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8 Nov 2009

Study finds dietary fat interacts with genes

- 10 Apr 2007
By Tufts University   
Page 2 of 3

“We have all known people that do not watch what they eat, but usually don’t see any effect on their weight,” says Ordovas. “This is the first study that enables us to identify this segment of the population using information on this gene.

“This does not mean that it is impossible for people with the specific SNP (-1131T>C) to become obese,” Ordovas continues. “While exact components of the diet may not be as critical to maintaining a healthy weight, excessive calories over time can still contribute to obesity. Also, since the specific SNP does not interact with carbohydrate or protein, and does not affect BMI when interacting with fat, it may be more problematic for people in this group to lose weight through dietary changes if they do, in fact, become obese. Our findings demonstrate that although genetics help to determine our risk of obesity, dietary and lifestyle habits are also important to consider.”

Ordovas determined that the interaction between the specific SNP (-1131T>C) and dietary fat was strongest for monounsaturated fatty acids (MUFAs), found in foods such as olive oil and canola oil. People with the specific SNP who consumed 11 percent or more of total calories as MUFAs had a lower likelihood of obesity. “Basically, it appeared that the interaction of the specific SNP with MUFAs was the reason that fat intake did not affect BMI for this group,” says Ordovas. “This interaction between APOA5 and dietary MUFA intake may explain why the Mediterranean diet, which is rich in MUFAs, is not generally associated with an increase in body weight. However, more studies are needed to confirm this.

“At this point, everyone is encouraged to follow current guidelines that recommend a well-balanced, healthful diet in order to maintain a healthy BMI and to reduce risk of certain diseases. But we study nutrigenomics with the idea that we can pinpoint people who may be at higher risk for certain conditions like cardiovascular disease, allowing these individuals to proactively alter the way nutrition affects their genes,” says Ordovas. “Once we are able to do this, we may develop several sets of guidelines for the public, based upon a person’s genotype.”

 
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