Genes Take Charge, and Diets Fall by the Wayside
Before the diet began, the fat subjects' metabolism was normal Ã¢Â€Â” the number of calories burned per square meter of body surface was no different from that of people who had never been fat. But when they lost weight, they were burning as much as 24 percent fewer calories per square meter of their surface area than the calories consumed by those who were naturally thin.
The Rockefeller subjects also had a psychiatric syndrome, called semi-starvation neurosis, which had been noticed before in people of normal weight who had been starved. They dreamed of food, they fantasized about food or about breaking their diet. They were anxious and depressed; some had thoughts of suicide. They secreted food in their rooms. And they binged.
The Rockefeller researchers explained their observations in one of their papers: "It is entirely possible that weight reduction, instead of resulting in a normal state for obese patients, results in an abnormal state resembling that of starved nonobese individuals."
It's an interesting read on some history of research into human weight loss, weight gain, and diet. It also has a compelling ending:
The message is so at odds with the popular conception of weight loss — the mantra that all a person has to do is eat less and exercise more — that Dr. Jeffrey Friedman, an obesity researcher at the Rockefeller University, tried to come up with an analogy that would convey what science has found about the powerful biological controls over body weight.
He published it in the journal Science in 2003 and still cites it:
"Those who doubt the power of basic drives, however, might note that although one can hold one's breath, this conscious act is soon overcome by the compulsion to breathe," Dr. Friedman wrote. "The feeling of hunger is intense and, if not as potent as the drive to breathe, is probably no less powerful than the drive to drink when one is thirsty. This is the feeling the obese must resist after they have lost a significant amount of weight."
It seems to me that discussion of the evolution of obesity-related genes has been wrongly directed toward the pathological result. Instead of the variation in weight gain, we need to consider how this variability in hunger would have affected people in the relevant populations.