OVERLAP BETWEEN ANOREXIA AND BULIMIA NERVOSA: UNDERSTANDING GENETIC ANDENVIRONMENTAL EFFECTS IN A SWEDISH POPULATION REGISTRY

Background Symptomatic flux and familial co-aggregation of anorexia nervosa and bulimia nervosa suggest etiological overlap between the two eating disorders. One previous twin study based on self-ratings has explored the genetic and environmental aspects of the overlap on symptom level [1]. No previous study, however, has used clinically diagnostic information to explore the genetic and environmental aspects of this etiological overlap on population scale. Methods We applied bi-variate structural equation modeling on large cohorts of full-sisters (334,433 pairs) and maternal half-sisters (57,036 pairs) that were randomly selected from the Swedish female population born 1970–2005. Our definition of anorexia nervosa included registered clinically diagnosed typical and atypical anorexia nervosa, and bulimia nervosa included registered clinically diagnosed typical and atypical bulimia nervosa. Results In the study population, heritability was estimated as .44 for anorexia nervosa (95% confidence interval [CI]=.38–.51) and .34 for bulimia nervosa (95% CI=.25–.44). The remaining variance was explained by unshared environmental effects (anorexia nervosa .56, 95% CI=.49–.62; bulimia nervosa .66, 95% CI=.56–.75). The phenotypic correlation between anorexia and bulimia nervosa was estimated as .59. The cross-sister-cross-disorder correlation was significantly higher in full-sisters (.16, sd.=.0019) than in maternal half-sisters (.022, sd.= .052). Around half of the phenotypic association between anorexia and bulimia nervosa was attributable to genetic influences (.52, 95% CI=.41–.63). We observed statistically significant genetic (.79, 95% CI=.63–.95) and environmental (.47, 95% CI=.37–1.00) correlations between the two disorders. Discussion We found high correlation and moderate environmental correlation between clinically diagnosed anorexia and bulimia nervosa. Our findings agree with previous twin study based on self-report symptomatic data [1], and points towards a shared mechanism that needs further attention in clinical practice and in future etiologic research.