CPT-1A – P479L Mutation in Inuit: Acknowledge It’s No Basis For A Ketogenic Diet; Recommend a “Ketogenic” Diet Anyway

Here’s the backdrop. A post by Peter at Hyperlipid. And then, A Second Post. Many comments on both threads, including Dr. Mike Eades participating in the second one. TL;DR: from what I gather of Peter’s posts: Inuit not in ketosis. It’s just a high fat diet.

Let’s look into this. First, Duck and I put together a series calling into question the very common practice of referring to the traditional Inuit population as clear, population-level justification for the long-term propriety of a ketogenic diet. Here’s all 17 posts and about 1,500 total comments: Leaving The Inuit Behind: Hormesis For The Rest Of Us.

The series has been generally dismissed by everyone I’m aware of that advocates for a ketogenic diet—both imagined ones (too high of protein intake) and real ones (very high fat, low—”chocolate cake”-like—protein, near nil carbohydrate). If that series had been dismissed on the basis of what we actually wrote—and the 75+ years of studies cited—then it would be upon us to look into the objections (we’d be delighted, as we have been with those raising legitimate questions all along the way in comments). But when the vast number of dismissals I’ve seen are mere scoffing at the idea of “a carb-munching Inuit;” or, their “high-carb diet” (neither of which remotely represents what we wrote), then it’s clear we’re dealing with disingenuous and dishonest posturing (from some who may, or may not, have actually read any of what we published—but same dishonesty and disingenuousness, either way). A commenter on Peter’s second post signals that the message got through to at least some.

All the FTA guys know the Inuit/glucose [via glycogen] consumption is a side issue anyway. The glucose discussion is to show how misinformed it appears we have been over the Inuits’ diet in general . But the FTA guys know that the elephant in the room is what appears to be their high level of protein consumption. This has to be addressed.

…Here, we’re talking about a specific gene mutation, CPT-1A, to be exact (P479L variant). Peter’s first post was the first I learned of it. Thanks to Google, one can get a “degree” in a matter of hours. In a nutshell, this gene provides instructions to make a liver enzyme (carnitine palmitoyltransferase 1A) that attaches to certain fatty-acid chains, allowing them to enter the inner “combustion chamber” of mitochondria, where they’re oxidized to produce energy.

From what I learned, Peter called it exactly right, on the surface.

From the evolutionary point of view we have here a mutation which is significantly lethal at well below reproductive age, so it should have been weeded out because affected individuals are less likely to live long enough to pass on the gene. But it has been highly positively selected for in several populations, the common factors being cold climate and minimal access to dietary carbohydrate. It’s a paradox. […]

LCFAs, unable to be metabolised, accumulate in the tissues as a storage disease. The advice is to avoid them as far as possible.

So the archetypical CPT-1a defect tolerant environment would seem to be a person sitting on a South Seas Island beach by a pile of coconuts chewing on a raw yam, with copious flatus night and day.

But it’s not.

The CPT-1a defect evolved in multiple non related populations where both starch and MCT were very notable by their near-complete absence. It’s an Arctic selected gene. No starches. No coconuts.

On the other hand, the mutation may be no big deal. Initially, Peter’s [1st] post was greeted by the LC peanut gallery with fireworks and confetti, thinking that the extremely high prevalence of the CPT-1A gene somehow proved that the Eskimo could not eat any carbs and ate the equivalent of a high fat ketogenic diet. Unfortunately for the gullible LCs, modern Inuit eat large quantities of sugar without immediate fatalities.

Few LCs seemed to realize that what Peter actually showed is that the Inuit could not easily produce ketones—something the literature has been showing for over 75 years. In fact, CPT-1A presents as a kind of ketogenesis disorder where the individual cannot rely on ketones for energy—it becomes dangerous for them to fast for significant periods. This may explain why Eskimos were known to snack constantly on their native diet.

The key point being that the Inuit could not have been in ketosis because they have difficulty making ketones!

Some VLCers have now latched onto the idea that free fatty acids are more important for energy than ketones, and seem oblivious to the fact that Westerners naturally produce ketones on a high fat diet while the Inuit cannot.

…I have a quibble with Peter, though. To me, this is a Bell Curve-esque situation, at an extreme. In that context, it’s difficult for me to say that it’s “highly positively selected for,” rather than, in the context of Planet Earth (a rotating-on-axis—on a tilt—orbiting spheroid with a single source of energy), a deleterious mutation that doesn’t get SELECTED OUT, owing to a very unique environment, As The World Turns. Simply, for me: a unique and very obscure environment with a weird-ass diet that allows an otherwise nefarious gene to propagate where it would have otherwise been selected out, because: As The [Rest of] World Turns.

Let me give you an aside.

Ever heard of PKU: Phenylketonuria? Well, when I was a kid, the only thing I knew about it was that Protein Kills U. See, I had a cousin not far from my age with that PAH gene mutation. His mom was so very diligent about his diet, 50 years ago. It was, essentially, a vegan diet that saved his life and brain (oh, NO!). Here’s what I recall growing up: Matt could never eat what we were all eating at any common family affair. I recall salads with tomato and cucumber, green beans, and fruits, mostly. When he was a teenager, he was over the hump and was able to eat normally. He’s still alive, 50-something by now. Has kids and grandkids.

Fucking YEA science!

So let me ask you: is that condition in any way relevant to the question of whether a vegan diet is likely optimally healthful long term for most people? Is that gene “highly positively selected for” in vegan populations (hypothetically: if there were such a thing)? If you think, if it were the case, of course not, then in what way does that Inuit “paradox” let ketosis qua lifestyle off the hook—much less suggest it’s the cat’s meow?

Are epileptics evidence that ketosis at 85% fat and minimal protein something you ought must look into?

Sound ridiculous? It’s intended to sound ridiculous. When I saw Peter’s post, it was the first thing that came to my mind and no, I didn’t jump up and say: SEE, the ‘highly positively selected for’ gene mutation responsible for PKU suggests that vegan DIETS MIGHT BE RIGHT FOR EVERYONE AND ANYONE WHO’S SAID DIFFERENTLY HAS NOW BEEN SCHOOLED!

The point of Duck’s and my series was this, and this time, it’s in order of emphasis:

  1. There is no shred of evidence leading to a rational conclusion that an Inuit-like diet is any justification for what our diet ought be (our = everyone). In fact, both of Peter’s posts lend weight to our primary thesis. Now, another piece: owing to a very unique environment, dietary necessity allowed the propagation of a genetic mutation that might otherwise have killed itself off.
  2. They were not in ketosis in any way ever measured, yet had reasonable glucose regulation in a fed state (although critiqued by Rabinowitch & Smith, 1936). Peter’s post gives insights but still, I’ve not yet seen an accounting for their high protein consumption (av. 270-300g per day: HUGE). In fact, I’ve rather seen every effort to avoid that exhaustively documented fact, in preference for an adventuresome Stefanssson.
  3. They prized every shred of carbohydrate they could get their hands on, and apart from whatever the earth wrought in appropriate months, they got some glycogen from fresh or frozen kills, unlike the way we eat animals.
  4. Nonetheless, they were a low carb society. But, by necessity, not preference. Home is where the heart is. Perhaps they thought they lived plenty long enough in that doG forsaken land, I suppose.

I could expound upon each of those points and they are not exhaustive. Feel free in comments.

Moving onto Peter’s second post; now, with a very substantial comment thread including moi-memme, Dr. Mike Eades, Tim Steele and Duck Dodgers. Significant snark at first, but eventually some pretty good and healthy dialog between Eades and Dodgers, eventually. As always, you are your own judge.

I don’t want to rehash what’s been hashed in comments, but for two things; one, in terms of Peter, and the other, in terms of Eades.

Peter first:

  1. He speculates that dietary PUFA from seafood may be the key here for the propagation of this mutation. Makes some sense in an evolutionary context.
  2. He says accurately: “People clearly have very differing ideas of what the Inuit did or did not eat as an ancestral diet.” I would say: People clearly have very differing tolerances for accepting 75 years of research that uniformly put the Inuit at a most notably high protein, not high fat ancestral diet. Fat was high (40-50%, according to research) by western standards, but protein is way more notable—unless you think the Tokoleans are more notable (highest recorded dietary fat and saturated fat consumption qua population).
  3. “”While it is perfectly possible to invoke a high protein diet to explain a lack of ketosis in the fed state this goes nowhere towards explaining the limited ketosis of fasting. P479L fits perfectly well as an explanation.” Of course, but it’s a point or explanation without a contravening argument. Shorter: P479L is a rare, weird mutation. Means nothing really, beyond a few more dots connected. People without it are not in ketosis in a fully fed or over-fed state, and they are in ketosis even on a sugar diet, if not fully fed. ketosis is primarily a starvation/significant energy deficit adaptation.
  4. “”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.” It looks like Peter and Mike Eades are at odds on this point.
  5. “…while systemic ketones are a useful adjunct, a ketogenic diet is essentially a fatty acid based diet with minimal glucose excursions and maximal beta oxidation. Exactly how important the ketones themselves are is not quite so clear cut.” Shorter version: it’s just a high fat diet. All the purple pee and magical numbers on a meter are probably hype.
  6. “”Confirming that the Inuit are not poster boys for ketosis is a ‘so what?’ moment for me.” I’d hesitate to say concession noted, but only because it’s Peter and I know quite well that he has never touted the virtue of perpetual ketosis and likes to stay just out of it. The problem is, so very many others point to these extreme environments as an excuse to be fat gluttons. I’m anti-glutton (with good reason), and I resent the suggestive marketing in that regard…unless you’re living on an ice sheet and it’s dark and below ZERO for several months of every year. If you are, please glutton away at every opportunity. Your life may depend on it. If you have a supermarket nearby, you’re foolishly fooling yourself. You know why you’re fat, or can’t lose weight. You eat too much, too often. Whether that’s a satiation root problem is another issue. It’s certainly not a macronutrient issue, per se.
  7. “”Using their P479L mutation to argue against ketogenic diets is more of a problem. It’s a massive dis-service to any one of the many, many people out there who are eating their way in to metabolic syndrome to suggest that a ketogenic diet is a Bad Thing because no one has lived in ketosis before.” Uh, this was brought up (by You, Peter) long after my blog series with Duck demonstrating over and over, backed by 100% of the actual research, that the Inuit were not in perpetual ketosis because of insane protein consumption. In other words, even without the mutation, people in fed states consuming 270-300g daily of protein would have to walk 15 miles, without eating, to pee pink. You brought it up, man, and I have a hard time thinking it wasn’t to distract from the real issue: a high protein diet, well documented.
  8. “Ultimately, point scoring on the internet about what the Inuit did or didn’t eat shouldn’t destroy people’s chances of health. Destroying a circular argument about Inuit diets may may the destructor feel good. Destroying the feet, eyes and kidneys of a person with type 2 diabetes, who need a ketogenic diet, as a spin off from that victory must be difficult to live with. I don’t know how anyone can do this.” Appeal to emotion. But more notably, the idea that lying to people is cool, if for a “good cause.” I submit that in the final analysis, lies kill and maim more people than anything else. Moreover, whatever the root cause or what got them there, we have the technology. We have brains, meters, insulin, and needles. Some may find an LC/VLC approach the method they like best to manage their diabetes. Others, millions of them, find that those technological tools can come pretty close to doing what a pancreas does.

That last point makes me laf, and cry. How very often is it that a falsehood becomes so very valuable, so commonplace, so widely believed and practiced that telling the PLAIN FUCKING TRUTH is tantamount to “destruction?” And not just plain destruction. We’re talking dismembering humans, here.

Mike Eades:

  1. He still will not take on the question of high protein, instead preferring to argue the finer points of glycogen degradation, all while plain old readers got the point we were trying to make (see above). I even asked in Peter’s comments: why “Protein Power” and not “Fat Power?” Have your views changed over the years, or are you just going with the flow?
  2. He explains away the failure of researchers being unable to detect measurable ketones 100% of the time over about 75 years to “keto adaptation.” I asked if he still held to that, in light of the mutation. He said: The short answer is probably.”

He explained it in a blog post too:

“What he fails to understand is that the Inuit are keto-adapted. Their lifelong diet of high-fat meat has gotten their ketone-producing-and-consuming systems working in precisely controlled fashion. Like, dare I say it, a well-oiled machine.

The Inuit burn ketones as they make them, so it stands to reason that they might not have measurable ketones under normal circumstances.”

If anyone has a more precise definition of “keto-adapted,” or any literature, please drop in comments, by all means. Because, I’m having a serous logical problem here. In essence: if demand equals supply in a dynamic flow system, then supply cannot be detected.

Or, as one commenter elegantly put it, paraphrasing: if there’s traffic, but no traffic jam, you can’t see the cars.

Or, how about this? Human respiration. It’s so elegant, both a positive feedback loop, and the negative one that dominates nature and keeps everything from going hog wild, fission chain-reaction at all times. When asleep, your breathing is very light. It’s just what you only need to provide oxidation in that rested state (sleep is the ultimate anti-oxidant?). When you wake, you breathe more deeply…and if into that morning run or treading the mill like a hamster—only for a smoothie, not nuts—you’re going to huff and puff.

The thing is, it’s a very tightly controlled positive-negative feedback mechanism. When sleeping, they’re probably so close as to be not worth mentioning. When running, it’s going to be a way wider distinction between which is predominately in play. But, as you initially gasp for air, uptake gets on line, and eventually, negative feedback comes into play and you eventually find a groove. Charted, it’s going to look like a wave with initially high amplitude over (positive) and under (negative) the x-axis, with the amplitude diminishing over time to a narrow band of positive-negative feedback handoffs.

Here’s the kicker: at every point along the whole process, you can precisely measure blood oxygen.

Dr. Eades: you have some serious explaining to do about keto-adaptation meaning they’re producing lots of ketones, using them at roughly the same rate, and hence, they are not detectable. It’s an extraordinary claim. One way to do that would be to acknowledge that calories really do count, importantly. You also mentioned that in your practice, you noticed that over time, less and less ketones were detected by your patients. I have no doubt. You explain this by “keto adapted,” but calories count makes more sense.

I explained it here: Synthesis: Low-Carb and Food Reward/Palatability, and Why Calories Count. TL;DR: LC, VLC, and/or “ketogenic” diets are renowned for initial satiation factors (in spite of the fact that boiled potatoes are the most satiating—why the “potato hack” is so effective). So, for example, on a moderate to high protein and fat diet with minimal carbohydrate, it’s easier for a person to run a 700+ kcal deficit than on a low-fat diet of any color (veg*n, Weight Watcher’s, etc.).

It’s that deficit that’s primarily producing ketones because of significant fat oxidation, just like our “potato hack subjects” in comments were measuring significant ketones (significant caloric deficit due satiation, fat mobilization, ketones).

But what happens when that 700 kcal deficit becomes homeostatic; i.e., as is so typical for so many, when energy requirements via weight loss reduce to about the same level as the person is eating—10-30 pounds from target weight and they “stalled?” They didn’t “stall.” They’re burning calories at the rate they’re expending them. Let’s call it “caloric adaptation,” only in this adaptation, you can measure the various associated parameters, as should be expected.

They aren’t invisible.

…Only magical, flying, rainbow-farting ketones are invisible.

Thanks to Duck, Tim, Gemma, and Philip for checking up on my work and providing valuable input in the final draft.

Since Covid killed my Cabo San Lucas vacation-rental business in 2021, this is my day job. I can't do it without you. Memberships are $10 monthly, $20 quarterly, or $65 annually. Two premium coffees per month. Every membership helps finance this work I do, and if you like what I do, please chip in. No grandiose pitches.


  1. Bret on December 3, 2014 at 20:36

    [Eades] still will not take on the question of high protein, instead preferring to argue the finer points of glycogen degradation…

    The only time I recall seeing him address this issue at all is in the comment section of his confirmation bias post, in response to commenter annique. To say he ‘addressed’ it is, as you’ll see, a bit of a stretch. Here it is, dated April 20, 2014 at 7:38 p.m. (sorry, can’t figure out how to link to the comment itself):

    “I don’t think the Inuit ate five to eight pounds of meat per day. And I’m not sure that the protein in a lot of fatty meat would interfere with ketosis. Why would it? The liver converts protein to glucose as the body needs it – it isn’t substrate driven. In other words, more protein doesn’t necessarily mean more glucose. Insulin controls gluconeogenesis, and it is known that protein stimulates the release of insulin. The insulin will inhibit gluconeogenesis.”

    In short:
    1. I don’t believe the literature on the protein consumption.
    2. High protein doesn’t interfere with ketosis.

    I’m not even going to address #1. It is wholly self explanatory.

    As for #2, why in the hell do Volek, Phinney, Jimmy Moore, and other nutritional ketosis advocates doubly emphasize the need to limit dietary protein in order to stay in ketosis? Perhaps they are misinformed about how it works. Perhaps Jimmy’s year-long ketogenesis, which resulted only after he limited protein below a certain threshold (way, way, way below the mid-200s, of course), was just a huge coincidence. Maybe Phinney & Volek were also flat out wrong on p. 66 of The Art and Science of Low Carbohydrate Performance, where they said that excess protein can result in conversion to glucose, and the resultant insulin will prevent ketosis.

    The high protein content has always been the elephant in the room. This glycogen degradation thing, which Eades seems completely obsessed with, is a huge, barely relevant distraction.

    • Duck Dodgers on December 3, 2014 at 21:37

      Additionally, the Inuit observational studies show evidence of significant urea metabolism—as Draper 1977 noted.

      The Aboriginal Eskimo Diet in Modern Perspective (Free Download)

      “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.”

      Although the urine volumes simply depended on the amount of water/coffee/tea they were given in the various studies, you can find more evidence and discussion of this large metabolic load of urea—along with high measurements on nitrogen in both blood and urine—in a number of studies, for example: Krogh & Krogh 1914, Rabinowitch 1936, Kaare Rodahl 1952.

      Krogh & Krogh had very detailed measurements. So, there’s all that to consider, but it’s hard to have a conversation or debate with someone who doesn’t want to acknowledge a century of scientific data. It’s crazy.

      And it’s even harder to have a conversation with someone who constantly misreads things.

      Frankly, unless Eades actually wants to participate in the discussion—and I think it’s pretty clear he doesn’t have much interest—the debate is now over. All of the scientific literature over the past century shows very high protein and significant urea metabolism in the Eskimos. And the Inuit have difficulty making ketones—presenting as a ketogenesis disorder. They have trouble fasting—which is probably why they were known to snack constantly.

      From: Overland to Starvation Cove, by Heinrich W. Klutschak

      “The Inuit have only two main meals but they take snacks at every hour of the day and night.”

      The LCHF camp is now scrambling to redefine themselves with FFAs (and PUFA?) to stay relevant in the Paleo world now that they have no ancestral basis to fall back on. It’s a mess.

      Imagine them trying to explain the ancestral basis to a newcomer…

      “Well, the Inuit didn’t make ketones, but you will, but don’t worry about it. It’s all the same thing…even though it’s totally different.”

      What a train wreck.

    • Duck Dodgers on December 4, 2014 at 14:09

      My favorite part of the Hyperlipid conversation (in Peter’s second post) is when Eades comes in and claims that no “serious” anthropologist would ever agree that the Eskimos were high protein.

      I then show him Draper (1977), who’s a biochemist and Eskimo expert (according to Discover Magazine) who argues that they were high protein and also obtaining 10g of glucose as glycogen per 2,500 calories of their meat diet (supporting everything I’ve been saying all along). Eades attempts to discredit Draper by misreading it and then goes back into hiding when I point out that he keeps misreading the table.

      Draper made it pretty clear in the 2004 Discover article that the Eskimos were relying heavily on gluconeogenesis based on the available data.

      So, unless Eades wants to come back out of hiding, I think we’re all done here.

    • Bret on December 4, 2014 at 13:49

      …unless Eades actually wants to participate in the discussion—and I think it’s pretty clear he doesn’t have much interest…

      No interest beyond taking the occasional pot shot at others’ knowledge of “basic biochemistry” while unwittingly exposing his own selectively applied knowledge/understanding of the same.

      Not to mention the refusal to acknowledge the protein thing, as well as his insistence that he never cared to debate Inuit ketosis (it’s not hard to see why) but to use the debate to showcase confirmation bias.

      I’m overwhelmed by the irony.

  2. Duck Dodgers on December 3, 2014 at 10:38

    Lots to take in here. Though, I probably would have titled the post…

    “Newsflash: Chronic Ketosis Has No Ancestral Basis Whatsoever”


  3. anarch on December 3, 2014 at 12:50

    TL;DR but that’s some pretty specific SEO you’ve got going on in the title…

  4. LeonRover on December 3, 2014 at 13:04

    As I understand it, a non-Inuit becomes keto-adapted after 2-3 weeks. This is the time it takes for upregulation of muscle tissues etc to use ketones for energy. Schwatca found this in his expedition in the 1840’s which was the basis for Steve Phinney’s experiments on cyclists decades ago.

    “Examining the results of these two ketogenic diet performance studies together indicates that both groups experienced a lag in performance across the first week or two of carbohydrate restriction, after which both peak aerobic power and sub-maximal (60–70% of VO2max) endurance performance were fully restored.” http://www.nutritionandmetabolism.com/content/1/1/2

    caloriesproper refences many studies, as does theeatingacademy on his self-experimentation.

    BTW, fleeting manifestation of BHB etc occur during intermittent fasting – starvation is not intermittent, so appearance of ketones is strong and permanent, until death.


    • Richard Nikoley on December 3, 2014 at 13:22

      With a quick read, Leon, this still does not explain.

      What you have said, essentially, is that they become more adapted to accessing fat for energy, perhaps more rapidly.

      My question is, how did they detect that? Measure it?

      Get it? Takes some thinking.

    • LeonRover on December 3, 2014 at 13:42


      “The duration of treadmill exercise to subjective exhaustion was 80% of base line after 1 wk of the PSF, but increased to 155% after 6 wk. Despite adjusting up to base line, with a backpack, the subjects’ exercise weight after 6 wk of dieting, the final exercise test was performed at a mean of 60% of maximum aerobic capacity, whereas the base-line level was 76%. Resting vastus lateralis glycogen content fell to 57% of base line after 1 wk of the PSF, but rose to 69% after 6 wk, at which time no decrement in muscle glycogen was measured after >4 h of uphill walking. The respiratory quotient (RQ) during steady-state exercise was 0.76 during base line, and fell progressively to 0.66 after 6 wk of the PSF. Blood glucose was well maintained during exercise in ketosis. The sum of acetoacetate and beta hydroxybutyrate rose from 3.28 to 5.03 mM during exercise after 6 wk of the PSF, explaining in part the low exercise RQ.”

      Indeed, the usual meaning of keto-adaption is that ketones are both produced and used. These observations suggest that adaptation results in a more efficient use of produced ketones resulting in higher circulating levels. :0 :)


    • Richard Nikoley on December 4, 2014 at 11:05

      “These observations suggest that adaptation results in a more efficient use of produced ketones resulting in higher circulating levels. :0 :)”

      So, they must have been able to detect and measure his level of keto adaptation.

      Far cry from flying, rainbow farting unicorns.

  5. Steven on December 3, 2014 at 13:11

    For me the moment Eades decides to eat rotten flesh in the form of high meat and such then I will take him and his ilk serious. I want to see them really embrace the things the Eskimo really eat.

    I was LC for a while and it seemed to work. But like most others it began to fall apart after a few months. Mine is not a weight issue but an autoimmune issue.

    The high meat issue for me came as part of my anagnorisis that VLC is bad. All the cultures that eat “LC” also eat a lot of rotting/fermenting meats and such. After reading all the posts here about the whys and hows it all clicked. Bacteria.

    My own n=1 has shown me how important starches are since I am in no mood to allow meats to fester for months. With out them my arthritis really hurts. I also can not eat the wide variety of foods I believe we are meant to eat as well. By starving my gut of fermentable matter and killing the gut biome I lost my ability to eat raw milks, cheeses and such. Eggs became an issue. Tomatoes and chilies were a no no. Coffee and chocolate as well. I never had issues with these foods until I went LC for a few months.

  6. Chuck on December 3, 2014 at 15:06

    Richard, did you see Roddy’s video on ketosis and stress?


    • GTR on December 4, 2014 at 11:14

      @Chuck – if a person starts from being fat then the increased mobilization of the body fat from it’s stores are a desirable state. And yes this fat mobilization is controlled by the the cortisol, a stress hormone.

      Here a low-carb proponent (John Kiefer) explains this:

      “When you first wake up in the morning, your body is primed to start burning fat before you eat, and cortisol is a key part of this process. At this point, your body is operating in the absence of both carbs and insulin—and when there’s no insulin around, cortisol doesn’t go after your muscle. See, the term catabolic doesn’t cover strictly muscle. It simply refers to the tearing down of more complex tissue in the body for a different use. When acting without insulin, cortisol triggers the breakdown of triglycerides into free-fatty acids (FFAs) for metabolization—a process known as lipolysis. In other words, without insulin, cortisol is an incredibly effective fat burner. ”

      Basically a very useful, or even indispensible hormone for those who need to loose weight.

      There remains a queistion about those who are slim, who just want to stay at the pysiquest they are at, how they should manage their stress hormones.

  7. Duck Dodgers on December 4, 2014 at 10:02

    Leaving this here for posterity. I’m getting quite tired of the subject.

    CPT1A is apparently now being used as a way to screen for heart disease.

    Scientists ID Genetic ‘On-Off Switch’ for Heart Disease

    The study the article refers to was mostly based on CPT1A causing the mainstream biomarkers like LDL and triglycerides to skyrocket. Though, they also apparently found that those with CPT1A also had far less Adiponectin—a protein hormone secreted from adipose tissue that modulates a number of metabolic processes, including glucose regulation and fatty acid oxidation. Hmm…

    We know the literature suggests that the Eskimos were eating very high protein and 50%-60% fat, while Stefansson and Anderson ate ~80% fat. Incidentally, the Eskimos were known to have lower cholesterol than Stefansson and Anderson when eating a the all-meat diet.

    This is one of the most interesting quotes in the early literature that scratches the surface of what we now know about the Eskimos and how their metabolisms are so different from ours:

    A Study Of The Blood Lipoids and Blood Protein In Canadian Eastern Arctic Eskimos, by Rabinowitch and Corcoran (1936)

    That the Eskimo differs from civilized peoples, at least with respect to tolerance of fat, is suggested from the findings of Tolstoi [1929] in two healthy men [Stefansson and Anderson] who lived for one year on lean and fat meats exclusively. In both of these subjects, these diets resulted in a definite increase of total fat and cholesterol; whereas, the average concentrations of these lipids were not only lower than the standard in the group of Eskimos as a whole, but, also, lower in those natives whose diets consisted chiefly of meat (Table III).

    Also suggestive of an unusual mechanism for the utilization of fat is the absence of ketosis in these natives, whereas the urines of both of Tolstoi’s subjects contained acetone. The explanation of this absence of ketosis is not entirely clear. As shown previously [Rabinowitch & Smith, 1936], though the small amount of carbohydrates in the diets may be more than balanced by the potential sugar production from the large amount of protein to keep the ratio of fatty acid to glucose below the generally accepted level of ketogenesis, the respiratory quotient data suggest another mechanism also. That the Eskimo possesses a very active fat metabolism is suggested from some of the data. One of the theories of fat metabolism is that fat which has been ingested or mobilized from the fat stores is brought to the liver where it undergoes desaturation and transformation into highly unsaturated phospholipins and it is the latter which are carried to the tissues for oxidation. Assuming this theory to be correct,a very active fat metabolism is suggested from the high ratios of phospholipins tototal cholesterol not only in the group as a whole (Table II) but also following ingestion of the soya bean oil (Table IV).

    The low cholesterol values are of interest, since they fit in with the high basal metabolic rates which were found amongst these natives [Rabinowitch & Smith, 1936]. However, interpretation is difficult here also because of the many variables which had to be considered in the calculations of these rates. The chief purpose, therefore, of this communication is to record the facts for future use and better interpretation with accumulation of more knowledge of the metabolism of fat.

    Amazing what they were figuring out before the genetics were even known.

  8. Per+Wikholm on December 4, 2014 at 03:07

    Great post Richard!
    My understanding is also that the tale of the invisible ketone body is an Eads only story, not backed up by Phinney and Volek.

    Both Stefansson and Andersen showed detecteble ketones during the whole year long Bellevue experiment with an 80 % fat diet. Did they both have problems getting “ketoadapted”?

    The measured levels declined somewhat during the year but was never undetectable. Pissing on stripes isn´t as accurate as blood measurements of ketones and measurements of acetone in your breath. I remember seeing a YouTube lecture with Volek stating that acetone in breath is pretty much reliable. Inuits have been measured for ketones with both methods – no ketoses.

    Besides no ketoses found, Inuits have also during several trials been tested for nitrogen in both urine and blood with results suggesting a high protein diet. All availible data suggests the Inuits were Protein Powered.

  9. Per+Wikholm on December 4, 2014 at 08:10

    Eades is pretty much alone on this planet stating that a high protein intake does not effect ketosis. Did +90 years of practice and science with the strictly protein restricted ketogenic diet for epilepsy control get it all wrong?

    In the beginning of the 1920`s there was a Swedish doctor named Karl Petren who run a diabetes clinic in the city of Lund. Insulin was just about to be discovered and later commersially availible but in his clinic diabetes was treated with a low carb high fat diet. He was aware of that there were two types of diabetes and in the severe form (later to be called type 1 diabetes) protein was strictly restricted.

    He instructed the nurses at his clinic to carefully remove even the tiniest shreds of muscle (protein) with a pincette from the chunks of lard that was served to the type 1 diabetics. For Karl Petrén this very strict protein (and of cause carb-) restriction was a matter of life and death for his patients.

    But Eades says anything goes… a nice stake won´t effect your ketosis/blood sugar levels.

  10. Duck Dodgers on December 4, 2014 at 10:36

    Here’s a cool fact. We know that CPT1A, found in virtually all full-blooded Eskimos, makes fasting dangerous, especially in children. Turns out the Eskimos had a way to combat the problem:

    From: The Incidence Of Anaemia In Infancy And Early Childhood Among Central Arctic Eskimos, by Sellers, et al. (1959)

    “In questioning the Eskimos about the diet fed to children, it was found that infants usually receive breast milk only and that other foods are not begun until after the first year of life. Even then, the diet consists largely of bannock [i.e bread] and breast milk. Breast feeding continued until three or four years of age or until another child makes it impossible to continue. It is only after this that meat becomes a staple in the diet. Rarely do Eskimo mothers masticate meat in order to feed it to the young child—a common practice found in former times.”

    So, basically breast milk as long as possible.

  11. LeonRover on December 4, 2014 at 10:50

    “Eades is pretty much alone on this planet stating that a high protein intake does not effect ketosis. ”

    He is the company of Bill CaloriesProper:


    • GTR on December 4, 2014 at 11:45

      @Duck – “Therefore, their metabolism is so rare and unique that it isn’t even remotely applicable to Westerners.”
      Notice that the Westeners metabolism of fats is special too:

      “They found that Europeans inherited three times as many genes involved in lipid catabolism, the breakdown of fats to release energy, from Neandertals as did Asians. (As expected, Africans did not carry any of these Neandertal variants.) The difference in the number of Neandertal genes involved with lipid processing was “huge,” Khaitovich says.”

      Kind of makes you wonder why high-fat diets pop up among Europeans, while civilized groups refrain from inventing them?

      Another interesting “special metabolism” genes are found in Sherpas, and they give them the ability to function at high altitudes. So making a Sherpa diet an example to follow for everyone also wouldn’t make much sense.


    • Duck Dodgers on December 4, 2014 at 10:59

      Bill’s post is inapplicable to the protein levels observed in the Inuit. I’m yawning as I write this (this is getting sooo boring), so I’ll just quote what I wrote in an earlier comment:

      Bill’s post clearly says that “Negative energy balance promotes ketosis even with relatively high protein intake…It was, however, a rather severe caloric restriction…The point is that high protein won’t ‘knock you out of ketosis’ if you’re losing weight.” In the comments of that post, Bill clarifies, “You can easily maintain ketosis with 30% protein if it’s divided into a few meals, and especially if there is a mild energy deficit. That’s how most of the studies in this post were designed (except Phinney 1983 which had no energy deficit). The participants in Phinney 1980 were able to get 50% protein and still maintain ketosis because of a larger energy deficit.” Phinney’s 1983 subjects were eating 45% less protein than the Inuit and twice the levels of fat, according to detailed measurements from Krogh & Krogh (1914) and Rabinowitch (1936). So, unless we can show that the Inuit were chronically starving themselves every day, or at the very least obtaining most of their calories from fat, Bill’s post doesn’t show us anything that relates to the observed Eskimo diet.

      Secondly, even if they approached a diet that was “ketogenic” to Westerners, their CPT1A gene was an anti-ketosis gene that presents as a kind of ketogenesis disorder. They couldn’t make very many ketones even if they wanted to. Therefore, their metabolism is so rare and unique that it isn’t even remotely applicable to Westerners.

      In other words, the most carnivorous humans on the planet resisted ketosis. So, the ancestral basis for a “ketogenic” diet is nothing more than a fantasy at this point. Even if we were to reproduce the ingredients, we wouldn’t be able to metabolize it like they do.

    • LeonRover on December 4, 2014 at 11:34

      Well then Per should state that his irony re Eades only applied if Eades was not talking generally.

      Double yawn.

    • Richard Nikoley on December 4, 2014 at 11:48

      “Well then Per should state that his irony re Eades only applied if Eades was not talking generally.”

      Agreed! Per, you have to make sure to account for that 1%.

      Start with veto adaptation. Oh, wait….

    • Per+Wikholm on December 4, 2014 at 13:20

      Bedtime here in Sweden now. Don´t know what LeonRover is actually trying to say… maybe that’s because my native language isn´t English but anyway here is a clarification on my position:

      No, my comment on Eades was not at all ironical. Either he has it right that invisible ketones exist or the rest of the science community got it right (including Volek and Phinney).

      And the counter argument is that you found some blogpost that agrees with Eades that Duck Dogers has already debunked?

    • GTR on December 4, 2014 at 13:27

      Apparently Native Americans are another group that has “special metabolism” genes (who’s the norm by the way then?).


  12. Michael44 on December 4, 2014 at 20:39

    Well, there may be a bit of yawning going on here, but it seems they’ve all gone to sleep at Peter’s site! ;)

  13. GTR on December 7, 2014 at 05:58

    There’s an interesting, supplementay to tiger nuts, fuel that apes could use for transformation from the tree animals to open space animals. Right now known to be utilized at a right moment in time: when the hot and wet climate, good for tree dwellers that eat fruit, started changing into the dryer climate, leading to more savanah.

  14. Phil on December 20, 2014 at 08:16

    Recent research ) explains the paradox of why VLCers/Ketoists see the evidence that Eskimos were never in ketosis as a good reason for everyone to eat a ketogenic diet and was summed up with: “When people are misinformed, giving them facts to correct those errors only makes them cling to their beliefs more tenaciously.” (Marty Kaplan, This cartoon illustrates the problem:

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