We note that the etiological influences of molecular genetic overlap and phenotypic correlation are not mutually exclusive (i.e., shared risk can be operating through multiple pathways). Researchers have posited several frameworks linking the two disorders. In the high-risk hypothesis, for example, individuals with a genetic predisposition for AD have been shown to engage in a range of risky (externalizing) behaviors prior to the onset of alcohol use problems (Meyers et al., 2014), increasing exposure to potentially traumatic experiences. The selfmedication hypothesis posits that individuals potentially self-medicate their PTSD with alcohol, ultimately increasing risk for AD (Haller and Chassin, 2014). Although present study findings suggest overlapping genetic risk may influence these different pathways linking PTSD and AD, the current study design does not allow us to disentangle these possible causal mechanisms. In an informative review of shared genetic risk across psychiatric disorders, Martin and colleagues (2017) describe the multiple, not mutually exclusive, interpretations of a given genetic correlation, which may signify: 1) the same risk variants are directly, causally impacting different phenotypes; 2) the same risk variants could be impacting a
