News
Tue, 12 Jul 2011 19:40:53 By: Paul Armentano, NORML Deputy Director
The White House yesterday, with little fanfare, issued its annual (and long overdue) 2011 National Drug Control Strategy report.
As usual, the White House’s official justification for the ongoing multigenerational drug war was light on facts and heavy on rhetoric, particularly as it pertained to the federal government’s fixation with criminalizing cannabis. Here are just a few examples (all of which are excerpted from a section of the report, entitled ironically enough, ‘The Facts About Marijuana‘) of your government on pot.
“[C]onfusing messages being conveyed by the entertainment industry, media, proponents of ‘medical’ marijuana, and political campaigns to legalize all marijuana use perpetuate the false notion that marijuana use is harmless and aim to establish commercial access to the drug. This significantly diminishes efforts to keep our young people drug free and hampers the struggle of those recovering from addiction.”
“Marijuana and other illicit drugs are addictive and unsafe. … The science, though still evolving in terms of long-term consequences, is clear: marijuana use is harmful. Independent from the so called ‘gateway effect’ — marijuana on its own is associated with addiction, respiratory and mental illness, poor motor performance, and cognitive impairment, among other negative effects.”
“The Administration steadfastly opposes drug legalization. Legalization runs counter to a public health approach to drug control because it would increase the availability of drugs, reduce their price, undermine prevention activities, hinder recovery support efforts, and pose a significant health and safety risk to all Americans, especially our youth.”
You get the idea.
Of course, none of these allegations represent anything new for this (or previous) administrations, and NORML has responded in detail to most of the Drug Czar’s claims previously. I did, however, take notice of this particular paragraph in the report, which appears under the title ‘Medical’ Marijuana.’
“In the United States, the Drug Enforcement Administration (DEA) has approved 109 researchers to perform bona fide research with marijuana, marijuana extracts, and marijuana derivatives such as cannabidiol and cannabinol. Studies include evaluation of abuse potential, physical/psychological effects, adverse effects, therapeutic potential, and detection. Fourteen researchers are approved to conduct research with smoked marijuana on human subjects.”
Only in an environment of absolute criminal prohibition can the administration imply, with a straight face, that allowing a grand total of 14 legally permitted scientists to study a substance consumed by tens of millions of Americans for therapeutic and/or recreational purposes is somehow to be construed as ‘progress.’ That total doesn’t even legally allow for one scientist per medical marijuana state to actively assess how cannabis is impacting that state’s patient population.
Moreover, this acknowledgment comes from the very same administration that on Friday flat out rejected the notion of even allowing hearings on the question of marijuana’s schedule I classification because, in their opinion, “there are no adequate and well-controlled studies proving efficacy.” Of course, with only a dozen or so scientists in the whole county even permitted to interact with pot and humans can there be any wonder why such studies aren’t more prevalent?
(By the way, remember the results last year of the series of FDA-approved ‘gold standard’ clinical trials assessing the safety and efficacy of inhaled cannabis in severely ill patients? Apparently neither does the DEA. Nor are they aware of these ‘well-controlled’ studies of medical cannabis. Or these.)
Interestingly, according to the DEA’s 2010 white paper on cannabis (no longer online), last year there were a total of 18 scientists licensed by the government to work with marijuana in a clinical setting. Perhaps next year there will only be ten. If the DEA and NIDA have there way perhaps by 2013 there will be zero.
As for the other 95 US scientists legally authorized by the federal government to assess the efficacy of ‘marijuana extracts and marijuana derivatives’ in animals, most of them were here last week — at the annual meeting of the International Cannabinoid Research Society. But even these ‘chosen few’ acknowledge that their work has next to no influence on the very administration that authorizes it.
Marijuana Researchers Meet At Pheasant Run
Researchers from around the world studying the effects of marijuana and exploring possible medical uses meet each year to compare notes and share their findings
About 250 scientists from around the world have gathered this weekend at Pheasant Run Resort sitting through seminars titled “Endocannabinoid Signaling in Periimplantation Biology,” and “Cannabinoids and HIV Pathogenicity,” to name a few, for the 21st Annual Symposium of the International Cannabinoid Research Society.
ICRS members meet once a year to compare notes on research studying how cannabinoids, compounds from the cannabis plant (more commonly known as marijuana) or from the brain called endocannabinoids, affect the body and how it functions.
While most attendees are scientists, many are graduate students or training scientists as well as physicians interested in learning how these chemicals might be useful in treating human disease.
“We are all around the world working on our own projects,” said Cecilia Hillard, ICRS executive director, professor of pharmacology and director of the Neuroscience Research Center at the Medical College of Wisconsin.
“That’s why it’s so wonderful for us to get together once a year so we can really share things that we learn,” she said.
For example, she said someone may be studying how bone is formed, and she is studying how the brain works.
“I learn a lot by learning how the bone is formed, and they learn about how neurons work,” Hillard said. “It’s really a lot of what we call a ‘cross-fertilization’ of ideas.”
While the society is not political, Hillard says the type of research that is done on the controversial topic of medical and personal use of marijuana is nonetheless important.
“We’re carrying out scientific investigations trying to understand what these molecules do,” Hillard said. “What we try to contribute to the debate is the reality.”
She said scientific investigation is done in a very neutral way, trying to understand what these molecules do.
“The mass appeal is, ‘is there a good use for this in the treatment of human disease?’” Hillard said. “Most of us really have a passion for looking at these molecules because there is a lot of potential for treatment of human disease.”
The findings of this research are published in scientific journals so that the information is available to anyone. She said sometimes “you have no idea the impact your work is having.” Hillard said part of the mission of the ICRS is to educate the public.
“I wish the politicians would (look at the data) but I don’t think they do,” she said.
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http://norml.org/index.cfm?Group_ID=7002
Emerging Clinical Applications For Cannabis & Cannabinoids
A Review of the Recent Scientific Literature, 2000 — 2011
Despite the ongoing political debate regarding the legality of medical marijuana, clinical investigations of the therapeutic use of cannabinoids are now more prevalent than at any time in history.
For example, in February 2010 investigators at the University of California Center for Medicinal Cannabis Research publicly announced the findings of a series of randomized, placebo-controlled clinical trials on the medical utility of inhaled cannabis. The studies, which utilized the so-called ‘gold standard’ FDA clinical trial design, concluded that marijuana ought to be a “first line treatment” for patients with neuropathy and other serious illnesses.
Among the studies conducted by the Center, four assessed smoked marijuana’s ability to alleviate neuropathic pain, a notoriously difficult to treat type of nerve pain associated with cancer, diabetes, HIV/AIDS, spinal cord injury and many other debilitating conditions. Each of the trials found that cannabis consistently reduced patients’ pain levels to a degree that was as good or better than currently available medications.
Another study conducted by the Center’s investigators assessed the use of marijuana as a treatment for patients suffering from multiple sclerosis. That study determined that “smoked cannabis was superior to placebo in reducing spasticity and pain in patients with MS, and provided some benefit beyond currently prescribed treatments.”
Around the globe, similarly controlled trials are also taking place. A 2010 review by researchers in Germany reports that since 2005 there have been 37 controlled studies assessing the safety and efficacy of marijuana and its naturally occurring compounds in a total of 2,563 subjects. By contrast, most FDA-approved drugs go through far fewer trials involving far fewer subjects.
While much of the renewed interest in cannabinoid therapeutics is a result of the discovery of the endocannabinoid regulatory system (which we describe in detail later in this booklet), some of this increased attention is also due to the growing body of testimonials from medical cannabis patients and their physicians. Nevertheless, despite this influx of anecdotal reports, much of the modern investigation of medical cannabis remains limited to preclinical (animal) studies of individual cannabinoids (e.g. THC or cannabidiol) and/or synthetic cannabinoid agonists (e.g., dronabinol or WIN 55,212-2) rather than clinical trial investigations involving whole plant material. Because of the US government’s strong public policy stance against any use of cannabis, the bulk of this modern cannabinoid research is predictably taking place outside the United States.
As clinical research into the therapeutic value of cannabinoids has proliferated – there are now an estimated 20,000 published papers in the scientific literature analyzing marijuana and its constituents — so too has investigators’ understanding of cannabis’ remarkable capability to combat disease. Whereas researchers in the 1970s, 80s, and 90s primarily assessed cannabis’ ability to temporarily alleviate various disease symptoms — such as the nausea associated with cancer chemotherapy — scientists today are exploring the potential role of cannabinoids to modify disease.
Of particular interest, scientists are investigating cannabinoids’ capacity to moderate autoimmune disorders such as multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease, as well as their role in the treatment of neurological disorders such as Alzheimer’s disease and amyotrophic lateral sclerosis (a.k.a. Lou Gehrig’s disease.) In fact, in 2009, the American Medical Association (AMA) resolved for the first time in the organization’s history “that marijuana’s status as a federal Schedule I controlled substance be reviewed with the goal of facilitating the conduct of clinical research and development of cannabinoid-based medicines.”
Investigators are also studying the anti-cancer activities of cannabis, as a growing body of preclinical and clinical data concludes that cannabinoids can reduce the spread of specific cancer cells via apoptosis (programmed cell death) and by the inhibition of angiogenesis (the formation of new blood vessels). Arguably, these latter findings represent far broader and more significant applications for cannabinoid therapeutics than researchers could have imagined some thirty or even twenty years ago.
THE SAFETY PROFILE OF MEDICAL CANNABIS
Cannabinoids have a remarkable safety record, particularly when compared to other therapeutically active substances. Most significantly, the consumption of marijuana – regardless of quantity or potency — cannot induce a fatal overdose. According to a 1995 review prepared for the World Health Organization, “There are no recorded cases of overdose fatalities attributed to cannabis, and the estimated lethal dose for humans extrapolated from animal studies is so high that it cannot be achieved by … users.”
In 2008, investigators at McGill University Health Centre and McGill University in Montreal and the University of British Columbia in Vancouver reviewed 23 clinical investigations of medical cannabinoid drugs (typically oral THC or liquid cannabis extracts) and eight observational studies conducted between 1966 and 2007. Investigators “did not find a higher incidence rate of serious adverse events associated with medical cannabinoid use” compared to non-using controls over these four decades.
That said, cannabis should not necessarily be viewed as a ‘harmless’ substance. Its active constituents may produce a variety of physiological and euphoric effects. As a result, there may be some populations that are susceptible to increased risks from the use of cannabis, such as adolescents, pregnant or nursing mothers, and patients who have a family history of mental illness. Patients with hepatitis C, decreased lung function (such as chronic obstructive pulmonary disease), or who have a history of heart disease or stroke may also be at a greater risk of experiencing adverse side effects from marijuana. As with any medication, patients should consult thoroughly with their physician before deciding whether the medical use of cannabis is safe and appropriate.
HOW TO USE THIS REPORT
As states continue to approve legislation enabling the physician-supervised use of medical marijuana, more patients with varying disease types are exploring the use of therapeutic cannabis. Many of these patients and their physicians are now discussing this issue for the first time and are seeking guidance on whether the therapeutic use of cannabis may or may not be advisable. This report seeks to provide this guidance by summarizing the most recently published scientific research (2000-2010) on the therapeutic use of cannabis and cannabinoids for 19 clinical indications:
* Alzheimer’s disease
* Amyotrophic lateral sclerosis
* Chronic pain
* Diabetes mellitus
* Dystonia
* Fibromyalgia
* Gastrointestinal disorders
* Gliomas/other cancers
* Hepatitis C
* Human Immunodeficiency Virus
* Hypertension
* Incontinence
* Methicillin-resistant Staphyloccus aureus (MRSA)
* Multiple sclerosis
* Osteoporosis
* Pruritus
* Rheumatoid arthritis
* Sleep apnea
* Tourette’s syndrome
In some of these cases, modern science is now affirming longtime anecdotal reports of medical cannabis users (e.g., the use of cannabis to alleviate GI disorders). In other cases, this research is highlighting entirely new potential clinical utilities for cannabinoids (e.g., the use of cannabinoids to modify the progression of diabetes.)
The conditions profiled in this report were chosen because patients frequently inquire about the therapeutic use of cannabis to treat these disorders. In addition, many of the indications included in this report may be moderated by cannabis therapy. In several cases, preclinical data and clinical data indicate that cannabinoids may halt the progression of these diseases in a more efficacious manner than available pharmaceuticals.
For patients and their physicians, this report can serve as a primer for those who are considering using or recommending medical cannabis. For others, this report can serve as an introduction to the broad range of emerging clinical applications for cannabis and its various compounds.
Paul Armentano
Deputy Director
NORML | NORML Foundation
Washington, DC
January 7, 2011
* The author would like to acknowledge Drs. Dale Gieringer, Dustin Sulak, Gregory Carter, Steven Karch, and Mitch Earleywine, as well as Bernard Ellis, MPH, former NORML interns John Lucy, Christopher Rasmussen, and Rita Bowles, for providing research assistance for this report. The NORML Foundation would also like to acknowledge Dale Gieringer, Paul Kuhn, and Richard Wolfe for their financial contributions toward the publication of this report.
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Gliomas/Cancer
A review of the modern scientific literature reveals numerous preclinical studies and one pilot clinical study demonstrating cannabinoids’ ability to act as antineoplastic agents, particularly on glioma cell lines.Gliomas (tumors in the brain) are especially aggressive malignant forms of cancer, often resulting in the death of affected patients within one to two years following diagnosis. There is no cure for gliomas and most available treatments provide only minor symptomatic relief.
Writing in the September 1998 issue of the journal FEBS Letters, investigators at Madrid’s Complutense University, School of Biology, first reported that delta-9-THC induced apoptosis (programmed cell death) in glioma cells in culture.[1] Investigators followed up their initial findings in 2000, reporting that the administration of both THC and the synthetic cannabinoid agonist WIN 55,212-2 “induced a considerable regression of malignant gliomas” in animals.[2] Researchers again confirmed cannabinoids’ ability to inhibit tumor growth in animals in 2003.[3]
That same year, Italian investigators at the University of Milan, Department of Pharmacology, Chemotherapy and Toxicology, reported that the non-psychoactive cannabinoid, cannabidiol (CBD), inhibited the growth of various human glioma cell lines in vivo and in vitro in a dose dependent manner. Writing in the November 2003 issue of the Journal of Pharmacology and Experimental Therapeutics Fast Forward, researchers concluded, “Non-psychoactive CBD … produce[s] a significant anti-tumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent.”[4]
In 2004, Guzman and colleagues reported that cannabinoids inhibited glioma tumor growth in animals and in human glioblastoma multiforme (GBM) tumor samples by altering blood vessel morphology (e.g., VEGF pathways). Writing in the August 2004 issue of Cancer Research, investigators concluded, “The present laboratory and clinical findings provide a novel pharmacological target for cannabinoid-based therapies.”[5]
More recently, investigators at the California Pacific Medical Center Research Institute reported that the administration of THC on human glioblastoma multiforme cell lines decreased the proliferation of malignant cells and induced cell death more rapidly than did the administration of WIN 55,212-2. Researchers also noted that THC selectively targeted malignant cells while ignoring healthy ones in a more profound manner than the synthetic alternative.[6]
Most recently, Guzman and colleagues reported that THC administration decreases recurrent glioblastoma multiforme tumor growth in patients diagnosed with recurrent GBM. In the first ever pilot clinical trial assessing the use of cannabinoids and GBM, investigators found that the intratumoral administration of THC was associated with reduced tumor cell proliferation in two of nine subjects. “The fair safety profile of THC, together with its possible anti-proliferative action on tumor cells reported here and in other studies, may set the basis for future trials aimed at evaluating the potential antitumoral activity of cannabinoids,” investigators concluded.[7] Several additional investigators have also recently called for further exploration of cannabis-based therapies for the treatment of glioma.[8-10]
In addition to cannabinoids’ ability to moderate glioma cells, separate studies demonstrate that cannabinoids and endocannabinoids can also inhibit the proliferation of other various cancer cell lines, including breast carcinoma,[11-15] prostate carcinoma,[16-18] colorectal carcinoma,[19] gastric adenocarcinoma,[20] skin carcinoma,[21] leukemia cells,[22-23]neuroblastoma,[24] lung carcinoma,[25-26] uterus carcinoma,[27] thyroid epithelioma,[28] pancreatic adenocarcinoma,[29-30], cervical carcinoma,[31] oral cancer,[32] biliary tract cancer (cholangiocarcinoma)[33] and lymphoma.[34-35]
Studies also indicate that the administration of cannabinoids, in conjunction with conventional anti-cancer therapies, can enhance the effectiveness of standard cancer treatments.[36] Most recently, investigators at the University of California, Pacific Medical Center reported that cannabinoids possess synergistic anti-cancer properties — finding that the administration of a combination of the plant’s constituents is superior to the administration of isolated compounds alone.[37]
Consequently, many experts now believe that cannabinoids “may represent a new class of anticancer drugs that retard cancer growth, inhibit angiogenesis and the metastatic spreading of cancer cells.”[38-39]
REFERENCES
[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] 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).
[8] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomas. Expert Reviews of Neurotherapeutics 8: 37-49
[9] Galanti et al. 2007. Delta9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells. Acta Oncologica 12: 1-9.
[10] Calatozzolo et al. 2007. Expression of cannabinoid receptors and neurotrophins in human gliomas. Neurological Sciences 28: 304-310.
[11] Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation. Cancer Research 66: 6615-6621.
[12] 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.
[13] 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.
[14] 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.
[15] Cafferal et al. 2010. Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition. Molecular Cancer 9: 196.
[16] Sarfaraz et al. 2005. Cannabinoid receptors as a novel target for the treatment of prostate cancer. Cancer Research 65: 1635-1641.
[17] Mimeault et al. 2003. Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines. Prostate 56: 1-12.
[18] 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.
[19] 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.
[20] Di Marzo et al. 2006. op. cit
[21] 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.
[22] Powles et al. 2005. Cannabis-induced cytotoxicity in leukemic cell lines. Blood 105: 1214-1221
[23] 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.
[24] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.
[25] Ibid.
[26] 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.
[27] Manuel Guzman. 2003. Cannabinoids: potential anticancer agents (PDF). Nature Reviews Cancer 3: 745-755.
[28] Baek et al. 1998. Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research: 21: 353-356.
[29] Carracedo et al. 2006. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. Cancer Research 66: 6748-6755.
[30] Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and pain. International Journal of Cancer 122: 742-750.
[31] 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.
[32] Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cells. Pharmacology 85: 328-335.
[33] 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.
[34] 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.
[35] 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.
[36] 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.
[37] 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.
[38] Natalya Kogan. 2005. Cannabinoids and cancer. Mini-Reviews in Medicinal Chemistry 5: 941-952.
[39] Sarafaraz et al. 2008. Cannabinoids for cancer treatment: progress and promise. Cancer Research 68: 339-342.
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NCI Recognizes Cancer-Killing Properties Of Cannabis
April 4, 2011
The website of the National Cancer Institute (NCI), a component of the United States National Institutes of Health (NIH), has acknowledged the cancer-fighting properties of marijuana’s active components, but stopped short of recognizing that oncologists may recommend cannabis as an anti-proliferative treatment therapy.
The agency last week added a new section to its cancer.gov website to address the issue of marijuana and cancer. The section, entitled ‘Cannabis and Cannabinoids (PDQ),’ provides “an overview of the use of cannabis and its components as a treatment for people with cancer-related symptoms caused by the disease itself or its treatment.”
The website states that preclinical trials have shown that marijuana’s active compounds may selectively target and inhibit cancer cell growth. “Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis,” the site reads. “Cannabinoids appear to kill tumor cells but do not affect their non-transformed counterparts and may even protect them from cell death.”
The site further states: “The potential benefits of medicinal Cannabis for people living with cancer include antiemetic effects, appetite stimulation, pain relief, and improved sleep.”
However, previous language included in this section of the website stating, “In the practice of integrative oncology, the health care provider may recommend medicinal Cannabis not only for symptom management but also for its possible direct antitumor effect” was removed by site administrators on Monday, March 28.
That portion of the website has been modified to now read, “Though no relevant surveys of practice patterns exist, it appears that physicians caring for cancer patients who prescribe medicinal Cannabis predominantly do so for symptom management.”
New language added to the page further states, “The U.S. Food and Drug Administration (FDA) has not approved the use of Cannabis as a treatment for any medical condition.”
The NCI amended its language after several media outlets reported that their initial assessment “could have an impact on the classification of marijuana as a schedule I drug.” Under federal law, cannabis is defined as a schedule I controlled substance with no recognized medical utility.
In a prepared statement, the NCI stated that its online material should not be viewed as “treatment recommendations and are not representative of any federal policy.” The agency added, “In light of the attention garnered by the PDQ summary statement on ‘Cannabis and Cannabinoids,’ reviewers … reexamined the recently posted statement and decided to change the wording, in order to clarify the meaning that the Board originally intended to convey and to correct several possible misinterpretations.”
For several decades, preclinical studies have documented the anti-cancer activity of cannabinoids and endocannabinoids in various types of cancerous cells, including breast carcinoma, prostate cancer, colorectal carcinoma, skin carcinoma, lung carcinoma, oral cancer, and lymphoma.
United State’s researchers initially documented the anti-tumor effects of cannabinoids in a 1975 study published in the Journal of the National Cancer Institute.
Source: norml.org
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http://www.cannabis-med.org/studies/study.php
I think you should add this link. I am not sure the best way to do it, but it has some good information on it. The heading for the information is below.
Clinical Studies and Case Reports
On this site you will find clinical studies with cannabis or single cannabinoids in different diseases and case reports on the use of cannabis by patients.
You may search for diseases (indications), authors, medication, study design (controlled study, open trial, case report etc.) and other criteria.
Article 7) http://www.safeaccessnow.org/article.php?id=4177
Medical Cannabis Research: What Does the Evidence Say?
Health and Human Services claims that “marijuana has no currently accepted medical use in treatment in the United States.” However, more than 6,500 reports and journal articles from around the world support the medical value of cannabis (marijuana). In addition, dozens of public health organizations have endorsed medical use of marijuana including the National Association of People Living With AIDS, AIDS Action Council, the American Public Health Association, the American Academy of Family Physicians, the American Nurses Association, the Federation of American Scientists, Kaiser Permanente, the New England Journal of Medicine, the National Association for Public Health Policy, the California Medical Association, the Whitman- Walker Clinic, the Lymphoma Foundation of America, and many more.
Here is an overview of the latest research.
CANNABIS SMOKE DOES NO HARM
1. Cannabis Smoking Does Not Cause Cancer
Sources: Tashkin D. Marijuana Use and Lung Cancer: Results of a Case-Control Study. American Thoracic Society International Conference. May 23, 2006, San Diego, California
According to Dr. Donald Tashkin and his colleagues at the University of California in Los Angeles results from a case-controlled study demonstrate that even heavy and long-term smoking of cannabis is not associated with lung cancer and other types of upper aerodigestive tract cancers.
The study included 1,209 residents of Los Angeles aged 18-59 with cancer (611 lung, 403 oral/pharyngeal, 90 laryngeal, and 108 esophageal). Interviewers collected lifetime histories of cannabis, tobacco, alcohol and other drug use, and data on other factors that may influence cancer risk, including diet, occupational exposures, and family history of cancer. Exposure to cannabis was measured in joint years (1 joint year = 365 joints). The cancer patients were compared to 1,040 cancer-free controls. Among the controls 46 per cent had never used cannabis, 31 per cent had used it for less than one joint year, 12 per cent for 10-30 joint years, 2 per cent for 30-60 joint years, and 3 per cent for more than 60 joint years.
Compared with subjects who had used less than one joint year, the risk for lung cancer was 0.78 for 1-10 joint years, 0.74 for 10-30 joint years, 0.85 for 30-60 joint years, and 0.81 for more than 60 joint years. A risk below 1.0 means that the risk for cannabis users was slightly lower than for non-users. Similar results were obtained for the other cancer sites. There was no dose-response relationship of cancer risk, which means that there was no increased risks for more intensive users.
2. Cannabis Does Not Accelerate HIV-infection
Sources: Abrams DI, Hilton JF, Leiser RJ, Shade SB, Elbeik TA, Aweeka FT, Benowitz NL, Bredt BM, Kosel B, Aberg JA, Deeks SG, Mitchell TF, Mulligan K, Bacchetti P, McCune JM, Schambelan M. “Short-term Effects of Cannabinoids in Patients with HIV-1 Infection: A Randomized, Placebo-controlled Clinical Trial.” Annals of Internal Medicine 2003;139(4):258-266
According to a study led by Dr. Donald Abrams at the University of California in San Francisco, smoked cannabis and oral THC given over a course of 21 days did not adversely affect CD4+ cell counts or viral loads in HIV-infected patients. Instead, researchers found that there was a small non-significant positive effect of cannabis and THC on these laboratory parameters compared to placebo. Cannabis and THC also increased appetite and caused weight gain.
All of the patients had been receiving the same anti-HIV medication for at least 8 weeks before the study began. 67 patients with HIV-1 infection were randomly assigned to a 3.95%-tetrahydrocannabinol marijuana cigarette, a 2.5-mg dronabinol (delta-9- tetrahydrocannabinol) capsule, or a placebo capsule three times daily before meals. Although not statistically significant, compared with placebo use the application of marijuana and THC was associated with a slight drop in viral load of 15% and 8%, respectively.
CANNABIS PROVIDES SYMPTOM MANAGEMENT FOR HIV/AIDS, HEP-C, MS and COPD
1. Smoked Cannabis Reduces HIV-Related Painful Peripheral Neuropathy
Sources: Abrams DI, Jay CA, Vizoso H, Shade SB, Reda H, Press S, Kelly ME, Rowbotham M, Petersen K. “Smoked cannabis therapy for HIV-related painful peripheral neuropathy: results of a randomized, placebo-controlled clinical trial.” Abstract, IACM 3rd Conference on Cannabinoids in Medicine, September 9-10, 2005, Leiden
The results of a randomized, placebo-controlled clinical trial demonstrates that smoked marijuana is effective in reducing HIV-related chronic ongoing neuropathic and acute pain. Neuropathy is a nerve disease, which often results in numbness, weakness, and spontaneous muscle twitching. Neuropathy is a serious medical problem with unsatisfactory treatment options.
In a clinical trial at the University of California, research participants smoked one marijuana cigarette containing 3.56% THC or a placebo three times daily for 5 days. Researchers concluded that smoked cannabis provided greater than a 30% reduction of pain in 13 of 25 randomized patients, who averaged 6 years of neuropathic pain.
2. Cannabis Reduces Neuropathic Pain In Multiple Sclerosis Patients
Sources: Rog DJ, Nurmikko TJ, Friede T, Young CA. “Randomized, controlled trial of cannabis-based medicine in central pain in multiple sclerosis”. Neurology 2005;65(6):812-9;
Researchers for the Walton Centre for Neurology and Neurosurgery in Liverpool conducted a single-center, 5-week, randomized, placebo-controlled group trial on patients with MS of a whole-plant cannabis-based medicine delivered via an oral spray. Each spray delivered 2.7mg of THC and 2.5mg of CBD (THC and CBD are two active compounds produced naturally by the cannabis plant), and patients could gradually selftitrate to a maximum of 48 sprays in 24 hours.
The researchers concluded that the cannabis-based extract Sativex, manufactured by GW Pharmaceuticals, is effective in reducing central neuropathic pain and sleep disturbance in people with multiple sclerosis (MS). Based on these study results, which were published now in the journal Neurology, Sativex was approved as a prescription medicine in Canada for the symptomatic relief of neuropathic pain in adults with MS and is available in pharmacies since 20 June 2005.
3. Smoked Cannabis May Help Hep-C Treatment
Sources: Sylvestre, Diana L. a b; Clements, Barry J. b; Malibu, Yvonne b. “Cannabis use improves retention and virological outcomes in patients treated for hepatitis C.” European Journal of Gastroenterology & Hepatology. 18(10):1057-1063, October 2006.
Research published by the European Journal of Gastroenterology and Hepatology conducted at the University of California, San Francisco medical school and the Organization to Achieve Solutions in Substance-Abuse (OASIS) conclude that: “modest cannabis use may offer symptomatic and virological benefit to some patients undergoing HCV treatment by helping them maintain adherence to the challenging medication regimen.” Bottomline, Hep-C patients who used cannabis in combination with their conventional medical treatment were three times more likely to have an undetectable virus level six months after the end of treatment.
Patients with hepatitis C virus (HCV), whose drug regimens include interferon and ribavirin treatments that produce notoriously difficult to manage side effects, researchers discovered that those using cannabis as an adjunct therapy were much more likely to adhere to their prescribed treatment. Researchers found that the HCV patients “were significantly more likely to remain on HCV treatment for at least 80% of the projected treatment duration, 95% versus 67%.”
In a companion article by six addiction treatment specialists, who consider the implications raised by this research, the authors note that “there is substantial evidence that cannabis use may help address key challenges faced by drug users in HCV treatment (e.g., nausea, depression), especially when such treatment occurs in the context of methadone maintenance treatment which may amplify these consequences.” They conclude with a call to action on behalf of patients: “we advocate that in the interim existing barriers to cannabis use are removed for drug users undergoing HCV treatment….”
4. THC Is Effective in Appetite and Weight Loss in Severe Lung Disease
Source: Lecture by K-C Bergmann on 17 March 2005 at the Meeting of the German Society of Pulmonology in Berlin
Patients with the severe lung disease (COPD, chronic obstructive pulmonary disease) often suffer from appetite loss and cachexia (weight loss) resulting in reduced general wellbeing and early mortality. In an open clinical study at the Clinic for Allergies and Asthma in Bad Lippspringe, Germany, 18 COPD patients aged 49 to 81 years with a mean body weight of 48.5 kg received 3.3-4.2mg of THC two times daily for 16 days as oily drops delivered by THC Pharm, one-half an hour before breakfast and dinner. In the six months before entering the clinic 7 participants had a constant body weight and 11 lost 2.3 kg on average.
After 16 days of treatment, results indicated a considerable improvement of appetite, general well-being and functional performance (36 per cent mean increase in walking distance) and an average gain in body weight of 1.5 kg, which is significant given the short treatment period.
CANNABIS COMPOUNDS AND THE POTENTIAL FOR CURES
1. Cannabinoids Reduce the Progression of Alzheimer’s Disease in Animals
Sources: Ramirez BG, et al. “Prevention of Alzheimer’s disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation.” Journal of Neuroscience 2005;25(8):1904-13;
Research by scientists of Madrid’s Complutense University and the Cajal Institute published in the Journal of Neuroscience has demonstrated that cannabinoids can reduce pathological processes associated with Alzheimer’s disease. Researchers hope that cannabinoids may be used to develop new drug therapies against the disease.
They began by comparing the brain tissue of patients who died from Alzheimer’s disease against the brain tissue of healthy people who had died at a similar age. The researchers found a dramatically reduced functioning of cannabinoid receptors in diseased brain tissue and markers of microglia activation. Microglia activate the brain’s immune response and are found near the plaque deposits associated with Alzheimer’s disease. When active, microglia cause inflammation. Nerve cells with cannabinoid-1 receptors (CB1), present in high numbers in control subjects, were greatly reduced in areas of microglial activation.
Next, rats were injected with amyloid-beta peptide. This protein plays an important role in Alzheimer’s disease, since increased brain levels of amyloid-beta are supposed to result in aggregation of this protein to form plaques. Animals who also received different cannabinoids performed better in tests of their mental functioning.
Analyses showed that cannabinoids had prevented microglial activation and thus had reduced inflammation. These effects were also mediated by cannabinoids that only bind to CB2 receptors. Researchers concluded: “Our results indicate that cannabinoid receptors are important in the pathology of AD and that cannabinoids succeed in preventing the neurodegenerative process occurring in the disease.”
2. Derivatives of Cannabis May Unlock Anti-Cancer Treatment
Source: Kogan, N.M., Blaquez, C., Gallily, R., Guzman, M., and Mechoulam, R. “Quinone Type Cannabinoids as AntiCancer Compunds.” Abstract, IACM 3rd Conference on Cannabinoids in Medicine, September 9-10, 2005, Leiden
Researchers at the Hebrew University in Israel have demonstrated that derivatives of the cannabis plant can be effective in arresting cancerous growths in laboratory and animal tests. Natalya Kogan, a Ph.D student working under the direction of Professors Raphael Mechoulam and Michael Schlesinger, has developed new compounds- known as quinonoid cannabinoids – that parallel a group of anti-cancer drugs, the best known which is daunomycin. However, whereas daunomycin is toxic to the heart the quinonoid compounds are significantly less toxic. The development of quinonoid compounds that display anticancer activity, but are less toxic is a major therapeutic goal.
Researchers are particularly interested in the cannabinoid quinone known as HU-331, which was very effective against human cancer cell lines in-vitro and also against in-vivo tumor grafts in nude mice. At 35 days after cancer cell injection, the tumors in the treated group were half the size of the tumors in the control group. Researchers conclude that HU-331 has a high potential as a new anti-cancer drug.
3. Cannabinoids May Promote the Development of New Brain Cells
Sources: Jiang W, Zhang Y, Xiao L, Van Cleemput J, Ji SP, Bai G, Zhang X. “Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects.” Journal of Clinical Investigation. October, 2005
According to animal research at the University of Saskatchewan, Canada, cannabinoids that bind to the CB1 receptor promote the development of new nerve cells in the hippocampus, a brain region that is very important for memory and behavior. This cannabinoid effect may decrease anxiety and depression.
Scientists used the synthetic cannabinoid HU210 that acts similar to THC on CB1 receptors in the brain. Chronic, but not acute treatment with this cannabinoid promoted nerve cell proliferation in the hippocampus of adult rats and exerted anxiolytic- and antidepressant-like effects.
Other illegal and legal drugs, including opiates, alcohol, nicotine and cocaine, have been shown to suppress the formation of new brain cells when used chronically, but the effect of cannabis on that process was uncertain. Cannabis appears “to be the only illicit drug whose capacity to produce increased … neurons is positively correlated with its (antianxiety) and anti-depressant-like effects,” Dr. Xia Zhang and his colleagues wrote in an article for the November issue of the Journal of Clinical Investigation, of which an advance was posted online on 13 October 2005.
Source: safeaccessnow.org