It should be no surprise that, against controls, cannabidiol (CBD) has recently been shown to reduce cigarette consumption in tobacco smokers. There appears to be some indirect anti-addictive activity built into the endocannabinoid system, part of the body’s onboard cell-signaling network. CBD, and any other agent that modulates this system, ought to have some effect on nicotine’s own effects (particularly since the cannabinoid receptor sites also function indirectly with the body’s built-in nicotinic receptors). Blocking fatty acid amide hydrolase (FAAH), the main catabolic enzyme of the endocannabinoid arachidonoylethanolamine (anandamide), is known to exacerbate withdrawal responses in nicotine-dependent mice, in inhibition of monoacylglycerol lipase, the most important hydrolytic enzyme of another endocannabinoid, 2-arachidonylglycerol (2-AG), reduces nicotine withdrawal symptoms. Moreover, enhancing levels of kynurenic acid, which is a neuro-inhibitory product of tryptophan metabolism that counteracts the effects of cannabinoids, does so as a negative allosteric modulator of α7 nicotinic receptors. So it is, that pharmacological manipulation of endocannabinoid modulators should be of promise in the treatment of nicotine dependence and relapse prevention. 

It is probably only cannabinoid receptor site 1 (CB1) that is pivotal in these actions. Evaluation of the selective CB2 antagonists AM630 and AM1241, at least, do not support any involvement of CB2 receptors in nicotine-seeking behavior. At CB1, rimonabant (SR141716),the very first experimental type 1 receptor antagonist, originally trialled as an anorectic anti-obesity drug, has been investigated in smoking cessation, and found, arguably, to have increased the odds of quitting 1.5-fold, though subsequent studies were inconclusive. Its efficacy was about the same as that of nicotine-replacement therapy. The same was found with taranabant, a CB1 inverse agonist. For adverse psychiatric effects, both drugs were withdrawn from use in 2008. The fact that they had these effects and also appeared to work in nicotine-seeking was useful in suggesting that they acted on at least two distinct neuronal pathways. 

A CB1 neutral antagonist, AM4113, has been tested head-to-head against rimonabant. Both reduced drug-taking behavior and priming- or cue-induced reinstatement of drug-seeking behavior in abstinent subjects. AM4113 worked as well as rimonabant, and showed better psychiatric tolerability. 

CB1 receptor stimulation with WIN 55,212-2, a widely used experimental CB1 and CB2 agonist, finally, has been shown to increase the reinforcing effects of nicotine and precipitate relapse in abstinent subjects. 

At this point it is safe to say that modulating CB1 receptor signaling should have some therapeutic value for treating nicotine dependence. 

DiolPure products contain PureForm CBD™ transformed from aromatic terpenes for pharmaceutical-grade purity. PureForm CBD™ is bioidentical to CBD extracted from hemp and cannabis, but free of any residual cannabinoids like THC or impurities or chemicals that can associate with traditional plant-derived production processes. 

The foregoing is a report on trends and developments in cannabinoid industry research. No product description herein is intended as a recommendation for diagnosis, treatment, cure or prevention of any disease or syndrome.