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Obesity gene may not be easy excuse

By EMILY WALKER, UPI Health Correspondent

WASHINGTON, April 30 (UPI) -- A variant of a common gene can make a person more likely to be obese than those without the gene, according to a recent British study.

The research also marks the first large-scale trial to pinpoint a genetic link between obesity and type 2 diabetes.

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Zeroing in on a genetic link may explain why so many Americans and Europeans are overweight and obese. Could the new evidence cause those with the gene to feel helpless to overcome their weight problem, or could identifying the gene help people avoid gaining weight? Perhaps both, experts say, although it's too early to tell.

"The main controversy is whether it is good to know (whether) how fat you are is partially genetic," said Andrew Hattersley of Peninsula Medical School in Exeter, co-author of the study that was published April 12 in the journal Science.

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For the study, researchers reviewed 13 previous studies of 39,000 white Europeans and evaluated their genetic susceptibility to type 2 diabetes. The researchers found a variant located in a gene called FTO that made certain people more likely to be overweight or obese and subsequently develop type 2 diabetes.

The link was detected in kids as young as 7. About 16 percent of the study sample had the gene, which put them at a 67 percent greater risk for being obese, or having a body mass index of 30 or more. BMI is a measure of body fat derived from a person's height and weight.

From 2003 to 2004, 66 percent of the U.S. population was classified as overweight, or having a BMI more than 25; 32 percent of that number were obese. A 5'5'' woman weighing 180 pounds would be classified as obese; a 5'11'' man weighing 215 would also be obese.

The study looked only at white Europeans, so the results could certainly be applied to white Americans, Hattersley said. But among other racial and ethnic groups, the effect of the gene may be different.

In addition, about one-third of those in the study with the fat gene were not obese, which means many factors, especially diet and exercise, influence a person's weight.

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While the study authors said uncovering this genetic link may lead to "novel pathways" in reducing the risk for obesity, going to the doctor and getting tested for the variant for obesity-prevention purposes is not currently an option.

"It wouldn't do anyone any good to know they have the gene at this time," said Dr. Robert Karp of the National Institute of Diabetes and Digestive and Kidney Diseases. For one thing, the research was not conclusive that the FTO variant caused obesity -- rather, it could be a number of genes located near the FTO gene play a role in a person's weight.

Still, Karp considers the study a landmark because scientists have been unable to replicate results from past studies establishing a link between genetics and obesity. But Karp estimates that it will be at least another five years before studies establish a definitive link, and perhaps much longer before that knowledge benefits those with weight problems.

In the meantime, researchers do know the FTO gene is expressed in an area in the brain called the hypothalamus, which controls hunger urges, so it is possible that appetite suppressants could lessen the effects of the predisposing gene. The gene is also expressed in the pancreas, which regulates insulin, so taking medication to regulate insulin production may also help counteract weight gain.

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But even with those potential remedies, knocking out the fat gene's power would have a limited effect on weight gain. The researchers found the gene itself was responsible for only an extra 3 pounds of fat and an extra 1 centimeter around the waist -- suggesting lifestyle may trump genetics when it comes to weight.

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