Cannabinoids Decrease the Th17 Infla... [J Neuroimmune Pharmacol. 2013] - PubMed - NCBI

Marijuana's cannabinoids improve human health by reducing systemic inflammation which is a root cause for many degenerative diseases. J Neuroimmune Pharmacol. 2013 Jul 28. [Epub ahead of print]

Cannabinoids Decrease the Th17 Inflammatory Autoimmune Phenotype.

Kozela E, Juknat A, Kaushansky N, Rimmerman N, Ben-Nun A, Vogel Z.

Source

The Dr Miriam and Sheldon G. Adelson Center for the Biology of Addictive Diseases, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, ewa.kozela@weizmann.ac.il.

Abstract

Cannabinoids, the Cannabis constituents, are known to possess anti-inflammatory properties but the mechanisms involved are not understood. Here we show that the main psychoactive cannabinoid, Δ-9-tetrahydrocannabinol (THC), and the main nonpsychoactive cannabinoid, cannabidiol (CBD), markedly reduce the Th17 phenotype which is known to be increased in inflammatory autoimmune pathologies such as Multiple Sclerosis. We found that reactivation by MOG35-55 of MOG35-55-specific encephalitogenic T cells (cells that induce Experimental Autoimmune Encephalitis when injected to mice) in the presence of spleen derived antigen presenting cells led to a large increase in IL-17 production and secretion. In addition, we found that the cannabinoids CBD and THC dose-dependently (at 0.1-5 μM) suppressed the production and secretion of this cytokine. Moreover, the mRNA and protein of IL-6, a key factor in Th17 induction, were also decreased. Pretreatment with CBD also resulted in increased levels of the anti-inflammatory cytokine IL-10. Interestingly, CBD and THC did not affect the levels of TNFα and IFNγ. The downregulation of IL-17 secretion by these cannabinoids does not seem to involve the CB1, CB2, PPARγ, 5-HT1A or TRPV1 receptors. In conclusion, the results show a unique cannabinoid modulation of the autoimmune cytokine milieu combining suppression of the pathogenic IL-17 and IL-6 cytokines along with boosting the expression of the anti-inflammatory cytokine IL-10.

via Cannabinoids Decrease the Th17 Infla... [J Neuroimmune Pharmacol. 2013] - PubMed - NCBI.

THC from marijuana is an anticancer drug

How long will this government-perpetrated fraud that there is no such thing as medical marijuana endure in the face of an overwhelming tsunami of science which proves that marijuana delivers health-building and protecting cannabinoids which fight disease and enhance our vitality? Promote adult marijuana use! From the following report, "THC has shown therapeutic potential as an anticancer drug." J Drug Target. 2013 Jun 18. [Epub ahead of print]

Preparation and characterization of Δ9-tetrahydrocannabinol-loaded biodegradable polymeric microparticles and their antitumoral efficacy on cancer cell lines.

de la Ossa DH, Gil-Alegre ME, Ligresti A, Aberturas MD, Molpeceres J, Torres AI, Di Marzo V.

Source

Department of Pharmacy and Pharmaceutical Technology, School of Pharmacy, Complutense University of Madrid , Madrid , Spain .

Abstract

Abstract: Cannabinoids present an interesting therapeutic potential as antiemetics, appetite stimulants in debilitating diseases (cancer, AIDS and multiple sclerosis), analgesics, and in the treatment of multiple sclerosis and cancer, among other conditions. However, despite their high clinical potential, only few dosage forms are available to date. In this paper, the development of Δ9-tetrahydrocannabinol (THC) biodegradable microspheres as an alternative delivery system for cannabinoid parenteral administration is proposed. Tetrahydrocannabinol was encapsulated into biodegradable microspheres by the oil-in-water (o/w) emulsion solvent evaporation method. Several formulations were prepared using different drug:polymer ratios. The influence of antioxidant (α-tocopherol acetate) concentration on the release of THC from the microparticles was studied. Elevated process yield and entrapment efficiencies were achieved. The in vitro drug release studies showed that the encapsulated drug was released over a two week period. As THC has shown therapeutic potential as anticancer drug, the efficacy of the microspheres was tested on different cancer cell lines. Interestingly, the microspheres were able to inhibit cancer cell proliferation during the nine-day study period. All the above results suggest that the use of biodegradable microspheres would be a suitable alternative delivery system for THC administration.

via Preparation and characterization of Δ9-tetrahy... [J Drug Target. 2013] - PubMed - NCBI.

Cannabinoids fight pancreatic cancer

Cannabinoids which work via the CB1 and CB2 receptor, as does THC from marijuana, interfere with pancreatic cancer's cellular metabolism, causing the cancer cells to die off. The following abstract is quite technical but what you need to consider is the final line which reports that cannabinoids killed off and stunted the growth of pancreatic cancer cells. Cell Death Dis. 2013 Jun 13;4:e664. doi: 10.1038/cddis.2013.151.Cannabinoids inhibit energetic metabolism and induce AMPK-dependent autophagy in pancreatic cancer cells.Dando I, Donadelli M, Costanzo C, Dalla Pozza E, D'Alessandro A, Zolla L, Palmieri M.SourceDepartment of Life and Reproduction Sciences, Biochemistry Section, University of Verona, Verona, Italy. Abstract: The anti-tumoral effects of cannabinoids have been described in different tumor systems, including pancreatic adenocarcinoma, but their mechanism of action remains unclear. We used cannabinoids specific for the CB1 ACPA and CB2 GW receptors and metabolomic analyses to unravel the potential pathways mediating cannabinoid-dependent inhibition of pancreatic cancer cell growth. Panc1 cells treated with cannabinoids show elevated AMPK activation induced by a ROS-dependent increase of AMP/ATP ratio. ROS promote nuclear translocation of GAPDH, which is further amplified by AMPK, thereby attenuating glycolysis. Furthermore, ROS determine the accumulation of NADH, suggestive of a blockage in the respiratory chain, which in turn inhibits the Krebs cycle. Concomitantly, inhibition of Akt/c-Myc pathway leads to decreased activity of both the pyruvate kinase isoform M2 PKM2, further downregulating glycolysis, and glutamine uptake. Altogether, these alterations of pancreatic cancer cell metabolism mediated by cannabinoids result in a strong induction of autophagy and in the inhibition of cell growth.

via Cannabinoids inhibit energetic metabolism and... [Cell Death Dis. 2013] - PubMed - NCBI.

Majority of Doctors Would Recommend Medical Marijuana

Most Docs OK With Medical Marijuana: SurveyMajority would give a prescription to an advanced cancer patient in pain

By Serena Gordon HealthDay Reporter

WEDNESDAY, May 29 (HealthDay News) -- Three-quarters of doctors who responded to a survey about medical marijuana said they would approve the use of the drug to help ease pain in an older woman with advanced breast cancer.

In a February issue of the New England Journal of Medicine, doctors were presented with a case vignette, as well as arguments both for and against the use of medical marijuana. Doctors were then asked to decide whether or not they would approve such a prescription for this patient.

The results now appear in the May 30 edition of the journal.

Seventy-six percent of the 1,446 doctors who responded said they would give the woman a prescription for medical marijuana. Many cited the possibility of alleviating the woman's symptoms as a reason for approving the prescription.

"The point of the vignette was to illustrate the kinds of patients that show up on our doorstep who need help. This issue is not one you can ignore, and some states have already taken matters into their own hands," said Dr. J. Michael Bostwick, a professor of psychiatry at the Mayo Clinic in Rochester, Minn.

Bostwick wrote the "pro" side for the survey, but said he could've written the "con" side as well, because there are valid arguments on both sides of the issue.

"There are no 100 percents in medicine. There's a lot of anecdotal evidence that this is something we should study more. Forgive the pun, but there's probably some fire where there's smoke, and we should investigate the medicinal use of marijuana or its components," Bostwick said.

Marijuana comes from the hemp plant Cannabis sativa. It's a dry, shredded mix of the plant's leaves, flowers, stems and seeds. It can be smoked as a cigarette or in a pipe, or it can be added to certain foods, such as brownies.

The case presented to the doctors was Marilyn, a 68-year-old woman with breast cancer that had spread to her lungs, chest cavity and spine. She was undergoing chemotherapy, and said she had no energy, little appetite and a great deal of pain. She had tried various medications to relieve her pain, including the narcotic medication oxycodone. She lives in a state where the use of medical marijuana is legal, and asks her physician for a prescription.

Dr. Bradley Flansbaum, a hospitalist at Lenox Hill Hospital, in New York City, said he sided with the majority for this particular case.

"I think there's some context that needs to be considered," Flansbaum said. "This was a woman with stage 4 cancer who wasn't responding to [anti-nausea medications]. I'm not saying let's legalize marijuana, but this is a woman at the end of her life, so what's the downside, given that there might be a benefit. In a different situation, medical marijuana might not be so well embraced."

For his part, Bostwick said that while he approved the use of medical marijuana in this case, he feels it's important that the prescription of marijuana as medicine only be done within the confines of an already-established doctor-patient relationship.

"My concern is doctors who see someone once and give them a prescription for medical marijuana. That's bad medicine," Bostwick said.

While many physicians felt as if there was no harm in allowing the breast cancer patient to try marijuana to see if it helped, Dr. Gary Reisfield, who co-wrote the "against" side for survey, expressed concern about a patient with lung disease smoking marijuana.

"Marijuana smoke irritates the airways," he said. The smoke can also cause airway inflammation and symptoms of bronchitis, and decreases the ability of the lungs to fight off fungal and bacterial infections, said Reisfield, chief of pain management services at the University of Florida's department of psychiatry.

What's more, marijuana isn't as safe a drug as many believe it to be. "Heavy marijuana use is associated with numerous adverse health and societal outcomes including psychomotor, memory and executive function impairments; marijuana use disorders; other psychiatric conditions such as psychosis; poor school and work performance and impaired driving performance," he said.

Many of the physicians who responded pointed out that drugs already approved and in use also have the potential for addiction, such as narcotics. "Similar arguments could be made against alcohol, opiates and stimulants," Bostwick said.

For his part, Reisfield pointed out that there are two FDA-approved prescription cannabinoid pills -- dronabinol (Marinol) and nabilone (Cesamet) -- that don't begin working as quickly as smoked marijuana, but provide longer symptom relief without the high of marijuana. They also don't appear to have any addictive properties, he said.

What many doctors would like to see, according to the survey, is more evidence on the use of marijuana as medicine, so they could make a better-informed decision one way or the other.

More information

Learn more about marijuana and its potential for medical use from the U.S. National Cancer Institute.

SOURCES: J. Michael Bostwick, M.D., professor, psychiatry, Mayo Clinic, Rochester, Minn.; Bradley Flansbaum, M.D., hospitalist, Lenox Hill Hospital, New York City; Gary Reisfield, M.D., chief, pain management services, department of psychiatry, University of Florida College of Medicine, Gainesville; May 30, 2013, New England Journal of Medicine

A Response to “Going to Pot” by Roxanne Khamsi

By Clint Werner, author of “Marijuana Gateway to Health”

In the June 2013 issue of Scientific American, “Science of Health” columnist Roxanne Khamsi wrote a surprisingly unscientific and biased piece on the health ramifications of legalizing marijuana that was sadly tainted with residue from last century’s reefer madness campaign. The title of the piece itself, “Going to Pot” is a loaded term that confers a negative association on the subject via cultural symbolism having nothing to do with the reality of what science is telling us about marijuana and how it affects the human organism and society. First, Ms. Khamsi is mistaken when she writes that doctors “may prescribe marijuana to treat or manage ailments.” In states with medical marijuana provisions, physicians write recommendations for their patients that allow access to dispensaries or cultivation cooperatives. Ms. Khamsi then asserts that “the safety of recreational use is poorly understood” and that “researchers worry that both short- and long-term use of the drug may harm the body and mind.” Researchers who are up-to-date on the science of marijuana have no such concerns regarding adult use. In terms of harming the body, recent research has revealed that regular use of marijuana actually seems to improve physical health. Population studies have shown that regular marijuana users have a reduced risk for developing lung cancer (Hashibe, Cancer Epidemiological, Biomarkers and Prevention, 2006), head and neck cancers (Liang, Cancer Prevention Research, 2009), bladder cancer (Thomas, American Urological Association meeting, 2013), lymphomas (Holly, American Journal of Epidemiology, 1999), as well as diabetes (Rajavashisth, BMJ Open, 2012). The diabetes protection data from the enormous NHANES report also revealed that subjects who smoked marijuana three times per week had a profound (> 50%) reduction in their blood levels of C reactive protein, a inflammation marker for heart disease, indicating that they experienced significant protection from developing cardiac disease. Research also revealed that regular, moderate marijuana smokers have improved lung function compared to non-marijuana smokers with no risk for developing COPD (Pletcher, JAMA, 2012). National Institute of Drug Abuse pulmonary researcher, Dr. Donald Tashkin has said that he now endorses legalization since there is no basis for concern about the substance’s negative effects on lung function. Given the nearly century-long reefer madness campaign waged with untold billions of government dollars, it is hard for people to grasp that a denigrated and criminalized substance could have such positive health effects, especially when smoked, but science trumps myth and superstition with evidence. In terms of mental health, a just-published paper reports that “marijuana use consistently buffered people from the negative consequences associated with loneliness and social exclusion” (Deckman, Social Psychological and Personality Science, 2013), which could be one of the reasons that researchers found a truly startling drop in suicides, especially among young adult men, following the enactment of state medical marijuana laws (Anderson, IDEAS, 2012). Other research has shown that marijuana’s anti-depressant effects could be the result of neurogenesis, the production of healthy and functional new brain cells, which is promoted by the cannabinoids in marijuana (Jiang, Journal of Clinical Investigation, 2005). Another recently-published study found that “mortality risk was lower in cannabis users than in non-cannabis users with psychotic disorders” (Koola, Journal of Psychiatric Research, 2013), indicating that marijuana is a beneficial treatment for mental problems rather than, as increasingly inferred, a causative agent. In attempting to explain the activity of marijuana’s cannabinoid molecules on the endocannabinoid receptors, Ms. Khamsi once again employs loaded language to imply a negative effect, writing that THC “triggers domino chains” which implies a collapse of order and function rather than an alteration in order and function, which is what is truly occurring. Ms. Khamsi then frets that using marijuana impairs “working memory.” Yes marijuana alters mental functioning; it shifts the mind into a blissful euphoria that redirects thought from the ordered and analytical to the relaxed and free-association style of thought that characterizes relaxation and insight. And unlike alcohol, which serves a similar function of quieting the work day mental noise, marijuana is not carcinogenic or lethal. Ms. Khamsi expresses the understandable concern that marijuana users will make our roadways more dangerous but this is not supported by data that shows us what actually happens when legal restrictions are eased. A comprehensive review of data from states with medical marijuana laws found that enactment of the laws led to a significant drop in traffic accident deaths by allowing for marijuana to substitute for alcohol, a far more impairing substance. Traffic accident fatalities dropped by 9 percent in medical marijuana states. (Anderson, pending publication in the Journal of Law and Economics, 2013). That is essentially the same level of protection afforded by the passage of mandatory sea belt laws and by increasing the age for alcohol consumption from 18 to 21 years. According to research conducted by the automobile insurance company 4autoinsurance.com, marijuana users are safe drivers because, unlike alcohol drinkers, they are aware of their level of impairment and either refuse to drive, delay driving or drive more carefully than normal by reducing speed and not changing lanes. Regular marijuana users showed far less evidence of impairment than did novice and occasional users. Impairment testing is the only way to effectively police for marijuana-impaired drivers without ruining the lives of people who pose no threat on the roadways. The cannabinoid CBD steers THC away from the CB1 receptor, thus dulling or nullifying the mind-altering effects, but CBD does not reduce THC levels in the blood. Therefore, a driver using a high CBD strain of marijuana could test over the THC limit while experiencing no psychoactive effects whatsoever. Consequently, effective and fair impairment assessment techniques will need to be developed. Ms. Khamsi then returns to the health effects of marijuana, but ignores the previously cited benefits of reduced risks for developing numerous cancers, diabetes and other inflammation- and oxidation-based degenerative illnesses, such as Alzheimer’s disease and arthritis. She then refers to the recent study of data from New Zealand that indicates that teenagers who use marijuana heavily have up to an 8 percent drop in IQ points. Those results were called into question upon review but still indicate a disturbing effect of heavy marijuana use on the developing adolescent brain. Neurologist Dr. Gary Wenk, who has written “a puff is enough” to protect the adult brain from age-related dementia, says that the effect of marijuana on a developing brain, especially in those under 15 years of age, is impairing. Regular use of marijuana by teens may also interfere with social and professional skill development by monopolizing the time and consciousness of teens that enjoy it. Ms. Khamsi correctly notes that black market marijuana is sometimes contaminated with “sand or glass beads” which are far more harmful to the user than cannabis itself. Black market marijuana is also frequently contaminated with insecticides not intended for use on plants that are consumed. Some of these products are neurotoxic and, ironically, may induce neurodegenerative illnesses by interfering with the functions of the endocannabinoid system. (Casida, Annual Review of Entomolgy, 2013) Smuggled marijuana is also stale and often riddled with mold. Given these threats to heavy teenage users, the question needs to be asked: How do we best reduce access to marijuana, especially the most harmful forms of marijuana, by teenagers? One study suggests that multidimensional family therapy (MDFT) is the most effective approach for treating teenagers with what is termed “cannabis use disorder” (Rigter, Drug and Alcohol Dependence, 2012). MDFT essentially reestablishes parental authority and time management in teens’ lives. If parents remain involved in all aspects of their teenage children’s lives, MDFT would not be necessary to correct a deficit in parenting. The best way to prevent teenage substance abuse is for parents to rigorously monitor and guide their children’s activities. By doing this, parents might not prevent experimentation but they can create an environment where regular access to and use of marijuana is impossible. Shrinking and killing off the black market via legalization and regulation can assist parents in this task, by making marijuana more difficult for teens to obtain. Dealers do not card and taking marijuana away from the illicit drug black market will also protect teens from the multiple drug offerings of those dealers. If teens do obtain marijuana on the sly, at least, having been diverted from legal and tested supplies, it will be less likely to be contaminated with more harmful substances. Commercial medical marijuana venders such as Harborside Health Center, which Khamsi mentioned, contract with growers and test their marijuana for safety and potency. Legalization transforms marijuana cultivators from shady criminals into proud artisans. And despite the possible risk of heavy marijuana use to teenagers’ cognition, a study of adolescent binge drinkers found that those who used marijuana suffered significantly less alcohol-related brain damage than the booze-only drinkers (Jacobus, Neurotoxicology and Teratology, 2009). Consider the irony: Marijuana protects the brains of booze binge drinkers. Ms. Khamsi also mentions increases in emergency room visits and those seeking treatment for marijuana use. The emergency room statistic most frequently cited by opponents of legalization involve the detection of marijuana use via urinalysis, a method that only indicates if marijuana has been used within the last two to four weeks, therefore the data does not indicate that marijuana use caused the emergency room visit. It merely indicates that more people seem to be using marijuana overall (DAWN Drug Abuse Warning Network, HHS, 2008). In fact, two studies have found direct associations between marijuana use and a decrease in emergency room visits (Vinson, Missouri Medicine, 2006 and Gmel, BMC Public Health 9, 2009). The BMC study found that “relative risks decreased with increasing levels of use,” in other words, when more marijuana was used, fewer injuries occurred. This might seem odd until one recalls that a cannabinoid-blocking drug (rimonabant) was rejected for approval by the FDA due to its side-effects, which included an increase in accidents and injuries. Given that smoking marijuana reduces our risks for developing various cancers, diabetes, heart disease, COPD, Alzheimer’s disease, and other inflammation-based illnesses along with depression, suicidal tendencies and alcohol-caused traffic accidents, shouldn’t it’s use by adults be encouraged and safe, legal outlets be established? Science has spoken.

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A Response to “Going to Pot” by Roxanne Khamsi

By Clint Werner, author of “Marijuana Gateway to Health” In the June 2013 issue of Scientific American, “Science of Health” columnist Roxanne Khamsi wrote a surprisingly unscientific and biased piece on the health ramifications of legalizing marijuana that was sadly tainted with residue from last century’s reefer madness campaign. The title of the piece itself, “Going to Pot” is a loaded term that confers a negative association on the subject via cultural symbolism having nothing to do with the reality of what science is telling us about marijuana and how it affects the human organism and society. First, Ms. Khamsi is mistaken when she writes that doctors “may prescribe marijuana to treat or manage ailments.” In states with medical marijuana provisions, physicians write recommendations for their patients that allow access to dispensaries or cultivation cooperatives. Ms. Khamsi then asserts that “the safety of recreational use is poorly understood” and that “researchers worry that both short- and long-term use of the drug may harm the body and mind.” Researchers who are up-to-date on the science of marijuana have no such concerns regarding adult use. In terms of harming the body, recent research has revealed that regular use of marijuana actually seems to improve physical health. Population studies have shown that regular marijuana users have a reduced risk for developing lung cancer (Hashibe, Cancer Epidemiological, Biomarkers and Prevention, 2006), head and neck cancers (Liang, Cancer Prevention Research, 2009), bladder cancer (Thomas, American Urological Association meeting, 2013), lymphomas (Holly, American Journal of Epidemiology, 1999), as well as diabetes (Rajavashisth, BMJ Open, 2012). The diabetes protection data from the enormous NHANES report also revealed that subjects who smoked marijuana three times per week had a profound (> 50%) reduction in their blood levels of C reactive protein, a inflammation marker for heart disease, indicating that they experienced significant protection from developing cardiac disease. Research also revealed that regular, moderate marijuana smokers have improved lung function compared to non-marijuana smokers with no risk for developing COPD (Pletcher, JAMA, 2012). National Institute of Drug Abuse pulmonary researcher, Dr. Donald Tashkin has said that he now endorses legalization since there is no basis for concern about the substance’s negative effects on lung function. Given the nearly century-long reefer madness campaign waged with untold billions of government dollars, it is hard for people to grasp that a denigrated and criminalized substance could have such positive health effects, especially when smoked, but science trumps myth and superstition with evidence. In terms of mental health, a just-published paper reports that “marijuana use consistently buffered people from the negative consequences associated with loneliness and social exclusion” (Deckman, Social Psychological and Personality Science, 2013), which could be one of the reasons that researchers found a truly startling drop in suicides, especially among young adult men, following the enactment of state medical marijuana laws (Anderson, IDEAS, 2012). Other research has shown that marijuana’s anti-depressant effects could be the result of neurogenesis, the production of healthy and functional new brain cells, which is promoted by the cannabinoids in marijuana (Jiang, Journal of Clinical Investigation, 2005). Another recently-published study found that “mortality risk was lower in cannabis users than in non-cannabis users with psychotic disorders” (Koola, Journal of Psychiatric Research, 2013), indicating that marijuana is a beneficial treatment for mental problems rather than, as increasingly inferred, a causative agent. In attempting to explain the activity of marijuana’s cannabinoid molecules on the endocannabinoid receptors, Ms. Khamsi once again employs loaded language to imply a negative effect, writing that THC “triggers domino chains” which implies a collapse of order and function rather than an alteration in order and function, which is what is truly occurring. Ms. Khamsi then frets that using marijuana impairs “working memory.” Yes marijuana alters mental functioning; it shifts the mind into a blissful euphoria that redirects thought from the ordered and analytical to the relaxed and free-association style of thought that characterizes relaxation and insight. And unlike alcohol, which serves a similar function of quieting the work day mental noise, marijuana is not carcinogenic or lethal. Ms. Khamsi expresses the understandable concern that marijuana users will make our roadways more dangerous but this is not supported by data that shows us what actually happens when legal restrictions are eased. A comprehensive review of data from states with medical marijuana laws found that enactment of the laws led to a significant drop in traffic accident deaths by allowing for marijuana to substitute for alcohol, a far more impairing substance. Traffic accident fatalities dropped by 9 percent in medical marijuana states. (Anderson, pending publication in the Journal of Law and Economics, 2013). That is essentially the same level of protection afforded by the passage of mandatory sea belt laws and by increasing the age for alcohol consumption from 18 to 21 years. According to research conducted by the automobile insurance company 4autoinsurance.com, marijuana users are safe drivers because, unlike alcohol drinkers, they are aware of their level of impairment and either refuse to drive, delay driving or drive more carefully than normal by reducing speed and not changing lanes. Regular marijuana users showed far less evidence of impairment than did novice and occasional users. Impairment testing is the only way to effectively police for marijuana-impaired drivers without ruining the lives of people who pose no threat on the roadways. The cannabinoid CBD steers THC away from the CB1 receptor, thus dulling or nullifying the mind-altering effects, but CBD does not reduce THC levels in the blood. Therefore, a driver using a high CBD strain of marijuana could test over the THC limit while experiencing no psychoactive effects whatsoever. Consequently, effective and fair impairment assessment techniques will need to be developed. Ms. Khamsi then returns to the health effects of marijuana, but ignores the previously cited benefits of reduced risks for developing numerous cancers, diabetes and other inflammation- and oxidation-based degenerative illnesses, such as Alzheimer’s disease and arthritis. She then refers to the recent study of data from New Zealand that indicates that teenagers who use marijuana heavily have up to an 8 percent drop in IQ points. Those results were called into question upon review but still indicate a disturbing effect of heavy marijuana use on the developing adolescent brain. Neurologist Dr. Gary Wenk, who has written “a puff is enough” to protect the adult brain from age-related dementia, says that the effect of marijuana on a developing brain, especially in those under 15 years of age, is impairing. Regular use of marijuana by teens may also interfere with social and professional skill development by monopolizing the time and consciousness of teens that enjoy it. Ms. Khamsi correctly notes that black market marijuana is sometimes contaminated with “sand or glass beads” which are far more harmful to the user than cannabis itself. Black market marijuana is also frequently contaminated with insecticides not intended for use on plants that are consumed. Some of these products are neurotoxic and, ironically, may induce neurodegenerative illnesses by interfering with the functions of the endocannabinoid system. (Casida, Annual Review of Entomolgy, 2013) Smuggled marijuana is also stale and often riddled with mold. Given these threats to heavy teenage users, the question needs to be asked: How do we best reduce access to marijuana, especially the most harmful forms of marijuana, by teenagers? One study suggests that multidimensional family therapy (MDFT) is the most effective approach for treating teenagers with what is termed “cannabis use disorder” (Rigter, Drug and Alcohol Dependence, 2012). MDFT essentially reestablishes parental authority and time management in teens’ lives. If parents remain involved in all aspects of their teenage children’s lives, MDFT would not be necessary to correct a deficit in parenting. The best way to prevent teenage substance abuse is for parents to rigorously monitor and guide their children’s activities. By doing this, parents might not prevent experimentation but they can create an environment where regular access to and use of marijuana is impossible. Shrinking and killing off the black market via legalization and regulation can assist parents in this task, by making marijuana more difficult for teens to obtain. Dealers do not card and taking marijuana away from the illicit drug black market will also protect teens from the multiple drug offerings of those dealers. If teens do obtain marijuana on the sly, at least, having been diverted from legal and tested supplies, it will be less likely to be contaminated with more harmful substances. Commercial medical marijuana venders such as Harborside Health Center, which Khamsi mentioned, contract with growers and test their marijuana for safety and potency. Legalization transforms marijuana cultivators from shady criminals into proud artisans. And despite the possible risk of heavy marijuana use to teenagers’ cognition, a study of adolescent binge drinkers found that those who used marijuana suffered significantly less alcohol-related brain damage than the booze-only drinkers (Jacobus, Neurotoxicology and Teratology, 2009). Consider the irony: Marijuana protects the brains of booze binge drinkers. Ms. Khamsi also mentions increases in emergency room visits and those seeking treatment for marijuana use. The emergency room statistic most frequently cited by opponents of legalization involve the detection of marijuana use via urinalysis, a method that only indicates if marijuana has been used within the last two to four weeks, therefore the data does not indicate that marijuana use caused the emergency room visit. It merely indicates that more people seem to be using marijuana overall (DAWN Drug Abuse Warning Network, HHS, 2008). In fact, two studies have found direct associations between marijuana use and a decrease in emergency room visits (Vinson, Missouri Medicine, 2006 and Gmel, BMC Public Health 9, 2009). The BMC study found that “relative risks decreased with increasing levels of use,” in other words, when more marijuana was used, fewer injuries occurred. This might seem odd until one recalls that a cannabinoid-blocking drug (rimonabant) was rejected for approval by the FDA due to its side-effects, which included an increase in accidents and injuries. Given that smoking marijuana reduces our risks for developing various cancers, diabetes, heart disease, COPD, Alzheimer’s disease, and other inflammation-based illnesses along with depression, suicidal tendencies and alcohol-caused traffic accidents, shouldn’t it’s use by adults be encouraged and safe, legal outlets be established? Science has spoken.

Marijuana use reduces alcohol and tobacco users' risk for developing head and neck cancer

Marijuana use protects tobacco smokers and alcohol drinkers from head and neck cancer! Legalization is on its way to the USA! A population-based case-control study of marijuana use and head and neck squamous cell carcinoma.Liang C, McClean MD, Marsit C, Christensen B, Peters E, Nelson HH, Kelsey KT.SourceDepartment of Community Health, Department of Pathology and Laboratory Medicine, Division of Biology and Medicine, Brown University, Providence, RI, USA.

Abstract: Cannabinoids, constituents of marijuana smoke, have been recognized to have potential antitumor properties. However, the epidemiologic evidence addressing the relationship between marijuana use and the induction of head and neck squamous cell carcinoma HNSCC is inconsistent and conflicting. Cases n = 434 were patients with incident HNSCC disease from nine medical facilities in the Greater Boston, MA area between December 1999 and December 2003. Controls n = 547 were frequency matched to cases on age +/-3 years, gender, and town of residence.  After adjusting for potential confounders including smoking and alcohol drinking, 10 to 20 years of marijuana use was associated with a significantly reduced risk of HNSCC [odds ratio OR10-<20 years versus never users, 0.38; 95% confidence interval CI, 0.22-0.67]. Among marijuana users moderate weekly use was associated with reduced risk OR0.5-<1.5 times versus <0.5 time, 0.52; 95% CI, 0.32-0.85. The magnitude of reduced risk was more pronounced for those who started use at an older age OR15-<20 years versus never users, 0.53; 95% CI, 0.30-0.95; OR> or =20 years versus never users, 0.39; 95% CI, 0.17-0.90; Ptrend < 0.001. These inverse associations did not depend on human papillomavirus 16 antibody status. However, for the subjects who have the same level of smoking or alcohol drinking, we observed attenuated risk of HNSCC among those who use marijuana compared with those who do not. Our study suggests that moderate marijuana use is associated with reduced risk of HNSCC.

Marijuana use reduces alcohol and tobacco users' risk for developing head and neck cancer

Marijuana use protects tobacco smokers and alcohol drinkers from head and neck cancer! Legalization is on its way to the USA! A population-based case-control study of marijuana use and head and neck squamous cell carcinoma.Liang C, McClean MD, Marsit C, Christensen B, Peters E, Nelson HH, Kelsey KT.SourceDepartment of Community Health, Department of Pathology and Laboratory Medicine, Division of Biology and Medicine, Brown University, Providence, RI, USA.

Abstract: Cannabinoids, constituents of marijuana smoke, have been recognized to have potential antitumor properties. However, the epidemiologic evidence addressing the relationship between marijuana use and the induction of head and neck squamous cell carcinoma HNSCC is inconsistent and conflicting. Cases n = 434 were patients with incident HNSCC disease from nine medical facilities in the Greater Boston, MA area between December 1999 and December 2003. Controls n = 547 were frequency matched to cases on age +/-3 years, gender, and town of residence.  After adjusting for potential confounders including smoking and alcohol drinking, 10 to 20 years of marijuana use was associated with a significantly reduced risk of HNSCC [odds ratio OR10-<20 years versus never users, 0.38; 95% confidence interval CI, 0.22-0.67]. Among marijuana users moderate weekly use was associated with reduced risk OR0.5-<1.5 times versus <0.5 time, 0.52; 95% CI, 0.32-0.85. The magnitude of reduced risk was more pronounced for those who started use at an older age OR15-<20 years versus never users, 0.53; 95% CI, 0.30-0.95; OR> or =20 years versus never users, 0.39; 95% CI, 0.17-0.90; Ptrend < 0.001. These inverse associations did not depend on human papillomavirus 16 antibody status. However, for the subjects who have the same level of smoking or alcohol drinking, we observed attenuated risk of HNSCC among those who use marijuana compared with those who do not. Our study suggests that moderate marijuana use is associated with reduced risk of HNSCC.

via A population-based case-control stud... [Cancer Prev Res Phila. 2009] - PubMed - NCBI.

[Marihuana and cannobinoids as medicaments]. [Przegl Lek. 2012] - PubMed - NCBI

Przegl Lek. 2012;69(10):1095-7. [Marihuana and cannobinoids as medicaments].

[Article in Polish]

Tkaczyk M, Florek E, Piekoszewski W.

Source Krakowska Wyzsza Szkoła Promocji Zdrowia, Kraków.

Abstract

Biological activity of cannabinoids is caused by binding to two cannabinoid receptors CB1 and CB2. Psychoactive is not only tetrahydrocannabinol (THC) but also: cannabidiol, cannabigerol or cannabichromen. Formerly, the usefulness of hemp was assessed in the relation to temporary appeasement of the symptoms of some ailments as nausea or vomiting. Present discoveries indicates that cannabis-based drugs has shown ability to alleviate of autoimmunological disorders such as: Multiple sclerosis (MS), Rheumatoid arthritis (RA) or inflammatory bowel disease. Another studies indicates that cannabinoids play role in treatment of neurological disorders like Alzheimer disease or Amyotrophic lateral sclerosis (ALS) or even can reduce spreading of tumor cells. Cannabinoids stand out high safety profile considering acute toxicity, it is low possibility of deadly overdosing and side-effects are comprise in range of tolerated side-effects of other medications.

via [Marihuana and cannobinoids as medicaments]. [Przegl Lek. 2012] - PubMed - NCBI.

Cannabinoids selectively inhibit proliferation ... [J Neurooncol. 2005] - PubMed - NCBI

This is an important study because it shows that the naturally-occurring cannabinoid molecule THC was safer, and more effective against cancer cells than was a synthetic cannabinoid, WIN 55,212-2. Yet researchers are discouraged from using cannabinoids from marijuana in lieu of the synthetic ones, because good findings about THC might "send the wrong message to young people." So now young people are getting a hold of far more dangerous synthetic cannabinoids and using them recreationally...the Law of Unintended Consequences. Neurooncol. 2005 Aug;741:31-40.Cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells.McAllister SD, Chan C, Taft RJ, Luu T, Abood ME, Moore DH, Aldape K, Yount G.  Abstract: Normal tissue toxicity limits the efficacy of current treatment modalities for glioblastoma multiforme GBM. We evaluated the influence of cannabinoids on cell proliferation, death, and morphology of human GBM cell lines and in primary human glial cultures, the normal cells from which GBM tumors arise. The influence of a plant derived cannabinoid agonist, Delta9-tetrahydrocannabinol Delta9-THC, and a potent synthetic cannabinoid agonist, WIN 55,212-2, were compared using time lapse microscopy. We discovered that Delta9-THC decreases cell proliferation and increases cell death of human GBM cells more rapidly than WIN 55,212-2. Delta9-THC was also more potent at inhibiting the proliferation of GBM cells compared to WIN 55,212-2. The effects of Delta9-THC and WIN 55,212-2 on the GBM cells were partially the result of cannabinoid receptor activation. The same concentration of Delta9-THC that significantly inhibits proliferation and increases death of human GBM cells has no significant impact on human primary glial cultures. Evidence of selective efficacy with WIN 55,212-2 was also observed but the selectivity was less profound, and the synthetic agonist produced a greater disruption of normal cell morphology compared to Delta9-THC.PMID: 16078104 [PubMed - indexed for MEDLINE]

via Cannabinoids selectively inhibit proliferation ... [J Neurooncol. 2005] - PubMed - NCBI.

Use of cannabinoid rece... [Best Pract Res Clin Endocrinol Metab. 2009] - PubMed - NCBI

THC from marijuana is a safe, effective and thoroughly enjoyable cannabinoid receptor agonist. Best Pract Res Clin Endocrinol Metab. 2009 Feb;                                                                                                      Use of cannabinoid receptor agonists in cancer therapy as palliative and curative agents.                                            Pisanti S, Malfitano AM, Grimaldi C, Santoro A, Gazzerro P, Laezza C, Bifulco M.Source Department of Pharmaceutical Sciences, University of Salerno, Italy.                                                                                           Abstract: 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.PMID: 19285265 [PubMed - indexed for MEDLINE]

via Use of cannabinoid rece... [Best Pract Res Clin Endocrinol Metab. 2009] - PubMed - NCBI.

Cannabinoids induce apoptosis of pancreatic tumor... [Cancer Res. 2006] - PubMed - NCBI

Cancer Res. 2006 Jul 1;6613:6748-55.Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes.Carracedo A, Gironella M, Lorente M, Garcia S, Guzmán M, Velasco G, Iovanna JL.SourceDepartment of Biochemistry and Molecular Biology I, School of Biology, Complutense University, c/José Antonio Novais s/n, 28040 Madrid, Spain                                                                                   .     Abstract: Pancreatic adenocarcinomas are among the most malignant forms of cancer and, therefore, it is of especial interest to set new strategies aimed at improving the prognostic of this deadly disease. The present study was undertaken to investigate the action of cannabinoids, a new family of potential antitumoral agents, in pancreatic cancer. We show that cannabinoid receptors are expressed in human pancreatic tumor cell lines and tumor biopsies at much higher levels than in normal pancreatic tissue. Studies conducted with MiaPaCa2 and Panc1 cell lines showed that cannabinoid administration a induced apoptosis, b increased ceramide levels, and c up-regulated mRNA levels of the stress protein p8. These effects were prevented by blockade of the CB2 cannabinoid receptor or by pharmacologic inhibition of ceramide synthesis de novo. Knockdown experiments using selective small interfering RNAs showed the involvement of p8 via its downstream endoplasmic reticulum stress-related targets activating transcription factor 4 ATF-4 and TRB3 in Delta9-tetrahydrocannabinol-induced apoptosis. Cannabinoids also reduced the growth of tumor cells in two animal models of pancreatic cancer. In addition, cannabinoid treatment inhibited the spreading of pancreatic tumor cells. Moreover, cannabinoid administration selectively increased apoptosis and TRB3 expression in pancreatic tumor cells but not in normal tissue. In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress-related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer. via Cannabinoids induce apoptosis of pancreatic tumor... [Cancer Res. 2006] - PubMed - NCBI.

OnMedica - News - Alcohol major contributor to cancer deaths

Marijuana has powerful anti-cancer activity. Alcohol is a powerful cancer promoting agent. If you're going to drink, you damn well need to be toking too! Alcohol major contributor to cancer deaths

A drink a day can increase breast cancer risk by 5%2     Even light drinking raises breast cancer risk   Alcohol major contributor to cancer deaths                                                                                     15 February 2013                                Alcohol is a major contributor to cancer deaths and years of potential life lost, researchers have found.These findings, published in the American Journal of Public Health, also show that reducing alcohol consumption is an important cancer prevention strategy as alcohol is a known carcinogen even when consumed in small quantities.Previous studies consistently have shown that alcohol consumption is a significant risk factor for cancers of the mouth, throat, oesophagus and liver. More recent research has shown that alcohol also increases the risk of cancers of the colon, rectum and female breast. Estimates have shown that alcohol accounts for about 4% of all cancer-related deaths worldwide.In this new study, researchers from the Boston University School of Medicine BUSM and Boston University School of Public Health BUSPH examined recent data from the US on alcohol consumption and cancer mortality. They found that alcohol resulted in approximately 20,000 cancer deaths annually, accounting for about 3.5% of all cancer deaths in the US.Breast cancer was the most common cause of alcohol-attributable cancer deaths in women, accounting for approximately 6,000 deaths annually, or about 15% of all breast cancer deaths. Cancers of the mouth, throat and oesophagus were common causes of alcohol-attributable cancer mortality in men, resulting in a total of about 6,000 annual deaths.The researchers also found that each alcohol-related cancer death accounted for an average of 18 years of potential life lost. In addition, although higher levels of alcohol consumption led to a higher cancer risk, average consumption of 1.5 drinks per day or less accounted for 30% of all alcohol-attributable cancer deaths."The relationship between alcohol and cancer is strong, but is not widely appreciated by the public and remains underemphasised even by physicians," said senior author Timothy Naimi from the Department of Medicine at BUSM."Alcohol is a big preventable cancer risk factor that has been hiding in plain sight," he added.

via OnMedica - News - Alcohol major contributor to cancer deaths.

Cannabinoids: a new hope for breast cancer ... [Cancer Treat Rev. 2012] - PubMed - NCBI

Marijuana fights beast cancer, why wait for "officials" to approve it? Use it now! Family history of breast cancer? Use it now! History of poor diet and alcohol consumption? Use it now! Cancer Treat Rev. 2012 Nov;10. 2012

Cannabinoids: a new hope for breast cancer therapy?               Caffarel MM, et al., Dept. Biochemistry and Molecular Biology I, School of Biology, Complutense University-CIBERNED-IRYCIS, Madrid, Spain.                                                                                          Abstract: Breast cancer is a very common disease that affects approximately 1 in 10 women at some point in their lives. Importantly, breast cancer cannot be considered a single disease as it is characterized by distinct pathological and molecular subtypes that are treated with different therapies and have diverse clinical outcomes. Although some highly successful treatments have been developed, certain breast tumors are resistant to conventional therapies and a considerable number of them relapse. Therefore, new strategies are urgently needed, and the challenge for the future will most likely be the development of individualized therapies that specifically target each patient's tumor. Experimental evidence accumulated during the last decade supports that cannabinoids, the active components of Cannabis sativa and their derivatives, possess anticancer activity. Thus, these compounds exert anti-proliferative, pro-apoptotic, anti-migratory and anti-invasive actions in a wide spectrum of cancer cells in culture. Moreover, tumor growth, angiogenesis and metastasis are hampered by cannabinoids in xenograft-based and genetically-engineered mouse models of cancer. This review summarizes our current knowledge on the anti-tumor potential of cannabinoids in breast cancer, which suggests that cannabinoid-based medicines may be useful for the treatment of most breast tumor subtypes.Copyright © 2012 Elsevier Ltd. All rights reserved.

via Cannabinoids: a new hope for breast cancer ... [Cancer Treat Rev. 2012] - PubMed - NCBI.

Towards the use of cannabinoids as antitumour agents : Abstract : Nature Reviews Cancer

PerspectivesNature Reviews Cancer 12, 436-444 June 2012 | doi:10.1038/nrc3247                                                                      Opinion: Towards the use of cannabinoids as antitumour agents Guillermo Velasco1,2,3, Cristina Sánchez1 & Manuel Guzmán1,2,4 Various reports have shown that cannabinoids the active components of marijuana and their derivatives can reduce tumour growth and progression in animal models of cancer, in addition to their well-known palliative effects on some cancer-associated symptoms. This Opinion article discusses our current understanding of cannabinoids as antitumour agents, focusing on recent insights into the molecular mechanisms of action, including emerging resistance mechanisms and opportunities for combination therapy approaches. Such knowledge is required for the optimization of preclinical cannabinoid-based therapies and for the preliminary clinical testing that is currently underway.

via Towards the use of cannabinoids as antitumour agents : Abstract : Nature Reviews Cancer.

US Investigators Praise Cannabinoids As Chemo Treatment

US Investigators Praise Cannabinoids As Chemo Treatment“ Cannabinoids inhibit cancer cell proliferation and should be clinically tested as chemotherapeutic agents, according to a review published in the January issue of the journal Cancer Research.Investigators at the University of Wisconsin School of Medicine and Public Health reported that the administration of cannabinoids halts the spread of a wide range of cancers, including brain cancer, prostate cancer, breast cancer, lung cancer, skin cancer, pancreatic cancer, and lymphoma. Researchers suggested that cannabinoids may offer significant advantages over standard chemotherapy treatments because the compounds are both non-toxic and can uniquely target malignant cells while ignoring healthy ones.“Cannabinoids … offer potential applications as anti-tumor drugs, based on the ability of some members of this class to limit inflammation, cell proliferation, and cell survival,” authors concluded. “[T]here is overwhelming evidence to suggest that cannabinoids can be explored as chemotherapeutic agents for the treatment of cancer.”"Read more: http://norml.org/news/2008/01/31/us-investigators-praise-cannabinoids-as-chemo-treatment

via US Investigators Praise Cannabinoids As Chemo Treatment | www.thctotalhealthcare.com.

Local delivery of cannabinoid-loaded microparticles... [PLoS One. 2013] - PubMed - NCBI

What will the prohibitionists say if marijuana turns out to be the most effective form of chemotherapy ever discovered? PLoS One. 2013;81:e54795. doi: 10.1371/journal.pone.0054795. Epub 2013 Jan 22.

Local delivery of cannabinoid-loaded microparticles inhibits tumor growth in a murine xenograft model of glioblastoma multiforme.Hernán Pérez de la Ossa D, Lorente M, Gil-Alegre ME, Torres S, García-Taboada E, Aberturas Mdel R, Molpeceres J, Velasco G, Torres-Suárez AI.SourceDepartment of Pharmacy and Pharmaceutical Technology, School of Pharmacy, Complutense University, Madrid, Spain.AbstractCannabinoids, the active components of marijuana and their derivatives, are currently investigated due to their potential therapeutic application for the management of many different diseases, including cancer. Specifically, Δ9-Tetrahydrocannabinol THC and Cannabidiol CBD - the two major ingredients of marijuana - have been shown to inhibit tumor growth in a number of animal models of cancer, including glioma. Although there are several pharmaceutical preparations that permit the oral administration of THC or its analogue nabilone or the oromucosal delivery of a THC- and CBD-enriched cannabis extract, the systemic administration of cannabinoids has several limitations in part derived from the high lipophilicity exhibited by these compounds. In this work we analyzed CBD- and THC-loaded poly-ε-caprolactone microparticles as an alternative delivery system for long-term cannabinoid administration in a murine xenograft model of glioma. In vitro characterization of THC- and CBD-loaded microparticles showed that this method of microencapsulation facilitates a sustained release of the two cannabinoids for several days. Local administration of THC-, CBD- or a mixture 1∶1 w:w of THC- and CBD-loaded microparticles every 5 days to mice bearing glioma xenografts reduced tumour growth with the same efficacy than a daily local administration of the equivalent amount of those cannabinoids in solution. Moreover, treatment with cannabinoid-loaded microparticles enhanced apoptosis and decreased cell proliferation and angiogenesis in these tumours. Our findings support that THC- and CBD-loaded microparticles could be used as an alternative method of cannabinoid delivery in anticancer therapies.

via Local delivery of cannabinoid-loaded microparticles... [PLoS One. 2013] - PubMed - NCBI.

Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI

CBD a plant cannabinoid found in marijuana/cannabis is a possible, effective treatment for Kaposi sarcoma. It's been about 16 years since effective anti-viral medicines were released for AIDS patients so many of you have never seen someone covered in and disfigured by purple KS lesions but anything that offers relief should be made available, not kept on Schedule one of the Controlled Substances Act. KS is not a disease that is exclusive to AIDS patients therefore CBD might benefit those who cannot use anti-retroviral drugs. Legalize the plant for goodness sake! Genes Cancer. 2012 Jul;37-8:512-20.

.Cannabidiol inhibits growth and induces programmed cell death in kaposi sarcoma-associated herpesvirus-infected endothelium.   Maor Y, Yu J, Kuzontkoski PM, Dezube BJ, Zhang X, Groopman JE.  SourceDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Abstract: Kaposi sarcoma is the most common neoplasm caused by Kaposi sarcoma-associated herpesvirus KSHV. It is prevalent among the elderly in the Mediterranean, inhabitants of sub-Saharan Africa, and immunocompromised individuals such as organ transplant recipients and AIDS patients. Current treatments for Kaposi sarcoma can inhibit tumor growth but are not able to eliminate KSHV from the host. When the host's immune system weakens, KSHV begins to replicate again, and active tumor growth ensues. New therapeutic approaches are needed. Cannabidiol CBD, a plant-derived cannabinoid, exhibits promising antitumor effects without inducing psychoactive side effects. CBD is emerging as a novel therapeutic for various disorders, including cancer. In this study, we investigated the effects of CBD both on the infection of endothelial cells ECs by KSHV and on the growth and apoptosis of KSHV-infected ECs, an in vitro model for the transformation of normal endothelium to Kaposi sarcoma. While CBD did not affect the efficiency with which KSHV infected ECs, it reduced proliferation and induced apoptosis in those infected by the virus. CBD inhibited the expression of KSHV viral G protein-coupled receptor vGPCR, its agonist, the chemokine growth-regulated protein α GRO-α, vascular endothelial growth factor receptor 3 VEGFR-3, and the VEGFR-3 ligand, vascular endothelial growth factor C VEGF-C. This suggests a potential mechanism by which CBD exerts its effects on KSHV-infected endothelium and supports the further examination of CBD as a novel targeted agent for the treatment of Kaposi sarcoma.

via Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI.

Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI

CBD a plant cannabinoid found in marijuana/cannabis is a possible, effective treatment for Kaposi sarcoma. It's been about 16 years since effective anti-viral medicines were released for AIDS patients so many of you have never seen someone covered in and disfigured by purple KS lesions but anything that offers relief should be made available, not kept on Schedule one of the Controlled Substances Act. KS is not a disease that is exclusive to AIDS patients therefore CBD might benefit those who cannot use anti-retroviral drugs. Legalize the plant for goodness sake! Genes Cancer. 2012 Jul;37-8:512-20.

.Cannabidiol inhibits growth and induces programmed cell death in kaposi sarcoma-associated herpesvirus-infected endothelium.   Maor Y, Yu J, Kuzontkoski PM, Dezube BJ, Zhang X, Groopman JE.  SourceDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Abstract: Kaposi sarcoma is the most common neoplasm caused by Kaposi sarcoma-associated herpesvirus KSHV. It is prevalent among the elderly in the Mediterranean, inhabitants of sub-Saharan Africa, and immunocompromised individuals such as organ transplant recipients and AIDS patients. Current treatments for Kaposi sarcoma can inhibit tumor growth but are not able to eliminate KSHV from the host. When the host's immune system weakens, KSHV begins to replicate again, and active tumor growth ensues. New therapeutic approaches are needed. Cannabidiol CBD, a plant-derived cannabinoid, exhibits promising antitumor effects without inducing psychoactive side effects. CBD is emerging as a novel therapeutic for various disorders, including cancer. In this study, we investigated the effects of CBD both on the infection of endothelial cells ECs by KSHV and on the growth and apoptosis of KSHV-infected ECs, an in vitro model for the transformation of normal endothelium to Kaposi sarcoma. While CBD did not affect the efficiency with which KSHV infected ECs, it reduced proliferation and induced apoptosis in those infected by the virus. CBD inhibited the expression of KSHV viral G protein-coupled receptor vGPCR, its agonist, the chemokine growth-regulated protein α GRO-α, vascular endothelial growth factor receptor 3 VEGFR-3, and the VEGFR-3 ligand, vascular endothelial growth factor C VEGF-C. This suggests a potential mechanism by which CBD exerts its effects on KSHV-infected endothelium and supports the further examination of CBD as a novel targeted agent for the treatment of Kaposi sarcoma.

via Cannabidiol inhibits growth and induces program... [Genes Cancer. 2012] - PubMed - NCBI.

Cannabinoid-associated cell death mechanisms in ... [Int J Oncol. 2012] - PubMed - NCBI

Marijuana=The Anti-Cancer Plant The cannabinoids in marijuana are powerful anti-cancer agents which work in many ways to suppress and destroy malignant cells. These actions are the dreams of cancer researchers and yet, marijuana remains illegal. Spread the news, using marijuana lowers your risk for developing cancer as well as diabetes and Alzheimer's disease!

Int J Oncol. 2012 Aug

.Cannabinoid-associated cell death mechanisms in tumor models review.Calvaruso G, Pellerito O, Notaro A, Giuliano M.SourceDepartment of Experimental Biomedicine and Clinical Neuroscience, University of Palermo, Palermo, Italy.

Abstract: In recent years, cannabinoids the active components of Cannabis sativa and their derivatives have received considerable interest due to findings that they can affect the viability and invasiveness of a variety of different cancer cells. Moreover, in addition to their inhibitory effects on tumor growth and migration, angiogenesis and metastasis, the ability of these compounds to induce different pathways of cell death has been highlighted. Here, we review the most recent results generating interest in the field of death mechanisms induced by cannabinoids in cancer cells. In particular, we analyze the pathways triggered by cannabinoids to induce apoptosis or autophagy and investigate the interplay between the two processes. Overall, the results reported here suggest that the exploration of molecular mechanisms induced by cannabinoids in cancer cells can contribute to the development of safe and effective treatments in cancer therapy.

via Cannabinoid-associated cell death mechanisms in ... [Int J Oncol. 2012] - PubMed - NCBI.