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.

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  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

 

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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

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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).

The Big Fat Surprise: A Critical Review; Part 2

The-Big-Fat-Surprise

[go to The Big Fat Surprise: A Critical Review; Part 1]

Introduction to Part Two

Note: I am actually publishing part two of my critique prior to part one for reasons that have nothing to do with anything.

The Big Fat Surprise (BFS) by Nina Teicholz is yet another book in a long line of books that informs the reader that everything you thought you knew about nutrition is wrong: saturated fat from animals is actually quite good for you, cholesterol isn’t really important, the government lied to you, nutritionists and dietitians lied to you, the American Heart Association lied to you, etc… Leaving aside that the concept of that kind of a conspiracy actually existing is really absurd, what I’m surprised about is that publishers can keep churning out books like this and people are gullible enough to keep buying them.

There wasn’t even much of a positive case for why, as Teicholz states in her subtitle, butter, meat, and cheese belong in a healthy diet. Even in Chapter 10, which is titled Why Saturated Fat is Good for You, there was hardly any evidence of why saturated fat is good for you. The bulk of the chapter — and indeed the book — instead focused on why a low-fat diet is not good for you. Of course she can poke all the holes she wants into a low-fat diet, but that still does not make a case for a high-fat diet, much less a diet high in butter, meat, and cheese. She still has all her work ahead of her.

This brings me to another problem with the book, and perhaps the low-carb community in general. Teicholz reduces the multiplicity of diets that exist in the world to a low-fat or high-fat dyad. To say that this kind of dietary binarism is myopic would be an understatement. This thinking really overlooks the complexity of diets and, in my opinion, totally ignores the kinds of issues that make nutrition science so interesting: issues like bioactive compounds, the gut microbiome, and nutritional epigenetics to name a few.

Unfortunately there are quite a few instances of inaccuracies in the book ranging from simple citation errors to deliberate misrepresentations of scientific studies to outright plagiarism. These are bold claims that I am leveling against the author. I don’t take these lightly, and I stand by them. I have checked many of her references and the results of my efforts are below. If I have made any mistakes please inform me in the comments. Furthermore, if you would like to go to the source and view the original text please let me know and I will provide the publication.

Chapter 6: How Women and Children Fare on a Low-Fat Diet

Page 136

Jerry Stamler expressed in 1972, that fat was “excessive in calories… so that obesity develops.” This seemingly obvious but nonetheless unproven assumption was that fat made you fat.

If you actually read the cited paper you will note that Stamler was not referring to fat when he said that, he was instead referring to the “habitual diet of Americans.”1 Stamler’s quote is taken out of context and put into a different context that is inaccurate.

* * *

Cribbing Taubes Alert

Teicholz seemingly copy-pastes Taubes work on page 136 when she discusses an amazingly obscure 1995 pamphlet by the American Heart Association. According to Teicholz the pamphlet:

told Americans to control their fat intake by increasing refined-carbohydrate consumption. Choose “snacks from other food groups such as . . . low-fat cookies, low-fat crackers, . . . unsalted pretzels, hard candy, gum drops, sugar, syrup, honey, jam, jelly, marmalade” […]

Leaving aside the fact that the pamphlet never actually advises anyone to increase their refined-carbohydrate consumption, what’s interesting is that Taubes says the very same thing in chapter sixteen of WWGF:

[T]he AHA counseled, “choose snacks from other food groups such as … low-fat cookies, low-fat crackers … unsalted pretzels, hard candy, gum drops, sugar, syrup, honey, jam, jelly, marmalade (as spreads).”

The ellipses are even in the same place! What a coinkydink.

She goes on to say:

In short, to avoid fat, people should eat sugar, the AHA advised.

No. That’s a gross and highly misleading oversimplification. There’s no way you can distill 20 pages of dietary advice into “eat sugar” and think you’re even approaching a decent approximation.

* * *

Page 138:

Jane Brody, the health columnist for the New York Times and the most influential promoter of the low-fat diet in the press, wrote, “If there’s one nutrient that has the decks stacked against it, it’s fat” […]

That quote does not appear in the cited NYT article.2

* * *

On page 143 Teicholz attempts to make the argument that plant-based diets aren’t all they’re cracked up to be:

Vegetarian diets generally have not been shown to help people live longer. The 2007 report by the World Cancer Research Fund and the American Institute for Cancer Research, discussed in the last chapter, found that in no case was the evidence for the consumption of fruits and vegetables in the prevention of cancer “judged to be convincing.”

This has got to be one of the most selective and misleading interpretations of the Second Expert’s Report. I mean, my god… So for those who are not familiar with it, the Second Expert’s Report (what Teicholz discusses above) is an incredible text that outlines ALL of the quality evidence on a given cancer topic regarding food, nutrition, and the prevention of cancer. All the evidence is evaluated by a large panel of elite doctors and researchers and given one of the following labels: unlikely, suggestive, probable, and convincing. To reach the convincing level you really need some rock solid evidence.3 None of the evidence regarding fruits and vegetables reached the venerable convincing level, but there was a ton of probable and suggestive evidence for many cancers. You really have to scour that section to find a quote that might fit an anti-vegetable narrative. Read it yourself for all the juicy details, but here are some remarks from the conclusion on page 1144:

Non-starchy vegetables probably protect against cancers of the mouth, pharynx, and larynx, and those of the oesophagus and stomach. There is limited evidence suggesting that they also protect against cancers of the nasopharynx, lung, colorectum, ovary, and endometrium. Allium vegetables probably protect against stomach cancer. Garlic (an allium vegetable, commonly classed as a herb) probably protects against colorectal cancer.

Fruits in general probably protect against cancers of the mouth, pharynx, and larynx, and of the oesophagus, lung, and stomach. There is limited evidence suggesting that fruits also protect against cancers of the nasopharynx, pancreas, liver, and colorectum.

 

veg second experts

* * *

On page 144 Teicholz derides the study that low-carbers love to hate, T. Colin Campbell’s China Study:

These books are based on one epidemiological study, with a number of significant methodological problems, that was never published in a peer-reviewed issue of a scientific journal. Campbell’s two papers were instead published as part of conference proceedings in journal “supplements,” which are subject to little or no peer review.

As evidence she cites a BLOG POST by then-undergraduate Chris Masterjohn, published by a private organization that is explicitly biased in favor of animal-based diets.5 Just let that sink in…

* * *

After discussing the Ornish diet for a bit, Teicholz mentions a paper on page 145 that reviews the evidence for (very) low-fat diets:

Tufts University nutrition professor Alice Lichtenstein and a colleague reviewed the very low-fat diet for the AHA […] Lichtenstein concluded that very low-fat diets “are not beneficial and may be harmful.”

Teicholz both takes the quote out of context and mangles it somewhat. Here’s the actual quote (emphasis mine):

At this time, no health benefits and possible harmful effects can be predicted from adherence to very low fat diets in certain subgroups.

The “in certain subgroups” part is vital to the accuracy of the statement. You can’t just cut it out. And Dr. Lichtenstein’s conclusion is quite a bit more nuanced than Teicholz would have you believe. The paper is actually a very objective look at low-fat diets.6 It acknowledges that more research needs to be done on these diets in order for a definitive recommendation. Moreover, as alluded to above, it states that until more evidence comes in young children, the elderly, pregnant women, and those with eating disorders should probably avoid the diet. However, it also acknowledges that a low fat diet can be beneficial and there is evidence for that. Here’s an actual quote from the conclusion:

There is overwhelming evidence that reductions in saturated fat, dietary cholesterol, and weight offer the most effective dietary strategies for reducing total cholesterol, LDL-C levels, and cardiovascular risk.

* * *

On page 146 Teicholz discusses the idea of reducing cholesterol levels In young children:

Indeed, in the late 1960s, the NHLBI had been putting children as young as four years old on cholesterol-lowering diets and also giving them cholestyramine, the same drug that would be used in the LRC trial. Convinced that cholesterol was a crucial part of the heart disease puzzle, the NHLBI went so far as to propose universal umbilical cord blood screening in order to start treatment as early as possible, even at birth. In 1970, mass screening of cord blood at “no more than” five dollars per baby was given serious consideration. Such was the preoccupation with heart disease that researchers believed healthy children ought to start out life in a position of defense.

These people are obsessed with cholesterol! Won’t somebody pleeease think of the children?? Of course to the average person reading this it sounds absurd, and it would be absurd if Teicholz had not removed a key bit of information that makes it very not absurd. According to the JAMA article she cited for this paragraph, the NHLBI was not proposing we give all or even most kids cholesterol-lowering drugs or cholesterol screenings.7 The article makes it abundantly clear that these are for children with familial type 2 hypercholesterolemia, a genetic condition associated with chronically high cholesterol levels. People with familial hypercholesterolemia have heart attacks and can die far younger than normal lipid folks. It makes perfect sense to go on a cholesterol-lowering diet or a statin if you have that condition. But of course, Teicholz wants to stoke your outrage a bit so you think the NHLBI are a bunch of incompetent boobs that are completely absorbed (pardon the pun) with the idea of cholesterol.

* * *

Teicholz continues to make the argument against vegetarianism on page 148:

One of the more important early nutrition researchers looking at these questions was Elmer V. McCollum, an influential biochemist at Johns Hopkins University. He performed endless feeding studies on rats and pigs because they, like humans, are omnivores and are therefore considered instructive for human nutritional needs. His book The Newer Knowledge of Nutrition (1921) is populated with pictures of scrawny, scruffy-furred rats raised on poor nutrition, compared to large, lustrously furred ones raised on better nutrition. He found that animals on a vegetarian diet had an especially difficult time reproducing and rearing their young.

She goes on to quote a passage from the book with the author explaining that the vegetarian rats were smaller and lived about half as long as the non-vegetarians. While I was looking for the quoted passage I noticed that basically the entire book is a discussion of rats on deprivation diets of some sort; rat experiments where the researchers deprive them of one or more essential amino acids, vitamins, and breast milk at birth to see what happens.8 This is what the pics of “scrawny, scruffy-furred rats” she refers to are; not necessarily vegetarian rats.

Moreover, I’m not sure that rats make a great proxy for humans. At least I would not be convinced to change my diet based only on rat studies. At any rate, much like her scholarship on the Second Expert’s Report, to find a quote that puts vegetarianism in a negative light you have to ignore paragraphs immediately preceding and immediately following her quoted passage. I’ll give you an idea of what I’m talking about. On page 1599:

The more valid arguments concerning the use of meat as contrasted with the fleshless dietary regimen, are based upon the view that meat is unwholesome and that it contains waste products, which, because of their poisonous properties, tend to do damage to the body tissues. This view is upheld by experimental results. Professor Irving Fisher of Yale conducted extensive experiments with flesh abstainers and flesh eaters, and found the former possessed of much greater endurance than the latter.

After discussing the experiment where the rats’ growth were stunted on a vegetarian diet, McCollum goes on to describe a different vegetarian diet that was more successful. Page 161:

The diet induced growth at approximately the normal rate, and reproduction and rearing of a considerable number of young. The young grew up to the full adult size and were successful in rearing a considerable number of their offspring (see Chart 7).

McCollum then describes another successful experiment where rats were fed another iteration of a vegetarian diet and thrived. He even explains why the diet that Teicholz mentioned did not permit the rats to thrive. Page 164:

[T]he diet was of such a nature that the animals could hardly do otherwise than take a rather low protein intake. Secondly, the leaves, which formed the only components of the food supply containing enough mineral elements to support growth, were fed in the fresh condition. In this form the water content and bulk are so great that it would be practically impossible for an animal whose digestive apparatus is no more capacious than that of an omnivorous rat to eat a sufficient amount of leaf to correct the inorganic deficiencies of the rest of the mixture […]

Ladies and gentlemen, this is cherry-picking at its finest.

* * *

On page 152 Teicholz tries really hard to find a reason to dismiss the results of a study:

[The NHLBI] funded a trial called the Dietary Intervention Study in Children (DISC). Starting in 1987, three hundred seven- to ten-year-old children were counseled, along with their parents, to eat a diet in which saturated fat was limited to 8 percent of calories and total fat to 28 percent, and this group was compared to an equal-sized group of controls. Investigators found that those put on the diet low in fat (and animal fat) grew just as well as the children eating normally during the three years of the experiment, and the authors emphasized this point.

Yet it was problematic for the study that the boys and girls in the trial did not represent a normal sample. For their study population, the DISC leaders had selected children who had unusually high levels of LDL cholesterol (in the 80th to 98th percentile). In other words, these children could very well have had familial hypercholesterolemia, the genetic condition that causes heart disease through a metabolic defect, which is entirely different from the way that cholesterol is altered by diet. These at-risk children were chosen because they were thought to need help more urgently in fighting the early onset of a life-threatening disease, yet their unusually high cholesterol levels meant that the results could not be generalized to the larger population of normal children.

I would totally agree with Teicholz here if there was significant evidence that hypercholesterolemia would confound growth results in some way. However, it seems obvious to me that she is trying real hard to find reasons to discount the results, and if this is the best she can do then it must be a good study design. Also, the diet is nearly one-third fat. How is this a “diet low in fat”??

* * *

Teicholz hits the vegetarian diet from all possible angles, including the idea that vegetarian children show retarded growth. Page 153:

Slightly stunted growth was consistently found among children eating vegetarian diets. Children were also found to experience growth spurts when incorporating more animal foods in their diets. Growth faltering was particularly pronounced among children on a vegan diet, which cuts out all animal foods.

As evidence she cites a twenty-two year-old review article on reduced fat diets.10 Refreshingly, Teicholz doesn’t really misrepresent the article nearly as much as her other claims. However, she does leave out some important details. One important distinction that is not made by Teicholz and is only kind-of made in the review article is the content of the vegetarian diets. What I mean is that the terms vegetarian diet, low fat diet, and low calorie diet are used almost interchangeably in the text. Now a vegetarian diet can of course be low fat or low calorie or both, but it certainly does not have to be.

The author also implies that ridiculously strict vegetarian diets are also included in the review including the Zen macrobiotic diet which the author claims as consisting only of brown rice and water. He also mentions some limitations of this review stating “[N]early all of the studies focus on diets that provide undernourishment in nutrients.” I think it’s reasonable to assume that this can and almost certainly does account for the slight growth stunting and not, as Teicholz would claim, a lack of animal fat.

* * *

Similar to the DISC trial above there was also another study done to test the outcomes of a low saturated fat diet on kids called STRIP (Special Turku Coronary Risk Factor Intervention Project). Teicholz refers to it as a low fat diet, but it simply replaces saturated fat with unsaturated. Evidently there were no adverse effects to growth or coronary disease risk factors. But that doesn’t stop Teicholz from doing her damnedest to try and convince you that the study is bunk. Page 154:

[A]lthough investigators found no vitamin deficiencies, the supplements they provided may have masked this problem. It is also significant that 20 percent of the families in both groups left before the end of the study.

* * *

Page 157:

The British biochemist and nutrition expert Andrew M. Prentice, for instance, hypothesized that the lack of high-fat animal foods was possibly “the major contributor of growth failure” among babies he studied in Gambia. He compared some 140 Gambian infants to a slightly larger group of relatively affluent babies in Cambridge, England; early on, the Gambians and British infants grew almost equally well. When they started to be weaned off breast milk at six months of age, however, their growth curves steadily diverged. The Gambians ate an equal number of calories as did the Cambridge babies for the first eighteen months of life, but the fat content of their diet steadily declined to just 15 percent of calories by the age of two, and most of that fat was polyunsaturated from nuts and vegetable oils. The Cambridge babies, by contrast, ate a majority of calories from eggs, cow’s milk, and meat—a minimum of 37 percent of calories as fat, most of it saturated. By the age of three, the Gambian babies weighed 75 percent less than they should, according to standard growth charts, while the Cambridge babies were growing according to expectations and weighed on average 8 pounds more than the Gambians.

The cited paper does make the case that essential fatty acids are needed for proper growth, and that a lack of dietary fat might explain the stunted growth in the Gambians.11 But some important details in the paper that Teicholz gets wrong or leaves out are that the Gambians did in fact consume less kcals and that Gambian children suffer from infection, disease, and diarrhea more than their Cambridge counterparts.

* * *

Page 158:

Reports from poorer countries in Latin America and Africa, however, revealed that children were eating less fat, with clear implications for nutrition and growth: diets with less than 30 percent of calories as fat started to get nutritionally worrisome, and at 22 percent, they were associated with growth faltering.

If look at the paper she cites for this data, you will find that the poorer countries such as Haiti also consumed FAR LESS kcals than their counterparts from more developed countries. Of course this doesn’t rule out fat as a factor, but I would argue that it definitely confounds the results.

 

You should also note that this is a cross-sectional analysis which is extraordinarily weak in terms of showing any kind of cause-effect relationship. Teicholz makes this very argument earlier in the book, but you can see here that she has no problem invoking these types of studies when it fits her narrative.

* * *

Teicholz then tries to make the argument that HDL was ignored by the major institutions as a predictor of heart disease. Page 162:

[W]hen diet and disease experts finally began to sidle away from total cholesterol, they did not turn to HDL-cholesterol. Instead, they chose to focus on LDL-cholesterol. By 2002, the NCEP was calling elevated LDL-cholesterol a “powerful” risk factor. The AHA and other professional associations agreed.

LDL was and is a powerful risk factor, but HDL was not ignored. The 2002 report that Teicholz cites has an entire section titled “Low HDL cholesterol as an independent risk factor for CHD.” I could quote about a hundred parts in that report that make the case that low HDL is a risk factor, but I’ll spare you. The report is open access so you can find it and peruse it if you’d like.

* * *

On page 165 Teicholz discusses the Boeing employees trial12 and its implication for women:

[The Boeing women] had followed the most stringent NCEP guidelines for an entire year and had apparently increased their risk of having a heart attack.

She bases this on the study results that the women with high cholesterol levels had a 8% decrease in HDL levels. In the book she doesn’t mention that these HDL reductions only occurred in hypercholesterolemic women, instead implying that all women had their HDL levels go down. Moreover, if one’s HDL levels are at, say, 72 mg/dl and decrease 8% they are still high enough to be considered protective. High HDL levels are not unlikely for women with high cholesterol. HDL as a risk factor for heart disease only occurs when HDL levels get below 40 mg/dl.

* * *

Page 166:

The idea that fat might lead to cancer was first aired at the McGovern committee hearings in 1976, when Gio Gori, director of the National Cancer Institute (NCI), testified that men and women in Japan had very low rates of breast and colon cancer and that those rates rose quickly upon emigrating to the United States. Gori showed charts demonstrating the parallel rising lines of fat consumption and cancer rates. “Now I want to emphasize that this is a very strong correlation, but that correlation does not mean causation,” he said. “I don’t think anybody can go out today, and say that food causes cancer.”

That’s not nearly all Gori presented, but the source of this quote, according to Teicholz is the testimony of Gori in Volume 2 of Diet Related to Killer Diseases (July 28, 1976): 176-182. However, that quote is not found in those page numbers. A similar quote is found on page 185, but it doesn’t include the “I don’t think anybody can…” bit, so I don’t know where Teicholz got those page numbers or that quote.

* * *

Page 167:

It is therefore surprising to learn that as far back as 1987, the epidemiologist Walter Willett at the Harvard School of Public Health had found fat consumption not to be positively linked to breast cancer among the nearly ninety thousand nurses whom he had been following for five years in the Nurses’ Health Study. In fact, Willett found just the opposite to be true, namely, that the more fat the nurses ate, particularly the more saturated fat they ate, the less likely they were to get breast cancer. These results held true even as the women aged. After fourteen years of study, Willett reported that his team had found “no evidence” that a reduction in fat overall nor of any particular kind of fat decreased the risk of breast cancer. Saturated fat actually appeared protective.

The first sentence is actually true. Willett found that breast cancer incidence among those that ate more total fat (even saturated fat) was not higher than those women that ate less total or saturated fat.13 But to claim that total fat or even saturated fat is protective of breast cancer is not supported by the evidence.

 

Cribbing Taubes Alert

Taubes makes the same mistake regarding the same study on page 72 of GCBC. Coincidence?

* * *

Cribbing Taubes Alert

Page 167:

[T]he most effective fats for growing tumors were polyunsaturated—the fats found in vegetable oils that Americans were being counseled to eat. Saturated fats fed to rats had little effect unless supplemented with these vegetable oils.

On page 73 of GCBC Taubes makes a similar statement:

Adding fat to the diets of lab rats certainly induced tumors or enhanced their growth, but the most effective fats by far at this carcinogenesis process were polyunsaturated fats—saturated fats had little effect unless “supplemented with” polyunsaturated fats.

The reason I am suggesting Teicholz cribbed from Taubes here is not just that both statements are very similar, but also because both cite the same (somewhat obscure) paper and draw the same erroneous conclusion from it. It’s a rather long and dense (and old) paper that very persuasively makes the case that differences in dietary fat – both amount and type – lead to wildly variable results.14 I looked real hard for any kind of definitive statement on dietary fat and cancer in lab rats and this was the best that I found:

Corn and safflower oils and lard consistently enhance tumorigenesis when fed at high levels; coconut oil and fats high in n-3 fatty acids do not, and beef tallow and olive oil are variably effective […]

Go ahead and read the paper. I defy you to come to the honest conclusion that vegetable oils are the only fats that will cause cancer in lab rats.

* * *

Page 168:

Even the NCI’s own studies came up empty-handed—the most recent of those being the Women’s Intervention Nutrition Study in 2006. This trial managed to get women to drop their fat intake to 15 percent or less, thereby answering criticisms that the women in earlier studies had not seen any results because they failed to lower their intake of fat enough. But even at 15 percent, the NCI still could not find a statistically significant association between fat reduction—of any kind or amount—and reduced rates of breast cancer.

The study in question does not study rates of breast cancer in general, but rather breast cancer relapses. And according to the results the lower fat intervention did in fact significantly reduce relapses by 24%.15

* * *

Page 169-170, Teicholz discusses the Women’s Health Initiative (WHI) study results:

Yet to everyone’s alarm and bafflement, the results, published in a series of articles in JAMA, did not come out remotely as expected. […] They had apparently met all their targets, but after a decade of following this diet, they were no less likely than a control group to contract breast cancer, colorectal cancer, ovarian cancer, endometrial cancer, stroke, or even heart disease. Nor did they lose more weight.

Teicholz is actually right about most of the results, except for the ovarian cancer and weight loss. Evidently there was significantly less ovarian cancer and weight among the intervention group.16,17

 

Cribbing Taubes Alert

Taubes makes this same mistake on page 75 of GCBC.

* * *

Page 172:

A review in 2008 of all studies of the low-fat diet by the United Nation’s Food and Agriculture Organization concluded that there is “no probable or convincing evidence” that a high level of fat in the diet causes heart disease or cancer.

This is absolutely true. However, here are some other conclusions by the same text that were intentionally left out because it runs contrary to the saturated-fat-is-sacred-and-unsaturated-fat-is-the-devil narrative18:

  • There is convincing evidence that replacing SFA with PUFA decreases the risk of CHD.

  • There is convincing evidence that replacing carbohydrates with MUFA increases HDL cholesterol concentrations.

  • There is insufficient evidence for relationships of MUFA consumption with chronic disease end points such as CHD or cancer.

  • There is insufficient evidence for relationships of MUFA consumption and body weight and percent adiposity.

  • There is insufficient evidence of a relationship between MUFA intake and risk of diabetes.

  • There is insufficient evidence for relationships of MUFA consumption with chronic disease end points such as CHD or cancer.

  • There is insufficient evidence for relationships of MUFA consumption and body weight and percent adiposity.

  • There is insufficient evidence of a relationship between MUFA intake and risk of diabetes.

  • There is insufficient evidence for establishing any relationship of PUFA consumption with cancer.

  • There is insufficient evidence for relationships of PUFA consumption and body weight and percent adiposity.

  • There is a possible positive relationship between SFA intake and increased risk of diabetes.

And these aren’t found in some obscure or deep part of the text. They are found in the EXACT same place she found the above quote.

* * *

Page 172:

The USDA and AHA have both quietly eliminated any specific percent fat targets from their most recent lists of dietary guidelines.

If by “quietly” Teicholz means “publicly published in their popular journal that has received widespread attention and 1773 academic citations since 2006,” then, yes, they “quietly” did that. And if by “eliminated any specific percent fat targets” Teicholz means “recommended consuming no more than 7% of kcals from saturated fat,” then, yes, they “eliminated any specific percent fat targets.”19

 

Chapter 7: Selling the Mediterranean Diet: What Is the Science?

Page 174:

The Mediterranean diet is now so famous and celebrated that it barely needs introduction. The regime recommends getting most of the body’s energy from vegetables, fruits, legumes, and whole grains. Seafood or poultry may be eaten several times a week, along with moderate amounts of yogurt, nuts, eggs, and cheese, while red meat is allowed only rarely, and milk, never.

 

Anyway, I don’t know why she claims that milk is not allowed. Her cited source does not say that. In fact, it says that dairy is allowed on a daily basis in low to moderate amounts.20*

* * *

Page 180:

In a meticulous, landmark paper in 1989, Ferro-Luzzi tried to create a workable definition of the nutritional patterns characterizing European countries bordering the Mediterranean Sea.

This “landmark” paper has only 145 citations according to Google Scholar, and it’s 25 years old.

* * *

Page 182:

Ferro-Luzzi also took a magnifying glass to Keys’s Greek data expressly to see if she could find some flaw with his 40-percent-fat number. She concluded that his data, like all of those available on the Greek diet of that period, were so scanty and unreliable that there were “few scientific grounds” for the claim of a traditional Greek diet ever being high in fat.

As evidence Teicholz cites a paper published by Ferro-Luzzi in 2002 in the European Journal of Clinical Nutrition.21 The paper makes the argument that the diets on Crete and Corfu are not exactly representative of Greek diets as a whole. She actually appears to conclude that Keys’s Seven Countries Study is THE ONLY reliable data on Greek diets so far; it’s all the other data that is scanty and unreliable. Let’s take some quotes from the paper:

In conclusion, the great value of these Key’s studies is that they provide a coherent basis for the only cohort diet-health study published from anywhere in Greece so far.

AND

Our first finding is that there are few reliable dietary studies from Greece in relation to dietary fat, other than the detailed Seven Countries Study. [emphasis mine]

Ferro-Luzzi’s attempt here is to associate the Seven Countries Study with her lower fat version of the Greek diet, claiming that Keys’s data confirms her argument. Do you see how this is basically the opposite of what Teicholz claims?

* * *

On page 188 Teicholz makes the argument that because Willett’s Mediterranean Diet pyramid was published in a journal supplement, it should not be regarded as serious scientific work.

The journal articles that Willett’s team wrote to establish the pyramid were not subject to the peer-review process that scientific papers normally undergo; they had only one reviewer, not the usual two to three. This was because the papers were published, along with the entire 1993 Cambridge conference proceedings, in a special supplement of the American Journal of Clinical Nutrition funded by the olive oil industry. These kinds of journal supplements sponsored by industry are standard in the field of diet and disease research, although a lay reader is unlikely to be aware of this financial backing, because sponsorship is not noted in the articles themselves.

If this is the case, then surely Teicholz would never cite a journal supplement in favor of her arguments. Y’know, since the science is tainted by industry money and all. If she did that would make her a hypocrite, right?

  • On page 111 Teicholz cites a supplement that favors meat in a healthy diet and downplays its effects on carcinogenesis.22

  • On page 75 and 101 she cites a supplemental paper to try and make the case that polyunsaturated fats are dangerous.23

  • On pages 165 and 367 she cites an American Journal of Clinical Nutrition supplement.24

  • On page 281 she cites a supplement as part of a claim that unsaturated fats play a role in atherosclerosis.25

  • Page 109 she cites a supplement to argue that Seventh-Day Adventist vegetarians weren’t so better off than others.26 (Note: I am not exactly sure this is a journal supplement, though. Teicholz cites it as one and so does PubMed, but the AJCN does not.)

  • Page 230 she uses a supplement to claim that tropical oils containing saturated fat are not harmful.27

  • Page 160 she cites a supplement as evidence that low-fat diets can lower HDL.28

  • Page 202 when she discusses a food frequency questionnaire.29

  • Page 144 when she claims vegetarians are not any better off than non-vegetarians.30

  • When she discusses Ancel Keys and his research on pages 38, 39, 40, 195, and 205.31

  • On page 158 where she makes the claim that more fat = healthier children.11,32–35

  • Page 318 when discussing LDL subfractions.36

  • On page 92 when she discusses two “scholarly estimates” claiming that polyunsaturated fat was nearly unheard of before 1910.37

  • When talking about trans fats and 7-11 on 261.38

  • When claiming that vegetarian women don’t fare better than omnivorous women on page 108.39

  • On page 324 when she claims that the evidence against SFAs is thin. 40

  • On pages 221-222 when she claims that meat consumption in Spain has “skyrocketed” while heart disease has “plummeted.”41

  • Page 223, when she claimed that sugar consumption in Spain fell dramatically.41

  • On page 154 when she discusses a study on babies.42

  • When she claims that children have reduced their intakes of fat in recent decades on page 158.43

* * *

Page 191 Teicholz claims that Keys and Company wooed people to their way of thinking by inviting them to Greece and describing the diet in a very romantic way.

[T]hese getaways were an easy sell. The enormous appeal of the Mediterranean had of course been a factor in influencing Keys and his colleagues from the start, and their rapture for the region came even to suffuse their scholarly work. Henry Blackburn, for instance, who worked closely with Keys, wrote a description of the Cretan male who was “free of coronary risk” for the American Journal of Cardiology in 1986, using language that is unusually florid for a scientific journal:

He walks to work daily and labors in the soft light of his Greek Isle, midst the droning of crickets and the bray of distant donkeys, in the peace of his land…. In his elder years, he sits in the slanting bronze light of the Greek sun, enveloped in a rich lavender aura from the Aegean sea and sky. He is handsome, rugged, kindly and virile.

The beauty of the landscape and lifestyle, its people, and its diet became united in one, overwhelming swoon.

But what Teicholz does not mention is that the above passage was from an journal editorial and it was satirizing an earlier piece that took a sardonic look at the “Low Risk Coronary Male.”44

* * *

Page 201:

Experts suggested that olive oil might help prevent breast cancer, for instance, but the evidence so far is very weak.

I would argue that the paper she cites to support that statement doesn’t really say that.45 Although the statement is phrased in such a way that reasonable people may disagree. Here’s the relevant portion of the paper. I’ll let you decide.

Overall, these observations suggest that olive oil or other oils high in monounsaturated fatty acids may decrease the risk of breast cancer, although more work is necessary before such inferences can be made with confidence. A practical implication may be that animal fat sources in the diet should be minimized, whereas monounsaturated fat sources, such as olive oil, need not be restricted, a recommendation that would be consistent with those for dietary prevention of heart disease.

Teicholz also leaves out what the authors would consider strong evidence regarding red meat and cancer:

In the case of colorectal cancer, associations with fat intake appear to be attributable to red meat intake; indeed, red meat intake is also strongly associated with colon cancer risk in international correlations. In the case of prostate cancer, red meat is also relatively consistently associated with risk, although whether some of this is the result of fat intake remains unclear.

* * *

On page 201, Teicholz claims that the bioactive compounds in olive oil have no benefits.

In “extra-virgin” olive oil, investigators identified a host of “nonnutrients,” such as anthocyanins, flavonoids, and polyphenols, that are believed to work their own minor miracles. They are present in olives because the fruit is dark-colored, a defense developed over thousands of years against exposure to the hot sun. Not all of the effects of these nonnutrients have been adequately explored, but in one case, flavonoids, sizable clinical trials on humans have been unable to show benefits to health.

Apparently by “health” Teicholz actually means CVD and nothing else, since she cites a meta-analysis that only focuses on CVD.46 Not cancer, not diabetes, not anything else. In any case I think she misunderstood the meta-analysis because after reading it I get the distinct impression that flavonoids do, in fact, play a beneficial role in CVD. I’m not sure why I get that impression, but maybe it has something to do with the forest plots that nearly all favor flavonoids and bits of text like this:

[T]his review provides evidence that some flavonoids or foods rich in flavonoids, such as chocolate or cocoa, and black tea, may modulate important risk factors.

AND

The changes in risk factors observed after flavonoid intake are clinically significant.

Also, if you’re curious, meta-analyses on flavonoids and outcomes like cancer and diabetes conclude that they are indeed beneficial.47–49

* * *

Page 203:

[A] few recent studies on animals suggest that olive oil may even provoke heart disease, by stimulating the production of something called cholesterol esters.

This is classic. To support her war on olive oil, Teicholz cites a review article that states in no uncertain terms that unsaturated fatty acids are far more beneficial to cardiovascular health than saturated fatty acids.50 In fact, here’s a quote from the text:

The best types of fat, in terms of improving the lipid ratio, were canola (rapeseed) oil, soybean oil, and olive oil, whereas the worst types were butter and stick margarine. Not surprisingly, all types of fat were better than pure SFA because even the worst of them do contain some unsaturated fats.

Hilarious, but getting back to the olive oil and provoking heart disease… There is a section that questions whether olive oil is as good as we think it is. The author discusses a couple studies using nonhuman primates that were fed dietary cholesterol (to induce atherosclerosis) and three types of oil: palm oil (saturated), safflower oil (monounsaturated), and some oil high in linoleic acid (polyunsaturated). The author then explains that the polyunsaturated oil had the most favorable outcomes in terms of atherosclerosis, while the monounsaturated fat was as bad as the saturated fat in the promotion of atherosclerosis. So if Teicholz wants to use that as evidence that olive oil provokes heart disease because it is high in MUFAs like safflower oil then she better also say that saturated fat also provokes heart disease.

 

However, other than a couple of animal studies, the article is generally favorable toward both MUFAs and PUFAs and quite unfavorable to SFAs.

* * *

Page 203:

Only because olive oil has been so wildly hyped does the disappointing news about actual scientific findings come as any surprise. Indeed, “surprisingly” is the word that two Spanish researchers used when confronting the data purporting to show olive oil’s heart-healthy effect, and concluding, in 2011, that there was “not much evidence.”

This may be another one of those reasonable-people-may-disagree type things, but I don’t really think the paper concludes that there is “not much evidence.” They do say those words in the abstract, though.51 Here is the sentence: “Surprisingly, there is not much evidence coming from analytical epidemiological studies about this issue.” Which is slightly, but I would argue distinctly, different from how Teicholz phrases that. They say there are not many epidemiological studies on the issue, while Teicholz claims they say there is not much evidence showing a heart-healthy effect. Is there a difference? You decide.

 

In any case, the paper actually goes on to describe the evidence that exists, and it seems quite positive for ol’ olive oil. In fact, Table 4 and Table 5 show the lowest odds ratios I have ever seen in real life. Most of the studies they review show a significant inverse association between olive oil and some form of heart disease.

OR table 4

OR table 5

* * *

On page 208 she mentions that Antonia Trichopoulou was steeped in bias and not a great scientist (which is… amusing coming from Teicholz).

“Antonia is perhaps guilty, as we all were, of thinking with her heart,” says her former colleague Elisabet Helsing, who, as the Advisor on Nutrition for WHO Europe, was involved in all the early work on the Mediterranean diet.”Many of us in this field, we were led not by the head but by our hearts. The evidence was never so good.” Or, as Harvard epidemiologist Frank B. Hu wrote in 2003, in a break with his colleagues, the Mediterranean diet “has been surrounded by as much myth as scientific evidence.”

The first quote is personal correspondence, so it can’t be verified, but the Hu quote can be. It does appear in the paper, but this is another classic example of Teicholz’s quote-mining. The whole article is what I would consider the opposite of an indictment of the Mediterranean Diet: Hu makes the case that the diet is quite beneficial and versatile. That quote is the only sentence that – when taken out of context – could possibly be construed as incriminating. In fact, much of this book is based on personal interviews with people to which I am not privy. I am uncovering an uncomfortable level of quote-mining by Teicholz which really makes me skeptical of the interviews.

* * *

Page 209, Teicholz discusses a randomized clinical trial of the Mediterranean Diet (the Lyon Diet Heart Study).52 The results clearly indicate CHD benefits, so naturally Teicholz has to do some serious spinning to explain-away these results:

Yet the study had enough methodological problems to give any reasonable person pause: It was small (“hopelessly underpowered,” meaning not enough subjects, as one researcher commented).

I find it strange that a trial that contains 605 participants would be characterized as “hopelessly underpowered.” Let’s take a look at that quote and see what the researcher’s explanation of this is… The cited source of that quote is a paper by Ness et al.53 The “hopelessly underpowered” quote does not appear in the text, nor is there anything similar that might be interpreted as hopelessly underpowered. In fact, there is no mention whatsoever of the Lyon Diet Heart study.

Teicholz continues the dubious Lyon-bashing on page 210 where she states the following:

These problems are described in a paper for the American Heart Association, which found itself in the awkward position of trying to reconcile its own recommended low-fat diet with the success of the relatively high-fat diet used in the Lyon study. The authors concluded that the diet had been “so poorly assessed in both groups” […]

Much like the hopelessly underpowered quote the “so poorly assessed in both groups” quote does not appear in the cited source.54 Teicholz’s next sentence says:

It’s quite possible that the better health outcomes seen in the experimental group were due entirely to what is called the “intervention effect,” they wrote.

They didn’t write that, either. I don’t even think a paraphrasing argument could be made here.

* * *

On page 211 Teicholz discusses the interesting case of Indian researcher Dr. Ram B. Singh who conducted a dietary trial in the early 90s examining common Indian fruits and vegetables and nuts and their effects on heart health.55,56 As it turns out Singh may have fabricated some of his data.57–61 Scandalous!

Teicholz could have left it there as an interesting and accurate anecdote of research malfeasance exposed, but she has to take it a step further and lie about something that didn’t happen.

Years later, however, the Singh study was still being included in scientific literature reviews of the Mediterranean Diet, including an influential one by Lluis Serra-Majem in 2006.

The review in question does not mention or cite that study at all.62 Teicholz is on a roll here with the lies. Maybe she thinks that if you have got this far reading the book then you’re pretty much on board with her arguments and doesn’t really need to provide actual evidence for her claims. The review does cite another study by Singh63 (presumably the same guy), but that study was published in 2002 and has not been linked with any kind of impropriety that I know of.

* * *

Page 215:

If the Israeli trial had never existed, everyone could have assumed that the Mediterranean option in PREDIMED was the best possible regime for health. But that third, low-carb arm in Israel had revealed that an even better option was possible. (Previous shorter trials had found the same thing, as we will see in Chapter 10.)

As evidence for the parenthetical claim she cites a meta-analysis comparing low-fat diets to Mediterranean diets!64 There is no discussion or mention of any low-carb diets in that paper.

* * *

Page 218 Teicholz makes the argument that the people of the Mediterranean did not eat lean meats like Keys and others recorded, but fatty meats. As evidence she cites a work of fiction:

Nor were the ancient Greeks feasting on chicken. The Iliad describes the dinner given by Achilles for Odysseus this way: “Patrokles put a big bench in the firelight and laid on it the backs of a sheep and a fat goat and the chine of a great wild hog rich in lard.”

Alright everyone, pack it up. Clearly Homer’s poetry written about a thousand years before Jesus was born trumps any kind of scientific research.

* * *

Page 221:

As Italy and Greece slowly grew more prosperous following the war, they started to leave the near vegetarian diet behind. From 1960 to 1990, Italian men came to eat ten times more meat on average, which was by far the biggest change in the Italian diet, yet the sizable spike in heart disease rates that might have been expected did not occur; in fact, they declined. And the height of the average Italian male during this time increased by almost three inches.

Is Teicholz implying that meat consumption decreased heart disease rates and increased height? Is that what she is doing here? It sure looks like it. Is this evidence from a randomized controlled dietary trial? Does Teicholz need to be reminded that correlation does not equal causation?

 

Her supporting evidence for this is a paper by Ferro-Luzzi (remember her?).65 The paper states that meat consumption increased about 3X not 10X. Sugar consumption increased about 4X. Both fruit and vegetable consumption doubled, as did eggs and fish. At the risk of spelling this out for everyone, even if we were to assume that something like height was due only to diet (which is a stretch), Teicholz still has all her work ahead of her to find good reasons to eliminate all the other dietary changes as a possible factor.

* * *

Page 221-222:

It was the same in Spain: since I960, meat and fat consumption have skyrocketed, while at the same time deaths from heart disease have plummeted. In fact, coronary mortality over the past three decades has halved in Spain, while saturated fat consumption during roughly this period increased by more than 50 percent.

Her evidence for this claim is a cross-sectional study by Lluís Serra-Majem.41 If you were not aware, cross-sectional studies are the least informative and least robust of all epidemiology, except for perhaps a case series. Funny how Teicholz claims throughout the book that epi studies like this one are basically meaningless if they purport to show some link between meat or saturated fat and some negative health outcome, but are just fine to invoke if they fit her narrative.

Meanwhile, if you actually read the study the author says something that Teicholz might not want you to hear:

This paradoxical situation can be explained by expanded access to clinical care, increased consumption of fruit and fish, improved control of hypertension, and a reduction in cigarette smoking.

The author goes on to state that bioactive compounds and dietary antioxidants such as beta-carotene likely also played a role in decreasing CHD. Of course Teicholz never informs her readers of this, because she wants you to think that meat brought CHD rates down.

Teicholz continues:

The trends are the same in France and Switzerland, whose populations have long eaten a great deal of saturated fat yet never suffered much from heart disease. The Swiss ate 20 percent more animal fats in 1976 than in 1951 while deaths from heart disease and hypertension fell by 13 percent for men and 40 percent for women.

True according to one of those cross-sectional, observational studies she cites (which according to her are crappy and meaningless).66 But what she doesn’t say is that other things happened in Switzerland in those years as well according to the analysis: use of anti-hypertensive drugs increased, the economy got much better, there was a migration to urban areas, intake of vegetable fats increased, there was an increased use of oral contraceptives. All of these factors are associated in some way with the decline of heart disease. Do they play a role? It is unclear, and it CANNOT be clear from this study. But that doesn’t stop Teicholz from letting you think that meat may have caused the downturn.

Continuing to the very next paragraph:

This apparent contradiction holds true even on the island of Crete. When the lead researcher for the Greek portion of the Seven Countries study, Christos Aravanis, went back to Crete in 1980, two decades after his initial research, he found that the farmers were eating 54 percent more saturated fat, yet heart attack rates remained extraordinarily low.

The Aravanis paper actually says the opposite of that67:

The 10-year adjusted MCHD [mortality from coronary heart disease] was correlated with total fat in the diet; the correlation with saturated fatty acids was much more significant.

AND

The 10-year incidence rate for CHD was correlated in low order with percentage of calories from total fats, but its correlation with percentage of calories from saturated fatty acids was significantly positive.

Chapter 8: Exit Saturated Fats, Enter Trans Fats

Cribbing Schleifer Alert

It would appear that Teicholz lifts much of the first few pages of chapter 8 from the works of David Schleifer, specifically his 2010 dissertation and a 2012 article which is essentially a condensed version of his dissertation. Schleifer is not attributed in the references section, either. Teicholz doesn’t blatantly copy-paste verbatim, but instead changes enough words to where she has plausible deniability. If you read through both chapter 8 and Schleifer’s dissertation, though, you can easily tell that it’s the same information in the same order.

 

For instance, Schleifer writes on page 64 of his dissertation “Philip Sokolof founded NHSA in Omaha, Nebraska in 1985 to increase public awareness of cholesterol. Sokolof was motivated by a near-fatal heart attack to spend approximately $15 million of his own money on public education campaigns related to saturated fat and cholesterol.”68 On page 228 of BFS Teicholz writes “Another force pushing food companies to ditch saturated fats for hydrogenated oils was a lone multimillionaire in Omaha, Nebraska, Philip Sokolof […] after suffering a near-fatal heart attack in his forties, made it his mission in his retirement to inform Americans about the dangers of saturated fats.”

 

  • Schleifer: “He seems to have operated the organization mostly by himself, spending approximately $15 million of his own money […]”69

  • Teicholz, page 230: “Sokolof founded a group called the National Heart Saver Association, funded by his own millions, and ran it mostly by himself.”

  • Schleifer: “Sokolof mailed ‘thousands of letters’ to food manufacturers urging them to eliminate saturated fats.”69

  • Teicholz, page 230: “[Sokolof] had mailed ‘thousands of letters’ to food manufacturers urging them to eliminate tropical oils from their products […]”

  • Schleifer, page 65: “Irritated at receiving form letters in response, he mounted his first of three ‘Poisoning of America’ campaigns in October 1988.”68

  • Teicholz, page 230: “[A]n irritated Sokolof decided that a campaign to shame these manufacturers publicly was his best option.”

  • Schleifer, page 65: “These consisted of full-page advertisements in The New York Times, Washington Times, The New York Post, USA Today, The Wall Street Journal and other newspapers […]”68

  • Teicholz, references page 383: “Identical full-page ads were also placed in the Wall Street Journal, Washington Times, New York Post, and USA Today, among other papers.”

Both Teicholz and Schleifer even publish the same Sokolof figure and use the same quotes from it.

 

But that’s not all: it appears Teicholz also takes most of her information on CSPI from Schleifer as well.

  • Both discuss the “Saturated Fat Attack” campaign, even though the source material from the 80s is nearly impossible to find.

  • Both pluck the same quotes from the same texts, even though the original texts might be 200+ page books.

  • Teicholz, page 228: “Hydrogenated oils were therefore ‘not a bad bargain’ when it came to heart disease, the group concluded.” Schleifer uses the same “not a bad bargain” quote in both of his texts.68,69 What are the odds?

  • Schleifer: “But it praised Burger King for switching to vegetable shortening in 1986, which it described as ‘a great boon to Americans’ arteries.’”69

  • Teicholz, page 228: “Another CSPI campaign successfully convinced movie theaters across America to switch from butter and coconut oil to partially hydrogenated oils in their popcorn poppers. This was ‘a great boon to American arteries’ CSPI judged.” Notice how Teicholz makes it seem like CSPI is referring to movie theaters here, when in fact it is actually Burger King.

The argument about the fight between the American Soybean Association and the Malaysian palm oil industry is also part of Schleifer’s dissertation. They both use the same quote from a NYT article.

  • Schleifer, page 71: “’A trade issue is not our concern,’ said Stuart Greenblatt, a spokesman for the Keebler Company, which has said it will remove tropical oils from all its products. ‘American consumers and their health is our concern, and they are telling us they don’t want it. We get piles of mail every day, from everywhere’”68

  • Teicholz, page 235: “’We are getting piles of mail every day, from everywhere,’ a spokesman for the Keebler Company told the New York Times. ‘American consumers and their health is our concern, and they are telling us they don’t want it [tropical oils].’”

  • Schleifer, page 77-78: “[…] General Mills’ Bugles brand corn chips were the only major American brand that did not reformulate; they were unable to find a technically viable alternative and continued to use coconut oil.”68

  • Teicholz, page 235: “Nor could Bugles, the cornucopia-shaped snack made by General Mills, be easily reformulated without coconut oil.”

It is amusing to me that Teicholz accuses Time magazine of lifting her arguments when she pretty blatantly lifts arguments from others. Again, I think it is worth mentioning that Schleifer is not mentioned in her references section, and he most definitely should be. To be fair, she puts his stuff in the bibliography, but never references it. I have no idea why the references/bibliography sections are structured like they are. It just makes everything monumentally confusing when attempting to look something up, plus it takes up an extra 100 or so pages that would not be necessary if they were cited the traditional way. My guess is that she just copied the way Taubes did GCBC, references and all.

* * *

Page 234:

In preliminary studies, palm oil seemed to protect against blood clots.

Nope. The study she cites actually shows that sunflower seed oil protects against blood clots… in rats.70

 

Chapter 9: Exit Trans Fats, Enter Something Worse?

Page 275:

Research over the past twenty years has allayed the health concerns raised about palm oil during the “tropical oil wars”; the oil may actually be beneficial for health in some ways […]

As evidence she cites a supplemental paper written by the Malaysian Palm Oil Council.71

* * *

Page 276:

More speculatively, research over the past decades has shown that omega-6s are related to depression and mood disorders.

The cited paper actually makes the case that low omega-3 intake is related to depression.72 I suppose if you really stretch your brain you can somehow argue that eating omega-6 will necessarily lead to low omega-3s, which might then cause depression, but that’s way out there.

 

Chapter 10: Why Saturated Fat Is Good for You

On page 288 Teicholz discusses Dr. Atkins and says

The diet was a tremendous success for him and then for his patients. Atkins tweaked the Wisconsin paper and expanded it into an article for Vogue magazine (his regime was called the Vogue Diet for a while).

I decided to check her bibliography and download the Vogue issue in question via ProQuest. She cites it as “Take It Off, Keep It Off Super Diet . . . Devised with the Guidance of Dr. Robert Atkins,” Vogue 155, no. 10 (1970): 84—85.” I looked on pages 84-85 and it wasn’t there. Strange, right? Where did she come up with that citation? As it turns out (as of this writing, at least) it is cited that way on Dr. Robert Atkins’s Wikipedia page: It turns out that the actual Vogue article is located in the same issue, but different page numbers. My guess is that Teicholz simply copy-pasted the Wikipedia reference and never even saw the original magazine issue.

vogue wiki reference_

* * *

Page 298, Teicholz discusses the memoirs of a physician:

With patients on his meat-all-the-time diet, Donaldson found himself “less and less likely to resort to drugs” to combat these diseases.

Her references indicate that the quote is found on page three of his memoir Strong Medicine. It is not. Nor is it clear, if it was the case that Donaldson prescribed fewer drugs, that it was the result of his meat-heavy diets.

* * *

Teicholz then discusses a doctor and researcher Otto Schaefer who visited some “Eskimo” populations. On page 299 she states:

To Schaefer, it seemed obvious that the Inuit were “unable to cope with starches and sugars” to which they had been introduced.

As the source of that quote Teicholz cites a paper titled “Glycosuria and Diabetes Mellitus in Canadian Eskimos.”73 The above quote does not exist in the text. The paper actually makes the case that diabetes was considerably overdiagnosed in Eskimo/Inuit populations, perhaps contrary to the case Teicholz is trying to make in this section, namely that CHOs led to chronic diseases in the Inuit.

* * *

Page 304:

[F]or peak performance during long-distance efforts such as marathons, the common wisdom has been that athletes should eat a lot of carbohydrates the night before. His was the first idea that Phinney wanted to test. “We were pretty sure we’d prove that the carb-loading concept was correct” Phinney told me. To his surprise, he found just the opposite: athletes in his experiments could perform at their best on nearly zero carbohydrates.

These “athletes” were actually obese study subjects.74 These subjects were on a low-carb, calorie-restricted diet and there was no control group of moderate or high-carbohydrate dieters with which to compare the results. In my interpretation the best thing you can say about this study is that obese people are capable of exercise on a reduced-calorie, ketogenic diet.

* * *

Page 305:

[O]ur bodies have no requirement for carbohydrates and can sustain themselves perfectly well, if not better, on ketones.

For this claim she cites a paper from 1956 that measured fatty acids in the blood.75 I don’t know if you can claim that we have no requirements for CHOs and can sustain ourselves as well or better on ketones. The only thing you can really say is that unesterified fatty acids exist in human plasma.

* * *

Page 306:

[T]he ability of blood vessels to dilate (known as endothelial function,” which many experts believe to be an indicator of heart attack risk) has also been shown to improve on the low carbohydrate diet, compared to people on one low in fat. Surprised and skeptical, Volek wondered if all these gains could simply be due to weight loss, since his subjects inevitably slimmed down on the Atkins diet. So he did further experiments keeping his subjects weight constant and found that the low-carb diet yielded the same improvements, even so.

My beef here is with that last statement, the rest is just for context. If you look at the “further experiments” Teicholz mentions you’ll find that the source of this statement is no trial, but rather a letter to the editor of AJCN that criticizes another study that claims that weight loss causes the improved endothelial function and not a load of fat.76,77

* * *

Page 306:

Carbohydrate restriction as a cure for diabetes had been reported by physicians as far back as the late nineteenth century, but Westman’s trials were among the first to give solid scientific backing to the treatment.

On page 398 of the Notes section Teicholz cites a study that predated Westman’s that ostensibly gives “solid scientific backing” to the idea that diabetes could be cured via CHO restriction. Except that the study was done on obese patients and given only 300-700 kcals of nearly pure protein, plus Tums and iron supplements.78 The patients ended up losing a lot of weight. A couple things: 1) “Cure” is certainly a strong word; 2) Can Teicholz be sure that it was not the weight loss alone or the Tums or the iron or the protein or the lack of fat that played a role in the improvement? It must be CHO restriction?

* * *

Page 307:

[T]he American Diabetes Association (ADA) has stood by its low-fat advice, based on the fact that diabetics have a very high risk of heart disease, and since authorities advise a low-fat diet to fight that disease, that is what the ADA recommends to prevent diabetes, too.

The publication she cites actually favorably mentions both a low-fat AND a low-carbohydrate diet.79 In fact, it seems that the ADA might be inclined toward a low-carb diet. Don’t believe me? From the text:

  • For weight loss, either low-carbohydrate or low-fat calorie-restricted diets may be effective in the short term (up to 1 year).

  • Although low-fat diets have traditionally been promoted for weight loss, two randomized controlled trials found that subjects on low-carbohydrate diets lost more weight at 6 months than subjects on low-fat diets.

  • Another study of overweight women randomized to one of four diets showed significantly more weight loss at 12 months with the Atkins low-carbohydrate diet than with higher-carbohydrate diets.

  • Changes in serum triglyceride and HDL cholesterol were more favorable with the low-carbohydrate diets.

  • In one study, those subjects with type 2 diabetes demonstrated a greater decrease in A1C with a low-carbohydrate diet than with a low-fat diet.

  • It is possible that reduction in other macronutrients (e.g., carbohydrates) would also be effective in prevention of diabetes through promotion of weight loss […]

  • Low-carbohydrate diets might seem to be a logical approach to lowering postprandial glucose.

Why not mention this? I don’t know. I suppose it is in keeping with the narrative throughout the book that nutrition authorities are incompetent, corrupt, and/or extremely rigid in their advice.

* * *

Page 308:

One of the more extraordinary experiments involved 146 men suffering from high blood pressure who went on the Atkins diet for almost a year. The group saw their blood pressure drop significantly more than did a group of low-fat dieters—who were also taking a blood-pressure medication.

Barely any of that statement is true: blood pressure went down a bit among the low-carbohydrate group, but not enough to be statistically significant.80 Also there was no mention of any group taking a blood pressure lowering medication. I don’t know where she gets that. Also, the study lasted for 24 weeks, not one year. She must have cited the wrong article, this is just too wrong to even be lying.

* * *

Page 309-310:

In 2008, results from a two-year trial were finally published. This was the study in Israel, discussed in the Mediterranean diet chapter, on 322 overweight men and women. The trial was exceptionally well controlled by the standards of nutrition research, with lunch, the principal meal of the day in Israel, provided at a company cafeteria.

The study separated subjects into three groups: one eating the AHA’s prescribed low-fat diet, another on the Mediterranean diet, and a third on the Atkins diet. […]

Shai found that for nearly every marker of heart disease that could be measured during the two years of the study, Atkins dieters looked the healthiest—and they lost the most weight. For the small subset of diabetics in the study, the results looked about equal for the Atkins and Mediterranean diets. And in every case, the low-fat diet performed the worst.

[…] Kidney function and bone density, two primary concerns, were found to be perfectly fine, if not improved, on the Atkins diet.

For these claims Teicholz cites a 2008 study by Shai published in NEJM.81 However, she leaves out a few facts from the study.

  1. The participants in the low-carbohydrate arm of the study were counseled to consume vegetarian sources of fat and protein.

  2. The participants were nearly all male, something Teicholz takes umbrage with in chapter 6.

  3. Although the low-fat diet did seem to “perform” the worst of the three, the Mediterranean diet and the low-carbohydrate diet fared similarly in most respects, not just in diabetics. So I doubt you can say unequivocally that the Atkins dieters were the healthiest when there’s another diet that leads to the same measured outcomes.

Although not discussed by Teicholz there were some other papers published using data from this particular study (referred to as DIRECT, Dietary Intervention Randomized Controlled Trial). One of which was a four year follow-up to the study that showed that the Atkins-style dieters gained back most of the weight that was lost.82 The Mediterranean dieters ended up losing nearly double the weight of the Atkins dieters. The low-fat group still had the least amount of weight lost. The Mediterranean dieters also had the most favorable cholesterol and triglycerides.

 

In another publication kidney function was found to be similarly improved among all three diets.83 Although the authors mention that since the improvement was so similar between diets, the improvement among participants was likely due to weight loss alone rather than the constituents of the diet. The same was said in a publication examining the effect of the three diets on atherosclerosis.84

Another publication from the same trial suggests that the Mediterranean diet is the most beneficial of the three for type 2 diabetics.85

For a more detailed discussion of the Shai study see CarbSane’s posts: Part 1, Part 2, Part 3, and Part 4.

* * *

Page 314:

In 2011, a group of top nutrition experts published the first high-level, formal consensus paper stating that refined carbohydrates were worse than saturated fats in provoking heart disease and obesity (Astrup et al. 2011).

This is not true. The paper stated that no clear benefit of replacing saturated fatty acids with carbohydrates has been shown, not that refined carbohydrates are worse.86 Moreover, the authors state unambiguously that replacing saturated fatty acids with polyunsaturates does decrease risk of heart disease – something Teicholz unsurprisingly leaves out.

* * *

Page 315:

Remember that the Shai study in Israel found that the Mediterranean diet group, eating a high proportion of calories as these “complex” carbohydrates, turned out to be less healthy and fatter than the group on the Atkins diet, although they were healthier than the low-fat alternative.

Umm… No.

* * *

Page 315:

The Women’s Health Initiative, too, in which some 49,000 women were tested on a diet high in complex carbohydrates for nearly a decade, showed no reduction in disease risk or weight.

Wrong again. There was decreased risk in ovarian cancer and weight.16,17

* * *

Page 317:

[I]n more than a few major studies, LDL-cholesterol levels were found to be completely uncorrelated with whether people had heart attacks or not.

Let’s take a look at these “major studies” she cites, shall we?

 

The first is by de Lorgeril et al.52 I won’t go into detail, but those in the intervention group had fewer heart attacks and also had lower LDL. From the text: “[T]he trend with time was a decrease in total and low density lipoprotein (LDL) cholesterol […]” Although it was not statistically significant, so we’ll give this one to Teicholz.

The second is not a study, but a short commentary by Despres.87 It argues that we should not focus exclusively on LDL, which is not the same as saying LDL is not correlated with anything.

The third is a statin trial that showed reducing LDL cholesterol also reduced coronary events.88 In other words, the opposite of Teicholz’s claim. Some choice quotes from the paper:

This trial provides evidence that the use of intensive atorvastatin therapy to reduce LDL cholesterol levels below 100 mg per deciliter is associated with substantial clinical benefit in patients with stable CHD.

Our findings indicate that the quantitative relationship between reduced LDL cholesterol levels and reduced CHD risk demonstrated in prior secondary-prevention trials of statins holds true even at very low levels of LDL cholesterol.

The fourth is a meta-analysis on statins and all-cause mortality.89 Basically irrelevant because it’s only slightly related to the claim of no relationship between LDL and heart attacks.

The fifth is by Castelli et al and is again pretty much the opposite of what Teicholz said.90 Want some more choice quotes?

There is a very regular increase of CHD prevalence rates with increasing LDL cholesterol level at each level of HDL cholesterol.

The inverse relationship between HDL cholesterol and CHD, when taken over the three levels of LDL cholesterol, is significant (P < 0.001) by a method of Mantel, as are the positive trends of CHD prevalence on LDL cholesterol level.

Cross-classification of triglyceride with LDL cholesterol level (fig. 3) leads to the conclusion that either lipid has a statistically significant association with CHD prevalence […]

In general, then, when contingency tables are constructed for the three lipids considered two at a time, HDL and LDL cholesterol emerge as consistently significant factors in CHD prevalence […]

Does Teicholz even read the studies she cites?

* * *

Page 324:

Krauss and his colleagues concluded that “saturated fat was not associated with an increased risk” for heart disease or stroke.

Krauss did not conclude that, according to the cited study.91 What was said is that replacing saturated fat with carbohydrate is not associated with an increased risk of heart disease in women. Notice how they are very different statements?

What about stroke? The paper mentions a couple things:

[S]aturated fat intake may be inversely related to ischemic and/or hemorrhagic stroke, but a meta-analysis including results from 6 other studies did not yield a statistically significant risk reduction.

Notably, in humans, the risk of stroke has been related to both the saturated and monounsaturated fatty acid content of plasma cholesteryl esters, which further supports the possibility that the dietary intake of these fatty acids may influence CVD risk by altering cholesteryl ester composition.

Bonus factoid: the paper also states that polyunsaturated fats are inversely associated with developing type 2 diabetes.

* * *

On page 325-326 she discusses a panel event at FNCE in 2010 and produces a quote by Mozaffarian: “its not really useful anymore to focus on saturated fats,” he said. She cites a subsequent publication of the event in the Journal of the American Dietetic Association.92 However, that paper does not contain that quote. Nor does the quote appear in other publications by JADA discussing that event and quoting Mozaffarian.93,94

* * *

Page 326: “Americans have dutifiilly followed official dietary advice […]” Pretty sure that’s not true.95 Even by the admission of the USDA.96

 

Conclusion

After reading The Big Fat Surprise by Nina Teicholz I am frankly disappointed – yet unsurprised – that a book like this was even published. We as readers need to start demanding better fact-checking from our publishers, especially the enormously successful ones like Simon & Schuster. Misinformation like this can actually affect people’s health in a potentially very negative way. I get that publishing companies want to make a profit, but you can publish a compelling pop science book that people buy without misinforming your audience.

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*EDIT: The original post contained this statement: I find it interesting that Teicholz uses the word “regime” to describe a diet. Regime means a system of government and is almost always associated with the types of government that are oppressive, totalitarian, dictatorial, despotic, etc. Is she subtly attempting to associate the Mediterranean diet with oppression and death? But I removed it because I had forgotten Teicholz also uses “regime” when describing other diets, such as Atkins.

 

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2. BRODY, J. E. Tending to Obesity, Inbred Tribe Aids Diabetes Study: Inbred Tribe Aids Research Into Obesity and Diabetes Samples Are Preserved 6,000 Involved in Study. N. Y. Times C1 (1980).

3. As it happens, if you look under the meat category, except for fish, meat does nothing BUT increase cancer risk. And the evidence is even ‘convincing’ when it comes to colorectal cancer.

4. Marmot, M. et al. Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective. (World Cancer Research Fund / American Institute for Cancer Research, 2007). at <http://www.dietandcancerreport.org/policy_report/index.php>

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9. I found two versions of this text: one published on 1918 and another in 1922. Teicholz cites a version apparently published in 1921. My page numbers correspond to the 1922 version.

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23. 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).

24. Ernst, N. D., Sempos, C. T., Briefel, R. R. & Clark, M. B. Consistency between US dietary fat intake and serum total cholesterol concentrations: the National Health and Nutrition Examination Surveys. Am. J. Clin. Nutr. 66, 965S–972S (1997).

25. Esterbauer, H. Cytotoxicity and genotoxicity of lipid-oxidation products. Am. J. Clin. Nutr. 57, 779S–785S (1993).

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63. Singh, R. B. et al. Effect of an Indo-Mediterranean diet on progression of coronary artery disease in high risk patients (Indo-Mediterranean Diet Heart Study): a randomised single-blind trial. Lancet 360, 1455–1461 (2002).

64. Nordmann, A. J. et al. Meta-Analysis Comparing Mediterranean to Low-Fat Diets for Modification of Cardiovascular Risk Factors. Am. J. Med. 124, 841–851.e2 (2011).

65. Ferro-Luzzi, A. & Branca, F. Mediterranean diet, Italian-style: prototype of a healthy diet. Am. J. Clin. Nutr. 61, 1338S–1345S (1995).

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71. Khosla, P. & Sundram, K. A supplement on palm oil–why? J. Am. Coll. Nutr. 29, 237S–239S (2010).

72. Hibbeln, J. R. & Salem, N. Dietary polyunsaturated fatty acids and depression: when cholesterol does not satisfy. Am. J. Clin. Nutr. 62, 1–9 (1995).

73. Schaefer, O. Glycosuria and diabetes mellitus in Canadian Eskimos. Can. Med. Assoc. J. 99, 201–206 (1968).

74. Phinney, S. D. et al. Capacity for Moderate Exercise in Obese Subjects after Adaptation to a Hypocaloric, Ketogenic Diet. J. Clin. Invest. 66, 1152–1161 (1980).

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76. Westman, E. C., Volek, J. S. & Feinman, R. D. Carbohydrate restriction is effective in improving atherogenic dyslipidemia even in the absence of weight loss. Am. J. Clin. Nutr. 84, 1549–1549 (2006).

77. Krauss, R. M., Blanche, P. J., Rawlings, R. S., Fernstrom, H. S. & Williams, P. T. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am. J. Clin. Nutr. 83, 1025–1031 (2006).

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83. Tirosh, A. et al. Renal Function Following Three Distinct Weight Loss Dietary Strategies During 2 Years of a Randomized Controlled Trial. Diabetes Care 36, 2225–2232 (2013).

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85. Ben-Avraham, S., Harman-Boehm, I., Schwarzfuchs, D. & Shai, I. Dietary strategies for patients with type 2 diabetes in the era of multi-approaches; review and results from the Dietary Intervention Randomized Controlled Trial (DIRECT). Diabetes Res. Clin. Pract. 86, Supplement 1, S41–S48 (2009).

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Gary Taubes is a Blowhard

Imagine if you will that you make a living by selling an idea. You are a merchant in the marketplace of ideas, and you sell an idea that we will call Idea X. You sell books that promote Idea X, you give lectures across the country extolling the virtues and benefits of Idea X, etc. Turns out that Idea X is somewhat controversial but quite lucrative. You tried selling other stories and ideas in the past, but none have been nearly as profitable to you as Idea X. Espousing this idea has afforded you the ability to provide your spouse and children a comfortable living in these tough economic times. Imagine also that a scientific study was recently conducted by prominent researchers and the results are published in a prestigious scientific journal. As it happens the results of the study are pretty devastating to Idea X and contradict some of its main points. In the following days the study results are much-discussed in various media outlets, and some people begin to doubt the idea that you’re selling. The study results have left the more loyal adopters of your idea confused as to what to believe, and they beg you to respond to the study.

What do you do?

There are probably a few different choices you could make in this case.

  1. You could ignore the study and hope this bad news blows over soon. Then after the media gets bored of discussing the study results and moves on, you can try to resume preaching your idea to the people still adhering to your idea. As time goes on you can try to re-convert those who left Idea X.
  2. You could follow where the evidence leads and come out and say “I don’t want to mislead anybody. It looks like Idea X is not supported by the evidence. I was wrong, and I’m sorry.” Then you face the very tough challenge of trying to find another idea that is both as profitable as your last idea with the caveat that it is also evidence-based and grounded in reality. If you don’t find another profitable idea then you’ll have to move your family out of your nice neighborhood and into a lousier one while you work unappealing jobs to put food on the table.
  3. You could denounce the study and the scientists who conducted it. You could try and poke holes in the evidence and muster your greatest argument for why no one should believe the results. It may not be intellectually honest, but the truth must be an unfortunate casualty when you and your family’s quality of life is at stake.

Gary Taubes has chosen #3, except he takes it even further and denounces not only the specific study and the researchers that conducted it, but the field of epidemiology as a whole. This is actually pretty shrewd since most epidemiological evidence is against him anyway. Taubes’s Idea X in this analogy is the assertion that, contrary to popular belief, foodstuffs like red meat, saturated fat, and cholesterol are actually healthy and pose no threat of disease while just about any and all carbohydrates are unhealthy.

Mr. Taubes recently wrote a blog post responding to a recent study titled Red Meat Consumption and Mortality published in Archives of Internal Medicine. The study concludes “red meat consumption is associated with an increased risk of total, CVD, and cancer mortality.”1 If I had to summarize Mr. Taubes entire blog post it would be something like: Epidemiology is a pseudoscience. Well, not all epidemiological research, just any research suggesting that eating red meat for every meal might not be healthy. Any scientist or nutrition researcher claiming that is practicing a junk science. Those that come to other conclusions are the real scientists, the good scientists. Also, I will never accept any scientific claim unless there are randomized, placebo-controlled clinical trials to back it up. Except for the claim that smoking causes lung cancer. I will accept that one without RCTs.

Let’s Break it Down

To start things off Taubes does not refute any specific thing in the actual paper. He leaves that job to someone else.

Zoe Harcombe has done a wonderful job dissecting the paper at her site.

Taubes prefers instead to respond to the paper’s general tone and the tone of some of the researchers involved with the paper, notably Dr. Walter Willett and Dr. Meir Stampfer.

Who is this Zoe Harcombe and why should I trust her judgment? The biography on her webpage does not tell me much about her credentials other than she is a

[Q]ualified nutritionist with a Diploma in Diet & Nutrition and a Diploma in Clinical Weight Management, but she is first and foremost an obesity researcher.

A “qualified nutritionist”? What does that even mean? Who “qualified” her and gave her “Diplomas”? Were these actual universities or did she just pay 30 bucks (or pounds perhaps, since she’s from the UK) for some shady online certification that means nothing? We are not told, and I suspect for good reason.

She is also an obesity researcher, huh? A quick Google Scholar search of her name came up with no publications. Is she actually a researcher or does she just call herself one? I suspect the latter. I love how Taubes apparently thinks she is some sort of authority on the matter but the Harvard School of Public Health is full of incompetent boobs.

Here is one of her “key problems with this study”

1) This study can at best suggest an observed relationship, or association. To make allegations about causation and risk is ignorant and erroneous.

Nowhere in the study did the authors claim to have a causal relationship. It is always stated as an association. Harcombe misrepresents the results.

Eventually her “key problems” devolve into irrelevant and unverifiable ad hominem

[O]ne of the authors (if not more) is known to be vegetarian and speaks at vegetarian conferences

It is like the author is a communist or something!  As if being a vegetarian would have any bearing on the results of the study. Are vegetarians not supposed to conduct nutrition research now, only omnivores? What about Jews or Muslims? If they do research involving meat should their results not be published? What’s more is this claim isn’t even verified. She has a citation but it takes me to this page that tells me nothing. I also went to the page with the 2013 speakers but none of them authored the study in question.

Okay, back to Taubes now.

The problem with observational studies like those run by Willett and his colleagues is that they do none of this [testing hypotheses]. That’s why it’s so frustrating. The hard part of science is left out and they skip straight to the endpoint, insisting that their interpretation of the association is the correct one and we should all change our diets accordingly.

You mean like how you do, Taubes, with your books and lectures? Except that you are not a scientist and have no medical training or research experience like Willett et al. I don’t want to engage too much in tu quoque, but pointing out hypocrisy is so much fun. Let me get in one more jab, and then I’ll move on.

I’m no expert in Taubesian hermeneutics, but I think he meant to say The problem with observational studies like those run by Willett and his colleagues is that they are so devastating to my position that everyone should eat truckloads of meat. Okay now I’ll get to the substance of his point.

Mr. Taubes seems to be accusing Willett et al. of laziness despite the fact that they churn out hundreds of studies that take decades to complete and are peer-reviewed and published in top-tier journals.2 The reason for this is because, according to Mr. Taubes, epidemiology is not a true science, and if Willett and his colleagues really wanted to study certain dietary aspects and their link to colon cancer mortality or cardiovascular disease mortality they have to conduct randomized, double-blind, placebo-controlled human clinical trials (I will abbreviate as RCTs). Anything less is not “good science.”

I’m not about to give you a lecture on what epidemiology is and why it is important. It may be a good subject for a future post, but for now I will say that it is a useful field when studying large populations, incidence and prevalence of disease, or when RCTs would be unethical or impossible.

Here is a visual reference to help understand the hierarchy of evidence a little better. At the top of the triangle you have the most rock-solid evidence that we have on a given subject and the bottom is the least valuable evidence.

As you can see, the cohort studies in question are not quite as good as RCTs, but they are as close as you can get. They are not meant to replace RCTs in evidence-based medicine, but they can be a good proxy when conducting a RCT would be impossible. Here’s another visual that explains each method.

Mr. Taubes asserts that the experts are wrong and red meat does not lead to any kind of mortality. He asserts this with barely any evidence and zero RCTs to back up his assertion, yet if anyone would disagree he demands they provide RCTs because Taubes will not accept cohort studies. Conveniently for him the RCTs he demands will  almost certainly never take place. Let me explain.

Mr. Taubes seems to think that RCTs examining specific dietary constituents and their roles in disease mortality are low-hanging fruit. I’d like to see Taubes design one for, say, red meat and colon cancer. It would be worth a read just to see how he deals with the problem of blinding alone. Furthermore, what would be a good placebo? I get that one group would be assigned red meat every meal, but how do you get the control group to eat placebo meat without the subjects really knowing if they are in the meat-eating group? Surely people can tell the difference between a tofu steak and a genuine ribeye. Plus cancer is not something that you get only a few weeks into a feeding study. It takes decades to arise, so it would mean that a RCT would also have to take as much time. There are many more difficult study design issues Mr. Taubes would need to tackle before he could begin.

This is all assuming of course that the study would be funded (it almost certainly wouldn’t because it would be the single most costly RCT in history) and that it would pass IRB approval (it wouldn’t because the study itself would be unethical considering there is a fair amount of evidence that red meat does in fact lead to colon cancer3, Red Meat Consumption and Mortality notwithstanding).

 

Throw it Against the Wall and See if it Sticks

If you don’t buy into his Epidemiology Sucks theory Taubes also hurls some other arguments against the study hoping at least one of them will stick. One is that the increase in mortality from red meat eaters is only an increase of 0.2 so it’s basically nothing and you should just forget about it. Of course another way to present that increase is 20%. An increase of only 0.2 seems like such a small number compared to 20%, doesn’t it? What if I told you that drinking Generic Beverage That You Sort Of Enjoy everyday increases your risk of developing esophageal cancer by twenty percent? My guess is you would cut down on Generic Beverage That You Sort Of Enjoy, even if you enjoyed it.

Another argument Taubes uses is admitting the following:

[T]he people who avoided red meat and processed meats were the ones who fundamentally cared about their health

If I may paraphrase: Okay, sure, vegetarians are healthier than meat-eaters. But is it because of the meat? I say it’s because vegetarians are just generally healthier than meat-eaters. They are more health-conscious and they smoke less. It has nothing to do with meat! It’s simply the “healthy cohort effect”!

Are you sitting down? I hope so because I’m about to rock your world: I agree with Taubes here. This is a legitimate concern with epidemiological studies. If you are not careful with your study design and statistical analysis these kinds of things can bias your results. However, there are many ways you can adjust for things like this, and I think it goes without saying that if you have a poor study design or no adjustments then you don’t get published in the top tier journals in which Willett and Stampfer get published. Furthermore, sampling biases like the healthy cohort effect are stronger in smaller cohorts of 10 or 20, but when you increase sample size to 100 or 1,000 the effect becomes negligible. In the case of Red Meat Consumption and Mortality the authors use cohorts of 37,698 men and 83,644 women, so if they did their due diligence with the statistical analysis (and I’m not about to check their math, that’s what the peer-review process is for) if the effect is even present it should be so weak as to be nonexistent.

As it stands the authors of the paper in question did in fact adjust for smoking status as well as a host of other lifestyle factors.4

Watch now as Taubes removes any possible hope you might have about his scientific literacy.

So do an experiment to see which is right. How do we do it? Well you can do it with an N of 1. Switch your diet, see what happens.

The ol’ do-it-yourself randomized controlled trial. The very pinnacle of oncological research. Have you switched to a high-beef, low-carb diet? Check. Have you died from colon cancer and/or cardiovascular disease? No? Well then the experts were wrong! Help yourself to some more mutton. Take note future lawyers: this is special pleading at its finest.

Credit Where Credit is Due

Although completely irrelevant to a discussion of Red Meat Consumption and Mortality Taubes does cite one randomized trial (not placebo-controlled) that kind of shows some benefits in a low-carb Atkins diet over other somewhat popular diets such as Zone or Ornish. It is totally a red herring, but let’s touch on it anyway. The study takes premenopausal women that are either overweight or obese and assigns them to one of several diets. They all receive instructions on how to follow their assigned diets and are followed-up on after one year. Turns out the Atkins people lost more weight than the other people. They also had a slightly more favorable lipid profile (i.e. higher HDL levels lower triglyceride levels) but elevated LDL levels compared to the other diets.5

A few things to note:

  • I think it is hilarious that earlier in his post Taubes criticizes the Red Meat Consumption and Mortality study because he claims “they use questionnaires that are notoriously fallible” to collect dietary information.6 Meanwhile he praises this “A to Z” study for its design without mentioning that the authors use telephone-administered dietary recalls, which are not bad per se but chosen mainly for their efficiency rather than robustness.
  • One could make an argument that simply giving people some instruction on the diets in the beginning and then coming back in a year to measure outcomes is not the best study design. For example, many nutrition labs in the Fred Hutch (including mine) will actually provide all of the meals to be eaten during the study free of charge. This accomplishes a couple things: 1) It increases compliance with the diet7 and 2) It allows the researchers to strictly control the calories, vitamins, fat content, etc. I don’t think the above study was a poor design, but there are stronger (albeit more costly and time-consuming) feeding designs one could use when studying diet.
  • I was not surprised that the Atkins group lost more weight. There are actually good and interesting reasons for why low-carb diets are very effective in that area, but I won’t get into that now. What did surprise me at first was that the Atkins group had lower triglyceride levels. But then I remembered that weight loss in general will produce that effect, especially if subjects are overweight at baseline. If the other diets produced as much weight loss as Atkins I would expect a similar reduction of triglycerides.8
  • This study uses exclusively disease-free, non-diabetic, non-pregnant or lactating (etc…9) overweight and obese premenopausal women, so to extrapolate these results and suggest that the general population would be healthier if they adopted this diet is certainly dubious.
  • This is a diet study that examines carbohydrates and weight loss and lipid profiles after 12 months. The Red Meat Consumption and Mortality study in question deals with red meat and cancer, CVD, and other mortalities after 28 years. The former does not and cannot refute the latter. They are almost unrelated. You can eat meat three times a day and have the bulk of your calories come from carbohydrates. You can be a vegan that eats a ton of fat and protein but very few carbs. They are not mutually exclusive.

Stunning Hypocrisy

Now you may be thinking that this is a guy who simply demands the highest levels of evidence. Sure Taubes may miss out on a ton of great knowledge obtained from epi studies but the man takes a hard line on evidence. He will only accept findings from human randomized controlled trials and you can’t fault him for that.

Except that he doesn’t.

If you take a look at some of Taubes’s other posts you will see he makes other controversial claims that run contrary to mainstream science.10 In other posts he conveniently uses epi studies to bolster his narrative while impugning the RCTs that run contrary to his point.

Some examples of this are his posts on sodium. He cherry-picks cohort studies and case-control studies as evidence that the sodium-hypertension link is one big hoax. He even cites ecological and cross-sectional studies which are among the least substantial types of studies not just in epidemiology but in all of science (they would be blue or green-ish on the above pyramid), and he misrepresents their results to claim that sodium does not cause hypertension. Cross-sectional and ecological studies literally cannot show causation; they are not designed to do so.

Meanwhile, Taubes tries to downplay one of the strongest and most-lauded RCTs on the subject (The DASH trials) saying that blood pressure change was only “modestly lower.” If you call nearly a ten-point decrease in blood pressure by only manipulating sodium intake11 “modest” then sure. I suppose I can’t argue with such vague wording.*  He also says that while the researchers measured blood pressure, they failed to measure other things such as lifespan. Big deal, right? Let’s just forget about that stupid study that completely contradicts me. He says basically the same thing about the Cochrane reviews that do not support his position on the subject. Sure the reviews state that cutting back on salt will lower blood pressure, but it doesn’t prove that cutting back will make you live longer so who cares, amiright? By the way, Cochrane reviews are at the very tip of the aforementioned evidence pyramid.

At least he doesn’t sink to the level of anecdotal evidence and personal testimony to prove a point. I take that back; he does:

All I knew was that I had played high school football in suburban Maryland, sweating profusely through double sessions in the swamplike 90-degree days of August. Without salt pills, I couldn’t make it through a two-hour practice; I couldn’t walk across the parking lot afterward without cramping.

You know what? Of all the evidence on the subject that story of Taubes in high school is the smoking gun we have all been waiting for, so I take it all back. You were right all along Taubes. Go collect your Nobel Prize. You have earned it, my friend.

 

In Conclusion

Mr. Taubes takes the position that red meat does not contribute to cancer or CVD mortality.  He took this position without any evidence from RCTs since, as he said, they have never been done.12 Moreover, he claims that any epidemiological evidence against his position is meaningless because the epidemiology field itself is meaningless.13 The only evidence Mr. Taubes is willing to accept are those of RCTs which are nearly impossible when it comes to things like diet and cancer mortality. So Mr. Taubes has set things up to where he cannot be proven wrong even if he is wrong.

You know what? I can do that, too! I contend that parachutes are not beneficial and life-saving when it comes to falling out of the sky. Prove me wrong. Oh and you can’t point to instances where groups of people have jumped out of an airplane and the parachute has slowed their velocity toward earth allowing a safe landing while those who had a malfunctioning parachute or no parachute at all suffered major trauma or death. Those would have to be either cohort or case-control studies and therefore meaningless. There have been zero RCTs studying the effect of parachutes and gravitational challenge.14 The basis for parachute use is purely observational, and its apparent efficacy could potentially be explained by a “healthy cohort” effect. My contention stands!

If Mr. Taubes had any intellectual consistency he would have to agree with that point. At best he would have to remain neutral on parachutes, since there are no RCTs to prove they do anything.

Some Additional Nit-Picky Stuff

Nutritionists and public health authorities have gone off the rails in their advice about what constitutes a healthy diet.

Wow, that’s painting with a pretty broad brush now isn’t it? It’s like saying “Government bureaucrats are wrong.” Much like government bureaucrats there are quite a few “nutritionists and public health authorities” in the world and they hold a variety of positions on a variety of topics. You mind picking one, telling me what it is, and why it is wrong? Or do you just want to construct a straw man that grossly misrepresents what a few people may or may not be saying so you can more easily refute it?

Are you talking about the advice of dietitians? What specific piece of advice do you object to? Do you have a problem with the following statement that I took off the AND website: “A well-balanced diet filled with whole grains, fruits, vegetables, healthy fats, low-fat dairy and lean protein is important for health and wellness.” Is that advice “off the rails”? Here’s a statement I copy-pasted from ChooseMyPlate.gov: “Limit the amount of foods and beverages with added sugars your kids eat and drink.” Is this bad advice? If so, why?

I first wrote about the pseudoscience of epidemiology in Science back in 1995, “Epidemiology Faces It’s Limits”[sic]… my Science article has since been cited by over 400 articles in the peer-reviewed medical literature…

Over 400 citations? Wow! Congratulations Mr. Taubes. You should be proud of yourself. Although I’m confused as to why you put that bit of self-aggrandizement in your post. Is it to imply that because your article has so many citations your thesis (Epidemiology is a bogus science) is correct? If citations = truth then I’m afraid that Willett (the villain in your narrative) is right and you are wrong. Why? Because Willett has actually published far more papers than you have, many of which have well over 1500 citations each. Furthermore, Willett’s papers are actual peer-reviewed scientific studies as opposed to simply lay commentary.

One last (petty) thing.

I’m writing this post with a little more haste than is my wont.

What are you doing Taubes? How about you quit pretending to be an 18th century British aristocrat and start acting like a 21st century American, you pretentious windbag. You are not Christopher Hitchens. Knock it off.

Way down at the bottom of the blog post Taubes admits a correction to an earlier version of the post. Evidently he instructed Dr. Willett to go read a chapter in a textbook titled Modern Epidemiology and learn how the “best epidemiologists” conduct real research. As it turns out Dr. Willett actually wrote the chapter in question. I won’t add any commentary here. Just let that bit of delicious schadenfreude wash over you like a warm bath.

*EDIT: This sentence originally said “more than ten-point decrease.” As it was pointed out to me by a commenter the more than 10 point decrease in blood pressure was between a low-sodium DASH diet compared to a typical high sodium diet. The data where ONLY sodium is manipulated resulted in decreases of 6-7 points.

  1. Pan A, PhD, Sun Q, MD, ScD, Bernstein AM, MD, ScD, et al. (2012) Red Meat Consumption and Mortality Results from 2 Prospective Cohort Studies. Arch Intern Med. 172(7):555-563.
  2. The number of studies published by Willett is currently at 1279 according to Pub Med
  3. WCRF/AICR (2007) Food, Nutrition, Physical Activity, and the Prevention of Cancer: A Global perspective. Second Expert Report. London, UK: World Cancer Research Fund; 280-288
  4. From the article: “The results were adjusted for age (continuous); body mass index (calculated as weight in kilograms divided by height in meters squared) category (<23.0, 23.0-24.9, 25.0-29.9, 30.0-34.9, or ≥35); alcohol consumption (0, 0.1-4.9, 5.0-29.9, ≥30.0 g/d in men; 0, 0.1-4.9, 5.0-14.9, or ≥15.0 g/d in women); physical activity level (<3.0, 3.0-8.9, 9.0-17.9, 18.0-26.9, or ≥27.0 hours of metabolic equivalent tasks per week); smoking status (never, past, or current [1-14, 15-24, or ≥25 cigarettes per day]); race (white or nonwhite); menopausal status and hormone use in women (premenopausal, postmenopausal never users, postmenopausal past users, or postmenopausal current users); family history of diabetes mellitus, myocardial infarction, or cancer; history of diabetes mellitus, hypertension, or hypercholesterolemia; and intakes of total energy, whole grains, fruits, and vegetables, all in quintiles.)”
  5. Gardner CD, Kiazand A, Alhassan S, et al. (2007) Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women the A to Z Weight Loss Study: a Randomized Trial. JAMA. 297(9):969-977.
  6. By the way the food frequency questionnaires used in Red Meat Consumption and Mortality as well as many other studies certainly have their limitations. No one disputes that. But they have been repeatedly verified for validity and reproducibility in many other studies, especially when looking at overall dietary patterns.
  7. something that the authors of this study were concerned with by stating: “limitations included the lack of a valid and comparable assessment of individual adherence to the 4 different diets”
  8. In fact the authors mentioned exactly that: “[T]he trajectories of weight change between 6 and 12 months suggest that longer follow-up would likely have resulted in progressively diminished group differences.”
  9. “Women were excluded if they self-reported hypertension (except for those whose blood pressure was stable using antihypertension medications); type 1 or 2 diabetes mellitus; heart, renal, or liver disease; cancer or active neoplasms; hyperthyroidism unless treated and under control; any medication use known to affect weight/energy expenditure; alcohol intake of at least 3 drinks/d; or pregnancy, lactation, no menstrual period in the previous 12 months, or plans to become pregnant within the next year”
  10. Omigosh! I did not see that coming (/sarcasm)
  11. Sacks FM, Svetkey LP, Vollmer WM, et al. (2001) Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med. 344:3-10.
  12. and in this author’s estimation won’t be done in our lifetimes, if at all
  13. unless we’re talking about smoking, of course
  14. Smith GC, Pell JP. (2003) Parachute use to prevent death and major trauma related to gravitational challenge: systematic review of randomised controlled trials. BMJ. 20;327(7429):1459-61.