Due to demonstrated effects on neurophysiology, nicotine dependence (Durazzo et al., 2007), anxiety (van Tol et al., 2010), depression (Drevets et al., 2008; Peterson and Weissman, 2011), family history of AUD (Gilman et al., 2007), presence of Wernicke-Korsakoff syndrome (Kril et al., 1997), liver disease (Pfefferbaum et al., 2004), and comorbid drug use disorders (Berman et al., 2008; Lorenzetti et al., 2010; O'Neill et al., 2001) merit further consideration as factors influencing WM atrophy in AUDs. In particular, brain abnormality in AUDs overlaps considerably with changes found in mood, anxiety, and other substance use disorders. Because epidemiological data have linked AUD treatment-seeking to higher lifetime incidence of mood, personality, and other substance use disorders (Cohen et al., 2007), it is plausible that an overall greater burden of psychopathology accounts in part for the significantly larger ES observed in treatment-seeking samples in the present study. One limitation of the present study is that these variables could not be coded reliably due to inconsistent reporting in the original studies. Future studies systematically investigating the influence of comorbid disorders will assist in identifying shared versus unique effects on neurobiology.
