Selenium deficiency has been implicated as a cause of hepatic injury, possibly from accentuated lipoperoxidation due to decreased activity of the selenoenzyme, glutathione peroxidase. Because of possible clinical and biochemical links between selenium and alcohol, we performed nutritional assessment and assayed red blood cell, plasma, and whole blood selenium by spectrofluorometry in 27 normals (group I), 30 asymptomatic alcoholics on admission to a detox unit (group II), and 16 alcoholics with severe liver disease (group III). We found a mean (±sd) whole blood selenium of 0.109 μg/ml±0.014 for group I vs 0.076±0.010 for group II (P<0.001), and 0.047±0.006 for group III (P<0.001 vs group I and II). For plasma, the mean (±sd) selenium was 0.095 μg/ml±0.016 for group I versus 0.065 μg/ml±0.012 in group II and 0.038 μg/ml± 0.007 in group III (AllP<0.001). Calculated red blood selenium levels were also significantly reduced in alcoholics versus controls. Whole blood and plasma selenium correlated directly with serum albumin. For whole blood selenium versus albumin,r=0.73 (P<0.01), and for plasma selenium versus albumin,r=0.71 (P<0.01). A significant inverse correlation was noted between whole blood selenium and the height of the total serum bilirubin (r=−0.46), alkaline phosphatase (r=−0.50), and AST (r=−0.51) (P<0.01 for all). Among alcoholics admitted for detoxification, selenium was diminished despite the absence of severe malnutrition, as determined by standard nutrition assessment parameters. We conclude that blood selenium levels are diminished in alcoholics, even in the absence of severe liver disease or malnutrition. This abnormality is markedly accentuated in the presence of severe liver disease and correlates directly with albumin and inversely with bilirubin. Associations between this finding and its role in liver disease, as well as other pathologic states attributed to alcoholism, deserves further consideration.