First, the strongest evidence supporting the stomach as the main site of FPM was the identification of several classes of ADH in the human stomach, particularly the gastric ADH class IV (21, 22). This enzyme is active at a range of alcohol concentrations that are typically achieved after alcohol ingestion, which are in the molar range (85, 86). Notably, the administration of non-competitive inhibitors of stomach ADH, such as Cimetidine, increases alcohol bioavailability when alcohol is ingested but has no effect when the same dose of alcohol is administered intravenously (87, 88).
