One interpretation of these results is that we could remove the carbohydrates from the diet and replace them with fat, and weight would be lost, perhaps without hunger, because insulin levels would drop, even if the total calories consumed did not. Kipnis’s results, as the University of Heidelberg clinicians Gotthard Schettler and Guenter Schlierf wrote in 1974, underlined the “necessity of restricting carbohydrates in obesity in order to restore insulin levels to normal, thus hopefully decreasing appetite and fat deposition….”

Kipnis, however, refused to believe that carbohydrates might cause obesity, or that avoiding carbohydrates might ameliorate the problem. When I interviewed him over thirty years later, he described the findings of his research as “very obvious.” “You manipulate the amount of carbohydrates you give a human,” he said, “you can manipulate his or her basal insulin level.” He also said that “insulin causes deposition of fat in fat cells.” But when it came to the cause of human obesity or weight gain, Kipnis rejected the relevance of these physiological phenomena. “Most people are obese because they eat more than they need to sustain the energy requirements that they have,” he said. “They eat too damn much.”

For the past quarter century, Americans have become progressively heavier and more diabetic. By 2004, one in three Americans was considered clinically obese; two in three were overweight. One in ten adult Americans had Type 2 diabetes—one in five over the age of sixty. It is now clear that the roots of this epidemic are evident even in infants and in the birth weights of newborns. Among middle-income families in Massachusetts, for example, as a team of researchers led by Matthew Gillman of Harvard reported last year, the prevalence of excessively fat infants increased dramatically between 1980 and 2001. This increase was most conspicuous among children younger than six months of age.

The probable explanation is that as women of childbearing age get heavier and more of them become diabetic, they pass the metabolic consequences on to their children through what is known technically as the intrauterine environment. The nutrient supply from mother to developing child passes across the placenta in proportion to the nutrient concentration in the mother’s bloodstream. If the mother has high blood sugar, then the developing pancreas in the fetus will respond to this stimulus by overproducing insulin-secreting cells. “The baby is not diabetic,” explains Boyd Metzger, who studies diabetes and pregnancy at Northwestern University, “but the insulin-producing cells in the pancreas are stimulated to function and grow in size and number by the environment they’re in. So they start over functioning. That in turn leads to a baby laying down more fat, which is why the baby of a diabetic mother is typified by being a fat baby.”