We found no association of alcohol dependence with any SNPs in NPY, which is consistent with some previously reported results (Hu et al., 2005; Mottagui-Tabar et al., 2005; Zhu et al., 2003). The bulk of evidence of the evidence for a role of the entire NPY system in alcohol-related phenotypes comes from animal models. While alcohol preference and consumption in rats and mice mimic similar traits of alcohol dependence in humans, their equivalence is still unclear (Crabbe, 2007). Our examination of the secondary phenotype of alcohol withdrawal provides another means to examine the nature of the association of these SNPs in the NPY system with alcohol dependence and provide important insights regarding disease heterogeneity.
