The Co-Occurrence of Eating and Substance Use Disorder: A Genetic Perspective

BY: Melissa Munn-Chernoff, PhD

DATE: March 18, 2016

Eating disorders and substance use disorders – including alcohol abuse and dependence, nicotine dependence, and illicit drug abuse and dependence – frequently co-occur. This means that individuals with an eating disorder are much more likely to have a substance use disorder than individuals without an eating disorder (and vice versa). Scientific research over the past several decades has tried to answer the question as to why we see this significant co-occurrence. One hypothesis is that eating disorders and substance use disorders may share genetic risk factors. In other words, the same genes that influence the risk for developing an eating disorder may influence the risk for developing a substance use disorder. In this month’s issue of the European Eating Disorders Review, Dr. Jessica Baker and I reviewed the research on the shared genetic factors between eating disorders and substance use disorders. Overall, the findings suggest that genetic factors are at play in influencing the co-occurrence of both disorders in women.

What does the research say exactly?

The most consistent findings have come from twin studies. A twin study compares the resemblance of identical and fraternal twins for a given trait or traits to determine how much liability in that trait(s) is due to genetic and environmental factors. One really cool thing about twin studies is that we can also determine the amount of shared genetic risk factors between two different traits from what is called a “genetic correlation.” The term “genetic correlation” represents the degree of genetic association between two traits, where 0 indicates no shared association and 1 indicates a complete overlap.

To date, research in this area has focused on the overlap between bulimia nervosa and substance use disorders. The genetic correlations between bulimia nervosa and alcohol use disorder range from 0.23 to 0.53; for bulimia nervosa and regular smoking, the genetic correlation was 0.35; and for bulimia nervosa and illicit drug use, it was approximately 0.38. Researchers have also examined binge eating and compensatory behaviors and found significant genetic correlations with alcohol use. For alcohol use, this correlation with binge eating was approximately 0.30 and with compensatory behaviors, it ranged from 0.32 to 0.61. Finally, using a combined assessment of binge eating and compensatory behaviors, the genetic correlation with an alcohol use disorder was similar to previous studies at 0.33; this correlation was the same for European American and African American women. Thus, shared genetic factors for these eating disorder symptoms and alcohol use disorder may be the same in both of these racial/ethnic groups. Taken together, the findings indicate that some (between 5% and 37%) of the genetic factors that influence the liability to bulimia nervosa and the symptoms of binge eating and compensatory behaviors also influence the liability to substance use disorders.

Where do we go from here?

Despite the emergence of information indicating shared genetic factors for eating and substance use disorders in the past decade, this area of research is really in its infancy. More studies are needed to examine substance-specific associations with eating disorders since much of the existing research has included alcohol use. This will help us better understand whether a similar genetic association is observed between eating disorders and other substance use disorders as is observed with alcohol use. Additionally, modern molecular and statistical techniques now permit the identification of the specific genes that play a role in both disorders – a question that twin studies cannot answer and an area that has not yet been explored. This genetic information should also be included with environmental factors to give us the best chance of understanding why these disorders co-occur, eventually aiding in their prevention and treatment. For instance, once specific genes have been identified and can be used to “predict” who may develop eating and substance use disorders, especially in those individuals who are exposed to a high-risk environment (e.g., trauma), we will be able to identify the pathways by which someone may develop these two classes of disorders. Finally, it will be important to determine whether other psychopathology (e.g., depression) and specific personality traits (e.g., impulsivity) impact the genetic association between eating and substance use disorders, as they are common in individuals with both disorders. For example, it is possible that individuals who tend to be impulsive are at greater genetic risk for co-occurring eating and substance use disorders. Needless to say, much work is needed to further understand why eating disorders and substance use disorders co-occur and how this information can be used to better treat individuals. At least this is a start in the right direction.


Munn-Chernoff, M.A., Baker, J.H. (2016). A primer on the genetics of comorbid eating disorders and substance use disorders. European Eating Disorders Review, 24, 91-100.