Preliminary linkage analyses were conducted with MERLIN-REGRESS(33), using a panel of SNPs selected for high minor allele frequency and low linkage disequilibrium (r2<0.02). Family-based association analyses of quantitative phenotypes were conducted using the FASTASSOC option in MERLIN (34); family-based analyses of the categorical DSM-IV alcohol dependence diagnosis were conducted using MQLS (35) as implemented in GDT (36). Results for our primary phenotypes were compared to those from the COGA (10), SAGE (9) and German (11) alcoholism GWAS studies. Finally, case-population control analyses were implemented using Huber-White adjustment for familial clustering in STATA (37). We use alpha=1.67E-7 (Bonferroni correction for 300,000 SNPS) as the threshold for genomewide significance for a single phenotype, thus alpha = 8.35E-8 for our primary HOD and AUD-FS outcome measures, allowing for testing of 2 phenotypes. We also report some key findings for other consumption phenotypes that would be more readily available in other data-sets. We looked for consistency of evidence of genetic effects across phenotypes – between HOD and AUD-FS; for each with dependence diagnosis, and with other consumption measures. Finally, we used case-population control comparisons
