Benzodiazepines reliably produce overconsumption of food and fluids. Opiate antagonists, naloxone and naltrexone, block the benzodiazepine-induced hyperphagia and hyperdipsia at low doses. Hence, activation of endogenous opioid mechanisms may be closely involved in the benzodiazepine facilitatory effects on ingestional behavior. Evidence is reviewed that opiate antagonists diminish feeding and drinking responses, and may enhance satiety processes in feeding and drinking, in addition to selectively diminishing the palatability of attractive foods and fluids. It is proposed that a single mechanism of action of the opiate antagonists would be sufficient to account for both effects on feeding and drinking. Biochemical data confirm that acute benzodiazepine treatment in vivo is associated with a naloxone-reversible release of striatal enkephalin. It is possible therefore that there is a close association between the behavioral and biochemical data, which both show that acute benzodiazepine effects are reversed by opiate antagonists. The implied relationship between benzodiazepine and endogenous opioid mechanisms may be relevant to the question of concurrent opiate-benzodiazepine abuse.