Good Calories, Bad Calories

In the past decade, the National Institutes of Health finally began funding randomized-control trials of 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 The Lancet phrased it 140 years ago—that cause fattening and obesity to begin with. Rather, the underlying assumption here, too, is that weight loss is caused inevitably by negative caloric balance—consuming fewer calories then we expend—and the investigators perceive these trials as testing whether carbohydrate restriction allows us to do so with more or less facility than semi-starvation diets that reduce calories directly or reduce fat calories specifically.

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