Alcoholic beverages contribute an appreciable percentage (4-6%) to the total caloric intake in Western societies. The caloric value of ethanol as fuel may be dose-related. Most evidence suggests that at moderate intake levels of less than 45 g/day (3 drinks) ethanol is efficiently utilized as a fuel by the liver. At high intakes, ethanol calories may not be utilized for cellular synthesis of ATP and maintenance of weight. The exact mechanism for this inefficient utilization remains unknown but may be related, in part, to metabolism of ethanol by the microsomal ethanol-oxidizing system, a reaction that does not contribute to generation of reducing equivalents for ATP synthesis. Although ethanol is utilized for ATP synthesis after single-dose administration, chronic consumption leads to morphological changes in hepatic mitochondria and to decreased ATP synthesis. Reductions in the activities of the enzymes of the mitochondrial electron transport chain have been reported after alcohol feeding and may help to explain decreases in hepatic ATP synthesis. There is some evidence that ATP degradation by "Na-K ATPase" is increased after ethanol feeding and that hepatic O2 consumption is likewise enhanced. However, other studies have failed to demonstrate enhanced O2 consumption. Current evidence suggests that malnutrition alone is not sufficient to explain the pathogenesis of chronic liver disease in alcoholics. Although the daily amount of alcohol consumed and the duration of excessive consumption are clearly important factors in the development of alcoholic hepatitis and cirrhosis, other factors, particularly nutritional deficiencies, may modulate the risk of developing alcohol-related liver damage. The prevalence of malnutrition is exceedingly high in alcoholics with clinically severe liver disease. Nutritional deficiencies are better correlated with a clinical index of severity than with histologic severity of alcoholic hepatitis. Prognosis and outcome of patients with alcoholic liver disease may be affected by nutritional deficiencies, which thus provides a rationale for aggressive nutritional management of these patients.