A candidate with considerable promise for association studies of cannabis use disorders is the gene that encodes the fatty acid amide hydrolase enzyme (FAAH)[54-57]. FAAH catalyzes the conversion of both AEA (anandamide) and 2-AG to arachidonic acid and ethanolamine (AEA) or glycerol (2-AG) [58,59]. In animal studies, inhibiting FAAH activity (and thereby reducing breakdown of endogenous cannabinoids) increases non-opioid induced analgesia [60]. In murine knock-out models, FAAH −/− mice are reported to be more responsive to exogenous cannabinoids and to have lower pain sensitivity [61].
