Well first, from a best-laid-plans scenario, this was supposed to be the final post in this matter: Lies, Damned Lies, and The Inuit Diet. That’s an excellent background overview. But then, Dr. Mike goes and posts this comment on his ironically titled “Beware the Confirmation Bias” post, that begins in what has become his typical dismissive tone when implying that he just can’t be bothered—but then gets bothered anyway, pretending to be doing everyone a favor.
This whole issue is like a vampire that refuses to die. It would be less aggravating if it were of any consequence, but in my view it isn’t.
Doesn’t he know that Original Vampires can’t be killed? And while I may tend towards the troublesome comportment of Claus, Duck’s conscientious Elijah persona tends to keep me in check. Moreover, what Dr. Eades means by “of [no] consequence” is actually his own insistence on completely avoiding the central point of the whole issue (the mythical very high-fat, ketogenic diet of the Inuit); instead, choosing to focus primarily on glycogen degradation which, while a point, is a minor one (very high protein consumption with attendant gluconeogenesis is The Point).
So with that, here’s Duck’s 10-point rebuttal to Dr. Eades, submitted in his comments about 5 days ago, but still “awaiting moderation.” I held up posting this in order to give a fair chance for him to put it through moderation—so I could merely link to it in a link roundup—but then yesterday, I saw he approved two other comments; so I have to rule out that he was just tied up.
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Dear Dr. Eades,
While I appreciate the sentiment of your “confirmation bias” post, there are a number of errors in this post that should be corrected.
1) You cited John Murdoch incorrectly in your comments. His observations did not match up with Stefansson’s as Murdoch observed the Eskimo’s moderate fat intake (as stated in your quote). At Point Barrow he observed their blubber conservation for lamp fuel, low reindeer availability and consumption of seal as a “staple”.
From: Ethnological Results of the Point Barrow Expedition, By John Murdoch (1892)
Page 56: “The most important sea animal is the little rough seal, which is very abundant at all seasons. Its flesh is the great staple of food, while its blubber supplies the Eskimo lamps, and its skin serves countless useful purposes.”
Page 268: “The flesh of the smaller seals forms such a staple of food, and their blubber and skin serve so many important purposes, that their capture is one of the most necessary pursuits at Point Barrow, and is carried on at all seasons of the year and in many different methods.”
Page 264: “Reindeer are comparatively scarce within the radius of a day’s march from Point Barrow, though solitary animals and small parties are to be seen almost any day in the winter a few miles inland from the seacoast.”
Murdoch even went out of his way to make this clear in another paper:
From: On Some Popular Errors in Regard to the Eskimos, by John Murdoch (1887)
“The enormous consumption of fat, supposed to be a physiological necessity to enable them to withstand the excessive cold, is probably the exception rather than the rule, to judge from the accounts of actual observers. It seems quite probable that the amount consumed in most cases is little, if any, greater than that eaten by civilized nations, when we consider that the people who eat the fat of the seal with the flesh and use oil for a sauce to their dried salmon, have no butter, cream, fat bacon, olive oil, or lard.
We found, indeed, at Point Barrow, that comparatively little actual blubber either of the seal or whale was eaten, though the fat of birds and the reindeer was freely partaken of. Seal or whale blubber was too valuable,—for burning in the lamps, oiling leather, and many other purposes, especially for trade.”
Murdoch’s observations clearly disagree with Stefansson’s. And even when they were able to find reindeer, even Stefansson admits that the reindeer are too lean to support ketosis.
2) While it’s true that researchers use liquid nitrogen to eliminate errors in a warm lab environment, it’s been well established that glycogen degradation falls on a curve and is temperature-dependent. The colder the temperature, the slower the degradation. Rigor mortis, which is the process of exhausting glycogen in the muscle to lactic acid, takes hours to complete, and takes a particularly long time in colder temperatures. It’s odd that you don’t mention this.
However, you seem to be unaware that diving marine mammals have even larger glycogen stores than had been previously assumed—particularly in their organs, blubber and skin [1][2][3][4]—and B) marine fish and marine mammals are unique in that they are unusually resistant to postmortem glycogen degradation and can even take days to degrade at 0°C (whales are particularly resistant even at 98°F).
3) Simply pointing out that researchers use liquid nitrogen to freeze glycogen does not tell us what the freezing point of glycogen metabolism is. Studies have shown that fish glycogen degradation can be halted at -10°C, while bovine glycogen degradation can be completely halted for months at -18°C (0°F) according to a 1980 study. Interestingly, some fish don’t easily deplete their glycogen when they struggle. Did you really think that glycogen metabolism can only be stopped by liquid nitrogen? I hope you have evidence to support such a claim.
Nevertheless, the slow degradation of marine-based glycogen has been known for a very long time.
From: Observations On The Glycogen Content of Certain Invertebrates and Fishes, By L.G. Kilborn and J.J.R. MacLeod (1919)
Until recently very little information existed concerning the presence of glycogen in the fishes. That some at least is present in the tissues of marine fish had been shown by Cl. Bernard, Pavy, Brücke, and others. It was stated by Bernard that this glycogen is unusually resistant to the influence of post-mortem changes, and that it does not readily disappear during hunger. During asphyxia, however, the glycogen rapidly disappears.
And, while you are correct that most muscle glycogen degrades via ATP (making at least land-based muscles a poor source of glycogen), you neglected to mention postmortem glyocgenolysis, until now, which is the conversion of glycogen to sugar particularly in non-muscle organs, such as the liver. For instance, glycogen in the liver (which is obviously not a muscle) will degrade via glycogenolysis, converting nearly all of the glycogen into sugar.
Interestingly, blood sugar will actually rise in the body of a dead animal, mainly due to postmortem glycogenolysis and bacterial breakdown of carbohydrates in the tissues and GI tract. When we consider that an average human liver has roughly 100g of glycogen in it, we can see that a liver has the potential to be very sugary. And in fact, universally, livers were eaten quickly and highly prized by hunters in virtually every culture—including the Inuit.
If the Inuit were consuming dietary glycogen (which does happen with carnivores, by the way) they likely got much of it from non-muscle organs, such as skins, hearts, livers and glycogen pools. These happen to be in locations in an animal that do not “contract” in the way that muscles do. For instance, Muktuk (narwhale skin) is said to be rich in glycogen and tastes sweet, like hazelnuts.
I’m unsure why you pointed us in the direction of “post-mortem glycogenolysis” since that was exactly my original point in that some glycogen degrades to sugar postmortem. And the very first study you asked us to look up when searching, “post-mortem glycogenolysis” says, “In all tissues glycogen was degraded rapidly and was accompanied by an increase in tissue glucose and lactate concentrations.” Even your own citations show us that you aren’t telling us the whole story when you say that, “the glycogen to lactic acid conversion upon death is all really basic science, not in dispute by anyone.” Well, actually, it’s clearly more complex than you are letting on. Granted I already pointed this out to you in the beef industry time tables, which you dismissed.
4) You stated that early Inuit researchers didn’t know what keto-adaptation was or how to test for it; however Joslin, Heinbecker, Rabinowitch, DuBois, McClellan and others all wrote about keto-adaptation and used a half dozen approaches to rule it out, including urine testing of acetone, diacetic, and β-hydroxybutyric acid; acetone bodies in the breath; respiratory quotient; as well as documenting protein intake. Their tests were sensitive enough to detect keto-adaptation in the Bellevue Experiment as well as in the Inuit during starvation ketosis, which they even mention in their writing.
5) In the comments, you claimed early 20th century researchers did not know about the speed of glycogen degradation. However, the rapid degradation of glycogen at room temperature was how Claude Bernard discovered glycogen in the first place.
From: Claude Bernard and The Discovery of Glycogen
At this time Bernard’s estimations of the sugar content of extract of liver tissue were made in duplicate by titration with copper reagent of Barreswil, a modified Fehling’s solution. He relates (Bernard, 1865, pp. 2291-295) how one day he was pressed for time and was unable to make his duplicate determinations simultaneously. He made one estimation immediately after the death of an animal and postponed the other until the following day. The second estimation gave a value very much higher than the first, and the difference was so great that Bernard investigated the reason for this discrepancy. Hitherto he had not ascribed significance to the length of time which elapsed between the death of an animal and the determination of the sugar content of the liver tissue. He now found that time was of great importance. Immediately after the death of an animal the liver was found to contain very little sugar, but within only a few minutes the amount of sugar had substantially increased, and at the end of two hours a large quantity had usually made its appearance.
So, from day one, glycogen was known to degrade rapidly. However, it was also known early on that glycogen in marine life was observed to degrade more slowly.
From: Observations On The Glycogen Content of Certain Invertebrates and Fishes (1920)
Until recently very little information existed concerning the presence of glycogen in the fishes. That some at least is present in the tissues of marine fish had been shown by Cl. Bernard, Pavy, Brücke, and others. It was stated by Bernard that this glycogen is unusually resistant to the influence of post-mortem changes, and that it does not readily disappear during hunger. During asphyxia, however, the glycogen rapidly disappears.
We can see that it is well known that glycogen in marine mammals was observed to degrade more slowly. So, perhaps it should not come as no surprise that, in 1952, Marsh found that whale glycogen depletion to rigor mortis took an exceptionally long time, even at 98°F!
And in the Simpson & MacLeod study you referenced, it clearly says, “It is well known that sugar accumulates as glycogen disappears when liver is allowed to stand after death.” So, again, we can see that you are not giving us all the details when you focus on muscle glycogen at room temperature. The literature is very clear that liver glycogen degrades to sugar, via post-mortem glycogenolysis, and this is what contributes to post-mortem blood sugars rising.
6) Their glycogen intake is probably not even worth scrutinizing given the well-documented very high protein and moderate fat consumption in every published study.
7) An article by Per Wikholm was published in this month’s LCHF Magasinet, where Per demonstrates that the Inuit could not have been in ketosis given that the scientific literature is abundantly clear, over and over again, that the Inuit consumed too much protein and not enough fat. And more importantly, Per debunks Stefansson’s claims for high fat with writing from his own books—Stef admitted in the pemmican recipes that Arctic caribou was too lean to support ketosis. And as the literature shows, the Inuit were saving their blubber and fat for the long dark Winter to power their oil lamps and heat their igloos. Again and again, we see that in the literature, as even Stefansson admits this.
As was stated above, the most popular LCHF bloggers in Sweden, Andreas Eenfeldt/Diet Doctor and Annika Dahlquist have reluctantly agreed with Per’s findings—admitting that the Inuit were likely not ketogenic from their diet.
8) You referenced a post by Bill Lagakos, on how “relatively” high protein consumption can be ketogenic, however the 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 you 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.
I already showed evidence that the Inuit went through times when food was scarce, and this is why even in the early 1930s the Inuit were only shown by Heinbecker to be adapted to starvation ketosis. If your argument is that the Inuit were only in ketosis while they were starving, I would agree.
9) I should point out that NOBODY is saying that the Inuit were a high carb culture. I have no idea where you ever got that idea from. In fact, nobody (not even Ho, 1972) is saying that the Inuit obtained 15%-20% of their calories from glycogen. The Kroghs clarified in their 1914 paper that glycogen accounted for a little more than half of the 54g/d of carbs in the diet (the rest was from bread and sugar, which had been available since at least 1855). That’s what Ho meant when he said “largely.” So, the estimation of glycogen is actually fairly low. But as far as I know, you are the only scientist to dispute the idea of dietary glycogen. In fact, the main reason marine fish evolved amylase is to digest the glycogen in the tissues of their prey.
From: Amylase activity of fingerlings of freshwater fish Labeo rohita fed on formulated feed, by M.P. Bhilave (2014)
“In fish amylase is needed to digest glycogen, an energy source which is found in animal tissue.”
10) And let’s be clear here. I did not go out of my way to pick 20+ studies from Google to confirm a bias. I honestly could not find any studies confirming ketosis from the traditional diet of the Inuit. And I honestly could not find any reliable evidence that the Inuit consumed a high fat diet beyond Stefansson’s contradictory statements or Schwatka’s sledging diet. Even when we look at a dietary survey of Inuit food preferences (Free Download), we still don’t see a preference for high fat! The idea that the Inuit were eating a lot of fat is nothing more than a myth that Stefansson perpetuated. I challenge you to find scientific evidence that concurs with Stefansson. Even McClellan and DuBois admitted in the published literature for the Bellevue Experiment that their Western ketogenic diet did not replicate the Eskimo diet.
Frankly, I find your post and follow-up comments to be more than a little ironic. Here I’ve been unable to find any evidence that the Inuit were in ketosis from their traditional diet, or that they even consumed a high fat diet. And I’ve found a large body of evidence showing that they have never been observed in ketosis or consumed large quantities of fat, and all you’ve done is casually dismiss 150 years of research, while only referring to Stefansson’s flawed observations. If that’s not the very definition of confirmation bias, I don’t know what is.
As to why you are reluctant to accept 150 years of detailed research on the Inuit diet—while only accepting the words of just one explorer who was well known to lie and exaggerate—only one reason comes to mind. It seems, to me at least, that rather than showing an interest in what the scientific literature actually says about the Inuit, you are hoping that Stefansson’s loose observations absolve you from having to show long term safety of a LCHF diet. The evidence suggests that LCHF is the modern invention of white polar explorers who needed to pack lightly while sledging. Shouldn’t the long term safety of a diet rise to higher standards than the word of a controversial polar explorer? I should certainly hope so.
Cheers.
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I await the next hand-brushing dismissal from Dr. Eades.
