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.

It was Margaret Albrink who extended Gofman’s observations to diabetes and set the stage for the science that would eventually evolve into our current understanding of metabolic syndrome. In 1931, Albrink’s advisers at Yale, John Peters and Evelyn Man, had set out to test the speculation voiced by Elliot Joslin, among others, that the atherosclerosis that plagues diabetics is caused by the fat and cholesterol in their carbohydrate-restricted diets. Man and Peters measured cholesterol in seventy-nine diabetics treated at Yale and reported in 1935 that the high-fat diets then prescribed for diabetics did not increase cholesterol: only nine of the seventy-nine had abnormally high cholesterol—the ones who “were extremely ill and profoundly emaciated.” Man and Peters continued collecting blood samples from diabetic patients for another quarter-century. In 1962, Albrink reported that the average triglycerides in these samples had increased by 40 percent over the years, and this was accompanied by a dramatic increase in the proportion of diabetics with atherosclerotic complications—from 10 percent in the early 1930s to 56 percent by the late 1950s. This coincided with a doubling of the proportion of carbohydrates in the prescribed diabetic diet and a reduction in fat calories from 60 percent to 40 percent, in accord with the increasing suspicion that fatty diets caused heart disease. (Joslin made a similar observation in 1959.) Albrink also confirmed Gofman’s observation that weight gain was accompanied by high triglyceride levels: adding ten pounds in middle age was associated with a 50 percent increase in triglycerides. Almost invariably, the greater the body fat, the higher the triglycerides in the circulation.