Genetic overlap between alcohol use disorder and bulimic behaviors in European American and African American women. (1st August 2015)

• Record Type: Journal Article
• Authors: Munn-Chernoff, Melissa A.; Grant, Julia D.; Agrawal, Arpana; Sartor, Carolyn E.; Werner, Kimberly B.; Bucholz, Kathleen K.; Madden, Pamela A.F.; Heath, Andrew C.; Duncan, Alexis E.
• Is Part Of: Drug and alcohol dependence. Volume 153(2015)
• Page Start: 335
• Page End: 340
• Publication Date: 2015-08-01
• Subjects: Twins -- African American -- Alcohol use disorder -- Eating disorders -- DSM-5 -- Heritability; Drug abuse -- Periodicals; Alcoholism -- Periodicals; 616.86
• DOI: 10.1016/j.drugalcdep.2015.05.043
• Languages: English
• ISSNs: 0376-8716

Abstract

Highlights: Alcohol use disorder (AUD) and bulimic behaviors co-occur, yet it is unknown why. Few studies have included African American women in genetic research. We examined their shared etiology in European American and African American women. Common genetic and environmental factors underlie liability to these behaviors. There were no significant differences between racial/ethnic groups. Abstract: Background: Despite substantial evidence that alcohol use disorder (AUD) and bulimic behaviors (i.e., binge eating and compensatory behaviors) co-occur, insufficient information exists regarding a possible shared etiology. Moreover, although numerous twin studies of European ancestry individuals have reported moderate heritability estimates for AUD and bulimic behaviors, with little evidence for shared environmental factors, research on genetic and environmental risk in African American (AA) individuals is lacking. Methods: We investigated specific and overlapping genetic and environmental influences on AUD and bulimic behaviors in 3232 European American (EA; 55.38% monozygotic) and 549 AA (42.81% monozygotic) young adult female twins from the Missouri Adolescent Female Twin Study (age range = 18–29 years). A structured clinical interview assessed lifetime DSM-5 AUD (minus craving) and bulimic behaviors. Biometrical twin modeling was conducted to generate age-adjusted estimates of genetic and environmental influences on AUD, bulimic behaviors, and their comorbidity. Results: Estimates of genetic and environmental contributions on AUD and bulimic behaviors could be equated across EA and AA women. Additive genetic effects accounted for 59% (95% CI: 50%, 66%) and 43% (33%, 52%) of the variance in AUD and bulimic behaviors, respectively, with the remainder due to non-shared environmental effects. Shared genetic factors ( r g = .33 (.18, .49)) were solely responsible for the correlation between phenotypes; the non-shared environmental correlation was not significant ( r e = .10 (−.05, .25)). Conclusions: Findings indicate similar magnitudes of genetic and environmental effects on AUD and bulimic behaviors for EA and AA women and implicate common genetic mechanisms underlying liability to these problem behaviors.