Previous analyses that have compared the MNB/NIDA European-American to African-American results have identified genomic regions that are labeled by clustered, nominally-positive SNPs from both samples, supporting roles for some allelic variants that are likely to be old in relation to human history [6], [7], [9], [21]. Data from analyses that combine results from individuals with different racial/ethnic backgrounds also provide suggestive results in regions such as the GABA receptor gene cluster on chromosome 4 for evolutionarily-old variants [16], [35]. Identification in both studies of SNP markers whose allelic frequencies distinguish controls from addicts of different ethnicities supports “common disease/common allele” genetic architecture [36] for part of the genetics of addiction vulnerability. However, the substantially greater convergence, noted here, for data from the same racial/ethnic groups also points to possibly-substantial roles for variants that have been accumulated more recently in human populations that have been more separate until relatively recently.
