Kentucky Medical Association’s Willful Ignorance

In an article on the Louisville Business First website the President of the Kentucky Medical Association is quoted as saying that its members need more information on medical marijuana before they could support medical marijuana legalization.   Dr. David Bemsema said that, ‘if there was a well-designed study that showed a positive medical benefit from marijuana use , Kentucky Doctors would have to consider an alternative delivery method. It wouldn’t consider smoking it as a delivery method because the group is opposed to smoking.”

Let’s just start with the willful ignorance of the members of the KMA.  There are numerous studies proving the efficacy and safety of medical marijuana.  Actually too many to list here but let’s just review the ones listed in the National Organization for the Reform of Marijuana Laws web library under the listing Gliomas/cancer.

[1] Guzman et al. 1998. Delta-9-tetrahydrocannabinol induces apoptosis in C6 glioma cells. FEBS Letters 436: 6-10.

[2] Guzman et al. 2000. Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation. Nature Medicine 6: 313-319.

[3] Guzman et al. 2003. Inhibition of tumor angiogenesis by cannabinoids. The FASEB Journal 17: 529-531.

[4] Massi et al. 2004. Antitumor effects of cannabidiol, a non-psychotropic cannabinoid, on human glioma cell lines. Journal of Pharmacology and Experimental Therapeutics Fast Forward 308: 838-845.

[5] Guzman et al. 2004. Cannabinoids inhibit the vascular endothelial growth factor pathways in gliomas (PDF). Cancer Research 64: 5617-5623.

[6] Allister et al. 2005. Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells. Journal of Neurooncology 74: 31-40.

[7] Torres et al. 2011. A combined preclinical therapy of cannabinoids and Temozolomide against glioma. Molecular Cannabis Therapeutics 10: 90.

[8] Guzman et al. 2006. A pilot clinical study of delta-9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer (E-pub ahead of print).

[9] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomas. Expert Reviews of Neurotherapeutics 8: 37-49

[10] Galanti et al. 2007. Delta9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells. Acta Oncologica 12: 1-9.

[11] Calatozzolo et al. 2007. Expression of cannabinoid receptors and neurotrophins in human gliomas. Neurological Sciences 28: 304-310.

[12] Foroughi et al. 2011. Spontaneous regression of septum pellucidum/forniceal pilocytic astrocytomas — possible role of cannabis inhalation. Child’s Nervous System 27: 671-679.

[13] Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation. Cancer Research 66: 6615-6621.

[14] Di Marzo et al. 2006. Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. Journal of Pharmacology and Experimental Therapeutics Fast Forward 318: 1375-1387.

[15] De Petrocellis et al. 1998. The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation. Proceedings of the National Academy of Sciences of the United States of America 95: 8375-8380.

[16] McAllister et al. 2007. Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells. Molecular Cancer Therapeutics 6: 2921-2927.

[17] Cafferal et al. 2010. Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition. Molecular Cancer 9: 196.

[18] Sarfaraz et al. 2005. Cannabinoid receptors as a novel target for the treatment of prostate cancer. Cancer Research 65: 1635-1641.

[19] Mimeault et al. 2003. Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines. Prostate 56: 1-12.

[20] Ruiz et al. 1999. Delta-9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism. FEBS Letters 458: 400-404.

[21] Ramos and Bianco. 2012. The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications. Journal of Urology 28: 9-14.

[22] DePetrocellis et al. 2013. Non-THC cannabinoids inhibit prostate carcinoma growth in vitro and in vivo: pro-apoptotic effects and underlying mechanisms. British Journal of Pharmacology 168: 79-102.

[23] Pastos et al. 2005. The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase-2. Gut 54: 1741-1750.

[24] Aviello et al. 2012. Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. Journal of Molecular Medicine [E-pub ahead of print]

[25] Di Marzo et al. 2006. op. cit

[26] Casanova et al. Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. 2003. Journal of Clinical Investigation 111: 43-50.

[27] Powles et al. 2005. Cannabis-induced cytotoxicity in leukemic cell lines. Blood 105: 1214-1221

[28] Jia et al 2006. Delta-9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemic T cells in regulated by translocation of Bad to mitochondria. Molecular Cancer Research 4: 549-562.

[29] Liu et al. 2008. Enhancing the in vitro cytotoxic activity of Ä9-tetrahydrocannabinol in leukemic cells through a combinatorial approach. Leukemia and Lymphoma 49: 1800-1809.

[30] Scott et al. 2013. Enhancing the activity of cannabidiol and other cannabinoids in vitro through modifications to drug combinations and treatment schedules 33: 4373-4380.

[31] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.

[32] Marcu et al. 2010. Cannabidiol enhances the inhibitory effects of delta9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival. Molecular Cancer Therapeutics 9: 180-189.

[33] Guzman. 2003 op. cit.

[34] Preet et al. 2008. Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 10: 339-346.

[35] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.

[36] Baek et al. 1998. Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research: 21: 353-356.

[37] Carracedo et al. 2006. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. Cancer Research 66: 6748-6755.

[38] Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and pain. International Journal of Cancer 122: 742-750.

[39] Ramer and Hinz. 2008. Inhibition of cancer cell invasion by cannabinoids via increased cell expression of tissue inhibitor of matrix metalloproteinases-1. Journal of the National Cancer Institute 100: 59-69.

[40] Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cells. Pharmacology 85: 328-335.

[41] Leelawat et al. 2010. The dual effects of delta(9)-tetrahydrocannabinol on cholangiocarcinoma cells: anti-invasion activity at low concentration and apoptosis induction at high concentration. Cancer Investigation 28: 357-363.

[42] Gustafsson et al. 2006. Cannabinoid receptor-mediated apoptosis induced by R(+)-methanandamide and Win55,212 is associated with ceramide accumulation and p38 activation in mantle cell lymphoma. Molecular Pharmacology 70: 1612-1620.

[43] Gustafsson et al. 2008. Expression of cannabinoid receptors type 1 and type 2 in non-Hodgkin lymphoma: Growth inhibition by receptor activation. International Journal of Cancer 123: 1025-1033.

[44] Natalya Kogan. 2005. Cannabinoids and cancer. Mini-Reviews in Medicinal Chemistry 5: 941-952.

[45] Sarafaraz et al. 2008. Cannabinoids for cancer treatment: progress and promise. Cancer Research 68: 339-342.

[46] Study shows non-hallucinogenic cannabinoids are effective anti-cancer drugs. October 14, 2013.

[47] Haartz. Israeli researchers say more doctors should recommend marijuana to cancer patients. January 30, 2012.

Marijuana has shown promise or actual benefits for many conditions to include epilepsy, cancer, Alzheimer’s, fibromyalgia, dystonia, hepatitis C, diabetes, pruritus, osteoporosis, MRSA, Huntington’s disease, multiple sclerosis, ALS, chronic pain, Tourette’s syndrome, HIV, hypertension, and arthritis.  All of these can be researched at this link—

http://norml.org/library/recent-research-on-medical-marijuana

The members of the KMA need to bone up on the facts.  The medical benefits of medical cannabis are undeniable.  As far as delivery method, the work of Dr Tashkin reported in the Journal of thoracic medicine shows that marijuana smokers get head neck and lung cancer at the same rate as non-smokers.  Vaporizing whole plant marijuana has shown to be the most effective and safe method of delivery with smoking second.  Vaporizing is 80% effective versus 60% effective for smoking.  I’m sure if there was a problem with smoking as delivery method it would have surfaced in the last 20 years medical marijuana has been available to the citizens of California.

So lets put this nonsense behind us and move forward.  Kentucky’s sick and disabled need compassion and support, they need medical marijuana, and they need their Doctors to be up to date on the facts.

Advertisements
This entry was posted in Uncategorized. Bookmark the permalink.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s