Our current state of medical marijuana distracts so many from the honest science behind the Endocannabinoid System. This alternative viewpoint I will lay out is neutral on whether cannabis should be legal or illegal; rather, I would like to succinctly provide reasons as to why the government should immediately reschedule cannabis from schedule I to maybe III or IV. An alternative to this request could be to reschedule the individual cannabinoids, like CBD and THC, as to give the public and science community more and better information. This is very simple.
Cannabidiol (CBD) is a cannabinoid molecule produced in the Cannabis plant. Cannabinoids play a role in the life of the plant because they serve as a defense mechanism. Generally, cannabinoids are sticky organic resins and are not water soluble. It is possible that in the wild the resins act to trap bugs from eating the leaves. This is the distinction I would like to make: phytocannabinoids are cannabinoids derived from plants and endocannabinoids are endogenous cannabinoids produced inside the body. It is important to note, we call them cannabinoids for no particular reason other than our Endocannabinoid receptors were found due to compounds from Cannabis (THC, primarily) activating these previously unknown receptors. Cannabinoids are just a class of molecules.
Contrary to common misinformation, Cannabidiol has low affinity for both CB1 and CB2 receptors. Instead, therapeutic action is achieved using other pathways by using other, less famous Endocannabinoid receptors.
- Suppression of Fatty Acid Amide Hydroxylase to suppress the quick degradation of endogenous cannabinoids
- Binding to other Endocannabinoid G-Protein Coupled Receptors
- GPR55, TRPV-1, PPAR type receptor
The second point is of great interest. Recently, scientists were able to produce 3D images of G-Protein Coupled Receptors. This feat allows researchers to observe the surface of the receptors on a computer. Future implications of this technology include finding the active sites for cannabinoids. This type of research could lead to a chemical alteration of CBD, for example, into a molecule that binds more effectively to this active site. That is one of my hopes and dreams for this new frontier.
Cannabidiol is directly correlated to an increased expression of Intercellular Adhesion Molecule 1 (ICAM-1). ICAM-1 is a gene that subsequently codes for its protein ICAM-1. This protein enhances the susceptibility of cancer cells to cytolysis (destruction) by Lymphokine Activated Killer Cells (LAK Cells). I see ICAM-1 as a sticky protein that allows for specific adhesion of LAK Cells to diseased cells. LAK Cells are a part of our immune system and classified under White Blood Cells. This mechanism provides an interesting lead to safer chemotherapies.
LAK Cells contain a receptor for ICAM-1 called Lymphocyte Function-Associated Antigen-1 (LFA-1). However, studies have shown LAK Cells treated with CBD do not affect the production of LFA-1 proteins. The link between ICAM-1 and LFA-1 is crucial to a successful linkage of the LAK Cell to cancer cell and thus vital for the cytotoxic action of the LAK Cell.
Studies have shown and continue to show that CBD acts in a concentration-dependent manner in increasing the expression of ICAM-1 and thus indirectly causing cancer cell lysis. More importantly, these effects seem to be absent in healthy cells. Healthy cells are unaffected while diseased and cancerous cells are prompted to produce ICAM-1 proteins. Diseased cells express Endocannabinoid receptor genes at a much higher rate than healthy cells.1
In the near future, I would like to see more discussion about this topic. I think so many of us know too many people who have suffered through cancer. This is an old meets new area of research. Cannabinoids present a natural therapy for cancer eradication. Why aren’t we pursuing this? Luckily, President Trump has repeatedly expressed positive thoughts towards medical marijuana and I do believe if he read this article, just like you, he would have more questions and be left wondering why CBD is still classified as a Schedule I Narcotic.
References
- Haustein, Maria; Ramer, Robert; Linnebacher, Michael; Manda, Katrin; Hinz, Burkhard. “Cannabinoids Increase Lung Cancer Cell Lysis by Lymphokine-activated Killer Cells via Upregulation of ICAM-1.”ScienceDirect. Elsevier B.V., 15 Nov. 2014. Web. 23 Apr. 2016.
- http://www.sciencedirect.com/science/article/pii/S0006295214004201
- This is a protected text from ScienceDirect. I am able to access it through my school’s account. To view the full text, you must be a student in college or pay to view.
- Sun, Yan; Bennet, Andy. “Cannabinoids: A New Group of Agonists of PPARs.” NCBI. 15 Nov, 2007.
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2220031/
- NCBI is the go to resource for most scientific research. They provide a wide range of services from genetic sequence data to peer reviewed articles such as this one.
