You may know that correlation studies have shown that the risk of becoming obese is 2.5 times higher for those who have double copies of the best known risk gene for being overweight or obese, the FTO gene (fat mass and obesity associated).

New discoveries of that sort have led to a resurgence in concern that we may be slaves to our genes, but is that the case?  No, in every study obesity still required high calorie consumption, especially fat.   A low fat diet neutralizes the harmful effects of the gene.

Several studies have found that exercise diminishes the effect of the risk gene but a new study is the first to examine the effect of the gene in relation to food habits. The risk variant of the FTO gene is common in the general population. 17 percent have double copies, meaning they have inherited it from both parents.   Another 40 percent have a single copy.

“This means that the critical factor is what you eat. At least in the case of the FTO gene, the most important obesity gene identified so far” says Emily Sonestedt, member of Marju Orho-Melanders research group at Lund University Diabetes Centre.  “It is difficult to calculate how much people eat with any certainty, which is one of the reasons why no one has done this before. But we have good data.”

The information comes from the large Malmö Diet and Cancer study where food habits were carefully documented using, among other things, an extensive questionnaire, a long interview and a food diaries kept by the participants themselves. When the eating habits of the carriers of the double risk variant for obesity was analyzed the pattern was clear. The risk of obesity was dramatically increased only in the case of high fat consumption.

“Yes, for those who had a diet where less than 41 percent of the energy consumed came from fat, obesity was not more common, in spite of the inherited risk” said Sonestedt.

The FTO genes acts in the hypothalamus, the part of the brain that regulates appetite and satiety, and the risk variant has been connected to an increased energy intake, especially in the form of fat.

“It could be that the carriers of the risk gene don’t feel as full from eating fat and therefore consume more and gain weight.”

The finding that the harmful effects of the gene can be cancelled by changing eating habits could, combined with mapping of the effects of other obesity genes, lead to better and more individualized nutritional counseling for those that want to avoid gaining weight. 

“This shows that we are not slaves to our genes. Even if we are born with an inherited predisposition to obesity, life style is important” says Sonestedt.

Article: American Journal of Clinical Nutrition, 'Fat and carbohydrate intake modify the association between genetic variation in the FTO genotype and obesity',