Category Archives: Disease Mechanisms

The Cure for Cancer is Illegal – The Mistake of The American Justice System

Devin Bost

Jan 26, 2014

Imagine an America where cancer patients could take only one drug that would stop their cancer from spreading[1], target and fix the genetic code of malignant cells[2], and prevent the cancer from ever returning[3]. Wouldn’t life be easier if American families never experienced contention resulting from the rising costs of health care, the rising costs of medications, and the increasingly dangerous side effects of novel drugs? This America is the America of tomorrow because these concepts are deeply rooted in the greatest medical discovery of the 21st century, but there is a catch. We have a malignant law that is withholding research and development of these compounds; we have a fractured law that is preventing our businesses from developing these medicines. This broken law is a great and powerful law that has protected our children[4] from intoxicated drivers[5], protected our families from violent crimes, and protected our property from drug related thefts. However, when Congress enacted the Controlled Substances Act – there is one scientific discovery that our Congressional representatives never could have anticipated: Cannabidiol, the greatest medical discovery in our nation’s history, is derived from one of the most dangerous plants on Earth. (That plant is cannabis, and it is commonly known by the public as “marijuana.”) Due to the miraculous medical properties of cannabidiol, we the People of the United States have an ethical duty to regulate the lawful research, manufacturing, and distribution of pharmaceutical cannabinoids.

The United States is one of the only countries worldwide in which it is a felony to grow industrial hemp[6] for purposes such as exporting biofuel substrates, exporting textiles or fibrous materials, or researching and developing novel drugs.  There is a reason: Types of cannabis have been selectively bred[7] by drug cartels and addicts to produce a dangerous[8], intoxicating[9], and addictive[10] compound called tetrahydrocannabinol (THC). THC changes the way cannabidiol acts upon the body[11] – thereafter producing a narcotic effect and inducing reinforcing properties when consumed. THC prevents learning[12], impairs spatial memory,[13] and induces psychosis – especially if consumed during adolescence.[14] Furthermore, prenatal exposure[15] to THC causes behavioral birth defects[16], mutated brain development[17], permanent reduction in infant brain functions[18], and fetal death[19]. THC exacerbates schizophrenic symptoms, psychotic behavior, learning and recall deficits, and cognitive deficits.[20] THC also sensitizes the brain to become more easily addicted[21] to other dangerous drugs[22] (e.g. heroin[23] and methamphetamine)[24].[25] So, what happens when we remove the THC from cannabis? We are given a miracle compound: cannabidiol.

Cannabidiol permanently changes the parts of our genetic code, even the parts of our genetic code that create dangerously[26] aggressive[27] cancerous cells[28] and result in inevitable death.[29] Cannabidiol selectively targets[30] these cancerous cells[31] and destroys[32] them (i.e. apoptosis), prevents tumors[33] from creating new blood[34] vessels[35] (i.e. inhibition of angiogenesis), and removes the genes in our bodies that produce the proteins[36] that are causing[37] the cancerous cells[38] to form in the first place[39] (i.e. genetic refactoring). Therefore, cannabidiol stops cancer from growing[40] and prevents cancer[41] from invading[42] other cells (i.e. inhibition of proliferation).[43] Never before has man discovered a drug that treats cancer by simultaneously leveraging apoptosis, inhibiting angiogenesis, inhibiting proliferation, and refactoring mutated genes. Cannabidiol is the single greatest hope for cancer patients that scientists have ever discovered.[44] Until we make it legal for cancer patients to obtain this compound, our law is obliterating any hope that these people deserve.

When we consider that radiation and many chemotherapy[45] drugs are actually carcinogenic,[46] cause permanent sterility[47], create serious occupational[48] safety[49] hazards,[50] and produce environmental hazards[51], it becomes clear that there is nobody physically[52] and psychologically[53] suffering more[54] than the people receiving chemotherapy[55] and radiation[56] treatment.  Many chemotherapy drugs are classified as chemical weapons (e.g. nitrogen mustard agents), according to the international Chemical Weapons Convention of 1993. Yet, according to our laws, it is legal to administer these weapons to the sick! Meanwhile, cannabidiol is still a felony to manufacture! How ethical is that? Radiation therapy also causes cognitive decline[57], heart disease[58], and a myriad of disturbing and painful side effects[59].[60] Perhaps the second most valuable[61] area of contemporary drug development research[62] is the beacon of light that cannabinoids[63] offer for novel[64] treatment[65] of multiple sclerosis (MS)[66]. Cannabidiol prevents the progressive disability[67] and symptoms[68] that occurs in multiple sclerosis. Recently, the neuroprotective potential of cannabidiol was discovered to ameliorate (i.e. reverse)[69] disease progression due to numerous properties[70] of these types of cannabinoids[71]. Are we going to wait idly for somebody to inform our congressional leaders of the injustice that is destroying the lives of these people? Or are we going to solve this problem now?

We the People of the United States must regulate the lawful manufacturing, distribution, sale, and exportation of commercial cannabis and hemp derivatives. Such a law will promulgate the fiscal incentives for future research and development on this subject, provide the American people with a new private sector and industry for job growth and provide the American people with an innovative means for financing our rising budget deficit (without inflicting further taxes upon our existing businesses). [72] In an interpretive ruling, the DEA stipulated, “Congress would not have adopted the 1970 statute in its present form if it had been aware of the effect on cultivation of plants for industrial uses. . . [T]he 1970 Congress did not address the possibility that portions of the cannabis plant excluded from the definition of marijuana might contain THC.”[73] What does this mean? It means: As a result of this failure to differentiate between marijuana (i.e. THC-containing) and hemp (i.e. THC-free), according to the UCLA law review, “[O]bstructions to the development and commercialization of industrial hemp could actually have the effect of harming the health, safety and well-being of the American people.”[74] Economic studies conducted by the US Government have notably and consistently overlooked the economic side-effects (i.e.  fiscal consequences) of ignoring the damage inflicted upon the health care, pharmaceutical, and biomedical industries[75] by withholding cannabinoid-based medicines from the people[76]. Moreover, as uncertain supply hurts businesses[77] – health care, pharmaceutical, and biomedical organizations have limited fiscal incentive to capitalize on (or invest in) cannabinoid related research. We, the people, must strengthen our existing drug policies,[78] conquer international[79] corruption,[80] and stop mutilating our afflicted people by enacting into law a mechanism for enabling private businesses to develop and manufacture cannabinoid medicines before this injustice destroys us.


Devin G. Bost

[1] Caffarel, M. M., et al. (2012) “Cannabinoids: A new hope for breast cancer therapy?” Cancer treatment reviews 38(7):911-8

[2] McAllister, Sean D., et al. “Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis.”Breast cancer research and treatment 129.1 (2011): 37-47.

[3] Velasco, Guillermo, Cristina Sánchez, and Manuel Guzmán. “Towards the use of cannabinoids as antitumour agents.” Nature Reviews Cancer 12.6 (2012): 436-444.

[4] Martin and Abood, “Neurobiology of marijuana abuse,” Trends in Pharmacological Sciences (1992); 13(5): 201-206

[5] Kuypers et al. (2012), “Medicinal Δ9-tetrahydrocannabinol (dronabinol) impairs on-the-road driving performance of occasional and heavy cannabis users but is not detected in Standard Field Sobriety Tests.” Addiction, 107: 1837–1844. doi: 10.1111/j.1360-0443.2012.03928.x

[6] Jean M. Rawson, “Hemp as an Agricultural Commodity,” CRS Report for Congress (2005); RL32725

[7] Lata, Hemant, et al. “Molecular analysis of genetic fidelity in Cannabis sativa L. plants grown from synthetic (encapsulated) seeds following in vitro storage.” Biotechnology letters 33.12 (2011): 2503-2508.

[8] Hjorthøj et al. (2012), “Correlations and agreement between delta-9-tetrahydrocannabinol (THC) in blood plasma and timeline follow-back (TLFB)-assisted self-reported use of cannabis of patients with cannabis use disorder and psychotic illness attending the CapOpus randomized clinical trial.” Addiction, 107: 1123–1131.

[9] Bhattacharyya et al. “Modulation of Mediotemporal and Ventrostriatal Function in Humans by Δ9-Tetrahydrocannabinol: A Neural Basis for the Effects of Cannabis sativa on Learning and Psychosis.” Arch Gen Psychiatry.2009; 66(4):442-451. 
[10] Cadoni et al. (2008), “Behavioral sensitization to Δ9-tetrahydrocannabinol and cross-sensitization with morphine: differential changes in accumbal shell and core dopamine transmission.” Journal of Neurochemistry, 106: 1586–1593.

[11] Morgan et al. (2010), “Cannabidiol Attenuates the Appetitive Effects of Δ9-Tetrahydrocannabinol in Humans Smoking Their Chosen Cannabis” Neuropsychopharmacology; 35(9): 1879–1885.

[12] Bhattacharyya, Sagnik, et al. “Modulation of mediotemporal and ventrostriatal function in humans by {Delta} 9-tetrahydrocannabinol: a neural basis for the effects of Cannabis sativa on learning and psychosis” Archives of general psychiatry 66.4 (2009): 442.

[13] Wise et al. (2011), “Δ9-Tetrahydrocannabinol-dependent mice undergoing withdrawal display impaired spatial memory” Psychopharmacology (Berl). 217(4): 485–494.

[14] Harte, Lauren C., and Diana Dow-Edwards. “Sexually dimorphic alterations in locomotion and reversal learning after adolescent tetrahydrocannabinol exposure in the rat.” Neurotoxicology and teratology 32.5 (2010): 515-524.
[15] Asghari-Roodsari, Alaleh, et al. “Tocolytic Effect of Δ9-Tetrahydrocannabinol in Mice Model of Lipopolysaccharide—Induced Preterm Delivery: Role of Nitric Oxide.” Reproductive Sciences 17.4 (2010): 391-400.
[16] Newsom, R. J., and S. J. Kelly. “Perinatal delta-9-tetrahydrocannabinol exposure disrupts social and open field behavior in adult male rats.”Neurotoxicology and teratology 30.3 (2008): 213-219.
[17] Psychoyos, Delphine, et al. “A cannabinoid analogue of Δ9‐tetrahydrocannabinol disrupts neural development in chick.” Birth Defects Research Part B: Developmental and Reproductive Toxicology 83.5 (2008): 477-488.
[18] Silva, Lindsay, et al. “Prenatal tetrahydrocannabinol (THC) alters cognitive function and amphetamine response from weaning to adulthood in the rat.”Neurotoxicology and teratology (2011).
[19] Scott, Katherine, and Karin Lust. “Illicit substance use in pregnancy–a review.” Obstetric Medicine 3.3 (2010): 94-100.
[20] D’Souza et al., “Delta-9-Tetrahydrocannabinol Effects in Schizophrenia: Implications for Cognition, Psychosis, and Addiction,” Biological Psychiatry (2005); 57(6): 594-608

[21] Morel, Lydie J., Bruno Giros, and Valérie Daugé. “Adolescent exposure to chronic delta-9-tetrahydrocannabinol blocks opiate dependence in maternally deprived rats.” Neuropsychopharmacology 34.11 (2009): 2469-2476.

[22] Robledo, Patricia, et al. “Advances in the field of cannabinoid–opioid cross‐talk.” Addiction biology 13.2 (2008): 213-224.

[23] Ranganathan, Mohini, et al. “Naltrexone does not attenuate the effects of intravenous Δ9-tetrahydrocannabinol in healthy humans.” The international journal of neuropsychopharmacology/official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP) (2012): 1.

[24] Vršková, Dagmar. “Endocannabinoid Brain System Involvement in dopamine mechanisms of behavioural sensitization to psychostimulants.”Acta Veterinaria Brno 78.3 (2009): 491-496.

[25] Asghari-Roodsari, Alaleh, et al. “Tocolytic Effect of Δ9-Tetrahydrocannabinol in Mice Model of Lipopolysaccharide—Induced Preterm Delivery: Role of Nitric Oxide.” Reproductive Sciences 17.4 (2010): 391-400.

[26] Maruyama et al., “Id-1 and Id-2 Are Overexpressed in Pancreatic Cancer and in Dysplastic Lesions in Chronic Pancreatitis,” The American Journal of Pathology (1999); 155(3): 815-822

[27] Schindl et al., “Overexpression of Id-1 Protein Is a Marker for Unfavorable Prognosis in Early-Stage Cervical Cancer,” Cancer Research (2001); 61(5): 5703-6

[28] McAllister et al., “Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells,” Molecular Cancer Therapeutics; 2007; 6(11): 2921-7

[29] Li et al., “Id-1 promotes tumorigenicity and metastasis of human esophageal cancer cells through activation of PI3K/AKT signaling pathway,” International Journal of Cancer (2009), 125(11): 2576-2585

[30] Ramer, Robert, et al. “Decrease of plasminogen activator inhibitor-1 may contribute to the anti-invasive action of cannabidiol on human lung cancer cells.” Pharmaceutical research 27.10 (2010): 2162-2174.

[31] Velasco, G., et al. “Cannabinoids as Potential Antitumoral Agents in Pancreatic Cancer.” Juan Iovanna• Uktam Ismailov (2009): 39.

[32] McKallip et al., “Cannabidiol-Induced Apoptosis in Human Leukemia Cells: A Novel Role of Cannabidiol in the Regulation of p22phox and Nox4 Expression,” Molecular Pharmacology (2006); 70(3): 897-908

[33] Qamri et al., “Synthetic cannabinoid receptor agonists inhibit tumor growth and metastasis of breast cancer,” Molecular Cancer Therapy (2009); 8(11): 3117-29

[34] Kogan et al., “A Cannabinoid Quinone Inhibits Angiogenesis by Targeting Vascular Endothelial Cells,” Molecular Pharmacology (2006); 70(1): 51-59

[35] Ramer et al., “Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1,” Biochemical Pharmacology (2010); 79(7): 955-966

[36] Zigler, Maya, et al. “Expression of Id-1 is regulated by MCAM/MUC18: a missing link in melanoma progression.” Cancer research 71.10 (2011): 3494-3504.

[37] Flygare, Jenny, and Birgitta Sander. “The endocannabinoid system in cancer—Potential therapeutic target?.” Seminars in cancer biology. Vol. 18. No. 3. Academic Press, 2008.

[38] Van Dross, Rukiyah, et al. “Receptor-dependent and Receptor-independent Endocannabinoid Signaling: A Therapeutic Target for Regulation of Cancer Growth.” Life Sciences (2012).

[39] Vaccani et al., “Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism,” British Journal of Pharmacology (2005); 144(8): 1032-1036

[40] Zajicek et al., “Role of Cannabinoids in Multiple Sclerosis,” CNS Drugs (2011); 25(3): 187-201

[41] Ligresti et al., “Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma,” The Journal of Pharmacology And Experimental Therapeutics (2006); 318(3): 1375-1387

[42] Jacobsson et al., “Inhibition of Rat C6 Glioma Cell Proliferation by Endogenous and Synthetic Cannabinoids. Relative Involvement of Cannabinoid and Vanilloid Receptors,” The Journal of Pharmacology And Experimental Therapeutics (2001); 299(3): 951-959

[43] McAllister et al., “Pathways mediating the effects of cannabidiol on the reduction of breast cancer cell proliferation, invasion, and metastasis,” Breast Cancer Research and Treatment (2011); 129(1): 37–47

[44] Prasad et al., “Cannabidiol Induces Programmed Cell Death in Breast Cancer Cells by Coordinating the Cross-talk between Apoptosis and Autophagy,” Molecular Cancer Therapeutics (2011); 10(7): 1161-72

[45] Steger-Hartmann, T. K. K. H. A., K. Kümmerer, and A. Hartmann. “Biological degradation of cyclophosphamide and its occurrence in sewage water.”Ecotoxicology and environmental safety 36.2 (1997): 174-179.

[46] Cardis, Elizabeth, et al. “Effects of low doses and low dose rates of external ionizing radiation: cancer mortality among nuclear industry workers in three countries.” Radiation research 142.2 (1995): 117-132.

[47] Lushbaugh, C. C., and George W. Casarett. “The effects of gonadal irradiation in clinical radiation therapy: a review.” Cancer 37.S2 (1976): 1111-1120.

[48] Sorsa, Marja, and Diana Anderson. “Monitoring of occupational exposure to cytostatic anticancer agents.” Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 355.1 (1996): 253-261.

[49] Sugiura et al., “Risks to health professionals from hazardous drugs in Japan: A pilot study of environmental and biological monitoring of occupational exposure to cyclophosphamide” Journal of Oncology Pharmacy Practice (2011); 17(1): 14-19

[50] Selevan, Sherry G., et al. “A study of occupational exposure to antineoplastic drugs and fetal loss in nurses.” New England Journal of Medicine 313.19 (1985): 1173-1178.

[51] Pacheco, M., and M. A. Santos. “Induction of Liver EROD and Erythrocytic Nuclear Abnormalities by Cyclophosphamide and PAHs in Anguilla L.” Ecotoxicology and environmental safety 40.1 (1998): 71-76.

[52] Portenoy, Russell K., and Pauline Lesage. “Management of cancer pain.”The lancet 353.9165 (1999): 1695-1700.

[53] Lee, Tsoy-Ing, Hsing-Hsia Chen, and Mei-Ling Yeh. “Effects of chan-chuang qigong on improving symptom and psychological distress in chemotherapy patients.” The American Journal of Chinese Medicine 34.01 (2006): 37-46.

[54] Herskovic, Arnold, et al. “Combined chemotherapy and radiotherapy compared with radiotherapy alone in patients with cancer of the esophagus.” New England Journal of Medicine 326.24 (1992): 1593-1598.

[55] Schumacher, A., et al. “Quality of life in adult patients with acute myeloid leukemia receiving intensive and prolonged chemotherapy–a longitudinal study.” Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, UK 12.4 (1998): 586.

[56] Curt, Gregory A., et al. “Impact of cancer-related fatigue on the lives of patients: new findings from the Fatigue Coalition.” The Oncologist 5.5 (2000): 353-360.

[57] New, Pamela. “Radiation injury to the nervous system.” Current opinion in neurology 14.6 (2001): 725-734.

[58] Weinberg, Clarice R., Kenneth G. Brown, and David G. Hoel. “Altitude, radiation, and mortality from cancer and heart disease.” Radiation research112.2 (1987): 381-390.

[59] Peters III et al., “Concurrent Chemotherapy and Pelvic Radiation Therapy Compared With Pelvic Radiation Therapy Alone as Adjuvant Therapy After Radical Surgery in High-Risk Early-Stage Cancer of the Cervix,” Journal of Clinical Oncology (2000); 18(8): 1606-1613

[60] D’Amico et al., “Pretreatment PSA Velocity and Risk of Death From Prostate Cancer Following External Beam Radiation Therapy,” The Journal of American Medical Association (2005); 294(4): 440-447

[61] Baker et al., “The biology that underpins the therapeutic potential of cannabis-based medicines for the control of spasticity in multiple sclerosis,” Multiple Sclerosis and Related Disorders (2012); 1(2): 64-75

[62] Melissa Brown, “The Garden State Just Got Greener: New Jersey Is The Fourteenth State in the Nation to Legalize Medical Marijuana,” Seton Hall Law Review (2011); 41(4):1519-67

[63] Celia Oreja-Guevara, “Clinical efficacy and effectiveness of Sativex ®, a combined cannabinoid medicine, in multiple sclerosis-related spasticity,” Expert Review of Neurotherapeutics (2012); 12(4): 3-8

[64] Michael Philip Barnes, “Sativex®: clinical efficacy and tolerability in the treatment of symptoms of multiple sclerosis and neuropathic pain,” Expert Opinion on Pharmacotherapy (2006); 7(5): 607-615

[65] Derick Wade, “Evaluation of the safety and tolerability profile of Sativex®: is it reassuring enough?” Expert Review of Neurotherapeutics (2012); 12(4): 9-14

[66] Docagne, Fabian, et al. “Therapeutic potential of CB2 targeting in multiple sclerosis.” (2008): 185-195.

[67] Baker et al., “Cannabinoid control of neuroinflammation related to multiple sclerosis,” British Journal of Pharmacology (2007); 152(5): 649-654

[68] Pryce and Baker, “Control of Spasticity in a Multiple Sclerosis Model is mediated by CB1, not CB2, Cannabinoid Receptors,” British Journal of Pharmacology (2007); 150(4): 519-525

[69] Fernández‐Ruiz, Javier, et al. “Cannabidiol for neurodegenerative disorders: important new clinical applications for this phytocannabinoid?.”British Journal of Clinical Pharmacology (2012).

[70] Lago et al., “Cannabinoids ameliorate disease progression in a model of multiple sclerosis in mice, acting preferentially through CB1 receptor-mediated anti-inflammatory effects,” Neuropharmacology (2012); 62(7): 2299-2308

[71] Lago et al., “Cannabinoids, multiple sclerosis and neuroprotection,” Expert Review of Clinical Pharmacology (2009); 2(6): 645-660

[72] Affidavit – David West, Ph.D., para. 34 United States v. White Plume, 447 F.3d 1067, 1072 (8th Cir. 2006) (No. CIV02-5071)

[73] Asa Hutchinson, “Interpretation of Listing of “Tetrahydrocannabinols” in Schedule I,” Federal Register (2001); 66(195): 51530-51534

[74] Christine A. Kolosov, J.D., “Evaluating The Public Interest: Regulation Of Industrial Hemp Under The Controlled Substances Act,”57 UCLA Law Review 237  (2009)

[75] Renee Johnson, “Hemp as an Agricultural Commodity,” CRS Report for Congress (2012)

[76] USDA – Economic Research Service, “Industrial Hemp in the United States: Status and Market Potential,” Agricultural Economic Report (2000); AGES-001E: 1-43

[77] Cho, S. H., & Tang, C., “Advance Selling in a Supply Chain under Uncertain Supply and Demand,” (2012) Available at SSRN 1557090.

[78] Irwin & Fry, (2007) “Strengthening drug policy and practice through ethics engagement: An old challenge for a new harm reduction,” International Journal of Drug Policy 18: 75-83

[79] Marcus Patrick Capetillo, Honors Thesis (2012), “Drug Trafficking in Mexico: Causes and Consequences of the Militarization of Mexico,” Baylor University Honors Program

[80] Katherine Michaud (2011) “Mexico’s Militarized Anti-Drug Policy: Understanding Its Origins Through Examination of Institutional Legacies, Democratization, and Public Opinion,” Sanford Journal of Public Policy 2(1):