We also employed an estimate of phenotypic variance in alcohol-related phenotypes attributable to a given set of SNPs (GCTA; Yang et al., 2011). For both the set of GABA system SNPs (737 markers), and the entire set of available genome-wide SNP markers (527,829 markers), separately, a SNP-based measure of genetic relatedness between each pair of individuals included in the analysis was computed. For each analysis, the matrix of the genetic relatedness estimates for all pairs of individuals was then included as random effects in a linear mixed model (along with the covariates as fixed effects), using restricted maximum likelihood estimation (REML), in order to estimate the proportion of phenotypic variance attributable to the SNPs used to compute inter-individual genetic relatedness. In order to derive an estimate of variance attributable solely to the SNPs included in the analysis, unburdened by the shared environment or other sources of phenotypic variance, and unbiased by cryptic relatedness between individuals, one member of each pair with full-genome SNP-based genetic relatedness estimated at greater than 0.025 was removed from subsequent analyses. For both the set of
