Implication of the endogenous opioid system in excessive ethanol consumption.

Numerous human and animal studies suggest that certain genetic factors may increase an individual's vulnerability to excessive alcohol consumption. Human and animal studies suggest that some of the reinforcing effects of ethanol may be mediated by the endogenous opioid system. In human studies, plasma levels of subjects genetically at high risk for excessive alcohol consumption showed lower basal activity of beta-endorphin, and more pronounced release of beta-endorphin in response to ethanol. In animal studies, the hypothalamus of mice bred for ethanol preference showed high basal activity of beta-endorphin and more pronounced release of beta-endorphin in response to ethanol than control mice. An important factor in the development of excessive ethanol consumption is the increase in opioidergic activity shortly after individuals begin drinking ethanol. Increased opioidergic activity could mediate the rewarding effects of ethanol, reinforce the act of drinking, and increase ethanol consumption. Human and animal studies, in which the administration of the opioid antagonists naloxone and naltrexone decreased ethanol consumption both by ethanol-preferring animals and by recovering alcoholics, support this hypothesis.