than a single pound to almost nine; “fat gain varied ten-fold among our volunteers,” Levine reported.
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.”
Something more is going on than mere immoderation in lifestyle—metabolic or hormonal factors in particular. Yet the accepted definitions of the cause of obesity do not allow for such a possibility. Why?
The answer dates back to the birth of modern nutrition research in the late nineteenth century. Until then, obesity had been considered no more likely to be cured by any facile prescription than was any other debilitating disease. As early as 1811, one French physician’s list of the curative agents promoted for obesity included several that might, naively, be considered the last resorts of desperate individuals: bleeding from the jugular vein, for example, and leeches to the anus. In the 1869 edition of
The paradox developed with the understanding of the energy content of foods—the calorie—and the development of a technology, known as calorimetry, that could measure the heat production and respiration of living organisms and so equate the caloric content of foods to the calories expended as energy in the process of living. This was the culmination of a hundred years of science, beginning in the mid-eighteenth century with the Frenchman Antoine-Laurent Lavoisier, who demonstrated that the heat generated by an animal (literally a guinea pig in his experiments) was directly related to how much oxygen it consumed and carbon dioxide it exhaled. Living organisms are burning or combusting just as any other fire or flame does, which is why both will expire without sufficient oxygen. By 1900, a succession of legendary German chemists—Justus von Liebig, his students Max von Pettenkofer and Carl von Voit, and their student Max Rubner, among others—had worked out how organisms burn protein, fat, and carbohydrates and the basics of both metabolism and nutrition science. “The amount of information [the Germans] acquired within a comparatively few years past is remarkable,” wrote Wilbur Atwater the pioneer of nutrition research in the United States, in 1888.
It was Rubner who discovered that fat had more than twice as many calories per gram as did protein or carbohydrates. He also demonstrated, in 1878, what he originally called the
Rubner gets credit for being the first to demonstrate that the law of conservation of energy holds in living organisms. Rubner studied the heat expenditure and respiration of a dog for forty-five days and published his findings in 1891. Eight years later, Francis Benedict and Wilbur Atwater confirmed the observation in humans: the calories we consume will indeed either be burned as fuel—metabolized or
It was with the application of these laws to the problem of human obesity that the paradoxes emerged. This work was done in the first years of the twentieth century by Carl von Noorden, the leading German authority on diabetes, the author-editor of several multivolume medical texts, and author of one 1900 monograph on obesity entitled, in the original German,
Von Noorden proposed three hypotheses for the cause of obesity. One of these, what he called diabetogenous obesity, was remarkably prescient, but so far ahead of its time that it had no influence on how the science evolved. (We will discuss this hypothesis later, in Chapter 22.) Von Noorden’s other two hypotheses, however, which he called exogenous and endogenous obesity, though simplistic in comparison, have dominated thinking and research on obesity ever since.
Von Noorden worked directly from the law of energy conservation: “The ingestion of a quantity of food greater than that required by the body,” he wrote, “leads to an accumulation of fat, and to obesity should the disproportion be continued over a considerable period.” This left open the question of what would cause such a positive energy balance,*80 and von Noorden suggested that it was due either to an immoderate lifestyle (exogenous obesity, driven by forces external to the body) or to the fact that some people seemed predestined to grow fat and
