Good Calories, Bad Calories (55 page)

Even if it could be established that al obese individuals eat more than do the lean—which they don’t—that only tel s us that eating more is associated with being obese. It tel s us nothing about what causes obesity, because it doesn’t tel us why the obese don’t respond to an increase in food intake by expending more energy. After al , this must be the case when a lean person has a healthy appetite. “The statement that primary increase of appetite may be a cause of obesity does not lead us very far,” Rony explained, “unless it is supplemented with some information concerning the origin of the primarily increased appetite…. What is wrong with the mechanism that normal y adjusts appetite to caloric output? What part of this mechanism is primarily disturbed…?”

Slightly more relevant are prospective studies, in which a population of individuals is observed to determine what distinguishes those who go on to become obese from those who don’t. These studies, however, also fail to establish cause and effect. Such studies have repeatedly demonstrated that those who are pre-obese expend less energy—even at the age of three months—than those who wil remain lean, which means that the low energy expenditure is a risk factor for obesity. This suggests that the pre-obese do indeed have a retarded metabolism, as von Noorden suggested, but it does not imply that relatively low energy expenditure causes obesity, only that it is associated with the condition of being pre-obese, and perhaps facilitates the drive to become obese.

As we’ve discussed, obesity is associated with al the physiological abnormalities of metabolic syndrome and al the attendant chronic diseases of civilization. For this reason, public-health authorities now assume that obesity causes or exacerbates these conditions. The alternative logic, with the causality reversed, implies a different conclusion: that the same metabolic-hormonal disorder that drives us to fatten also causes metabolic syndrome and the attendant chronic diseases of civilization.

The second misinterpretation of the law of energy conservation inevitably accompanies the first and is equal y unjustifiable. The idea that obesity is caused by the slow accumulation of excess calories, day in and day out, over years or decades, and the associated idea that it can be prevented by reductions in caloric intake and/or increases in physical activity, are both based on an assumption about how the three variables in the energy-balance equation—energy storage, energy intake, and energy expenditure—relate to each other. They assume that energy intake and energy expenditure are what mathematicians cal independent variables; we can change one without affecting the other. “We cannot get away from the fact that, given no change in physical activity [my italics], increased food means increased weight,” as John Yudkin phrased it in 1959. “Yet this simple expression of the laws of conservation of mass and of energy is stil received with indignation by very many people.” But Yudkin’s purportedly inescapable truth included an assumption that may not be physiological y plausible: “given no change in physical activity.” The question is whether one can actual y change energy intake in a living organism without prompting compensatory changes in energy expenditure.

When Carl von Noorden suggested in 1900 that obesity could be caused by eating one extra slice of bread every day or climbing fewer flights of stairs, so that a few extra dozen calories each day would accumulate over a decade into tens of pounds, and when the USDA Dietary Guidelines, over a century later, evoked the same concept with the suggestion that “for most adults a reduction of 50 to 100 calories per day may prevent gradual weight gain,” they were treating human beings as though they are simple machines. “There is only one trouble,” as Hilde Bruch commented about von Noorden’s logic—“human beings do not function this way.”

If we consume an average of twenty-seven hundred calories a day, that’s almost a mil ion calories a year; almost twenty mil ion calories consumed over the course of two decades—more than twenty-five tons of food. Maintaining our weight within a few pounds for twenty years requires that we adapt our food intake to our expenditure over that period with remarkable accuracy. It’s al too easy, therefore, to imagine how a metabolic or hormonal defect might lead to obesity by inducing the slightest compensatory inclination to consume more calories than we expend, and why it would be so subtle as to go undetected by virtual y any imaginable diagnostic technology. “It is conceivable,” as Eugene Du Bois of Cornel University suggested seventy years ago in his classic textbook Basal Metabolism in Health and Disease, “that common obesity is the only manifestation of an endocrine disturbance…so slight that it upsets the balance of intake and output by less than 0.1 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 mil ion 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 al our homeostatic systems, via what George Cahil of Harvard and Albert Renold of the University of Geneva in 1965 cal ed “multiple metabolic control mechanisms.” This idea evolved in the 1970s into the popular set-point hypothesis, that our bodies wil defend a certain preferred amount of body fat against either an excess or a deficit of calories. It fel 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 homeostatical y is that energy intake and expenditure are very much dependent variables—that they are physiological y linked so that a change in one forces a corresponding change in the other—and it is energy storage that is determined biological y 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, tel s us that any increase in energy expenditure wil have to induce a compensatory increase in intake, and so hunger has to be a consequence. And any enforced decrease in intake wil 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 wil lead to long-term weight loss, as the body natural y compensates. We get hungry, and if we can’t satisfy that hunger, we’l get lethargic and our metabolism wil 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 wil 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 wel -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 mil ions of years precisely to minimize its effects…. As food in take drops, the level of thyroid hormone fal s 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 wil power, Bruch, Rony, and others have argued that this failure is precisely the evidence that tel s 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 wil 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 col aborators described them, and anyone wil experience them, regardless of weight.

Obese patients who try to reduce their weight by semi-starvation, as Rony noted, wil always be fighting what he cal ed their “spontaneous impulses of eating and activity.” Once they give in to these impulses, which is effectively preordained, they wil 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 wil the caloric deprivation address the metabolic and hormonal forces at work.

Just as we wil decrease energy expenditure in response to caloric deprivation, we wil 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 smal excesses, they observed, on the order of a few hundred calories a day, is “wel 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 of Newburgh’s argument that obesity is caused by a perverted appetite. “The idea that people burned off excess energy when overfed was regarded with great disfavor by respectable nutritionists,” as the British clinician John Garrow later noted. “It was a story put about by charlatans to justify magic cures, or by self-indulgent obese people as a justification for their obesity.” It experienced a renaissance in the 1960s, sparked by the British physiologist Derek Mil er, who reported that young pigs fed a low-protein diet would consume five times as many calories as those fed a high-protein diet, and yet could burn off the excess so as not to gain weight. This led Mil er to speculate that the pigs would eat until they satisfied their protein requirements, and while doing so would stay lean through this process of Luxuskonsumption.*88 It was thought that the ability to burn off excess calories would be of particular survival advantage when confronted with a poor-quality diet, when excessive amounts of food had to be consumed to achieve a requisite amount of protein or essential vitamins or minerals. Mil er’s observations prompted the renewed interest in overfeeding experiments of the kind we discussed in the last chapter (Chapter 16). The one consistent finding in these studies has been that individuals vary dramatical y in response to prolonged and enforced gluttony. Some wil fatten easily, and some wil not. The conclusion, seemingly unavoidable, is that a critical variable in the facility with which we gain weight is whether we respond to superfluous calories by storing them away as fat and/or muscle or by converting them to heat and physical activity—i.e., Luxuskonsumption.