The alcohol-addictive metabolite hypothesis of alcohol addiction is reviewed. The status of monoamine oxidase in this clinical condition is also discussed and possible reasons for low platelet activity proposed. An endogenous monoamine oxidase inhibitor, which is also a benzodiazepine receptor ligand, denominated tribulin, is produced in excess following alcohol withdrawal and may, in fact, be a predisposing factor for or the actual agent precipitating delirium tremens. Alcohol suppresses tribulin production and predisposed individuals may drink it to counter the dysphoric effects of a baseline overproduction of this compound.