We first performed a sex-stratified genome-wide association meta-analysis and genotype-sex interaction meta-analysis including autosomes and the X chromosome. We then developed an approach to identify SNPs with Sexually Differentiated Effects (SDEs), and assessed whether the SDEs regulate gene expression and are enriched for associations with sexually-differentiated anthropometric traits (i.e. height, weight, body mass index, hip and waist circumference) as observed in autism spectrum disorders (Mitra et al. 2016). Third, we performed SNP-based heritability analysis to (a) assess the proportion of overall OCD heritability explained by the X chromosome, and (b) test for evidence of sexually-dependent liability threshold for OCD between males and females. An important correlate of the sex-dependent liability threshold is that the sex with the lower prevalence/milder presentation requires a higher genetic burden to become affected and therefore is more likely to have affected children, also known as the Carter effect. This has been reported for several complex traits (Kruse et al. 2012; Kantarci et al. 2006). Fourth, we performed a sex-stratified genetic correlation analysis with other traits which may play a role in OCD development (e.g. brain
