Heritability explained by common variants (h2SNP) and genetic correlations with 23 other traits chosen because of previous findings or hypothesised relationships (including cannabis use; appendix pp 15–17) were estimated using LDSR22, 32 on the results of the meta-analysis of case-control individuals of European ancestry (the number of unrelated cases of African ancestry was less than the acceptable sample size threshold for LDSR). Conversion of h2SNP estimates from observed scale to liability scale was done using a range of estimated population prevalences from 1%3 to 8·5% (because in some samples we used DSM-IV cannabis abuse or dependence).33 Significance of genetic correlations with other traits was determined using a Bonferroni correction for 23 tests (including with cannabis use; α=0·002). Finally, we examined whether the genetic correlations for cannabis use disorder were significantly different than those for cannabis use5 using the jackknife procedure implemented through LDSR.32
