The Case Against The Case Against Sugar

the-case-against-sugar

Introduction

As I read through Gary Taubes’s The Case Against Sugar – or as I sometimes refer to it “CAS” for short – one question kept popping up in my mind: Was this a book that needed to be written? The answer is a resounding NO.

Why do I say this? Is it because I have some personal grudge against Taubes? No. Rather, I say this book doesn’t need to exist for the following reasons:

  1. Is anyone under the impression that we need MORE sugar in our diets? That we would be healthier if people drank MORE high-calorie sugar water and ate MORE Oreos? Are doctors and nutritionists and policy-makers saying things like “In order to fight this obesity epidemic, all we need to do is get people to start adding cokes, cookies, candy, cake, cream-puffs, and corn syrup into their diet”? Of course not.
  2. But for the sake of my introductory argument, let’s say that the unwashed idiot masses are somehow under the impression that they need to be disabused of the idea that sugar is what they need more of in their diet. Would these dum-dums spend $24.95 for a rather academic book by an author who has a reputation of boring scientific works so dense that he basically had to re-issue Good Calories, Bad Calories (GCBC) into a version that was actually readable? Not likely.
  3. Okay, forget about my unwashed masses theory. Maybe you are the type of person that wants information on sugar. You’d like to know the history of sugar farming and sugar consumption, the chemical structure of sugar, the different types of sugar (fructose, sucrose, glucose, galactose, maltose, etc.), how sugar is made, where it’s made, the health effects, and the nutrient content. Then just look at the Wikipedia entry on sugar and you can find all that and more! Maybe Wikipedia is beneath you and you’d prefer a more curated, scholarly text on sugar. There are dozens of academic and peer-reviewed papers on sugar and its effects on dental caries, cardiovascular disease, weight gain, and diabetes. Simply look it up on Google Scholar or PubMed or whatever. I’ll get you started. Here are links to just a few of the systematic (and non-systematic reviews) in just the past few years.

But maybe you still want to read The Case Against Sugar because you just really enjoy the pleasure of Taubes’s… beautiful…writing? There’s surely no accounting for taste. But if you want a book that’s all about sugar, then you might be disappointed. That’s because although the title might lead you to believe that the book is chiefly about sugar, the reality is that much of the book is devoted to making the case that low-fat diets are bad and the government is bad for ostensibly forcing them on you. That’s right, it’s Good Calories, Bad Calories all over again.

Why does Taubes retread these old waters? My guess would be because there are only so much words you can write about the health effects of sugar. If you asked me to write a similar book I might be able to write 50 pages. If I double-spaced and wrote superfluous and over-extended sentences I might be able to stretch it out to 100 pages. But a publishing company is not going to be able to charge 25 bucks for a 100-page book. There’s no money there. You gotta give them 300 pages or more before you can justify that price. A sugar novella may not be worth the editing and cover art and printing and marketing you put behind it. Because of this Taubes discusses things like tobacco, cereal, why low-fat diets are bad, why the government sucks, and why the link between salt and hypertension is overblown. He literally copy-pastes passages from GCBC into CAS. But I’m actually working on a future post that addresses just that.

In the meantime, what follows is a non-exhaustive critical review and fact-check of some claims advanced in CAS. In short, much like GCBC, it is exceptionally dishonest and a misrepresentation of much of the source material. There’s not even a good reason why Taubes is dishonest. You’d think that a muckraking text on sugar would be a lay-up, but here we are.

 

Not the Introduction

In the Prologue of CAS, it becomes evident that Taubes attempts to pin the cause of diabetes on sugar. We will discuss the merits of this soon enough, but on page 13 Taubes says the following:

And on those very rare occasions when sugar consumption declined—as it did, for instance, during World War I, because of government rationing and sugar shortages—diabetes mortality invariably declined with it. “Rises and falls in sugar consumption,” wrote Haven Emerson and Louise Larimore in 1924, “are followed with fair regularity . . . by similar rises and falls in the death rates from diabetes.”

The text that is cited for support is a 1924 analysis by Emerson and Larimore.(1) This is a totally legitimate quote from the source text. My point in highlighting this is not that Taubes misrepresented the authors, although they did mention that sedentary behavior is also correlated with diabetes – something that Taubes leaves out. What I want to mention is that this is an epidemiological study. Not only is it epidemiological, but it is also a cross-sectional which is one of the weakest analyses when it comes to suggesting causation.

I want to remind readers that there has been no love lost between Taubes and the enterprise of epidemiology. He has repeatedly maligned the study of population health, calling it unreliable and a pseudoscience. Anytime an epidemiological study is published that is devastating to Taubes’s bizarre pet theories of nutrition he claims the entire field of study is nonsense. However, this has never stopped him from citing epidemiological studies when it suits his needs. The Case Against Sugar is no different. I am not going to write a paragraph each time cites an observational study in support of his arguments because that would really muddy the waters of this review, but he does cite them quite often here and I will point them out when I feel it is appropriate.

* * *

On page 33 in a chapter titled “Drug or Food?” Taubes states the following:

Certainly, people and populations have acted as though sugar is addictive, but science provides no definitive evidence. Until recently, nutritionists studying sugar did so from the natural perspective of viewing sugar as a nutrient—a carbohydrate—and nothing more. They occasionally argued about whether or not it might play a role in diabetes or heart disease, but not about whether it triggered a response in the brain or body that made us want to consume it in excess. That was not their area of interest.

In short, Taubes claims that the neurobiological effects of sugar were not studied. No one cared. Except several times throughout the same chapter Taubes cites research on the neurobiological effects of sugar, including one 435-page tome published in 1977 by the NIH titled Taste and Development: The Genesis of Sweet Preference that does nothing but dive into the research.(2) Not a major gaffe on Taubes’s part, exactly, but which is it: Was research conducted in this field or wasn’t it?

* * *

On page 38, Taubes doesn’t understand evolutionary adaptations and so demands nutritionists fill in the gaps:

This raises the question of why humans evolved a sweet tooth, requiring intricate receptors on the tongue and the roof of the mouth, and down into the esophagus, that will detect the presence of even minute amounts of sugar and then signal this taste via nerves extending up into the brain’s limbic system. Nutritionists usually answer by saying that in nature a sweet taste signaled either calorically rich fruits or mother’s milk […] so that a highly sensitive system for distinguishing such foods and differentiating them from the tastes of poisons, which we recognize as bitter, would be a distinct evolutionary advantage. But if caloric or nutrient density is the answer, the nutritionists and evolutionary biologists have to explain why fats do not also taste sweet to us.

Firstly, does fat not have a pleasurable flavor? Is it not also desired for its texture, mouthfeel, and palatability? Secondly, I’m no molecular biologist, but for all nutrients and calories to taste the same (sweet) I would imagine that the receptors would need to be able to bind to hydrophilic, hydrophobic, and amphipathic molecules of varying sizes, while also not binding to non-nutritive substances. Is that possible? Thirdly, would having the ability to differentiate nutrients based on flavor (salt, sweet, savory, etc.) confer some sort of selective advantage? If Taubes had asked himself these questions would he have still written the above paragraph?

* * *

On page 44 Taubes concludes the first chapter with a straw man:

Nutritionists have found it in themselves to blame our chronic ills on virtually any element of the diet or environment […] before they’ll concede that it’s even possible that sugar has played a unique role in any way other than merely getting us all to eat (as Harvard’s Fred Stare put it forty years ago) too damn much.

“Nutritionists” is such a nebulous term, but this is wrong, nevertheless. There is a large body of scientific research on sugar that has been ongoing for as long as the enterprise of science has been around. Taubes even cites some of it himself. Moreover, no nutritionist or dietitian that I know of has ever advocated consuming more sugar or that sugar is healthy or even that sugar is blameless when it comes to rising obesity.

* * *

In Chapter 3: The Marriage of Tobacco and Sugar, Taubes puts the blame on sugar (not tobacco!) for lung cancer deaths that have been increasing over the past century. The chapter is only eight measly pages, and is essentially a Reader’s Digest version of another book published a few years earlier titled Golden Holocaust, and peppered with a few choice quotes from a 1950s report published by the Sugar Research Foundation.(3,4) In fact, much of what Taubes writes in this chapter (much like the previous chapter) is basically copy-pasted from Golden Holocaust. Consider the following excerpt from page 33 of Golden Holocaust:

page 33 golden holocaust

And now page 65 of CAS:

page 65 CAS

To be fair to Taubes, there is no plagiarism here; everything is appropriately cited and quoted, but the whole chapter is like this. Very little of it is original writing.

* * *

On page 98 Taubes copies his own work:

Influential British and Indian physicians working in the Indian subcontinent had discussed the high and apparently growing prevalence of diabetes among the “lazy and indolent rich” in their populations, and particularly among “Bengali gentlemen” whose “daily sustenance . . . is chiefly rice, flour, pulses, sugars.”

“There is not the slightest shadow of a doubt that with the progress of civilization, of high education, and increased wealth and prosperity of the people under the British rule, the number of diabetic cases has enormously increased,” observed Rai Koilas Chunder Bose, a fellow at Calcutta University, noting that perhaps one in ten of the “well-to-do class of Bengali gentleman” had the disease.

Compare this to pages 102-103 of GCBC:

To British investigators, it was the disparate rates of diabetes among the different sects, castes, and races of India that particularly implicated sugar and starches in the disease. In 1907, when the British Medical Association held a symposium on diabetes in the tropics at its annual conference, Sir Havelock Charles, surgeon general and president of the Medical Board of India, described diabetes among “the lazy and indolent rich” of India as a “scourge.” “There is not the slightest shadow of a doubt,” said Charles’s colleague Rai Koilas Chunder Bose of the University of Calcutta, “that with the progress of civilization, of high education, and increased wealth and prosperity of the people under the British rule, the number of diabetic cases has enormously increased.” The British and Indian physicians working in India agreed that the Hindus, who were vegetarians, suffered more than the Christians or the Muslims, who weren’t. And it was the Bengali, who had taken on the most trappings of the European lifestyle, and whose daily sustenance, noted Charles, was “chiefly rice, flour, pulses and sugars,” who suffered the most—10 percent of “Bengali gentlemen” were reportedly diabetic.

The recycling of his own work notwithstanding, it’s a bit of a selective interpretation of the source material.(5) The following are some choice quotes that Taubes does not mention:

[The Hindus] generally eat more than is actually necessary for the maintenance of health, are more susceptible to diabetes than their Mohammedan or Christian brethren. It is difficult to state the part food plays in the production of diabetes, and what part gluttony supplies in the manufacture of sugar within the system. True it is that our diet chiefly consists of rice, flour, pulse, and cereals of diverse kinds; but so long as there does not exist the essential cause of diabetes, which Is still unknown, they exert little or no deleterious effects upon our health, and a man may continue to take carbohydrates and sugar lifelong, and still may not suffer from diabetes; he might suffer from temporary glycosuria. I do not agree with those who believe that carbohydrates are the only factors of diabetes, for meat-eaters are not immune against the disease.

[…]

The following articles of diet are recommended [for diabetics]: New rice, curd, flesh of animals living in swamps, fish, sweets, wines, vinegar, excess of oil, and onions. […] The following articles of diet are especially recommended, for they are considered to be very beneficial: Barley, flour of old wheat, Moong dal, Arabar dal, Chena dal (Bengal grain), fried rice, sesamum seeds, meat juice, old wines, old honey, whey, sparrows, pigeons, rabbits, snipe, peacock, venison.

[…]

And, although the carbohydrate excess in the food of the Indian is very great, still, just as in Europe, where the consumption of sugar, vegetables, and beer may be also in excess, the essential cause of diabetes must be present, or otherwise the factors mentioned will not determine the disease. So it is in the East.

[…]

Exercise, as a rule, is disliked by the gentlemen class of Bengal after a certain age, and members of this service form no exception. Further, in addition to sedentary habit, excessive mental labour, often in over crowded court-rooms, and ingestion of heavy, fatty, starchy, and saccharine meals, seem to be no unimportant factors in the causation of the disease among this class of highly useful Indian public officers.

If we take the whole of the text into account, we find that these Bengali gentlemen not only consume starches and pulses, but also heavy fatty foods, and they consume it all in excess. Additionally, they don’t like to exercise according to these physicians. Might these lifestyle factors play a role in diabetes? Moreover, the physicians themselves make it clear that they do not think sugar and carbs cause diabetes since diabetes can also be present in those that do not eat carbs and be absent in those that consume a lot of carbs. If these physicians thought carbs promoted the development of diabetes they would not be prescribing diets that included honey, flour, rice, sweets, and wine in the treatment diets. Why doesn’t Taubes mention this?

Continuing… Taubes claims that this point about Indian diabetics was “singularly compelling” to an influential diabetes specialist named Frederick Allen.

Allen found this point singularly compelling. These early Hindu physicians, after all, were linking diabetes to carbohydrate consumption and sugar more than a millennium before the invention of organic chemistry and its revelations that sugar, rice, and flour were carbohydrates and that carbohydrate “in digestion is converted into the sugar which appears in the urine.” “This definite incrimination of the principal carbohydrate foods,” Allen wrote, “is, therefore, free from preconceived chemical ideas, and is based, if not on pure accident, on pure clinical observation.”

First, there is no evidence that Allen found this “singularly compelling.” Secondly, unlike Taubes, Allen discusses evidence both for and against the theory that carbohydrate consumption is associated with diabetes.(6) Let’s look at the full quote (emphasis mine):

This definite incrimination of the principal carbohydrate foods is, therefore, free from preconceived chemical ideas, and is based, if not on pure accident, on pure clinical observation. But Bose himself, with a more modern viewpoint, states that he does not know how much the heavy carbohydrate diet and the gluttony of the Hindus may have to do with the great prevalence of the disease among them; but unless the unknown cause of diabetes is present, a person may eat gluttonously of carbohydrate all his life and never have diabetes.

Having the full quote changes Allen’s tone, wouldn’t you say? Let’s look at what else Allen wrote immediately following the out-of-context quote:

Among the authorities on diabetes, von Noorden declares against any relation between the eating of carbohydrate and the incidence of the disease. […] A. L. Benedict considers that though some diabetics give a history of excessive eating of sugar or carbohydrates, many non-diabetics are guilty of equal excesses, particularly young girls who live on candy. Supporters of the sugar-theory call attention to the concomitant increase of diabetes and of sugar- consumption. But if sugar were a cause, diabetes should be more prevalent among the young, especially girls; and a larger proportion of case-histories should show sugar-excess. The products of carbohydrate digestion and metabolism are not toxic, and indigestion generally stops the excess before long.

* * *

Relating back to the Prologue of this book, on page 100 Taubes describes the intrepid research of Emerson and Larimore:

By the mid-1920s, the rising mortality rates from diabetes in the United States had become the fodder of newspapers and magazines; Joslin, the Metropolitan Life Insurance Company, and the New York State commissioner of health were all reporting publicly what Joslin was now calling an epidemic. When Haven Emerson, head of the department of public health at Columbia University, and his colleague Louise Larimore discussed this evidence at length at two conferences in 1924—the American Association of Physicians and the American Medical Association annual meetings—they considered the increase in sugar consumption that paralleled the increasing prevalence of diabetes to be the prime suspect.

But is this actually true? Was sugar the “prime suspect”? From the Emerson and Larimore article:

The food shortage expressed itself not so much in the lack of sugar and carbohydrates as in lack of fats, which should make one suspect that it is not the quality but the gross quantity of food (calories) that plays the chief part in development of a high diabetes death rate in a community where more food is eaten than is required. (1)

So, the sugar shortage, in effect, was the shortage of all foods. Sugar consumption was used only as a proxy. This is repeated in the text:

One index of the tendency of our people to use larger amounts of food is the record of per capita consumption of sugar, which is offered here not as an explanation of the increased death rates from diabetes in recent years, but more as a sign of the tendency to excesses in the use of foods of all kinds, beyond the needs of persons for foods in proportion to their expenditure of energy at the different ages of life, and in particular in the later decades.

If any prime suspect is fingered by the authors, it is the difference in physical activity between those that have diabetes and those that do not. This point is bought up many times in the text and is the closing sentence from Emerson.

Nevertheless, Taubes’s deliberate misreading of this text becomes his basis for claiming that it’s basically a capital-F Fact that sugar consumption causes diabetes. Now, Taubes doesn’t say this explicitly, but there’s a significant tonal shift for the rest of the book. From here on out, any scientist offering contrary views to this (misinterpreted) theory is a hack, and any growing body of evidence against it is part of a conspiracy. I wish I was making this up.

* * *

One of Taubes’s hacks in this narrative is a British physician named HP Himsworth. On page 104 Taubes states “But he was only in his mid-twenties in 1931, when he proposed that a diet relatively rich in carbohydrates was ideal for diabetics, implying that a diet rich in fat might be a cause of the condition.” Nope. Never said that. In fact, Himsworth said the opposite:

Ketosis is much better controlled [compared to a high-carbohydrate diet], there is less tendency to coma and to infection, and the general health is better. Furthermore, the diet is cheaper, less obvious to others, more palatable, and therefore more likely to be adhered to. The disadvantage is that when put on to the diet the patient, if not carefully watched, may drift during the first week when his urine is just becoming sugar-free into acute hypoglycaemia.(7)

The reason Taubes hates him is because Himsworth suggested that if someone drifts into a hypoglycemic coma you should give them sugar. This is something that is true even today, but if you speak of sugar favorably under any conditions, even one as life-threatening as a diabetic coma, you go on Taubes’s shit list and he’ll twist your words around while you’re in the grave and can’t defend yourself.

 * * *

Taubes continues to smear Himsworth on pages 105-106 saying:

In a 1949 lecture to the British Royal College of Physicians, Himsworth described the problem with the hypothesis as a paradox: even though populations that consumed more fat tended to have more diabetes, “the consumption of fat has no deleterious influence on sugar tolerance, and fat diets actually reduce the susceptibility of animals to diabetogenic agents.”

Taubes cites the source of this quote as being from a 1949 publication in Proceedings of the Royal Society of Medicine.(8) However, that quote does not exist in that text. Do you know where it does exist? It exists unsourced on page 104 of Yudkin’s Pure, White and Deadly, which Taubes then copy-pastes into GCBC and subsequently this book.(9)

himsworth trio

For a larger image go here: http://imgur.com/a/zCKR0

Continuing with the above quote…

Now Himsworth suggested that maybe dietary fat wasn’t the culprit, after all, and perhaps there were “other, more important, contingent variables” that tracked with fat in the diet. He suggested total calories as a possibility—overeating of all foods—because of the association between diabetes and obesity, and because “in the individual diet, though not necessarily in national food statistics, fat and calories tend to change together.” Himsworth omitted mention of sugar, however, which is another contingent variable that tracks together with fat and calories in both national food statistics and individual diets.

Have you ever heard of Karl Rove’s playbook? It’s allegedly a collection of Rove’s most insidious but effective strategies for manipulating public opinion and winning elections. Tactic #3 in this playbook involves accusing your opponent of your own weakness before they bring it up. Examples of this tactic include the Swiftboating of John Kerry or whenever Donald Trump claims one of his opponents is unhinged or corrupt.

Taubes deploys it brilliantly here in that last bolded sentence. Because A) Himsworth, in fact, does mention it. He even creates a nice graph illustrating the whole thing. (8) And B) TAUBES IS THE ONE THAT DOESN’T MENTION THAT SUGAR TRACKS WITH CALORIES. REMEMBER EMERSON AND LARIMORE?

himsworth fat and mortality

 

 * * *

Page 108:

[P]astoral populations like the Masai in Kenya, or South Pacific Islanders like those on the New Zealand protectorate of Tokelau, consumed less fat (and in some cases less meat) over the course of their relevant nutrition transitions, and yet they, too, experienced more obesity, diabetes, and heart disease (and cancer as well). These populations are the counterexamples that suggest that this dietary-fat hypothesis is wrong

Ugh, enough with Masai and Tokelau. Can we stop repeating nonsense? I guess not since Taubes also devotes a few pages to talking about how calories don’t have anything to do with obesity.

Continuing…

The same is true of populations like the French and Swiss, who eat fat-rich and even saturated-fat-rich diets but are notably long-lived and healthy. Mainstream nutrition and chronic-disease researchers would ignore these populations entirely or invoke ad hoc explanations (the French paradox, for instance) for why their experience is not relevant.

The reason the French and the Swiss are generally healthier than Americans is not because they eat more chocolate and cheese, nor is it much of a paradox. Both France and Switzerland consume 200-300 kcals less per day than the US, according to the FAO. They also are more physically active, according to the WHO. No one is ignoring this data, except for Taubes.

 * * *

On pages 104-105 Taubes takes a few more uncharitable shots at Himsworth:

To make his argument that fat caused diabetes, Himsworth had to reject evidence that populations like the Inuit or the Masai, eating very-high-fat diets, also had very low diabetes rates, or at least they did at the time that Himsworth was making his claims. He did so by insisting that the evidence regarding the Masai was “so scanty” that it could be ignored […]

And

Neither Himsworth nor Joslin apparently bothered to ask whether the Japanese consumed less sugar than the Americans or the British—which they did.

Let’s be clear on the timeline here: Taubes is explicitly describing a period in the 1930s and 1940s citing texts from those decades. Are we all clear on that? So regarding the Masai, Taubes doesn’t cite anything in CAS about the Masai, but he does in GCBC and the earliest study he mentions is by the late, great George Mann published in 1964.(10) Mann was involved in a lot of Masai diet and health research. In fact, he was probably the first person to publish hard-hitting research on the Masai. However, before Mann, there was only a trickle of Masai research coming in and it was mainly about dentistry and venereal disease, the earliest if these published in 1946. (11–13) Here is a graph I made using data extracted from PubMed.

publications in pubmed of masai

Like I said, the very earliest is 1946 and it’s about teeth. It wasn’t until George Mann came around that people started to become interested in the diet of the Masai.(14) Looking at this chart one could reasonably assume that perhaps the evidence on diet and diabetes w/r/t the Masai people was “so scanty” that it could be ignored. But the thing is HIMSORTH DOESN’T EVEN IGNORE IT. He mentions the scanty data available on the Masai in his paper, and also mentions that there’s not enough evidence to draw any good conclusions. (15)

Moving on to the Japanese…. Taubes shits on Himsworth for allegedly not mentioning that the Japanese consumed less sugar than the US. As evidence for this claim Taubes cites a paper from the AJCN published in 1968.(16) Why would Taubes cite a paper from 1968? Was there good nutrition data from the 30s and 40s? Turns out, no, there wasn’t. Japan did not start doing a National Nutrition Survey until 1949. This is why the data from the paper doesn’t start until 1950. This is even explicitly stated in the paper.

insull

IN. SPITE. OF. THIS. Himsworth still digs up three papers that estimate macronutrients in the Japanese diet, discusses the data in several paragraphs, and creates this chart:

japan graph

Lastly, Himsworth never claimed to have discovered the cause of diabetes. At best, he describes the fat-diabetes relationship as an association. But I guess if Taubes wants to smear him because it makes for a better story that he can sell his audience then who am I to question it?

 * * *

Cranky, Old Man Taubes then gets on his soapbox and claims that the thought that calories or physical activity might have anything to do with the development of obesity is totally absurd. Page 109-110:

By this energy-balance logic, the close association between obesity, diabetes, and heart disease implies no profound revelations to be gleaned about underlying hormonal or metabolic disturbances but rather that obesity is driven, and diabetes and heart disease are exacerbated, by some combination of gluttony and sloth.

This whole passage is really a non compos mentis rant on his crackpot theories that have been debunked so many times I don’t have time to cite everything. Nevertheless, he cites a source for the above statement that makes no sense at all. It’s a short blurb by the FAO about why it’s important (on a global level) to eat a heathy diet. It makes no mention of hormones or endocrinology or that obesity can’t be a symptom of a metabolic disorder or any of that. Taubes apparently doesn’t realize he’s promoting a (nutty) mechanism of obesity development at the cellular level via dietary means, and the FAO is simply advocating a better diet to benefit a nation’s economy and improve global health.

Taubes then fleshes out his conspiracy theory a bit for the next few pages. For those uninitiated to his crackpottery, Taubes’s thinking is that German researchers like Gustav von Bergmann actually cracked the case w/r/t obesity: it’s not a case of energy intake and physical activity, but rather a hormonal disorder. However, this “good science” was buried after WW2 when Germans became personae non gratae among the scientific and cultural elite. “They didn’t see any reason to read the German-language literature, even though most of the significant science had been published in these journals,” claims Taubes. Nevertheless, there were still brave researchers willing to investigate this German research and do the “real” science. One such researcher was a fellow named Julius Bauer (pg 115):

In a series of articles written from the late 1920s onward, Bauer took up Bergmann’s thinking and argued that obesity was clearly the end result of a dysregulation of the biological factors that normally work to keep fat accumulation under check.

However, if one actually reads the series of articles, one might conclude that they are not exactly the ringing endorsement that Taubes claims:

The question of obesity has occupied the minds and pens of so many workers that it seems scarcely necessary to add another publication. Endocrinologists, especially, have taken a great interest in the subject, and as a result we find the literature filled with references to the relation between endocrine disorders and obesity. While we grant that endocrine dysfunction may be a cause of obesity we feel that these cases form a small, numerically almost insignificant part of the obese patients that present themselves in the clinic. It shall be the purpose of this report to review briefly the present concepts of the nature of obesity and to present a case that illustrates the dangers of an “endocrine diagnosis” in cases which, on careful study, reveal another, more likely, basis for the obesity. (17)

(bolding mine, italics in the original)

And what does Dr. Bauer recommend in treating obesity? Why low calorie diets and more exercise, of course!

In no case should obesity be treated without the prescription, first of all, of a dietetic regimen. All other therapeutic procedures are secondary to this one. Not only a general quantitative reduction of calories should be instituted, but their quality should also be considered. […] The output of energy should be increased as far as possible by the prescription of greater muscular activity, in the form of walking and other physical exercises, with due regard to the patient’s cardiac state. (18)

Unfortunately, Dr. Bauer also recommends some treatments that most experts would consider a bit hokey today, such as massages to “loosen fatty masses,” mercurial diuretics, limiting “as far as possible the intake of fluids of all kinds,” thyroid hormones, and wearing “elastic stockings” to prevent water retention.

Continuing on page 116, Taubes writes:

By 1938, Russell Wilder, the leading expert on diabetes and obesity at the Mayo Clinic and soon to become director of the Food and Nutrition Board of the National Academy of Sciences, was writing that this German-Austrian hypothesis “deserves attentive consideration” […]

Interestingly, Wilder prefaces the above quote with “Even though one grants, as one must, that the caloric balance will determine in the end whether fat is deposited or released from storage in the body as a whole […]” (19) Why Taubes excises this bit of text should be obvious to anyone paying attention.

Taubes puts a coda on this bit of conspiracy:

By 1940, the Northwestern University endocrinologist Hugo Rony, in the first academic treatise written on obesity in the United States, was asserting that the hypothesis was “more or less fully accepted” by the European authorities. Then it virtually vanished.

I think it’s important to note a few things here. First, Rony did not claim it was accepted by “the European authorities” (Taubes also makes this mistake in GCBC by stating it was accepted “in Europe”), but rather that it was accepted in Germany. Minor point, but worth mentioning because Taubes clearly expands the acceptance from one country to an entire continent to make it seem more legitimate. Second, Rony also mentions a few things immediately following the “more or less fully accepted” quote that are less than charitable to the theory. Notably on page 174,

[T]he main elements of this attractive theory remain as hypothetical as they were thirty years ago. Thus, there is as yet no direct evidence that the fat tissues of obese subjects have an increased affinity to the glucose (and fat) of the blood. […] The results of glucose and fat tolerance tests made on obese and non-obese persons do not support the assumption that ingested glucose and fat disappear from the blood of obese subjects faster land at lower thresholds than from the blood of non-obese subjects. (Chapter VI). Neither is there any material evidence to show that the fat depots of obese persons resist fat mobilization at times of caloric need for energy consumption more than the fat tissues of non-obese subjects do. On the contrary, it appears from data concerning the basal metabolism and nitrogen output in undernutrition (page 72 and 149), that the fat of the fat depots of most obese subjects is more readily available for energy consumption than that of non-obese subjects. Furthermore, we have no valid proof that glandular or nervous system disturbances, in producing generalized obesity, act primarily upon the fat tissue. (20)

Emphasis mine. In fact, the entire Rony text is really devastating to Taubes’s theory, in that it fully supports what Taubes calls the “energy-balance theory” and effectively rejects the fringe theories like those Taubes promotes.

 * * *

At this point it is worth mentioning the intentional conflation of three ideas: energy balance, energy partitioning, and a set-point.

Energy partitioning is what happens to your food once you eat it. Do dietary carbohydrates become stored as liver glycogen, muscle glycogen, fat, burned for energy, used to synthesize or repair DNA, become advanced glycation end-products…? Similar questions could be asked about dietary proteins or fats: Converted to triglycerides? Incorporated into phospholipid bilayers of cells? Used in maintenance of skeletal tissue? Cardiac tissue? Myelinogenesis? Metabolized for energy? Milk production? A thousand different factors influence where the calories go after mastication in your pie-hole. But it won’t change the fact that once those calories end up in the bloodstream you’re going to use them in one way or another, and if you don’t use them you store them. Related to this is where fat gets preferentially stored: on visceral organs, breasts, butt, thighs, back…whatever. This is determined largely by genetics and sex.

A set-point is shorthand for the weight range that one’s body maintains in homeostasis. I don’t know if the theory is universally accepted among obesity researchers, but I think there’s quite a bit of evidence supporting it and it’s well understood in the academic nutrition community.

These are not mutually exclusive ideas. In fact, in many ways they are complimentary. Why do I bother to bring this up? Because Taubes likes to make the confusing argument that if fat can be preferentially stored in certain areas then energy balance is false. Or if something can influence appetite or physical activity, such as hormones or hypothalamic lesions, then energy balance is false. If that makes absolutely no sense to you then you’re not alone. It’s a complete non sequitur.

On page 117 and 118 Taubes writes:

This perspective [energy balance] might have been more understandable if not for two developments. First, animal models of obesity consistently refuted Newburgh’s arguments and supported the European school of thinking. […]

For this “development” he cites a series of rodent studies that, if anything, run contrary to his point by providing evidence for energy balance.(21–26) Some studies damage the hypothalamus of a rodent, causing it to become lethargic, thus gaining weight. Some induce fasting only to reintroduce food later to find that the rodent overeats to kind of make up for the lost calories during the fast. Here’s another that takes genetically obese mice and varies their caloric intake:

alonso

Looks like calorie intake might play a big role in body weight after all. The interesting thing here is that mice can be genetically bred to defend a higher “set-point” than other mice, but it is certainly not evidence against energy balance.

 * * *

Much of Chapter 7 and Chapter 8 is devoted to shitting on “Big Sugar,” which in my humble opinion is completely fine. The sugar industry (loosely made up of growers, processors, and manufacturers) has been involved in funding research favorable to sugar consumption, promoting sugary products, lobbying government of behalf of sugar, and whatever is necessary to increase profits. In all likelihood, this has had a detrimental effect on public health and probably confused people about how beneficial sugar might actually be. SOAPBOX ALERT: I don’t like this aspect of our society. I hate that industries can get together to form these institutions and consortiums where their only goal is to manipulate markets and manipulate public opinion and confuse the science in the name of wringing a few more dollars from hardworking Americans. Profit is the only goal here, while the health and well-being of everyone else is a secondary concern at best.

Having said that, the sugar industry is not unique in this respect. All food industries – indeed, all industries — have these kinds of organizations with the exact goals. Potatoes, beef, chicken, pork, milk, salt, cheese… even fruits and vegetables. They all have lobbying arms, they all fund scientific research they hope will be flattering to their commodities, they all engage in public relations and advertising campaigns to get you to buy their products, and none of them really give a shit about your health.

So Taubes can shit on Big Sugar all he wants, but it’s curious that he has nothing negative to say about the meat, cheese, or dairy industries, and in fact parrots some of their propaganda. The meat industry even uses his writing in their own propaganda. Just so you know.

 * * *

Not content to merely libel deceased researcher Ancel Keys in his previous two books, Taubes also libels him here on page 150:

[H]is thinking and the strength of his personality—both his competitors and his friends described him as combative and ruthless—would drive nutrition research for the next thirty years.

Nope. Not at all. As evidence Taubes cites a eulogy by Keys’s longtime colleague Henry Blackburn who had nothing but favorable things to say about Keys.(27)

Continuing with lies about scientists that cannot defend themselves:

In 1957, the AHA published a fifteen-page assessment of the evidence, compiled by some of the leading cardiologists of the era, concluding that the dietary-fat/heart-disease hypothesis was highly questionable, and castigating researchers—presumably Keys—for taking “uncompromising stands based on evidence that does not stand up under critical examination.”

Notice the “presumably Keys” part. There is no evidence at all that the authors were referring to Ancel Keys here, but Taubes throws his name in there anyway for good measure. Maybe he has those special glasses from National Treasure and he can read text that no one else can see just like Nic Cage did.

ben-gates-glasses

The report seems to have somewhere between a neutral and a favorable view of Keys, as evidenced by the following quotes:

  • “Mayer et al. found that high-fat animal or vegetable diets increased and low-fat diets decreased serum cholesterol of normal subjects, confirming earlier data of Keys.”
  • “Keys, in particular, has placed emphasis on the proportion of total dietary calories contributed by the common food fats […] Certainly there is an abundance of data, both clinical and experimental, that tends to relate excess fat intake to atherosclerosis.” (28)

 * * *

On page 151 Taubes claims that plenty of research was conducted over the years to try and answer the diet-heart hypothesis, but they results were, at best, ambiguous.(29) Then he hits you with this (emphasis mine):

Some of the trials suggested a modest reduction in heart disease from decreasing the saturated fat content of the diet; one even suggested that it might lengthen lives. But others suggested it wouldn’t, and one even suggested that eating less saturated fat would shorten our lives.

Nope. Not at all. Not even close. The paper he cites even suggests the opposite.(30) See for yourself. Note: The control diet was high in saturated fat and the treatment diet was high in unsaturated fat.

death

Apart from one trend point (in yellow), all other trends indicate less cardiac events and less overall death on the unsaturated fat diet. The most charitable thing you could say about Taubes here is that his interpretation of the text is highly selective, but I would just call it a lie (or perhaps an alternative fact).

 * * *

On page 160 Taubes shows he doesn’t know what words mean when he states the following:

In 1963, in a seminal article in The Lancet, Yudkin took up Cleave’s idea that species are adapted—”anatomically, physiologically, and biochemically”—to a particular diet and combination of foods, and that the most dramatic departures from this diet are likely to be the harmful ones.

I’m going to pick on the word “seminal” here. Per the Google machine “seminal” means “(of a work, event, moment, or figure) strongly influencing later developments.” Synonyms include influential, formative, groundbreaking, pioneering, original, and innovative. First of all, the idea of species adapting to their environment was not at all groundbreaking or original thought in 1963. Nor was it particularly groundbreaking in Darwin’s time, because this idea had been around since before the common era.

Perhaps the Lancet paper was influential in some other way in the nutrition science community. Maybe this particular paper that Taubes refers to as seminal actually inspired a ton of research and is the cornerstone of an entire field of nutrition research. Let’s see how many times it’s been cited over the past half century.

yudkin seminal

Not much as it turns out. Certainly not the impact that I imagine a “seminal” paper having, especially for being in the public domain for 53 years now.

Maybe you don’t think it’s a big deal, and maybe it’s not. But I think it’s clear that Taubes is biasing his writing.

 * * *

On page 163 Taubes beats up the non-profit organization he loves to hate:

When cardiologists and the American Heart Association thought about the role of triglycerides or lipoproteins in heart disease, perhaps not surprisingly they considered them from a physician’s perspective—not what they (or we) could learn about the genesis of heart disease by studying these other substances [sugar]

As proof that the AHA refuses to consider sugar a possible culprit he cites a conference report from 1989.(31) A couple of things are worth mentioning here:

  1. This was a conference explicitly on cholesterol, not EVERY SINGLE potential risk factor. This is, of course, mentioned in the introduction: “Cholesterol was selected as the first conference topic because of the timeliness of the subject. Future conferences on hypertension, smoking, and possibly other risk factors are planned.” A single risk factor was selected for focus and simplicity, not because it was the exclusive risk factor. Can we get a little intellectual honesty here, please?
  2. As a matter of fact a conference specifically on sugar was held later that advocated the reduction of dietary sugars.(32) I wonder why that was not mentioned. And studies examining sugar intake and CVD were conducted and discussed, with recommendations to reduce sugar intake. (33–46)
  3. Even Ancel Keys, the Devil himself, wrote an editorial for AHA’s journal back in 1968.(47) A recommendation was offered that “consumption of sugar and products containing sugar should be reduced,” but Taubes would never mention that because then Keys couldn’t be the villain in his story anymore.

Taubes continues, writing “The American journals, like the research communities in the United States, remained focused on fat and largely quiet on the sugar question.” This is so blatantly false that I can’t even. I’m not about to begin citing all the research that would rebut that notion, but I will refer you to the Circulation papers that I cite above as a start.

 * * *

Page 173:

The point man for the Sugar Association’s Food and Nutrition Committee was Fred Stare, founder and longtime chairman of the department of nutrition at the Harvard School of Public Health. The sugar industry had been supporting Stare and his department since the early 1940s […]

This is true, but it’s worth noting (because Taubes won’t mention it) that Big Sugar was not the only industry providing gifts to HSPH. Pretty much all sectors of the food market were providing gifts to Harvard, including the beef industry, the pharmaceutical industry, the fruit and vegetable industry, the poultry industry, the fish industry…. I could go on.(48) Is this good evidence that Harvard has been compromised?

But if you find that compelling, then I have story for you. Let me put on my tinfoil hat… A few months ago a commentary was published in JAMA Internal Medicine about the sugar industry’s attempt to influence public opinion.(49) The authors of this commentary cite an article by Taubes as well as the same sugary industry documentation Taubes does in CAS. This commentary was published in November of 2016, and CAS was published in December 2016. Might there have been some collusion between Taubes and the authors?

As a matter of fact there was, although it wasn’t disclosed at the time. It was later revealed that Taubes personally funded the research of that paper.(50) As you are aware, Taubes has a financial stake in making Big Sugar look bad in order to sell more books and collect more fees for speaking engagements. Clearly there’s a conflict of interest here.

*takes off tinfoil hat* What I mentioned above is all true, but that doesn’t mean that there’s no merit to the JAMA text.

 * * *

On pages 186-187, Taubes trods some familiar ground:

[T]he NIH invested a quarter-billion dollars in two trials that tested variations on the same theme, or links in a hypothetical chain of reasoning. The first trial would test the supposition that men with high cholesterol levels who were told to eat a low-fat diet […] would live longer than men who weren’t. The results of this study were published in 1982 and failed to confirm the hypothesis. The men on the low-fat diet suffered more deaths than the men who were left to their own devices. […] The second trial tested the hypothesis that a cholesterol-lowering medication given to men with very high levels of cholesterol would lengthen their lives, compared with men who took no such medication. The results of this study, published in 1984, indicated that the medication helped, albeit just barely.

The first study Taubes is referring to is the multiple risk factor intervention trial (MRFIT).(51) I don’t want to get into the weeds on MRFIT, but in my opinion it was not a very well-designed or well-executed trial for reasons that include:

  • Multiple variables of interest (smoking, diet, hypertension) were not isolated, so it was impossible to point to one risk factor as a potential cause even if there was a clear difference in outcomes.
  • There was no attempt to minimize any potential observer effect, it seems. The participants in the control group were informed that they were at high risk of dying from CHD, the controls’ physicians were also informed, and the participants were obviously subjected to having data collected on them for many years, at least according to the JAMA editor.(52) Although it’s kinda funny to watch him try to polish the turd that MRFIT became.
  • There was not much of a structured diet to follow, rather, the intervention focused broadly on improving shopping, cooking, and eating patterns.(53) For example, participants were encouraged to set goals such as “no more eating while watching TV.” (54)
  • Adherence to the recommended eating patterns was poor. Only about 50% of the intervention group “were judged to adhere well to recommended food patterns.” But the people that did adhere to the “food patterns” had better outcomes than the poor adherents. (55)

So perhaps because of that type of intervention, there was no statistically significant difference between the groups w/r/t deaths from CHD or any kind of death. However, there are clear trends that show a general risk reduction in the intervention in any death, but especially death from CHD.

mrfit

So when Taubes says you’re more likely to die on the diet, that’s exceptionally misleading since, with the exception of maybe two very brief time points, you’re more likely to die from either CHD or anything else eating your normal fare.

Another thing Taubes misrepresents is the diet. The intervention diet was not a low-fat diet, but rather a diet that replaced saturated fats with unsaturated fats.(56)

With regard to the second trial, Taubes minimizes some good results. Namely, his claim that death “just barely” reduced is actually a figure of 19% reduced risk of definite CHD death and 24% reduced risk of a definite myocardial infarction. If you include suspected CHD deaths (as in there was clear evidence of CHD prior to death such as severe substernal pain, diagnostic enzymes met certain values, or a certain ECG pattern, but it was not immediately prior to the death) then that number increases to 30%.(57) Moreover, according to the results, those that reduced their total cholesterol levels by 25% had a CHD risk that was half that of the controls.(58) But a conspiracy theory is a little sexier, I guess, and presumably sells more books, so WHO CARES, RIGHT?

By the way, did you notice that this book was supposed to be about sugar’s relationship to obesity, but it somehow morphed into some pro-fat propaganda nonsense? Maybe Taubes had to hit a certain word count for his publisher, but really, how much can you say about sugar in 350 pages? Maybe he ran out of bad things to say at about page 100, so he began to copy-paste his old stuff from Good Calories, Bad Calories and didn’t think anyone would notice.

 * * *

Taubes continues with the recycled lies from GCBC which have nothing to do with sugar on pg 187:

Had scientific progress stopped there, we wouldn’t know whether the leap of faith was justified. But we do. The NIH eventually spent between half a billion and a billion dollars, depending on the estimate, testing the hypothesis that a low-fat diet would prevent chronic disease in women and bestow on them a longer life. The authorities involved had little doubt that it would, and were responding to political pressure to include women in medical trials; women had been underrepresented until then. The trial, known as the Women’s Health Initiative, was launched in the early 1990s, and the results were reported in 2006. Once again, it failed to confirm the hypothesis. The roughly twenty thousand women in the trial who had been counseled to consume low-fat diets and to eat more fruits, vegetables, and whole grains, and less red meat) saw no health benefits compared with the women who had been given no dietary instructions whatsoever.

Again, not true. The intervention group weighed less and reduced their incidence of ovarian cancer.(59,60)  Unless “saw no health benefits” means “lost weight and had a reduced risk for cancer,” in which case they saw no health benefits. I wrote about this in a previous blog post, and I even emailed Taubes about this mistake a few years ago. He didn’t seem to care much, and clearly still does not. Although the results were statistically significant, Taubes did not think this was worth mentioning and claimed “journalistic license” on his part to report the results the way he did.

Imagine, if you will, if the results were different. Imagine that the results of this enormous trial showed that a low-carbohydrate, high-fat (LCHF) diet conferred similar weight loss and reduction of cancer risk. You think Taubes would claim that a LCHF diet was no better than a normal western diet or even a low-fat diet? There is no way that would happen.

 * * *

Page 188:

A quarter century later, the most authoritative review of the evidence—from an international organization known as the Cochrane Collaboration—claimed that no health benefits derived from eating a diet low in fat, although the evidence “suggest[ed]” a small benefit if a diet high in fat replaced saturated fat with polyunsaturated fat. The leap of faith had turned out to be, well, a leap of faith.

Enough with the low-fat stuff! We get it, you don’t like low-fat diets. You wrote two other books on the topic, wasn’t this supposed to be about sugar? At any rate, this is not a lie and I want to take some credit for that, even if it’s wholly undeserved. Back in, say, 2013 or something when I first embarked on the Sisyphean task that is reviewing Good Calories, Bad Calories, I wrote Taubes to point out that he had made an erroneous claim on this Cochrane review. He wrote back and seemed surprised about the error and evidently modified the claim to be technically accurate here; unlike the previous point about the WHI trials. Nevertheless, the summary of that Cochrane review is actually pretty devastating to Taubes’s overall argument in his last two books. However, it really shouldn’t be relevant in this book… and yet here we are. Summary below:

Modifying fat in our food (replacing some saturated (animal) fats with plant oils and unsaturated spreads) may reduce risk of heart and vascular disease, but it is not clear whether monounsaturated or polyunsaturated fats are more beneficial. There are no clear health benefits of replacing saturated fats with starchy foods (reducing the total amount of fat we eat). Heart and vascular disease includes heart attacks, angina, strokes, sudden cardiovascular death and the need for heart surgery. Modifying the fat we eat seems to protect us better if we adhere in doing so for at least two years. It is not clear whether people who are currently healthy benefit as much as those at increased risk of cardiovascular disease (people with hypertension, raised serum lipids or diabetes for example) and people who already have heart disease, but the suggestion is that they would all benefit to some extent.(61)

 * * *

Page 190:

Scientists had tested the hypothesis that sugar consumption caused chronic disease in rats, because they could do those experiments: they could feed the rodents sugar-rich diets, or not, and see what happened over the lifetime of a rat. But it wasn’t a human’s lifetime. They had no idea whether rats were good models for humans.

True, but that’s never stopped Taubes from citing rodent studies when it fit into his narrative.

 * * *

Pages 204-205:

First, feed animals enough pure fructose or enough sugar (glucose and fructose) and their livers convert much of the fructose into fat—the saturated fat palmitic acid, to be precise, which is the one that supposedly gives us heart disease when we eat it, by raising LDL cholesterol. The biochemical pathways involved are clear and not particularly controversial.

Reading that paragraph was such a trip. I can almost hear Taubes struggling with what to write:

“Gawd, I wanna tell everyone all the reasons sugar is so bad. It’s so bad that fructose gets converted into palmitic acid, which is, like, THE WORST of all the saturated fatty acids. There’s so much evidence that palmitic acid raises LDL cholesterol immensely, and we all know what raising LDL does! It raises your chances of heart diseases BIG LEAGUE. It’s bad stuff. Really bad stuff. Oh shit! Fuck! I wrote books on how cholesterol is meaningless, and all those studies that connected it to heart disease were bunk. I told people to eat more steak which has more palmitic acid than any other saturated fatty acid! Jeez, what do I do here?? I’m in a tight spot. How about I write ‘supposedly’ in there… yeah, that’s the ticket! Now I got plausible deniability if there are any bad hombres that want to review my book.”

I don’t know why I made Taubes sound a little like Donald Trump. I guess I’ve been reading too much POLITICO lately.

 * * *

On page 208 Taubes laments the lack of human studies on the gravest of all concerns, sugar:

The number of researchers interested in studying sugar and fructose and worrying about the metabolic effects of consuming them is certainly growing, as is the willingness of health organizations worldwide to fund laboratory research, or at least to discuss such funding. But this has yet to be accompanied by the kind of human trials that might identify what happens when we consume sugar or high-fructose corn syrup for years, and at what level of consumption we incur a problem. As of the fall of 2016, fewer than a dozen clinical trials—all small and of short duration – were ongoing in the United States that might actually establish anything that the researchers who pay attention to the literature haven’t known for decades.

Stupid government! Why won’t it fund some damn human trials on sugar?? Let’s take a look at how Taubes arrives at this claim of a paucity of research. In the notes section we find this reference:

From search on clinicaltrials.gov for “sucrose OR fructose AND United States.”

So I typed exactly this and received the following result:

clinical trials dot gov

457 studies! One would imagine you could get a decent picture of the effects of sugar from the data from 457 human clinical trials. But to be fair to Taubes, he used the word “ongoing” and many of these trials had concluded. But if you filter out the ones that have concluded you get the following result:

clinical trials.gov

It appears that there are 79 ongoing studies in the United States involving sucrose and/or fructose. Do you think that in the few months that CAS was published and I wrote this review the number of trials increased by 900 percent? Not likely. There is probably a combination of filters that one can use to whittle the trials to a number less than twelve, but is it honest to claim there just is not the data or the funding to come to any conclusions on sugar?

On a related note, if Taubes is so concerned about human trials that investigate sucrose/fructose maybe he should fund them with the $10 million he was given by a Hedge fund manager (who apparently has more money than brains) to design and fund the studies that Taubes deems fit. If you look at ClinicalTrials.gov you will notice he has not done so.

This brings me to another related point. Here Taubes is advocating for more nutrition research, yet on page 150 Taubes strongly implies that some research is not worth doing if it’s funded by the sugar industry:

Keys had a conflict of interest: his research had been funded by the sugar industry—the Sugar Research Foundation and then the Sugar Association […]

For a bit of context here, the Sugar Industry did give Keys $36,000 in research funding.(62) That’s a lot of scratch in 1944. But if you look at the research that resulted from that funding, you will see that is was starvation research which ended up being the foundation of a lot of further research and data that helped the US Government develop military rations. I have not been able to find any research by Keys that promotes sugar consumption or anything like that. In fact, I mentioned statements earlier by Keys that would suggest the opposite. Presumably Taubes has not found such evidence either, because if he had you can be sure he would have trumpeted it to the skies as evidence of clear scientific corruption. Instead he can only really imply it because of the funding source.

I don’t like to get into the research funding game, because I think that discussion of funding can distract from the actual merits of the research itself. Nevertheless, if it turns out that good, high-quality research is performed by skilled scientists that is funded all or in part by an industry lobbying group then that can’t help but taint the results. Personally, I prefer to focus on the methodology of a given study and if the results jive with the bulk of other research that has been conducted on the topic rather than the funding.

However, if Taubes wants to be consistent and intellectually honest then if he impugns either research or a specific researcher for receiving industry backing, like Ancel Keys, then he should do it for everyone, right? Except that he doesn’t. Take John Yudkin, for example: an English food researcher that Taubes has lauded many times in this book (and others) has also received funding throughout his career from the Dairy Council, the flour industry, and Unilever (which manufactures about half of all the products you find in the supermarket).(9) Curiously, Taubes makes no mention of Yudkin’s conflicts of interest. If you look at other researchers Taubes cites positively you will find similar funding from the Dairy Council, Egg Nutrition Board, the Cattleman’s Association, etc., but you will never hear Taubes decrying their supposed conflicts of interest.

 * * *

Chapter 10 is largely devoted to discussing a handful of reports from the early 20th century on Native Americans. Now, I want you to keep in mind that these are observational studies, and the most observasional-ly of observational studies at that: usually one or two guys going to live near some Native Americans for a time and write about what they see. There’s no hypothesis, no rigorous statistical analysis, and only the mildest of data collection. The scientific method is employed in these reports only in the most superficial manner.

Why do I ask you to keep this in mind? Do I have an axe to grind against observational reports? Certainly not, but Gary Taubes does, and it doesn’t seem to matter if they are high-quality prospective cohort studies that adhere strictly to scientific principles, have a massive amount of peer review, or are published in the most reputable journals. Consider this statement from Taubes:

The catch with observational studies like the Nurses’ Health Study, no matter how well designed and how many tens of thousands of subjects they might include, is that they have a fundamental limitation. They can distinguish associations between two events […] But they cannot inherently determine causation […] As a result, observational studies can only provide what researchers call hypothesis-generating evidence — what a defense attorney would call circumstantial evidence. Testing these hypotheses in any definitive way requires a randomized-controlled trial — an experiment, not an observational study […] (63)

So Taubes is not a fan of the observational study. In fact, he wrote a whole magazine article about how observational studies like the Nurses’ Health Study have steered nutrition science in the wrong direction because they don’t provide valuable data. It makes perfect sense, then, why he would devote an entire chapter to some first-hand accounts and come to unwarranted conclusions, like sugar gave Native Americans diabetes.

Take the following statement from page 217:

Sugar seemed to be a prime suspect, and that was a recurring theme in a century’s worth of observations and discussion. When Hrdlička had commented that the Pima were already eating Western foods in 1906, he had been referring largely to sugar, white flour, and lard purchased at local trading posts or included in the government rations.

But the cited source for this claim – a 1906 report published in American Anthropologist – barely mentions food at all.(64) In fact, the one time food is mentioned it doesn’t mention sugar, flour, or anything that might substantiate Taubes’s claim:

Unlike the Apache, Navaho, and some other southwestern tribes, these people eat fish, ducks, chickens, and indeed everything obtainable that enters into the dietary of the white man.

Taubes must be using those Benjamin Franklin glasses again.

On page 218 Taubes discusses more incontrovertible evidence that sugar alone is to blame for the diseases among Native Americans:

When Indian Health Service physicians studied the living conditions on the Pima, Papago, and Navajo reservations half a century later, they reported purchases of Western foods—particularly sugar and sweets […]

Let’s take a look at the source of this claim that purportedly shows that the Navajo were dieting particularly on sugar and sweets (the italics are Taubes’s, not mine). (65)

Traders have reported an increased sale of meats in recent years. The meat is either locally grown and killed or purchased from packers in the larger cities such as Phoenix. […] White wheat flour is the most popular staple and is usually purchased in 25-pound sacks or larger.

They also have a table of the most common purchases at the white man’s trading posts and sugar does not even crack the top five:

navajo purchases

The authors also include a typical meal stratified by economic status.

navajo meal pattern

 

Taubes makes it seem like the Navajo are subsisting on cakes, cookies, ice cream, Twizzlers, and chocolate, but aside from some sugar in their coffee their main diets appear to be mutton, potatoes, and tortillas.

 * * *

Page 216:

Throughout these decades, the Indian Health Service physicians and the NIH researchers struggled to explain what they were witnessing. […] One NIH researcher who arrived in Arizona in 1983 to study the Pima later said he was “shocked” by “the amount of suffering” he was seeing.

According to the reference section of the book, the NIH researcher is Dr. Eric Ravussin, a rather well-known figure in the nutrition science realm that has co-authored many publications on the Pima. The quote is from a personal interview that Taubes conducted with Ravussin. Clearly Taubes is aware of his research; however, aside from that five-word quote above, there is no mention or reference of Ravussin’s work on a chapter that largely focuses on the Pima. So why did Taubes not see fit to include some of Ravussin’s work? Would it surprise you to know that Ravussin’s work does not perfectly align with Taubes’s narrative? Of course it wouldn’t.

It turns out that Dr. Ravussin has published several studies that look at Mexican Pimas and American Pimas. Although essentially genetically identical, the Mexican Pimas are much leaner and have 1/6th of the prevalence of NIDDM than their Arizonan counterparts. Why the difference? Taubes would have you believe it’s sugar, but Ravussin’s work says different. According to several of his papers, the Mexican Pimas were far more physically active, and ate a diet low in fat and high in carbohydrates and fiber from corn, wheat, and beans. Moreover, the fat the Mexican Pimas ate were largely unsaturated compared to their brothers and sisters in Arizona.(66–69)

What I imagine Taubes is thinking when quoting Ravussin: “Gosh, I know about Ravussin’s contributions to the Pima literature. I mean, he was so important that I even wanted to interview him about his work, but should I include his actual research? My story won’t be as plausible, but should I give my readers a fair interpretation of the available evidence? Nah, I’ll just say it is sugar’s fault.” Either that, or when interviewing Ravussin, Tabues hears acquires info that he can’t use because it runs contrary to the fiction Taubes is trying to craft, so he just quotes Ravussin in a very neutral way.

 * * *

Taubes makes some rather byzantine connections throughout this chapter. Take page 214 for instance where Taubes discusses a couple of anthropologists that wrote about the Pima near the turn of the 20th century. Taubes claims they were fat even back then when anthropologists were poking around their teepees:

Both Frank Russell, for instance, and a physician-turned-anthropologist named Aleš Hrdlička commented during the first years of the twentieth century on the surprising presence of obesity among the Pima, despite their extreme poverty, although almost exclusively among the older members of the tribe, and particularly the women. They “exhibit a degree of obesity,” Russell wrote, “that is in striking contrast with the ‘tall and sinewy’ Indian conventionalized in popular thought.” […] Russell suggested that some item of the diet was “markedly flesh-producing,” but without making any speculations about what it might be.

And then Taubes says “As for diabetes, if it was present among the Pima in the early years of the twentieth century, neither Russell nor Hrdlička had thought it worth mention.” This very statement is ludicrous. The only way to diagnose diabetes is a blood test, and it’s not like anthropologists were in the habit of carrying portable centrifuges, chromatography machines, ELISA equipment, sterile syringes, and vials in their backpacks around the American Southwest in 1906 and testing random natives for high HBA1c and performing OGTTs. That’s just a hunch, though. This claim is about as absurd as saying “As for microorganisms, if they were present among the Europeans in the years 1346–1353, no doctor had thought it worth mention.” There is a crude way to indicate that you might have diabetes, though, that doesn’t involve fancy equipment, but it does involve tasting someone’s urine. Again, I doubt Russell was walking around the reservations asking to taste their piss, but if Russell did drink Pima piss in the early years of the twentieth century, he had not thought it worth mention.(70,71)

Let’s unpack the rest of this mess. Now the diet of these Native Americans in early 1900 were, according to Russell, a “mixed diet in which vegetable food predominates.” Taubes uses this narrative in Good Calories, Bad Calories to conclude that a high vegetable diet makes one fat (because of the carbohydrates), but in this book it’s deployed in a much more confusing manner. The argument Taubes is trying to make here is that The Pima were fine in the early 1900s, then the white man came along with his sugar and flour in the midcentury years which correlated with increased numbers of Pimas diagnosed with diabetes. Therefore, sugar → diabetes.

However, Taubes’s overriding thesis is that sugar → diabetes → obesity → almost every modern chronic disease. The problem is that Taubes’s dumb theories don’t even make sense in the alternate reality that he’s constructed. According to Russell, the Pima were already obese before the white man’s sugar! And they could very well have had diabetes, too – there’s no way to know. The fact that diabetes was not mentioned in some turn-of-the-century anthropology texts is certainly not a diagnosis either way. So Taubes contradicts himself, but apparently is not aware that he does it because there is no attempt to square this circle.

 * * *

Taubes performs a little sleight of hand on page 223:

The vital question is: What initially triggers insulin resistance and metabolic syndrome and thus diabetes and obesity in all these populations—including the Pima and other indigenous populations, in which diabetes exploded through the populations over the course of a few generations, and those in which the prevalence has been increasing steadily over the course of half a century or more?

Did you catch that? It seems that at this point in the book Taubes has concluded that insulin resistance definitely causes obesity, and the only question now is what causes the insulin resistance? But what evidence has he provided to that effect? Chapter 10, where this quote is found, is largely about Native Americans getting fat sometime in the first half of the 20th century. He tries to pin the blame solely on sugar, but can’t really do that since the diet, lifestyle, and pretty much the entire landscape changes during that period. The mental leap that Tubes makes appears like it might have happened at the end of chapter 9 where he is claiming that not enough studies have been done to come to a conclusion. He then rhetorically asks:

So the answer to the question of whether sugar, in the form of sucrose and HFCS, is the primary cause of insulin resistance and metabolic syndrome and therefore obesity, diabetes, and heart disease is: it certainly could be.

I want to make it clear the Taubes spends quite a lot of ink in chapter 9 telling you that it is a mistake to conclude anything about sugar. Here are some choice quotes (72):

  • We’re unlikely to learn anything more definitive in the near future […]
  • [W]hat’s still needed is experiments […]
  • There is clearly a need for intervention studies […]
  • [E]very experiment can still be easily criticized as falling short of being conclusive […]
  • The studies with rodents aren’t necessarily applicable to humans.
  • [I]t’s unclear how to extrapolate from what happens in just a few months when we’re talking about conditions—metabolic syndrome, obesity, diabetes, heart disease—that develop over years […]
  • The data that would be definitive are ungettable […]
  • The kind of randomized controlled trials over the course of ten or twenty years that would truly test the hypothesis that sugar caused heart disease or diabetes […] were no different from the kind the NIH was then considering and would soon reject for the dietary-fat/cholesterol hypothesis. Such trials were certainly far beyond the budget of any single researcher or even collaboration of researchers […]
  • Thousands if not tens of thousands of subjects have to be randomized to high- and low-sugar diets and then followed for years […] Such studies are exorbitantly expensive, and few researchers in this field think they’ll ever be conducted.

Despite all this rhetoric about the need for rigorous science to come to any conclusions, Taubes apparently concludes that insulin resistance causes diabetes. When he comes to this conclusion is not exactly clear and the “definitive” scientific evidence that led him to conclusion is equally unclear, yet here we are. Who wants to bet that Taubes concludes that sugar causes insulin resistance with equally murky evidence?

 * * *

Taubes also misrepresents the Tokelau Island Migrant Study (TIMS) in this chapter. To briefly summarize, there was a group of islands in the middle of the Pacific that had not been penetrated by the “Western” diet and “Western” lifestyle until relatively recently in the 20th century. They had their share of problems such as high rates of infectious disease, but low levels of the “Western” diseases like obesity, diabetes, heart disease, etc. However, there were some of the Tokelauans that eventually emigrated to New Zealand in the 1960s and 70s, and those migrant populations ended up adopting a more Western diet, Western lifestyle, and ended up taking on Western diseases as well. Shocking, I know. There was an epidemiological study commissioned to study these populations called the TIMS.

Taubes, of course, attributes this increase in Western diseases attributable to… what else? Sugar. However, all of the evidence from the TIMS indicates that changes in lifestyle were multifactorial.

  • “Diet in New Zealand was much more diversified; though fish was still frequently eaten, immigrants also used eggs, dairy products, and red meat. Simple carbohydrate and salt intake increased while fat supplied a smaller proportion of total energy. On the whole, life for migrants was very different from that on the atolls.” (73)
  • “The migrants to New Zealand studied in Taupo in 1974/75 chose meat to supply one third of their daily energy cereals one fifth, dairy products and eggs one sixth and sugar, one seventh.” (74)
  • “The factors most likely contributing to this difference, are changes to a higher calorie, high protein diet, higher alcohol consumption, a greater weight gain and altered levels of physical activity in the migrants.” (75)
  • “Migrants had more diabetes and smoked more, drank more alcohol, and exercised less. Migrants tended to have higher levels of ‘incipient coronary disease,’ with mean cholesterol levels near those of the host New Zealand society, while non-migrant levels remain relatively low.” (76)
  • “In Tokelau, male adults engage in considerable physical activity meeting the demands of coconut harvesting and fishing in a subsistence economy. The diet while adequate is limited in variety, and alcohol is consumed in small quantities. In N.Z., the men work in factories, travel in automobiles and public transport rather than canoes […]” (77)
  • “An important part of this undesirable progression can probably be attributable to lifestyle changes which could in principle be prevented: excessive smoking and drinking, lack of exercise, unwise dietary indulgence, etc.” (78)

 * * *

This next bit is dishonest, but not exactly surprising given the track record here. On page 228 Taubes describes a visit to Africa by Dr. Hugh Trowell:

When Trowell arrived in Kenya, he would later write, hypertension and diabetes were absent. The native population was also as thin as “ancient Egyptians,” despite consuming relatively high-fat diets and suffering no shortage of food. *

There’s also a footnote to this passage:

* During World War II, according to Trowell, the British government sent a team of nutritionists to the region to learn why local Africans recruited into the British Army could not gain sufficient weight to meet army entrance requirements. “Hundreds of x-rays,” Trowell wrote, “were taken of African intestines in an effort to solve the mystery that lay in the fact that everyone knew how to fatten a chicken for the pot, but no one knew how to make Africans . . . put on flesh and fat for battle. It remained a mystery.”

Let’s deal with the claims in the main text first. The source of these claims comes from a book titled The Truth about Fiber in your Food.(79) There is no mention of anything related to the Africans having a high fat diet. In fact, it was quite the opposite. Trowell claims the Africans were not eating enough calories:

During World War II, he was aware, a team of British medical experts had been formed and sent to Africa to advise the military authorities about army diets because Africans refused to eat the number of calories that nutritionists, and Trowell himself, advised. (79)

Emphasis mine. Related to this is Tabues footnote and the bottom of the page. What’s intriguing to me is the ellipsis that marks where Taubes omitted some words. Reprinted below is the full quote (again, emphasis mine):

“Hundreds of x-rays,” he [Trowell] recalls, “were taken of African intestines in an effort to solve the mystery that lay in the fact that everyone knew how to fatten a chicken for the pot, but no one knew how to make Africans eat their caloric requirements and put on flesh and fat for battle. It remained an unsolved mystery.”

Obviously, this kind of dishonesty is troubling. The use of ellipses in writing is to omit extraneous text for overall clarity. However, by omitting these statements of caloric intake and falsely introducing the idea of Africans eating high fat diets is journalistic malfeasance. It changes the original meaning of the text to something that was clearly not intended by original author in order to support a false narrative by Taubes.

By the way, if you’re curious about the mystery of the thin Africans, the answer lies in the consumption of fiber, which is unsurprising given the title. Later in the chapter the author explains:

Africans on high fiber diets, Trowell points out, not only have colons twice the size of modern Western man, and stool weight double and transit time three times as rapid, and a low incidence of certain diseases of the colon, they have all this together with full stomachs after meals on bulky fiber-rich carbohydrates, which are digested and absorbed more slowly, allowing satiety mechanisms to operate normally to preserve normal weight throughout life, even when physical activity decreases during middle age.

 * * *

Page 236: “The simplest hypothesis—as encapsulated in Occam’s Razor—is always the most likely.”

Clearly, which is why a global conspiracy led by one man with no wealth or power to suppress high-quality nutrition science that demonstrated calories aren’t real and that unlimited amounts of bacon and lard are good for you while sugar and bread is quite literally slow-acting poison IS NOT AT ALL SIMPLE NOR LIKELY.

 * * *

At the end of the book, Taubes attempts to blame the world’s ills on sugar and trots out a small parade of chronic diseases that are apparently caused by sugar consumption. The first in this procession is gout.

Gout

Taubes starts talking about vegetarian diets for some reason. Not because they are relevant in a book about sugar, but mainly because I think Taubes must have been insulted by a vegetarian once and now hates all their smug, self-satisfied kind. On page 239 he discusses high uric acid levels, the end product of purine metabolism and one of the primary causes of gout:

As it turns out, a nearly vegetarian diet is likely to have only a very modest effect on uric acid levels […] This is why purine-free diets are no longer prescribed for the treatment of gout, as the physician and biochemist Irving Fox noted in 1984, “because of their ineffectiveness” and their “minor influence” on uric acid levels.

Vegetarian diets are not at all mentioned in the Hydrick and Fox text that Taubes cites here.(80,81) Vegan, plant-based, and meat-free are not mentioned, either. Hydrick and Fox do mention that sometimes people replace meats (which are generally high in purine, but not exclusively found in meats) with eggs and cheese under the mistaken assumption that this replacement will reduce their gout. However, eggs and cheese are high in saturated fat and cholesterol, which are contraindicated in dietary treatment of gout because hyperlipidemia is associated with the condition. H&F also note that ketosis is not at all recommended, either, because it will “elevate the serum urate level and precipitate acute gout.” To be fair, ketosis is not even mentioned in CAS, but it is usually considered to be the whole point of carbohydrate restriction. Ketosis is referred to many times in GCBC and is tacitly endorsed as a method of weight loss.

What about Taubes’s evidence showing sugar causes gout? Well, it’s pretty shoddy. Get this: first Taubes talks about how gout has increased alongside Westernization; “Westernization” in this case = sugar intake, presumably. If you think that’s conclusive evidence of sugar leading to gout, the I have some spurious correlations for you, buddy. Then Taubes mentions some research where six kids were given some fructose and ended up with high uric acid levels.(82) However, this was a study on “hereditary fructose intolerance,” which is a disease where not all the necessary enzymes to break down fructose are available which leads to an accumulation of purines. In other words, not exactly generalizable to the population at large. Still, if one eats a ton of fructose there is evidence to suggest that one may have slightly higher uric acid levels, although the effects are “minimal for healthy individuals on normal diets.”(83) Or, as Taubes puts it citing the same exact study as I just did: “likely” to cause gout.

For good measure, Taubes throws in a paper stating that hyperuricemia is associated with metabolic syndrome which Taubes never demonstrated was the result of sugar consumption — and poof! – you got yourself some Taubesian proof that sugar → gout. (84)

Hypertension

In this section Taubes does not actually make much of a positive case that sugar leads to hypertension. Instead he relies on trying to take down salt as a risk factor and hopes that he can slide sugar in to fill the void. Page 245:

For fifty years, the consensus of opinion in the medical community has been that the dietary trigger of hypertension is salt consumption. Eating too much salt raises blood pressure; hypertension is the pathological, chronic state that in turn increases risk of both heart disease and cerebrovascular disease (strokes). It’s a simple hypothesis and a concise one—and it’s all too likely wrong. But to suggest that sugar causes hypertension is to suggest that salt doesn’t (or not as much), and public-health authorities typically take umbrage. So it’s necessary to talk this through, beginning with some history.

The “history” Taubes provides here is really recycled garbage from his previous work. It has nothing to do with sugar and hypertension, of course, is primarily in the book to take up space (in my opinion), and is misleading to boot.

For instance, on page 249 Taubes claims: “As with saturated fat and heart disease, though, this salt/hypertension hypothesis has resolutely resisted confirmation in clinical trials.” He cites two systematic reviews that don’t support his statement. This first is a Cochrane review that concludes

A modest reduction in salt intake for 4 or more weeks causes significant and, from a population viewpoint, important falls in BP in both hypertensive and normotensive individuals, irrespective of sex and ethnic group. (85)

The other claims that salt reduction does not do much for people with normal blood pressure, but helps reduce blood pressure in those with hypertension:

A mean daily sodium reduction of 118 mmol/24 h for 28 days decreases BP by 3.9/1.9mm Hg in hypertensive persons. This effect indicates that reduced sodium intake may be used as a supplementary treatment in hypertension. (86)

But what of the actual research on the topic of sugar and blood pressure? Here Taubes cites a few things that aren’t definitive but hopes you’ll fill in the gaps with your imagination. Much like in movies where the actors throw a punch that doesn’t connect, you hear some Foley sound of slapping meat, and the stuntman falls dramatically to the ground it’s enough to suspend disbelief because your mind puts it all together. Except in this case, Taubes punches are miles away from the fall guy. I know, I know, my metaphors could use some work. Anyway, take this example on page 250:

Not surprisingly, there’s a long history of evidence implicating sugar—now in the laboratory and the clinic, as well as in the study of populations. As early as the 1860s, the German nutritionist Carl von Voit, a legendary figure in nutrition research, had suggested that something about eating carbohydrates made the human body retain water […]

Ah, so you’re supposed to believe something causes people to retain water. Presumably that something is actually sugar, and the water volume you retain is enough to make you chronically hypertensive, but you have to fill in those gaps yourself. Additionally, the source material is a bit more nuanced than Taubes would have you believe:

It has been known for many years that high caloric, high carbohydrate diet leads to notable accumulation of water in the tissues. However, the carbohydrate content of the diet is not the sole factor determining water balance. In the first place, the protein content of the diet, too, has a definite effect on water balance in that high protein content favors water elimination. Furthermore, other than dietary factors may play a role in water exchange, and may compensate or even reverse the effect of diet. Thus, one of Newburgh and Johnston’s own cases retained, instead of lost, water on a low carbohydrate, low caloric diet. (20)

Taubes eventually gets to some positive evidence for a link between sugar and hypertension, though it’s rather murky and kind of contradicts his point about sodium. It turns out that hyperinsulinemia may lead to an increase in blood pressure by increasing sodium retention.(87–89) So what causes hyperinsulinemia? The cited literature makes the case for insulin resistance as the primary factor. Taubes would have you believe that sugar intake causes insulin resistance and diabetes, but the evidence for that claim just is not very abundant nor is it mentioned as a risk factor in the texts. However, you might imagine someone who is constantly swilling sodas all day, every day to have elevated insulin levels.

And that’s pretty much it for the evidence that sugar leads to hypertension. Compelling, right?

Cancer

Again, here Taubes spends several pages on the proposition that Westernization leads to cancer, and in Taubes’s mind Westernization = sugar and he hopes you’ll think so, too. When discussing cancer deaths he even drags out our old friend tobacco to attempt to blame sugar: “Some of this, of course, was due to the dramatic increase in lung cancers that in turn was a product of the epidemic cigarette smoking that was aided and abetted by sugar.” But aside from the general “Western” diet and lifestyle that is made up of hundreds of factors, what direct evidence does Taubes provide that sugar → cancer?

Well, none. Seriously. Taubes provides no actual evidence that sugar consumption leads to cancer. The best he can do is very murky indirect evidence that insulin resistance and diabetes are associated with cancer. He concludes the cancer section with this statement:

If the sugars we consume—sucrose and HFCS specifically—cause insulin resistance, then they are prime suspects for causing cancer as well, or at the very least promoting its growth.

That’s a big IF, and one that Taubes has not demonstrated.

Dementia

This is the same scenario as the above. No actual evidence that sugar consumption leads to dementia is presented, only a series of associations like Alzheimer’s and dementia are associated with other diseases like diabetes, metabolic syndrome, and obesity. So if sugar consumption is the primary cause of obesity and diabetes then it may also contribute to dementia. Again, you must take it on faith that these associations are actually causations and that sugar actually is the primary cause of obesity, diabetes, and metabolic syndrome to the exclusion of other risk factors.

Conclusion

What did we learn after reading The Case Against Sugar? We learned that Taubes is not presenting a good faith interpretation of the evidence. If you removed the misinterpretations and the non-sequiturs like low-fat and tobacco use you would basically have about as much as you could find for free in one of those reviews I linked to in the introduction.

cloud

References

  1. Emerson H, Larimore L. Diabetes mellitus: A contribution to its epidemiology based chiefly on mortality statistics. Arch Intern Med [Internet]. 1924 Nov [cited 2015 Oct 11];34(5):585–630. Available from: http://dx.doi.org/10.1001/archinte.1924.00120050002001
  2. Weiffenbach JM, editor. Taste and Development: The Genesis of Sweet Preference [Internet]. Bethesda, MD: U.S. Dept. of Health, Education, and Welfare, Public Health Service, National Institutes of Health; 1977 [cited 2017 Jan 9]. Available from: https://catalog.hathitrust.org/Record/002479177
  3. Proctor R. Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition. University of California Press; 2011. 737 p.
  4. Weiss FJ. Tobacco and Sugar [Internet]. 1950 [cited 2017 Jan 9]. Available from: https://www.industrydocumentslibrary.ucsf.edu/tobacco/docs/#id=jmvc0212
  5. Charles RH, Bose RKC, Bose CL, Chakravarti S, Roy RD, Sandwith FM. Discussion On Diabetes In The Tropics. Opening Papers. Br Med J [Internet]. 1907 Oct [cited 2015 Oct 11];2(2442):1051–64. Available from: http://www.jstor.org/stable/20296272
  6. Allen FM. Studies concerning glycosuria and diabetes [Internet]. W. M. Leonard; 1913. Available from: http://books.google.com/books?id=aDcSAAAAYAAJ
  7. Himsworth HP. Recent Advances in the Treatment of Diabetes. Lancet [Internet]. 1931 Oct;218(5644):978–9. Available from: http://linkinghub.elsevier.com/retrieve/pii/S0140673600859474
  8. Young FG, Richardson KC. Discussion on the cause of diabetes. Proc R Soc Med [Internet]. 1949 May;42(5):321–30. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18149426
  9. Yudkin J. Pure, White and Deadly. Penguin; 1972.
  10. Mann GV, Shaffer RD, Anderson RS, Sandstead HH, Prendergast H, Mann JC, et al. Cardiovascular disease in the masai. J Atheroscler Res [Internet]. 1964 Jul [cited 2013 Aug 6];4(4):289–312. Available from: http://www.sciencedirect.com/science/article/pii/S0368131964800417
  11. SCHWARTZ J. Teeth of the Masai; second report. East Afr Med J [Internet]. 1952 Jan [cited 2017 Jan 21];29(1):27–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14926670
  12. SCHWARTZ J. The teeth of the Masai. J Dent Res [Internet]. 1946 Feb [cited 2017 Jan 21];25:17–20. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21015792
  13. McKAY DH. Venereal disease in Masai; a field survey–June and July 1950. East Afr Med J [Internet]. 1950 Nov [cited 2017 Jan 21];27(11):451–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14802312
  14. Also, I know that “Maasai” is an alternate spelling. I tried that in PubMed, too, but got far fewer hits.
  15. HIMSWORTH HP. Diet and the incidence of diabetes mellitus. Clin Sci. 1935;2:117–48.
  16. INSULL W, OISO T, TSUCHIYA K. Diet and Nutritional Status of Japanese. Am J Clin Nutr. 1968;21(7):753–77.
  17. Silver S, Bauer J. Obesity, constitutional or endocrine? Am J Med Sci. 1931;181:769–77.
  18. BAUER J. OBESITY. Arch Intern Med [Internet]. 1941 May 1;67(5):968. Available from: http://archinte.jamanetwork.com/article.aspx?doi=10.1001/archinte.1941.00200050076006
  19. WILDER RM. DISEASES OF METABOLISM AND NUTRITION. Arch Intern Med [Internet]. 1938 Feb 1;61(2):297. Available from: http://archinte.jamanetwork.com/article.aspx?doi=10.1001/archinte.1938.00180080139009
  20. Rony HR. Obesity and Leanness [Internet]. Lea & Febiger; 1940 [cited 2017 Mar 10]. Available from: https://books.google.com/books/about/Obesity_and_Leanness.html?id=SSm0AAAAIAAJ
  21. Hetherington AW, Ranson SW. Experimental Hypothalamico-Hypophyseal Obesity in the Rat. Exp Biol Med [Internet]. 1939 Jun;41(2):465–6. Available from: http://ebm.sagepub.com/content/41/2/465.short
  22. Hetherington AW, Ranson SW. The spontaneous activity and food intake of rats with hypothalamic lesions. Am J Physiol [Internet]. 1942 Jun;136(4):609–17. Available from: http://ajplegacy.physiology.org/content/136/4/609.short
  23. Mayer J. Decreased Activity and Energy Balance in the Hereditary Obesity-Diabetes Syndrome of Mice. Science (80- ) [Internet]. 1953 May [cited 2013 Aug 6];117(3045):504–5. Available from: http://www.jstor.org/stable/1680214
  24. ALONSO LG, MAREN TH. Effect of food restriction on body composition of hereditary obese mice. Am J Physiol [Internet]. 1955 Nov;183(2):284–90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/13268678
  25. Mrosovsky N. Lipid Programmes and Life Strategies in Hibernators. Am Zool [Internet]. 1976;16(4):685–97. Available from: http://www.jstor.org/stable/3882135
  26. BROOKS CM, LAMBERT EF. A study of the effect of limitation of food intake and the method of feeding on the rate of weight gain during hypothalamic obesity in the albino rat [Internet]. Vol. 147, American Journal of Physiology. American Physiological Society; 1946 [cited 2017 Mar 13]. 695-707 p. Available from: https://www.cabdirect.org/cabdirect/abstract/19471400649
  27. Blackburn H. Ancel Keys [Internet]. Available from: http://www.sph.umn.edu/epi/history/keys/
  28. Page IH, Stare FJ, Corcoran AC, Pollack H, Wilkinson CFJ. Atherosclerosis and the fat content of the diet. Circulation [Internet]. 1957 Aug;16(2):163–78. Available from: http://www.ncbi.nlm.nih.gov/pubmed/13447160
  29. They weren’t. I’m not going to re-litigate all that nonsense; I have written many a post on Taubes’s misrepresentations and lies.
  30. Frantz IDJ, Dawson EA, Ashman PL, Gatewood LC, Bartsch GE, Kuba K, et al. Test of effect of lipid lowering by diet on cardiovascular risk. The Minnesota Coronary Survey. Arter Thromb Vasc Biol [Internet]. 1989 Feb;9(1):129–35. Available from: http://www.ncbi.nlm.nih.gov/pubmed/2643423
  31. AHA Conference Report on Cholesterol. Circulation [Internet]. 1989 Sep 1;80(3):715–48. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.80.3.715
  32. Van Horn L, Johnson RK, Flickinger BD, Vafiadis DK, Yin-Piazza S. Translation and Implementation of Added Sugars Consumption Recommendations: A Conference Report From the American Heart Association Added Sugars Conference 2010. Circulation [Internet]. 2010 Dec 7;122(23):2470–90. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/CIR.0b013e3181ffdcb0
  33. Johnson RK, Appel LJ, Brands M, Howard B V., Lefevre M, Lustig RH, et al. Dietary Sugars Intake and Cardiovascular Health: A Scientific Statement From the American Heart Association. Circulation [Internet]. 2009 Sep 15;120(11):1011–20. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/CIRCULATIONAHA.109.192627
  34. Oken E, Radesky JS, Wright RO, Bellinger DC, Amarasiriwardena CJ, Kleinman KP, et al. Maternal fish intake during pregnancy, blood mercury levels, and child cognition at age 3 years in a US cohort. Am J Epidemiol [Internet]. 2008 May 15 [cited 2013 Sep 17];167(10):1171–81. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2590872&tool=pmcentrez&rendertype=abstract
  35. Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, Franch HA, et al. Diet and Lifestyle Recommendations Revision 2006 A Scientific Statement From the American Heart Association Nutrition Committee. Circulation [Internet]. 2006 Jul [cited 2014 May 27];114(1):82–96. Available from: http://circ.ahajournals.org/content/114/1/82
  36. Dhingra R, Sullivan L, Jacques PF, Wang TJ, Fox CS, Meigs JB, et al. Soft Drink Consumption and Risk of Developing Cardiometabolic Risk Factors and the Metabolic Syndrome in Middle-Aged Adults in the Community. Circulation [Internet]. 2007 Jul 9;116(5):480–8. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/CIRCULATIONAHA.107.689935
  37. Kumanyika SK, Obarzanek E, Stettler N, Bell R, Field AE, Fortmann SP, et al. Population-Based Prevention of Obesity: The Need for Comprehensive Promotion of Healthful Eating, Physical Activity, and Energy Balance: A Scientific Statement From American Heart Association Council on Epidemiology and Prevention, Interdisciplinary Commi. Circulation [Internet]. 2008 Jul 22;118(4):428–64. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/CIRCULATIONAHA.108.189702
  38. Howard B V. Sugar and Cardiovascular Disease: A Statement for Healthcare Professionals From the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation [Internet]. 2002 Jul 23;106(4):523–7. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.0000019552.77778.04
  39. SoRelle R. Good Blood Sugar Control Keeps Patients Healthier for Years. Circulation [Internet]. 2000 Mar 7;101(9):e9013–e9013. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.101.9.e9013
  40. Wylie-Rosett J. Fat Substitutes and Health: An Advisory From the Nutrition Committee of the American Heart Association. Circulation [Internet]. 2002 Jun 11;105(23):2800–4. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.0000019402.35632.EB
  41. Libby P. Diabetic Macrovascular Disease: The Glucose Paradox? Circulation [Internet]. 2002 Nov 26;106(22):2760–3. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.0000037282.92395.AE
  42. Krauss RM, Eckel RH, Howard B, Appel LJ, Daniels SR, Deckelbaum RJ, et al. AHA Dietary Guidelines: Revision 2000: A Statement for Healthcare Professionals From the Nutrition Committee of the American Heart Association. Stroke [Internet]. 2000 Nov;31(11):2751–66. Available from: http://stroke.ahajournals.org/content/31/11/2751.short
  43. Assmann G, Carmena R, Cullen P, Fruchart J-C, Jossa F, Lewis B, et al. Coronary Heart Disease: Reducing The Risk : A Worldwide View. Circulation [Internet]. 1999 Nov 2;100(18):1930–8. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.100.18.1930
  44. Kromhout D. Prevention of Coronary Heart Disease by Diet and Lifestyle: Evidence From Prospective Cross-Cultural, Cohort, and Intervention Studies. Circulation [Internet]. 2002 Feb 19;105(7):893–8. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/hc0702.103728
  45. Taegtmeyer H. Insulin Resistance and Atherosclerosis : Common Roots for Two Common Diseases? Circulation [Internet]. 1996 May 15;93(10):1777–9. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.93.10.1777
  46. Kendall FE. Does the Pattern of Carbohydrate Nutrition Hold a Clue to Atherosclerosis? Circulation [Internet]. 1967 Sep 1;36(3):340–4. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.36.3.340
  47. Keys A. Prevention of Coronary Heart Disease Official Recommendations from Scandinavia. Circulation [Internet]. 1968 Aug 1;38(2):227–8. Available from: http://circ.ahajournals.org/cgi/doi/10.1161/01.CIR.38.2.227
  48. Hess J. Harvard’s Sugar Pushing Nutritionist. The Saturday Review [Internet]. 1978 Aug;10–4. Available from: https://www.unz.org/Pub/SaturdayRev-1978aug-00010
  49. Kearns CE, Schmidt LA, Glantz SA. Sugar Industry and Coronary Heart Disease Research. JAMA Intern Med [Internet]. 2016;9:1–19. Available from: http://archinte.jamanetwork.com/article.aspx?doi=10.1001/jamainternmed.2016.5394
  50. Error in Acknowledgments. JAMA Intern Med [Internet]. 2016 Nov 1;176(11):1729. Available from: http://archinte.jamanetwork.com/article.aspx?doi=10.1001/jamainternmed.2016.6774
  51. Multiple Risk Factor Intervention Trial [MRFIT] Research Group. Multiple risk factor intervention trial. Risk factor changes and mortality results. Multiple Risk Factor Intervention Trial Research Group. JAMA [Internet]. 1982 Sep;248(12):1465–77. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7050440
  52. Lundberg GD. MRFIT and the Goals of The Journal. JAMA J Am Med Assoc [Internet]. 1982 Sep 24;248(12):1501. Available from: http://jama.jamanetwork.com/article.aspx?doi=10.1001/jama.1982.03330120059033
  53. Dolecek TA, Milas NC, Van Horn L V, Farrand ME, Gorder DD, Duchene AG, et al. A long-term nutrition intervention experience: lipid responses and dietary adherence patterns in the Multiple Risk Factor Intervention Trial. J Am Diet Assoc [Internet]. 1986 Jun;86(6):752–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/3519737
  54. Benfari RC. The multiple risk factor intervention trial (MRFIT). Prev Med (Baltim) [Internet]. 1981 Jul;10(4):426–42. Available from: http://linkinghub.elsevier.com/retrieve/pii/0091743581900591
  55. Van Horn L, Dolecek TA, Grandits GA, Skweres L. Adherence to dietary recommendations in the special intervention group in the Multiple Risk Factor Intervention Trial. Am J Clin Nutr [Internet]. 1997;65(1 Suppl):289S–304S. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8988943
  56. Or at least it was supposed to be.
  57. The lipid research clinics coronary primary prevention trial results: I. reduction in incidence of coronary heart disease. JAMA [Internet]. 1984 Jan [cited 2014 Mar 7];251(3):351–64. Available from: http://dx.doi.org/10.1001/jama.1984.03340270029025
  58. The lipid research clinics coronary primary prevention trial results: II. the relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA [Internet]. 1984 Jan [cited 2014 Mar 7];251(3):365–74. Available from: http://dx.doi.org/10.1001/jama.1984.03340270043026
  59. Howard B V, Manson JE, Stefanick ML, Beresford SA, Frank G, Jones B, et al. Low-fat dietary pattern and weight change over 7 years: the Women’s Health Initiative Dietary Modification Trial. JAMA [Internet]. 2006 Jan;295(1):39–49. Available from: http://jama.jamanetwork.com/data/Journals/JAMA/5006/JOC50164.pdf
  60. Prentice RL, Thomson CA, Caan B, Hubbell FA, Anderson GL, Beresford SAA, et al. Low-Fat Dietary Pattern and Cancer Incidence in the Women’s Health Initiative Dietary Modification Randomized Controlled Trial. J Natl Cancer Inst [Internet]. 2007 Oct [cited 2014 May 27];99(20):1534–43. Available from: http://jnci.oxfordjournals.org/content/99/20/1534
  61. Hooper L, Summerbell CD, Thompson R, Sills D, Roberts FG, Moore HJ, et al. Reduced or modified dietary fat for preventing cardiovascular disease. In: The Cochrane Collaboration, editor. Chichester, UK: John Wiley & Sons, Ltd; 2012 [cited 2014 Mar 15]. Available from: http://doi.wiley.com/10.1002/14651858.CD002137.pub3
  62. Sugar Research Foundation Inc. Some facts about the sugar research foundation, Inc. and its prize award program. New York; 1945.
  63. Taubes G. Do We Really Know What Makes Us Healthy? The New York Times Magazine. 2007 Apr 11;52(L).
  64. Hrdlička A. Notes on the Pima of Arizona. Am Anthropol [Internet]. 1906;8(1):39–46. Available from: http://www.jstor.org/stable/659164
  65. Adams CM, Bridgforth EB, Dalton E, Darby WJ, Efner JA, Houk N, et al. A study of the dietary background and nutriture of the Navajo Indian. J Nutr [Internet]. 1956 Nov [cited 2017 Apr 17];60(Suppl 2):1–85. Available from: http://jn.nutrition.org/content/60/2_Suppl/63.extract
  66. Schulz LO, Bennett PH, Ravussin E, Kidd JR, Kidd KK, Esparza J, et al. Effects of traditional and western environments on prevalence of type 2 diabetes in Pima Indians in Mexico and the U.S. Diabetes Care. 2006;29(8):1866–71.
  67. Ravussin E, Valencia ME, Esparza J, Bennett PH, Schulz LO. Effects of a Traditional Lifestyle on Obesity in Pima Indians. Diabetes Care [Internet]. 1994 Sep 1;17(9):1067–74. Available from: http://care.diabetesjournals.org/cgi/doi/10.2337/diacare.17.9.1067
  68. Esparza-Romero J, Valencia ME, Martinez ME, Ravussin E, Schulz LO, Bennett PH. Differences in insulin resistance in Mexican and U.S. Pima Indians with normal glucose tolerance. J Clin Endocrinol Metab. 2010;95(11):358–62.
  69. Valencia ME, Bennett PH, Ravussin E, Esparza J, Fox C, Schulz LO. The Pima Indians in Sonora, Mexico. Nutr Rev. 1999;57(5 Pt 2):S55-NaN-S58.
  70. Russell F. The Pima Indians [Internet]. 1908. 387 p. (Annual report). Available from: https://books.google.com/books?id=vu0NAAAAIAAJ
  71. Although Russell did write on page 459 that “Food products collected at low tide, especially mussels and clams, were talked to, so that they would not bring sickness upon those eat ing them. If a person took tobacco just after eating mussels he would be. poisoned and was sure to die unless small cuts were made on top of his head and urine poured into them.;
  72. Note: two of these quotes are actually quotes of people Taubes is quoting, but nevertheless he is clearly promoting the ideas.
  73. Joseph JG, Prior IAM, Salmond CE, Stanley D. Elevation of systolic and diastolic blood pressure associated with migration: The Tokelau Island migrant study. J Chronic Dis [Internet]. 1983 Jan [cited 2017 Apr 13];36(7):507–16. Available from: http://linkinghub.elsevier.com/retrieve/pii/0021968183901285
  74. Harding WR, Russell CE, Davidson F, Prior IAM. Dietary surveys from the Tokelau Island migrant study. Ecol Food Nutr [Internet]. 1986 Nov [cited 2017 Apr 17];19(2):83–97. Available from: http://www.tandfonline.com/doi/abs/10.1080/03670244.1986.9990951
  75. Østbye T, Welby TJ, Prior IAM, Salmond CE, Stokes YM. Type 2 (non-insulin-dependent) diabetes mellitus, migration and westernisation: The Tokelau Island Migrant study. Diabetologia [Internet]. 1989 Aug;32(8). Available from: http://link.springer.com/10.1007/BF00285332
  76. Tokelau Island Studies « Heart Attack Prevention [Internet]. [cited 2015 Feb 16]. Available from: http://www.epi.umn.edu/cvdepi/study-synopsis/tokelau-island-studies/
  77. Stanhope JM, Sampson VM, Prior IAM. The Tokelau island migrant study: Serum lipid concentrations in two environments. J Chronic Dis [Internet]. 1981 Jan [cited 2017 Apr 13];34(2–3):45–55. Available from: http://linkinghub.elsevier.com/retrieve/pii/0021968181900503
  78. Howden-Chapman P, Woodward A, Wellington School of Medicine. The health of Pacific societies: Ian Prior’s life and work: A celebration at the Wellington School of Medicine [Internet]. Steele Roberts; 2001 [cited 2017 May 30]. 112 p. Available from: http://catalogue.nla.gov.au/Record/849782
  79. Galton L. The truth about fiber in your food [Internet]. Crown Publishers; 1976 [cited 2017 Jul 15]. 246 p. Available from: http://agris.fao.org/agris-search/search.do?recordID=US201300529282
  80. By the way, why does Taubes only mention Fox and not Constance Hydrick, who is the lead author of the paper anyway?
  81. Hydrick C, Fox I. Nutrition and Gout. In: Olson RE, Broquist HP, Chichester CO, Darby WJ, Kolbye AC, Stalvey RM, editors. Nutrition Reviews’ Present Knowledge in Nutrition. 5th ed. Washington, D.C.: Nutrition Foundation; 1984. p. 740–56.
  82. Perheentupa J, Raivio K. FRUCTOSE-INDUCED HYPERURICÆMIA. Lancet [Internet]. 1967 Sep;290(7515):528–31. Available from: http://linkinghub.elsevier.com/retrieve/pii/S0140673667904941
  83. Mayes PA. Intermediary metabolism of fructose. Am J Clin Nutr [Internet]. 1993 Nov;58(5 Suppl):754S–765S. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8213607
  84. Reaven GM. The kidney: an unwilling accomplice in syndrome X. Am J Kidney Dis [Internet]. 1997 Dec;30(6):928–31. Available from: http://linkinghub.elsevier.com/retrieve/pii/S0272638697901062
  85. He FJ, Li J, MacGregor GA. Effect of longer-term modest salt reduction on blood pressure. In: The Cochrane Collaboration, He FJ, editors. Chichester, UK: John Wiley & Sons, Ltd; 2013 [cited 2013 Jun 18]. Available from: http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0013125/
  86. Graudal NA, Galløe AM, Garred P. Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: A meta-analysis. JAMA [Internet]. 1998 May [cited 2014 Mar 7];279(17):1383–91. Available from: http://dx.doi.org/10.1001/jama.279.17.1383
  87. Landsberg L. Diet, obesity and hypertension: an hypothesis involving insulin, the sympathetic nervous system, and adaptive thermogenesis. Q J Med [Internet]. 1986 Dec;61(236):1081–90. Available from: http://www.ncbi.nlm.nih.gov/pubmed/3310065
  88. DeFronzo RA. Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. J Cardiovasc Pharmacol [Internet]. 1992;20 Suppl 1:S1-16. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1284137
  89. DeFronzo RA. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidaemia and atherosclerosis. Neth J Med [Internet]. 1997 May;50(5):191–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/9175399

 

Good Calories, Bad Calories: A Critical Review; Chapter 23 – The Fattening Carbohydrate Disappears

 

cover

Introduction

This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

In this particular chapter Taubes attempts to make the case that the notion that low-carb diets were optimal for nearly everyone was pretty much settled science, until a cabal of highly influential obesity researchers decide to deliberately and systematically bury the “truth.”

Tabues on page 424

[A] generation of obesity authorities were determined to dismiss the practical significance of carbohydrate-restricted diets, they dismissed the potential theoretical significance at the same time. Obesity researchers today say they still have no hypothesis of weight regulation that can explain obesity and leanness, let alone account for a century of paradoxical observations.

Let’s explore some of his evidence for this consipracy.

 

The Fat Mafia

One thing I have discovered while fact-checking this book is that often Taubes will cite some text as evidence for a claim; sometimes it actually substantiates the claim and sometimes it does not. But even when it does support a claim it’s often useful to read the entire document for context. Frequently, all or part of the rest of the cited text is actually contrary to much of what Taubes says. Of course, rarely is this contrary evidence mentioned. You can call it the suppression of evidence or cherry picking. I’ve even heard the term “Occam’s Broom” (sweeping inconvenient data under the carpet). Here is one such example. The opening paragraph of chapter 23 discusses a portion of what Taubes seems to believe is a cataclysmic event in the history of nutrition: The McGovern Committee on Nutrition and Human Needs.

The tenor of the hearing was inquisitorial, and a pithy condemnation of Atkins and his diet by the Harvard nutritionist Fred Stare was read into the record by Senator Charles Percy of Illinois (Stare did not attend). “The Atkins diet is nonsense,” Stare declared. “Any book that recommends unlimited amounts of meat, butter and eggs, as this does, in my opinion is dangerous. The author who makes the suggestion is guilty of malpractice.”

This is a completely legitimate quote, at least according to the transcripts. But the quote is not what I want to explore; it’s everything surrounding it. In particular Dr. Atkins himself testifies on behalf of his 1972 diet book titled Dr. Atkins’ Diet Revolution: The High Calorie Way to Stay Thin Forever. I haven’t read it, to be honest, but apparently in the book he argues that counting calories is a hoax.1 However, under oath he walks that back.2 Below is a smattering of what he says:

[When confronted with a statement mentioning that a majority of human beings remain lean on diets extremely high in carbohydrate and correspondingly low in fat in Asia and Africa] Is this not explained by the low total caloric intake of these cultures?

[Talking about his own diet] The control of pathologic hunger patterns as well as the increased satiety value of this diet do, in general, lead to a significant decrease in caloric consumption. This, indeed, represents the principal advantage the diet provides […]

[When asked if calorie reduction for weight loss is a hoax] No, clearly not. I would never deny that a person who had the stomach for it could lose weight by cutting calories. That would be sheer nonsense.

Again, I haven’t read Dr. Atkins’s infamous treatise, but whatever he wrote he appears to be “clarifying” his position to some degree to indicate that low-CHO diets are really a means of achieving the caloric deficit that would lead to weight loss.

If anyone is wondering why I bring this up it’s because Dr. Atkins is considered The Godfather of the low-cab diet by many, including Taubes. Indeed Taubes’s theories on nutrition are clearly derived from Atkins and his books. And if you have read GCBC or any of Taubes’s other writings on nutrition you will be aware that one of Taubes’s central (and controversial) theories is that calories are unconnected to weight loss or gain; the real culprit is the carbohydrate. However, any mention otherwise, especially from The Godfather himself, is scrubbed.

* * *

The next page is another example of Occam’s Broom. I’m going to quote a bit more text here than usual because there’s some unpacking to do, but starting on page 405:

Three years later, in July 1976, McGoverrn’s committee returned to the subject of diet and disease in the hearings that would lead, a half year later still, to the publication of Dietary Goals for the United States. The first witness was Assistant Secretary of Health Theodore Cooper, who repeatedly emphasized the need for further research to establish reliable knowledge about the diet-disease connection. McGovern and his fellow congressmen, however, wanted to tell the American public something more definitive, so McGovern asked Cooper if he could, at least, agree with the proposition that “overconsumption may be as serious a problem of nutrition as underconsumption.”

“Particularly overconsumption of the wrong things,” Cooper replied. “Very often in the poor we see people who are plump who might be called obese, and people would then conclude that they do not have a deficiency because they look rotund, healthy in one sense of the word. But it is true that the consumption of high carbohydrate sources with the induction of obesity constitutes a very serious public health problem in the underprivileged and economically disadvantaged. I would agree with that.”

This response seems clear enough: the overconsumption of “high carbohydrate sources”-a phrase used to describe carbohydrate-dense starches and refined carbohydrates rather than leafy green vegetables and fruits-was associated with obesity in the poor, and perhaps even the cause. McGovern then asked Cooper to provide a “general rule of thumb” about eating habits that would help prevent disease and lengthen our lives, and Cooper reluctantly agreed to do so.

“What kinds of foods in general should we be consuming less of and what should we be eating more of?” McGovern asked.

“I think what we need to consider doing is to reduce our total fat intake,” Cooper replied. “Fat adds a caloric substance-almost twice as much-nine calories per gram-as compared to sugar. I think in order to have an effective reduction in weight and realignment of our composition we have to focus on reducing fat intake.”

With that answer, Cooper had contradicted himself, and the conventional wisdom on diet and health in America had shifted. The problem was no longer overconsumption of high-carbohydrate sources, but the overconsumption of fatty foods. And if Cooper realized that reducing our total fat intake meant increasing our consumption of carbohydrates, he neglected to say so.

Can’t you feel the smugness dripping off the page with that last sentence? I imagine Taubes made this face after typing the period:

smug face

Okay, let’s unpack this a little. When reading the above passage you may get the impression that Dr. Cooper looks like a jackass because he immediately contradicted himself, while the rest of the committee is blithely unaware of the incongruity. But nothing gets past Taubes, right? He is here to shed a light on these ignoramuses that made us all fat and sick. First off, let’s go back and look at the references section.

chapter 23 refs

So when McGovern asked Cooper about overconsumption in the testimony transcript it’s found on pages 9 and 10. When McGovern asks Dr. Cooper about the rule of thumb it’s found on pages 19 and 20. So there’s a FULL 10 PAGES OF COOPER’S TESIMONY that is concealed, in which Cooper discusses a number of public health and nutrition concerns including malnutrition, prenatal nutrition, lipids and atherosclerosis, the importance of exercise, etc. Moreover, Cooper’s response to the rule-of-thumb question is slightly more verbose that what Taubes elects to quote. And by “slightly” I mean “considerably.”

Here’s a bit more of Cooper’s response to McGovern’s rule-of-thumb question:

Well my first advice would be to eat less. As a general rule, I think the American public eats too much. With very few exceptions, and there are people obviously who would suffer from a weight reduction, most of us would not be terribly affected if we could reduce our total caloric intake.

[…]

I personally believe there is some benefit to reducing our preoccupation with sweet things.

[…]

I would recommend an appropriate amount of protein intake which we could give some recommendations to by group and target populations. A healthy intake of fresh fruits and vegetables with substantial fiber content.

[…]

It is very attractive for me to say stop eating commercially prepared foods.

Taubes suppresses all of this, of course, because it’s Taubes’s goal to make Cooper and the rest of the government look like clueless hacks. So instead he provides the most uncharitable characterization of Cooper’s testimony.

For that last sentence… Taubes uses a tried and true tactic oft-used by the more disingenuous low-carbers: intentionally conflating total and relative amounts. For example, it has often been said that once Big Brother began recommending “low-fat” diets the obsequious populace complied: eating less fat, more carbohydrates, and getting fat as a result. However, since 1971 Americans have been steadily eating more daily calories. In terms of macronutrients we have been eating more of everything. More CHOs, more protein, more fat, but we increased our CHO intake slightly more than we have increased our fat and protein intake. So it might appear that we have decreased our fat intake and increased our CHO intake if you look at only the % change in macronutrient intake, when in reality TOTAL FAT ACTUALLY INCREASED & TOTAL CALORIES INCREASED. Make sense?

So back to that last sentence: “And if Cooper realized that reducing our total fat intake meant increasing our consumption of carbohydrates, he neglected to say so.” Reducing total fat does not mean increasing total carbohydrates. One could reduce or elevate total fat consumption completely independent of whether or not one increased or decreased total CHOs. Or total protein for that matter. However, if one adjusted their proportion of calories from fat, that may affect their proportion of calories from carbohydrate. Or it might not affect it at all, depending on how one’s protein intake is adjusted. It’s the difference between relative amounts and actual amounts. And if you were to ask me the former is rarely more relevant than the latter.

So to summarize, Cooper neglected to mention that reducing total fat intake would necessarily lead to an increase in carbohydrate consumption because he has a few brain cells to rub together.

* * *

On pages 407-408 Taubes discusses an obesity symposium held on the other side of the pond way back in the Summer of ’69. A text was published on the proceedings of this symposium.3 If you read through the text you will find it a relatively sober look at obesity that discusses its etiology and treatment. Some time is clearly spent in the text examining the multi-factorial causes of obesity: genetic, environmental, psychological, metabolic, and social & lifestyle factors. But Taubes doesn’t want to mention any of this to his readers; it’s too messy and confusing and doesn’t exactly fit with the narrative he is trying to craft. So instead he tries to find a sentence or two that would make his audience believe that all those smart Englishmen got together and concluded the carbohydrate was the scourge of the obesity epidemic.

At the London conference, Howard reviewed the literature on carbohydrate restriction dating back to Banting and concluded that this was the only effective method to induce and maintain weight loss. “A common feature of all who have written on the subject,” he said, is “that the patient’s hunger is satisfied whilst on a diet high in carbohydrate of the same caloric value, patients complain of hunger.”

Again, legitimate quote, but removed from a broader context because the broader context is unkind to Taubes. Elsewhere in Dr. Alan Howard’s presentation he effectively disproves Taubes’s entire thesis. There’s even a nice graph that Taubes would not want you to see.

Howard 103

And on page 103 Howard states

In conclusion, therefore, one can state that there is no evidence that over a long period, fat, carbohydrate and protein calories are substantially different, and the loss in body weight still depends on the total number of calories consumed.

I could quote endlessly from the proceedings that contrast starkly with how Taubes presents the symposium specifically and his arguments generally, but in the interest of readability I will refrain. I am not going to say that sugars and other carbohydrates can’t play a role in the development of obesity, but it’s certainly not nearly as one-dimensional as Taubes makes it out to be.

* * *

On pages 412-413, Taubes discusses a paper by Edgar Gordon, MD that influenced Atkins:

Gordon’s diet, as described in JAMA, began with a forty-eight hour fast-“not to produce a spectacular loss of weight, but rather to break a metabolic pattern of augmented lipogenesis”-and then allowed protein and fat as desired but limited carbohydrates to minimal fruits, green vegetables, and a half-slice of bread every day. “The total caloric value is quite high in terms of reducing diets,” wrote Gordon. Atkins later said his attention was caught by Gordon’s observation that his subjects lost weight without ever complaining of hunger.

This is a minor point so skip over it if you wish, but I’d like to note some things about the diet. First, it does not allow protein and fat as desired. It’s actually very specific in the amounts you are allowed (100 grams of protein, 80 grams of fat, and 50 grams of CHO totaling 1,320 calories daily), and it’s somewhat specific in the types of fat (emphasis is placed on polyunsaturated, while saturated fat is very limited – butter is a contraindicated food in this diet).4 I’m not sure where Taubes gets this “protein and fat as desired” claim, but it’s possible he misinterpreted a sentence in the paper. For instance, Gordon is a big proponent of having several meals (or “feedings”) per day as opposed to one or two larger meals. He explicitly stated that the prescribed diet be divided into at least six meals per day or more if desired. Maybe Taubes got confused and thought more meals = unlimited fat and protein.

A couple other things worth noting about the diet is that patients were also prescribed triiodothyronine (a lipolytic hormone) 3X daily in addition to diuretics: either injections of mercurials or daily administration of ammonium chloride.

* * *

As I mentioned in the intro, essentially this chapter attempts to make the case that the nutrition “elite” are terrified of the idea of low-carbohydrate diets so they systematically attempt to invalidate the idea by subtly impugning low-carb diets in obscure medical texts. If you think that idea is absurd then you’re not alone. Taubes however, seems to think it’s perfectly reasonable.

One example of this is page 420 where Taubes writes:

He [George Bray] dismissed as irrelevant the work of those investigators who did actively study the dietary treatment of obesity, like Charlotte Young, who gave the presentation on dietary therapy at the NIH conference on obesity that Bray organized and chaired in 1973. Young specialized in the study of body composition, and she had been studying diets and obesity at Cornell since 1950. In the official NIH report on the conference, Obesity in Perspective, Bray treated her discussion of carbohydrate-restricted diets as naïve and of no consequence. In the book he coedited the year after the conference, Treatment and Management of Obesity, Young’s observations on carbohydrate- restricted diets are described as still requiring further “confirmation before they can be fully accepted …. The question of the value of a low carbohydrate diet and its effectiveness in weight loss is still unresolved.” In The Obese Patient, published three years after the NIH conference, Bray wrote of Young’s studies, “The data are suggestive and require careful replication with larger groups of individuals.”

The first cited text is page 43 of Obesity in Perspective.5 The whole book is a summary of the conference and what each presenter discussed. Below is the paragraph where Young is mentioned.

In her presentation, DR. YOUNG noted that conventional nutritional treatment of the obesities has not been an outstanding success, although we know of people for whom it has been of great value. The use of behavioral modification, a technique introduced by DR. STUART, seems to be a move in the right direction since, in at least some cases, it is behavior which needs to be modified. Some questions which need probing are whether the obesities are primarily behavioral and consequences of habits or whether they are symptoms of some more fundamental psychologic or psysiologic abnormality. Dr. Young also asked whether there were alterations in the efficiency with which energy was utilized by obese and lean subjects. She also questioned the role of the changes in the number of fat cells in juvenile and adult onset forms of obesity. Finally, in reviewing nutritional approaches to treatment, she raised questions about the mechanisms by which the hypothalamus senses the abnormalities present in the obese state.

I’m gonna leave it up to you to decide if in his summary of Young’s presentation he editorialized it in such a way as to indicate her ideas were “naïve and of no consequence.” Actually, I’m not gonna leave it up to you. I’m just gonna tell you that it didn’t. Taubes just made that up. In no way did anything in that paragraph characterize Young as naïve and of no consequence. It’s not even Bray’s opinion: it’s just a summary of what Young presented herself.

In Treatment and Management of Obesity the full context of the quote is thus: The author of this chapter of the text – which was actually written by Grant Gwinup and not George Bray as Taubes implies – discusses some studies on the topic of diet and exercise and their effects on obesity.6 In one paragraph he mentions some studies where people were put on diets that varied greatly in proportions of carbohydrates, protein, and fat, yet weight loss was consistent despite the fraction of macronutrients. Then he follows with this paragraph:

Recent studies by Young et al. has suggested, on the other hand, that a very low carbohydrate diet may indeed increase the rate at which body fat is catabolized. Their studies, on a small number of college students, require confirmation before they can be fully accepted. However, they suggest that a carbohydrate content of less than 50 g/day in the diet is sufficient to cause increased rates of weight loss compared to 60-104 g of carbohydrate in a diet with the same total number of calories. Thus, the question of the value of a low carbohydrate diet and its effectiveness in weight loss is still unresolved.

Does that sound at all dismissive of Young or her studies? Or is it the exact same thing you will find in any good piece of scientific writing that discusses a given topic (i.e. some studies demonstrate X, while these others suggest Y)? Hint: It’s the latter.

And as for that quote in The Obese Patient I can’t find it.7 I found three times in the book where Young is cited and none have anything to do with that quote. Perhaps it’s in there, but if it is I cannot find it. If you’re interested in the context where Bray does cite Young… Regarding changes in body composition over a lifetime on page 22 he writes “The data from several cross sectional studies of men and women have been summarized by Forbes and Reina (1970) (see also Behnke, 1963; Krzywicki and Chinn, 1967; Young et al., 1963; Norris, Lundy and Shock, 1963; Flynn et al., 1968).” And on page 179 in discussing how smaller, more frequent meals affects cholesterol levels where Bray writes “This reduction of cholesterol with frequent ingestion of small meals has been confirmed in several other studies (Gwinup et al., 1963; Jagannathan et al., 1964; Irwin and Feeley, 1967; Young et al., 1972). Glucose tolerance curves are also improved when eating three or more meals as compared with one or two large meals (Fabry et al., 1964; Gwinup et al., 1963l Young et al., 1972).”

Bray is so devastatingly cruel to Young, right? How could Bray live with himself after saying such harsh things?

* * *

The Carb Cosa Nostra is at again! Time for good research to sleep with the fishes. An example of this is found on page 421:

When M. R. C. Greenwood discussed the effect of insulin on the enzyme lipoprotein lipase, LPL, the “gatekeeper” for fat accumulation in cells, at the Fourth International Congress on Obesity, Hirsch ignored the implications in his review of dietary therapy, even though Greenwood had received her doctoral degree with Hirsch.

Let’s unpack this because there is quite a bit of bullshit in that single sentence. First off, Taubes cites the same source for Greenwood’s LPL presentation and Hirsch’s presentation that allegedly “ignored” Greenwood: The Proceedings of the 4th International Congress on Obesity.8 I think it’s worth pointing out a few things:

  1. Hirsch was Greenwood’s thesis advisor. Hirsch was also the chair of the Fourth International Congress on Obesity. I think it’s reasonable to assume that Hirsch played a role in Greenwood’s presence at the conference, so he’s not trying to silence her.
  2. Taubes stating that Greenwood “discussed the effect of insulin on the enzyme lipoprotein lipase” is generous. She does discuss LPL, but insulin in mentioned literally one time and not in context of LPL – at least not directly.
  3. In regards to both of the presentations, they were given at the same conference. Hirsch appeared to have given two very brief presentations on diet and obesity; both very generalized, like an overview. Did Taubes expect that Hirsch was in the audience for Greenwood’s presentation, fully absorbed everything Greenwood had to say about normal and abnormal growth and maintenance of adipose tissue vis-à-vis LPL and insulin (which was mentioned only once), amend his original presentation that he had prepared on a basic overview of diet, and get into the weeds of the cellular mechanisms of fat cell regulation? I mean, really? Is this how Taubes operates at conferences? Does he incorporate details of all the previous presentations at the same conference, even if it is outside the scope of his talk? If he doesn’t do this does some asshole accuse him of ignoring research?

* * *

Another instance of the above is found on page 420-421 where Taubes states:

Donald Novin, director of the Brain Research Institute at UCLA, discussed what he called the “carbohydrate hypothesis of ingestive behavior” at Bray’s Second International Congress on Obesity. Novin suggested that the “widespread popularity of the low carbohydrate diets” could be explained by the effect of carbohydrates on insulin, and then of insulin on fat deposition and thus hunger. Bray, who had worked closely with Novin at UCLA, gave the summary talk at the conference on obesity therapies and omitted mention of Novin’s hypothesis.

And the same bullet-points apply.

  1. Bray chaired the goddamned 2nd International Congress on Obesity and edited its proceedings. I’m sure he wasn’t trying to bury Novin’s research, but if he was he was doing a real bad job at it.
  2. I’m not sure Novin’s presentation has much overlap with Bray’s. If you read Novin’s presentation you will discover that he discusses how glucose infusion suppresses feeding in rabbits, but if you perform a vagotomy on the rabbits the infused glucose will stimulate feeding to some extent.9 (At the time Novin doesn’t even know why this is stating “We have no explanations, only speculation.”) While Bray’s presentation is about the risk-benefit ratio of certain dietary treatments of obesity.
  3. Taubes shits on Bray for not performing the completely absurd and irrational practice of revising and incorporating a pre-prepared talk on risk-benefit analysis with some preliminary and inconclusive research on rabbits that was given earlier in the day. Presumably Bray should have also revised and incorporated the results of all 25 talks that preceded his own, lest someone like Taubes accuse him of “omitting” important research and attempting to stifle scientific progress some thirty years later.

Conclusion

If you didn’t read the wall of text above I will attempt to summarize. Throughout this chapter Taubes attempts to craft the narrative that the TruthTM of the efficacy of low carb diets were systematically buried or conspicuously ignored by unscrupulous diet researchers (which inevitably led to the rise of Coke and Pepsi and the obesity epidemic). However, the evidence presented for this cover-up is either very weak or completely made up. The only cover-up presented in this chapter is Taubes’s use of Occam’s Broom: where inconvenient facts are swept under the carpet.

cloud

Refs

1. It seems pretty clear in his newspaper ad, though, which looks pretty scammy if you ask me.‘Only 10 years out of medical school I was already a fat man. 40 pounds overweight, with 3 chins! Yet I have no willpower – even the idea of hunger scares me. I knew I could not follow a low-calorie diet for even a single day.’ He read about FMH, and by using his own body as a laboratory, discovered that he could command it to make this miracle hormone whenever he wished.” FMH by the way stands for Fat Metabolizing Hormone according to the ad, and as far as I know it’s completely made up.

2. United States. Nutrition and diseases–1973 [-1974] Hearings, Ninety-third Congress, first[-second] session. (U.S. Govt. Print. Off., 1973).

3. Obesity: Medical and Scientific Aspects : Proceedings of the 1st Symposium of the Obesity Association of Great Britain Held in London, October 1968. (E. & S. Livingstone Limited, 1969).

4. Gordon ES, Goldberg M & Chosy GJ. A new concept in the treatment of obesity: A 48-hour total fast followed by six meals a day and later by stepwise increases in food and calorie intake has permitted patients to lose weight that they show no tendency to regain for periods of up to 6 months. it also promoted spontaneous evolution of good dietary habits. JAMA 186, 50–60 (1963).

5. Bray, G. Obesity in Perspective. Vol 2. (DHEW, 1973).

6. in Treatment and Management of Obesity (eds. Bray, G. A. & Bethune, J. E.) 93–102 (Harper and Row, 1974).

7. Bray, G. A. The obese patient. (W. B. Saunders, 1976).

8. Hirsch, J. & VanItallie, T. B. Recent Advances in Obesity Research, Volume IV: International Congress Proceedings: 4th. (CRC Press, 1985).

9. Recent Advances in Obesity Research: International Congress Proceedings: 2nd. (Hemming Information Services, 1978).

Good Calories, Bad Calories: A Critical Review; Chapter 24 – The Carbohydrate Hypothesis III: Hunger and Satiety

cover

Introduction

This is another post in my ongoing series of posts on Gary Taubes’s Good Calories, Bad Calories (GCBC). One of the main challenges I have encountered while reviewing this chapter is that Taubes devotes several pages to discussing the work of Jacques Le Magnen and attempting to associate Le Magnen’s research with Taubes’s own theories. My undergraduate advisor actually spent some time in France and worked directly with Le Magnen, so of course all his students were educated on Le Magnen’s work. However, Taubes cites a number of texts by Le Magnen that I was either unable to find or are written entirely in French. For that reason I cannot comment on the specifics of the texts, and unless I find some of the specific texts Taubes cites these pages are outside the scope of this chapter review.

Not the Introduction

On pages 425-426 Taubes describes a diet that was designed by JB Sidbury and RP Schwartz to help obese children lose weight, stating “The diet that Sidbury eventually used in his clinic and claimed to be uniquely effective contained only 15 percent carbohydrates-‘the remaining being apportioned approximately equally between protein and fat […]’” Taubes makes great hay of Sidbury’s diet and how it reduced insulin levels and therefore fat mass, stating also “insulin will ‘facilitate lipogenesis’ and inhibit the release of fat in the adipose tissue, this in turn created what Sidbury called the ‘milieu for positive fat balance’ in the cells of the adipose tissue” and “’decreased insulin levels would then permit normal fatty acid mobilization’” and “he [Sidbury] described an approach to obesity therapy that differed from Robert Atkins’s only in the details of the application.”

Leaving aside that Sidbury and Schwartz never claimed their diet was “uniquely” effective, they do claim that their dietary treatment was effective to some degree, which is really no surprise if you read the details of their diet.1 From page 67 of Childhood Obesity:

Prior to our interest in the subject, we routinely had the dietitian give the mother a 1000 calorie diet for an obese child, whether 4 or 14 years old. The results could have been predicted with a little reflection. Indeed an adult should be given a 700 or 800 calorie diet if weight loss at a reasonable rate is the goal. We then arbitrarily designed a 300 calorie diet to be used for children 3 to 8 years, 500 calories from 8 years to puberty, and 700 calories over puberty. This schedule has been effective; hence we have continued it.

This is all to be expected, except that it essentially contradicts items 5 & 6 of Taubes’s “inescapable” conclusions found on page 454. For those that haven’t read GCBC, Taubes attempts to make the case that overeating, exercise, or caloric intake of one’s diet is of no real consequence with regard to weight loss or gain. The only factor that really matters, according to Taubes, is insulin which can be manipulated by dietary carbohydrates.

Of course if Taubes is correct then Sidbury and Schwartz could have prescribed diets of 6000 kcals or more and weight loss would have been just as effective so long as the diet was ketogenic.

* * *

Starting on page 436 Taubes attempts to make the case that carbohydrates cause infertility! So if you’re trying to get pregnant and you’re sitting down to a nice meal of meat and potatoes, put your fork down, discard your potatoes, and help yourself to some more meat.

He starts off by setting up the straw man of Conventional WisdomTM, or in this case Common Belief.

[T]he critical variable in fertility is not body fat, as is commonly believed, but the immediate availability of metabolic fuels.

I’m not even sure why he brings this part up. I guess to add to the list of all the Conventional WisdomTM he has “debunked.” At any rate, as evidence for what is commonly believed he cites a paper by Frisch and MacArthur titled “Menstrual Cycles: Fatness as a Determinant of Minimum Weight for Height Necessary for Their Maintenance or Onset” that concludes the following “The data suggest that a minimum level of stored, easily mobilized energy is necessary for ovulation and menstrual cycles in the human female.”2 The authors also mention that “If a minimum of stored fat is necessary for normal menstrual function, one would expect that women who live on marginal diets would have irregular cycles, and be less fertile, as has been observed, and that poorly nourished lactating women would not resume menstrual cycles as early after parturition as well-nourished women, as also has been observed.” Notice anything funny here? And he contrasts this with two papers by Schneider and Wade that conclude the exact same thing, only they used animals for their studies instead of people.3,4

Whatever. Not a big deal, but strap in because this next one is a whopper. Continuing on pg 436-437 Taubes tries to make the argument that insulin is responsible for infertility, citing some research by Wade and Schneider.

[I]nfusing insulin into animals will shut down their reproductive cycles. In hamsters, insulin infusion “totally blocks” estrous cycles, unless the animals are allowed to increase their normal food intake substantially to compensate.

However, if you actually read the research you will find that it wasn’t the insulin they were studying, but hypoglycemia.4 Insulin was simply a way of artificially inducing hypoglycemia in the hamsters. The authors even mention this:

[I]nsulin was used as a tool to demonstrate the effects of fuel partitioning on reproductive function. Treatments with high doses of insulin that produced hypoglycemia inhibited reproductive function. The results do not support a role for insulin per se, independent of effects on fuel availability.

Emphasis mine. Unless something was really wrong with you, you likely are not going to experience hypoglycemia if you consume a diet that includes at least some carbohydrates. Indeed, those deciding to consume low-carbohydrate diets would be at greater risk of hypoglycemia.5

* * *

If you’re still not convinced that meat = magic then Taubes has a tobacco tale for you on page 437; and a tall tale it is.

Consider nicotine, for instance, which may be the most successful weight-loss drug in history, despite its otherwise narcotic properties.

I wanna stop right here. This is a bold claim. The most successful weight loss drug IN HISTORY? If that’s true then the majority of smokers that I know should be thin. As a matter of fact they should be downright anorexic considering their frequency. Actually, the reverse is true if my experience is any indication. Of course using anecdotal arguments like this is not at all scientific, but c’mon has Taubes never heard of ephedrine? Sibutramine? Dinitrophenol? Amphetamines for god’s sake? Even cocaine?

Absurd historical claim nothwithstanding, he attempts to make the claim that if and when people gain weight after they stop smoking is because smoking is hormonally similar to eating a low-carb diet.

There seems to be nothing smokers can do to avoid this weight gain. The common belief is that ex-smokers gain weight because they eat more once they quit.

[…]

[A]s Judith Rodin, now president of Rockefeller University, reported in I987, smokers who quit and then gain weight apparently consume no more calories than those who quit and do not gain weight. (They do eat “significantly more carbohydrates,” however, Rodin reported, and particularly more sugar.) Smokers also tend to be less active and exercise less than nonsmokers, so differences in physical activity also fail to explain the weight gain associated with quitting.

There’s the ol’ Common BeliefTM again. I guess he figures he wore out Conventional Wisdom so he’ll go with another phrase that means the same thing. Nevertheless, reading this passage Taubes would have you believe that people lose weight after they quit smoking and weight gain in these instances is completely divorced from the amount of calories they eat. As evidence he cites a paper by Judith Rodin, but perhaps more importantly he does NOT mention contradicting evidence from other papers that he cited on the very same page! Por ejemplo, when discussing other aspects of nicotine he cites a review paper titled “Smoking Cessation and Weight Gain” published in 2004, which states

Mechanisms of weight gain [following smoking cessation] include increased energy intake, decreased resting metabolic rate, decreased physical activity and increased lipoprotein lipase activity (14–16,20–23). Nicotine significantly decreased body weight and food intake via a decrease in meal size and a longer inter-meal interval […]6

Another review titled “Weight Gain Following Smoking Cessation” that Taubes cites on this very page relates the following:

Nicotine has commonly been called an anorectic, an agent that suppresses eating. Consistent with this view, the vast majority of prospective studies have found a sharp increase in eating during the first few weeks of smoking cessation (e.g., Hatsukami, Hughes, Pickens, & Svikis, 1984; Perkins, Epstein, & Pastor, 1990; Spring, Wurtman, Gleason, Wurtman, & Kessler, 1991). The magnitude of this increase (approximately 250-300 kcals/day) is strikingly similar across studies, despite important differences in food measurement methodology (e.g., observation of food intake in in-patients, subject self-report by means of food diaries) and subject populations (female subjects, male subjects, or both).7

But Taubes dismisses all of this evidence by glossing over it and highlighting the single Rodin publication, which looks at current smokers and those that recently quit.8 If you actually read the text of the study you’ll find that the quitters on average did not gain significantly more weight than the smokers. Moreover, almost half actually lost weight after quitting. It is also worth noting that the measurement of caloric intake was self-reported, and self-reporting energy intake has been shown to be notoriously unreliable. But I’m sure this singular study with self-reported intake and non-significant results trumps all the other evidence to the contrary.

* * *

On page 446 Taubes says the following:

Avoiding carbohydrates will lower insulin levels even in the obese […]

Now this is a pretty anodyne and uncontroversial statement. I doubt you’ll find any nutrition professional worth their salt that would disagree with the above statement. What is interesting about this is not the statement, but the source Taubes cites for this. It absolutely backs up that claim, but it is devastating to his other claims. Namely, #6 and #9 of his “inescapable” conclusions found in the epilogue.*

The cited study take obese individuals and feeds them isocaloric high and low carb diets as well as hypocaloric high and low carb diets.9 All participants on the isocaloric diets10 maintained their weight whether fed high or low carb diets. All participants fed the hypocaloric diets lost weight regardless of the relative amount of CHO was in the diet. This is actually a pretty damn good experiment to test Taubes’s main hypothesis of calories vs carbs, and the good old calorie wins.

high low carb insulin

* * *

Not a major point but on page 446 Taubes says

It also makes us question the admonitions that carbohydrate restriction cannot “generally be used safely,” as Theodore Van Itallie wrote in 1979, because it has “potential side effects,” including “weakness, apathy, fatigue, nausea, vomiting, dehydration, postural hypotension, and occasional exacerbation of preexisting gout.”

It’s basically a misquotation on two accounts. Van Itallie actually states that low calorie diets “can generally be used safely.”11 Secondly, he states that low calorie diets that are ALSO low in carbohydrates have potential side effects. He is not speaking of carbohydrate restriction in general terms as Taubes implies.

* * *

Page 447, Taubes contends that, although cholesterol levels may rise on a low-CHO diet, it is by no means permanent.

The existing evidence suggests that this effect will vanish with successful weight loss, regardless of the saturated-fat content of the diet. Nonetheless, it’s often cited as another reason to avoid carbohydrate-restricted diets and to withdraw a patient immediately from the diet should such a thing be observed, under the mistaken impression that this is a chronic effect of a relatively fat-rich diet.

Maybe this is another minor point, but the “often cited” part of his claim is in reality a single newspaper article about a guy that sues the Atkins estate for his high cholesterol.12 The article seems to imply that the case is kind absurd and that a judge would almost certainly throw out the suit.

 

 

*For those that don’t have the book…
“6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.”
“9. By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.”

cloudReferences

1. in Childhood Obesity (ed. Collip, P. J.) (Distributed by Medical and Technical Publishing Co, 1975).

2. Frisch, R. E. & McArthur, J. W. Menstrual cycles: fatness as a determinant of minimum weight for height necessary for their maintenance or onset. Science 185, 949–951 (1974).

3. Schneider, J. E. & Wade, G. N. Availability of metabolic fuels controls estrous cyclicity of Syrian hamsters. Science 244, 1326–1328 (1989).

4. Wade, G. N. & Schneider, J. E. Metabolic fuels and reproduction in female mammals. Neurosci. Biobehav. Rev. 16, 235–272 (1992).

5. Colle, E. & Ulstrom, R. A. Ketotic hypoglycemia. J. Pediatr. 64, 632–651 (1964).

6. Filozof, C., Fernández Pinilla, M. C. & Fernández-Cruz, A. Smoking cessation and weight gain. Obes. Rev. 5, 95–103 (2004).

7. Perkins, K. A. Weight gain following smoking cessation. J. Consult. Clin. Psychol. 61, 768–777 (1993).

8. Rodin, J. Weight change following smoking cessation: The role of food intake and exercise. Addict. Behav. 12, 303–317 (1987).

9. Grey, N. & Kipnis, D. M. Effect of Diet Composition on the Hyperinsulinemia of Obesity. N. Engl. J. Med. 285, 827–831 (1971).

10. (except for one that did not consume all of the prescribed diet).

11. Bray, G. A. Obesity in America: a conference. (U.S. Dept. of Health, Education, and Welfare, Public Health Service, National Institutes of Health, 1979).

12. Burros, M. Dieter Sues Atkins Estate and Company. New York Times 1 (2004).

Good Calories, Bad Calories: A Critical Review; Chapter 8 – The Science of the Carbohydrate Hypothesis

coverIntroduction

This is another post in my ongoing series of posts on Gary Taubes’s Good Calories, Bad Calories (GCBC). Several of the publications that Taubes cites for various claims are amazingly obscure. I’m working on getting a couple of them right now, so perhaps this post will be updated in the future when I receive and look through them. In the meantime this post is the fact-checking I have done of chapter eight so far.

Surprisingly it doesn’t contain that much “science of the carbohydrate hypothesis.” It’s really more of an introduction to the similarly-named chapters toward the end of the book. He spends some time with Tokelau (which I will get to soon), discusses what homeostasis is, and then reworks one of his earlier articles about salt toward the end of the chapter.

Not the Introduction

God, I love the beach. I bet it's paradise over there.

Ian Prior in Tokelau, 1971

For the first several pages of chapter eight Taubes discusses a rather interesting cohort study involving the people of the Tokelau Islands in the south pacific. Briefly, Ian Prior, an epidemiologist from New Zealand, decided to study the residents of Tokelau while the New Zealand government wanted to organize a large voluntary migration effort of the peoples from the islands to NZ. Some opted to stay on the Tokelau Islands rather than migrate, which provided Prior an excellent opportunity to study the two populations and compare their lifestyles, diet, and health. As you might guess, the islanders that “immigrated” to NZ ended up having more health problems than those that stayed behind.

Why? What happened? According to the University of Minnesota synopsis of the study, it is due to “the tendency for migrants at all ages to be heavier than non-migrants. Migrants had more diabetes and smoked more, drank more alcohol, and exercised less.1 These factors make the poorer health among the migrants pretty easy to explain. Taubes, however, doesn’t want you to think that any of this has to do with the study results so he straight-up lies to you on page 138:

A number of factors combined to make this higher disease incidence among the migrants difficult to explain. For one thing, the Tokelauans who emigrated smoked fewer cigarettes than those who remained on the atolls, so tobacco was unlikely to explain this pattern of disease.

He goes on to state that the migrants were far more physically active and had a much more “rigorous” lifestyle than the non-migrants because they worked in sewing factories and had to walk to shops. I’m not even kidding. Again, this directly contradicts the actual study results.

So how does Taubes explain the health discrepancy? Why, it’s exclusively due to saturated fat intake, of course! Yes, as it turns out the native diet of the Tokelauans ate a diet largely composed of fish, coconuts, and fruit. According to Taubes it was the coconut oil in the Tokelauan diet that was apparently uniquely protective because coconut oil has saturated fats. Moreover, Taubes also mentions that the migrants to NZ started eating bread and potatoes which contributed to their health problems. And, of course, he has to drag Keys into this saying “If Keys’s hypothesis was correct, the migrants should have manifested less evidence of heart disease, not more.”

Actually, no. The non-migrants should have manifested less heart disease. Taubes is conflating the fatty acids in coconuts with all saturated fatty acids. The fatty acids in coconuts are quite a bit different from that fatty acids found in the foods that Taubes promotes throughout the book (beef tallow, bacon, cheese, etc.) It has been demonstrated to the satisfaction of most people that coconut oil does not have a huge impact on serum cholesterol levels and by extension heart disease. Matter of fact, the first person to demonstrate this was none other than Ancel “Beelzebub” Keys himself!2,3

Aside from alcohol consumption, diet was not even mentioned in the study synopsis as being a potential factor in the health decline. Nevertheless, Taubes credits the saturated coconut oil for the good health of the non-migrants, and blames the bread and potatoes on the poor health of the migrants. What Taubes glosses over are other dietary components introduced to the migrants which include salt, eggs, dairy, and red meats.4

* * *

One of the main goals of GCBC is to upend everything we all thought we knew about nutrition: Saturated fats from animals are actually good for you! Carbohydrates from fruits, vegetables, or grains are actually the enemy! Calories don’t matter! You can gorge yourself of whatever you like, and as long as it doesn’t include carbohydrates you’re in the clear! Dietary fiber is meaningless! I suspect Taubes does this not because these things are true or even that he believes these things are true, but rather because it sells more books. It’s a shame people have to get wildly inaccurate information about how to take charge of their own health for the financial gain of one individual, but that seems to be the case.

Another one of these bits of “conventional wisdom” that he upends is the idea that salt has anything to do with high blood pressure. Page 146:

[P]ublic-health authorities for the past thirty years have insisted that salt is the dietary cause of hypertension and the increase in blood pressure that accompanies aging. […] That’s the hypothesis. But in fact it has always been remarkably difficult to generate any reasonably unambiguous evidence that it’s correct.

He goes on to state that even if by some miracle salt really does somehow influence blood pressure, it has such a negligible effect that cutting salt intake “makes little difference” to our overall health. As evidence he cites a 2004 Cochrane Review by He and MacGregor. Old versions of Cochrane reviews are difficult to find. It seems they usually replace the old ones every time the data gets updated. In this case I was only able to find the 2013 version of the same title by He and MacGregor.5 Let me quote from the end of the review (emphasis mine):

Our meta-analysis of randomised trials of longer-term modest reductions in salt intake demonstrates a significant effect on blood pressure in individuals with both elevated and normal blood pressure. The blood pressure fell, on average, by 5/3 mmHg in hypertensives and 2/1 mmHg in normotensives. These falls in blood pressure would have an immediate and significant impact on population blood pressure and would, therefore, be predicted to reduce stroke deaths by approximately 14% and ischaemic heart disease (IHD) deaths by 9% in individuals with elevated blood pressure, and in individuals with normal blood pressure reduce stroke and IHD deaths by approximately 6% and 4% respectively. It is important to note that these reductions in stroke and IHD deaths were estimated from a previous meta-analysis of prospective observational studies. A recent meta-analysis of 1 million adults in 61 prospective studies demonstrates that the relationship between blood pressure and cardiovascular risk is much stronger than previously estimated. Therefore, the reductions in stroke and IHD with the modest reductions in salt intake might be even greater. Since raised blood pressure is also a major risk factor for heart failure, a reduction in salt intake would likely reduce the incidence of heart failure.

I’ll leave it up to you if you think if a modest reduction in salt intake in fact “makes little difference.”6

* * *

Taubes tries to make the case that CHOs are the real culprit leading to insulin resistance which leads to hypertension and ultimately atheroslcerosis. Page 150 of the hardback Taubes states:

Finally, by the mid-1990s, diabetes textbooks, such as Joslin’s Diabetes Mellitus, contemplated the likelihood that chronically elevated levels of insulin were “the major pathogenetic defect initiating the hypertensive process” in patients with Type 2 diabetes. But such speculations rarely extended to the potential implications for the nondiabetic public.

Taubes is quoting out of context here. The actual quote states7:

Should hyperinsulinemia be the major pathogenetic defect in initiating the hypertensive process in patients with NIDDM, it is unlikely that it sustains the hypertension indefinitely. With increasing insulin resistance, the pancreas must secrete higher levels of insulin. Eventually, its reserve capacity is exhausted and plasma insulin levels fall. Other mechanisms must then sustain the hypertension.

Interestingly, immediately before the cherry-picked quote from Taubes is a statement that contradicts Taubes’s argument:

[H]ypertension and insulin resistance may be different clinical manifestations of a common underlying cellular defect by which the level of cytosolic free calcium is increased and the level of intracellular free magnesium is decreased.

As a matter of fact the entire paper makes the argument that the cause of hypertension is clearly multifactorial.

* * *

Page 150:

Though this carbohydrate-induced water retention and the hypertensive effect of insulin were occasionally discussed in nutrition and dietetics textbooks-Modem Nutrition in Health and Disease, for example, which was published in 1951 and was in its fifth edition by the 1970s-they would appear solely in the technical context of water and electrolyte balance (sodium is an electrolyte), whereas the discussion of hypertension prevention would focus exclusively on the salt hypothesis.

Nope. Not even close. Modern Nutrition in Health and Disease describes a variety of factors associated with hypertension. And when it comes to prevention does not “focus exclusively on the salt hypothesis.” Example from the 1999 edition that I have:

In hypertensives whose blood pressures have been controlled with medications, weight loss or NaCl restriction more than doubles the likelihood of maintaining normal blood pressure after withdrawal of drug therapy. The following lifestyle modifications have been recommended as adjunctive or definitive therapy for hypertension: weight reduction if overweight; aerobic exercise; limited NaCl and alcohol intake; maintenance of adequate dietary potassium, calcium, and magnesium intake; smoking cessation and reduced dietary saturated fat and cholesterol intake for overall cardiovascular health.

It’s a shame Taubes never reads what he cites.

cloud

Refs

Good Calories, Bad Calories: A Critical Review; Chapter 12 – Sugar

Introduction

This post is another in a long line of self-abusive posts in which I spend way too much time combing Gary Taubes’s Good Calories, Bad Calories (GCBC), and usually end up disappointed at the publishing industry and feel depressed for the masses of people that actually trusted Taubes’s “research.”

This chapter is not as bad as many of the others, though. It happens to be about sugar, and the fact is that you don’t need to heavily distort scientific publications to indict sugar. Taubes still manages it, however. If you’d like to read other chapter reviews of GCBC by yours truly, visit my Book Reviews page.

As you read this post you might leave with the impression that I advocate sugar consumption. Nothing could be further from the truth: it is clearly an ingredient that Americans (and perhaps any country with a Pepsi presence) consume far too much. It would only benefit your health to reduce your consumption of it. What I do advocate is intellectual honesty which is why I come to sugar’s defense when journalists like Taubes make up or distort evidence against it.

Not the Introduction

On page 200 Taubes states 

The more fructose in the diet, the higher the subsequent triglyceride levels in the blood. For this reason, fructose is referred to as the most lipogenic carbohydrate.*

*Credit for this observation dates to 1916, to Harold Higgins of the Nutrition Laboratory of the Carnegie Institution.

I’m not sure that Taubes can really state this. The Higgins paper he cites does not really measure lipogenesis. It measures respiratory quotient. In the paper Higgins does say that one might say that levulose (fructose) and galactose, judging by the RQ, could preferentially turn into fat.1 However, Higgins actually observed the sugars being burned:

A study of figure 1 shows clearly that levulose [fructose], sucrose, probably lactose and possibly maltose give indications by the respiratory quotients of being metabolized, and in all probability burned by the fourth to the seventh minute after ingestion “on an empty stomach,” which is quite as rapidly as alcohol in the same subject and much quicker than alcohol in four other subjects.

* * *

On page 200, Taubes states

Although sugar also seemed to raise cholesterol levels, particularly LDL, as would be expected for any nutrient that increased triglyceride synthesis in the liver. In 1992, John Bantle reported that LDL cholesterol in diabetic patients was elevated more than 10 percent on a high-fructose diet after a month, which is comparable to what can be achieved by saturated fats.

For this claim he cites two references. One is a study co-authored by Bantle (although he is not the lead author, Joyce Swanson is).2 That study does show that at a couple of points in the study LDL was elevated compared to the controls, as was triglycerides at one point and total cholesterol at one point. (See pic below) However, contrary to Taubes’s claim this study used normal, healthy patients – not diabetics.

Metabolic effects of dietary fructose in healthy subjects

Dietary fructose effects on lipoprotein metabolism and risk for coronary artery disease

The other citation for his claim that fructose elevates LDL is a review article that makes more of a point to state that the evidence on this issue is quite conflicting.3 (see pic above) From the author’s conclusion:

Perhaps the most general conclusion that could be drawn from this review of the effects of dietary fructose on lipoprotein metabolism is how little we actually know.

Does Taubes even read the studies he cites? And shockingly Taubes now admits that sat fat can raise LDL cholesterol levels!

Also from the conclusion:

[I]t would seem unlikely, based on available data, that dietary fructose at quantities obtainable from natural sources provided in a well-balanced diet would result in any deleterious metabolic effects.

* * *

On page 201 Taubes claims:

[F]ructose elevates blood pressure more than an equivalent amount of glucose does, a phenomenon called fructose-induced hypertension.

What you might think after reading this statement is that if you consume fructose this might lead to some degree of hypertension, but unless you’re a rat you would be wrong. Taubes cites two publications for this claim: one by Hodges and Rebello and one by Hwang et al.4,5 Both mention that fructose consumption leads to hypertension in rats. In fact the title of the Hwang paper is “Fructose-Induced Insulin Resistance and Hypertension in Rats.” However, you will find the opposite is true in humans. The other paper makes it clear that fructose has no effect on blood pressure in humans. From the text: “Fructose ingestion produced no significant changes in blood pressure […]” The authors also mention that lactose and galactose also showed no increase in blood pressure. Although to be fair to Taubes the study does mention that both sucrose and glucose increased blood pressure in humans so he’s not way off base here. Nevertheless, he seems to give all the studies he cites a mere cursory glance before writing about their results and very often getting them wrong.

* * *

Page 202, Taubes claims: “The American Journal of Clinical Nutrition dedicated an entire issue to the deleterious effects of dietary fructose.” Not exactly true. The AJCN did do a supplement of one issue that focused on fructose, and it wasn’t focused on the deleterious effects, either. Some of the reports had nothing to do with fructose and health. Just look at some titles like “Manufacturing, composition, and applications of fructose” and “Worldwide production of high-fructose syrup and crystalline fructose.” Other reports indicated neutral to favorable data regarding fructose and health. For example, one report on diabetes concluded6:

In summary, the side effects of fructose supplementation do not seem at this time to be of particular concern when fructose is ingested in modest amounts.

Another report on the public health implication of fructose states7:

On the basis of currently available information, as reviewed in this monograph, fructose is a valuable, traditional source of food energy, and there is no basis for recommending increases or decreases in its use in the general food supply on in special dietary use products.

Another report says that fructose aids in mineral absorption.8 Another says that fructose may increase physical performance.9 These are all from the same supplement that Taubes mentions. I know this because Taubes even cites yet another report on fructose and thermogenesis that concludes the following10:

The greater thermic effect of fructose, its nondependence on insulin for its metabolism, and its greater sweetening potency compared with glucose are factors that may speak in favor of fructose as a valuable carbohydrate for the dietary management of obesity and NIDDM [non insulin-dependent diabetes mellitus].

But of course there was no way in hell Taubes was going to mention this part of the conclusion. Instead he mentions the part that says more research is needed – a sentiment you can find at the end of literally all nutrition studies and likely any scientific study period.

* * *

Page 203:

In 2002, the Institute of Medicine of the National Academies of Science released its two-volume report on Dietary Reference Intakes (subtitled Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids), and spent twenty pages discussing the possible adverse effects of sucrose and high-fructose corn syrup. It then concluded that there was still “insufficient evidence” to set up an upper limit for sugar consumption in the healthy diet.

Despite Taubes’s attempt to make this seem like a huge scandal because of a wildly incompetent Institute of Medicine, this is pretty standard stuff. No tolerable upper limits (UL) were set for any macronutrient. ULs are set for things like vitamin A and iron; micronutrients at which there is a point where they start to become acutely toxic.

Refs

1. Higgins, H. L. The Rapidity with Which Alcohol and Some Sugars May Serve as Nutriment. Am. J. Physiol. 41, 258–265 (1916).

2. Swanson, J. E., Laine, D. C., Thomas, W. & Bantle, J. P. Metabolic effects of dietary fructose in healthy subjects. Am. J. Clin. Nutr. 55, 851–856 (1992).

3. Hollenbeck, C. B. Dietary fructose effects on lipoprotein metabolism and risk for coronary artery disease. Am. J. Clin. Nutr. 58, 800S–809S (1993).

4. Hodges, R. E. & Rebello, T. Carbohydrates and blood pressure. Ann. Intern. Med. 98, 838–841 (1983).

5. Hwang, I. S., Ho, H., Hoffman, B. B. & Reaven, G. M. Fructose-induced insulin resistance and hypertension in rats. Hypertension 10, 512–516 (1987).

6. Gerrits, P. M. & Tsalikian, E. Diabetes and fructose metabolism. Am. J. Clin. Nutr. 58, 796S–799S (1993).

7. Glinsmann, W. H. & Bowman, B. A. The public health significance of dietary fructose. Am. J. Clin. Nutr. 58, 820S–823S (1993).

8. O’Dell, B. L. Fructose and mineral metabolism. Am. J. Clin. Nutr. 58, 771S–778S (1993).

9. Craig, B. W. The influence of fructose feeding on physical performance. Am. J. Clin. Nutr. 58, 815S–819S (1993).

10. Tappy, L. & Jéquier, E. Fructose and dietary thermogenesis. Am. J. Clin. Nutr. 58, 766S–770S (1993).

Good Calories, Bad Calories: A Critical Review; Chapter 9 – Triglycerides and the Complications of Cholesterol

cover

Introduction

This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

Page 158 Taubes discusses a paper1 by Pete Ahrens

By 1957, Ahrens was also warning about the dangers of oversimplifying the diet-heart science: maybe fat and cholesterol caused heart disease, or maybe it was the carbohydrates and triglycerides. “We know of no solid evidence on this point,” wrote Ahrens, “and until the question is further explored we question the wisdom of prescribing low-fat diets for the general population.”

However, that quote is taken out of context. Taubes makes you think Ahrens is saying that there is “no solid evidence” regarding whether or not carbohydrates caused heart disease, but Ahrens is really referring to the ambiguity (at the time) of whether HDL or LDL causes heart disease. Actual quote:

[W]e are tempted to ask whether the lower density lipoproteins are less “atherogenic” than the higher-density lipoproteins rich in cholesterol and phospholipids. We know of no solid evidence on this point […]

I don’t think it’s a big deal, but it is misleading. What is even more misleading, though, is the information that is in the Ahrens paper that was purposefully ignored by Taubes because it runs contrary to his argument.

In this chapter (among other chapters) Taubes tries to make the case that cholesterol is not very relevant in discussions of atherosclerosis. The real culprit, according to Taubes, is triglycerides which are raised by those evil carbohydrates. Triglycerides are the only biomarker that matters. But while the Ahrens paper cited by Taubes does indicate that high CHOs can lead to elevated triglycerides it also makes clear a few other things, like vegetarian diets and very low fat diets are best for reducing lipids (triglycerides and cholesterol) and that plant-based fat is preferable to animal fats in the same regard.

Don’t believe me? Here are a few quotes from the paper:

  • “Experience to date has shown that two regimens are effective in lowering serum lipid levels of our outpatients. The first is total vegetarianism, in which all dairy products are omitted except for skim milk, washed cottage cheese, skim milk cheeses, and egg whites.”
  • “The second regimen consists of a very low fat diet (less than 25 Gm. per day) supplemented by an ounce or more of corn oil at least three times daily.”
  • “Serum lipids can be altered by dietary means, and experimental data lead to the presumptive conclusion that unsaturated fats in the diet cause depressions in levels of cholesterol and phospholipids.”
  • “[P]atients with existent or threatening arteriosclerosis may be justifiably advised to eat higher proportions of unsaturated fats.”

There is even a nice graph in the paper that Taubes would probably prefer you not see.

ahrens

I don’t think it needs any editorializing, but in case you can’t tell ALL of the lipid measurements – triglycerides, phospholipids, free cholesterol, and total cholesterol – are higher when fed animal fats at ALL points compared to plant fats.

* * *

On page 159 Taubes discusses a publication by Kuo2 that Taubes uses to support his carbohydrate-leads-to-hypertriglyceridemia-and-therefore-CHD argument. The study in question does show that his study patients with high levels of serum triglycerides were able to lower them when on a low-CHO diet. However, what is made clear in the study is that this is only true for patients with an abnormal condition of carbohydrate sensitivity, and that a diet with moderate carbs does not lead to hypertriglyceridemia in normal patients. In fact, Kuo mentions that one would need to eat an absurd amount of CHOs to induce elevated triglycerides. From the paper (emphasis mine):

A moderately high dietary sugar and other carbohydrate intake, amounting to 35% to 40% of total daily calories, did not appear to exert a significant effect on the blood lipid levels of young normolipemic subjects with negative family history of coronary disease and abnormality in carbohydrate metabolism. It was necessary to raise the carbohydrate intake to 85% to 90% of total calories to induce hyperglyceridemia in patients who were not abnormally sensitive to carbohydrates.

In the same paragraph in which he mentions the Kuo paper, Taubes claims the CHO-triglyceride-CHD hypothesis was confirmed by two other big studies at the time (Goldstein et al. and Carlson and Bottiger).3,4 Except they don’t even mention the pièce de résistance of Taubes’s argument: the carbohydrates. They simply discuss the association between CHD and triglycerides, which has never been disputed as far as I know. No mention of carbs at all in these papers.

* * *

On page 160 Taubes claims that the US government – and, by extension, researchers – ignored triglycerides as a risk factor for CHD in favor of studying cholesterol because everyone had a huge hard-on for Keys, apparently:

The National Institutes of Health, which was effectively the only source of funding for this research in the United States, had already committed its resources to three enormous studies-the Framingham Heart Study, Keys’s Seven Countries Study, and the pilot programs of the National Diet-Heart Study. These studies would measure only cholesterol and so test only Keys’s hypothesis. No consideration was given to any alternative hypothesis.

I’m sure you’ll be shocked to discover that Taubes is not exactly being honest here. Two out of the three studies that he said measured only cholesterol in fact measured both cholesterol and triglycerides (among other things).5-7 In fact, one of the Framingham papers mentions that triglycerides are a risk factor, albeit not as predictive as cholesterol is (emphasis mine):

The data presented suggest that in men the moderately elevated cholesterol values commonly encountered in the general population, regardless of the metabolic aberration responsible or how it is transported or partitioned among the lipoproteins, are associated with increased risk of coronary heart disease. Elevated endogenous triglyceride values appear significant in coronary atherogenesis only when accompanied by high cholesterol values.

* * *

On pg 160 of hardback Taubes states:

By 1961, Keys and his collaborators in the Seven Countries Study had measured cholesterol in over ten thousand men. By 1963, they had completed the exams on another eighteen hundred men. Even had it been technically possible to include triglycerides in the measurements, or to return to the original locales and retest for triglycerides, the cost would have been astronomical. The result, as we’ve seen, was considered a resounding victory for Keys’s fat-cholesterol hypothesis.

His citation for this is page I-7 in the study program and objectives which is a table of causes of death and a table of death rates from US vital statistics.8 There is no reference for cholesterol or triglycerides or exams or cost or really anything that Taubes claims here.

* * *

On page 161 Taubes discusses a series of papers published in the NEJM that report on various disorders of lipoprotein metabolism….. aaaaaaand makes some claims about them that are not backed up by the evidence in the actual papers (emphasis mine):

Four of the five lipoprotein disorders described in this series were characterized by abnormally elevated levels of triglycerides in the very low density lipoproteins. For this reason, Fredrickson, Levy, and Lees also warned against the dangers of advocating low-fat diets for all patients, because these diets increased carbohydrate consumption and so would elevate triglycerides[…]

As evidence for the claim Taubes cites page 219 of Fredrickson et al. 1967.9 That paper neither advocates for or warns against low-fat diets. In fact it’s never mentioned, but here are a few things that are mentioned in the section on dietary management of this disorder:

  • “[A] patient with a marginal Type II pattern who has neither of the other components of the triad diagnostic for the familial syndrome and who has a high intake of foods rich in cholesterol and saturated fats warrants dietary advice, for the expectation is good that he will respond.”
  • “The 2 components in dietary treatment of the Type II abnormality are limited intake of cholesterol and the substitution of polyunsaturated for saturated fats. Cholesterol and saturated (usually from animal) fats occur together in foods, and many therapists today are more concerned with their elimination […]”
  • “Substitution of skim-milk over whole-milk products, severe restriction or even elimination of egg yolks and reduction in meat intake for a daily intake of about 100 mg of cholesterol and 20 to 30 g of fat is one of the most effective dietary regimens.”
  • “Most Type II patients (provided they have normal glucose tolerance) can tolerate carbohydrate intakes of approximately 4 or 5 gm. Per kilogram of body weight per day without significant rise in their glyceride concentrations.”

That particular paper he cited dealt with only Type II of the five types of abnormal lipoprotein metabolism. Just FYI. He cites others though. Continuing with Taubes on that same paragraph:

By far the most common of the five lipoprotein disorders was the one designated Type IV, characterized by elevated VLDL triglycerides-“sometimes considered synonymous with ‘carbohydrate-induced hyperlipemia,'” they wrote-and it had to be treated with a low-carbohydrate diet.

Wrong on so many levels. Let’s take a look at the quote first. Taubes excises what follows that quote because the authors go on to say that while some might classify Type IV as “carbohydrate-induced,” it is really not true. Here’s the entire quote on page 273 of the same Fredrickson series, bolding mine:

The Type IV pattern (hereafter called simply “Type IV”) is a valuable indicator of metabolic imbalance; it does not describe a specific disease. It is sometimes considered synonymous with “carbohydrate-induced hyperlipemia.” This is probably too narrow a concept since most patients who have this pattern on a regular diet do not lose it entirely when their diet is changed so that 10 per cent of their calories come from carbohydrate, and an occasional patient does not have an abnormal increase in plasma glycerides when fed 80 per cent of his calories as carbohydrate.

That deals with the blatant quote-mining. What about the claim that the treatment had to be a low-carb diet? The authors also clearly state that carbohydrates should not be assumed to be the cause of the hyperlipemia, at least regarding Type IV, and that weight loss should be considered the primary treatment of such a disorder.

How does Taubes get away with this?

* * *

From page 168 in the hardback:

When they finally were tested in two clinical trials in the 1990s—the Lyon Diet Heart Trial and an Italian study known as GISSI-Prevenzione—both supported the contention that the diet prevented heart attacks, but neither provided evidence that it did so by either raising HDL or lowering LDL, which was how it was now alleged to work

The GISSI study does not measure diet.10 The diets remain the same throughout. The variable of interest in the study is one omega-3 gel capsule with the primary endpoints being death, non-fatal myocardial infarction, and stroke (i.e. not cholesterol). Conclusion: Dietary supplementation with n-3 PUFA led to a clinically important and statistically significant benefit. This study does not prove his claim.

Regarding the Lyon Diet Heart trial, Taubes’s inclusion of HDL and LDL makes his claim technically correct. However, the results of the Lyon Diet Heart trial are actually pretty devastating to Taubes’s overall thesis. What Taubes leaves out is that total cholesterol was very predictive of a second myocardial infarction. From the study: “[E]ach increase of 1 mmol/L of total cholesterol increased the risk of recurrence by 20% to 30%.”11 Not to mention the experimental diet contained – among other things – less saturated fat.

* * *

On pages 168-169:

Consider a porterhouse steak with a quarter-inch layer of fat. After broiling, this steak will reduce to almost equal parts fat and protein. Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid. Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL. (Stearic acid is metabolized in the body to oleic acid, according to Grundy’s research.) The remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL. In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed. The remaining 30 percent will raise LDL cholesterol but will also raise HDL cholesterol and will have an insignificant effect, if any, on the ratio of total cholesterol to HDL. All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.

For this paragraph of claims Taubes cites two studies, one by Katan and one by Grundy.12,13 He also cites the USDA National Nutrient Database for the fatty acid profile of his hypothetical steak.

If you actually look at the National Nutrient Database for a porterhouse steak you will note that Taubes is correct when he breaks down the fatty acid composition. However, you’ll notice that he focuses on the stearic acid (18:0) which is only one-third of the SFAs, the other two-thirds that he neglects to mention is palmitic acid (16:0) which according to the Katan study he cites raises LDL cholesterol monumentally compared to stearic acid.
Nutrient data for 23002, Beef, short loin, porterhouse steak, trimmed to 0.12 fat, cooked, broiled

fatty acids and cholesterol

As for the claim that the “remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL,” this is blatantly untrue, even by the studies Taubes himself cites.

fatty acids and cholesterol2

Again, does Taubes even bother to read the studies he cites?

“All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly.”

I’m not sure he can make that claim. Based on his own references, carbs seem to decrease both HDL and LDL. That would suggest a more-or-less neutral effect on the HDL/LDL ratio and therefore a neutral effect on CVD.
fatty acids and cholesterol3

By the way, does Taubes now accept that cholesterol plays a role in heart disease? It seems that the reason red meat is beneficial for you, according to Taubes, is that is helps lower LDL and raise HDL. The same notion he was arguing against the entire chapter! Moreover, it seems that the source of the cholesterol-mitigating properties is the unsaturated fats that are found more abundantly in vegetable oils. Here’s Taubes again:

The observation that monounsaturated fats both lower LDL cholesterol and raise HDL also came with an ironic twist: the principal fat in red meat, eggs, and bacon is not saturated fat, but the very same monounsaturated fat as in olive oil.

So why not just go for the olive oil? Oh yeah, because vegetable fats cause cancer or some such nonsense. But not meat, of course; it’s perfect.

Refs

 

1. Ahrens, E. H., Jr et al. Dietary control of serum lipids in relation to atherosclerosis. JAMA 164, 1905–1911 (1957).

2. Kuo PT. Hyperglyceridemia in coronary artery disease and its management. JAMA 201, 87–94 (1967).

3. Goldstein, J. L., Hazzard, W. R., Schrott, H. G., Bierman, E. L. & Motulsky, A. G. Hyperlipidemia in Coronary Heart Disease I. Lipid Levels in 500 Survivors of Myocardial Infarction. J. Clin. Invest. 52, 1533–1543 (1973).

4. Carlson, L. & Böttiger, L. E. Ischaemic heart-disease in relation to fasting values of plasma triglycerides and cholesterol. Stockholm prospective study. The Lancet 299, 865–868 (1972).

5. Chapter XIII: Serum Triglyceride Changes. Circulation 37, I–224–I–226 (1968).

6. Kannel, W. B., Castelli, W. P., Gordon, T. & McNamara, P. M. Serum Cholesterol, Lipoproteins, and the Risk of Coronary Heart Disease: The Framingham Study. Ann. Intern. Med. 74, 1–12 (1971).

7. In fact, Taubes’s citation for Framingham here is actually a newspaper article that doesn’t even mention Framingham. I am assuming it is an innocent citation error.

8. Keys, A. Coronary heart disease in seven countries. I. The study program and objectives. Circulation 41, I1–8 (1970).

9. Fredrickson, D. S., Levy, R. I. & Lees, R. S. Fat Transport in Lipoproteins — An Integrated Approach to Mechanisms and Disorders. N. Engl. J. Med. 276, 34–44 (1967).

10. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. The Lancet 354, 447–455 (1999).

11. De Lorgeril, M. et al. Mediterranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications After Myocardial Infarction: Final Report of the Lyon Diet Heart Study. Circulation 99, 779–785 (1999).

12. Katan, M. B., Zock, P. L. & Mensink, R. P. Dietary oils, serum lipoproteins, and coronary heart disease. Am. J. Clin. Nutr. 61, 1368S–1373S (1995).

13. Grundy, S. M. Influence of stearic acid on cholesterol metabolism relative to other long-chain fatty acids. Am. J. Clin. Nutr. 60, 986S–990S (1994).
 

The Big Fat Surprise: A Critical Review; Part 1

The-Big-Fat-Surprise

[go to The Big Fat Surprise: A Critical Review; Part 2]

Introduction to Part 1

Nina Teicholz’s The Big Fat Surprise (BFS) is a book that claims to reveal “the unthinkable: that everything we thought we knew about dietary fats is wrong.” This is a trope that is often exploited to sell diet/nutrition books, and it works surprisingly well.

What makes this particular book interesting is not so much that it is bad (which it is) or that it is extravagantly biased (which it also is). No, what really fascinates me about this book is that the author excessively and shamelessly lifts other people’s material. Most notably Teicholz lifts from another popular low-carb book called Good Calories, Bad Calories (GCBC) by Gary Taubes.

If I had written a book and I had “borrowed” other people’s work, here’s what I would do: I would cross my fingers and pray that no one ever notices. I would never bring it up, and diffuse it as quickly as I could if someone else brought it up. Not Teicholz. She gets in there and picks fights, accusing others of plagiarizing her work if they write a piece that is also critical of low-fat diets.

 

Despite all this finger-wagging Teicholz does try to bring something new to the table. She makes an effort to speak to some people involved that Taubes did not. Although given the excessive misrepresentation of not only her work but those of others I am deeply skeptical that Teicholz fairly represented her conversations with some of these individuals.

Teicholz also attempts to appeal to the soccer mom demographic by writing a chapter about how women and children are not adequately studied when it comes to low-fat diets. However, any study she might cite in favor of her low-carb narrative (Shai, for example) has similar male:female ratios, and most don’t include children. There are good reasons for this, of course, but I won’t discuss them here.

At any rate, to wrap up this introduction, the results of fact-checking the first five chapters of BFS are below. I posses all of the texts that are discussed. I will be happy to provide them if you like. Let me know.

Chapter 1: The Fat Paradox: Good Health on a High-Fat Diet

On page 11-12 Teicholz discusses the Masai tribe of Africa and how they consume quite a bit of milk daily yet have very low cholesterol (much like Taubes does in ch. 2 of GCBC). She also mentions that they are not fat and they don’t have high blood pressure. I don’t know why she throws the blood pressure and leanness in there since no one claims that milk causes high blood pressure, nor that these African tribes that walk about 30 miles per day and burn 300-500 kcals/hour would be fat because they drink milk. The real crime here is one of omission.

In support of her argument that diets heavy in saturated fat won’t lead to high cholesterol because the Masai do it, she cites an article published in the NEJM titled “Some Unique Biologic Characteristics of the Masai of East Africa.”1 The entire point of that article was to claim that the reason that the Masai have such low cholesterol levels despite a diet heavy in saturated fats was because they have a unique feedback mechanism that suppresses endogenous cholesterol synthesis that most of us don’t have. Yet there of course is no mention of this in the text (or GCBC) because to suggest that their low cholesterol was due to genetics would hurt her meat-is-good-for-you narrative.

Continuing with the Masai on page 12, Teicholz discusses George Mann and his findings:

If our current belief about animal fat is correct, then all the meat and dairy these tribesmen were eating would have caused an epidemic of heart disease in Kenya. However, Mann found exactly the opposite—he could identify almost no heart disease at all.

As evidence for this she cites a paper titled “Atherosclerosis in the Masai” that does indicate very little evidence of infarctions, but does state the following:

We find the Masai vessels do show extensive atherosclerosis; they show coronary intimal thickening which is equal to that seen in elderly Americans.

Mann goes on to say that the reason why there are so few occlusions despite the extensive atheroslcerosis is that the Masai’s blood vessels enlarge as they age.2

Now that we have uncovered some very important points that were concealed by Teicholz, we are still confronted with an odd reality. The Masai consume a ton of milk and likely a fair amount of meat and yet they do not have elevated cholesterol levels due to a unique biological mechanism. Despite the low cholesterol they still get atheroslcerosis. Enough that men in their prime have the blood vessels of elderly Americans. Yet despite even this they manage to escape heart attacks because their vessels are larger than average. Wow. I don’t know what to make of the Masai, except that they are indeed a unique people. In this case I think we can treat the Masai as outliers and not assume that we can live like they do and remain free of heart disease.

* * *

On page 14 Teicholz discusses a text by Hrdlicka3,4 published near the turn of the (last) century and states:

The Native Americans he visited were eating a diet of predominantly meat, mainly from buffalo, yet, as Hrdlicka observed, they seemed to be spectacularly healthy and lived to a ripe old age.

However, if you go look at the text you will find that the diet of Native Americans is based around, y’know, the most abundant crops in the Americas: corn and wheat. There are several pages devoted to describing the diet, so I don’t want to quote all of it, but perhaps this will give you an idea of what Hrdlicka really found. Page 19:

The principal article of diet among the Indians throughout the Southwest and Mexico is maize, which is eaten in the form of bread of various kinds, or as mush, or boiled entire. It is also parched on charcoal and eaten thus, or is ground into a fine meal, which, sweetened, constitutes the nourishing pinole of some of the tribes. Wheat is used in similar ways but less extensively. Next in importance to corn and wheat in the Indian diet are meat and fat and beans. Meat is scarce.

For a more nuanced view of the issue see this post and scroll down to “Hrdlička and the diet of Southwestern Native Americas.”

* * *

Page 15, Teicholz attempts to make the case that Africans living in British colonies nearly 100 years ago ate a ton of meat and had basically no cancer. As evidence for both of these claims she cites what amounts as a Letter to the Editor in the BMJ by George Prentice.5

The British Medical Journal routinely carried reports from colonial physicians who, though experienced in diagnosing cancer at home, could find very little of it in the African colonies overseas. So few cases could be identified that “some seem to assume that it does not exist,” wrote George Prentice, a physician who worked in Southern Central Africa, in 1923.

If you bother to look at the publication by Prentice you will notice that right after he says that some seem to assume that cancer does not exist, he immediately states why this is both a false and dangerous belief that has led to a patient of his dying of cancer because he himself believed that Africans did not get cancer when he was a younger doctor. He didn’t remove a breast tumor when he could have and should have and that his patient died because of this. Prentice also says in addition to breast cancer he sees other cancers all the time:

I have also seen epithelioma of the face. In this case the eyelids and the whole of one eye were completely destroyed, and the bone of the eye socket was attacked; the case was inoperable. I have seen a tumour, fungating and evidently malignant, that had practically split the bones of the face, causing the eyes to bulge laterally and giving a strange chameleon look to the patient. It was inoperable. I have seen cancer of the left ovary that proved fatal. I believe I have seen cases of malignant disease of the liver, but as there was no autopsy the diagnosis was not confirmed. I have removed many large tumours of the testicle which, if not cancerous, are of a nature unknown to me. Keloids and fatty tumours are very common.

In case you could not tell, Teicholz takes Prentice’s words completely out of context to make it appear he was communicating the opposite of what he was actually communicating.

I’m sure she’s also hoping that the reader won’t realize that – true or not – all she has been discussing so far in the book are very tenuous and unscientific correlations, and that by the time the readers get to the part where she bashes these types of associations that they won’t realize she’s being wildly inconsistent and even hypocritical in how she deals with studies and observations.

* * *

Page 16:

It is true that American beef from a cow raised on grain does have a different fatty-acid profile from an ox hunted in the wild. In 1968, the English biochemist Michael Crawford was the first to look at this question in detail. […] His paper seemed to confirm that modern-day people should not consider their domesticated meat to be anywhere near as healthy as hunted meat from the wild. And for the past forty-five years, Crawford’s paper has been widely cited, forming the general view of the subject. What Crawford buries in his data, however, is that the saturated fat content of the wild and domesticated animal meats hardly differed at all.

Yep. Crawford “buries” it by making it Figure 1 in his paper.6 I know when I want to bury data in a paper I visualize it and put it at the head of the results.

fatty acid ratios

By the way, this “widely cited” paper has been cited only 183 times since it’s publication in 1968. Truly a landmark paper, this one.

Chapter 2: Why We Think Saturated Fat Is Unhealthy

Cribbing Taubes Alert

In GCBC on page 14 Taubes discusses a century-old document that was published by a German journal that is both very difficult to find and written in German.

The evidence initially cited in support of the hypothesis came almost exclusively from animal research-particularly in rabbits. In 1913, the Russian pathologist Nikolaj Anitschkow reported that he could induce atherosclerotic-type lesions in rabbits by feeding them olive oil and cholesterol.

Do you think Taubes both A) possesses that obscure text AND B) is fluent in German? It’s possible, although my money would be on Taubes simply reading what others had written about the study and simply paraphrasing.

BFS page 22:

Early evidence suggestively linking cholesterol to heart disease also came from animals. In 1913, the Russian pathologist Nikolaj Anitschkow reported that he could induce atherosclerotic-type lesions in rabbits by feeding them huge amounts of cholesterol.

What are the odds that Teicholz also speaks German and has the German text that was published over 100 years ago? Again, possible, but given the similarity of how she and Taubes discuss the paper my guess is that she simply paraphrased Taubes without attribution.

* * *

Here’s something interesting… On page 16 of GCBC Taubes says the following:

In 1937, two Columbia University biochemists, David Rittenberg and Rudolph Schoenheimer, demonstrated that the cholesterol we eat has very little effect on the amount of cholesterol in our blood.

As evidence he cites Rittenberg and Schoenheimer’s 1937 paper titled “Deuterium as an indicator in the study of intermediary metabolism XI. Further studies on the biological uptake of deuterium into organic substances, with special reference to fat and cholesterol formation.”7

On page 23 of BFS Teicholz writes the following:

The notion that cholesterol in the diet would translate directly into higher cholesterol in the blood just seemed intuitively reasonable, and was introduced by two biochemists from Columbia University in 1937.

She also cites the same exact paper. You see the problem, right? Both Taubes and Teicholz claim opposite things yet cite the same paper as evidence. So who is correct? Actually neither of them are correct because the cited text doesn’t address the issue. The paper discusses experiments on animals such as rodents and chicks, not humans as is implied by both Taubes and Teicholz. Furthermore, the only thing these experiments demonstrate is that these animals are capable of synthesizing cholesterol, and has essentially nothing to do with dietary cholesterol influencing or not influencing serum cholesterol.

* * *

Continuing with the dietary cholesterol controversy, on page 23 immediately after the above statement Teicholz claims:

It was Ancel Keys himself who first discredited this notion. Although in 1952 he stated that there was “overwhelming evidence” for the theory […]

She then accuses him of being a hypocritical flip-flopper for arrogantly walking the statement back three years later by saying that tremendous amounts of cholesterol have only a trivial effect on serum cholesterol and that “this point requires no further consideration.”

Damn, this guy sounds like an arrogant prick considering he wholly endorsed the theory a few years before, right?!

…Except if you look at the 1952 paper where Teicholz pulls that quote Keys says the EXACT OPPOSITE of what Teicholz claims.8 In the paper Keys argues that the animal experiments that have shown that feeding high cholesterol to, say, rabbits have no relevance to humans, going on to say

No animal species close to man in metabolic habitus has been shown to be susceptible to the induction of atherosclerosis by cholesterol feeding.

AND

From the animal experiments alone the most reasonable conclusion would be that the cholesterol content of human diets is unimportant in human atherosclerosis.

AND

Direct evidence on man in this connection is unimpressive.

Besides, even if he did hold an erroneous belief beforehand, why would you want to knock a guy for simply following the evidence? This is science: you are supposed to always be self-correcting.

* * *

Page 23-24:

In 1992, one of the most comprehensive analyses of this subject concluded that the vast majority of people will react to even a great deal of cholesterol in the diet by ratcheting down the amount of cholesterol the body itself produces. […] Responding to this evidence, health authorities in Britain and most other European nations in recent years have rescinded their advisories to cap dietary cholesterol.

Emphasis mine. The reason for bolding “in recent years” is because the evidence cited for this sentence is a paper published in 1987!!9 And of course the evidence they were apparently responding to was a meta-analysis published in 1992.10 There’s a chronology problem here. A meta-analysis, by the way, whose first sentence of the summary states:

Serum cholesterol concentration is clearly increased by added dietary cholesterol but the magnitude of predicted change is modulated by baseline dietary cholesterol.

Again, emphasis mine.

* * *

On page 25 you will see this structure:

fatty acid

This structure is incorrect on many levels. For one it is not even a fatty acid. It’s actually not anything because it is not a legitimate chemical structure, but it’s closest to pentane which no one would want to consume. In order for it to be a fatty acid it would at least need a carboxyl group at one end. However, that would make the structure into valeric acid which is not commonly found in foods (especially the butter, meat, and cheese Teicholz promotes) and not commonly consumed unless you’re eating valerian root.

I pointed this out on my Amazon review of the book and I got pilloried because apparently I was supposed to simply know that the Fisher projection was not really supposed to be a fatty acid, but was supposed to be a simple, generic structure to illustrate how hydrogens are arranged around carbon atoms. However, if Teicholz didn’t want to put a proper carboxyl group because she was afraid it might confuse her audience she could have at least put an “R” or ellipses or something to indicate that part of the fatty acid is being left out in order to concentrate on the hydrogens. Even so, if it is indeed just a generic structure used to illustrate how hydrogens are arranged then why are the end hydrogens arranged incorrectly, and why are there two missing hydrogens? This structure is absolutely wrong no matter how you slice it.

* * *

The lies about Ancel Keys continue on page 27 when Teicholz discusses a paper of his called “Atherosclerosis: A Problem in Newer Public Health” and says this paper received “enormous attention” and was the genesis of America’s alleged fear of fat.

There is no evidence at all that Keys’s 1953 paper received “enormous attention.” In fact, the evidence that exists would suggest the opposite. There was no mention of the paper in the lay press. That is until relatively recently when Gary Taubes began lying about it. What about academia? According to Google Scholar this highly influential paper has only been cited 247 times since its publication, which spans 61 years as of this writing. An average of four citations per year. It was cited merely 99 times from the time it was published to 1973, a full twenty years after its publication. For comparison, on page 159-160 Teicholz mentions a study whose results she claims were “ignored.” That study was published in 1992 and has received 682 citations.

* * *

Page 31:

Keys found further ammunition for his hypothesis from a compelling observation made during World War II, which is that deaths from heart disease dropped dramatically across Europe during wartime and rebounded soon afterward. These events led Keys to presume that the food shortages— particularly of meat, eggs, and dairy—were very likely the cause. There were, however, other explanations: for instance, sugar and flour were also scarce during the war; people breathed fewer car-exhaust fumes due to gasoline shortages and got more exercise by cycling or walking to get around. Other scientists noted these alternative explanations for the decline in heart disease, but Keys dismissed them outright.

The paper that noted the alternative explanations was published in 1957, yet Keys was apparently dismissing them in 1956.11,12

* * *

On page 34, Teicholz discusses a paper by Yerushalmy and Hilleboe that criticized a graph in Keys’s “Atherosclerosis: A Problem in Newer Public Health” paper mentioned above.13

Yerushalmy’s objection was that Keys seemed to have selected only certain countries that fit his hypothesis. There were other factors that could equally well explain the trends in heart disease in all these countries, he asserted.

If you actually read Keys’s paper you will note that Keys mentioned that he left out some less-developed countries because they had very poor vital health statistics.14 Some more developed European countries he claims he would have included if the Nazi’s had not very recently invaded, occupied, and rationed food which would confound his simple cross-sectional analysis. It wasn’t that he was a diabolical scientist bent on lying to the public about the cause of heart disease. Or if he was he had a damn fine excuse for not using those countries.

It’s funny because on pages 34-36 Teicholz criticizes Keys for not including more European countries like France and Switzerland (which incidentally would have fallen right in line with Keys’s graph). Then a few pages later on 37-38 Teicholz discusses Keys’s Seven Countries Study and criticizes him for including countries that Nazi Germany had invaded and occupied several years before.

At any rate, Yerushalmy and Hilleboe did indeed point out some other factors in their paper, most prominently they pointed out that both animal fat and animal protein were far better correlated with heart disease than total fat. Many different types of heart disease, in fact. This held true whether or not it was calculated as total amounts or as a percentage of total calories. Moreover, vegetable protein and vegetable fat were negatively correlated with heart disease.

Of course there was no way that Teicholz was ever going to mention this.

* * *

Page 40:

I looked more closely into the dietary data on Greece, because it became the exemplar for the Mediterranean diet (see Chapter 7), and I found one of the most stunning and troubling errors. In that country. Keys had sampled the diets on Crete and Corfu more than once, in different seasons, in order to capture variations in the food eaten. Yet in an astonishing oversight, one of the three surveys on Crete fell during the forty-eight-day fasting period of Lent.

Astonishing oversight? One of the most stunning and troubling errors? Despite what appears to be insincere hand-wringing over this gravest of all scientific errors, I don’t really see the problem here. The question that needs to be asked here is: Does collecting dietary information during a period where some Christians adhere to a quasi-fasting ritual invalidate the dietary data? I suppose it would if a sufficient number of participants were strictly adhering to the fast. Was this the case? According to the 211-page write-up of the study programs and objectives this was not the case15:

The seasonal comparisons in Crete and Corfu were of interest because the survey in Crete in February and part of the survey in Corfu in March-April were in the 40-day fasting period of Lent of the Greek Orthodox church, but strict adherence did not seem to be common in the populations of the present study.

How would the scientists come to the conclusion that there was no strict adherence? They could simply compare the dietary data collected during the spring with the dietary data collected during other times of the year. What if the participants were all lying on their dietary surveys? The researchers also collected the actual foods eaten by participants, lyophilized them, and sent them out for chemical analysis. Apparently there were no significant differences with that data either.

Even if the alleged “error” of collecting data in the spring was so insurmountable it had to be thrown out, it would not invalidate the other two dietary collections in Crete and it would certainly not be nearly enough to nullify the entire study. It seems pretty clear to me that while writing this book Teicholz is actively searching for any hint of impropriety. She discovered a mention of Lent, decided to ignore the rest, and enthusiastically proclaimed that she had unearthed some alarming facts about the study.

Additionally she tries to make the case on pages 41 and 42 that Keys tried to sheepishly bury the flawed methodology of his crappy study. If this is true he did an exceedingly poor job of it, considering in addition to all of the analyses published from the data. Keys published:

  • A 211-page paper describing the study objectives and methods15
  • A 300+ page monograph describing the particular details of data collection in each country16
  • A 300+ page book describing in great detail the study and its results17

In addition there were other entire books published on the study.18,19 Keys is not being obfuscatory.

Chapter 3: The Low-Fat Diet Is Introduced to America

Cribbing Taubes Alert

On page 49 Teicholz discusses an AHA nutrition committee report:

Committee members went so far as to rap diet-heart supporters like Keys on the knuckles for taking “uncompromising stands based on evidence that does not stand up under critical examination.” The evidence, they concluded, did not permit such a “rigid stand.”

On page 20 of GCBC, Taubes makes a similar statement regarding the same report and uses the same quotes.20 I would argue that both get it wrong. The report seems to have somewhere between a neutral and a favorable view of Keys, as evidenced by the following quotes:

  • “Mayer et al. found that high-fat animal or vegetable diets increased and low-fat diets decreased serum cholesterol of normal subjects, confirming earlier data of Keys.”
  • “Keys, in particular, has placed emphasis on the proportion of total dietary calories contributed by the common food fats […] Certainly there is an abundance of data, both clinical and experimental, that tends to relate excess fat intake to atherosclerosis.”

* * *

Cribbing Taubes Alert

On page 49 Teicholz continues discussing the views of the AHA:

The AHA committee swung around in favor of their ideas, and the resulting report in 1961 argued that “the best scientific evidence available at the present time” suggested that Americans could reduce their risk of heart attacks and strokes by cutting the saturated fat and cholesterol in their diets.

On page 21 of GCBC Taubes says essentially the same thing and uses the same quote from the same paper.21

Continuing on the report, page 50:

Keys himself thought that the 1961 AHA report he had helped write suffered from “some undue pussy-footing” because it had prescribed the diet only for high-risk people rather than the entire American population […]

On page 21 of GCBC Taubes says almost the exact same thing, including the undue pussy-footing quote. However, Taubes cites the quote correctly as being from Time magazine’s article titled Fat in the Fire, whereas Teicholz cites it incorrectly as The Fat of the Land.22,23

* * *

Cribbing Taubes Alert

There is getting to be too many of these alerts. On page 4 of GCBC Taubes states:

“People should know the facts,” Keys told Time. “Then if they want to eat themselves to death, let them.”

BFS page 50:

“People should know the facts,” he said. “Then, if they want to eat themselves to death, let them.”

This quote is found in Time magazine’s The Fat of the Land article.23 Continuing…

GCBC page 21:

The Time cover story, more than four pages long, contained only a single paragraph noting that Keys’s hypothesis was “still questioned by some researchers with conflicting ideas of what causes coronary disease.”

BFS page 51:

In the Time article, there is only a brief mention of the reality that Keys’s ideas were “still questioned” by “some researchers” with conflicting ideas about what causes coronary disease.

* * *

On page 54 Teicholz educates the reader on case-control studies:

These studies are understood to suffer from “recall bias,” whereby patients may inaccurately remember past consumption.

Immediately after this disclaimer Teicholz goes on to produce several case-control studies that fit her narrative. By doing so, this is what I hear as a reader: “Case-control studies suck. Don’t try to use them as evidence. But here are a few whose results I like and you should know about them.”

* * *

Cribbing Taubes Alert

GCBC page 26:

[JAMA] reported that the mostly Italian population of Roseto, Pennsylvania, ate copious animal fat – eating prosciutto with an inch-thick rim of fat, and cooking with lard instead of olive oil – and yet had a “strikingly low” number of deaths from heart disease, Keys said it warranted “few conclusions and certainly cannot be accepted as evidence that calories and fats in the diet are not important.”

BFS page 55:

[T]he mostly Italian population living there had a “strikingly low” number of deaths from heart disease […] the local diet included copious amounts of animal fats, including prosciutto with fat an inch thick around the rim, and most meals cooked in lard. […] Keys concluded that the Roseto data “certainly cannot be accepted as evidence that calories and fats in the diet are not important.”

There is so much information in both those publications, yet surprisingly the same exact quotes are independently plucked by Teicholz.24,25

* * *

Page 56:

F. W. Lowenstein, a medical officer for the World Health Organization in Geneva, collected every study he could find on men who were virtually free of heart disease, and concluded that their fat consumption varied wildly.

I suppose that’s true according to the study.26 Fat intake varied from 21 g/day to 355 g/day in the case of the Somalis. Although, if you remove the Somalis as something of an outlier (they also consume 6,247 kcals/day according to the paper), then fat intake in all the other populations drops to 100 grams of fat per day or less.

* * *

Cribbing Taubes Alert

Teicholz uses Taubes’s Karl Popper quote.

GCBC page 24-25:

[The scientific method requires] that scientists not just test their hypotheses, but try to prove them false. “The method of science is the method of bold conjectures and ingenious and severe attempts to refute them,” said Karl Popper.

BFS page 56-57:

A scientist must always try to disprove his or her own hypothesis. Or, as one of the great science philosophers of the twentieth century, Karl Popper, described, “The method of science is the method of bold conjectures and ingenious and severe attempts to refute them.”

* * *

Page 57:

[…] Keys was not on the lookout for his own biases. He considered the burden of proof to be on those opposing him. He made no attempts to refute his own ideas, as Popper advised. He promoted the “idol of his mind” without hesitation.

OMG. What?! How?? Can I get some evidence for that?

* * *

 

Page 65 Teicholz then pivots to Framingham and mentions how they found cholesterol to be a big predictor of death. BUT…

However, thirty years later, in the Framingham follow-up study—when investigators had more data because a greater number of people had died— it turned out that the predictive power of total cholesterol was not nearly as strong as study leaders had originally thought.

Is she talking about the paper that states in the conclusion “This study and the Coronary Drug Project results on nicotinic acid therapy show a direct association of cholesterol levels with mortality, which becomes stronger with lengthy follow-up”?28 Is that the one she’s talking about? Because that’s the one she cited. The paper also states that the association holds strong even after adjusting for individual differences in blood pressure, smoking, relative weight, and diabetes.

* * *

Page 67:

Not until 1992, in fact, did a Framingham study leader publicly acknowledge the study’s findings on fat. “In Framingham, Mass, the more saturated fat one ate . . . the lower the person’s serum cholesterol. . . and [they] weighed the least” wrote William P. Castelli […]

What the reader doesn’t know is that 1) this quote is taken from an editorial that extols the virtues not of meat and cheese, but of the unsaturated fat in nuts, 2) there is literally a half page of text between the ellipses, 3) the italics are not part of the original quote, and most importantly 4) Teicholz cuts off the quote immediately before the author mentions that he is talking about the people that were the most physically active.29 But I’m sure their physical activity has no effect on their weight or cholesterol levels, right?

* * *

Cribbing Taubes Alert

On page 159 of GCBC Taubes quotes from a 1967 JAMA editorial30:

JAMA published an editorial in response to Kuo’s article, suggesting that the “almost embarrassingly high number of researchers [who had] boarded the ‘cholesterol bandwagon'” had done a disservice to the field. “This fervent embrace of cholesterol to the exclusion of other biochemical alterations resulted in a narrow scope of study,” the editorial said.

On page 71 of BFS Teicholz uses the same exact quote:

An “almost embarrassingly high number of researchers boarded the ‘cholesterol bandwagon,'” lamented the editors of the Journal of the American Medical Association in 1967, referring to the narrow, “fervent embrace of cholesterol” to the “exclusion” of other biochemical processes that might cause heart disease.

Chapter 4: The Flawed Science of Saturated versus Polyunsaturated Fat

Cribbing Taubes Alert

Much like elsewhere in BFS, Teicholz appears to take an incredible amount of what might be called “inspiration” from GCBC. Much like in GCBC, Teicholz discusses the Anti-Coronary Club trial, plucks the same quotes, and discusses the same media reactions.

GCBC, page 36:

The first and most highly publicized was the Anti-Coronary Club Trial, launched in the late 1950s by New York City Health Department Director Norman Jolliffe.

BFS, page 73:

An early and celebrated trial was called the Anti-Coronary Club, launched by Norman Jolliffe, director of the New York City Health Department, in 1957.

 

GCBC, page 36:

The eleven hundred middle-aged members of Jolliffe’s Anti-Coronary Club were prescribed what he called the “prudent diet,” which included at least one ounce of polyunsaturated vegetable oil every day. The participants could eat poultry or fish anytime, but were limited to four meals a week containing beef, lamb, or pork.

BFS, page 73:

He signed up eleven hundred men to his Anti-Coronary Club and instructed them to reduce their consumption of red meat, such as beef, lamb, or pork, to no more than four times a week (which would be considered a lot by today’s standards!) while consuming as much fish and poultry as they liked.

GCBC, page 36:

[T]wenty-six members of the club had died during the trial, compared with only six of the men whose diet had not been prudent.

BFS, page 74:

[T]wenty-six members of the diet club had died during the trial, compared to only six men from the controls.

 

Okay, maybe both Taubes and Teicholz did independent research and came across the same study and both found it was compelling enough to include in their books. And maybe they both independently included the same info from the study as well. It’s certainly possible. But would they mention the same NYT article?

GCBC, page 36:

“Diet Linked to Cut in Heart Attacks,” reported the New York Times in May 1962.

BFS, page 74:

“Diet Linked to Cut in Heart Attacks,” reported the New York Times in 1962 […]

Would they independently use the same quote from the multiple trial publications?

GCBC, page 36:

Eight members of the club died from heart attacks, but none of the controls. This appeared “somewhat unusual,” Christakis and his colleagues acknowledged.

BFS, page 74:

[I]nvestigators began to find “somewhat unusual” results: […] Eight members of the club had died of heart attacks, but not one of the controls.

They also both misrepresent the study:

GCBC, page 36:

They discussed the improvements in heart-disease risk factors (cholesterol, weight, and blood pressure decreased) and the significant reduction in debilitating illness “from new coronary heart disease,” but omitted further discussion of mortality.

BFS, page 74:

In the discussion section of the final report, the authors […] emphasized the improved risk factors among the men in the diet club but ignored what those risk factors had blatantly failed to predict: their higher death rate.

Notice how both Taubes and Teicholz minimize the main results of the study, namely that the prudent diet did exactly what researchers imagined it would do: reduce not only risk factors for heart disease, but also actual coronary events.31–33 Further, they both misrepresent the study by claiming those devious scientists omitted discussion of death rate when nothing could be further from the truth. Both cited publications discuss death rate and mortality among participants very clearly. In fact, the slight difference in death from causes other than heart disease was not even significant. From the 1966 publication31 (emphasis mine):

The rates for these deaths in the 50-59 age group were 689 per 100,000 person-years in the experimental group, and 666 per 100,000 in the control group. The difference between these two rates is slight and not statistically significant.

* * *

Cribbing Taubes Alert

In GCBC, Taubes immediately segues from discussing the Anti-Coronary Club trial to discussing the Dayton’s LA Veterans trial.34–36 Strangely enough Teicholz does the exact same thing.

GCBC, page 37:

In July 1969, Seymour Dayton, a professor of medicine at the University of California, Los Angeles, reported the results of the largest diet-heart trial to that date. Dayton gave half of nearly 850 veterans residing at a local Veterans Administration hospital a diet in which corn, soybean, safflower, and cottonseed oils replaced the saturated fats in butter, milk, ice cream, and cheeses. The other half, the controls, were served a placebo diet in which the fat quantity and type hadn’t been changed. The first group saw their cholesterol drop 13 percent lower than the controls […]

BFS, page 75:

It was conducted by UCLA professor of medicine Seymour Dayton on nearly 850 elderly men living in a local Veterans Administration (VA) home in the 1960s. For six years, Dayton fed half the men a diet in which corn, soybean, safflower, and cottonseed oils replaced the saturated fats in butter, milk, ice cream, and cheese. The other half of the men acted as controls and ate regular foods. The first group saw their cholesterol levels drop almost 13 percent more than did the controls.

Is it just me or do those paragraphs sound very similar?

GCBC, page 37:

“Was it not possible,” Dayton asked, “that a diet high in unsaturated fat…might have noxious effects when consumed over a period of many years? Such diets are, after all, rarities […]”

BFS, page 75:

“Was it not possible,” he asked, “that a diet high in unsaturated fat. . . might have noxious effects when consumed over a period of many years? Such diets are, after all, rarities.”

Both Taubes and Teicholz introduce the author and gives a brief background of the trial, then relate the conditions and methods of the study, then they cherry-pick from the results. They both then interpret the results for you. ONLY AFTER ALL THAT do Teicholz and Taubes reproduce a couple sentences from the journal article questioning whether a diet of unsaturated fat might have “noxious effects” presumably because of the study results. What they likely want the reader to think is that after the results of the study are in and the numbers have been crunched and the data has been analyzed Dr. Seymour Dayton is sitting at his desk and ruminating on what could have produced these results. As if he is asking a rhetorical question or providing a hypothesis for a future dietary trial.

In reality Dayton actually asks that question in the beginning of the paper to kind of whet the reader’s appetite. He then goes on to answer that very question in the text with an answer that would not be favorable to Teicholz’s (or Taubes’s) argument. Do you want to know if the experimental diet has noxious effects? Well there’s a section in the results portion of the study titled “Does the Experimental Diet Have Noxious Effects?” where Dr. Dayton states34:

As indicated in table 29 and discussed in some detail above, the excess mortality in nonatherosclerotic categories was not sufficiently impressive to justify the conclusion that harmful effects had been demonstrated.

AND

One may also wonder whether the experimental diet may have exerted its effect on mortality data primarily by accelerating nonatherosclerotic deaths (see table 28), decreasing the atherosclerotic mortality by inducing early death due to other cause. Such a mode of action would be associated with higher numbers of deaths in the experimental group compared with the controls, whereas the reverse was true in this trial (fig. 13).

AND

The other observation which raised some question of a possible toxic effect was the low arachidonic acid concentrations in atheromata of long-term, high-adherence subjects on the experimental diet (tables 37 to 40). For reasons already cited, this may be more appropriately viewed as evidence of a salutary rather than a toxic effect.

Teicholz both 1) Uses the exact same quote Taubes does in GCBC, phrases it the exact same way, and removes the same exact words from within the quote; and 2) Takes the quote out of context just like Taubes does in order to imply something antithetical to what Dayton actually meant.

Moreover, both Taubes and Teicholz either minimize or outright ignore results of the study that they do not like (ironically, a trait they accuse the big, bad nutrition researchers of doing). Remember the control group was high in saturated animal fat, and the experimental group was high in unsaturated fats from plants.

The number of men sustaining events in major categories, in the control and experimental groups, respectively, was: definite silent myocardial infarction, 4 and 9; definite overt myocardial infarction, 40 and 27; sudden death due to coronary heart disease, 27 and 18; definite cerebral infarction, 22 and 13. The difference in the primary end point of the study-sudden death or myocardial infarction was not statistically significant. However, when these data were pooled with those for cerebral infarction and other secondary end points, the totals were 96 in the control group and 66 in the experimental group; P = 0.01. Fatal atherosclerotic events numbered 70 in the control group and 48 in the experimental group; P < 0.05. Life-table analysis in general confirmed these conclusions. For all primary and secondary end points combined, eight year incidence rates were 47.7% and 31.3% for the control and experimental groups, respectively; P value for the difference between the two incidence curves was 0.02.

If you don’t want to read the above block quote, I’ll summarize it for you: in all but one endpoint that was measured the experimental diet of unsaturated fats had less overt myocardial infarction, sudden death, cerebral infarction, fatal atherosclerotic events, etc. And not by a tiny margin – a significant margin.

* * *

Page 75:

[V]egetable oils had been introduced into the food supply only in the 1920s, yet suddenly the oils were being recommended as a cure-all. In fact, the upward curve of vegetable oil consumption happened to coincide perfectly with the rising tide of heart disease in the first half of the twentieth century […]

Not true. At least not true by the study she cites.37 The study by Blasbalg et al simply shows the trends of fatty acid consumption from various sources. Specifically, it shows from which foods Americans have been getting their linoleic acid and alpha linolenic acid. It has absolutely zero analysis of heart disease or any other disease for that matter. Nor does she cite a separate paper that shows trends in heart disease to compare the paper on fatty acid consumption.

Just for kicks, let’s do Teicholz’s work for her. Let’s start with the Blasbalg paper. It appears that in the 20th century butter and lard dropped precipitously at about mid-century. Shortly afterward poultry and shortening consumption rose. Soybean oil also rose concurrently with shortening probably because it was a prominent ingredient. Canola oil consumption also increased in the 90s.

oils1

oils2

What about heart disease? According to a paper by Cooper et al CVD rose until about mid-century, but then begins a steady decline into the millennium.38

F1.large

You have to ask yourself: does the vegetable oil correlate perfectly with CVD?

Cribbing Taubes Alert.

In GCBC, after discussing the LA Veterans trial, Taubes moves immediately to discuss the Helsinki Mental Hospital Study. Strangely enough Teicholz does the exact same thing! What are the odds that they would both independently discuss the same trials in the very same order!

GCBC, page 37:

Ordinary milk was replaced with an emulsion of soybean oil in skim milk, and butter and ordinary margarine were replaced with a margarine made of polyunsaturated fats. These changes alone supposedly increased the ratio of polyunsaturated to saturated fats sixfold.

BFS, pages 76-77:

Ordinary milk was replaced with an emulsion of soybean oil in skim milk, and butter was replaced by a special margarine high in polyunsaturated fats. The vegetable oil content of the special diet was six times higher than in a normal diet.

* * *

Page 86:

[R]emarkably, when Jerry Stamler reissued his 1963 book. Your Heart Has Nine Lives, it was published as a “professional” red leather edition by the Corn Products Company and distributed free of charge to thousands of doctors. Inside, Stamler thanks both that company and the Wesson Fund for Medical Research for “significant” research support.

The very same point was also made by Taubes in GCBC, but that’s not my point here. What I’d like to say about this is that there is roughly half a page in the book that lists people and organizations that have lent financial support to the research in the book. Taubes and Teicholz, however, only list the vegetable oil manufacturers. However, neither list the National Dairy Council which is also named among the research supporters. The reason for leaving out organizations like the NDC should be pretty obvious by now. But let me spell it out for you just in case you’re confused: Both Teicholz and Taubes are attempting to craft a narrative where Big Vegetable Oil and greedy nutrition researchers are in cahoots with each other (and also the government) to dupe the American consumer into eating less butter and cheese. If Teicholz or Taubes were to mention that the National Dairy Council funded the same research, well, then that conspiracy narrative would be weakened.

* * *

On pages 94-95, Teicholz makes the case that low cholesterol is associated with cancer in some studies, and strongly implies that low cholesterol might cause cancer:

By 1981, nearly a dozen sizable studies on humans had found a link between lowering cholesterol and cancer, principally for colon cancer.

This is kind of nit-picky, but notice how Teicholz uses the words “lowering cholesterol” and not “low cholesterol.” This implies that the act of lowering cholesterol leads to cancer and not that the condition of low cholesterol is somehow linked to cancer. To the average Joe Schmo this may seem like I’m being petty and unreasonably contrarian, but if you ever take an epidemiology class you will know that how you phrase things matters a great deal.

Anyway, let’s take a look at the studies Teicholz cites…

Cribbing Taubes Alert

The first thing to notice is that ALL of the studies she cites in favor of the link between low cholesterol and cancer are also cited by Gary Taubes in GCBC when he makes the same argument. Hmmm…

  • Pearce and Dayton 197136: Cited by Taubes, and as previously mentioned it is a bad study to cite in favor of this association.
  • Nydegger and Butler 197039: Cited by Taubes. Does show a link between cancer and low lipoprotein levels. However, the authors point out this is likely due to some cholesterol-lowering effect of cancer and not the other way around, since people with chronically low cholesterol levels do not show an increased incidence of cancer.
  • Oliver et al 197840: Cited by Taubes. The high-cholesterol group had a lower cancer rate than the two low-cholesterol groups, but it was not significant. From the paper: “These figures are surprisingly close to the rates observed in trial subjects in Groups I and III. Thus the data for all cancer do not give rise to special concern.”
  • Beaglehole et al. 198041: Cited by Taubes. Shows a significant inverse relationship.
  • Kark et al. 198042: Cited by Taubes. Also shows an inverse relationship between low cholesterol and cancer, but the authors suggest that the cancer is not likely a result of low cholesterol. From the paper: Were high cholesterol levels associated with improved survival, one would expect that those prevalent cases surviving until 1974 as well as live incident cases (surviving until 1974) would also have high cholesterols. The reverse was true.
  • Garcia-Palmieri et al. 198143: Cited by Taubes. Shows a significant inverse relationship.
  • Stemmermann et al. 198144: Cited by Taubes. Shows a significant inverse relationship with colon cancer, but also shows a positive relationship with CHD but that, of course, is never mentioned.
  • Miller et al. 198145: Cited by Taubes. Shows a significant inverse relationship, but makes it clear that suggesting low cholesterol might cause cancer is almost certainly wrong: “Although we found colon cancer patients to have significantly lower serum cholesterol levels than controls, the observed differences may partially reflect the metabolic influence of advancing disease, since there were no significant differences in serum cholesterol levels between controls and cases with early tumors. Our data suggest that low serum cholesterol levels in colon cancer patients do not necessarily precede tumor formation but may be a consequence thereof.”
  • Kozarevic et al. 198146: Cited by Taubes. Shows a non-significant relationship. Also mentions the following that is never discussed: “Serum cholesterol, as expected, was positively related to the incidence of coronary heart disease death.”
  • Rose et al. 197447: Cited by Taubes. Shows a significant inverse relationship with colon cancer. Again, the authors suggest that low-cholesterol might be a result of colon cancer. And again, this is not mentioned.
  • Williams et al. 198148: Cited by Taubes. Shows a significant inverse relationship with colon cancer, but also mentions that it is possible that cancer of the colon can affect cholesterol absorption and excretion leading to low serum levels. I’m shocked this was not mentioned. Shocked.

* * *

Page 94:

[E]ver since corn oil had been shown to double the rate of tumor growth in rats in 1968, there had been a baseline level of concern about vegetable oils and cancer.

There has? I don’t think so. But anyway, the study Teicholz cites is waaayy off the mark.49 For some brief detail some rats were fed either a low-fat diet, a diet high in coconut oil, or a diet high in corn oil. Then they were injected with a carcinogen known to cause breast cancer. Turns that the rates of uptake and clearance of the carcinogen was equal on all three diets.

* * *

Page 94:

Other studies from this time led to the supposition that corn oil might cause cirrhosis of the liver.

As evidence she cites a very obscure study on rats that were fed a diet explicitly designed to induce cirrhosis where some were also supplemented with corn oil. The researchers found that the corn oil did not exert a protective effect.50 Not preventing cancer DOES NOT EQUAL CANCER-PROMOTION. This is possibly the most twisted and misleading claim Teicholz has made so far in the chapter.

* * *

Page 94:

NIH investigators found that Japanese people with cholesterol levels below 180 mg/dL suffered strokes at rates two to three times higher than those with higher cholesterol.

The cited text does state that the people with the lowest cholesterol did have the highest incidence of stroke51, but I want to note a few things. First, this is not a study, but a letter to the editor. Second, these were not NIH investigators nor do I think it had anything to do with the NIH considering the NIH is never mentioned and the studies discussed in the letter were conducted by Japanese researchers on Japanese participants in Japan. Why would American taxpayer money fund this effort? Please correct me if I am wrong.

* * *

Page 94-95:

The NHLBI became so concerned about the cancer findings that it hosted three workshops in 1981, 1982, and 1983. The evidence on the topic was reviewed and rereviewed by an extremely prominent group of scientists […] One suggestion was that low cholesterol might be an early symptom of cancer, rather than a cause. It was a plausible bit of logic. In the end, however, although the assembled researchers could find no convincing explanation for the cancer findings, they concluded that they did “not present a public health challenge” and did not “contradict” the more urgent, “commonsense” public health message for everyone to lower their cholesterol.

A couple of minor things, but I could not find the word “commonsense” that was quoted above in either of the Feinleib papers that were cited.52,53 Moreover, as I recall the public health message for everyone to lower their cholesterol never even existed. The message was/is for those with high cholesterol to lower their cholesterol. There’s a difference.

The scientists involved included nearly all of the above authors of the scary observational studies that indicated a link between low serum cholesterol and cancer.52 Furthermore, the consensus of the panelists was unanimous in that there was not nearly enough evidence to suggest that lowering cholesterol is a risky behavior.

If Teicholz was not an extraordinarily biased journalist, and she wanted to write BFS with a modicum of honesty she could have easily included some more recent studies that show no association with cholesterol-lowering and an increased risk of cancer.54–58 Some even indicate a protective effect of low serum cholesterol on cancer. But when has the truth ever been able to move books?

* * *

Page 95:

When I mentioned all this to Stamler, he didn’t remember any part of this cancer-cholesterol debate. In this way, he is a microcosm of a larger phenomenon that allowed the diet-heart hypothesis to move forward: inconvenient results were consistantly ignored; here again, “selection bias” was at work.

WOW… Pot. Kettle. Black!

* * *

Cribbing Taubes Alert

GCBC, page 38:

The principal investigator on the trial was Ivan Frantz, Jr., who worked in Keys’s department at the University of Minnesota. Frantz retired in 1988 and published the results a year later in a journal called Arteriosclerosis, which is unlikely to be read by anyone outside the field of cardiology. […] When I asked Frantz in late 2003 why the study went unpublished for sixteen years, he said, “We were just disappointed in the way it came out.”

BFS, page 96:

Frantz, who worked in Keys’s university department, did not publish the study for sixteen years, until after he retired, and then he placed his results in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, which is unlikely to be read by anyone outside the field of cardiology. When asked why he did not publish the results earlier, Frantz replied that he didn’t think he’d done anything wrong in the study. “We were just disappointed in the way it came out,” he said.

At least Teicholz cites Taubes as the source of the Frantz quote.

* * *

On page 97, Teicholz discusses the Western Electric study:

But the results, after twenty years of study, actually showed that diet affected blood cholesterol only a tiny bit and that the “amount of saturated fatty acids in the diet was not significantly associated with risk of death from CHD [coronary heart disease],” as the authors wrote.

Strangely enough, on page 29 of GCBC Taubes discusses the very same study and quotes the very same line. Whooda thunk? Well, by now everyone shoulda thunk.

Anyway, it is true that Western Electric found only non-significant relationships between saturated fat and CHD mortality.59 But yet again, evidence that runs contrary to the overall thesis is left out. From the paragraph immediately before the saturated fat quote (emphasis mine):

When the risk of death from CHD was analyzed in terms of the component dietary variables, it was inversely related to intake of polyunsaturated fatty acids and positively related to intake of dietary cholesterol.

Those evil vegetable oils that are toxic and cause all kinds of disease evidently protect from CHD death. And all that cholesterol from the butter, meat, and cheese that Teicholz wants people to eat is evidently increasing it. What was that Teicholz was saying about “selection bias”?

* * *

Page 98, Teicholz discusses a study in which participants were from either Hiroshima or Nagasaki and tries really hard to convince you to not to pay attention to the results by saying:

The possible radiation exposure of these men to the atomic bombs dropped on their cities at the end of World War II was not factored into the analysis.

If the only participants are from areas with essentially the same amount of radiation then the results are controlled for. If one cohort had been from Osaka and the other from Nagasaki AND their diet or lifestyle was different then she would have a point, but that is clearly not the case. Not to mention the lead author on the publication in question is a STATISTICIAN working in Japan’s ATOMIC BOMB CASUALTY COMMISSION. Ladies and gentlemen, this is what you call a hail mary.

* * *

On page 99, Teicholz discusses the results of a large cohort study she refers to as the Ni-Hon-San. The results indicate that a diet high in saturated fat increases risk of pretty much “all manifestations of CHD” and that you might do well to eat less of it. Of course Teicholz will have none of this so she again scours the publications to find a molehill to portray as a mountain:

So I dug up the paper on NiHonSan’s diet methodology, published two years earlier. It seems that the team in the San Francisco Bay Area had completely fallen down on the job. Not only did they get diet information from only 267 men, compared to the 2,275 interviewed in Japan and a whopping 7,963 in Honolulu, but they had done these interviews only one time and in only one way (a twenty-four-hour recall questionnaire), whereas the other two teams had assessed diet on two different occasions, several years apart, and in four different ways; this was clearly not the “same method” that the authors claimed. Yet these issues were never mentioned […]

These issues are “never mentioned” except where they are explicitly mentioned… in a published article… by the most widely-read nutrition journal… that is completely free and does not require any kind of subscription to access… which is where Teicholz found them.

A few things:

  • Teicholz seems to think that because CA completed less diet records that somehow invalidates the results.
  • California did more than just the 24-hour recall, according to the methods paper.60 They also did a 7-day food record and a food acculturation questionnaire.
  • Teicholz assumes incompetence by the CA researchers, when in fact it was funding issues. It is described in detail in the book Honolulu Heart Program.61 Books are often compiled from large cohort studies like these (e.g. The Seven Countries Study and The China-Cornell-Oxford Project). Investigative journalism, anyone?

* * *

Page 100:

[T]he Japanese have recently been eating far more meat, eggs, and dairy than they used to since the end of World War II, rates of heart disease have dropped to levels seen by Keys in the 1950s. This means that although the story of diet and disease in Japan is complex, we can pretty well say that based on this trend alone, a diet low in saturated fat was not the factor that spared the Japanese from heart disease in the postwar years.

That’s a bold claim for which Teicholz cites a review article not on heart disease, but on stroke – a particular subset of heart disease.62 Additionally, the article never even mentions meat or even fat consumption. It does mention cholesterol as a risk factor, though. Perhaps Teicholz should have read the conclusion:

The atherogenic effect of hypercholesterolemia is well established and is based on evidence from numerous epidemiological, pathological, and biological studies. Furthermore, the proportion of atherothrombotic cerebral infarctions may have recently increased in Japan, because this subtype currently accounts for approximately one third of cerebral infarctions in the Japan Standard Stroke Registry Study (JSSRS). We should formulate a confirmed strategy for lipid management to prevent cerebral infarction.

Teicholz cites no evidence for the increased meat consumption, but no matter. I know how to Google. It seems that meat consumption has increased in Japan over the years, although it still pales in comparison to US consumption which is probably why Japanese heart disease remains comparatively low.

meat_consumption_per_capita_graph-1024x682

Source here and here.

* * *

Page 101:

Seymour Dayton was concerned about the extremely low levels of arachidonic acid, an essential fatty acid present mainly in animal foods, among his prudent dieters.

A few things: 1) Arachidonic acid is one of those evil polyunsaturates, 2) Arachidonic acid is not an EFA, and 3) Here’s what Dayton said about AA on the exact page from the exact paper Teicholz cites34 (emphasis mine)

The other observation which raised some question of a possible toxic effect was the low arachidonic acid concentrations in atheromata of long-term, high-adherence subjects on the experimental diet (tables 37 to 40). For reasons already cited, this may be more appropriately viewed as evidence of a salutary rather than a toxic effect.

* * *

Page 101-102:

In the United States, Pete Ahrens, who was still the prudent diet’s most prominent critic, continued to publish his central point of caution: the diet-heart hypothesis “is still a hypothesis … I sincerely believe we should not. . . make broadscale recommendations on diets and drugs to the general public now.”

A few things:

  1. Ahrens is not referring to the diet-heart hypothesis in this text, he is referring to the lipid hypothesis. There is a difference. Teicholz actually clips the words “lipid hypothesis” from one of the quotes: “The Lipid Hypothesis is still a hypothesis.” In fact, he never even mentions the diet-heart hypothesis in the text.
  2. Ahrens does write those words, but all three phrases are out of order. As a journalist, are you allowed to do that? Take bits of text and arrange them however, as long as you put ellipses in there? If they were to go in order of appearance it would be “[…] make broadscale recommendations on diet and drugs to the general public now […] I sincerely believe we should not […] is still a hypothesis […]” By the way there is about one and a half paragraphs between the last two quotes.
  3. This is another example of quote-mining by Teicholz, because Ahrens actually says some not-so-bad things about the Lipid hypothesis in the text and cholesterol-lowering in general. Two can play the quote-mining game. For instance:

[When asked whether we should abandon the Lipid Hypothesis] My reply to the last question is “no”: I submit that the Lipid Hypothesis has never really been put to an adequate test, and that therefore we cannot conclude that the premise is false.

AND

[I]t seems entirely logical, indeed essential, for internists to screen routinely for hyperlipidemia […] If hyperlipidemia persists, a full year’s evaluation should be made of a low-cholesterol, low-saturated, high polyunsaturated-fat diet, with moderation in alcohol intake.

AND

The Lipid Hypothesis is still a hypothesis. I have tried to show that it is a viable one, and how in the future we may better put it to test.

* * *

Cribbing Taubes Alert

On page 22 of GCBC Taubes states the following:

The resulting literature very quickly grew to what one Columbia University pathologist in 1977 described as “unmanageable proportions.”

On page 102 of BFS Teicholz writes:

By the late 1970s, however, the number of scientific studies had grown to such “unmanageable proportions,” as one Columbia University pathologist put it, that it was overwhelming.

This quote is from Dietary Goals for the United States—Supplemental Views publication which is an 881-page text, at least in PDF format. What are the odds that Teicholz independently arrived at “unmanageable proportions” in that enormous publication? Do you think this is original research?

* * *

Page 102:

The ambiguities inherent to nutrition studies opened the door for their interpretation to be influenced by bias— which hardened into a kind of faith. There were simply “believers” and “nonbelievers,” according to cholesterol expert Daniel Steinberg.

Interestingly enough, this person that Teicholz calls a “cholesterol expert” would almost certainly disagree with the entire thesis of BFS, since he appears to accept that high cholesterol plays a role in heart disease, and that serum cholesterol can be controlled to some degree via the diet. This is made pretty clear if you read the publication Teicholz cites for this.63 In fact, Ahrens himself (whom Teicholz describes above as the biggest critic of the diet-heart hypothesis – although she confuses it with the lipid hypothesis) was, according to Steinberg, one of the first to conduct “the definitive demonstration that saturated fats tend to raise while polyunsaturated fats tend to lower blood cholesterol in humans […]” Steinberg’s entire review series on the pathogenesis of atherosclerosis is both quite interesting and readable. I highly suggest reading them if you are interested in the topic. They are open access papers, but if you didn’t want to go to the trouble of finding them here is a link to the series.

Chapter 5: The Low-Fat Diet Goes to Washington

 

Cribbing Taubes Alert

BFS, page 112:

[W]hen Senator McGovern announced his Senate committee’s report, called Dietary Goals, at a press conference in 1977, he expressed a gloomy outlook about where the American diet was heading. “Our diets have changed radically within the past fifty years,” he explained, “with great and often harmful effects on our health.”

The problem here is that Teicholz cites the source of this quote as “Select Committee on Nutrition and Human Needs of the United States Senate, Dietary Goals for the United States (Washington, DC: US Government Printing Office, 1977); 1.” However, this quote does not appear on page 1. It appears on page XIII. Normally I would chalk this up to a simple citation error.64 The reason I mention it is because Taubes uses the same exact quote on page 10 of GCBC, and also mistakenly cites the source of the quote as being on page 1. I would argue (as I have done previously many times) that this is good evidence that Teicholz is simply lifting sentences from others and simply citing what they cite – likely without ever even seeing the source material.

* * *

Cribbing Taubes Alert

Page 112:

The New York Times health columnist Jane Brody perfectly encapsulated this idea when she wrote, “Within this century, the diet of the average American has undergone a radical shift away from plant-based foods such as grains, beans and peas, nuts, potatoes, and other vegetables and fruits and toward foods derived from animals—meat, fish, poultry, eggs and dairy products.”

This Brody quote appears word-for-word on page 10 of GCBC. It’s from a book Brody published 30 years ago. Isn’t it astonishing that both Taubes and Teicholz can do completely independent research, find the exact same publications, and use the same quotes from those publications?

* * *

Page 122:

Ahrens chose a nine-member task force representing the full range of scientific views on the diet-heart hypothesis. The panel deliberated for several months over each link in the chain of the diet-heart hypothesis, from eating saturated fat, to total cholesterol, to heart disease. The results, however, were not exactly welcome news to diet-heart supporters […] The final report from the Ahrens task force in 1979 made it clear that the majority of its members remained highly skeptical of the idea that reducing fat or saturated fat could deter coronary disease.

Actually, the task force didn’t make that clear at all.65 I actually blogged about this not too long ago because Taubes cites the same obscure paper and comes to a similar but still erroneous conclusion.

The paper gives a score of 0-100 to associations between a given dietary issue and atherosclerosis, where 0 is the weakest evidence for the association and 100 is the most rock-solid evidence. The final score is an aggregation of scores by several experts in the field based on epidemiological evidence, animal studies, human interventions, autopsies, biological plausibility, etc. Cholesterol alone received a score of 62. Saturated fat alone received a 58. Cholesterol and fat together received a 73. For comparison the association between alcohol and liver disease received an 88, and the association between carbohydrate and atherosclerosis got an 11. Carbohydrate and diabetes got a 13.

I don’t want to tell you how you should interpret that data, but it seems pretty clear to me that the evidence that cholesterol and fat play a role in atherosclerosis is quite strong: well above the halfway point and approaching the level of alcohol and liver disease. Teicholz, however, tells her readers that the committee was “highly skeptical” for reasons that should be pretty clear by now.

 

* * *

Cribbing Taubes Alert

On pages 56-59 of GCBC Taubes discusses lipid trial and a consensus conference. On page 127-134 Teicholz discusses the same trial and conference in a strikingly similar way.

GCBC page 56:

The second trial was the $150 million Lipid Research Clinics (LRC) Coronary Primary Prevention Trial. The trial was led by Basil Rifkind of the NHLBI and Daniel Steinberg, a specialist on cholesterol disorders at the University of California, San Diego. The LRC investigators had screened nearly half a million middle-aged men and found thirty-eight hundred who had no overt signs of heart disease but cholesterol levels sufficiently high-more than 265 mg/dl-that they could be considered imminently likely to suffer a heart attack.

BFS page 127:

The other trial was the $150 million Lipid Research Clinic Coronary Primary Prevention Trial (LRC) […] LRC was led by Basil Rifkind, chief of NHLBl’s Lipid Metabolism Branch, together with Daniel Steinberg, a cholesterol specialist at the University of California, San Diego. They screened nearly half a million middle-aged men and found 3,800 with levels of cholesterol high enough (265 mg/dL or above) to be considered likely to have a heart attack soon […]

GCBC page 57:

To call these results “conclusive,” as the University of Chicago biostatistician Paul Meier remarked, would constitute “a substantial misuse of the term.”

BFS page 130:

The biostatistician Paul Meier commented that to call the results “conclusive” would constitute “a substantial misuse of the term.”

GCBC page 57:

As Rifkind told Time magazine, “It is now indisputable that lowering cholesterol with diet and drugs can actually cut the risk of developing heart disease and having a heart attack.”

BFS page 130:

[…] Rifkind told Time magazine, “It is now indisputable that lowering cholesterol with diet and drugs can actually cut the risk of developing heart disease and having a heart attack.”

sorry it's true gcbc

sorry it's true bfs

Conclusion

 Some have called this review mere quibbling or nit-picking, and that the true thesis of BFS still stands. I would strenuously argue the opposite. If I was nit-picking I would have also brought up one or more instances where Teicholz misquotes someone, but the actual quote is not substantively different. I imagine those are innocent mistakes. Nor do I think that Teicholz’s main arguments still hold up. The arguments in this book are scientific claims that are purportedly supported by scientific evidence. If it turns out, however, that the evidence was never really there in the first place then you can no longer make the claim.

The issues I bring up in this review are too substantial and too numerous to be ignored. If you were to remove all of the instances where Teicholz deeply distorts a study or publication, and you were to remove all conclusions that she draws from the distortions you would be left with nothing but a pamphlet.

 cloud

Refs

1. Biss, K., Ho, K.-J., Mikkelson, B., Lewis, L. & Taylor, C. B. Some Unique Biologic Characteristics of the Masai of East Africa. N. Engl. J. Med. 284, 694–699 (1971).

2. Mann, G. V., Spoerry, A., Gray, M. & Jarashow, D. Atherosclerosis in the Masai. Am. J. Epidemiol. 95, 26–37 (1972).

3. How the hell does one even pronounce that, by the way??

4. Hrdlicka, A. Physiological and medical observations among the Indians of southwestern United States and northern Mexico. (Washington, Govt. Print. Off., 1908). at <http://archive.org/details/physiologicalmed00hrdl>

5. Prentice, G. Cancer Among Negroes. Br. Med. J. 2, 1181 (1923).

6. Crawford, M. A. Fatty-acid ratios in free-living and domestic animals: Possible Implications for Atheroma. The Lancet 291, 1329–1333 (1968).

7. Rittenberg, D. & Schoenheimer, R. Deuterium as an indicator in the study of intermediary metabolism XI. Further studies on the biological uptake of deuterium into organic substances, with special reference to fat and cholesterol formation. J. Biol. Chem. 121, 235–253 (1937).

8. Keys, A. Human Atherosclerosis and the Diet. Circulation 5, 115–118 (1952).

9. Truswell, A. S. Evolution of dietary recommendations, goals, and guidelines. Am. J. Clin. Nutr. 45, 1060–1072 (1987).

10. Hopkins, P. N. Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review. Am. J. Clin. Nutr. 55, 1060–1070 (1992).

11. Mann, G. V. The epidemiology of coronary heart disease. Am. J. Med. 23, 463–480 (1957).

12. Keys, A. The diet and the development of coronary heart disease. J. Chronic Dis. 4, 364–380 (1956).

13. Yerushalmy, J. & Hilleboe, H. E. Fat in the diet and mortality from heart disease; a methodologic note. N. Y. State J. Med. 57, 2343–2354 (1957).

14. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y. 20, 118–139 (1953).

15. Keys, A. Coronary heart disease in seven countries. I. The study program and objectives. Circulation 41, I1–8 (1970).

16. Keys, A. Epidemiological Studies Related to Coronary Heart Disease: Characteristics of Men Aged 40–59 in Seven Countries. Acta Med. Scand. 180, (1966).

17. Keys, A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. (Harvard University Press, 1980).

18. Kromhout, D., Menotti, A. & Blackburn, H. W. The Seven Countries Study: A Scientific Adventure in Cardiovascular Disease Epidemiology. (Brouwer, 1994).

19. Toshima, H., Koga, Y. & Blackburn, H. Lessons for Science from the Seven Countries Study: A 35-Year Collaborative Experience in Cardiovascular Disease Epidemiology. (Springer Japan, 2011).

20. Page, I. H., Stare, F. J., Corcoran, A. C., Pollack, H. & Wilkinson, C. F., Jr. Atherosclerosis and the fat content of the diet. Circulation 16, 163–178 (1957).

21. Page, I. H. et al. Dietary Fat and Its Relation to Heart Attacks and Strokes. Circulation 23, 133–136 (1961).

22. Medicine: Fat in the Fire. Time (1960). at <http://content.time.com/time/magazine/article/0,9171,895155,00.html>

23. The Fat of the Land. Time 77, 48 (1961).

24. STOUT, C., MARROW, J., BRANDT, E. N., Jr & WOLF, S. UNUSUALLY LOW INCIDENCE OF DEATH FROM MYOCARDIAL INFARCTION. STUDY OF AN ITALIAN AMERICAN COMMUNITY IN PENNSYLVANIA. JAMA 188, 845–849 (1964).

25. Keys, A. Arteriosclerotic heart disease in Roseto, Pennsylvania. JAMA 195, 93–95 (1966).

26. Lowenstein, F. W. Epidemiologic Investigations in Relation to Diet in Groups Who Show Little Atherosclerosis and Are Almost Free of Coronary Ischemic Heart Disease. Am. J. Clin. Nutr. 15, 175–186 (1964).

27. Ahrens, E. H., Jr, HIRSCH, J., OETTE, K., FARQUHAR, J. W. & STEIN, Y. Carbohydrate-induced and fat-induced lipemia. Trans. Assoc. Am. Physicians 74, 134–146 (1961).

28. Anderson, K. M., Castelli, W. P. & Levy, D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA 257, 2176–2180 (1987).

29. Castelli WP. Concerning the possibility of a nut… Arch. Intern. Med. 152, 1371–1372 (1992).

30. Coronary heart disease and carbohydrate metabolism. JAMA 201, 1040–1041 (1967).

31. Christakis G, Rinzler SH, Archer M & Kraus A. Effect of the anti-coronary club program on coronary heart disease risk-factor status. JAMA 198, 597–604 (1966).

32. Christakis, G., Rinzler, S. H., Archer, M. & Maslansky, E. Summary of the research activities of the anti-coronary club. Public Health Rep. 81, 64–70 (1966).

33. Jolliffe, N., Rinzler, S. H. & Archer, M. The Anti-Coronary Club; Including a Discussion of the Effects of a Prudent Diet on the Serum Cholesterol Level of Middle-Aged Men. Am. J. Clin. Nutr. 7, 451–462 (1959).

34. Dayton, S., Pearce, M. L., Hashimoto, S., Dixon, W. J. & Tomiyasu, U. A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis. Circulation 40, II–1 (1969).

35. Dayton, S. & Pearce, M. DIET AND ATHEROSCLEROSIS. The Lancet 295, 473–474 (1970).

36. Pearce, M. L. & Dayton, S. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet 1, 464–467 (1971).

37. Blasbalg, T. L., Hibbeln, J. R., Ramsden, C. E., Majchrzak, S. F. & Rawlings, R. R. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am. J. Clin. Nutr. 93, 950–962 (2011).

38. Cooper, R. et al. Trends and Disparities in Coronary Heart Disease, Stroke, and Other Cardiovascular Diseases in the United States Findings of the National Conference on Cardiovascular Disease Prevention. Circulation 102, 3137–3147 (2000).

39. Nydegger, U. E. & Butler, R. E. Serum Lipoprotein Levels in Patients with Cancer. Cancer Res. 32, 1756–1760 (1972).

40. A co-operative trial in the primary prevention of ischaemic heart disease using clofibrate. Report from the Committee of Principal Investigators. Br. Heart J. 40, 1069–1118 (1978).

41. Beaglehole, R., Foulkes, M. A., Prior, I. A. & Eyles, E. F. Cholesterol and mortality in New Zealand Maoris. Br. Med. J. 280, 285–287 (1980).

42. Kark, J. D., Smith, A. H. & Hames, C. G. The relationship of serum cholesterol to the incidence of cancer in Evans County, Georgia. J. Chronic Dis. 33, 311–322 (1980).

43. Garcia-Palmieri, M. R., Sorlie, P. D., Costas, R. & Havlik, R. J. An apparent inverse relationship between serum cholesterol and cancer mortality in Puerto Rico. Am. J. Epidemiol. 114, 29–40 (1981).

44. Stemmermann, G. N., Nomura, A. M., Heilbrun, L. K., Pollack, E. S. & Kagan, A. Serum cholesterol and colon cancer incidence in Hawaiian Japanese men. J. Natl. Cancer Inst. 67, 1179–1182 (1981).

45. Miller, S. R., Tartter, P. I., Papatestas, A. E., Slater, G. & Aufses, A. H., Jr. Serum cholesterol and human colon cancer. J. Natl. Cancer Inst. 67, 297–300 (1981).

46. Kozarevic, D. et al. Serum cholesterol and mortality: the Yugoslavia Cardiovascular Disease Study. Am. J. Epidemiol. 114, 21–28 (1981).

47. Rose, G. et al. Colon cancer and blood-cholesterol. Lancet 1, 181–183 (1974).

48. Williams, R. R. Cancer Incidence by Levels of Cholesterol. JAMA 245, 247 (1981).

49. Gammal, E. B., Carroll, K. K. & Plunkett, E. R. Effects of Dietary Fat on the Uptake and Clearance of 7,12-Dimethylbenz(α)anthracene by Rat Mammary Tissue. Cancer Res. 28, 384–385 (1968).

50. Patek, A. J., Kendall, F. E., De Fritsch, N. M. & Hirsch, R. L. Cirrhosis-enhancing effect of corn oil. Protection by choline. Arch. Pathol. 82, 596–601 (1966).

51. Ueshima, H., Iida, M. & Komachi, Y. Is it desirable to reduce total serum cholesterol level as low as possible? Prev. Med. 8, 104–105 (1979).

52. Feinleib, M. Summary of a workshop on cholesterol and noncardiovascular disease mortality. Prev. Med. 11, 360–367 (1982).

53. Feinleib, M. On a possible inverse relationship between serum cholesterol and cancer mortality. Am. J. Epidemiol. 114, 5–10 (1981).

54. Jacobs, E. J., Newton, C. C., Thun, M. J. & Gapstur, S. M. Long-term Use of Cholesterol-Lowering Drugs and Cancer Incidence in a Large United States Cohort. Cancer Res. 71, 1763–1771 (2011).

55. Murai, T. et al. Low Cholesterol Triggers Membrane Microdomain-dependent CD44 Shedding and Suppresses Tumor Cell Migration. J. Biol. Chem. 286, 1999–2007 (2011).

56. Hu, J. et al. Dietary cholesterol intake and cancer. Ann. Oncol. 23, 491–500 (2012).

57. Bardou, M., Barkun, A. & Martel, M. Effect of statin therapy on colorectal cancer. Gut 59, 1572–1585 (2010).

58. Law, M. R., Thompson, S. G. & Wald, N. J. Assessing possible hazards of reducing serum cholesterol. Br. Med. J. 308, 373–379 (1994).

59. Shekelle, R. B. et al. Diet, Serum Cholesterol, and Death from Coronary Heart Disease. N. Engl. J. Med. 304, 65–70 (1981).

60. Tillotson, J. L. et al. Epidemiology of coronary heart disease and stroke in Japanese men living in Japan, Hawaii, and California: methodology for comparison of diet. Am. J. Clin. Nutr. 26, 177–184 (1973).

61. Kagan, A. Honolulu Heart Program. (CRC Press, 1996).

62. Tanaka, T. & Okamura, T. Blood Cholesterol Level and Risk of Stroke in Community-based or Worksite Cohort Studies: A Review of Japanese Cohort Studies in the Past 20 years. Keio J. Med. 61, 79–88 (2012).

63. Steinberg, D. Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy: part II: the early evidence linking hypercholesterolemia to coronary disease in humans. J. Lipid Res. 46, 179–190 (2005).

64. Let’s face it. They are bound to happen. There are surely citation errors in this blog post.

65. Ahrens, E. H. The evidence relating six dietary factors to the Nation’s health. Introduction. Am. J. Clin. Nutr. 32, 2627–2631 (1979).

66. Broad, W. J. NIH deals gingerly with diet-disease link. Science 204, 1175–1178 (1979).