(Beatty et al., 1996; Bowden, 1988; Corral-Varela and Cadaveira, 2002; De Renzi et al., 1984; Matthews and Morrow, 2000; Nixon et al., 1987; Oscar-Berman and Ellis, 1987; Riege, 1987; Shelton et al., 1984). Damaging effects on the hippocampus are believed to result from the combined effects of ethanol-induced glucocorticoid elevation, compromised nutrition, and oxidative stress. In previous research on long-term abstinent alcoholics (LTAA) in our laboratory, (Sameti et al., 2011) we did not find reduced subcortical (including hippocampal) volumes in LTAA, but did find significantly lower hippocampus (and amygdala) volumes in multi-year abstinent alcoholics with co-morbid psychiatric disorders.