Release of CRF by alcohol and/or stress also elicits release of beta-endorphin, an endogenous opioid peptide. Beta-endorphin plays a role in brain reward pathways and is affected by all drugs of abuse, including alcohol, with alcohol’s induction of beta-endorphin appearing to be at least in part under genetic control (Froehlich et al. 2000). Moreover, it has been suggested that low levels of endogenous opioid peptides including beta-endorphin may characterize individuals at genetic risk for developing AD. Changes in beta-endorphin synthesis, processing and release after chronic alcohol have been studied frequently, and a confusing array of results have been reported, probably due to differences in subjects, exposure regimens, doses of alcohol, and timing of hormone assessments [for review, see (Gianoulakis 2004)]. The mu opioid receptor antagonist naltrexone is one of the few available treatments for AD, with a polymorphism of the OPRM1 (opioid receptor mu 1) receptor gene providing some predictability for naltrexone’s clinical efficacy [e.g., (Ooteman et al. 2009)].
