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.

* * *

*Edit

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 brought up many times in the text and is the closing sentence from Emerson.

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

* * *

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

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

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

 * * *

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

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

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

himsworth trio

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

Continuing with the above quote…

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

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

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

himsworth fat and mortality

 

 * * *

Page 108:

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

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

Continuing…

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

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

 * * *

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

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

And

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

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

publications in pubmed of masai

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

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

insull

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

japan graph

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

 * * *

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

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

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

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

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

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

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

(bolding mine, italics in the original)

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

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

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

Continuing on page 116, Taubes writes:

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

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

Taubes puts a coda on this bit of conspiracy:

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

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

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

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

 * * *

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

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

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

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

On page 117 and 118 Taubes writes:

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

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

alonso

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

 * * *

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

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

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

 * * *

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

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

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

Continuing with lies about scientists that cannot defend themselves:

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

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

ben-gates-glasses

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

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

 * * *

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

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

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

death

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

 * * *

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

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

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

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

yudkin seminal

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

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

 * * *

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

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

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

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

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

 * * *

Page 173:

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

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

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

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

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

 * * *

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

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

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

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

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

mrfit

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

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

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

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

 * * *

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

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

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

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

 * * *

Page 188:

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

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

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

 * * *

Page 190:

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

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

 * * *

Pages 204-205:

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

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

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

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

 * * *

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

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

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

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

So I typed exactly this and received the following result:

clinical trials dot gov

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

clinical trials.gov

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

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

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

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

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

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

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

 * * *

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

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

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

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

Take the following statement from page 217:

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

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

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

Taubes must be using those Benjamin Franklin glasses again.

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

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

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

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

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

navajo purchases

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

navajo meal pattern

 

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

 * * *

Page 216:

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

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

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

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

 * * *

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

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

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

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

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

 * * *

Taubes performs a little sleight of hand on page 223:

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

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

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

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

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

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

 * * *

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

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

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

 * * *

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

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

There’s also a footnote to this passage:

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

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

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

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

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

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

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

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

 * * *

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

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

 * * *

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

Gout

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

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

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

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

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

Hypertension

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

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

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

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

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

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

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

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

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

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

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

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

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

Cancer

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

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

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

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

Dementia

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

Conclusion

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

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  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

*Edit: I removed the text below that was included in the main body of the original blog post. I did this because I was made aware from this post that I was being less than charitable on this point. Taubes does in fact discuss some of what I accuse him of not discussing on page 99. The original point I removed is reprinted below for transparency.

 

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?

 

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.

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Refs

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).
 

Good Calories, Bad Calories: A Critical Review; Chapter 1 – The Eisenhower Paradox

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

Early in the chapter Taubes claims that most mainstream nutrition authorities were saying that the American diet changed during the 20th century, from a plant-based diet to a diet heavy in meat. On pages 10 and 11 he attempts to refute this notion by saying that the USDA statistics from which this notion is drawn is very flawed, citing a personal interview with David Call and a paper on food disappearance data.1 Specifically he says

  • “The USDA statistics, however, were based on guesses, not reliable evidence.”

  • “The resulting numbers for per-capita consumption are acknowledged to be, at best, rough estimates.”

  • “The reports remained sporadic and limited to specific food groups until 1940 […] Until then, the data were particularly sketchy…”

However, the very next paragraph he makes the argument that the US has always been a meat-eating country, and as evidence he cites data from the USDA! “By one USDA estimate, the typical American was eating 178 pounds of meat annually in the 1830s, forty to sixty pounds more than was reportedly being eaten a century later.” Either the food stats are reliable before 1940 or the are not. Pick a side and be consistent.

He’s really all over the map in this section because he then claims that in fact we did eat less meat in the early 20th century due to a few reasons: the cattle industry could not keep up with population growth, meat rationing during WW1, and Upton Sinclair’s The Jungle. He then makes the argument that Americans started eating more fruits and vegetables and decreased consumption of animal products. Following this change, incidents of heart disease skyrocketed to become an epidemic – an epidemic that earlier in the chapter he claims was completely bogus.

* * *

On pages 14 and 15 Taubes talks a bit about cholesterol and says

Despite myriad attempts, researchers were unable to establish that patients with atherosclerosis had significantly more cholesterol in their bloodstream than those who didn’t. “Some works claim a significant elevation in blood cholesterol level for a majority of patients with atherosclerosis,” the medical physicist John Gofman wrote in Science in 1950, “whereas others debate this finding vigorously. Certainly a tremendous number of people who suffer from the consequences of atherosclerosis show blood cholesterols in the accepted normal range.”

It’s interesting to note that immediately after that sentence in the cited text Gofman also wrote2

There does exist a group of disease states (including diabetes mellitus, nephrotic nephritis, severe hypothyroidism, and essential familial hypercholesteremia) in which the blood cholesterol level may be appreciably elevated. Such patients do show, in general, earlier and more severe atherosclerosis than the population at large.

In fact, most of the text makes the case that there are particular cholesterol particles to blame for atherogenesis, specifically those with a density of 10-20 Svedberg units that are currently known as LDL. However, since this paper was published in 1950 they are referred to as the Sf 10-20 class of cholesterol molecules. Gofman also noted – prior to even anything that Keys published on the subject – that dietary lipids affect these Sf 10-20 molecules, stating:

Our preliminary study of a group of 20 patients whose diet we have restricted in cholesterol and fats has demonstrated that the concentration of the Sf 10-20 class of molecules is definitely reduced or even brought down to a level below resolution ultracentrifugally in 17 of the cases studied within two weeks to one month.

I can’t understand why Taubes didn’t mention that, can you?

* * *

Taubes knocks me for a loop on page 15 when he states:

The condition of having very high cholesterol—say, above 300 mg/dl—is known as hypercholesterolemia. If the cholesterol hypothesis is right, then most hypercholesterolemics should get atherosclerosis and die of heart attacks. But that doesn’t seem to be the case.

Actually that seems to be exactly the case… even by the study Taubes cites.

Coronary Artery Disease in 116 Kindred with Familial Type II Hyperlipoproteinemia

click to embiggen

click to embiggen

That study even seems to be in agreement with the other studies on familial hypercholesterolemia at the time3:

Our results are qualitatively similar to analyses on a smaller scale which have established an enhanced risk of premature CAD in affected members of families with familial hypercholesterolemia.

But since certain thyroid and kidney disorders might also cause hypercholesterolemia I suppose Taubes can just ignore all that evidence linking cholesterol to heart disease.

* * *

Pg. 15

Autopsy examinations had also failed to demonstrate that people with high cholesterol had arteries that were any more clogged than those with low cholesterol. In 1936, Warren Sperry, co-inventor of the measurement technique for cholesterol, and Kurt Landé, a pathologist with the New York City Medical Examiner, noted that the severity of atherosclerosis could be accurately evaluated only after death, and so they autopsied more than a hundred very recently deceased New Yorkers, all of whom had died violently, measuring the cholesterol in their blood. There was no reason to believe, Sperry and Landé noted, that the cholesterol levels in these individuals would have been affected by their cause of death (as might have been the case had they died of a chronic illness). And their conclusion was unambiguous: “The incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.”

I was unable to find the cited Landé and Sperry paper. It is so old and obscure that not only was I unable to find it, the databases I used (PubMed, WorldCat, Academic Search Complete) could not find a record of it even existing. But let’s do something we probably should not do and take Taubes at his word here. It is still interesting to note that this is an example of an observational study, specifically a cross-sectional study. Later in the book Taubes will make the case that observational studies are worthless. In fact, you will see throughout the book that Taubes will cite observational studies, usually without caveat, if it fits his meat-is-good narrative. However, if he doesn’t like the conclusion of a study (observational or otherwise) you will find that he impugns the methodology, the authors, or even the entire field of science of which it is a part. Get your popcorn ready.

* * *

Like the above point, this is not a real significant issue, but it shows that Taubes is not above quote mining to try and paint someone in a negative light. On page 16:

Henry Blackburn, his longtime collaborator at Minnesota, described him as “frank to the point of bluntness, and critical to the point of sharpness.” David Kritchevsky, who studied cholesterol metabolism at the Wistar Institute in Philadelphia and was a competitor, described Keys as “pretty ruthless” and not a likely winner of any “Mr. Congeniality” awards.

I imagine the point of these quotes is to paint Keys as kind of an asshole, just in case any reader might find themselves sympathizing with Keys when Taubes takes massive, diarrhea-like shits all over Keys’s research and Keys personally. I cannot verify the Kritchevsky quote above because it was from a personal interview, but adding a bit of context to the Blackburn quote can change the tone entirely4:

Ancel Keys has a quick and brilliant mind, a prodigious energy, and great perseverance. He can also be frank to the point of bluntness, and critical to the point of sharpness. But by the boldness of his concepts, the vigor of his pursuits, and the rigor of his methods, as well as by his personal example, he led several generations of investigators in making powerful contributions to the public health.

The entire article is actually quite praiseworthy.

* * *

Pg. 15:

This was a common finding by heart surgeons, too, and explains in part why heart surgeons and cardiologists were comparatively skeptical of the cholesterol hypothesis. In 1964, for instance, the famous Houston heart surgeon Michael DeBakey reported similarly negative findings from the records on seventeen hundred of his own patients. And even if high cholesterol was associated with an increased incidence of heart disease, this begged the question of why so many people, as Gofman had noted in Science, suffer coronary heart disease despite having low cholesterol, and why a tremendous number of people with high cholesterol never get heart disease or die of it.

I’m not sure why Taubes names DeBakey as the primary source here, since he was actually the fourth author in the study that was cited, but no matter… It’s interesting to find that if you check the 1964 paper that is cited, it’s a type of observational study called a case series that examines 1,700 surgical patients treated for some sort of atherosclerosis.5 Turns out 1,416 out of the 1,700 (or 83%) have what the Mayo Clinic would describe as “high” cholesterol levels (over 200 mg/dL).

Does Taubes even read the studies he cites? Or does he read them and deliberately misrepresent them?

A second paper he cites in support of that paragraph is not even a study, but a statement by the president of the American Heart Association6 (wait… they’re supposed to be the bad guys, right?). He says many things in that statement, but what is most relevant to this paragraph is he says that

In a nation of over a quarter of a billion people we are a remarkably heterogeneous lot, and in truth there are no two of us alike. Those with low cholesterols as a group seem to have less coronary disease than those with high cholesterols, but this is too often extrapolated to apply directly to one individual.

He goes on to expound that, sure, cholesterol levels are important, but sometimes people get heart disease and don’t have high cholesterol levels so we should individualize our advice. I don’t think it really helps or hurts Taubes’s argument, but evidently he cited it anyway. Probably to pad his references.

* * *

If Taubes’s irrational contempt for Keys was not obvious before, it should be crystal clear after this passage on page 16:

When Keys launched his crusade against heart disease in the late 1940s, most physicians who believed that heart disease was caused by diet implicated dietary cholesterol as the culprit. We ate too much cholesterol-laden food—meat and eggs, mostly—and that, it was said, elevated our blood cholesterol. Keys was the first to discredit this belief publicly, which had required, in any case, ignoring a certain amount of the evidence.

Before Keys came along all of the “evidence” that dietary cholesterol substantially affects serum cholesterol was from animal studies. Studies that, just two pages earlier, Taubes argues have no bearing on human physiology. So Keys decides to conduct some cholesterol research on actual humans, and concludes that dietary cholesterol actually doesn’t have a substantial effect on serum cholesterol.7 If this were anyone else other than Keys Taubes would likely praise them for not following the conventional wisdom of the day and conducting proper scientific research, but instead Keys is accused of “ignoring” evidence. I think that’s fair.

In the same paragraph as above Taubes discusses a cholesterol study:

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

Although the statement “the cholesterol we eat has very little effect on the amount of cholesterol in our blood” is true for most people, as we have just discovered, the Rittenberg/Schoenheimer study that Taubes mentions has almost nothing to do with that statement.8 Firstly, the study was conducted on mice, and extrapolating results on people from cholesterol studies on animals are certainly dubious as Taubes himself admits. Moreover, the study itself involves feeding mice water labeled with deuterium then measuring deuterium in their cholesterol and fatty acids in the mice’s tissues to see how much deuterium had been incorporated into those molecules. As far as I can tell it has nothing to do with feeding them cholesterol and seeing if that impacts their blood cholesterol levels. But correct me if I am wrong.

Pg. 16 continued:

As a result, Keys insisted that dietary cholesterol had little relevance to heart disease. In this case, most researchers agreed.

Most researchers agreed… 16 years later.9

* * *

On page 17 Taubes writes:

By 1952, Keys was arguing that Americans should reduce their fat consumption by a third, though simultaneously acknowledging that his hypothesis was based more on speculation than on data: “Direct evidence on the effect of the diet on human arteriosclerosis is very little,” he wrote, “and likely to remain so for some time.”

This is another minor point, but it should be pointed out that THAT IS WHAT A HYPOTHESIS IS. It’s a guess based on little or no evidence, and all scientists have them. Just for context, here’s the quote from Keys that Taubes plucked with a bit more… umm… context10:

[W]e may remark that direct evidence on the effect of the diet on human atherosclerosis is very little and is likely to remain unsatisfactory for a long time. But such evidence as there is, plus valid inferences from indirect evidence, suggests that a substantial measure of control of the development of atherosclerosis in man may be achieved by control of the intake of calories and of all kinds of fats, with no special attention to the cholesterol intake. This means: (1) avoidance of obesity, with restriction of the body weight to about that considered standard for height at age 25; (2) avoidance of periodic gorging and even temporary large calorie excesses; (3) restriction of all fats to the point where the total extractable fats in the diet are not over about 25 to 30 per cent of the total calories; (4) disregard of cholesterol intake except, possibly, for a restriction to an intake less than 1 Gm. per week.

Taubes gets the quotation a smidge wrong, but it still keeps the spirit of the original. The bigger picture here is that Keys is recommending (in an academic journal, by the way) to avoid becoming obese, avoid gorging on food, a diet that’s about 30% fat, and to not worry too much about cholesterol intake. Pretty uncontroversial stuff, if you ask me. Yet Taubes portrays Keys here and elsewhere as some kind of radical crusader, religious zealot, idiot, and kind of an asshole.

* * *

On page 18 Taubes discusses a 1957 paper by Jacob Yerushalmy and Herman Hilleboe, which is something of a response to Ancel Keys’s 1953 paper Atherosclerosis: A Newer Problem in Public Health.11 If you’re not familiar with the Keys paper I will give you a brief synopsis. Keys published some data that suggested a remarkable relationship between fat in the diet and heart disease. Included in the paper was a striking (if oversimplified) figure looking at several countries and their population’s typical fat intake juxtaposed with deaths from heart disease.

YH4

Taubes says:

Many researchers wouldn’t buy it. Jacob Yerushalmy, who ran the biostatistics department at the University of California, Berkeley, and Herman Hilleboe, the New York State commissioner of health, co-authored a critique of Keys’s hypothesis, noting that Keys had chosen only six countries for his comparison though data were available for twenty-two countries. When all twenty-two were included in the analysis, the apparent link between fat and heart disease vanished. Keys had noted associations between heart-disease death rates and fat intake, Yerushalmy and Hilleboe pointed out, but they were just that. Associations do not imply cause and effect or represent (as Stephen Jay Gould later put it) any “magic method for the unambiguous identification of cause.”

I have actually written about this in a previous blog post, but I will revisit this again. Aside from the fact that Keys never claimed a cause-and-effect relationship (much less an unambiguous one) and always identified it as an association, Taubes completely misrepresents the results of the study. It’s true that after Yerushalmy and Hilleboe added more data into the graph the relationship becomes a bit more muddied, but it certainly does not vanish as Taubes claims. There is still a noticeable relationship.12 See for yourself.

YH1

What’s even more interesting is that Y&H actually conclude that consumption of animal fat and/or animal protein is much more strongly associated with heart disease than total fat. Moreover, vegetable fat and/or vegetable protein is actually negatively correlated with heart disease. The resolution is not very sharp, but here are the results. I’ll leave it to you to wonder why Taubes ignores this highly pertinent information.

YH3

YH-2

click to embiggen

See Taubes response #1

* * *

On pages 19-20 Taubes claims that Keys “insisted” that fat elevated cholesterol. I am not sure what Keys was doing that made him so insisting, other than writing a few academic articles concluding that there was an association between dietary fat and serum cholesterol (which there was), while also making sure to point out that there are many details about this association that have yet to be discovered (which there also were). Taubes then goes on to mention some studies that examined those details:

In 1952, however, Laurance Kinsell, director of the Institute for Metabolic Research at the Highland–Alameda County Hospital in Oakland, California, demonstrated that vegetable oil will decrease the amount of cholesterol circulating in our blood, and animal fats will raise it. That same year, J. J. Groen of the Netherlands reported that cholesterol levels were independent of the total amount of fat consumed: cholesterol levels in his experimental subjects were lowest on a vegetarian diet with a high fat content, he noted, and highest on an animal-fat diet that had less total fat. Keys eventually accepted that animal fats tend to raise cholesterol and vegetable fats to lower it, only after he managed to replicate Groen’s finding with his schizophrenic patients in Minnesota.

In other words, Keys did what any good scientist should do: he followed the evidence. Yet the syntax of the last sentence would have you imagine that Keys was some sort of stubborn asshole that refused to accept the truth until the evidence overwhelmed him.

* * *

This may be another nitpicky issue, but the following quote is misleading. Page 20:

This kind of nutritional wisdom is now taught in high school, along with the erroneous idea that all animal fats are “bad” saturated fats, and all “good” unsaturated fats are found in vegetables and maybe fish. As Ahrens suggested in 1957, this accepted wisdom was probably the greatest “handicap to clear thinking” in the understanding of the relationship between diet and heart disease.

First of all, I was never taught that kind of “nutritional wisdom” in high school. Come to think of it I was never taught any nutritional wisdom in high school, but that’s neither here nor there. My issue with this is that in the text that Taubes cites as the source of that quote, Ahrens does not say that the animal fat = bad / vegetable fat = good binarism is the greatest handicap to clear thinking. What he does say is that the good-bad dyad was a greater handicap than the confusion about why experimental diets were designed to be eucaloric.13

* * *

Tabues uses a 1957 review article titled “Atherosclerosis and the Fat Content of the Diet” as a source for three claims in this chapter. One is simply a block quote on page 8. The other two claims are very tenuous, especially the following found on page 20:

In 1957, the American Heart Association opposed Ancel Keys on the diet-heart issue.

The article does mention Keys a few times, as well as a number of other researchers involved with dietary research involving atherosclerosis, but it is very neutral on Keys. In fact, you might even say the author mildly endorses Keys at a couple of points: “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.” And “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.”14

After reading the article I certainly didn’t get the idea that the AHA opposed Keys. Even if they did they never explicitly stated this.

* * *

On page 21 Taubes pulls some numbers from thin air:

As Time reported, Keys believed that the ideal heart-healthy diet would increase the percentage of carbohydrates from less than 50 percent of calories to almost 70 percent, and reduce fat consumption from 40 percent to 15 percent.

The Time article actually does report that Keys suggested American reduce their fat intake from 40 to 15 percent. However, there is no mention in the entire article about Keys recommending an increase in carbohydrates.15

Go to Good Calories, Bad Calories: A Critical Review; Chapter 2 – The Inadequacy of Lesser Evidence

cloud

Refs

1. Call, D. L. & Sánchez, A. M. Trends in fat disappearance in the United States, 1909-65. J. Nutr. 93, Suppl:1–28 (1967).

2. Gofman, J. W. et al. The Role of Lipids and Lipoproteins in Atherosclerosis. Science 111, 166–186 (1950).

3. Stone, N. J., Levy, R. I., Fredrickson, D. S. & Verter, J. Coronary artery disease in 116 kindred with familial type II hyperlipoproteinemia. Circulation 49, 476–488 (1974).

4. Blackburn, H. Ancel Keys. at http://www.mbbnet.umn.edu/firsts/blackburn_h.html

5. Garrett H, Horning EC, Creech BG & De Bakey M. Serum cholesterol values in patients treated surgically for atherosclerosis. JAMA 189, 655–659 (1964).

6. James, T. N. Presidential address. AHA 53rd scientific sessions, Miami Beach, Florida, November 1980. Sure cures, quick fixes and easy answers. A cautionary tale about coronary disease. Circulation 63, 1199A–1202A (1981).

7. Keys, A., Anderson, J. T., Mickelsen, O., Adelson, S. F. & Fidanza, F. Diet and Serum Cholesterol in Man: Lack of Effect of Dietary Cholesterol. J. Nutr. 59, 39–56 (1956).

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

9. Quintão, E., Grundy, S. M. & Ahrens, E. H. Effects of dietary cholesterol on the regulation of total body cholesterol in man. J. Lipid Res. 12, 233–247 (1971).

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

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

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

13. Ahrens, E. H., Jr. Seminar on atherosclerosis: nutritional factors and serum lipid levels. Am. J. Med. 23, 928–952 (1957).

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

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

Good Calories, Bad Calories: A Critical Review; Chapter 3 – Creation of Consensus

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

Near the beginning of chapter three Taubes makes some serious unfounded claims. From page 44:

This alliance between the AHA and the makers of vegetable oils and margarines dissolved in the early 1970s, with reports suggesting that polyunsaturated fats can cause cancer in laboratory animals. This was problematic to Keys’s hypothesis […]

Polyunsaturated fats cause cancer?!?!?! That’s a bold claim for which Taubes cites two supporting texts. One is a New York Times article from 1973 titled “Heart Association Strengthens its Advice: Cut Down on Fats,” and it barely has anything to do with Taubes’s claim.1 It mostly deals with atherosclerosis (not cancer), and hardly discusses polyunsaturated fats. The closest thing you will find that even comes close to supporting the claim that “polyunsaturated fats can cause cancer in laboratory animals” is near the end of the article. There is a section titled Challenges and Answers that states the following:

Despite this evidence, doubts and doubters remain. Some of the challenges to the heart disease-fatty diet thesis, and the answers from the heart association, follow: […] Polyunsaturates are dangerous. Dr. Mueller says that there is no evidence that consumption of polyunsaturates is harmful at the recommended levels or even considerably above these levels. While such consumption is known to increase the body’s need for vitamin E, most vegetable oils contain enough vitamin E to satisfy the need.

Hmmm… Is that strong evidence for his claim? Nope. What about the other citation? It not a study involving laboratory animals, but rather a trial of elderly veterans.2 Turns out the data from that trial show a few more people dying from cancer on a diet high in polyunsaturated fat. But the results from the study were something of an outlier. The authors even mention this:

The experience of other investigators using similar diets has not been the same. […] Many of the cancer deaths in the experimental group were among those who did not adhere closely to the diet. This reduces the possibility that the feeding of polyunsaturated oils was responsible for the excess carcinoma mortality observed in the experimental group. […] In both groups, the numbers of cancer deaths among the various adherence strata are compatible with random distribution (table v). A high incidence among high adherers would be expected if some constituent of the experimental diet were contributing to cancer fatality.

Again you must ask yourself “Is this evidence strong enough to justify the claim that polyunsaturated fats cause cancer in laboratory animals?” It’s up to you to decide. I might even ask myself a few more questions like “Is this an innocent citation error? Certainly a book of this depth and magnitude is bound to have a few simple human errors. If it is an honest mistake, why do all the mistakes happen to be in favor of a low-carb, high-fat diet?”

Taubes also uses this study later in the chapter so we’ll revisit this soon. See Taubes response #2 and #3.

 * * *

In chapter three Taubes devotes much ink to slandering discussing the 1977 publication of Dietary Goals for the United States by a committee led by George McGovern. Now I have no problem criticizing the government. In fact, I think that one of the great things about living in the US is the right to just trash the hell out of the government and politicians either in private or in the public eye. I encourage everyone to exercise that right if they see fit; however, criticisms have a little more bite to them when they are actually legitimate. Much of the cited evidence against the Dietary Goals comes from what were ostensibly personal interviews with a few people involved with its drafting. Of course, no one is privy to this information so we can only go on what is publicly available.

On page 46-47 Taubes claims:

Dietary Goals was couched as a plan for the nation, but these goals obviously pertained to individual diets as well. Goal number one was to raise the consumption of carbohydrates until they constituted 55–60 percent of the calories consumed. Goal number two was to decrease fat consumption from approximately 40 percent, then the national average, to 30 percent of all calories, of which no more than a third should come from saturated fats. The report acknowledged that no evidence existed to suggest that reducing the total fat content of the diet would lower blood-cholesterol levels, but it justified its recommendation on the basis that, the lower the percentage of dense fat calories in the diet, the less likely people would be to gain weight, and because other health associations—most notably the American Heart Association—were recommending 30 percent fat in diets. To achieve this low-fat goal, according to the Dietary Goals, Americans would have to eat considerably less meat and dairy products.

When Taubes says “The report acknowledged that no evidence existed to suggest that reducing the total fat content of the diet would lower blood-cholesterol levels…” he is using a straw man that I’m fairly certain is not even discussed in Dietary Goals. By this point total fat was not the issue, but type of fat was and Dietary Goals discusses the evidence that a diet low in saturated fat and high in unsaturated fat will decrease blood-cholesterol levels. Also, I saw no recommendations for eating “considerably less meat and dairy products,” but please correct me if I am wrong.

Taubes’s arguments against Dietary Goals are not even internally consistent at times. For instance on page 45 Taubes writes “McGovern’s staff were virtually unaware of the existence of any scientific controversy” and “They believed that the relevant nutritional and social issues were simple and obvious.” Yet on page 47 Taubes writes “Though the Dietary Goals admitted the existence of a scientific controversy, it also insisted that Americans had nothing to lose by following the advice.” So did the authors know about a controversy or not? I suppose you could imagine a scenario where the authors knew nothing of a controversy yet wrote about one in an official government document anyway, but it seems specious to me.

Let’s go further into Taubes’s Dietary Goals bloodbath shall we? On page 46…

Having held one set of hearings before publishing the Dietary Goals, McGovern responded to the ensuing uproar with eight follow-up hearings. Among those testifying was Robert Levy, director of the National Heart, Lung, and Blood Institute, who said that no one knew whether lowering cholesterol would prevent heart attacks, which was why the NHLBI was spending several hundred million dollars to study the question.

Would Gary Taubes, a New York Times columnist and alumnus of the Ivy Leagues, possibly take someone out of context to misrepresent their position in order to fit his own low-carb narrative? Surely not. But just to be sure let us add a bit more context to Dr. Levy’s statements.3

We have no doubt from the vast amount of epidemiological data available that elevated cholesterol is associated with an increased risk of heart attack, especially some specific types of high cholesterol. We have no doubt that [blood] cholesterol can be lowered by diet and/or medication in most patients. Where the doubt exists is the question of whether lowering [blood] cholesterol will result in a reduced incidence of heart attack; that is still presumptive. It is unproven, but there is a tremendous amount of circumstantial evidence. Not only is there circumstantial epidemiologic data, but there is very exciting animal data. Here is one of many studies that have been done over the last decade with nonhuman primates. It shows that not only can we prevent atherosclerosis from progressing by making dietary changes, but that regression actually occurs. Atherosclerosis will lessen if we lower [blood] cholesterol levels in animals through diet. The problem is we can’t do these kinds of studies in man; it is not ethical. There is no doubt that [blood] cholesterol can be lowered by diet in free-living populations. It can be lowered by 10 to 15 percent.

You have to ask yourself whether Taubes’s characterization of Levy’s testimony is really an accurate representation of Levy’s actual testimony. As a reader are you at all angry that a science journalist like Taubes misrepresents people over and over again? I am genuinely curious. Let me know in the comments section.

 * * *

Taubes makes stuff up again on page 49:

The ASCN committee concluded that saturated-fat consumption was probably related to the formation of atherosclerotic plaques, but the evidence that disease could be prevented by dietary modification was still unconvincing.*

*It also affirmed the suspicion that polyunsaturated fats might be dangerous, and so further diminished the role of margarines and corn oils in dietary recommendations.

As evidence Taubes cites a paper titled The Evidence Relating Six Dietary Factors to the Nation’s Health by Dr. Ahrens.4 The paper gives a score of 0-100 to associations between a given dietary issue and atherosclerosis, where 0 is the weakest evidence for the association and 100 is the most rock-solid evidence. The final score is an aggregation of scores by several experts in the field based on epidemiological evidence, animal studies, human interventions, autopsies, biological plausibility, etc. Cholesterol alone received a score of 62. Saturated fat alone received a 58. Cholesterol and fat together received a 73. For comparison the association between alcohol and liver disease received an 88, and the association between carbohydrate and atherosclerosis got an 11. Carbohydrate and diabetes got a 13.

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

He also tells his readers that the ASCN committee affirmed that polyunsaturated fats might be dangerous, which apparently diminishes the role of margarine and corn oil. However, the committee claims nothing of the sort; there is no implied subtext either. In fact, there is literally no mention of polyunsaturated fats, corn oil, or margarine.

He does cite a separate paper that, as far as I can tell, has nothing to do with the ASCN committee paper other than being published by the same journal.5 There is still no mention of corn oil or margarine or any kind of affirmation that polyunsaturated fats might be dangerous. In fact, the text claims that polyunsaturated fats are generally beneficial, but that the long term effects of specific concerns such as lipid peroxidation of polyunsaturates have yet to be studied.

* * *

On page 54 Taubes strongly implies (like he has done before) that polyunsaturated fats and low levels of cholesterol leads to cancer and death:

The other disconcerting aspect of these studies is that they suggested (with the notable exception of three Chicago studies reported by Jeremiah Stamler and colleagues) low cholesterol levels were associated with a higher risk of cancer. This link had originally been seen in Seymour Dayton’s VA Hospital trial in Los Angeles, and Dayton and others had suggested that polyunsaturated fats used to lower cholesterol might be the culprits.

Dayton actually suggests the opposite in that very study. Pearce and Dayton actually do conduct a trial with elderly veterans where two groups are fed more-or-less the same diet, except one diet has more polyunsaturated fats in it. The results do indicate that in fact the group eating the diet with more polyunsaturates does have a few more cancer deaths in the group. But, as Taubes would say, there were caveats. I’ll let the authors explain:

The experience of other investigators using similar diets has not been the same. […] Many of the cancer deaths in the experimental group were among those who did not adhere closely to the diet. This reduces the possibility that the feeding of polyunsaturated oils was responsible for the excess carcinoma mortality observed in the experimental group. […] In both groups, the numbers of cancer deaths among the various adherence strata are compatible with random distribution (table v). A high incidence among high adherers would be expected if some constituent of the experimental diet were contributing to cancer fatality.

Indeed, other investigators’ experiences was not the same. A survey of five similar dietary trials published that same year suggested there was no link between low serum cholesterol and cancer.6 There are a handful of studies you can find that will support the link between cancer and low cholesterol, though. You can find them. But perhaps those results are due to the cholesterol-lowering effects of cancer, not the other way around.7

In fact, the authors of the MRFIT study (of which Taubes displays the results in the next chapter) explicitly mention this.8 In case you’re interested:

The increased total mortality at the lowest cholesterol levels has been noted before. It is primarily due to an increased risk of cancer death in those with the lowest cholesterol concentrations and is probably explained by a cholesterol-lowering effect of cancer. The most recent evidence for this explanation is an analysis of the MRFIT screening cohort which showed that the association between low serum cholesterol and cancer incidence does not persist beyond 5 years of follow-up, whereas that between high serum cholesterol and CHD incidence remains after 5 years.

In any case, regardless of whether or not it was evident to Taubes at the time GCBC was published, the results are in: a recent meta-analysis of 27 large-scale human trials confirmed no association between low cholesterol levels and cancer.9 Of course Taubes would probably demand a large, randomized clinical trial where healthy people are randomly assigned to get cancer and then have their cholesterol levels measured before accepting it. Hell, even then he would probably find a way to dismiss it. Dismissing good evidence that contradicts him is one of Taubes’s greatest skills.

* * *

On pages 53-54 Taubes discusses several studies that have found negative correlations between carbohydrate intake and heart disease.10,11 In other words, studies that have found that carbohydrates may be slightly protective against heart disease. Uh, oh! It’s time for Taubes to do some serious spinning. But remember what I said above? This is his specialty. He has a PhD in spinning science. You might even call him a Spin Doctor! Get it? Okay, here’s what he says:

When one is reading this report, it’s hard to avoid the suspicion that once the government began advocating fat reduction in the American diet it changed the way many investigators in this science perceived their obligations. Those who believed that dietary fat caused heart disease had always preferentially interpreted their data in the light of that hypothesis. Now they no longer felt obliged to test any hypothesis, let alone Keys’s. Rather, they seemed to consider their obligation to be that of “reconciling [their] study findings with current programs of prevention,” which meant the now official government recommendations. Moreover, these studies were expensive, and one way to justify the expense was to generate evidence that supported the official advice to avoid fat. If the evidence didn’t support the recommendations, then the task was to interpret it so that it did.

Now scientists can’t even be trusted!! Why? They’re greedy whores, of course; willing to do and say anything to keep those sweet, sugary NSF grants rolling in. Researchers have to maintain their lavish lifestyle, and if that means lying to the public and a few people get diabetes and die because of it, well, so be it. Health scientists didn’t get into the field of research because of a love of science or truth or the public good – they did it for the cold, hard cash.

Not only is that sentiment one of the most cynical things I have ever read, it is completely absurd and without merit. (I wonder if there are issues of psychological projection here; like when a cheating spouse unreasonably accuses their partner of cheating.) And lest you think Taubes took that quote from some secret literature of the Scientist Guild that shares tips and tricks on how to bilk the government out of research funding and promote chronic diseases for shits and giggles, here is a little more context:

Although the findings reported here – particularly those related to starch intake – may eventually be found to have practical implications, it would be premature to propose dietary alterations before the findings are examined more carefully. We consider the inverse relation of CHD incidence to the total daily caloric intake as a prescription for greater physical activity rather than for greater caloric intake.

[…]

The apparently protective effect of starch consumption against CHD seems to imply that the proportion of calories coming from starch should be increased. In isocaloric diets, increased intake of starch is a logical way to balance decreased intake of fat. Thus, from a practical point of view there is no difficulty in reconciling our study findings with current programs for prevention of CHD.

Doesn’t really sound so evil, does it? And by the way, there was never any official government “advice to avoid fat.” Never. The Dietary Goals for the United States that Taubes keeps hammering away at recommended a diet consisting of one-third fat. ONE-THIRD. This is not in any way a low-fat diet or advice to avoid fat. What it is is Taubes’s favorite straw man. For the record Dietary Goals recommended Americans cut their sugar intake by nearly 50%, yet no praise was given for that decision. I wonder why.

* * *

On page 57 Taubes discusses a study, the results of which he doesn’t like because they show that lowering cholesterol reduced nonfatal heart attacks, fatal heart attacks, and overall death. Watch the master of spin work his magic:

Nonetheless, these results were taken as sufficient by Rifkind, Steinberg, and their colleagues so they could state unconditionally that Keys had been right and that lowering cholesterol would save lives. Rifkind and his collaborators also concluded that the cholesterol-lowering benefits of a drug applied to diet as well. Although the trial included only middle-aged men with cholesterol levels higher than those of 95 percent of the population, Rifkind and his colleagues concluded that those benefits “could and should be extended to other age groups and women and…other more modest elevations of cholesterol levels.”

Isn’t he good? By the way, the cited source for that Rifkind quote is a National Heart, Lung, and Blood Institute consensus conference, and those words do not appear in it.12

Go to Good Calories, Bad Calories: A Critical Review; Chapter 4 – The Greater Good

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Refs

1. Brody, J. Heart Association Strengthens Its Advice: Cut Down on Fats. N. Y. Times 54 (1973).

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

3. United States. Dietary goals for the United States. (U.S. Govt. Print. Off., 1977). at <http://catalog.hathitrust.org/Record/011389409&gt;

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

5. Glueck, C. J. Appraisal of dietary fat as a causative factor in atherogenesis. Am. J. Clin. Nutr. 32, 2637–2643 (1979).

6. Ederer, F., Leren, P., Turpeinen, O. & Frantz, I. Cancer among men on cholesterol-lowering diets: Experience from five clinical trials. The Lancet 298, 203–206 (1971).

7. Rose, G. & Shipley, M. J. Plasma lipids and mortality: a source of error. The Lancet 315, 523–526 (1980).

8. Martin, M. J., Browner, W. S., Hulley, S. B., Kuller, L. H. & Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. The Lancet 328, 933–936 (1986).

9. Cholesterol Treatment Trialists’ (CTT) Collaboration. Lack of Effect of Lowering LDL Cholesterol on Cancer: Meta-Analysis of Individual Data from 175,000 People in 27 Randomised Trials of Statin Therapy. PLoS ONE 7, e29849 (2012).

10. Yano, K., Rhoads, G. G., Kagan, A. & Tillotson, J. Dietary intake and the risk of coronary heart disease in Japanese men living in Hawaii. Am. J. Clin. Nutr. 31, 1270–1279 (1978).

11. Gordon, T. et al. Diet and its relation to coronary heart disease and death in three populations. Circulation 63, 500–515 (1981).

12. Consensus Conference. Lowering blood cholesterol to prevent heart disease. JAMA 253, 2080–2086 (1985).

Good Calories, Bad Calories: A Critical Review; Chapter 4 – The Greater Good

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

On pages 60-62 Taubes discusses a publication by the National Academy of Sciences titled Diet and Health: Implications for Reducing Chronic Disease Risk.

I’m not sure that Taubes actually reads it because he gets a few things wrong about it. First (and this is a minor point) he says the publication is thirteen hundred pages long, when in fact it is not even eight hundred pages long. At least that’s the version I have.

Second — and this is probably a more important point — he says about the publication:

It was no longer about the validity of the underlying science, which was no less ambiguous than ever, but about whether Americans should be eating low-fat diets or very low-fat diets.

Actually, Diet and Health recommends a diet of 30% of total calories from fat.1 I don’t see how this could be seen as a low-fat diet, much less a very low-fat diet. Clearly Taubes wants the committee to have recommended something like a very low-fat diet, but they did no such thing so he just lies and says they did anyway. (See: straw man)

Taubes then says:

One striking fact about this evolution is that the low-fat diets now being recommended for the entire nation had only been tested twice… The results of those trials had been contradictory.

Clearly Taubes didn’t bother to actually read Diet and Health. If he did he would have noticed the literally TWENTY-SEVEN PAGES of references regarding dietary fat alone! In fact, the bulk of the publication was devoted to explaining the evidence behind the recommendations. I don’t really blame Taubes for not reading it, though; it was quite long and it didn’t really fit nicely into the narrative he was attempting to craft. As a matter of fact one of the cited trials, titled Low-fat Diet in Myocardial Infarction in The Lancet, had a group consuming about half the percentage of calories from fat than what the National Academy of Sciences was recommending in Diet and Health so the results aren’t really comparable. Nevertheless, the low-fat group actually had beneficial effects to weight and serum lipids compared to the control group.2

* * *

Taubes does some really excellent minimizing on pages 63 and 64 when he discusses some data from the MRFIT trial:

For every one thousand middle-aged men who had high cholesterol—between, say, 240 and 250 mg/dl—eight could expect to die of heart disease over any six-year period. For every thousand men with cholesterol between 210 and 220, roughly six could expect to die of heart disease. These numbers suggest that reducing cholesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand). If we were to stick rigorously to a cholesterol-lowering diet for thirty years—say, from age forty to seventy, at which point high cholesterol is no longer associated with an increased risk of heart disease—we would reduce our risk of dying of a heart attack by 1 percent.

By the way, I find it humorous that in the previous chapter Taubes was talking about what a disaster the MRFIT trial was, but here he’s discussing it as if it were the capital-T truth.

I think his data is actually wrong, too. He publishes a graph on the same page taken from a MRFIT article, and I think he’s simply guesstimating. The actual data from the trial says that a serum cholesterol value of 220 mg/dl would correspond to a CHD death rate of 5.81/1,000 and a cholesterol value of 250 mg/dl would have a death rate of 9.1/1,000.3,4 I suppose it’s a minor point, but I am going to use the real data in a second.

His choice of how to present the results is a great study of how to deceive with statistics. It also reminds of a scene in Pulp Fiction. You’ve probably seen it, but if you haven’t I’m not going to explain the context because I don’t really need to to make my point.

                                     VINCENT
                         What do you think about what happened 
                         to Antwan?

                                     MIA
                         He fell out of a window.

                                     VINCENT
                         That's one way to say it. Another 
                         way is, he was thrown out. Another 
                         was is, he was thrown out by 
                         Marsellus. And even another way is, 
                         he was thrown out of a window by 
                         Marsellus because of you.

So Taubes says “These numbers suggest that reducing cholesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand).” That’s certainly one way to say it. Another way is that it reduces your risk of dying from a heart attack by 36%. Another way is it reduces your relative risk of CHD death from 2.88 to 1.84 (with 1.0 being optimal). And even another way to say it is that this data suggests that 205,954 lives in the US could be spared by lowering serum cholesterol from 250 to 220, assuming 20% of the population has cholesterol in excess of 250 mg/dl.

* * *

Page 65-66

Between 1987 and 1994, independent research groups from Harvard Medical School, the University of California, San Francisco, and McGill University in Montreal addressed the question of how much longer we might expect to live if no more than 30 percent of our calories came from fat, and no more than 10 percent from saturated fat, as recommended by the various government agencies. All three assumed that cholesterol levels would drop accordingly, and that this low-fat diet would have no adverse effects, which was still speculation rather than fact.

The Harvard study, led by William Taylor, concluded that men with a high risk of heart disease—such as smokers with high blood pressure—might gain one extra year of life by shunning saturated fat. Healthy nonsmokers, however, might expect to gain only three days to three months. “Although there are undoubtedly persons who would choose to participate in a lifelong regimen of dietary change to achieve results of this magnitude, we suspect that some might not,” the Harvard investigators noted.

The UCSF study, led by Warren Browner, was initiated and funded by the Surgeon General’s Office. This study concluded that cutting fat consumption in America would delay forty-two thousand deaths each year, but the average life expectancy would increase by only three to four months. To be precise, a man who might otherwise die at sixty-five could expect to live an extra month if he avoided saturated fat for his entire adult life. If he lived to be ninety, he could expect an extra four months.* The McGill study, published in 1994, concluded that reducing saturated fat in the diet to 8 percent of all calories would result in an average increase in life expectancy of four days to two months.

Browner reported his results to the Surgeon General’s Office, and only then submitted his article to JAMA. J. Michael McGinnis, the deputy assistant secretary for health, then wrote to JAMA trying to prevent publication of Browner’s article, or at least to convince the editors to run an accompanying editorial that would explain why Browner’s analysis should not be considered relevant to the benefits of eating less fat. “They would have liked it to come out the other way,” explained Marion Nestle, who had edited the Surgeon General’s Report on Diet and Health and had recruited Browner to do the analysis. This put Browner in the awkward position of protecting his work from his own funding agents. As he wrote McGinnis at the time, “I am sensitive to the needs of your office to put forward a consistent statement about what Americans should do, and to your dismay when a project that you have sponsored raises some questions about current policy. I am also concerned that the impacts of recommendations that apply to 240 million Americans are clearly understood. This manuscript estimates the effects of one such recommendation—altering dietary fat intake to 30 percent of calories—based on the assumptions that underlie that recommendation. Shooting the messenger—or creating a smoke screen—does not change those estimates.” JAMA published Browner’s article—“What If Americans Ate Less Fat?”—without an accompanying editorial.

*Browner’s analysis also assumed that restricting dietary fat would reduce cancer deaths, which was speculative then and is even more speculative now.

Although the analysis is perhaps more pessimistic about the benefits of reducing saturated fat, it is also a bit more nuanced than Taubes makes it seem.5 The figures of 42,000 saved lives are in there as is the extra four months of life, but there’s also the following:

The analysis indicates that if those assumptions are valid, restricting dietary fat to a maximum of 30% of total energy intake could reduce CHD mortality rates by between 5% and 20%. Mortality due to cancers of the breast, colon, and prostate might be reduced by an even greater proportion. Similar reductions would also occur in the incidence of these diseases.

AND

From the public health point of view, an increase of 3 months in life expectancy multiplied by 240 million Americans results in about 60 million years of additional life […]

Browner also points out that since the 3-4 month estimate is a statistical average, the real effects of lowering saturated fat would probably translate to several extra years in some individuals and possibly no increased lifespan in others.

But that is not the interesting part… The interesting part is where Taubes states that J. Michael McGinnis tried to shut down the publication of the article. This is based on a letter (presumably) that Browner wrote to McGinnis back then. I have contacted both Dr. Browner and Dr. McGinnis to see if they can confirm this. As of this writing I have received no response from Dr. Browner, but I did receive one from Dr. McGinnis that was very interesting. McGinnis claims he was never contacted by Taubes for his side of the story and that what Taubes wrote “certainly doesn’t ring either familiar or true.” In McGinnis’s own words:

Neither Marion nor I worked in the Surgeon General’s office—rather in a parallel office in HHS—but if the paper was done when she worked with me, it would have been nearly 30 years ago. I really have no recollections on any of what is reported in the passage—including the commissioning of the paper. I do recall the general reported finding on the limited impact on heart disease deaths of the lipid intake reduction indicated, although not the individuals or center (or centers) making the reports. Given the fact that the finding of small effects of isolated dimensions was not unusual (recall MRFIT), it would not have been particularly surprising. It is certainly possible that I would have been of a mind that a narrowcast analysis could be misleading if interpreted as reflecting on the impact of broader associated dietary changes. But unless I was a reviewer commenting on methodologic limits, it would be very unlike me—I cannot recall a single instance—to separately suggest that an article not be published. Indeed, to the contrary, I am squarely in the camp that there is great merit in publicly “calling the question” on these issues to prompt further analytic advances.

Dr. McGinnis also said that he will happily recant if someone were to produce the letter in question. I also contacted Dr. Marion Nestle and she claims that, while she can’t remember the specifics, what Taubes wrote about her remarks are generally true.

* * *

On page 72 Taubes discusses the famous Nurses Health Study and states

In 1992, Willett published the results from eight years of observation of the Nurses cohort. Fifteen hundred nurses had developed breast cancer, and, once again, those who ate less fat seemed to have more breast cancer. In 1999, the Harvard researchers published fourteen years of observations. By then almost three thousand nurses had contracted breast cancer, and the data still suggested that eating fatty foods (even those with copious saturated fat) might protect against cancer.

Walter Willett and Meir Stampfer are two of several authors of these obervational studies.6,7 (Interestingly, Taubes says in a blog post that Willett and Stampfer are not real scientists, they don’t do “real” science, and epidemiology is not to be trusted.) The cited studies do not provide evidence for his claim that copious amounts of saturated fats might protect against cancer. The best thing he can say is that consumption of SATURATED fat doesn’t appear to increase one’s risk of BREAST cancer. Of course the same could also be said of MONOUNSATURATED, POLYUNSATURATED, and even TRANS fats, at least according to these studies.

* * *

On page 73 Taubes gets on the polyunsaturated-fats-cause-cancer bandwagon again stating:

This laboratory evidence that dietary fat caused breast cancer began to evaporate as soon as Diet, Nutrition, and Cancer was published, and researchers could get funding to study it. By 1984, David Kritchevsky, one of the authors of Diet, Nutrition, and Cancer, had published an article in Cancer Research reporting on experiments that had been explicitly designed to separate out the effects of fat and calories on cancer, at least in rats. As Kritchevsky reported, low-fat, high-calorie diets led to more tumors than high-fat, low-calorie diets, and tumor production was shut down entirely in underfed rats, regardless of how fatty their diet was.

However, the results from the study itself are different:8

The data from 3 separate studies altering caloric and fat intake support the conclusions that a high-fat diet influences initiation as well as promotion of DMBA-induced mammary tumorigenesis, that high caloric intake increases tumor yield, and that restriction of caloric intake (even concomitant with the provision of twice as much dietary fat) inhibits tumor formation during the promotion period.

At least he got part of the study correct. By the way, I wonder how Taubes squares this circle in his mind when he later advocates eating all the calories you want — as long as it’s all meat, of course.

* * *

Pg 74

Nonetheless, the pervasive belief that eating fat causes breast cancer has persisted, partly because it once seemed undeniable. Purveyors of health advice just can’t seem to let go of the notion. […] By 2006, with the next release of cancer-prevention guidelines by the American Cancer Society, the ACS was acknowledging that “there is little evidence that the total amount of fat consumed increases cancer risk.” But we were still advised to eat less fat and particularly meats (“major contributors of total fat, saturated fat and cholesterol in the American diet”), because “diets high in fat tend to be high in calories and may contribute to obesity, which in turn is associated with increased risks of cancers.” (Saturated fats, in particular, the ACS added, “may have an effect on increasing cancer risk,” a statement that seemed to be based solely on the belief that if saturated fat causes heart disease it probably causes cancer as well.)

Of course, Taubes ignores the reference in the text that immediately follows “may have an effect on increasing cancer risk” and instead tells his readers that the statement is based on some unfounded belief. In case you’re wondering the reference is a review article that pours over several relevant studies on fat and cancer.9 What Taubes also omits is that the main reasons the ACS recommends avoiding red and processed meats have little to do with fat content.10 I’ll let the ACS explain:

Many epidemiologic studies have examined the association between cancer and the consumption of red meats (defined as beef, pork, or lamb) and processed meats (cold cuts, bacon, hot dogs, etc.). Current evidence supports an increased risk of cancers of the colon and/or rectum and prostate. More limited evidence exists for other sites. Studies that have examined red meat and processed meat separately suggest that risks associated with processed meat may be slightly greater than red meat, but the consumption of both should be limited.

Meat contains several constituents that could increase the risk of cancer. Mutagens and carcinogens (heterocyclic amines and polycyclic aromatic hydrocarbons) are produced by cooking meat at high temperatures and/or by charcoal grilling. The iron content (heme) in red meat may generate free radicals in the colon that damage DNA. Substances used to process meat (nitrates/nitrites and salt) contribute to the formation of nitrosamines that can damage DNA. It is also possible that the fat content in meat contributes to risk. For example, foods that are high in fat increase the concentration of secondary bile acids and other compounds in the stool that could be carcinogens or promoters of carcinogenesis.

These cancer properties of red and processed meats have been well-documented over the years. There is a mountain of evidence for them. But of course Taubes has never been one to let evidence ruin a good story about how people that disagree with him are pinheaded schmucks.

* * *

Pg 75, Taubes lies about the results when discussing a study by the Women’s Health Initiative claiming that

The women on the diet also consumed fewer calories—averaging 120 calories a day less than the controls over the eight years of the study.*

*They did not, however, lose any weight because of this, which is paradoxical, and an issue we will discuss later.

Actually, everyone on the diet lost a significant amount of weight.11

See Taubes response #4

* * *

On page 84 Taubes discusses the results of a Cochrane review*:

The review concluded that the diets, whether low-fat or cholesterol-lowering, had no effect on longevity and not even a “significant effect on cardiovascular events.”

The first part of that claim is actually true. The second lies about the results of the systematic review. It actually reduced cardiovascular events by 16%. The same authors published the Cochrane results in BMJ and they concluded then12:

The findings on cardiovascular events are broadly in keeping with benefits that might be expected from modest lowering of cholesterol concentration and certainly provide support, at an individual level, for the central role of dietary fat intake in the causation of cardiovascular disease.

The results also indicated a reduction in mortality by 9%, but that figure was within the 95% CI. In any case, if you’re curious about the updated results they are basically unchanged.13 From the 2012 Cochrane review:

Dietary change to reduce saturated fat and partly replace it with unsaturated fats appears to reduce the incidence of cardiovascular events, but replacing the saturated fat with carbohydrate (creating a low fat diet) was not clearly protective of cardiovascular events (despite small improvements in weight, body mass index, total and LDL cholesterol).The protective effect was seen almost exclusively in those who continue to modify their diet over at least two years, and in studies of men (not those of women). Dietary advice to those at high risk of cardiovascular disease (particularly where lipid lowering medication may not be available), and probably also to lower risk population groups, should continue to include dietary fat modification, possibly as part of a Mediterranean dietary pattern, and it should be stressed that this is a permanent pattern of eating.

*Something Taubes holds in high regard, unless of course a result might contradict his thesis (as is the case with a Cochrane review of salt and hypertension) in which case they are meaningless. But more on that later.

See Taubes response #5

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1. National Academy Press. Diet and Health: Implications for Reducing Chronic Disease Risk. (1989). at <http://www.nap.edu/openbook.php?record_id=1222&gt;

2. A Research Committee. Low-fat Diet in Myocardial Infarction: A Controlled Trial. The Lancet 286, 501–504 (1965).

3. Martin, M. J., Browner, W. S., Hulley, S. B., Kuller, L. H. & Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. The Lancet 328, 933–936 (1986).

4. Stamler J, Wentworth D & Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded?: Findings in 356 222 primary screenees of the multiple risk factor intervention trial (MRFIT). JAMA 256, 2823–2828 (1986).

5. Holmes, M. D. et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA 281, 914–920 (1999).

6. Browner WS, Westenhouse J & Tice JA. What if americans ate less fat?: A quantitative estimate of the effect on mortality. JAMA 265, 3285–3291 (1991).

7. Willett, W. C. et al. Dietary fat and fiber in relation to risk of breast cancer. An 8-year follow-up. JAMA 268, 2037–2044 (1992).

8. Kritchevsky, D., Weber, M. M. & Klurfeld, D. M. Dietary Fat versus Caloric Content in Initiation and Promotion of 7,12-Dimethylbenz(a)anthracene-induced Mammary Tumorigenesis in Rats. Cancer Res. 44, 3174–3177 (1984).

9. Kolonel, L. N. Fat, meat, and prostate cancer. Epidemiol. Rev. 23, 72–81 (2001).

10. Kushi, L. H. et al. American Cancer Society Guidelines on Nutrition and Physical Activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA. Cancer J. Clin. 56, 254–281; quiz 313–314 (2006).

11. Howard, B. V. et al. Low-fat dietary pattern and weight change over 7 years: the Women’s Health Initiative Dietary Modification Trial. JAMA 295, 39–49 (2006).

12. Hooper, L. et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst. Rev. Online CD002137 (2001). doi:10.1002/14651858.CD002137

13. Hooper, L. et al. in Cochrane Database Syst. Rev. (The Cochrane Collaboration) (John Wiley & Sons, Ltd, 2012). at <http://doi.wiley.com/10.1002/14651858.CD002137.pub3&gt;