Cannabidiol (CBD), the main non-psychoactive and non-addictive constituent of Cannabis sativa, has long received interest as a therapeutic for numerous psychiatric and neurologic disorders (e.g., ref. [1]). Recently, investigations on the scope of CBD’s medical benefits have encompassed its potential to treat substance use disorders. Both clinical and preclinical data are overall promising in this regard. However, presently available data are scattered across several classes of abused drugs (i.e., tetrahydrocannabinol, nicotine, opiates, alcohol) and several stages of the addiction cycle (i.e., self-administration, withdrawal, drug seeking, abstinence). Moreover, both positive and negative findings have been obtained such that scope and nature of CBD’s effects on addictive behavior remained to be more clearly established [2].

Among the studies of CBD’s “anti-addiction” potential, a major positive finding reported by Hurd and colleagues [3] was that CBD attenuates cue-induced heroin reinstatement with effects that outlasted treatment by two weeks. Intrigued by these findings, we focused our efforts specifically on the anti-relapse potential of CBD and identified distinct leads in the literature suggestive of potential for several indications critical for relapse prevention. Many general behavioral effects of CBD, including anxiolytic, anti-stress, anti-depressant, and anti-compulsive actions (e.g., ref. [1]), are predictive of therapeutic benefit also for drug seeking and relapse. Moreover, CBD interacts with signaling mechanisms within the brain circuitry that regulates anxiety, drug desire associated with drug-related cues/contexts, and effects of stress on drug seeking. Lastly, CBD has both neuroprotective and proneurogenic actions [4]. The former includes attenuation of ethanol-induced neurodegeneration, an intoxication-induced deficit contributing to impaired impulse control in alcoholics. The proneurogenic effects of CBD have been implicated in the drug’s anti-anxiety actions, and are predictive of anti-craving effects given emerging evidence implicating neurogenesis as an important factor in inhibiting drug seeking.

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