Results of the present study also showed that 31% of the variance in MDD liability was explained by the joint effect of all common SNPs. This perfectly replicates the h2SNP estimate (0.32) obtained by a previous study based on the GAIN MDD dataset (26), including overlapping cases with the current study and different controls genotyped on a different platform. Estimates of h2SNP were higher for the subtypes: 38% for MDD with decreased and 43% for MDD with increased appetite/weight. This suggests that subtypes may be genetically more homogeneous. It is important to remark, however, that due to the limited sample size the standard errors around the estimates were large. Nevertheless, our results are in line with recent twin-based estimates(52) showing higher heritability for atypical depression defined according to DSM-III (0.51) as compared to MDD (0.43). Major strengths of the current study include the availability of GWAS data in a large sample well-characterized in terms of psychiatric diagnoses, the use of different sub-phenotyping strategies to identify MDD subtypes and GPRS based on large international consortia. An important limitation is that the
