Good Calories, Bad Calories (65 page)

This brings us back to the questions we asked earlier: If people eat less on carbohydrate-restricted diets, why aren’t they hungry. And if they don’t eat less, why do they lose weight? If the restriction of carbohydrates works to ameliorate this defect in fat metabolism, as Pennington speculated, then weight wil be lost, hunger wil be absent, and calorie consumption may decrease, while energy expenditure wil increase. This is no more than the consequences of the law of energy conservation applied to a biological system that works to conserve body composition and maintain a healthy flow of fuel to the cel s and tissues.

In an ideal world, Pennington’s metabolic-defect hypothesis of obesity would have been tested directly. Instead, it was ignored. Pennington made this easier by speculating that the root cause of obesity was an inability to metabolize properly a compound cal ed pyruvic acid. This made physiological sense, but further research quickly refuted it. Pennington’s error al owed his contemporaries in nutrition and obesity research to dismiss him as just another renegade who refused to accept the reality of energy conservation. He deserved far better, as it wouldn’t be long before researchers pinned down the precise nature of the metabolic-hormonal defect that appears to be the driving force in the accumulation of excess fat.

THE CARBOHYDRATE HYPOTHESIS, I: FAT METABOLISM

Looking at obesity without preconceived ideas, one would assume that the main trend of research should be directed toward an examination of abnormalities of the fat metabolism, since by definition excessive accumulation of fat is the underlying abnormality. It so happens that this is the area in which the least work has been done.

HILDE BRUCH, The Importance of Overweight, 1957

IN JUNE 1962, EDWIN ASTWOOD OF Tufts University gave the presidential address to the annual meeting of the Endocrinology Society in Chicago. Although Astwood was not known as an obesity researcher, he nonetheless took the opportunity to present what he considered the obvious explanation for its cause. A physician who had spent thirty years studying and treating hormone-related disorders, Astwood had discovered the reproductive hormone luteotropin (now known as luteinizing hormone), and he had created the standard technique for purifying pituitary hormones. He had performed what The New England Journal of Medicine would cal a “bril iant series of experiments” to demonstrate that hyperthyroidism could be control ed with anti-thyroid drugs. By 1976, when Astwood died, three dozen of his former students had become ful professors; eight were department chairmen—“a record perhaps unequaled in medicine,” according to his obituary in the journal Endocrinology. He was a man who knew what he was talking about, even when he was speculating, as he was in his 1962 address, entitled “The Heritage of Corpulence.”

Astwood believed that obesity and a disposition to fatten are genetic disorders. If genes determine stature and hair color, the size of our feet, and a

“growing list of metabolic derangements,” he asked, then “why can’t heredity be credited with determining one’s shape?” Although it’s possible to fatten animals by stuffing them, “and doubtless we could do the same thing to ourselves if we put our minds to it,” Astwood did not consider this a cause of overweight. “Not many people try to get into the circus this way,” he said—“they become candidates spontaneously.” He also considered inactivity to be of dubious importance. “Many of our moderately fat patients sit like bumps on a log,” he said, but that could be an effect, not a cause. “It would be interesting to know whether adiposity and inertia go together for some reason common to both. If fatty acid is needed for energy, a deficit could indeed promote lethargy and indolence.”

Astwood then described what had been learned over the past thirty years about the hormonal regulation of fat metabolism. “To turn what is eaten into fat, to move it and to burn it requires dozens of enzymes and the processes are strongly influenced by a variety of hormones,” he explained. Sex hormones, for instance, determine where fat is stored, as evidenced by the differences in fat distribution between men and women. Thyroid hormones, adrenaline, and growth hormone accelerate the release of fatty acids from fat depots, as does a hormone known as glucagon, secreted by the pancreas.

“The reverse process,” Astwood said, “the reincorporation of fat into the depots and the conversion of other food to fat, tends to be reduced by these hormones, but to be strongly promoted by insulin.” Al of this demonstrated “what a complex role the endocrine system plays in the regulation of fat.”

Final y, Astwood speculated on what he considered the simplest possible explanation for obesity, and here he echoed Alfred Pennington, although, if he had read Pennington’s work, he neglected to mention it. “Now just suppose that any one of these (or other unlisted) regulatory processes were to go awry,” Astwood said.

Suppose that the release of fat or its combustion was somewhat impeded, or that the deposition or synthesis of fat was promoted; what would happen? Lack of food is the cause of hunger and, to most of the body, [fat] is the food; it is easy to imagine that a minor derangement could be responsible for a voracious appetite. It seems likely to me that hunger in the obese might be so ravaging and ravenous that skinny physicians do not understand it.

There is no reason to suppose that only one of these mechanisms ever goes wrong…. There are so many possibilities here that I am wil ing to give odds that obesity is caused by a metabolic defect. I would not want to wager about how many enzymes determine the shape of voluminous pulchritude.

This theory would explain why dieting is so seldom effective and why most fat people are miserable when they fast. It would also take care of our friends, the psychiatrists, who find al kinds of preoccupation with food, which pervades dreams among patients who are obese. Which of us would not be preoccupied with thoughts of food if we were suffering from internal starvation? Hunger is such an awful thing that it is classical y cited with pestilence and war as one of our three worst burdens. Add to the physical discomfort the emotional stresses of being fat, the taunts and teasing from the thin, the constant criticism, the accusations of gluttony and lack of “wil power,” and the constant guilt feelings, and we have reasons enough for the emotional disturbances which preoccupy the psychiatrists.

For the past century, the conspicuous alternative to the positive-caloric-balance hypothesis has always been, as Pennington, Astwood, and Hilde Bruch suggested, that obesity is caused by a defect in the regulation of fat metabolism. At the risk of repetition, it is important to say this is, by definition, a disorder of fat accumulation, not a disorder of overeating. For whatever reason, the release of fat or its combustion is impeded, or the deposition or synthesis of fat is promoted, as Astwood said, and the result is obesity. That in turn wil cause a deficit of calories elsewhere in the body—Astwood’s

“internal starvation”—and thus a compensatory hunger and sedentary behavior.

This alternative hypothesis differs in virtual y every respect from the positive-caloric-balance/overeating hypothesis. It implies a cause of weight gain and a treatment that stand in contradiction to virtual y everything we have come to believe over the past fifty years. For this reason, it’s a good idea to compare the basic propositions of these two competing hypotheses before we continue.

The positive-caloric-balance/overeating hypothesis dictates that the primary defect is in the brain, in the “regulation of ingestive behaviors, particularly at the cognitive level,” as it was described by the University of California, Santa Cruz, biologist M.R.C. Greenwood in 1985. This defect purportedly causes us to consume more calories than we expend, and thus induces weight gain. Overeating and sedentary behavior are defined (tautological y) as the causes of obesity. The treatment is to create a caloric deficit by eating less and/or expending more. This hypothesis presupposes that excess calories accumulate in the body and thus are effectively “pushed” into the fat cel s, which play a passive role in the process. And the calories remain bound up as fat only because we never expend sufficient energy to require their use.

Implicit in this hypothesis is the assumption that energy expenditure and energy intake are independent variables. Because they are independent, one of these variables can be manipulated, consciously or unconsciously, so that the primary result wil be an increase or a reduction in energy stores—i.e., the amount of fat we carry—without the other responding. It is almost impossible to overstate the extent to which this hypothesis now pervades al thinking and research on obesity and weight, and underlies every accepted method of treatment and prevention. As Greenwood observed, “The vast majority of the notoriously unsuccessful weight control programs are predicated on this assumption.”

By contrast, the alternative hypothesis proposes that the primary defect is hormonal and metabolic—in fat storage and/or the burning of fat for fuel (oxidation)—and is in the body, not the brain. This defect causes the excessive accumulation of calories as fat and compensatory urges to eat more and expend less energy. In this hypothesis, overeating and inactivity (hunger and lethargy) are side effects of this underlying metabolic defect; they are not causes. The hypothesis presupposes that calories are effectively “pul ed” into the fat cel s, rather than pushed, with our fat tissue playing a very active role in this process. It assumes that energy intake and expenditure are dependent variables: a change in one induces a compensatory change in the other, because the body constantly works to maintain a healthy body composition and a dependable flow of energy to the cel s. Immoderate eating and physical inactivity do not induce obesity, because the body adjusts intake to expenditure and expenditure to intake. Neither eating less nor exercising more addresses the cause of the problem, and that’s why these approaches fail. The only effective treatments, according to this hypothesis, would be those that remedy the fundamental regulatory defect.

The only thing missing from this hypothesis as it was original y conceived a century ago, or as reconceived by Pennington and then Bruch and Astwood, was an explanation for the epidemiological observations. In other words, obesity may be caused by a hormonal or metabolic defect determined primarily by genetic inheritance, but the epidemiology tel s us that this defect is triggered by environmental factors. Genetics determines our propensity to put on weight, but those genes (nature) have to be triggered by an agent of diet or lifestyle (nurture) to explain the association of obesity with poverty, the present obesity epidemic, and the emergence of obesity in recently Westernized populations. A change in the environment is also necessary to explain why man alone seems to grow chronical y obese, not other species of animals. “Something has happened in the past twenty, thirty, forty years in the incidence of obesity, and that has to be environmental,” as George Cahil has said about the present obesity epidemic.

The likely explanation is the effect of diet on this regulation of fat metabolism and energy balance. Since insulin, as Astwood noted, is the hormone responsible for promoting the incorporation of fat into our adipose tissue and the conversion of carbohydrates into fat, the obvious suspects are refined carbohydrates and easily digestible starches, which have wel -documented effects on insulin. This is what Peter Cleave argued, albeit without understanding the underlying hormonal mechanisms at work, and what the geneticist James Neel, father of the thrifty-gene hypothesis, came to believe as wel . And it’s the effect of these carbohydrates on insulin that would explain the dietary observations—the futility of calorie restriction, the relative ease of weight loss when carbohydrates are restricted, and perhaps two centuries of anecdotal observations that sweets, starches, bread, and beer are uniquely fattening.

In this hypothesis, obesity is another variation on the theme of insulin dysfunction and diabetes. In Type 1 diabetes, the cause is a lack of insulin. The result is an inability to use glucose for fuel and to retain fat in the fat tissue, leading to internal starvation, as Astwood put it, excessive hunger, and weight loss. In obesity, the cause is an excess of insulin or an inordinate sensitivity to insulin by the fat cel s; the result is an overstock of fuel in the adipose tissue and so, once again, internal starvation. But now the symptoms are weight gain and hunger. In obesity, the weight gain occurs with or without satisfying the hunger; in Type 1 diabetes, the weight loss occurs irrespective of the food consumed.

This alternative hypothesis of obesity ultimately vanished in the 1980s, a casualty of the official consensus that fat was the dietary evil and carbohydrates were the cure. Ironical y, it disappeared just as al the relevant physiological mechanisms had been worked out and a causal path established from the carbohydrates in the diet through insulin to the regulatory enzymes and molecular receptors in the adipose tissue itself.

This alternative hypothesis of obesity constitutes three distinct propositions. First, as I’ve said, is the basic proposition that obesity is caused by a regulatory defect in fat metabolism, and so a defect in the distribution of energy rather than an imbalance of intake and expenditure. The second is that insulin plays the primary role in this fattening process, and the compensatory behaviors of hunger and lethargy. The third is that carbohydrates, and particularly refined carbohydrates—and perhaps the fructose content as wel , and thus the amount of sugars consumed—are the prime suspects in the chronic elevation of insulin; hence, they are the ultimate cause of common obesity. These latter two propositions—that insulin regulates fat deposition and carbohydrates regulate insulin—have never been controversial, but they’ve been dismissed as irrelevant to obesity, given the ubiquitous belief that obesity is caused by overeating. That, I wil argue, was a mistake.

Through the beginning of World War I , the notion that a defect in fat metabolism causes obesity was known as the lipophilia hypothesis. “Lipophilia”