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Shared Genetic Risk of Eating Disorders and Substance Use Disorders

By Melissa A. Munn-Chernoff, Ph.D.

Eating disorders and substance use disorders frequently co-occur. Individuals with a lifetime history of bulimia nervosa and the binge-eating/purging subtype of anorexia nervosa have a higher prevalence of substance use disorders than women with the restricting subtype of anorexia nervosa and women without a history of an eating disorder. Eating disorder and substance use disorder comorbidity complicates treatment, is associated with elevated co-occurring psychiatric and somatic conditions, relapse rates, mortality, and longer recovery times than having an eating disorder or substance use disorder alone.1 Treatment for this comorbid presentation is lacking, with patients often toggling between eating disorder and substance use disorder treatment programs.2,3 Therefore, identifying mechanisms underlying this comorbidity is a crucial step in supporting prevention and treatment approaches.

One possible mechanism contributing to the comorbidity between eating disorders and substance use disorders is shared genetic risk. Twin studies suggest that some of the genetic factors influencing liability to eating disorders also influence vulnerability to substance use disorders. The strongest genetic association is between bulimia nervosa symptoms—in particular binge eating—and problematic alcohol use, with genetic correlations ranging from approximately 0.20 to 0.50.4 Less research has investigated other substance use disorders. One study found that the genetic correlation between bulimia nervosa symptoms and regular smoking was 0.35, whereas the genetic correlation between bulimia nervosa symptoms and illicit drug use disorder was about 0.40.5,6 Indeed, these findings can be extended to adolescents.7,8 Differentiating between classes of illicit drugs is difficult in twin studies because of their low prevalence. However, recent advances in genetic methods now allow for a comprehensive examination of shared genetic risk across multiple traits, where assessment of all disorders of interest in a single sample is not necessary.

Genome-wide association studies, which scan the entire genome to examine whether any genetic markers are more common in cases than controls, have identified significant genetic variants for anorexia nervosa and use of multiple substances. Using these data, we recently investigated genetic correlations between eating-disorder-related and substance-use-related traits.9 Three key findings emerged. First, there was a significant positive genetic correlation—same genes, same direction of effect—between anorexia nervosa and alcohol use disorder (0.18), which is consistent with prior twin studies. Second, there was a significant positive genetic correlation (0.23) between anorexia nervosa and cannabis initiation (i.e., trying cannabis for the first time), as well as between anorexia nervosa with binge eating and cannabis initiation (0.27). Finally, negative genetic correlations—same genes, but opposite direction of effect—emerged between anorexia nervosa without binge eating and several smoking-related traits (genetic correlations ranged from -0.23 to -0.19). These results indicate that genes do partly explain the relation between eating disorders and problematic substance use and highlight the potentially complex associations among these behaviors.

Although the genetic studies described above cannot identify the specific genes influencing comorbid eating disorders and substance use disorders, they do provide initial evidence about patterns of shared genetic factors across different eating disorders and use of certain substances.

Furthermore, they provide important clinical implications, which include guiding prevention efforts and improving treatment. For example, it is important to screen for the presence of eating disorder symptoms in individuals who misuse substances, and vice versa, especially in adolescence, as interventions targeting eating disorder (or substance use) prevention may have the additional benefit of reducing the presence of symptoms of the other disorder. This is especially important for individuals with a family member who has a history of either disorder to identify who may be at high-risk for developing this comorbid presentation.

Second, in treatment settings, providing psychoeducation to patients and their loved ones about the role that genes, and how they may interact with environmental factors, play in the risk for eating disorders and substance use disorders is critical. Discussing that there is a biological component to these disorders and their comorbidity can reduce guilt, shame, and stigma. Knowing that these disorders are not controlled by simply “eating more”, “eating less”, or “stopping substance use” can be powerful for patients and their loved ones. These disorders are not choices—they are serious illnesses that have a biological component. If individuals have a high genetic risk for these disorders, it may make it harder, but certainly not impossible, to achieve full recovery.

In summary, understanding specific patterns of association for these disorders provides important information regarding the role of genetics for individuals who experience both conditions. Additional research that can identify the genes contributing to the comorbidity between eating disorders and substance use disorders will provide a powerful tool to inform the development of biologically informed prevention and treatment interventions.

About the author:

Melissa A. Munn-Chernoff, Ph.D., is an Assistant Professor at the University of North Carolina at Chapel Hill Center of Excellence for Eating Disorders in the Department of Psychiatry. She received her B.A. in Psychology at Michigan State University in 2003 and a Master’s in Psychiatric Epidemiology (M.P.E.) at Washington University School of Medicine in St. Louis, Missouri in 2006. Dr. Munn-Chernoff then received her M.A. in Psychology in 2009 and her Ph.D. in Psychology and Behavior Genetics in 2011, both from the University of Colorado Boulder. Upon graduation, she completed post-doctoral training in psychiatric and genetic epidemiology, with an emphasis on substance use disorders, at Washington University School of Medicine in St. Louis. Dr. Munn-Chernoff has three primary programs of research: (1) elucidating the comorbidity of eating disorders and substance use disorders from a genetic epidemiology perspective; (2) identifying genetic vulnerability to eating disorders and their symptoms; and (3) investigating eating disorder and comorbid psychopathology in underrepresented populations. To complete this work, she has received grants from the National Institute of Mental Health and the National Institute on Alcohol Abuse and Alcoholism. In 2021, Dr. Munn-Chernoff was elected as a Fellow of the Academy for Eating Disorders.


1.         Gregorowski C, Seedat S, Jordaan GP. A clinical approach to the assessment and management of co-morbid eating disorders and substance use disorders. BMC Psychiatry 2013;13:289.

2.         Center on Addiction and Substance Abuse. Food for thought: Substance abuse and eating disorders. In: Columbia University, ed. New York, NY: The National Center on Addiction and Substance Abuse at Columbia University; 2003:1-83.

3.         Dennis AB, Pryor T, Brewerton TD. Integrated treatment principles and strategies for patients with eating disorders, substance use disorder, and addictions. In: Brewerton TD, Dennis AB, eds. Eating Disorders, Addictions and Substance Use Disorders. Berlin Heidelberg: Springer-Verlag; 2014:461-89.

4.         Munn-Chernoff MA, Baker JH. A primer on the genetics of comorbid eating disorders and substance use disorders. European Eating Disorders Review 2016;24:91-100.

5.         Baker JH, Mazzeo SE, Kendler KS. Association between broadly defined bulimia nervosa and drug use disorders: Common genetic and environmental influences. International Journal of Eating Disorders 2007;40:673-8.

6.         Baker JH, Mitchell KS, Neale MC, Kendler KS. Eating disorder symptomatology and substance use disorders: Prevalence and shared risk in a population based twin sample. International Journal of Eating Disorders 2010;43:648-58.

7.         Baker JH, Johnson NK, Munn-Chernoff MA, et al. Illicit drug use, cigarette smoking, and eating disorder symptoms: Associations in an adolescent twin sample. Journal of Studies on Alcohol and Drugs 2018;79:720-4.

8.         Baker JH, Munn-Chernoff MA, Lichtenstein P, Larsson H, Maes H, Kendler KS. Shared familial risk between bulimic symptoms and alcohol involvement during adolescence. Journal of Abnormal Psychology 2017;126:506-18.

9.         Munn-Chernoff MA, Johnson EC, Chou YL, et al. Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies. Addiction Biology 2021;26:e12880.


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