Why Both Genetics and Lifestyle Matter in the Obesity Epidemic

People with a specific mutation in one gene are substantially more likely to be obese than those without it. But they are also at higher risk of suffering from environmental factors.
Author:
Publish date:
Social count:
0
People with a specific mutation in one gene are substantially more likely to be obese than those without it. But they are also at higher risk of suffering from environmental factors.
(Photo: joe_13/Flickr)

(Photo: joe_13/Flickr)

We’ve all heard the caveats about the role of our genes in our lives: Genes aren't destiny, nor are nature and nurture mutually exclusive. Humans may not be blank slates, but we're not DNA robots either. Yet it's easy to forget those caveats when bombarded, week after week, with genetic studies that describe the influence of genetics on our health, our personalities, our educational attainment, and even our bad habits.

Take obesity, for example. It's a major public health issue that affects more than one third of adults in the United States, and it exacts an enormous toll on the economy and our well-being. Childhood obesity has tripled in a generation, a clear sign that this problem is being triggered by recent changes in how we live. But researchers have discovered an important genetic basis for obesity too. In 2007, several groups found that an extremely common version of a gene called FTO puts people at risk. In one study, a remarkably large fraction—16 percent—of the study subjects had inherited two copies of this risky version of FTO (one each from their mother and father), and they were substantially more likely to be obese. In other words, a very common mutation in one gene alone likely plays an important role in our obesity epidemic. With genetic results like these, it's easy to get tunnel vision and forget about the environment.

Without question, our genes play a big role in making us who we are. But in the renaissance of genetic research, it's easy to forget that genes don't act in isolation—they act on the stage set by our environment.

But we shouldn't. Even in the earliest days of genetics, scientists understood that the environment often has a strong influence on how genes manifest themselves. They recognized that intrinsic physical differences between individuals aren’t necessarily a reflection of genetic differences. "Every student of genetics ought to know this," wrote Wilhelm Johannsen, coiner of the term "gene," in 1911. He went on to provide some well-known agricultural examples: "Temperature has great influence upon the intensity of color in flowers.... Pure lines of beans may in one year be different in size.... Some strains of wheat yield relatively much better than others on rich soil, while the reverse is realized on poorer soils."

Johannsen's example of the yields of different wheat strains in different soils illustrates a particularly important fact about genes and the environment: How the environment affects you depends on your genetic make-up. Genetically different individuals will respond differently to the same environment. Geneticists call this a "gene by environment interaction," a phrase which refers to the representation of the effect in their mathematical models. It's a formal acknowledgement that everyone encounters the world differently.

Gene by environment interactions are very common, but don't be fooled by the fact that scientists can represent them mathematically. These interactions are often unmeasurable because, except under highly controlled conditions, it's almost impossible to isolate discrete environmental factors from the complex and variable total environment in the real world. As a result, geneticists try to put careful limits on their claims when they talk about the effects of our genes on our traits, though this is often ignored when people speculate about the genetic underpinnings of cultural and racial differences.

While everyday experiences tell us that a given social or physical environment affects different individuals in different ways, scientists struggle to measure this. This poses a challenge when trying to address something like the obesity epidemic, in which both genes and the environment play a role. On the one hand, we have the genetic studies. On the other, researchers have tracked the influences of specific social and environmental factors on obesity, such as fast food, social networks, income inequality, parenting, and changing means of transportation. Reconciling these two lines of research is not easy, because many of these environmental factors are difficult to measure precisely and to isolate from other confounding variables of the environment. This makes it hard to tease out the environmental risk factors that actually interact with the genetic ones, like the FTO gene.

How the environment affects you depends on your genetic make-up. Genetically different individuals will respond differently to the same environment.

Recently, one team of researchers found a way to solve this problem by bypassing the difficult measurements of environmental factors altogether. Instead, they looked at a different variable: time. In a study out in Proceedings of the National Academy of Sciences this month, these researchers showed that the obesity risk posed by the risky version of the FTO gene has actually changed over the past several generations. Regardless of what the specific social and environmental changes have been, the total environment has in some way altered the influence of genetics on obesity.

To show this, the researchers turned to a valuable long-term study called the Framingham Offspring Study, which has tracked the health of more than 5,000 subjects since 1971. The researchers divided the study subjects into three groups, based on the status of their FTO gene: those who did not have a risky version of the gene, those who carried only one copy of the risky version (inherited from only one parent), and those who carried two copies of the risky version.

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 supported in a second study published this month, which found that children with the non-risky version of FTO "seem to be more protected by a favourable social environment” than children with copies of the risky version.

Without question, our genes play a big role in making us who we are. But in the renaissance of genetic research, it's easy to forget that genes don't act in isolation—they act on the stage set by our environment.

Related