Losing weight isn’t easy, and it’s harder still when your genes are working against you. But a new study by University of Maryland researchers shows that even people with a genetic predisposition to gain weight can exert some control over how big they get.
Led by Dr. Soren Snitker at the University of Maryland and his postdoctoral fellow, Evadnie Rampersaud, who is now at the University of Miami, the team studied 704 Amish men and women. Although the Amish are a genetically homogeneous group, the study of volunteers’ genotypes still showed a genetic diversity that reflected the makeup of the general Caucasian population: Specifically, they exhibited a range of variations on the FTO gene, which previous studies have associated with obesity and high body mass index, or BMI. Experts say about half of all people of European descent possess at least one “heavy” variant of the FTO gene. Within the Amish study group, some volunteers had two copies of a fattening variant; these people were 67% more likely to be obese and were on average 7 lbs. heavier than people without any copies of this form of the gene.
But researchers also discovered a subgroup of volunteers who had two copies of the heavy FTO variant, but still managed to avoid being fat. Their simple trick Exercise. Rampersaud found that the most physically active men and women in the study were able to stay within a normal BMI range, despite their genetic predisposition; other people with the same gene variants, who were relatively inactive, were overweight. “This is the first time that we can show the direct gene-environment interaction for a gene related to obesity,” Rampersaud says. “It re-emphasizes the role that physical activity plays in our daily life — it’s not just something people preach. There actually is something related to the outcome of exercising, and we showed that in this study.”
There’s a hitch. The people who successfully overrode their genes were burning a stunning 900 kilocalories more per day than their less active counterparts, which amounted to three to four hours of moderate exercise daily. “That’s a lot,” acknowledges Rampersaud, who tracked participants’ physical activity for seven days using accelerometers. By contrast, the volunteers in the “low” activity group were doing about two to three hours of gardening, housework or brisk walking each day. That’s the kind of activity many people in the general American population — which, unlike the Amish, relies on cars and dishwashers and washing machines — would consider a serious workout.
That’s not to say the study’s lessons aren’t useful. In a previous Danish trial that studied a more urban population that was slightly less active than the agrarian Amish, scientists found that those with the obesity-prone copies of FTO did not have to exercise that much to reduce their weight and BMI. Notes Dr. David Katz, director of the Yale-Griffin Prevention Research Center, the current study, which was published in the Archives of Internal Medicine, highlights a critical new understanding in the relationship between genes and our lifestyle. It’s long been known that we can compensate for our genetic makeup by our lifestyle choices — by watching what we eat and how much we exercise, for example — but as this study shows, it’s now becoming clear that our lifestyle patterns may actually alter our genes and the way they are expressed as well. “We can nurture nature,” he says, “and the idea that you can alter genetics through lifestyle is an emerging theme. The power of lifestyle is dramatic.”
To what exact degree physical activity can influence the effect of the FTO gene isn’t clear yet, but, says Rampersaud, at least we now know that genes — especially the “wrong” genes — don’t necessarily spell out destiny when it comes to weight. And that’s a useful lesson to keep in mind when making small daily decisions — taking the stairs instead of the elevator, say, or passing up a dessert. Every little bit can make a difference.
