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Skinny genes: How DNA shapes weight-loss success Add to ...

Researchers, who discovered it in diabetes studies with mice in 2007, originally nicknamed it the "fatso gene" because it spanned a large stretch of DNA code. Only later did they learn it plays a major role in becoming fat. Acting on the brain's hypothalamus, the FTO gene seems to fuel appetite even after a person is full, increasing the risk of obesity by as much as 70 per cent. What's more, almost half of all people of European descent carry it.

A recent European study of 752 teenagers found those who carry the FTO gene had more body fat than non-carriers unless they exercised for an hour each day. A study of Amish adults in Pennsylvania found that carriers needed three to four hours a day of moderate exercise to keep the weight off.

Even so, large population studies show that while the gene hinders weight loss, it actually has a mild effect, relatively speaking. People who carry two copies of FTO tend to weigh only about six to seven pounds more than those who do not carry any copies. The difference is only three to five pounds at Dr. Hegele's clinic, where there are also patients without the gene who weigh 300 pounds.

"We're just at the kindergarten stage of understanding how to integrate genetic testing into risk prediction in the clinic," Dr. Hegele says. After learning that they carry the FTO gene, "a few patients see the glass as being half empty and react fatalistically: They think there's nothing to be done and so they are not inclined to act. ... Others do become motivated, but they are not the majority."

The reactions are further complicated in that genes related to weight confer only a predisposition, Dr. Hegele says. This means they might be mitigated not only by efforts to stay fit, but also by other genes - and the vast majority of genes involved in weight gain have yet to be identified.

Many of these genes are thought to be involved in the complex connections between our minds and bellies. For example, research from McGill University suggests that weight struggles and obesity should be considered neurobiological disorders - mediated by a small but powerful group of hormones that can push us to feast when we're full, slow our metabolism and zap the motivation to climb on that treadmill.

Most weight-loss efforts fail because the solutions fail to take the root causes into account, says Dr. Sharma, who is also scientific director of the Canadian Obesity Network. Those causes are the product of an individual's genes and experience - and there is no "one-size-fits-all" solution.

"It comes down to seeking professional help," to tailor a personal plan, Dr. Sharma says. For instance, not everyone has experienced exercise as a positive endeavour and DNA, he says, is a blueprint shaped very much by experience.

"There is no point in prescribing an obesity treatment to people to do things they do not enjoy - people don't like doing things they are not good at. If you're not a natural-born athlete, … taking up regular running, for example, is going to be very difficult."

So how does such a person tackle long-term weight loss?

Those not inclined to take up a vigorous exercise regimen should do "whatever it is that they can enjoy," Dr. Sharma suggests. "Even small bouts of activity - using the stairs, standing rather than sitting in meetings, parking farther away - can help manage weight."

After all, some research has found that a natural-born fidgeter can slay up to 700 calories a day, doing little more than spontaneous muscle contractions and sitting up straight.

Many people can also limit weight gain just by watching how and when they eat, Dr. Sharma adds.

If a person needs, say, 2,000 calories a day but consumed only 400 by dinnertime, he says, the additional 1,600 calories needed is bound to come by way of a huge dinner and dangerous couch-side snacking. Yet if you didn't eat breakfast, or much of a lunch, the body's furnace shifts into starvation mode by evening, he says, meaning that it will cling to every calorie consumed.

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