“…Both preclinical and clinical studies suggest that the endogenous opioid system may modulate the intake of alcoholic beverages (Froehlich et al, 1988; Reid & Hunter 1984; Reid, Delconte, Nicols, Bilsky, & Hubbell, 1991; Volpicelli, Davis, & Olgin, 1986). The two major theories of endogenous endorphin modulation of drinking, opioid deficit / compensation hypothesis (Volpicelli, 1987) and opioid surfeit hypothesis (Reid, 1990; Reid et al, 1991), suggest that opiate antagonists’ effects on the endogenous opioid system should decrease baseline levels of alcohol craving, decrease levels of craving after drinking is initiated (Berg, Volpicelli, Alterman, & O’Brien, 1990), or both. Consistent with this hypothesis, Volpicelli and colleagues (1992) found that subjects on naltrexone reported significantly less craving at the end of a 12-week trial than subjects on placebo.…”