ALDH6A1, and ALDH18A1) was attained through the genome-wide component of the study (Bierut et al., 2007). Since these genes were not initially targeted in the candidate gene component of the study, SNP coverage is generally sparser. Because this study is evaluating alcohol-related phenotypes, we have chosen to analyze all available ADH and ALDH genes. Initial SNP genotyping was performed by Perlegen Sciences for the Genome Wide Association and Candidate Gene Studies of Nicotine Dependence and details are available in (Bierut et al., 2007 and Saccone et al., 2007). Additional genotyping was then performed at the Center for Inherited Disease Research (CIDR) to improve coverage of the ADH and ALDH genes. Data cleaning to insure high quality genetic data included a missing genotype rate < 2%. Out of 190 SNPs successfully typed, 15 were not analyzed; two SNPs were out of Hardy-Weinberg equilibrium (P < 0.001), and thirteen had a minor allele frequency less than 1%, leaving 175 SNPs across the seven alcohol dehydrogenase(ADH) and ten aldehyde dehydrogenase (ALDH) genes for association tests.
