The study was conducted by the Marju Orho-Melanders research group at Lund University Diabetes Centre, and is being published in the American Journal of Clinical Nutrition. While previous studies have shown that the effect of the obesity risk gene is reduced through exercise, this is the first study to look at the gene in relation to food intake. The researchers note that the study was a challenge to conduct because it is difficult to know with any certainty how much people really eat. Food habits were meticulously recorded throughout the study, and the results showed that the risk of obesity among double gene carriers was significantly increased only for people who consumed high fat diets. Those who consumed diets of less than 41% fat did not become obese more often than anyone else, despite carrying the gene.
The gene is known as FTO, the best known obesity-related gene so far. It operates on the hypothalamus, the part of the brain that regulates appetite. People with the gene tend to consume more energy, particularly 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" says Emily Sonestedt, main author of the study and member of Marju Orho-Melanders research group. "This shows that we are not slaves to our genes. Even if we are born with an inherited predisposition to obesity, lifestyle is important."
The findings are considered significant because they could lead to better individualised weight management and nutrition counseling for people with the gene. About 17 percent of the general population has a double copy of the gene, meaning they inherited it from both parents. Around 40 percent of the population has a single copy of the gene.
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