Good Calories, Bad Calories (51 page)

endocrinologist Ethan Sims beginning in the late 1960s. Sims first used students for his experiments, but found it difficult to get them to gain significant weight. He then used convicts at the Vermont State Prison, who initial y raised their food consumption to four thousand calories a day. They gained a few pounds, but then their weights stabilized. So they ate five thousand calories a day, then seven thousand (five ful meals a day), then ten thousand, while remaining sedentary.

There were “marked differences between individuals in ability to gain weight,” Sims reported. Of his eight subjects that went two hundred days on this mildly heroic regimen, two gained weight easily and six did not. One convict managed to gain less than ten pounds after thirty weeks of forced gluttony (going from 134 pounds to 143). When the experiment ended, al the subjects “lost weight readily,” Sims said, “with the same alacrity,” in fact, as that with which obese patents typical y return to their usual weights after semi-starvation diets. Sims concluded that we’re al endowed with the ability to adopt our metabolism and energy expenditure “in response to both over-and undernutrition,” but some of us, as with any physiological trait, do it better than others.

Another overfeeding study, led by Claude Bouchard, who is now head of the Pennington Biomedical Research Center in Louisiana, was published in 1990. Bouchard and his col eagues overfed twenty-four young men—twelve pairs of identical twins—by a thousand calories a day, six days a week, for twelve weeks. The subsequent weight gain varied from nine to thirty pounds. The amount of body fat gained also varied by a factor of three. In 1999, James Levine from the Mayo Clinic reported that he had overfed sixteen healthy volunteers by a thousand calories a day, seven days a week, for eight weeks. The amount of fat these subjects managed to put on ranged from less 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 col eagues 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 al 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 wil 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 recal s, “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 “stil 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 virtual y everything they eat turns to fat, and this was precisely what was happening with Mayer’s obese mice. “These mice wil 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 al ow for such a possibility. Why?

An obese Zucker rat will be fatter than a lean one, even if it’s semi-starved from birth onward. (Photo courtesy of Charles River Laboratories.) 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, naïvely, 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 Practice of Medicine, the British physician Thomas Hawkes Tanner added to these “ridiculous”

prescriptions, those of Thomas King Chambers, whose 1850 book, Corpulence; or Excess of Fat in the Human Body, recommended eating “very light meals of substances that can be easily digested” and devoting “many hours daily to walking or riding.” “Al these plans,” wrote Tanner, “however perseveringly carried out, fail to accomplish the object desired; and the same must be said of simple sobriety in eating and drinking.”*79

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 (literal y 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 wil 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 original y cal ed the isodynamic law, which has since been distil ed by nutritionists to the phrase “a calorie is a calorie.” A calorie of protein provides the same amount of energy to the body as a calorie of fat or carbohydrate. Lost in this distil ation is the fact that the effects of these different nutrients on metabolism and hormone secretion are so radical y different, as is the manner in which the body employs the nutrients, that the energetic equivalence of the calories themselves is largely irrelevant to why we gain weight. As Rubner suggested more than a century ago, “the effect of specific nutritional substances upon the glands” may be the more relevant factor.

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 wil indeed either be burned as fuel—metabolized or oxidized—or they’l be stored or excreted. The research of Rubner, Benedict, and Atwater is the origin of the pronouncement often made by nutritionists with regard to weight-reducing diets that “calories in are equal to calories out.” As Marian Burros of the New York Times observed, there’s no violating the laws of thermodynamics.

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, Die Fettsucht. “His work contains many ideas which have become so incorporated, and in such a matter of fact way, into medical thinking, that his name is no longer mentioned with them,” noted Hilde Bruch fifty years ago. The same is stil true today.

Von Noorden proposed three hypotheses for the cause of obesity. One of these, what he cal ed diabetogenous obesity, was remarkably prescient, but so far ahead of its time that it had no influence on how the science evolved. (We wil discuss this hypothesis later, in Chapter 22.) Von Noorden’s other two hypotheses, however, which he cal ed 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 stay fat, regardless of how much they ate or exercised (endogenous obesity, driven by internal forces, not external).

In the cases where immoderate lifestyle was to blame—by “far the most common” of the two, von Noorden believed—the metabolism and physiology of the obese individual are normal, but “the mode of living” is defective, marked by that now familiar combination of “overeating or deficient physical exercise.” In endogenous obesity, the lifestyle is normal, and the weight gain is caused by an abnormal y slow metabolism. These unfortunate individuals might eat no more than anyone else, but their metabolisms use a smal er proportion of the calories they consume, and so a greater proportion is stored as fat.

Just as heart-disease researchers came to blame cholesterol because it seemed to be an obvious culprit and they could measure it easily, von Noorden and the clinical investigators who came after him implicated metabolism and the energy balance because that’s what they could measure and that, too, seemed obvious. In 1892, a German chemist named Nathan Zuntz had developed a portable device to measure an individual’s oxygen consumption and carbon-dioxide respiration. This, in turn, al owed for the calculation, albeit indirectly, of energy expenditure and the metabolism of anyone who had the patience to remain immobile for an hour while breathing into a face mask. Within a year, Adolf Magnus-Levy, a col eague of von Noorden, had taken this calorimeter to the hospital bedside and begun a series of measurements of what later became known as basal metabolism, the energy we expend when we’re at “complete muscular repose,” twelve to eighteen hours after our last meal. By the end of World War I, calorimetric technology had been refined to the point where measuring metabolism had become “an extremely popular, almost fashionable field.”

Von Noorden’s focus on metabolic expenditure set the science of obesity on the path we stil find it. The evolution of this research, however, proceeded like a magician’s sleight-of-hand. By the 1940s, common sense, logic, and science had parted ways.

The most obvious difficulty with the notion that a retarded metabolism explains the idiosyncratic nature of fattening is that it never had any evidence to support it. Before von Noorden proposed his hypothesis, Magnus-Levy had reported that the metabolism of fat patients seemed to run as fast if not faster than anyone else’s.*81 This observation would be confirmed repeatedly: The obese tend to expend more energy than lean people of comparable height, sex, and bone structure, which means their metabolism is typical y burning off more calories rather than less. When people grow fat, their lean body mass also increases. They put on muscle and connective tissue and fat, and these wil increase total metabolism (although not by the same amount).

The tendency of the obese to expend more energy than do the lean (of comparable height, age, and sex) led to the natural assumption that they must eat more than the lean do. Otherwise, they would have to lose weight. Researchers from Magnus-Levy onward avoided this conclusion by calculating energy expenditure as a metabolic rate—the total metabolism divided by weight, for instance, or by the skin-surface area of the subject. The obese could then be said to have a metabolic rate that seemed, on average, to run slower than that of the lean. That was beside the point, though, at least when it came to the amount of calories that must be consumed either to cause obesity or to reverse it. The factor of interest, noted the British physiologists Michael Stock and Nancy Rothwel in 1982, is “the metabolism of the individual and not a unit fraction of that individual.”

One of the most tel ing observations that emerged from these studies of metabolic rate was how greatly it might differ between any two individuals of equal weight, or how similar it might be among individuals of vastly different weights. In 1915, Francis Benedict published his studies of the basal metabolism translated into the minimal amount of energy expended over the course of a day, as measured in eighty-nine men and sixty-eight women.