Good Calories, Bad Calories

of 1 percent.”

Less easy to imagine, though, is how anyone avoids this fate, particularly if we believe that the balancing of intake and expenditure is maintained not by some finely tuned regulatory system, one honed over a few million years of evolution to accomplish its task under any circumstances, but, rather, by our conscious behavior and our perspicacity at judging the caloric value of the foods we eat. Looked at this way, as Du Bois suggested, “there is no stranger phenomenon than the maintenance of a constant body weight under marked variation in bodily activity and food consumption.”

In 1961, the Cambridge University physiologist Gordon Kennedy discussed the paradoxes of obesity and weight regulation in the context of two propositions that he described as “common sense rather than physiology.” The first was that “there must be long-term regulation of energy balance.” The second was that “there is no a priori reason why this balance should be maintained by control of appetite alone, since it depends as much on calorie expenditure as on calorie intake.”

Like Kennedy, most researchers who studied metabolism and the science of bioenergetics and growth through most of the twentieth century assumed that energy balance must be regulated involuntarily, without conscious intent, and that the mechanisms that do so adapt both intake to expenditure and expenditure to intake. Our bodies work to minimize long-term fluctuations in energy reserves and maintain a stable body weight, and they do so, as with all our homeostatic systems, via what George Cahill of Harvard and Albert Renold of the University of Geneva in 1965 called “multiple metabolic control mechanisms.” This idea evolved in the 1970s into the popular set-point hypothesis, that our bodies will defend a certain preferred amount of body fat against either an excess or a deficit of calories. It fell out of favor because it implied that neither calorie-restricted diets nor exercise would lead to long- term weight loss.

The fundamental assumption of this idea that body weight is regulated homeostatically is that energy intake and expenditure are very much dependent variables—that they are physiologically linked so that a change in one forces a corresponding change in the other—and it is energy storage that is determined biologically within a certain range set by the interaction between genetics and the environment. Now the same law of energy conservation that decrees that calories in equal calories out, tells us that any increase in energy expenditure will have to induce a compensatory increase in intake, and so hunger has to be a consequence. And any enforced decrease in intake will have to induce a compensatory decrease in expenditure—a slowing of the metabolism and/or a reduction in physical activity.

In the nineteenth century, Carl von Voit, Max Rubner, and their contemporaries demonstrated that this was indeed what happened, at least in animals. Francis Benedict, Ancel Keys, George Bray, Jules Hirsch, and others have demonstrated this in humans, showing that neither eating less nor exercising more will lead to long-term weight loss, as the body naturally compensates. We get hungry, and if we can’t satisfy that hunger, we’ll get lethargic and our metabolism will slow down to balance our intake. This happens whether we’re lean or obese, and it confounds those authorities who recommend exercise and calorie restriction for weight loss. They operate on the assumption that the only adjustment to the caloric deficit created by either dieting or exercise will be a unilateral reduction in fat tissue. This would be convenient, but the evidence argues against it.

Among researchers who study malnutrition, as opposed to those whose specialty is obesity, these compensatory effects to caloric deprivation are taken for granted, as is the fact that hormones regulate this process. “Changes in…hormones such as insulin and glucagon^*87 play an important role in this metabolic response to energy restriction,” explains Prakash Shetty, director of the Nutrition Planning, Assessment and Evaluation Service of the United Nations’ Food and Agriculture Organization. “These physiological changes may be considered as metabolic adaptations which occur in a previously well-nourished individual and are aimed at increasing the ‘metabolic efficiency’ and fuel supply of the tissues at a time of energy deficit.” We should not be surprised that “dieting is difficult,” as Keith Frayn of Oxford University says in his 1996 textbook, Metabolic Regulation. “It is a fight against mechanisms which have evolved over many millions of years precisely to minimize its effects…. As food in take drops, the level of thyroid hormone falls and metabolic rate is lowered. Food intake has to be reduced yet further to drop below the level of energy expenditure. Hunger mechanisms, including the feeling of an empty stomach, lead us to search for food….”

Though the traditional response to the failure of semi-starvation diets to produce long-term weight loss has been to blame the fat person for a lack of willpower, Bruch, Rony, and others have argued that this failure is precisely the evidence that tells us positive caloric balance or overeating is not the underlying disorder in obesity. No matter what technique is used to achieve a caloric deficit, whether eating less or exercising more, it will only serve to induce hunger and/or a compensatory decrease in energy expenditure. These are the “usual symptoms resulting from reduced food intake,” as Ancel Keys and his collaborators described them, and anyone will experience them, regardless of weight.

Obese patients who try to reduce their weight by semi-starvation, as Rony noted, will always be fighting what he called their “spontaneous impulses of eating and activity.” Once they give in to these impulses, which is effectively preordained, they will get fat again. This is exactly what we would expect to see if obesity were merely a consequence of an underlying disorder, much as high blood sugar and glycosuria—i.e., sugar in the urine—are symptoms and consequences of diabetes. Consuming fewer calories can serve only to address the symptoms temporarily, just as with diabetes. It does not remove the underlying abnormality.

This is why the long-term failure of semi-starvation diets is significantly more informative about the true nature of obesity than is the short-term weight loss. This failure is an important “clue to the puzzle,” as Bruch suggested in 1955. The obese, Bruch noted, “react exactly like normal people after starvation. They continue overeating.” This drive to become fat can be inhibited or even temporarily reversed by restricting calories—just as a child’s growth can be stunted by starvation or malnutrition—but in neither case will the caloric deprivation address the metabolic and hormonal forces at work.

Just as we will decrease energy expenditure in response to caloric deprivation, we will also increase expenditure in response to caloric surplus. This compensatory effect of overeating was also demonstrated in the late nineteenth century by Carl von Voit and Max Rubner, although they disagreed about the mechanisms at work. It has since been encapsulated in a German word, Luxuskonsumption, which means a spendthrift metabolism that wastes excess calories as heat or superfluous physical activity. The term was first used in this context in 1902 by the German physiologist R. O. Neumann, who spent three years studying how his own body weight responded to extended fluctuations in caloric intake. Luxuskonsumption was Neumann’s explanation for the apparent disassociation between the calories he consumed and the ease with which he maintained his weight.

Through the first half of the twentieth century, this capacity for Luxuskonsumption was assumed to be a critical factor in the genesis of obesity or leanness. To borrow Gordon Kennedy’s phrase, this seemed like common sense rather than physiology. “Food in excess of immediate requirements and not needed to replenish stores can be readily disposed of, being burnt up and dissipated as heat,” wrote David Lyon and Sir Derrick Dunlop, clinicians at the Royal Infirmary of Edinburgh, in 1932. “Did this capacity not exist, obesity would be almost universal.” And so the ability to burn up small excesses, they observed, on the order of a few hundred calories a day, is “well within the capacity of the ordinary person, but in the obese individual the power of flexibility is much less evident.”

Investigators studying obesity argued about the same handful of studies on Luxuskonsumption, and then the subject went out of fashion with the general acceptance