None of these experiments could explain what happened to the extra calories in those subjects who did not fatten easily, and why some of these subjects fattened more than others. Why is it that when two people eat a thousand calories a day more than they need to otherwise maintain their weight, and this overfeeding continues for weeks on end, one barely adds a pound of fat while the other puts on nearly ten? Bouchard and his colleagues used identical twins for their study to determine whether genetics contributed to this ability to fatten, and they reported that, indeed, pairs of twins gained similar amounts of weight and fat. “Genetic factors are involved” was all they could say. “These may govern the tendency to store energy as either fat or lean tissue and the various determinants of the resting expenditure of energy.”

Those engaged in the practice of animal husbandry have always been implicitly aware of the genetic, constitutional component of fatness. This is why they breed livestock to be more or less fatty, just as they breed dairy cattle to increase milk production, racehorses for speed and endurance, or dogs for hunting or herding ability. It’s conceivable, as the logic of overeating and sedentary behavior might suggest, that breeders of fat cattle or pigs have merely identified genetic traits that determine the will to eat in moderation and a propensity to exercise, but it strains the imagination that these are the relevant factors.

Much of the laboratory research on both obesity and diabetes is carried out on strains of rats and mice that grow reliably obese (sometimes monstrously so) eating no more than others that remain lean. The German physiologist Ingrid Schmidt says that when she first saw an example of an obese Zucker rat her immediate response was disbelief. “Up until that moment,” Schmidt recalls, “I thought if someone is too fat he should eat less. Then I saw that animal and thought, That’s incredible, one gene is broken, and this is the result. And once they get fat, you have the same problem you do with fat humans: everything is changed, and you have no idea what’s the cause and what’s secondary to this underlying defect.”

When Jean Mayer began studying a strain of obese mice in 1950, he observed that if he starved them sufficiently he could reduce their weight beneath that of normal rats, but they’d “still contain more fat than the normal ones, while their muscles have melted away,” which made them sound suspiciously like rodent versions of Sheldon’s emaciated endomorphs. For centuries, fat men and women have been complaining that virtually everything they eat turns to fat, and this was precisely what was happening with Mayer’s obese mice. “These mice will make fat out of their food under the most unlikely circumstances,” he wrote, “even when half starved.”