BY: Jessica Baker, PhD

DATE: October 31, 2016

Hopefully you read Part 1 of this blog series, Overview of Genetics and Genetic Research Methods, which provided a basic introduction to how genetics research in eating disorders and psychiatry is conducted. If not, click the link and have a read before you dive into this post. In this second blog of the series, we provide you with an overview of the current status of research on the role of genetics in developing eating disorders.

We simply have to quash the misbelief that eating disorders are caused solely by society, culture, and the media. This myth trivializes eating disorders as a choice—a choice made by the individual to attain the “perfect body” as determined by society, culture, and the media. Importantly however, this myth fails to take into account that most of us are exposed to societal, cultural, and media pressures to be thin yet only a fraction of these same people develop an eating disorder. Nor does it take into account that individuals not exposed to these same cultural pressures can also develop an eating disorder.

Interest and research in examining the genetic risk for psychiatric disorders and eating disorders specifically, has skyrocketed over the past several decades. In part, in an effort to explain some of the conflicting ideas about why a disorder develops. For example, as just described, if a group of individuals is exposed to the same societal, cultural, and media pressures to be thin (and this is the cause of an eating disorder) why do only a small number of these people actually develop an eating disorder? Perhaps individual differences in the genetic makeup of these people plays a role in who gets an eating disorder and who stays well.

In Part 1 of this blog series, Dr. Munn-Chernoff provided an introduction to how genetic studies are conducted and a basic glossary of important genetics terms. If you need a refresher you can refer back to her blog and to the glossary.

The first step in determining whether there is a genetic risk for eating disorders was to examine whether eating disorders run in families. Research was clear: eating disorders do run in families. Specifically, individuals who have a family member with an eating disorder are up to 11-times more likely to develop an eating disorder themselves than individuals who do not have a family member with an eating disorder.¹ It’s important to note that not everyone with an eating disorder has a family member with an eating disorder. Sporadic (or nonfamilial) cases also occur. Eating disorders can run in families for two reasons: 1) genes are involved and eating disorders are heritable; or 2) families model eating disorder behaviors (e.g., if you see a family member dieting you might learn that behavior and develop it yourself—having nothing at all to do with your genes).

The twin study approach that allows us to disentangle genetics from exposure/modeling have revealed that 40-60% of the risk for anorexia nervosa, bulimia nervosa, and binge-eating disorder in adults is accounted for by genetic factors.¹ Thus, the answer to why eating disorders run in families appears to be genes—and this has been replicated in several studies around the world.

Even though Part 1 of our series introduced several genetic methods whose goal is to determine the specific genes involved in risk for a disorder, we do not yet know which genes influence eating disorders risk. Many small candidate gene studies over the past decade have failed to pinpoint specific genes that influence risk. But, we now know that these studies included far too few participants and took an approach that was destined to fail. Genetics is a rapidly advancing field and it comes as no surprise that we are developing more powerful and effective methods every day to isolate the genes that increase risk. We now know that tens-to-hundreds of thousands of individuals are needed in order to identify the hundreds of genes that are likely to influence risk for eating disorders. And this is now our goal. In fact, UNC has led the way in the largest global eating disorders genetic study ever, the Anorexia Nervosa Genetics Initiative (ANGI) and is about to launch a second large study the Binge Eating Genetics INitiative (BEGIN). More on those studies in a later post in our series.

Although we now know that genetics plays a role in the risk for eating disorders, we also know that genes do not act alone! If eating disorders risk were all genetic, then the heritability would be 100%, but we know that it is more like 40-60%. What accounts for the rest of the risk? Environment. Thus, the reigning theory as to how eating disorders develop is that these genetic and cultural factors (among other factors) work together to increase risk. As described in our Eating Disorders: Nature and Nurture blog, there are two main ways that genetic and environmental (e.g., society, culture, media) factors may work in concert to increase risk for an eating disorder. First, one’s genetic predisposition may influence what types of environments one exposes oneself to. For example, an individual’s genetic predisposition towards an eating disorder may influence whether she or he takes up activities that tend to be highly weight focused (e.g., ballet, wrestling).

A second way that genes and environment co-act is that an individual’s genetic predisposition might influence how he or she responds to an environmental stressor. For example, although most of us are exposed to the fashion industry and its unrealistic standards of thinness, only those individuals who are more genetically predisposed to an eating disorder might find that the extreme measures they take to achieve this measure of thinness would lead to a frank eating disorder. Others might engage in these behaviors for a while and they give up the quest and change careers!

Thus, the working theory as to how eating disorders develop is that genes and environment work together to influence risk—like a “perfect storm.” Just the particular genetic predisposition put in just the particular environment at a particular point in development can set the stage for an eating disorder.

When we talk about the genetics of eating disorders, it’s important to know what we are NOT saying. We are NOT saying that society, culture, and media are not important. They ARE important and we need to continue to work toward size and shape acceptance and diversity in the world. We are also NOT saying that genes are destiny. You can be at high genetic risk for an eating disorder and never develop the illness. Likewise, you can be at low genetic risk and be exposed to a heavy dose of unhealthy environments and still develop an eating disorder.

Eating disorders are complex and require complex explanations. By just focusing on genes OR environment, we are ignoring a very important piece of the puzzle. Later in our blog series we will discuss how genetic research can inform prevention and treatment strategies for eating disorders.

1. Trace, SE, Baker, JH, Penas-Lledo, E, and Bulik, CM. The genetics of eating disorders. Annual review of clinical psychology 2013. 9: 589-620.

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