One possible explanation for these findings is that these drugs may serve as a substitute for one another. Ethanol and cannabis both have depressant effects on central nervous system function. In laboratory rodents, administration of either ethanol or Δ9-tetrahydrocannabinol (THC; the main psychoactive compound in cannabis) produces hypolocomotion, hypothermia, and ataxia (Crabbe et al., 2005; Martin et al., 1991). In human subjects acute administration of either compound produces euphoria and feelings of intoxication (Heishman et al., 1997; Jones and Stone, 1970), and both substances decrease response time and accuracy on neuropsychological tests measuring memory, attention, and psychomotor performance (Chait and Perry, 1994; Heishman et al., 1997; Heishman et al., 1988). In addition, daily cannabis users significantly increased self-reported ethanol craving and consumption during a two-week abstinence from marijuana (Peters and Hughes, 2010) and individuals in treatment for CUDs increased the frequency of ethanol use during 12 months following treatment (Stephens et al., 1994). However, there are conflicting data with respect to combined ethanol and cannabis use. Findings from other studies of post-treatment outcomes for CUDs show a decrease (Stephens et al., 2000) or no change (Kadden et al., 2009) in ethanol consumption associated with decreased use of cannabis.
