carbohydrate-restricted diets, as has the Dr. Robert C. Atkins Foundation, but these trials have been designed to test only the hypothesis that such diets can be used safely and effectively as a means to lose weight. The subjects are overweight and obese, and the studies compare weight loss and heart-disease risk factors with the results of low-fat or calorie-restricted diets. These trials are neither planned nor interpreted as tests of the hypothesis that it is the carbohydrates in the diet—“the sugar and starchy elements of food,” as
A direct test of the carbohydrate hypothesis asks the opposite question: not whether the absence of refined and easily digestible carbohydrates and sugars causes weight loss and is safe, but whether the presence of these carbohydrates causes weight gain and chronic disease. Such a trial would ideally be done with lean, healthy individuals, or with a spectrum of subjects from lean through obese, including those with metabolic syndrome and Type 2 diabetes. They would be randomized into two groups, one of which would consume the sugary and starchy elements of food and one of which would not, and then we would see what happens. We might randomly assign a few thousand individuals to eat the typical American diet of today—including its 140–50 pounds of sugar and high- fructose corn syrup a year, nearly 200 pounds of flour and grain, 130-plus pounds of potatoes, and 27 pounds of corn—and we could assign an equal number to eat a diet of mostly animal products (meat, fish, fowl, eggs, cheese) and leafy green vegetables. Since the latter diet would be relatively high in fat and saturated fat and calorically dense, the conventional wisdom is that it would cause heart disease and, perhaps, obesity and diabetes. So this would test the dietary-fat/cholesterol hypothesis of heart disease, as well as the carbohydrate hypothesis.
Such a trial would not be ideal, because many dietary variables would differ between the two groups—calories and fats among them. The subjects would also know what diet they’re consuming, and so the study would not be done blindly (although, ideally, the physicians who treated the subjects and the investigators themselves would be unaware). Nonetheless, it would be a good starting point. Would those eating the carbohydrate-rich diet be more likely to become glucose-intolerant, hyperinsulinemic, and insulin-resistant? Would they be fatter and have a greater incidence of obesity, metabolic syndrome, and Type 2 diabetes? Would they have more heart disease and cancer? Would they die prematurely or live longer? These are the questions we need to answer.
Another question that needs to be addressed urgently regards the health effects of sugar and high-fructose corn syrup alone. Since the 1980s, as we discussed (see Chapter 12), sugar and high-fructose corn syrup have been exonerated as causes of chronic disease on the basis that the evidence was ambiguous. Since then, virtually no studies have been funded; there have been no attempts to clarify the picture. Today I can imagine no research more important to the public health than rigorous, controlled trials of the long-term health effects of sugar and high-fructose corn syrup.
For the past decade, the National Institutes of Health has been funding trials that test whether “lifestyle modification” will prevent diabetes and metabolic syndrome. But these trials are done only in the context of the conventional wisdom on diet, obesity, and disease. In the largest of these trials to date, the $150 million Diabetes Prevention Program, the lifestyle modification included 150 minutes of exercise each week and a low-fat, low-calorie diet. The results confirmed that such a program of diet and exercise will indeed prevent or delay the appearance of diabetes and metabolic syndrome, but they said nothing about what aspect of this lifestyle modification was responsible. Was it the reduction in fat calories or total calories? Was it the exercise? Or was it a change in the type of carbohydrates consumed or a reduction in the total amount of carbohydrates? As we discussed (see Chapter 19), even if the goal of a diet is to reduce calories by preferentially reducing fat, it will inevitably cut back on carbohydrates as well, and usually sugars in particular.*138
The NIH is currently spending $200 million on a decade-long trial called Look AHEAD to test the hypothesis that if obese diabetics lose weight they’ll be healthier for the effort. This is “the largest, most expensive trial ever funded by NIH for obesity outcome research,” says the Baylor University psychologist John Foreyt, who is one of the trial’s principal investigators. But once again, the trial tests only the conventional wisdom. The goal of Look AHEAD is to induce five thousand obese diabetics to lose weight by the same lifestyle modification used in the Diabetes Prevention Program: cutting calories and fat calories, and exercising. If these obese diabetics do lose weight, and if they do end up healthier for it, we still won’t know whether it was the calories, the fat calories, the exercise, some combination of all three, or maybe just the carbohydrates or the sugar that made the difference. And we won’t know whether, if they restricted carbohydrates alone and ate protein and fat to their hearts’ content, they would have been healthier still.
Because these trials are planned as a test of only one hypothesis—and a poorly defined hypothesis at that—the research ensures that we won’t have the kind of reliable answers that we so desperately need. If the Diabetes Prevention Program had included a test of the carbohydrate hypothesis, the investigators could have compared the effect of a low-fat, low-calorie diet and exercise to the effect of carbohydrate restriction alone, and that would have told us whether it’s the carbohydrates or the calories and the sedentary behavior that cause these chronic diseases. If Look AHEAD were to include a test of the carbohydrate hypothesis, we might at least know the answer in another decade. It doesn’t, and we won’t.
The scientific obligation, as I said in the prologue, is to establish the cause of obesity, diabetes, and the chronic diseases of civilization beyond reasonable doubt. By doing so, we can take the necessary steps to prevent these disorders, rather than trying to cure them or ameliorate them after the fact. If there are competing hypotheses, it does us little good to test one alone. It does little good to continue basing public-health recommendations and dietary advice on association studies (the Framingham Heart Study and the Nurses Health Study are prominent examples) that are incapable of reliably establishing cause and effect. What’s needed now are randomized trials that test the carbohydrate hypothesis as well as the conventional wisdom. Such trials would be expensive. Like the Diabetes Prevention Program and Look AHEAD, they’ll cost tens or hundreds of millions of dollars. And even if such trials are funded, it might be another decade or two before we have reliable answers. But it’s hard to imagine that this controversy will go away if we don’t do them, that we won’t be arguing about the detrimental role of fats and carbohydrates in the diet twenty years from now. The public will certainly not be served by attempts of interest groups and industry to make this controversy go away. If the tide of obesity and diabetes continues to rise around the world, it’s hard to imagine that the cost of such trials, even a dozen or a hundred of them, won’t ultimately be trivial compared with the societal cost.
PROLOGUE: A BRIEF HISTORY OF BANTING
“…corpulence notoriety”: Anon. 1864b. “…size or weight”: Banting 1864:14.
“Knowing too that…”: Harvey 1872:69–70.
Banting began dieting: Banting 1864:18–19. “I have not felt better…”: Banting 1869.
United States, Germany: Banting 1869. “the emperor of the French…”: Anon. 1864c. “If he is gouty…”: Quoted in “banting” entry, OED 1989.
