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Interplay between genes and environment offers new clues in obesity puzzle

Interplay between genes and environment offers new clues in obesity puzzle

Picture of Ryan White

In a sense the good news has also been the bad news: U.S. obesity rates haven’t budged much over the last decade, either for adults or children. More than a third of adults and about 17 percent of kids and adolescents are obese. (The one bright spot is among 2- to 5-year-olds, for whom obesity rates have plummeted.)

The ongoing obesity epidemic and its attendant health risks (type 2 diabetes, heart disease and cancer among them) make efforts to better understand what’s driving and sustaining the epidemic seem all the more urgent.

The usual explanations dwell on diet (mounting heaps of highly processed foods laden with salt, sugar and fat) and lack of exercise (an increasingly sedentary nation). But there’s also been growing awareness of the ways in which social factors such as “food deserts,” the built environment and social networks shape our diet and fitness regimens.

The rising profile of “social determinants” raises a question then: Is America’s obesity epidemic merely a tale of changing social and cultural norms, or do our genes play a starring role as well? Or perhaps the key lies in the nexus between the two?

A new study published by the Proceedings of the National Academy of Sciences could help shed some new light on the way in which genetics and the environment interact to promote obesity. The research suggests that the power of a specific gene – called FTO or “fat mass and obesity associated” – actually increased over time, as the environment changed throughout the 20th Century. While the FTO gene in question has been present in some individuals all along, changes in the environment may, in fact, have boosted its ability to bring about physiological changes in people harboring the genetic variant in question. It’s the environment working on our genes, which in turn are working on our bodies.

The new PNAS study used longitudinal data from the 30-year Framingham Heart Study to look at the link between the FTO gene and body mass index (BMI) over time. Michael White, a geneticist at Washington University School of Medicine, did an enviable job translating the science into lay terms in a superb post for Pacific Standard. White writes:

By looking at four decades’ worth of body measurements for these subjects, the researchers found a clear example of genetics interacting with the environment. People who carried one or two copies of the risky FTO were even more at risk for obesity if they were born after 1942. For those with no copies of the risky version of FTO, when they were born didn’t matter—their obesity risk stayed the same. While the overall effect was relatively small, it’s clear that how our changing environment affects people’s risk for obesity depends, in part, on their DNA.

This is interesting for at least two reasons. For one, it suggests that our genes are “historical” in the sense that even if they themselves don’t change, their physiological effects or “expression” can change over time. Second, this research implies that something significant changed in the larger world that impacted those growing up in the years following 1942, at least for individuals carrying one or more copies of the “risky” FTO gene.

The PNAS study wasn’t designed to sort out which historical factors might account for the growing obesity risk among this subset of individuals, but the authors do detail a few of the changes getting underway at the time:

Many hypothesized environmental influences on the rise in obesity did indeed occur after the early 1940s, including technological advances reducing energy expenditure at work as well as increases in the caloric content of processed foods, whose effect may be experienced most strongly by individuals whose tastes and habits would be influenced at a young age.

Future research may begin to untangle the relative importance of those factors, but the suggestion seems clear: History changes everyone, but owing to our genetic variability, not necessarily in the same ways. Some are more at risk than others to new diets and behaviors. The obesity epidemic, according to this telling, is explained by the interplay between genetics and the environment:

Our results suggest that the well-documented rise in BMI in the United States over the past 40 years may have been disproportionately driven by individuals for whom genetic factors interacted with environmental changes encountered in their development due to their era of birth — in this case, being born later.

A great deal of reporting on obesity tends to emphasize the role of genetics or the role of the environment, depending on the latest bit of research. But nuanced studies like this one remind us that it’s always wise to keep both in mind at once.

Photo by Dave Fayram via Flickr.

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