rising breath alcohol concentrations, as compared to those participants homozygous for the 118A allele. These findings are not consistent with the findings in the present study for the 118G allele, nor are they particularly consistent with studies that have found a less intense response to opioid agonists. However, the findings of Ray and Hutchinson [94,95] are consistent with the findings in the present study of an association between expecting to experience a more intense response to alcohol and carrying at least one minor allele for eight other SNPs in the opioid receptor gene. Since, in the study of Ray and Hutchinson [94,95], only one SNP was genotyped and the ethnic characteristics of the sample were not specified, it is possible that the findings reflected stratification of the sample or that the A118G variant was in linkage disequilibrium with several other alleles that may encode for a more intense response to alcohol. These data further suggest that making conclusions on the role of the mu opioid receptor gene in the development of alcohol-related behaviors may be limited if only one polymorphism in the gene is evaluated in isolation.
