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 classically 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 “will 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 will 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 virtually every respect from the positive-caloric-balance/overeating hypothesis. It implies a cause of weight gain and a treatment that stand in contradiction to virtually 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 (tautologically) 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 cells, 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
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 “pulled” into the fat cells, rather than pushed, with our fat tissue playing a very active role in this process. It assumes that energy intake and expenditure are
The only thing missing from this hypothesis as it was originally 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 tells 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 chronically 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 Cahill 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 well-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 well. 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 cells; 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. Ironically, it disappeared just as all 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 well, 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 will argue, was a mistake.
Through the beginning of World War II, the notion that a defect in fat metabolism causes obesity was known as the
