June 3

The Role of Genes in the Obesity Epidemic

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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

To date, about 100 genetic markers have been linked to obesity. But put all of them together and overall, they account for less than 3 percent of the difference in BMI between people. The “fat gene” you may have heard about (called FTO, short for “FaT mass and Obesity associated’’) is the gene most strongly linked to obesity, but it explains less than 1 percent of the difference between people––a mere 0.34 percent.

FTO codes for a brain protein that appears to affect your appetite. Are you one of the billion people that carry the FTO susceptibility genes? Who cares, as it only appears to result in a difference in intake of a few hundred extra calories a year. The energy imbalance that led to the obesity epidemic is on the order of hundreds of calories a day. And that’s the gene so far known to have the most effect. The chances of accurately predicting obesity risk based on FTO status is only slightly better than flipping a coin. In other words, no; those genes don’t make you look fat.

When it comes to obesity, the power of your genes is nothing compared to the power of your fork. Even the small influence the FTO gene has appears to be weaker among those who are physically active, and may be abolished completely in those eating healthier diets. FTO only appears to affect those eating diets higher in saturated fat (predominantly found in meat, dairy, and junk food). Those eating healthier appear to be at no greater risk of weight gain––even if they inherited the “fat gene” from both their parents.

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Physiologically, FTO gene status does not appear to affect your ability to lose weight. Psychologically, knowing you’re at increased genetic risk for obesity may motivate some people to eat and live healthier, but may cause others to fatalistically throw their hands up in the air and resign themselves to thinking that it just runs in their family. Obesity does tend to run in families, but so do lousy diets.

Comparing the weight of biological versus adopted children can help tease out the contributions of lifestyles versus genetics. Children growing up with two overweight biological parents were found to be 27 percent more likely to be overweight themselves, whereas adopted children placed in a home with two overweight parents were 21 percent more likely to be overweight. So, genetics plays a role, but this suggests that it’s more the children’s environment than their DNA.

One of the most dramatic examples of the power of diet over DNA comes from the Pima Indians. The Pima Indians of Arizona have among the highest rates of obesity and the highest rates of diabetes in the world. This has been ascribed to their relatively fuel-efficient genetic makeup. Their propensity to store calories may have served them well in times of scarcity when they were living off of corn, beans, and squash. But, when the area became “settled”, their source of water, the Gila river, was diverted upstream. Those who survived the ensuing famine had to abandon their traditional diet to living off of government food programs, and chronic disease rates skyrocketed. Same genes, but different diet, different result.

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In fact, a natural experiment was set up. The Pima living over the border in Mexico come from the same genetic pool, but were able to maintain more of their traditional lifestyle––sticking with their beans, tortillas, and potatoes. Same genes, but seven times less obesity, and about four times less diabetes. Genes may load the gun, but diet pulls the trigger.

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