able to find a robust association with alcohol consumption using our risk scores suggesting they are valid tools to investigate the genetic overlap between disorders. The variation in weekly alcohol consumption explained by the alcohol dependence PGRS is low, less than 0.1 percent. We created a meta‐analysed PGRS that utilized summary statistics from the Yale‐Penn and SAGE GWAS combined (n = 5127) to try to increase the amount of variance explained in our traits of interest. This score explained 0.3 percent of the variance in alcohol consumption. A large GWAS of schizophrenia (N ∼ 150 000) was used to create PGRS in an independent schizophrenia cohort. These scores explained 7 percent of the variance in schizophrenia (Schizophrenia Working Group of Psychiatric Genetics Consortium 2014) and demonstrate that as the size of a discovery GWAS increases the amount of variance explained by PGRS increases. Considering that the genetic overlap between alcohol consumption and abuse is not perfect (rG = 0.61) (Dick et al. 2011) and the original GWAS for alcohol dependence had fewer individuals, it is understandable that the variance explained by PGRS is low. Finally, not all of the associations we report withstand correction for multiple testing. The associations between
