Plasma amino acid abnormalities are frequently reported in alcoholics, with the most common abnormalities being those of depressed branched chain amino acids (BCAA) and increased aromatic amino acids. The depression in branched chain amino acids is due to multiple factors including portal-systemic shunting, hyperinsulinemia, hyperglucagonemia (all due to advanced liver disease) as well as dietary deficiency. alpha-Amino-n-butyric acid is a nonessential amino acid derived primarily from the catabolism of methionine, threonine, and serine. Increased levels due to chronic alcohol consumption may reflect altered glutathione metabolism and lipid peroxidation due to alcohol and may be used empirically as a biochemical marker of heavy drinking. The high levels of aromatic amino acids such as tyrosine and tryptophan as well as their breakdown products may be due to impaired hepatic metabolism and appear to play a role in the pathogenesis of hepatic encephalopathy. The effects of high levels of aromatic amino acids may be potentiated by depressed BCAA; these normally compete with each other for CNS transport. Alterations in these amino acids may have implications for nutritional requirements for amino acids in these patients as well as therapeutic approaches.