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A war on obesity, not the obese
In their efforts to lose weight, obese individuals are fighting biology, evolution and a culture that misunderstands them
Food consumes our interest. To the hungry, it is the focal point of every thought and action. To hundreds of millions of obese and overweight individuals, it is the siren’s song, a constant temptation that must be avoided lest one suffer health consequences and stigmatization. To the non-obese, it is a source of sustenance and often pleasure. To the food and diet industries, it is big business. And to those interested in public health, it is at the root of one of the most pressing public health problems in the developed and developing world.
Alarm about the health crisis associated with an emerging “obesity epidemic” is sounded almost weekly in response to reports that its incidence has greatly increased over the past decade. Many argue that this explosive increase over a short period of time indicates that the obesity problem is primarily a result of our modern lifestyle. The facts, however, do not support this conclusion. For example this argument fails to take into account that the increasing incidence of obesity in the population, from 23.3 percent in 1991 to 30.9 percent today, is not reflected by a proportionate increase in the weight of the average American, which grew by just 7 to 10 pounds.
Thus while we can’t minimize the importance of the fact that more than half of the U.S. population is now overweight or obese, we should highlight the fact that the change in weight attributable to any recent change in our environment, such as a change in diet or a more sedentary lifestyle, is much smaller than the enormous differences in weight, often numbering in the hundreds of pounds, that can be observed among individuals. The question might as well be, in our current environment where almost everyone has essentially free access to unrestricted calories, why is anyone thin?
The answer appears to reside in our genes and the way in which they interact with environmental factors. Numerous studies have shown that the heritability of obesity is equivalent to that of height and exceeds that of many disorders for which a genetic basis is generally accepted.
Consider the case of a 200-pound, 9-year-old English girl whose legs were so large she could barely walk. She was found to lack a weight-regulating hormone called leptin, and often consumed as much as 1100 calories in a single meal, approximately half the amount an average adult would require in an entire day. After leptin treatment, this was reduced to 180 calories, the typical intake for a child her age. Her weight is now normal. About five percent of severely obese children have been shown to carry defects in known single genes, and there are likely to be other forms of genetic obesity that have yet to be identified.
In general, obesity genes encode the molecular components of the system that regulates energy balance, matching food intake to energy expenditure and maintaining constant energy stores in the form of fat. Normally, the system is incredibly precise. Over the course of a decade, a typical person consumes approximately 10 million calories, generally with only a modest change in weight. To accomplish this, energy intake and output must match with just a 0.17 percent margin for error. This extraordinary level of precision exceeds by several orders of magnitude the ability of nutritionists to accurately count calories and suggests that conscious factors alone are incapable of precisely regulating caloric intake.
So why are some individuals obese and others not? Feeding is a complex motivational behavior, and many factors influence when we start eating and when we stop. These factors include the unconscious urge to eat that is regulated by leptin and other hormones, the conscious desire to eat less (or more), sensory factors such as smell and taste, emotional state, and others. The brain somehow processes this diverse information. Though there is clearly cross-talk between brain regions that produce a basic drive to eat and those that express your conscious wishes, the feeling of hunger is intense and, even if not as potent as other basic drives, such as the drive to breathe, it is the powerful force that the obese must resist in order to sustain weight loss. For most dieters, sooner or later a primal hunger trumps the conscious desire to be thin.
There’s also an environmental component. As a species, we carry the genetic legacy of two environments. One is passed down from hunter-gatherers, who had only sporadic access to food. In such an environment, genes that predispose to obesity increase energy stores and provide a survival advantage in times of famine. The second, passed down from more recent societies, is the result of a decreased risk of starvation but a higher risk of obesity related health problems. In this environment, genes that resist obesity and its complications would have a selective advantage. It may be that it is the obese who carry the hunter-gatherer genes and the lean that carry the Western genes, an idea supported by the observation that populations that were historically more prone to starvation (Pima Indians, Pacific Islanders and others) become the most obese when exposed to a Western diet and lifestyle.
The challenge we face now is to build a molecular framework for the system that regulates weight and to identify these genes and genetic variants that cause obesity. As we learn more about the physiologic system that balances energy, the impact of the environment on its function will also become better understood and new therapeutic approaches will be developed.
In the meantime, a different kind of understanding is called for. Obesity is not a personal failing. In trying to lose weight, the obese are fighting a difficult battle. It is a battle against biology, a battle that only the intrepid take on and one in which only a few prevail.

Adapted with permission from A War on Obesity, Not the Obese, Science, 299:856, February 7, 2003. 2003 AAAS. To read the article in its entirety, visit http://www.sciencemag.org/cgi/content/full/299/5608/856?ijkey=I8k8M9ZPdI83U&keytype=ref&siteid=sci

May 13, 2005



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