its historical norm and with other Western countries.

                    So, again, I have to wonder how Taubes and others have missed all this history.

                    1. My granddad talked about his diet as a kid, back in Germany in 1890 or so. It was oat porridge and potatoes, and lucky to get it. Plus whatever vegies they could grow, and goat milk. He did eventually take a job as a servant in a castle where he could get “meat every day”, but he counted himself lucky.

                      There was a huge gulf between what “rich people” ate and everyone else, and there weren’t all that many rich people. If you look at the pictures, a number of the rich were quite obese and sick (Henry 8 comes to mind, and Ben Franklin, and Genghis Khan for that matter).

                      Still, when granddad moved to the US circa 1930, he could eat anything he wanted and so could grandma. Neither got fat, or cancer, or high blood pressure, and grandma lived to a healthy old age, died at 96.

                    2. Duck, in your first post, your question: “If carbs caused everyone to gain weight, then how does he explain that Americans were once thin eating a high carb diet?” Then you follow with this: “As far as I can tell, Americans consumed roughly 56% carbs / 12% Protein / 32% Fat in 1909, and consumed even more carbohydrates during the 19th century.” You conclude your post with this: “Unless I missed something (entirely possible) Taubes seems to have skipped right over that part of American history. This ignored historical data implies that there is something else causing significant weight gain in Americans.”

                      First Duck, I agree with part of your last statement: “…there is something else causing significant weight gain …” I think there are other factors besides macronutrient balances that affect us. A big concern are the ubiquity of estrogenic hormone-disrupting compounds such as BPA and phthalates in so much of what we handle and consume. These days we are *constantly* exposed to them. More on these endocrine disruptors and other factors in another post. We’ll be busy enough covering the possible confounders here. Let’s start with “thin eating a high carb diet.” The closer you are to eating a subsistence diet, the less the macronutrient mix matters. The closer to a subsistence diet, the hungrier for calories your bod’s cell are, and so the less insulin it takes to admit those calories–be they from carbs or fats–into these maximally receptive cells meanwhile staying below the fat-storage threshold. Americans in 1889 did a lot more physical labor than today and food cost a much bigger part of the budget than the mere 11% it does today. Look how thin Chinese people were a few gens ago. Rural Chinese farmers ate mainly rice and greens yet stayed thin because they ate comparatively little and did lots of physical labor. As China grows more prosperous, obesity and diabetes there is taking off, and they still love to eat noodles and rice. Going back to the 19th cen, if you look at people of comfortable means who could regularly eat their fill, obesity WAS in fact a problem. Taubes starts GCBC with the example of William Banting who started a low-carb movement in England in the 1860s. This is well documented. Your questions and comments focus on America and this is in England. But the physiology is the same.

                      Duck, if we could somehow adjust for the subsistence diet confounder, would we find that Americans really *did* get fatter from 1889 to 1961? Might they have even gotten a little thinner? It’s possible. I don’t know as if we’ll ever know this for sure. I’ve never seen obesity rates for those years. Have you?

                      For the two AJCN reports, the data starts at 1889, missing all but the last 11 years of the 19th century. That’s important because we were well into the period of producing great surpluses of ever more refined flour and plenty of sugar. Here’s this from GCBC on pp 96–97: “It wasn’t until the mid 19th century that white flour became suitably inexpensive for popular consumption…sugar was also a luxury until the mid 19th century.” Other readings suggest that flour truly took off starting in 1875 when we saw a spate of process refinements over the next 25 years to the turn of the century and then “…mills after 1900 manufactured breakfast cereals and special pastry, cake, and pancake flours—some including leavening ingredients. Marketing specialists realized that the best way to sell flour was to make it easy to use. General Mills introduced “Bisquick” in 1930.” You can read about those here:

                      http://www.encyclopedia.com/topic/Flour_mills.aspx
                      http://www.angelfire.com/folk/molinologist/america.html

                      As for your statement “The high demand for white flours during the 19th century were said to be responsible for the dyspepsia epidemic.” Duck, do you have a link for the ‘”dyspepsia epidemic?” I could not find any such discrete event. But many of my search results found “Graham Bread” as the Dyspepsia Bread.” Graham bread is *not* a white bread but rather it’s made from non-sifted whole-wheat flour. https://en.wikipedia.org/wiki/Graham_bread. That only makes sense since this bran bread is high in fiber, roughly a fifth being indigestible cellulose: http://medical-dictionary.thefreedictionary.com/Wheat-bran. White flour has only a fraction of the fiber of whole wheat; see here the two entries in the USDA Nutrient Database:

                      http://ndb.nal.usda.gov/ndb/foods/show/6546 (white)
                      http://ndb.nal.usda.gov/ndb/foods/show/6543 (whole wheat)

                      As for sweeteners (sugar, molasses, honey, etc), Duck, again, I refer you to that table from Guyenet et al showing a *20-fold* increase in US sugar consumption since 1820 as refined cane and beet sugar production kept rising and becoming more affordable. Table 1 at that first link you supplied earlier (http://ajcn.nutrition.org/content/14/3/169.full.pdf) shows a similar pattern to Guyenet’s table: a dramatic increase in sugars (Antar et al call it “simple CHO”). The “complex carbs” (wheat, corn, flours, cereals, potatoes) appear to have steadily gone down in that time. Still Duck, to say that “American’s total carbohydrate consumption fell ~30% between 1889 to 1961” tells only part of the story at best, and may even be misleading. As a percentage of total calories, carb consumption fell less, only from 58% in 1909 to 48% in 1961. And that’s assuming these studies are even correct–they come with many caveats. These are not ward studies, but rather calculate macronutrient balances indirectly, using the food supply, and had to resort to different info sources, which those researchers may have used their own methodologies to collect their data. The data in the Antar study trends in eerily consistent straight line curves through the years, not at all what you’d expect during disruptive events like the Great Depression (1932) and WWII (1942–45), both times of rationing and food shortages which tend to favor carb-rich plant-sourced foods. Interestingly, the Antar studies disclosure includes: “This work is supported in part by grants from the Cereal Institute Inc…” Hardly a lack of conflict of interest!

                    3. The reason Graham bread was the “dyspepsia bread” is because Graham bread was the cure for dyspepsia. People weren’t getting enough fiber due to all the white flour that had become fashionable.

                      Rich obese people (like Henry VIII) ate significantly more meat and sugar than poor people. The peasant diet was mainly complex carbohydrates, dating back to Ancient times.

                      William Banting may have founded the low carb movement in the mid 1800s, but even Banting’s doctor didn’t believe that low carb was necessary for everyone. Dr. William Harvey stressed that Banting could have lost weight if he exercised more and ate less refined foods. Banting had an affinity for refined foods/sugar.

                      On corpulence in relation to disease, by William Harvey, 1872

                      (p.137) We may see the proof of this, in the fact that Mr. Banting became fatter as long as he lived what is called “low,” i.e., when he ate principally bread and potatoes, with the addition of large quantities of beer, milk, and sugar; whilst, when he lived “well,” i.e., principally on meat, he became thinner…

                      (p.145) …In many villages the inhabitants live chiefly on potatoes and cider, and only eat meat occasionally in the course of the year, and yet in spite of this plentiful supply of “the means of respiration,” we seldom meet a “Banting figure” amongst them. It can easily, therefore, be understood why medical men have always earnestly recommended all corpulent people to take much exercise, to sleep little, and to undertake some mechanical labour.

                      There really wasn’t much need for a Banting diet before refined sugars and flours entered the America diet. If there was, it would have been popularized much earlier.

                      “*20-fold* increase in US sugar consumption since 1820”

                      Sugar consumption? Or Sugar production?

                      My sources clearly showed that simple sugar was replacing complex carbohydrates. But simply looking at wholesale sugar production is misleading because most Westerners would have relied on local or backyard honey hives for their own sugar needs. For instance, In England in about AD 1350, honey cost approximately 7 pence per gallon (equivalent to 1.3 pence/kg), which is what the same volume of butter cost. (Rogers, 1866). This was much less than one would expect if it was a scarce and highly prized food item:

                      Honey revisited: a reappraisal of honey in pre-industrial diets, by Allsop & Miller (1996) (Free Download)

                      A reappraisal of the evidence from the Stone Age, Antiquity, the Middle Ages and early Modern times suggests that ordinary people ate much larger quantities of honey than has previously been acknowledged. Intakes at various times during history may well have rivaled our current consumption of refined sugar. There are implications therefore for the role of sugar in modern diets. Refined sugar may not have displaced more nutrient-rich items from our present-day diets but only the nutritionally comparable food, honey.

                      Mind you that people needed beeswax for all the candles they were burning before animal-fat candles became popular in the mid-1800s. Mead was also a very popular drink in the middle ages, leading up to the 17th century. It’s made by fermenting the final washings of honey from the comb in a solution with water.

                      Pointing to mollasses production, as some indicator that the American diet became sugar crazy, omits the fact that people have had access to their own local or backyard sugar production. This is the selective history I’m talking about.

                      “Rural Chinese farmers ate mainly rice and greens yet stayed thin because they ate comparatively little and did lots of physical labor…Americans in 1889 did a lot more physical labor than today.”

                      Offices are not new inventions. This line of thinking ignores the fact that sedentary occupations have been common for centuries (artisans, watchmakers, clergy, lawyers, scholars) and many Americans had slaves for their labor.

                      In the 19th century, one of the hallmark features of a sedentary life was a loss of appetite, particularly as people aged and could no longer do manual labor.

                      See: The Diseases of Sedentary and Advanced Life: A Work for Medical and Lay Readers (1885)

                      Incidentally, there is a strong correlation in the Western world between fortification of foods and obesity. Countries that fortify have significantly more obesity. As it turns out, before feed, rat chow, and carbs could be fortified, people and animals would lose their appetites when they ate refined grains, because the refined foods lacked the B vitamins that stimulate appetite. In fact, it was the appetite stimulating effect of B vitamins that led to their discovery by Osbourne and Mendel in the 1920s. Apparently the tastebuds crave the taste of B vitamins (this effect may be bypassed if you swallow B vitamin pills).

                      Once it was discovered, the ‘patent medicine’ industry quickly began to sell “ironized yeast” to encourage people to increase their appetites and gain weight. Most people were too thin and it was unpopular to be skinny and scrawny in the 1920s and 30s, as people wanted curves and vitamins were seen as the way to fatten up.

                      See: Ironized Yeast advertisements

                      By the 1950s, it was discovered that you could fatten animals with a combination of antibiotics and vitamins, and it could be done without much extra food intake. It only worked with a combination of antibiotics and vitamins. Just giving antibiotics or vitamins alone didn’t work. To this day, the combination is used to fatten animals.

                      France has a high rate of antibiotic abuse but their food isn’t fortified. This might explain why they have such a low obesity rate despite lots of refined flour. The B vitamins added to our refined grains are known appetite stimulants. It appears to be why food producers are so eager to add them to foods.

                      Without those fortificants, people would likely not have the voracious appetite for refined foods– the lack of vitmains (especially B vitamins) is supposed to result in a loss of appetite. It’s an innate and protective mechanism so that animals and humans do not gravitate towards nutritionless staples.

                      I doubt it’s a coincidence that the wholesale baking industry (not doctors) pushed to increase fortification in the 1970s along with the US Dietary Guidelines. It appears they figured out that they could sell more refined foods by adding appetite-stimulating vitamins to them.

                      It’s amazing nobody has noticed this. Everyone here talks about macronutrients, but nobody realizes that one of the macronutrients is now laced with appetite-stimulants, unlike in the 1800s when people lost their appetites. Banting loved beer and sugar. The beer was a good source of appetite-stimulating B vitamins.

                      Interesting stuff.

                    4. Duck Dodgers, wbryanh- Wow, you 2 have written “books”! All while I’ve been sleeping, then going to work- (I live in Europe, so I’m on a different schedule/writing plan from you probably). Hmmmm, where to begin? First off, when I said that Gary Taubes “delved into the history” in his book, what I meant was he wrote about the history of obesity research, not about every diet of every time period. I don’t see this as “selective writing”. His book is long and dense enough- (in fact, many people complain about this!)- it would be hard to include absolutely everything. And as far as I know, he never actually said that all people who eat a high carbohydrate diet automatically get fat; what he *did* say is that fatness is mostly caused by hormonal factors, and where obesity is found, it is generally found together with high carbohydrate diets- (i.e., not with hunter-gatherers who eat just meat and fat). Most of his book was a debunking of the “calories in, calories out” theory. In any case, according to the Weston A. Price Foundation, in the time period you were talking about, people did eat pretty many carbs- (this is confirmed by John Nicholson, though in England, in his book “The Meat Fix”). According to both sources, although people ate carbs, they also ate a lot of meat, fat, and offal, *and* they exercised a lot, many of them doing outdoor labor. When there is no metabolic syndrome, the appetite and energy expenditure regulates itself, and the body weight remains relatively constant.

                      In any case, during the 1800’s and early 1900’s, obesity and diabetes did exist, they were just more rare than they are now; the obesity epidemic as we know it hadn’t taken off yet. Around this time, many explorers noticed that hunter-gatherers in various parts of the world did not get diabetes, obesity, or other “diseases of civilization” that Westerners were getting- (appendicitis, gallstones, dental caries, constipation, diverticulitis, heart disease and cancer). Gary Taubes did write an extensive chapter about that (mentioning obesity and diabetes briefly, among all the other diseases listed). They also noticed that when these native people switched to a “Western” diet, these diseases started to crop up; some of them immediately, some of them took a generation or two, but there was always a distinct pattern. In this chapter, also, I would like to mention that he did speak quite a lot about “refined” versus “complex” carbs; partly because the theories of the day (Cleaves, Reaven)- were that the newer, refined carbohydrates were the main problem. But when Denis Burkitt- (not sure if I spelled it right) “discovered” fiber, these theories gave way to the general belief that disease/obesity is caused by lack of fiber rather than refined carbohydrate and sugar in the diet. (This fiber theory has never actually been proven, but it’s become a “fact” which people take for granted today). In any case, I was under the impression that Gary Taubes also implicated mainly refined carbs and sugar. (I know he’s currently working on a book about sugar, which should come out soon).

                      Duck Dodgers- I think your theory about B-vitamins is interesting; although I didn’t comment on it, I read your earlier posts on the subject. (Does it apply only to synthetic vitamins?) There could really be something in that, at least regarding Americans. The only thing is that I live in Europe, and the foods here are not fortified; however, I have seen first hand how obesity and diabetes is spreading like wildfire; quite sad, really. What I also see is that there are way more fast food places and sugary drinks, and people seem to be eating those things more.

                    5. Duck, again, I agree there are other factors beside dietary fat-carb balances driving our chronic disease and obesity. Likely many other factors, including environmental toxins (like the estrogenics I mentioned earlier), massive GI microbiome disruption due to routine use of antibiotics, massive external microbiome disruption due to antibiotic chemicals like triclosan impinged in everything from soaps to clothes, big changes to the gluten content of wheat since Norman Borlaug intensive selective breeding, and chronic disruptions of our circadian rhythms from working odd shifts and simply being able to stay up late due to cheap bright light. And yes Duck, for me that includes food fortification. These are just a few of the very many changes we’ve seen in our modern world, esp since 1945.

                      Still, these numerous other mitigating factors don’t necessarily exonerate HCLF. Just because many earlier peoples ate high-carb diets doesn’t mean they necessarily enjoyed better health than their LCHF peers. We can’t say that HCLF *didn’t* promote chronic disease like diabetes. We have too many unknowns. Until well into the 20th cen, acute conditions–deadly infections, workplace accidents, wars–killed way more people than chronic disease. In 1900 the average life span of an American male was 47 years. Plus, until recently chronic diseases were massively under-diagnosed. Diabetes is a terrific example. We didn’t have urine test strips till the ’40s, no glucometers until the early ’80s. Even today hundreds of millions of people unknowingly suffer from diabetes. Here’s a history of diabetes dx’ing: http://www.bjbs-online.org/pdf/pp83-93%20BJBS69(2).pdf

                      Duck, I do find issues with a lot of the evidence you present here. Before launching into all that, about “dyspepsia bread” you are quite right about it being used to help with dyspepsia! On that point I stand corrected. As far as people eating it to help with eating it to counter-effects of eating refined flour products, that could very well be the case–I just can’t say. I haven’t been able to find any history on it to support your claim. Do you have that link I asked for earlier? That’d be great, but if not, no worries, not gonna debate it.

                      About Henry VIII and Banting, yes, what you say appears to go along or at least not contradict what I said, when you bear in mind what I said about macronutrients mattering less when eating closer to a subsistence diet and doing more physical work. The passage you quote:

                      “(p.145) …In many villages the inhabitants live chiefly on potatoes and cider, and only eat meat occasionally in the course of the year, and yet in spite of this plentiful supply of “the means of respiration,” we seldom meet a “Banting figure” amongst them. It can easily, therefore, be understood why medical men have always earnestly recommended all corpulent people to take much exercise, to sleep little, and to undertake some mechanical labour.”

                      That is one man’s anecdotal observation, and his reporting is clearly not immune to error. These days I very much doubt we’d advise corpulent people to “… sleep little…” Could well be most of those villagers he observed did a lot of physical labor and ate closer to a subsistence diet, not necessarily due to lack of availability, but that a diet mainly of potatoes and cider is not very interesting. Not much “food reward” as Stephan Guyenet says.

                      As for what you say here: “There really wasn’t much need for a Banting diet before refined sugars and flours entered the America diet. If there was, it would have been popularized much earlier.” It’s easy to assert Duck, but we can’t know it for sure. It’s amazing how obtuse we can be for so long. Wealthy Romans drank out of lead goblets for 1500 years without realizing the lead drove their insanity. But again, I can readily believe that the increasing cheapness and availability of refined carbs drove matters to a crisis point.

                      About sugar consumption vs production and honey, Duck, can you seriously suggest that sugar (cane, honey, molasses, etc) pre-mid 19th cen was anywhere near as available as today’s sugar like HFCS, which you have to work to avoid?! What you say “In England in about AD 1350, honey cost approximately 7 pence per gallon (equivalent to 1.3 pence/kg), which is what the same volume of butter cost. (Rogers, 1866).” That may seem cheap, Duck, but 7 pence was an enormous amount of money in 1350. Per this site, a pound in 1350 had the spending power of nearly *7000* pounds today. Thus that gallon of honey today would cost 490 pounds! Butter has historically been expensive. So has beeswax. Per the wiki on it: https://en.wikipedia.org/wiki/Candle

                      “…Beeswax candles were expensive, and relatively few people could afford to burn them in their homes in medieval Europe…” Typically the candle-makers used animal fats.

                      As far as the link you posted: “Honey revisited : a reappraisal of honey in pre-industrial diets” the authors of this speculative study you cite (Allsop and Miller) are the first to admit its limitations: “…There are no precise figures for per capita [honey] consumption during most periods in history…” Even with all this, I’m ready to accept that for at least a few groups, honey may well have served as a main food source. Again, these groups likely did more physical work and ate closer to a subsistence diet. And again, their generally short life spans and lack of diagnostics prevent us from knowing if their HCLF diet promoted chronic disease or not.

                      Duck, about what you say here: “Offices are not new inventions. This line of thinking ignores the fact that sedentary occupations have been common for centuries (artisans, watchmakers, clergy, lawyers, scholars) and many Americans had slaves for their labor.” Duck, your line of thinking ignores the fact until relatively recently, a much greater part of the population *did* do a lot of physical labor. E.g. from https://en.wikipedia.org/wiki/Agriculture_in_the_United_States#History:

                      “In 1870, 70-80 percent of the US population was employed in agriculture.[15] As of 2008, less than 2 percent of the population is directly employed in agriculture.” And those few remaining farmers use many more “labor-saving devices” E.g. they replaced the ox-pulled hand plow with motorized tractors with air-conditioned cabs and cupholders for the 64oz Big Gulp sugar water.

                      About food fortification, it’s an area I want to research a lot more, and I appreciate all the links you posted on this! Duck, there’s so much to add to this discussion, including the common “more is merrier” mentality when it comes to micronutrients like Vitamin C and iron. Made worse by our RDAs which we determined in the 30s and 40s mainly through WAG (wild-ass guessing) Our need for these micros can vary hugely on specific conditions which is why we evolved to store many of the them, esp Vits A and B12, and to adapt to episodic shortages of them, e.g. potassium. More later Duck. Thanks for reading. –Bryan

                    6. I have to agree with wbryanh, that there is more to the obesity epidemic than B-vitamins and fortified food- (although I do find it an interesting concept and I think it may contribute). I finally had a look at that fortification link, and, though it’s interesting, it doesn’t explain everything. First off, it seems that the reasoning is that B-vitamins mainly stimulate appetite- (unless I missed something?) But that doesn’t explain why poor people who don’t have enough food and don’t eat lots of calories get fat. It has been documented that some Native American cultures who are very poor literally eat too little food. Though what they eat is mostly “industrial food”, white flours, sugars, government rations, they are eating too little, not overeating…..why do they get fat, or even obese?

                      Also, I’d like to give my own n=1, (and part of the reason why I’ve been interested in Gary Taubes’ work). Back when I was a young woman, I was anorexic for a few years. In an attempt to lose weight, I ate a low fat, mostly low-calorie but high carb diet. (This was back in the 80’s, when I didn’t know any better). I could not lose weight this way, so I reduced my diet lower and lower, to create a greater caloric deficit. During this time, I never ate more than 700 calories per day. Very often I would only eat something like 2 ears of corn for the whole day, or maybe 1 small container of blueberries, and that was it. All unrefined foods, and so few calories it couldn’t have been high in B-vitamins. And yet, I actually gained weight during this time! Luckily, I wasn’t anorexic for long, since it didn’t *work* anyway. And as soon as I started eating meat and fat again, and loads more calories, I lost the weight. At the time I just thought I was an anomaly, and that I was *weird*. However, when I read Good Calories, Bad Calories, I realized that something hormonal was going on with me- (it may not be like this for everyone). I personally think that in my case, it has something to do with eating fat. When I go too low fat, I tend to put on weight (the bad kind of weight too). With book titles like “Eat Fat, Lose Fat”, obviously some other people have noticed this phenomenon too.

                      A few more things: I live in Germany, and yes, the people do drink a lot of beer. However, they have traditionally drunk beer, but were not always fat; I have seen them progressively get fatter, but I don’t think they’re drinking more beer. In the Middle Ages people drank mainly beer, but there was no obesity epidemic then. Also, one of the observations that Weston Price made when he visited native cultures was that most of them ate far more vitamins and minerals than the people of his time; his main theory, aside from avoiding industrial foods, was to eat a “nutrient dense” diet. There was no obesity or diabetes among these groups (hence my question about “synthetic B-vitamins”). In the link, it was not specified that the B-vitamins only caused weight gain when they were synthetic; the implication was that generally too many vitamins, even from meat or vegetables, could be too much. (?)

                      wbryanh, you mentioned modern wheat as being a possible factor- (I definitely think it is!)- let me also mention that modern corn is not what it used to be either. It’s gotten much sweeter. Whereas it used to be a complex carbohydrate, it has now become quite high glycemic. (And in America corn is ubiquitous). In addition, soy is an endocrine disrupter, and soy, in this quantity, is a relatively recent addition to our diet. (Soy is also used to fatten animals). Also, in my lifetime, I’ve noticed that many fruits and vegetables have been bred to be sweeter. Some fruits that I remember as having a “complex” taste when I was young, I no longer like because they now taste cloyingly sweet. I absolutely think people are eating more refined sugar than ever before, because- not only have I read about it- but I’ve even observed it in my lifetime.

                    7. Hi Morgana! I haven’t dived into Duck’s fortification links yet, but will when I can carve out some more time. I suspect there’s a lot there, for reasons I wrote to Duck just now, about megacorps devising ways to drive us to eat ever more. About what you say here:

                      “poor people who don’t have enough food and don’t eat lots of calories get fat. It has been documented that some Native American cultures who are very poor literally eat too little food. Though what they eat is mostly “industrial food”, white flours, sugars, government rations, they are eating too little, not overeating…..why do they get fat, or even obese?”

                      I’d very much like to see the docs on it, because we simply can’t escape the basic thermodynamics. If we spend more energy than we take in, we have no choice but to lose weight! I suspect these kids don’t get enough healthy real whole food to eat, but WIC etc supplies them plenty of the the high refined carb and rancidifying omega-6-bomb veggie and legume oil loaded food-like substances. About you eating super-low-cal in the 80s, again, if you are taking in fewer cals than you burn then you simply have to lose weight, and you can down-regulate only so much and still be ambulatory :-). Maybe on your “cheat” days you ate more than you remember? But certainly your experience protein and fat and losing weight, that’s mine experience too, and I could stop cal-counting after a while.

                      About what you say here: “[The Germans] have traditionally drunk beer, but were not always fat; I have seen them progressively get fatter, but I don’t think they’re drinking more beer. In the Middle Ages people drank mainly beer, but there was no obesity epidemic then.” Morgana, they may not be drinking any more beer, but over the course of years, we can steadily become more insulin resistant forcing more the beer (and bread and pasta and other high carb foods) into adipose tissue.

                      About this you say: “the observations that Weston Price made when he visited native cultures was that most of them ate far more vitamins and minerals than the people of his time; his main theory, aside from avoiding industrial foods, was to eat a “nutrient dense” diet. There was no obesity or diabetes among these groups (hence my question about “synthetic B-vitamins”). In the link, it was not specified that the B-vitamins only caused weight gain when they were synthetic; the implication was that generally too many vitamins, even from meat or vegetables, could be too much. (?)” Morgana, vitamins we get from real foods may act much differently in/on us than the fortifying ones which can have novel formulation our bods don’t quite know how to deal with. In general, I have a tough time thinking that we need to carefully measure out the micronutrients we take in. Life just isn’t like that. Sometimes we’ll get loads of a given micronutrients, other times we won’t get it at all for a while. Thus our bods had to evolve ways to conserve, store and eliminate as needed. I certainly worry about micronutrient formulations like supplements and fortifications, and stopped ingest these in 2009.

                      About your corn comments, absolutely it’s gotten sweeter! I’m 55 and remember the solid super-starchy stuff from the 60s-70s you had to cook to eat. One day in the 90s, I decided on a whim to chomp into an ear and was amazed how good and sweet it tasted! About soy, I cut virtually all of it out, only eating organic locally produced non-GMO natto once in a while. Fermenting soy allegedly mitigates the estrogenic compounds (incl isoflavones) as well of course to reduce carbs. Definitely they’ve bred to make fruits sweeter and likely veggies, too, though no examples of those jump to mind at the moment (maybe some squashes?) About eating more refined sugar, how could we NOT be?! Truly we have to always work, to have our wits about us to not to take it in. E.g. Hebrew National Kielbasa dogs. In the supermarket, the Nutrition Facts panel shows they have no carbs, and indeed my BGs stay low when I eat those from the store. So one day I ordered the dog with the VERY SAME name at Costco’s food court (sans bun), and my BGs popped to 150. I went back to add to the court to get the bulk hot dog box, and learned from the label they jammed a load of HFCS into the dogs! That’s yet another example of where the food comps take every opportunity to sneakily press our evolutionary hot buttons to lead us to buy more of their junk. After all, it costs a fraction of a cent of HFCS to add a certain pleasant and enticing je ne sais quoi to the dog which may be enough to get you to plunk down $2 for another. You can NEVER win with these guys–except to leave the table entirely. Which I did. For years now, I almost never eat out, though I go out plenty with friends, but have only coffee/tea and that’s been working out super well.

                    8. wbryanh- Thanks for answering me. A few things:

                      1) I know I’ve read about poor people who become fat on an insufficient calorie diet. Gary Taubes mentions it in his book- (it may have been “Why We Get Fat”, not sure….”)- but I’ve read about it independently of Taubes. It was an American Indian tribe, (not the Pima, though they may have had the same problem). Possibly the Sioux. I would have to look up the link again, I don’t know where I saw it. I will do that as soon as I have time- (which is not today unfortunately, sorry….) Also, I saw a documentary a few years ago about Global Obesity, where they showed some very poor people, living at subsistence level who were obese. (The documentary might have been called “Globesity”?) They were eating crap, like soda, but they had too little food to eat. Basically, one of the problems with being poor is that- with little money to spend- they will often choose to spend it on cheap foods that will fill them up fast, like sugar, or starchy carbohydrates. I do not believe in the “law of thermodynamics” in regards to calories/fat burning. If you want to read a good book debunking the law of thermodynamics, I recommend Zoe Harcombe’s book, “The Obesity Epidemic”.

                      2) When I was anorexic, there were no “cheat days”; I was anorexic! A normal woman should consume between 1500 to 2000 calories, I believe; I cut mine down to 1000 calories (half), then, when that didn’t work, I went to about 700 on a “top” day- (on other days I ate even less than that. Also, one must keep in mind that I was exercising constantly). Anorexics control their calories to the point of obsession. And, I gained weight. I think it probably had partly to do with hormones; I was 21, probably the peak childbearing age, so I think my hormones might have been doing something crazy to compensate. Our bodies are not like a car that you fill up with gas, and then we have “fuel”; although our food does give us energy to burn, we also need the calories for certain processes within the body. When those calories are not forthcoming, the body will “ramp down” on certain processes- (whatever is “less important”), and the body will compensate in whatever way it needs to. (This certainly happened to me, in more ways than one). My theory is that people who eat too few calories may, in some cases, become extremely insulin resistant; almost like a bear in preparation for hibernation. (Animals that don’t have access to excessive food before winter will still gain weight- for instance, in captivity- if they are hibernating animals). Again, if you want to read about this concept of body processes versus low calorie diets, I recommend Zoe Harcombe’s book.

                      That doesn’t mean that reducing calories can’t help with weight loss; sometimes it does, sometimes it doesn’t. In any case, the hormonal aspect of fat gain- (not only insulin, that’s just one factor)- is also a very interesting subject, which I am still researching.

                      3) Yes, I do know that B-vitamins act very differently in the body when they are synthetic as opposed to when they are found naturally in foods. I was momentarily confused, because the link I had a look at also seemed to implicate diets that are high in meat, as well as the fact that presently, we eat more B-laden fruits and vegetables in the winter when traditionally these were unavailable. But Duck Dodgers straightened me out on that one, I think I understand the theory better now.

                      Finally, I meant to thank you for reminding me- (in another post of yours, on another subject)- that even lean people *can* fast, and that we have more fat preserves than we may realize. That’s true; and actually, I have absolutely no problem with 16 hour fasts, and don’t even have any blood pressure effects. So, yeah…..maybe I’ll give it a try sometime. In any case, wbryanh, I have enjoyed having a good “this and that” with you.

                    9. I kind of wonder if there isn’t a “hibernation switch” that gets thrown. If you look at omnivores like, say, bears … they are very thin when they get out of hibernation. They eat like mad, and get bigger again, but not obese. Come fall they overeat again, and they store a lot of fat, which gets them through the winter.
                      Now, during the winter you don’t want a lot of muscle … it’s expensive and eats calories. So to get ready for hibernation, you need to store fat … lots of fat.
                      In the fall, what bears eat tends to be a lot of fruit, and honey if they can. That’s when the fruit gets ripe and there is a lot of it. In the spring, there are grubs and fish (salmon!) and greens. I’m not sure where tubers fall in there. They are typically available all the time. Bears are also active in both fall and spring, gathering food.
                      But at any rate, it makes sense to me that there is some epigenetic switch that tells the bears when to make muscle and when to make fat. Possibly the “poor people food” of THIS era hits that switch, where the “poor people food” of a century ago did not. I’ve certainly known obese people that really don’t eat all that many calories, and then people that eat huge meals.
                      To find those foods though, might mean testing each food type individually?

                    10. Beer is an especially interesting case. Yes, it is full of B vitamins, and has been traditionally used to “fatten up” people. The monks that brewed beer were noted as being fat in the plays and stories of the time, and in fact when they look at the bones in abbeys … the monks that brewed beer were fat, while the ones that made say, brandy, were not.

                      One other thing about beer though, is *hops*. Hops are a narcotic and antibiotic in their own right, and in beer, it helps raise the ethanol content by suppressing the lactobacilli. But the hops also give you that nice “beer buzz”.

                      Through much of European history, both beer and cider were drunk throughout the day, in preference to water. Both have vitamin B and plenty of calories, though usually not so much in the way of sugars. The dead yeast are a calorie source too, in unfiltered beer? We don’t drink unfiltered beer much these days, but if you make homebrew there is a nice layer of yeast at the bottom of each bottle.

                      Queen Victoria was into her beer and also she was rather obese. She had a 50-inch waist.

                      “Give my people plenty of beer, good beer and cheap beer, and you will have no revolution among them” – Queen Victoria

                    11. heathertwist- Thanks for joining our conversation; you’ve posted some interesting ideas, which has given me “food for thought”. I like learning things I didn’t know about before.

                    12. Also, the dyspepsia epidemic of the 19th century was well known to be caused by eating too many refined foods. Again, the fiber-rich Graham bread was a cure for dyspepsia. John Harvey Kellog used fiber-rich cereals at his sanitarium to cure dyspepsia.

                      But the 19th century diet that became too high in refined flour was known to cause an interesting side effect. It resulted in constipation from lack of fiber, but it also caused a loss of appetite.

                      The Cincinnati Lancet and Clinic, Volume 8; Volume 47 (1882)

                      “The appetite may remain intact in dyspepsia; but, as a rule, it decreases or disappears entirely.”

                      …and…

                      The Dyspepsia of phthisis (1894)

                      “In the early stages of the complaint, the appetite may present little or not deviation from the normal, but as the disease progresses it tends to diminish and may even disappear.”

                      The second source goes on to explain that the appetite might change considerably depending on what was presented in the meal. Osbourned and Mendel showed the same thing in the 1920s, only they figured out that the appetite-stimulating factor was the B vitamins. This is why pellagra (a B vitamin deficiency) causes lack of appetite. So, we might deduce that Banting’s beer drinking is what stimulated his appetite. I wouldn’t be surprised if the obese Depression-era children were given yeast cakes (or yeasted breads) to stimulate their appetites. Yeast cakes were the main B vitamin supplements before B vitamin pills and wafers were created.

                      The effect is supposed to only happen when the subject is deficient in B vitamins, but obese people are now known to have micronutrient deficiencies. And, of course, people surviving on mainly white flour during the 19th century would have been deficient in B vitamins. So, it all makes sense in terms of appetite.

                      Today, companies fortify water with B vitamins (Vitamin water). It’s unlikely done for health purposes. More likely it’s done to stimulate the tastebuds. Tastebuds are well known to change with deficiencies. For instance, people who are deficient in copper or zinc do not taste the offending metallic taste of those aqueous minerals.

                    13. “Does it apply only to synthetic vitamins?”

                      The early literature on B vitamins suggests that the “reward” side of the appetite-stimulating effect is mainly about the vitamins hitting the tongue of deficient animals. If you swallow B vitamin pills (and you have good methylation) you might not crave the taste of B vitamins the same way because you might not be deficient. Animals will naturally gravitate towards B vitamin flavors when they start start to become deficient from eating nuritionless chow. They will tend to avoid the completely nutritionless foods as they become deficient. And they can “learn” about these tastes and create preferences for them (See Harris 1933, in my other comments). In other words, the animals can be “educated” to associate the taste of B vitamins with other flavors that are associated with them (i.e. you can remove the enrichments and the animals will still associate the flavor with those enrichments, even if the enrichments are removed). The “education” side of the equation might be equivalent to say, “dietary guidelines”.

                      “The only thing is that I live in Europe, and the foods here are not fortified; however, I have seen first hand how obesity and diabetes is spreading like wildfire; quite sad, really. What I also see is that there are way more fast food places and sugary drinks, and people seem to be eating those things more.”

                      Obviously sugar can be quite addictive, caloric and not very filling. But there are probably other ways for companies to stimulate appetites without techinical enrichments (besides sugar). Yeast extracts are a “taste” of B vitmains. Marmite, an enriched yeast extract, is known to stimulate appetite. It’s actually banned in Denmark because it contains enrichments. But, of course, drinking beer is a B-vitamin yeasty flavor, so that too should stimulate appetite with a meal. You get the idea. Just the yeasty umami flavor added to processed foods can stimulate appetite if the tastebuds are trying to guide us to obtain these vitamins.

                      A single slice of enriched bread is laced with as many stimulating vitamins as a medium sweet potato—and almost as many B vitamins as a cup of beans. The sweet potato and beans are far more filling than a slice of enriched bread.

                      Anyhow, all of these diet gurus, like Taubes, seem to have overlooked the main difference between refined carbs in the 19th and 20th century in American. Everyone focuses on just macronutrients, but that misses a big part of what happens to appetite when you eat truly unenriched and nutritonless foods as staples.

                    14. “Duck Dodgers- I think your theory about B-vitamins is interesting”

                      I wouldn’t call it my theory. Dr. Ss Zhou, et al. (from the studies I mentioned, above) is the one who figured it out. I just extrapolated his ideas into various points of history. It’s his theory though. You’d have to look at his studies to see the details and correlations, etc.

                    15. Ok. Everyone calm down. 🙂 I don’t think that fortification is the only factor in obesity. I never said that.

                      Obviously obesity is multi-factoral. However, I think that fortification is a majorly overlooked factor that everyone has been oblivious too. But, once you look at the correlations and the history, it becomes apparent that fortification in developed countries are now only done to sell more food. If the fortifications were not there, you would eventually lose your appetite trying to eat mainly refined foods—as what happened during the dyspepsia epidemic.

                      @wbryanh, I don’t think anything can ever “exonerate” any diet. 🙂 The way I see it is that grains, and wheat in particular, were always considered to be the healthiest foods from the days of Hippocrates right up until the 19th century. Hippocrates recommended wheat, barley and periodic bloodletting for good health. Bloodletting waned in the 19th century, but for all we know it may have been protective of some Western diseases like diabetes.

                      Borlaug wheat seems to be a distraction. Yes, it’s a sub-par wheat, but unfortified countries seem to do well on it. For instance, according to FAOSTAT, France consumes 40% more wheat, as food, than Americans do—and it’s unfortified. They produce predominantly semi-dwarf hard winter wheat. But the French have one of the lowest obesity levels in the developed world and very little Non-Celicac Gluten Sensitivity (good luck finding gluten free menus in France). So, while Borlaug is a poor specimen of wheat, it doesn’t seem to be deleterious for unfortified countries. 72% of Pakistan’s daily caloric intake per capita comes from unfortified wheat and they have one of the lowest obesity rates on the planet (5.5% in 2008). It would seem that unfortified Borlaug wheat does not cause obesity.

                      Anyhow, enough about that. I agree it’s all very complex and multi-factoral. Fortification is just one of many factors. We agree.

                      Here are my basic notes for when you decide to research this:

                      Zhou et al, found the correlations, but I have no idea if his theories on B vitamins are right or not. He seems to think that niacin overload is to blame. Apparently most researchers think that obese people have micronutrient deficiencies, but Zhou says obese people may be storing unmetabolized synthetic niacin. Either way, Zhou et al references that B vitamins like niacin are known to be appetite stimulants, but he doesn’t go into detail. I also found research that obese people are deficient in thiamin, but at the same time store lots of thiamin in their cells. (Don’t ask me what that means). Zhou also points out that obese people have high serum folate levels, which is indicative of unmetabolized folic acid from fortification. There is some research saying that high serum folate is associated with increased appetite. At any rate, obese people certainly have abnormal B vitamin metabolisms. It’s plausible that obese people are deficient in micronutrients (despite high serum of some B vitamins) which may make them crave the taste of B vitamins. Again, I have no idea if Zhou’s research is right or not, but his correlations are eye opening to say the least. To my mind, the appetite-stimulating effect is very interesting and could explain a lot about the paradoxical history of weight gain in the US.

                      Anyhow, Scientists during the 1920s knew that when animals are fed pure, nutritionless flours and refined grains as staples, the animals quickly lose their appetite and lose weight.

                      Studies In Deficiency Disease, Chapter VI, by Sir Robert McCarrison (1921)

                      Distaste and loathing of food, loss of appetite, and it may be also depraved appetite, are thus cardinal symptoms of deficiency disease, and their significance is great. They are due in part to the monotony of the food, but in the main to insufficient supply of vitamins, and of vitamin B in particular. Thus Osbourne and Mendel have found that if animals, fed on purified dietaries, free from this vitamin are given yeast separately, it increases their appetite for the deficient food, no doubt inconsequence of its high content of vitamin B. The well-known effect of yeast in improving the appetite in human beings is probably due to the same cause. Drummond finds the addition of this vitamin to a synthetic diet, causes a greatly increased intake of food and consequently increased rate of growth…The animals are impelled to eat more in order to satisfy the cells stimulated to growth by the vitamin. Vitamins are thus indirect stimulants of appetite, they induce the desire for food, and are, therefore, indirect stimulants of digestive juices. It seems to me that “loss of appetite” is one of the most fundamental signs of vitamin deprivation. It is a protective sign, the first danger signal of impending disaster. It should at once excite suspicion as to the quality of the food in any patient who may exhibit it.

                      In other words, humans and animals have a natural tendency to become less hungry when fed deficient and nutritionless food. It’s an innate, protective mechanism to prevent the cravings of nutritionless staples. In the early 1920s, George Cowgill found that B vitamins could increase the appetites of mice, rats, pigeons and dogs. He coined term “appetite vitamin” for vitamin B1 (thiamine). Small amounts of dried brewer’s yeast (for B vitamins), were soon commonly added to the feeds of cattle.

                      The key thing to understand is that Thomas Osborne & Mendel discovered that they only needed to provide a taste via a “small daily dose” of B vitamins to stimulate appetite and make the rats gain their weight back. Osborne later said…

                      The Water-Soluble Vitamine (1920)

                      “For a long time it has seemed that the problems presented by feeding our young rats were in many ways similar to those of infant feeding. Until Mendel and I learned how to supply the vitamines to young rats we had endless troubles which are now overcome.”

                      Soon “ironized yeast” was sold as an appetite stimulant. In addition to thiamin, riboflavin and niacin are now known to be appetite stimulants in deficient animals.

                      In 1933, Harris et al. published an exhaustive study observing the appetites of rats and vitamin-enriched foods. The experiments showed that rats deficient in B vitamins overwhemingly craved the taste of B vitamins, but could be “educated” to associate the vitamins with flavors.

                      Before WWII, bakers were mainly against enrichments because it made the product expensive and people were suspicious. It was the military that made enrichments commonplace by requiring their addition for War purchases during WWII. The enrichments were useful for soldiers who needed to survive on combat rations for weeks at a time (the Russians just used whole wheat with great success).

                      But somewhere after WWII, bakers—represented by the American Bakers Association—began to realize that enrichments would help them sell more flour. With carbohydrate consumption falling, they set out to raise enrichment levels. The first thing they did was get congress to pass the Vitamins and Minerals Amendments. The new law prevented the FDA from classifying excessive levels of vitamins or minerals as a drugs.

                      Next, in the mid-1970s the ABA convinced the FDA to triple iron enrichment levels. It was known as super-enrichment. William H. Crosby (the father of modern hematology) wrote two letters in JAMA expressing his outrage for the ABA’s move. Crosby wrote:

                      William H. Crosby (1975)
                      “…the data were manipulated to suggest a national catastrophe, especially in the area of anemia”[1]

                      “One nutritionist with whom the plans were discussed has written to me: “I was particularly pleased to see your criticism of the Ten-State Nutrition Survey. It was apparent from the protocol that there were no controls, or I should say random sampling techniques, for which I was very critical, and the response was simply, This is what McGovern wants.”[2]

                      In 1981, the ABA finally succeeded in convincing the FDA to raise enrichment levels on flour to where they stand today. At the same time the ABA also lobbied the government to “educate” the US population to eat enriched grains via the Food Pyramid. Rice enrichment levels were not raised, however flour enrichment levels for iron and B vitamins were increased significantly. Thiamine was increased ~28% from the previous average range. Niacin was increased ~33% from the previous average range. And iron was increased by ~38 increase from the previous average range. The industry also expanded enriched flour into virtually all wholesale refined grain products. The total amount of iron compounds in the US food supply increased by 19-fold from 1970 to 1987. The FDA no longer has much control in regulating how much fortification goes into foods.

                      To this day, the ABA lobbies the government to promote enriched foods. Take a look at the ABA’s press releases and annual reports and you will see that they are firmly committed to lobbying enriched foods to the US dietary guidelines committee.

                      As far as I can tell, iron fortification is poorly absorbed and mainly just causes lots of inflammation in the gut. It’s not very good at solving anemia (they would have fortified with copper if they were trying to solve anemia). However, Progesterone receptor membrane component 1 (PGRMC1) as an iron binding protein in yeast which co-purifies with progesterone binding proteins in the liver and ovary. Makes me wonder if the adding free iron to yeasty dough results in something that would otherwise not happen with phytate-bound iron.

                      If I think of anything else, I’ll let you know. Thanks for listening!

                      (Again, I agree this is just one factor. Yes, obesity is multi-factoral, I know).

                    16. Duck, to correct the record, things are not so ducky in France. You say: “Borlaug wheat seems to be a distraction…the French have one of the lowest obesity levels in the developed world and very little Non-Celicac Gluten Sensitivity…”

                      Actually, France and the US have roughly the *same rates* of celiac disease, about 1% of the pop:

                      http://www.afdiag.fr/intolerance-au-gluten/la-maladie-coeliaque/
                      http://www.medscape.com/viewarticle/770529

                      The French link says: “One estimates that one person out of 100 can develop this disease in Europe. The prevalence seems to be identical in North America. In France only 10–20% of the cases to date are diagnosed.” (“On estime qu’une personne sur 100 peut développer cette maladie en Europe. La prévalence semble identique dans le continent nord-américain. En France, seulement 10 à 20% des cas seraient aujourd’hui diagnostiqués.)

                      About obesity, Duck it is relatively low in France as you say, but strong cultural eating norms–like no snacking ever between meals–may have been largely responsible for that suppression. As these norms have eroded since the 1990s, obesity begun to soar in France, doubling from 1995–2004. See here: https://en.wikipedia.org/wiki/Obesity_in_France

                      The same norms may have also suppressed rates of diabetes in the past, but it too, greatly increased in a decade, from 2.6 to 4.4% (“En 2000, le taux de prévalence du diabète était de 2,6%. En 2006, il était déjà à 3,95%. En 2009, il atteint les 4,4%”)
                      http://www.afd.asso.fr/diabete/chiffres-france#

                    17. Duck, you say “I don’t think anything can ever “exonerate” any diet. :)”

                      If you mean “no amount of meta-analyses, systematic reviews, RCTs, and cohort, case control, historical, anthropological, and molecular mechanistic modeling studies can exonerate any diet,” then I agree with you!

                      All those things above have great value. But our best option is for each of us to test each food- and lifeway on ourselves, tracking what we consume and do as carefully as feasible. To cut out of our lives as many modern complex products as possible, e.g. plastics, chemical-filled soaps, shampoos. And to get as many health measures as we can wheedle out of our docs and we can do at home.

                    18. Duck, thank you for getting me fired up about this fortification angle. At least one thing you said about it, that producers fortify in part to fire up our appetites, especially resonates with me. As Michael Pollan discussed, food producers went from being Mom and Pop shops serving their local communities, to huge multinational corporations beholden to their shareholders who always have the imperative to increase profits–a tall order when we should eat only so many calories each day. I will be diving down this rabbit hole as soon as time allows.

                    19. Another thing about “mom and pop” food … if you were say, Korean and living at a barely sustenance level, you would feed your kids food that kept them FED as long as possible. So you chose foods that kept them full and happy, whatever that was.
                      The modern food system is very opposite. You choose foods that let people overeat, so they buy more.

                      As Duck Dodgers has pointed out, the factors aren’t all that simple. For me I figure you have to adopt the entire cuisine … eat like a French person and see what happens. Eat like a Korean person. It’s more than just recipes … it’s about timing, food sources, additives, drinks (tea vs. coke?).

                      But I can say that well, a Korean or Japanese mountain person menu just makes you a lot more full for a lot longer than the typical American fare. I’ve never been able to pinpoint it to a macronutrient profile or set of allowed foods.

                      However, there ARE good studies that were done on say, chickens, which are also omnivores. I turns out that if you are growing chickens, you can have 3 food mixes. One makes fast-growing, very lean chickens. Second makes very fat fast-growing chickens. The third makes slow-growing lean chickens that don’t eat much.

                      The difference for chickens has to do with methionine. The methionine acts like a “stop eating” switch. If the food is too high in methionine, the chickens undereat and grow slowly, although they are healthy. If there is too little methionine, they overeat and get fat. If there is “just enough”, they grow fast but don’t get too fat.

                      So for people that get a lot of fish or eggs, they tend to have too much methionine? So they undereat? That doesn’t explain the Japanese yam-eaters though. I can tell you from experience that yams just plain fill you up (more so than a potato or bread, for sure).

                    20. Duck Dodgers- thanks for clarifying your position on the fortification issue! I guess I jumped to the conclusion that you were promoting that as the only/main cause to obesity; my mistake. I definitely find it interesting, and I definitely want to pursue it further, so thanks for giving information on what to look up. Frankly, I’ve been rather skeptical of fortified foods all along. And, yes, food companies will do all they can to get people to overeat; (adding sugar to food will have the same effect, which may be one reason why sugar is added to most processed food).

                      A.k.a. blood letting: the blood letting would have been a way to get rid of excess iron in the blood. Excess iron has been correlated with disease- (though, aside from the case of hemophiliacs, I’m not sure if it’s a correlation or causation). But this could have had an effect on health.

                    21. …and yes, the Pima were obviously eating lots more sugar and fat at the same time too. I just thought that the increased access to enriched flour was another “coincidence”, perhaps making them hungrier for all the other crap. Just thought it was interesting.

                    22. “Queen Victoria was into her beer and also she was rather obese. She had a 50-inch waist. ”

                      Great info there!

                      One thing I would point out is that the overwhelming majority of our B vitamins come from our microflora. Which means that someone eating fiber-rich complex carbohydrates should be feeding their microflora with enough fiber to avoid B vitamin deficiencies, particularly if their diet was sufficient in B vitamins.

                      But a queen eating lots of sugar and (white) flour and meat would likely have a B vitamin deficiency (particularly if obese) and in that case, the beer might stimulate appetite in her situation. And since she had access to unlimited food, she could satisfy that increased hunger.

                      At least in the 19th century, most peasants drank small beer all day, since the water was not safe to drink. Besides the fact that small beer is very weak, they probably didn’t have appetite stimulation if their guts were making sufficient B vitamins from all the fiber they were eating.

                      So, again, someone who has adequate B vitamin production in their gut should not have appetite stimulation from tasting B vitamins as far as I can tell.

                      Also, a poor person wouldn’t have access to unlimited food like a rich person would. So, even if they were actually hungrier, they just went hungry. :/

                    23. WBryanH said: “Actually, France and the US have roughly the *same rates* of celiac disease, about 1% of the pop:”

                      Oh, heh, I never said that France has less celiac than Americans do. I said they have less Non-Celiac Gluten Sensitivity. Gluten free options are extremely rare in France. I imagine that the inflammation from iron fortification makes it harder for Americans to digest gluten.

                      My reading on the subject is that virtually every country (with a few exceptions) has a ~1% celiac rate no matter what the diet is. The only reason why some countries have higher celiac is because it’s just diagnosed more in some countries.

                      True celiac is also believed to be rising all over the world, but nobody really knows why.

                      Anyhow, my point was mainly that the French (and Pakistan) eat far more Borlaug wheat but the non-celiacs there seem to have less problems digesting it. Here in the US everyone here thinks they have gluten sensitivity from Borlaug wheat. But, eat Borlaug wheat in France and somehow it’s not addictive nor as problematic. As I said, it’s extremely rare to find gluten free options in France. Yes, they have the same celiac rates, but not the so-called “sensitivity” we do.

                      Non Celiac Gluten Sensitivity is also believed by many to be a bogus disease. There’s no true biomarker for it. Not saying people aren’t sensitive to gluten, but the research is shifting to other potential causes (like ATIs or other gut inflammation). That’s why I think it’s curious that fortified countries seem to have gluten free options. In the US I think it’s a $10 billion industry. In France, nobody really cares much about it.

                    24. Not to mention the obvious, but they don’t add iron to bread in France.
                      Now, if you want to create a vaccine, what you do is to pair a protein (a bit of virus) with an irritant (adjuvant: like aluminum or iron). Then the immune system learns that the protein bit (the virus) is bad, because “obviously” it caused an irritation.
                      Frankly American baby formula and hamburger buns seem like custom-made vaccines to teach the immune system to hate casein and gliadin. Maybe not to the celiac level, but something like 30% of Americans have IgA antibodies to gliadin.
                      Celiacs actually have IgA immune factors to the tTG in bread. tTG also happens to hold your gut cells together, so an immune reaction to tTG is bad stuff … it means you attack your own gut cells and destroy the villi.
                      High IgA levels to gliadin… no one knows what that causes exactly. But disturbingly, the anti-gliadin IgA ends up in the blood, which means there is some gut permeability going on there too.

                      Now … I’m celiac. I get REALLY SICK off tiny bits of wheat. My family isn’t though. When I had to change my diet, I got depressed about the whole thing and stopped cooking with wheat just in self-defense. My family hardly noticed, and the deal was that they could eat anything they wanted when they went out. So my husband was happy to go out and get “real” pizza and my daughter would eat the birthday cupcakes happily. Both stopped though, because they said they made them “feel sick” compared to the similarly rich versions we made at home.

                      There could be multiple reasons for that. One might be just that I made them afraid of wheat. Although, this didn’t have any effect on them with dairy, which I also don’t eat. Other factors though:

                      — FODMAPS. Wheat is full of fructans, while rice flour etc. is not. Fructans are hard for some people to digest.
                      — Enrichment, bromine and other additives: white flour in this country is loaded with other stuff.
                      — Different breeds of wheat.
                      — Different cooking methods.

                      My daughter and husband routinely “cheat” when they go out and it’s difficult to find GF food. They often get ill as a result, though their “ill” is just a mild upset stomach. Anyway, my daughter did eat gluten-free when she was in France because she didn’t want to deal with the stress of an upset tummy. She would go into a restaurant, point to herself, and say “celiac”. The waiter would nod and they’d figure it out. It is way easier to be celiac in Europe than in the US.
                      What I’ve heard is that in Europe celiac is just a routine test (like we test for diabetes) so the people that have it know they have it. Maybe fewer people have the “minor” reactions to wheat because they didn’t grow up on iron-fortified baby foods.

                    25. Duck, again it’s wrong what you say: “…[The French] have less Non-Celiac Gluten Sensitivity [than the Americans.] First, sources estimate rates of Non-Celiac Gluten Sensitivity (NCGS) in the US and in France being roughly the same–up to 6%. Second, these can only be estimates because NCGS is notoriously difficult to diagnose. Which, interestingly, you DO allude to at the bottom of your post.

                    26. Similar rates celiac and NCGS between the US and France only makes sense. Celiac disease is the frankest manifestation, the tip of the iceberg of gluten sensitivities if you go by what Dr Davis writes in Wheat Belly. And in your last post you do cite him for evidence. If celiac rates are similar in the US and in France, we should not be surprised to find the same for NCGS.

                      Duck, I’m not saying fortification plays no role. Like you, I believe it may play even a large role. What I am saying: You have no evidence to support your dismissal of Borlaug wheat strains to support your statement that “Borlaug wheat seems to be a distraction.“ It may be as you say. Or Borlaug wheat may play a very important role, as Dr Davis, Dr Perlmutter (author of Grain Brain) and many others assert. We simply don’t know either way. This can only be your opinion. So far you haven’t shown any real evidence to support it.

                      OK, this is the last of my of three-part comment. Sorry to break it up like this. These were originally one comment but Rawfoodsos was blocking *something* in the full comment. But the site wouldn’t tell me what, so had to guess at it.

                    27. Oh guys, I forgot to mention that Zhou believes that high meat consumption may contribute to the problems he describes, as meat is high in niacin (the B vitamin he focuses on most). In reality, you do see the correlations he mentions with countries that have high meat consumption and do not fortify. But, I agree it’s complex and I have no idea if he’s barking up the wrong tree or not. I only mention this because he does believe it’s possible to have the same end result from high meat consumption. I can’t quite follow his explanations, but I suppose it’s possible that someone with a compromised methylation cycle could end up storing (or not properly metabolizing) excess vitamins from a high meat diet. I really don’t know though.

                      B vitamins in food are supposedly only a minority of the B vitamins we get from our microflora. So, it’s possible that eating too much (muscle) meat results in some compromised B vitamin production due to lack of fiber. Just thought I’d mention it to clarify what Zhou said. Indeed, it’s complex.

                      As for the US government’s position on fortification, the US government does not require fortification. I believe individual states did at one time, but I think there may have been a court position that made it illegal to force fortification. So, the FDA’s position is that it’s “suggested” but not mandatory, and companies are free to create lots of fortified products, so long as they adhere to the suggested levels—even though fortifying virtually every product was not the original intention of fortification. The FDA has also said that widespread fortification is “not necessary” for the US.

                      So, it is possible to buy unfortified flour in the US (generally organic flour is unfortified these days) but the UK and Canadian governments do, in fact, require fortification for all white flour.

                      At the end of the day, what you see is that it’s the companies that want to fortify and add it to the Food Pyramid, and the government sort of goes along, maybe even reluctantly. The American Bakers Association leads a group of lobbyist groups known as the “Grain Chain” that continues to pressure the DGAC to promote enriched grains in the government’s MyPlate icon.

                      Comments to the 2015 Dietary Guidelines Advisory Committee Regarding the Importance of Grains in the Diet

                      The crucial role of enriched grains in the diet

                      The Grain Chain endorses maintaining the 2010 DGAC grain consumption recommendation that Americans consume six servings daily with at least half of all grains as whole grains. We also urge the Committee to continue to recognize the valuable role of enriched grains in a healthy diet, a key component of which is fortification with folic acid, in the 2015 Dietary Guidelines.

                    28. heathertwist said: “Maybe fewer people have the “minor” reactions to wheat because they didn’t grow up on iron-fortified baby foods.”

                      Yes, I had the exact same thought. Actually there are some who believe that autism may be a result of the enormous levels of iron in baby formula (note: not a reliable source).

                      Anyhow, I got in touch with one researcher about the high iron levels in baby formula and they wrote back:

                      “Giving iron or formula supplemented with 100X iron eliminates breastfed flora and changes gut/microbiome development. Iron for babies is very controversial and is deliberately manipulated by formula companies to make breastfeeding problematic”

                      That’s kinda scary.

                      I decided to look into this a bit further, and without much effort I came upon a pair of related papers.

                      Effect of iron on neonatal gut flora during the first week of life (1985)

                      Effect of iron on neonatal gut flora during the first three months of life (1985)

                      The studies concluded that compared to fortified cow-milk preparation, a low iron content in standard preparations of cow’s milk enhances resistance of the neonatal gut to colonization of pathogens.

                      There are also studies showing that high levels of iron in baby formula appears to have negative consequences on development.

                      What a mess.

                  2. Morgana said: “Though what they eat is mostly “industrial food”, white flours, sugars, government rations, they are eating too little, not overeating…..why do they get fat, or even obese?”

                    The Pima? While some got fat before enrichment (could be from any number of reasons, since we agree that obesity is multi-factoral), the health of virtually all Native American are well known to have deteriorated rapidly after the 1950s. In 1959, most Pima were still somewhat healthy eating lots of beans and lard-fried white-flour tortillas—part of their diet since the late 19th century when the government began giving them white flour as part of their rations. Hesse wrote in his paper, “The flour is almost exclusively of the non-enriched variety, and because it has a higher gluten content than enriched flour, it ‘makes better tortillas.’ Little enriched flour is sold at the trading posts.”

                    Within 10 years their health completely deteriorated. By 1971, the Pima had a very high prevalence of obesity and diabetes. The Pima were still eating their beans and lard-fried white flour tortillas, but they were now also indulging in soft drinks, enriched pastries, they were more sedentary, and they were eating considerably more enriched flour.

                    Morgana said: “I live in Germany…I have seen them progressively get fatter, but I don’t think they’re drinking more beer.”

                    Could be from any number of reasons. Nobody ever said that fortification or B vitamins are the only reason.

                    Morgana said: “In the Middle Ages people drank mainly beer, but there was no obesity epidemic then.”

                    Yes, though they would have been eating complex carbohydrates, which tend to have bitter tannins and fiber that are satiating signals. If we say beer is an appetite stimulant, then it’s probably mainly problematic if it entices you eat lots of sugar and white flour.

                    Morgana said: “Also, one of the observations that Weston Price made when he visited native cultures was that most of them ate far more vitamins and minerals than the people of his time; his main theory, aside from avoiding industrial foods, was to eat a “nutrient dense” diet. There was no obesity or diabetes among these groups (hence my question about “synthetic B-vitamins”).”

                    As I said, the appetite-stimulating effect is only true if the person is deficient in B vitamins (or, say, has abnormal B vitamin metabolism as Zhou suggests).

                    Morgana said: “In the link, it was not specified that the B-vitamins only caused weight gain when they were synthetic; the implication was that generally too many vitamins, even from meat or vegetables, could be too much. (?)”

                    I actually wrote Zhou and he did think that synthetic B vitamins are very problematic for some people. For instance, not everyone has the enzymes to metabolize (synthetic) folic acid. So, they build up unmetabolized folic acid in the body and the serum levels rise, even though the person is deficient (since they cannot use the folic acid well). I believe Zhou would call this “overload” even though the person is technically deficient.

                    I do not think you could easily get B vitamin overload from real foods. B vitamins from real foods are easily excreted. But the synthetic B vitamins are not easily excreted in some situations (like folic acid for instance). I believe Zhou thinks that synthetic niacin is particularly problematic.

                    To my mind, Zhou may have made some mistakes as he dives into the complexity. But, I think he was on to something when he pointed out the correlations and the possibility for appetite-stimulation.

                    At the very least, fortification makes it so that people can survive on nutritionless foods. If the fortification were not there, most people would lose their appetites eating nothing but pure white flour (as we saw with dyspepsia and Osbourne & Mendels rats and many other studies). On the other hand, I did see one study that rats deficient in thiamine may still crave sugar and fat, but still lose weight as their appetite diminishes.

              2. And as I said wbryanh this is fine if you’re writing a fictional romantic history about nutrition. But we’re talking about the construction of GT’s carb insulin assertion. If this were scientific writing the assertion would be on page one in the abstract, FOLLOWED by the 200 pages of defense.

            3. @morgana, no, GT does not say in the NY Mag article that everyone gains weight if they exercise. But he doesn’t cite examples of people who have lost or maintained weight. He’s biased the article by doing that. Do you understand that the article was written to be read in 5 minutes by someone waiting for a bus, not someone who would spent 12 hours deconstructing it on a blog? The immediate impression GT makes is that exercise is futile, and he says this in a judgemental and assertive manner.

              It shows tremendous bias to cling to GCBC the way you (and wbryanh) do. If you cite that book, please cross reference the position of Ancel Taubes and other nutritionists and physiologists. Answer arguments with more than prooftexting and precisionism! Don’t presume that the rest of the world knows or cares about the GCBC chapter on exercise, or the section on the Pimas, etc etc etc!

              1. thhq- I don’t think I’m unduly biased towards Taubes; the problem is, you’ve criticized things that he’s supposedly said, but I can’t find any evidence that he’s even said those things. Basically, I don’t really know to what you are referring…..the link you sent me was a New York Times article on salt, and I saw nothing in there about exercise or weight gain. And I can’t find any “chapter on exercise” in Good Calories, Bad Calories either; I looked at the table of contents today, and there was nothing- (unless there are a few words about exercise in one of the other chapters).

                Basically, my stance on diet is pretty much where Denise Minger stands; it does appear that different diets seem to work for different people. I would never criticize someone for the way that they’ve chosen to eat. However, when people criticize low carb diets, I feel the need to defend them; partly because this way of eating works really well for me, mostly because there is enough slander and bad press about them anyway (mostly wrong, I may hasten to add). Likewise, if I feel that someone like Gary Taubes or Atkins is being misrepresented, I feel the need to defend them, for the truth. If I appeared dogmatic, I apologize. But I did read Good Calories, Bad Calories, so I know what Gary Taubes did and didn’t say. I see online bloggers constantly misrepresenting him, and this bothers me, partly because people tend to repeat what they’ve heard (even if they didn’t get it from the source).

                In any case, I’m glad you lost weight and became healthy by exercising. This is truly great! Since this very positive thing has happened to you, why should you even care what Gary Taubes thinks of it? I say- (in a positive, non-criticizing way)- maybe just “let it go”?

                1. I’ll leave you with this Morgana. If you haven’t read Dixon’s series on Keys you may find this interesting.

                  http://jleonarddixon.com/2014/06/17/science-unintended-consequences-ancel-keys-cholesterol-and-the-transition-to-an-obese-society-foreword-why-i-wrote-this-book/

                  If GT, Eades, Sisson or anyone else in the HFLC community has done this kind of respectful discussion of the greatest 20th century nutritionist give me the links. This man’s association with George McGovern and the food pyramid is unfortunate, he does not deserve to be mocked and pilloried. Why did he live to be 100? That is the question to be answered.

                2. In “Why We Get Fat”, Taubes explains that there’s little scientific evidence that exercise is a significant factor in weight loss. He does say that there are many health benefits to exercise, though.

                  As with anything, people respond differently to exercise. Since reading what Taubes wrote, whenever someone tells me that he lost weight through exercise, I ask further questions.

                  When someone starts an exercise program, I thind that the person changes other variables too. Usually they are changing their diet, meal schedule, cutting back on beer consumption, and sleeping more.

                  I’m guessing that when scientists are studying this in the clinic they have a control group and for the exercise group they are not changing a lot of different factors along with the introduction of exercise.

  32. Denise, have you ever explored the notion of cellular/acellular fats (like it’s popular to do with carbs these days) in a carby meal? Aka, the difference between eating a bunch of walnuts vs the same amount of fat from an oil. The different digestion speed and pattern might very well create a scenario where there’s very little ffa released into the blood at any given time, thereby annulling the effect typically seen in research with starch+oil.

  33. I’m starting to get confused. . . Maybe that’s the point. So this is the girl that “debunked” the China Study? She seems to not know what she believes or thinks as she is constantly changing. It looks to me that she likes to be the rebel, the outlier, different to whatever group she happens to be in. At a young age, she decides to become a vegetarian, not for ethical motivations she says . . . So the reason is unclear. Then I guess when vegetarianism was too “normal” for her she decides to become raw 100% plant-based. This is when all her health problems started. She would have to be doing something pretty extreme for all her hair to fall out and teeth to be rotting in her mouth. Then she decides to write a critique on the China Study and join the paleo, low carb movement. Now that she is part of the paleo movement she now wants to come out and say “Hang on! I’ve just discovered all this information on the health benefits of a low fat, high carb diet!”
    What shocks me is that she had not read earlier about all the scientific literature that supports a low fat, high carb diet. She could have read about it when she was vegetarian or when she was a raw foodist or in the very least when she decided to argue against the works on Dr Colin Campbell, Neal Barnard, John Macdougall etc. However, it looks like she is only discovering this information now. So basically my point is, while this girl chops and changes and goes from one diet to the next and one belief system to the next and writes lengthy blogs about each change . . . Millions of people are on a whole foods plant-based diet and are thriving . . . For years . . . She criticizes Colin Campbell for fudging his data to get the results he wants. However I think I prefer to follow the advice of a man who has 60 years experience in the field and has followed what he preaches for over 40 years, is fit and healthy today (in his 80s?) and is free of cancer, heart disease, diabetes, Alzheimer’s, arthritis etc. His children also follow a whole foods plant-based and so do his grandchildren! I’ve been on a whole foods plant-based diet for 6 years and I have had one cold in all that time when I was pregnant, apart from that I’ve been fit and healthy, had a great pregnancy and have since nursed my child for 11 months (who has never been sick). So I’m not sure what Denise Minger did that was so extreme that made her hair fall out and subsequently make her believe that carbs are bad and lots of meat and fat are good . . . But I will not be following her advice . . . on anything. Ordinarily I don’t mind if people disagree with a plant-based diet but people actually refer to this unstable girl as “evidence” that the China Study has been debunked.

    1. Lily, you may genuinely and ardently feel you follow the right foodway for you. Millions feel the same way about grain-free LCHF. But your gratuitous put-downs e.g. “this unstable girl” are uncool and work against your message. That’s even before I clued into your logic fails and your apparent ignorance of Denise Minger’s remarkably well elucidated arc of her journey, her evolving dietary positions. Highly educated researchers also take serious issue with The China Study. e.g this: http://www.cholesterol-and-health.com/China-Study.html from Chris Masterjohn PhD. T. Colin Campbell fails to deliver a satisfactory defense, as Chris Kresser discusses here (http://chriskresser.com/rest-in-peace-china-study):

      “Campbell’s response to previous critics of the China Study has been something to the effect of: “I’m a trained scientist. Therefore you should believe me and not my critics.” That is a weak argument – to put it mildly. You don’t need six years of graduate school to learn to think critically. Nor does having a lot of letters after your name make you immune to biased thinking or intellectual blindness. A lot of smart, educated people believed the cholesterol hypothesis for decades. But that never made it true.””

    2. I’m on a similar track @Lily, and I’ll look into Colin Campbell. I don’t think either of the extremes -below 15% fat or below 15% carbs – is the best way to go for healthy longevity, though either of those diets works fairly well if they are not over or under eaten. I’d recommend reading Eat Well and Stay Well by Ancel and Margaret Keys if you can find a copy.

      There are lots of ways to live a healthy hundred years, from Paleo to vegetarian, but there are a lot more ways to barely make it to a sick seventy. It’s not rocket science. Don’t pay attention to the picky precisionists who will say that you are an idiot because you are not a devoted acolyte of Taubes, Atkins, Sisson, Eades, Pritikin, Keys, McGovern, etc. etc. etc. It’s your health and you have to figure it out for yourself.

    3. The five minute read leaves me with the impression that Campbell is another persona in search of acolytes and book sales. I give Denise Minger a lot of credit for looking at the broad scope of diets rather than taking the single rifle shot.

      My dad made it to 88 on cookies, tuna sandwiches, pancakes, scrambled eggs, bacon and canned pears. Ancel Keys made it to 100 drinking wine, eating pasta and bread, seafood, fruit and lots of olive oil. My diet doesn’t need to be anymore complicated than those. What I do with my life between meals is what makes the difference between being healthy and unhealthy.

  34. Bit off topic here. But whilst Denise was criticizing the China Study, (Which I personally haven’t read), she was also knee deep in nonsense and delusion during that time. She was referencing and recommending Anthony Colpo and Malcolm Kendrick. That’s right, Dr Malcomn Kendrick, the author of “The Great Cholesterol Con”. I actually read that book when I was into the Paleo/Cholesterol denialism ideology. Re-reading that book 6 years later I feel like I was seriously deluded because of my preference for certain food products.

    I seriously hope Denise stops calling her a scientific blogger and seperaters herself from these Paleo pseudoscientist. It might be hard considering she occasionally gets paid by Sisson to write low carb defending blogs and even had a book published by this supplement salesmen “paleo” guru, but I think if she was honest she would separate herself from all of those hucksters.

    Come on Denise. You were able to separate yourself from the crazy raw food crowd, I think you are able to separate yourself from the “paleo” crowd.

  35. Duck/Bryan,

    I did some ketosis reading to learn more and to refresh my memory, so I have a few points and questions to add to this discussion.

    1. Duck, after all the reading, I agree with you, inuits were not in ketosis, according to our traditional definition of it. So we can’t really use them as a poster child for ketosis.

    2. May be inuits are “better” at burning fat then us, that’s why they are adapted to produce much less ketones as a byproduct of their FFA metabolism? Inuits may well have evolved a mechanism to promote FA metabolism over ketones.

    3. Duck, I don’t think inuits have difficulty fasting, their children may, but not adults. And Peter has a theory that it has to do with omega-3 metabolism, which they have a lot in their diet and which the CPT1a evolved to deal with.
    http://high-fat-nutrition.blogspot.com/2014/11/the-p479l-gene-for-cpt-1a-and-fatty.html?m=1

    4. Chronic cold exposure depletes glucose/raises FFA, so this mutation is an adaptation to Inuits’ cold surroundings and has to do with using UCP for free heat. There is more from Peter here:
    http://high-fat-nutrition.blogspot.com/2014/11/coconuts-and-cornstarch-in-arctic.html

    5. Another interesting point that has been touched upon here is how do we define ketogenic diet and if the level of ketones in the blood even matters. I like Peter’s definition from the link above: “ a ketogenic diet is essentially a fatty acid based diet with minimal glucose excursions and maximal beta oxidation. Exactly how important the ketones themselves are is not quite so clear cut.”

    6. So yes, as Bryan said, can we thrive long term on persistent LCHF? Even VLC? Besides possible liver issues (that can be tested using AST, ALT, ALP), or thyroid issue (which I”m not concerned about either) are there any other known concerns/issues with VLC dieters who feel well on it?

    7. I have an issue with medical tests, most of the reference ranges are based on people eating a “normal’ HC diet, not LCHF, so how useful are these tests? Besides, may be there are some things we are not even testing for? Basically, what is that we don’t know yet and how do we decide what’s best in this incomplete information environment? Can we go on how we feel and look 🙂 ?

    8. I think fasting insulin so far is one of the best markers that correlate with longevity in population studies.

    1. Anna, you are correct. The adults can definitely fast. However, typically the children cannot safely fast.

      Additionally, the Inuit have always been known to snack constantly throughout the day, as first reported by Franklin in 1845.

      The Alaska Dispatch News article I mentioned earlier states:.

      Clues emerging about Arctic gene, diet and health

      Anecdotal evidence is that some adults have long coped with the effects of this gene, if unknowingly, Hirschfeld said. They may talk about how they make sure to carry along snacks if they are engaged in strenuous activity like hunting, he said. After a few hours of exertion and no eating, as these adults describe it, they get sluggish, sleepy and “real jittery,” classic signs of hypoglycemia, Hirschfeld said. “They’d have a candy bar, and they’d snap out of it.”

      Most adults can fast pretty well when they need to, but it sounds like their fasting doesn’t mix well with strenuous exercise.

      Heinbecker showed that (rested) Eskimos could certainly fast in his studies during the early 1930s, but they struggles to make ketones. Perhaps they were just drawing down on fat stores. Only his fasting pregnant/lactating women were really able to produce ketones, but pregnant women are known to have exaggerated ketone production and Heinbecker’s subjects were well below what we would expect from pregnant women. His pregnant/lactating subjects weren’t ketoadapted because he said that due to their employment they were accustomed to eating a carby Western diet.

      Anyhow, you get the idea. They have to be careful when they fast and they prefer to snack all the time.

      A friend of a friend of mine got a license to kill a muskox in Alaska several years ago. He flew out to Nunivak, got in touch with his Eskimo guides and went out in a boat to go find the muskox.

      He said that as they were riding this boat in rough seas, the Eskimo guides started pointing to the shore excitedly. They pulled into a little cove, jumped out of the boat, and started eating from a tub of cream cheese mixed with salmon. Then they used a small gas stove to make some tea. After a short bit they jumped in the boat and continued on.

      His friend said that during the several days they were hunting for muskox, this same scene played out several times a day. He was perturbed, because even if they were getting close to muskox, the guides would drop everything and take a cheese and tea break. His interpretation was that the Eskimo Hunting Guide Union had strict rules about ‘break-time’ and these guides were just taking advantage of it. But they were probably just hungry. lol 🙂

      1. Duck, may be they eat to warm up, not because they are “hungry”. It takes a lot of energy to generate heat there…

        But either way, I doubt they have difficulty fasting any more then us. They should be even more adapted to survive the fasting, given the conditions they live in, especially if they indeed have a bigger liver, as you are saying, they can store more fuel.

    2. Anna, I’ve had a chance to look more at your post. Honestly it’s one of the better ones I’ve seen recently. It does more to further the Inuit discussion than anything else I’ve seen here to date. Possibly even settle it for the purposes of non-Inuit contemplating a LCHF foodway.

      Hyperlipid Peter sums it up esp well: “…Confirming that the Inuit are not poster boys for ketosis is a “so what?” moment for me. Using their P479L (i.e. for CPT1a deficiency) mutation to argue against ketogenic diets is more of a problem. It’s a massive dis-service to any one of the many, many people out there who are eating their way into metabolic syndrome to suggest that a ketogenic diet is a Bad Thing…”

      Anna, I address your points here:

      1) “…inuits were not in ketosis, according to our traditional definition of it. So we can’t really use them as a poster child for ketosis…” Anna, ketosis appears to mean different things to different people and we have no agreed def for it. I’m willing to accept the idea that Inuit aren’t drawing the bulk of their kcals from ketones. More like ketones + FFAs.

      2) “…Inuits may well have evolved a mechanism to promote FA metabolism over ketones.” Anna: Agreed. We often say “ketotic” and “glycolytic.” But I hardly ever hear “lipolytic.” The CPT1a deficiency variant may have been allowed spread due to lack of selective pressure, having nothing to do with purported liver damage from extra fat load. Maybe the selective pressure was greater for the Inuit to quickly get FFAs from white adipose tissue directly to thermogenic tissue like brown adipose tissue. Greater than the downside of maybe having to freq feed their children.

      3) “…I don’t think inuits have difficulty fasting, their children may, but not adults. And Peter has a theory that it has to do with omega-3 metabolism, which they have a lot in their diet and which the CPT1a evolved to deal with.” Anna, I also haven’t heard of fasting issues in Inuit adults, and would like to learn how they adapt to fasting as Inuit grow older. Given their huge and harsh environment and often subsistence diet, it’s very hard to imagine the Inuit are always snacking all the time. It’s likely there were plenty of times they had to go hours or even days without eating anything. Peter’s comment I will (as usual with him) have to spend more time with it, but these comments jumped out to me: “…while systemic ketones are a useful adjunct, a ketogenic diet is essentially a fatty acid based diet with minimal glucose excursions and maximal beta oxidation. Exactly how important the ketones themselves are is not quite so clear cut…”

      4) “Chronic cold exposure depletes glucose/raises FFA, so this mutation is an adaptation to Inuits’ cold surroundings and has to do with using UCP for free heat…” Anna: Yup. Like like my example in 2)

      5) “a ketogenic diet is essentially a fatty acid based diet with minimal glucose excursions and maximal beta oxidation. Exactly how important the ketones themselves are is not quite so clear cut.” Anna: Again, yup.

      6) “…can we thrive long term on persistent LCHF? Even VLC? Besides possible liver issues …or thyroid issue … are there any other known concerns/issues with VLC dieters who feel well on it? Anna, I haven’t heard of other issues beyond what you list, and would really like to.

      7) “I have an issue with medical tests, most of the reference ranges are based on people eating a “normal’ HC diet, not LCHF, so how useful are these tests? Besides, may be there are some things we are not even testing for? …Can we go on how we feel and look…” Anna: Yes, I also have plenty of issues with the current state clinical health measures, as I discuss elsewhere in this forum. We shouldn’t rely much on any single health measure but interpret them in their totality with an eye for mitigating factors. Even a lot of doctors fail to do in this age of push-button medicine, e.g. “Got high LDL? Take this statin.” I agree we have to look at as many factors as feasible–including how we feel and look as you note Anna. Together, tests + qualitative personal observation further our individual health states way more than the vast body of research–even peer-reviewed-“science” out there that people can sling at each other till the cows come home. Best of all is to look at all three things: research, clinical health tests and qualitative personal observations (e.g. “how do I feel?”)

      8) “I think fasting insulin so far is one of the best markers that correlate with longevity in population studies. Anna, that is my sense too, and I’m looking forward to when we will develop a home test for serum insulin that’s as cheap easy and reliable as checking blood glucose. There’s plenty of evidence to suggest that chronically elevated insulin can further metabolic syndrome and lead to a host of pathologies, including Alzheimer’s disease. –Bryan