Evidence from animal models, human linkage studies, twin studies, and association studies of large populations suggests that this variation in our susceptibility to obesity has a genetic component. But rather than being controlled by a single gene, susceptibility to common obesity is thought to be affected by many genes polygenic. Twin studies offer some insight into the genetics of common obesity.
Based on data from more than 25, twin pairs and 50, biological and adoptive family members, the estimates for mean correlations for body mass index BMI are 0. These studies can be used to find gene variations that play a role in common, complex diseases such as obesity. The second obesity-associated gene variant that researchers identified lies on chromosome 18, close to the melanocortin-4 receptor gene the same gene responsible for a rare form of monogenic obesity.
To date, genome-wide association studies have identified more than 30 candidate genes on 12 chromosomes that are associated with body mass index. Genetic changes are unlikely to explain the rapid spread of obesity around the globe. It takes a long time for new mutations or polymorphisms to spread. So if our genes have stayed largely the same, what has changed over the past 40 years of rising obesity rates?
Our environment: the physical, social, political, and economic surroundings that influence how much we eat and how active we are.
Environmental changes that make it easier for people to overeat, and harder for people to get enough physical activity, have played a key role in triggering the recent surge of overweight and obesity. Work on obesity-related gene-environment interactions is still in its infancy. Rather, it seems that eating a healthy diet and getting enough exercise may counteract some of the gene-related obesity risk. In , for example, Andreasen and colleagues demonstrated that physical activity offsets the effects of one obesity-promoting gene, a common variant of FTO.
The study, conducted in 17, Danes, found that people who carried the obesity-promoting gene, and who were inactive, had higher BMIs than people without the gene variant who were inactive. Having a genetic predisposition to obesity did not seem to matter, however, for people who were active: Their BMIs were no higher or lower than those of people who did not have the obesity gene.
Subsequent work on the relationship between the FTO gene, physical activity, and obesity yielded contradictory results. But once again, being physically active lowered the risk: Active adults who carried the obesity-promoting gene had a 30 percent lower risk of obesity than inactive adults who carried the gene.
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