Fat: Fighting the Obesity Epidemic

Fat: Fighting the Obesity Epidemic

Fat: Fighting the Obesity Epidemic

Fat: Fighting the Obesity Epidemic


When the leptin gene was discovered in 1994, news articles predicted that there might soon be an easy, pharmaceutical solution to the growing public health crisis of obesity. Yet this scientific breakthrough merely proved once again how difficult the fight against fat really is. Despite the many appetite-suppressants, diet pills, and weight-loss programs available today, approximately 30 percent of Americans are obese. And that number is expanding rapidly. Fat is the engaging story of the scientific quest to understand and control body weight. Covering the entire twentieth century, Robert Pool chronicles the evolving blame-game for fat--from being a result of undisciplined behavior to subconscious conflicts, physiological disease, and environmental excess. Readers in today's weight-conscious society will be surprised to learn that being overweight was actually encouraged by doctors and popular health magazines up until the 1930s, when the health risks associated with being overweight were publicly recognized. Thus began decades of research and experiments that subsequently explained appetite, metabolism, and the development of fat cells. Pool effectively reanimates the colorful characters, curious experiments, brilliant insights and wrong turns that led to contemporary scientific understanding of America's epidemic. While he acknowledges the advances in the pharmacological fight against flab, he underscores that the real problem of obesity is not losing the weight but keeping it off. Drugs offer a quick fix, but they aren't the ultimate answer. American society must remedy the unhealthy daily environments of its cities and towns, and those who have struggled with their weight and have experienced the "yo-yo" cycle of dieting must understand the underlying science of body weight that makes their struggle more than a question of willpower.


The twenty-two-year-old Turkish man, identified only as Patient 24, was discovered in early 1997 by Metin Ozata. Ozata, a doctor at Turkey's Gulhane School of Medicine in Etlik-Ankara, was assembling subjects for a study of obesity in Turkey, and the twenty-two-year-old male was the fattest he had yet found. In the words of the bland clinical report, Patient 24 was “markedly hyperphagic”—which, translated into layman's terms, means roughly “eats as much as any two normal people.” Five-foot-six and 330 pounds with a fifty-five-inch waist and fifty-nine-inch hips, the man could not walk a city block without stopping to rest. Strangely enough, his four brothers and one sister were of normal weight, actually quite thin by American standards. The five had an average body mass index—the standard measure of fatness—of just 23, which works out to 143 pounds on a five-foot-six frame, well below anyone's definition of overweight. Their brother's body mass index was, by contrast, a massive 55.8.

Besides his weight, Patient 24 was unusual in a number of other ways, Ozata found. He had never gone through puberty. He had no beard and very little hair in his pubic region or, except for his head, anywhere else on his body. He had higher-than-normal levels of insulin in his bloodstream and exceptionally low levels of male hormones. His penis and testicles had never gotten larger than a small boy's, while his breasts were more like a woman's than a man's.

To anyone acquainted with the history of obesity research, the set of symptoms displayed by Patient 24 was strikingly familiar. In 1950, researchers at the Jackson Laboratory in Maine had discovered a mutant mouse that grew to three times the weight of normal mice, with immense deposits of fat that left it so round that it had trouble walking. The researchers named the mutation obese and bred it into an inbred strain of mice. When the researchers further studied these obese mice, they found that they had exceptionally high insulin levels, did not develop sexually, and were infertile.

If Patient 24 had been discovered five years earlier, his resemblance to the obese mouse might have been noted, but most likely he would have been written off as nothing more than an interesting case, an obesity of unknown origin accompanied by further hormonal disturbances. In 1994, however, a researcher at the Rockefeller University in New York City had, after years of searching, tracked down the gene affected by the obese mutation. The gene, it turned out, instructs the body how to create a hormone called leptin, which is produced in . . .

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