Behavioral, Neurodevelopmental, Psychiatric


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Literature Discussion & Clinical Trials

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July 2020

What is Addiction

Addiction is a mental disorder causing a psychological and physical inability to stop consuming a chemical and/or substance and an inability to stop partaking in certain activities, even though it may cause harm to oneself or the addict’s social circle and surroundings.1

It is important to distinguish between addiction and misuse, as misuse refers to incorrect or excessive use of e.g. substances whilst addiction is a long-term inability or loss of control over substance intake or participation in activities.1

Common substance addictions:

  • Alcohol
  • Drugs
  • Smoking

Common activity addictions:

  • Gambling
  • Sport/fitness
  • Work


  • Uncontrollably seeking chemicals or substances
  • Uncontrollably participating in harmful “habits”
  • Losing interest and neglecting activities that do not involve the addiction
  • Inability to stop harmful behavior though it may cause personal-, professional- and health problems.
  • Increased risk-taking to engage in the addiction
  • Exercising secrecy about problems that may occur as a result of the addiction.
  • Change in appearances

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Uncontrollably participating in either harmful activities and/or abusing chemicals and substances.


Clinical data suggests CBD and THC among cannabinoid receptors may be therapeutic in Addiction.


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The connection between Cannabinoids & Addiction

Studies find that CBD and THC may have great therapeutic potential and may be used to help treat Addiction. CBD and THC are well-known cannabinoids, however, they do not have the same psychoactive effects. THC is psychoactive while CBD does not possess psychoactive effects. According to WHO guidelines, the cannabidiol CBD is generally well tolerated with a good safety profile.

Clinical data propose that THC and CBD may be used in the therapeutic treatment of addiction, as many cannabinoid receptors can be found in the  dopaminergic neurons system.2

As such, THC and CBD may offer opportunities for beneficial interaction for different types of addictions here among alcohol, food, nicotine, or opioids.

Furthermore, recent findings support that CBD may help in reducing relapse in two beneficial ways; 1) it may support actions between several vulnerability states, and 2) have a long-lasting positive effect in preventing relapse with only brief treatment.3

The literature discussion is an overview of the published results from scientific studies investigating if and how cannabinoids can be beneficial in the treatment of Addiction. The overview will be updated regularly to ensure the newest and most accurate information.

Inhibition of MAGL may have therapeutic potential
Cancer, neurogenerative diseases, ischemic injuries, inflammation, pain, anxiety, nausea, and drug-withdrawal symptoms could possibly be treated by MAGL inhibitors, which showed potential therapeutic action.4

DAGL is a potential target in addiction treatment
Biosynthesis of 2AG was increased in the ventral tegmental area (VTA) after rats were exposed to nicotine. GABA signaling is reduced by 2-AG, leading to an increased VTA sensitivity to nicotine and increased sensitization of DA release in the nucleus Nucleus accumbens Abiotic stress. GABA signaling in the VTA was restored by suppression, suggesting that DAGL can be a good target when treating addictions.5

Following the same line, DAGL expression in rat nucleus accumbens and depolarization-induced suppression of inhibition were increased by morphine withdrawal. This suggests that 2-AG plays a role in mediating this process.6

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Moreover, very similar results were found in a study that focused to test the effects of cocaine in orexin neurons.7

Cannabinoid interaction in addiction risk
CB1 is a member of the G protein-coupled receptor and can be found in the parts of the brain that mostly play a role in addictive behavior. It was shown that increased receptor binding and increased CB1 -mediated neuronal activation in the prefrontal cortex can be connected to at least one genetic variation/polymorphism in CB1. 8

Activation of the nucleus accumbens, ventromedial prefrontal cortex , simple_tooltip content=’Part of the brain involved in the cognitive process of decision making.’] orbitofrontal cortex ‘][/simple_tooltip], and ventral tegmental area as well as subjective appreciation of alcohol can be increased by alcohol exposure. Similar linkage to addiction risk showed that interaction between THC and Mu opioid receptors is weak, suggesting that Mu opioid can be considered as a cannabinoid receptor.8,9

Cannabinoid receptor CB1 may be involved in reward signal blocking
Post-mortem research proposes that though the expression is not affected, CB1 receptors have been shown to have hyperactivity in the caudate nucleus and hypoactive in the cerebellum of alcoholics.10
Dopaminergic signaling in the nucleus accumbens can be blocked and alcohol craving and consumption can be reduced through blocking the reward signal with CB1 antagonists.8

The endocannabinoid system may be involved in addiction inhinition
In one study in rats, addictive behavior (cocaine-seeking) can be reduced via chronic stimulation of the endocannabinoid system, anandamide.11
This proposes that the endocannabinoid system can be involved in inhibiting addiction.

Cannabinoid receptor CB2 may be a target for addiction treatment
Mice that drink more alcohol and eat more food have been shown to be genetically deficient for CB2 . This proposes that CB2 could be a target to treat addiction.12


Clinical trials are research studies that examine new treatments and evaluate their effects on human health outcomes.

The ECS may be involved in addiction
In one fMRI study , it was demonstrated that THC can help in decreasing the anticipatory nucleus accumbens response to nicotine. This suggests that the endocannabinoid system is involved in addictive behavior.13

CBD may decrease addictive behavior
A pilot, randomized double-blind placebo-controlled study aimed to assess the effect of CBD in people who wanted to stop smoking. It was found that cigarette consumption was significantly reduced in smokers by the treatment with CBD.14

  3. Gonzalez-Cuevas, G., Weiss, F. (2018). Unique treatment potential of cannabidiol for the prevention of relapse to drug use: preclinical proof of principle
  4. Chen, R., Zhang, J., Wu, Y., Wang, D., Feng, G., Tang, Y.-P., … Chen, C. (2012). Monoacylglycerol lipase is a therapeutic target for Alzheimer’s disease. Cell Reports2(5), 1329-1339.
  5. Buczynski, M. W., Herman, M. A., Hsu, K.-L., Natividad, L. A., Irimia, C., Polis, I. Y., … Parsons, L. H. (2016). Diacylglycerol lipase disinhibits VTA dopamine neurons during chronic nicotine exposure. Proceedings of the National Academy of Sciences of the United States of America113(4), 1086-1091.
  6. Wang, X.-Q., Ma, J., Cui, W., Yuan, W.-X., Zhu, G., Yang, Q., … Gao, G.-D. (2016). The endocannabinoidsystem regulates synaptic transmission in nucleus accumbens by increasing DAGL-α expression following short-term morphine British Journal of Pharmacology173(7), 1143-1153.
  7. Tung, L.-W., Lu, G.-L., Lee, Y.-H., Yu, L., Lee, H.-J., Leishman, E., … Chiou, L.-C. (2016). Orexins contribute to restraint stress-induced cocaine relapse by endocannabinoid-mediated disinhibition of dopaminergic neurons. Nature Communications7, 12199.
  8. Hutchison, K.E., Haughey, H., Niculescu, M., Schacht, J., Kaiser, A., Stitzel, J., Horton, W.J., and Filbey, F. (2008). The incentive salience of alcohol: translating the effects of genetic variant in CNR1. Arch. Gen. Psychiatry 65, 841–850.
  9. Pertwee, R.G., Howlett, A.C., Abood, M.E., Alexander, S.P.H., Di Marzo, V., Elphick, M.R., Greasley, P.J., Hansen, H.S., Kunos, G., Mackie, K., et al. (2010). International Union of Basic and Clinical Pharmacology. LXXIX. cannabinoidreceptors and their ligands: beyond CB1 and CB2. Pharmacol. Rev. 62, 588–631.
  10. Erdozain, A.M., Rubio, M., Meana, J.J., Fernández-Ruiz, J., and Callado, L.F. (2015). Altered CB1receptor coupling to G-proteins in the post-mortem caudate nucleus and cerebellum of alcoholic subjects. J. Psychopharmacol. Oxf. Engl.
  11. Chauvet, C., Nicolas, C., Thiriet, N., Lardeux, M.V., Duranti, A., and Solinas, M. (2014). Chronic Stimulation of the Tone of Endogenous AnandamideReduces Cue- and Stress-Induced Relapse in Rats. Int. J. Neuropsychopharmacol. Off. Sci. J. Coll. Int. Neuropsychopharmacol. CINP.
  12. Pradier, B., Erxlebe, E., Markert, A., and Rácz, I. (2015). Interaction of cannabinoid receptor 2 and social environment modulates chronic alcohol consumption. Behav. Brain Res. 287, 163–171.
  13. Jansma, J.M., van Hell, H.H., Vanderschuren, L.J.M.J., Bossong, M.G., Jager, G., Kahn, R.S., and Ramsey, N.F. (2013). THCreduces the anticipatory nucleus accumbens response to reward in subjects with a nicotine Addiction. Transl. Psychiatry 3, e234.
  14. Morgan, C.J.A., Das, R.K., Joye, A., Curran, H.V., and Kamboj, S.K. (2013). Cannabidiol reduces cigarette consumption in tobacco smokers: preliminary findings. Addict. Behav. 38, 2433–2436.





Below you find the plant cannabinoidscannabinoid receptors, and endocannabinoids that are associated with the potential therapy.

If you have any further information relevant to the connection between Addiction and cannabinoids or find any of the information inaccurate, outdated or incomplete please contact us here.