Third, whatever the flaws in Gary Taubes's books, he is ultimately convincing on two points:
Sugar is very, very bad. I will say more below on why convincing people of that is an important accomplishment.
What the nutrition establishment is telling us needs to be closely examined and cross-checked by scientists outside the nutrition establishment. It is very unwise to simply trust the nutrition establishment.
On the second point, what Stephan Guyenet says about nutrition scientists is not very reassuring. Gary Taubes emphasizes that many of the scientists who tried to exonerate sugar were in the pay of the sugar industry. Stephan does not inspire confidence in the interpretations made by nutrition scientists with his response that a key scientist who attacked sugar was in the pay of the egg, edible oil, and dairy industry. Stephan does say
... 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.
But even if the conflict-of-interest is currently completely solved (which I doubt) there is hysteresis (history dependence) in science. Points of view that became dominant in the industry-funding free-for-all period still affect where the science is coming from today.
Let me turn to a more point-by-point discussion of Stephan's post.
A. In his second paragraph Stephan writes:
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.
Here Stephan seems to be saying "Sensible people like me realize that sugar is one of several coequal causes of obesity, diabetes, heart disease etc., not the only cause." But walking down the aisles of any grocery store and comparing the number of "lowfat" offerings to the number of "no sugar added" offerings makes it clear that in the popular imagination the dangers of sugar are rated far, far below the dangers of dietary fat. So there is a lot of work to be done to get people's perception of the dangers of sugar up to the level of being "sugar is bad on a par with four or five other things" that Stephan seems to give as his own view. If Gary overstates the harm from sugar (and I will argue Gary overstates the harm from sugar less than Stephan thinks) it may show Gary's inferiority to real scientists (a key part of Stephan's message), but it does not make Gary a danger to public health; given the public's underestimation of the dangers of sugar, Gary's overstatement is a countervailing error.
B. A little further down, this passage is an important part of Stephan's argument:
... 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).
Here, Gary has made himself a real-life straw man by pushing too hard the idea that sugar is the one and only problem. Here I won't defend Gary; let me defend instead my own view—which draws on the arguments in Gary's books, but interprets them by my own lights. In my view, which is very much in the spirit of what Gary is saying but I hope is more subtle, the two main causes of the rise in obesity are:
The shift toward consumption of foods that are high on the insulin index. (See "Forget Calorie Counting; It's the Insulin Index, Stupid.") Many of these are high in sugar, but some are not. For example, processed "lowfat" foods are higher on the insulin index than the corresponding full fat foods. So the spread of lowfat foods could be contributing to the rise in obesity even in a period when sugar consumption itself is declining somewhat.
The expansion of the "eating window" within each day, with the corresponding shortening of the biggest chunk of time with no food consumption. (See "Stop Counting Calories; It's the Clock that Counts.")
Unfortunately, good data on the timing of food consumption for a representative sample is not available, but having lived through the 1970s and all the decades after (I was born in 1960), it is my sense that attitudes have become much more favorable to snacking than they were when I was young. So I suspect that the average daily eating window has, in fact lengthened since the 1970s.
Looking over the last 120 years instead of just the last 45, there is little question that consumption of foods high on the insulin index (most of which have their insulin index raised by their sugar content) has gone up in a big way since the late 19th century.
C. Stephan's next paragraph is:
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).
What are I thought were some of Gary's best arguments were his arguments about the likely role of sugar and flour in bringing to indigenous populations what in an age before political correctness were called the "Diseases of Civilization." These discussions about the transition to the "Diseases of Civilization" or "Western Diseases" are some of the best parts of Gary's books. Stephan does not discuss all of the places where Gary's historical argument based on the transition from indigenous diets to Western diets looks good, and I cannot do it justice here.
Gary argues that other than Western diets adding sugar and flour, every other aspect of Western diets was duplicated by at least some indigenous diet, so sugar and flour must be the culprit. This is a strong argument. However, I would add in the possibility that people in almost every indigenous population had substantial chunks of time when they had no food consumption. Whether their fasts were involuntary or not, they probably fasted reasonably frequently. So in my view, the key aspects of Western diets that brought Western Diseases were sugar, flour and a reduction in periods of time with no food consumption.
The protective effects of fasting could be crucial for explaining the lack of Western diseases among the Hadza and the Mbuti that Stephan points to as evidence against the evils of sugar. Following Jason Fung's logic that I lay out in "Obesity Is Always and Everywhere an Insulin Phenomenon," the periods when the Hadza and Mbuti ate a lot of sugar would have been high-insulin periods, but those high-insulin periods would have been counteracted by the low-insulin periods of low or zero food consumption. I wouldn't recommend to anyone an alternation between high sugar consumption and fasting—it would be quite painful because sugar consumption when you do eat makes fasting a lot harder (or so I believe based on my own experience and hope to demonstrate for other people someday if no one else has)—but the fasting component might be sufficient to avoid the worst of the Western Diseases.
D. Next, after invoking the "Igon Value Problem," to remind his readers of the greater merit of scientists as compared to journalists, Stephan writes:
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.
If you actually read the abstracts of the four papers that Stephan flags, and assume that there isn't something brilliant in the papers that the authors didn't bother to put in the abstracts, they don't contradict the idea that both obesity and diabetes are caused (probabilistically) by chronic high insulin levels rather than diabetes being caused by obesity per se. This distinction matters for the reason I give in my post "Obesity Is Always and Everywhere an Insulin Phenomenon":
There is an interesting theoretical case in which chronically high insulin levels would be de-linked from obesity. Suppose the fat cells of someone caught in a carb rebound cycle became resistant to insulin, but his or her muscle cells retained their normal sensitivity to insulin. Because the fat cells would not respond much to the insulin signal telling them to take in glucose from the bloodstream and convert it into triglycerides and then fat, he or she would not gain much weight. But to keep blood glucose levels in line, insulin levels would have to go up even further to get the job done just from the muscle cell response to insulin. If high insulin levels cause most of the chronic diseases we associate with obesity, then while still normal in weight, he or she would be at risk for all of these chronic diseases. This is someone others might envy for being able to eat anything without gaining weight—right up until he or she died of a heart attack.
The abstracts emphasize two results:
Both of these results are consistent with the idea that it is chronically high levels of insulin that tend to cause both obesity and diabetes, rather than obesity per se causing diabetes. There is a third result mentioned:
Although quite indirectly, if anything this supports the idea that sugar tends to cause diabetes.
E. Gary Taubes is at his most confused when discussing calories in/calories out. This is one of the first things I had to straighten out theoretically in my own mind after readings Gary's books. That effort is reflected in the title of my early foray into a Twitter discussion on diet: "How the Calories In/Calories Out Theory Obscures the Endogeneity of Calories In and Out to Subjective Hunger and Energy." In my view, two key channels through which high insulin makes people fat are
making people hungry so they want to eat more and
making people feel sluggish so they want to do less activity.
Keep that in mind as you read the following passage from Stephan:
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.
In a metabolic ward, the number of calories consumed is so tightly controlled that the first channel can't operate and the range of possible activity is probably less than normal, reducing the magnitude of the second effect. Unless a metabolic ward study is exceptionally high-powered, it may then be unable to detect the remaining effects on activity levels plus the reduction in resting metabolism that high insulin levels might lead to.
On the low power of metabolic ward studies to identify effects, this quotation from the second flagged study is revealing:
The abstract of the first flagged study doesn't mention sample size at all, and the rest of the paper is still behind a paywall. (If funded by the government, I think it has to come out from behind its paywall a year or so after publication, which is in a couple of months.)
Gary Taubes' invocation of folks in Africa who sometimes become obese or diabetic on a diet of 1600 calories with a lot of sugar is only a research topic. I wouldn't dismiss the possibility too quickly, but it needs verification or disproof, perhaps with a study putting people on a 1600 calorie high-sugar diet for a longer period of time. If I were on a human subjects review panel, I don't know that I would approve such a study. If I am right about that, it speaks to people's beliefs (correct or not) that sugar is likely to be harmful.
F. After scolding Gary for not recognizing the great interest diet scientists have had in hormones, including insulin, Stephan writes this about insulin and sugar:
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.
Let me emphasize that Stephan thinks the idea "that insulin resistance is the primary cause of common noncommunicable diseases like coronary heart disease, diabetes, Alzheimer’s disease, and gout ... can be reasonably argued." What Stephan questions is the role of sugar in causing insulin resistance.
I am inclined to agree with Stephan that rodent data do not support the idea that sugar is more harmful than fat (though it does seem to support the idea that fat plus sugar is worse than fat alone). But I am struck by the possibility that rodents might be much better adapted to highcarb diets than humans are. This may even allow them to eat sugar with less harm than humans. Am I wrong in thinking that for many, many generations rodents outside laboratories have tended to eat highcarb diets? The "many, many generations" is important. Even if rodents had only been eating highcarb diets for the same number of years as humans, the larger number of generations per century would have allowed rodents that hang around humans to be naturally selected to tolerate highcarb diets more than long-generationed humans.
Every discipline tends to develop conventions that the best research that is feasible for the typical researcher should be treated with respect. But if the best experimental research that is feasible is studies on rodents that might be much better adapted to highcarb diets than humans and small-sample-size human studies, it shouldn't make it any more persuasive to those of us who are not acculturated diet scientists for them to say "This is the state of the art."
G. Stephan's next paragraph is consistent with my hypothesis that involuntary fasting protected the Hadza from Western Diseases despite their high sugar consumption:
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.
Of course, Stephan is emphasizing the number of calories consumed. But I think of the number of calories consumed as highly endogenous. Outside of metabolic wards—and a few people with freakishly strong self-control applied to a misguided task—the number of calories people consume (relative to how big they are) is mostly determined
by how active they are—or more generally, by how many calories they burn
by what types of food they eat
by when they eat.
Because eating sugar or other high-insulin-index foods makes people feel hungry a couple of hours later, sugar helps induce the food overconsumption that in combination with the fructose from the sugar itself can overload the liver.
H. One of my contentions has been that for a high fraction of people, chronically high insulin levels lead to obesity. Chronically high insulin levels also lead at a somewhat later stage to insulin resistance, which leads the body to amp up its insulin production. Although exercise is, in general, disappointing to people hoping it will lead to weight loss (see the article I linked to on my blog with the retitling "Julia Belluz and Javier Zarracina: Why You'll Be Disappointed If You Are Exercising to Lose Weight, Explained with 60+ Studies"), it is effective in averting or reducing the great danger of insulin resistance—and through averting insulin resistance averting more severe weight gain. Gary goes overboard in talking down the benefits of exercise. Leaving aside what he says here about calories (where I would definitely recast things) on exercise, I think Stephan is more on target than Gary when he writes:
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.
I. After catching Gary in a serious misquotation, Stephan begins to wind down with this 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.
When people in the food industry want to redesign food to make it more attractive to us, one of the first things they usually do is to add sugar. But unlike Stephan, I don't think it is just about the immediate rewards of eating things with sugar in them. Those immediate rewards are there, and they matter. But in addition, sugar in any serious quantity causes an insulin spike that pushes blood sugar down below its normal range a little while later, leading to hunger.
Conclusion. I learned a lot from reading Gary Taubes's books. But I am also grateful to Gary Taubes as providing part of the trail that led me to Jason Fung's The Obesity Code. Jason Fung's The Obesity Code is one of the five books I featured in "Five Books That Have Changed My Life." Where I think Gary Taubes's work has value added even given the existence of Jason Fung's work is in providing a much more detailed history of nutritional thought. I would love to read a comparably detailed history of nutritional thought by another author with a different point of view that was as engaging as Gary Taubes's books, but I don't know of any.
Let me end by repeating the two things Gary Taubes convinced me of:
Link to the Facebook discussion of this post
Don’t miss my other posts on diet and health:
I. The Basics
II. Sugar as a Slow Poison
III. Anti-Cancer Eating
IV. Eating Tips
V. Calories In/Calories Out
VI. Other Health Issues
VII. Wonkish
Evidence that High Insulin Levels Lead to Weight Gain
Framingham State Food Study: Lowcarb Diets Make Us Burn More Calories
Anthony Komaroff: The Microbiome and Risk for Obesity and Diabetes
Evidence that Gut Bacteria Affect the Brain
Prevention is Much Easier Than Cure of Obesity
A Conversation with David Brazel on Obesity Research
Don't Tar Fasting by those of Normal or High Weight with the Brush of Anorexia
Magic Bullets vs. Multifaceted Interventions for Economic Stimulus, Economic Development and Weight Loss
Carola Binder: The Obesity Code and Economists as General Practitioners
The Heavy Non-Health Consequences of Heaviness
After Gastric Bypass Surgery, Insulin Goes Down Before Weight Loss has Time to Happen
Biohacking: Nutrition as Technology
A Low-Glycemic-Index Vegan Diet as a Moderately-Low-Insulin-Index Diet
David Ludwig, Walter Willett, Jeff Volek and Marian Neuhouser: Controversies and Consensus on Fat vs. Carbs
Analogies Between Economic Models and the Biology of Obesity
Layne Norton Discusses the Stephan Guyenet vs. Gary Taubes Debate (a Debate on Joe Rogan’s Podcast)
Sutton, Beyl, Early, Cefalu, Ravussin and Peterson: Early Time-Restricted Feeding Improves Insulin Sensitivity, Blood Pressure, and Oxidative Stress Even without Weight Loss in Men with Prediabetes
Critiquing `All-Cause and Cause-Specific Mortality with Low-Carbohydrate Diets' by Mohsen Mazidi, Niki Katsiki, Dimitri P. Mikhailidis, Naveed Sattar and Maciej Banach
VIII. Debates about Particular Foods and about Exercise
IX. Gary Taubes
X. Twitter Discussions
XI. On My Interest in Diet and Health
See the last section of "Five Books That Have Changed My Life" and the podcast "Miles Kimball Explains to Tracy Alloway and Joe Weisenthal Why Losing Weight Is Like Defeating Inflation." If you want to know how I got interested in diet and health and fighting obesity and a little more about my own experience with weight gain and weight loss, see “Diana Kimball: Listening Creates Possibilities” and my post "A Barycentric Autobiography. I defend the ability of economists like me to make a contribution to understanding diet and health in “On the Epistemology of Diet and Health: Miles Refuses to `Stay in His Lane’.”
