During the last 16 years an increasing number of studies have indicated a new diagnostic marker of alcohol abuse, unrelated to any of the conventional markers of alcoholism. This marker, now called carbohydrate-deficient transferrin, consists mainly of one or two isoforms of transferrin that are deficient in their terminal trisaccharides. Such isoforms have so far been detected by methods based on charge, i.e., isoelectric focusing, chromatofocusing, and anion-exchange chromatography of various designs combined with immunological detection techniques. This transferrin abnormality measures an accumulated effect of alcohol consumption, appearing after regular intake of 50-80 g of ethanol/day for at least one week and normalizing slowly during abstinence (half-life = about 15 days). To summarize all studies to date, approximately ˜2500 individuals have been examined, with a total clinical sensitivity of 82% and a specificity of 97%. False-positive results have only occasionally been reported: in a few patients with severe liver disease, usually primary biliary cirrhosis and chronic active hepatitis; in patients with genetic D variants of transferrin; and in patients with (and some carriers of) a recently identified inborn error of glycoprotein metabolism. The mechanism behind the transferrin abnormality is unknown but an acetaldehyde-mediated inhibition of glycosyl transfer has been suggested. Carbohydrate-deficient transferrin may thus offer a new possibility of diagnosing alcohol-related disorders. Its measurement is little affected by other conditions and, contrary to conventional markers of alcohol abuse, is apparently largely independent of concomitant liver disease.