Consistent with the hypothesis of a shared endophenotype for OCD and substance misuse,7,8,9 we found shared genetic factors to explain approximately 56% to 68% of the covariance. The validity of our results was increased by the use of 2 separate cohorts and study designs with different assumptions. However, a genetic correlation by itself is insufficient to confirm the hypothesis because it might reflect some other genetically influenced trait instead of the hypothesized compulsivity endophenotype. A genetic correlation might reflect vertical pleiotropy (ie, phenotypic mediation) instead of shared genetic etiology.55 These hypotheses can be tested in future OCD GWAS benefiting from a substantially increased sample size28 compared with previous efforts.56
