BACKGROUND: This clinical laboratory study evaluated how the timing of drinking and subjective responses to alcohol are effected by the opioid antagonist naltrexone. METHODS:Forty non-treatment seeking alcoholics were randomly assigned to treatment with 50 mg naltrexone or matching placebo for 7 days. On day 7, they were administered an "initial drink" of alcohol (blood alcohol levels of between 20 and 30 mg%) in a bar-like setting. In a random fashion, half of the subjects in each group (naltrexone and placebo) had either immediate or delayed (40 min) access to up to 8 additional mini-drinks over a 2-h period. In the delayed group subjective reactions to alcohol were measured prior to access to more drinks. RESULTS: In the immediate access condition, subjects had similar drinking patterns, irrespective of whether they were taking naltrexone or placebo. However, in the delayed condition, naltrexone-treated subjects consumed fewer drinks and had a slower progression of drinking. There was a positive relationship between alcohol-induced stimulation and the number of drinks consumed in the placebo subjects but a negative correlation in the naltrexone subjects. CONCLUSIONS: These data suggest that the effectiveness of naltrexone on alcohol consumption may be somewhat dependent on pattern of consumption. Since naltrexone seems to disrupt the connection between alcohol-induced stimulation and further alcohol consumption, there may be a time-critical period between drinks necessary for alcoholics to benefit from its effects. These findings are consistent with clinical trial data that suggest a potential synergistic effect between relapse prevention therapies and opiate antagonist pharmacotherapy.
RCT Entities:
BACKGROUND: This clinical laboratory study evaluated how the timing of drinking and subjective responses to alcohol are effected by the opioid antagonist naltrexone. METHODS: Forty non-treatment seeking alcoholics were randomly assigned to treatment with 50 mg naltrexone or matching placebo for 7 days. On day 7, they were administered an "initial drink" of alcohol (blood alcohol levels of between 20 and 30 mg%) in a bar-like setting. In a random fashion, half of the subjects in each group (naltrexone and placebo) had either immediate or delayed (40 min) access to up to 8 additional mini-drinks over a 2-h period. In the delayed group subjective reactions to alcohol were measured prior to access to more drinks. RESULTS: In the immediate access condition, subjects had similar drinking patterns, irrespective of whether they were taking naltrexone or placebo. However, in the delayed condition, naltrexone-treated subjects consumed fewer drinks and had a slower progression of drinking. There was a positive relationship between alcohol-induced stimulation and the number of drinks consumed in the placebo subjects but a negative correlation in the naltrexone subjects. CONCLUSIONS: These data suggest that the effectiveness of naltrexone on alcohol consumption may be somewhat dependent on pattern of consumption. Since naltrexone seems to disrupt the connection between alcohol-induced stimulation and further alcohol consumption, there may be a time-critical period between drinks necessary for alcoholics to benefit from its effects. These findings are consistent with clinical trial data that suggest a potential synergistic effect between relapse prevention therapies and opiate antagonist pharmacotherapy.
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