To date, more than 400 distinct genes have been linked to the causes of overweight or obesity, although only a handful appear to be significant factors. Genes influence the causes of obesity in many ways, by affecting appetite, satiety, metabolism, food cravings, body-fat distribution, and the tendency to use eating as a way to cope with stress.

The strength of the genetic influence on weight disorders varies quite a bit from person to person. According to research, genes account for just 25% of the predisposition to be overweight, while for others the genetic influence is as high as 70% to 80%.

The researchers analyzed the data from 45 studies to determine the real influence of the genes on adult weight status.

What they discovered was actually encouraging: Adults bequeathed with their parents' “fat” genes were not condemned to a life of obesity. Those with the gene did indeed have a higher chance of being heavier, but regular physical activity reduced the gene's impact on obesity by about a third. Furthermore, the researchers discovered that having one copy of the gene appeared to be responsible for, on average, only about two extra pounds of excess weight. Not fifty pounds, not even twenty. Even having two copies of this version of the gene, one from each parent, is associated with only about seven extra pounds on average.


In fact, in many cases, these gene variants may only “kick in” once other lifestyle factors trigger them. Researchers at Harvard found that among those who had genetic variants linked to being overweight, a sedentary lifestyle, in this case, defined as watching more than forty hours of TV each week—appeared to be the trigger for weight gain. The effects of the fat genes in these subjects were about four times greater than the effects seen in others who had these same genetic variants but who spent less than an hour per week watching TV. Moreover, those who had such a genetic predisposition but instead used their leisure time to engage in physical activity equivalent to an hour per day of brisk walking cut the effect of their fat genes nearly in half.

It’s not just our level of physical activity that can determine whether these genes kick in or not. In another study, researchers examined a similar connection in those with a genetic variant linked to obesity and their consumption of sugary beverages. They found that the more servings per week of sugar-sweetened beverages that an individual with the fat gene variants reported, the more of an effect these genes appeared to have on their weight. So again, the research reveals that while these genes increase the risk of gaining weight, it is the lifestyle-related risk factor of high-calorie beverage consumption that “springs the trap,” leading to weight gain.

So for most people, the factors that tip the scales toward weight gain are things we can control. This is a very hopeful message. When we consider the conclusions of these researches, it should be clear that even in the face of gene variants that influence our weight, the real power lies in our own hands.

This may go a long way in explaining why weight problems are so common in the United States. Despite the prevalence of these gene variants worldwide, you would be hard-pressed to find a country in which a significant percentage of the population does not have them. The bottom line, in other words, is that genetics cannot explain the obesity epidemic. The explosion of weight problems that Americans now face is a relatively recent phenomenon that has come about too quickly to blame genetic change, which happens very slowly. More importantly, we know that Americans are genetically similar to other people living in countries from which their ancestors emigrated—yet obesity rates vary largely across countries. For example, in Japan and Sweden, the obesity rates are about 5 percent in women, but in the United States, the rates are almost 40 percent.

Interestingly, when women relocate from Sweden or Japan to the United States, research shows that they tend to fatten up and look much more like Americans. If it were all up to these genes alone, rates of overweight and obesity would be roughly the same everywhere. And we know they are not.





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