Gene Linked to Binge Eating

Flawed Appetite Suppression Gene Found in Obese Binge Eaters

From the WebMD Archives

March 19, 2003 -- A mutation in a gene related to appetite suppression has been linked to binge eating in obese people. The finding could someday lead to better weight-loss weapons for people who have had little success fighting the battle of the bulge, researchers say.

Investigators found that a particular gene involved with the signaling of suppression of appetite was abnormal in obese binge eaters. In the study, melanocortin 4 receptor (MC4R) mutations occurred in roughly 5% of morbidly obese people, all of whom reported having been diagnosed with binge eating. The findings appear in the March 20 issue of TheNew England Journal of Medicine.

People with binge-eating disorder frequently eat huge amounts of food over a short period of time until they feel uncomfortable or even sick. Unlike the similar, but distinct, eating disorder bulimia nervosa, people with the syndrome do not purge, take laxatives, or over-exercise after bingeing. The National Institutes of Health estimates that 2% of people in the United States suffer from binge-eating disorder, but a much higher percentage of obese people -- as many as 70% -- are believed to be binge eaters.

In the newly published study, an international team of researchers assessed the prevalence of three distinct genetic mutations in 469 severely obese patients. In addition to MC4R, the investigators looked for mutations in the leptin receptor gene and the proopiomelanocortin gene, both of which have been implicated in obesity.

They found that 24 of the obese patients (5%) had MC4R mutations and all 24 reported binge eating, while just 14% of obese people without the mutation considered themselves binge eaters. Neither of the other mutations was linked to binge eating.

"We found that binge eating appears to be a characteristic of people with this MC4R mutation," researcher Fritz F. Horber, MD, tells WebMD. "That is not to say that all binge eating is due to this gene mutation. There are many environmental and genetic factors associated with binge eating."

What the findings might do, Horber says, is help doctors identify obese patients who are particularly likely to fail at weight-loss interventions because their overeating is driven by a specific genetic abnormality. But he adds that most of his obese patients with the mutation seem relieved to find a genetic reason for their weight problems.

"There is always a lot of guilt among people who are very overweight, because they believe, and are told, that it is totally their fault," he says. "My patients with this mutation seem to be much less depressed because we have given them a reason for why they are the way they are."

While this specific mutation appears to be the cause of obesity in, at most, one in 20 obese people, Horber believes genetic factors play some role in almost all obesity. Dozens of different genes have been implicated in human obesity, but molecular endocrinologist Joel F. Habener, MD, says obesity is rarely caused by just one genetic mutation.

"Obesity is a complex disease that is likely to have multiple genetic and environmental influences," says Habener, who wrote an editorial published along with the study. "Environmental factors appear to be driving an epidemic of obesity. We live in an increasingly sedentary society and have ready access to inexpensive calories." Habener is a professor of medicine at Harvard Medical School, and is director of the laboratory of molecular endocrinology at Massachusetts General Hospital.

Both researchers say the search for the genetic cause of obesity should lead to better drugs to treat the problem. In his editorial, Habener wrote that drugs already under development may prove effective for the treatment of binge-eating disorder in overweight patients.

"Right now there are really no effective drugs to treat morbid obesity," Habener tells WebMD. "But I think within the next decade we will see better treatments based on genetic research."

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SOURCES: The New England Journal of Medicine, March 20, 2003. Fritz E. Horber, MD, Klinik Hirslanden, Zurich, Switzerland. Joel F. Habener, MD, director, laboratory of molecular endocrinology, Massachusetts General Hospital; professor of medicine, Harvard Medical School; investigator, Howard Hughes Medical Institute.
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