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[DRAFT] How cannabis works in the treatment of addiction

While mainstream medicine has not yet embraced cannabis as a treatment option for substance addictions, there is plenty of anecdotal (and some scientific) evidence to backup this claim.

For full transparency, I’m letting you (the reader) know that I personally used cannabis to finally put an end to my addiction to alcohol. It was actually that experience that really changed my perspective on what cannabis is and is not.

From that newfound perspective, I decided that cannabis was not the harmful ‘illicit’ drug that mainstream society projects onto the subject. In fact, as I learned more about the properties of cannabis, I began to see it as a plant with a complex set of chemicals that offered a wide-range of benefits to the user who understood them. For example, I soon learned that cannabis with modest levels of CBD offers greater pain-relieving benefits that cannabis without CBD. With that information, I started using cannabis to treat the pain and inflammation I encountered after strenuous exercise. This enabled me to be more productive in the evenings after a good workout. Nowadays, you can find top athletes promoting CBD for this exact purpose.

To get back to the main topic, let’s explore how cannabis works to help overcome substance addictions. To understand how this is possible, we need to be aware of the basic mechanism behind most physiological addictions. In the case of alcoholism, sugar cravings, and opiate addiction [for example], alterations in dopaminergic pathways are cited as a factor in the cycle of drug-seeking behavior. Typically, these substances induce a marked increase in either dopamine production and/or uptake. The body may respond either by producing more dopamine receptors or desensitizing the response to dopamine. In both cases, the brain now needs more dopamine to illicit the same response as before. The result an increase in tolerance leading to an increase in consumption.

The way in which cannabis alleviates cravings is through the action of a common petrochemical found in most varieties. Beta-caryophyllene (BCP for short) is a terpene that [when combined with THC] produces a strong regulatory effect on dopamine within certain regions of the brain. Without getting too technical, BCP reduces cravings by inhibiting the release of dopamine [1].

References

[1] He, Yi, et al. “β‐Caryophyllene, a Dietary Terpenoid, Inhibits Nicotine Taking and Nicotine Seeking in Rodents.” British Journal of Pharmacology, vol. 177, no. 9, 15 Feb. 2020, pp. 2058–2072, bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/bph.14969, 10.1111/bph.14969. Accessed 28 Aug. 2021.

[2] Galaj E, Bi GH, Moore A, et al. Beta-caryophyllene inhibits cocaine addiction-related behavior by activation of PPARα and PPARγ: repurposing a FDA-approved food additive for cocaine use disorder. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology. 2021 Mar;46(4):860-870. DOI: 10.1038/s41386-020-00885-4. PMID: 33069159.

‌[3] Basha, Rafeek Hidhayath, and Chandrasekaran Sankaranarayanan. “β-Caryophyllene, a Natural Sesquiterpene, Modulates Carbohydrate Metabolism in Streptozotocin-Induced Diabetic Rats.” Acta Histochemica, vol. 116, no. 8, Oct. 2014, pp. 1469–1479, pubmed.ncbi.nlm.nih.gov/25457874/, 10.1016/j.acthis.2014.10.001. Accessed 28 Aug. 2021.

[4] Gonzalez-Cuevas, Gustavo, et al. “Unique Treatment Potential of Cannabidiol for the Prevention of Relapse to Drug Use: Preclinical Proof of Principle.” Neuropsychopharmacology, vol. 43, no. 10, 22 Mar. 2018, pp. 2036–2045, www.ncbi.nlm.nih.gov/pmc/articles/PMC6098033/, 10.1038/s41386-018-0050-8. Accessed 28 Aug. 2021.

[5] Francomano, Fabrizio, et al. “β-Caryophyllene: A Sesquiterpene with Countless Biological Properties.” Applied Sciences, vol. 9, no. 24, 11 Dec. 2019, p. 5420, www.mdpi.com/2076-3417/9/24/5420/htm, 10.3390/app9245420. Accessed 28 Aug. 2021.

[6] Foll, Bernard Le, et al. “Peroxisome Proliferator-Activated Receptor (PPAR) Agonists as Promising New Medications for Drug Addiction: Preclinical Evidence.” Current Drug Targets, vol. 14, no. 7, 1 May 2013, pp. 768–776, pubmed.ncbi.nlm.nih.gov/23614675/, 10.2174/1389450111314070006. Accessed 28 Aug. 2021.

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