Editor’s note: Pending an FDA decision, 23andMe no longer offers new customers access to health reports referred to in this post. Customers who purchased prior to November 22, 2013 will still be able to see their health reports, but those who purchased after that time will not. Those customers will have access to ancestry information as well as access to their uninterpreted raw data.
In 2009, 27% of Americans met the clinical criteria for obesity—a body mass index (BMI) of 30 or greater—7 percentage points higher than a mere 9 years earlier. Even this staggering 27% estimate may be too low. A large National Health and Nutrition Examination Study (NHANES) study estimated the prevalence of obesity at 34%. No wonder losing weight is a national preoccupation.
But how much control do we really exert over our weight? We all know people who seemingly gorge themselves at every meal but never gain an ounce and others who all too easily pack on the pounds.
In a paper published in PLoS Medicine, Shengxu Li and colleagues tackled a piece of that puzzle. Using a sample of 20,000 Europeans, they compared the predictive power of 12 SNPs known to influence BMI in sedentary and physically active individuals. While carrying a greater number of risky versions of these SNPs was associated with higher BMI in both groups, the association was much weaker in the physically active.
In the sedentary group, each additional risky variant translated to a 0.21 increase in BMI, or an extra 1.3 lbs (592 g) for someone 5’7 (170 cm). By comparison, in the physically active people, each additional risky variant translated to a 0.13 increase in BMI, or an extra 0.8 lbs (397 g) for someone 5’7 (170 cm). Leading a physically active lifestyle, they concluded, was associated with a 40% reduction in the genetic predisposition to obesity.
(23andMe customers can check their data for these variants using the information in the table at the end of this post and the Browse Raw Data feature.)
Although we only have 9 of the 12 SNPs covered in our database, a quick analysis using our customers’ data replicated their findings. Carrying more risky variants was predictive of a higher BMI overall, but this effect was much more pronounced among our customers who reported low levels of physical activity.
Of course, the 12 SNPs under investigation do not represent the totality of genetic predisposition to obesity. In fact, the 12 SNPs combined accounted for only 1.2% of the variation in weight among the sedentary individuals, and even less, 0.6%, among the physically active. Other genetic factors not measured in this research, such as rare variants associated with BMI, likely play a role as well.
SNPs associated with BMI
|SNP||Nearest Gene||Risk Version|
* In some cases, 23andMe cannot report data for the original SNP, so a proxy SNP that correlates perfectly with the original in Europeans is reported instead.
SNPwatch gives you the latest news about research linking various traits and conditions to individual genetic variations. These studies are exciting because they offer a glimpse into how genetics may affect our bodies and health; but in most cases, more work is needed before this research can provide information of value to individuals. For that reason it is important to remember that like all information we provide, the studies we describe in SNPwatch are for research and educational purposes only. SNPwatch is not intended to be a substitute for professional medical advice; you should always seek the advice of your physician or other appropriate healthcare professional with any questions you may have regarding diagnosis, cure, treatment or prevention of any disease or other medical condition.