Despite a growing number of reports
and case studies regarding the cancer-busting properties of cannabis, the clinical use of cannabinoids as a treatment for cancer is unlikely to get the green light until scientists can figure out exactly how it interacts with tumors. While research on this subject has been frustratingly slow, a series of new studies have begun to shed light on the potent anti-cancer properties of CBD.
Among these is a research project currently being conducted at the University of Newcastle in Australia, where scientists have been comparing the efficacy of different cannabis cultivars in fighting cancer. Results have indicated that a high-CBD strain known as ‘Eve’ is significantly better at killing cancer cells than other varieties containing less CBD but more THC.
Commenting on these findings,
lead researcher Dr. Matt Dun explained that “we initially used leukemia cells and were really surprised by how sensitive they were [to Eve]”. The team later tested their high-CBD cannabis on pediatric brainstem glioma cells and found that it was equally effective at killing off these cancerous cells.
Significantly, though, Dun says that “the cannabis didn’t kill normal bone marrow cells, nor normal healthy neutrophils [white blood cells].” This is hugely important, as it suggests that CBD works via some sort of “cancer-selective mechanism,” whereby it is able to recognize and target tumors while leaving healthy cells untouched.
So far,
studies have indicated that CBD targets cancer via a number of different pathways. For instance, it is generally accepted that CBD differs from other cannabinoids like THC in that it has a low affinity for the body’s cannabinoid receptors, and instead binds with other kinds of receptors known as G-protein coupled receptors (GPCRs). One such receptor, known as GPR55, has been found to play a significant role in the development of numerous types of cancer, and researchers theorize that CBD may interfere with this process by binding to this receptor[i].
Other studies, however, have indicated that CBD does interact with cannabinoid receptors and that this mediates the formation of two key enzymes that synthesize reactive oxygen species. These, in turn, stimulate apoptosis in cancer cells, essentially causing them to self-destruct[ii].
While CBD is widely seen as a potential game-changer in cancer treatment, several other compounds found in cannabis have also been found to help kill tumors. Cannabigerol (CBG), for instance, has shown great promise as a treatment for colon cancer, while the activation of cannabinoid receptors has been found to stimulate the release of proteins that prevent prostate cancer from developing[iii].
In spite
of all this evidence, however, many questions still remain regarding how cannabis interacts with cancer cells, as well as which cannabinoids are most effective for treating which types of cancer. Because of this, doctors are not yet in a position to prescribe cannabis to cancer patients or to advise those suffering from the condition to self-medicate with marijuana.
Yet as interest in medical cannabis as a treatment for cancer continues to skyrocket, many within the scientific community are now optimistic that marijuana could soon become a key ally in the fight against the deadly illness.
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[i] Afrin F, Chi M, Eames AL, Duchatel RJ, Douglas AM, Schneider J, Gedye C, Woldu AS, Dun MD. Can Hemp Help? Low-THC Cannabis and Non-THC Cannabinoids for the Treatment of Cancer. Cancers. 2020 Apr;12(4):1033. – https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7226605/
[ii] McKallip RJ, Jia W, Schlomer J, Warren JW, Nagarkatti PS, Nagarkatti M. Cannabidiol-induced apoptosis in human leukemia cells: a novel role of cannabidiol in the regulation of p22phox and Nox4 expression. Molecular Pharmacology. 2006 Sep 1;70(3):897-908. – https://pubmed.ncbi.nlm.nih.gov/16754784/
[iii] Sarfaraz S, Afaq F, Adhami VM, Malik A, Mukhtar H. Cannabinoid receptor agonist-induced apoptosis of human prostate cancer cells LNCaP proceeds through sustained activation of ERK1/2 leading to G1 cell cycle arrest. Journal of Biological Chemistry. 2006 Dec 22;281(51):39480-91. – https://pubmed.ncbi.nlm.nih.gov/17068343/
