Alcohol abuse has serious consequences on physical and mental health and represents a major public health burden. Chronic alcohol consumption has been shown to have detrimental neurologic effects, inducing widespread neuronal loss in both fetuses and adult organisms. One proposed mechanism of ethanol-induced cell loss with sufficient exposure is an elevation in concentrations of bioactive lipids that mediate apoptosis, including the membrane sphingolipid metabolites ceramide and sphingosine. While these naturallyoccurring lipids serve as important physiological modulators of normal neuronal development, differentiation, and apoptosis, elevated levels resulting from various extracellular insults have been implicated in pathological apoptosis of neurons and oligodendrocytes in several neuroinflammatory and neurodegenerative disorders. Previous work has shown that acute administration of ethanol to developing mice increases levels of ceramide and sphingosine in multiple brain regions, hypothesized to be a mediator of fetal alcohol-induced neuronal loss. Elevated ceramide levels have also been implicated in contributing to ethanol-mediated neurodegeneration in adult animals and humans. The present study aimed to determine the effect of chronic voluntary ethanol consumption on lipid profiles in brain and peripheral tissues from adult selectively bred alcohol-preferring (P) rats to further examine alterations in lipid composition as a potential contributor to ethanolinduced cellular damage. Nondeprived P rats were exposed for 13 weeks to either a 20% ethanol intermittent access drinking paradigm (45 ethanol drinking sessions total) or were given access only to water (non ethanol-exposed control). Following the final experimental session, brain, liver, heart, muscle, adipose tissue, and blood were collected for subsequent thin layer chromatographic analysis of lipid content. Ethanol intake and microstructural measures of ethanol ingestive behavior were analyzed to determine levels and patterns of ethanol consumption across time. It was hypothesized that chronic voluntary ethanol intake in adult alcohol-preferring rats would increase levels of ceramides and other pro-apoptotic lipids compared to non-exposed controls, consistent with dysregulated lipid signaling as a potential mediator of alcohol-induced pathology. Contrary to expectations, genetically selected alcohol-preferring (P) rats exposed chronically to a 20% ethanol intermittent access drinking paradigm displayed substantial reductions in concentrations of ceramides in both forebrain and heart relative to non-exposed controls, as well as modest but significant decreases in liver cholesterol. These data are opposite in nature to previously observed elevated levels of pro-apoptotic lipids in developing rodents following acute ethanol administration, believed to contribute to fetal alcohol-induced neuronal loss. The present findings indicate that ethanol intake levels achieved by alcohol-preferring P rats as a result of chronic voluntary exposure may have favorable vs. detrimental effects on lipid profiles in this genetic line, consistent with prior data supporting beneficial cardioprotective and neuroprotective effects of moderate ethanol consumption. These data add to a growing literature that moderate ethanol intake has beneficial effects on specific physiological and behavioral indices of disease risk, and may contribute to a more thorough understanding of the underlying mechanisms mediating ethanol's cardioprotective and neuroprotective effects.