than individuals with treatment histories. Not surprisingly, inadequate diet and nutritional deficiencies are commonly reported in clinical samples of alcoholics. Thiamine deficiency is increasingly identified as an important contributor to alcohol-related brain damage of all kinds (See Martin et al. (2003) for a review), especially disruption of fronto-cerebellar and cerebellothalamocortical circuitry affecting abstract problem solving, visuospatial processing, verbal memory and perceptual motor skills (Sullivan, 2003; Sullivan et al., 2005). Given that treated alcoholics are less likely than TNAD to attend to everyday activities, or to be cohabitating or employed, it is reasonable to hypothesize that TNAD individuals are more likely to attend adequately to their diet and, hence, are less likely to suffer the effects of thiamine deficiency, especially given that TNAD also have lower alcohol doses after meeting criteria for heavy alcohol use (Fein et al., 2005). Future research may focus on comparing nutritional histories of TNAD and treated alcoholics.
