Posts Tagged ‘cannabis studies’
Investigators at the University of Melbourne and the Australian National University, Center for Mental Health Research assessed the impact of cannabis use on various measures of memory and intelligence in over 2,000 self-identified marijuana consumers and non-users over an eight-year period.
Among cannabis consumers, subjects were grouped into the following categories: ‘heavy’ (once a week or more) users, ‘light’ users, ‘former heavy’ users, ‘former light’ users, and ‘always former’ — a category that consisted of respondents who had ceased using marijuana prior to their entry into the study.
Researchers reported: “Only with respect to the immediate recall measure was there evidence of an improved performance associated with sustained abstinence from cannabis, with outcomes similar to those who had never used cannabis at the end point. On the remaining cognitive measures, after controlling for education and other characteristics, there were no significant differences associated with cannabis consumption.”
They concluded, “Therefore, the adverse impacts of cannabis use on cognitive functions either appear to be related to pre-existing factors or are reversible in this community cohort even after potentially extended periods of use.”
Separate studies have previously reported that long-term marijuana use is not associated with residual deficits in neurocognitive function. Specifically, a 2001 study published in the journal Archives of General Psychiatry found that chronic cannabis consumers who abstained from the drug for one week “showed virtually no significant differences from control subjects (those who had smoked marijuana less than 50 times in their lives) on a battery of 10 neuropsychological tests. … Former heavy users, who had consumed little or no cannabis in the three months before testing, [also] showed no significant differences from control subjects on any of these tests on any of the testing days.”
Additionally, studies have also implied that cannabis may be neuroprotective against alcohol-induced cognitive deficits. A 2009 study by investigators at the University of California and San Diego reported that binge drinkers who also used cannabis experienced significantly less white matter damage to the brain as compared to subjects who consumed alcohol alone.
For more information regarding the impact of cannabis on brain function, see NORML’s factsheet ‘Cannabis and the Brain: A User’s Guide,’ here.\
[Editor's note: This post is excerpted from this week's forthcoming NORML weekly media advisory. To have NORML's media alerts and legislative advisories delivered straight to your in-box, sign up here.]
Only fourteen researchers in the United States are legally permitted to conduct research assessing the effect of inhaled cannabis in human subjects, according to data included in the White House’s 2011 National Drug Control Strategy, released last week.
In a section of the report entitled ‘Medical Marijuana,’ the administration states, “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.” However, it later clarifies that of these 109 scientists, only fourteen “are approved to conduct research with smoked marijuana on human subjects.”
Among those scientists licensed to work with either cannabis or its constituents — primarily in animal models — most are involved in research to assess the drug’s “abuse potential, physical/psychological effects, [and] adverse effects,” the report stated.
In 2010, a spokesperson for the US National Institute on Drug Abuse (NIDA) — the federal agency that must approve any US clinical trial involving marijuana – told the New York Times: “[O]ur focus is primarily on the negative consequences of marijuana use. We generally do not fund research focused on the potential beneficial medical effects of marijuana.”
Earlier this month, DEA Administrator Michele Leonhart denied a nine-year-old petition seeking to initiate hearings regarding the federal classification of cannabis as a schedule I substance, stating in part, “[T]here are no adequate and well-controlled studies proving efficacy.”
Commenting on the report, NORML Deputy Director Paul Armentano said: “Only in an environment of absolute criminal prohibition would this or any administration purport to the public that it is acceptable to allow no more than fourteen researchers to clinically study a substance consumed by tens of millions of Americans for therapeutic or recreational purposes. This acknowledgement illustrates once again the administration’s supposed commitment to ‘scientific integrity’ does not apply to cannabis.”
For more information, please contact Allen St. Pierre, NORML Executive Director, at (202) 483-5500 or Paul Armentano, NORML Deputy Director at: email@example.com.
10) MARIJUANA USE HAS NO EFFECT ON MORTALITY:
A massive study of California HMO members funded by the National Institute on Drug Abuse (NIDA) found marijuana use caused no significant increase in mortality. Tobacco use was associated with increased risk of death. Sidney, S et al. Marijuana Use and Mortality. American Journal of Public Health. Vol. 87 No. 4, April 1997. p. 585-590. Sept. 2002.
9) HEAVY MARIJUANA USE AS A YOUNG ADULT WON’T RUIN YOUR LIFE:
Veterans Affairs scientists looked at whether heavy marijuana use as a young adult caused long-term problems later, studying identical twins in which one twin had been a heavy marijuana user for a year or longer but had stopped at least one month before the study, while the second twin had used marijuana no more than five times ever. Marijuana use had no significant impact on physical or mental health care utilization, health-related quality of life, or current socio-demographic characteristics. Eisen SE et al. Does Marijuana Use Have Residual Adverse Effects on Self-Reported Health Measures, Socio-Demographics or Quality of Life? A Monozygotic Co-Twin Control Study in Men. Addiction. Vol. 97 No. 9. p.1083-1086. Sept. 1997
8) THE “GATEWAY EFFECT” MAY BE A MIRAGE:
Marijuana is often called a “gateway drug” by supporters of prohibition, who point to statistical “associations” indicating that persons who use marijuana are more likely to eventually try hard drugs than those who never use marijuana – implying that marijuana use somehow causes hard drug use. But a model developed by RAND Corp. researcher Andrew Morral demonstrates that these associations can be explained “without requiring a gateway effect.” More likely, this federally funded study suggests, some people simply have an underlying propensity to try drugs, and start with what’s most readily available. Morral AR, McCaffrey D and Paddock S. Reassessing the Marijuana Gateway Effect. Addiction. December 2002. p. 1493-1504.
7) PROHIBITION DOESN’T WORK (PART I):
The White House had the National Research Council examine the data being gathered about drug use and the effects of U.S. drug policies. NRC concluded, “the nation possesses little information about the effectiveness of current drug policy, especially of drug law enforcement.” And what data exist show “little apparent relationship between severity of sanctions prescribed for drug use and prevalence or frequency of use.” In other words, there is no proof that prohibition – the cornerstone of U.S. drug policy for a century – reduces drug use. National Research Council. Informing America’s Policy on Illegal Drugs: What We Don’t Know Keeps Hurting Us. National Academy Press, 2001. p. 193.
6) PROHIBITION DOESN’T WORK (PART II):
(DOES PROHIBITION CAUSE THE “GATEWAY EFFECT”?): U.S. and Dutch researchers, supported in part by NIDA, compared marijuana users in San Francisco, where non-medical use remains illegal, to Amsterdam, where adults may possess and purchase small amounts of marijuana from regulated businesses. Looking at such parameters as frequency and quantity of use and age at onset of use, they found no differences except one: Lifetime use of hard drugs was significantly lower in Amsterdam, with its “tolerant” marijuana policies. For example, lifetime crack cocaine use was 4.5 times higher in San Francisco than Amsterdam. Reinarman, C, Cohen, PDA, and Kaal, HL. The Limited Relevance of Drug Policy: Cannabis in Amsterdam and San Francisco. American Journal of Public Health. Vol. 94, No. 5. May 2004. p. 836-842.
5) OOPS, MARIJUANA MAY PREVENT CANCER (PART I):
Federal researchers implanted several types of cancer, including leukemia and lung cancers, in mice, then treated them with cannabinoids (unique, active components found in marijuana). THC and other cannabinoids shrank tumors and increased the mice’s lifespans. Munson, AE et al. Antineoplastic Activity of Cannabinoids. Journal of the National Cancer Institute. Sept. 1975. p. 597-602.
4) OOPS, MARIJUANA MAY PREVENT CANCER, (PART II):
In a 1994 study the government tried to suppress, federal researchers gave mice and rats massive doses of THC, looking for cancers or other signs of toxicity. The rodents given THC lived longer and had fewer cancers, “in a dose-dependent manner” (i.e. the more THC they got, the fewer tumors). NTP Technical Report On The Toxicology And Carcinogenesis Studies Of 1-Trans- Delta-9-Tetrahydrocannabinol, CAS No. 1972-08-3, In F344/N Rats And B6C3F Mice, Gavage Studies. See also, “Medical Marijuana: Unpublished Federal Study Found THC-Treated Rats Lived Longer, Had Less Cancer,” AIDS Treatment News no. 263, Jan. 17, 1997.
3) OOPS, MARIJUANA MAY PREVENT CANCER (PART III):
Researchers at the Kaiser-Permanente HMO, funded by NIDA, followed 65,000 patients for nearly a decade, comparing cancer rates among non-smokers, tobacco smokers, and marijuana smokers. Tobacco smokers had massively higher rates of lung cancer and other cancers. Marijuana smokers who didn’t also use tobacco had no increase in risk of tobacco-related cancers or of cancer risk overall. In fact their rates of lung and most other cancers were slightly lower than non-smokers, though the difference did not reach statistical significance. Sidney, S. et al. Marijuana Use and Cancer Incidence (California, United States). Cancer Causes and Control. Vol. 8. Sept. 1997, p. 722-728.
2) OOPS, MARIJUANA MAY PREVENT CANCER (PART IV):
Donald Tashkin, a UCLA researcher whose work is funded by NIDA, did a case-control study comparing 1,200 patients with lung, head and neck cancers to a matched group with no cancer. Even the heaviest marijuana smokers had no increased risk of cancer, and had somewhat lower cancer risk than non-smokers (tobacco smokers had a 20-fold increased lung cancer risk). Tashkin D. Marijuana Use and Lung Cancer: Results of a Case-Control Study. American Thoracic Society International Conference. May 23, 2006.
1) MARIJUANA DOES HAVE MEDICAL VALUE:
In response to passage of California’s medical marijuana law, the White House had the Institute of Medicine (IOM) review the data on marijuana’s medical benefits and risks. The IOM concluded, “Nausea, appetite loss, pain and anxiety are all afflictions of wasting, and all can be mitigated by marijuana.” While noting potential risks of smoking, the report added, “we acknowledge that there is no clear alternative for people suffering from chronic conditions that might be relieved by smoking marijuana, such as pain or AIDS wasting.” The government’s refusal to acknowledge this finding caused co-author John A. Benson to tell the New York Times that the government “loves to ignore our report … they would rather it never happened.” Joy, JE, Watson, SJ, and Benson, JA. Marijuana and Medicine: Assessing the Science Base. National Academy Press. 1999. p. 159. See also, Harris, G. FDA Dismisses Medical Benefit From Marijuana. New York Times. Apr.
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NORML Foundation/Senior Policy Analyst“Cannabinoids possess … anticancer activity [and may] possibly represent a new class of anti-cancer drugs that retard cancer growth, inhibit angiogenesis (the formation of new blood vessels) and the metastatic spreading of cancer cells.” So concludes a comprehensive review published in the October 2005 issue of the scientific journal Mini-Reviews in Medicinal Chemistry.Not familiar with the emerging body of research touting cannabis’ ability to stave the spread of certain types of cancers? You’re not alone.For over 30 years, US politicians and bureaucrats have systematically turned a blind eye to scientific research indicating that marijuana may play a role in cancer prevention — a finding that was first documented in 1974. That year, a research team at the Medical College of Virginia (acting at the behest of the federal government) discovered that cannabis inhibited malignant tumor cell growth in culture and in mice. According to the study’s results, reported nationally in an Aug. 18, 1974, Washington Post newspaper feature, administration of marijuana’s primary cannabinoid THC, “slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent.”Despite these favorable preclinical findings, US government officials dismissed the study (which was eventually published in the Journal of the National Cancer Institute in 1975), and refused to fund any follow-up research until conducting a similar — though secret — clinical trial in the mid-1990s. That study, conducted by the US National Toxicology Program to the tune of $2 million concluded that mice and rats administered high doses of THC over long periods experienced greater protection against malignant tumors than untreated controls.Rather than publicize their findings, government researchers once again shelved the results, which only came to light after a draft copy of its findings were leaked in 1997 to a medical journal, which in turn forwarded the story to the national media.Nevertheless, in the decade since the completion of the National Toxicology trial, the U.S. government has yet to encourage or fund additional, follow up studies examining the cannabinoids’ potential to protect against the spread cancerous tumors.Fortunately, scientists overseas have generously picked up where US researchers so abruptly left off. In 1998, a research team at Madrid’s Complutense University discovered that THC can selectively induce apoptosis (program cell death) in brain tumor cells without negatively impacting the surrounding healthy cells. Then in 2000, they reported in the journal Nature Medicine that injections of synthetic THC eradicated malignant gliomas (brain tumors) in one-third of treated rats, and prolonged life in another third by six weeks.In 2003, researchers at the University of Milan in Naples, Italy, reported that non-psychoactive compounds in marijuana inhibited the growth of glioma cells in a dose dependent manner and selectively targeted and killed malignant cancer cells.The following year, researchers reported in the journal of the American Association for Cancer Research that marijuana’s constituents inhibited the spread of brain cancer in human tumor biopsies. In a related development, a research team from the University of South Florida further noted that THC can also selectively inhibit the activation and replication of gamma herpes viruses. The viruses, which can lie dormant for years within white blood cells before becoming active and spreading to other cells, are thought to increase one’s chances of developing cancers such as Karposis Sarcoma, Burkitts lymphoma, and Hodgkins disease.More recently, investigators published pre-clinical findings demonstrating that cannabinoids may play a role in inhibiting cell growth of colectoral cancer, skin carcinoma, breast cancer, and prostate cancer, among other conditions. When investigators compared the efficacy of natural cannabinoids to that of a synthetic agonist, THC proved far more beneficial – selectively decreasing the proliferation of malignant cells and inducing apoptosis more rapidly than its synthetic alternative while simultaneously leaving healthy cells unscathed.Nevertheless, US politicians have been little swayed by these results, and remain steadfastly opposed to the notion of sponsoring – or even acknowledging – this growing body clinical research, preferring instead to promote the unfounded notion that cannabis use causes cancer. Until this bias changes, expect the bulk of research investigating the use of cannabinoids as anticancer agents to remain overseas and, regrettably, overlooked in the public discourse.”
Gliomas/Brain Cancerby Paul ArmentanoNORML Foundation/Senior Policy AnalystGliomas (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.A review of the modern scientific literature reveals numerous preclinical studies and one pilot clinical study demonstrating cannabinoids’ ability to act as anti-neoplastic agents, particularly on glioma cell lines.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. 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. Researchers again confirmed cannabinoids’ ability to inhibit tumor growth in animals in 2003.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 anti neoplastic agent.”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.”
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, gastric adenocarcinoma, skin carcinoma, leukemia cells,[22-23]neuroblastoma, lung carcinoma,[25-26] uterus carcinoma, thyroid epithelioma, pancreatic adenocarcinoma,[29-30], cervical carcinoma, oral cancer, biliary tract cancer (cholangiocarcinoma) 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. 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.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]
 Guzman et al. 1998. Delta-9-tetrahydrocannabinol induces apoptosis in C6 glioma cells. FEBS Letters 436: 6-10.
 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.
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.
 Allister et al. 2005. Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells. Journal of Neurooncology 74: 31-40.
 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
 Galanti et al. 2007. Delta9-Tetrahydrocannabinol inhibits cell cycle progression by downregulation of E2F1 in human glioblastoma multiforme cells. Acta Oncologica 12: 1-9.
 Calatozzolo et al. 2007. Expression of cannabinoid receptors and neurotrophins in human gliomas. Neurological Sciences 28: 304-310.
 Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation. Cancer Research 66: 6615-6621.
 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.
 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.
 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.
 Cafferal et al. 2010. Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition.Molecular Cancer 9: 196.
 Sarfaraz et al. 2005. Cannabinoid receptors as a novel target for the treatment of prostate cancer. Cancer Research 65: 1635-1641.
 Mimeault et al. 2003. Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines.Prostate 56: 1-12.
 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.
 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.
 Di Marzo et al. 2006. op. cit
 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.
 Powles et al. 2005. Cannabis-induced cytotoxicity in leukemic cell lines. Blood 105: 1214-1221
 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.
 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.
 Baek et al. 1998. Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Archives of Pharmacal Research: 21: 353-356.
 Carracedo et al. 2006. Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. Cancer Research 66: 6748-6755.
 Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and pain. International Journal of Cancer 122: 742-750.
 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.
 Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cells. Pharmacology 85: 328-335.
 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.
 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.
 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.
 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.
 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.
 Sarafaraz et al. 2008. Cannabinoids for cancer treatment: progress and promise. Cancer Research 68: 339-342.
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|Mr. Worth Repeating: former NYPD cop, former high school health teacher, the unstoppable Ron Marczyk, R.N., Toke of the Town columnist|
Editor’s note: Ron Marczyk is a retired high school health education teacher who taught Wellness and Disease Prevention, Drug and Sex Ed, and AIDS education to teens aged 13-17. He also taught a high school International Baccalaureate psychology course. He taught in a New York City public school as a Drug Prevention Specialist. He is a Registered Nurse with six years of ER/Critical Care experience in NYC hospitals, earned an M.S. in cardiac rehabilitation and exercise physiology, and worked as a New York City police officer for two years. Currently he is focused on how evolutionary psychology explains human behavior.