The twin studies demonstrated that OCD, or at least its dimensional representation, is not only familial but also heritable, with twin correlations ranging from 0.52 and 0.43 in MZ twins compared to 0.27 and 0.20 in DZ twins (in children and adult samples, respectively). These findings are in line with previous reports [1, 71, 72], and indicate that both genetic and environmental characteristics are important in the etiology of OCS. The analyses of the specific roles of additive genetic effects (A) and non-shared environment (E) components of the ACE model in the etiology od OCD revealed that our findings are in line with previous results [1] with each accounting for 46% and 54% of the variance, respectively. Interestingly, single-nucleotide polymorphisms -based heritability of OCD is still considerably lower, in the region of 30% [73], which indicates that further research is needed to understand the “missing heritability”. It is plausible to assume that while the majority of inherited liability for OCD is due to common genetic variation, rare variation may also contributes to some extent. Thus, future genetic studies should focus on common as well as rare genetic variants as a way to capture more of the unexplained phenotypic heritability.
