Good Calories, Bad Calories

Finally, 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 willing 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 all 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 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 independent variables. Because they are independent, one of these variables can be manipulated, consciously or unconsciously, so that the primary result will 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 all 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.”