I’ve been asked by a number of people to review Gary Taubes’s new book, The Case Against Sugar. I reluctantly agreed that it would probably be a good idea for me to do so. In this post, I’ll provide something that is not available anywhere else (to my knowledge): a review of the book from the perspective of a former researcher who is an expert in some of the topics it discusses. [update 7/22/17: there is now a second detailed expert review of the book available here]

The Case Against Sugar is a journey through sugar history and science that argues the point that sugar is the principal cause of obesity, diabetes, coronary heart disease, and many other common noncommunicable diseases. This differs from the prevailing view in the research and public health communities that obesity and noncommunicable disease are multi-factorial, with refined sugar playing a role among other things like excess calorie intake, physical inactivity, cigarette smoking, alcohol and illegal drug use, and various other diet and lifestyle factors. I side with the latter view. In case anyone is wondering, I’ve never had any contact with the sugar industry and I have no other relevant conflicts of interest.

I’ll break the review into two parts, the first covering the historical aspects of the book, and the second covering its scientific aspects.

The History

Taubes excels at constructing detailed historical narratives to make his points. In The Case Against Sugar, he presents a colorful and informative history of sugar and the sugar industry. He also provides a history of the use of sugar in tobacco processing and how it may have contributed to the rise of cigarette smoking, which I wasn’t aware of.

His discussion of the history of research on sugar, dietary fat, obesity, and noncommunicable disease is less compelling due to its one-sided nature. For example, The Case Against Sugar portrays an epic struggle decades ago between researchers who believed that saturated fat was the primary cause of coronary heart disease, and those who believed that sugar was. These views are embodied by the American researcher Ancel Keys and the British researcher John Yudkin, respectively.

Taubes makes hay of the fact that Keys was supported in part by the sugar industry, painting Yudkin as a righteous underdog standing up to a corrupt and aggressive Keys. Yet he never gives serious consideration to the strength of the evidence supporting each man’s beliefs, instead using a historical narrative to imply that Keys was a stooge of the sugar industry who unfairly won the argument due to his sharp elbows (whether or not this is true, it’s also true that Yudkin’s evidence was not as compelling as Keys’s). This tactic of using historical narratives as a substitute for evidence is one that recurs throughout the book.

In his haste to undermine Keys, Taubes neglects to mention that Yudkin had his own conflicts of interest: he was funded by the egg, edible oil, and dairy industries, all of which had an interest in pinning the blame for obesity and chronic disease on sugar (1). It’s interesting to note that if we substitute the egg, meat, and dairy industries for the sugar industry, Taubes’s arguments about the corrupting influence of industry on science sound very similar to those that are made by certain people in the vegan community about animal foods.

The truth is that both sides have somewhat of a point, but both are also exaggerated and incomplete. Each industry jockeys to promote its own interests, and those that are sufficiently well heeled often do so by supporting research. This includes the sugar industry, as well as the egg, edible oil, meat, and dairy industries. If Taubes wants to decry research funded by the sugar industry, he should apply the same principle to research funded by other industries, including Yudkin’s. Yet Yudkin gets a pass, while Taubes probes every nook and cranny of history to uncover the dastardly Keys’s conflicts of interest.

A related point is that in 2017, research institutions and reputable scientific journals have policies in place for disclosing and limiting conflicts of interest. These policies aren’t perfect, but they’re much better than what we had two decades ago. In contrast, the book industry has no policies for managing the conflicts of interest of its authors, and it also has virtually no accountability for what it publishes. Taubes points his finger at others while never disclosing his own conflict of interest, which is that his fame and fortune rely on perpetuating his controversial ideas to an audience that has little basis for evaluating them.

In chapter 8, The Case Against Sugar discusses the process that led the Food and Drug Administration to designate sugar as “generally recognized as safe” (GRAS). GRAS is a designation that is given to substances that have been consumed for a long time and are not overtly toxic, like vinegar. Taubes implies that sugar was unjustly given GRAS status by the FDA due to food industry influence, but this reveals a lack of understanding of the GRAS designation (he repeated this claim in a recent article; 2). The purpose of the FDA is not to be a nanny that prevents us from eating food that has long-term health consequences, and consequently GRAS status doesn’t imply that a substance supports leanness or health when consumed regularly. You can eat your way to obesity and heart disease on an all-GRAS diet: Everything in pizza, white bread, French fries, soda, ice cream, potato chips, and bacon is GRAS. By all logic, sugar should be GRAS, but that doesn’t make it healthy.

Also, revoking GRAS status means that a substance cannot be sold as food. Is Taubes suggesting that the FDA should have made the sale of sugar illegal, yet continue to allow us to buy cigarettes, whiskey, and cheese crust pizza? That seems a bit extreme.

The Science

Scientifically, The Case Against Sugar suffers from a condition Steven Pinker has called the “Igon Value Problem”. This term describes the tendency of certain science journalists to arrive at obtuse conclusions due to a superficial understanding of their subject matter (3). There are many examples of this in The Case Against Sugar, but the underlying theme is that Taubes misunderstands (or chooses not to apply) the scientific method itself.

Evidence of this can be found on the first page:

The purpose of this book is to present the case against sugar– both sucrose and high-fructose corn syrup– as the principal cause of the chronic diseases that are most likely to kill us, or at least accelerate our demise, in the twenty-first century… If this were a criminal case, The Case Against Sugar would be the argument for the prosecution.

Trials proceed by very different principles than science does. The prosecutor is not expected to present a balanced case– he is expected to be biased against the defendant. What ensures balance in the legal process is the inclusion of a defendant who is equally biased in favor of himself. Yet in The Case Against Sugar, the defendant is nowhere to be found. What results is an argument that is carefully crafted to support the prosecution, while facts that support the defense are omitted, minimized, or misrepresented.

This is the opposite of the scientific method, which emphasizes objective analysis of facts and seeking evidence that might falsify your beliefs. This might be forgiven in a popular book, but in this case Taubes attempts to take the scientific high ground, portraying his views as rational and evidence-based and those prevailing in the scientific community as biased, irrational, and corrupt.

The Igon Value Problem doesn’t take long to rear its ugly head. In the introduction, Taubes deploys an argument that he believes is sufficient to negate most of the scientific literature on obesity and chronic disease… drumroll please… Occam’s Razor:

If this were a criminal investigation, the detectives assigned to the case would start from the assumption that there was one prime suspect, one likely perpetrator, because the crimes (all the aforementioned diseases [including obesity, diabetes, cardiovascular disease, Alzheimer’s, and several others- SG]) are so closely related. They would only embrace the possibility that there were multiple perpetrators when the single suspect was proved insufficient to explain all the evidence. Scientists know this essential concept as Occam’s Razor.

What if I were to tell you that the structure of DNA is actually a single straight strand rather than a double helix? Would you believe me just because my hypothesis is simpler than the conventional one? Of course not, and for good reason: evidence suggests the more complex hypothesis is correct. The truth is that Occam’s Razor is a weak argument that only applies when two hypotheses are equally well supported (or equally unsupported). As soon as one hypothesis has a stronger evidence basis than another, Occam’s Razor becomes irrelevant. Yet for Taubes, this flimsy argument is sufficient to throw most of the relevant scientific literature out the window, besides, of course, a few tidbits that support the prosecution.

Besides its misapplication of Occam’s Razor, the passage above manifests the Igon Value Problem in a second way: the diseases in question are actually not all correlated with one another, or even with sugar intake. Statistics demonstrating this are readily available. For example, sugar intake is higher today in the US than it was in the 1970s, and while obesity has increased three-fold, coronary heart disease mortality has declined by over 60 percent (4, 5, 6). Taubes neglects to inform the reader that sugar intake has been declining since 1999 in the US, a period over which obesity and diabetes rates have increased substantially (7, 8, 9).

Taubes argues that sugar is the only factor that reliably shows up when a culture develops Western noncommunicable diseases, supporting the point with examples of cultures that adopted sugar-rich diets and became ill. Yet he makes no effort to look for a counterexample that could refute his argument: a traditionally-living culture that has a high intake of sugar and does not suffer from Western noncommunicable diseases. If such a culture can be found, this piece of evidence is sufficient to reject Taubes’s argument that sugar reliably associates with the onset of these diseases in a population. Let’s do Taubes’s research for him. A well-studied Tanzanian hunter-gatherer tribe called the Hadza gets 15 percent of its average year-round calorie intake from honey, plus fruit sugar on top of it. This approximates US sugar intake, yet the Hadza do not exhibit obesity, cardiovascular disease, or any of the other disorders Taubes attributes to sugar (10, 11). In fact, many hunter-gatherer groups relied heavily on honey historically, including the Mbuti of the Congo whose diet was up to 80 percent honey during the rainy season (10). Yet they do not exhibit obesity or insulin resistance (12).

The Igon Value Problem frequently appears in Taubes’s portrayal of opposing viewpoints from the scientific community. For example, Taubes repeatedly asserts that researchers, physicians, and nutritionists simply assume that obesity causes diabetes. In fact, there is abundant and compelling evidence supporting this “assumption”, and such evidence is only a few keystrokes away on Google Scholar (13, 14, 15, 16). Yet it receives no mention in the book. Instead, the reader is gravely informed that today’s scientists, physicians, and nutritionists simply inherited the idea from the previous generation of scientists, who themselves essentially plucked it out of thin air. This is followed by Taubes’s alternative viewpoint, which seems downright reasonable by comparison despite the weak evidence offered to support it.

Here’s a third example. Taubes upbraids the research community for its belief that body fatness is determined by calorie intake, rather than the impact of foods on insulin. He supports the latter proposition with semi-anecdotal observations from Africa suggesting that a group of people eating a high-sugar diet supplying “as little as sixteen hundred calories per day” were sometimes obese and diabetic.

A person who actually wants to get to the bottom of this question should conduct their investigation in a very different manner. The first order of business is to look up the relevant metabolic ward studies, which are the most tightly controlled diet studies available. These studies consistently show that calorie content is the only known food property that has a meaningful impact on body fatness. This is true across a wide range of carbohydrate-to-fat ratios and sugar intakes, and a correspondingly wide range of insulin levels (17).

What makes Taubes’s oversight so extraordinary is that he was involved in funding one of these metabolic ward studies, which compared two diets that differed more than tenfold in sugar content. The results showed that a 25 percent sugar, high-carbohydrate diet caused slightly more body fat loss than a 2 percent sugar, very-low-carbohydrate (ketogenic) diet of equal calories (18). Despite these clear and consistent findings, Taubes continues to insist that calorie intake is not an important determinant of body fatness, and he offers the reader questionable evidence in support of this while omitting high-quality evidence to the contrary. All while exuding righteous indignation about the scientific community’s misguided beliefs.

A fourth and final example of the Igon Value Problem. Taubes states that obesity researchers have been barking up the wrong tree since World War II because they are so focused on calories that they have no interest in the influence of hormones on body fatness. This is another instance in which a cursory Google Scholar search could have prevented a colossal mistake: the search term “leptin obesity” alone returns 385,000 results, all since 1994. In fact, researchers are extremely interested in hormonal influences on body fatness, which is why the topic has been studied extensively and so many relevant hormones have been identified (for example, leptin, ghrelin, glucagon, GLP-1, epinephrine, and amylin).

Taubes’s revisionist history of obesity research allows him to argue that the reason why insulin’s central role in obesity hasn’t been uncovered is that no one is looking. The truth is that researchers have examined insulin up, down, and sideways, and found that it is unlikely to contribute to common obesity. Yet this evidence isn’t discussed in The Case Against Sugar, nor in Taubes’s previous book Good Calories, Bad Calories— it is simply assumed not to exist.

In the final chapters of The Case Against Sugar, Taubes argues that insulin resistance is the primary cause of common noncommunicable diseases like coronary heart disease, diabetes, Alzheimer’s disease, and gout, and that sugar is the primary cause of insulin resistance (he goes out of his way to emphasize that dietary fat, calorie intake, and physical activity are irrelevant). The former proposition can be reasonably argued, while the latter is a case of Taubes cramming a square peg into a round hole. Taubes leans heavily on the animal literature, correctly stating that high intakes of refined sugar sometimes cause insulin resistance in rodent models. But he omits two inconvenient facts: First, sugar is not very fattening in rodents, particularly relative to added fats like lard; and second, added fats also tend to cause more severe insulin resistance than sugar (19, 20, 21, 22, 23, 24).

The combination of added fat and sugar is even more harmful than fat alone, and the most fattening and insulin-resistance-inducing diet of all is to give rodents free access to a variety of highly palatable human foods (25, 26). Sugar alone cannot remotely explain the effects of palatable human food on body fatness and health in rodents– or in humans– although it does contribute.

The mechanism Taubes proposes for how sugar causes insulin resistance is that the fructose component, making up 50 percent of table sugar, overloads the liver, rendering it less sensitive to the insulin signal, and this eventually causes whole-body insulin resistance. Taubes is correct about the impact of fructose on the liver, although again he leaves out critical information: realistic doses of fructose primarily overload the liver if a person is overconsuming calories and liver energy stores are already full (25). This is probably why hunter-gatherer groups such as the Hadza can eat as much sugar as Americans and not develop health problems (26, 27). These facts do not fit Taubes’s narrative that calories are irrelevant, and they are not shared with the reader.

Here are two other inconvenient facts that Taubes omits from his finely crafted narrative: Both sedentary behavior and overeating calories cause pronounced insulin resistance, and conversely, physical activity and eating fewer calories powerfully combat insulin resistance (28, 29, 30, 31). Physical activity almost instantaneously increases the insulin sensitivity of muscle tissue, which is a major determinant of whole-body insulin sensitivity. Again, abundant evidence of this is only a few keystrokes away on Google Scholar, yet Taubes dismisses the idea out of hand.

During the course of his argument, Taubes uses sleight of hand to portray the views of researchers as more favorable to his ideas than they really are. For example, in chapter 9 he argues that obesity and physical inactivity are not the real causes of insulin resistance, rather sugar causes both insulin resistance and obesity. To support his theory, he invokes the work of Stanford endocrinologist Gerald Reaven, claiming that he “was bringing back the notion that carbohydrates were bad”. This seemed mighty fishy to me, so I looked up what Reaven actually thinks. Here’s a quote from a review paper he wrote (emphasis mine) (32):

Since being overweight/obese and sedentary decreases insulin sensitivity, it is not surprising that the prevalence of the manifestations of the [insulin resistance syndrome] is increasing at a rapid rate. From a dietary standpoint, there are two approaches to attenuating the manifestations of the [insulin resistance syndrome]: (a) weight loss to enhance insulin sensitivity in those overweight/obese individuals who are insulin resistant/hyperinsulinemic; and (b) changes in macronutrient content of diets to avoid the adverse effects of the compensatory hyperinsulinemia [i.e., replacing carbohydrate with unsaturated fat- SG].

Taubes neglects to inform the reader that Reaven thinks obesity and physical inactivity cause insulin resistance, and that these factors explain the rising prevalence of metabolic disease– precisely what Taubes is arguing against in that passage. Furthermore, Reaven explains in no uncertain terms that he does not think insulin resistance causes weight gain.

Rather than straightforwardly reporting what Reaven’s studies revealed and what the man believes, Taubes takes Reaven’s argument that people with existing insulin resistance may benefit from carbohydrate restriction and warps it to make it appear as if Reaven supports Taubes’s beliefs about the origins of insulin resistance. In doing so, Taubes flips Reaven’s position by 180 degrees. If you want the real scoop on Reaven’s important work, go straight to Reaven’s book Syndrome X.

I’ll end this section on a positive note. In The Case Against Sugar, Taubes finally acknowledges the importance of food reward in eating behavior and obesity. As a reminder, food reward is the seductiveness of certain foods (like ice cream and chips) that motivates us to eat them, and as common sense suggests, it’s an important influence on what and how much we eat. Previously on his blog, Taubes argued at length that food reward has nothing to do with obesity, and (remarkably) that the brain itself is unimportant (33). In The Case Against Sugar, he argues that the seductiveness of sugar is precisely why we eat it, ultimately leading to obesity. He even briefly discusses dopamine, the chemical mediator of reward, acknowledging both the importance of food reward and the brain generally in food intake and obesity. This is progress.

Conclusion

Science is imperfect, and scientists are as well. Pioneers such as John Ioannidis, Brian Nosek, Vinayak Prasad, Adam Cifu, Chris Chambers, and David Allison are making a good faith effort to identify flaws in the scientific process and address them. Journalists have an important role to play here as well, by helping to identify problems and raising awareness about how to fix them. Taubes also views science as flawed, but primarily where it disagrees with his personal beliefs. Rather than contribute to the solution, Taubes adds to the problem by promoting an unscientific thought process that systematically excludes opposing evidence.

To answer the question posed in the title, refined sugar is bad, although not the singular cause of all humankind’s ills. A core principle of journalism is the accurate, objective, and complete transmission of pertinent facts to the reader. The Case Against Sugar is a journey through sugar history and science that is heavily distorted through the lens of Taubes’s personal beliefs. By this metric, it is not journalism, but advocacy. To a general audience that has little basis for evaluating its claims, the book will be misleading. Yet for readers who are willing to take The Case Against Sugar with a case full of salt, it does contain some interesting history.