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