Inter-individual differences in neurobiological circuits, due to genetic variation and their downstream effects, alter susceptibility to developing addiction. Although addiction is multifactorial, heritability estimates have indicated that around 40%–60% of the population variability in becoming addicted to nicotine, alcohol, or illicit drugs is attributable to genetic factors [3, 5]. Some genetic factors may influence an overarching susceptibility to developing addiction; thus, their effects are shared across different drugs of abuse. In contrast, other genetic factors may underlie susceptibility to developing specific drug addictions. To pinpoint the genetic factors underlying addiction, variants selected from biologically plausible candidate genes were long-studied in hypothesis-driven studies, but genetic variant associations were not firmly established until the advent of the agnostic, hypothesis-generating genome-wide association study (GWAS) approach. As seen across the field of complex human disease genetics, the potential of GWAS to make novel discoveries continues today with ever increasing sample sizes and statistical power, denser genomic coverage, and phenotype harmonization. This review outlines GWAS reports to date for nicotine, alcohol, or other drug addictions and focuses on common variants (mostly, single nucleotide polymorphisms [SNPs]) with robust evidence for association (i.e., identified at the standard genome-wide significance threshold [P<5×10−8] and replicated in an independent dataset).
