Posts Tagged ‘marijuana studies’

Genetic Code of Cannabis Reported Unlocked

(CBS News)  A small Massachusetts-based company says it has successfully sequenced a marijuana plant, paving the way for more research into the therapeutic effects of Cannabis – including its potential for treating cancer and inflammatory diseases.
Medicinal Genomics published the raw sequence strings at midnight. The company’s findings have not yet undergone peer review. Medicinal Genomics put the data up on Amazon.com’s EC2 cloud- computing system.The more than 131 billion bases of sequence, which is believed to constitute the largest known gene collection of the Cannabis genomes so far, will be made available to the scientific public sometime this fall.
The breakthrough also raises the possibility that researchers will eventually be able to weed out – no pun intended – the psychoactive effects pot smoking has on people while enhancing the medicinal aspects of Cannabis.
It’s only happenstance but Medicinal Genomics is headquartered both in Marblehead, Mass. and Amsterdam, where the company’s research facilities are found.
“This is the beginning of a more scientific approach to the genetics of the species,” Richard Gibbs, director of the Human Genome Sequencing Center at the Baylor College of Medicine in Houston, told Bloomberg. “This is not really about marijuana; it’s about pharmacology.”

Marijuana Users Ain’t “Stupid Stoners”

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By NORML on Jul 27, 2011

The consumption of cannabis, even long-term, poses few adverse effects on cognitive performance, according to clinical trial data to be published in the scientific journal Addiction.

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.]

Marijuana Does Not Cause Long Term Cognitive Impairment

Cannabis Brain

Study: Marijuana Not Linked With Long Term Cognitive Impairment

By Maia Szalavitz

The idea that “marijuana makes you dumb” has long been embodied in the stereotype of the slow, stupid stoner, seen in numerous Hollywood movies and TV comedies and going unquestioned by much of American culture. But a new study says no: the researchers followed nearly 2,000 young Australian adults for eight years and found that marijuana has little long-term effect on learning and memory— and any cognitive damage that does occur as a result of cannabis use is reversible.

Participants were aged 20-24 at the start of the study, which was part of a larger project on community health.  Researchers categorized them as light, heavy, former or non-users of cannabis based on their answers to questions about  marijuana habits.

Light use was defined as smoking monthly or less frequently; heavy use was weekly or more often. Former users had to have not smoked for at least a year. Fully 72% of the participants were non-users or former users; 18% were light users and 9% were heavy current users. Prior studies have found that drug users do accurately report their consumption levels in surveys like this as long as anonymity is guaranteed and there are no negative consequences for telling the truth.

Participants took tests of memory and intelligence three times over the eight year period the study. They were also asked about how their marijuana use had changed. When the results were at last tabulated, researchers found that there were large initial differences between the groups, with the current marijuana smokers performing worse on tests that required them to recall lists of words after various periods of time or remember numbers in the reverse order from the one in which they were presented.

However, when the investigators controlled for factors like education and gender, almost all of these differences disappeared.  The lower education levels of the pot smokers — and their greater likelihood of being male — had made it look like marijuana had significantly affected their intelligence.  In fact, men simply tend to do worse than women on tests of verbal intelligence, while women generally underperform on math tests. The relative weighting of the tests made the impact of pot  look worse than it was.

Researchers then explored whether quitting cannabis would affect the one difference that remained, which was poorer performance by heavy users on a test that required immediate recall of a list of nouns.  They found that heavy users who had quit by the end of the study were no longer distinguishable on this measure from those who had never used.

The authors, who were led by Robert Tait at the Centre for Mental Health Research at Australian National University, conclude:

[T]he 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. These findings may be useful in motivating individuals to lower cannabis use, even after an extensive history of heavy intake.

But what about all the prior research linking cannabis with lasting negative effects on cognition? Those studies may have been confounded by the fact that in many cases, heavy users were tested after being abstinent for only one day — so their performance could have been affected either by residual marijuana in their systems or by irritability or other effects of withdrawal.  Studies that have looked at heavy users after longer periods of abstinence generally concur with the new research, finding no lingering effect on cognition.

Other research concludes that the “stupid stoner” image itself can impair performance, with subjects essentially living down to what’s expected of them.  But the literature overall now suggests that those “I’m not as think as you stoned I am,” moments are likely limited to the high itself.

The research was published in the journal Addiction.

Medical Marijuana Research Conference To Be Held in Illinois

cannabis science

International Medical Marijuana Research Conference Held This Week Near Chicago
White House sponsors conference only days after it threatens medical marijuana states

Chicago, IL — Starting tomorrow, the International Cannabinoid Research Society (ICRS) will hold its 21st annual symposium in St. Charles, Illinois, just outside of Chicago . Notably, this year’s symposium is sponsored in part by an array of pharmaceutical companies, the U.S. National Institute on Drug Abuse (NIDA), and ElSohly Laboratories, Inc., the federal government’s only licensed source of research-grade cannabis (marijuana) used in therapeutic studies. The symposium features poster presentations by four members of the Multidisciplinary Scientific Advisory Board of Americans for Safe Access — Dr. William Courtney, Dr. Jeff Hergenrather, Jahan Marcu and Dr. Amanda Reiman.

This important public health symposium is taking place less than a week after Deputy Attorney General James Cole inconspicuously issued a memorandum on June 29th to U.S Attorneys, defending the government’s threats of criminal prosecution against local and state officials, as well as others producing or distributing medical marijuana even if such actions are legal under state law. Rarely has the federal government threatened public officials over the development and passage of their own public health laws.

“This symposium and its sponsors shows that medical cannabis is a valid medication that has been recognized and studied by scientists right under our noses,” said Steph Sherer, Executive Director of Americans for Safe Access (ASA), the country’s leading medical marijuana advocacy group. “meanwhile, the federal government continues its antiquated, political campaign to undermine the ability of millions of patients to safely and legally obtain their medication.”

Part of what’s happening this week includes a presentation by Temple University doctoral student, ASA Advisory Board member, and cannabinoid researcher Jahan Marcu, focusing on research around cannabinoid receptors in the brain to better understand how and which parts of the cannabis plant work best with the human body. Marcu previously published findings in the Journal of Molecular Cancer Therapeutics on a study showing enhanced anti-cancer effects with certain compounds found in the cannabis plant. For his presentation in 2009, Marcu received the prestigious “Billy Martin Award” from the ICRS.

Dr. Amanda Reiman will be presenting on dispensary-based research and models for patient access to whole-plant medicine. While an ASA Advisory Board member, Reiman was also a postdoctoral fellow in the School of Public Health at the University of California, Berkeley, and is currently a medical cannabis researcher who regularly presents at ICRS and other related conferences. Reiman’s research on the impact of localized medical marijuana distribution on patients is particularly relevant given the federal effort to undermine the regulation of such facilities.

“The federal government cannot both support medical marijuana and undermine its legal implementation,” continued Sherer. “This contradictory policy must end.” The government has multiple options currently available, not the least of which is a 9-year-old petition to reclassify marijuana now pending before the Drug Enforcement Administration, as well as Congressional legislation recently introduced by Rep. Barney Frank (D-MA), HR 1983, which also calls for rescheduling marijuana from its position as a dangerous drug with no medical value.

Available for Interviews:
ASA Advisory Board members presenting at the ICRS symposium
Dr. Jeff Hergenrather 707-823-3000
Dr. Amanda Reiman 510-847-2405
Jahan Marcu 215-828-9183
Dr. William Courtney 707-353-0627

Further information:
International Cannabinoid Research Society symposium: http://www.icrs2011.org/
Last week’s memo from U.S. Deputy Attorney General James Cole: http://AmericansForSafeAccess.org/downloads/James_Cole_memo_06_29_2011.pdf

Top 10 Cannabis Studies The Government Wishes It Didn’t Fund

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.
21, 2006

Worth Repeating: Over 50 Studies Show Cannabis is Medicine

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Graphic: The Truth Source

​Welcome to Room 420, where your instructor is Mr. Ron Marczyk and your subjects are wellness, disease prevention, self actualization, and chillin’.


Worth Repeating
​By Ron Marczyk, R.N.
Health Education Teacher (Retired)
The quote below, from a news release, is a political statement that is based on incomplete and biased science. Remember, once science is politicized, it is no longer science.
“No sound scientific studies supported medical use of marijuana for treatment in the United States, and no animal or human data supported the safety or efficacy of marijuana for general medical use.”
Not true! An overwhelming number of studies exist to firmly support cannabis as all-purpose medicine and very possibly a strong candidate as a cure for cancer as was originally reported by the National Cancer Institute.
There has never been a single documented primary human fatality from overdosing on cannabis in its natural form in any amount. How’s that for safety!

In addition, cannabis can be vaporized or eaten in sweets, which takes the smoking issue off the table!  And as counter-intuitive as its sounds, evidence exists that cannabis offers a mild protective effect against cancer.
marijuana-bottle.jpeg
Photo: THC Finder
​ I would like to bring attention to the 50+ empirical studies (footnoted below) that may have been overlooked by the FDA in their “thoroughly analyzed search of all the relevant medical, scientific data” on medical cannabis.
“In 2001, the Food and Drug Administration (FDA) and the Drug Enforcement Administration thoroughly analyzed the relevant medical, scientific, and abuse data and concluded that marijuana continues to meet the criteria for placement in schedule I of the Controlled Substances Act. The Food and Drug Administration reiterated this determination in April 2006, stating in a news release:
“Marijuana is listed in Schedule I of the Controlled Substances Act (CSA), the most restrictive schedule. The Drug Enforcement Administration (DEA), which administers the CSA, continues to support that placement and FDA concurred because marijuana met the three criteria for placement in Schedule I under 21 U.S.C. 812(b)(1) (e.g., marijuana has a high potential for abuse, has no currently accepted medical use in treatment in the United States, and has a lack of accepted safety for use under medical supervision).
“Furthermore, there is currently sound evidence that smoked marijuana is harmful. A past evaluation by several Department of Health and Human Services (HHS) agencies, including the Food and Drug Administration (FDA), Substance Abuse and Mental Health Services Administration (SAMHSA) and National Institute for Drug Abuse (NIDA), concluded that no sound scientific studies supported medical use of marijuana for treatment in the United States, and no animal or human data supported the safety or efficacy of marijuana for general medical use. There are alternative FDA-approved medications in existence for treatment of many of the proposed uses of smoked marijuana.” (Source: justice.gov)
Empirically Based Evidence Supporting Medical Cannabis
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.”
Thanks, Paul.
The following current research studies all provide overwhelming evidence that THC holds the promise of being a non-toxic multipurpose chemotherapy agent that may have anti-tumor action on many different types of cancer.
THC and synthetic cannabinoids both have similar action on CB1/2 receptors, and seem to work best in combination, just as ingesting cannabis as a whole plant produces its wide spectrum healing effects, such as relieving vomiting, being able eat, having no physical pain and being able to sleep. This is how the body heals itself.
Medical cannabis is a family of unique cannabinoids  that also have antiemetic effects, appetite stimulation, pain relief, and improved sleep, as reported by the National Cancer Institute:   http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page5
These four medically proven cancer treatment effects of cannabis on their own totally disprove the FDA statement, but with an anti-tumor effect added, as also reported by NCI, this plant becomes a “Swiss survival knife”of medicines.  Imagine that – one drug that treats five different medical conditions at once!
A quick search of Wikipedia yields the following five studies:
“Investigators at Madrid’s Complutense University, School of Biology, first reported that THC induced apoptosis (programmed cell death) in glioma cells in culture”[1a]
“Investigators followed up their initial findings, reporting that the administration of both THC and the synthetic cannabinoid agonist WIN55-212-2 induced a considerable regression of malignant gliomas in animals” [2b]
“Researchers again confirmed cannabinoids’ ability to inhibit tumor growth in animals in 2003″[3c]
“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”[4d]
“Consequently, many experts now believe that cannabinoids may represent a new class of anticancer drugs that retard cancer growth, inhibit angiogenesis and the metastic spreading of cancer cells [5e] and have recommended that at least one cannabinoid, cannabidiol, now be utilized in cancer therapy.”
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Gliomas/Brain Cancer
by Paul Armentano
NORML Foundation/Senior Policy Analyst
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.
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.[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 anti neoplastic 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]
Five Other Studies Found on pub.Med. Relating to Gliomas
1. Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells.
J Clin Invest. 2009 May;119(5):1359-72     Department of Biochemistry and Molecular Biology, Complutense University, Madrid, Spain.
FINDINGS:
Autophagy can promote cell survival or cell death, but the molecular basis underlying its dual role in cancer remains obscure. Here we demonstrate that delta(9)-tetrahydrocannabinol (THC), the main active component of marijuana, induces human glioma cell death through stimulation of autophagy.
The finding of this study describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.
From this study:
Glioma photo 1.jpeg
Graphic: J. Clin. Invest.
In the image above, the blue is just staining for the nucleus, and it shows where the nucleus is and that there are cells there. The green is staining for the LC3 with or without treatment (shown on the top) in the presence of small inhibitors made of RNA (siC, sip8, siTRB3)-(shown on the side of each panel). The red is control for those inhibitors used (random siRNA) that just shows that the inhibitors that they used targeted the intended genes.

Cancer Res. 2001 Aug 1;61(15):5784-9. Dept of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.
FINDINGS:
The development of new therapeutic strategies is essential for the management of gliomas, one of the most malignant forms of cancer. We have shown previously that the growth of the rat glioma C6 cell line is inhibited by psychoactive cannabinoids.  These compounds act on the brain and some other organs through the widely expressed CB(1) receptor. By contrast, the other cannabinoid receptor subtype, the CB(2) receptor, shows a much more restricted distribution and is absent from normal brain. Cannabinoid receptor expression was subsequently examined in biopsies from human astrocytomas.
A full 70 percent (26 of 37) of the human astrocytomas analyzed expressed significant levels of cannabinoid receptors. Of interest, the extent of CB(2) receptor expression was directly related with tumor malignancy.
Nat Med. 2000 Mar;6(3):313-9.  Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040-Madrid, Spain.
FINDINGS:
Delta 9-Tetrahydrocannabinol, the main active component of marijuana, induces apoptosis of transformed neural cells in culture. Here, we show that intratumoral administration of Delta9-tetrahydrocannabinol and the synthetic cannabinoid agonist WIN-55,212-2 induced a considerable regression of malignant gliomas in Wistar rats and in mice deficient in recombination activating gene.
Cannabinoid treatment did not produce any substantial neurotoxic effect in the conditions used. Experiments with two subclones of C6 glioma cells in culture showed that cannabinoids signal apoptosis by a pathway involving cannabinoid receptors, sustained ceramide accumulation and Raf1/extracellular signal-regulated kinase activation. These results may provide the basis for a new therapeutic approach for the treatment of malignant gliomas.
Neuropharmacology. 2004 Sept.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Avenida Complutense, sn, 28040 Madrid, Spain.
Abstract
Gliomas, in particular glioblastoma multiforme or grade IV astrocytoma, are the most frequent class of malignant primary brain tumours and one of the most aggressive forms of cancer. Current therapeutic strategies for the treatment of glioblastoma multiforme are usually ineffective or just palliative. During the last few years, several studies have shown that cannabinoids — the active components of the plant Cannabis sativa and their derivatives –slow the growth of different types of tumours, including gliomas, in laboratory animals.
Remarkably, cannabinoids kill glioma cells selectively and can protect non-transformed glial cells from death. These and other findings reviewed here might set the basis for a potential use of cannabinoids in the management of gliomas.

British Journal of Cancer 2006   Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid 28040, Spain
FINDINGS:
Delta 9-Tetrahydrocannabinol (THC) and other cannabinoids inhibit tumour growth and angiogenesis in animal models, so their potential application as antitumoral drugs has been suggested. However, the antitumoral effect of cannabinoids has never been tested in humans. Here we report the first clinical study aimed at assessing cannabinoid antitumoral action, specifically a pilot phase I trial in which nine patients with recurrent glioblastoma multiforme were administered THC intratumorally.
The patients had previously failed standard therapy (surgery and radiotherapy) and had clear evidence of tumour progression. The primary end point of the study was to determine the safety of intracranial THC administration. We also evaluated THC action on the length of survival and various tumour-cell parameters. A dose escalation regimen for THC administration was assessed. Cannabinoid delivery was safe and could be achieved without overt psychoactive effects. Median survival of the cohort from the beginning of cannabinoid administration was 24 weeks (95% confidence interval: 15-33). 9-Tetrahydrocannabinol inhibited tumour-cell proliferation in vitro and decreased tumour-cell Ki67 immunostaining when administered to two patients. The fair safety profile of THC, together with its possible antiproliferative action on tumour cells reported here and in other studies, may set the basis for future trials aimed at evaluating the potential antitumoral activity of cannabinoids.
CANCER IN GENERAL 
From Paul Armentano at NORML:
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]
Studies found on Pub. Med.
Cancer Cell. 2006 Apr;9(4):301-12.
Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain.
FINDINGS: One of the most exciting areas of current research in the cannabinoid field is the study of the potential application of these compounds as antitumoral drugs. Here, we describe the signaling pathway that mediates cannabinoid-induced apoptosis of tumor cells. By using a wide array of experimental approaches, we identify the stress-regulated protein p8 as an essential mediator of cannabinoid antitumoral action. Activation of this pathway may constitute a potential therapeutic strategy for inhibiting tumor growth.
Curr Clin Pharmacol. 2010 Nov 1;5(4):281-7.
Division of Cellular and Molecular Medicine (Oncology), St George’s University of London, London, UK. w.liu@sgul.ac.uk
FINDINGS:
• Cannabinoids, the active components of the cannabis plant, have some clinical merit both as an anti-emetic and appetite stimulant in patients. Recently, interest in developing cannabinoids as therapies has increased following reports that they possess anti-tumour properties.
• Research into cannabinoids as anti-cancer agents is in its infancy, and has mainly focused on the pro-apoptotic effects of this class of agent. Impressive anti-cancer activities have been reported; actions that are mediated in large part by disruptions to ubiquitous signalling pathways such as ERK and PI3-K.
• However, recent developments have highlighted a putative role for cannabinoids as anti-inflammatory agents. Chronic inflammation has been associated with neoplasia for sometime, and as a consequence, reducing inflammation as a way of impacting cancer presents a new role for these compounds. This article reviews the ever-changing relationship between cannabinoids and cancer, and updates our understanding of this class of agent. Furthermore, the relationship between chronic inflammation and cancer, and how cannabinoids can impact this relationship will be described.
Neuropharmacology. 2004 Sept
Chemoprevention Program, Paul P. Carbone Comprehensive Cancer Center and Dept of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin 53706, USA.
FINDINGS:
Cannabinoids are a class of pharmacologic compounds that offer potential applications as antitumor drugs, based on the ability of some members of this class to limit inflammation, cell proliferation, and cell survival. In particular, emerging evidence suggests that agonists of cannabinoid receptors expressed by tumor cells may offer a novel strategy to treat cancer. Here, we review recent work that raises interest in the development and exploration of potent, nontoxic, and nonhabit forming cannabinoids for cancer therapy.

Best Pract Res Clin Endocrinol Metab. 2009 Feb.
Department of Pharmaceutical Sciences, University of Salerno, Italy.
FINDINGS:
Cannabinoids (the active components of Cannabis sativa) and their derivatives have received renewed interest in recent years due to their diverse pharmacological activities. In particular, cannabinoids offer potential applications as anti-tumour drugs, based on the ability of some members of this class of compounds to limit cell proliferation and to induce tumour-selective cell death.
Although synthetic cannabinoids may have pro-tumour effects in vivo due to their immunosuppressive properties, predominantly inhibitory effects on tumour growth and migration, angiogenesis, metastasis, and also inflammation have been described. Emerging evidence suggests that agonists of cannabinoid receptors expressed by tumour cells may offer a novel strategy to treat cancer. In this chapter we review the more recent results generating interest in the field of cannabinoids and cancer, and provide novel suggestions for the development, exploration and use of cannabinoid agonists for cancer therapy, not only as palliative but also as curative drugs.
BREAST CANCER
Cancer Lett. 2009 Nov 18;285(1):6-12. Epub 2009 May 12.Dept of Pharmacology and Toxicology, University of Otago, Dunedin, New Zealand.
FINDINGS:
Cannabinoids, the active components of the hemp plant Cannabis sativa, along with their endogenous counterparts and synthetic derivatives, have elicited anti-cancer effects in many different in vitro and in vivo models of cancer. While the various cannabinoids have been examined in a variety of cancer models, recent studies have focused on the role of cannabinoid receptor agonists (both CB(1) and CB(2)) in the treatment of estrogen receptor-negative breast cancer. This review will summarize the anti-cancer properties of the cannabinoids, discuss their potential mechanisms of action, as well as explore controversies surrounding the results.
CERVICAL CANCER
J Natl Cancer Inst. 2008 Jan 2;100(1):59-69. Epub 2007 Dec 25.
Institute of Toxicology and Pharmacology, University of Rostock, Schillingallee 70, Rostock D-18057, Germany.
BACKGROUND:
Cannabinoids, in addition to having palliative benefits in cancer therapy, have been associated with anticarcinogenic effects. Although the antiproliferative activities of cannabinoids have been intensively investigated, little is known about their effects on tumor invasion. we found that ..
FINDINGS:
Increased expression of TIMP-1 mediates an anti-invasive effect of cannabinoids. Cannabinoids may therefore offer a therapeutic option in the treatment of highly invasive cancers.
PROSTATE CANCER
Cancer Res. 2005 Mar 1;65(5):1635-41
Department of Dermatology, University of Wisconsin, Madison, Wisconsin 53706, USA.
FINDINGS:
Cannabinoids, the active components of Cannabis sativa  (marijuana) and their derivatives have received renewed interest in recent years due to their diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory effects and tumor regression.
Here we show that expression levels of both cannabinoid receptors, CB1 and CB2, are significantly higher in CA-human papillomavirus-10 (virally transformed cells derived from adenocarcinoma of human prostate tissue), and other human prostate cells LNCaP, DUI45, PC3, and CWR22Rnu1 than in human prostate epithelial and PZ-HPV-7 (virally transformed cells derived from normal human prostate tissue) cells. WIN-55,212-2 (mixed CB1/CB2 agonist) treatment with androgen-responsive LNCaP cells resulted in a dose- (1-10 micromol/L) and time-dependent (24-48 hours) inhibition of cell growth, blocking of CB1 and CB2 receptors by their antagonists SR141716 (CB1) and SR144528 (CB2) significantly prevented this effect. Extending this observation, we found that WIN-55,212-2 treatment with LNCaP resulted in a dose- (1-10 micromol/L) and time-dependent (24-72 hours) induction of apoptosis (a), decrease in protein and mRNA expression of androgen receptor (b), decrease in intracellular protein and mRNA expression of prostate-specific antigen (c), decrease in secreted prostate-specific antigen levels (d), and decrease in protein expression of proliferation cell nuclear antigen and vascular endothelial growth factor (e). Our results suggest that WIN-55,212-2 or other non-habit-forming cannabinoid receptor agonists could be developed as novel therapeutic agents for the treatment of prostate cancer.
COLORECTAL CANCER
Int J Cancer. 2007 Nov 15;121(10):2172-80.
Department of Cellular and Molecular Medicine, Cancer Research UK, Colorectal Tumour Biology Group, School of Medical Sciences, University of Bristol, University Walk, Bristol, United Kingdom.
FINDINGS:
Deregulation of cell survival pathways and resistance to apoptosis are widely accepted to be fundamental aspects of tumorigenesis. As in many tumours, the aberrant growth and survival of colorectal tumour cells is dependent upon a small number of highly activated signalling pathways, the inhibition of which elicits potent growth inhibitory or apoptotic responses in tumour cells. Accordingly, there is considerable interest in therapeutics that can modulate survival signalling pathways and target cancer cells for death.
There is emerging evidence that cannabinoids, especially Delta(9)-tetrahydrocannabinol (THC), may represent novel anticancer agents, due to their ability to regulate signalling pathways critical for cell growth and survival. Here, we report that CB1 and CB2 cannabinoid receptors are expressed in human colorectal adenoma and carcinoma cells, and show for the first time that THC induces apoptosis in colorectal cancer cells. These data suggest an important role for CB1 receptors and BAD in the regulation of apoptosis in colorectal cancer cells. The use of THC, or selective targeting of the CB1 receptor, may represent a novel strategy for colorectal cancer therapy. 
FOOTNOTES

1a.       Guzman, C; et al.. “Delta-9-tetrahydrocannabinol induces apoptosis in C6 glioma cells”. FEBS Letters 436 (1): 6-10.doi:10.1016/S0014-5793(98)01085-0.        PMID 9771884.
 2b.    Guzman, I; et al.. “Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation.”. Nature Medicine 6 (3): 313-319. doi:10.1038/73171PMID 10700234.
3c.    Liu, WM; et al. (2008). “Enhancing the in vitro cytoxic activity of Delta9-tetrahydracannabinol in leukemic cells through a combinatorial approach.”. Leukemia and Lymphoma 49 (9): 1800-1809. doi:10.1080/10428190802239188PMID 18608861.

5d.   Natalya, Kogan. “Cannabinoids and cancer”. Mini-Reviews in Medicinal Chemistry 5 (10): 941-952.doi:10.2174/138955705774329555PMID 16250836

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

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

3] Guzman et al. 2003. Inhibition of tumor angiogenesis by cannabinoidsThe 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 cellsJournal of Neurooncology 74: 31-40.

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

8] Parolaro and Massi. 2008. Cannabinoids as a potential new drug therapy for the treatment of gliomasExpert 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 cellsActa Oncologica 12: 1-9.

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

[11] Cafferal et al. 2006. Delta-9-Tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulationCancer 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 carcinomaJournal 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 proliferationProceedings 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 cancerCancer 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 mechanismFEBS 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-2Gut 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 linesBlood 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 mitochondriaMolecular 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 vivoOncogene 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 genesCancer Research 66: 6748-6755.

[30] Michalski et al. 2008. Cannabinoids in pancreatic cancer: correlation with survival and painInternational 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-1Journal of the National Cancer Institute 100: 59-69.

[32] Whyte et al. 2010. Cannabinoids inhibit cellular respiration of human oral cancer cellsPharmacology 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 concentrationCancer 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 lymphomaMolecular 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 activationInternational 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 approachLeukemia and Lymphoma 49: 1800-1809.

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

[38] Natalya Kogan. 2005. Cannabinoids and cancerMini-Reviews in Medicinal Chemistry 5: 941-952.

[39] Sarafaraz et al. 2008. Cannabinoids for cancer treatment: progress and promiseCancer Research 68: 339-342.

2011-04-14_14-18-03_72.jpeg
Photo: Ron Marczyk
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.



Everything You Need To Know About Marijuana Legalization

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