Good Calories, Bad Calories Part 11

This conviction that positive caloric balance causes weight gain is founded on the belief that this proposition is an incontrovertible implication of the first law of thermodynamics. "The fact remains that no matter what people eat, it is calories that ultimately count," as Jane Brody explained in the New York Times. "Eat more calories than your body uses and you wil gain weight. Eat fewer calories and you wil lose weight. The body, which is after al nothing more than a biochemical machine, knows no other arithmetic."

For fifty years, clinicians, nutritionists, researchers, and public health officials have used this logic as the starting point for virtual y every discussion of obesity. Anyone who chal enges this view is seen as wil ful y disregarding a scientific truth. "Let me state," said the Columbia University physiologist John Taggart in his introduction to an obesity symposium in the early 1950s, "that we have implicit faith in the validity of the first law of thermodynamics." "A calorie is a calorie," and "Calories in equals calories out," and that's that.

But it isn't. This faith in the laws of thermodynamics is founded on two misinterpretations of thermodynamic law, and not in the law itself. When these misconceptions are corrected, they alter our perceptions of weight regulation and the forces at work.

The first misconception is the a.s.sumption that an a.s.sociation implies cause and effect. Here the context is the first law of thermodynamics, the law of energy conservation. This law says that energy is neither created nor destroyed, and so the calories we consume wil be either stored, expended, or excreted. This in turn implies that any change in body weight must equal the difference between the calories we consume and the calories we expend, and thus the positive or negative energy balance. Known as the energy-balance equation, it looks like this: Change in energy stores = Energy intake-Energy expenditure The first law of thermodynamics dictates that weight gain-the increase in energy stored as fat and lean-tissue ma.s.s-wil be accompanied by or a.s.sociated with positive energy balance, but it does not say that it is caused by a positive energy balance-by "a plethora of calories," as Russel Cecil and Robert Loeb's 1951 Textbook of Medicine put it. There is no arrow of causality in the equation. It is equal y possible, without violating this fundamental truth, for a change in energy stores, the left side of the above equation, to be the driving force in cause and effect; some regulatory phenomenon could drive us to gain weight, which would in turn cause a positive energy balance-and thus overeating and/or sedentary behavior. Either way, the calories in wil equal the calories out, as they must, but what is cause in one case is effect in the other.

Al those who have insisted (and stil do) that overeating and/or sedentary behavior must be the cause of obesity have done so on the basis of this same fundamental error: they wil observe correctly that positive caloric balance must be a.s.sociated with weight gain, but then they wil a.s.sume without justification that positive caloric balance is the cause of weight gain. This simple misconception has led to a century of misguided obesity research.

When the law of energy conservation is interpreted correctly, either of two possibilities is al owed. It may be true that overeating and/or physical inactivity (positive caloric balance) can cause overweight and obesity, but the evidence and the observations, as we've discussed, argue otherwise. The alternative hypothesis reverses the causality: we are driven to get fat by "primary metabolic or enzymatic defects," as Hilde Bruch phrased it, and this fattening process induces the compensatory responses of overeating and/or physical inactivity. We eat more, move less, and have less energy to expend because we are metabolical y or hormonal y driven to get fat.

In 1940, Hugo Rony, former chief of the endocrinology clinic at Northwestern University's medical school, discussed this reverse-causation problem in a monograph ent.i.tled Obesity and Leanness, which is easily the most thoughtful a.n.a.lysis ever written in English on weight regulation in humans.*86 Rony's goal, as he explained it, was to "separate recognized facts from suggestive evidence, and reasonable working hypothesis from mere speculations." This set Rony apart from Louis Newburgh, Jean Mayer, and others who were more interested in convincing their col eagues in the field that their speculations were correct.

When Rony discussed positive energy balance, he compared the situation with what happens in growing children. "The caloric balance is known to be positive in growing children," he observed. But children do not grow because they eat voraciously; rather, they eat voraciously because they are growing.

They require the excess calories to satisfy the requirements of growth; the result is positive energy balance. The growth is induced by hormones and, in particular, by growth hormone. This is the same path of cause and effect that would be taken by anyone who is driven to put on fat by a metabolic or hormonal disorder. The disorder wil cause the excess growth-horizontal, in effect, rather than vertical. For every calorie stored as fat or lean tissue, the body wil require that an extra calorie either be consumed or conserved. As a result, anyone driven to put on fat by such a metabolic or hormonal defect would be driven to excessive eating, physical inactivity, or some combination. Hunger and indolence would be side effects of such a hormonal defect, merely facilitating the drive to fatten. They would not be the fundamental cause. "Positive caloric balance may be regarded as the cause of fatness," Rony explained, "when fatness is artificial y produced in a normal person or animal by forced excessive feeding or forced rest, or both. But obesity ordinarily develops spontaneously; some intrinsic abnormality seems to induce the body to establish positive caloric balance leading to fat acc.u.mulation. Positive caloric balance would be, then, a result rather than a cause of the condition."

An obvious example of this reverse causation would be pregnant women, who are driven to fatten by hormonal changes. This hormonal drive induces hunger and lethargy as a result. In the context of evolution, these expanded fat stores would a.s.sure the availability of the necessary calories to nurse the infants after birth and a.s.sure the viability of the offspring. The mother's weight loss after birth may also be regulated by hormonal changes, just as it appears to be in animals.

What may be the single most incomprehensible aspect of the last half-century of obesity research is the failure of those involved to grasp the fact that both hunger and sedentary behavior can be driven by a metabolic-hormonal disposition to grow fat, just as a lack of hunger and the impulse to engage in physical activity can be driven by a metabolic-hormonal disposition to burn calories rather than store them. Obesity researchers wil immediately acknowledge that height, and thus the growth of skeletal bones and muscle tissue, is determined by genetic inheritance and driven by hormonal regulation, and that this growth wil induce the necessary positive caloric balance to fuel it. But they see no reason to believe that a similar process drives the growth of fat tissue. What they believe is what they were taught in medical school, which was and is the conventional wisdom: the growth of skeletal muscle and bones, and thus our height, is driven by the secretion of growth hormone from the pituitary gland; the growth of fat tissue, and thus our girth, is driven by eating too much or physical inactivity.

This notion that fattening is the cause and overeating the effect, and not vice versa, also explains why a century of researchers have made so little progress, and why they keep repeating the same experiments over and over again. By this logic, those who become obese have a const.i.tutional tendency to fatten, whereas those who remain lean have a const.i.tutional tendency to resist the acc.u.mulation of fat. This tendency is the manifestation of very subtle deviations in metabolism and hormonal state. The obese have a const.i.tutional predisposition to acc.u.mulate slight excesses of fat in their adipose tissue, which in turn induces compensatory tendencies to consume slightly more calories than the lean or expend slightly less. Obese individuals wil put on fat until they have counterbalanced the influence of this underlying disorder. Eventual y, these individuals achieve energy balance-everyone does-but only at an excessive weight and with an excessive amount of body fat.

The essential question, then, is: what are the metabolic and hormonal deviation that drives this fattening process? When we have that answer, we wil know what causes obesity.

For the past half-century, obesity researchers have focused on a different question: establishing the characteristics that distinguish fat people from lean.

Do fat people expend less energy? Do they consume more? Are they aware of how much they're eating? Are they less physical y active? Is their metabolism slower? Are they more or less insulin-sensitive? Al of these address factors that may be a.s.sociated with the condition of being obese, but none address the question of what causes it initial y.

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 a.s.sociated 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 appet.i.te. "The statement that primary increase of appet.i.te 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 appet.i.te.... What is wrong with the mechanism that normal y adjusts appet.i.te 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 r.e.t.a.r.ded metabolism, as von Noorden suggested, but it does not imply that relatively low energy expenditure causes obesity, only that it is a.s.sociated with the condition of being pre-obese, and perhaps facilitates the drive to become obese.

As we've discussed, obesity is a.s.sociated with al the physiological abnormalities of metabolic syndrome and al the attendant chronic diseases of civilization. For this reason, public-health authorities now a.s.sume 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 acc.u.mulation of excess calories, day in and day out, over years or decades, and the a.s.sociated idea that it can be prevented by reductions in caloric intake and/or increases in physical activity, are both based on an a.s.sumption about how the three variables in the energy-balance equation-energy storage, energy intake, and energy expenditure-relate to each other. They a.s.sume 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 ma.s.s and of energy is stil received with indignation by very many people." But Yudkin's purportedly inescapable truth included an a.s.sumption 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 acc.u.mulate 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 cla.s.sic 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 circ.u.mstances, 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 appet.i.te 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 a.s.sumed 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 a.s.sumption 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 a.s.sumption 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, a.s.sessment 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 disa.s.sociation 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 a.s.sumed 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 appet.i.te. "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.

At least some of these excess calories are lost in the various chemical reactions required to digest and store the nutrients. Rubner referred to this as the heat generated by the "thermochemical tangle of breakdowns" that occur during the process of digestion. Physicians measure basal or resting metabolism after a twelve-to-eighteen-hour fast because by then this diet-induced thermogenesis has played itself out. The protein in the diet, as Rubner discovered, dominates this effect. The more protein digested over the amount necessary to maintain tissues and organs, the greater the heat generation.

It's what Rubner cal ed the specific dynamic effect of protein that is usual y invoked as the rationale to eat high-protein diets for weight loss; excessive calories lost as heat in the process of digesting and utilizing protein can't then be stored as fat or used for fuel.

As the external environment changes, though, our bodies change the manner in which they utilize this heat. Maintaining our bodies at a constant temperature (roughly 98.6F) requires more energy when it's cold than when it's warm. More of the heat from this thermochemical tangle of breakdowns, as Rubner reported, wil go to that purpose when it's cold, as it wil when our energy reserves are low-when we're undernourished-and we need to conserve the biological y useful energy for other purposes. In short, we wil put this heat to use when we need to conserve energy, and we wil waste it when it might be to our benefit to avoid the acc.u.mulation of excess calories as fat.

The primary source of controversy today remains the question that Rubner and Voit disputed a hundred years ago: whether the excess calories consumed have to be dissipated entirely as heat, or whether they can also be used biological y. Rubner argued that the energy requirements of our cel s are basical y constant. Under some set requirement, determined by temperature among other factors, our cel s wil adjust by conserving energy. Anything greater, and the energy is wasted as heat. Voit believed that the metabolic rate of our cel s responds to the fuel available. The more fuel, the more energy generated. According to Voit, overeating leads to an increase in the available energy for cel s, tissues, and muscles, and so perhaps to what the clinical investigators studying obesity in the first half of the century cal ed the "impulse to physical activity" or the "impulse to move." That feeling of restlessness, they believed, is the manifestation of cel s and tissues, literal y, having energy to burn.

Both interpretations suggest the same fundamental conclusion about how our bodies work. We have thrifty metabolisms when we are undernourished and so need to use efficiently every calorie we consume, and we have spendthrift metabolisms when we're overnourished, so as to avoid excessive weight gain and obesity. Our cel s may have a certain maximal or ideal capacity for metabolizing nutrients, but the amount that they actual y metabolize is ultimately determined by the quant.i.ty and perhaps the quality of the nutrients delivered in the circulation. This determination is made on a cel ular and hormonal level, not a cognitive or conscious one.

This idea that energy expenditure increases to match consumption, and that the ability to do this differs among individuals, also serves to reverse the cause-and-effect relationship between weight and physical activity or inactivity. Lean people are more active than obese people, or they have, pound for pound, a higher expenditure of energy,*89 because a greater proportion of the energy they consume is made available to their cel s and tissues for energy.

By this conception, lean people become marathon runners because they have more energy to burn for physical activity; their cel s have access to a greater proportion of the calories they consume to use for energy. Less goes to making fat. That's why they're lean. Running marathons, however, wil not make fat people lean, even if they can get themselves to do it, because their bodies wil adjust to the extra expenditure of energy, just as they would adjust to calorie-restricted diets.

Our propensity to alter our behavior in response to physiological needs is what the Johns Hopkins physiologist Curt Richter cal ed, in a heralded 1942 lecture, "total self-regulatory functions." Behavioral adaptation is one of the fundamental mechanisms by which animals and humans maintain homeostasis. Our responses to hunger and thirst are manifestations of this, replenishing calories or essential nutrients or fluids. Physical activity, as Richter suggested, is another example of this behavioral regulation, in response to an excess or dearth of calories. "We may regard the great physical activity of many normal individuals, the play activity of children, and perhaps even the excessive activity of many manic patients, as efforts to maintain a constant internal balance by expending excessive amounts of energy," he explained. "On the other hand, the low level of activity seen in some apparently normal people, the almost total inactivity seen in depressed patients, again may be regarded as an effort to conserve enough energy to maintain a constant internal balance."

In 1936, when Eugene Du Bois published the third edition of his metabolism textbook, Basal Metabolism in Health and Disease, he described the system that accomplished the regulation of a stable body weight as it was then understood. How much we want to eat on any given day, Du Bois explained, is determined by how much we've depleted whatever our body considers the necessary reserves of protein, fat, and carbohydrates. If we then consume more calories than we need, the excess wil either be burned off as heat or induce physical activity: "When wel nourished, the individual tends to become more energetic and it is quite possible that he wil soon burn up his stored fat by extra work or exercise which would not have been undertaken had it not been for the overfeeding." If we consume less food than we might require to replenish our reserves, then the amount of heat generated in response to a meal is minimized, and the stores of carbohydrates (glycogen), fat, and protein are used to make up the difference. Should the caloric deficit continue, the result is "a gradual lowering of metabolism and a tendency toward restriction of activities, due to a lack of energy and initiative."

However this homeostatic system works to balance energy intake and output and thus maintain a steady supply of fuel to the cel s and a stable body weight, it is extraordinarily complex and involves the entire body. Rony discussed this: "The appet.i.te mechanism, which is but a part, although the most important one, of body weight regulation is in itself a highly complex mechanism involving [the central nervous system], endocrine glands, the gastric neuro-muscular apparatus, and the organs of the glycogen, protein, and fat reserves." This notion was supported by a host of experimental and clinical studies, as we'l discuss in Chapter 21, which demonstrated that disturbances in body-weight regulation-like obesity-could be caused by "pathological changes in certain parts of the nervous system, endocrine system and depot organs."

It is also vital to understand that it's our cel s and tissues that require and expend the energy we consume, so this adjustment of intake to expenditure is occurring first and foremost on a cel ular level. "Whatever may be the mechanisms control ing food intake," as the University of California, Berkeley, nutritionist Samuel Lepkovsky wrote in 1948, "the chief site of their action must be the cel ." A fundamental requirement of any living organism is to provide a steady and reliable supply of fuel to its cel s, regardless of the circ.u.mstances. We apparently evolved an intricate and extraordinarily robust regulatory system of hormones, enzymes, and the nervous system to accomplish this task. If the necessary fuel fails to reach the cel s, the body compensates. The crucial factor is not how much is eaten-how many calories are consumed-or how much is expended, but how those nutrients or the energy they contain is ultimately distributed, how those calories are utilized and made available when needed. It's not the energy balance that is driving this system, but the distribution of that energy, the demand for energy at the cel ular level.

Chapter Eighteen.

FATTENING DIETS.

Oversupply of food does not necessarily produce excessive nutrition. The appropriation depends in part on the character of the food and the ease or difficulty with which it is converted into a condition suitable for absorption, in part on such extrinsic and intrinsic influences as heredity, age, s.e.xual and psychical habits, exercise and sleep; but to a great extent also on personal peculiarities of the metabolic processes....

JAMES FRENCH, The Practice of Medicine, 1907 IN 1857, JOHN HANNNING SPEKE AND Richard Burton set off through West Africa to search for the source of the Nile River. After Burton fel il, Speke discovered the river's origin on his own. When he returned to the region five years later, according to his memoirs, he heard about the custom of local Abyssinian n.o.bility to fatten up their wives to "such an extent that they could not stand upright." He went to see for himself. "There was no mistake about it,"

he recal ed. "On entering the hut I found the old man and his chief wife sitting side by side on a bench.... I was struck with the extraordinary dimensions, yet pleasing beauty, of the immoderately fat fair one his wife. She could not rise; and so large were her arms that, between the joints, the flesh hung down like large, loose stuffed puddings." Two weeks later, when Speke visited "another one of those wonders of obesity," he took the opportunity to measure her. Her chest was fifty-two inches around. Her arms were nearly two feet in circ.u.mference and her thighs over two and a half feet.

With the notable exception of the current prevalence of obesity in Western societies, there is little reason to believe that fattening up the const.i.tutional y lean is any easier than inducing leanness in the obese. For successful fattening, the excess calories consumed have to be stored as fat, rather than expended in metabolism or physical activity or stored as muscle. This isn't a given, considering these alternative uses for the calories. Continuing to consume excess calories is necessary, too-the person being fattened has to continue eating long after becoming sated-and these calories also have to be stored as fat.

In the early 1970s, the British physician John Garrow attempted to add twelve hundred calories a day to his daily diet, hoping to sustain it for a hundred days. After failing with several methods, he found that he could accomplish his goal by keeping chocolate biscuits on hand and, "whenever the prospect didn't seem too revolting, eating however many of these biscuits that I could." He managed to gain fifteen pounds in sixty days and then gave up the experiment and lost the weight in fifty days. "I learned that for me it is difficult to move my weight at al rapidly in any direction," he said, "and I saw absolutely no reason to suppose that obese people would find it easier than I did."

Various foods have been used to induce extensive fattening. The tribes that Speke visited relied on milk to fatten their women. In the mid-1970s, the French ethnologist Igor de Garine doc.u.mented two male fattening sessions of the Ma.s.sa tribe of northern Cameroon. In an individual ritual, the man ingests both milk and a porridge made from sorghum, a cornlike grain that provides, like sugarcane, a sweet syrup from the stalk. In 1976, Garine reported, one Ma.s.sa tribesman gained seventy-five pounds on this ceremonial binge, apparently averaging ten thousand calories a day throughout. In a group fattening ritual, the men consume thirty-five hundred calories a day, rather than their usual twenty-five hundred, the excess consiting of milk and porridge. The weight gain tends to be fifteen to twenty pounds. The Ma.s.sa are cattle herders, and their staple diet is primarily milk. This fattening, therefore, is accomplished by the addition of carbohydrates almost exclusively-one thousand to seventy-five hundred calories a day of sorghum.

The sumo wrestlers of j.a.pan, whose weight commonly exceeds three hundred pounds, typical y reach that level by their early twenties. In 1976, a University of Tokyo col aboration, led by Tsuneo Nishizawa, published an article in The American Journal of Clinical Nutrition that stil const.i.tutes the most comprehensive a.n.a.lysis in the English medical literature of the sumo diet, body composition, and health. The world of professional sumo wrestling, according to Nishizawa, is divided into an "upper group," const.i.tuting the best wrestlers in the country, and a "lower group." The members of the upper group consumed on average some fifty-five hundred calories' worth of chanko nabe (a pork stew) a day, out of which 780 grams were carbohydrates, 100 grams fat and 365 grams protein. This const.i.tuted more than twice the calories and carbohydrates of the typical j.a.panese diet of the era,*90 slightly less than twice the fat, and four and a half times the amount of protein. The sumo diet was very high in carbohydrate by our standards-57 percent of the calories-and very low in fat-16 percent-considerably beneath what most public-health authorities in America consider a feasible low-fat target. The lower group of sumo weighed as much as their more accomplished col eagues, but were significantly fatter and less muscular. They consumed, on average, only 5,120 calories of chanko nabe a day, consisting of 1,000 grams of carbohydrates, 165 grams of protein, and only 50 grams of fat; these lesser sumo attained and maintained their corpulence on a diet of nearly 80 percent carbohydrate calories and 9 percent fat.

It seems that if we wanted to design a diet capable of inducing pathological obesity in young men in their prime, we might start with just such a very low-fat, high-carbohydrate diet. The diet would provide an enormous amount of calories, which might be the salient factor, but we would have to wonder what it is about this dietary composition that al ows for such extraordinary overconsumption, not just for a few days, but for years or perhaps decades.

For the past quarter century, public-health authorities and obesity researchers have insisted that it is dietary fat, not carbohydrates, that fattens most effectively and causes obesity. This is why low-fat, low-calorie diets are recommended for weight loss as wel as prevention of heart disease. This notion is based on four pieces of evidence, al of which are easily chal enged.

The one that has been most influential is the a.s.sociation between heart disease, obesity, and diabetes. If heart disease is caused by high-fat diets, as is commonly believed, then so are obesity and diabetes, since these diseases appear together in both individuals and populations. But there is no evidence linking obesity to dietary-fat consumption, neither between populations nor in the same populations.*91 And, of course, if dietary fat is not responsible for heart disease, then it's unlikely that it plays a role in obesity and diabetes.

Second, laboratory rats wil become obese on a high-fat diet. This is the evidence that convinced George Bray that excessive dietary fat would cause obesity in humans, too, and Bray has been among the most influential obesity authorities and the foremost proponent of this dietary-fat/obesity hypothesis. According to Bray, the rats used in his laboratory experiments would grow reliably obese on high-fat diets. "I could feed them any kind of composition of carbohydrates I want," Bray said, "and in the presence of low fat, they don't get fat. If I raised the fat content, particularly saturated fat, in susceptible [my italics] strains I would get obesity regularly."

But some strains of rats, perhaps most of them, wil not grow obese on high-fat diets, and even those that do wil grow fatter on a high-fat, high-carbohydrate diet than a high-fat, low-carbohydrate diet. Moreover, to induce obesity even in susceptible rodents, the percentage of fat in the diet has to be greater than 30 percent, and usual y closer to 40 or even 60 percent (which stil makes only some strains of rats fat). Though 30 percent sounds like a low-fat or moderate-fat diet for humans, it's far greater than anything rats would normal y consume, either in the wild or in the laboratory. It's what researchers wil cal a pharmaceutical dosage of fat. Rat chow is typical y 26 percent fat calories. Rats wil also fatten when fed large amounts of carbohydrates in the form of sugar. Moreover, other animals fatten on carbohydrates, including pigs-whose digestive apparatus is most like that of humans among experimental animals-cattle, and monkeys.

In the 1970s, Anthony Sclafani of Brooklyn Col ege demonstrated that rats get "super obese" if al owed to freely consume a selection of foods from the local supermarket. This made their eating habits and subsequent obesity seem particularly like ours in character. But, as Sclafani explained, his rats fattened preferential y on sweetened condensed milk, chocolate-chip cookies, and bananas. Among the foods they didn't eat to excess were cheese, pastrami, and peanut b.u.t.ter-the items that were high in fat and low in carbohydrates.

The third supporting leg of the hypothesis that fat is particularly fattening is an a.s.sumption that the density of fat calories fools people into eating too many. Density was original y invoked to explain why some rats would eat fat to excess and become obese. Because the fat used in these experiments is typical y an oil-Crisco cooking oil poured over the rat chow-it was hard to imagine that palatability was the deciding factor. As a result, researchers suggested that the density of the fat calories-nine calories per gram, compared with four for protein and carbohydrates-fooled the rats into consuming too many.

This was in line with the belief that we match our intake to expenditure by simple mechanisms such as those that limit the volume of food consumed in a single meal. It also led to the notion that eating fiber-rich, leafy vegetables wil prevent weight gain by fil ing our stomachs with fewer digestible calories than if we consumed the densely packed calories of fat or refined carbohydrates. The more rigorous experiments with laboratory animals, however, suggest otherwise. The seminal experiments on this question were done by the University of Rochester physiologist Edward Adolph back in the 1940s.

Adolph diluted the diets of his rats with water, fiber, and even clay, and noted that the rats would continue to eat these adulterated diets until they consumed the same amount of calories they had been eating when he had fed them unadulterated rat chow. The more Adolph diluted the chow with water, the more the rats consumed-until the meals were more than 97 percent water. At these very low dilutions, the rats apparently expended so much energy drinking that they couldn't consume enough calories to balance the expenditure. When Adolph put 90 percent of their daily calories directly into the rats'

stomachs, "other food was practical y refused for the remainder of the twenty-four hour period." Putting water directly into their stomachs had no such effect. Adolph's conclusion was that rats adjust their intake in response to caloric content, not volume, ma.s.s, or even taste, and this is presumably true of humans as wel .

The fourth piece of evidence is thermodynamic. The idea dates to the late nineteenth century and its revival by the University of Ma.s.sachusetts nutritionist J. P. Flatt was coincident with the rise of the dietary-fat/heart-disease hypothesis in the 1970s. According to Flatt's calculations, the "metabolic cost" of storing the calories we consume in adipose tissue-the proportion of energy dissipated in the conversion-and-storage process-is only 7 percent for fat, compared with 28 percent for carbohydrates. For this reason, when carbohydrates are consumed in excess, as the University of Vermont obesity researchers Ethan Sims and El iot Danforth explained in 1987, the considerable calories expended in converting them to fat wil "blunt the effect on weight gain of high-carbohydrate, high-caloric diets." High-fat diets, on the other hand, would lead "to a metabolical y efficient and uncompensated growth of the fat stores." Flatt's a.n.a.lysis omitted al hormonal regulation of fuel utilization and fat metabolism (as wel as a half-century's worth of physiological and biochemical research that we wil discuss shortly) but it has nonetheless been invoked often during the last twenty years to make the point, as Sims and Danforth did, that obesity is yet another "penalty for living off the fat of the land rather than the carbohydrate."

Like much of the established wisdom on diet and health, this conclusion was based on very little experimental evidence. In this case, its only supporting evidence came from Sims's overfeeding studies. These began in the mid-1960s with four smal trials that led to the observation that some people wil gain weight easily and others won't, even when consuming the same quant.i.ty of excess calories. Another half dozen trials fol owed, each with only a handful of subjects, intending to shed light on what Sims and his col aborators cal ed the "obvious question" of whether a carbohydrate-rich diet, independent of the calories consumed, could raise insulin levels, cause obesity, and induce hyperinsulinemia and insulin resistance. Sims and his col aborators varied the composition of the diets that their volunteers would then eat to excess. Some diets were "fixed carbohydrate" regimens, in which the amount of fat was increased as much as possible but the carbohydrates were limited to what the subjects would have normal y consumed in their pre-experiment lives; others were "variable carbohydrate" regimens, in which both fat and carbohydrates were added to excess.

In the mid-1970s shortly after finishing their research, Sims and Danforth believed that obesity was most likely caused by chronical y elevated levels of insulin, and that the elevated levels of insulin were likely the product of carbohydrate-rich diets. In the 1980s, their opinions changed and fel into step with the prevailing consensus on the evils of dietary fat. Sims and Dansforth now found in their decade-old results an observation that supported Flatt's argument that it was thermodynamical y more efficient to fatten on fat than on carbohydrates. When excess calories were provided in the form of fat alone, they now explained, the subjects converted a greater proportion of the excess into body fat than when the excess calories included both fat and carbohydrates. "Simply stated, when taken in excess, fat is more fattening than carbohydrate," Danforth wrote in 1985. "Therefore, if one is destined to overeat and desires to suffer the least obesity, overindulgence in carbohydrate rather than fat should be recommended." "In view of these considerations and the tendency toward overnutrition in most affluent societies," he added, "main attention should be toward reducing both caloric and fat intake."

What the Vermont investigators failed to take into account, however, was their own previous observation that the nutrient composition of the diet seemed to affect profoundly the desire to consume calories to excess. One potential y relevant observation that Sims and his col eagues neglected to publish, for example, was that it seemed impossible to fatten up their subjects on high-fat, high-protein diets, in which the food to be eaten in excess was meat. According to Sims's col aborator Edward Horton, now a professor of medicine at Harvard and director of clinical research at the Joslin Diabetes Center, the volunteers would sit staring at "plates of pork chops a mile high," and they would refuse to eat enough of this meat to const.i.tute the excess thousand calories a day that the Vermont investigators were asking of them. Danforth later described this regimen as the experimental equivalent of the diet prescribed by Robert Atkins in his 1973 diet book, Dr. Atkins' Diet Revolution. "The bottom line," Danforth said, "is that you cannot gain weight on the Atkins diet. It's just too hard. I chal enge anyone to do an overfeeding study with just meat. You can't do it. I think it's a physical impossibility."

Getting their volunteers to add a thousand calories of fat to their daily diet also proved surprisingly difficult. Throughout their numerous publications, Sims and his col eagues comment on the "difficult a.s.signment of gaining weight by increasing only the fat." Those fattening upon both carbohydrates and fat, on the other hand, easily added two thousand calories a day to their typical diet. Indeed, subjects in some of his studies, Sims and his col eagues reported, experienced "hunger late in the day...while taking much greater caloric excesses of a mixed diet"-as much as ten thousand calories a day.

Sims and his col aborators evidently did not wonder why anyone would lose appet.i.te-develop "marked anorexia," as they put it-on a diet that includes eight hundred to a thousand excess fat calories a day, and yet feel "hunger late in the day" on a diet that includes six to seven thousand excess calories of fat and carbohydrates together. It would seem there is something about carbohydrates that al ows the consumption of such enormous quant.i.ties of food and yet stil induces hunger as the night approaches.

By perceiving obesity as an eating disorder, a defect of behavior rather than physiology, and by perceiving excessive hunger as the cause of obesity, rather than a symptom that accompanies the drive to gain weight, those investigators concerned with human obesity had managed to dissociate the perception of hunger and satiety from any underlying metabolic conditions. They rarely considered the possibility that hunger, satiety, and level of physical activity might be symptomatic of underlying physiological conditions. Imagine if diabetologists had perceived the ravenous hunger that accompanies uncontrol ed diabetes as a behavioral disorder, to be treated by years of psychotherapy or behavioral modification rather than injections of insulin. These researchers simply never confronted the possibility that the nutrient composition of the diet might have a fundamental effect on eating behavior and energy expenditure, and thus on the long-term regulation of weight.

There is one way to test this latter notion, and, in fact, such tests were done from the 1930s onward. Alter the proportion of fats and carbohydrates in experimental diets and see what happens. Test low-fat diets versus low-carbohydrate diets, keeping in mind that a diet low in fat must be high in carbohydrates and vice versa. This would test the notion that these nutrients have unique metabolic and hormonal effects that influence weight, hunger or satiety, and energy expenditure. Such trials provide the means of answering these fundamental questions: What happens when we eat a diet restricted in carbohydrates, but not calories? Do we lose or gain weight? Are we as hungry as we are when calories are restricted? Do we eat more or less? Do we expend more or less energy? And what about when fat is restricted, but carbohydrates or calories are not? What are the effects on hunger, energy expenditure, and weight?

Chapter Nineteen.

REDUCING DIETS.

Concentrated carbohydrates, such as sugars and breadstuffs, and fats must be restricted. Diets, therefore, should exclude or minimize the use of rice, bread, potato, macaroni, pies, cakes, sweet desserts, free sugar, candy, cream, etc. They should consist of moderate amounts of meat, fish, fowl, eggs, cheese, coa.r.s.e grains and skimmed milk.

ROBERT MELCHIONNA of Cornel University, describing the reducing diet prescribed at New York Hospital in the early 1950s THE AMERICAN HEART a.s.sOCIATION TODAY insists that severe carbohydrate restriction in a weight-loss diet const.i.tutes a "fad diet," to be taken no more seriously than the grapefruit diet or the ice-cream diet. But this isn't the case. After the publication of Banting's Letter on Corpulence in 1863, physicians would routinely advise their fat patients to avoid carbohydrates, particularly sweets, starches, and refined carbohydrates, and this practice continued as the standard treatment of obesity and overweight through the better part of the twentieth century. Only after the AHA itself started recommending fat-restricted, carbohydrate-rich diets for heart disease in the 1960s and this low-fat prescription was then applied to obesity as wel , was carbohydrate restriction forced to the margins. "In the instruction of an obese patient," as Louis Newburgh of the University of Michigan explained in 1942, "it is a simple matter to teach him to omit sugar because sweet flavors are not easily disguised. It is also relatively simple to teach him to limit the use of foods high in starch."

Those early weight-loss diets were meant to eliminate fat tissue while preserving muscle or lean-tissue ma.s.s. The protein content of the diet would be maximized and calories reduced. Only a minimal amount of carbohydrates and added fats-b.u.t.ter and oils-would be al owed in the diet, because these were considered the nonessential, i.e., nonprotein, elements. When physicians from the Stanford University School of Medicine described the diet they prescribed for obesity in 1943, it was effectively identical to the diet prescribed at Harvard Medical School and described in 1948, at Children's Memorial Hospital in Chicago in 1950, and at Cornel Medical School and New York Hospital in 1952. According to the Chicago clinicians, the "general rules" of a successful reducing diet were as fol ows: 1. Do not use sugar, honey, syrup, jam, jel y or candy.

2. Do not use fruits canned with sugar.

3. Do not use cake, cookies, pie, puddings, ice cream or ices.

4. Do not use foods which have cornstarch or flour added such as gravy or cream sauce.

5. Do not use potatoes (sweet or Irish), macaroni, spaghetti, noodles, dried beans or peas.

6. Do not use fried foods prepared with b.u.t.ter, lard, oil or b.u.t.ter subst.i.tutes.

7. Do not use drinks such as Coca-Cola, ginger ale, pop or root beer.

8. Do not use any foods not al owed on the diet and [for other foods use] only as much as the diet al ows.

With the carbohydrates and added fats minimized in these diets, meat was inevitably the primary const.i.tuent. This would provide the protein necessary to ensure that weight loss came mostly from the patient's fat and not the muscle. The idea was to keep the body in what is cal ed nitrogen equilibrium, with the nitrogen consumed from the protein in the diet balancing out the nitrogen being excreted in the urine from the breakdown of muscle protein.

When these clinicians discussed what plant foods they would al ow in their diets, they typical y did so on the basis of the carbohydrate content: potatoes are nearly 20 percent carbohydrate by weight (the rest is mostly water), so they were known as 20-percent vegetables. Green peas and artichokes are 15-percent vegetables. Onions, carrots, beets, and okra are 10-percent vegetables. Most of the green vegetables-including lettuce, cuc.u.mbers, spinach, asparagus, broccoli, and kale-are 5-percent, which means carbohydrates const.i.tute at most 5 percent of their weight. These weight-loss diets al owed only 5-percent vegetables, which ruled out al starchy vegetables, like potatoes. Because a one-cup serving of a 5-percent vegetable wil yield only twenty to thirty calories, as the University of Toronto physician Walter Campbel wrote in 1936, "the inclusion of an extra portion or omission of an undesired portion is of little moment in the [dietary] scheme as a whole." Some of these diets did al ow an ounce or two of bread-usual y whole-grain, because white bread had too few vitamins to make it worth including. But most did not. "Al forms of bread contain a large proportion of carbohydrate, varying from 4565 percent," noted H. Gardiner-Hil of London's St Thomas's Hospital Medical School in 1925, "and the percentage in toast may be as high as 60. It should thus be condemned."

When these physicians talked about lean meat as the basis of a weight-reducing diet, they did not mean a chicken breast without the skin, as has been the iconic example for the past twenty years. They meant any meat, fish, or poultry (bacon, salt pork, sausage, and duck occasional y excepted) in which the visible fat had been trimmed away.

Once weight was satisfactorily lost, weight-maintenance diets were also restricted in carbohydrates, although not so drastical y. For maintaining a reduced weight, as described by the Pittsburgh physician Frank Evans in the 1947 edition of the textbook Diseases of Metabolism, the daily diet should include at least one egg, a gla.s.s of skimmed milk, a portion of raw fruit, "a generous portion of any cut of lean fresh lamb, beef, poultry or fish," and a portion of each of three 5-percent vegetables. Individuals trying to maintain their weight loss could then eat anything else they wanted, Evans wrote, but they could do so only as long as they maintained a stable weight and were sufficiently "sparing with" alcohol, added fats and oils, "concentrated carbohydrate foods," "starches," "mealy vegetables, which are potatoes, beans, peas," and "cereals, used as vegetables, which are: macaroni, spaghetti, rice, corn."

Evans provided one of the few variations on this regime that caught on as an obesity therapy in the years before World War I . This was a very low-calorie diet, of 360 to 600 calories a day, rather than the common prescription of 1,200 to 1,500 calories, then considered the minimal amount that a patient would tolerate and that would produce a safe and consistent weight loss. Evan's diet could induce a loss of up to five pounds a week, rather than the two pounds predicted for the more typical semi-starvation diets. The daily menu, explained Evans in 1929, was "composed of fresh meat and egg white. Approximately 100 [grams] of lean steak was the backbone of each of the two largest meals. When necessary, fresh fish was given at intervals." No starches or sugars were al owed, but the patient could eat a few ounces of 5-percent vegetables and one ounce of bread each day. These minimal carbohydrates-perhaps twenty grams-were included to "spare" the protein in the diet, so that it would be utilized for balancing out nitrogen losses rather than having some of it converted to glucose to fuel the brain and central nervous system. "The secret of the success of this procedure depends, almost certainly, on giving enough protein," Russel Wilder of the Mayo Clinic wrote after first prescribing the diet for his patients in 1931. Evans's very low-calorie diet may also have been popular because it appealed to the puritanical sense of those clinicians like Louis Newburgh, who believed that gluttony had to be vigorously curbed in obese patients. One of the fundamental rules of Evans's diet was: "No concession to gustatory sensualism is permitted."

In the century before the medical community began prescribing fat-restricted, carbohydrate-rich diets for weight loss, one point of controversy was whether carbohydrates should be avoided because they are uniquely fattening or perhaps even cause obesity-as Jean Anthelme Bril at-Savarin and Wil iam Banting would have suggested-in which case they would be the only nutrient restricted, or because they const.i.tute superfluous calories, in which case dietary fat was restricted as wel , by avoiding oils, lard, and b.u.t.ter. "The next question to decide," wrote the Chicago physician Alfred Croftan in the Journal of the American Medical a.s.sociation in 1906, "is whether the carbohydrates or the fats are to be chiefly restricted."

One observation made repeatedly through the 1960s was that the obese favor carbohydrates, and that these const.i.tute the great proportion of al calories they consume. Though the obese did not appear to eat more calories, on average, than the lean, they did consume more carbohydrates. Such a dietary a.s.sessment was inevitably difficult to make with any accuracy, explained Sir Derrick Dunlop of the Royal Infirmary in Edinburgh, when he reported in 1931 on the lessons he had learned from treating 523 obese patients. Nonetheless, Dunlop believed that "obesity does occur in persons without showing any direct relationship to food intake, and that a certain group of patients do become overweight on an apparently normal wel -balanced diet,"

and, second, "that an outstanding dietetic abnormality was an excessive intake of carbohydrate." "In some extreme cases," he noted, "the diet had consisted almost exclusively of sweet tea, white bread and scones."

This observation was echoed in The Lancet in 1935 by the British physician John Anderson, and in the 1940s by Hilde Bruch, Hugo Rony, and the Harvard physician Robert Wil iams and his col eagues, al of whom had questioned their fat patients extensively about their diets. Their common finding was an excessive consumption of starches and sweets. Rony reported that the craving for sweets and starches among his patients was so common that it suggested an underlying physiological mechanism at work, possibly related to a greater need for or reduced availability of glucose. "It is easier to induce the gluttonous obese to control his general appet.i.te than to control his craving for sweets," Rony noted. One common rationale for restricting carbohydrates in weight-reducing diets was that it eliminated a disproportionately large share of the calories that the obese would normal y eat.*92 When carbohydrates are restricted, however, calories may also be cut-and the reverse is nearly always true. One of the revolutionary aspects of Frank Evans's very low-calorie diet was that it also restricted carbohydrates almost entirely.93 When Louis Newburgh subsequently concluded that al obese patients can sustain a significant rate of weight loss for months or years if their diet is sufficiently draconian-as was the case with his patient who lost over 360 pounds-he was using Evans's very low-calorie, very low-carbohydrate diet to generate this weight loss. His patient lost the weight while eating at most a hundred calories of carbohydrates daily. It could have been the restriction of carbohydrates that was responsible for the weight loss. It could also have been the calorie restriction.

This same confounding of calories and carbohydrates might also explain the success stories attributed to low-calorie diets-Albert Stunkard's one patient in a hundred, as he reported in 1959, who lost as much as forty pounds and managed to keep it off. It's effectively impossible to restrict calories significantly without also reducing the carbohydrates. Any calorie-restricted diet that restricts al calories equal y, restricts carbohydrates, too. Even diets that preferential y reduce fat wil have to reduce carbohydrates to achieve a significant reduction in calories (unless the dieters are wil ing to sacrifice protein in fish and meat, for instance, in order to avoid the fat that accompanies it). If dieters avoid sweets and snacks, and if they drink sugar-free soda but not regular soda, they're reducing their carbohydrate consumption significantly, and they're changing the type of carbohydrates they consume. Any benefit may be due to the calories reduced, or the carbohydrates, or even just the relative absence of sugar.