Heritability of binge-eating and broadly defined bulimia nervosa

Using diagnostic information obtained at two different times, we incorporated error of measurement into structural equation twin models to evaluate the contribution of additive genetic, common environmental, and individual-specific environmental factors to the liability to binge-eating and broadly defined bulimia nervosa (BN). We also evaluated the validity of the equal environment assumption (EEA) with reference to these two phenotypes.

We interviewed 1897 female twins (including both members of 854 twin pairs) from a population-based register about their lifetime history of binge-eating and of broadly defined BN twice, approximately 5 years apart.

The reliabilities of a lifetime history of binge-eating (kappa = .34) and of broadly defined BN (kappa = .28) were low. Based on single interviews, the heritability of binge-eating was estimated to be 50% and broad BN 60%, with the remaining variance attributable to individual-specific environment. Common environmental influences had no effect on liability to either trait. By combining information from two interview waves and thereby incorporating error of measurement into a structural equation model, the estimated heritability of the latent vulnerability to binge-eating (82%) and broadly defined BN (83%) increased substantially. Although there were no violations of the EEA detected for binge-eating, cosocialization influenced twin concordance for broadly defined BN.

Lifetime histories of binge-eating and broadly defined BN appear to be highly heritable conditions of low reliability.