The Case for Keto: A Critical Review

I also cross-posted this review to substack, because that’s where all the cool kids are publishing stuff nowadays.

Introduction

Here we are again. Another Gary Taubes book. After reading it, I have pretty much the same feelings about this book as I did his previous books. To the lay reader it probably has the veneer of a thoroughly researched book by an author who sees through all the BS that’s out there and presents a no-nonsense recitation of the facts. But the reality is quite the opposite: Taubes seems to ignore a lot of evidence that is contrary to his ideas and the evidence he presents is usually taken out of it’s original context and placed into a new context that is created to really change the original meaning. I would say that this is Taubes’s biggest failing in writing the book, but I’m fairly certain this is not simply incidental human error.

Another flaw of the book (in my opinion) is a heavy reliance on a kind of anti-intellectual rhetoric mixed with a weird version of classism. What I mean by this is that nutritional experts and nutrition researchers are treated with contempt. It should be noted that he only treats the researchers that publish findings contrary to Taubes’s theories with contempt. If they happen to align with his theories they are treated with reverence. The narrative is very much infused with an elite ruling class of oppressive nutritional authorities and an innocent proletariat that just want to lose weight and go about their lives. You can believe all that if you want. I can’t stop you. Conspiracy theories are certainly in vogue nowadays.

Anyway, I am writing this introdution in between trying to sooth my finicky 4 month old son, so my thoughts my not be totaly coherent, but I think you are picking up what I’m laying down. But you didn’t come here for the introduction. You came here to witness me pick apart a book.

Not the Introduction

The first paragraph of TCFK is how we should have listened to a guy name Edwin Astwood:

On June 22, 1962, a Tufts University Medical School professor named Edwin Astwood tried and failed to correct how we think about the cause of obesity. We have been living with that failure ever since.

Taubes spends the next two pages building Astwood up by stating what a brilliant guy he is and listing his credentials, but he does not mention any of Astwood’s dietary arguments or what he believed and why. The thing Taubes does mention is the first sentence of a 1962 speech that Astwood gave in Chicago where Astwood says that obesity is similar to a sexually transmitted infection, in that the patient is often blamed.

So what are some of Astwood’s theories on obesity? Dr. Astwood argues that obesity is actually a heritable condition caused by a “defective enzyme” and dieting won’t help.

I wish to propose that obesity is an inherited disorder and due to a genetically determined defect in an enzyme; in other words, that people who are fat are born fat, and nothing much can be done about it. (1)

Big, if true. That would render the whole point of Taubes’s book moot, because why follow a ketogenic diet? It won’t matter if you’re fat or thin. Astwood goes on to argue that that there’s nothing wrong with being fat; in fact, it can be quite desirable in women if the fat is deposited in the right places. Seriously, he spends several paragraphs on this point. In doing so he gives us a phrase that I haven’t been able to forget: “I would not want to wager about how many enzymes determine the shape of voluminous pulchritude.” Quite a turn of phrase!

On page 23 Taubes invokes a narrative that he’s used before. To wit, German scientists developed the correct idea that obesity was caused by poor hormone regulation, but after Germany lost WW2 the science that had come from Germany fell out of favor. What replaced it was the incorrect notion that a calorie surplus caused obesity. The good German research was all but forgotten. Or that’s how Taubes tells it, at least.

Does he provide the slightest bit of evidence for this? Not at all, and in fact there is evidence to the contrary. German scientists were highly valued in the United States and elsewhere both during and after WW2. In fact, the US (and other countries like England) made a great effort to poach German scientists as a kind of “brain drain” operation. But nevertheless it is an interesting story for why Taubes’s pet theory of obesity has not been widely accepted for nearly a century.    

On page 27-28 Taubes dismisses the idea that issues of psychology could play a role in obesity, and seems to denigrate psychiatrists as something akin to grifters.

[O]besity treatment had become the purview primarily of psychiatrists and psychologists. These were the medical professionals charged with teaching fat people to get thin and supposedly elucidating our understanding of the disorder. They saw the obese and overweight, not surprisingly, from their own unique perspective and context, as clearly suffering from mental, emotional, and behavioral disorders. They found it easy to ignore a revolution in endocrinology, because that wasn’t their area of study.

A couple paragraphs later Taubes goes back to Germanophobic theory of obesity and writes the following:

Astwood’s proposition and his theory, and the thinking of the prewar German and Austrian authorities, effectively disappeared. In 1973, after forty years of research had worked out the science of fat metabolism and storage in great detail, Hilde Bruch, the leading U.S. authority on childhood obesity, remarked on its absence. It was “amazing how little of this increasing awareness,” she wrote, “is reflected in the clinical literature on obesity.”

Hilde Bruch was a German-born psychiatrist that emigrated to the US in the 1930s. And that quote is taken from a text where she is absolutely not referring to a dearth of German research in the literature or even a lack of discussion on hormonal regulation. Rather, she was referring to the lack of behavioral science and family systems theory in obesity research. In other words, Bruch does not refer to what Taubes states and instead the “leading U.S. authority on childhood obesity” says precisely the opposite of what Taubes claimed a couple paragraphs earlier.

Taubes likes to cite Bruch in his other works, too, but fails to really put her works into context. Because if he did it would hurt his case for keto. One example is from the text Taubes cites here. As she explains in the text, there are really only two obesity treatments in her view: “manipulate the energy balance so that an obese person expends more than he takes in and thus loses weight.”  The other is to “effect a change in the person himself so that he no longer abuses the eating function in futile efforts to solve other problems of living, and to help him gain sufficient inner strength so that he can face the task of reducing without undue mental strain.” (2)

She also discusses the impact of family dysfunction to obesity in her earlier work:

In such an environment which does not offer adequate emotional security, food gains an inordinate importance. Food is offered and received not alone for the appeasement of a bodily need but it is highly charged with emotional value. To many mothers the offering of food represents the only way of expressing their affection and devotion. The child increases his demands as his need for gratification and security in other respects remains unsatisfied. On the other hand, enjoyment of physical activities and social relation is greatly restricted. The atmosphere of fearful apprehension confers upon them the meaning of danger, threat, and insecurity. The development of obesity in such surroundings becomes comprehensible. Overeating and inactivity bring about the increasing storage of fat. But these symptoms do not befall a child suddenly; they are closely connected with his whole development. (3)

On page 29 Taubes is incredulous that medical textbooks don’t present alternative hypotheses that “compete” with the calorie model of obesity, stating “The absence of a competing theory is remarkable, especially given the stakes and the profound implications.”

One wonders if Taubes is equally incredulous that alchemy isn’t taught as a competing theory in chemistry textbooks, or that intelligent design is not included in (most) biology textbooks as a “competing” theory to evolution.

On page 30 Taubes mentions Dr. Reginald Passmore whom Taubes says was the author of “definitive” nutrition information for a generation of British medical professionals.

Passmore coauthored an article in the British Journal of Nutrition that began with the declaration: “Every woman knows that carbohydrate is fattening: this is a piece of common knowledge, which few nutritionists would dispute.” This observation resonated almost perfectly with what laboratory researchers were learning at the time about the hormonal orchestration of fat storage and fat metabolism.

That article certainly began with that declaration but ended quite differently. The article was about a study where people were fed excessive amounts of carbohydrate, with the expectation that the extra carbs would be converted to fat. But what Passmore found didn’t support that conclusion:

In each of the three series of experiments described above, it was found to be difficult to raise the RQs of the subjects significantly above 1.00. Thus, despite the large intakes of carbohydrate, there was no evidence of the net conversion of carbohydrate into fat in substantial amounts within 24 h. (4)

Emphasis mine. Taubes has a nasty habit of taking the words of researchers out of context and making them fit his own narrative. When writing an article, authors like to inject the mildest bit of drama into what would otherwise be a dry recitation of findings, so they craft their findings as if their results were surprising in some way. In this case the story was: Everyone knows carbohydrates are fattening, but we put this common wisdom to the test and our results might surprise you. Here’s what we did and how it challenges the conventional wisdom.

So it’s funny that when Taubes writes “this observation resonated almost perfectly with what laboratory researchers were learning at the time” it certainly wasn’t what that author was learning at the time. Or it would be funny if you think lying to a gullible audience is funny.

Throughout the text Taubes takes a very anti-establishment stance. He has taken similar stances in his other books, but I think TCFK is the most explicit and most pointed when it comes to attacks on “nutritional authorities.” Here’s a representative example on page 37:

[T]he nutritional and academic authorities have failed us, and they and we should acknowledge that. Had they not failed us, we would, almost by definition, never have reached this point of epidemic obesity. That’s the context of this discussion and all that follows. I believe it should be the context of every public discussion on obesity and weight control. If the conventional thinking and advice worked, if eating less and exercising more were a meaningful solution to the problem of obesity and excess weight, we wouldn’t be here. If the true explanation for why we get fat were that we take in more calories than we expend and the excess is stored as fat, we wouldn’t be here. So many more of us would be lean and healthy, and books like this one would not be necessary.

Emphasis in the original. It should be noted that, although Taubes frequently attacks the experts, when he finds one to quote that advances his pro-ketogenic argument, he goes out of his way to list his/her educational credentials, make sure you know they held professorships, mention how many years they did research, etc. You can see this very clearly in the first few pages of the book where Taubes lauds Dr. Astwood for pages, even describing an award he had won and comparing it to the Nobel Prize (“He won the Lasker Award, considered one step below the Nobel Prize, for the thyroid work”). So when it comes to attacking authorities versus embracing authorities, Taubes definitely wants to have his cake and eat it, too.

But I would like to address the maligning of the experts here. As I write this, the United States is mired in the depths of the COVID-19 pandemic. We have by far the most cases of the disease, and we are tied with the European Union for the most deaths.

Other countries have managed to get this pandemic under control. Where the US has over 200,000 new confirmed cases per day, South Korea has 745 cases/day, China has 100 cases/day, Taiwan has 5 cases/day, and New Zealand has 2 cases/day.

Why is that? Are those countries getting better health advice that the US? No, their public health officials were saying the same thing ours were: mask up, social distance, stay home if possible, wash your hands, etc. But there was clearly a difference in the application and execution of this advice.

Many factors led to the US being the hardest hit country: the White House’s efforts to “play down” the importance of the virus, inability to mobilize the resources of the federal government to acquire and effectively distribute supplies like ventilators and masks, our inability to perform widespread testing and contact tracing, nearly an entire political party that pretended the virus wasn’t real and openly participated in super spreader events… we could go on. But the advice of the epidemiologists and public health experts like Dr. Tony Fauci, Dr. Vin Gupta, and Dr. Peter Hotez is not to blame. These experts have been communicating every day exactly what we need to do to mitigate the spread of the virus for nearly a year now, but as a society we have been unable to universally coalesce around these messages and engage in effective mitigation and prevention.

This is similar to the obesity “epidemic.” The US also has the most overweight and obese people per capita. Again, why are other countries leaner and healthier in this respect? Other countries have nutrition experts and authorities that say basically the same thing our experts say. The problem in the US is that we are unable or unwilling to really apply those recommendations. It also does not help when people like Taubes write nutrition books full of deliberate misinformation.  

One of the key elements in Taubes’s argument is that some people are simply “born” thin, while others are less fortunate and are born with a metabolic deficiency which causes them to become fat. This argument is distilled on page 45-46:

Those who fatten easily are profoundly different from those who don’t and may have been from the womb onward. Their physiology is different; their hormonal and metabolic responses to foods are different.

If these differences are so pronounced, you would think that there would have been ways to identify and differentiate these individuals long ago. Much like how you can identify people with diabetes with a simple OGTT. But I know of no such test and Taubes doesn’t present evidence of any type of test or even hypothetical investigative tool that would do so. One would imagine that (if Taubes is correct) such a tool would be very valuable for identifying those people at very high risk of developing obesity and therefore a likely milieu of other chronic diseases such as heart disease, cancer, diabetes, hypertension, etc.

In fact, the topic has been widely studied and no enterprising researcher has been clever enough to cash in on creating such an important diagnostic tool. Taubes tries to conceal that from you, though. Take, for example, a passage from this very same page as the above. Taubes discusses the hearings before the Select Committee on Nutrition and Human Needs of the United States Senate in 1977:

I want to be sure we don’t oversimplify,” Bellmon said. “We make it sound like there is no problem for those of us who are overweight except to push back from the table sooner. But I watched Senator [Robert] Dole in the Senate dining room, a double dip of ice cream, a piece of blueberry pie, meat and potatoes, yet he stays as lean as a west Kansas coyote. Some of the rest of us who live on lettuce, cottage cheese and RyKrisp don’t do nearly as well. Is there a difference in individuals as to how they utilize fuel?”

The doctor in the hearing replies “We constantly hear anecdotes of this type, but, to date, people doing research in this field have been unable to find clear evidence that people remain thin because of some special metabolic characteristic.” But Taubes would have you believe that a slavish devotion to an ancient religion led the good doctor to this belief and not a lack of clear and compelling evidence.

Taubes does this throughout the book; framing a conclusion based on facts and evidence as if it is some sort of irrational, unscientific dogma. In reality, Taubes is guilty of the very thing that he accuses others of doing. Taubes himself has not meaningfully changed his beliefs on why people get fat in nearly 20 years despite all evidence to the contrary. He has called scientific studies that don’t fit his beliefs pseudoscience, and he has denounced the researchers and results he himself funded (through his organization NuSI) that he expected would prove his theories correct. He has even openly admitted that he would not alter his beliefs no matter what the evidence demonstrates.  

Whenever I go back and read ones of Taubes’s references I very often find that Taubes took the original author out of context, and something immediately following (or immediately preceding or both) will undercut the point Taubes is trying to make. I imagine Taubes at home on his computer writing a draft of TCFK, pulling an old nutrition book off his bookshelf, flipping though it while his finger traces the words and thinking “Can’t use that… Nope… That’s no good… Hmmm, doesn’t really support what I’m saying… Definitely not that… Okay, I could probably use that sentence as long as I make sure to leave it ambiguous as to what he’s actually talking about… And that’s it. Can’t use anything else.”

One such example is Taubes’s mention of a 1936 textbook on metabolism as an example of why thinking that the body strictly regulates calorie intake and fat accumulation is ridiculous. Page 52:

[O]ther experts in the early decades of the twentieth century saw it as a reason to question the whole way of thinking. Eugene DuBois, for example, the leading authority on human metabolism in the United States in the 1920s and 1930s, suggested in his seminal textbook that this simple mathematics tossed the whole energy balance (gluttony and sloth) concept of body weight regulation into the realm of the absurd. Considering how exquisitely accurate the imbalance has to be to avoid obesity, how few calories actually have to be stored in excess as fat every day to become obese, to lead to tens of pounds of excess fat every decade, he said, “There is no stranger phenomen[on] than the maintenance of a constant body weight under marked variation in bodily activity and food consumption.” (Another phrase used by physicists to describe this kind of problem is “spherically senseless,” meaning it makes no sense no matter which way you look at it.)

DuBois then goes on to illustrate in pretty striking detail how exactly this phenomenon occurs. Like I mentioned earlier, many researchers like to present problem/conundrum/question upfront, then go on to answer the question they proposed with their work. Much like Darwin is taken out of context by creationists to make it seem like Darwin himself didn’t believe in natural selection, Taubes does the same with the authors he cites.

DuBois actually seems to endorse the gluttony and sloth concept of obesity that Taubes rails against:

[I]n some individuals, with apparently normal endocrine glands, the weight increases to the point where it exceeds the normal limits. These are the cases of so-called simple or exogenous obesity. The term exogenous indicates that there is no endocrine disturbance, but that the fault lies either in too much food or too much laziness. It is not strictly exogenous because greediness and laziness certainly rest within the body. (5)

DuBois also throws cold water on Taubes’s metabolic defect theory:

We must conclude that simple or constitutional obesity, which seems to be in many cases an hereditary disease, is accompanied by no abnormality of metabolism striking enough to be demonstrated by our present methods.

On page 45 Taubes attacks Jean Mayer for accepting the fact that it’s pretty difficult to gain weight if you exercise a lot or don’t eat anything.

Our current obsession with physical activity is largely rooted in Mayer’s proselytizing in the 1970s. But at the beginning of his career in the 1950s, he studied a strain of obese mice. “These mice,” he wrote, “will make fat out of their food under the most unlikely circumstances, even when half starved.” […] Mayer’s mice did not get fat by overeating. They got fat by eating. Half-starving them didn’t make them lean.

Emphasis mine. That quote comes from a book on overweight that Mayer wrote in 1968. Taubes doesn’t cite any page number for this quote, but it’s found on page 49 for those that are curious.

Taubes has to remove quite a bit of context here to make this passage fit his anti-exercise narrative. If you bother to read the couple paragraphs preceding the above quote you will find that

  • The mice are inbred to create abnormalities like obesity to make it easier to study the condition. I’m not sure Taubes wants to equate obese people with inbred mice.
  • One of the reasons the mice are obese is because they don’t exercise like normal mice. Mayer describes them as “extraordinarily inert” and basically don’t move. He states that you can get them to lose weight by putting them on a treadmill or by introducing genes that cause them to pace around their cages all day. Sounds like this could be evidence that physical activity can cause weight loss after all.
  • Another thing that Mayer mentions is that if you put the obese mice on a reducing diet they will lose weight, but interestingly they lose much more muscle and less fat than you might expect. Mayer explains that this is because their particular abnormality makes it easier to burn lean muscle for fuel rather than fat. Kind of an interesting factoid, but I’m not sure that this aberration in inbred mice is terribly relevant to humans. (6)

If it’s not obvious to you, there are a lot of problems when you try to apply some logic to this bizarre thinking. Let’s take an example of ex-athletes. After an elite athlete retires from their sport, it’s not uncommon for these athletes to then gain some (or quite a bit) of weight. See Charles Barkley or Mike Tyson. For Taubes’s mice analogy to be true in humans you would have to believe that elite sportsmen like Tyson, Barkley, and others were actually just born obese. Their training and physical activity played little to no role in their lean periods while they were professional athletes, and the lack of intense training and playing at an elite level played no role in gaining weight after their retirement. Moreover, what appeared to be lean muscle on their bodies during their heyday was really just extra fat, since they can never be truly lean. Maybe what appeared to be muscle on Mike Tyson was just hardened fat, and much like the obese mice on low calorie diets didn’t actually have much lean muscle.

Or maybe all these obese athletes were on strict ketogenic diets while training and playing and just as they retired, they all went back on bread and pasta. I mean, this thought experiment really strains credulity.

There was a period of time around the 1940s to the 1960s where incoming freshman to Ivy League universities like Harvard would be asked to strip naked and be photographed from different angles as part of the new student orientation. The students were told this was for purposes of posture and if anyone’s posture was extremely bad they were sent to posture classes. However, that was not true and the students were not informed as to what the photos were really being used for, which was to lend an air of scientific respectability to a eugenicist.

What does that all mean? And what does it have to do with TCFK? Great questions I will soon answer. The eugenicist in question is a man named William H. Sheldon, and he had certain ideas about undesirable people and how to make a great society. To help humanity achieve this great society Sheldon believed we needed a way to identify undesirables, and so began Sheldon’s somatotyping project. Sheldon believed that one look at your body type revealed volumes about you: how intelligent you were, how ambitious you were, how sexually deviant, how lazy, how confident, and all other types of traits and behaviors. So he set out to prove this when he was at Harvard using these questionably-obtained photographs of college freshmen.

Long story short he writes some really racist things (like “Negro intelligence” comes to a “standstill at about the 10th year”), gets accused multiple times by his assistants of doctoring data, is not taken seriously by his fellow academics, leaves Harvard and has to rely on financial support from other rich eugenicists that liked his views, and fades into relative obscurity leaving behind a set of controversial racist, chauvinistic, and extreme eugenicist texts. (7,8)

Gary Taubes, however, seems to find value in his work and thinks it’s great to cite Sheldon on page 48 to support Taubes’s theories on obese people being born that way:

Cut back enough on the calories a fat person is allowed to eat, and the result is a less fat person. But as the Harvard psychologist William Sheldon observed in the late 1940s, starving a fat man (an endomorph, in his terminology) doesn’t actually turn him into a lean man (an ectomorph) or a muscular, athletic one (a mesomorph) any more than starving a mastiff turns it into a collie or a greyhound.

To reiterate, Sheldon was a deeply unscientific person and no one really takes his somatotyping work seriously. But even if we were to do so, Sheldon doesn’t even make the point that Taubes wants him to make in the book that he cites, because Sheldon mentions that endomorphs are generally lazy, not too bright, and eat a lot. I’m not going to copy-paste everything Sheldon wrote about endomorphs, but it’s deeply unflattering stuff that is written in some flowering language. I’ll mention a few here, just because I find them to be quite funny:

  • “There is an essential dislike of bodily exercise. The arms often show a limp relaxation like that of a seal’s flipper, and the hands are likely to be soft and flaccid.”
  • “The individual has a primary desire to be comfortable, and to bask in his comfort. He shows relatively great interest in being comfortable, and if he has any ingenuity, a considerable proportion of it is devoted to making himself comfortable.”
  • “All responses are conspicuously slow. Movement is slow and deliberate. Both verbal and motor reactions are slow, as revealed by the common reaction time experiments of the psychological laboratory. Eye movements are slow, including those involved in reading. The eye wink is observed to be slow, like that of a sleepy child.”
  • “There is a deep joy in eating, and a considerable fuss and ceremony are made overeating. Usually there is a history of having overeaten and of having desired more food than was needed to maintain normal weight or growth. In a true motivational sense the individual lives, partially at least, to eat.”
  • “The greatest of social satisfaction is to be derived from the festive board, and from lingering over a fine, well-served meal.” [I mean, who can argue?]
  • “Digestion is excellent and is a primary pleasure. To sit with a full belly and do nothing but digest, is to experience the fullness of life. Elimination too is pleasant and free from unpleasant psychological complications. It is especially pleasant to sit on the stool with the Sunday paper. If the individual is free from social inhibition, a fine belch is an excellent thing, and often flatus is most agreeable.” (9) [Who among us hasn’t enjoyed this from time to time?]

So if these are the primary traits of an endomorph, I’m not sure that it helps Taubes sell the idea that fat people aren’t fat because they eat too much and exercise too little.

On page 52 Taubes does his classic move of taking the introductory question of a paper out of context and ignoring the rest of the text:

Russell Wilder, the leading pre–World War II authority on obesity and diabetes at the Mayo Clinic, did ask precisely this question in 1930: “Why then do we not all grow fat?” After all, he wrote, “we continue to be protected against obesity, most of us, even though we hoodwink our appetite by various tricks, such as cocktails and wines with our meals. The whole artistry of cookery, in fact, is developed with the prime object of inducing us to eat more than we ought.” (That was almost ninety years ago when Wilder said “most of us” are protected against obesity. Today he might have to say “some of us,” but his point is still a good one.)

Wilder then goes on to answer his question with statements that are directly opposed to what Taubes is trying to argue. Wilder says that there is no difference in metabolism between the thin and the obese (contrary to Taubes’s earlier statements) but the difference lies in the brain, as obese/overweight people defend a higher setpoint than thin people. (Although he doesn’t explicitly say setpoint, as I don’t think that term was coined in 1930.)

Wilder also says the management of obesity is to control “calorie intake and output so that the latter will exceed the former” and “we can accomplish this reduction by either by limiting the food or increasing the outlets, that is, the expenditures of energy.” He also says that “I hope to have made it clear that there can be no gain of weight if the calories in the intake fail to meet those in the output.” (10) Wilder seems to have made it clear to anyone who does not want to deliberately misrepresent him.

Starting on page 67, Taubes brings up Hilde Bruch again, “a psychiatrist and psychoanalyst, known foremost for her work on eating disorders and obesity” as Wikipedia puts it.

“Researchers— physiologists, notably, and so not physicians or nutritionists and certainly not psychiatrists or psychologists— had discovered that the storage of fat in fat cells and the liberation of that fat from storage and its use for fuel (oxidation, in the lingo) wasn’t in any way the simplistic process that was implied then and is implied still by the nutritional authorities. Columbia University’s Hilde Bruch, who was the leading midtwentieth-century authority on childhood obesity, understood this and waxed indignant about it in a book she wrote in 1957 called The Importance of Overweight, which should still be required reading for anyone interested in understanding obesity.”

He devotes a few pages to Bruch and selectively quoting her. He brings up quotes from her on fat metabolism and fat regulation and how overeating is not a cause of obesity, but rather a symptom of some other issue. Taubes is again doing what I am going to now call the “Taubes Shuffle,” where you take quotes out of their original context and place them in a new context that makes it seem to a trusting reader like the author is supporting Taubes’s crackpottery, when that’s obviously not the case when you read the original text. In this instance, the Taubes shuffle makes it appear that Bruch’s book The Importance of Overweight is about the storage and metabolism of fat, but it’s really not. It’s really about environmental factors that lead children to overeat. Bruch focuses on family dynamics and domestic issues that influence how much children eat: overbearing parents, childhood trauma, chaos at home, overindulgent parents… All of these things, argues Bruch, can lead people to develop an unhealthy relationship to food, where food is a form of comfort, security, and self-soothing. Or weight is gained as a kind of armor against the cruel world. Many of the cases that are included in the book are heartbreaking. Bruch also argues that diets may work in the short term, but unless these psychological issues are addressed the weight will be regained later.

But of course Taubes’s book is not about how you need to get over your daddy issues to lose weight, it’s about how following a certain diet can make you lose weight—pretty much the exact opposite of what Bruch is stating in her book. In fact, if you look back at the passage in TCFK, immediately before Taubes introduces Bruch, he poohpoohs the idea that psychiatrists and psychologists would have any knowledge of the matter.

Another Taubes shuffle on page 69:

Researchers studying fat accumulation in animals would note how fat cells and the animals themselves could accumulate fat or mobilize it and burn it for fuel “without regard to the nutritional state of the animal,” as though how much or how frequently the animal ate was irrelevant to whether it was using up its fat stores or building them up.

A 1948 study is cited for this and immediately after that quote the authors discuss how “lowering of the fat content of the tissue during hunger is the result of mobilization exceeding deposition.” (11) So if words still have meaning this would be the opposite of the phrase “how much or how frequently the animal ate was irrelevant to whether it was using up its fat stores or building them up.”

Back to another Taubes shuffle on page 79 when bringing up low-carbohydrate diets in the treatment of obesity:

These unbalanced diets restricted in sugars, grains, and starches, fat-rich instead, induced significant weight loss without hunger. This was the case in report after report, independent of how many calories the patients in these various institutions were fed, whether fewer than five hundred calories a day (as at the Mayo Clinic) or whether the patients were encouraged to eat as many calories as they could, as was often the prescription. “The absence of complaints of hunger has been remarkable,” the Mayo Clinic’s Russell Wilder wrote in 1933.

But if you read the study that Taubes takes the Wilder quote from, Wilder is clearly talking about a low-calorie diet he prescribed to patients. The diet in question is not fat-rich and not unlimited in calories. It’s a diet that is between 500-600 calories/day and includes 100 grams of lean steak, 500 grams of vegetables, and alternating days of 100 mL of whole milk or 100 mL of orange juice with 50 grams of brewer’s yeast.(12) All with plenty of salt and a precise amount of vitamins and minerals.

So just to spell it out, Taubes put a quote by Wilder claiming that a lack of hunger is remarkable immediately after talking about fat-rich diets where patients are encouraged to eat as much as they could, when the quote refers to something completely different. The Taubes Shuffle.

This next one is not exactly a Taubes Shuffle, but it’s definitely a deliberate omission. Here Taubes lists foods from an old textbook that are contraindicated for obesity:

Here’s the British endocrinologist Raymond Greene’s version from his seminal 1951 textbook The Practice of Endocrinology: Foods to be avoided:

  1. Bread, and everything else made with flour
  2. Cereals, including breakfast cereals and milk puddings
  3. Potatoes and all other white root vegetables  
  4. Foods containing much sugar
  5. All sweets

Funny thing is there are eight items on that list, but Taubes only includes five. The other three being salt, fluids, and fats. I’m not sure why Taubes left fluids off (although drinking excessive amounts of water is popular in the keto diet community), but he has been a stout proponent of consuming more salt for years because that’s contrary to “conventional wisdom” and therefore he’s in favor of it. I think the reason he left fat off is obvious. A funny thing to read after reading Greene’s list is that Greene himself states that “this diet makes no claim to scientific accuracy […]” (13)

Since this is a text that is nearly 70 years old, there are some other interesting things about Greene’s recommendations, like that he also supports Turkish baths, amphetamines, diuretics, and dinitrophenol for weight loss.  

This next passage is almost worthy of leaving out because it’s not totally wrong, but I’ll mention it anyway. On page 81 Taubes mentions an Obesity conference in 1973:

Charlotte Young, a Cornell University professor, gave the only talk on dietary therapy, reviewing the hundred- year history of diets restricting sugar, starchy carbohydrates, and grains, and the results of the multiple clinical trials even back then, including Young’s own trials at Cornell. All these LCHF diets, Young said, “gave excellent clinical results as measured by freedom from hunger, allaying of excessive fatigue, satisfactory weight loss, suitability for long-term weight reduction and subsequent weight control.”

A couple things. 1) Young wasn’t exactly referring to all of the LCHF diets in the hundred-year history as Taubes says. She’s not even technically referring to a LCHF diet at all. She’s referring to a diet that she explicitly says is “moderate fat.” (14) Last I checked, moderate fat does not mean the same thing as high fat. 2) Young states that she tested 1800 calorie diets on obese men with varying degrees of carbohydrate: 30 grams, 60 grams, and 104 grams. All groups lost weight and were all successful in controlling hunger. She then says “In terms of practical interest, I concluded that the highest of the low carbohydrate levels used, 104 gm., was the most suitable for long term use.”* 3) Young wasn’t the only one with discussion of dietary therapy of obesity. She was the only one that had those words in the title of her talk, but many of the talks included discussions of how to treat obesity in different ways, from diet to exercise to fasting to pharmacological methods.

We have another Taubes Shuffle on page 87-88. He discusses insulin resistance and then basically states the thesis of his book: that any diet that works is not because it creates a calorie deficit, but rather that it creates in insulin deficit. Then he quotes Roxane Gay:

“I know the math,” Roxane Gay says in her memoir Hunger, as though that should be enough to solve her unruly body and reduce her excess fat. “In order to lose a pound of fat you burn 3,500 calories.” She then goes on to observe that this knowledge has clearly been useless to her.

I think the implication here is clear. When you link those two ideas you give the impression that Gay has attempted to lose weight by burning excess calories, but that’s useless because calorie deficits don’t work. Gay needs to reduce her insulin to lose weight, right?

Well, in fact if you read Hunger you’ll discover that chapter 46, where that quote is from, is all about how Gay doesn’t exercise. It’s about how much she hates it and considers it a waste of time. Gay says “I have a membership to Planet Fitness, though I have never visited the local facility. Basically, I donate $19.99 a month to their corporate existence and the idea that I can walk into a Planet Fitness, anywhere in the country, should I feel like working out.” (15) So to overly-explain what’s going on: it’s not that Gay is burning a ton of calories and not losing weight; it’s that she is not burning a ton of calories despite “knowing the math.” As a addendum, in chapter 65 she states that she tried low-carb diets. Those seemed to have been useless to her as well.  

Page 91:

Nutritionists and dietitians of the conventional school of thinking have been instructed and will tell us that carbohydrates are the preferred fuel for our bodies and our brains, thus implying that they are indispensable. But these nutritionists and dietitians are thinking about it the wrong way. The observable fact is that when carbohydrates are available in our diet, we do use them for fuel and we use them first.

That’s what “preferred” means.

Page 100:

Most of those who had been mentored in science weren’t particularly good at it. They didn’t understand what it meant to be skeptical of their own ideas and so to check and triple- check their assumptions. (“The first principle” of science, as the Nobel laureate physicist Richard Feynman put it so aptly, “is that you must not fool yourself and you’re the easiest person to fool.”)

If that ain’t the pot calling the kettle black, I don’t know what is.

Taubes continues to discuss the merits of LCFH diets, because, well, that’s what the book is about. He mentions a pediatrician named James Sidbury on page 118:

Sidbury knew that carbohydrates stimulate insulin and insulin facilitates fat formation and traps fat in fat tissues. He also knew, as he noted in a 1975 book chapter on this work, that kids with obesity crave carbohydrate- rich foods— “crackers, potato chips, french fries, cookies, soft drinks, and the like.” Restrict the carbohydrates and feed these kids only fat and protein, he reasoned, and their insulin would come down, and their fat metabolism would work as it does in lean kids. These children would burn their stored fat and lose weight without obsessive hunger and without constantly grazing on carbohydrates. He instructed parents to feed their children with obesity only 300 to 700 calories a day, made up of virtually all protein and fat. The kids lost weight as if by magic.

Funny how Taubes attributes all this magic weight loss to lack of carbohydrates and not to the extremely low calories. (16) Abracadabra!

Continuing:

Another example of this thinking also dates to the 1970s and comes from George Blackburn and Bruce Bistrian at Harvard Medical School. Bistrian and Blackburn developed what they called a “protein-sparing modified fast” to treat patients with obesity: 650 to 800 calories a day of nothing but lean fish, meat, and fowl. It had effectively no carbohydrates, making it a ketogenic diet, albeit a very low-calorie version. Bistrian and Blackburn prescribed the diet to thousands of patients, as Bistrian told me when I interviewed him in January 2003, and half of them lost at least forty pounds.

It’s wild how these ketogenic diets are very effective as long as they are very low calorie. But calories don’t matter of course because Taubes tells us so.

I’ve accused Taubes before of having it both ways in the most promiscuous manner. It is true in his other books like it’s true in this one. In chapter 11 he states that exercise doesn’t work, but if it does work it’s only because exercising is like being on a ketogenic diet:

I haven’t discussed exercise in this book in part because precious little evidence exists to suggest that we can lose any meaningful amount of fat and keep it off merely by increasing the amount of energy we expend through exercise or physical activity. We all may know people, though, who swear they lost weight merely by upping their workouts or returning to them after a lengthy absence. If that’s true, then the physical activity had to increase the length of time their insulin levels stayed under the threshold for mobilizing fat.

It’s not just about exercise, though. He also says that if low calorie diets happen to work for some people, it’s only because they restrict carbohydrates. Fasting type diets? They’re ketogenic, too, of course.

He loves to have it both ways in his rhetoric. Throughout the text Taubes denigrates so-called experts and nutritional authorities. He treats them with such contempt. His rhetoric is very anti-establishment and treats any author or nutrition researcher as just another pezzonovante. Yet when he wants to quote someone that ostensibly supports his ideas, they are introduced reverently often as a “leading authority” with a list of their bona fides and pedigree. (But when looking at what this person actually wrote, it’s usually clear his/her work doesn’t totally support Taubes’s ideas.)

He cites studies that support his ideas, but also says that other studies are most likely wrong. (“The best reason to ignore the latest study results, the latest media reports suggesting we should eat this and not that, is that the interpretation of these latest studies is most likely wrong.”)

Page 139:

After my 2002 article suggesting that Atkins was right all along, I was accused of taking a contrarian perspective not because I really thought the evidence supported it, but because it was more newsworthy and would earn me a large book contract. Reporting that the conventional wisdom was indeed right would not. The editors of The New York Times Magazine might not have even published such a version because it wouldn’t have been news.

Yes.

What’s interesting is that he doesn’t even argue against this notion. He just states it. And I would have to agree with him here. It’s much less likely that a longform article about how eating a plant based diet is usually pretty healthy and backed by evidence would have been published and led to a major seven-figure book deal.

Taubes wrote “What if it’s all been a Big Fat Lie?” Tell you what, I’ll pitch an article titled “What if You Already Know Pretty Much what a Healthy Diet Is?” to the New York Times and see if they bite.

A few years back I was working in a manufacturing plant. My boss was a smoker and one day when he was talking to me he excused himself to go outside and have a cigarette. And because I am was a smug prick I said “You know smoking takes years off your life, right?” He jokingly replied “Yeah, the worst years. It’s the ones at the end! It’s the wheelchair, kidney dialysis, adult diaper years. I don’t want that.” He was paraphrasing a Denis Leary bit.

Gary Taubes must have heard that bit, too, but instead of thinking it was a joke he must have thought it was a great argument for shortening your life because he makes that argument earnestly in chapter 12. He mentions that some “experts” claim that LCHF diets are bad for you and can shorten your life. His response is basically “So What? Do you really want to live a few more years in your nineties?” He even likens avoiding saturated fat to rearranging the deck chairs on the Titanic. We’re all gonna die anyway, so who cares? Live it up! (17)  

Page 151-152 Taubes mentions the article he wrote in 2002, claiming he was right all along:

In my [NYT] article, I noted that five clinical trials had recently been completed (albeit not yet published) comparing the LCHF/ketogenic Atkins diet to the kind of low-fat, calorie-restricted (semistarvation) diet recommended then and still by the American Heart Association. The trial participants ranged from overweight adolescents in Long Island, who followed the diets for twelve weeks, to Philadelphia adults weight averaged 295 pounds and who followed these diets for six months. The results of those five studies were consistent. The participants eating the LCHF/ketogenic high-fat diet lost more weight, despite the advice to eat to satiety, than those who ate the AHA recommended low-fat, low-saturated-fat diet. Moreover, their heart disease risk factors showed greater improvement.

A few things:

  • Taubes provides no evidence that the AHA recommends a low-fat, semistarvation diet, because there isn’t any. Read the org’s own nutrition recommendations yourself.
  • The results of the trials Taubes cites were not consistent and they did not all show greater improvement in heart disease risk factors.
    • For example, one study he cites by Foster et al., showed no significant differences in weight loss (low fat vs low carb) after one year. (18) That same study had mixed effects on risk factors. Comparatively, HDL was increased and triglycerides decreased in the low carb group (an improvement), but the LDL and total cholesterol were both increased (the opposite of greater improvement).

Figure 1 From the Foster Study

  • Additionally, two of the authors Taubes cites here (Brehm and Yancy) author a meta-analysis of low carb vs low fat diets a couple years later, and their findings show that it’s not all roses for low carb diets. (19) They show that at 6 months weight loss is greater on low carb, but at one year weight loss in the same. Moreover, some heart disease risk factors (like total cholesterol and LDL) show greater improvement on low fat diets, while HDL and triglycerides show greater improvement on low carb. Also, weight loss favors low carb in the short term, but after a year there is no difference between the diets. Basically, the results from several trials mirror the results of the Foster trial described above.  

The following piece is almost not worthy of inclusion, but I wanted to say a couple things about it anyway. On pages 152-153 Taubes discusses a study by Dr. Sarah Hallberg that got quite a bit of positive attention from the low-carb community a couple years ago. (20) Probably because Hallberg and two other authors, Steve Phinney and Jeff Volek, are part of the low-carb money-making ecosystem.

The study in question compares a group of obese diabetics following a low-carb, ketogenic diet to another obese group following no prescribed diet. Turns out the group that followed a diet lost weight, and with that weight loss some other benefits were gained as well, like improved insulin sensitivity, blood pressure, and other risk factors. Taubes evidently finds these results “particularly compelling” and the study is reinforcement of Taubes’s thesis that ketogenic diets can cure diabetes.

But in my humble opinion, there is nothing noteworthy about the results. I say this because pretty much any diet that results in an obese person losing a significant amount of weight will lead to those outcomes. This trial didn’t compare low carb to another diet, but other studies have done this before. Weight loss from low-carb or low-fat diets produce the same improvement in insulin sensitivity. (21) In fact, it doesn’t seem to matter much how you lose the weight (diet, physical activity, weight loss drugs, bariatric surgery) because they all will improve insulin sensitivity, with greater weight loss producing greater glucose control. (22) In other words, there is nothing uniquely beneficial to following a keto diet in this respect.   

Back in the salad days of Good Calories, Bad Calories, Taubes misleads the reader about the results of a Cochrane review:

In 2001, the Cochrane Collaboration published a review of “reduced or modified dietary fat for preventing cardiovascular disease.” The authors combed the literature for all possibly relevant studies and identified twenty seven that were performed with sufficient controls and rigor to be considered meaningful. These trials encompassed some ten thousand subjects followed for an average of three years each. The review concluded that the diets, whether low-fat or cholesterol-lowering, had no effect on longevity and not even a “significant effect on cardiovascular events.”

The deception here was that the review he cited actually stated a significant risk reduction in cardiovascular events if you replace saturated fat with unsaturated fat. (23) Here in TCFK he does much the same thing but is not quite as blatant about it. He cites a more recent version of essentially the same Cochrane analysis:

Now, thirty years later, the most recent unbiased review of this evidence—from the Cochrane Collaboration, an international organization founded to do such impartial reviews— concluded that clinical trials have failed to demonstrate any meaningful benefit from eating low-fat diets and so, implicitly, any harm from eating fat-rich foods.

To be fair to Taubes, the review does state that if you were to replace all the saturated fat in your diet with carbohydrate in your diet you wouldn’t be any better off. But the most interesting part of the review and the part that you’ll be interested in if you care bout health is that the review (again) found a significant benefit from replacing the saturated fats with unsaturated fats. (24)**

Another pretty obvious lie that can be easily verified are the statements made that there has been no clinical trial evidence that fruits and vegetables and such are good for you. It’s just something we collectively decided to believe despite zero evidence. Page 157:

As for the idea that a healthy diet must be mostly plants, that it must include fruits, vegetables, whole grains, pulses, and legumes, we don’t have even the ambiguous 1960s- era studies to support it. We have no meaningful clinical trial evidence to support this idea, as Michael Pollan infers in In Defense of Food, the book that brought us the mantra “Eat food. Not too much. Mostly plants.”

Emphasis mine. This statement is pretty egregious. You can do what I just did and go to PubMed, type in “plant based diet” and filter results to only show randomized clinical trials. I got 521 results.

Moreover, these results are not demonstrating how plant-based diets promote ill health, quite the opposite. The first result is a trial that concludes those that followed a plant-based diet (ad libitum consumption of “whole grains, legumes, vegetables and fruits”) resulted in “significant improvements in BMI, cholesterol and other risk factors.” If you’d rather use the search terms vegetarian diet, you get 216 results.

The only thing that Taubes can use to defend his use of that claim is the adjective “meaningful,” but only if he wants to claim that literally all of the trails that were conducted were personally meaningless to him for some reason.

Taubes even tries to argue that salt does not lead to hypertension, it’s actually insulin because insulin must be the cause of all human’s chronic diseases, I guess. Page 164:

By the mid- 1990s diabetes textbooks, such as Joslin’s Diabetes Mellitus, described chronically elevated levels of insulin as likely to be “the major pathogenic defect initiating the hypertensive process” in patients with type 2 diabetes.

Not surprisingly, Taubes takes this quote waaaay out of context, such that he changes it’s intended meaning. Here’s the full quote:

Should hyperinsulinemia be the major pathogenetic defect in initiating the hypertensive process in patients with NIDDM, it is unlikely that it sustains the hypertension indefinitely. (25)

Some of this stuff I don’t even know how to respond to it. Sometimes he sounds like an alien. Page 167:

Eating abundant fruits and vegetables, as a recent New York Times article said, “can promote health,” as though these foods contain indispensable ingredients that work to make us healthy and keep us healthy. By this logic, the more fruits and vegetables in a diet, the better.

Ummm…. Yeah. Yep.

At the end of chapter 12 Taubes actually brings up the climate change problem, but only briefly. His position is basically the following: Does eating animals contribute to climate change? Probably. But can we really know for sure? No, we can’t. So just go ahead and eat the cows. He doesn’t do the least bit of effort to actually investigate or evaluate the science. I imagine that is because he has done so and the results are not favorable to his keto diet promotion, therefore he pretends like it’s unknowable.

Much of the remainder of the book is devoted to unsourced and unverified anecdotes, testimonials, and claims from low-carb proponents that it really works for me! Or It really works for my patients! One example is Sean Bourke, a physician who owned a chain of for-profit weight loss clinics:

Bourke, a Yale- educated emergency medicine physician, is the cofounder of the dozen JumpstartMD clinics in the San Francisco Bay Area. He told me that some fifty thousand patients had come to these clinics looking for advice on controlling their weight since he opened the first one in January 2007. This is, in effect, his clinical experience. (With his JumpstartMD colleagues and a collaborator at the Lawrence Berkeley National Laboratory, Bourke recently published a paper in the Journal of Obesity on the results from over 24,000 of these patients, for whom he had complete clinical data.

The paper is not cited, but I believe I have found it and want to note a couple things: there is not data from over 24,000 patients included, the diets are explicitly low-calorie (spoiler: that’s the real weight loss sauce, not the ratio of carbs to fat), and the attrition rate is pretty high. Half the patients drop out at 6 months and about 2/3rds are gone after one year. I thought that adherence to LCHF was supposed to be easier.

Refs

1.          Astwood EB. The Heritage of Corpulence. Endocrinology [Internet]. 1962 Aug;71(2):337–41. Available from: https://academic.oup.com/endo/article-lookup/doi/10.1210/endo-71-2-337

2.          Bruch H. Eating disorders; obesity, anorexia nervosa, and the person within. [Internet]. New York,; 1973 [cited 2020 Dec 9]. Available from: http://hdl.handle.net/2027/mdp.39015000282544

3.          Bruch H, Touraine G. Obesity in Childhood: V. The Family Frame of Obese Children. Psychosom Med [Internet]. 1940 Apr;2(2):141–206. Available from: http://www.psychosomaticmedicine.org/content/2/2/141.abstract

4.          Passmore R, Swindells YE. Observations on the respiratory quotients and weight gain of man after eating large quantities of carbohydrate. Br J Nutr [Internet]. 1963;17:331–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14045336

5.          DuBois EF. Basal metabolism in health and disease [Internet]. Philadelphia: Lea & Febiger; 1936. p. 494 p. Available from: file://catalog.hathitrust.org/Record/002076603

6.          Mayer J. Overweight: Causes, Cost, and Control [Internet]. Englewood Cliffs, New Jersey: Prentice-Hall; 1968 [cited 2020 Dec 28]. Available from: https://books.google.com/books/about/Overweight_causes_cost_and_control.html?id=4bRktQEACAAJ

7.          Rosenbaum R. The great Ivy League nude posture photo scandal. New York Times [Internet]. Late Editi. 1995 Jan 15; Available from: https://www.proquest.com/newspapers/great-ivy-league-nude-posture-photo-scandal/docview/430004640/se-2?accountid=14784

8.          Vertinsky P. Embodying Normalcy: Anthropometry and the Long Arm of William H. Sheldon’s Somatotyping Project. J Sport Hist [Internet]. 2002 [cited 2020 Dec 16];29(1):95–133. Available from: https://www-jstor-org.offcampus.lib.washington.edu/stable/43610055?sid=primo&seq=1#metadata_info_tab_contents

9.          Sheldon WH. The varieties of temperament: A psychology of constitutional differences. [Internet]. New York and London: Harper and Brothers; 1942 [cited 2013 Jul 9]. Available from: http://archive.org/details/TheVarietiesOfTemperamentAPsychologyOfConstitutionalDifferences

10.        Wilder RM. The Management of Obesity. J Am Diet Assoc. 1930;6(2):91–100.

11.        Wertheimer E, Shapiro B. THE PHYSIOLOGY OF ADIPOSE TISSUE. Physiol Rev [Internet]. 1948 Oct 1;28(4):451–64. Available from: http://physrev.physiology.org/content/28/4/451.short

12.        Wilder RM. The Treatment of Obesity. Int Clin [Internet]. 1933 [cited 2020 Dec 30];4(43):1–21. Available from: https://babel.hathitrust.org/cgi/pt?id=mdp.39015070332682&view=1up&seq=17&q1=remarkable

13.        Greene R. The Practice of Endocrinology [Internet]. Philadelphia: Lippincott; 1951 [cited 2020 Dec 30]. Available from: https://catalog.hathitrust.org/Record/001580458

14.        Bray G, editor. Obesity in Perspective. Vol 2 [Internet]. Washington: U.S. Govt. Print. Off; 1975. Available from: https://catalog.hathitrust.org/Record/000040052

15.        Gay R. Hunger: A Memoir of (My) Body [Internet]. Harper Perennial; 2018 [cited 2021 Jan 1]. Available from: https://www.amazon.com/Hunger-Memoir-Body-Roxane-Gay/dp/0062420712

16.        The diet is 300 daily calories up to age 8, 500 to puberty, and 700 after puberty. That’s really low. That’s less calories than my infant son drinks in formula every day. But weight is lost “as if by magic.” Truly this is sorcery.

17.        He contentedly quotes another physician that prescribes LCHF diets who says her patients tell her “I don’t care if I die in ten years, I feel like crap today, I want to stop feeling like crap today.”

18.        Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, et al. A Randomized Trial of a Low-Carbohydrate Diet for Obesity. N Engl J Med [Internet]. 2003 [cited 2013 Jun 9];348(21):2082–90. Available from: http://www.nejm.org/doi/full/10.1056/NEJMoa022207

19.        Nordmann AJ, Nordmann A, Briel M, Keller U, Yancy Jr WS, Brehm BJ, et al. Effects of low-carbohydrate vs low-fat diets on weight loss and cardiovascular risk factors: a meta-analysis of randomized controlled trials. Arch Intern Med [Internet]. 2006 [cited 2013 Mar 2];166(3):285. Available from: http://archinte.ama-assn.org/cgi/reprint/166/3/285.pdf

20.        Hallberg SJ, McKenzie AL, Williams PT, Bhanpuri NH, Peters AL, Campbell WW, et al. Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study. Diabetes Ther [Internet]. 2018;9(2):583–612. Available from: https://doi.org/10.1007/s13300-018-0373-9

21.        Bradley U, Spence M, Courtney CH, McKinley MC, Ennis CN, McCance DR, et al. Low-fat versus low-carbohydrate weight reduction diets – Effects on weight loss, insulin resistance, and cardiovascular risk: A randomized control trial. Diabetes. 2009;58(12):2741–8.

22.        Grams J, Garvey WT. Weight Loss and the Prevention and Treatment of Type 2 Diabetes Using Lifestyle Therapy, Pharmacotherapy, and Bariatric Surgery: Mechanisms of Action. Curr Obes Rep. 2015;4(2):287–302.

23.        Hooper L, Summerbell CD, Higgins JP, Thompson RL, Clements G, Capps N, et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst Rev [Internet]. 2001;(3):CD002137. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11687015

24.        Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in saturated fat intake for cardiovascular disease. Cochrane database Syst Rev [Internet]. 2015 Jun 10;(6):CD011737. Available from: http://doi.wiley.com/10.1002/14651858.CD011737

25.        Christlieb AR, Krolewski AS, Warram JH. Hypertension. In: Kahn CR, Weir GC, editors. Joslin’s Diabetes Mellitus. 13th ed. Philadelphia: Lippincott Williams & Wilkins; 1994. p. 817–35.

*Editorial note 4/15/2021: In this sentence I originally wrote “Young states that she tested 1800 calorie diets on obese men with varying degrees of carbohydrate: 30 grams, 60 grams, and 104 grams. She then says that the highest level of carbohydrate was the best.” However, Young didn’t really claim it was “the best.” That was my paraphrase. I have added Young’s actual quote for clarity.

**Editorial note 4/15/2021: It was brought to my attention that I was being unfair to Taubes and may have been a bit misleading about the results myself. I amended this section to be more accurate. Previously I had written “Taubes blatantly lies about the results of a Cochrane review” and “the review does not examine low fat diets” but a strict interpretation of a replacement of saturated fat with CHO would be considered a de facto low fat diet.

The Case Against The Case Against Sugar

the-case-against-sugar

Introduction

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

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

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

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

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

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

 

Not the Introduction

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

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

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

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

* * *

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

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

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

* * *

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

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

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

* * *

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

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

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

* * *

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

page 33 golden holocaust

And now page 65 of CAS:

page 65 CAS

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

* * *

*Edit

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

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

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

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

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

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

* * *

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

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

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

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

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

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

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

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

* * *

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

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

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

 * * *

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

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

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

himsworth trio

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

Continuing with the above quote…

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

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

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

himsworth fat and mortality

 

 * * *

Page 108:

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

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

Continuing…

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

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

 * * *

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

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

And

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

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

publications in pubmed of masai

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

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

insull

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

japan graph

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

 * * *

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

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

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

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

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

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

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

(bolding mine, italics in the original)

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

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

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

Continuing on page 116, Taubes writes:

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

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

Taubes puts a coda on this bit of conspiracy:

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

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

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

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

 * * *

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

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

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

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

On page 117 and 118 Taubes writes:

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

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

alonso

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

 * * *

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

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

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

 * * *

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

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

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

Continuing with lies about scientists that cannot defend themselves:

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

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

ben-gates-glasses

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

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

 * * *

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

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

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

death

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

 * * *

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

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

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

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

yudkin seminal

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

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

 * * *

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

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

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

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

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

 * * *

Page 173:

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

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

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

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

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

 * * *

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

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

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

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

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

mrfit

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

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

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

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

 * * *

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

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

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

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

 * * *

Page 188:

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

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

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

 * * *

Page 190:

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

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

 * * *

Pages 204-205:

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

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

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

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

 * * *

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

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

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

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

So I typed exactly this and received the following result:

clinical trials dot gov

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

clinical trials.gov

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

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

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

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

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

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

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

 * * *

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

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

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

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

Take the following statement from page 217:

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

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

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

Taubes must be using those Benjamin Franklin glasses again.

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

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

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

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

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

navajo purchases

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

navajo meal pattern

 

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

 * * *

Page 216:

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

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

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

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

 * * *

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

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

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

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

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

 * * *

Taubes performs a little sleight of hand on page 223:

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

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

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

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

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

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

 * * *

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

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

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

 * * *

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

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

There’s also a footnote to this passage:

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

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

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

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

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

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

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

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

 * * *

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

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

 * * *

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

Gout

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

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

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

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

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

Hypertension

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

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

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

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

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

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

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

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

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

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

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

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

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

Cancer

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

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

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

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

Dementia

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

Conclusion

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

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*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?