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Chronic inflammation is caused by abnormal behavior in the immune system and can lead to tissue, joint and organ damage. Studies have shown marijuana is effective at reducing chronic inflammation associated with a variety of diseases and can help patients manage the pain associated with their inflammation-related condition.
Overview of Inflammation
While inflammation is an essential response by the body’s immune system to injury, bacteria and viruses, at times the inflammatory response is called upon unnecessarily. When called upon appropriately, the inflammatory response effectively removes the infectious or damaging stimuli so that the body can initiate the healing process. However, when called upon unnecessarily, in the case of autoimmune diseases, the immune system reacts as if tissues are infected or abnormal when in actuality they are normal. As a result, the body causes damage to its own tissues.
Acute inflammation that comes and goes as necessary to deal with injuries and diseases represents a well-balanced and effective immune system. With chronic inflammation, however, the immune system is essentially “out-of-wack” as it won’t shut off the inflammatory response.
Examples of diseases that are associated with inflammation include rheumatoid arthritis, a chronic inflammatory disease that causes joint destruction, deformity and loss of function, psoriatic arthritis, which causes joint pain, stiffness and swelling, as well as red patches on the skin, Crohn’s and other inflammatory bowel diseases where the digestive tract becomes inflamed, atherosclerosis, the inflammation of arterial walls that can limit or block blood flow and cause heart attacks and stroke, and some cancers.
Treatment of inflammatory diseases typically involves anti-inflammatory and pain medications and the modifying or avoidance of particular activities that stress the inflamed area. In certain cases, surgery is required.
Findings: Effects of Cannabis on Inflammation
Medical marijuana has been found to be effective at both reducing chronic inflammation and at curtailing the pain associated with inflammatory-related diseases, thanks to its cannabinoids, including tetrahydrocannabinol (THC).
Cannabinoids have demonstrated success at reducing inflammation related to a variety of conditions. Studies have shown that THC is able to reduce the development of atherosclerosis, the chronic inflammatory disease and a major risk factor of heart attacks and strokes, and at reducing airway inflammation related to the flu virus (Fimiani, et al., 1999) (Buchweitz, et al., 2008).
Inflammatory pain is a common symptom of a number of chronic inflammation diseases, such as sickle cell disease and cancer, but cannabis has proven helpful in pain management. The cannabinoids in cannabis act upon the cannabinoid receptors 1 and 2 (CB1, CB2), which are involved in the mediation of pain associated with inflammation (Clayton, Marshall, Bountra & O’Shaughnessy, 2002).
States That Have Approved Medical Marijuana for Inflammation
Inflammation is not specifically included on the list of approved conditions for medical marijuana in any state. However, many states do include specific inflammation-related conditions. Medical marijuana is approved for patients with arthritis in Connecticut (psoriatic arthritis), California, Illinois, and New Mexico.
Patients diagnosed with Crohn’s disease are allowed to legally use marijuana for treatment in Arizona, Arkansas, Connecticut, Florida, Georgia, Hawaii, Illinois, Louisiana, Maine, Massachusetts, Michigan, Minnesota, Montana, New Hampshire, New Jersey, New Mexico, New York, North Dakota, Ohio, Pennsylvania, Rhode Island, Washington, and West Virginia. Connecticut has also approved medical marijuana to treat ulcerative colitis, another type of inflammatory bowel disease.
If an inflammation-related condition is causing chronic pain, medical marijuana has been approved for treatment in Alaska, Arizona, California, Colorado, Delaware, Hawaii, Maine, Maryland, Michigan, Montana, New Mexico, Ohio, Oregon, Pennsylvania, Rhode Island, Vermont, and West Virginia. The states of Nevada, New Hampshire, North Dakota, Montana, Ohio and Vermont allow medical marijuana to treat “severe pain.” The states of Arkansas, Minnesota, Ohio, Pennsylvania, Washington, and West Virginia have approved cannabis for the treatment of “intractable pain.”
A number of other states will consider approving medical marijuana for the treatment of other conditions, but require an approval or a recommendation by a physician. These states include: California (any debilitating illness where the medical use of marijuana has been recommended by a physician), Connecticut (other medical conditions may be approved by the Department of Consumer Protection), Massachusetts (other conditions as determined in writing by a qualifying patient’s physician), Nevada (other conditions subject to approval), Oregon (other conditions subject to approval), Rhode Island (other conditions subject to approval), and Washington (any “terminal or debilitating condition”).
In Washington D.C., any condition can be approved for medical marijuana as long as a DC-licensed physician recommends the treatment.
Recent Studies on Cannabis’ effect on Inflammation
- Acharya, N., Penukonda, S., Shcheglova, T., Hagymasi, A.T., Basu, S., and Srivastava, P.K. (2017, March 27). Endocannabinoid system acts as a regulator of immune homeostasis in the gut. Proceedings of the National Academy of Sciences of the United States, 114(19), 5005-5010. Retrieved from http://www.pnas.org/content/114/19/5005.full.
- Adhikary, S., Li, H., Heller, J., Skarica, M., Zhang, M., Ganea, D., and Tuma, R.F. (2011). Modulation of Inflammatory Responses by a Cannabinoid-2–Selective Agonist after Spinal Cord Injury. Journal of Neurotrauma, 28(12), 2417–2427. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3235339/.
- Buchweitz, JP., Karmaus, PW., Williams, KJ., Harkema, JR. and Kaminski, NE. (2008, March). Targeted deletion of cannabinoid receptors CB1 and CB2 produced enhanced inflammatory responses to influenza A/PR/8/34 in the absence of presence of Delta9-tetrahydrocannabinol. Journal of Leukocyte Biology, 83(3), 785-96. Retrieved from http://www.jleukbio.org/content/83/3/785.long.
- Clayton, N., Marshall, FH., Bountra, C., and O’Shaughnessy, CT. (2002, April). CB1 and CB2 cannabinoid receptors are implicated in inflammatory pain. Pain, 96(3), 253-60. Retrieved from http://journals.lww.com/pain/pages/articleviewer.aspx?year=2002&issue=04000&article=00005&type=abstract.
- Craft, R.M., Kandasamy, R., and Davis, S.M. (2013, September). Sex differences in anti-allodynic, anti-hyperalgesic and anti-edema effects of Δ9-tetrahydrocannabinol in the rat. Pain, 154(9), 1709-17. Retrieved from http://journals.lww.com/pain/pages/articleviewer.aspx?year=2013&issue=09000&article=00028&type=abstract.
- Croxford, J.L., and Yamamura, T. (2005, September). Cannabinoids and the immune system: potential for the treatment of inflammatory diseases? Journal of Neuroimmunology, 166(1-2), 3-18. Retrieved from http://www.jni-journal.com/article/S0165-5728(05)00160-8/fulltext.
- De Laurentiis, A., Araujo, H.A., and Rettori, V. (2014). Role of the Endocannabinoid System in the Neuroendocrine Responses to Inflammation. Current Pharmaceutical Design, 20(29), 4697-706. Retrieved from http://www.eurekaselect.com/120077/article.
- De Petrocellis, L., Melck, D., Bisogno, T., and Di Marzo, V. (2000, November). Endocannabinoids and fatty acid amides in cancer inflammation and related disorders. Chemistry and Physics of Lipids, 108(1-2), 191-209. Retrieved from http://www.sciencedirect.com/science/article/pii/S0009308400001961.
- Fimiani, C., Liberty, T., Aquirre, AJ., Amin, I., Ali, N. and Stefano, GB. (1999, January). Opiate, cannabinoid, and eicosanoid signaling converges on common intracellular pathways nitric oxide coupling. Prostaglandins & Other Lipid Mediators, 57(1), 23-34. Retrieved from http://www.sciencedirect.com/science/article/pii/S0090698098000689.
- Fukuda, S., Kohsaka, H., Takayasu, A., Yokoyama, W., Miyabe, C., Miyabe, Y., Harigai, M., Miyasaka, N., and Nanki, T. (2014). Cannabinoid receptor 2 as a potential therapeutic target in rheumatoid arthritis. BMC Musculoskeletal Disorders, 15, 275. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4243420/.
- Kinsey, S.G., Mahadevan, A., Zhao, B., Sun, H., Naidu, P.S., Razdan, R.K., Selley, D.E., Imad Damaj, M., and Lichtman, A.H. (2011). The CB2 cannabinoid receptor-selective agonist O-3223 reduces pain and inflammation without apparent cannabinoid behavioral effects. Neuropharmacology, 60(2-3), 244–251. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021987/.
- Klein, T.W. (2005, May). Cannabinoid-based drugs as anti-inflammatory therapeutics. Nature Reviews Immunology, 5, 400-411. Retrieved from http://www.nature.com/nri/journal/v5/n5/full/nri1602.html.
- Matthews, A.T., and Ross, M.K. (2015). Oxyradical Stress, Endocannabinoids, and Atherosclerosis. Toxics, 3(4), 481–498. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4686160/.
- Michalski, C.W., Maier, M., Erkan, M., Sauliunaite, D., Bergmann, F., Pacher, P., Batkai, S., Giese, N.A., Giese, T., Friess, H., and Kleeff, J. (2008). Cannabinoids Reduce Markers of Inflammation and Fibrosis in Pancreatic Stellate Cells. PLoS ONE, 3(2), e1701. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253501/.
- Panikashvili, D., Shein, N.A., Mechoulam, R., Trembovler, V, Kohen, R., Alexandrovich, A. and Shohami, E. (2006, May). The endocannabinoid 2-AG protects the blood–brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines. Neurobiology of Disease, 22(2), 257-264. Retrieved from http://www.sciencedirect.com/science/article/pii/S0969996105003074.
- Parker, J., Atez, F., Rossetti, R.G., Skulas, A., Patel, R., and Zurier, R.B. (2008, May). Suppression of human macrophage interleukin-6 by a nonpsychoactive cannabinoid acid. Rheumatology International, 28(7), 631-5. Retrieved from http://link.springer.com/article/10.1007%2Fs00296-007-0489-0.
- Wright, K.L., Duncan, M., and Sharkey, K.A. (2008). Cannabinoid CB2 receptors in the gastrointestinal tract: a regulatory system in states of inflammation. British Journal of Pharmacology, 153(2), 263–270. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219529/.