Scientists have long researched the fat-boosting gene FTO to find out why people with the high-risk mutation of the gene correlated so highly with being overweight. New findings suggest the connection stems from FTO's overproduction of ghrelin, the hormone responsible for hunger, in high-risk cases.

Published in The Journal of Clinical Investigation, the study found that a mutation of the gene made fatty foods more tempting and increased production of the hormone ghrelin, which controls levels of hunger in the brain. These findings led researchers, who operated out of the University College London, to believe FTO's high-risk presence in the subjects "biologically programmed" them to eat more.

As a gene, FTO appears as a pair on the 16th chromosome — where each parent passes on one copy to the child. Each copy comes as either a high-risk or low-risk form. Those with high-risk pairs have been associated with greater rates of obesity compared to people with low-risk pairs. By one study's estimate, people with the high-risk pairs are 70 percent more likely to be obese.

The University College London study examined ghrelin levels on either side of a meal to see how the hormone curbed appetite in both high- and low-risk cases. All subjects were normal weight.

After the meal, the ghrelin levels in the high-risk group never reached as low as the low-risk group's levels. Moreover, the levels climbed back much more quickly in the high-risk group.

In subsequent tests, a series of brain scans after a meal showed further gaps between the two groups. Men with the high-risk genes found pictures of high-fat foods more appealing than the low-risk men. One expert heaped the blame on faulty genetic wiring.

"Their brain is set up to be particularly interested in anything to do with high-calorie food," Dr. Rachel Batterham, head of the Center for Obesity Research at University College London, told the BBC. The high-risk subjects were, in effect, "biologically programmed to eat more," she added.

Batterham's suggestions to counteract this predisposition hinge on awareness. The more people understand their genetic makeup and why they're driven to fattier foods, the more they can take an active role in performing exercises that decrease ghrelin levels. Batterham recommends cycling, for instance, to curb the hormone's production.

"Also protein meals do lower ghrelin more," she continued. "So anything that suppresses ghrelin is more likely to be effective in FTO patients."

Professor Steve Bloom from Imperial College London offered an explanation for this gene's role in earlier societies.

"We know the tendency to overeat in a society with too much food and no need for exercise is inherited," Bloom said. "Slowly we are discovering the factors which make us overweight and this study, encompassing not only demonstration of a higher level of hunger hormone, ghrelin, but also changes in the brain associated with ghrelin's action, is an important step forward."

Source: Karra E, O'Daly O, Choudhury A. A link between FTO, ghrelin, and impaired brain food-cue responsivity. The Journal of Clinical Investigation. 2013.