Epidemiologic studies report high co-occurrence between PTSD and both problematic alcohol use and AUD (Brown, Stout, & Mueller, 1999; Debell et al., 2014; Kessler, Chiu, Demler, Walters, & Walters, 2005; Mills, Teesson, Ross, & Peters, 2006; Pietrzak, Goldstein, Southwick, & Grant, 2011). One model for understanding this comorbidity is the shared liability model, which suggests that shared, common factors (e.g. trauma, genetics, physiological, and psychological traits) contribute to increased risk for alcohol use behaviors, AUD, and PTSD (Danovitch, 2016). Indeed, twin and molecular studies suggest correlated genetic risk (Bountress et al., 2022; Sartor et al., 2011; Sheerin et al., 2020; Xian et al., 2000). Growing research has begun to explore the role of shared neurobiological mechanisms (Brady & Sinha, 2005; Gilpin & Weiner, 2017). Neurophysiological and neuropsychological measurement can further our understanding of shared risk beyond self-report data (Davis et al., 2013). Some work has focused on the role of early stress in producing a cascade of neurobiological changes, such as reduced functional activity and/or structural alterations in key brain areas, that may act to increase risk for psychiatric disorders (Teicher et al., 2003). More research is needed to uncover possible mechanisms by which early trauma may influence neuropsychological development.
