Large scale GWAS have identified significant hits for PTSD phenotypes (e.g. Nievergelt et al., 2019), problematic alcohol use (PAU) (Zhou et al., 2020a), (e.g. alcohol dependence; Walters et al., 2018), and alcohol consumption (Clarke et al. 2017). Recent analyses have allowed for examination of genetic associations across alcohol consumption (Kranzler et al., 2019; Liu et al., 2019; Sanchez-Roige et al., 2019b), PAU (Gelernter et al., 2019a; Sanchez-Roige et al., 2019a; Walters et al., 2018; Zhou et al., 2020b), as well as PTSD and re-experiencing symptoms (Gelernter et al., 2019b; Nievergelt et al., 2019). Single nucleotide polymorphism (SNP) -based heritability of PTSD suggests modest to moderate heritability (∼15%), with these estimates larger in women than men (i.e. 36% v. 5%; Duncan et al., 2017). SNP-based heritability of problem alcohol phenotypes suggests modest heritability, ranging from 5.6–9.4% for AD (h2 = 0.090, s.e. = 0.019; Walters et al., 2018), AUD (Kranzler et al. 2019: h2 = 0.056, s.e. = 0.004; Zhou et al. 2020a: h2 = 0.094, s.e. = 0.005), and PAU (h2 = 0.068, S.E. = 0.004; Zhou et al., 2020a).
