The pathogenesis of alcoholic pancreatitis continues to be a puzzle. Of the many theories as to how alcohol might cause pancreatic damage, none satisfactorily explains why only a minority of alcoholics develop clinical pancreatitis. Hypertriglyceridemia and inherited factors could be important antecedents in some individuals, and high fat and protein diets may favour the development of the disease. Disturbances of the sphincter of Oddi have been postulated, but there are experimental and theoretical objections to the view that alcoholic pancreatitis generally results from sphincter dysfunction (obstruction-hypersecretion, biliary-pancreatic reflux and duodeno-pancreatic reflux). Biochemical studies of the effect of alcohol on pancreatic tissue have so far been relatively unrewarding. The most widely held view is that alcohol causes the deposition of protein in peripheral ducts leading to obstruction, inflammation and degeneration. However, it remains to be shown that these deposits are the cause rather than a result of pancreatic inflammation. Research might be facilitated by the development of a suitable animal model of the disease.