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 For many years it has been observed that eating disorders (EDs) sometimes run in families, but it has not been known why. Do EDs develop because family members model disordered eating behaviors/attitudes that are emulated by those who observe them? On the other hand, is there a genetic cause that has nothing to do with modeled behavior? Or, is it a combination of both factors? These questions address the classic nature vs. nurture debate. Fortunately, as technology has become more sophisticated over the last 10 years, there has been much research into the role of genetics in EDs, and the results have already begun to help guide prevention and treatment efforts.

Family studies have produced the following conclusions:

• If an individual’s mother or sister has had Anorexia Nervosa (AN), they are twelve times more likely than someone without a family history of AN to develop AN.
• If an individual has a family member with Bulimia Nervosa (BN), they are four times more likely to develop BN than people without a family history of BN.
• If an individual has a family member with Binge Eating Disorder (BED) they are two times more likely to develop BED than people without a family history of BED.

Twin studies that compare identical twins and fraternal twins have been helpful in detecting the genetic contribution to the development of EDs. This is because twins “share” the same family environment. However, while identical twins share 100% of their genes, fraternal twins only share 50% of their genes.

Twin studies have found that:

• AN and BN are more likely to occur in both twins when they are identical (100% of the same genes) than in fraternal twins (50% of the same genes), suggesting that genetics play a very important role.

In genetic linkage studies, researchers collect genetic samples from multiple generations of family members in which at least two members have EDs. They look for common variations and “linkages” in the actual genes that may be passed from parent to child. Linkages are areas on a chromosome that contain several hundred genes. In genetic association studies, specific genes of interest are compared between people who do and do not have EDs.

Genetic studies have produced the following findings:

• Significant linkages have been found on chromosome 10 for BN and chromosome 1 for AN. At this point it is unknown which genes in the identified linkages are involved in EDs and what these genes control.
• Genes that control the neurotransmitter serotonin have received a lot of study and results suggest these genes may play an important role in EDs, particularly AN. Serotonin is involved in the regulation of appetite and eating behavior.
• Certain personality traits common in people with EDs are also considered moderately heritable. Traits seen in childhood before people develop AN or BN include obsessionality and perfectionism. These traits are neither good nor bad; for instance, perfectionism that is directed towards achieving a “perfect body” might exacerbate an ED while perfectionism that is directed towards achieving “perfect grades” can make people successful in school.

What Are the Implications?

EDs are complex illnesses caused by multiple factors. While it appears that people may inherit a genetic vulnerability for EDs, this does not guarantee development of an ED. Rather, researchers think inherited genes may be “turned on” when an individual is exposed to particular environmental factors such as a culture that emphasizes thinness, dieting behavior, a traumatic event, participation in high-risk sports, or a combination of triggers. Ultimately, the hope is that a better understanding of the genetics of EDs will continue to inform prevention and treatment efforts and reduce stigma associated with the illness.

For more information, see http://www.anbn.org/.

Submitted by: Sarah Hubbard, PhD