BACKGROUND: We present a bivariate twin analysis of anorexia nervosa and bulimia nervosa to determine the extent to which shared genetic and environmental factors contribute to liability to these disorders. METHOD: Focusing on females from the Swedish Twin study of Adults: Genes and Environment (n = 7000), we calculated heritability estimates for narrow and broad anorexia nervosa and bulimia nervosa and estimated their genetic correlation. RESULTS: In the full model, the heritability estimate for narrow anorexia nervosa (AN) was (a(2) = .57; 95% confidence interval [CI]: .00-.81) and for narrow bulimia nervosa (BN) (a(2) = .62; 95% CI: .08-.70), with the remaining variance accounted for by unique environmental factors. Shared environmental factors estimates were (c(2) = .00; 95% CI: .00-.67) for AN and (c(2) = .00; 95% CI: .00-.40) for BN. Moderate additive genetic (.46) and unique environmental (.42) correlations between AN and BN were observed. Heritability estimates for broad AN were lower (a(2) = .29; 95% CI: .04-.43) than for narrow AN, but estimates for broad BN were similar to narrow BN. The genetic correlation for broad AN and BN was .79, and the unique environmental correlation was .44. CONCLUSIONS: We highlight the contribution of additive genetic factors to both narrow and broad AN and BN and demonstrate a moderate overlap of both genetic and unique environmental factors that influence the two conditions. Common concurrent and sequential comorbidity of AN and BN can in part be accounted for by shared genetic and environmental influences on liability although independent factors also operative.
BACKGROUND: We present a bivariate twin analysis of anorexia nervosa and bulimia nervosa to determine the extent to which shared genetic and environmental factors contribute to liability to these disorders. METHOD: Focusing on females from the Swedish Twin study of Adults: Genes and Environment (n = 7000), we calculated heritability estimates for narrow and broad anorexia nervosa and bulimia nervosa and estimated their genetic correlation. RESULTS: In the full model, the heritability estimate for narrow anorexia nervosa (AN) was (a(2) = .57; 95% confidence interval [CI]: .00-.81) and for narrow bulimia nervosa (BN) (a(2) = .62; 95% CI: .08-.70), with the remaining variance accounted for by unique environmental factors. Shared environmental factors estimates were (c(2) = .00; 95% CI: .00-.67) for AN and (c(2) = .00; 95% CI: .00-.40) for BN. Moderate additive genetic (.46) and unique environmental (.42) correlations between AN and BN were observed. Heritability estimates for broad AN were lower (a(2) = .29; 95% CI: .04-.43) than for narrow AN, but estimates for broad BN were similar to narrow BN. The genetic correlation for broad AN and BN was .79, and the unique environmental correlation was .44. CONCLUSIONS: We highlight the contribution of additive genetic factors to both narrow and broad AN and BN and demonstrate a moderate overlap of both genetic and unique environmental factors that influence the two conditions. Common concurrent and sequential comorbidity of AN and BN can in part be accounted for by shared genetic and environmental influences on liability although independent factors also operative.
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