The Case Against The Case Against Sugar

the-case-against-sugar

Introduction

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

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

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

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

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

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

 

Not the Introduction

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

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

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

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

* * *

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

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

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

* * *

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

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

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

* * *

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

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

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

* * *

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

page 33 golden holocaust

And now page 65 of CAS:

page 65 CAS

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

* * *

On page 98 Taubes copies his own work:

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

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

Compare this to pages 102-103 of GCBC:

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

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

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

[…]

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

[…]

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

[…]

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

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

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

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

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

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

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

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

* * *

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

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

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

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

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

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

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

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

* * *

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

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

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

 * * *

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

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

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

himsworth trio

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

Continuing with the above quote…

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

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

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

himsworth fat and mortality

 

 * * *

Page 108:

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

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

Continuing…

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

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

 * * *

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

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

And

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

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

publications in pubmed of masai

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

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

insull

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

japan graph

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

 * * *

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

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

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

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

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

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

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

(bolding mine, italics in the original)

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

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

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

Continuing on page 116, Taubes writes:

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

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

Taubes puts a coda on this bit of conspiracy:

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

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

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

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

 * * *

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

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

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

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

On page 117 and 118 Taubes writes:

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

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

alonso

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

 * * *

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

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

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

 * * *

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

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

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

Continuing with lies about scientists that cannot defend themselves:

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

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

ben-gates-glasses

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

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

 * * *

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

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

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

death

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

 * * *

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

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

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

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

yudkin seminal

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

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

 * * *

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

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

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

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

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

 * * *

Page 173:

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

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

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

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

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

 * * *

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

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

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

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

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

mrfit

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

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

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

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

 * * *

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

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

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

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

 * * *

Page 188:

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

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

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

 * * *

Page 190:

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

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

 * * *

Pages 204-205:

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

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

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

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

 * * *

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

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

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

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

So I typed exactly this and received the following result:

clinical trials dot gov

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

clinical trials.gov

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

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

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

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

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

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

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

 * * *

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

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

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

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

Take the following statement from page 217:

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

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

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

Taubes must be using those Benjamin Franklin glasses again.

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

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

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

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

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

navajo purchases

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

navajo meal pattern

 

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

 * * *

Page 216:

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

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

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

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

 * * *

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

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

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

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

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

 * * *

Taubes performs a little sleight of hand on page 223:

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

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

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

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

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

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

 * * *

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

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

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

 * * *

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

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

There’s also a footnote to this passage:

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

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

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

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

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

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

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

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

 * * *

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

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

 * * *

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

Gout

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

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

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

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

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

Hypertension

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

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

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

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

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

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

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

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

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

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

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

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

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

Cancer

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

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

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

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

Dementia

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

Conclusion

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

cloud

References

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

 

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

 

cover

Introduction

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

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

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

Tabues on page 424

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

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

 

The Fat Mafia

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

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

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

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

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

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

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

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

* * *

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

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

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

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

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

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

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

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

smug face

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

chapter 23 refs

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

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

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

[…]

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

[…]

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

[…]

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

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

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

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

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

* * *

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

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

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

Howard 103

And on page 103 Howard states

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

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

* * *

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

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

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

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

* * *

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

One example of this is page 420 where Taubes writes:

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

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

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

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

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

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

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

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

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

* * *

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

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

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

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

* * *

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

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

And the same bullet-points apply.

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

Conclusion

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

cloud

Refs

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

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

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

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

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

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

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

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

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

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

cover

Introduction

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

Not the Introduction

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

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

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

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

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

* * *

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

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

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

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

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

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

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

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

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

* * *

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

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

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

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

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

[…]

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

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

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

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

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

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

* * *

On page 446 Taubes says the following:

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

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

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

high low carb insulin

* * *

Not a major point but on page 446 Taubes says

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

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

* * *

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

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

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

 

 

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

cloudReferences

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

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

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

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

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

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

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

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

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

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

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

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

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

coverIntroduction

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

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

Not the Introduction

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

Ian Prior in Tokelau, 1971

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

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

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

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

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

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

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

* * *

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

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

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

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

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

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

* * *

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

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

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

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

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

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

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

* * *

Page 150:

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

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

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

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

cloud

Refs

Adele Hite, Nina Teicholz, and Logical Fallacies

Introduction

Some weeks ago I got a call from a reporter.1 This reporter had just attended an event called “Politics of the Plate: The Evolution of American Food Policy” presented by Real Clear Politics that included Nina Teicholz and Adele Hite. You can view the event below, but the gist of the event was that the US government’s nutrition policy is bad, it has been based on bad science for years, it advocates a low-fat/high-carbohydrate diet, is anti-fat, and has contributed to the rise in obesity and many chronic diseases we see today.

According to this reporter, the event was compelling enough that he or she wanted to write a piece on it and kind of examine the merits of our nutrition recommendations.2 I was told the piece would be published about a week after our conversation, but as of this writing many weeks later it has not come out. Perhaps I was successful in convincing the reporter that Teicholz and Hite did not know what they were talking about. Or maybe the senior editor of the news outlet didn’t feel it was something that needed to be published. I don’t know. But what I’d like to do here is give something of an expanded version of what I told the reporter.

[Link to the video on Real Clear Politics]

False Dichotomies

I’m going to get into the merits of the arguments in a moment, but before I do I would like to spend several paragraphs on one logical fallacy I have encountered often when I engage the work of popular low-carb authors and increasingly when the more zealous low-carb adherents engage with me: the false dichotomy.

One employs the false dichotomy when there is little evidence for their position, but there is another position for which there is even less evidence (or there is good evidence against the other position). If the charlatan can convince their audience that these are the only two positions available then their job becomes much easier. All they need to do is poke some holes in the opposing position, and then the charlatan’s position is accepted by default – the charlatan doesn’t even need to provide positive evidence for their own position. In other words, reduce the spectrum of positions, of which there may be countless, to only two, and make sure the opposing position is a rather weak one.

Okay, that last paragraph was perhaps too abstract. Let’s talk about something more concrete. What I see very, very often among proponents of low-carb diets is that there are essentially only two diets out there to follow: the low-fat/high-carbohydrate diet or the high-fat/low-carbohydrate diet. When low-carbers are asked why one should follow a low-carbohydrate diet, often they begin by telling you that a low-fat diet is bad. Nina Teicholz does this in her recent book The Big Fat Surprise: Why Butter, Meat, and Cheese Belong in a Healthy Diet. You might think that the book is a collection of evidence for butter, meat, and cheese being healthy, but it is not. The bulk of the book is dedicated to pointing out how and why a low-fat diet might not be healthy. Very little ink in the book is actually dedicated to making the case for butter, meat, and cheese.

This is actually a pretty smart move on her part, since not a lot of evidence exists that butter, meat, and cheese are healthy. So instead of trying to show legitimate evidence in favor of her position, she reduces the spectrum of diets in the world to essentially low-fat or low-carb and pokes holes in the low-fat diet, hoping her readers accept her low-carb position by default.3

This logical fallacy is also used by the young-earth creationist community. If you follow that issue at all you will notice that the cornerstone of the creationists’ argument is not “Let me present all the scientific evidence suggesting that our deity created life and the universe…” But rather their argument is “Here are some possible inconsistencies with evolution by natural selection…” Now of course creationists can try to poke all the holes they want in evolution, but doing this does not make the scientific case for why young-earth creationism is true. They still have all their work ahead of them.

FalseDilemma

I feel like I need a picture to break up the wall of text.

 

Teicholz also employs this tactic when trying to create a bizarre crusade against the USDA. For decades official dietary guidelines have consistently recommended a diet that is 1/3rd fat. A diet that includes ~33% calories from fat may not be considered a high-fat diet, but nobody in their right mind would call this a low-fat diet. No one, that is, except for hyper-dogmatic low-carb proponents like Teicholz. You see, since there are only two diets in existence, and the USDA does not recommend a high-fat/low-carbohydrate diet, it must therefore be recommending a low-fat diet.

Although this kind of argumentation is clearly based on flawed reasoning it seems to be quite effective at both convincing the less-skeptical among the audience and at rallying the troops for the ridiculous anti-government crusade du jour. I have criticized false and misleading statements by low-carbohydrate proponents like Teicholz and Taubes on this website, and I have also made evidence-based criticisms other places online such as Reddit. I am always accused of both following and promoting a low-fat diet.4 It never fails. Nevermind that there is no evidence of this promotion because I have never advocated such a diet; if I point out dishonesty by low-carbers then I must follow a low-fat diet. There is no alternative.

For those too busy to read the long-winded explanation above, I will sum it up as I did in an earlier post: Many LCHF proponents reduce the multiplicity of diets that exist in the world to a low-fat or high-fat dyad. This is overly-simplistic and creates a false dichotomy, which only benefits people interested in deception.

Adele Hite Wants to Change the Dietary Guidelines

If you watched the above video, you’ll notice that Adele Hite is not a big fan of the dietary guidelines. She blames the guidelines for the rise in obesity over the last several years as well as a major contributor to chronic diseases such as heart disease, diabetes, and cancer. She has written a manifesto on her website, complete with a letter-writing campaign where you can print a pre-written letter by Hite and send it to the USDA.

In Hite’s blog post she says the letter “is not a call for low-carb, high-fat dietary recommendations,” but it kind of is. She criticizes what she says are plant-based recommendations, and lists a series of “specific recommendations” that she takes issue with because they are apparently anti-fat and too focused on carbohydrates. By the way, I’m pretty sure these “specific recommendations” are straw men (another logical fallacy!), because I can’t find them anywhere in the full 95-page document of the 2010 Dietary Guidelines for Americans. At least not in the specific wording she uses.

As an aside, I doubt very highly that the Dietary Guidelines for Americans have any meaningful influence over our food consumption. I don’t have any evidence to back this up, but neither do I think Hite or Teicholz have any evidence to the contrary. I bet you dollars to donuts that you could do a man-on-the-street style interview and grab 100 random people and ask them questions about the dietary guidelines like

  • According to the Dietary Guideline for Americans, how much folic acid should a woman who wishes to become pregnant consume daily? Answer in micrograms, please.
  • According to the Dietary Guideline for Americans, persons aged 51 years or older should consume no more than how many milligrams of sodium per day?
  • According to the Dietary Guideline for Americans, pregnant or breast-feeding women should consume seafood ranging from ______ oz to ______ oz per week?

…and NONE of them would know the answers. I bet you could even repeat the experiment with actual medical doctors and you wouldn’t do much better. Besides most of the guidelines are so freaking vanilla that I have a hard time understanding why anyone would be against them? Who could possibly be against recommending a variety of vegetables? Who could be against recommending physical activity? Only people with personality disorders that need attention.

In the video Teicholz says that the guidelines are aggressively influential and she makes ridiculous claims like the NSF and the NIH will only fund research that conforms to the guidelines, ALL nutritionists must conform to the guidelines, ALL doctors must use the guidelines to educate their patients, ALL the Health and Human Services programs are required to abide by the guidelines, school lunch programs must conform to the guidelines… methinks there is a teensy bit of exaggeration going on. I could explain why these claims are ridiculous, but this post is long enough as it is.

 

Apparently this plate is the worst thing to happen to public health since the cigarette.

Apparently this plate is the worst thing to happen to public health since cigarettes.

In any case, Hite makes some claims in her manifesto that have actual citations. If you are a follower of the blog you know how much I love citations. Let’s dive in!

The DGA have contributed to the rapid rise of chronic disease in America.

In 1977, dietary recommendations (called Dietary Goals) created by George McGovern’s Senate Select Committee advised that, in order to reduce risk of chronic disease, Americans should decrease their intake of saturated fat and cholesterol from animal products and increase their consumption of grains, cereal products, and vegetable oils. These Goals were institutionalized as the DGA in 1980, and all DGA since then have asserted this same guidance. During this time period, the prevalence of heart failure and stroke has increased dramatically. Rates of new cases of all cancers have risen. Most notably, rates of diabetes have tripled. In addition, although body weight is not itself a measure of health, rates of overweight and obesity have increased dramatically. In all cases, the health divide between black and white Americans has persisted or worsened.

obesity-trends-cdc-2009-chartbook

From the video

 

Right off the bat, before we even check any sources, Hite is shown to be a hypocrite. How? I’ll tell you. Hite discusses supposed increases in chronic disease since the DGA have been introduced, arguing that “the DGA have contributed to the rapid rise of chronic disease in America.” She also makes this same case in the video with the fancy graph she had made at Kinkos. To break this down a bit: Event happened (dietary guidelines); then some other things happened (increased disease, allegedly); therefore the event caused the things.5 In case you can’t tell this is the post hoc ergo propter hoc fallacy. Some might know it better as “correlation does not equal causation.” Its use is often criticized by people who know the difference between spurious correlations and causes. People like Adele Hite.

Now let’s get into the claims and the evidence. Since the DGAs were introduced…

Claim: The prevalence of heart failure and stroke has increased dramatically.

Facts: Hite cites the Morbidity and Mortality: 2007 Chart Book on Cardiovascular, Lung, and Blood Diseases. Don’t know why she doesn’t cite the more up-to-date 2012 chart book, but it’s the one I’m going to use. According to the report, heart failure has pretty much stayed constant since the 1980s, with a slight increase for blacks over the years. She is right about stroke, though, at least partly. Prevalence of stroke rose quite a bit up until 2008 when it started declining. But there’s a lot of data in the chartbook that was not mentioned. Why? Because it doesn’t fit nicely into the story Hite is trying to craft. For example:

  • The death rates for cardiovascular disease have dropped precipitously since 1980. [chart]
  • The death rates for stroke have fallen since 1980. [chart]
  • Age-adjusted death rates for coronary heart disease have plunged. [chart] This remains true even when stratifying by race. [chart] [chart]
  • Hospital case-fatality rates for acute myocardial infarction have plummeted. [chart]
  • Hospital case-fatality rates for heart failure have dropped like crazy. [chart]
  • Hospital case-fatality rates for stroke have sunk dramatically. [chart]
  • Age-adjusted death rates for stroke have cratered. [chart] Again, this remains true when stratifying by race. [chart] [chart]

Now if Hite wants to blame the DGAs for an increase in stroke prevalence (which she has no business doing in the first place, considering the evidence) then she must also say that the above improvements are also due to the DGAs.

Claim: Rates of new cases of all cancers have risen.

Facts: Her evidence for this is a decade-old publication on cancer statistics.6 The way Hite words that claim you might think each subgroup of cancer (lung, brain, colorectal, ovarian, etc.) have all risen, but this is not the case. Incidence of most cancers has dropped, but if you average all the cancer incidence over the past several years they have risen very slightly as a whole. It seems that the substantial increase in lung cancers skews the average upward. Although, if you look at cancer death rates they have all decreased slightly. Technically correct, but potentially misleading.

Claim: Rates of diabetes have tripled.

Facts: According to the cited source, the total number of persons with diabetes has tripled – not the rate.7 Technically incorrect, but I’ll let this one slide.

Claim: Rates of overweight and obesity have increased dramatically.

Facts: Absolutely true.8 Well, at least obesity rates have increased dramatically. Overweight actually has remained pretty stable through the years.

Claim: All available data show Americans have shifted their diets in the direction of the recommendations.

Facts: This is a juicy one that needs unpacking. This is kinda something that has been batted about on all sides of the nutrition spectrum for several years. Hite cites another old statistics report based on self-reported dietary intakes from 1971-2000.9 Here’s the low-down on that and similar reports: Since 1971 (and even earlier, I’m sure) Americans have been steadily eating more daily calories. In terms of macronutrients we have been eating more of everything. More CHOs, more protein, more fat.10 Thing is we have increased our CHO intake more than we have increased our fat and protein intake, which means that if you look at the relative changes in macronutrient intake we will have narrowly increased our percentage of calories from carbohydrate, and narrowly decreased our percentage of calories from fat and protein. Then what happens is people like Teicholz, Hite, and anyone else with a moneyed agenda claim that the DGAs forced Americans on a low-fat diet which has caused a rise in obesity, diabetes, and all that which is extraordinarily misleading because TOTAL FAT ACTUALLY INCREASED & TOTAL CALORIES INCREASED. This highly relevant context is left out to hornswoggle an unskeptical audience. Don’t be deceived.

Claim: Current choline intakes are far below adequate levels, and choline deficiency is thought to contribute to liver disease, atherosclerosis and neurological disorders. Eggs and meat, two foods restricted by current DGA recommendations, are important sources of choline. Guidance that limits their consumption thus restricts intake of adequate choline.

Facts: Almost entirely false. The source for this claim is a review article on choline.11 An article funded by the American Egg Board if you were curious. The article kinda says that intakes among women are suboptimal. According to the paper the Nurses Health cohort has intakes of about 411 mg/day which is not quite the recommended 450 mg/day. But the eggs and meat statement is preposterous on two levels. One, the current DGAs don’t restrict eggs or meat. In fact they explicitly recommend an increase in egg consumption and lean meat consumption. Secondly, choline is widely available in plant foods as well. In fact the article mentions soy flour as having one of the highest concentrations of choline, along with quinoa and wheat germ.

Claim: In young children, the reduced fat diet recommend by the DGA has also been linked to lower intakes of a number of important essential nutrients, including calcium, zinc, and iron.

Facts: Again, the DGAs do not recommend a reduced fat diet, unless your idea of “reduced fat” is simply “not extremely high in fat.” Further, the study she cites for this claim actually makes the case that lower fat diets are actually healthy for children! From the conclusion: “Lower fat intakes during puberty are nutritionally adequate for growth and for maintenance of normal levels of nutritional biochemical measures, and are associated with beneficial effects on blood folate and hemoglobin.”

Claim: DGA guidance rejects foods that are part of the cultural heritage of many Americans and indicates that traditional foods long considered to be important to a nourishing diet should be modified, restricted, or eliminated altogether: ghee (clarified butter) for Indian Americans; chorizo and eggs for Latino Americans; greens with fatback for Southern and African Americans; liver pâtés for Jewish and Eastern European Americans.

Facts: Nope. At least not explicitly.

Claim: Recommendations to prevent chronic disease that focus solely on plant-based diets is a blatant misuse of public health authority that has stymied efforts of researchers, academics, healthcare professionals, and insurance companies to pursue other dietary approaches adapted to specific individuals and diverse populations, specifically, the treatment of diabetes with reduced-carbohydrate diets that do not restrict saturated fat. In contradiction of federal law, the DGA have had the effect of limiting the scope of medical nutrition research sponsored by the federal government to protocols in line with DGA guidance.

Facts: Nope. At least Hite provides no evidence for these absurd claims. Plus the DGAs even explicitly say that “plant-based sources and/or animal-based sources can be incorporated into a healthy eating pattern.”

Claim: The science behind the current DGA recommendations is untested and inconsistent. Scientific disagreements over the weakness of the evidence used to create the 1977 Dietary Goals have never been settled. Recent published accounts have raised questions about whether the scientific process has been undermined by politics, bias, institutional inertia, and the influence of interested industries.

Facts: For fuck’s sake. Here Hite cites Gary Taubes’s Good Calories, Bad Calories and Teicholz’s The Big Fat Surprise. How many times must we revisit the lies??

Claim: Two recent meta-analyses concluded there is no strong scientific support for dietary recommendations that restrict saturated fat.

Facts: Actually the only one of the two cited studies is a meta-analysis; the other is a review article.12,13 The meta-analysis has been widely misinterpreted to suggest that saturated fatty acids are harmless, but that’s not the case. As we all know some saturated fatty acids are basically benign, like those found in coconut and other tropical oils. Typically the short and medium chain fatty acids. But the data from that paper show that the longer chain fatty acids definitely increase the risk of heart disease, especially stearic and palmitic acids which are the most abundant in animal fats. http://i.imgur.com/H72g1eP.png The only one that appears to decrease risk is margaric acid, a synthetic fat found in margarine. Even when you pool all the saturated fatty acids the net effect is an increased risk of heart disease, although a modest one. All the polyunsaturates, however, were shown to decrease risk of heart disease: http://i.imgur.com/e7lJ6PL.png http://i.imgur.com/YfC1qMx.png

The review article also gets misinterpreted, willfully it seems. It states that replacing saturated fatty acids in the diet with polyunsaturated fats has been conclusively shown to reduce the risks of CVD. It also says replacing saturated fats with carbohydrate offers no real benefit. However, low-carbers like Hite and Teicholz take that last result and make the leap to “saturated fats are good” or “restricting saturated fat is bad.” It is truly deceitful.

Claim: Federal dietary guidance now goes far beyond nutrition information. It tells Americans how much they should weigh and how to lose weight, even recommending that each American write down everything that is eaten on a daily basis.

My sarcastic response: How dare they?? This is clearly an attack. The horror… The horror…

Claim: This focus on obesity and weight loss has contributed to extensive and unrecognized “collateral damage”: fat-shaming, eating disorders, discrimination, and poor health from restrictive food habits.

My response: The government is responsible for fat-shaming now? The USDA caused eating disorders and discrimination because they recommended incorporating more fruits and vegetables? I can’t imagine that demonizing carbohydrates and vegetable oils would cause any kind of eating disorders, though.

At the end of the letter Hite ends with such vague and nonspecific recommendations that no matter what the committee actually decides you would have real difficulty making the case that Hite’s precepts were not followed. Seriously… have the recommendations apply to all Americans; expand nutrition research; include traditionally nourishing foods; are directed towards health and well being; are clear, concise, and useful… I mean, unless the committee recommends a diet of used tires and uranium and does so in an 800 page report written in pig latin, I imagine Hite will have difficulty proving that the USDA did not do just as she instructed.

Conclusion

There may indeed be a case for modifying the current dietary guidelines, but Hite and Teicholz make a bad case based on logical fallacies and the willful misinterpretation of nutrition science. Let’s hope that the people tasked with actually creating these recommendations rely on evidence instead of nonsense.

 cloud

1. A reporter, by the way, that writes for a legitimate news publication. It wasn’t like Bubba’s Food Blog or anything.

2. I’m keeping the identity of the reporter vague for a couple reasons. First, on the off-chance that he or she still is planning on publishing something I don’t want to scoop them. Secondly, I know from firsthand experience and secondhand knowledge that the more zealous of the low-carb bunch can be rather cruel, and I wouldn’t want the reporter to experience any of that just for speaking to me.

3. She also hopes her readers will assume that a low carbohydrate diet necessarily means a diet high in butter, meat, and cheese, even though the few studies she cites in favor of a low carb diet often use vegetarian sources of protein and plant-based fats in the low-carbohydrate groups.

4. Amusingly, very often I also get accused of being brainwashed by the government and/or being a paid shill for Big Vegetable. I wish I was kidding.

5. In case you want to argue semantics with me and say some crap like ‘she said CONTRIBUTED not caused,’ then I say that’s a distinction without much of a difference. Webster defines contribute as ‘to help to cause something to happen.’

6. Jemal, A. et al. Cancer Statistics, 2005. CA. Cancer J. Clin. 55, 10–30 (2005).

7. CDC – Number of Persons – Diagnosed Diabetes – Data & Trends – Diabetes DDT. at <http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm>

8. Products – Health E Stats – Overweight, Obesity, and Extreme Obesity Among Adults 2007-2008. at <http://www.cdc.gov/nchs/data/hestat/obesity_adult_07_08/obesity_adult_07_08.htm>

9. Wright, J., Kennedy-Stephenson, J., Wang, C., McDowell, M. & Johnson, C. Trends in Intake of Energy and Macronutrients — United States, 1971–2000. (National Center for Health Statistics, CDC, 2004). at <http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm>

10. Ford, E. S. & Dietz, W. H. Trends in energy intake among adults in the United States: findings from NHANES. Am. J. Clin. Nutr. 97, 848–853 (2013).

11. Zeisel, S. H. & da Costa, K.-A. Choline: An Essential Nutrient for Public Health. Nutr. Rev. 67, 615–623 (2009).

12. Siri-Tarino, P. W., Sun, Q., Hu, F. B. & Krauss, R. M. Saturated fat, carbohydrate, and cardiovascular disease. Am. J. Clin. Nutr. 91, 502–509 (2010).

13. Chowdhury, R. et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann. Intern. Med. 160, 398–406 (2014).

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

Introduction

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

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

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

Not the Introduction

On page 200 Taubes states 

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

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

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

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

* * *

On page 200, Taubes states

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

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

Metabolic effects of dietary fructose in healthy subjects

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

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

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

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

Also from the conclusion:

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

* * *

On page 201 Taubes claims:

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

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

* * *

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

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

Another report on the public health implication of fructose states7:

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

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

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

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

* * *

Page 203:

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

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

Refs

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

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

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

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

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

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

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

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

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

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

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

cover

Introduction

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

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

Not the Introduction

Page 158 Taubes discusses a paper1 by Pete Ahrens

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

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

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

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

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

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

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

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

ahrens

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

* * *

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

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

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

* * *

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

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

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

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

* * *

On pg 160 of hardback Taubes states:

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

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

* * *

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

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

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

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

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

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

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

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

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

How does Taubes get away with this?

* * *

From page 168 in the hardback:

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

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

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

* * *

On pages 168-169:

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

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

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

fatty acids and cholesterol

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

fatty acids and cholesterol2

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

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

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

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

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

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

Refs

 

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

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

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

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

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

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

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

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

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

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

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

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

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