Eating Disorders and Substance Abuse Disorders: Is There a Genetic Overlap?

Eating Disorders and Substance Abuse Disorders: Is There a Genetic Overlap?

By Jessica Baker, PhD

Individuals with an eating disorder are at higher risk for an alcohol or substance use disorder compared with people who do not have an eating disorder.1,2 For example, in a previous study examining how frequently a variety of substance use disorders occurred in females with an eating disorder,3 we found that 24 percent and 18 percent of women with bulimia nervosa had a history of an alcohol use disorder and an illicit drug use disorder, respectively. In addition, 22 percent of women with anorexia nervosa had a history of an alcohol use disorder, and 17 percent had a history of an illicit drug use disorder. For comparison’s sake, only 14 percent of females in the sample had an alcohol use disorder and 8 percent had an illicit drug use disorder. Thus, women with an eating disorder were significantly more likely to have a history of a substance use disorder. Interestingly, this increased risk is observed in both directions.4 People with alcohol or substance use disorders are also more likely to have a history of an eating disorder compared with people without an alcohol or substance use disorder. This pattern of comorbidity (or having more than one disorder) is most commonly observed in binge eating type eating disorders, such as bulimia nervosa or binge eating disorder; however, individuals with anorexia nervosa are also more likely to experience a substance use disorder compared with individuals without anorexia nervosa.5 But when we compare the prevalence of substance use disorders among the eating disorders, substance use disorders are generally observed at a higher rate among bulimia nervosa and binge eating disorder compared with anorexia nervosa.

Over the past five decades or so, research has established that people with an eating disorder are at increased risk for an alcohol or substance use disorder (and vice versa). What we still know very little about is why this increased risk exists. A review paper on this topic,6 published almost 20 years ago, described three possible explanations for why this comorbidity between eating disorders and alcohol and substance use disorders occurs:

  1. “Addictive” personality: An addictive personality style may predispose individuals to both eating disorders and substance use disorders—certain personality traits may make certain individuals vulnerable to addictive-like behaviors (e.g., alcohol, drugs, eating, gambling).
  2. Shared family risk: There is a family component that predisposes risk for both eating disorders and substance use disorders. For example, an individual with a family history of an alcohol use disorder may have heightened risk for an alcohol use disorder and/or an eating disorder.
  3. Shared societal factors/pressures: Certain individuals, girls specifically, may be more vulnerable to external societal or cultural pressures, such as social pressures toward thinness and experimenting with alcohol or drugs.

For this article, we will dive into #2 more in-depth—is there a family component that predisposes risk for both eating disorders and alcohol and substance use disorders? Such a shared family component could be genetic and/or environmental in nature. Genetic would refer to the genes passed down to you from your biological parents. Family environment would refer to the environment/home you grew up in, regardless of whether you grew up with your biological parents. In perhaps more familiar terms, this could be referred to as nature and nurture.

To date, research examining such a shared family risk has been completed using a twin study research design. And this research provides convincing evidence that a shared family component exists between eating disorders and alcohol and substance use disorders. Twin study designs capitalize on the natural fact that identical twins share, on average, 100 percent of their DNA and fraternal twins share, on average, 50 percent of their DNA. Therefore, in basic terms, the traits that identical twins are twice as likely to both exhibit (i.e., concordance) compared with fraternal twins are said to have a genetic component. Twin studies also allow us to calculate a genetic correlation, which represents the correlation between the genetic factors that influence risk for one trait and the genetic factors that influence risk for a second trait. In other words, this can help answer the question of whether there is shared genetic overlap between two traits (and how much).

We have completed a number of twin studies examining the genetic association between various eating-disorder-related traits and various aspects of alcohol and substance use and misuse. A majority of this work to date has focused on bulimia nervosa and related symptoms (e.g., binge eating), and the data are clear: A genetic overlap exists between eating disorders and alcohol and substance use disorders.3,7 For example, we have observed a genetic correlation of 0.53 between bulimia nervosa and an alcohol use disorder and of 0.39 between bulimia nervosa and an illicit drug use disorder.3 The take-home message of these genetic correlations is similar to that of other types of statistical correlations—the strength of the association between two traits. The correlations are not 1.0, so there is not complete overlap in genetic factors between eating disorders and alcohol and substance use disorders. Similarly, the correlations were not 0.0, so there is some overlap in genetic factors. Here, we would generally call it a moderate amount of overlap based on the correlation strength. Providing even more evidence of genetic overlap, shared genetic risk has also been observed among binge eating, purging, body dissatisfaction, drive for thinness, and alcohol use.7

As noted, twin studies have focused exclusively on bulimia nervosa (and related traits). Only one study to date has examined anorexia nervosa. That study,8 led by my colleague at the UNC Center of Excellence for Eating Disorders, used genome-wide association study results for anorexia nervosa to calculate genetic correlations between anorexia nervosa and a variety of substance use traits. These genetic correlations are similar to the correlations obtained in twin studies but are calculated based on genome-wide study findings. A significant genetic correlation between anorexia nervosa and alcohol use disorder was observed; however, this correlation (0.18) was lower than correlations observed in twin studies with bulimia nervosa. Significant genetic correlations were also observed between anorexia nervosa and trying cannabis for the first time (0.23), and between anorexia nervosa restricting subtype and smoking behaviors. Findings from this study are consistent with twin study results suggesting that some of the same genes influence risk for anorexia nervosa and alcohol and substance use.

Our understanding of the comorbidity between eating disorders and alcohol and substance use disorders has evolved greatly over the past two decades. Initial twin studies and genetic correlations paved the way for understanding that a genetic overlap exists; however, a limitation of genetic correlations is that they cannot identify the specific genes involved in risk. As genetics research evolves, we will be able to use more contemporary methods to identify the specific risk genes for both eating disorders and alcohol and substance use disorders. Such approaches have been successful in identifying shared genetic variants between schizophrenia, bipolar disorder, and major depression.9

An important caveat to all of this work: There is not a single gene that causes eating disorders or substance use disorders or their comorbidity. The genetic risk for complex behavioral traits such as eating disorders and substance use disorders is polygenic. This means that many genes, likely thousands, each of which only has a small effect, play a role in genetic vulnerability. Identifying the genetic factors that contribute to the comorbidity between eating disorders and alcohol and substance use disorders will aid in our understanding of why this comorbidity occurs. And answering the question as to why this comorbidity occurs will ultimately have important implications for prevention, detection, and treatment. An alcohol or substance use disorder can complicate treatment and recovery from an eating disorder (and vice versa). Unfortunately, few empirically supported, effective treatments exist for this comorbidity. Cracking the genetic code could lead to the next generation of personalized intervention and prevention programs.

About the author:

Jessica H. Baker, PhD has a B.S. in Psychology from Michigan State University and a Ph.D. in Clinical Psychology from Virginia Commonwealth University where she received training in behavior genetics at the Virginia Institute for Psychiatric and Behavior Genetics. She conducts research on and provides treatment for eating disorders. Broadly, Dr. Baker’s research focuses on the biological and genetic vulnerability for eating disorders, with a particular focus on: 1) the comorbidity between eating disorders and substance use disorders; 2) the role of gonadal steroids (e.g., estradiol) in the risk for and maintenance of eating disorders; and 3) changes in genetic and biological risk across the lifespan. As part of her work, Dr. Baker is also interested in college student mental health and examining how the transition to college may increase risk for disordered eating, substance use, or both.

References:

  1. Bahji, A, Mazhar, MN, Hudson, CC, Nadkarni, P, MacNeil, BA, and Hawken, E. Prevalence of substance use disorder comorbidity among individuals with eating disorders: A systematic review and meta-analysis. Psychiatry Research 2019. 273: 58-66.
  2. Bogusz, K, Kopera, M, Jakubczyk, A, Trucco, EM, Kucharska, K, Walenda, A, et al. Prevalence of alcohol use disorder among individuals who binge eat: A systematic review and meta-analysis. Addiction (Abingdon, England) 2020.
  3. Baker, JH, Mitchell, KS, Neale, MC, and 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.
  4. Holderness, C, Brooks-Gunn, J, and Warren, M. Co-morbidity of eating disorders and substance abuse. Review of the literature. International Journal of Eating Disorders 1994. 16: 1-35.
  5. Root, TL, Pisetsky, EM, Thornton, L, Lichtenstein, P, Pedersen, NL, and Bulik, CM. Patterns of comorbidity of eating disorders and substance use in a large population-based sample of Swedish females. Psychological Medicine 2010. 40: 105-115.
  6. Wolfe, WL and Maisto, SA. The relationship between eating disorders and substance use: Moving beyond co-prevalence research. Clinical Psychology Review 2000. 20: 617-31.
  7. Munn-Chernoff, MA and Baker, JH. A primer on the genetics of comorbid eating disorders and substance use disorders. European Eating Disorders Review: The Journal of the Eating Disorders Association 2016. 24: 91-100.
  8. Munn-Chernoff, MA, Johnson, EC, Chou, YL, Thornton, LM, Walters, RK, Yilmaz, Z, et al. Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies. Addiction Biology in press.
  9. Smoller, JW, Craddock, N, Kendler, K, Lee, PH, Neale, BM, Nurnberger, JI, et al. Identification of risk loci with shared effects on five major psychiatric disorders: A genome-wide analysis. The Lancet 2013. 381: 1371-9.

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