A pervasive myth about eating disorders is that they are somehow caused by the fashion and entertainment industry promoting images of the “perfect” skinny body. Anorexia and bulimia nervosa have been trivialized as girls or women trying to achieve this ideal which has led to the false belief that these are simply disorders of choice. This belief has hampered our understanding of and empathy for people who suffer from eating disorders and fails to account for the fact that although just about every woman is exposed to this societal thin ideal, only a fraction of them develop eating disorders.
However, research over the past decade has revealed that genetics play a role in eating disorders. But what does that mean? Genetic research is also challenging to understand for families and sufferers. First off, we know that eating disorders do run in families. Relatives of individuals with anorexia nervosa are over 10 times more likely to have an eating disorder themselves. But, everyone with an eating disorder doesn’t necessarily have a relative with an eating disorder—and given the stigma that surrounds eating disorders—even if they did have a relative with an eating disorder, they might not know.
But, disorders or traits can run in families for two reasons. They can run in families because genes are involved and they are heritable. Or they can run in families because of modelling or exposure. If you see a family member dieting or binge eating when stressed, you might learn that behaviour and develop it yourself with nothing to do with your genes.
One way of teasing out genetic from environmental reasons for a trait or a disorder running in families is through large twin studies. We have studied several large twin cohorts—many having over 40,000 twin pairs. The beauty of these large twin studies is that they contain both identical and fraternal twins. Identical twins actually share 100% of their genes. For most intents and purposes, they are clones. Fraternal twins are no more genetically similar than regular siblings—they share 50% of their genes. They do however share the womb, and grow up at the same time, so their environment is more similar than siblings who are different ages. By documenting the frequency with which both members of identical twin pairs have the disorder in comparison to both members of fraternal twin pairs, you can estimate how heritable a disorder is. So if you find that both members of a large population of identical twins have anorexia about 50% of the time, but both members of fraternal twin pairs only both have the disorder about 20% of the time—that is a strong clue that genes play a role. We can then put numbers to those statistics. Studies that have used this approach reveal that genetic factors account for approximately 28% to 58% of an individual’s likelihood to develop anorexia. For bulimia, those numbers have ranged from 54% to 83% and for binge eating disorder about half of the liability is due to genetic factors.
Now that suggests that genes play a role, but since those estimates aren’t 100%, genes don’t explain the entire picture. Environment is not off the hook because the rest of the liability is due to environmental factors. Extreme dieting, a toxic food environment, pervasive dissatisfaction with shape and weight, and pressures to attain picture perfect body ideals all can lead an individual down a path of restricting, binge eating, extreme exercise, and other behaviors that can be the first signs of the slippery slope towards an eating disorder.
We do not yet know which genes influence eating disorders risk. UNC is leading a 17 country study—the Genetic Consortium for Anorexia Nervosa (GCAN) which is funded by the Wellcome Trust in the United Kingdom and locally by the Foundation of Hope (http://www.walkforhope.com/ ). We have collected DNA from over 4000 individuals with anorexia nervosa to conduct a genomewide association study. This allows us to scan the entire genome and look for differences between these people with anorexia nervosa and a matched control group of people without anorexia. We are looking forward to results from that study in the summer of 2011.
We are very interested in how learning about the genetic contribution to eating disorders influences how people think about eating disorders. Many parents and loved ones have reported that understanding that biology is involved has helped them have more compassion for people with eating disorders and helped them understand how challenging recovery can be. Many patients have felt relieved that people are no longer saying that their disorder is because of vanity or is just a choice. This information helps them understand themselves more. But just because genes are involved does not mean that recovery is not possible. Many people are comforted to know that it simply means that recovery requires an uphill battle against your biology. Whereas for some people quitting smoking requires an uphill battle against their liability to become dependent on nicotine—for people with eating disorders, this can mean fighting against the urge to binge or fighting against the urge to restrict. Recovery is possible regardless of your genotype.
This biological understanding can help us all break through the stigma that has surrounded eating disorders. We support fighting stigma with science at every turn. The more we can learn about the causes of all eating disorders—binge eating disorder, bulimia nervosa, and anorexia nervosa, the more effective we will be at ridding the world of false myths and developing effective treatment and prevention strategies.