Good Calories, Bad Calories

This model also explains, as Pete Ahrens suggested in 1961, why high-carbohydrate diets appear innocuous in populations that are chronically undernourished. This was inevitably the case with those Southeast Asian populations extolled by Keys and others for their low total-cholesterol levels and apparent absence of heart disease. Such populations lived on carbohydrate-rich diets out of economic necessity rather than choice. Their diets were predominantly unrefined carbohydrates because that’s what they cultivated and it was all they could afford. As Ahrens had noted, the great proportion of individuals in such populations barely eked out enough calories to survive. This was true not only of Japan in the years after World War II, but of Greece and other areas of the Mediterranean as well. If these populations indeed had low cholesterol and suffered little from heart disease, a relative lack of calories and a near-complete absence of refined carbohydrates would have been responsible, not the low intake of saturated fat. In developed nations—the United States, for example—where calories are plentiful, it would be the carbohydrates pushing our metabolisms toward the production of atherogenic lipoproteins. Here, too, the saturated fat in the diet is of little significance.

Chapter Ten

THE ROLE OF INSULIN

The suppression of inconvenient evidence is an old trick in our profession. The subterfuge may be due to love of a beautiful hypothesis, but often enough it is due to a subconscious desire to simplify a confusing subject. It is not many years ago that the senior physician of a famous hospital was distinctly heard to remark, sotto voce, “medicine is getting so confusing nowadays, what with insulin and things.” It is a sentiment with which almost everybody who qualified more than a quarter of a century ago is likely to sympathize…. But ignoring difficulties is a poor way of solving them.

RAYMOND GREENE, in a letter to The Lancet, 1953

Scientific progress is driven as much by the questions posed as by the tools available to answer them. In the 1950s, when Ancel Keys settled on dietary fat and cholesterol as causes of heart disease, he did so because he sought to understand the disparity in disease rates among nations and what he believed was a growing epidemic of coronary heart disease in the United States. Those investigators whose research would eventually evolve into the science of metabolic syndrome—the physiological abnormalities common to obesity, diabetes, and heart disease—had different questions in mind. Why are the obese exceptionally likely to become diabetic and vice versa? Why is atherosclerosis so common with both diabetes and obesity? Are these coincidental associations, or do obesity, heart disease, and diabetes share a common cause?

In the decade after World War II, Jean Vague, a professor of medicine at the University of Marseille in France, extended these associations to what he called “android obesity,” where the excess fat sits predominantly around the waist. (“Beer bellies” are the archetypal example.) Vague reported that android obesity was associated with atherosclerosis, gout, kidney stones, and adult-onset diabetes. He speculated that some type of hormonal overactivity led to overeating, and that, in turn, to an increased secretion of insulin to store away the excess calories in fat tissue. This excessive secretion of insulin might then, over the years, cause what he called pancreatic depletion and thus diabetes. A similar hormonal overactivity, Vague suggested, might cause atherosclerosis, either directly or by inducing the secretion of “lipoprotein molecules,” as John Gofman was proposing, which would then cling to the artery walls and begin the accumulation of fats and cholesterol that is characteristic of atherosclerotic plaques.

Gofman also sought out common mechanisms to explain the association between obesity and heart disease. Because weight gain was associated with both higher blood pressure and increased triglyceride-rich VLDL, he suggested, that alone could explain why the obese had an increased risk of heart disease. But Gofman did not speculate whether weight gain elevated blood pressure and triglycerides or whether the same mechanism increased our weight and raised our blood pressure and triglycerides.