medicinal marijuana

I knew this was good for MS sufferers (and fishing) but I didn't know all this. Thought I'd pass it on.



(cannabis and cancer) "... we show that cannabinoid administration selectively down-regulates MMP-2 [matrix metalloproteinases] expression in mice bearing gliomas as well as in two patients with recurrent glioblastoma multiforme. Cannabinoid-induced inhibition of MMP-2 expression was also evident in cultured glioma cells, indicating that the changes observed in gliomas in vivo reflect?at least in part?the direct effect of cannabinoids on tumor cells. MMP-2 expression is upregulated in almost all human cancers, including gliomas, and this has been shown to be closely associated with negative prognosis."

"As MMP-2 up-regulation is associated with high progression and poor prognosis of gliomas and many other tumors, MMP-2 downregulation constitutes a new hallmark of cannabinoid antitumoral activity."

Source: Cristina Bla?zquez, Mar??a Salazar, Arkaitz Carracedo, Mar Lorente, Ainara Egia, Luis Gonza?lez-Feria, Amador Haro, Guillermo Velasco, and Manuel Guzman, "Cannabinoids Inhibit Glioma Cell Invasion by Down-regulating Matrix Metalloproteinase-2 Expression," Cancer Research (March 2008), pp. 1951 and 1945.
http://cancerres.aacrjournals.org/cgi/reprint/68/6/1945.pdf


(cannabis and cancer) "Cannabinoids have a favourable drug safety profile. Acute fatal cases due to cannabis use in humans have not been substantiated, and median lethal doses of THC in animals have been extrapolated to several grams per kilogram of body weight. Cannabinoids are usually well tolerated in animal studies and do not produce the generalized toxic effects of most conventional chemotherapeutic agents. For example, in a 2-year administration of high oral doses of THC to rats and mice, no marked histopathological alterations in the brain and other organs were found. Moreover, THC treatment tended to increase survival and lower the incidence of primary tumours. Similarly, long-term epidemiological surveys, although scarce and difficult to design and interpret, usually show that neither patients under prolonged medical cannabinoid treatment nor regular cannabis smokers have marked alterations in a wide array of physiological, neurological and blood tests."

Source: Guzman, Manuel, "Cannabinoids: Potential Anticancer Agents." Nature Reviews: Cancer (October 2003), p. 752.
http://www.brainlife.org/reprint/2003/guzm%C3%A1n_m031000.pdf


(cannabis and cancer) "In conclusion, a cannabinoid-based therapeutic strategy for neural diseases devoid of undesired psychotropic side effects could find in CBD [a cannabinoid] a valuable compound in cancer therapies along with the perspective of evaluating a synergistic effect with other cannabinoid molecules and/or with other chemotherapeutic agents as well as with radiotherapy. Whatever the precise mechanism underlying the CBD effects, the present results suggest a possible application of CBD as a promising, nonpsychoactive, antineoplastic agent."

Source: Massi, Paola; Vaccani, Angelo; Ceruti, Stefania; Colombo, Arianna; Abbracchio, Maria P., and Parolaro, Daniela, "Antitumor Effects of Cannabidiol, a Nonpsychoactive Cannabinoid, on Human Glioma Cell Lines," The Journal of Pharmacology and Experimental Therapeutics (Bethesda, MD: The American Society for Pharmacology and Experimental Therapeutics, March 2004) Vol. 308, p. 845.
http://jpet.aspetjournals.org/content/308/3/838.full.pdf


(cannabis and cancer) "Cannabinoids, the active components of marijuana and their other natural and synthetic analogues have been reported as useful adjuvants to conventional chemotherapeutic regimens for preventing nausea, vomiting, pain, and for stimulating appetite. Before the discovery of specific cannabinoid systems and receptors, it was speculated that cannabinoids produced their effects via nonspecific interaction with cell membranes. Cannabinoids are proving to be unique based on their targeted action on cancer cells and their ability to spare normal cells. Variation in the effects of cannabinoids in different cell lines and tumor model could be due to the differential expression of CB1 and CB2 receptors. Thus, overexpression of cannabinoid receptors may be effective in killing tumors, whereas low or no expression of these receptors could lead to cell proliferation and metastasis because of the suppression of the antitumor immune response."

Source: Sarfaraz, Sami; Adhami, Vaqar M.; Syed, Deeba N.; Afaq, Farrukh; and Mukhtar, Hasan, "Cannabinoids for Cancer Treatment: Progress and Promise," Cancer Research (Philadelphia, PA: American Association for Cancer Research, January 2008) Vol. 68, pp. 341-342.
http://cancerres.aacrjournals.org/cgi/reprint/68/2/339.pdf


(cannabis and breast cancer) "In conclusion, our data indicate that cannabidiol, and possibly Cannabis extracts enriched in this natural cannabinoid, represent a promising nonpsychoactive antineoplastic strategy. In particular, for a highly malignant human breast carcinoma cell line, we have shown here that cannabidiol and a cannabidiol-rich extract counteract cell growth both in vivo and in vitro as well as tumor metastasis in vivo. Cannabidiol exerts its effects on these cells through a combination of mechanisms that include either direct or indirect activation of CB2 and TRPV1 receptors and induction of oxidative stress, all contributing to induce apoptosis."

Source: Ligresti, Alessia; Moriello, Aniello Schiano; Starowicz, Katarzyna; Matias, Isabel; Pisanti, Simona; De Petrocellis, Luciano; Laezza, Chiara; Portella, Giuseppe; Bifulco, Maurizio; and Di Marzo, Vincenzo, "Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma," The Journal of Pharmacology and Experimental Therapeutics (Bethesda, MD: The American Society for Pharmacology and Experimental Therapeutics, March 2004) Vol. 318, No. 3, pp. 1386-1387.
http://jpet.aspetjournals.org/content/318/3/1375.full.pdf


(cannabis and breast cancer) "Our results, which were obtained in a clinically relevant animal model of ErbB2-positive breast cancer, suggest that these highly aggressive and low responsive tumors could be efficiently treated with nonpsychoactive CB2-selective agonists without affecting the surrounding healthy tissue."

From the abstract: "Conclusions: Taken together, these results provide a strong preclinical evidence for the use of cannabinoid-based therapies for the management of ErbB2-positive breast cancer."

Source: Caffarel, Mar?a M; Andradas, Clara; Mira, Emilia; P?rez-G?mez, Eduardo; Cerutti; Camilla; Moreno-Bueno, Gema; Flores, Juana; Garc?a-Realm, Isabel; Palacios, Jos?; Ma?es, Santos; Guzm?n, Manuel; S?nchez, Cristina, "Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition," Molecular Cancer (London, United Kingdom: July 22, 2010), p. 1 and P. 8.
http://www.molecular-cancer.com/content/9/1/196
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917429/pdf/1476-4598-9-196....


(cannabis and diabetic cardiomyopathy) "Remarkably, CBD attenuated myocardial dysfunction, cardiac fibrosis, oxidative/nitrative stress, inflammation, cell death, and interrelated signaling pathways. Furthermore, CBD also attenuated the high glucose-induced increased reactive oxygen species generation, nuclear factor-
B activation, and cell death in primary human cardiomyocytes.

"Conclusions: Collectively, these results coupled with the excellent safety and tolerability profile of CBD in humans, strongly suggest that it may have great therapeutic potential in the treatment of diabetic complications, and perhaps other cardiovascular disorders, by attenuating oxidative/nitrative stress, inflammation, cell death and fibrosis."

Source: Rajesh, Mohanraj; Mukhopadhyay,Partha; Batkai, Sandor; Patel, Vivek; Patel, Keita; Matsumoto, Shingo; Kashiwaya, Yoshihiro; Horvath, B?la; Mukhopadhyay, Bani; Becker, Lauren; Hasko, Gy?rgy; Liaudet, Lucas; Wink, David A.; Veves, Aristidis; Mechoulam, Raphael; Pacher, Pal, "Cannabidiol Attenuates Cardiac Dysfunction, Oxidative Stress, Fibrosis, and Inflammatory and Cell Death Signaling Pathways in Diabetic Cardiomyopathy," Journal of the American College of Cardiology (San Diego, CA: American College of Cardiology Foundation: December 2010) Vol. 56, No. 25, p. 2115.
http://www.natap.org/2010/newsUpdates/marijuana.pdf
http://content.onlinejacc.org/cgi/content/abstract/56/25/2115


(cannabis and diabetic retinopathy) "Inflammation-mediated neurodegeneration is of utmost clinical relevance. Inflammation in neural tissues involves production of reactive oxygen species that stimulate cellular release of proinflammatory cytokines. ... Adenosine has been shown to mitigate the proinflammatory cytokine release response in central neural tissue."

"CBD [cannabidiol (CBD), a nonpsychotropic and nontoxic cannabinoid] has been shown to block NMDA-, LPS-, or diabetes induced retinal damage (El-Remessy AB, et al., manuscript submitted),5,17 ... "

"Drugs that enhance extracellular adenosine signaling have been of clinical interest in treatment of inflammation after myocardial or cerebral ischemia.25,26 CBD as an anti-inflammatory drug is an attractive alternative to smoking marijuana because of its lack of psychoactive effects.27 CBD is known to be nontoxic in humans,28 which has previously been a problem for other nucleoside inhibitor drugs.29,30

Source: Liou, Gregory I.; Auchampach, John A.; Hillard, Cecilia J.; Zhu, Gu; Yousufzai, Bilal; Salman, Mian; Khan, Sohail; and Khalifa, Yousuf, "Mediation of Cannabidiol Anti-inflammation in the Retina by Equilibrative Nucleoside Transporter and A2A Adenosine Receptor," Investigative Ophthalmology & Visual Science (Rockville, MD: Association for Research in Vision and Ophthalmology, December 2008), Vol. 49, No. 12, pp. 5530-5531.
http://www.iovs.org/cgi/reprint/49/12/5526.pdf


(cannabis and diabetic retinopathy) "Recent evidence suggests that local inflammation plays a major role in the pathogenesis of diabetic retinopathy. The function of CBD as an antioxidant to block oxidative stress and as an inhibitor of adenosine reuptake to enhance a self-defense mechanism against retinal inflammation represents a novel therapeutic approach to the treatment of ophthalmic complications associated with diabetes."

Source: Loiu, George, " Diabetic retinopathy: Role of inflammation and potential therapies for anti-inflammation, " World Journal of Diabetes (Beijing, China: Beijing Baishideng BioMed Scientific Co., March 15, 2010), p. 15.
http://www.wjgnet.com/1948-9358/pdf/v1/i1/12.pdf


(endocannabinoid deficiency) "Baker et al. have described how endocannabinoids may demonstrate an impairment threshold if too high, and a range of normal function below which a deficit threshold may be crossed [112]. Syndromes of CECD [Clinical Endocannabinoid Deficiency] may be congenital or acquired. In the former case, one could posit that genetically-susceptible individuals might produce inadequate endocannabinoids, or that their degradation is too rapid. The same conditions might be acquired in injury or infection."

Source: Russo, Ethan, "Clinical Endocannabinoid Deficiency (CECD): Can this Concept Explain Therapeutic Benefits of Cannabis in Migraine, Fibromyalgia, Irritable Bowel Syndrome and other Treatment-Resistant Conditions?," Neuroendocrinology Letters (Stockholm, Sweden: Society of Integrated Sciences, Feb-Apr 2004) Nos.1/2, Vol.25, p. 38.
http://www.ncbi.nlm.nih.gov/pubmed/18404144
http://www.freedomtoexhale.com/clinical.pdf


(cannabis and the gastrointestinal tract) "The role of the endocannabinoid system in the control of GI functions under physiological and pathological conditions has recently received increased interest. Within the last 5 years, more than half of all studies on the roles of the endocannabinoid system in the GI tract have been published. The current state of knowledge of the physiology and pharmacology of cannabinoids has largely increased, providing new potential tools for the treatment of several GI diseases. The symptoms of the most common GI disorders, IBS and inflammatory bowel disease, affect more than 20% of the population in Western countries and cause great discomforts [106]. Intestinal cramping, nausea, chronic diarrhoea and inflammation are all symptoms onto which the cannabinoids may be effective. Cannabis derivatives and other newly developed cannabinoids may represent promising tools for the treatment of different GI disorders because they can act at multiple sites, covering a wide spectrum of symptoms."

Source: Massa, Federico; Storr, Martin; and Lutz, Beat, "The endocannabinoid system in the physiology and pathophysiology of the gastrointestinal tract," Journal of Molecular Medicine (Berlin, Germany: August 26, 2005) Vol. 83, p. 951.
http://www.springerlink.com/content/pj24p7323lp31105/fulltext.pdf


(cannabis in HIV and hepatitis C) "Short-term use of smoked cannabis did not affect viral load in 15 HIV-positive patients and also is associated with adherence to therapy and reduced viral loads in 16 patients with hepatitis C infections."

Source: American Medical Association, Council on Science and Public Health, "Report 3 of the Council on Science and Public Health: Use of Cannabis for Medicinal Purposes" (December 2009), p. 15.
http://americansforsafeaccess.org/downloads/AMA_Report.pdf


(cannabis and HIV) "This study provides evidence that short-term use of cannabinoids, either oral or smoked, does not substantially elevate viral load in individuals with HIV infection who are receiving stable antiretroviral regimens containing nelfinavir or indinavir. Upper confidence bounds for all estimated effects of cannabinoids on HIV RNA level from all analyses were no greater than an increase of 0.23 log10 copies/mL compared with placebo. Because this study was randomized and analyses were controlled for all known potential confounders, it is very unlikely that chance imbalance on any known or unknown covariate masked a harmful effect of cannabinoids. Study participants in all groups may have been expected to benefit from the equivalent of directly observed antiretroviral therapy, as well as decreased stress and, for some, improved nutrition over the 25-day inpatient stay."

Source: Abrams, Donald I., MD, et al., "Short-Term Effects of Cannabinoids in Patients with HIV-1 Infection - A Randomized, Placebo-Controlled Clinical Trial," Annals of Internal Medicine, Aug. 19, 2003, Vol. 139, No. 4 (American College of Physicians), p. 264.
http://www.annals.org/content/139/4/258.full.pdf+html


(cannabis and HIV) "Conclusions: Smoked and oral cannabinoids did not seem to be unsafe in people with HIV infection with respect to HIV RNA levels, CD4+ and CD8+ cell counts, or protease inhibitor levels over a 21-day treatment."

Source: Abrams, Donald I., MD, et al., "Short-Term Effects of Cannabinoids in Patients with HIV-1 Infection - A Randomized, Placebo-Controlled Clinical Trial," Annals of Internal Medicine, Aug. 19, 2003, Vol. 139, No. 4 (American College of Physicians), p. 258.
http://www.annals.org/content/139/4/258.full.pdf+html


(cannabis and lymphoma) "In conclusion, our study demonstrates that the cannabinoid receptor agonists R(+)-MA and Win55 induce a sequence of signaling events leading to cell death of MCL cells. The requirement of ligation of both CB1 and CB2 [receptors] raises the possibility that cannabinoids may be used to selectively target MCL cells to undergo apoptosis."

Note: MCL is a malignant B-cell lymphoma with an aggressive course and generally a poor clinical outcome. MCL tumors respond to chemotherapy, but the remissions are short and the median survival is only 3 years."

Source: Gustafsson, Kristin; Christensson, Birger; Sander, Birgitta; and Flygare, Jenny, "Cannabinoid Receptor-Mediated Apoptosis Induced by R(+)-Methanandamide and Win55,212-2 Is Associated with Ceramide Accumulation and p38 Activation in Mantle Cell Lymphoma," Molecular Pharmacology (Bethesda, MD: The American Society for Pharmacology and Experimental Therapeutics, August 2006), p. 1619.
http://molpharm.aspetjournals.org/content/70/5/1612.full.pdf


(marijuana and adolescents) In an ethnographic study of adolescents who were regular marijuana users, researchers at the University of British Columbia, concluded, "Thematic analysis revealed that these teens differentiated themselves from recreational users and positioned their use of marijuana for relief by emphasizing their inability to find other ways to deal with their health problems, the sophisticated ways in which they titrated their intake, and the benefits that they experienced. These teens used marijuana to gain relief from difficult feelings (including depression, anxiety and stress), sleep difficulties, problems with concentration and physical pain. Most were not overly concerned about the risks associated with using marijuana, maintaining that their use of marijuana was not 'in excess' and that their use fit into the realm of 'normal.'

Conclusion: Marijuana is perceived by some teens to be the only available alternative for teens experiencing difficult health problems when medical treatments have failed or when they lack access to appropriate health care."

Source: Bottorff, Joan L , Johnson, Joy L, Moffat, Barbara M, and Mulvogue, Tamsin, "Relief-oriented use of marijuana by teens," Journal of Substance Abuse Treatment, Prevention, and Policy (Vancouver, BC: April 2009), pp. 4-7.
http://www.substanceabusepolicy.com/content/pdf/1747-597X-4-7.pdf


(cannabis and memory) "Nevertheless, when considering all 15 studies (i.e., those that met both strict and more relaxed criteria) we only noted that regular cannabis users performed worse on memory tests, but that the magnitude of the effect was very small. The small magnitude of effect sizes from observations of chronic users of cannabis suggests that cannabis compounds, if found to have therapeutic value, should have a good margin of safety from a neurocognitive standpoint under the more limited conditions of exposure that would likely obtain in a medical setting."

Source: Grant, Igor, et al., "Non-Acute (Residual) Neurocognitive Effects Of Cannabis Use: A Meta-Analytic Study," Journal of the International Neuropsychological Society (Cambridge University Press: July 2003), 9, pp. 687-8.
http://www.csdp.org/research/348art2003.pdf


(cannabis and migraines) "The information reviewed above indicates that cannabis has a long established history of efficacy in migraine treatment. Clinical use of the herb and its extracts for headache has waxed and waned for 1200 years, or perhaps much longer, in a sort of cannabis interruptus. It is only contemporaneously that supportive biochemical and pharmacological evidence for the indication is demonstrable. Cannabis? unique ability to modulate various serotonergic receptor subtypes, inhibit glutamatergic-mediated toxicities, simultaneously provide antiinflammatory activity and provide acute symptomatic and chronic preventive relief make it unique among available treatments for this disorder."

Source: Russo, Ethan, "Hemp for Headache: An In-Depth Historical and Scientific Review of Cannabis in Migraine Treatment," Journal of Cannabis Therapeutics (September 2000) Vol. 1, pp. 73-74.
http://www.drugpolicy.org/docUploads/hemp_for_headache.pdf


(cannabis and morning sickness) "This study was designed to determine how therapeutic users of cannabis rate its effectiveness as an anti-emetic, and particularly as a treatment for nausea and vomiting of pregnancy. In general (not specific to pregnancy), the vast majority of our respondents considered cannabis to be extremely effective or effective as a therapy for nausea (93%) and vomiting (75%), and as an appetite stimulant (95%). In the context of pregnancy, cannabis was rated as extremely effective or effective by 92% of the respondents who had used it as a therapy for nausea and vomiting (morning sickness)."

Source: Westfall, Rachel E.; Janssen, Patricia A.; Lucas, Philippe; and Capler, Rielle, "Survey of medicinal cannabis use among childbearing women: Patterns of its use in pregnancy and retroactive self-assessment of its efficacy against ?morning sickness,;" Contemporary Therapies in Clinical Practice (United Kingdom: November 2009) Vol. 15, Issue 4, p. 32.
http://www.ncbi.nlm.nih.gov/pubmed/19880090
http://safeaccess.ca/research/cannabis_nausea2006.pdf


(cannabis and multiple sclerosis) "... there is evidence that cannabinoids may provide neuroprotective and anti-inflammatory benefits in MS. Neuroinflammation, found in autoimmune diseases such as MS, has been shown to be reduced by cannabinoids through the regulation of cytokine levels in microglial cells [25]. The therapeutic potential of cannabinoids in MS is therefore comprehensive and should be given considerable attention."

Source: Lakhan, Shaheen E and Rowland, Marie, "Whole plant cannabis extracts in the treatment of spasticity in multiple sclerosis: a systematic review," BMC Neurology (Los Angeles, CA: Global Neuroscience Initiative Foundation, December 2009) Vol. 9, p. 63.
http://www.biomedcentral.com/content/pdf/1471-2377-9-59.pdf


(cannabis and pain) "By providing a medical geographic patient utilization ?snapshot? of 236.4 patient-years of the use of MC at a regional pain clinic, this study provides further insight into the applicability of cannabinoid botanicals in the management of a broad range of refractory chronic pain conditions in adults, from myofascial pain and discogenic back pain to neuropathic pain and central pain syndromes. With physicians employing proper chart documentation of appropriate use, efficacy, and side effects at patient visits, in a manner similar to that used in opioid management of pain, there will hopefully be additional reports in the future on MC use in pain management to add to the clinical database.

"Such a literature can grow only if certain stereotypes and myths about MC use are dispelled amongst pain management specialists and their regulators. The results presented here should help to deconstruct mythologies about the kinds of patients accessing MC treatment, including their young age or their propensity to malinger or feign disease. One prominent mythology is that patients who receive treatment with MC are not ?truly sick.?45 An examination of the chart review data, which includes both subjective and objective diagnostic data substantiating patients? chronic pain illnesses, helps to deflate this concern."

Source: Aggarwal, Sunil K.; Carter, Gregory T.; Sullivan, Mark D.; ZumBrunnen, Craig; Morrill, Richard; and Mayer, Jonathan D., "Characteristics of patients with chronic pain accessing treatment with medical cannabis in Washington State," Journal of Opiod Management, (Weston, Massachusettes: September/October 2009), Vol. 5, p. 264.
http://www.ncbi.nlm.nih.gov/pubmed/19947069
http://students.washington.edu/sunila/JOM_5-5-05.pdf


(cannabis, pain, and HIV) "In this randomized clinical trial, smoked cannabis at maximum tolerable dose (1?8% THC), significantly reduced neuropathic pain intensity in HIV-associated DSPN compared to placebo, when added to stable concomitant analgesics. Using verbal descriptors of pain magnitude from DDS, cannabis was associated with an average reduction of pain intensity from ?strong? to ?mild to moderate?. Also, cannabis was associated with a sizeable (46%) and significantly greater (vs 18% for placebo) proportion of patients who achieved what is generally considered clinically meaningful pain relief (eg X30% reduction in pain; Farrar et al, 2001). Mood disturbance, physical disability, and quality of life all improved significantly for subjects during study treatments, regardless of treatment order."

Source: Ellis, Ronald J; Toperoff, Will; Vaida, Florin; van den Brande, Geoffrey; Gonzales, James; Gouaux, Ben; Bentley, Heather; and Atkinson, J. Hampton, "Smoked Medicinal Cannabis for Neuropathic Pain in HIV: A Randomized, Crossover Clinical Trial," Neuropsychopharmacology (Nashville, TN : American College of Neuropsychopharmacology, 2009), Vol. 34, p. 678.
http://www.nature.com/npp/journal/v34/n3/pdf/npp2008120a.pdf


(cannabis and neuropathic pain) "We found that 25 mg herbal cannabis with 9.4% tetrahydrocannabinol, administered as a single smoked inhalation three times daily for five days, significantly reduced average pain intensity compared with a 0% tetrahydrocannabinol cannabis placebo in adult participants with chronic post-traumatic or postsurgical neuropathic pain. We found significant improvements in measures of sleep quality and anxiety. We have shown the feasibility of a single-dose delivery method for smoked cannabis, and that blinding participants to treatment allocation is possible using this method."

Source: Ware, Mark A.; Wang, Tongtong; Shapiro, Stan; Robinson, Ann; Ducruet, Thierry; Huynh,Thao; Gamsa, Ann; Bennett, Gary J.; and Collet, Jean-Paul,"Smoked cannabis for chronic neuropathic pain: a randomized controlled trial" (Ottawa, ON: Canadian Medical Association, October 5, 2010), p. E697-E700.
http://www.cmaj.ca/cgi/reprint/182/14/E694.pdf


(cannabis and PTSD) "A chart review of patients diagnosed with PTSD who were referred to a private psychiatric clinic suggests that the synthetic cannabinoid, nabilone, has beneficial effects beyond its official indication in regard to abolishing or greatly reducing nightmares that persisted in spite of treatment with conventional PTSD medications.

"The subjects concomitantly received nabilone in addition to the one or more psychiatric medications that they were already taking for 2 years or more. No tolerance to nabilone was observed among the patients. This may indicate its potential longer-term safety and efficacy.

"... on the basis of these retrospective findings, nabilone appears to be a significant treatment for nightmares in the PTSD population."

Source: Fraser, George A., "The Use of a Synthetic Cannabinoid in the Management of Treatment-Resistant Nightmares in Posttraumatic Stress Disorder (PTSD)," CNS Neuroscience & Therapeutics (Hoboken, NJ: Wiley-Blackwell, Winter 2009), p. 87.
http://onlinelibrary.wiley.com/doi/10.1111/j.1755-5949.2008.00071.x/pdf


(cannabis and substance abuse treatment) "It is clear, however, that cannabis use did not compromise substance abuse treatment amongst the medical marijuana using group. In fact, medical marijuana users seemed to fare equal to or better than non-medical marijuana users in every important outcome category. Movement from more harmful to less harmful drugs is an improvement worthy of consideration by treatment providers and policymakers. The economic cost of alcohol use in California has been estimated at $38 billion [30]. Add to this the harm to individuals, families, communities, and society from methamphetamine, heroin, and cocaine, and a justification can be made for medical marijuana in addictions treatment as a harm reduction practice. As long as marijuana use is not associated with poorer outcomes, then replacing other drug use with marijuana may lead to social and economic savings."

Source: Swartz, Ronald, "Medical marijuana users in substance abuse treatment," Harm Reduction Journal (London, United Kingdom: March 2010) Vol. 7, p. 7-8.
http://www.harmreductionjournal.com/content/pdf/1477-7517-7-3.pdf


(cannabis as a treatment for schizophrenia and psychosis) "... a preliminary report from a 4-week, double-blind controlled clinical trial, using an adequate number of patients and comparing the effects of CBD with amisulpride in acute schizophrenic and schizophreniform psychosis, showed that CBD significantly reduced acute psychotic symptoms after 2 and 4 weeks of treatment when compared to baseline. In this trial CBD did not differ from amisulpride except for a lower incidence of side effects (49).

"In conclusion, results from pre-clinical and clinical studies suggest that CBD is an effective, safe and well-tolerated alternative treatment for schizophrenic patients."

Source: "Zuardi, A.W.; Crippa, J.A.S.; Hallak, J.E.C.; Moreira, F.A.; and Guimar?es, F.S., "Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug," Brazillian Journal of Medical and Biological Research (Ribeir?o Preto, Brazil: April 2006), Volume 39, Issue 4, p. 427-428.
http://www.scielo.br/pdf/bjmbr/v39n4/6164.pdf


(cannabis and substance abuse treatment) "The current study has revealed unique properties of the phytocannabinoid CBD and underscores the contrasting characteristics of the main constituents of cannabis in relation to addiction vulnerability. Compared with the documented effects of THC to enhance heroin self-administration (Solinas et al., 2004; Ellgren et al., 2007), the present data demonstrated that CBD specifically inhibited reinstatement of cue-induced heroin seeking. The specificity of CBD to cue-induced reinstatement was also emphasized by the observation that the compound still inhibited drug relapse behavior in animals extinguished to the environmental context (self-administration chamber) previously associated with heroin. The results are striking given the very selective and protracted effects of CBD."

"Overall, the observations of this study suggest the potential for CBD as a treatment strategy given its specificity to attenuate cue-induced drug-seeking behavior, preferential impact on mesolimbic neuronal populations, and enduring neural actions. Clearly, greater attention needs be given to the potential role of CBD in the treatment of addiction and other mental health disorders.Clearly, greater attention needs be given to the potential role of CBD in the treatment of addiction and other mental health disorders.

Source: Ren, Yanhua; Whittard, John; Higuera-Matas, Alejandro; Morris, Claudia V.; and Yasmin L. Hurd, "Cannabidiol, a Nonpsychotropic Component of Cannabis, Inhibits Cue-Induced Heroin Seeking and Normalizes Discrete Mesolimbic Neuronal Disturbances," The Journal of Neuroscience (Washington, DC: Society for Neuroscience, November 25, 2009), Vol. 29, No. 47, pp. 14767 and 14768.
http://www.jneurosci.org/cgi/reprint/29/47/14764.pdf


(cannabis and skin cancer) "The present data indicate that local cannabinoid administration may constitute an alternative therapeutic approach for the treatment of nonmelanoma skin cancer. Of further therapeutic interest, we show that skin cells express functional CB2 receptors. The synergy between CB1 and CB2 receptors in eliciting skin tumor cell apoptosis reported here is nonetheless intriguing because it is not observed in the case of cannabinoid-induced glioma cell apoptosis (21, 22). In any event, the present report, together with the implication of CB2- or CB2-like receptors in the control of peripheral pain (40?42) and inflammation (41), opens the attractive possibility of finding cannabinoidbased therapeutic strategies for diseases of the skin and other tissues devoid of nondesired CB1-mediated psychotropic side effects."

Source: Casanova, M. Llanos; Bl?zquez,Cristina; Mart?nez-Palacio, Jes?s; Villanueva, Concepci?n; Fern?ndez-Ace?ero, Jes?s; Huffman, John W.; Jorcano, Jos? L.; and Guzm?n, Manuel, "Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors," Journal of Clinical Investigation (Ann Arbor, MI: American Society for Clinical Investigation, January 2003), p. 49.
http://www.jci.org/articles/view/16116/version/1/files/pdf?disposition=a...


(cannabis and drug substitution) "Eighty five percent of the BPG [Berkeley Patients Group] sample reported that cannabis has much less adverse side effects than their prescription medications. Additionally, the top two reasons listed by participants as reasons for substituting cannabis for one of the substances previously mentioned were less adverse side effects from cannabis (65%) and better symptom management from cannabis (57.4%).

"Conclusion
"The substitution of one psychoactive substance for another with the goal of reducing negative outcomes can be included within the framework of harm reduction. Medical cannabis patients have been engaging in substitution by using cannabis as an alternative to alcohol, prescription and illicit drugs."

Source: Reiman, Amanda, "Cannabis as a Substitute for Alcohol and Other Drugs," Harm Reduction Journal (London, United Kingdom: December 2009).
http://www.harmreductionjournal.com/content/pdf/1477-7517-6-35.pdf


Even if you're against this stuff (I'm not) we should try and think of others and support it when it gets here IMO.