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:


Oh, Homer!

Over a year ago, I gave a presentation at the Ancestral Health Symposium called “Lessons From the Vegans: What the Paleo Movement Can Learn From the Success of Plant-Based Diets.” In retrospect, I probably should’ve called it “Lessons from the Low-Fatters: What the Paleo Movement Can Learn from the Success of People Who Eat Ridiculous Amounts of Carbs and Don’t Keel Over,” but that was too long for the conference brochure. And for my verbally dyslexic mouth. And also, I didn’t know it was really going to be about fat until I fell down an extended PubMed rabbit hole and, upon regaining consciousness two days later, realized I had found the Nerd Project to end all Nerd Projects.

In truth, though, this post started brewing long before my talk. Having witnessed some pretty impressive healing when I noshed among the low-fat raw vegans (and, after a decade of self-experimenting, concluding I do best on a lower fat diet myself), I just can’t get on board with the categorical “Fat rules, carbs drool!” trend infiltrating both mainstream and alternative nutrition. There are too many exceptions to the rule, too many gaps in the theory, and too many skinny fruitarians frolicking in the sun-dappled fig orchards.

But even beyond that, this post is born of a belief I hold dearly—one that guides my approach to research and underlies the very mission of this blog:

We can’t ignore evidence in order to preserve an ideology.

At least not under the guise of “science.”

When confronted with something that challenges our belief system, the worst possible thing we can do is clamp our hands over our eyes and say, “You do not fit into my understanding of reality; therefore, you do not exist. BE GONE, NON-EXISTING ANOMALY.” Yet that’s what so many of us do—often without even realizing it—when faced with outcomes our chosen philosophy can’t explain. On the flip side of cherry picking, we cherry-throw-out: selectively deleting data that threatens our version of the truth, nipping any cognitive dissonance in the bud before it has a chance to rattle our worldview. It’s easy to be “right” when we’ve shoved all competing evidence into the wood chipper!


For a long time in the nutrition world, our thrown-out cherries were the ones challenging the low fat ideology. We discarded the high fat Inuit cherries and the milky, bloody Masai cherries; the coconut-filled cherries of the Tokelau; the cherries of the traditional reindeer-herding Sami; even the smothered-in-butter French cherries—just to name a few.* It didn’t make sense that these populations could exist and be healthy with their fat-gorging ways, so we slapped them with a “paradox” sticker and deemed them weird exceptions to the Dietary Laws that govern the rest of us.

* For the record, all these examples come with some major caveats, and I don’t think they should be used as evidence to support the kind of high-fat diets many people are eating today (though they don’t necessarily stand as counter-evidence either). More on that in an upcoming post!

Only in more recent years have those cherries been rescued from the compost bin and plopped back into the world’s collective fruit bowl (please wash before consumption). Bestselling books like “Good Calories, Bad Calories” and “The Big Fat Surprise” carved new histories in which fat was an innocent bystander, dragged into the mud by bad science and even badder scientists. The phrase “healthy fat” moved from oxymoron status to popular catchphrase. People whir 80 grams of butter into their coffee and call it breakfast. Apparently Bob Dylan had it right in all but plurality: Time, it is a-changin’!


As awesome as the pro-fat movement has been for challenging outdated beliefs and reviving some truly nutritious foods, there’s been a dark side to the process as well. All of a sudden, the same rhetoric once leveled against high-fat diets is being slung against low-fat ones. Not only is low fat (and by consequence, high carb) not the dietary angel we once thought, the new story goes, but it’s actually the source of all edible evil: the driving force behind our obesity epidemic, a major contributor to heart disease, the puppet master pulling those blood-sugary strings of insulin resistance and diabetes. If only the USDA had recommended 6 to 11 servings of bacon instead of 6 to 11 servings of grains, we wouldn’t be in this mess!

See the problem here?

In the process of redeeming fat, we traded one form of oversimplified blame for another. And it’s led to a brand new wave of cherry genocide. We now dismiss (or paradox-sticker) high-carb populations in the same way we justified ignoring the high-fat ones. We snub decades of clinical success involving fat reduction (to the point where you might think such evidence doesn’t even exist—in which case, you’re in for a surprise with this post!). We deny the potential for low-fat diets to be anything other than a metabolic train wreck, ending in a smoking heap of shrapnel and insulin injections. “Surely those low-fatters are starving all the time,” we proclaim. “Surely they’re making themselves diabetic! They might feel okay right now, but won’t those carby diets go all Cujo on them as the years progress, eating their souls and whatnot?”


Let me be frank here.

If we’re really after the truth, we can’t keep throwing away perfectly good cherries. Seriously. It’s gotta stop. When we censor data we don’t like instead of revising our theories accordingly, we perpetuate the same problems we’ve been battling for decades: partial truths treated as gospel; public policies that do more harm than good; baffled consumers who can’t figure out if it’s the omelet that’s killing them or the OJ they wash it down with.

Do we really want to keep heading down that road? It probably goes somewhere awful! Like Stockton. (Sorry, Stockton.)

Hence why we’re gathered here today, around this massive compilation of pixels, delving into a decidedly hot topic. This post is my attempt to rescue some discarded cherries and return them to the Fruit Bowl of Our Lives. Which, if nothing else, will one day make a fantastic soap opera.

I do want to make one thing abundantly clear before we continue, though. The title “In Defense of Low Fat” doesn’t imply its inverse, “In Attack of High Fat.” Quite the opposite! My goal here is to create a space where two very different dietary approaches can sit down for tea, respectfully coexist, and interact without any subsequent homicide investigations. In fact, I’ll be arguing for a more panoramic view of nutrition where the success of both high-fat and low-fat diets are compatible, and maybe even make sense. It just requires zooming out farther than we’re used to looking, and acknowledging that our ever-rivaling communities could actually learn a lot from each other.

For the sake of reading ease, this sucker is divvied up into two parts: this one, which discusses the crazy-huge body of research behind truly low-fat diets (especially the really obscure stuff!), and the upcoming Part 2, which ties everything together with science, and whatnot. And because this post is long even by my standards, I’ve created a clickable Table of Contents to help you navigate the labyrinth. Good luck! (You’ll need it…)


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.


The Low-Fat History You Probably Never Heard

The popular version of events goes something like this:

America was happily eating its buttery, meaty, cholesteroley fare until Ancel Keys came along with the idea that fat causes heart disease. He cherry-picked data to make it seem like his theory was true, narrowed the culprit down to saturated fat, manipulated the Powers That Be into believing him, and then bull-horned the message far and wide until we all bought his myth. Low fat started with him!

Unfortunately, that’s a big, pre-chewed wad of baloney.

Here’s the deal. People were already whipping out low-fat diets to treat diabetes, multiple sclerosis, high blood pressure, kidney failure, heart disease, and obesity when Keys was a mere young’un shoveling bat poop in Arizona. Heck, the ancient Egyptians prescribed a near-fat-free diet of wheat, grapes, honey, and berries for what was almost certainly diabetes (“too great emptying of urine”). And contrary to popular belief, the early-1900s evidence supporting low fat didn’t come exclusively from rabbits and test tube experiments and correlative scatterplots: it came from actual human people eating actual food with their actual mouths.

If anything, our pal Keys was a latecomer to the idea that fat could play a role in chronic disease. The notion that he single-handedly criminalized fat is complete and utter fiction. He might’ve been the loudest and most unflappably confident voice in the choir, but he certainly wasn’t singing solo.

Here’s a more realistic timeline of the past century, albeit still very incomplete. (Click to make ‘er big!)


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

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


Here’s one for the Paradox Files.

In the 1930s, a man by the name of Walter Kempner fled an increasingly Jew-hostile Germany and landed square in the halls of Duke University… where he proceeded to totally blow the medical community’s mind. His mission: treat kidney disease. His solution: put renal-failing folks on a special diet low in sodium, protein, and fat—a menu devised from in vitro experiments he’d done on kidney tissue.

At the time, very few researchers believed that food could have any effect on kidney disease. Or high blood pressure. Or diabetes. Or heart disease. Or most other chronically wrong-going things in the body. As with Ancel Keys, who was pretty much laughed out of the WHO conference where he presented his “fat causes heart disease” idea, Kempner spent the first chunk of his career swimming upstream in a river of skepticism.

But his colleagues’ dubiousness didn’t last long. After placing patient after so-called-hopeless patient on his unique regimen, it became clear that Kempner’s diet worked. Really ridiculously well. And it became equally clear that the kidney wasn’t the only body part made happy by the new cuisine. Obesity, diabetes, high blood pressure, heart failure, coronary artery disease, psoriasis, and arthritis often saw major improvement or total reversal as a result of the diet. During the course of his career, Kempner treated over 18,000 patients with the above conditions—all by changing what went on the stabby end of their forks.

So what was in this mystical diet of his? Brace yourself!

  • White rice
  • Fruit
  • Fruit juice
  • Refined table sugar
  • In some cases, vitamin supplements (A, D, thiamine, riboflavin, and niacin)

…And not a darned thing else. Kempner summed up the details himself in a 1974 article, readable here:

A patient takes an average of 250 to 350 gm. of rice (dry weight) daily; any kind of rice may be used provided no sodium, chloride, milk, etc. has been added during its processing. … All fruit juices and fruits are allowed, with the exception of nuts, dates, avocados and any dried or canned fruit or fruit derivatives to which substances other than white sugar have been added. Not more than one banana a day should be taken. White sugar and dextrose may be used ad libitum; on an average a patient takes about 100 grams daily, but, if necessary, as much as 500 grams daily should be used. Tomato and vegetable juices are not allowed.

In other words, it was the CARBPOCALYPSE. Along with feasting on impressive amounts of white rice, people were averaging 100 grams of pure sugar a day, and some ate over a pound of it. That’s up to 2,000 calories from refined sugar alone—the same amount deliciously packed into 25 Cadbury Creme Eggs.

(Wisely, Kempner knew his diet was at no risk of being crowned Dietary Homecoming Queen. He apparently described it as a “monotonous and tasteless diet which would never become popular,” and whose only saving grace was the fact that it worked. And as I mentioned in my AHS presentation, he apparently whipped some of his patients in order to help them comply, as—in his words—”the risk to their life was so great that it warranted harshness.” Ouch!)

Here’s a breakdown of how the diet panned out, macronutrient-wise. Image from Duke University files; red graffiti my own doing, to indicate percent of total calories:


What’s really noteworthy is that the diet wasn’t automatically calorie restricted. In fact, some patients had to increase their energy intake to help them gain weight, or to stabilize their weight if they were losing too much. That’s important, because it means we can’t write this off as a diet that improved biomarkers solely by inducing weight loss (Twinkie Diet, I bow in your general direction). It also means that many people spontaneously ate less than they needed when stuffing their faces with unlimited amounts of starch and sugar… as long as fat intake was super low.

If this seems totally baffling and Twilight-Zoney, that’s because it is. According to my calculations, there is an 84% chance that you are now Googling “rice diet Snopes” or contacting my mother to inquire about my recent psychotic break (joke’s on you; she thinks I’m great!). I urge you to keep reading, though, because we’re about to get to the ooey, gooey data at the center of this carb-filled Tootsie Pop.

Let’s start with something weighty: an obesity paper published in 1975 in the Archives of Internal Medicine, which should be of particular interest to anyone convinced refined carbs are inherently fattening:

Here, Kempner compiled data from 106 slimmed-down patients—a mere slice of the thousands he treated over the years—who all dropped at least 100 pounds on his program and achieved a normal weight. (The average loss amongst them was 140 pounds, and one man melted away over 300). These particular losers ranged from 16 to 65 years old, and featured a mix of women and men.

When it came to blasting obesity, Kempner employed what he called a “rice-reduction diet”—the same protocol he’d designed for renal failure and hypertension, but with lower calories:

In the unmodified initial diet, 90% to 95% of the caloric intake is carbohydrate, taken as rice and fruit. As in the original rice diet, salt intake is exceedingly low (less than 60 mg of sodium per day) and fluid intake is thus markedly reduced to prevent water intoxication. Thus, the initial diet is low-calorie, low-salt, low-protein, low-fat, and essentially free of cholesterol.

After getting into that sugary, starchy groove for a month, the dieters could start eating veggies again (which were initially nixed due to their sodium content—kept low, in part, to help tame high blood pressure and “reduce the stimulatory effect of salt on food intake”). A bit later on, lean meats could also make a triumphant gustatory return.

Thanks to Kempner’s hawkish monitoring and dietary tweaking, obedient dieters were greeted with a steady (and often plateau-free) slide towards a healthy weight, like so:


And since we’re all such visual creatures, here are some photos demonstrating the rice diet in action, first published in Kempner’s aforementioned obesity paper. This young woman lost 123 pounds in just shy of a year:



And here we have 278 pounds obliterated in a bit over a year, doing the same. His fasting triglycerides dropped from 187 mg/dL to 85 mg/dL:


And this lovely lady lost 115 pounds in 33 weeks. Her fasting blood sugar dropped from 315 mg/dL to 100 mg/dL, and her triglycerides plummeted from 516 mg/dL to a peachy keen 79 mg/dL—after eating a diet literally made of refined sugar and starch.


Looking at these sugar-fueled Incredible Shrinking People brings an important point to mind. If we assume weight loss is just a matter of calories in versus calories out, the rice diet isn’t any more remarkable than other low-calorie bootcamps: folks ate less and lost weight. Dur. But if you’ve hung around the internet for very long, you might’ve seen the theory—popular within some corners of the low-carb world—that successful weight-loss diets are invariably low carbohydrate diets (or at least low refined sugar and starch diets), regardless of what other rationale those diets masquerade under (low fat, high fiber, low calorie, food combining, eating only on Tuesdays in the presence of an ovulating jackalope, etc.).

How? Because folks inevitably slash their carb intake when they eat less food overall, the theory goes. This rests on the premise that insulin is the wizard behind the curtain of obesity, and that quelling its wrathful swings—triggered by carbohydrates and refined carbohydrates in particular—is necessary for losing weight. Gary Taubes explained this concept in detail in a 2010 blog post:

Simply put, anyone who tries to diet by any of the more accepted methods (i.e., Weight Watchers), and anyone who decides to “eat healthy” as its currently defined, will remove the carbohydrates from the diet that may be — if the carbohydrate/insulin hypothesis is correct — the most fattening. And if they’re trying to cut calories, they’ll be removing some number of total carbohydrates as well. And if these people lose fat on these diets, this is a very likely reason why.

The rice diet might be the most compelling hole-poker we have for that theory. While most carby programs—say, Pritikin or McDougall or Ornish—eschew refined grains and sugar (and thus could fit snugly into the insulin-centric concept above), Kempner’s program sure didn’t. He fed folks almost nothing but the “most fattening” carbohydrates and still managed to slim them down. Does your brain hurt yet?

Of course, losing weight is a far different beast than maintaining a 100-pounds-lighter frame after the losing’s been done—leading us to the question: what happened to these folks in the long run? Did they maintain their weight loss? Gain it all back? Develop a crippling phobia of small, white, oblong granules, requiring years of psychotherapy and Riki Lake guest appearances to overcome?

Alas, Kempner noted that long-term results were “not yet available for the patients analyzed in this report,” and I’ve yet to find any follow-up papers revealing their fate. The only clue I’ve seen comes from the first page of the “Rice Diet Renewal” book, which states that 43% of rice dieters had maintained their weight loss (or lost even more) six years after their stint in the program. (For comparison’s sake, an Annual Review of Nutrition paper estimates that on average, about 20% of folks who’ve lost significant weight are able to maintain that loss for at least a year.)

All that said, the rice diet was about far more than impressively svelte before-and-after shots. As alluded to earlier, it also had the uncanny side effect of improving diabetes and insulin resistance—even when weight loss wasn’t part of the equation. I warned you this was gonna get weird! Kempner published a whole paper on the topic in 1958, which you wouldn’t know by looking at its hauntingly empty PubMed entry:

(Email me if you want the full text!)

For starters, Kempner was just as perplexed as us modern-day health enthusiasts might be when it comes to the effect his diet had on diabetics. As he penned in the paper you cannot see:

We have for the past 15 years treated numerous diabetic patients with the rice diet. Since more than 90 percent of the calories in this diet are derived from carbohydrates, it was anticipated that increased amounts of insulin would be necessary to keep the blood sugar at its previous level. However, the opposite proved to be true. … Not only is the rice diet well tolerated but in many instances the blood sugar and the insulin requirements decrease.

In this report, Kempner analyzed 100 diabetics who’d entered the rice diet program between 1944 and 1955. All of them strictly followed the diet for at least three months (often much longer), and they were observed an average of nearly two years—with some folks monitored for up to eleven years after they’d first embarked on the carby cuisine.

The findings? Ladies and gents, place your bets…

More than half of those 100 diabetic ricers—63%—actually saw their fasting blood sugar drop by at least 20 mg/dL during the diet. Only 15% had their blood sugar go up significantly. The remaining 22 saw little to no change.

To get a visual sense of those numbers, here’s an aptly named pie graph (don’t worry; it’s fat and carb free!). “Increased” or “decreased” is defined as a change of at least 20 mg/dL:


Let’s repeat that: eating almost nothing but starch and sugar and fruit, the majority of diabetic patients lowered their blood sugar levels. In fact, when everyone’s results were pooled together, the average blood sugar change was a drop of 47 points.

‘Twas a similar story in Insulin Land. Of the study’s participants, 68 entered the scene already dependent on insulin. As the carbs raged on, 21 of those insulin-injecters didn’t have to change their dosage; nine needed an increase (including four people who initially weren’t on any insulin at all); and—again comes the cruel, cruel defiance of prediction—42 slashed their usage significantly. In fact, 18 folks were able to discontinue their insulin entirely. Feasting on white rice. And sugar. And fruit juice.

Here’s another delicious graph of pie, calculated for the 72 patients who needed insulin at some point during the study:insulin_usage_rice_diet

Once again: eating virtually nothing but this…


…the majority of diabetics ended up with better glucose control and insulin sensitivity, and in some cases freed themselves from diabetes entirely.

Let that sink in for a minute.

Or two, if you need to grab a glass of water and ward off the vapours.

Just to be clear, the point here isn’t that the rice diet is the Best Thing Ever for diabetics and everyone should trade their insulin pumps for a metric ton of Skittles (nobody needs to taste that many rainbows). After all, 15% of the rice-dieting diabetics actually got worse, many of the improvers still had above-normal blood sugar (despite huge drops from baseline), and we could probably hack Kempner’s protocol to make it more nutritionally sound without ruining its therapeutic effects. Clearly, it ain’t perfect. All I’m saying is that these results totally fly in the face of what most of us consider possible. Sugar and white rice improving diabetes? Blasphemy!

All that said, an important critical-thinky question remains: was this all just a byproduct of weight loss? We know that restricting calories and dropping pounds can definitely boost insulin sensitivity and glucose control, regardless of whether the diet used is particularly healthy. It’s one thing to not be diabetic because you’re eating kale and grass-fed buffalo whose ancestors were blessed by Sacagawea, and another to not be diabetic because you’re living on napkins and crack. Can we at least say that the successful diabetics were the ones who lost weight throughout the program, spontaneously eating less, unamused by a diet that had exactly one-and-a-half flavors?

NOPE. As Kempner pointed out, any obese patients were indeed encouraged to lose weight—but the improvements in blood sugar levels and insulin requirements occurred “both in patients who lost weight and in those who did not have a significant weight change” (his words). Kempner’s data, both in this paper and in the massive collection of his work filed away at Duke University, showed that the diet could benefit diabetics even when their weight and energy intake didn’t budge.

And it didn’t end there. The rice diet also proved helpful for heart failure. It rapidly healed psoriasis. It excelled at its original goal of treating high blood pressure. The “good for” list stretched on nearly as far as those endless bowls of rice! As early as 1949, Kempner had observed that the rice diet was healing more than 70% of his seriously ill, not-responding-to-other-treatments patients from a wide spectrum of disease backgrounds. That figure stayed pretty stable as the decades rolled on.


Psoriasis obliteration on the rice diet.

Just last year, the Journal of Electrocardiology published something of a Rice Diet Resurrection, dredging up Kempner’s key findings and blasting open his oft-forgotten legacy: “An archaeologic dig: A rice-fruit diet reverses ECG changes in hypertension.” In it, the authors pointed out something pretty important regarding the ultimate success of the diet. A band-aid treatment it was not; the rice diet actually seemed to permanently reverse the conditions it set out to treat, at least for many adherents:

A poorly known but important observation was that patients who were able to follow the regime, and who were slowly guided through a gradual modification of the diet over many months, were able to transition into a very tolerable low fat, largely vegetarian diet, while leading a normal, active life, without medications, indicating that the disease state had been permanently modified.

“Permanently modified” probably needs a qualifier, since those folks couldn’t make a total return to their former gustatory ways. But over time, they could start eating a more diverse diet with (lean) animal foods, all manner of vegetables, a moderate level of salt, and the magnificent return of tastiness. Not too shabby, considering many of those folks were initially riding a bullet train towards death. (In another very recent article, “Who and what drove Walter Kempner?“, the authors noted that in Kempner’s day, life expectancy for anyone with malignant hypertension—one of Kempner’s main patient demographics—was only six months. The fact that he gave most of them decades of recouped earth time was pretty fantastic.)

So whatever became of the rice diet? Like most things in life, it lost out to stuff that was newer, prettier, shinier, and easier to squeeze inside an FDA-approved pill. Kempner relinquished the Rice Diet throne in 1992 (and in case you’re wondering, died of a heart attack five years later, at the age of 94—though it’s unclear what his own diet and lifestyle actually were). After his departure, the rice diet predictably loosened up: the program later allowed “a wider selection of largely vegetarian food choices,” though still with low sodium and protein intake (and ostensibly less whipping).

In his 1983 article “Kempner Revisited,” Eugene Stead—who’d worked at Duke alongside the Rice Man himself—summed up Kempner’s unorthodox legacy in a way that captures my own thoughts:

Who in his right mind would have ever thought that rice and fruit could modify vascular disease appreciably? Who would have fed a protein-deficient patient, losing large quantities of protein in his urine, a protein-poor diet? Who would have dared to give a more than 90% carbohydrate diet to a diabetic? Every expert knew that cholesterol levels were not influenced by diet. Nevertheless, all these leads have paid off richly.


Kempner walkin’ the talk. From Duke University files.

Ultimately, I find Kempner’s work both important and wildly uncomfortable.

Important, because it exposes some cracks in our current view of carbohydrates and sugar—areas where our thinking has room to grow and our assumptions have room to crumble.

Uncomfortable, because it demolishes my long-held rationale for why low fat, veganish diets can be successful: that they work because they involve switching to whole foods (Kempner’s sure didn’t!); that they work because they reduce refined sugar and starch intake (the very lifeblood of the rice diet!); that they work because they increase disease-fighting plant compounds (nary a vegetable to be seen under Kempner’s strictest watch). Let me go on record here: I TOTALLY stand corrected!

Perhaps the only areas of overlap with an ancestral framework are that all that rice would’ve provided a decent source of resistant starch, gluten was nowhere to be seen, and the uber-lean diet would’ve smashed polyunsaturated fat (PUFA) intake to smithereens. (If you haven’t caught wind of the PUFA-hatin’ yet, these fats are garnering quite a bad rap due to their unstable, oxidation-prone structure—especially omega-6 PUFAs, the pro-inflammatory Evil Cousins of omega-3s. But even PUFAs as a whole have taken a clobbering in some spheres (hello Ray Peat!), and higher-than-trivial intakes have been indicted as a cause of many terrible things.)

Indeed, after my AHS talk, a few people contacted me suggesting it may be the PUFA reduction that improved sugar metabolism and other aspects of health, thus allowing rice dieters to thrive on an otherwise nonsensical diet. And more broadly, that rock-bottom PUFA intake might be the biggest reason low fat, plant-based diets have any positive effect on chronic diseases to begin with. That would leave saturated and monounsaturated fat in the clear, needlessly nixed in the quest for better health.

I might be inclined to guess the same thing, if not for one human-sized monkey wrench by the name of Roy Swank.

Roy Swank: Kickin’ some multiple sclerosis butt… by nixing saturated fat


You might be familiar with our current diet-wielding, multiple-sclerosis-blasting warrior Terry Wahls, but less known is the fellow who preceded her by over half a century: Roy Swank. And what a story he had!

Swank exited the womb practically destined for greatness. Along with growing up near my beloved home city of Portland, young Swank was musically gifted, athletically inclined, and devastatingly suave. He spent his formative years wooing his future wife, Eulalia, in his dad’s mortuary hearse (chicks dig that stuff), and started driving a local doctor around town to see patients when he was just 13. It was then that his interest in medicine roared to life! By the time he was 26, Swank had racked up a Bachelor of Science, a PhD, a medical degree, and a fitting destiny for his surname.

But our relevant saga began in 1948, when Swank got invited to Montreal to research multiple sclerosis (MS)—a devastating autoimmune disease affecting the brain and spinal chord. He soon discovered a peculiar trend: across the globe, MS was rare in areas where saturated fat intake was low, but much more common where meat and dairy were a mainstay. And as he scoured disease patterns from the previous two decades, Swank noticed that World War II heralded a drop in MS rates wherever meat and dairy were rationed. The clincher came with a Norwegian survey he helped conduct, which showed MS was clustering around the country’s rural, mountainous, dairy-noshing farming regions, while coastal fishing communities—whose fat intake was lower and mostly polyunsaturated—were pretty much spared.

And you might get a kick out of this: when plotting MS prevalence against national intake of animal fat, Swank arrived at a perfect upward curve that was nearly indistinguishable from the one we vilified Ancel Keys for. Here’s Keys’ six-country graph overlaid with Swank’s MS data. Eerie, no?

From page 13 of

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!


FYI: average saturated fat intake for the lowest bracket was 17 grams per day; for the middle bracket, 25 grams per day; and for the highest bracket, 42 grams per day.

(In case you’re wondering, it didn’t seem to be a matter of having a longer but more miserable, enfeebled life for the low-fat adherents. As Swank noted, “Patients on our low-fat diet have been remarkably free of bacterial and viral infections, ‘colds and flu’ occur rarely, and recovering from urinary and other bacterial infections has been rapid when appropriately treated.” Indeed, quite a few measures of their health improved.)

The Swankers’ disease progression—as tracked by that neurological scale mentioned earlier—followed a similar trend. For the folks eating 20 or fewer grams of saturated fat per day, the disease remained relatively stable, with just over half a grade of progression (worsening) on average. But for the subset of folks eating between 20.1 and 30 grams per day, the disease progressed an average of 2.6 grades. And for those chowing down on more than 30 grams per day, the disease worsened by an average of 3.0 grades. (To help conceptualize that, a three-grade change is the equivalent of going from “mild physical impairments” to “confined to bed and chair.”)

Here are more Smurf-colored bars for the visually inclined:


And because I love me some graphs, here’s another one straight from Swank’s paper, showing the dramatic drop in exacerbation (flare-up) rates before and after folks got all Swanky:


Pretty impressive, no?

In addition to all this fun stuff, Swank commented (again, in his 1991 paper “Multiple sclerosis: fat-oil relationship“), that some patients needed an even steeper slash in their saturated fat intake—down to 10 grams per day, maximum—in order to “gain an improvement in energy and freedom from severe fluctuations of disease.” Swank wrote:

In recent years, this experience induced us to eliminate all meats and other sources of fat from the diet of many patients when first seen. We estimate that saturated animal fat was reduced to ~5 g/day plus the fractional or trace amounts of fat contained in many foods. It is our impression that these patients improved faster than others in whom this was not done.

In the vein of Devil’s Advocation, though, we should give our critical-thinking wheels a whirl and see if there are any alternative explanations for these findings. Could there be some suspicious lifestyle confounders like we see in studies today? Were saturated fats lumped in with hydrogenated ones and mutually given the boot, while only the latter was a true health-harmer? Was the supplementation of cod liver oil, chock full of omega-3 and vitamin-A-rich goodness, enough to explain the mortality patterns? Was the culprit saturated fat itself, or was it just guilty by association—maybe serving as a proxy for generalized I-Don’t-Give-A-Hoot-About-My-Health-itis, as the rebels who ignored Swank’s “eat less saturated fat!” message were more likely to ignore the “sugar is bad” or “vegetables are good” or “don’t run with scissors while chewing arsenic candy” messages as well?

As much as I love wailing my confounder alarms, I don’t think the usual suspects apply in this case. Here’s why!

  • Hydrogenated fats were indeed banned from the menu, but not until 1951—two or three years after folks started the diet, at which point they’d already seen profound improvements.
  • Likewise, cod liver oil (and other omega-3-rich fluid oils) weren’t allowed during the first couple years of the diet, and again, folks saw an 80% decrease in their MS flare-up rates during that time.
  • As for potential bad-guy carbs skewing the results? Remember, Swank developed his diet in the late 1940s—decades before refined grains and sugar joined the Dietary Villain ranks and were widely considered harmful. In fact, his diet didn’t restrict refined grains or sugar to begin with, so it wouldn’t make sense that a “screw it all” mentality would result in folks rebelliously downing processed carbs. (Heck, in Swank’s Multiple Sclerosis Diet book, there are plenty of recipes calling for white flour and sugar, and no indication that his patients—at least during the first few decades—were told to stick to whole-food sources of carbohydrate.)

And lest we wonder if the folks eating more saturated fat were also eating more of those gnarly, high-PUFA vegetable oils we so love to hate (thus obscuring the real relationship between saturated fat and MS progression): no dice! Swank’s data showed pretty clearly that the more saturated fat people ate, the less vegetable oil they were eating—an inverse correlation of -0.62 by the study’s 22nd year. Likewise, as Swank explained in the paper we’ve been discussing, higher unsaturated oil intake went hand-in-hand with better outcomes in terms of disability and mortality. The inclusion of vegetable oils “seemed to make patients feel better, increased their energy, and improved the condition of hair and skin,” even though Swank maintained they weren’t necessary for treating MS itself (since his patients took a fantastic turn for the better before those oils were added back to the diet).

Hence why I called Swank a “monkey wrench” a bit earlier on. In contrast to the theory that rock-bottom PUFA levels are the real reason very low fat diets work (while saturated fat would be an innocent, needlessly reduced bystander), Swank found the opposite to be true—that saturated fat had the strongest relationship with MS progression and mortality, while polyunsaturated fat levels could be scaled up or down without negatively impacting health. At least within that 10 to 40 gram range. And at least for multiple sclerosis (although mortality from other chronic diseases dropped during Swank’s diet as well).

That said, there is another possibility that could maybe, maybe, MAYBE be obscuring the saturated fat trend: Neu5Gc. This is a little sialic acid molecule that humans, rather uniquely, can’t synthesize. We produce a similar molecule called Neu5Ac, but lost the ability to make Neu5Gc after splitting from our last common ancestor with the great apes. Because gene mutations ‘n stuff. Other primates (and almost all mammals) can still synthesize Neu5Gc just fine!

Here’s why it matters: even though we can’t make Neu5Gc on our own, we can incorporate it into our tissues when we ingest it from food. And the prime sources of Neu5Gc happen to be red meat and dairy, the same food-vehicles that deliver most of our saturated fat. Because Neu5Gc looks like a foreign substance to our paranoid human innards, we’re capable of producing antibodies against it (although levels of those antibodies vary widely from person to person), which, in turn, can stir up all sorts of trouble. So far, we’ve got theories about a potential role for anti-Neu5Gc’s antibodies in systemic inflammation, cancer, heart disease, hypothyroidism, and also… WAIT FOR IT… multiple sclerosis. (See: “Why does multiple sclerosis only affect human primates?” and “Missing links in multiple sclerosis etiology. A working connecting hypothesis.“)


From “Quantitative analysis of sialic acids in Chinese conventional foods by HPLC-FLD,” 2014.

I waffled over whether to even include this speculation here, since Neu5Gc research is just a wobbly-kneed babe in the woods right now, and we’d need a lot more data before we could definitively link it to any disease. But, considering that 1) humans are the only primate that develops multiple sclerosis, 2) humans are the only mammal that can’t make Neu5Gc (and that produce antibodies against it), 3) multiple sclerosis tends to cluster around areas with a higher intake of Neu5Gc-containing foods (land meat and dairy), and 4) there’s a plausible mechanism linking Neu5Gc with the development of multiple sclerosis (through the effects of antibodies on the blood-brain barrier and axon-myelin unit)… well, all I’m sayin’ is it seems quite intriguing!

That said, Swank actually had some compelling, research-backed ideas about why saturated fat per se could trigger MS, which we’ll discuss in Part 2 of this post. It’s worth noting that he didn’t believe saturated fat causes multiple sclerosis, just that it “precipitates or accelerates it in susceptible individuals,” as he wrote in 1954. It’s not outside the realm of possibility that Neu5Gc somehow plays the role in the development of MS, while saturated fat, under specific conditions, aggravates it. So, even if this Neu5Gc stuff pans out, it doesn’t necessarily pardon saturated fat!

At any rate, we’re not quite at the end of Swank’s research rope. In 2003, he published the 50-year results of his never-ending study: “Review of MS patient survival on a Swank low saturated fat diet.” By that time, after 16 years of letting them do their own thang, he’d managed to track down 15 of his surviving participants and pull them in for interviews and in-person visits. They were all between 72 and 84 years old. (Swank himself was 94, and in case you’re wondering, was still goin’ strong until he passed away in 2008 at the age of 99). Amazingly, only two survivors needed help walking and had any sign of their disease; as for the others, Swank described it thusly:

The remaining 13 patients were remarkably well. They were very active, could care for themselves, could walk as necessary, and were normal mentally. … [They] stood and were active and unusually youthful looking, with very smooth facial skin devoid of wrinkles due to good subcutaneous circulation. They were all in friendly, good spirits, had joyful laughter, and generally quite youthful behavior. This study also indicated that patients with MS, if they rigorously follow the extremely low-fat diet proposed by Swank, which contains no more than 10 to 15 g/d of saturated fat, can expect to survive and be ambulant and otherwise normal to an advanced age.

Take note of that “good subcutaneous circulation” comment, because it’s at the crux of Swank’s theory about why saturated fat is harmful for MS patients (hint: it has to do with blood cell aggregation and oxygenation). More on that in the next blog-post installment! We’ll be coming back to some of Swank’s research and ideas when we discuss the science behind why low-fatting works, because he’s just that awesome.

In the meantime, we’re hardly done with our historical saga. Next up is another obscure figure from the dusty, carb-encrusted pages of science’s past: Lester Morrison.

Lester Morrison: ???

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.


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:


The Casa Del Mar building, later transformed into Pritikin’s healing grounds. From Santa Monica Library Archive.

It was in this magical palace, wringing patients through a 26-day diet overhaul and hawkishly watching their food intake, that Pritikin could document the effects of his program on a large-scale basis.

And document he did! Although his reputation was that of a heart-healer, Pritikin’s diet did far more than assuage troubled arteries. Just as Kempner saw, the uber-fatlessness had the fortunate side effect of rapidly—and often permanently—healing diabetes. The earliest PubMed-able record of Pritikin’s success with diabetics came in 1976, with this little gem:

(FYI: Pritikin’s name isn’t on this paper, but it darn well should be. Scandalous tidbit alert! In 1974, Pritikin divulged the details of his diet to a Dr. James W. Anderson—an internationally acclaimed diabetes researcher at the time—and proposed an official study to test the uber-low-fatness on diabetics. Pritikin designed every detail of the study, drummed up $10,000 to fund it, created meal plans, and then received a grand total of zero credit for any of his contributions once the study was completed and published. In fact, Anderson proceeded to repackage Pritikin’s diet under a different name (the “HFC Diet,” standing for the “High Fiber, High Carbohydrate Diet”) and claimed it as his own invention—conducting a number of additional studies so successful that, in 1979, the American Diabetes Association was inspired to downsize its recommended fat intake. Despite years of haranguing Pritikin for more funding money (and thanking him profusely in their private correspondences), Anderson never publicly mentioned his collaboration with Pritikin or credited him for originating the diet. Buuuurn.)

So what was this study all about? For one week, 13 diabetic men—all who needed either insulin or oral drugs to control their blood sugar—ate the standard American Diabetes Association diet of the time: 34% fat and 43% carbohydrate, the rest made up of protein and wishful thinking. After that, they spent at least two weeks in Carbsville, eating a diet of only 9% fat and 75% carbohydrate. (The two diets were isocaloric, meaning they had the same number of calories, and were designed to help folks maintain their weight rather than lose or gain any.)

Surely that carb palooza sent their blood sugar into a frenzy! …Except it didn’t. After switching from the ADA diet to Pritikin-hijacked-by-Anderson one, nine patients had their insulin and oral drugs completely discontinued—at which point their fasting blood sugar was actually lower than it had been when they were still on medication. (The cutoff for drug discontinuation was a fasting blood sugar of 120 mg/dL.) It only took nine days of low-fatting to make that happen! Another patient’s insulin needs dropped from 28 to 15 units per day. As a further head-scratcher, fasting triglycerides, contrary to what we might expect, dropped significantly for ten men. The only folks who didn’t see any benefit from the 9% fat diet were the three who had the most advanced diabetes at the study’s onset—needing 40 to 55 units of insulin per day.

A tabular and graph-ular representation of changes in fasting blood sugar, in case you’re curious:



Even more intriguing, those results weren’t just a result of weight loss. Only five patients dropped more than three pounds, and there was no difference in fasting blood sugar and triglyceride levels between them and the weight-stable folk. And most importantly, the results seemed to stick: after the study, the nine most successful patients were weaned onto more flexible diets—60 to 65% carbohydrate instead of 75%. And after at least four months of followup, the researchers noted their blood markers hadn’t changed and the “control of the diabetes has been satisfactory without any drug therapy.” Pretty neat, huh?

Okay, okay: this study was tiny and used only men and we could find plenty of things to complain about (more womenfolk! Longer time frame! More Instagram pictures of the researchers’ feet overlooking exotic and envy-inducing locales!). Those are fair criticisms, to be sure. But this study does offer something we hardly ever see: a direct comparison between a Swampland menu (34% fat) and a Carbosis menu (9%), with the subsequent revelation that Oh hey, they actually have totally different results!

Again, as I’m trying to hammer home in this post, most of our “low fat” studies are actually only comparing different shades of Swamplandness—without ever hitting that fantastical 10% that brings a dramatic metabolic shift. And that makes us think that low fat is just a sham that does nothing except make our food taste like rabbit chow. So finding a study-gem like this, where fat intake actually does dip into the magic zone, and where the impressive results challenge our “low fat is bunk” narrative, is a rare and valuable find—even if it could be better designed.

That said, we’re in luck because Pritikin actually published some of his own studies on diabetics, and they were bigger and longer. Two of those papers came out in 1982 and 1983, respectively:

  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:


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.


Hi, James!

And while part of me would love to sit here and write about EVERY SINGLE ONE of those studies in attempt to explode the internet with Literally the Longest Blog Post Ever, another part of me—the part that realizes even the most patient of my readers have sanity limits and day jobs—has vetoed that plan in favor of a briefer sampling. Behold!

ESCAPE HATCH FOR THE FATIGUED OF BRAIN: what follows is a pretty long and sciency scroll of scientific scienceness. I know this blog post is big. I know your brain is turning into soup. CLICK HERE if you want to bypass the study summaries and get back to Pritikin’s life narrative!

Note: the Pritikin Program involves both the Pritikin diet and an hour of daily walking. Although we could definitely consider exercise a confounder (since it can independently improve metabolic and hormonal markers), studies of walking alone haven’t demonstrated anything nearly as dramatic as what’s been achieved with the Pritikin Program. At best, we could wager that walking probably boosts the results of the program, but only contributes to a fraction of its overall effects.

Another note! Unless otherwise mentioned, all the studies below allowed an ad libitum (non-calorie-restricted) energy intake. The participants could eat as much as their hearts desired out of any Pritikin-friendly item except for fish and poultry, which were capped at three servings per week (combined).

Prostate Cancer Protection

  • Long-term adherence to the Pritikin Program was a major boon for squashing out insulin resistance and reducing prostate cancer risk. Folks who followed the diet between 1 and 28 years reduced fasting insulin by 52%, fasting glucose by 20%, HOMA IR (a measure of insulin resistance) by 62%, and fasting triglycerides by 45%. And in a group of overweight men, even a quick jaunt on the program (two weeks) reduced fasting insulin by 30%, fasting glucose by 14%, HOMA IR by 40%, and fasting triglycerides by 33%. Not impressed yet? Blood from the Pritikin-fed fellows (both two-week and long-term) drastically slowed the growth of prostate epithelial cells, suggesting benefit for the prevention of prostate cancer.

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


  • In a similar study of both short-term (11 days) and long-term (average 14.2 years) Pritikin followers, more evidence of prostate cancer protection emerged. The short-termers saw a 20% drop in insulin-like growth factor 1 (IGF-1) levels and a 53% rise (that’s a good thing!) in insulin-like growth factor binding protein 1 (IGFBP-1); the long-termers saw a solid 55% drop in IGF-1 and 150% rise in IGFBP-1. (IGF-1 has been strongly associated with cancer due to its role in regulating cell growth and death, and and IGFBPs are proteins that bind insulin-like growth factors and neutralize some of their unsavory activities.) Likewise, the short-term group saw a 25% drop in fasting insulin levels and the long-term group saw a 68% drop. As with the previous study, both groups’ Pritikin-ified blood was particularly awesome at fighting cancer: the serum from the short-termers caused a 30% decrease in the growth of LNCaP cells (a line of human prostate cancer cells) and serum from the long-termers caused a 44% decrease, compared to baseline. Both groups’ blood also increased the rate of death for those cancer cells.
  • Yet another study of Pritikin dieters (27 obese men) showed the program may be an excellent defense against the disease: the men saw a 28% increase of sex hormone-binding globulin (which binds androgens and appears to help protect against prostate cancer) and a 43% drop in fasting insulin; for three men who started out with slightly elevated PSA (prostate-specific antigen) levels, the diet also reduced that. According to the researchers, “The increase in SHBG would result in more testosterone being bound and, therefore, less of the androgen available to act on the prostate. The decrease in insulin might also decrease mitogenic activity in the prostate.”
  • One more on the prostate front! An analysis of post-Pritikin-Program blood shed light on the mechanisms behind the aforementioned anti-cancer effects: apparently, the Pritikin Program reduced tumor cell inflammation and resulted in lower NFκB activation in LNCaP cells. (NFκB, or “nuclear factor kappa-light-chain-enhancer of activated B cells” if you want to be fancy about it, is a protein complex involved in DNA transcription, cell death, and cytokine production.) The program’s results also seemed to hinge on reducing IGF-1 levels, because when the researchers added back IGF-1 back to the participants’ squeaky clean, post-Pritikin-Program serum, the results were completely reversed:

From “Analyzing serum-stimulated prostate cancer cell lines after low-fat, high-fiber diet and exercise intervention.” Barnard, et al., 2011.

Reduced LDL Oxidation and Spiffed-Up HDL

  • Three weeks on the Pritikin Program resulted in LDL particles that, even by paleo- and low-carb-advocate standards, were much less likely to oxidize and promote heart disease. In a group of 80 Pritikinning men and women, average LDL particle size increased (with larger LDL considered less atherogenic), and 27% of the folks who’d started out with LDL pattern B switched to LDL pattern A (again, considered less atherogenic). In vitro, the participants’ LDL also became more resistant to copper-induced oxidation—with a 21% drop in initial oxidation, 13% increase in lag time (the delay before oxidation happens, as the LDL’s antioxidants become depleted), a 20% reduction in peak diene formation (a way to measure oxidation), and a 17% reduction in maximal rate of diene formation. All of that jargon basically means the LDL had become far more resistant to oxidation—at least based on this particular assay (there’s always some uncertainty about how well in vitro (outside the body) studies translate to in vivo (inside the body)).

From “Effects of diet and exercise on qualitative and quantitative measures of LDL and its susceptibility to oxidation.” Barnard, 1996.

  • Similarly, a study in postmenopausal women found that the Pritikin Program led to more oxidation-resistant LDL particles.
  • Even though the Pritikin Program often reduces HDL (the so-called “good cholesterol” lipoprotein), it makes the existing HDL that much awesomer. A study of obese men found that after three weeks in Pritikin Land, the HDL inflammatory index (AKA the ability of HDL to prevent LDL from oxidizing) changed from “pro-inflammatory” to “anti-inflammatory.” The activity of platelet activating factor acetylhydrolase also increased, LDL decreased by 26%, and triglycerides decreased by 29%. Basically, even though HDL was lower than at baseline, its function was mucho improved—”suggesting increased turnover of proinflammatory HDL,” according to the researchers.

From “Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors.” Barnard, et al., 2006.

Breast Cancer Protection

  • In postmenopausal women, the Pritikin Program fantastically improved the major metabolic and hormonal risk factors for breast cancer: on average, insulin dropped 29%, insulin-like growth factor 1 (IGF-1) dropped 19%, insulin-like growth factor binding protein 1 (IGFBP-1) increased 32%, estradiol (among women who were on hormone therapy) dropped 34%, and estradiol (among women who weren’t on hormone therapy) dropped 37%. In vitro, serum from those Pritikinettes dramatically slowed the growth (and induced apoptosis, or programmed cell death) in three breast cancer cell lines (MCF-7, T-47D and ZR-75-1) compared to blood from the same ladies before they’d started the diet.
  • In a study of pre-menopausal women, two months of the Pritikin diet led to some fun breast-cancer-protective hormonal changes: serum estrone and estradiol (types of estrogens) fell during the women’s early folicular and late luteal phases (with decreases ranging from 18% to 26%), with no negative impact on ovulation. (Exposure to ovarian hormones, especially estrogen, appears to increase breast cancer risk, so these changes could be expected to reduce it.)

From “Effects of a very low fat, high fiber diet on serum hormones and menstrual function. Implications for breast cancer prevention.” Barnard, et al., 1995.

Colon Cancer Protection

Heart Disease, and Related Adventures

  • Here’s a goodie called, “Effects of an intensive exercise and nutrition program on patients with coronary heart disease: Five-year follow-up.” (There’s no link because for some awfully frustrating reason, this paper is nonexistent online, and I was only able to track it down via the library. Email me if you want a PDF copy!) This study followed the progress of 64 Pritikin adherents with coronary heart disease, five years after they left the sheltered, intensive clutches of the residential program. Prior to entering the program, 59% of the patients had experienced a heart attack and 80% had angina (chest pain). During that five-year follow-up, four people died (one of cancer, two of a heart attack, and one of heart failure during a mitral valve replacement), and two additional folks had non-fatal heart attacks. Reports of angina dropped from the initial 80% to only 32%. Fascinatingly, despite the fact that this was a highly diseased group with the odds stacked against them in terms of morbidity and mortality, their annual death rates ended up being close to that of the “regular” population after they Pritikinized their lives! (At the time the paper was written, post-heart-attack mortality was around 10 to 15% for the first year following the event, and as high as 50% by the third year.)



From “Effects of an intensive exercise and nutrition program on patients with coronary heart disease: Five-year follow-up.” Barnard et al. J Cardiac Rehab 1983;3:183-190.

  • In 31 obese men, the Pritikin Program brought awesome improvements in a huge range of risk factors for heart disease—including blood lipids, oxidative stress, inflammation, and cell adhesion. After just three weeks, there were significant drops in LDL (25% lower), triglycerides (28% lower), fasting glucose (12% lower), insulin (30% lower), HOMA IR (33% lower), C-reactive protein (39% lower), soluble cell adhesion molecules, inflammatory cytokines, and monocyte adhesion. And to sweeten the deal, nine out of the 15 men who entered the program with an official diagnosis of metabolic syndrome no longer met diagnostic criteria by the time their three weeks of low-fatting was up.
  • In 15 hyperlipidemic men, two weeks of the Pritikin bootcamp improved a number of risk factors for heart disease: it lowered the men’s blood pressure, slashed triglycerides, reduced the aggregation velocity and maximum aggregation of platelets, and reduced the formation of thromboxane (which is made by platelets and promotes blood clotting and constriction of blood vessels).
  • Combined with daily aerobic exercise, the Pritikin diet facilitated major improvements in myocardial blood flow. After six weeks, resting blood flow decreased by 12%, and hyperemic blood flow increased by 9%—leading to an improved myocardial flow. (It’s impossible to know how much diet versus exercise played a role in these results, though!)
  • In postmenopausal women on hormone replacement therapy, the Pritikin Program heralded some promising changes on the heart-disease-protection front. After just two weeks, 20 women saw significant drops in their BMI, glucose levels, insulin levels, all serum lipids, and HOMA IR. The researchers conclude that these “rapid improvements may reduce the risk of acute myocardial infarction (MI), and if sustained, these changes may mitigate the risk for atherosclerosis progression and its clinical consequences.” Not too shabby.
  • In a small study of 11 men, the Pritikin Program appeared to be uber protective against atherosclerosis progression. In the span of 21 days, the program dropped LDL by 23%, triglycerides by 41%, fasting insulin by 46%, and fasting blood sugar by 7%. Serum 8-iso-PGF 2 alpha (a product of lipid perodixation) also sank, whereas nitric oxide availability rose. In Barnard, et al.’s words: “The present study is the first to show that unrestricted consumption of a low-fat, high-fiber diet and daily exercise can mitigate oxidative stress, improve NO availability, and normalize BP in obese men within 3 weeks.”

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


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

Diabetes Damage Control!

  • For 70 diabetics, a 26-day jaunt in the world of Pritikin led to all sorts of disease-blasting perks: fasting blood sugar fell by 24%, blood pressure dropped by 10%—and even better, 71% of the folks who’d been taking oral hypoglycemic drugs pre-Pritikin were able to ditch their prescription (ditto for 44% of the folks taking insulin and 61% of the folks who’d been taking blood pressure medication)! Also, VO2max (“functional maximum oxygen uptake) improved by 41%.
  • In diabetic men, a three-week Pritikin Program reduced heart-disease risk factors associated with diabetes: the program whipped down fasting glucose by 20%, dropped fasting insulin by 30%, and totally clobbered markers of oxidative stress, inflammation, and monocyte-endothelial interaction (a major part of the heart disease process). Boom!
  • Among 652 non-insulin-dependent diabetics, three weeks of the Pritikin Program significantly improved their condition: fasting glucose dropped by 16%, and 71% of folks taking oral hypoglycemics (and 39% of the folks taking insulin) were able to discontinue those medications. Triglycerides and blood pressure also fell to delightful new lows.
  • In diabetics, the Pritikin Program reduced fasting insulin in diabetics by an average of 33% in just three weeks, and restored normal fasting insulin levels in 59% of insulin-resistant folks in the same time frame. (Triglycerides also dropped across the board!)

In the Elderly

  • Among 70 folks aged 70 and older (average age of the group being 78.7), 26 days of the Pritikin Program totally spiffed up their health: they lost an average of five pounds, total cholesterol and triglycerides fell significantly, their treadmill performance increased by 49%, the type II diabetics of the group reduced their fasting blood sugar by 27%, and half of the patients taking blood pressure medication were able to discontinue it.

But What About the Children?!

  • In overweight and normal-weight children, two weeks of the Pritikin Program yanked down multiple cardiometabolic risk factors: insulin levels fell (by 28.1% in overweight kiddos and 52.5% in normal-weight kiddos, respectively), HOMA-IR fell (28.4% and 53.1%, respectively), leptin levels fell (44.1% and 69.3%, respectively), and a variety of proinflammatory cytokines were reduced (molecules that increase inflammation in the body). LDL went down by 24.5% and 29.4%, while HDL hardly budged. Those changes didn’t correlate with weight loss, either!
Effect of Pritikin Program on inflammatory cytokines

Effect of Pritikin Program on inflammatory cytokines. From “Effects of an intensive short-term diet and exercise intervention: comparison between normal-weight and obese children.” Barnard, 2013.

  • Also in children, two weeks on the Pritikin Program (for 19 overweight kiddos) massively improved factors associated with heart disease: the program tanked LDL by 25.3% and triglycerides by 39.5% (HDL didn’t significantly change); 8-isoprostaglandin F2 alpha (a marker of lipid peroxidation) fell by 81%, CRP fell by 41%, and MMP-9 (a measure of plaque stability and progression) fell by 49%. Markers of endothelial cell activation (ICAM-1 and sE-selectin) also went kerplunk! As the researchers summed it up:

    “The primary findings of this study provide evidence that even a short-term lifestyle modification program may (1) improve the lipid profile; (2) decrease production of the reactive oxygen species superoxide and hydrogen peroxide and increase NO production; (3) decrease endothelial cell activation and adhesion; (4) decrease inflammation; (5) decrease monocyte chemoattraction; and (6) decrease MMP-9, a marker of plaque destabilization, all of which may contribute to a reduction in atherosclerosis progression.”


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


  • WE’RE NOT DONE WITH YOU YET CHILDRUNS. Yet another study on overweight youth found, again, a massive drop in insulin (33%), HOMA-IR (29%), triglycerides (40%), systolic blood pressure (10%), diastolic blood pressure (10%), and LDL (27%), with no change in HDL. All seven of the kiddos who were classified with metabolic syndrome at the start of the study had reversed their diagnosis by the end of it!

And that’s just a freakin’ handful of the research out there. Seriously. A handful. If you want to venture into the full-on Pritikin Research Safari, I recommend bringing snacks and water, ’cause you’ll be gone awhile!

Just to be clear, I’m not trying to say that the Pritikin Program is wildly successful for everyone who jumps aboard, or that it’s unequivocally the best treatment for the diseases it’s been used for. The point I want to make is more conceptual than anything. Contrary to the belief that low-fat, high-carb diets raise insulin levels, muck up glucose control, encourage obesity, and promote inflammation, the overwhelming majority of studies published on the Pritikin diet have shown the polar opposite. That doesn’t mean there isn’t a range of outcomes within each study; indeed, some participants do well, some do really well, and some don’t do well at all, even when the collective effect is positive. But seriously, the Pritikin Program yields impressive results, and it’d take a whole lotta’ somersaults of logic to conclude otherwise.

I know your brain is probably maxed out on scienceness now, so let’s resume our narrative of Mr. Pritikin’s life! First up, an interesting parallel between his way of thinking and that of the modern Paleo community.

In the early ’70s, Pritikin wrote a three-volume opus compiling his theories—dotted with hundreds of scientific references—about every major condition of the time: atherosclerosis, angina, high blood pressure, gout, arthritis, gallstones, kidney stones, diabetes, lung cancer, colon cancer, prostate cancer, breast cancer, as well as hearing and vision diseases. He was convinced they were all, essentially, manifestations of a huge mistake called “What Americans Typically Eat.” In fact, Pritikin had a fascinatingly ‘ancestral’ approach to nutrition (back at a time when linking diet to chronic disease period was considered cuckoo for Cocoa Puffs), which he discussed in the introduction to his three-volume work:

Such a postulation linking diet and the scourge of degenerative diseases may seem far-fetched, until one reflects upon some basic biological facts. All animals, man included, have a diet that emerged from the long-term experience of the species in nature over many thousands of years. Now, man no longer eats foods his body was designed to eat, but has created a synthetic diet—the penalty of which is to endure the adverse effects of short-term experience. The more man’s diet departs from foods to which he is biologically suited, the more the adverse effects.

Whereas the modern incarnation of Paleo has drawn heavily from higher-fat-eating societies (the Inuit and Masaai are particularly cherished), Pritikin found dietary consistency among the starch-based populations: the Tarahumara Indians, the Bantu, and the natives of New Guinea, whose traditional low fat intake and virtual freedom from heart disease fed into his overarching philosophy about food. Just keep that in mind if you find the idea of low-fat eating to be ancestrally preposterous!

For what it’s worth, Pritikin certainly walked his talk. Before his mortal departure, he’d requested an autopsy be performed so the world could have an honest look at his once-diseased heart. The results were published in a New England Journal of Medicine article called “Nathan Pritikin’s heart,” where the state of his ticker blew the pathologist away:

The epicardium was smooth, and no scars were visible. The endocardium and all valves were normal. … The coronary arteries were soft and pliable … there were no raised plaques and no compromise of the lumens. No clots were present. … No infarcts of any size, or other finding referable to vascular disease, were present in any organ.

The report concluded, “In a man 69 years old, the near absence of atherosclerosis and the complete absence of its effects are remarkable.”

Important note on Pritikin’s death: Critics of Pritikin (Priticritics?) often point to his departure from the world—death by suicide, amidst a painful battle with leukemia—as evidence that his low-fat diet either pulverized his mental health (suicide) or gave him cancer (leukemia). Those are both pretty bold claims, so let’s take a moment to assess them.

In the 1950s, Pritikin went through a series of high-dose radiation treatments for a skin condition, pruritus ani, that was stubbornly resisting all the pills and ointments he tried. Over the course of two months, he got blasted with a total of 220 rads (“radiation absorbed doses”) of unfiltered x-rays—the equivalent of getting 3700 chest x-rays or 22 million dental x-rays. Not surprisingly, it wreaked havoc: he soon ended up with a blood condition he’d battle for the rest of his life, later diagnosed as a rare form of leukemia. That all happened before he embarked on a low-fat diet.

Pritikin actually managed to keep his disease in remission for almost three decades, but in late 1984, saw an unfortunate resurgence of symptoms—including leg swelling so severe that he had to stop going on his beloved daily runs. His docs ushered him onto some experimental chemotherapy, telling him it was the only way he could ever resume jogging. Not only did the chemo not help, it also left Pritikin with crippling anemia, kidney failure, diabetes, all-consuming pain, and 30 pounds stripped off his already slender body. In February of 1985, he flew out to New York for a second opinion, was told his case was hopeless and he would certainly die within the next six months, and proceeded to take his own life in a hospital bed in Albany.

As George McGovern reflected, “He was always in charge of his life. It rather followed he’d want to be in charge of his death.”

With all that in mind, can we implicate Pritikin’s diet in his sad demise? With enough mental gymnastics and anti-low-fat bias, sure—but I don’t think it’s particularly logical or fair. Did his diet shorten his life, or lengthen what was originally a grim prognosis? And if we make an automatic diet-death jump, should we do the same for the recent passings we’ve seen in the high-fat community (low-carb guru Barry Groves, saturated-fat-redeemer Mary Enig, or “Carbohydrates Can Kill” author Robert Su)?

As drawn as our human brains are to stories and anecdotes, I think it’s wiser to look at bigger, statistically stable data instead of case studies. Everyone has to die of something, and food isn’t the only tool of the grim reaper.

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.

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.


  1. This is an excellent review of importance of fats, protein and carbohydrates on the prevention, treatment and reversal of major chronic diseases in the United States.

    I highly recommend this post to traditional and integrative physicians, as well as their patients.

    1. I just yesterday returned from a (Dr. John) “mcDougal 3-day weekend” that included Drs. Colin Campbell, Caldwell Esselstyn ( your grandpa wanna be, Denise), Michael Greger (author of How Not To Die), John McDougal, and several other like minded souls. Denise, these folks all follow a whole grain, plant based diet that you describe in your blog about Dr. Esselstyn and they are all strict vegans. Surely you know this so can you make the leap that yeah, there are more roads to Dublin, and a whole food plant based (WFPB) diet is one of them? Even if your analysis, for arguments sake, of The China Study is correct, Colin Campbell’s conclusion is to eat a WFPB diet, in his case a strict vegan diet. Can you declare that while his study had many faults yet his diet is in fact one road to Dublin?
      Ps you should come to one of Dr. McDougals events, with a disguise, maybe, but an open mind, which your discussion in this blog in general, and about Dr. Esselstyn in particular, convince me you have in spades. I love to read your blog, even if I come from the dark side (vegan), because I want to read both sides of this issue, health.

      1. Denise does not need a disguise as she has given her apology. She should come as she is. I applaud Denise for this superb article. There is a Turkish proverb that reads: “No matter how far you have gone on the wrong road, turn back.” Denise has done that and I give her kudos to admit some of the earlier faults and now become more of the writer she has become.

  2. There is something in all of this. Of course not everyone does well on high fat, low carb, high carb or low fat. We are all unique individuals. For people with metabolic syndrome who fail to lose weight on any diet, the scientific evidence seems to report better results with low carb high fat. But I am sure there are exceptions to this. Only the individual person can decide what diet is best for them. I had metabolic syndrome and the very low carb high fat diet did wonders for me, I am now a normal sized person, my diabetes has improved immensely. But I cannot digest fat very well, no gallbladder. I have since moved to eating lots of fruit and very little animal products and am continuing to lose weight without any negative impact on my blood sugars. So there are two extremes and they both had a purpose for me, but at different times, and they both worked well. There is no reason to think that one philosophy of eating is the only way to eat forever. We change. I believe as long as your diet is not full of processed foods, the unhealthy fats, and sugars – either low fat or high fat could be appropriate.

  3. OMG, I love that you wrote this post. I can’t wait to delve into this. But I first wanted to say how much I appreciate that you are on the scene. Finally, something that ties together the success of super low-fat plant-based diets and LCHF diets. Thank you Denise!!!!

  4. You are missing one key point. Not all fats are bad. In fact, essential fats are essential for cell homeostasis and cannot be made by your body. They are called essential fatty acids. Your low fat diet will starve your body for these essential fats causing a host of symptoms and facilitate over 60 chronic diseases according to the National Academy of Science. Your program is sound for trans, saturated and monounsaturated fat. It is dangerous for ignoring the need for essential fat which can easily be verified.

    1. And how much of these “essential fatty acids” does one need to get these alleged benefits? Nowhere have I seen it to be more than a couple of grams per day, which can covered by only a couple of eggs.

      1. I wish the answer to your question was simple. But it isn’t because each person responds to nutritional inputs differently for a number of reasons. For example, genetics is a huge wild card in fatty acid metabolism. That is why the “one size fits all” numbers you quote are incorrect and dangerous for some people.

        Thankfully there is a simple affordable pin prick serum mail-in test that will generate a comprehensive 3 page report of your complete fatty acid profile. Based on gas chromatography, it provides research-level accuracy that is certainly appropriate for consumer use. You can read about the technology here:

    2. You obviously haven’t heard that there is no such thing as an essential fatty acid. Once again, scientific fact becomes scientific false. Maybe Denise will do a blog post on this.

      1. I refer you to:

        The National Academy of Sciences which links 60 chronic diseases to Omega 3 essential fatty acid deficiency.

        The National Lipid Association that states the deficient Omega 3/6 ratio of the general public impacting all chronic diseases.

        The International Society for the Study of Fatty Acids and Lipids position papers

        Behind each statement are hundreds of studies supporting essential fatty acids.

        Please cites your studies that conclude “there is no such thing as essential fatty acids”.


          In 1938, a biochemist William Brown volunteered to go six months eating an extremely low-fat diet. He consumed a diet of defatted milk and cottage cheese, sucrose, potato starch, orange juice and some vitamin and mineral supplements. His blood lipids became more saturated and their concentrations of linoleic and arachidonic acids were cut in half. He experienced an absence of fatigue, his high blood pressure returned to normal, and migraines he had suffered from since childhood vanished, his metabolic rate increased and he lost weight, his respiratory quotient increased suggesting greater carbohydrate oxidation, lower respiratory quotients are associated with diabetes. The diet produced no deficiency, and likely corrected a PUFA excess. Six months on a specially prepared laboratory diet, no deficiency, if these fats are essential they’re essential in such tiny amounts that its almost meaningless to call them essential.


            1. 1 day’s supply of Vitamin D3 is ~125ug. ∴180 days’ supply of Vitamin D3 is ~22.5mg.
              1 day’s supply of EFAs is ~2g. ∴180 days’ supply of EFAs is ~360g. That’s a lot to store!

            2. Hi, Certain conditions, related to fat assimilation, prevent vitamin D storage, as Dr Trevor Marshall discusses in one or more videos on YouTube.

          1. Your cited review references classic studies and is very interesting in that, even though it dates to 1938, nothing in it is directly contradicted by the voluminous contemporary science I’ve read to date. But the INTERPRETATION of study results has changed greatly from yours. And there are some curious anomalies.

            For starters, the title includes the phrase “prolonged use” of the extremely low fat diet and yet the study is only over a few months and the conclusions specifically warn, “it cannot be assumed that the human subject could subsist indefinitely on a diet completely devoid of the unsaturated fatty acids”.

            All the observed good results you cite are due to reducing saturated fat in the subject diet, which is a really good thing on which we can all agree. But your interpretation that, “The diet produced no deficiency, and likely corrected a PUFA excess.” is dead wrong in light of new findings.

            Here is what is happening. Some of the stored fats in the human body are the essential ones which it draws on when the subject does not consume them. That is why immediate deficiency symptoms did not occur. Yet your study reports serum level of essential fats dropped by almost HALF. So the subject was in significant deficiency of essential fats and his body made up for it by drawing down on stores it had accumulated.

            A further complication is that the stored essential fat is mostly omega 6 because there is a huge amount of it in the modern diet. But a quicker major deficiency of omega 3 fat is inevitable. Since both level and ratio of these fats are deemed to play a role, reducing the excess omega 6 in fat stores is probably good as you claim. But the major problem is a GROSS DEFICIENCY of omega 3s. This is why the ISSFAL recommendation I cite posts no safe limit on omega 3 fat intake but a likely limit to omega 6 fat.

            The easy solution for consumers is to do the simple serum test which embraces contemporary science to determine their essential fatty acid status and then be guided by test results.


        2. I’m not discounting the deficiency in EFAs, as I’ve read about a rare case of it, but I just wonder how one, living a modern lifestyle would be unfortunate enough to develop such a deficiency. EFAs in all their forms are either added to our foods or naturally occur in fish and some plants. Even on an intentionally low PUFA diet like Peat’s it’s nearly impossible to go under 4g without compromising calories and nutrient density.

          And by the way, out of pure ignorance, what would constitute a deficiency? I’m not sure if the FDA/ AMA has made recommendations regarding the minimum daily value. Would such a deficiency stem from intentional avoidance or a genetic/ physiological malfunction?

          I also think the term “essential” is loaded with meaning. The public would understand essential as “necessary (for health) when in the original scientific terminology essential described fatty acids that, unlike cholesterol, cannot be produced by the body.

          I think Ray Peat’s argument (and his proponents) raise the question: If our body cannot produce them on its own, we must be able to survive without them? (The human body is often programmed to be able to sustain itself.) I’m not settled on this since I can’t see a logical reason to avoid fatty (and tasty) things like avocados, fish and olive oil. But I don’t know… I’m trying it out!

      2. Forsythia, salbers12 is right, omegas 6 and 3 ARE essential. Check out Susan Allport’s book “The Queen of Fats” for a great case example of someone suffering from too little Omega-3

    3. It is actually very difficult to avoid “essential fats”. You can go without nuts and seeds and olives and avocado, but all fruit and vegetables have some pufa!

      1. Your ignorance is dangerous. All pufa are not essential. It’s almost impossible to avoid the w6 essential fatty acid, linoleic acid found in seed oils, but the w3 essential fatty acids – linolenic acid or the elongated versions EPA and DHA – are simply not found in the diets of 25% of Americans according to William Lands. Since the same enzymes process both families and the prostaglandin progeny of w6 fatty acids are overwhelmingly inflammatory, while the prostaglandins derived from w3 fatty acids are anti-inflammatory, we are more or less likely to suffer chronic inflammation according to the w6/w3 ratio of our diets. Japan wins, we lose. “The potential attributable burden of disease ranged from 20.8% (all-cause mortality in men) to 99.9% (bipolar disorder)” Read and salve your ignorance.

        1. That paper assumes that differences in dietary percentages of “essential” fatty acids are responsible for mortality differences between Japan and the US!

          It also assumes that the ratio of n6 to n3 should be at lower.

          It then makes recommendations based on those assumptions.

          The best advice from that paper is to consume fewer n6 fats.

        2. An excellent citation that agrees with my extensive reading. I’m not entirely clear on several statements that may be worth exploring. The National Academy of Science now links over 60 chronic diseases to omega 3 deficiency. So it seems a pretty safe correlation whether it is justified by this paper or not. The the optimal cellular-level target appears to be equal amounts of LC omega 3 & 6 FA. How best to achieve this is the question? Two serum measurements that bear on this are the LEVEL of LC omega 3 and the RATIO of LC omega 3s to 6s. Both need to be addressed. For example, if the ideal ratio of 1 to 1 is achieved but the level of omega 3s is too low, there is not enough present for optimal cellular function. Additionally, if the optimum level of LC omega 3s is present but the ratio is too high the the omega 6s swamp cell receptors so that the 3s are not absorbed. The best plan is a personal blood test and be guided accordingly.

          1. I have begun sprinkling flax seeds and chia seeds, both excellent sources of 3’s, on one or two of my meals each day. I’ve cut out all animal products so have reduced my 6’s. Wanna make sure you actually use the stuff and don’t leave it in a container in the fridge? Go to the store ( I found it at Bed Bath and Beyond) little containers that you put the seeds in and are really easy to access and pour. Makes a big difference in how readily you use the stuff. I do it every day without thinking now. Experiment with different containers until you find the easiest. I did.

            1. The root source of DHA is algae: fish eat the algae and the DHA climbs up the food chain. The ALA that is in plants CAN be converted to DHA, but some people do it better than others. Seems to have to do with your genetics … people who lived inland have better ability to convert plant omega-3’s into the longer ones that people need. Anyway, if one does not want to eat fish for whatever reason, the next-best source is algae. supplements.

              “By now, everyone has heard that omega 3s are good for your brain. However, omega 3 is a generic name for a family of fats. Docosahexaenoic acid (DHA), a specific type of omega 3 found in fish, krill and algae, is what your brain is made from. While humans have the ability to convert the type of omega 3 in walnuts and seeds into DHA, new research has shown that the degree to which these omega 3s are converted is dictated by your genes.”


              I think this is particularly important for vegan women that are planning to have children. The development of the brain is very much dependent on the amount of DHA in the mother … if the mother is not genetically able to convert flax seeds to DHA, the baby will suffer.

        3. Um, Jonathan, YOU need to learn what you’re talking about before you start shooting off your arrogant piehole. First, learn what “essential” means in the context of nutrition. An essential nutrient is a nutrient required for normal human body function that the bod either can’t synthesize at all, or not enough for good health. The 18C omega fats linoleic acid and alpha-linolenic acid ARE indeed essential–we have to ingest them. As far as longer-chains, EPA and DHA, we can make them from ALA, but conversion rates are low enough (~8–21% to EPA, 0–9% to DHA) as to make them conditionally essential. You are correct that we can easily obtain w6 from our diet, but we don’t really know the minimum levels for w3. Nor the ideal 6:3 ratios: 2:1? 4:1? Read that “Queen of Fats” book and you’ll see a test case that went for years without any w3 before starting to suffer overt systems. Some people eating ancestral diets, e.g. the Pima Indians in Arizona and their Tarahumara cousins in Chihuahua State, were plenty healthy before Euro intervention even though these inland desert and arid land dwellers ate diets rich in beans and corn and got far less EPA and DHA than the Japanese, Inuit, and other peoples living near cold-water seas rich in high-w3 marine life. Leafy greens do include small levels of ALA because they need that w3 in the thylakoids for photosynthesis so Richiebogie is at least partially correct when he says “… vegetables have some pufa.” As far as that PubMed study you tout, that’s just one more of the zillions of meta-studies out there, completely correlative, nothing clinical about it, confirming nothing at all. The study leads even make that clear, putting “estimations” in the title. Correlation does not imply causation. Get off your high horse.

          1. Umm, feelings run high! Every word you say is true. I chose Lands’s pdf because it was to hand and because it gives a good overview. However …

   is an RCT which found raising w6 increased both all cause mortality and heart death quite dramatically

   is an RCT which showed that raising w3 halved heart deaths – I believe this is the most successful dietary intervention ever studied

            This one cut all-cause mortality too. So we have RCTs in which more w6 increased all-cause mortality, and more w3 reduced all-cause mortality. Yes, they’re secondary prevention trials, and, yes, Sydney probably ate more trans fats but this is the best data I can find to justify my dietary choices. My coronary artery calcium score is zero after 15 years of lowcarb (because I’m Type I, not because of dietary convictions), taking fish oil and avoiding seed oils.

            Had I been lulled into complacency by advice like richiebogie’s “It is actually very difficult to avoid “essential fats””, I think it likely I’d now have rampant atherosclerosis. Which is why I say it’s dangerous bollocks.

            1. Jonathon, is it this from richiebogie you reacted to?:

              “It is actually very difficult to avoid “essential fats”. You can go without nuts and seeds and olives and avocado, but all fruit and vegetables have some pufa!”

              If so, I think you may have read too much into his comments. I don’t see him advocating using seed oils or other w6 bombs.

              btw, I interpret this as him saying you get pufa in a great many foods. Do you think he’s wrong?

              In any event, you should have sought clarification from him before you adopted your high and arrogant tone. Just saying.

              1. He said its very difficult to avoid “essential fats”, no explanation, no references – seemed pretty arrogant to me – perhaps he can clarify that?

                All I know is that doctors have been selling me variations on the theme for 15 years and I’m hale and hearty while one of them retired prematurely with Parkinson’s, and a second died with dementia blind from ARMD, all conditions for which lchf has been found to help. Had I taken their advice, I’d probably be with them now.

                When people come on cocksure with what I know to be untrue, then I feel I must oppose them since this may help people who find themselves in the position I found myself in 15 years ago, fighting the conventional medical wisdom – which is turning out to be more and more wrong.

                If I come off as arrogant, then maybe it’s because I’ve got something to be arrogant about, like being alive

            2. Jonathan, I do mainly what you’re doing, only I don’t get pufa (or anything else) through supps, just through food (mainly canned salmon and sardines). I try to keep ALL pufas low because pufa is the most oxidizable of the fats, esp w3, I init did the spreadsheet work on those to make sure I was getting enough w3 (Mary Enig of “Know Your Fats” gives 3–4g/day), and obviously no seed/nut oils and limit fatty grain-fed meats.

              About the RCTs. The first one you cite, the Sydney Diet Heart Study, doesn’t test w3 at all, merely subs w6 with SFA. The Lyon Diet Heart Study does look at w6/w3 balances, but where’s the sample rate? Can’t seem to find it, maybe just overlooking it.

              Finally, your CA calcium score, Vit A/Vit D/Vit K balances can also greatly affect that. Those fat-solubles work together to transport serum ca to bone.

              1. Yes! I think your strategy has the best chance of lengthening healthspan.

                “Saturated fat protected the livers of rats given alcohol, but replacing the saturated fat with corn oil resulted in oxidative stress and severe liver damage (Ronis 2004). Moreover, there’s a robust inverse association between saturated fat intake and ischemic stroke in both American (Gillman 1997) and Japanese men (Yamagishi 2010) – the more saturated fat eaten, the less the likelihood of a stroke” from an essay I wrote.

                Ramsden’s meta-analysis concludes “Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death”

                I take the fish oil because I tested low in cell-wall w3’s, thought to be a diabetic trait where w3’s are burned for energy preferentially over glucose when insulin is high, causing insulin resistance. I do take K2, but I started after I got the zero calcium score.

                As you point out, the RCT evidence is woefully inadequate but what the hell we’ve got to eat something!

      2. Therese Dolacek found among about 6,000 middle-aged men with lousy risk factors for heart disease in the MRFIT Usual Care group that 20% of them reported zero intake of conditionally-essential w3 fatty acids. She went on to say “Analysis of the combined fatty acids predominantly found in fish … demonstrated significant inverse associations with CHD, CVD, and all cause mortality groups but not for cancers … The benefit … [at] 664 mg/day … [was] … 40, 41, and 24% lower [incidence respectively when compared to zero intake]”

        So I’d amend your gnomic utterance to: “It’s actually very difficult to avoid eating the pattern of ‘essential fats’ associated with heart health and less death if you eat fish”

        Pardon me for being a little insane on this topic, it’s the legacy of my 30-year fight against the conventional medical wisdom that diabetics should eat lfhc and avoid saturated fat. The way you put it implies you can’t help getting your “essential fats”, don’t worry about them – dangerously misguided advice IMO

        1. This is the medical wisdom my conventional MD handed me in 2007 when I was diagnosed Type 2 diabetic. It is anything but “lfhc and avoid saturated fat”.

          After two weeks of following this protocol my fasting blood glucose dropped from 200 to 100 without any other medication.

          Any doctor that would recommend lfhc to treat diabetes with lfhc is insane, certainly not conventional by 2007 Illinois standards.

          1. Wow! They advocate more than 50% carb calories, what were you eating before?? Dr Richard Bernstein suggests 6% as an upper limit of carb calories. Allick 2004 points out that such a low carb intake depletes liver glycogen by about half which prevents the liver from raising the blood sugar via glycogenolysis, allowing the diabetic to have normal fasting blood sugar Being Type I, I have to keep to that level to prevent high fasting blood sugars – you must have beta cells producing enough insulin to get away with such a high carb intake

            1. There’s no advocacy of carbs at any level (you don’t have to use the sample meals), and you could construct it VLC if you so desired. It’s biased against high glycemic carbs, and set up so typical SAD dieters will use it.

              My problems were overeating high glycemic carbs and fats and being sedentary. Specifically I was eating huge amounts of frosted mini wheats and raisin bran. I suppose that my carbs were 70% of total calories diabetic at 2500 total calories per day and no exercise, dropped to 40% of total calories at 1500 total calories per day and 350 calories per day exercise with the carb exchange system. After I’d controlled blood sugar and lost 25 lbs, I increased the exercise to 700 calories per day, the food to 1800 calories per day and started putting the high glycemics back in. I was able to maintain a 2 lb/week weight loss rate for 6 months doing this, stopping it after 50 lbs lost. Since then I’ve continued to increase the exercise. I aim for Cordain’s 1000 calorie per day historic Paleo exercise by walking and biking. I eat to maintain weight, typically 2300-2500 calories per day, on ca 50% carb, 35% fat, 15% protein, and have stayed at target weight for 8 years.

              VLC Paleos have called me asymptomatic in the past. However, I couldn’t eat this way without all the exercise or if I hadn’t lost the weight. I’m certain that I stopped what I was doing, my trigs would go from 35 back well above 100, my blood sugar would go from under 100 back to 200 fasting, my CRP from below 6 back to 8, and my HDL down from 70 to 30.

                1. My Dr. recommended getting CRP below 6, and the test shows a healthy range 4.8%-5.6%, so I don’t think this is the high sensitivity test. I started at 8.2% in 2/07, and by 8/07 was below 6% (after 6 months of the carb counting and 50 lbs weight loss). I’ve been at that level until the last test in 2/14. I moved in 2014 and my current Dr. doesn’t run it.

          2. Thhq, I agree with Jonathan here. If I stayed on this high-carb diet that Novo Nordisk proposes, I’d be injecting insulin by now. And I ask you the same question as Jonathan: What percent carb diet did you eat before?

            Bear in mind your BG levels don’t tell the whole story. With such a diet, you may have near-normal BGs but chronically high serum insulin levels, esp if you have insulin resistance. Chronically high serum insulin may also harm you in various ways, e.g. promote growth of amyloid plaque in the brain that lays the groundwork for Alzheimer’s. E.g. the same enzyme that dismantles insulin also dismantles the amyloid plaque, but works on insulin first. So chronically high insulin may mean never enough enzyme left over to break down the plaque. You can get an inkling of your insulin levels with the C-peptide test, but to really put a fine point on it, you need the euglycemic clamp, and expensive and involved test not regularly done.

      3. Wow, just WOW. Talk about cherry picking, dismissing anything that can, god forbid, brake the fabric of the little pattern we are trying to build, and leap frog from diet to MS with several other subjects in between to overcome reading sharpness with a totum revolutum devoid of unbiasedness.
        The agglutination of causalities without a minimal effort to look beyond the obvious first impression is flabbergasting, The dismissal with the wave of a hand of historical data is insulting.
        I will be honest, I did not read the very few last paragraph, cause though you write very well, your style is, simply put, chaotic, you are very capable of giving a headache to an aspirin.

        But with that said, the article is pseudo science, yes it is. It’s obvious that you don’t have a scientific background, you don’t challenge the methodology, you don’t provide articles where the testing hypothesis has being duplicated following the same program, and I don’t mean 10 or 15, but hundredths, that is how peer review works. You do make a half hearted attempt to play Devil´s Advocate, but excuse me if I am not overly convinced or satisfied by it.

        But let me address the first shortcoming. The P. diet, is a diet which is first and foremost high in fiber, then high in carbo and almost lacking fat and animal protein. It requires strict adherence to it for life, AND relies heavily on exercise. Of course you gonna get the improved body, of course you gonna get rid of type 2 diabetes, you are exercising. You just barely brushed aside the whole core of the diet like if it were an innocent passer jaywalking onto your fine article. Then you don’t address the number of maladies caused by a diet deprived of fat or with very low fat intakes, liver cancer, brain malfunction, cell membrane integrity, hormonal imbalance, etc. All of that without going into the trivial detail that not all fats are created equal, and the same goes for carbohydrates.

        You also take as example people from indigenous tribes, as role models for the diet benefits, since they don’t have heart disease, well yeah, but they suffered from severe malnutrition, anemia, are susceptible to viral infection and have a high incidence of certain types of tumors associated with low fat and animal protein intakes. The bantus don’t have that diet by choice, they have it by geography, and by the way, their infant mortality is enormous, cuz somewhat carbos are not sufficient to provide synthesis of mother’s milk.

        So stop pandering your neo sophism, reading nutrition books and science papers is not a magic wand to turn you into a scientist, or an expert on the matter. I read many books in quantum physics and relativistic theory, it does make me a physics expert either, because although I have the math background to understand the theory, I don’t have enough of it to propose hypothesis using a few cherry picked articles.


        1. Hilarious. The high carb cheerleaders sounded exactly like you when the China Study article was released here!

          3 paragraphs on how she’s not a “scientist” (even though she never claims to be one) and then more condescending babble about nothing.

          Get a life, dude.

    4. Please do more research into efa’s. Especially R. Peat’s. They are NOT essential. I feel making a statement like that without really researching will harm and may kill a lot of people.

  5. At last- -!! But I’m not going to read this tonight- – I shall waken in the morning but stay in bed and read and digest until I’ve ‘got it’. I’ve been wondering when it was going to appear, ever since you prematurely hit the ‘Publish’ button some months ago. Good night, from the South of Africa

  6. 1. Thank you / this is great / you’re awesome.
    2. I have absolutely no idea what to ever eat anymore…, ever.
    3. Do you happen to have some sort of magical machine that gives you more time in the day than the rest of us?!?!?!?
    4. Thank you!


    1. Eric, my reaction exactly (and I’ve written a diet book!). Thanks, Denise!


      P.S. I would add a 3b: I wish I also had a time machine to do a few N=1 trials, repeated with washout periods, of high-fat, low-fat (really low-fat), and a couple variants of in-the-middle-fat diets.

  7. I was a Registered Dietitian working in Marin County, California, at a very large cardiology group when low fat diets were popular. I am still an advocate of low fat eating and controlled, careful fat eating–I have not fallen for the “high fat, high protein” way of eating. (I see too many impaired renal function patients and colon/breast/prostate cancer patients to feel excess protein and fat are good for people.)

    What I find “hilarious” about the movement to blame “carbs for the obesity epidemic and the explosion of Type 2 diabetes” is that for that statement to be true, EVERYONE in the population would have needed to be eating a very low fat, very high carbohydrate diet–all the time for that to happen (if it was even true.) The truth was (and is) that it was very difficult for people to eat a very low fat diet–AND VERY FEW PEOPLE ACTUALLY DID IT–even those who were cardiac patients. It has always struck me as ironic that no one ever really checked to see if people were really eating low fat and high carbohydrate diets before they were blamed for the health disasters. The association was too “theoretical” without sufficient data to back it up. People self-identified with a low fat diet and would say they ate that way–but that did not mean they ate that way all the time.

    Keep up the good work–you are a brave soul. I envy your dedication.

    1. Like Denise was saying, the still are whole populations who eat very high fat and have very little cardiovascular disease – the Maasai, the Eskimo, some populations in China, etc. An idea is that it probably has to do with other factors, too – like level of physical activity and place of living (the Eskimo live in very cold weather most of the time, so fat is probably necessary for them anyways). The thing is, nobody even thinks of the fact that air is a nutrient too – so maybe, if you breath clean air, you can eat more fat and still not get sick – or something of the sort. Since most of the diseases are plurifactorial, fat cannot be the only one causing – or curing – heart disease…

      1. Not only that, but there is still no proof that dietary fat even causes heart disease in the first place- (or the corollary, that low fat “cures” heart disease). If any of these diets DO cure heart disease, then it could likely be due to any number of factors, not the low fat element. Based on all I’ve read, it still seems a bit unclear exactly what causes heart problems. There are a lot of theories out there, but nothing has been scientifically proven. And there are so many “paradoxes” as well……

  8. Very detailed post, must have been a lot of work! I know it might seem mysterious or surprising to some why low fat vegan works so well. Our bodies are natural starchivores (low fat plant based), just Google ‘omnivore vs frugivore’ and look at the chart – from teeth, to stomach, intestines, etc. Even Denise does a low fat diet. So it makes perfect sense when we eat our natural human diet why our bodies would perform so well, reverse heart disease, etc. But humans are uniquely able to adapt to lack of carbs by going into ketosis – an emergency state during starvation or illness. When no glucose is available (emergency state) our body switches to using fat to survive. Not something we want to do on a regular basis in a healthy state. We avoid all the nutrients, fiber and phytochemicals that plants have to offer. It’s fairly simple to understand.

    I know people here probably don’t accept the china study links between protein and cancer, so here are 5 other ways meat causes cancer that you may not have heard about for example estrogen, IGF-1, hydrogen sulfide, Neu5Gc. Sure we can scavenge some meat for calories and survival but it’s not going to help us thrive and live to 100+. People jumped all over your china study critique because they like to hear good things about their bad habits.

    The success of LCHF is usually based on short term weight loss (assuming caloric deficit and includes loss from glycogen stores and associated water depletion) which creates associated reductions in say blood pressure, but it’s not able to reverse heart disease such as with Dr. Esselstyn’s studies. They have bad breath, constipation and revert to caffeine or laxatives to stimulate the bowels. Check out the longest living populations in Okinawa and 7th day adventists they blow away the masai and eskimos (why we use small isolated tribal populations who didn’t live as long and were shown to have atherosclerosis is a question for another day). 🙂

    Keep up the great work!

      1. My system also runs much more smoothly when I reduce my fiber intake. In fact, I can’t do a high carb diet anymore, since I am intolerant to so many of the foods; there would be nothing left for me to eat.

        And- in response to Will- I eat LCHF, but I am underweight, and therefore am not even trying to lose weight. But I’ve seen massive improvements in my health since I started eating this way about 4 years ago. I had pretty massive health issues when I ate a plant based, low fat diet; (I also went through a phase of eating a very low fat diet, of exactly the kind that Denise describes). So my first point is that the benefits of LCHF- for many of us, anyway- are NOT solely due to “temporary weight loss”. My second point is that no one particular diet is the “absolute correct one” for all people.

    1. I lost 150+ pounds on LCHF, so I’ll assure it was not water weight alone. I have excellent bowel function. I think you miss her point, BOTH diets seem to work. Some people do well on one or the other, if vegan suits you great, go for it, but stop spreading the lie that LCHF doesn’t work for people like me, it’s simply not true.

    2. Vegan nonsense at its finest. Posting that in the comment section of a blog that clearly states how BOTH diets are perfectly fine show how narrow-minded you guys are. Shaking head really

      1. Then there is the notion that neither diet is ideal. And that swampland is only swampland when carbs and fats are combined in the one meal.
        My bet is Denise will have something to say in terms of following both diets, but not a mix of the two.
        We will see…

    3. “They have bad breath, constipation and revert to caffeine or laxatives to stimulate the bowels.”

      Is that so? I don’t know any LCHF eaters who have had bowel problems. I assume you must have access to a large database to make this assertion with such confidence.

      Many low-carbers who convert from the SAD find they actually consume more vegetables than before. Often their fiber intake increases substantially.

      I’m unaware of studies showing that LCHF is incapable of reversing heart disease. There are certainly studies that shows it reverses metabolic markers “associated” with heart disease, but these are questionable indicators. LCHF hasn’t been studied in depth, and in most cases the LCHF diets that have been trialed are in the “swampland” Denise has described.

      I think Denise is presenting objective analysis. And she didn’t prove anything regarding the superiority of low-fat diets (or try to), She is pointing out there is “magic” at both ends of the spectrum.

      And I might add that the “magic zone” at the LCHF end is far, far larger.

      1. I disagree. I run a Facebook group with LCHFers and that is a huge complaint, either they have very loose stools, or constipation. Either way, it is a common complaint. I have myself had extremely loose and often stools on LCHF. I eat higher carb, and the problem instantly disappears. In both diets, I am eating a lot of veggies/starches. The only difference is the amount of sugar and fat.

    4. Will . whey you aré in Ketosis you do not avoid all the nutrients because you can still eat as much as vegetables you want with all the micronutrients and phitochemicals

    5. What do you consider “short term”? I’ve lost 65 pounds in the last six months (30 pounds disappeared in the first 30 days) eating LCHF. I am no longer pre-diabetic, my LDL is down, my VLDL is way down, my HDL is up, etc, etc…. Oh, and I’m not friggen hungry all the time, which for a weight loss diet is VERY important to insure compliance. To drive that last point home, I even fast two days a week. That’s how “not hungry” this diet makes me feel. BTW, I had never been on a diet before more than two or three days in my entire life, and I had put off doing this diet on my doctors advice, as I didn’t want to have the severe hunger pains I had on my three day diet stint in high school 33 years ago.

      If your doing LCHF and have constipation, then your not doing the diet correctly (hint, your eating too much protein, and not enough low starch vegetables & fiber). The most common mistake people make on this diet is thinking that it is high fat AND high protein diet (it’s not). It is a high fat, very low carbohydrate, & MODERATE protein diet. Too much protein and two things happen. First you stop loosing weight, because your body tries to turn the excess protein into sugar. The other thing that happens, and yet another reason you stop losing weight, is that ya can’t poop anymore 8^].

      I DO think that the author may be onto something though, when speaking about the “magic” that happens on the extremes of fat & carbohydrate dietary intake levels, and the macro-nutrient swamp that is the Standard American Diet.

      I watched a Horizon (BBC’s version of NOVA) episode on weight loss and diets a few months ago, where they had taken two identical twins who were about the same weight, and fed them different diets. One was high fat & protein, almost no carbs. While the other was almost all Carbs, lowerish fat, minimum protein. What was interesting were the results. Both gained a little bit of weight, because neither was following a truly LCHF or VLF diet (too much processed foods, etc). Here’s the interesting part… Although allowed to eat as much as they wanted, both tended to eat about the same amount of calories. Hmmmm…..

      Near the end of the program, another scientist shared the results of a feeding study he did on 3 sets of rats. The 1st set of rats he fed a high carb very low fat diet. The 2nd set he fed a high fat very low carb diet. Neither of those two sets of rats gained any significant amount of weight, or had any significant disease problems. The 3rd set of rats gained weight like crazy, and were having various health problems, and way higher mortality rates… He fed the 3rd set of rats “cheesecake” exclusively. The cheesecake would be akin to a Standard American Diet (SAD). The scientist’s theory of why this was, is because the 3rd set of rats ate WAY more calories than the other two sets of rats.

      His example of why goes like this: Take a bowl of heavy cream, a spoon, and start eating. You’ll soon quit, as it won’t take much to have your fill. Now (sometime later), do the same thing, but this time with a bowl of sugar. Again, it won’t take long for you to stop eating spoonfuls of sugar. NOW (again, sometime later), pour the bowl of sugar into the bowl of heavy cream, mix them, and get out your spoon again. This time you’ll most likely consume the entire bowl… Why? Because when you add sugar and fat together at a certain ratio (something not found often in nature), it kind of turns off your brain’s satiety switch, and hence causes you to over eat. BTW, sugar+cream+cold=ice cream…. At a certain ratio of sweetness to fat, we can’t help but want to have more.

      They tested this hypothesis by giving out free donuts to random strangers. Of the 3 types of donuts they gave out (glazed, chocolate frosting, & powdered sugar), one type was consistently chosen the most. It was the glazed doughnut, as it has the same sugar to fat ratio as ice cream does.

      Now that’s food for thought ;-).

  9. The thing that’s missing in this whole discussion is protein. Of the ways we get calories, there’s pretty good evidence that protein is a better plan than either fat or carbohydrates. Indeed, one could argue that the success of low-carb diets is largely due to the fact that they are high-protein diets: Atkins’s own argument was that the fat was in the diet to make you less hungry, not because it was inherently good for you. Weightlifters and other health types have been advocating high-protein diets for years, and having generally good health with them.

    I think you are doing a disservice to your readers if you paint the diet question as “high fat vs. high carbs.” The most credible evidence I’ve seen favors diets featuring lots of protein, plenty of fruits and vegetables, enough fat to reduce food cravings, small amounts of sugar and simple carbohydrates, and less total food intake. I’m guessing you wouldn’t find any of that controversial?

    1. PO8:

      Sorry but a high (animal) protein diet is a disaster for someone like me who has high uric acid levels. I eat way less meat than most people and I can bring on a gout attack at will simply by upping my protein intake from fish, beef, poultry and pork. Through trial and error I do best on low fat. Vegetable protein doesn’t seem to have any effect on my uric acid/gout nor does dairy and eggs (as demonstrated in studies).

    2. The human liver simply cannot process enough protein to meet our energy needs. For that reason, we need to get more than half of our calories from some combination of carbohydrate and fat. This article suggests it should be one or the other, but not both.

      1. People keep saying the low carbohydrate diet is high protein. A properly formulated low carbohydrate diet supposed to be moderate protein, high fat and very low carb. This is like Atkins and what the other low carb gurus out there say it should be moderate protein.

  10. Fascinating! Excellent work. I’ve been checking your website for months looking for updates. I can only imagine the amount of research and work that went into writing this. Can’t wait for part 2 and wondering if genetics will help make sense of it all.
    I will be at the Anaheim conference in November. Looking forward to meeting you there.

  11. Am I really the first commenter or has it been so long in reading that a page refresh would show a different truth?

    Anyway, it’s post like this that show why I read your work and trust you. I don’t have a lot of time left over in life to read about nutrition science. Thank goodness for you thorough review and overall entertaining presentation. Can’t wait until part 2!

  12. “… we could nitpick about [Esselstyn’s studies]: … the patients were abnormally motivated and self-selected (rather than reflective of the general heart-disease population, who might not be so inclined to give up steak forever)”

    These issues may be relevant to the prospects for widespread adoption of the dietary regimen, but they do not confound the results of the studies.

    One of the largest impediments to widespread adoption is the conviction of medical professionals that it’s impossible for almost all patients to change the way they eat.

    Michael Greger ( analogizes thus, mimicking a hypothetical M.D. saying, several decades ago something like, “I’d try harder to get my patients to quit smoking, but I know how they love it so!”

  13. Wow! It is an incredibly good read, so far only read until the end of the Walter Kempner – Rice diet part, its great results was definitely what made me question the low carb ideologies. Now I think its effectiveness is due to its ability to increase the metabolic rate, by completely eliminating PUFA and fats, along with amino acids like tryptophan which supports Ray Peat’s work as you mentioned aswell.

    Have to go to bed to get some sleep gains, (living in EU) but can’t wait to wake up tomorrow and finish the rest of it, thank you so much for this Denise!

  14. Tremendous! Thank you! I have not read part two yet so am at this point a confused but open-minded paleo adherent. Always looking to optimize the program based on new information.

  15. “We can’t ignore evidence in order to preserve an ideology.”

    So fucking awesome to read this. Thank you.

  16. Excellent post: shows once again one size does not fit all. Hard to understand how Pritikin had some heart issue, yet clean coronary arteries. And yes, genetics do count. Many tout Jack LaLanne, and yet I believe he had a brother who was not health oriented who lived in to his 90’s.
    Many on a very low fat diet will have their LDL size shrink and an increase in Ldl_P and yet not be insulin resistent ( much to the chagrin of the paleo crowd) which appears to be contrary to the data you cite in your piece. Krauss and others say that 1/2 the population will experience it and perhaps those on the very low fat diet who did not have a positive outcome might fit in to this profile.

    1. Hi Steve,

      Thanks for your comments! As for your point here —

      “Many on a very low fat diet will have their LDL size shrink and an increase in Ldl_P and yet not be insulin resistent ( much to the chagrin of the paleo crowd) which appears to be contrary to the data you cite in your piece. Krauss and others say that 1/2 the population will experience it and perhaps those on the very low fat diet who did not have a positive outcome might fit in to this profile.”

      Indeed, there’s generally (but not always, as we saw in this post) a decrease in LDL size on very high-carb diets. I’m no longer convinced LDL particle size is as significant as some health figures are claiming. Large, fluffy, supposedly ‘protective’ LDL predominates in people with familial hypercholesterolemia, who develop atherosclerosis as early as their 20s and 30s (or even earlier for homozygotes!); likewise, low-fat doctors like Ornish have reversed heart disease in patients even when their LDL particles are small. I suspect in Western populations, LDL particle size is part of a cluster of hallmark elements for metabolic syndrome rather something inherently harmful, and that its association with heart disease diminishes in the context of non-SAD diets. I’ll be going into more detail about that in either the next blog post or the one after it!

    1. This post made me think of Tim’s potato diet too! I’m glad Denise mentioned the RS content of the rice diet, because I was curious about that.

      Denise, this was such an awesome read! Reading things you write is always an enjoyable experience, and makes me feel like I’m getting a brain massage. I’m also a sucker for myth-busting and paradigm-destruction, so that made it even more fun to read. I can’t even imagine how long this must’ve taken you to research and write.

      Now that you point it out, it is funny how so little attention is paid to some of the extremely high-carb/low-fat ancestral diets. And when attention is paid, it’s to defend “safe starch,” with little discussion of the accompanying low fat intake.

      I’m also glad you mentioned Ray Peat, because the rice/sugar diet made me think of him. I’ve been meaning to make myself understand his dietary recommendations for ages, and just haven’t gotten around to it. I’m super excited to read part 2!

  17. Revisiting cherished theories? Admitting that you were wrong? What a rare thing to find in the diet world. My hat goes off to you. Keep up the good work.

  18. You are brave, girl! It took guts and grace to do this piece–somewhere between a call-out to Thomas Kuhn and a confession to Pope Francis – :).

    I’ve followed your writings from the China Study on, agreeing and disagreeing here and there, but admiring your stamina, civility, smarts, good humor, inventiveness, insight and analytical prowess.

    I’ve followed even longer Pritikin (since his first book); Ornish (since before his publication of his study showing that a low-fat/et al ‘program’ can reverse heart disease); McDougall (since his first book) and Roy Swank via my first exposure to McDougall. Both McDougall and Pritikin have written about Kempner’s work & I read numerous of his earliest research studies on the Rice Diet website (not sure they’re still available at this site.)

    McDougall was/is one of Swank’s biggest fans and was instrumental in funding and designing a Swank-ish MS study in collaboration with OSHU about which one can read here:

    One has to wonder if the patients in the McDougall ‘arm’ might have done a bit better with a bit more PUFA, as per Swank…but that arm did get randomly assigned the sickest patients in the study. Love McDougall for his helping SO MANY PEOPLE but he’s not the first person I recommend to someone suffering from heart disease (or any of the other diseases that appear to improve, as you so ably demonstrate in your review of the low-fat research, in a significant majority of folks who stick to these low-fat diets). He’s dogmatic to a fault…and his recent coloring book for children borders on the offensive in so many ways (and I am a semi-vegan–for health and environmental reasons) that it makes it really difficult for me to send those in need to his website.

    Love Esselstyn too despite the similarities he shares with McDougall. He’s a kinder, gentler, more avuncular McDougall–and his latest study keeps adding to his cred.

    But my biggest thanks are for the intro to Lester Morrison! Must have read about him in one of Pritikin’s books but it’s been at least thirty years and it was really fun and educational to be re-informed and enlightened if in fact I had already been exposed to his work and then forgotten about it.

    I’m looking forward to part 2. And to the good news on HFLC diets.

    I’m sure you’ve seen the recent study by Kevin Hall et al purporting (by others…and Hall) to disprove the carbohydrate-insulin hypothesis in a head to head study of a low carb vs a very low fat diet-


    •19 adults with obesity were confined to a metabolic ward for two 2-week periods
    •Cutting carbohydrates increased net fat oxidation, but cutting fat by equal calories had no effect
    •Cutting fat resulted in more body fat loss as measured by metabolic balance
    •Mathematical model simulations predicted small long-term differences in body fat”

    Stephen Guyenet has two nice takes on this study:

    Both Hall and Guyenet ‘guess’ that an even lower carb diet might show more positive results.

    Here’s Hall’s response to the Taubes and Teicholz-like critics:

    Hall notes that he’s already finished a study that responds to the many complaints his team has received from the low-carb groups re the first study:

    He’s hinting…but the results haven’t been published yet. Love the suspense!

    I am sure I am one of many who truly appreciate the enormous amount of time you have spent on your newest endeavor….and I am really looking forward to whatever comes next: paradox, spoiler, or whatever! Sock it to us! 🙂

  19. Just for people who look at the magic of the rice diet, this extreme part of the program was not long term – just like atkins 20g/day thing was not long term. The rice diet contained extremely low levels of protein, and largely rice protein. Rice protein is great and all, but low in many amino acids, especially lysine, and even more so once you adjust for actual available lysine rather than just total. This is not a diet that is to be consumed for a long time.

  20. Well, haven’t read all 1.2 million words of Part ! yet…, but I did catch a great mixed metaphor possibility:

    BACON-SCENTED rainbow farts from flying, floating, or even incorporeal unicorns, as catechism may demand.

  21. Interesting read. But is there any practical application? Who is going to eat less than 10% fat as a lifestyle? Would be more useful to see an analysis of food combinations for realistic living. If you have a meal high in carbs, that is ok, just ensure its low in fat, etc. These are entertaining post and kudos on your dope writing style… but clinicians are left with the job of actually guiding patients to make realistic changes, which 65% fat or 10% fat are neither for most people.

    1. There are a ton of people already eating this way. Anyone following McDougall, Pritikin, Ornish, Barnard (forgetting any), and possibly Fuhrman are all eating a whole foods plant-based (i.e. vegan) diet. They also feed it at True North Health, the fasting center in northern CA, but it is inspired largely by McDougall as well.

      1. The ATOZ study showed that while Ornish says to eat less than 10% of calories from fat, people who follow (or think they are following) Ornish actually eat about 20-30% of calories from fat – too much for the benefits cited in this article.

      2. There’s also a ton of people eating at the other extreme: moderate animal source foods, low carb, high fat, who are doing very well indeed. Check out Mark’s Daily Apple, for multiple examples. Some people do well as vegans, others – with different biochemistries – don’t. Success on any diet depends far more on factors like the enzymes that our bodies are able to produce than adherence to ideology, at any position on the continuum. For every triumphant vegan story, there’s an equally triumphant ex-vegan story, just as there are people who trumpet their success on their paleo diet and others, once staunch disciples, who now call it the fail-eo diet.

        There never was any single ancestral diet, and humans don’t even have a clear ancestral line! More and more DNA work shows that early Homo sapiens interbred (in different times and in different places) with Neanderthals, Denisovans, and a species so far called Species X that some researchers think may prove to Homo erectus. Adding to the excitement, Neanderthals and Denisovans may have interbred. I look forward to the day when babies are food-typed at the same time and as routinely as they’re blood-typed.

    2. Thanks for your comments! My hope is that by understanding the mechanisms behind macronutrient interaction, we’ll be able to apply the relevant concepts to less rigid diets and create something sustainable. That said, there really are plenty of people out there eating less than 10% fat — folks following the McDougall program, etc. — so it’s not impossible. My own diet falls around 15% fat on many days, and I find it both easy and enjoyable.

      1. “My hope is that by understanding the mechanisms behind macronutrient interaction, we’ll be able to apply the relevant concepts to less rigid diets and create something sustainable.”

        +1, though I’m totally down with obtaining 90% calories from maple syrup.

        I’m very curious to hear what your research suggests on the topic of potential mechanisms. Your post above seems to foreshadow greater attention paid to the cellular environment, e.g. in your references to quality of blood flow and the levels of O/CO2 available to individual cells. A related theme concerns how the very low fat diets (VLFDs) above may affect electrolyte balance. Do you have any pet theories about the role that cellular metabolism plays in human health? Or whether or not VLFDs provide an “optimal” environment for cellular metabolism?

        Yours is my favorite nutrition blog. I’m staying tuned.

  22. Denise

    Have you seen these studies that use low fat high carbohydrate macrobiotic diets to reverse diabetes?
    The Effect of the Macrobiotic Ma-Pi 2 Diet vs. the Recommended Diet in the Management of Type 2 Diabetes
    The Randomized Controlled MADIAB Trial
    Ma-Pi 2 macrobiotic diet intervention during 21 days in adults with type 2 diabetes mellitus, Ghana 2011
    Ma-Pi 2 macrobiotic diet and type 2 diabetes mellitus: pooled analysis of short-term intervention studies
    Medium- and Short-Term Interventions with Ma-Pi 2 Macrobiotic Diet in Type 2 Diabetic Adults of Bauta, Havana
    Gut microbiota and Ma-Pi 2 macrobiotic diet in the treatment of type 2 diabetes
    Ma-Pi 2 Macrobiotic Diet Intervention in Adults with Type 2 Diabetes Mellitus

    1. With regard to Dr Morrison
      Prevention of Atherosclerosis in Sub-Human Primates by Chondroitin Sulfate A
      By Lester M. Morrison, M.D., Katsumi Murata, M.D., Ph.D., J. Joseph Quilligan, Jr., M.D., O. Arne Schjeide, Ph.D., and Leon Freeman, Ph.D.

  23. Fascinating! Those of us who’ve been around quite a spell (I’m 66) already know that reality is far more complex than our dearly-held beliefs would have it, but we so effortlessly forget that, as we slip into dietary dogma (and political dogma, etc., ad infinitum). I’ve just been thinking deeply about just this issue in regard to feeding the cats. Of all the dozen or two cats, and seven or eight dogs, I’ve had in my time, Tibey is the first one I had to take to the vet (UTI). Brought him home today, $6,000 in the hole. We have a first-rate vet who gave excellent medical care, but she gave a bag of kibble labeled Urinary Health. Ingredients? Chicken, corn, corn gluten, soybean oil, and on and on to pukedom. I’ve fed him and his brother a species-appropriate diet, based upon Kymythy Schultze’s recommendations, for about six years, since weaning. I also have Dr. Becker’s book, and, in rereading it I noticed that she says the diet of wild felines includes only 7% fat! So I’ve been giving them too much (they are lean, sleek, incredibly athletic, and, of course, lovable) I assumed that the negative effects of excess dietary fat would result partly from the displacement of other essential nutrients, but the studies you’ve discussed sound largely like starvation, junk food diets, so what gives? Food for a great deal more thought, a great deal. Thank you so much for this fine piece of work. It is good for us to shatter our myths from time to time-keeps us properly humble.

  24. my husband lived in taiwan from ’63 to ’97. yes, he was very thin on a traditional, low-fat, mostly rice diet in taiwan before the economic boom hit in his middle school years. he was thin because he was poor and went to bed hungry every night. he does have beautiful teeth, though. when i lived in taiwan off and on for 7 years i got a lot thinner, but my body i believe canabalized my muscle. i had been very athletic before the move to taiwan. living in taiwan i only walked a lot of exercise. when i got home and took a hike in the woods with a friend, my fingers swelled up i believe because my heart wasn’t pumping the way it should have been. i was only 24 at the time.

  25. Well, technically, ‘paleo’ can encompass high carb diets as well as low carb ones while still maintaining its’ core tenants. I wonder if I should try a high carb diet? It sounds pretty insufferable though…

  26. Dear Denise:

    Thank you very much for writing this. I really appreciate that you are willing to publicly change your mind and admit you were wrong about something. I really appreciate how you mostly refrained in this article for advocating for a new replacement theory to explain everything and allowed yourself instead to dwell on evidence against a current theory. And I really appreciate that you forced your attention onto uncomfortable evidence, and that in doing so you forced me to do likewise. I do indeed find these results surprising and discomforting, and I’m glad to be forced to think about them.

    I do have two objections, but before I launch into them I want to emphasize that these objections do not give my weary brain an “out” and let me shove this uncomfortable evidence out of sight and forget about it.

    The first objection is that these results are all from an earlier era, not randomized, and so it’s hard for me to know how this kind of treatment would compare to alternative treatments tested under better-controlled, randomized conditions. I did a quick bit of googling and hit upon this updated, randomized trial from McDougall:

    Apparently the results were so disappointing that it didn’t get written up into a paper but was instead merely a poster: . The actual results aren’t all there (it says “Click to enlarge” but it doesn’t enlarge for me). The excuse from McDougall at the end of that web page about randomization resulting in too many more-sick patients going into the test group doesn’t make any sense. They could still have reported improvement in those patients, if they had improved, or if their rate of decline had been lower than expected.

    So my first objection is that as far as I know (which isn’t far), these phenomenal results have failed to replicate when attempted under better-controlled conditions.

    My second objection is this: “We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.”

    No, that’s wrong. Earlier in your post you argued that reducing fat from 34% to 30%, and finding no improvement, shouldn’t be used as an argument that reducing fat to 10% wouldn’t be beneficial. That’s a good argument! And for the exact same reason, the fact that increasing carbohydrate to 90% was beneficial (in these non-randomized experiments) should not be used as an argument that increasing carb from 48% to 54% is not a chief cause of our current health crises.



    1. i think the takeaway lesson from this is that this writer is not, and should not be regarded as, a health authority. you’re doing the right thing in doing your own research; she has no credentials, she simply reads a lot about nutrition. as do i, and as you do as well, i take it.

    2. Dear Denise: if you could delete this comment, which is a slightly earlier version of my comment below, that would be cool. I don’t see a way to delete it myself.

    3. Hey Zooko,

      Thanks for the great comments! Those are some excellent points. In response —

      1) The lack of robust study design is definitely the biggest problem with studies from that era. Ideally, I would LOVE to see a “true” low fat diet and a “true” low carb or keto diet go head-to-head with a great study design, relatively large sample size, and sufficient follow-up period. Maybe one day the Funding Gods will descend and grant such a thing. Until then, I appreciate the older studies because, despite weaker designs, they’re free from other notorious forms of confounding plaguing research today (especially healthy user’s bias).

      That said, I’m very familiar with that McDougall study and will talk about it a bit in the next post. What I find fascinating is that the biggest difference between the two men’s studies is that McDougall used a strict vegan diet for his, and Swank allowed a wide variety of animal products (and considerably higher protein intake), so long as they were lean (trimmed meats, skim milk, egg whites, plenty of seafood). That raises the possibility that the vegan component was actually harmful (or less beneficial), that something in the lean animal products in the absence of saturated fat was also helpful, or any other of a variety of options; the mens’ diet were similar in fat intake but not identical elsewise. Relapse rates had already dramatically improved for the Swankers by one year, so I’m hesitant to suggest McDougall’s study just wasn’t long enough for the results to start manifesting, but I suppose that’s a possibility as well (seeing as Swank’s 50-year monitoring of some patients allowed a much fuller view of their disease progression than one year for the McDougall study).

      It also raises the intriguing possibilities about MS symptoms improving independently of improvements in brain lesions/MRI scans. Swank didn’t use MRIs in his study or measure brain lesions; he only went by objective changes in the patients’ physical capabilities and their number of relapses over the years. So we can’t even say for sure that his study improved MS on the basis of lesions. McDougall’s study does show a trend of improvement in FSS score and MFIS score between 0 and 12 months, especially a pretty dramatic jump when they first started the diet from baseline — so the patients WERE improving in some measure. Why did they improve without concurrent improvements in MRI scans? Could it be possible that the diet alleviates MS symptoms in a different way and sheds light on a different element of MS etiology? I find it fascinating as a possibility, though certainly inconclusive, and I’m not as well versed in MS as I’d need to be to know if that theory could even hold water.

      Anyway, Swank’s results (and rationale) will make a lot more sense after Part 2. He conducted (and drew from) a lot of additional research on both animal models and humans, showing some very specific changes in blood and tissue oxygenation from dairy fat (meals of nothing but pure cream — and in the 1940s, before dairy was largely crap). Anyway, stay tuned for that, as it does add more credence to Swank’s findings.

      2) “”“We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.”

      No, that’s wrong. Earlier in your post you argued that reducing fat from 34% to 30%, and finding no improvement, shouldn’t be used as an argument that reducing fat to 10% wouldn’t be beneficial. That’s a good argument! And for the exact same reason, the fact that increasing carbohydrate to 90% was beneficial (in these non-randomized experiments) should not be used as an argument that increasing carb from 48% to 54% is not a chief cause of our current health crises.”

      Ah, I disagree. We can’t blame low-fat, high-carb diets for heart disease and diabetes and obesity because the nations (America, etc.) suffering from these conditions have NEVER eaten low-fat, high carb diets. We’ve eaten moderate-fat, moderate-carb diets, which may be the worst of the worst. 🙂

      1. It would make sense that the well balanced proteins from lean meat, which tend not to be allergenic, would be much better with respect to an autoimmune disease like MS than plant proteins, which tend to induce immune system reactions.

        I think it’s ridiculous to assert that a 15% fat 80% carb diet isn’t “low fat, high carb”. 20% carb, 60% fat diets – typical strict paleo – are always referred to as low carb, high fat, after all. People who go below 10% carbs are usually referred to as being on “very low carb”, “ketogenic”, or in some cases, for those on 0% carbs, “zero carb”. Similar wording should be used for the other end of the spectrum.

        Heart disease has been with us for a while, but we can absolutely blame low fat, high carb for the obesity epidemic. What we can’t blame is VLF (very low fat) or no-fat diets.

      2. ”We’ve eaten moderate-fat, moderate-carb diets, which may be the worst of the worst.”

        Even worse yet, Denise.

        We have eaten mostly a moderate (SFAs, refined PUFAs, and trans-fat) fat, and moderate (sugar and refined carb) diets. That’s the SAD. Lots of meat, refined carbs, and junk. No wonder we’re in the state we’re in. Anyone blaming the low-fat diet for our current health state is not being honest. As you have shown, lots of population ate successfully a truly low-fat, high unrefined carbs diet with excellent health.

        Thanks for your article.

      3. ” We’ve eaten moderate-fat, moderate-carb diets, which may be the worst of the worst. :)”

        What about Ancel Keys Med Diet? It lies in the middle of Swampland, yet it allows the eating of all foods…in moderation. As a result it is the best of the worst, at a minimum.

        Pushing macronutrient extremes in search of a perfect health diet is an interesting game to play. But it takes extreme motivation, a flexible schedule and an open wallet. Most people can’t sustain these diets for more than a few months, so their usefulness is confined to emergencies like weight loss, celiac, and IBS.

  27. Dear Denise:

    Thank you very much for writing this. I really appreciate that you are willing to publicly change your mind and admit you were wrong about something. I really appreciate how you mostly refrained in this article for advocating for a new replacement theory to explain everything and allowed yourself instead to dwell on evidence against a current theory. And I really appreciate that you forced your attention onto uncomfortable evidence, and that in doing so you forced me to do likewise. I do indeed find these results surprising and discomforting, and I’m glad to be forced to think about them.

    I do have two objections, but before I launch into them I want to emphasize that these objections do not give my weary brain an “out” and let me shove this uncomfortable evidence out of sight and forget about it.

    The first objection is that these results are all from an earlier era, when randomization was not practiced, and so it’s hard for me to know how this kind of treatment would compare to alternative treatments under better-controlled, randomized conditions. I did a quick bit of googling and hit upon this updated, randomized trial from McDougall:

    Apparently the results were disappointing — no improvement in brain imaging or in disease burden for the low-fat diet arm. So disappointing, apparently, that they didn’t get written up into a paper but instead merely a poster: . The actual results aren’t all there (it says “Click to enlarge” but it doesn’t enlarge for me). The excuse from McDougall at the end of that web page about randomization resulting in too many more-sick patients going into the test group doesn’t make any sense. They could still have reported improvement in those patients, if they had improved, or if their rate of decline had been lower than expected.

    So my first objection is that as far as I know (which isn’t far), these phenomenal results have failed to replicate when attempted under better-controlled conditions.

    My second objection is this: “We can’t categorically blame low-fat, high-carb diets for heart disease and diabetes and obesity. We just can’t. NOT EVEN A LITTLE BIT. This needs to go away.”

    No, that’s wrong. Earlier in your post you argued that reducing fat from 34% to 30%, and finding no improvement, shouldn’t be used as an argument that reducing fat to 10% wouldn’t be beneficial. That’s a good argument! And for the same reason, the fact that increasing carbohydrate to 90% was beneficial (in these non-randomized experiments) should not be used as an argument that increasing carb from 48% to 54% is not a chief cause of our current health crises.



    1. Two follow-ups to my own comment:

      1. I realized that I didn’t find that McDougall trial through Google — I found it by reading admgm’s comment. Sorry to have forgotten that, admgm.

      2. There’s another way that trials from this era are unreliable, and that’s selection effects by the experimenter after the beginning of the experiment. For each subject who did well under their care, the experimenter would take credit for it, and for each subject who did badly, the experimenter would investigate and find some way that the subject was not following the protocol and blame the subject for it. Then they would write up a report showing that their treatment had a nearly perfect track record. To prevent such shenanigans is why nowadays we require Intention To Treat analysis.

      Some of the parts of your post about just counting the results in adherers reminded me of this, and so did the part about whipping the patients, because those experimenters who blamed patients for their failure would also tend to be the ones who bullied patients.

      (As an aside, I think that *both* Intention To Treat *and* adherer analysis should be standard instead of just ITT, but that’s a topic for another day.)

  28. Denise – beyond this post being, honestly, the most interesting thing I’ve read in the health-o-sphere this year, it’s inspiring.

    It takes big stones to backtrack on your beliefs and admit they were short/wrong/misguided/whatever – something that so few in this biz are willing to do (or are even capable of doing).

    Well done. Way to set the bar high. Looking forward to part 2.

  29. I respect how Denise is slowly and politely Denise is removing herself from the wacko paleo community she found herself involved with. Just have a look at the first few AHS talks she did. They must be pretty embarrassing to watch, especially considering the type of people she found her associated with. Leaving the Raw food wacko’s and jumping into the wacko paleo camp was probably a pretty big move for her.

    Finding out that the paleo sect that she jumped into is just as wacko or even worse than the raw food cult she left was involved in must of been pretty brutal.

  30. Personally I’ve tried both ends of the dietary spectrum. Both require an adjustment period. And while both may be magical in their own way, intuitively I’ve leaned toward the high carb pole.
    This diet war has raged for a good while now, but a clear and rational evaluation such as this represents a major push forward for the high carb camp.
    Essential fats and carbs don’t mix well. One option is to cut the fat, the other to cut the carbs. Cutting fat is evidently a health inducing option, whereas high fat has its issues longer term.

    1. Essential fats and carbs mix very well indeed, and have for millenia. The problem for millenia has been finding enough fat, at a price that the average person can afford. It’s only recently that people have had a problem with being in the middle of the swamp. That’s where I live, and eat my daily 1000 calories carb, 1000 calories high fat, 400 calories protein, and maintain healthy weight. You cannot overeat for what you do, and I get the 1000 calories a day Cordain recommends for a minimal level of Paleo exercise. Ditch the car/subway/bus, ditch the chair, and walk bike or run to the nearest bakery for the donut you need to get your needed calories for the day. They’re not empty calories if you metabolize them.

      Believe me the middle of the swamp is the sweet spot. Not an Atkins/Taubes/Eades/Jimmy Moore CVD risk-land, nor a Jobs/Pritikin wrecked liver-land. Every food every day, within reason.

  31. Wow, this was an amazing read, thank you for pulling this all together. It’s left me confused not really knowing if there is a way forward. I do wonder at the effect of all these extremes on the gut biome, and wonder that the restricted nature of some of these diets actually promote healing and remission by improving the gut health. I got diagnosed with Hashimotos this February, prior to the blood tests (out of desperation with ballooning weight), I went on the HCG diet which is virtually no fat. My symptoms improved amazingly (mainly the pain and fatigue), even though I didn’t loose as much weight as I hoped. It wasn’t until I started taking thyroid medication that the weight slipped away. I follow a restricted paleo diet. I look forward to reading part 2, is there going to be any help with a way forward?

  32. I appreciate your hard work in pursuing the truth, I lost 50Kgs and got rid of diabetes through low fat diet only to afterwards change my mind and admit publicly that a high fat diet is superior so I can definitely appreciate your humility and your science based rather than ego based approach. But I do have five comments/questions here –

    1) To get below the magic number of 10% fat – one has to reduce consumption of animal products and with that to reduce the consumption of DHA, EPA, B12, Iron, Zinc, Iodine, Glycine, etc, etc. What is the impact of such a diet on the *brain’s health*? What is the impact on our hormones? On our sex drive? On Homocysteine levels? On the activation of so many genes in our body. I am aware that you said that many of these low fat diets do allow some consumption of animal products – but the question is how much and whether that is enough. Health is not only about cardio vascular health and cancer prevention. I would love it if your part 2 (or part 3) will take that into consideration. Let’s see the whole picture.

    2) I wasn’t aware that we humans can’t synthesize Neu5GC and that actually we have antibodies against this thing. I was under the ancestral approach impression that whatever we were evolutionary accustomed to eat – was good for us – this is why we survived so far and so based on this understanding if really there was a problem with the Neu5GC then we would all become vegans by natural selection process. We know that this is not true because never ever has there been a vegan society lasting more than several generations.

    3) How easy it is to live one’s life on the low fat diet? I think you have to be quite the masochist to adhere to such a regime. So yea, suppose that after you answer points (1) and (2) above and indeed low fat diet is even a bit better than high fat diet – which diet should one pursue? How much can a person sustain such a harsh low fat diet and convince himself that he feels great? I would choose the easier diet, the one that I can pursue for the rest of my life.

    4) Why is it that you are focusing only on the extreme diets? Either very low fat or very high fat? Doesn’t it make sense that humans, throughout the last 2.5 million years ate a diet that is somewhere in the middle?

    5) Does this blog post mean that you now moved from advocating high fat to low fat? Or is it that you merely indicate that there’s a viable low fat diet option?

    1. Hi Aviel,

      Thanks for the great questions! I’ll address them as best I can, in order:

      “1) To get below the magic number of 10% fat – one has to reduce consumption of animal products and with that to reduce the consumption of DHA, EPA, B12, Iron, Zinc, Iodine, Glycine, etc, etc. What is the impact of such a diet on the *brain’s health*? What is the impact on our hormones? On our sex drive? On Homocysteine levels? On the activation of so many genes in our body.”

      — I’d say, first of all, that 10% of calories as fat is an average and not necessarily the goal of every single meal of every single day. I’ll be covering this in Part 2, but for folks who aren’t trying to reverse their diabetes or advanced heart disease, occasional (2 – 3 times per week) higher fat meals with nutrient-dense animal foods is unlikely to ruin the carbosis benefits and will make for a more nutritionally complete diet.

      That said, a low-fat diet doesn’t necessarily reduce intake of those micronutrients, apart from DHA and EPA. Liver (rich in vitamins A, D, E, K, B12, iron, copper, etc.) is only 25% fat, and can easily be integrated into a low-fat diet without pushing the macro averages above 10%. Clams are only 9% fat and also very high in B12; other shellfish like oysters supply a lot of animal-based nutrients as well and are relatively low in fat. Bone broth is low fat and rich in glycine. Insects are mostly protein, for those daring to go there! 😉

      As for DHA and EPA, the need isn’t particularly high if omega-6 intake is low, so small amounts of seafood will probably be sufficient here. Interestingly, it seems fat restriction actually increases omega-3 status — see “Consumption of a low fat diet alters fatty acid patterns in a manner similar to that observed with feeding of (n-3) long-chain fatty acids. This change is likely related to decreased competition for the enzymes of elongation and desaturation, with reduced total intake of 18:2(n-6) favoring elongation and desaturation of available (n-3) fatty acids.”

      As for the impact of very low-fat on brain health, sex hormones, etc., I’d love to see more research delving into that using non-vegan diets. Considering that many populations have successfully subsisted and reproduced on diets in the 10 – 15% fat range, I doubt it harms reproductive functions as long as energy intake and micronutrient content is sufficient. Neurological health deserves more attention, and my guess is that there will be a range of response due to individual variation and ApoE status. Homocysteine is unlikely to be a problem as long as folate and B12 status are good.

      “2) I wasn’t aware that we humans can’t synthesize Neu5GC and that actually we have antibodies against this thing. I was under the ancestral approach impression that whatever we were evolutionary accustomed to eat – was good for us – this is why we survived so far and so based on this understanding if really there was a problem with the Neu5GC then we would all become vegans by natural selection process. We know that this is not true because never ever has there been a vegan society lasting more than several generations.”

      — Per evolutionary theory, we only need to survive until reproductive years in order to keep our DNA in the gene pool. The problems associated with Neu5GC (in theory, anyway) wouldn’t show up until later in life, after reproduction; and historically, the biggest killers were immediate things like acute infections, traumatic injury, etc. before chronic disease had a chance to take hold. Also, if Neu5GC really is an issue (still highly speculative!), it involves interaction with bacteria that may be a more neolithic phenomenon.

      “3) How easy it is to live one’s life on the low fat diet? I think you have to be quite the masochist to adhere to such a regime. So yea, suppose that after you answer points (1) and (2) above and indeed low fat diet is even a bit better than high fat diet – which diet should one pursue? How much can a person sustain such a harsh low fat diet and convince himself that he feels great? I would choose the easier diet, the one that I can pursue for the rest of my life.”

      — I disagree here! I actually very much prefer a low-fat diet to a high-fat one (although my only experience with low carb, high-fat on a personal level was only a 6-week experiment a few years ago — I experienced no detectable advantages and had a few problems worsen). There are thousands (? I’m guessing) of followers of the McDougall program, Ornish, Pritikin, etc. who appear very content with their diet. Apart from my six-week experiment, my diet has been pretty low fat for the past 10 years and I actually prefer it taste-wise and texture-wise to higher-fat eating plans. If you’re interested, Angelo Coppola has a “Plant Paleo” diet plan that fits into the low-fat bracket but is very nutritionally replete and looks delicious:

      “4) Why is it that you are focusing only on the extreme diets? Either very low fat or very high fat? Doesn’t it make sense that humans, throughout the last 2.5 million years ate a diet that is somewhere in the middle?”

      — I’m focusing on the extreme diets as a way to explore macronutrient interaction and its impact on human health. I’ll explain more in Part 2 why I think we can isolate some of the effects from these extreme diets and apply them to more flexible eating plans. To get there though, we have to study what exactly is happening on a biological level — which is why these studies (and the more mechanistic research I’ll go through in Part 2) are valuable!

      I’d say it’s historically much more likely that we swung between macronutrient extremes than ate a diet in the middle: warmer seasons would feature abundant fruit and plant foods (high carb), winter would have lower high-energy plant food ability but perhaps more large game; and even in the shorter term, times of gathering (plant foods, small lower-fat/higher-protein mammals and insects and reptiles) would be punctuated by sporadic successful kills, in which case gorging on meat was likely. Even geographically, tropical areas tend to produce more sugary and starchy foods (fruits, tubers/roots) and polar regions are lower carb with more animal-derived nutrition.

      “5) Does this blog post mean that you now moved from advocating high fat to low fat? Or is it that you merely indicate that there’s a viable low fat diet option?”

      I’ve never advocated high fat (or any specific diet, for that matter), so I guess the technical answer is no. I’ve defended high fat when the science used to discredit it is bad, and I’ll continue to do so when the occasions arise — as well as recommend it when it seems the best choice for someone’s specific situation. But I’d be quite a hypocrite to advocate a high-fat diet when my own experience with it was unimpressive and I’ve been eating a low-fat diet for the last decade! 🙂

      1. We need to keep in mind that the body fat composition of the wild game, even the hooved mammals, that our Paleo ancestors ate was a far cry from that of today’s typical feedlot-fattened, selectively bred cattle and grain-fed poultry. Outdoor Life lists the fat content for various types of wild game commonly hunted today, and many of these animals have less than 10% fat in their meat. These include mule deer, elk, antelope and several others. So even during seasons when our ancestors consumed a fair quantity of red meat, it probably wasn’t hard for them to keep their intake in the 10-15% fat range. History buffs have probably encountered the term “rabbit starvation” in the diaries of early explorers, a situation where a person’s body fared poorly because the meat he was consuming was so lean.

        1. Wild game is about 10% fat by weight. That comes to about 50% fat by calories – more after accounting for bones and such. Our livers cannot handle more than about 40% of calories from protein – thus rabbit starvation – so at those times we ate meat, we were getting most of our calories from fat.

          I don’t think it’s a coincidence that the whole body body fat percentage of wild game is very similar to the fat percentage to which steaks are typically trimmed. Most of the extra fat on feedlot animals is trimmed and discarded.

          1. No. As a scientist, organic foodie, and math nerd, I DO know the pitfall of comparing calories on a weight vs. calorie basis. The Outdoor Life analysis was based on calorie percentages, NOT on weight. For example, 3.5 oz. of elk meat at 0.9 g fat, total 137 calories. See

            Wild game is very different from “trimmed steaks” from grain-fed beef, and one reason people complain of elk as being too “dry”. Most of the fat on beef cuts in grocery stores is NOT trimmed. Even when I buy grass-fed beef, I end up trimming a huge amount of fat from it. At certain seasons, yes, the fat in wild game is higher. The protein handling problem is likely just what was causing a problem for the folks suffering from rabbit starvation. And please remember that fat and protein are only two of the macronutrients — our Paleo ancestors ate a lot of carbs — root veggies and tubers and fruit and such. Despite what some bacon-addicted “modern Paleos” will tell you.

            1. That Outdoor Life analysis does not reflect the whole animal. It reflects a trimmed 3.5 oz serving. And most of the fat absolutely is trimmed off of beef cuts in grocery stores. To see what a steak from a feedlot animal looks like if it really isn’t trimmed, have a gander at the picture here:


              Yes, that’s more than half an inch of fat most of the way around the steak.

              Now, wild animals do not have that much fat, which in domestic cattle can be up to 40% of total carcass weight. However, even wild ungulates do have substantial amounts of fat in deposits in the belly and in the rump at the base of the tail, amounting typically to around 10% of the total carcass weight. That’s more than half of the total carcass caloric value. Paleolithic humans would have had no problem getting fat to eat.

              1. Yes….and I was under the impression also that early humans, and many modern hunter-gatherers, ate plenty of fat. Animals with fat were sought after; and though some wild animals are lower in fat, there are plenty that have fat on them. Early humans used to eat brain marrow, also high in fat, and Inuit and other native people ate fatty fish and sea mammals. Many hunter-gatherers processed the fat of certain animals, to be used later- (ever heard of oolichan grease? Not sure if I spelled it right….And then of course there’s pemmican….) So, yes; I agree with Psychohist.

              2. yes. Plus Paleolithic and Paleolithic-style cultures also selectively hunted the older animals late in the season who had really good stores of fat on them. Modern day “theorists” don’t ever consider these sorts of details.

                    1. There is no such thing as a paleolithic style culture. There are hunter gatherer style cultures but even then, little to none that do not also utilize some sort of agriculture or animal husbandry. Gathering data from these cultures no not in any way validate any theory of our paleolithic ancestors. And please don’t mention Inuit cultures, they are a very young culture and are about as far removed from any ancestors that have any influence on 99.99% of modern humans.

                    2. Zach: I believe you are talking about modern day hunter-gatherers. However, many of these observations were made in the 1800’s and early 1900’s, the time of the explorers. Back then, there were not only more hunter-gatherer cultures in existence, but they were also living a more “pure” hunter-gatherer lifestyle. Since you don’t want anyone to mention the Inuit, I won’t, but let me give another example: the Sioux Indian (as well as other Plains Indians). The Sioux lived mainly from buffalo meat, and it was noted that when they hunted, they did indeed choose the fatter animals.

                      Generally, since hunting expends a lot of calories, it has been noted by observers that hunting cultures tend to try to seek out the most nutrient dense foods; in other words, preferring to kill a bigger animal over a smaller one, or choosing the animals with the most fat on them- (at least they did this whenever possible. I may also hasten to add that modern day hunter-gatherers have fewer choices, due to encroachment, being pushed off their lands and into more marginal territory, etc.) It is theorized that Paleolithic people probably behaved in a similar manner, though I guess we don’t know this for sure. But it makes sense, seeing as we somehow survived through the ice age.

                      I’m not saying that all hunter-gatherers *have* to eat lots of fat.Those that have access to more plant foods and other carbohydrates could probably get by with less fat. But the “low carb” hunter-gatherers- and there were quite a few- would have had to have eaten adequate fat.

                    3. I spent some time on this site. That area had a rich history dating back centuries. There are links to a diary of white explorers living off of game, who reported eating currents they found made them sick, but they mentioned there was nothing really wrong with the currents. Perhaps due to a change in gut bacteria(my theory ). It may have been on this site that I read certain berries were added to the meat and fat to preserve them.


                      This book was at one time available to read free online.


                      I have never tried a diet of just meat and fat.

                    4. Zach, what you say makes no sense. People can argue the semantics of “paleo,” now a highly co-opted and abused word. But the fact that a society following an ancestral lifestyle, like the Hadza, even if they also practice agriculture and/or animal husbandry, doesn’t necessarily alter how they pursue their hunting and gathering, nor does it necessarily make it different from dedicated hunter-gatherers past or present. As far as “validating any theory” not sure what you mean by that either. It’s unlikely we’ll ever know in detail what pre-agricultural societies ate. We need to use the evidence at our disposal. This includes what direct evidence we do find (e.g. bones showing cut marks), analyses of bone and dentition, and, yes, examining the lifestyles and foodways of modern day hunter-gatherers. And absolutely we need to include Inuit cultures who migrate to the NA Arctic in ~900AD, and who come from the same common ancestors as nearly all of us only 40,000 yo. That’s only 2000 generations ago–time for a handful of successful SNPs to survive, like lactase persistence–but not for the very many conditions that are are determined multifactorially, such as Type 2 diabetes, driven by MNPs locvated on at least six genome sites.

                    5. Good points, wbryanh. And I’ll repeat one of the comments I made earlier above, that there is very good evidence that early humans broke open the brains of the animals they killed and sucked on the brain marrow. (Very high in fat). Some even theorize that this is what made our brains become bigger.

  33. Excellent overview, thank you Denise!

    For me, the problem with all of these studies is that they focus on the same type of person. Either they’re all overweight or they all suffer from some kind of disease. It would be very helpful if, at the very least, studies were designed that tested how overweight people and those with normal weight, or how sick and healthy people react to the same type of diet.

    My point is, there are basically two different kinds of people who, for simplicity’s sake, can be put in one of two categories – heat sensitive or cold sensitive. It’s actually a bit more complicated than that and environmental factors are tied to this as well, but in general these groups’ reaction to the different types of food is inherently different and they develop altogether different types of diseases when they eat the wrong diet for their type. Simply put – their bodies are unable to maintain a certain elemental balance and diseases develop because of that.

    Thus, when the same type of diet is tested on people from both groups, the results might be markedly different. While one group may do well on a certain diet, the other might actually develop all kinds of problems. To find out which diet is good for a person, one has to find out to which group the person belongs, without ignoring environmental factors and other individual differences in the person’s lifestyle, all of which have an effect on their metabolism and ultimately their health. For example, it makes a huge difference if a person does primarily physical or primarily mental exercise.

    1. Yes, I think that is the point. Denise is showing that there is not just one kind of diet that can help people. Frankly if you live long enough and have tried a great number of diets yourself for various purposes and at various times in your life and spoken with a number of other people who have done the same, you don’t need elaborate research or studies begin to understand that ( beyond eating real, well produced and fresh food) there is not one best way of eating. We need to better understand why some diets work best for specific conditions and specific people. The point is to get beyond trying to win the LCHF/HFLC wars and to collaborate on trying to discern how to target diets for individuals, healthy ones and sick ones. My bet is that there will be numerous variations.

  34. Hello,

    I think you have a typo. Search for “changges” which I think should be “changes” with only one ‘g’ letter.


  35. The sooner people lose their obsession with macronutrient ratios, the better. Carbs, fats & proteins can be obtained from:-
    1. Minimally-processed animal & vegetable produce.
    2. Over-processed crap-in-a-bag/box/bottle.

    We should be basing our diets on 1.
    The Food Product industry wants us to base our diets on 2 and uses every marketing trick in the book to “make it so”.

      1. No. In what way does your comment contradict the fact that we should be basing our diets on 1.?

        Just because it’s possible to be healthy on a diet of milled rice and refined sugar for *one* *year* doesn’t mean that it’s the optimum diet for *life*.

        Do you have any evidence that 1. isn’t a better choice over a lifetime? Kempner’s trial only lasted for one year, so there would have been no long-term health problems caused by micronutrients missing from his diet.

        1. The actual evidence Denise presents is that 1. doesn’t matter if you are on a very low fat diet.

          There is also evidence that whole grains are worse from an autoimmune perspective than refined white flour. In general, for nonpaleo foods, processed versions seem if anything healthier than unprocessed versions.

          1. Whole grains contain oils in the outer coat that can go rancid. Consuming rancid oils from stale whole grains is definitely not good for optimum health. Refining grains removes these oils, which is a good thing. However…

            Refined grains are lower in certain minerals (copper & manganese, for example). If this is compensated for by eating other foods that are high in those minerals, it’s not a problem. A diet comprising milled rice, refined sugar & fruit juice will be lacking in the above minerals.

            A very low fat diet comprising veggies, root veggies & tubers, legumes, whole grains and whole fruits will be high in the above minerals.

            Please provide evidence showing that fresh whole grains are worse from an autoimmune perspective than refined white flour.

            1. “Please provide evidence showing that fresh whole grains are worse from an autoimmune perspective than refined white flour.”

              It’s because whole grains have more toxins like gluten and wheat germ agglutinin. These toxins lead to more leaky gut and then trigger autoimmune responses due to molecular mimicry.

              As someone with an autoimmune disease, I’m perfectly happy avoiding both whole and refined grains. Doesn’t hurt anything, and I’ve got both bases covered.

              1. “It’s because whole grains have more toxins like gluten and wheat germ agglutinin. These toxins lead to more leaky gut and then trigger autoimmune responses due to molecular mimicry.”
                You’ve got it the wrong way round. Whole grains have an outer husk which *doesn’t* contain gluten, so the relative gluten content of whole grains is lower than for refined white flour. Also, despite thorough chewing, whole grains have a much smaller surface area than refined white flour, reducing absorption through the gut wall.

                As you have gut permeability issues & AI disease, you’re better-off sticking to meat & veg!

            2. The opposite is the case. There is much more missing in refined grains than just copper and manganese (althouth those trace minerals are crucial for phase II enzymes). We always have to be wary of the fallacy of reductionism when evaluating the health effects of a complex, natural food. There are many more differences between whole and refined grains, all being at least as significant as the content of micronutrients:

              1) Fiber, of course, but the term “fiber” is as much an overgeneralized umbrella term as the term “fat”. Both comprise a huge variety of compounds with very different health effects. While in contrast to fatty acids, all known types of fiber seem to have beneficial effects (well, except a well known side-effect from large doses), some excert their effects simply by increasing the mass of the intestinal lumen, some have probiotic effects, and some excert potent physiological effects even beyond acting as a prebiotic. Whole grains – particularly oats and barley, but also wheat and rye – contain large amounts of β-glucans in the bran – a type of fiber that is also found in fungi but fruits an vegetables are generally devoid of – that is partially absorbed and partially metabolized by gut bacteria. It excerts powerful immune-regulating effects, not only on the intestine (which we now know to be crucial on a systemic level) but also systemically through intestinal absorption of the β-glucans and their bacterial metabolites. Here is a comprehensive review on β-glucans done by a hobby researcher.

              2) An abundance of seconary plant metabolites concentrated in the bran, phenolic compounds such as simple phenolic acids and tannins, compounds related to B-vitamins such as PABA, and – probably most importantly – significant amounts of inositol hexaphosphate or phytic acid. The very compound that paleo lore has painted as a villain of whole grains may in fact have highly beneficial effects in well nourished Westerners, as it has a high binding affinity to iron and does chelate iron not only in the intestinal lumen but is also absorbed through passive diffusion and acts as an chelator of free iron in the blood stream, as testified by many people who suscessfully lowered their iron overload by taking supplemental IP6. Ironically, Paleo dieters who avoid phytic acid like the plague would probably derive the most benefit from it, given the high heme iron and saturated fat load of such dietary patterns and their well-known inflammatory effects.

              3) Last but not least: structure. Whole grains ain’t whole grains. The aspect that usually gets lost first when engaging in reductionist methodology of nutritional science is the three-dimensional, cellular structure in which nutrients are delivered within a whole food matrix. Usually it accounted for only as a factor in bioavailablity (e.g. carotenoids), but it may have effects far beyond this aspcect. By legal definition, whole grain products are all products made out of unrefined grains. However, the literal meaning would be a grain that is not milled to flour but still intact or coarsely cracked. Bread baked from grist instead of flour has a significantly lower glycemic and caloric load, because much of the starch that remains tightly contained within the cellular structure is indigestible and thus acts as a prebiotic fiber in the large intestine similar to resistant starch, further improving gut health.

              Of course, eating some refined grain know and then won’t hurt – it’s simply a wasted opportunity to eat something much more healthy. I’m the first to admit, though, that I sometimes happily waste this opportunity in exchange for a delicious, crispy croissant. 😉

              1. 1. & 2. If someone’s diet consists entirely of grains, then what you say would have a significant effect. Who eats a diet of rice and nothing else whatsoever?

                3. I totally agree. See

                I don’t like orthorexia a.k.a. “clean” eating. As long as the diet is *based* on whole, minimally-refined animal & vegetable produce, there’s some wiggle-room for refined foods. 😀

                1. Actually a huge number of people around the world DO live off mostly grains, sometimes for their entire lives. With very little in the way of vegetables. That is why the IIRC developed “golden rice” … to save the sight and lives of millions of children.

                  Oddly though, some of those grain-eaters are actually surprisingly healthy. Like this guy:

                  He’s from a culture that eats mainly sorghum, 3 meals a day. Other places in Africa eat mainly millet, or their own version of corn, or yams. Or peanuts or milk. One of the first questions one asks when meeting a stranger is, “What is your staple?” … I guess they define the culture by the main food. When you see the pictures though, the people are typically tall, with straight teeth and wide smiles … even when they are living at a barely subsistence level.

                  I haven’t yet seen a culture with healthy people living mainly off wheat or barley though. Even in the ancient Egyptian and Roman days … skeletons of the rich and the poor were both pretty bad. Even Oetzi, with all his exercise. The French are healthier than Americans, but not nearly as robust as your average Japanese mountain villager who lives off yams.

                  1. Well, in chapter 3 of Dr. Price’s “Nutrition and Physical Degeneration” he found the Swiss in perfect health eating mainly whole rye.

                    Major-General Sir Robert McCarrison’s “Studies in Deficiency and Disease” he found the Hunza eating mainly whole wheat, barley, maize, apricots and milk. He describes them as “unsurpassed in perfection of physique and in freedom from disease in general, whose sole food consists to this day of grains, vegetables, and fruits, with a certain amount of milk and butter, and goat’s meat only on feast days.” His findings are documented in Guy Wrench’s “Wheel of Health.”

                    Egyptians and Otzi had the unfortunate dental abscesses from millstone grit and sand which destroyed their teeth and their health. Difficult to know how they would have done without that issue.

                  2. Rice is so low in protein that I think of it as a “filler”, rather than a staple. Eating beans with rice improves the AA profile a lot. Tubers are good.

                    In the 1st world, the problem is over-consumption. For nearly 100 years, the 1st world masses have been manipulated to over-consume, as it keeps them happy & docile and it’s good for the economy.

                    Have you seen ?

                    1. I agree, white rice is totally nutrition-less. Which is what makes the Kempner studies so amazing. Even more amazing to me is that the Chinese railway workers were noted as being MORE healthy on a diet of mainly rice and vegetables and dried octopus, than the Irish beef and potatoes guys. OK, the Chinese boiled their water and did less whisky! But still … they worked 10-11 hour days at hard labor on mainly rice, lived in hard conditions, and were noted for being “healthy”.

                      Billions of people live off mainly rice. They DO get nutrition problems if they don’t also get some vegies and protein too. But given that, they do fine and tend to be healthier than the people getting the Western diet.

                      I think the idea that scarcity protected people is mostly a myth. Comparisons have been done calorie-for-calorie with Westerners, for the same exercise levels. The Chinese often eat MORE calories for the same exercise level, and yet tend to be skinnier and healthier. Your average Japanese doesn’t go to bed hungry either, and is likely more healthy than the average American.

                      However, the Chinese have *less* tolerance for “The Western Diet”, whatever that is .. and get diabetes with less weight gain. It seems to have something to do with the actual food choices.

                    2. Asians appear to have limited Sub-cutaneous Adipose Tissue (SAT) hyperplasia, which limits fat storage capacity below the skin. As a result, Visceral Adipose Tissue (VAT) stores are filled prematurely, leading to the Metabolic Syndrome, as VAT deposits are much more metabolically-active than SAT deposits. This is a.k.a. “Skinny-fat”.


                      The SAD/SED combination of refined carbs + fats results in fats being stored, as carbs are burned preferentially. A high-carb, low-fat diet suits Asians much better!

                    3. Having re-read what I wrote about Adipocyte Hyperplasia and the comments from June 2012, the following thought processes occurred:-

                      Adipocyte Hyperplasia occurs mostly during childhood, as that’s when rapid hyperplasia of other cells occurs a.k.a. growth.

                      A slim child which becomes a slim adult has few SAT adipocytes, predisposing said adult to get excess VAT rather than SAT if chronic over-eating occurs during adulthood.

                      A fat child which becomes a fat adult has lots of SAT adipocytes, allowing said adult to get rolls of SAT rather than VAT if chronic over-eating occurs during adulthood.

                  3. heathertwist said: “I haven’t yet seen a culture with healthy people living mainly off wheat or barley though. Even in the ancient Egyptian and Roman days … skeletons of the rich and the poor were both pretty bad. Even Oetzi, with all his exercise.”

                    Indeed there were healthy grain eating cultures that were observed in the early 1900s when various of prominent doctors were researching nutrition, at the time. The idea that grains are not a good food for humans comes from the “porotic hyperostosis” study of ancient skeletons. The bones of early farmers were found to have lesions which were thought to be due to iron deficiency as a consequence of eating grains instead of meat.

                    However, it only became clear a few years ago (2009) that the lesions were not due to iron deficiency, making the original hypothesis flawed.

                    The causes of porotic hyperostosis and cribra orbitalia: a reappraisal of the iron-deficiency-anemia hypothesis (2009)

                    So, the original hypothesis is obsolete—yet it is still used to claim that grains are problematic. The skeletal lesions were perhaps due to episodes of starvation or something else. We don’t really know. But, I’m not sure why grains would be assumed to be the only culprit of causing such lesions and skeletal issues. Now that the original hypothesis has been deemed obsolete, another explanation is needed.

                    Keep in mind that societies became larger, infections were more rampant, and food was scarce at times. Societies were adapting and there was a lot of turmoil. Mass starvation was also said to have happened as early farming practices depleted the soils to oblivion. Some say this turmoil and social stress is evident at archaeological sites like Göbekli Tepe and Caynou, where mass death, genocides or sacrifices appear may have happened.

                    Also the high levels of cavities in early Neolithic skeletons has been attributed to the wearing down of teeth from poor milling standards. Attrition broke the enamel, which led to dental abscesses and promoted cavities.

                    See: Teeth and Bread in Ancient Egypt (1972)

                    This is very different from the sugar-promoted cavities we have today. (Honey was their main sugar, but honey is believed to be protective of dental caries). Arteriosclerosis has been linked to dental infections. If we wanted to, we could probably link all of their health issues to poor dental health and starvation, but that too would be highly speculative. Incidentally even Paleolithic teeth have also been found to have significant wear and tear.

                    The point being is that it’s very easy to create a narrative both vilifying and defending grains by using ambiguous archaeology.

                    1. “Indeed there were healthy grain eating cultures that were observed in the early 1900s when various of prominent doctors were researching nutrition, at the time. ”

                      I would really like to see such a study! I’ve been looking. There are loads of healthy skeletons of “grain eaters” in general, just not wheat-eaters. Hard bran and everything, their teeth might wear down, but they didn’t have the soft enamel that has become common now. If you combine the soft enamel with sugar, it causes cavities. But most cultures don’t have soft enamel: just a few do, and those ones also have significant skeletal changes (crooked teeth, narrow mouth etc) which one associates with vitamin malabsorption.

                      It’s also not clear what the “prominent doctors” considered “healthy”. Price was rather specific: he counted cavities and took pictures of the dental arches! But the cultures he considered “healthy” were oat-eaters. And the Swiss, who ate barley bread. The Swiss also drank a lot of raw milk though, and it turns out that raw milk interferes with one of the factors in wheat that is a problem. Also, it turns out that the Swiss had gone through a big problem with goiter not long before Price studied them. The Swiss government started trucking in iodized salt because so many of the recruits failed their physicals because of goiter.

                      He did notice that English poor folk got healthier when supplemented with whole wheat bread, raw milk, and cod-liver oil. Which may show that whole wheat is better than white wheat, or that raw milk really does help, or that the vitamin involved happens to be in cod-liver oil. Anyway, the Chinese did fine on white rice and vegies and fish, for the most part, without extra raw milk or cod-liver oil.

                      The main reason I got curious about this was my daughter. Until she was 6, she ate a normal US diet, and her tooth enamel was really soft. “Sticky” as the dentist put it. She got cavities constantly. Then we switched from wheat to rice, and her next visit … no sticky teeth. Didn’t get any more cavities from that point, even though she ate (and eats) plenty of sugar.

                      So for some people, at least, it turns out that wheat messes with vitamin absorption and also with the gut biota, which is where Vit K is produced. I don’t know if it’s Vit K or Vit D or what else, but I think something is going on that interferes with skeletons and teeth.

                      It could well be that this happens a whole lot less with whole boiled or parched grains … those digest slower and feed bacteria less. The whole grains … of any type … also interfere with iron absorption but in general I think that’s a good thing (as was some level of hookworm!).

                      Anyway, sure, one can skew history, and skew statistics. But it’s a weak argument. Anyway, I’ve never made the argument that “grains” caused anything bad: just one or two particular grains which have weird effects on humans.

                    2. heathertwist said: “I would really like to see such a study! I’ve been looking.”

                      Are you not familiar with McCarrison’s observations on the Hunza? They ate a lot of whole wheat and milk and a few other foods, of course (even the bible says one cannot live on bread alone). McCarrison also did experiments on rats where he gave one set of rats a British diet (white flour, margarine, etc) and another set of rats the Hunza diet of whole wheat and milk. The rats eating a Hunza diet had no discernable disease. His study was done to prove that the success of the Hunza diet had nothing to do with genes.

                      Sir McCarrison presented his findings before the Royal College of Surgeons and his observations are summarized in the 1938 book, “The Wheel of Health,” by Dr. Guy Wrench. (Free on Google Books).

                      In his lectures, McCarrison remarked:

                      “In conformity with the constitution of their dietaries they are the finest races of India, so far as physique is concerned, and amongst the finest races of mankind. Familiar as I am with the [wheat]-fed races of northern India, I have little patience with those who would have us believe that ‘white flour’ is as good an article of diet as ‘whole wheat flour’.”

                      He was their doctor for 7 years and described them as one of the finest and physically fit races he had ever seen. The Hunza are no longer healthy now eating a modern diet.

                      heathertwist said: “There are loads of healthy skeletons of “grain eaters” in general, just not wheat-eaters.”

                      Well, if you dig into the history books, you’ll see that wheat was considered the healthiest and most revered of all foods. The word cereal comes from the name for the ancient Roman goddess, Ceres—the goddess of grains and agriculture. Ceres was said to have discovered wheat, and given the gift of agriculture to humankind.

                      Hippocrates not only recommended wheat bread, but experimented heavily with different preparations.

                      If wheat was so deleterious, you’d think that Hippocrates would have noticed it and warned against its consumption instead of recommending it for the prevention of disease.

                      Avicenna recommended bread as a key staple of the diet. Paracelsus believed that wheat had mystical properties, and Aristotle thought foods made from wheat suits our bodies best. A 19th century encyclopedia says that wheat is the most nutritious and most important edible plant in the entire vegetable kingdom. Surely if wheat was so terrible, we would see evidence in the history books.

                      Over 250 years ago, Swedish biologist Carl von Linné, the father of modern taxonomy and modern ecology, wrote two texts—Ceres noverca arctoum and De pane diaetetico—that were wholly devoted to bread and bread-making. Citing his own observations as well as those of the greatest medical authorities of antiquity, he wrote.

                      From: De pane diaetetico, by Carl von Linné (1757)

                      Of all foods bread is in truth the most noble. It is a food that is so necessary that we usually describe a true pauper with the words “he has not even a crumb of bread”. It is served on the tables of both the rich and the poor, is beneficial in all diseases and suitable for all temperaments and it imparts a pleasant taste to food that is of itself tasteless. Therefore, since bread is so widespread and strengthens us and pleases our taste, I beg you distinguished reader, to not feel disturbed by paying attention to a dietetic investigation of bread.

                      Von Linné also provided examples of how bread could prevent or cure specific diseases. Although rye was popular in his home country of Sweden, von Linné considered wheat bread to be “the most excellent of all.”

                      In the 19th century, Thomas Hodgkin, the prominent English physician and first to observe Hodgkin’s disease, wrote:

                      The means of promoting and preserving health. Lecture II, on the Articles of food, solid and fluid, by Thomas Hodgkin (1841)

                      The farinaceous seeds are unquestionably the most important of [alimentary vegetable substances]…

                      Of Wheat.—This appears to be the oldest and most valuable grain with which we are acquainted… It contains a large quantity of starch; a highly nutritive principle; and a larger quantity of gluten, the most nutritious of all the vegetable principles, than any other grain.(1) …It is far superior to every other kind of grain, for the formation of bread, which is emphatically termed the “staff of life” and, in all civilized countries, forms so large and considerable a part of our diet, that the word “bread” is become almost equivalent with that of “food.”

                      Seeing, then, that wheat, in the form of bread, is of so great importance as an article of diet, it will be worth while for us to dwell a little upon the varieties of bread, and on some points connected with its use…

                      heathertwist said: “Price was rather specific: he counted cavities and took pictures of the dental arches! But the cultures he considered “healthy” were oat-eaters. And the Swiss, who ate barley bread.”

                      Actually, Price said the Swiss ate whole rye bread and milk. Price wrote:

                      “The nutrition of the people of the Loetschental Valley, particularly that of the growing boys and girls, consists largely of a slice of whole rye bread and a piece of the summer-made cheese (about as large as the slice of bread), which are eaten with fresh milk of goats or cows. Meat is eaten about once a week…Of all the children in the valley still using the primitive diet of whole rye bread and dairy products the average number of cavities per person was 0.3.”

                      “Anyway, sure, one can skew history, and skew statistics. But it’s a weak argument.”

                      I’m mainly pointing out that people often use the Neolithic skeletons to demonize grains when in fact nobody actually knows what actually caused the bad skeletons. If wheat were so problematic, you’d think somebody would have noticed this before white flour triggered the dyspepsia epidemic in the 19th century. Yet, everyone who wrote about wheat seemed to think it was the best thing since, well, sliced bread.

                    3. OK, some people say the Hunzas are awesome. I don’t see a lot of evidence for that … unlike the Okinawans, Sardinians, Japanese mountain people, Masai … where are the studies? One visitor did write a book about them and noted:

                      “As their diet is deficient in oils and vitamin D, all Hunzas have soft teeth, and fully half of them have the barrel chests and rheumatic knees of sub-clinical rickets.”

                      As paleoedge noted:

                      “But there is a problem with this climate theory; why did the Inuits maintain their darker tone? The reason is theorized to be because northern Europeans switched vitamin D rich meat for low-fat vitamin D deficient grain, while the Inuit maintained a vitamin D rich meat based diet without grains. It turns out, Dr. Cordain found out that wheat contains an anti-nutrient called WGA, a lectin that binds to cellular glycoproteins. Once in the gut, WGA binds to a cell receptor, and then a nuclear pore found in every cell in the body that blocks the transport and absorption of vitamin D. According to Dr. Cordain, WGA has a half-life of four hours, which means if you are sunbathing while consuming wheat, the vitamin D is most likely being blocked from the sun. Whoa!”

                      However, my grandmother grew up in Germany, and lived to be 96. Her diet included wheat, but really not that much … like the Hunza, there were a lot of other vegetables, lots of dairy, and limited meat. The grains tended to be mainly oats. They rarely got wheat growing up (it was for rich people) and it was a lower-quality wheat at that.


                      Actually there is a theory that white skin actually developed in the Middle East, as an adaptation to eating wheat. The white skin people eventually moved North, and I guess the people that live there now are better adapted (or just sickly: what are the caries rates in the Middle East?).


                      “Then, the first farmers from the Near East arrived in Europe; they carried both genes for light skin. As they interbred with the indigenous hunter-gatherers, one of their light-skin genes swept through Europe, so that central and southern Europeans also began to have lighter skin. The other gene variant, SLC45A2, was at low levels until about 5800 years ago when it swept up to high frequency.”

                      Interestingly, Sardinia, which was one of the wheat-exceptions, appears to be no longer:


                      “According to Sarah Wilson who visited Sardinia with National Geographic, “the longevity phenomena seems to have come to an abrupt halt, even reversed. It’s almost like as soon as money came to the island (which it did about 50 years ago) the locals went from famine to feast, taking on the health consequences that come with abundance. Young Sardinians are incredibly overweight. And Sardinia has one of the highest incidences of celiac disease, I’m guessing from eating so much bread and pasta where the gluten content has shifted due to the more processed wheat strains available today.”

                    4. heathertwist, Duck Dodgers: I have also read that the health of the Hunza was not all that awesome, though it was better than most people’s health today. Like most native cultures, they did have an absence of diabetes, cancer and heart disease; however, compared to other native groups, they did have goiter, and a reasonable number of cavities.

                      heathertwist, I believe in another post you mentioned that you are a celiac? Me too! “Welcome to the club”. In researching celiac disease years ago, I remember reading that most of those cultures that did eat wheat traditionally also ate many more other grains, mostly gluten free, like millet or teff, buckwheat, etc. In other words, they varied their grains. It was stated that we as a culture today eat far more wheat than most cultures of the past, because we eat almost exclusively wheat. (For instance, I’m pretty sure I’ve read that the Hunza also eat buckwheat and millet). Some of these other types of grains have become obsolete, and few people in the West even know about them. (Apparently, wheat is more convenient to grow and transport). And my guess is that if the Swiss were eating lots of rye bread, it was most likely fermented sourdough; this would remove some of the anti-nutrients and make it more digestible- (I don’t know: Weston Price didn’t mention that they fermented it. However, wheat was traditionally fermented, so maybe he didn’t feel the need to mention it?) It could also be possible that drinking full fat milk, and/or eating meat (or cod liver oil) helps mitigate some of the harmful effects of wheat by replacing nutrients. So in other words, eating wheat in a traditional culture would be different from eating lots of wheat and sugar with low fat milk in a modern day culture.

                      In any case, wheat bread of the past was very different from modern wheat bread. Not only was the wheat different- (it was lower in gluten; the bread would have been flat, dense, and not “fluffy”)- it might have been fermented, and, nowadays, there are many shortcuts to bread making. Rather than relying on a long process of letting the dough rise, there are many additives that are used today to speed up the process. Not only are some of these additives questionable for human health, but also, in not using a slow, traditional process, it might make the wheat more deleterious.

                      Finally, I don’t think we can have a discussion about wheat without mentioning that which interests me the most: the opioid effects! Duck Dodgers, I wonder if many of these historical figures praised the benefits of wheat because it makes people “feel good”? It is definitely, absolutely addictive, like sugar; I see many people who are addicted to it, all around me. (I was addicted to it even while it was killing me). Some have even suggested that the widespread shift from hunting and gathering to farming may have had something to do with opiates and addiction. I find that theory very interesting……

                    5. “heathertwist, I believe in another post you mentioned that you are a celiac? Me too! “Welcome to the club”. In researching celiac disease years ago, I remember reading that most of those cultures that did eat wheat traditionally also ate many more other grains, mostly gluten free, like millet or teff, buckwheat, etc”

                      Well thanks! An interesting time to be part of that club … !

                      There is something interesting going on with the heritage wheat too. One of the aid organizations sent some wheat berries to a town that traditionally ate mainly wheat. But the kids developed celiac symptoms from the American wheat. It probably shouldn’t be toooo surprising … heritage corn and beans are sure different from the modern ones. But the heritage wheat didn’t seem to help the Egyptians or Romans, so it’s hard to say.

                      “And my guess is that if the Swiss were eating lots of rye bread, it was most likely fermented sourdough; this would remove some of the anti-nutrients and make it more digestible- (I don’t know: Weston Price didn’t mention that they fermented it. However, wheat was traditionally fermented, so maybe he didn’t feel the need to mention it?)”

                      I haven’t seen that rye and barley are anywhere near as harmful as wheat though. It is true that celiacs cross-react to rye and barley, but would a culture that ONLY ate rye and barley have the same issues? Celiac is a very specific kind of auto-immunity, but there doesn’t seem to be a similar kind of illness that is triggered by, say, millet or quinoa.

                      The “healthy Swiss” weren’t all that healthy either. They had a super-high rate of goiter until the Swiss government started trucking in iodized salt circa 1920.


                      Now, my grandma grew up in a German village and she did live to a grand old age (96) with no heart disease, high blood pressure, tooth loss, etc. She didn’t get white wheat much as a kid (they got a slice per week as a treat) but she certainly ate it a lot, esp. cookies, when she came to America. But further, she was somewhat sun-phobic and kept the shades drawn, and covered herself from head to toe with long sleeves, high necklines, thick stockings, hat … which was traditional for her growing up. So I always wondered why she never got rickets? Or goiter, for that matter.

                      The answer appears to be that in her day, one of the favorite foods were fish. Pickled herring was big, and river eel, and even salmon. Another favorite food was mushrooms, which they gathered themselves in the local forests. Mushrooms dry and keep very well, and guess what? They are an incredible source of Vit D, esp. if they are sun-dried, and actually high in protein too. Cheap food for anyone who wants to gather them. Otzi was found with a string of dried mushrooms!

                      “Placing regular mushrooms in direct sunlight for an hour (winter) will generate your daily needs of vitamin D in a serve (100g or three button mushrooms – See more at:

                      Price used cod liver oil as a magic cure of sorts, which would provide Vit D and Vit A (the two that tend to be problematic), and, I think, iodine?

                      So maybe that is part of the reason the Egyptians had more issues with wheat … it was too hot and dry there to have a lot of mushrooms!

                      ” It is definitely, absolutely addictive, like sugar; I see many people who are addicted to it, all around me. (I was addicted to it even while it was killing me).”

                      Amen to that! I think this is one reason that there is such a strong reaction to the “anti-gluten” people. I mean, in our culture, we have people who won’t drink milk, won’t eat sugar, won’t eat meat, won’t eat chocolate unless it’s fair trade … I’ve gone on my share of food experiments. But the “no wheat” food experiment had people talking to me like I’d joined an evil cult and they got seriously angry.

                      Also though when kids stayed overnight at our house, they would start going bonkers at the end of day 2. Got headaches and had anger fits. One, her Mom reported, started screaming on the drive home “I have to have spaghetti!” so they stopped for food. There was not spaghetti so the girl had a meltdown. Mind you we DO have spaghetti and bread, and these kids were too young to understand that our spaghetti was missing the gluten part. But they definitely were going through withdrawals.

                    6. heathertwist- I had a look at the link you posted about the Swiss. They mention that some “alpine villages” had problems with goiter, but there was no mention of the specific valley that Weston Price visited, where the people were so healthy: the Loetschental Valley. It was a very remote part of Switzerland where the people still ate only traditional, natural food, whereas in most other parts of Switzerland the people ate very differently. As I recall, he made the distinction that the people in this valley were much healthier than the average Swiss elsewhere. So I’m still not sure about that; unless there is a link somewhere that states specifically that those people had goiter?- (but even if they did, it may be hard to find the evidence). So, who knows?

                      That was very interesting what you wrote about people getting sick when their heritage wheat was replaced by American wheat!

                      There is also the theory that in some African countries, where the people are starving and are fed government rations of wheat, some of those children who still look emaciated may be suffering form celiac disease rather than actual starvation. I think there was no proof of this, just speculation, but I hope someone is looking into this possibility. When people suddenly eat lots of wheat when it’s not part of their traditional diet, celiac is likely to occur.

                      Also, I guess that was a good point about rye and barley. Although they both have gluten, they are most likely not harmful in the way that wheat can be. I guess it’s possible that a culture eating just rye and/or barley may not have the same problems as wheat eating cultures.

                      Last thing about wheat: Denise Minger, in her “China Study” rebuttal, noticed there seemed to be a correlation between wheat eating groups of Chinese and heart disease.

                    7. The bit I read about the wheat berries in food aide was an actual report, not just an anecdote. But it was years and years ago!

                      Yes, Denise did an amazing job of analyzing The China Study in terms of wheat, rather than meat. It is the case worldwide that the places that grow wheat tend to also be the places that have cows or goats … they are the inland people! The coastal people can get food more easily by eating fish, and rice grows better in warm or wet places (wheat gets moldy easily). Inland people have other confounding issues too, notably lack of iodine and lack of fish. The more fish people eat, the statistically more intelligent they tend to be.

                      Cordain is saying that the WGA in wheat is what blocks the Vit D … not the “gluten” (gluten is a total misnomer, but the term has stuck!). WGA stands for “Wheat Germ Agglutinin” Barley and Rye have something similar, but I don’t know that it is the same thing. Try baking bread from barley or rye and you get the idea … they are really different.

                      I also don’t know to what degree raw milk blocks the process. Apparently it DOES block a lot of it, which might be one reason why raw milk got suck kudos as a health food. Drinking raw milk with your wheat might be the magic bullet-dodger!

                      “On another note, not only does wheat contain gliadin, which upregulates zonulin, which increases intestinal permeability, it also contains an obscure compound (thaumatin like proteins) which also increase intestinal permeability. Hence wheat represents a triple time bomb (gliadin, WGA and thaumatin like proteins) which maintain physical and physiological characteristics that almost certainly impair gut function, interact with our immune systems to produce low level inflammation, and impair vitamin D metabolism (not a vitamin at all, but a hormone having receptors in virtually every cell in the body).” (Cordain)


                    8. Interesting link! There’s a lot about wheat there.

                      I have also read about wheat and vitamin D, in other sources. (As well as the idea that white skin might be a recent adaptation to grain eating). It’s all very interesting.

                      There’s also some evidence that wheat eating might interfere with magnesium absorption.

                    9. Oh yeah, and I forgot to mention, that was totally fascinating about the children going through wheat withdrawal! Yes, I can believe it too. I’ve seen this kind of thing; (with sugar too). As wheat and sugar often appear together in foods, that’s a double whammy.

                    10. heathertwist said: “Dr. Cordain found out that wheat contains an anti-nutrient called WGA, a lectin that binds to cellular glycoproteins.”

                      Matt LaLonde, and many others, have questioned Dr. Cordain’s overlooking the fact that people do not eat raw wheat…

                      Mat Lalonde said: “It turns out that most lectins, especially the most well-studied ones like wheat germ agglutinin, PHA, which is in legumes, which is phytohaemagglutinin, they are deactivated by heat. These proteins are very sensitive to heat, and they’re destroyed. So people waving their hands in the air like, ‘Oh my God, these things are really toxic!’ and whatnot. And it’s true. They are very toxic. We have the research to show that they are toxic in animals in vitro when they’re fed to animals, but it turns out that they’re feeding raw legumes or pure isolated proteins to these things, not cooked food…

                      …There are some lectins that are not deactivated by heat that do survive digestion, make their way into the bloodstream, and are likely very allergenic, and one of those is peanut lectin. And that research has been done. If you have people eat raw or roasted peanuts and you look at the level of lectin that goes into their blood within one hour of consuming those peanuts, you see the lectin levels rise. So there are some that are dangerous, but you should not assume that an entire class of chemicals is…that all of them are dangerous if they haven’t been individually tested.”

                      Even Dr. Ayers, an actual glycobiologist, says that cooked lectins are fine (see his user comments, below the post, where he discusses WGA).

                      heathertwist said: “On another note, not only does wheat contain gliadin, which upregulates zonulin,”

                      Actually, certain ancient types of tetraploid wheat (e.g.; Graziella Ra, Khorasan wheat/Kamut) have even greater amounts of total gliadin than modern accessions. Interestingly, during the 1800s, gluten (and gliadin) were considered to be the most nutritious vegetable compound. This may explain why cultures preferred wheat varieties with higher levels of gluten. For instance, Einkhorn was the least reactive wheat, and more reactive wheats were preferred by cultures, even during the Neolithic.

                      In the 19th century, doctors recommended gluten bread for diabetics. 6th century Chinese actually added wheat gluten to their foods as a protein source. It’s only been since about 1950 that people began to have problems with gluten. Of course, everyone blames “modern wheat varieties” but few seem to notice that wheat is now heavily processed (fumigated, reconstituted and sometimes bromated). Also, the protective oils often removed to improve shelf life. It’s a bit like adulterating, fumigating and removing the Vitamin E from a mongongo nut and wondering why someone eating those heavily processed nuts would have health issues.

                      heathertwist said: “which upregulates zonulin which increases intestinal permeability, it also contains an obscure compound (thaumatin like proteins) which also increase intestinal permeability. Hence wheat represents a triple time bomb (gliadin, WGA and thaumatin like proteins) which maintain physical and physiological characteristics that almost certainly impair gut function,”

                      Those who make this insinuation—that a temporary upregulation of zonulin promotes health issues—are often the same people who recommend using liberal amounts of coconut oil for cooking and eating. Ironically, these individuals don’t seem to realize that lauric acid, found concentrated in coconut oil, is known to upregulate zonulin and causes the same intestinal permeability that gluten does.

                      There’s little evidence that a temporary upregulation of zonulin is problematic in a healthy individual. For all we know, it may plat a role in oral tolerance.

                      Even celiac researcher Alessio Fasano explains that it’s no big deal for healthy people:

                      Alessio Fasano said: “I eat a Big Mac. I have gluten in there. These fragments release zonulin, which increases permeability. Stuff comes through, including gluten. My immune system that is tuned to do the job right will clean up the mess, and I will not even know that all that happened. Also because this open-and-close is short. It’s a matter of minutes that it will open and a matter of minutes that will turn to be closed.”

                      He goes on to explain that people with celiac secrete too much zonulin and their tight junctions stay open longer than it should.

                      Anyhow, it’s probably unhelpful wise to scare healthy people into fearing these normal processes, particularly when other popular foods, like coconut oil, have the same likely normal effect.

                    11. Uh oh….I do eat raw peanuts from time to time. But I don’t notice myself having issues with them at all. In fact, I’m normally quite sensitive to foods; I have trouble digesting most other legumes, even if they are soaked and cooked. Could it be that it’s personal, and our bodies react differently to lectins and other anti-nutrients?

                    12. Yeah, some groups have spent thousands of years adapting to wheat (and to milk!) and some groups have not. And some people don’t think they have any much reaction at all. There is just this amazing coincidence that the healthiest cultures are the ones with the least wheat, and that a lot of people drop wheat and suddenly feel a whole lot better. And things like the China Study. My prediction is it will be like say, “Sugar of Lead” … the rich Romans added it to their wine and no one could see any problem with it. Except rich people kept going crazy.

                      Anyway, lectins are not always destroyed by heat. Gluten for sure isn’t … the whole point of gluten is to get bread to rise. WGA maybe could be destroyed by cooking it enough, but apparently it is not:

                      “.whilst variable amounts of agglutinin were found in wholemeal pasta probably as a consequence of thermal inactivation during food processing..”


                      “The concentration of WGA in white flour is about 3 to 4 milligrams per 100 grams, whereas in whole wheat it’s 10 times that, it’s an order of magnitude higher. But at physiologic levels, we’re only talking nanogram concentrations in bloodstreams. We know from tissue studies, these in vitro studies, that cells respond at nanogram concentrations, so nanogram concentrations can easily be achieved by consuming 4 to 7 milligrams per 100 grams.”


                      So they are working with WGA as a drug-delivery system and it works it seems in really tiny amounts. There aren’t many lectins in canned beans, but there are some left in homemade beans, and it’s fairly common for people to get sick (and even die) from home-cooked kidney beans. Cooked bread has “variable amounts” of WGA in it, and some of it is inactivated by other foods with it. Or not. So the effect likely has to do with how it’s cooked, what you eat with it, and what your genes are. Hardly a glowing recommendation for a highly wheat-based diet.

                      Fasano is Italian, and hardly a health-food person. He’ll probably live a normal Italian life and get arthritis and heart disease at the usual age, like all the other Italians, who are in fact the most wheat-adapted. He likely takes Vit D pills or eats Vit D enriched foods too, and has his cavities filled like everyone else. He’ll get osteoporosis as expected as he gets older and likely a few root canals. So he’ll live longer than a celiac would who was eating wheat, and won’t live with a constant stomach-ache … and he’ll be able to eat Big Macs and pizzas, which is important to him. But will not live as long or be as healthy as the average Japanese mountain villager.

                      But what would his life be like if his Big Macs did NOT have wheat in them? (or added iron, for that matter). That is the question. The experimenters who are trying it out … the no wheat lifestyle … are beginning to answer that question. Maybe it’s just another odd dietary fad. Or maybe the non-wheat people will end up being quite a bit healthier. Right now we have these massively parallel food experiments going on with fat, sugar, meat, GMO, fish, and grains. I say the more the merrier … try something out, see how it works for you, and share with the rest of us.

                    13. “Could it be that it’s personal, and our bodies react differently to lectins and other anti-nutrients?”

                      It’s definitely personal, but our flora are likely responsible for much of our adaptations.

                      We find indigenous cultures take steps to minimize wild plant toxins, but wild plant toxins often make our domesticated foods look quite tame (domestication is a kind of toxin reduction). Their gut flora adapts to their diet.

                      This is a key point to understand because while on the surface we often don’t have the ability to digest certain foods, like dairy, seaweed, or grain toxins, our gut flora can quickly adapt to break down those foods. For instance, most Masai are lactose intolerant, but their flora adapts to their high dairy diet. Japanese individuals possess the genes for the consumption of the algal polysaccharide porphyran in their microbiomes, which are rarely found in North American and European individuals. We cannot digest phytate, but our flora can.

                      Plus most lectins and antinutrients are also known to have beneficial properties:

                      Potential health benefits and problems associated with antinutrients in foods (1993)

                      Phytic acid, lectins, phenolic compounds, amylase inhibitors and saponins have also been shown to reduce the blood glucose and insulin responses to starchy foods and/or the plasma cholesterol and triglycerides. In addition, phytic acid, phenolics, saponins, protease inhibitors, phytoestrogens and lignans have been related to reduced cancer risks. Because antinutrients can also be mitigating agents, they need re-evaluation and perhaps a change in name in the future…It is evident that both adverse and health benefits may be attributed to antinutrients in foods. It is also evident that, in many cases, the same interactions that make them antinutritive also are responsible for their beneficial effects.

                      The dreaded kidney bean lectins have anti-fungal and anti-viral activities and lectins in general have anti-cancer properties too. Phytates have anti-cancer functions and therapeutic properties against diabetes mellitus, atherosclerosis, coronary heart disease and reduces kidney stone formation. Toxic glycoalkaloids, found in potatoes and nightshades, have been shown to offer antiallergic, antipyretic, anti-cancer and anti-inflammatory effects; blood sugar-lowering effects, and anti-pathogenic effects against viruses, protozoa, and fungi. Cyanogenic glycosides have anti-cancer properties. Phytosterols, polyphenols, flavonoids and tannins, alkaloids, phytates all have anticancer, antioxidant or endocrine normalization properties as well.

                      Notice a pattern? Antinutrients are not so black and white after all. They aren’t always bad. In the context of adapted gut flora, I suspect they help maintain homeostasis (i.e. a proper balance of what we might consider “good” or “bad”… yin/yang).

                    14. Duck Dodgers- thanks for the clarification about lectins (and other anti-nutrients. Actually, I had read that about phytates before, but I didn’t know it applied to the others). This explains why I feel fine with peanuts (though I eat them in moderation), as well as nightshade vegetables, of which I eat a lot of! Not only do I digest them well, but they don’t seem to be causing me any harm and I feel very healthy when I eat them. However, I’m not sure about the “adaptation” theory; though I had exposure to foods like wheat and soy for a good part of my life, I never “adapted” to them. I think it probably has to do with more than just damaged gut flora- (if anything, I think those foods might have caused damaged gut flora, in my case). And there are so many vegetables and fruits that most people think of as being benign and even healthy, that I can’t digest at all! Basically, I just go by how I feel, and screw all those conventional “recommendations”.

                  4. “There is just this amazing coincidence that the healthiest cultures are the ones with the least wheat”

                    Yes, an amazing coincidence that those who eat the most white flour are unhealthy. Like most anti-wheat sentiments, this statement conflates the difference between white flour eating cultures and traditional whole wheat. It should be obvious that any refined food is problematic, and wheat is the king of refined grains in the modern world.

                    The problem with that conflation is that it ignores the cultures that thrived on, revered and worshiped wheat. Prescribed by Hippocrates, Paracelsus, Avicenna, Aristotle, favored by the Spartans, the Greeks and the Romans, and observed by countless scholars who wrote about its health effects. In every single instance, throughout Western history, wheat was unanimously considered to be the healthiest of all foods by the most prominent medical authorities—and this sentiment existed until the industrial revolution.

                    Furthermore, gluten was discovered in 1742 and even through the 19th century was believed to be the most nutritious plant compound. Not only did most cultures prefer higher gluten wheats, but it’s only since the 1950s that many people began to have trouble with gluten.

                    Anyhow, the “amazing coincidence” would be like condemning all meats without recognizing that processed meats are completely different from eating whole animals. It’s misleading. If you’ve never seen how modern flour is made, it’s extremely processed.

                    Let’s not pretend that modern wheat milling is indicative of traditional wheat consumption. It’s common knowledge that bread is broken.

                    1. Good points. Qualitative, mostly-opinion statements like “the healthiest populations eat the least wheat” are problematic for many reasons: their qualitative nature; their failure to define what “healthiest” is; their failure to present any quantitative analysis; their dependence on apparent correlations, rather than establishing causative relationships; their failure to deal with confounding factors; and many others. Of course, the statements in support of wheat suffer the same shortcomings. And many of the assertions are made without any backup from the historical record. For example, sea vegetables are not a food that only the Japanese began to eat in quantity, and then only in recent times. Coastal peoples throughout the world have used them for many centuries.

                    2. Qualitative? In terms of say, the Hunzas … there isn’t much data. But in terms of the China Study … it is much more studied. Also the Japanese mountain people. They exist NOW and aren’t hard to find or hard to study.

                      In terms of ancient peoples … we are getting good data now too. The plaque off Neanderthal’s teeth, or the contents of Oetzi’s stomach … yeah, we are understanding exactly what they were eating. The Romans kept records of what they fed their slaves, and we have the bones of the slaves to compare to. And of the nobles (a lot of them are full of lead!). The railroads in the 1800’s have exactly what they fed to their workers too, and loads of data about illnesses.

                      It’s basically an exciting time, I think. A lot of research is finally coming to a kind of “universal field theorem” of human nutrition. I’m not sure anyone knows where it will lead. Like Denise, I’ve gone down a lot of tracks in studying this, and I’m certainly not going to say “Hey, but THIS TIME I’m right!”. We should share though, because that’s how we get to the next step.

                    3. Absolutely, the statement I flagged as qualitative is exactly that. There are reams of data on many populations, but that does not make the statement. “the healthiest populations eat the least wheat” any less qualitative. Healthiest in terms of what criteria? Which populations were evaluated and by what criteria? Is there a positive correlation between quantity of wheat consumed and “healthiness”? If so, is it statistically significant? Is there a tabular or graphic illustration of the correlation? If such a correlation exists, what confounding factors may have influenced it? The statement as it was made is a classic illustration of a qualitative statement on the subject of diet and health.

                    4. “Is there a positive correlation between quantity of wheat consumed and “healthiness”? If so, is it statistically significant? Is there a tabular or graphic illustration of the correlation? If such a correlation exists, what confounding factors may have influenced it?”

                      And the problem is that the discussion around the qualitative statement usually goes like this:

                      Person A: Studies and published observations show that whole grains are considerably healthier than refined grains and refined grains tend to promote degenerative diseases.

                      Person B: There is evidence that wheat promotes chronic disease.

                      Person A: No, you found evidence that refined white flour promotes chronic disease. But we already knew that.

                      Repeat ad nauseam.

                    5. “Which populations were evaluated and by what criteria? Is there a positive correlation between quantity of wheat consumed and “healthiness”? If so, is it statistically significant?”

                      I’m basically pointing you to Denise’s excellent (and detailed) analysis of the China Study. There are books and studies that say more or less the same thing, though yes, most of them are not so detailed. The China Study though was of a large population, eating largely homegrown foods, in towns where the population typically ate the same kinds of foods day in and day out. Denise crunched the numbers. She does have the results.

                      “Wowza! By the way, wheat flour also correlates significantly with hypertensive heart disease and stroke, but I’m mainly going to look at coronary heart disease in this post. (And although wheat looks like it could have a nonlinear relationship with heart disease, with the highest wheat eaters having disproportionately steeper rates than non-wheat eaters, I’m going to treat it as linear for the sake of this analysis. That way, the worst that’ll happen is we’ll underestimate the potential effect of wheat, which—for now—is better than overestimating it.)”


                      I expect there will be a lot more hard data in the next decade or so, esp. as so many people are doing their various “diet experiments”. All those n=1 experiments do add up eventually. There have been some interesting studies though, done on correlations between, say, anti-gliadin IgA and the prevalence of certain diseases. Or the percentage of people whose symptoms get better on a non-wheat diet even though they are not celiac. Anyway, they are detailed and there are dozens of them.



                    6. Duck, you say to Heathertwist: “…One could easily create any narrative they wanted to with such vague clues. I’ve often wondered if the whole point of Paleo™ is to base a particular diet on extremely ambiguous data.” This to sum up your words on Oetzi, how there are many factors, not just diet, that affected his health…”

                      We can say the same about early grains! Even early grains may well have been much less healthy for us than a hunter-gatherer diet.

                      In an earlier post, you say: “…cultures that thrived on, revered and worshiped wheat…” Duck, we don’t need to fact-check your comment to know that the “thrived on” assertion is unknowable at best. And certainly suspect.

                      No question, the Ag Rev allowed humans to civilize. Our planet’s population explored 2500x since then. But because calories became much easier and more reliably available doesn’t mean they made us *healthier.* We have evidence for the opposite:


                      “…empirical studies of societies shifting subsistence from foraging to primary food production have found evidence for deteriorating health from an increase in infectious and dental disease and a rise in nutritional deficiencies…”

                      And this from Pulitzer-Prize winning anthropologist Jared Diamond (

                      “…The farmers gained cheap calories at the cost of poor nutrition, (today just three high-carbohydrate plants — wheat, rice, and corn — provide the bulk of the calories consumed by the human species, yet each one is deficient in certain vitamins or amino acids essential to life.)…”

                    7. Duck, about this you say:

                      “… Prescribed by Hippocrates, Paracelsus, Avicenna, Aristotle, favored by the Spartans, the Greeks and the Romans, and observed by countless scholars who wrote about its health effects. In every single instance, throughout Western history, wheat was unanimously considered to be the healthiest of all foods by the most prominent medical authorities—and this sentiment existed until the industrial revolution…”

                      Even if fact-checking bore out your high-flown assertions, should anyone be surprised if early prominents did extol wheat’s virtues? If you had a choice to eat nutritionally inferior food or to starve to death, which would you choose? That quickly became the option in many places after the Ag Rev when human population started exploding and developing large permanent communities, creating an absolute need for the most abundant reliable easiest-to-obtain calories. No government could possibly recommend against wheat–even to the current day. And of course the medical authorities from Hippocrates on up to the 1970s when the McGovern Committee developed the US’s disastrous dietary guidelines, they all lacked sufficient data on wheat to make properly informed pronouncements on it. Back in the day, they lacked blood serum tests to measure inflammation biomarkers, they lacked sophisticated IT to do large epidemiological studies, they lacked the basic nutritional biochem we know today. People usually didn’t live long enough for chronic disease to clearly manifest–until the past century. I submit to you that, over the 10–12k years from the Ag Rev, only now are we able to begin to properly assess wheat’s true health effects–even apart from all the processing such as fortification–which you so correctly point out.

                    8. heathertwist said: “or the contents of Oetzi’s stomach … yeah, we are understanding exactly what they were eating”

                      I think the problem is concluding skeleton/health conditions based on mainly diet when other factors are known to have a significant, or even greater, effect on bone and joint health. Many ancient civilizations and cultures had to deal with famines and plagues, and dental attrition which promoted abscesses and infections, and poor growth, etc. all of which may have had a significant effect on their skeletal remains and health. To link those problems to mainly diet alone can be more than a little misleading.

                      Case in point, it’s been insinuated that Otzi’s poor health and skeletal remains may have been due to his diet. However, Otzi was known to have dental attrition, was genetically pre-disposed to heart disease, and a rather serious infection (possibly the oldest known case of Lyme disease) that may be linked to poor skeletal and joint status. His diet was the least of his problems. He was a very sick individual.

                      One could easily create any narrative they wanted to with such vague clues. I’ve often wondered if the whole point of Paleo™ is to base a particular diet on extremely ambiguous data.

                    9. “We can say the same about early grains!”

                      Of course. I only pointed out the historical and written evidence to show that the anti-grain evidence is inconclusive at best, and misleading at worst. Nobody can ever really prove anything one way or the other. Though, I doubt it helps anyone to only have an anti-grain sentiment given the extremely vague data we are dealing with.

                      “Even if fact-checking bore out your high-flown assertions”

                      Please. I’ve already given the sources here.

                      Do note the references showing that bread, and specifically wheat, was considered to be the healthiest of all foods right up until the mid-19th century when plenty of other foods were available. The idea that grains are an ideal food is not just an ancient belief. The belief lasted right up until the industrial revolution when prominent scientists like Carl von Linné (1757) and Thomas Hodgkin (1841) documented the well known health promoting effects of (wheat) bread. It hardly seems like something we should easily dismiss—we’re talking about actual written opinions based on actual observations, all spanning thousands of years.

                      “People usually didn’t live long enough for chronic disease to clearly manifest–until the past century”

                      Let’s not conflate life expectancy at birth with life span. Hippocrates lived to between 83 and 90 years of age. Aristotle lived to 62. Von Linné lived to 70. Medieval scholars had an average lifespan of 59–84.3 years in the Middle East and 69–75 in Islamic Spain. New England colonists had lifespans of 62-65 years. Is that not long enough for chronic disease to clearly manifest? Spoiler alert. Eventually we all die. 🙂

                    10. Duck, very interesting observations on wheat, thanks for your comments. A few questions if you have some time.

                      1. Do you think that white flour is a problem and whole wheat is ok, or it doesn’t matter, any wheat flour is ok? Perhaps the milling process is what makes the difference?

                      2. I’m curious, do you have any theory on why americans are getting fatter and fatter and more and more people world wide are having Diabetes? If it’s not wheat, then what? Do you blame sugar or simply too much calories? and if it’s increased caloric intake, why did it happen?


                    11. It should be painfully obvious by now that unsaturated oils are the driving factor in the obesity AND disease epidemic. Secondary would be added food fillers such as fortification, lecithins, gums, dyes, etc.

                      Bottom line, if you eat real food and real food ingredients, life will be ok.

                    12. Zach, what is real food? is sugar real food? is flour real food? Is broccoli real? And if whole grains that are milled are real food, then why oil extraction from grains is not real food?

                    13. Hi Anna. I surfed through the forum (yet again) this time to revisit your other comments, including your exchange with Neisy. So I’m smiling in the possibility you include rhetorical elements in your questions to Duck’n’Zach 🙂

                      In any case, why don’t I take a crack at your Qs?

                      About your Zach Qs, it’s hard to know exactly what he means when he says “unsaturated” oil. Does he include the monounsaturates which, after all, qualify as “unsaturated?” Including that Mediterranean Diet darling, olive oil? From my reading and tracking my food and health numbers for the past nine years, I’m quite disposed to the idea that an overabundance of omega-6s polys you usu find in the SAD (Standard American Diet) could be raising systemic inflammation and setting the table for chronic disease. Legume/nut/seed oils (e.g. from soybean, peanut, corn, and sunflower seed) are exceptionally high in omega-6 (w6) and these are products most people consumed till researchers devised cost-effective ways to extract these oils in the late19th c and turn of the last century. Before then, people mainly used lard and suet (tallow). In this sense, what Zach may mean by “real food” is a food that has not undergo novel refinements, such as those hexane-processed high w6 oils which he may consider to not be “real foods.” But of course Zach should answer for himself. Back to olive oil, it has a long history and it is relatively low in w6. I used it almost every day. I get extensive blood panels every three months and check my blood sugars throughout the day, and all my number remain quietly in the normal zone, and I’m now 55. Many of my numbers were well out of whack when I was 46 and was diag’ed T2D. These have since steadily improved, most of all my BGs, which are now normal (mostly 75–95 mg/dL), and my C-Reactive Protein, a popular biomarker for systemic chronic inflammation, which steadily dropped over 3 years from from 4.6 (inflammatory) to 0.6 (anti-inflammatory). In fact, all my blood panel numbers are now normal.

                      As for your Duck Qs, my take is that we should regard warily *all* wheat flour. White flour, for the very fast carbs/gluten/lectins and loss of nutrients replaced by fortification plus chemicals introduced in its processing, the potential downsides of which Duck amply covers through the forum (search on “fortification”) Whole wheat includes the bran and comes with its own concerns, e.g. phytic acid that, in your GI, can steal essential minerals from your food. Though some will argue that, in the case of iron which we too often get too much of, phytic acid could be a *good* thing. You can find detailed explorations of this here: and of course in Wheat Belly and Grain Brain. For my part, I quit grains early on (2007) simply because grains are high in carbs–long before I faced the additional health questions of gluten, hemoagglutenating lectins, and phytic acid. I wrote a spreadsheet to track my meals, keyed detailed nutrient data into it from the USDA Nutrient Database (a tremendous resource if you get a chance to play with with it:, and found I could easily get all my micronutrients (vits + mins) without eating a single grain. Again Anna this is just my n=1. Please get as many health checks as you can, as often as you can. I can make specific suggestion for you on that if you want.

                      Finally your Q on why Americans are getting fatter and fatter and more and more people around the world are developing diabetes. I suspect this is very multifactorial, going way behind wheat and the threadbare “too-much-food/too-little-exercise” trope. We live in an unprecedented bewildering era of change. America was already well on its way to becoming sedentary in the 1950s/60s, and still much slimmer then. HFCS arrived to the US in 1975, and we kept upsizing sugar water esp since HFCS was so cheap. Chemical companies also keep creating new compounds, many of which are estrogenic and so promote metabolic syndrome–I can give you the proposed mechanistic chain for that for you if you want. Then there’s widespread use of antibiotics which can profoundly disrupt our microbiome, more and more violation of our circadian rhythms through working night shifts, and many many many other factors. Mark’s Daily Apple does an excellent job discussing these elements, And of course, I look forward to Zach and Duck’s answers, should they decide to respond to your questions.

                    14. Hi, Anna. To respond, I suppose real food would constitute foods that we can consume and get a net positive in terms of nutrition and also that are unadulterated with man made substances, i.e. they came from nature and required little to no preperation to eat. I would say that use of fire for cooking, rocks for pulverizing, water for soaking, etc is probably as far as one should go for prep.

                      So to answer your questions, no I don’t think that refined sugar or refined grains should be considered food, yes they are edible and give us calories but in terms of health, they are a net negative. Natural sources of sugar however (honey, cane, maple, etc) are probably healthy, same for whole grains which require little more than a rock, water and heat to eat.

                      Oils are anempty calorie and net negative. Before the industrial age, oil was hardly ever consumed and rendered fats were the norm. Of course it’s not completely black and white and not all oils are created equal. I would take an expeller pressed oil from a whole real food (coconut, olive) over a machine and chemical solvent extracted oil from a non edible food any day. (Cotton seed, rape seed, canola, etc)

                    15. Zach, your definition of real foods is very subjective and biased.

                      I think if one would eat a lot of honey and maple syrup, it will have a similar effect of eating a lot of table sugar. Btw, one can make sugar with water, flame and rocks.

                      it’s highly debatable what “net positive” is in terms of nutrition. We can’t possibly know how to calculate this.

                      Most of the veggies we eat are modified and bread by humans and required much more then water flame and rocks.

                      You can have expeller pressed canola oil, would it make it healthy? It has lots of omega-3s and some people consider it healthier then olive oil:

                    16. Whatevers clever, you can worry and fret, I’ll eat the grains and sugars and be lean, energetic and happy.

                      Done with this blog till the next post, love the carb love!

                    17. Bryan, thanks for your reply 🙂

                      To your point about fats, Zach doesn’t seem to like detailed discussions and precise definitions. It’s easier to debate this way.

                      You can see my view of why the world is getting fatter and fatter in my reply to Duck. It’s somewhat similar to yours. I’m not convinced about antibiotics because I’ve met many people who basically eat them for food, yet are very thin.

                      Thanks for sharing your health history, my experience was very similar, although I didn’t have diabetes or major health issues. I certainly feel healthier and more energized eating LC, even compared to whole soaked sprouted grains/nuts and freshly milled oats ala dr. Price. And I have objective markers to back it up. My fasting insulin is 1.8, triglycerides are 40, down from 135, CRP is 0.4. So high fat diet hasn’t increased my inflammation markers.

                      What other tests or health checks do you routinely do? Have you ever tested your leptin level?

                      As you’ve seen from my previous posts, thanks for reading btw, I’m leaning towards thinking that
                      CR and protein restriction matters more then the type of nutrients for the most part and if one has a metabolism that’s not damaged. But subjectively I enjoy LCHF diet more then HCLF (I prefer bacon to beans) and it’s easier for me to maintain it. For me LCHF is naturally CR and hunger is very rarely present compared to HC, when I felt the need to snack all the time.

                      How many carbs do you eat normally? And what do you think about ketosis long term?


                    18. Hi Anna, you’re very welcome. I like your style 🙂

                      About Zach, if you search for my handle in this forum, you’ll see the exchanges I had with him earlier and then finally put an end to, concluding it was a sheer waste of time. I find it’s pointless to argue with anyone who’s long on religious fervor and testosterone and short on science. Zach doesn’t want an genuine discussion and sharing of ideas that don’t jibe with his own. He just wants to beat into you how great HCLF is and how everyone should do it.

                      About what you say: “I’m not convinced about antibiotics because I’ve met many people who basically eat them for food,…” When you get a chance maybe clarify that? At the moment I’m picturing waifs honking down handfuls of Cipro caps 🙂

                      Once I left grains (July 2007) I left them totally, not even trying things like fermented teff which seems to work well for Ethiopians. That’s not because I harbor an anti-grain dogma–I don’t–as I’ve explained in posts to Duck and others. It’s only because I’ve never felt a compelling need to seek out fermented heirloom grains. My grain-free LCHF foodway, mainly organic and pasture-raised locally produced foods, satisfies me utterly. But I’m certainly open to trying fermented heirloom grains and see how I fare with them. I completely agree that CR transcends the HCLF/LCHF debates–esp for people who are not yet deep into metabolic syndrome.

                      About my carb intake, I usu eat ~40–80g per day. Some days it’s zero (fasting), Occasionally up to 100-120 grams during the summer when the high-sugar fruits ripen. In the latter case, I just put up with my higher BGs (110–135 post-prandrial)

                      About ketosis long-term, I simply haven’t seen a compelling argument against it.The only reason to eat carbs is for the glucose, and our bods make plenty for our needs, esp from excess protein. ~ 75% of the excess protein we eat, our liver makes glucose out of it. The only exception is when doing extended resistance training, like free weights at the gym, working out regularly to fail, trying to put on muscle mass. In that case I found I needed to chow a high-fast-carb meal within 45m after the workout in order to continue to grow muscle mass. In those cases, my post-meal BGs would often be in the 60s, even after a 100+ g carb meal! But this post-resistance recovery meal is the ONLY exception I’ve found for me for eating carbs.

                      Most of all, Anna, I’m very glad you get plenty of health tests. I truly feel that’s our best shot to learn what actually works for us. There’s so little true science out there, and of course it can’t account for individual metabolic diffs. I’m still eager to read research papers and listen to people steeped in the field, be they formerly credentialed folks or autodidacts. But ultimately it is for the ideas, for things to investigate further and to try. You also find plenty of caveats and shortcoming in the tests, but you learn to cross-ref your results, not to read too much into any one result. In this fashion we straggle and crawl toward something that might resemble the truth 🙂

                      For my tests, at home I check weight/BF%/BP/HR in the morning, and test BGs 4x/day, including at peak post-meal times. For blood panels, beyond the usual CBC, lipid panel, liver and kidney enzymes, etc. lineup, I get these:

                      – C Reactive Protein. Which you get. Congrats on your anti-inflamm 0.4!
                      – Hemoglobin A1c. Avg blood sugar over 60–90 days. Useful because you can have a normal FBG and still too-high post-prandrial BGs. Ideally <5.0%
                      – C Peptide. Proxy for basal serum insulin. S/b <1 ng/L adj
                      – Iron panel (TIBC, Transferrin, etc), since systemic iron overload *is* a common prob, and I eat meat and cook in cast iron
                      – T3 and T4 for Thyroid. TSH can give a false reading.
                      – Mercury. Get one to check, then repeat IF you eat a lot of fish high up on the thophic scale, e.g. tuna, king mackerel.
                      – Consider for other heavy metals too, e.g. lead, cadmium, selenium. If you eat lots of shellfish and esp if you eat lots of Brazil Nuts, you may want to check selenium.

                      About Lipid testing: the current standard is woefully inadequate and uninformative. It measures just total trigs and c'stol, and gives no idea of the number of size of the lipoproteins these lipids travel in though serum. Many researchers consider certain of the lipoproteins–not their lipid cargos–to be the actual atherogenic elements coursing through our blood. Esp older, smaller more highly oxidized LDL and–yes–HDL–lipos. The current direct-lipo measure tests like VAP and NMR may still not be ready for prime-time. Mark Sisson discusses them here: His post is already a few years old, but it's a good starting point.

                      Finally about leptin. I haven’t been able to wheedle this out of my doc, but I admit I haven’t pressed that hard either. I fast frequently (18h–3d) and almost never feel an acute desire to eat. At this point I can go pretty much as long as I want without eating, and feel fine, though I don’t see a point to go beyond three days. –Bryan

                    19. Bottom line bro is that you feel the need to writ short story sized posts that I bet are directly inverse to how healthy you are. I have great health and don’t feel the need to argue or post a mountain of studies yo get my point across.

                      I have read mountains of information and none of it makes a hill of beans compared to achieving true health. True health comes from being able to utilize carbohydrates, plain and simple. One can never be truly healthy restricting calories or carbs. Sorry but that’s the plain truth. You guys and girls restricting macros, fasting, searching out heirloom fermented teff (lol) will never experience true health until you get to the root issue of being under carbed.

                    20. Zach, my carb deprived brain can’t handle your comments full of assumptions, vague statements and lack of coherent thought process or quality references. May be my brain doesn’t have enough glucose to truly understand your point. So I hope you forgive me that I will not reply any further to your comments. Let’s agree to disagree.

                    21. Bryan, thanks for Zach warning 🙂

                      To clarify my antibiotic point, it was a gross exaggeration on my part. I meant to say that they take antibiotics so often, it’s almost like food. I think the gut flora influence on our health is grossly exaggerated as well. It’s a new FAD. I’m not saying it doesn’t matter, I’m saying it doesn’t matter as much for the vast majority of people compared with other abuses they take, especially metabolic syndrome.

                      My concern about ketosis is the lack of test subjects, so to speak. Inuits being a strange genetic exception, no population has subsisted in a constant ketosis for a prolonged amount of time, so we simply don’t know. That’s why I try to stay on the edge of it, coming out of it periodically with protein and carb binges, which are fun anyway.

                      I’ve noticed similar results to yours after my resistance training, although I’ve never had BG in the 60th!

                      I used to test my BG often, I’ve kind of relaxed and stopped it now for the most part and test occasionally after a carb binge to see it around 135-145.

                      I did ferritin testing as well, love cooking in cast iron! and had to do a few blood donations to bring it down to 80 from 140. I’ve heard lots of bad thing about iron, so trying to keep it at a lower range point.

                      I eat lots of sardines, salmon, shrimp, so not much large fish at all, thanks.

                      Also, how do you check for selenium? do you mean too much of it? I don’t eat much nuts, but take selenium 1xweek.

                      I agree on cholesterol testing, I don’t put much faith in it at all.


                    22. Hi Anna. Glad to save you some time and frustration 🙂

                      About antibiotics, those are one of the very many novel inputs in our lives that came along post WWII. Starting ~ decade ago, researchers started showing great interest in it as shown here: Michael Pollan wrote a compelling piece on it too:


                      There’s some though that gut microbes help mediate insulin response and blood sugars though it’s mostly correlative at this point, such as what you read here:


                      Mechanistically flora mediating BGs and insulin response is a plausible idea because so much of proper blood sugar regulation is about proper *signaling.* You can have plenty of insulin output and even decent insulin sensitivity, and still have BG issues.

                      You can think of our bods as a large corporation and those trillions of microbes as little temps workers which our bod gives room and board and “hires” and “fires” at will depending on the specific and ever-changing tasks it needs done.

                      About persistent ketosis, you’re right we haven’t seen much of it in the Ag Age starting ~12k years ago. We have many questions, many of which research may never be able to answer. E.g. can we all still thrive in persistent ketosis? If not, did some of permanently lose the ability to thrive in persistent ketosis since the dawn of Ag, e.g. through one or several SNP mutations? Or can those Ketosis intolerant people become tolerant once their gut microbiome adjusts. As for the Inuit’s genetic exception, I hope people don’t read too much into that. The Inuit may be much closer to us than some believe. Just because the Inuit have SNP variants that *may* (and I emphasize *may* since we have not directly tested this) preferentially direct dietary fat to skeletal muscle and brown adipose tissue doesn’t means the rest of the world will fare poorly on a high fat diet. E.g. it could be we have evolved more robust ways to vet dietary fat in the GI and send the excess to the exit, i.e. not bring it systemic. Bottom line, again, keep observing your own experience. I’ve been in steady ketosis almost nine years. I still regularly get as many tests as I can and monitor myself, and have been doing and feeling terrific.

                      About my low post-resistance-training BGs, they may have been a combo of keen insulin sensitivity brought on by my intense 90–120 minute workouts and my unstable sugar control due to my early and mild diabetes. It’s not uncommon for early diabetics to get slight hypos even without taking meds. Again, that could be due in part to bad signaling, possibly from unbalanced gut biome. Fortunately, I never get the “feak and weebles” unless my BG dropped below ~44 mg/dL, which happened only a handful of times. When I stopped taking supps, including chromium picolinate, I stopped getting those super low BGs.

                      About the fish you eat, excellent! Funny how many fish low on the food chain are also high in Omega-3, like the salmon and sardines you eat, herring, smelt, and other cold-water species. I eat shrimp too when I can find it (and afford it) wild. I totally avoid farmed raised shrimp as those ponds are often polluted, sometimes with heavy metal laden effluent from factories, esp in China. See Taras Grescoe’s book “Bottomfeeder” for scary details on that.

                      About serum selenium, I don’t check for it because I stopped taking all supplements in 2009–I could fill a book with the reasons why I stopped supps!–and I limit the only food source that’s outrageously high in selenium, which are Brazil Nuts. Selenium’s one of the easier minerals to overdose on, and supp makers occasionally flub up the formulations with tragic results:

                    23. Regardless of how you interpret their SNPs it would be at least worth pointing out that the Inuit have never been observed to be in ketosis.[1][2][3][4]

                      The one exception was Heinbecker showed in his follow-up experiments (in 1931 and 1932) that even (non-Pregnant/lactating) Eskimos who regularly ate carbohydrates had difficulty making ketones.*

                      Before their unique genetics were discovered, it was stated by the researchers that they were not in ketosis due to a high protein diet. However, the genetic evidence on CPT1a now explains why they had difficulty producing ketones and why Inuit children have difficulty fasting. (aka “hypoketotic hypoglycemia”).

                      Anyhow, I think it’s worth pointing out to Anna that the Inuit are not an example of a population in perpetual ketosis. They clearly metabolize fats differently than we do and they do not exhibit ketosis as we do.

                      * Pregnant/lactating women have exaggerated ketone production and the pregnant/lactating Eskimos in Heinbecker’s experiments made more ketones, while fasting, but were still well below what we would expect from pregnant/lactating women.

                    24. Hi Duck. What you say here: “I think it’s worth pointing out … the Inuit are not an example of a population in perpetual ketosis.” So far I’m left with a much different impression. That 1972 paper suggests the test subject Inuit *are* indeed ketotic.

                      It’s important to note someone could be in ketosis *at relatively low serum ketone levels.* Just like certain lucky folks can be in glycolysis and still enjoy low blood glucose levels. It’s possible that, due to his/her genetic variants and/or other adaptations and conditions, an Inuk may well be in ketosis even when serum ketone levels appear relatively low–low enough to show negative on test strips.

                      For the record, here’s a couple of ketosis defs: WebMD defines it as “…a normal metabolic process… your body … burns fat instead [of carbs]…”
             The Wiki ( says: “Ketosis is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood…”

                      OK, back to that 1972 paper. It has the most recent research of your links. I started with it with the idea that study results are the most accurate due to ongoing improvements in medical testing and diagnostics.

                      Duck, the paper never mentions “ketosis” or “glycolysis.” But the authors sure do imply ketosis. They say “…[The negative ketone body test result] does not preclude an increase in ketone body production during this time…” and “…the Eskimos had high serum FFA and low glucose levels (approximately 65 mg/100 ml) indicated that free fatty acids played a major role in body energy production…” Reading this, given their high level of serum FFAs, the subjects sure don’t seem glycolytic. What else could they be then except ketotic? –Bryan

                    25. Bryan, I’m well aware that they burn a lot of FFAs in other areas of their bodies. And I’m aware of ketoadaptions. But the genetics clearly explain how they could not burn much FFAs in their livers like we do—they literally have a deficiency of the liver enzymes to do this—hence their known tendency for hypoketotic hypoglycemia.

                      wbryanh said: “Reading this, given their high level of serum FFAs, the subjects sure don’t seem glycolytic. What else could they be then except ketotic?”

                      No one denies that they burn a lot of fat for heat. But the point being that their livers appear to be protected (or at least spared) from metabolizing a lot of FFAs due to their CPT1a mutations. They just don’t do ketosis like we do. And the studies show this as well. They evolved differently than we did, due to their harsh climate.

                    26. Duck, let’s be clear. Your evidence, however interesting, in NO WAY indicts persistent ketosis. Your assertions “the Inuit have never been observed to be in ketosis…” and “…the Inuit are not an example of a population in perpetual ketosis.” are misleading at best, and most likely wrong. Inuit on VLC foodways most likely *are* in persistent ketosis. You even lean toward that in places. E.g. in your previous post you appear to contradict yourself by saying: “…[The Inuit] just don’t do ketosis like we do.”

                      Persistent ketosis may well remain a terrific option for Inuit and non-Inuit alike. Here’s why:

                      In their 1972 report–by far the most relevant of the five links you supply–fully describes ketosis, however “hypoketotic” it may be.
                      Ho et al observed in the serum of those 168 Inuit “high FFAs” [free fatty acids], and “low BGs.” Sorry, Duck, but that’s ketosis. The only other energy-burning option is glycolysis, and given the high serum FFAs in these healthy test subjects, it sure isn’t glycolysis. Even the authors allow their results “do not preclude an increase in ketone body production during this time. Again, Duck, someone can be in ketosis even *at relatively low serum ketone levels* so long as glucose is not their primary fuel at that time.

                      What you say here: “…their livers appear to be protected (or at least spared) from metabolizing a lot of FFAs due to their CPT1a mutations…” You imply that that CPT1a mutation somehow evolved with the aim to prevent overloading and burdening the liver with FFAs. Please remember Duck this implication reflects your opinion. *It is not fact*. Even for folks lacking the CPT1a variant, you’ll find little evidence that a ketotic diet, even long term, burdens and harms their livers. There’s plenty of evidence to suggest a long-term ketotic diet does not harm the liver at all: e.g. here: Duck if you can present strong evidence to the contrary, I’ll gladly stand corrected. The Inuit CPT1a variant may have evolved for reason having nothing to do with purported liver sparing. Many ancestrally-living Inuit lived on subsistence VLC foodways in intensely cold environments requiring huge amounts of calories just to generate enough thermal energy to survive. It’s quite plausible that CPT1a may have stuck in order to direct more FFAs to the skeletal muscle and brown adipose tissue. We simply can’t say for sure what specific selection pressures drove the spread of this variant in the Inuit.

                      Bottom line (again!): Whatever foodway–HCLF, HFLC, “Swampland,” whatever–get regularly tested and see how you are doing. If anyone happens to have any qualms about persistent ketosis, please regularly test your liver enzymes and your blood for FFAs and ketone bodies. Get a ketone testing meter or ketone test strips. Easy enough to do. You absolutely shouldn’t let these Inuit studies dissuade you from exploring any foodway, including VLC. The still meager, poorly understood, and caveat-filled results we see from the Inuit studies–many from 70 or more years ago–no way confirms or even strongly suggests any danger of persistent ketosis for us. –Bryan

                    27. Relax, Bryan.. Nowhere in my comment did I ever say that the Inuit didn’t burn FFAs. And nowhere in my comment did I ever say this proves anything good or bad about ketosis. I could care less.

                      All I said is that they don’t do ketosis like Westerners do.

                      Do you deny that most Inuit have CPT1a deficiencies? Do you deny that a CPT1a deficiency tends to cause hypoketotic hypoglycemia?

                      Wikipedia: Carnitine-acylcarnitine translocase deficiency

                      The signs of carnitine-acylcarnitine translocase deficiency usually begin within the first few hours of life…This disorder may also cause extremely low levels of ketones (products of fat breakdown that are used for energy) and low blood sugar (hypoglycemia). Together, these two signs are called hypoketotic hypoglycemia…This disorder can cause sudden infant death.

                      That’s just what the research says about the Inuit. That’s all I’m pointing out. They do ketosis differently from the way we do. That’s all.

                    28. Duck why do you ask me these two questions?:

                      “Do you deny that most Inuit have CPT1a deficiencies? Do you deny that a CPT1a deficiency tends to cause hypoketotic hypoglycemia?”

                      If you had read my post carefully, you’d know I don’t deny either one.

                      What is your point? How are these relevant to the main message. That we should feel free and safe to experiment with persistent ketosis?

                    29. Bryan said: “Duck why do you ask me these two questions? If you had read my post carefully, you’d know I don’t deny either one.”

                      Ok.. just wasn’t sure if you were acknowledging it or not. Understood.

                      Bryan said: “What is your point? How are these relevant to the main message. That we should feel free and safe to experiment with persistent ketosis?”

                      Yes, people should feel free to experiment, if they wish. They just shouldn’t be doing it under the pretense that they will be burning fats like the Inuit do. The Inuit are not an example of what happens in Western metabolisms.

                      …Also, many studies point out that the Inuit also ate considerable quantities of protein, and apparently have enlarged livers (which happens to be a symptom of CPT1a) with increased capacity for gluconeogenesis, which is originally why the old researchers did not believe they were in ketosis, despite burning lots of FFAs throughout their bodies. As multiple studies have pointed out, the ratios of fatty-acid to glucose were observed to be well below the generally accepted level of ketogenesis. [1][2][3][4]

                      But, I agree, people should experiment if they want to. They should just understand that they are going to burn FFAs differently from the Inuit. That doesn’t make ketosis good or bad, of course.

                    30. Maybe many/most non-Inuit can handle a persistent ketogenic diet *better* than the Inuit. As ironic as that sounds, given the ancestral Inuit’s VLC foodway.

                      There’s little evidence to show that ketosis burdens the livers of people in the Western developed world. Even though we generally lack the CPT1a variant that appears to be more common in the Inuit.

                    31. Bryan said: “Maybe many/most non-Inuit can handle a persistent ketogenic diet *better* than the Inuit. As ironic as that sounds, given the ancestral Inuit’s VLC foodway.”

                      lol.. That’s certainly a perspective I’ve never heard before. 🙂

                      Bryan said: “There’s little evidence to show that ketosis burdens the livers of people in the Western developed world.”

                      I wouldn’t know. Has it really been that well studied? I do remember Tolstoi in 1936 tested Stef and Andersen’s glucose response after their year-long Bellevue experiment and found they had a “false diagnosis of diabetes” that tends to happen after a long fast (i.e. very poor glucose control and/or physiological insulin resistance). That seems to be a temporary and normal response to fasting/ketosis as far as I know.

                      Perhaps it’s no big deal and soon reverses after some time on a varied diet. But, I’m not sure anyone really knows the long term consequences of it. Probably something people should at least be aware of.

                    32. I just (superficially) tried to find a link about this, but couldn’t find anything off hand- (it takes time, which I just don’t have right at this moment). However, I do know that Dr.’s Phinney and Volek have done some long term testing with low carb diets, and found no harm. They write about some of this in their book “The Art and Science of Low Carbohydrate Living”. In addition, there are several doctors who have been in long term ketosis; I know Dr. Phinney himself, and I believe Dr. Volek also. And, Dr. Eric Westman has been on a long term ketogenic diet- (he mentions it in his debate with Dr. Colin Campbell, which is on You Tube). These people seem to be in pretty good health, and they are doctors, so they must be aware of their health markers. There is also a book called “Ketopia” (which I haven’t read, though it sounds interesting). This is also about ketogenic diets, all the health benefits, and long term effects I believe.

                      Having said all that, I will admit that constant ketosis may not be the best thing for everyone. Children can generally make metabolic adaptations pretty quickly, but some adults may have difficulty if it’s not what they’re used to. However, it does appear that many people thrive on a ketogenic diet.

                    33. The modern evidence we have for ketogenic diets are clinical studies which are overwhelmingly either positive or neutral on them. We don’t have epidemiological studies on them, but not sure how much that even matters. Epidemiological studies have debatable value given their inherently correlative nature and issues of self-reporting.

                      Most people who want to try a persistent ketosis foodway should have no compunctions whatsoever! Go for it!

                    34. Duck, right? That’d be funny if we (assuming you are not Inuit) *did* handle ketosis better than those far Northern peoples. But the more we discuss and analyze this issue, the more I’m thinking it’s plausible. We may have the advantages, e.g. adequate persistent ketone levels, with no apparent downsides, at least none broadly documented. I can’t speak to the 1936 Stef and Andersen experience, but I can speak about my own in 2015. I am in persistent ketosis and even then, my BGs can start to float stubbornly higher, likely due in part to my marginal insulin output. In such a case I fast anywhere from 18h to three days, however long it takes to push me back onto the “right side of the metabolic divide.” Fasting always corrected my BGs, and it appears to be getting more effective. When I first started fasting in 2009, for a few years I used to have to occasionally do 2- and 3-day fasts to get the desired effect. But since ~2012, 18h fasts has been reliably doing the trick, and even these I need to do less and less. –Bryan

                    35. Duck,

                      I know the whole Inuit/ketosis thing has been in the spotlight and is very controversial, so I’m not putting all my stakes on them being in ketosis.

                      Having said that, it’s their protein that they metabolize differently, that I find interesting. They have so much brown fat and are able to decouple lots of ATPs as free heat, so they could eat much more protein then us and still be in ketosis.

                      And if ketosis defined simplistically as burning and using mostly fat for fuel, they certainly were in ketosis. Their mutations may just affect how they get in and out of ketosis, not how they “do it” or stay in it.

                      I’d say there are more similarities then differences between how we and inuit burn FFA, after all we both evolved and have mitochondrion that can burn only carbs or fat for fuel. We burn most of the fat not in the liver anyway, so I think it’s very similar how we and inuit burn fat.


                      thanks for reminding me about Dr. Phinney, I meant to read his stuff and forgot.


                      what is the longest modern study of people in ketosis have you seen? preferably not epileptic kids, because their disease will screw the results anyway.

                    36. Anna said: “And if ketosis defined simplistically as burning and using mostly fat for fuel, they certainly were in ketosis. Their mutations may just affect how they get in and out of ketosis, not how they “do it” or stay in it.”

                      Well, according to Wikipedia, “Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood.”

                      Wikipedia also defines “ketone bodies” are defined as, “Ketone bodies are three water-soluble molecules that are produced by the liver from fatty acids during periods of low food intake (fasting) or carbohydrate restriction”

                      The article goes on to say, “Ketone bodies are produced from acetyl-CoA (see ketogenesis) mainly in the mitochondrial matrix of hepatocytes (liver tissue) when carbohydrates are so scarce that energy must be obtained from breaking down fatty acids”

                      So, no, I don’t believe that’s the actual definition of ketosis. The Inuit don’t do it like that.

                    37. Duck, technically you are correct, “Ketosis is a metabolic state where *most* of the body’s energy supply comes from ketone bodies”. Although I’m sure it’s debatable how “most” it is.

                      But ketone bodies are made mostly from FFA, some call ketones a byproduct of FFA metabolism. So in ketosis state our mitochondria uses ketones (made from FFA) and FFA (directly), so as I was saying in general terms, mitochondria is “using mostly fat for fuel”.

                      So I’m not sure what’s the argument here.

                      Anyway, if most of ketones are made in the liver, may be that’s why inuits’ liver is so enlarged? To produce more ketones? Idk.

                      But I still fail to see how they “do it” differently? both, us and them, burn ketones and FFA for energy while in ketosis. They may be able to get in and out easier, meaning their liver is more adapt at producing them, for example, or they have some other mechanism for additional ketone production, possibly.

                      But on a deep mitochondrial level we are exactly the same while in ketosis – we burn the same ketones and the same FFA to live.

                    38. “Anyway, if most of ketones are made in the liver, may be that’s why inuits’ liver is so enlarged? To produce more ketones? Idk.”

                      No. They do not produce more ketones. They struggle to produce ketones. As the research on CPT1a explains, the Inuit have difficulty producing ketones and this is why the Inuit can have difficulty fasting—particularly their children who tend to die of SIDS without regular breastfeeding around the clock. We don’t have difficulty fasting like that.

                      The mutation promotes “hypoketotic hypoglycemia” (low ketones, low blood sugar).

                      Wikipedia: Carnitine-acylcarnitine translocase deficiency

                      This disorder may also cause extremely low levels of ketones (products of fat breakdown that are used for energy) and low blood sugar (hypoglycemia). Together, these two signs are called hypoketotic hypoglycemia.

                      Anna said: “But I still fail to see how they “do it” differently? both, us and them, burn ketones and FFA for energy while in ketosis. .”

                      No.. the difference is that we burn “mostly” ketone bodies (acetoacetate and β-hydroxybutyrate) while they are known to have “extremely low levels of ketones”.

                    39. Anna,

                      I think Bryan had a rather accurate way of looking at it… Westerners appear to be “better” at ketosis than the Inuit.

                      It seems paradoxical, but I think Bryan is technically correct. The Inuit aren’t very good at producing ketones. But Westerners are quite good at it.

                    40. Duck, Anna–Anna I saw your recent comment and was thinking along your lines–this does seem like a distracting semantical snarl on “ketosis.” What does “ketosis” truly mean anyway? Duck, you pulled the def from the Wiki–not an unimpeachable source. But can I blame you? We can’t even find agreement on the def in the medical dictionaries. Many of those sources still imply it’s something pathological. Even doctors still confuse “ketosis” with “ketoacidosis.” We need to get past the surprisingly vague names of these metabolic states, which we use sloppily anyway. We often say “ketotic” to distinguish from the absence of the primacy of glycolysis. Maybe instead we should say “glycolysis” and “aglycolysis?”

                      In ant event, all that takes us away from the main question that triggered all the Inuit diet discussions. In search of what many of us want to know: Can we thrive on persistent LCHF? Even VLC?

                      The Inuit appear to do just that (with certain restrictions like freq child feeding) on VLC. Great. That’s a perfectly valid starting point for rest of us. Fellow humans being who diverged from us not so many thousands of years ago are up there in the Wild Blue North making VLC work. The Inuit are not from Mars. Genetically speaking we are still very very very very closely related. The fundamental mechanisms of energy production remain just the same. Our mitochondria oxidize glucose and beta-oxidize fats in just the same ways. It doesn’t at all mean we can’t take meaningful macronutrient lessons from the Inuit that we can effectively apply to our own lives. Their SNP variants appear to merely tweak the ketone body/FFA balance likely due to the Inuits’ special environment. So what if then that *may* make the Inuit not strictly “ketotic?”–whatever that means. So what if those with the CPT1a deficiency variant derive a greater proportion of their energy directly from the free fatty acids than non-variant VLCers? Our plasma albumin tows FFAs directly to the many types of cells that need the energy. Bypass the liver! Collect 200 ATPs!

                      Finally, let’s remember the idea that the Inuit with the CPT1a deficiency variant are “hypoketotic” Not “aketotic.” They are obviously producing *some* ketones. Plus that Wiki says the liver is the main but not the *sole* source of ketone bodies.

                      If anything, my recent discussions with you Duck makes me think that those of without the SNP variant may actually fare *better* on VLC than the Inuit. We have very little evidence that persistent VLC overloads and injures the liver. My little n=1 redux, I’ve been doing VLC it for over eight years. My extensive blood work has consistently improved in that time. Liver enzyme levels (AST, ALT, ALP) are always normal. –Bryan

                    41. What I haven’t heard here is any discussion of gluconeogenesis. Discover has a nice article about a lot of the issues with the Inuit:


                      At one point I was in a group where a researcher with a zoo chimed in. She was saying that true carnivores are NOT “in ketosis” at all … they convert protein to glucose. Which isn’t efficient, but it works. If a lion or bobcat in a zoo is throwing ketones … it is ill and needs treatment.

                      She said the same is true for the Inuit. You maybe could find some other researcher and see if they agree. It may well be true that Europeans don’t have that ability so much, but the low-carb hunters probably would. Same as a lion.

                    42. Heathertwist said: “What I haven’t heard here is any discussion of gluconeogenesis”

                      Yes, exactly (actually I did mention it briefly). As I had mentioned in an earlier comment, all of the researchers who actually studied the Inuit firsthand (not talking about those who just wrote about them) believed that they were relying too heavily on gluconeogenesis to be in “ketosis”. They were eating far too much protein.

                      Their enlarged livers were believed to assist in gluconeogenesis beyond what Westerners can do. And their significant excretion of urea was also seen as evidence of this.

                      Actually there was a paper that was just published this past September that summarized all of the available Inuit research, and it too explained how they were a high protein culture that relied heavily on gluconeogenesis.

                      The Importance Of Dietary Carbohydrate In Human Evolution (2015)

                      The diets of traditional Arctic populations are sometimes given as examples of successful high-protein diets (Lindeberg 2009). An estimate of their dietary composition suggested that about 50% of the calories come from fat, 30–35% from protein (or around 300 g per day and lower for pregnant women; Speth 2012), and 15–20% from carbohydrate principally in the form of glycogen from the meat they consume (Ho et al. 1972). Ethnographic evidence demonstrates that nutrients, including essential vitamins, minerals, and carbohydrates, were obtained from eating the stomach contents of terrestrial prey animals, and tundra plants and kelp (Kuhnleini and Soueida 1992; Speth 2012). Meat frozen soon after slaughter will retain much of its muscle glycogen (Varmin and Sutherland 1995), providing another source of available carbohydrate. It is likely that circumpolar peoples ate more carbohydrate than is generally thought (Rabinowitch 1936; Sinclair 1953). Nevertheless, Inuit have enlarged livers with an increased capacity for gluconeogenesis, and have greater capacity for excreting urea to remove ammonia, a toxic byproduct of protein breakdown (Kaleta et al. 2012). Indeed, a recent study has identified high frequencies of a nonsynonymous G>A transition (rs80356779) leading to a Pro479Leu change in the CPT1A gene—a key regulator of mitochondrial long-chain fatty-acid oxidation—in modern circum- Arctic populations (Clemente et al. 2014). Interestingly, the derived A-allele has been shown to associate with hypoketotic hypoglycemia and high infant mortality. Ethnographic texts record the Inuit habit of snacking frequently (Klutschak 1987). This custom may well be a direct consequence of the rs80356779 ‘A’ allele gene as fasting, even for several hours, can be deleterious for people with this allele. The high frequency of the CPT1A Pro479Leu change in circum-Arctic therefore suggests that it is an important adaptation to high meat, low- carbohydrate diets.

                      As you can see, they handle their food differently than we do. When white Arctic explorers lived with the Inuit, the white men had to eat a lot of fat and limit their protein to stay in ketosis. However, the Inuit were known to eat enormous quantities of meat, preferably dipped in fat. The point being that the Inuit did not limit their protein intake—they ate it constantly throughout the day to avoid fasting.

                      Interestingly, Stefannson never claimed that the Inuit ate 80% fat. In fact, his Inuit recipe for pemmican (when based on caribou rather than bison and the standard recepie was 2/3 lean caribou meat to only 1/3 melted fat) was relatively lean. LCHF Magasinet not only explained the Inuit/ketosis myth but they calculated the fat content of the Inuit pemmican would be less than 60%. You might get into mild ketosis if the fat content exeeds about 2/3 of calories, but but 60% wouldn’t achieve it even if the inuits ate 100% pemmican year around.

                      So, again, all of the evidence points to a high protein diet in the Inuit. They just weren’t eating enough fat to be in “ketosis”.

                    43. Duck, just curious, where’s the actual clinical proof that supports what you say about the Inuits’ “…enlarged livers…” and “…their significant excretion of urea…”?

                      I’ve been googling “Inuit liver autopsies” and “Inuit urine output” which so far turns up nothing except those comments from Harold Draper in Discover Mag and replicated elsewhere “recalling his 1970s studies.” Trouble is, I can’t find links to Draper’s actual studies. I’m not saying they don’t exist. Just saying I haven’t so far been able to find them.

                      Duck if you have links that prove what you assert, it’d be great if you post them here for us.

                      In the meantime, Duck, that new paper from Hardy et al is very interesting! Ever since I read Wrangham’s excellent little book “Catching Fire,” I’ve been following the research on the role starchy roots/tubers may have played in our pre Ag Rev evolution. Looking forward to digging into Hardy’s work. It’ll be a while till I have much to say on it. Most of the refs therein are books or stuck behind paywalls. At the moment, I’m ordering what cited pubs I can. Thanks –Bryan

                    44. Well, the Hardy paper references Kaleta, et al. 2012. But Harold Draper mentions increased urea in his 1977 paper. Both should be freely accessible.

                      I don’t know if Draper ever saw an Eskimo liver, but in his paper he just talks about urea clearance and high water intake with high protein.

                      The Aboriginal Eskimo Diet in Modern Perspective (1977)

                      Their high-protein diet imposed on Eskimos a need to dispose of an unusually large metabolic load of urea, a potentially toxic nitrogenous compound formed during the conversion of amino acids to glucose. Animals fed high-protein diets exhibit diuresis and an increase in water consumption, and it is of interest that early explorers commented on the high water intake of Eskimos. A feedback mechanism acts to prevent uremia under conditions of high protein intake by stimulating water consumption and thereby enhancing the dilution and excretion of urea. The need for efficient urea clearance implies that renal disease in Eskimos consuming the native diet has unusually serious clinical implications.

                      CPT1a deficiency is known to cause enlarged livers, so I don’t doubt that they have them.

                      Of course, at the time, Draper didn’t know about their CPT1a mutations, but I’m sure he would have found that fascinating.

                      Draper mentions lack of fiber, but actually glycans in (raw?) animal tissue can be broken down by some bacteria (how meat is tenderized, for instance), so I imagine they had biomes similar to a carnivore might. They also ate rotting meats, a traditional delicacy which was claimed to offer health benefits.

                    45. ???

                      Duck these don’t answer the question at all!

                      In the Draper paper, he says *nothing* about enlarged Inuit livers. Draper does say this about urea: “…their high-protein diet imposed on Eskimos a need to dispose of an unusually large metabolic load of urea…” But he doesn’t give a shred of evidence on how he determined that. It’s a completely unsupported comment.

                      In the Kaleta, et al. 2012 paper, I searched on “liver” and “urea” and came up with -nada-. Where are the relevant passages?

                      Again Duck… Where’s the actual clinical proof that supports what you say about the Inuits’ “…enlarged livers…” and “…their significant excretion of urea…”?

                      So far you’ve shown -NADA-

                      You made that assertion. It is reasonable for us to ask you to list the specific text that backs up your assertion. Duck, it is not asking too much of you. –Bryan

                    46. Bryan,

                      I specifically said that Draper never explained the evidence, beyond the very high urea excretion. See this quote from Discover Magazine, who interviewed Draper:

                      The Inuit Paradox (2004)

                      “On a truly traditional diet, says Draper, recalling his studies in the 1970s, Arctic people had plenty of protein but little carbohydrate, so they often relied on gluconeogenesis. Not only did they have bigger livers to handle the additional work but their urine volumes were also typically larger to get rid of the extra urea.”

                      “Bigger livers”. At any rate, the high urea excretion is the byproduct of high protein intake.

                      I too could not find where Draper actually saw the bigger livers, but that’s what Draper appears to have told Discover when they interviewed him. Or perhaps Discover was getting their sources elsewhere. They are generally considered to be a reputable source, however.

                      Regardless, CPT1a deficiency is known to cause enlarged livers:

             Carnitine palmitoyltransferase I deficiency

                      “People with CPT I deficiency can also have an enlarged liver (hepatomegaly).”

                      So, according to the NIH, enlarged livers is a common symptom of CPT1a deficiency.

                    47. So Duck, we’ve established you totally lack clinical evidence for Inuit having bigger livers. Or having to pee excessively. That your statement saying “Their enlarged livers … And their significant excretion of urea …” may well be complete nonsense. OK.

                      You cite an NIH paper that says “…People with CPT I deficiency can also have an enlarged liver…” We can chuck this out too. It’s only a general discussion that applies to all peoples with the deficiency, e.g. Hutterites as well as Inuit. It includes no evidence about enlarged Inuit livers. Duck if we buy your argument that “The Inuit are different from us” shouldn’t we then avoid to assume their livers will respond like ours to that deficiency?

                      Actually this is fascinating discussion. For years I’ve heard these “Inuit enlarged liver, Inuit pee a lot” factoids, you being the latest purveyor of them. I never questioned them till now. Now I find out we have no true evidence for them after all! I can regard this as the latest stool of med-anthro bullsh*t to scoop away till someone does real actual observations on the Inuit and their livers and urinary patterns. Thanks for this. –Bryan

                    48. Bryan, I found it!

                      It seems Draper was just referring to the well known observations of enlarged livers commonly observed in Eskimos:

                      Western Diseases, Their Emergence and Prevention (1981)

                      “Little is known concerning the pathology of the liver enlargement reported some 20-30 years ago in mainly healthy Eskimo hunters (Brown, 1955; Hildes, 1958; Schaefer, 1971). The hepatic enlargement may have reflected increased gluconeogenesis from protein because of the relatively deficiency of dietary carbohydrate in the traditional Eskimo diet. The high composition of protein necessitated high urinary excretion of nitrogen. The increased consumption of carbohydrate and decreased intake of protein in the modern Eskimo diet lessened the metabolic load on kidneys and liver.”

                      So there you go. It was just an observation referenced in the literature. And there is plenty of evidence of high urinary nitrogen excretion in the Eskimo literature. They were well known to have a high protein diet.

                      Ya know… there’s no need to scream “nada” every time you think there’s a gotcha. We can both easily look into this stuff. No need for me to do all the work here!

                    49. Duck, I posted my last frustrated note to you before I got this evidence from you. I’ve reviewing it now. I’m sorry if I showed some frustration here, but it’s what happens when someone’s trying to snow us, when trying to back up their statements with really flimsy evidence as has been the case on this topic till now. If you had said “I know there’s real evidence, please give me time to find it” or somesuch, that be great! Will be back soon –Bryan

                    50. But what you say Duck, “We can both easily look into this stuff. No need for me to do all the work here!” I respectfully disagree. You make the assertion, you do the work to back it up. Down to the actual text to support what you’re asserting. We all should be doing that and I try to do AMAP. Otherwise we could be tossing out there all kinds of assertions without being sure what we’re talking about and letting “others sort it out.” We are dealing with fascinating but enormously complex material than directly affects our lives. We need to be as rigorous with ourselves as possible. Don’t mean to lecture Duck, but you have to admit, you haven’t been consistently great about that 🙂 –Bryan

                    51. Bryan,

                      This is not some flimsy assertion. I have yet to find a single paper or study—referencing actual measurements on actual Eskimos—that did not conclude that the Eskimos were eating a high protein diet. For example, the following researchers all concluded that the Eskimo diet was a high protein diet and were not in ketosis:

                      Krogh & Krogh 1914 (Nobel Prize winner)
                      Lusk 1914
                      Joslin 1917 (first doctor to ever specialize in diabetes in the US)
                      Schaffer 1921
                      Heinbecker 1928, 1931, 1932
                      Tolstoi 1929
                      McClellan & DuBois 1930 (Stefansson’s own doctors)
                      Rabinowitch 1936
                      Rabinowitch & Corcoran 1936
                      Rabinowitch & Smith 1936
                      Kaare Rodahl 1952
                      Sinclair 1953 (A detailed review of the literature)
                      Ho 1972
                      Hui 1975
                      Bang, Dyerberg & Hjorne 1976
                      Draper 1977
                      Bang, Dyerberg & Sinclair 1980
                      VanItallie & Nufert 2003
                      Leonard & Snodgrass 2005
                      Hardy 2005

                      They all say the Inuit ate high protein, because they did. So, the scientific literature says—without a doubt—that the Inuit were high protein. Therefore, I believe it is you who needs to show otherwise.

                      Bryan said: “You make the assertion, you do the work to back it up.”

                      Sorry, but it’s not my assertion. It’s just what the literature says. All of the literature says high protein and no ketosis. If you disagree, it’s you who will have to show otherwise.


                    52. Duck, to be clear, I wasn’t questioning you about the Inuit protein intake. I’m not ready yet to do that. Like I said earlier, I can’t yet get near enough data from the Hardy paper. Thanks for all the links. Most of them you’ve already posted and I’ve reviewed them to varying degrees. But you’ve included a few new ones; thank you for those. Looks like I’ll have to learn Danish 😉

                      What I did question: The enlarged liver/freq peeing thing. Most of the comments addressing that presumed issue point back to that Discover mag article. That site quality is mostly OK–I’ve worked for large consumer tech and general interest pubs for over 20 years and ex-colleagues went on to edit and write at Discover, Popular Science, etc. But that article’s simply a reporting job and doesn’t cite any studies, at least not for our topic here. One of the things I’ve learned in the biz is how the internet can propagate and replicate CW till it gets to the point that even a lie told enough times looks like the truth.

                      About assertion, Duck indeed you were asserting: “Their enlarged livers … their significant excretion of urea …” Sorry, but that is the case. It’s right there in your post. It’s up to you to supply solid credible evidence to back that up. If I disagree with your assertion, yes, it is up to me to find credible rebuttals. But if you fail to provide strong and relevant evidence to back it up, I’m well within my rights to ask you for it. I am sometimes willing to do your work. But you shouldn’t *expect* me to do your work.

                      Duck what you say here: “All of the literature says … no ketosis.” Of course that’s false. You yourself quoted literature saying “hypoketotic…” “Hypoketotic” is not “aketotic.” We know the Inuit *do* in fact produce ketones, if not to our level. Only how much? I’ve yet to see serum ketone measurement actually listed in mmol/L (millimolar) or in any other concentration units. Maybe they are there in one of those linked you posted, and I haven’t seen it yet. But Duck, the larger issue has to do with the fact that “ketosis” is a surprisingly nebulous and ill-defined term. Someone can assert that if an Inuk has 0.000001 mmol/L of serum ketones, he is in “ketosis.” Who are we to say he’s wrong? What is the minimum mmol/L of serum ketones to declare someone “ketotic?” You don’t know. No-one else knows either. –Bryan

                    53. Sounds good, Bryan. If ketosis is a surprisingly nebulous and ill-defined term, then I don’t even know what to say about it. 🙂 At this point the literature says what the literature says. There’s not much more to say!

                    54. About decided the term “ketosis” is nigh near meaningless, it’s funny to arrive at that point isn’t it Duck? After all the keyboard sturm und drang about Nanook and his ketones.

                      As for what you say “At this point the literature says what the literature says…” that’s right. And much of the literature saying quite different things!

                      So Duck, what definition of “ketosis” will you stick with? –Bryan

                    55. “what definition of “ketosis” will you stick with?”

                      Probably the classical definition mentioned by Sinclair 1953 and others. It seems like there is a recent movement to redefine what ketosis is—and that’s fine—but I’ll leave that to others to sort out.

                    56. OK, once again I posted to you before seeing your answer.

                      That 1953 Sinclair paper is behind a paywall. If you wouldn’t mind posting his ketosis def here …

                      Thanks –Bry

                    57. “…If ketosis is a surprisingly nebulous and ill-defined term, then I don’t even know what to say about it. 🙂 …”

                      Duck, why don’t we start with that Wiki def you cited earlier:

                      “Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood.”

                      Using that def, are the Inuit in “ketosis” or not? Do we know? How many calories do they derive from serum ketones? Serum glucose? Serum FFAs? BTW, when the liver breaks down excess protein, not *all* of it become glucose. About a quarter of it becomes fat.

                      Who’s actually measured these things in our far northern friends? Do you know?

                      And Duck, most important, if insulin levels remain low, low enough to continue to allow release of fats from adipose tissue, *does it all really matter?*

                      Is it like arguing how many angels can dance on the head of a pin? –Bry

                    58. I hear you Bryan. It’s impossible to define the diet. I get it. Nevertheless, they are known to be a high protein culture. There’s really nothing left to say. I’m getting on a plane in the morning and have to head to bed. It’s been fun. Be well and take care.

                    59. To be clear, Duck, you *do* furnish a lot of links. It’s only that the quality of the evidence you cite can really vary. But you have a lot of great ideas. Given the state of most “science” out there, I’ll take the ideas! –Bryan

                    60. Hi Duck. Sorry. But if you are trying to imply that enlarged Inuit livers were somehow “unhealthy” you’re still batting zero.

                      What you said: “…It seems Draper was just referring to the well known observations of enlarged livers commonly observed in Eskimos…” Draper offers three refs for these “well known observations” as you call them. They are “Brown, 1955; Hildes, 1958; and Schaefer, 1971.”

                      Once again these texts prove elusive. However, thanks to our Jonathan Christie here, we have Dr Schaefer’s 1959 glowing report on exceptionally robust Inuit health. In it Schaefer refs Brown and Hildes works for the same years that Draper cites:

                      “…Many seal-eating Eskimos *though perfectly healthy*, have a relatively large liver. This hepatomegaly was first described by Brown and confirmed by Hildes….” You can see his report here:

                      Duck, this strongly suggests that Schaefer found nothing in the earlier Brown and Hildes works that suggests these Inuits’ livers were pathologically enlarged. Nothing from Brown and Hildes to suggest their livers were in any way “unhealthy.”

                      And Duck, about what you said “…And there is plenty of evidence of high urinary nitrogen excretion in the Eskimo literature…” Even now, you persist to fail to show even one shred of real evidence to back up your claim.

                      Finally Duck what you say here “…[the Inuit] were well known to have a high protein diet…”

                      So what? Where’s the evidence that the Inuits’ protein intake, whatever percent of the diet that was, harmed their health in any persistent way?

                      As you requested Duck, I’m rating your work on this topic to date a quieter all-lower-case “nada.”

                      It still means “nada.” –Bryan

                    61. “Hi Duck. Sorry. But if you are trying to imply that enlarged Inuit livers were somehow “unhealthy” you’re still batting zero.”

                      Thanks for the straw man argument, but no that’s not what I was saying. The scientists I cited believed that their enlarged livers were due to their high protein diet. Of course, I explained that already, but you’re having trouble following that point for some reason.

                      “Once again these texts prove elusive. However, thanks to our Jonathan Christie here, we have Dr Schaefer’s 1959 glowing report on exceptionally robust Inuit health.”

                      Wonderful. And guess what? Schaefer beleived their glowing health was due to their, high protein diet.

                      Normalization effect of preceding protein meals on “diabetic” oral glucose tolerance in Eskimos (1972)

                      “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.”

                      That’s what I’ve been trying to tell you all this time. They don’t even eat like you do.

                      “And Duck, about what you said “…And there is plenty of evidence of high urinary nitrogen excretion in the Eskimo literature…” Even now, you persist to fail to show even one shred of real evidence to back up your claim.”

                      Enough with the lies. I already gave you links to all of the literature. Krogh & Krogh 1914 showed high nitrogen from high protein. As did Rodahl 1952 and others.

                      “Finally Duck what you say here “…[the Inuit] were well known to have a high protein diet…” So what? Where’s the evidence that the Inuits’ protein intake, whatever percent of the diet that was, harmed their health in any persistent way?”

                      It’s all documented in the links I’ve provided earlier. ALL of the research says they were high protein—even Schaefer. Even the LCHF Magasinet Swedes understand what you are having trouble seeing.

                      But once again you’ve missed the point. The point is not whether they were healthy or not. We really don’t know since even Inuit mummies are well known to have had significant arterioclerosis (possibly from inhaling soot from their lamps). That’s not the point.

                      The point is that the Inuit were eating so much protein that all of the researchers who looked into their enlarged livers believed they were relying heavily on gluconeogensis for much of their energy. And a grand total of ZERO believed that they were relying heavily on ketones.

                      Is that how you eat, Bryan? Do you eat a high amount of protein and reserve most of your fat for burning lamp fuel for heat? If you are able to eat a high protein diet and can stay in ketosis, then I agree with Peter on this one, who says:

                      “I have some level of discomfort with using the Inuit as poster people for a ketogenic diet. That’s fine. They may well have eaten what would be a ketogenic diet for many of us, but they certainly did not develop high levels of ketones when they carried the P479L gene.”

                      Peter sums it up nicely. Why on Earth would you want to use this extreme culture with unique genes and a high protein diet as the poster boys for a ketogenic diet anyhow? Makes zero sense.

                      “As you requested Duck, I’m rating your work on this topic to date a quieter all-lower-case “nada.” It still means “nada.”

                      And once again you’ve resorted to argument from fallacy.

                      I really have no interest in debating your fallacies any further, Bryan. If you want to know my opinion, then you should read all of the links I provided which actually observed real Eskimos. The literature stands on its own. The literature says they were not in ketosis (the original definition, which you are now trying to change) and that they ate a high protein diet. All of those references I provided refer to the Inuit’s observed high protein diet, which the researchers believed furnished their carbohydrate via gluconeogenesis.

                      And if you yourself eat a raw, high protein diet, then you can feel proud that you eat like an Inuit and are super healthy. However, if you are into protein restriction, then I have no idea what you are doing looking into a culture that doesn’t even eat like you do. It’s mind boggling.

                      There’s really nothing else left to say.

                    62. Duck, about the Inuit Paradox, to remind you why so many of us care and what we really want to know:

                      – Can the Inuit Paradox inform our decision–us non-Inuit folks–to try a persistent VLC foodway?
                      – Does the Inuit Paradox offer real evidence to consider to optimize dietary omega 6/omega 3 balance to lower our systemic inflammation?

                      The Inuit Paradox keeps offering tremendously exciting and relevant evidence to suggest the above approaches may indeed work to greatly improve our health. Duck, to date, no amount of “evidency-ness” you’ve shoveled onto this forum, when we closely or often even merely cursorily examine your sources, even begins to discredit the Inuit Paradox. Your slew of links have never–and I mean *never*–delivered rigorous evidence to discredit that Paradox. Your vague implied warnings against adopting lessons from the ancestral Inuit foodway: “…they are not like us,” “they burn fatty acids very differently,” “they do not exhibit ketosis as we do” and so forth, are simply that–vague and wholly unsupported warnings. Nothing you said and shown should even remotely dissuade anyone from experimenting with VLC. Ancestrally-living Inuit can and routinely DID thrive on VLC, even a near no-carb diet. By nearly all measures, many ancestrally-living Inuit enjoyed all-around robust health. Here’s a summary of the info that recently surfaced that we bat around here:

                      – the Inuit have one or a few genetic SNP variants (And so? In re: VLC, why should we care?)
                      – they “eat a high-protein diet” (So what? Why should we care? What’s “high?” anyway?)
                      – they “may or may not be in ketosis” (So what? Why should we care?)
                      – the conflicting accounts/non-accounts of CVD in ancestrally-living Inuit like those found in the 1940 Bertelsen report (I finally have this report. **Bertelsen utterly fails to say what the people who referenced it–including Ottawa Heart’s Dr Fodor–have been saying or implying it says.** Stay tuned for details.)

                      These points above are either wrong or fail to relate to our goals to find an optimum foodway to preserve and enhance our health.

                      So Duck, with your impressive ark of non-evidence, can I blame you for trotting out your tired litany of distractions? You recycle your irrelevant points accented with argumenta ad hominem: “…The scientists I cited believed that their enlarged livers were due to their high protein diet…Of course, I explained that already, but you’re having trouble following that point for some reason…That’s what I’ve been trying to tell you all this time. They don’t even eat like you do…” Meanwhile Duck you pose a silly rhetorical question, with a side of unsupportable assumption (the lamp fat thing), for which you already know the answers: “…Is that how you eat, Bryan? Do you eat a high amount of protein and reserve most of your fat for burning lamp fuel for heat?…” Again Duck, of course I don’t eat high protein and you know it. The point is that the diet is VLC–remember? I’ve made clear here I eat 15% protein and mostly fat. There’s plenty of evidence to suggest even the Inuit prefer fat. Maktaaq (Muktuk) is blubber that’s well over 90% fat by calores: In that 2004 Discover Mag link you’ve cited before Duck, , raw muktuk… to many [Inuit], it’s a mainstay.” Canadian Arctic explorer and ethnologist Vilhjalmur Stefansson spent a great deal of time researching the Inuit. His observations and his own experiences and further experiments with a very high meat diet led Stefansson in his book “Fat of the Land.” to propose a diet that is mostly fat. Ho et al in 1972, , says “…Approx 50% of the calories were derived from fat and 30 to 35% from protein.”

                      Then Duck we see this old saw from you–“I’ve Posted The Links…” You say: “…It’s all documented in the links I’ve provided earlier. ALL of the research says they were high protein—even Schaefer. Even the LCHF Magasinet Swedes understand what you are having trouble seeing…” complete with yet more ad hominem, accusing me of “…having trouble seeing…” something which I’ve never denied to begin with. Sure it’s perfectly plausible, even likely, the Inuit ate a higher percentage of protein than many others following their ancestral foodways. Duck, so what? I’ve seen zero evidence to suggest a higher protein has in any way impacted Inuit health, except possibly episodically and temporarily when sparse food availability forced them to eat ultra high protein.

                      Duck what you say here, in your one bolded comment in your post: “…the Inuit were eating so much protein that all of the researchers who looked into their enlarged livers believed they were relying heavily on gluconeogenesis for much of their energy…” Duck, I give that a big bolded “So What?” See my protein/fat discussion above. How much are their livers “enlarged?” Marginally bigger,like 5%? Who’s actually measured it? Does it even matter? You’ve yet to show even one researcher to determine this was an unhealthy adaptation. Indeed Schaefer said in 1959 “…Many seal-eating Eskimos *though perfectly healthy*, have a relatively large liver…”
                      Also your phrase “relying heavily on gluconeogenesis” is meaningless. “Heavily” as compared to what? Just ketosis? What about lipolysis? In that Ho report linked above, we read this: “The fact that the Eskimos had high serum FFA and low glucose levels (approximately 65 mg/100 ml) indicated that free fatty acids played a major role in body energy production…”

                      Here Duck you quote an irrelevant passage from Hyperlipid’s Peter:


                      and yet completely ignore his main message: You quote from Peter: “I have some level of discomfort with using the Inuit as poster people for a ketogenic diet. That’s fine. They may well have eaten what would be a ketogenic diet for many of us, but they certainly did not develop high levels of ketones when they carried the P479L gene.”

                      Duck what you conveniently leave out: Peter actually ardently *supports* VLC and ketosis. He writes further down in that same blog post:

                      “I’m always amazed by the concept that a ketogenic diet might be temporarily therapeutic but must be discontinued because it eventually becomes Bad For You… point-scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health…”

                      Finally Duck, you emerging fave distraction: Your spurious charges of “argument of fallacy.” You say “I really have no interest in debating your fallacies any further…” Duck, sure, that’s easy to say when you conveniently leave out specifics and examples to support your charges, or even show proof I’ve made even one argument to you “from fallacy.” Whatever. We’re used to that from you. Duck, if it makes you feel better to believe all that–whatever all that’s even supposed to be or to mean–then please be my guest. It won’t change the fact that I and very very many other folks derived health-saving and even life-saving lessons from the Inuit Paradox.

                      Duck, I’ll conclude with Peter’s conclusion out of his same post you cited:

                      “…point-scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health. Destroying a circular argument about Inuit diets may may the destructor feel good. Destroying the feet, eyes and kidneys of a person with type 2 diabetes, who need a ketogenic diet, as a spin off from that victory must be difficult to live with. I don’t know how anyone can do this.”



                    63. Bryan said: “Can the Inuit Paradox inform our decision–us non-Inuit folks–to try a persistent VLC foodway?”

                      No it cannot. Because they do not eat anything like Western VLC dieters do. To imply otherwise is dishonest.

                      Bryan said: “Does the Inuit Paradox offer real evidence to consider to optimize dietary omega 6/omega 3 balance to lower our systemic inflammation?”

                      Unknown. They possess unique genetic adaptions to apparently metabolize fats differently than we do. Incidentally, Hugh Sinclair once attempted to consume a high n-3 PUFA diet and it caused him to have difficulty with clotting and hemorrhages.

                      Bryan said: “Nothing you said and shown should even remotely dissuade anyone from experimenting with VLC.”

                      This is a straw man argument (which seems to be your expertise). I am not trying to dissuade anyone from experimenting with VLC. I am pointing out that the whole of the scientific literature says that the Inuit diet is not a proxy Western VLC diets.

                      Bryan said: “Ancestrally-living Inuit can and routinely DID thrive on VLC, even a near no-carb diet.”

                      Wonderful. And they did it by eating excessive levels of protein. The exact opposite of what Western VLC diets promote. They were converting enormous amounts of protein into carbohydrates via gluconeogensis. gluconeogensis = production of glucose. Glucose inhibits ketosis.

                      Bryan said: “the Inuit have one or a few genetic SNP variants (And so? In re: VLC, why should we care?)”

                      Because Westerners don’t have those SNPs and we don’t know if they are necessary for thriving on a VLC diet. That should be an obvious variable to consider.

                      Bryan said: they “eat a high-protein diet” (So what? Why should we care? What’s “high?” anyway?)”

                      Because protein is restricted in Western VLC diets. Protein knocks people out of ketosis. You should know this of course. And if you have difficulty understanding this, then I will point you to Peter’s article on the subject.

                      Peter writes:

                      “I just wanted to throw out a few comments about the inhibition of ketogenesis by protein. The obvious effect, that of stimulating gluconeogenesis, appears to be at best a partial explanation of what happens…At around 65kg bodyweight nowadays keeping to 1g/kg is not the easiest target. A decent steak and I miss it. Life is too short to stress about this, but I certainly don’t eat steak every day…Eating a steak is not very ketogenic.”

                      Read that again. (See my next post for documented Inuit protein consumption).

                      The Inuit eat an excessive amount of protein, they do not restrict it. Therefore, they cannot be used as a proxy for a Western VLC or ketogenic diet.

                      Bryan said: “I’ve seen zero evidence to suggest a higher protein has in any way impacted Inuit health”

                      Another straw man argument. I never said their high protein intake was deleterious. Rather, my point is that their high protein diet is the exact opposite of the protein restriction advocated by Western VLC dieters. Please do your best to understand that point. You should never imply that the Inuit diet is a proxy for Western VLC. Peter’s post on protein and ketosis proves this. And yes, I’m aware that Peter promotes Western VLC diets. That’s why he’s uncomfortable with using them for “poster boys” of ketogenic diets.

                      Bryan said: “Canadian Arctic explorer and ethnologist Vilhjalmur Stefansson spent a great deal of time researching the Inuit. His observations and his own experiences and further experiments with a very high meat diet led Stefansson in his book “Fat of the Land.” to propose a diet that is mostly fat.”

                      Yes, his “own experiences” are the key there. Stefansson was advocating a Western version of the Eskimo VLC diet. However, Stefansson was a white man who claimed to have gotten sick when he tried to eat a high protein diet. The only way Stefansson could survive in the Arctic was to restrict protein and eat high fat. You’ve just proven my point. White people cannot eat the high protein diet that the Inuit consume. Stefansson’s experience proved it and his own doctors admitted that he was unable to consume the observed high protein intake in an Eskimo’s traditional diet .

                      Bryan said: “Ho et al in 1972, says “…Approx 50% of the calories were derived from fat and 30 to 35% from protein.”

                      Yes. Ho is getting figures from Krogh & Krogh 1914. Krogh & Krogh observed excessive protein intakes. Again, you are proving my point. Western VLC dieters do not consume that much protein, particularly if they want to remain in ketosis.

                      Bryan said: “How much are their livers “enlarged?” Marginally bigger,like 5%? Who’s actually measured it? Does it even matter? You’ve yet to show even one researcher to determine this was an unhealthy adaptation.”

                      Straw man. I never said it was an unhealthy adaptation. The point is that they are relying protein to produce a lot of glucose, which inhibits ketosis. This glucose production is why no scientist ever claimed they were in ketosis. A Western VLC dieter restricts protein to stay on a VLC diet. That’s my point.

                      Bryan said: “your impressive ark of non-evidence”

                      I don’t see how presenting you with a century of scientific evidence is “non-evidence.” See my next post if you aren’t going to bother reading it.

                      Bryan said: “It won’t change the fact that I and very very many other folks derived health-saving and even life-saving lessons from the Inuit Paradox.”

                      I do not deny that a ketogenic diet can be therapeutic for some. However, since the Inuit were not in ketosis, whatever “life-savings lessons” you think are derived from the Inuit Paradox are based on a misunderstanding of what the Inuit actually consumed (in reality a high protein diet).

                      Bryan said “Duck, I’ll conclude with Peter’s conclusion… “…point-scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health. Destroying a circular argument about Inuit diets may may the destructor feel good. Destroying the feet, eyes and kidneys of a person with type 2 diabetes, who need a ketogenic diet, as a spin off from that victory must be difficult to live with. I don’t know how anyone can do this.”

                      Lol. I agree with Peter. And his statement would be relevant if someone here was trying to use the Inuit’s non-ketosis to dissuade others from trying a trying a VLC diet. But no one here is doing that, so again… it’s a straw man (once again).

                      It makes no difference if the Inuit were healthy or not because their diet has nothing to do with a Western VLC diet. As you like to say… “Nada”.

                      We agree that they burn a lot of FFAs, but they also produce a lot of endogenous glucose from their excessive protein intake (see my next post). How is that like a Western VLC diet? It’s not.


                    64. Duck, the Inuit Paradox absolutely can and *should* inform non-Inuit who contemplate a persistent VLC foodway, esp them who fear it because “no one’s ever done it before.” I never suggested we should eat all the same things as the Inuit. It’s the nutrient lessons we learn from them. I’m not going to start eating muktuk. But I’m making sure to eat salmon with the skin and bones. Both have high long-chain w3 and plenty of other nutrients. Nothing “dishonest” about that Duck. That’s very valuable to know and act on.

                      About Hugh Sinclair’s tissues with clotting on high w3, again you fail to read my comment correctly. I said “*optimize* dietary omega 6/omega 3 balance.” I had a similar clotting issue till I dialed back down my w6/w3 ratio from 1:1 to 3–4:1. I was fine afterwards and still kept getting lower CRPs.

                      Duck if “Nothing you said and shown should even remotely dissuade anyone from experimenting with VLC.” is a straw man argument as you claim, then why do you keep flogging the ill-defined idea that “the Inuit diet is not a proxy [for] Western VLC diets?” Do you do this out of a burning academic interest? People here want to learn how to get and remain healthier. If they need reassurance that they can safely achieve that on LCHF, the Inuit experience can help them hugely. Does that mean we have to eat 50% fat/35% protein like the Inuit do? Of course not. I eat 80% fat/15% protein. Point is Duck, it’s to reassure people they may well do very well on *persistent low-carb* and should not be the least bit afraid to experiment with it.

                      About what you say here: “Wonderful. And the [Inuit] did it by eating excessive levels of protein. The exact opposite of what Western VLC diets promote. They were converting enormous amounts of protein into carbohydrates via gluconeogensis. gluconeogensis = production of glucose. Glucose inhibits ketosis.” Duck, where to start with this flabby mess you spilled here? Again, your view that it’s “excessive” protein has never been proven. That’s simply your opinion. About it being “opposite to Western VLC” of course that’s wrong. Both are low carb. It’s a matter of setting the fat/protein balance that works best. About gluconeogenesis you have no idea how much of this ancestrally-living Inuit generate. Ditto for “enormous amounts of protein”–“enormous” is simply your personal feeling. Duck, obviously you’re welcome to all your opinions on all this. Just please understand they are not supported by the actual science. None in that “century of scientific evidence” you stuck up here.

                      Duck you say “Because Westerners don’t have those [Inuit] SNPs and we don’t know if they are necessary for thriving on a VLC diet…” *Sigh* Been there, done that already Duck. If anything, westerners are *better* at producing ketones. In any event, I’ve always suggested that people going on VLC get blood tests if only to assuage any concerns they may have.

                      About my comment: “Bryan said: they “eat a high-protein diet” (So what? Why should we care? What’s “high?” anyway?)” and your answer: “Because protein is restricted in Western VLC diets…” Duck yes you persist to misunderstand me. Where have I ever said we should eat a high-protein diet? Take a look round. You won’t find me saying that anywhere. And of course you’ve never answered what you think what constitutes “excessive.” Not holding my breath for that.

                      What you say here “The Inuit eat an excessive amount of protein…” Duck, you think if say this enough times maybe one day it’ll come true? Just wondering.

                      Oh but wait, then we get this from you! “I never said [the Inuit’s] high protein intake was deleterious.” Oh really? Duck, sure, you didn’t *say* their “high” protein intake doesn’t harm them. But do you believe it does? If not, then Duck why do you just say “The Inuit eat an excessive amount of protein…”? Pray reconcile these two statements for us.

                      About what you say. “You should never imply that the Inuit diet is a proxy for Western VLC.” Gee Duck. Maybe if you say it enough times, that’ll become true too. Maybe Bryan blog comments exhorting folks to chow unseemly amounts of protein will start spontaneously popping up all round the webosphere 🙂

                      Duck, you say: “… You’ve just proven my point. White people cannot eat the high protein diet that the Inuit consume. Stefansson’s experience proved it and his own doctors admitted that he was unable to consume the observed high protein intake in an Eskimo’s traditional diet…” Yes Duck. If you want to take Stefansson n=1 as “proof” that “white people” can’t eat the high protein diet the Inuit consume, sure, be my guest. Whatever. I’ve never advocated a high-protein foodway anyway. You know. Just in case I haven’t told you that before. And Duck, a news flash: You’ll find other kinds of non-Inuit folks out there besides “white people.”

                      Our exchange here: Bryan says: “Ho et al in 1972, says “…Approx 50% of the calories were derived from fat and 30 to 35% from protein.” Duck says: ”Ho is getting figures from Krogh & Krogh 1914. Krogh & Krogh observed excessive protein intakes…” Sure Duck. I’ suppose you’ll actually bother to back up that assertion of “excessive protein intakes” with actual K & K text? I’ve learned not to hold my breath for actual proof from you. If that text evidence actually exists and you actually post it, please remember this is nutrition science from over a hundred years ago around the time we were discovering “vital amines.” Duck, if this becomes yet another assertion you fail to support, I won’t mind.

                      About this: “I never said [high protein intake] it was an unhealthy adaptation.” Hmm. You’ve gone on about “enlarged livers” and “…their significant excretion of urea…” OK Duck whatever you say.

                      About this mess: “The point is that they are relying protein to produce a lot of glucose, which inhibits ketosis. This glucose production is why no scientist ever claimed they were in ketosis. A Western VLC dieter restricts protein to stay on a VLC diet. That’s my point.” Oh really Duck? “Glucose inhibits ketones” is your point? Gee, all this time I thought it was the Inuit “hypoketotic hypoglycemic” state you kept going on about. You know, yielding those raging 65mg/dL serum glucose levels ready to put the boots to any ketones with enough temerity to try to leave the liver. And I was thinking all this due to that CPT1a deficiency variant gene you kept going on about–you know, the deficiency that inhibits ketone production. Silly me Duck. Please enlighten us: What mg/dL of serum glucose do you need to start inhibiting ketosis? Enquiring minds want to know.

                      You say: “I do not deny that a ketogenic diet can be therapeutic for some. However, since the Inuit were not in ketosis, whatever “life-savings lessons” you think are derived from the Inuit Paradox are based on a misunderstanding of what the Inuit actually consumed (in reality a high protein diet).” Yes Duck, been around this block with you too a few times. What’s up with your amnesia? Mon pauvre, try to remember. Hint Q: Compared to Inuit, how well might non-Inuit handle “ketosis?”

                      And finally this Duck–good job putting words in my mouth: Duck says:“I agree with Peter. And his statement would be relevant if someone here was trying to use the Inuit’s non-ketosis to dissuade others from trying a trying a VLC diet. But no one here is doing that…” Well, Duck, that’s wrong too. You can sure find folks here inveighing against VLC. But Duck, please consider this: You’ve come up with one argument after the next to drive home the idea that the Inuit–the world’s top success story of ancestral VLC–are so “different” from us that their experience can serve little or no use to us. You efforts have the effect to cast doubt on what is perhaps the most inspiring example of low-carb success our planet offers. You upbraid people including me for imagined arguments of fallacy, meanwhile doggedly perpetuating the fallacy of insisting that people who suggest we take lessons from the Inuit are advocating “their high-protein diet” and even that we should eat their foods. Your insistence in this matter borders on an odd obsession. Your stubbornly refuse to see that VLC advocates, in the main, are *not* advocating a high-protein. Why do you do this? Your verbal contortions would be risible except this is very important stuff we’re discussing. Our diet decisions directly impact our health and lives. Duck, I’m not saying you shouldn’t spin your academic arguments regarding the Inuit. That stuff’s great fun and, most of all, we should feel free to voice our views here. But I say again to you, in this important matter, I *will* call bullsh*t when I see it. Most of all, people–especially people with high blood sugar issues–need to know they should feel absolutely free and SAFE to try VLC and even consider it as a lifetime choice, not just a “therapy.” The evidence suggests a low-carb moderate-protein very-high-healthy-fat foodway is perfectly safe. –Bryan

                    65. Bryan,

                      You’ve accused me of not presenting evidence, despite that I provided links to over 100 years of scientific observations on the Eskimos. Since you won’t take the time to read any of it, here’s what the scientists who observed the Eskimos found with their protein consumption (and nitrogen production) from high protein and high gluconeogenesis production.

                      Krogh & Krogh put a handful of Eskimos individually into a respiration chamber for 4 days at a time and fed them lots of Seal meat. They wrote:

                      Study Of The Diet And Metabolism Of Eskimos Undertaken In 1908 On An Expedition To Greenland by Krogh & Krogh (1914)

                      “The normal diet of Eskimos contains an excessive amount of animal protein (280 gr.) and much fat (135 gr.) while the quantity of carbohydrate is extremely small (54 gr. of which more than 1/2 is derived as glycogen from the meat eaten). Their dietary habits are vey like those of the carnivorous animals…The maximum quantity of nitrogen found in the urine of one day was 53 gr…According to our experiments the Eskimos would appear therefore to be able to retain a large amount of protein for a certain period exceeding 24 hours and to utilize it as a source of energy with very little loss.”

                      This was the first of many observations of high nitrogen excretion—a sign of significant glucose production from gluconeogenesis and not ketosis.

                      The Kroghs explained in their highly detailed report that the Eskimos would not enter the chamber unless they were promised various quantities of bread (and sugar for their coffee) during the experiment. The Kroghs agreed and gave them lots of bread/sugar some days and only a little bread/sugar on the VLC days. On VLC days, the Kroghs found that roughly half of their 54g of carbs came from bread/sugar and more than half came from glycogen in the meats. According to Rink 1855, Inuit were known to source bread and sugar since white man appeared in the 1800s, so we don’t know if these modern carbs craved by the Eskimos replaced other traditional carbs in their diet (Angelica, for instance) or if they were new additions to their diets.

                      In 1931, Heinbecker wrote:

                      Studies of the Metabolism of Eskimos, by Peter Heinbecker (1931)

                      “According to [Shaffer’s] analysis the metabolism of the foodstuffs contained in the Eskimo dietary would not be expected to cause ketosis, because the calculated antiketogenic effect of the large protein ingestion was somewhat more than enough to offset the ketogenic effect of fat plus protein…The results indicate no retention of nitrogenous products in the blood from the habitual high protein diets.”

                      Again, See Peter’s post on the importance of protein restriction in Western VLC diets.

                      In a review of all the available literature by 1953, Hugh Sinclair wrote:

                      The Diet of Canadian Indians and Eskimos, by Hugh Sinclair (1953)

                      “It is, however, worth noting that according to the customary convention (Woodyatt, 1921 ; Shaffer, 1921) this diet is not ketogenic since the ratio of ketogenic(FA) to ketolytic (G) aliments is 1.09. Indeed, the content of fat would have to be exactly doubled (324 g daily) to make the diet ketogenic (FA/G > 1-5). The Eskimo is apparently able to digest and absorb very large amounts of protein and fat at a single meal. In times of plenty, 4 kg of meat daily is a common amount and much is taken at a single meal…The high ingestion of protein alters blood and urinary composition : non-protein nitrogen and amino-acids are raised in plasma, and urinary nitrogen is increased (Rabinowitch & Smith, 1936), even during fasting (Heinbecker, 1931).”

                      4 kg of meat daily? Half the fat of what would be needed to reach ketosis? Hmm… And Peter says steaks aren’t ketogenic. So, Western VLCers do not eat this way, of course. Unlike the Eskimos, Western VLC dieters restrict protein. That’s been my point all along. You cannot use the Eskimo diet as a proxy for a Western VLC diet.

                      Clinical and Other Observations on Canadian Eskimos in The Eastern Arctic, by I.M. Rabinowitch (1936)

                      “It is also of interest to note that, though whale, walrus and seal have enormous layers of blubber, the accumulations of fat in the musculature seen in some land animals are practically unknown; the meat is, therefore, lean. When consideration is given to these facts and to the additional fact that about 58 per cent of protein is convertible into sugar, it is obvious that the ratio of fatty-acid to glucose is well below the generally accepted level of ketogenesis. I estimate that when food is abundant, the average daily diet of the adult Eskimo consists approximately of 30 to 40 grams of carbohydrate (which includes glycogen), 250 to 300 grams of protein, and about 150 grams of fat (FA/G=1.2)… Of particular interest are the high non-protein values of the blood (urea, amino-acids)…due apparently to the high protein diets.”

                      Not only did Rodahl observe high protein, but observed even higher protein intake during the Winter:

                      Basal Metabolism of The Eskimo, by Kaare Rodahl (1952)

                      “It is hardly fair to compare the metabolism of Eskimos on high protein diets with White people on comparatively low protein diets, and perhaps one would be justified in speaking of an “Eskimo basal condition.”… It was also observed that the basal metabolism was higher in the winter when the protein intake was increased, than in the summer…

                      …It is well known that considerably higher amounts of protein are regularly consumed by the Eskimos (DuBois, ’28), who generally speaking, prefer a diet where approximately 50% of the calories come from protein and the greater part of the remaining 50% are derived from fat. August and Marie Krogh (’13) report that the normal diet of the West Greenland Eskimos contained an excessive amount of animal protein—280 gm daily—and they noted that there seemed to be a considerable delay in the metabolism of protein and excretion of nitrogen, only 60% of the nitrogen being excreted during the first 24 hours after eating large meals rich in protein. In East Greenland the Eskimos consume an average of 300 gm of protein daily (Hoygaard, ’41). In Alaska a daily protein consumption of more than 300 gm has been observed among the most primitive Eskimos.”

                      Bryan, do any Western VLC dieters regularly consume 300gm of protein per day? Is it advocated as part of a VLC lifestlye? No, of course not. Because doing so would result in a metabolism that relied too heavily on gluconeogenesis (i.e. glucose) for energy.

                      Therefore, you cannot use the Inuit as a proxy for the health of a Western ketogenic diet. They don’t eat anything like Western VLCers do. Nor do any of us have their genes or metabolisms that allow them to eat this way.

                      My overarching point is that the Inuit cannot be a proxy for Western VLC or ketosis. To imply otherwise is dishonest when we see that all of the scientific literature shows otherwise.

                      This is not to say that a Western VLC diet is unhealthy—I have no idea if it is or is not. It may very well be that VLC is the best diet in the world! Who knows? All I’m saying is that you cannot use the Inuit as an example of Western VLC. That should be obvious given what was actually observed about the Eskimo diet.

                      Feel free to dig into the Inuit all you like. And feel free to advocate a ketogenic diet to those who may need it. Just be aware that at 300gm of protein per day, the Eskimos are not eating anything like a Western VLC diet.

                      Peter is wise to distance himself from the Inuit. You should follow his lead.


                    66. Duck, thank you for this very interesting material. Really, I do visit your links or had been. But it does get discouraging when so many you’ve posted go to material that’s stuck behind paywalls or in books or doesn’t address the issue.

                      Like I made clear in my last mail, you don’t need to sell me on the idea that the Inuit can eat a lot of protein. I never disputed it. I’m not convinced all Inuit around the north ate whopping amounts of protein all the time. There’s plenty of evidence to suggest they eat more fat when given the choice. They land a big bowhead whale, and they’re literally savoring the maqtaak for days. Since most Inuit live near the sea and hunt blubber-rich marine mammals, they often get a chance to eat a lot of fat, and can give the excess protein to their dogs. Nonetheless, I can imagine they need to eat high protein often enough that they’d have to adapt to it.

                      And how do they adapt? Duck I had to laugh when you asked me: “Bryan, do any Western VLC dieters regularly consume 300gm of protein per day?“ That was *me* from July–October 2007! During those four months I was averaging 300g protein per day. That was 40–50% of my calories. I know this because, during that time, I carefully weighed everything I ate down to the gram and entered all that into my spreadsheet. During that high-protein time, this “white boy” actually felt fine as I recall. At that time I walked 8–10 miles per day, and had plenty of strength to do that. The two main downsides: people told me I had ammonia breath and I had to get up several times per night to pee. Reading this about the Inuit makes me more curious about high protein. Who knows how my bod would have adapted if I carried it beyond those four months? But starting in October, I start systematically dialing up the fat percent till I got to my current level (80%) in spring 2008. I much preferred to eat the fat–the “flavor carrier”–over the protein.

                      This is also interesting: “Inuit were known to source bread and sugar since white man appeared in the 1800s” Reading through Bertelsen’s report in 1940, I was a little surprised to learn many of his Inuit patients had already adopted a lot of western-style food and habits, especially smoking and drinking alcohol. More on that later.

                      I want to spend more time looking at what you posted, and especially to crunch a few of their numbers. I’m going to bed now and will come back to this tomorrow. –Bryan

                    67. Bryan, you probably didn’t notice, but I had already provided the Krogh & Krogh many days ago (remember, you thought you’d “have to learn Danish,” but all you had to do was scroll past the Danish introduction). Due note the high levels of gluconeogenesis as shown by their high nitrogen excretion, which shows the Inuit rely heavily on glucose production. Those enlarged livers appear to be a (healthy?) symptom of that glucose production—I never said it was deleterious. If we can agree on that, then we’re in good shape here.

                      None of what I presented here was intended to prove that the Inuit were unhealthy. It was only done to show that they were not in ketosis and therefore cannot be used as an example of a “healthy” ketogenic culture (as has often been done by LCHF advocates).

                      It’s simply erroneous to use the Inuit as “poster boys” for a ketogenic diet or somehow to prove the safety of a ketogenic diet. You can’t do that given what the scientific literature says about their high protein diet and their unique genetic adaptations for fat burning. I say it’s dishonest to use them as poster boys, but even if you disagree with me, relying on the Inuit to prove the safety of a ketogenic diet so is to commit the fallacy of affirming the consequent—a logical fallacy of inferring the converse from the original statement.

                      An example of this fallacy would be:

                      “All cats are animals. Ginger is an animal. Therefore, Ginger is a cat.”

                      I think anyone can see the problem with that logical fallacy. One can easily commit this exact same fallacy by saying:

                      “The Inuit VLC diet is healthy. A ketogenic diet is VLC. Therefore, a ketogenic diet is healthy.”

                      I’m trying to get you to understand that this logical fallacy illustrates why the Inuit cannot be used as “poster boys” for a ketogenic diet.

                      If you want to argue it’s possible that a culture can exist and thrive on VLC, then that’s fine. But that’s an entirely different statement and you’d need to clarify that they did not eat a Western ketogenic diet.

                      But arguing that Ginger is a cat is unacceptable and fallacious.


                    68. I’ve been reading this back-and-forth about the Inuit for awhile, but haven’t commented until now. A few things come to mind: first off, who exactly are *the Inuit*? Aren’t they a series of different tribes in the Arctic region? Couldn’t they conceivably be eating slightly different diets? If we monitored the glucose reaction and ketone production of 4 Americans, could we come to any conclusions about the American diet and the health of all Americans?

                      I was under the impression that at least some of the Inuit ate pretty high fat diets. If you watch the documentary “My Big Fat Diet”- (you can google it on You Tube), those Inuit traditionally used a liberal amount of oolichan grease (not sure if I spelled that right). They dipped their fish in it, synonymous with dipping lobster in butter. Some Inuit ate mostly seal meat, which is pretty high in fat. Many groups rendered fat which they used to make pemmican. And I had read that berries preserved in seal fat was a delicacy which many of them ate in the winter. So I believe some of the tribes could have been eating a ketogenic diet; at least, I’m not convinced you can rule it out entirely.

                      About the protein issue: protein turns into glucose *only* if you eat more protein than what is needed for body processes, like tissue and cell regeneration. So it only turns into glucose if you eat an excess of what the body requires. This means that that amount will be different for each person. Some can eat a higher amount of protein and still be in ketosis- (I believe I may be one of those people). It could be that, living in a cold climate, exercising as they do, and eating zero to minimal carbohydrate might mean that they require more protein. Some of the papers you gave links to simply claimed “they couldn’t be in ketosis because they ate too much protein”, but I’m not convinced that’s true. Again, I’m not sure you can rule it out. In western, very low carb diets the protein recommendation may be on the low side in order to ensure that the majority get into ketosis, as that varies from person to person.

                      If they used urine ketones to measure whether or not they were in ketosis- (I’m pretty sure blood ketone meters are a more recent thing)- that method is notoriously inaccurate, as when people are keto-adapted they often utilize the ketones rather than excrete them.

                      I’m not saying they definitely were in ketosis all the time; I don’t know this one way or the other. And, as I said, this may have varied between different groups of Inuit; it may have even varied between the seasons. These are just a few thoughts I had.

                    69. Morgana, The Inuit are a group of culturally similar indigenous peoples inhabiting the Arctic regions of Greenland, Canada, and Alaska. They used to be called “Eskimos” but that was considered to be offensive since it supposedly translated to “raw meat eaters”. Of course, their tendency of eating raw meat is yet another reason why they do not eat like Westerners do. I don’t see too many Western VLCers eating lots of raw meat.

                      Morgana said: “I’m not convinced that’s true”

                      As it has been explained by Peter, and others, the majority of Inuit have CPT1a mutations that while they burn FFAs, they struggle to produce ketones. As Peter wrote,

                      “They may well have eaten what would be a ketogenic diet for many of us, but they certainly did not develop high levels of ketones when they carried the P479L gene.”

                      Even if you could prove that high protein is ketogenic, they cannot be used as an example of a “ketogenic” culture because of their highly prevalent CPT1a mutation. Everyone produces some ketones, including me, but we wouldn’t consider me to be “ketogenic” just because I produce some ketones.

                      Interestingly, the Inuit deficiency of CPT1a appears to force FA oxidation to brown fat. See the main graphic here, in this paper:

                      Adipose Fatty Acid Oxidation Is Required for Thermogenesis and Potentiates Oxidative Stress-Induced Inflammation

                      Since we don’t have CPT1a deficiencies, this suggests that we are burning fat in different cells than they do (mainly brown fat). They need to produce heat, after all. They were known to be warm to the touch, even on the coldest days.

                      Anyhow, the high protein diet is just another reason on top of their unique deficiency in CPT1a why they were not considered to be ketogenic.

                      It seems like people now suddenly want to redefine what “ketogenic” is, however the classic therapeutic ketogenic diet contained a specific ratio by weight of fat to combined protein and carbohydrate. (This is the “customary convention” of ketosis that Sinclair 1953 referred to). We should all be able to agree that the Inuit did not satisfy the classic “customary convention” of ketosis. Certainly the children did not as they have been known to die when their bodies attempt to rely on ketones for survival. If there is a brand new definition of what “ketogenic” is, that would be news to me.

                      Now, if you want to redefine what a “ketogenic” diet is, then you ought to institute a name change since the Inuit obviously do not produce many ketones. Otherwise we are conflating the medically recognized definitions.

                      Morgana said: “Some can eat a higher amount of protein and still be in ketosis”

                      If you have evidence showing a lowering of the ketogenic dietary fat requirement for people who are not using one of the three known changes in fat sourcing and protein demand (weight-loss, athletic demand or MCT oils), you’ll have to provide evidence. That would be groundbreaking (you should publish it!) and it would be great to have a citable reference for that. I have yet to find any evidence to change the ketogenic/anti-ketogenic macro-nutrients ratio for situations outside of those three known changes.

                      Of course, the Inuit were not trying to lose weight and they are known to have difficulty fasting after hours of strenuous work—they require snacks to avoid hypoketotic hypoglycemia.

                      This is not to say that the adult Inuit could never be in a mild ketosis. I’m sure some did enter ketosis in some situations, like starvation. Nevertheless, as Bryan has pointed out, they don’t do ketosis as well as Westerners do. And they don’t satisfy the customary convention of a ketogenic diet and they burn fats very differently than we do.

                      So, again, I have no idea why anyone would think they are a proxy for a Western customary ketogenic diet. A VLC diet? Yes, albeit a very unique one (very high n-3 PUFA with extremely rare PUFA-burning genes).

                      As you can see, there was a reason why Peter distanced himself from the Inuit. And he wasn’t alone. This debate first happened in Sweden and prominent Swedish LCHF advocates Andreas Eenfeldt[1][2] and Annika Dahlquist[3] quickly distanced themselves from the Inuit after they reviewed the evidence.

                      The Inuit are Genetically Adapted to a High-Fat Diet, Study Says

                      “Is a strict low-carb diet super healthy for everyone? People who argue for this often bring up the Inuit people. However, this particular argument has never been a very strong. And now it got even weaker.

                      According to a study released in Science yesterday, the Inuit, who have lived in the extreme conditions of the Arctic for a long time, seem to have developed genes that make them especially well suited to eat large amounts of omega-3 fat.”

                      Those are the words of one of the most prominent LCHF doctors in Sweden. So, I don’t see what the fuss is here.

                      Obviously this revelation does not detract from the efficacy of a ketogenic diet. It just means that the Inuit are not a proxy for such a diet. The Swedes, and Peter, seem to understand this quite well. I’m surprised others here aren’t able to reach the same conclusion.

                    70. Duck Dodgers- I think you misunderstood much of what I was trying to say, and, although you supplied several links, you didn’t really supply many answers. My main point was that there are different groups of people who are called “Inuit”, and it’s unclear to me how many of them have actually been studied, how many of them really eat a high protein diet- (I know at least some Inuit eat a higher fat diet), how many of them really have this genetic mutation- (according to the link you posted some, but not all)- and if we can make a generalization about all Inuit based on- (at least, the link I looked at)- 4 people. It doesn’t matter to me what Andreas Eenfeldt believes about the situation, I like to see evidence and come to my own conclusion. By the way, I’m not saying you’re wrong, it’s just that the links you’ve posted have raised more questions for me than answers.

                      But first: about raw meat: yes, I do eat raw meat, and I’m sure that at least some low carbers do too. I eat raw herring this time of year, and occasionally raw salmon. I eat salted, hung dried ham in the form of Parma ham or Serrano ham. I also eat a venison salami sometimes; I like carpaccio of all sorts, and many people eat steak tartare, so yes, some of us do eat raw meat. I’m not sure what the point is, it might be neither “here nor there”, but I just thought I’d mention that I do eat it.

                      Also, I don’t think I was “changing the definition of ketosis”. Ketosis is normally defined by a blood ketone reading of at least .5 Mm to about 3.0- (this is the optimal range). The classic ketogenic diet used to treat epilepsy in the past is neither here not there; it is not necessary to use that diet to go into ketosis, and actually, nowadays they’ve discovered that the less restrictive Atkins diet works just as well for people with epilepsy. The ability to get into ketosis varies from person to person; there is no “one size fits all” in terms of a certain macronutrient profile. According to Dr. Seyfried, women often can get into ketosis easier than men; and according to Dr. Jeff Volek, thin people and athletes also generally have an easier time getting into ketosis. (I won’t supply links, sorry, it’s too late here and I’m getting ready for bed. These were 2 interviews I saw on You Tube. Unfortunately they are long, and I don’t know at exactly what mark they said these things). In any case, what that means is that some people are able to eat more carbohydrate than others and still be in ketosis, i.e., the blood meter range; this goes for protein as well. Of course, obviously eating a huge amount of protein will keep one out of ketosis, it’s just that I’m not totally convinced that *all* Inuit ate a huge amount of protein, though it looks like some did.

                      Not sure if you’ve bowed out of this discussion or not, but I thought I’d clarify those few points.

                    71. Morgana, to chime in about the raw meat (and fermented meat since Inuit do that too), more non-Inuit folks eat it than we may realize. Many eat raw oysters. Sashimi is quite popular in Japan and in many metro areas in North America. Some sauces, like true fish sauce and Worcestershire sauce has fermented anchovies in it. About the herring, I get that in our season for it (this month and next) and pickle them, except I eat the milt and roe sashimi-style (raw) as is common in Japanese cuisine. Same with uni (sea urchin) when I can find it in the store. I gently split the uni open clamshell-style with a cleaver, squeeze some Meyer lemon juice on the orange-y egg sacs and down the hatch yum. Tastes like the sea. Also, like you, I make tartare, from meat and salmon. You find cultures all over the world fermenting fish:
                      Swedes ferment herring (surströmming) and the Icelanders ferment shark (Hákarl). Granted those two ferments are acquired tastes to be sure! But few people think the Swedes and Icelanders are fundamentally “different from us” because they eat raw meats. –Bryan

                    72. Why would eating raw meat make anyone think the eaters are “fundamentally different”? Many European nations, as well as Asian ones, have their raw meat dishes: carpaccio, ceviche, etc. In the early 1900s, when forensic medicine was in its infancy, German immigrants in large cities contracted trichinosis by eating raw pork — they did it in the motherland, and had no problem there because they didn’t feed their hogs garbage as we did in the US (As an aside, the fascinating, and, I fear, now out-of-print, book, “Eleven Blue Men” has some fascinating stories of early medical forensics, including how the trichina problem was identified). It seems only in the second half of the 20th Century that Americans got turned off on the idea of raw flesh. Perhaps that was a a good thing, with the mass production of beef.

                    73. Annie what you ask: “Why would eating raw meat make anyone think the eaters are ‘fundamentally different’?” This traces back to what Duck wrote to Morgana a couple of days ago (the 13th):

                      “Of course, their [the Inuit] tendency of eating raw meat is yet another reason why they do not eat like Westerners do…”

                      This is part of Duck’s persistent efforts to categorically portray “the Inuit” and “the Inuit diet” as profoundly different from “us” and “our diet.” As though “the Inuit” are some monolithic block of people who all share the same special adaptive genes and eat just the same type of diet at all times, however far-flung they may be around the circum-Arctic. Duck categorically asserts things like “…the Inuit diet is not a proxy Western VLC diets”, that “ [the Inuit] …evolved differently than we did,” and “The Inuit are not an example of what happens in Western metabolisms.” He even suggests “the Inuit diet” is somehow unsuitable and even harmful, saying things like: “…they [stayed in gluconeogenesis] by eating excessive levels of protein…” and “…Krogh & Krogh observed excessive protein intakes…” and “…they …produce a lot of endogenous glucose from their excessive protein intake…”

                      All this to imply that “the Inuit” are so different from us that the rest of the world can derive no lifeway or foodway lessons from them. As Morgana, I, and some others here have been suggesting, the picture is much more complex and nuanced. I maintain that the Yupik-Inuit ancestral foodways are likely much healthier than how Duck portrays them and that they can serve as a tremendous inspiration and guide for the many millions of metabolically sick people who are considering VLC but viscerally fear it due to life-long massive pro-carb anti-fat acculturation. However much I may have misunderstood certain details of it at the time I learned about it in 2007, the Inuit experience critically aided my journey back to health. –Bryan

                    74. Hi Morgana. Good question “who exactly are *the Inuit*? The nomenclature’s a WIP. I attended high school in Canada with lots of First Peoples including Inuit from Quebec and Iqaluit in the part of former NWT now called Nunavut. My Inuit classmates were already eating loads of SAD of course, but still hunted (on snowmobiles, in power boats) and did seem partial to maktaaq (muktuk = blubber = 90+% fat). This was back when Canada started moving to call them Inuit. We slid into referring to all the closely related circumpolar peoples “Inuit” even though the Yupik of far eastern Siberia and Alaska don’t call themselves that. Many sources still collectively refer to all of them as “Eskimo” though some promote “Inuit-Yupik.” These two links offer more detail on them and somewhat complement Wikis and US/Canada gov’t sources:


                      Ancestrally, Inuit-Yupik typically didn’t live so much in “tribes” as in very small single- or several-family units. Most live near the sea and traditionally derive most of their calories from large very blubber-rich marine life, like seals and the bowhead whale. Morgana you said “I was under the impression that at least some of the Inuit ate pretty high fat diets.” and all I’ve learned agrees with that: Fat was the Inuit-Yupik’s main calorie source. At least for the coastal peoples, and most Inuit-Yupik are coastal dwellers. Morgana, you ask “Couldn’t they conceivably be eating slightly different diets?” yes they do, depending on where they live and the season. Veg-wise at one end of the spectrum, some ancestrally-living Siberian Yupik (at least in Chukotka) most consistently included veg, even using root cellars. Alaskan Inuit and Yupik Some regularly ate sea veg, other not so much. At the other end of the spectrum are the far Northern Greenland Inuit, like those around Qaanaaq, who ate virtually no veg because it was rarely available. The inland Inuit, like the reindeer Yupik in Siberia and caribou hunters in Alaska, had a harder time getting iodine, so ate the thyroid glands of these big ungulates, esp during the typical times to conceive children.

                      For the ancestral foodway stuff I expect you’ll want my sources and I’m busy trying to find them! This is from my research 5–7 years ago, early on in my LCHF journey. Please bear with me while I find them. Meanwhile you can find some of it in Susan Allport’s book “The Queen of Fats.”

                      Finally Morgana about what you say: “… I believe some of the tribes could have been eating a ketogenic diet…” The more I delve into this matter with Duck and others, the more the Inuit experience raises a fascinating question. What conditions define their energy metabolic state(s)? Indeed what conditions define the energy metabolic states of any of us?

                      For example, let’s look at one of the most recent direct measures we have on this matter. In their 1972 report, Ho et al say:

                      “…Each Eskimo’s serum was tested for the presence of ketone bodies … and all serums were negative. This does not preclude an increase in ketone body production during this time… The fact that the Eskimos had high serum FFA and low glucose levels (~65 mg/dL) indicated that free fatty acids played a major role in body energy production…”

                      Picking this apart, I began to realize that terms like “ketosis” and “glycolysis” sorely lack comprehensive definition. No-one can give us a broadly accepted def for those two terms. We foodway-focused folks typically–perhaps sloppily–default to the term “ketosis” as a default state in which *all* fat-derived energy–ketones and FFAs–predominate over glucose derived energy (glycolysis). Maybe we need a more precise term to encompass all fat-derived energy. How about “keto-lipolysis?” How does that sound to everyone?

                      Let’s go with keto-lipolysis for the moment. Morgana, we still don’t know how to determine which energy-metabolic state predominates–glycolysis or keto-lypolysis. Do we go by sheer millimolars of glucose and fats+ketones in serum at any given moment–whichever has the greatest concentration wins? Or rather is it by calories delivered to our tissues at any given moment–the one that delivers the most calories at any one time wins? Or rather is it whether or not the metabolic conditions at any given moment trip the insulin switch to start/stop mobilizing fats from adipose tissue? Is it some combo of these three conditions? Again, we have no broadly accepted defs. Indeed I find remarkably few *proposed* defs. However, when you look at what Ho et al found–very low serum glucose (65mg/dL) and highly mobilize FFAs, keto-lipolysis wins hands-down by all three defs.

                      By the FFA-excluding definition of ketosis that Duck promotes, these Inuit are most likely not in ketosis. But for those of us looking at LCHF, that is a moot point, esp since non-Inuit appear to be much better at ketosis anyway. For us seeking to optimize our health through diet, Duck’s strict def of ketosis is utterly irrelevant. Much more important: are these Inuit in glycolysis? Regardless of how much gluconeogenesis they may or may not be doing? By the above defs, these Inuit are definitely not in glycolysis. For us seeking to optimize our health through diet, that’s what we care about. For us, to dwell solely on how much gluconeogenesis the Inuit or anyone else are doing is an utter waste of time. What we care about is whether or not we are in keto-lipolysis or glycolysis. By as many relevant measures of these states as possible –Bryan

                    75. Bryan said: “Duck’s strict def of ketosis is utterly irrelevant”

                      lol. You’ve got to be kidding me. This is yet another fallacymoving the goalposts.

                      As if I invented the actual definition of ketosis. Give me a break. What universe do we live in where you get to redefine ketosis as being something that isn’t ketosis?

                      Do yourself a favor and look up the word “ketosis” in any medical dictionary and textbook. You’ll find that it says that ketosis is a “raised levels of ketone bodies in the body tissues.” The Inuit do not fit that definition.

                      But feel free to reinvent the definition if you like. lol

                    76. Duck, maybe you’ve been missing the message.

                      For people looking to improve their health with LCHF, looking at ketosis in isolation DOESN’T WORK.

                      Just wondering Duck. What part of that don’t you understand?

                      Also, you utterly fail to produce a broadly accepted comprehensive definition for ketosis. We’ve been around this block before. You didn’t do it in your last post. You’ve never done it in any previous posts. You won’t in the future until when and even if the global establishment agrees it. To simply say “raised levels of ketone bodies in the body tissues” doesn’t even begin to cut it. Raised from what level? To what level? Is fat mobilized from adipose tissue or not? What are the serum glucose levels? All those considerations matter greatly for our overall health.

                      Duck, you can’t even keep your own various defs of “ketosis” straight. On December 3rd, you posted this: “Ketosis /kɨˈtoʊsɨs/ is a metabolic state where most of the body’s energy supply comes from ketone bodies in the blood.” Guess what Duck? “Raised” levels of ketones do not necessarily mean “most of the body’s energy supply comes from ketone bodies.” And the def you gave on the 3rd says “ketone bodies in the *blood*” But the def you give today says “ketone bodies in the *body tissues*” So which is it Duck? “blood” or “body tissues?”

                      Duck, if you want, keep flogging your “Inuit are different” “low ketosis,” “high gluconeogenesis” stuff in your craftily crafting way. Just please don’t expect me to stop calling you on the bullsh*t I find in it. –Bryan

                    77. Bryan said: “So which is it Duck? “blood” or “body tissues?”

                      lol. It makes no difference since the Inuit cannot manage to produce many ketones either way!

                      And with that, I’m afraid our time is done here, Bryan. As I mentioned earlier, the Inuit debate already happened in Sweden last year and it was decided by LCHF advocates that the Inuit have no business being compared to a ketogenic diet. Peter obviously agrees. As do I. So, there’s nothing left to say. That debate ended a year ago. Let it go.

                      Take care, Bryan. I’m out.

                    78. wbryanh- My question “who are the Inuit” was basically a rhetorical question. The point I was trying to make to Duck Dodgers is that- since “the Inuit” consists of many groups of people- it’s not clear to me at all that every single one of them eats a high protein diet, has enlarged livers, and has trouble producing ketone bodies, though I see by the research that at least some do. According to the link that Duck Dodgers posted, in the groups where this mutation appears, approximately 68% of them have this genetic mutation. Although that is a high number, what can we say about the others who don’t have it? (Apparently, according to that same link, the native peoples of inland Alaska don’t have that mutation at all). It is thought that this mutation used to confer a metabolic advantage in the past, but has become detrimental in the present day. In the link below, it is mentioned that this mutation might have ensured that they didn’t over-produce ketone bodies, due to their unique living situation and diet. (This is all conjecture of course, but the article does mention “high fat diets” and “ketosis”, implying that at least some Inuit are, or were, in ketosis):


                      By the way wbryanh, you don’t need to supply any links or “proof” for me that the Inuit ate a high fat diet; I’ve read many times that they did, and it was mentioned in the documentary that I wrote about in my post to Duck Dodgers. The “high fat” aspect was even mentioned in the link that Duck Dodgers posted, as it is in the link above. I hadn’t read in the past that they ate huge amounts of protein- (I didn’t realize it was even possible to eat that much protein, as I thought it made people sick). It’s possible I guess that some did and some didn’t. In any case, I’m not saying that all that was said about the Inuit was all wrong, it’s just that- natural skeptic that I am- some of the evidence seemed a bit conflicting to me, and raised a few questions.

                    79. Oh OK Morgana. Thanks. That (probably missense) CPT1a variant does intrigue me. My thought is that it compels more FFAs to go straight to thermogenic tissue, e.g. brown adipose tissue. But who knows? I can’t warm to the idea thought that it’s some “liver-sparing” thing. My sense is that our GIs are too good at vetting trigs in the duodenum to allow a whopping load of long-chain polys to go systemic. –Bryan

                    80. I said … “to allow a whopping load of long-chain polys to go systemic.” That is, Morgana, except to let them in to burn right away, e.g for thermal energy. –Bryan

                    81. Morgana, rereading your post, I’m absorbing more good points you made. 68% of northern indigenous peoples in far eastern Siberia with the variant means almost *a third* of them have the normal CPT1a gene per that link you gave, making them “less different than us:”


                      That gene variant rate could be greater or less for the Yupik-Inuit in Alaska, Canada, and Greenland.

                      To dilute the message and muddy the waters still further, the researchers tested Chukchi and Koryaks as well as “Eskimo” (I assume here they mean Yupik, the only Eskimo people I know of in Siberia). I couldn’t find anywhere it says how many of each group they tested. Was it an even mix of the three groups? Or weighted toward one or two of those groups? It’s likely the “Eskimos” were a minority in this little cohort.

                      The Koryak are especially interesting because they live south of the Yupik and Chukchi and appear to eat more plant-sourced food. This Koryak Wiki,, says:

                      “… Salmon and other freshwater fish as well as berries and roots played a major part in the diet…”

                      The last point on that CPT1a gene variant: How much weight can we put in a sample rate of only 25 people?

                      Morgana, about the article quote you cited: “…mutation could be protective against overproduction of ketone bodies…” Yes, interesting that this piece also points to a high fat diet with the Yupik and other indigenes. And like you say the risk of “overproduction of ketones” is conjecture. I’ve heard of plenty of accounts of people on high-fat diets testing negative for ketones, and that was my experience too. When I went 80% fat 15% protein 5% digestible carb in early 2008, I tested my ketones for several months and it always came up negative on the strip. That makes sense. Our bods have at least several ways to regulate our ketone body levels. Our very neuron-rich GI constantly communicates with our brain regarding energy needs, and is able to vet to a great degree the dietary fats in the duodenum, deciding whether the body needs them (for structure and energy) or not, letting the excess wend down to the exit. Even if some excess fat goes systemic we may have ways besides CPT1a variants to gate conversion to ketone bodies, like storing the fat in adipose tissue. Finally, we can easily purge unused ketone bodies that exist at physiological levels. β-hydroxybutyrate and acetoacetate spontaneously break down into acetone, a volatile compound we eliminate through our pores and breath. –Bryan

                    82. wbryanh- yes, good point about the ketones. Ketosis isn’t “dangerous”, like some people seem to think, and the body has ways to regulate it. In any case, it’s curious why and how that mutation came about. I wonder how prevalent it was in their ancestral past- (before the introduction of modern foods into their diet?) I think it was mentioned somewhere that most of the people who were tested were already eating at least some non-traditional foods, though I don’t know if that has any relevance at all. In any case, I’d like to study this further….(not tonight though, I just got back from a long day of work). I’ll let you know if I find anything.

                    83. Morgana, yes, I’m curious to know too. More and more, I wonder what life factors select for it. Duck posted something recently about how the CPT1a deficiency variant is common among the Hutterites. It’s also common in the Koryaks even though they have more consistent access to veg than the Yupik and Chukchi. Anyway the research is there waiting for you when you get rested up. 🙂 –Bryan

                    84. wbryanh- Been looking for information about this mutation. It’s hard to find what I’m looking for- (maybe not much is known about it)- but most of the medical literature looks at it as a “deficiency disease”- (it’s the cause of a high infant mortality rate). Since it’s relatively prevalent in certain Arctic communities, it’s suspected that it served an advantage at one time, though no one seems to be in agreement as to what this advantage might have been. I thought this was an interesting link- it states once again that not all Inuit have this mutation (they give some specific information about the percentages). They also mention that the Inuit ate a high fat diet, not necessarily a high protein diet (although I guess one doesn’t preclude the other):

                      It has been mentioned that this mutation seems to protect against diabetes (though I don’t understand the mechanism). I’ve been trying to discover exactly when in time this mutation became prevalent, and if it was before or after the introduction of “Western” foods- (which I guess many of them have been eating for quite awhile). Could be interesting…..

                      Like always, there’s a bit of conflicting information. I’ll keep looking though.

                    85. Hi Morgana. About CPT1a deficiency, I’m into a house repair right now, but the Pediatrics piece you posted is very interesting and I’ll come back to read it more closely. I’m wondering if it has more to do with lots of long-chain w3 in the diet, regardless of calories burned and extreme cold? The highest verified rate of the deficiency I know of are for those 25 indigenes in Siberia that got their genomes sequenced, and they were a mix of Eskimo (Yupik), Chukchi and Koryak, the latter who lived further south, and that 68% or roughly 2:1 for having the homozygote. (Btw, I don’t know of any such sequencing studies for Alaska, Canada, and Greenland Yupik-Inuit.) But all these people are coastal and eat sea life. Then in that Pediatrics piece you posted, on page e1166, you see 1:4 for the coastal BC indigenes on Vancouver Island, where the weather is very mild, and usually don’t have to spend so much energy hunting for food and warding off cold. The ratio drops down dramatically as you move inland away from big w3 sources. The Hutterites in NA are 1:16, but many lived in coastal Europe (Amsterdam, Leeuwarden, Danzig (i.e. Gdansk) before coming to NA, so maybe lots of herring? Anyway, these are my quick thoughts on it.

                      About the Inuit eating a high fat diet, it makes sense to me. I don’t doubt they eat very high protein at times when they have to. But from just about all I’ve read and heard, the Inuit favor fat. About what level “excessive” protein may be, I found this Wiki that suggests actual numbers:


                      which has this: ” …It has been observed that the human liver cannot safely metabolise much more than 221–301 g of protein per day (for an 80 kg/176 pound person)…” Ducks posted studies of Inuit eating up to that much, 280–300g. I don’t recall any going beyond that, but quite possibly overlooked them. I even have personal experience with a high protein diet. I spent a month in 2007 dialing up to 300g/day protein, and kept it there from Aug–Nov 2007 (not July–Oct like I said earlier) and felt fine except for ammonia breath and peeing 3–4x/night. Fact is, no-one commits to any figure that constitutes “excessive.” That Wiki continues:

                      “…given the lack of scientific data on the effects of high-protein diets, and the observed ability of the liver to compensate over a few days for a shift in protein intake, the US Food and Nutrition Board does not set a tolerable upper intake level nor upper acceptable macronutrient distribution range for protein.”

                      Per this anyway, our livers adjust very quickly to a high-protein diet.

                      OK Morgana back to carpet-laying. Lots to follow up on! –Bryan

                    86. wbryanh- okay, in looking further, it seems that this mutation appeared thousands of years ago; though it’s hard to know how widespread it was, or exactly when it became so prevalent. What about life before this mutation developed: were the Inuit in ketosis? It is a recessive gene, and apparently both parents need to carry the gene in order for it to appear- (I can re-find the links if you need). It’s considered a “deficiency disease”, so researchers have wondered why it’s so prevalent in these Arctic groups. It can cause problems (as we know), like hypoglycemia and high infant mortality, which wouldn’t bode well for the people. It’s been called a “paradox”. Researchers theorize that it probably incurred some kind of benefit in the past, when they were on their traditional diets. One of the common theories is that it “protected them from their high fat diet”; (that is, of course, assuming that high fat diets are “dangerous” and that we need “protection” from them). I haven’t figured out what the mechanism would be that would “protect” them, nor has that been explained. In addition, there are several other theories as to why this mutation might be advantageous (for instance, it keeps them warm, which makes more sense to me).

                      But looking at it from another angle: what is the “cure” for hypoglycemia? A low carb, or even a ketogenic diet. It was bandied about in the comment section of an article about the Inuit on the blog of Dr. Eades (“Protein Power”) that possibly this mutation appeared in the gene pool, but since they were fat burners (possibly even ketogenic)- the gene just “stuck around”, not doing any damage, whereas in other populations who eat higher carbohydrate diets it would have been selected out. This might explain why it’s far more prevalent in certain populations (the coastal), as you mentioned. Do the inland Inuit eat more carbohydrates? (I believe you said they did). In any case, that’s another possibility, the way I see it; that rather than incurring an evolutionary advantage- (some liken it to sickle cell anemia)- maybe it simply wasn’t causing too many problems on their native diet, but now it is problematic on their modern diets. I’m not saying this is definitely the case; I just believe it could be plausible.

                      Below is a link explaining how breastfed infants (when they are exclusively breast fed) are in a state of ketosis. I believe the Inuit, like most hunter gatherer cultures, breastfed their babies for a pretty long time. And I guess Duck mentioned that the babies with this gene mutation had to be fed very often- (at least, the ones who had been exposed to modern foods, or formula). It’s kind of hard to ascertain how things were on their native diet, as the Inuit have been exposed to modern foods for quite awhile now. (So, as you mentioned before, maybe they are burning fatty acids, but do “ketosis differently” than we do?)


                    87. Morgana, what you say here: “…the gene just “stuck around”, not doing any damage…” I definitely want to explore more that option. The longer the fat chain, the less polar it is, thus the less of it travels directly from the duodenum through the hepatic portal because long-chain fats simply don’t travel well in serum. Rather the vast majority of these very long chain w3 fats (20-C and 22-C long) have to take the long roundabout “milk-run” (fat-run?) on chylomicron “buses.” Our GIs load these long-chain fats onto chylomicrons and send them into our lymph system where they travel all the way up to our left subclavian vein where they finally enter serum. (Here’s a Wiki with details on it: ) I suspect for Yupik-Inuit and related circum-Arctic folks who adapted to such a rugged and intensely cold place, their bods suck up loads of these fats into thermogenic tissue, like brown adipose tissue, long before they ever have a chance to make it down to the liver. So maybe it’s that, despite a diet hugely high in these w3s, remarkably few of these Inuit lipos ever make it to the liver, and so CPT1a fell into disuse. As for evol selective pressures, maybe the need to generate the max thermal energy simply to not freeze to death trumps the problem of need to frequently feed Inuit infants. Of course on all this hard tellin’ not havin’ the actual isotope-tracer tests to show us. But this is one of the ideas I’m noodling around. –Bryan

                    88. Expanding on my last comment Morgana, could be the relatively high rates of the CPT1a deficiency homozygote in coastal BC indigenes, like those on Vancouver Island, may be vestigial? At least in part? Left over from when the original First Peoples crossed the Bering Land Bridge 15–20k years ago? We have evidence the homozygote is quite common in current day Siberians from those 25 gene sequences showing the 68% presence for the deficiency in Yupik/Chukchi/Koryak. Could be CPT1a deficiency traveled across the Land Bridge in these original First Peoples, stayed prevalent in the Yupik-Inuit and others in the far north due to enviro pressures, and had time over the relatively few millennia to go only partially heterozygotic. Esp for their relatives such as the coastal indigenes who migrated south and who still eat a high w3 fish diet so less enviro pressure to go heterozygotic. Meanwhile those who migrated inland like the BC interior, away from high w3 and possibly more carbs, experienced more evol pressure to go heterozygotic but even so they still retain vestigially the deficiency. Again all this from reasoning, no proof. –Bryan

                    89. Morgana, you bring up other points I’d like to address, but have to stay on the hateful toxic task of laying wall-to-wall. I hope to come back this evening, early morning your time. BTW, It’s Duck who’s been saying the Inuit “…do ketosis differently from the way we do.” I’m not sure what Duck fully and exactly means when he says that. But I’m willing to consider the idea it includes fewer ketones. Which brings up an interesting question: Why do Yupik-Inuit infants need to eat frequently, but the adults can fast? What life-time adaptations allow the adults to do that? I may be overlooking simple answers here, but have my mind on the carpet task. OK Morgana, to be continued. –Bryan

                    90. wbryanh- below is a link explaining how glycogen is converted to lactic acid after the animal is killed. One of the points made is that if the animal is stressed, or exercising- (like if it is being hunted?) the glycogen goes into the bloodstream and basically gets used up. Of course, they are talking about muscle meats here, so I don’t know how that applies to liver or to sea animals and their skin:


                      Generally, there are small amounts of carbohydrate in meat (more in liver), but usually it is considered minimal, and therefore not included in macronutrient ratios. (Well, in the meat that *we* eat anyway). There are also small amounts of carbohydrates in eggs; (the eggs of sea birds were also eaten quite a lot by the Inuit).

                    91. Morgana, thanks for the FAO link. I’ve been meaning to look more into glycogen depletion during animal stress like during hunts. The Yupik-Inuit going on often protracted hunts and taking sometimes hours, like in the case of whales, to chase and make the kill. So it’s easy to imagine these creatures convert at least some (most? all?) of their glycogen to lactic acid.

                      Shellfish–at least bivalves–have a lot of glycogen. I wonder how much the bivalve feels stress and drives its glycogen to lactic acid? –Bryan

                    92. wbryanh- below is a link about the carbohydrate content of shellfish after death. (There is a table as well). You will note that although shellfish does contain carbohydrate, it’s still pretty minimal (at least the ones listed). By the way, I don’t agree with everything he writes in this article (mainly his opinion on cheese). But I thought the information about shellfish might interest you:


                    93. Hi Morgana. Thanks for Cordain’s shellfish carb missive. I hadn’t read anything by him for ages. Shellfish carb loads aren’t negligible and in my early days of taking control of my metabolic health (2007–2009), eating a bowlful of mussels definitely popped my blood glucose levels, though as usual I can’t discount other possible drivers. But even the most carb-filled shellfish (cooked whelks) at 15g/100g are still less carb dense than starchy tubers like boiled potato at 19g/100g of active carbs ( and not all that much more than some legumes like lentils at 11.5g/100g of active carbs. ( Lentils are on a par with carby shellfish runners-up mussels and abalone. Plus, shellfish comes with a big load of vitamins and minerals which may help offset the BG-popping effect of the carbs.

                      Interesting, I don’t remember Cordain him being interested in food acid-base issues. I haven’t yet found much research to lead me to put much stock in dietary pH regimens. For healthy people anyway. Our bods offer plenty of ways to balance serum pH. About cheese, some people feel it sits in an ancestral murky zone. But I’ve never had much trouble with it. The path to cheese seems built on completely natural processes. Ruminants like sheep have rennet in their rumen which begins to curdle mother’s milk right in the rumen so the lamb can more easily and completely digest the dairy. –Bryan

                    94. Bryan: One note on blood glucose and shellfish. At one point I looked into the whole issue after a long conversation with an insulin-dependent diabetic. He very carefully tracked his sugar intake and blood glucose and dosed with insulin as needed, and had been quite successful at keeping his blood sugar steady.

                      But what surprised and confused me was that “carbs” were not the main issue. His BG would spike when he ate proteins too, but especially *certain* foods, not protein in general. Gluconeogenesis can be used by the body to produce glucose, but it takes time, and one dish of oysters wouldn’t do it.

                      What does spike BG quickly is anything that causes the body to release stored glycogen. And this is where one protein meal can have way more effect than another protein meal. Some of the factors have to do with how much assimilatable iron is in the meal, which is also affected by the Vit. C content, and probably polysaccharides and fat, and things like lactoferrin. Shellfish are super-high in minerals, including iron. So is liver, of course. Not so much in fat or “white meat”.

                      This doesn’t have much to do with the argument about “are Inuit in ketosis” of course, but it does affect the average low-carber who is looking at their BG. There is an excellent full-text article on the subject:


                      “Reciprocally, iron influences insulin action. Iron interferes with insulin inhibition of glucose production by the liver. Hepatic extraction and metabolism of insulin is reduced with increasing iron stores, leading to peripheral hyperinsulinemia (48). In fact, the initial and most common abnormality seen in iron overload conditions is liver insulin resistance (49). There is some evidence that iron overload also affects skeletal muscle (50), the main effector of insulin action.”

                      Anyway, I just think it’s another factor to consider. When I hear from people who are trying to “stay in ketosis” (as measured by ketostix) they often say that “eating too much protein” is an issue, and that they need to just eat mostly fat. But I don’t think “protein” is the only issue with the high-protein foods … the high mineral content has an effect too.

                    95. Hi Heather, thanks for the link on iron and T2D. Before I continue on that topic, let me address what you say here:

                      “Gluconeogenesis can be used by the body to produce glucose, but it takes time, and one dish of oysters wouldn’t do it…”

                      To be clear Heather, *dietary* glycogen, like what we find in shellfish, doesn’t need to pass through our livers. Our GIs’ α-amylases set upon this “animal starch” like they do on plant-sourced starches we eat like amylose and amylopectin.


                      Starch digestion starts with salivary amylases in our mouths and continues in our duodena. So yes, the glycogen in shellfish may well be responsible for popping fragile BGs. I certainly saw that effect in the early days of my efforts to recover what I could of my broken glucose metabolism.

                      I can’t discount other possible factors like you point out. E.g. shellfish with its abundance of vits and mins, and esp of certain proteins like tropomyosin which can be quite allergenic for many people, causing an immune response, which is an inflammatory event that can pop fragile BGs.


                      That said, though the years I saw my carb tolerance generally improved regardless of my carb sources, e.g. shellfish, fruits, etc. So I do lean toward the idea that glycogen was largely responsible for those early effects.

                      Back to iron, that’s truly one of the big takeaways for me in our forum here. Of many takeaways; we’ve had so many excellent exchanges. I do think iron it could be a big issue that Duck and other people here have discussed. When I carefully tracked my meal nutrients in the spreadsheet (2008–2010), iron was one of those that routinely exceeded the RDI. Because of that, I started getting Iron/TIBC panels in 2009, and found my iron levels ride at the very high end of the normal ranges. I donate blood to lower them, but that effect doesn’t seem to last long. I need to keep digging into this. –Bryan

                    96. Yes, I agree the starches get into one’s system very quickly, esp. the dextrose starches. I had not thought about the carb content of seafood much until it came up here. But I do eat a lot of “Asian” style seafood, and shellfish are big on the menu! What is interesting is that a lot of them are just naturally and obviously sweet. I think some of them might even get sweeter as they dry. There might be some reaction that happens … like what happens with mushrooms, when dried in the sun the Vit D content gets very high.

                      But another weirdness in the Inuit diet may be that it would be high in taurine. There is a lot of taurine in seafood anyway, but it tends to get destroyed by cooking. Populations that tend to eat raw fish … like the Japanese and Inuit … get higher dosages of it. The more taurine, the better the heart-health markers.

                      So this could affect the Inuit in a few ways that aren’t related to genetics or carb content:

                      1. Taurine protects against heart disease, regardless of the other factors in the diet.


                      2. Taurine helps with fat digestion. It’s used to make bile.


                      3. Taurine affects ketone production in the liver (in rats anyway: makes the liver more prone to produce ketones).


                      4. Taurine is key to glucose transport.


                      In theory human beings can synthesize taurine, but it appears that getting more from your diet has really good health effects.



                      My body tends to hoard iron also, and after donating blood my hemoglobin just shoots right back up. I’m guessing that’s an adaptation to constant parasites in past ages. But it could also be an adaptation to thousands of years of eating whole grains. My ancestors lived mainly off oatmeal, and whole oatmeal is a big iron-blocker.

                    97. Morgana: You are welcome! I learn so much here.

                      So far it appears that all the “healthy” diets are in fact high-taurine diets (and most of them are also wheat-free, except the French). The Inuit have raw fish and meat. The Japanese and Okinawans, of course, have their raw fish, plus octopus which is super-high in taurine. The French have raw milk cheese, and maybe stuff like pickled herring (which is not cooked). The Maasai and Swiss have raw dairy. The Maasai also have (or used to have) raw blood.

                      There is a nice PDF here of the world-wide study:


                      Has a nice graph of mortality rates vs. taurine excretion. Oddly, Finland and Sweden are low on the Taurine excretion graph.

                      The outliers to this theory are the healthier vegans: the Rice diet and the Japanese mountain people especially. Vegans though, often have *more* heart diseases than average, which is thought to be either the lack of B12 or the lack of “sulfated amino acids”. Also vegans in the US are low on taurine excretion:

                      So how do some vegans stay healthy? I’m kind of wondering if the vegans that are super-healthy are also the ones that appear to have a high-sulfur diet (and some other source of B12). The Japanese mountain people live near a volcano and eat mainly roots which happen to be high in sulfur … maybe those roots happen to make it easier for the body to synthesize taurine. High-sulfur vegies might do the same thing: broccoli, cabbage etc., which are the backbone of many low-meat diets. Garlic of course, is high sulfur and noted for being “healthy”. Some water supplies are high in sulfur, and some are not.

                      It really would be ironic if the common feature of “healthy human diets” ends up being the secret of Pottinger’s cats …

                    98. Hi Heather, sorry to not write sooner. I was delving into your taurine links. Esp on its sulphur (S) content. Very interesting–thanks for these!

                      What surprises me a little, I rarely see discussion about vegans getting enough S. It’s so easy to get enough S on a non-vegan diet that those folks don’t have to think about it. But conceivably could be an issue for vegans who don’t eat enough brassicas like broc and cabbage and alliums (allia?) like garlic and onions. Here’s a WAP piece on it:


                      After the “Organic Four” (C,H,O,N) and phosphorus (P) and calcium (Ca), S is one of the most common elements in our bods. We need it for all kinds of critical processes, including to make amino acids and to shuttle electrons in cells in addition to the reasons you gave Heather:


                      About our bods making enough of their own taurine from raw S from raw meat, cooked meat, S-rich veg etc. I eat raw meat/shellfish and love it, but could it be we can do fine on dairy/eggs/cooked meat/S-rich veg? I’m still trying to put a finer point on it. Here’s the links that Life Extension supp comp author gave us for it if you guys want to have pokes at it:

                      6) (full)
                      7) (abstract)
                      8) (full)
                      9) (full)
                      10) (abstract)
                      11) (abstract)
                      12) (abstract)
                      13) (abstract)


                    99. Heather btw, on endogenous vs supp taurine, I didn’t yet check the quality of the citation-containing journals. That’s a biggie cuz we’ve seen an explosion of bogus pay-for-print research journals the past decade. Even if you see an impressive ref in PubMed, all rich and science-y full of big words and graphs, you still could be getting a low-worth or even worthless report. You can go here to vet journals:


                      Any journal I don’t immediately recognize (Lancet, BMJ, etc) I go to that site to check it. Free full texts more often come from bogus journals that the paywalled stuff. But you can find plenty of paywalled junk too.

                      Also, some of these links call taurine and “amino acid.” Some argue that’s wrong cuz taurine lacks the carboxyl group (-COOH). Anyway FYI: and of course Wiki’s not an unimpeachable source. –Bryan

                    100. Yeah, there are a lot of bogus studies out there now! On taurine though there is SO MUCH study and it mostly seems in agreement. Taurine was one of the first nutrition issues studied … Pottinger’s cats! What amazes me is that I haven’t heard about it much til now. Probably because I assumed that us meat eaters get plenty of it.

                      The surprising thing though is that it is not the case that a meat-eating diet automatically has enough taurine. When taurine *excretion* is measured, countries like Finland and England come out LOW in taurine. Clearly something else is going on. Likely how much the food is cooked is one big issue. And some foods compete with it. And some people seem to synthesize it better than others. There is so much to still be studied!


                      The French come out higher than Finland … maybe all that nice raw cheese. The variation in taurine excretion is kind of odd, given that it is supposedly easy to produce in the body.

                      I could see how some vegans get more sulfur than others, just based on the types of vegies they eat. Some of the popular vegan diets do stress eating lots of sulfur-vegies. But the rice diet seemed like an anomaly. And then it hit me: in the descriptions of the Rice diet, it was specified that fresh or dried fruit could be used! Given this is in the days when refrigerators were rarer, I’d guess there was a fair bit of dried fruit. And guess what? Dried fruit is often treated with sulfur!

                      Good set of links, thanks. I’ll peruse them.

                      And yeah, a lot of places call taurine an amino acid or a “conditionally essential amino acid”. It’s kind of a weird chemical in any case. It doesn’t actually get “used” all that much.

                    101. Heather, interesting! About what you say “…The surprising thing though is that it is not the case that a meat-eating diet automatically has enough taurine…” I’ll retract what I said “It’s so easy to get enough S on a non-vegan diet…” till we know more.

                      And great catch on the hidden sulphur in Kempner’s Rice Diet!

                      About Pottenger’s cats, first I heard of them, and have to laugh, makes me think of Schrödinger’s cat 🙂 But seriously the raw protein vs cooked animal-protein sources are interesting. Pottenger’s cats cough up confounderballs of course. First they are cats not people (as much as some beg to differ), we’ve had up to nearly two million years (per Richard Wrangham and others) of cooking our food, so we may have evolved adaptations to get/make/conserve taurine, and the results of Pottenger’s work, we can view them only correlatively. But those caveats said, it’s still exciting! About measuring taurine excretion, how to interpret the results? Can we simply say that greater taurine passing comes from greater taurine consumption and/or endogenous production? Or can it mean the excretor is more ably absorbing the available taurine than those who pass more of it, leaving less to go into urine? Or something else? So many variables.

                      About what you say here Heather, “…a lot of places call taurine an amino acid or a ‘conditionally essential amino acid’…” I agree there’s a lot of confusion about it out there in the web-o-sphere. I think most folks, when they hear “amino acid” they think “protein building block” which taurine almost certainly isn’t. I couldn’t find a single example of a protein that incorporates taurine into its AA chain. And don’t see how it could; its sulfonyl hydroxide sits right where the carboxyl group needs to be in order to link AAs together. See on page 9:


                      All that said, Heather, seems little doubt that our little oddball taurine is important! The relevant section out of this:

                      “…Taurine is the most abundant free amino acid in animal tissues…In addition to its role in the synthesis of the bile salt taurocholate, taurine has been proposed…to act as an antioxidant, an intracellular osmolyte, a membrane stabilizer, and a neurotransmitter. …Taurine is found in mother’s milk, may be conditionally essential for human infants…recent work has begun to reveal taurine’s action in the retina. It appears that taurine, via an effect on a glycine receptor, promotes the generation of rod photoreceptor cells from retinal progenitor cells…”

                      BTW, another important S-containing compound is the vaunted antioxidant α-lipoic acid, which sports a disulfide bond.


                      I took ALA (cheapo TJ’s racemic mix because I couldn’t afford ALA-R) as part of my gaggle of supps in 2008–2009. –Bryan

                    102. Bryan:

                      “About measuring taurine excretion, how to interpret the results? Can we simply say that greater taurine passing comes from greater taurine consumption and/or endogenous production? Or can it mean the excretor is more ably absorbing the available taurine than those who pass more of it, leaving less to go into urine? Or something else? So many variables.”

                      My daughter made an analogy I found interesting. She said maybe taurine is like oil in a watch. It just SITS there and doesn’t really “do anything” … but if the oil isn’t there the watch stops.

                      The people doing the Esselstyn protocol wouldn’t be ingesting any taurine to speak of. Since they are alive and actually healthy you can figure they are making as much taurine as they need. The studies seem to show that vegans do excrete taurine, so they create a little more than what they need? So they would be excreting the extra? And left to ones own devices, one creates more taurine than one actually currently needs? But the vegans do seem to excrete a lot less than non-vegans. And it seems pretty clear that the more taurine you excrete, the healthier you are and the longer you live? So again, where do the Esselstyn and Pritkin vegans fit in here?

                      So … which would be better: eating very little taurine, plenty of sulfur vegies, and very little fat … or eating lots of taurine with a generally healthy diet? What happens if you heat a high-fat vegan diet anyway?

                      I don’t know either. Doesn’t seem like it would be a difficult thing to study though.

                      Yes on the middens! It’s amazing, just how BIG some of those are. Well, if I had the choice of chasing a gazelle or picking through tide pools, I’d vote for the tide pool! Chimps sometimes kill mammals and eat them, but it takes them a lot of time to chew them. Bonobos pick food out of swamps, including shellfish and snails. The bonobos get more Omega 3’s.

                    103. Morgana, about excess dietary protein forcing (nor not) gluconeogenesis (GNG), thanks for that link. I’ve wondered about it too, though I admit I generally assumed more GNG till now. With your link I’ll delve more into this. Even before we discuss other possible GNG gating factors, I’d like to point out that a quarter or more–maybe way more–of the protein could be converted to ketones/fats, depending on protein’s amino acid mix. Of the 20 AAs, 13 are obligate glycogenic, 2 are obligate ketogenic (lipogenic?), and the remaining 5 swing either way depending on the bod’s conditions/needs.


                      Also Morgana even if we *do* see increased GNG, people with exquisite insulin sensitivity may do such a bang-up job rapaciously sucking glucose into their cells the moment it hits serum that these people keep enjoying very low mg/dL of blood glucose–low enough to still allow fat mobilization. Aren’t low BGs what really matter? Whatever the mix of energy metabolic states we’ve batted around ad naseum–glycolysis, ketosis, lipolysis–what may matter most is whether or not we trip the insulin switch which decides whether we keep fats stuck in adipose or mobilize fat into serum. IOW, it appears the *sustained* concentration* of glucose in serum is what matters, not how glucose is hitting serum at any one time. For ancestrally-living Inuit, all the direct measure evidence fits the bill–low serum glucose, lots of mobilized FFAs.

                      For the Yupik-Inuit, besides their subsistence foodways, steady hard work and frequent warding off of cold, they appear to have a unique advantage–exceptionally permeable cell membranes. w6 and w3 are our only “essential” fats, meaning we have to get them from diet, and they also appear to populate our cell membranes in proportion to how we get them in our diet. I.e. the less w6 and the more w3, the more w3 in relation to w6 we find in our cell membranes. w3 is slightly more flexible than w6, so a higher w3/w6 cell membrane ratio results in more permeable cells. The ancestrally living Inuit eat the highest w3/w6 ratio foodway of anyone on Earth, so possibly enjoy the most permeable cell membranes. This increased cell membrane porosity may maximize nutrient ingress including glucose and its closely related downstream metabolite, Vitamin C. This may help explain why the Yupik-Inuit seem to do so well on quite low glucose and Vitamin C. We need to look at the effects of high w3/w6 ratio cell membranes on the GLUT1 transporters: –Bryan

                    104. Thanks for that information on amino acids! Wow, I did not know that before. I feel like I’m learning a lot from this thread.

                    105. Happy New Year Morgana! Hope your holidays were peaceful and relaxing and healthful. OK, at least two of those three.

                      I finally returned to your link–via some intriguing stuff on fat-driven gluconeogenesis. Chris Masterjohn looks at the mounting evidence to suggest that our bods can make pyruvate/glucose from…ketone bodies! Specifically, from acetone:


                      That’s what circled me back to your link which suggests GNG output–even in the presence of excess AAs–remains more or less constant. Until now, I couldn’t picture what else could happen to excess (glucogenic) AAs except to go off to GNG, thus “necessarily forcing BGs higher.” I now consider other GNG processes might be going on at the same time, which the bod dials down as AA-driven GNG ramps up, all to maintain the same net output. Those other GNG sources include glucose from glycerol, the backbone compound for triglycerides. And now, apparently, glucose from acetone. Another candidate example of how we remain the robustly exquisitely homeostatic beings we are (or should be). –Bry

                    106. Thanks wbryanh, Happy New Year to you too! Also, thanks for that link, it was interesting. I especially thought that all those ketogenic diet “debunkers”- you know, the people who say the ketogenic diet is “unhealthy” and “unnatural” and is going to kill us- need to have access to this information!

                    107. Good timing on your post Morgana. I just made my first post at Chris’ site. I’m afraid I’m a little effusive about the his acetone → pyruvate discussion (thanks to a pair of gin and sodas). But maybe you’ll want to check it out anyway.


                      I included that link you posted showing stable net GNG under varying inputs. –Bryan

                    108. Just noticed that this my first post on Masterjohn’s site (–yesterday at 2:20pm–it calls me “Unknown.” My followup post calls me WBryanH as expected. –Bryan

                    109. The post I looked at (yesterday) called you just “Bryan”. This new link you sent me doesn’t seem to take me to the same article on ketones; there were things about cod liver oil and other stuff. In any case, it was clear yesterday which comment was yours, so no worries.

                      I’ve been thinking more about this theme. First off, it debunks the idea on “Perfect Health Diet” that there is a such thing as “glucose deficiency”- (I never believed in it in the first place, since I couldn’t find anything to back it up scientifically. I think Jaminet might have just made it up; although, generally, in regards to other matters I do respect much of what he says).

                      Also, I’m wondering if it might be harder for people who are not yet keto-adapted and used to eating high carb diets to make this conversion? I remember reading on Peter Attia’s blog that when he first started experimenting with the ketogenic diet, it was harder for him to generate enough energy in the beginning, whereas later on his body adapted and it became much easier. I noticed something similar when I first tried a low carb, keto-type diet- (though granted, I was also recovering from chemotherapy and a lot of other horrible treatments, so who knows how much that might have played a part). Eventually though, I noticed I had far more energy, and on a much more “even keel”, than when I was high carb.

                      In any case, it brings up a lot of questions. Hopefully Chris Masterjohn will do a follow up post.

                    110. Morgana, yes, I remember the “low-carb flu” in the first half of August 2007. I noticed it mainly in the first week. I’ve never heard that it lasts more than a few weeks. But evidently even that short time is enough to thwart many people. The only longer-term symptom I experienced was when I smelled baking bread and other baking wheat-based foods. Made it momentarily a little hard to walk past bakeries, doughnut shops and pizza parlors. Took ~ nine months for the fragrance to stop triggering me. Then one day, it magically stopped. I still love the smell of baking grain-based foods. I just don’t think about eating them.

                      About glucose deficiency–or more like carb deficiency to make clear we’re talking about *exogenous* and not our “home-grown” glucose from glycogen, GNG, etc. I’ve concluded it’s simply impossible for us to quantitatively determine such a problem can ever exist in healthy people. No-one can do this. Not the Jaminets. Nor anyone else.

                      Even keto champions like Mark Sisson, Emily Deans, etc, keep telling us “some brain cells need glucose.” But, again, no-one seems to have any proof of this.

                      Our *only* cells I’ve been able to confirm that absolutely positively require glucose at all times are our red blood cells. This because, afaik, our RBCs are our ONLY cells out of our 200+ cell types that *completely lack mitochondria.* Thus, our RBCs–which are essentially hollowed-out hemoglobin “tote sacks”–need to lacto-ferment glucose to generate enough energy for their very modest energy needs. E.g. to keep active nutrient (and maybe ion?) gradients across the cell membrane. Yes, Morgana, I said “lacto-ferment.* Just like we lacto-ferment sauerkraut and kimchi. Our RBCs are little fermenters! Amazing eh? BUT, no-one seems to have any idea how much glucose these cells require. Again, their energy needs are quite modest. They have little else to do besides passively course through our blood to deliver oxygen to cells and cart away the carbon dioxide. But as low as our RBCs’ energy needs are, that constant need may explain why we have to maintain some minimal level of blood glucose at all times. For BG to always be around to serve as little on-the-fly Gluco Happy Meals for the RBCs’ endless trips around our bods.

                      Here’s the only argument I’ve seen that even begins to make the case for some level of glucose dependency in non-RBC cells:

                      Biochemical, Physiological, and Molecular Aspects of Human Nutrition
                      By Martha H. Stipanuk, Marie A. Caudill. Page 211, near top of first column.

                      “…Other specialized cells are also primarily glycolytic because of a relative lack of mitochondria or limited blood or oxygen supply relative to their rates of metabolism; these include leukocytes, white muscle fibers, cells of the testis, the renal medulla, and some cells of the cornea, lens, and retina of the eye…”

                      But even here, Morgana, who’s actually *measured* any of this? E.g. who actually measured respiration in our eyes’ lenticular cells? Even for these “remote” cells, how do we know ketones can’t deliver all the energy goods? Those little ketone bodies diffuse through blood and tissue pretty fast and effectively. Esp acetone.

                      Could it be our RBCs are the *only* reason our bods need to produce glucose at all? At least for energy purposes?

                      It’s all such a massive load of “WE DON’T KNOW.” –Bryan

                    111. There are obligate glucose-requiring cells of the nervous system and/or brain – as a Type I diabetic on a very low-carb diet, I’m not affected by hypoglycemia until my blood sugar has been <60mg% for a long time. Then, I notice purple patches in my visual field, I feel the cold (even if it's not very cold), my thinking slows and I'm prone to errors of judgement. Ketosis protects against the hypoglycemic symptoms we want to avoid – seizures, coma, death – but hypoglycemia still leaves the brain sucking wind

                    112. Jonathan, remember I said “it’s …impossible for us to quantitatively determine such a problem can ever exist *in healthy people.*” E.g. people who can rely on appropriate levels of endogenous insulin and don’t have to inject insulin. Injecting insulin can overwhelm the bod’s “home-grown” glucose, disposing too much of in into cells, driving BGs dangerously low. When we bring med interventions into the picture, all bets are off.

                      In such a case, your symptoms may come from under-fed RBCs that begin to fail to deliver enough oxygen to your cells. How do you know that’s not the case? We simply have no direct measurement of what’s really going on. We can propose and infer pathways, mechanisms and causes & effects all we want. But it’s very hard hard to prove any of them till we actually measure them. That’s what I’ve been talking about. –Bryan

                    113. Jonathan, I also read Emily Deans’ post where she makes that startling assertion. She doesn’t source it. She doesn’t tell us what we call those cells. She doesn’t even tell us if they are neuronal or glial cells.

                      Frankly, her claim makes no sense to me.

                      Our brains have two main classes of cells: neuronal and glial:

                      Some of the smallest neurons in the brain are Cerebellar granule cells
                      and they come with mitochondria:

                      The smallest glial cells are the microglia:
                      and they too contain mitochondria:

                      In fact, astrocytes, our brains’ most abundant glial cells, not only sport mitos but even appear to make their own ketone bodies!

                      Looking at this another way, the smallest mitos are 0.5 um in diam while the smallest cells are ten times bigger, 4–5 um. So plenty of room for mitos to fit inside even the smallest cells. RBCs (~ 5um) ditched their mitos. But that’s likely because they didn’t need them since they are basically hemoglobin cargo vessels. RBCs even lack nuclei.

                      Jonathan, that brain cells have mitos only makes sense. You expect these cells to be extremely active metabolically, which requires lots of energy. Without mitochondria (and thus without a place to perform the Krebs Cycle) the only way cells can produce energy is through anaerobic fermentation, a very inefficient and low-energy-yield process.

                      I wanted to ask Emily about her comment. But that appears to be a non-starter. I couldn’t post my question to her blog post because she closed the comments. Her FAQ makes it clear “…my email volume is incredible, and I simply do not have the time to respond…”

                      Jonathan, I do question if Emily’s statement is correct. And even if these mysterious mito-less brain cells do indeed exist, how abundant can they be? If we have just a small number of them, they’d require a vanishingly small amount of glucose to power them. But again, I’m far from convinced they even exist. In my research, time and again, the only cells I read about that completely lack mitochondria are red blood cells. If you find evidence that these mito-less brain cells do indeed exist, I’d love to see it and will gladly stand corrected. –Bryan

                    114. Jonathan, thanks for sending me down a glial tendril. Found some interesting stuff that brings up more questions than answers.

                      Here’s an Emily Deans piece that describes more her suggestion that tendrils rely on glucose:

                      In it she gives a smidge more detail: “…Certain long nerve tendrils are too spindly to carry mitochondria. Those spindly bits need to run on pure glucose. Glucose becomes ATP… directly via glycolysis…”

                      At least we now know Emily’s talking about mito-less tendrils, not the brain cell cores the tendrils emanate from. But she gives no idea how many such “certain long nerve (glucose-dependent) tendrils” we find in a “typical” brain. What portion of the brain’s energy do these sop up?

                      And do these tendrils run on locally made glucose? Of the brain cells, astrocyte glial cells seem to have an exceptionally high number of very thin tendrils. Astrocytes are also the one brain cell type that produces ketones. Chris Masterjohn gave evidence of multiple pathways from acetone (a ketone body) to glucose. So did astrocytes evolve the ability to produce ketones to generate fuel for their own tendrils? Via a pathway to glucose?

                      I can’t find what a “spindly tendril” is composed of. Or what its energy needs are. Or where the glycolysis takes place to feed the tendril.

                      On another note, this link tells us brain cells are not wild for free fatty acid fuel, even though FFAs can easily cross the blood-brain barrier: So for brain fuel, looks like it’s mainly ketones and glucose.

                      Just my random findings and thoughts on the matter before I head to bed. Good night –Bryan

                    115. Anyway Jonathan, your statement:

                      “…In those [brain’s] places, we must use glucose itself (via glycolysis) to create ATP” – seems more plausible.”

                      the “seems more plausible” part may not at all relate to your symptoms and your low BGs. IF you were also cranking out plenty of ketones at the time.

                      Sure, glial (and/or neuronal?) cell “spindly tendrils” may indeed need glucose for their ATPs. And so? Maybe your spindly tendrils were getting all the glucose they needed from one or more of the (acetone→glucose) pathways Chris Masterjohn spells out here:


                      Pathways fed by acetones streaming from your liver and/or your astrocytes.

                      So, to sum up Jonathan, what caused your brain fog and other symptoms? Did they result from:

                      1) low BGs underfeeding your brain cells, as you suggest? Or,

                      2) under-glucosed faltering RBCs failing to deliver enough oxygen to your brain and to clear enough carbon dioxide from your brain? Or,

                      3) both? Or something else?

                      I couldn’t even venture a guess which scenario “seems most plausible.”

                      We’ve often heard the human brain is bioscience’s final frontier. Still, I’m amazed how little we know about it. –Bryan

                    116. It’s uncontested that by some mechanism hypoglycemia is less severe in the insulin-dependent if they are keto-adapted, by whatever mechanism – yet the dolts at the American Diabetes Association do not acknowledge even this observation – so IMO there’s no point in waiting for the Catholic church to look through the proverbial telescope before taking action …

                    117. Jonathan, if I listened to my Kaiser doc/ADA/mainstream, I’d be injecting insulin now. Instead of enjoying the totally med-free life I currently have.

                      But I’ll never forget one visit in 2007, when I put my doc on the spot about the macros I should eat. I asked him, in essence: “The higher carbs will surely kill me faster. We can eat only so much protein. That leaves dietary fat. What do you recommend?”

                      He looked very uncomfortable and anxiously looked around his office like the walls had ears.

                      He then leaned over toward me and–I kid you not–he *whispered* to me:

                      ( “I’d eat a high-fat diet” )

                      The he looked around anxiously again, and quickly added:

                      “Make sure you come in often for your lipid panel!!”


                    118. Jonathan, to make clearer.

                      You assert: “There are obligate glucose-requiring cells of the nervous system and/or brain…”

                      To back up your assertion, you give your symptoms:

                      “…I’m not affected by hypoglycemia until my blood sugar has been <60mg% for a long time. Then, I notice purple patches in my visual field, I feel the cold (even if it's not very cold), my thinking slows and I'm prone to errors of judgement…"

                      All I’m saying: Your symptomatic evidence fails to prove your assertion that the brain has obligate glucovore cells. Why? Could be your symptoms *don't* stem from a glucose shortfall. Instead, it could be your under-glucosed RBCs fail to deliver enough O2 to your brain cells. And maybe those same underfed RBCs fail to remove enough CO2 from your brain cells.

                      Too little O2 and accumulating CO2 can definitely slow your thinking and cause other troubles!

                      Jonathan, just trying to make clear your evidence in no way proves or disproves any obligate glucovory in the brain. We aerobically respire fatty acids as well and glucose. That is to say, both energy-producing processes–originated either from fatty acids or from glucose–require sufficient oxygen to work. Perhaps a shortfall of oxygen–not glucose–helped cause your symptoms. Perhaps CO2 buildup helped cause your symptoms. We can't say for sure. But we can’t discount those possible causes. Bottom line: WE DON’T KNOW. –Bryan

                    119. Well, as some people say- (Tim Noakes, among others)- there is no such thing as “essential carbohydrates”. We need protein and we need fat, but we don’t need to eat carbohydrate, as our bodies can make them from protein, and even from fat.

                      And I agree, we probably don’t really know to what extent some of our cells need glucose. Some people (like Jaminet again) claim that ketogenic diets cause dry eyes, or dry mucous membranes in other tissues (like the intestine?) I’ve never noticed this at all in my case. Oh sure, I do seem to have less mucous and post nasal drip on a low carb diet (I assumed that was a good thing?) I don’t notice any problem with eyes, and my digestion is much better on low carb, so I’m assuming that’s another myth.

                      A propos the smell of fresh bread baking: to this day, the smell of wheat bread fills me with longing. As a celiac, I experienced bread (gluten) addiction; in people with leaky gut, the opiates in gluten can go into the bloodstream and cause something like a “high”; a.k.a. addiction. My whole wheat bread addiction was one of the main things that clued me in to the fact that I was a celiac. But even though the smell is tempting, I know that gluten makes me very, very ill, so that’s enough to stop me eating bread! I guess other people are not so “lucky”, and I can understand how it must be difficult not to give into cravings. When I first found out I was a celiac, and had to go on a gluten free diet- (I was still high carb for years, even though gluten free)- I would smell people’s bread, bagels, pizza crust, etc., just to get the vicarious pleasure!

                      Going low carb was relatively easy for me, in terms of cravings. Those gluten free breads and carbs taste pretty grim, so I never really missed those foods at all. Sugar was a little more tricky; however, once I stopped for a time, I’ve now come to the point that I actually dislike sugar. I’m highly sensitive to cloyingly sweet foods. Many fruits just taste too sweet for me now. Eating out in restaurants can be hard, as the food is sometimes too sweet, to suit “normal people’s” palates. I feel sometimes like I’m an anomaly in a world of sugar loving people!

                    120. Morgana, about sugar, “cloying” is a terrific word for it. Definitely you and I are still exceptions. Every once in awhile I’ll taste something that has a lot of added sugar, and it’s too much and unpleasant. To look at this another way, foods that never tasted sweet to me before now taste quite sweet, e.g. broccoli and *esp* cabbage. When I first started my VLC journey in late July 2007, I went a year without cabbage. When I finally returned to it, I couldn’t believe how sweet it tasted. I googled to see if Big Food was sugaring up cabbage like they did corn! When I was a kid (60s/70s) corn was very starchy. You had to cook it to eat it. But by the 90s, you could eat it raw off the cob and it tasted very sweet.

                      If there’s one thing that’s come home to me during my journey, it’s that we know *so d*mn little.* So much stubbornly remains beyond our ability to measure. Even something so seemingly basic like: How many cells actually compose us? I was like: “How can we NOT know that?!” And yet our cell-count estimates span almost *two magnitudes:*

                      Carl Zimmer, posted Wed 10/23/2013

                      “…estimates sprawled over a huge range, from 5 billion [I’m guessing CZ meant 5 trillion –B] to 200 million trillion cells…If scientists can’t count all the cells in a human body, how can they estimate it? The mean weight of a cell is 1 nanogram. For an adult man weighing 70 kilograms, simple arithmetic would lead us to conclude that that man has 70 trillion cells. On the other hand, it’s also possible to do this calculation based on the volume of cells. The mean volume of a mammal cell is estimated to be 4 billionths of a cubic centimeter…Based on an adult man’s typical volume, you might conclude that the human body contains 15 trillion cells…”

                      Much as I try to quantify and ferret out robust evidence, at a certain point Morgana, I had to go with my gut (haha ba dum tss) and choose *some* foodway. Of course Tim Noakes et al can’t *prove* that carbs are wholly optional calories. We have few if any direct measures. Nor can we reasonably expect to see such measures over a long term with a sufficiently large sample rate to let us say “Yes, for sure, that’s the way to go alright!” People reasonably ask: Where are the broad long-term studies for VLC-VHF? I don’t know of any.

                      That said Morgana, my eight + years living VLC-VHF have been exceptionally and uniformly positive. It may well be the single best thing I’ve ever done for myself. Since I embarked on VLC in 2007 at age 46, EVERYTHING improved by all observed measures I’ve done to date. Without exception. Like you noticed with lowered mucus production and still properly moist eyes, my symptoms cleared up and all else that was well stayed well. Even my springtime allergies nearly totally cleared up. I’m far from the only one who’s experienced frankly wondrous improvements. I’ve heard and read endless accounts about people who radically improved when they went grain-free VLC. Whatever their various mitigating factors may be.

                      Even mainstream biochem grudgingly mumbles and tilts toward inherent superiority of keto. Oxygen is a necessary evil. It’s key to aerobic respiration, which we humans have to do. But oxygen is… oxidizing! It attacks unstable fats like w3 and causes them to quickly rancidify. It helps create oxidized species like free radicals that rampage through our systems, that appear to wreak havoc and accelerate aging. Well guess what? When we respire fatty acids, kcal-to-kcal, we generate way less O–*6+x* less O–than when we respire glucose. That’s way less O that hangs around the cytosol to attack hapless cellular byfloaters. It’s easy to do the math. Glucose yields only 4 kcal/g and sports a whopping six Os per molecule. A long-chain fat (e.g 18C stearic acid) yields 9+ kcal/g and carries only two Os. Way less O means way less damage to our sensitive mitochondrial tissue and other organelles that bobble around in the cytoplasm and can stray in the path of bully oxygen which rapaciously steals electrons from anything within reach.

                      Morgana, If you accept the current biochem, it suggests that, at the deepest cellular level, keto lets us work BETTER. In the short term and esp in the long term.

                      But because we have a surprising paucity of direct empirical evidence, I have to rely on the circumstantial evidence I can find in all the relevant disciplines, which include paleoanthropology, paleoethnography, paleofornesics, organic chemistry, biochemistry, genetics, and nutrition science. I continually review anecdotal evidence, meanwhile always look at its depth, breadth and quality. I collect all the the clinical measures I can coax out of my doc. I often simply stop and ask myself: How do I feel? Even with all that evidence, I feel like pioneer forging (foraging?) into the old known/new unknown. I am my own Grand Experiment, though I meet a growing number of fellow-travelers. At this point, I have to say, I feel great and pretty great about it! To this point, even now, it astounds me that VLC it appears to have only numerous upsides and zero downsides in my regular daily life. I know of no other life change I’ve made that rewarded me with such strong and unalloyed positive results. –Bryan

                    121. Cloying is the perfect word for too much sweetness, and is the word I’ve used for decades. A couple of times, when I’ve accidentally sipped iced tea that someone “presweetened”, it’s literally made me gag. The thought of sweetened coffee is gruesome, especially if black without the cream to tone down the sugar. Needless to say, I don’t waste money on those cloying synthetic coffee drinks that are so popular. Fruit is fine usually, but some overripe types, even with no sweetener added, are awful. People think it’s weird that I can’t understand why anyone would add sugar to berries (or even grapefruit). Maybe some of us are different from the general public in the lack of a “sweet tooth”. I’ll have to research to see if there is any indication of a genetic factor. But, even as a child, I preferred dark, dark chocolate to milk chocolate, and literally gagged on things like pineapple upside down cake. The very thought of it makes my throat tighten. When my Mom would make it, I’d beg off on dessert.

                    122. annielaurie- I guess there could be a genetic component, though in my own case I highly doubt it, as I come from a family of sugar addicted people. In fact, as a child, I myself was a sugar-o-holic! I know many people say we are “hard wired” to like sugar, but I’m not sure that it’s that simple. (I agree that we are probably hard wired to like the very subtle sweetness of natural fruits and vegetables, the rest I’m not sure about…..) Basically, our taste for sweetness is cultivated. Usually babies and very young children are fed sugar and fast carbs, first thing, while weaning. Actually, it might even start in the womb- (my mother definitely ate lots of sweet foods! Especially chocolate). At one time I loved sugar so much I never imagined I could possibly give it up, but low and behold, after a few weeks on a ketogenic diet, not eating sugar, I grew to dislike the taste. (Though I still like the sweetness of vegetables and some fruits, and of course very dark chocolate; nothing below 85%). Because of my experience with sugar, I am a firm believer that the taste for sugar- (in it’s “cloying” form)- is largely cultivated- (though there may be other aspects at play here too, like genetics, possibly certain deficiencies, etc.)

                    123. wbryanh- I know what you mean about corn! I loved corn as a child, but somewhere along the line- (even before I went low carb)- I just decided I didn’t really feel like eating it anymore. It used to have a certain “nutty” taste, which it doesn’t have now. Funny enough, my brother (independently) came to the same conclusion; we talked about it years later. And I know what you mean about the sweetness of vegetables. For me, this is a huge benefit of eating low carb; all my food tastes so much better now! I hadn’t realized how much sugar dulls the taste buds. (Actually, not just sugar. Before I even gave up sugar, I stopped eating all grains, and when I did, other food tasted so much better! So I think something about eating high carb- for me, at least- affected my taste buds). I enjoy the flavors of food so much now. This is one of the things that has kept me wanting to eat low carb, and it also keeps me from wanting to cheat.

                      Of course, I’ve also experienced a whole slew of health benefits. Too many to mention here…..

                    124. Morgana on one level it seems self-evident that if we cut out added sugar that we’ll get more sensitized to what we still eat, that smaller amounts will taste sweet, right? But still, in the months after I went LC, my sense of taste returned so dramatically I wondered, how could that be? Finally this idea hit me: My incipient neuropathy had gone away. My nerve endings everywhere were healing–and beginning to sense more and feel more.

                      In late 2006/early 2007–the months preceding my T2D diag–I had tingling in my fingers and toes at night. After the diag (29 Mar 2007), I started to restrict cals and exercise like mad, meanwhile kept following the gov’t guidelines (50% carb, “wholehealthygrains,” etc). For a while my RC and all-day walks brought my BGs down from the troposphere, but then they started going up again, till they peaked of 245 on 29 Jul 2007. And this was after a 30 mile hike during which I ate nothing but a Clif Bar every 2–3 hours!

                      That was it. I went LC that day. That’s how I’ve been rolling ever since.

                      Constant keto really does seem too good to be true. I keep half expecting some bombshell to drop, that we’ve just discovered some horrible consequence of following LCHF long-term. Doesn’t everything have downsides? Yet the more I follow it and read the latest research on it, the better it looks. For me, there just don’t seem to be any trade-offs. –Bryan

                    125. I may have experienced a downside to keto – after 15 years, I got GERD from Helicobacter – fixed with two antibiotics, but then chronic diarrhea which lasted for three years, nothing made much difference – SCD, FODMAPs, food sensitivity testing, Elixa probiotics – I had Candida and high levels of a couple of commensal bacteria (“possible pathogens”) and C. diff so was treated with Nystatin, Cipro and Flagyl with little result. I read Richard Nikoley on potato starch, I’d done psyllium husks and Acacia senegal without improvement but I thought what the hell – and mirabile dictu it’s working! It’s plausible (to me at least) that my low carb diet starved out some desirable bacteria like the bifidos that make sfca’s – I tested low in 2ndary bile acids which inhibit C. diff – so I’m convinced (in spite of n=1, many possible confounders, perhaps coincidence) it’s prudent to add prebiotics to the keto diet, especially potato starch since neither psyllium husks nor Acacia senegal made much of a difference …

                    126. Jonathan, I’m sorry you had to suffer all that! Ugh!

                      Did you ever find a proposed mechanism for how long-term keto may have led to your GERD? Besides possibly low bifidos? What I’ve read up to now, eg this:


                      links H Pylori more to carbs, in particular malabsorbed carbs in the GI which start to ferment. Which surprises me, at first glance, that potato starch seemed to clear up the problem that may involve SIBO! Btw, I had one excellent experience with PS, and then nothing after that, neither good nor bad. You can search this forum for my discussion on that.

                      I’d love to see a site where people doing long-term keto record their experiences and symptoms. To follow LCHF long-term is to ultimately go into the unknown, since relatively few people these days do it. For me, to this point (8.5 years) I’ve had absolutely no negative experience with it. But that’s only a little over half the years you’ve spent in keto. And it could be problems may in fact crop up even after such a long time. I ate HC for my first 46 years, but didn’t get hints of a problem till I was maybe 40. Of course, I wasn’t so focused on the matter either! I’m sure then I missed symptoms that now would look as big as barns.

                      I have to leave for an appt so will look at your bifido link when I get back. –Bryan

                    127. wbryanh, Jonathan Christie- First off, thanks for that Chris Kresser link….that was very interesting! I’ve read lots of his stuff, but not that one.

                      In any case, my own reason for going low carb in the first place was mainly to help my digestive issues- (though I did not have GERD; that was about the only thing I didn’t have, ha ha). I am a celiac, so I was already gluten free, but I seem to also have issues with fructose and high FODMAP foods in general. Going low carb helped my digestive issues immensely- (among other things), but it still wasn’t perfect. Then last Spring I decided to go on a low FODMAP diet, which I did for about 2 months, and then slowly added back the foods one at a time to see what I was sensitive to. This helped me immensely, as I discovered that even some low carb vegetables cause me problems. And, luckily, I’m not sensitive to all high FODMAP foods, so I can still eat some things like asparagus and shiitake mushrooms; I even discovered, through the diet, that I can eat some fruits- (when I originally went low carb I didn’t eat any, thinking fruits didn’t agree with me at all). I stopped eating grains completely because I notice I feel better when I don’t eat them- (apparently this is true of many celiacs). Luckily for me, the low carb diet- as well as knowing which FODMAP foods I can and can’t eat- totally cured all my digestive problems.

                      However, as some say, there are times in our lives when one thing works, and then it can happen that things in the body change, and we need to make little tweaks in our diets. My theory is that in this day and age, it’s particularly difficult to eat the very varied diet of our ancestors- as well as the fact that so many foods today just aren’t of the same quality as they used to be. It could be that a particular way-of-eating can work for awhile, but eventually some problems may occur, possibly due to nutrient deficiencies, or changes in gut bacteria. This is why we need to always be vigilant and continue to tweak the diet when we find something has changed. It looks like you’ve done that, Jonathan Christie, by adding in potato starch. I am also aware of the fact that if something ceases to work for me, I need to re-evaluate, and find answers. You’re right, wbryanh, that so little is known about long terms effects of ketogenic diets! (Though there seem to be plenty of people online who have done fine long term. One good example is Dr. Phinney, who looks quite healthy at his age).

                      Also, since we all have such different microbiomes, I’m convinced that there’s no one-size-fits-all…..just like Denise always points out! In the Chris Kresser link, he talks about stomach acid (or lack thereof) as being a major issue with GERD. I used to be mostly vegan, and I think that that diet caused low stomach acid for me. I was also unwittingly eating a lot of foods that I was intolerant to, causing yet more problems. In my own case, low carb seems to have greatly improved my stomach acid (as well as bile, another thing that was insufficient in my case). All of these digestive enzymes and hormones work together, so if one is off, it can affect all the others. I also think that for some of us, after years on a low fat diet, it can be difficult to suddenly digest high fat foods; the body isn’t used to it, so there may be malabsorption. This is my theory (one of them) as to why some people have problems on a ketogenic diet. If you can’t properly digest the food you’re eating- (my case on a vegan diet)- you won’t be able to absorb the nutrients you need and imbalances will occur.

                      In any case, this way-of-eating works for me now; but I am aware of the fact that if that ever changes, I need to be flexible.