A newly published animal study is shedding important light on the gateway theory of substance use, perhaps opening the door to eventual new treatment strategies to combat addiction.
The journal Science Translational Medicine this month published research identifying a molecular mechanism that appears to explain the progression from tobacco use to cocaine use. Researchers using mice were able to show a gateway effect that operated in only the direction from tobacco to cocaine, with the reverse not being true, says Eric Kandel, MD, a senior author of the study with Columbia University Medical Center.
This research for the first time identified nicotine’s effect of inhibiting an enzyme and thereby reprogramming gene expression patterns, resulting later in an altered behavioral response to cocaine. These results could suggest similar effects in humans; it has already been seen in drug use surveys that cocaine dependence rates are higher among users who had smoked prior to initiating cocaine use.
Kandel explains that along with the possibility that smoking prevention efforts could have added benefits in preventing other drug use, the latest findings could have implications for treatment as well. The thought of creating compounds that would produce the opposite effect from what was seen with nicotine in this study “holds up the possibility of identifying a therapeutic approach,” he says.
Kandel adds that researchers have just begun to conduct a similar analysis of alcohol’s possible mechanisms of action as a gateway substance. The field certainly seems to be on the brink of a clearer biological understanding of the gateway theory.