Furthermore, the meta-analysis lacked tests of discriminant validity, that is, it did not test whether these nicotine-related hits were also relevant for other substance use disorders, or what the mechanisms of that action may be. In the present study we evaluate the relationship between the nicotine SNPs identified by (Thorgeirsson, et al., 2010) and alcohol use. There are multiple etiological pathways that would result in an association with nicotine SNPs and alcohol use; we discuss two. First, it may be that the SNPs are not etiologically specific for smoking, but rather are relevant for more pervasive behavioral systems that impact general risk for substance use like disinhibition or impulsivity. Second, if a genotype is related to nicotine use then this, by definition, indicates that an individual with the risk genotype will experience increased environmental exposure to nicotine. That is, the genotype causes smoking, but it also causes the environment of nicotine intake. Some have theorized that environmental exposure to drugs and alcohol acts as a “gateway,” in which the experience of drug effects cause further use of other, possibly “harder”
