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Uh oh. I just found out that I might be slightly wrong in my last post. I just found out that things like cimetidine and ranitidine that decrease the production of stomach acid cause an increased rate of gastric emptying. This means that the alcohol reaches the small intestine quicker where is it more effectively absorbed.
So cimetidine wouldn't really potentiate the effects of alcohol but it does speed up the onset of the effects and the peak blood alcohol level would be increased. So it might seem like it potentiates the effects since you will feel more intoxicated at the peak than you otherwise would have, but it would also shorten the duration of the effects since elimination of the alcohol from your body would a start sooner.
Haha only potentiators of alcohol i know of are other downers and that is never a good idea! Alcohol hardly needs potentiation unless you are a really big guy with a huge tolerance... Or just afraid of the calories haha. I have heard of people using alternate ROAs for alcohol but never heard anything GOOD about them!
Personally I think it might but have yet to experiment.
If cytochrome affects Alcohol dehydrogenase (which is what breaks down alcohol in the first stage of metabolism, I think) it would mean that it could potentially potentiate . I think it's likely.
If this was true doing so would cause extensive liver damage which is why I'm hesitant even to test with controlled dosages in a safe environment. Using cimetidine to potentiate alcohol is analogous to distracting your liver then twisting a broken bottle into it while it's got it's back turned .
Section of Liver Diseases and Nutrition, Bronx Veterans Affairs Medical Center 10468.
JAMA 1992 Nov 18;268(19):2652.
To determine whether the H2-receptor antagonist, ranitidine, which is a potent inhibitor of gastric alcohol dehydrogenase activity in vitro, increases the bioavailability of orally administered ethanol (0.3 g/kg of body weight) and to compare the resulting blood alcohol concentrations with those of two other H2-antagonists, cimetidine and famotidine, the latter of which does not inhibit gastric alcohol dehydrogenase. DESIGN:
For each of the H2-receptor antagonists, a different group of subjects was used. In each group, a paired design was adopted with each subject serving as his own control. SETTING:
Hospital laboratory. SUBJECTS:
Normal, healthy men aged 24 to 46 years. INTERVENTION:
Eight men were treated for 1 week with ranitidine (300 mg/d), six with cimetidine (1000 mg/d), and six with famotidine (40 mg/d). MEASURES:
Peak blood alcohol concentrations, areas under the blood alcohol curve, first-pass metabolism, and bioavailability of orally consumed ethanol. RESULTS:
Relative to baseline, ranitidine increased the mean peak concentration and the area under the curve of blood alcohol concentrations by 34% (P less than .05) and 41% (P less than .01), respectively. First-pass metabolism of ethanol was decreased from 70 +/- 10 to 31 +/- 9 mg/kg of body weight, with a corresponding increase in ethanol bioavailability of 79.6% to 92.6%. By comparison, cimetidine had even a greater effect on blood alcohol levels, while famotidine had no significant effects. CONCLUSION:
Patients treated with ranitidine or cimetidine should be warned of possible functional impairments after consumption of amounts of ethanol considered safe in the absence of such therapy.