as far as statistics...not sure there is anything. it is like alcohol...to much can affect a person...or the chemical make up of a person can have a negative reaction. just as not everyone that takes a drink commits crimes....alot has to do with the individual. the mind set of someone plays a part in it as well.

IMO...it's just like alcohol.

OH BTW...ty juliet
sorry...slow reaction here lol

According to the prestigious European medical journal, The Lancet, "The smoking of cannabis, even long-term, is not harmful to health.

The Lancet
(The Lancet is a British medical journal)
Volume 346, Number 8985, November 11, 1995, p. 1241
Editorial

Deglamorising cannabis

The smoking of cannabis, even long term, is not harmful to health. Yet this widely-used substance is illegal just about everywhere. There have been numerous calls over the years for the legalisation, or at least decriminalisation, of soft drugs, among which cannabis remains the most popular with all social groups. In this highly contentious area, the Dutch attitude has been often mentioned as the voice of sanity. In the Netherlands, customers of coffee shops can buy up to 30 g of cannabis for about 10 pounds ($15) although the drug is technically illegal. The shops are not allowed to advertise, or to sell cannabis to individuals aged under 16 years.

Prominent among those currently calling for legislative reform -- and going further by making constructive proposals -- are police chiefs and city medical officers, people who know only too well that the existing policies in most countries are ineffective and unworkable.

Meanwhile, politicians have largely remained silent, seemingly afraid of offending powerful segments of the electorate or merely of being perceived as weak in the face of rising crime figures. When the occasional politician raises her head above the parapet -- as the British opposition MP Clare Short did recently in calling for a fresh debate on decriminalisation of cannabis -- the response is tediously predictable: widespread condemnation from political colleagues and overwhelming support from those who have to cope with the end result of political inertia.

In the case of Ms. Short, not only was she speedily reprimanded by the party leader, but also party officials claimed that their non-legalisation stance was entirely logical since legalisation of cannabis would "increase the supply, reduce the price, and increase the usage". According to a Home Office report earlier this year, the number of people taking cannabis has doubled in a decade -- without any help from "liberal" measures. Perhaps the politicians' real fear was that freedom to use soft drugs would automatically progress to increased use of substances such as cocaine and heroin. If so, they must have overlooked the recent Dutch government review which pointed out that decriminalisation of possession of soft drugs has not led to a rise in the use of hard drugs.

If the Dutch approach is so successful, why are changes afoot in The Hague to tighten up that country's drug policy? First Amsterdam's mayor proposed closing down half the city's coffee shops that sell cannabis, and in doing so he rejected a report by his health department in favour of legalisation of soft drugs. Then the Dutch government, which had made an election promise to legalise cannabis, last month issued a discussion paper which mirrored the Amsterdam plan. If, as expected, the Dutch parliament agrees the latest proposals, half the country's 4000 cannabis-selling coffee shops will close and the amount that can be sold to an individual will be cut to 5 g. Since the government's own review provides no ammunition for such a change in policy, the real reason behind the new measures must lie elsewhere. One need look no further than the Netherlands' neighbours and co-signatories of the Schengen agreement, which introduced a border-free zone between the Netherlands, France, Germany, Spain, Luxembourg, and Belgium. When France, in particular, threatened to end the agreement, claiming that the Netherlands was the major supplier of Europe's drugs, some action had to be taken and the coffee shops became the scapegoat.

Leaving politics aside, where is the harm in decriminalising cannabis? There is none to the health of the consumers, and the criminal fraternity who depend for their succour on prohibition would hate it. But decriminalisation of possession does not go far enough in our view. That has to be accompanied by controls on source, distribution, and advertising, much as happens with tobacco. A system, in fact, remarkably close to the existing one in Dutch coffee shops. Cannabis has become a political football, and one that governments continually duck. Like footballs, however, it bounces back. Sooner or later politicians will have to stop running scared and address the evidence: cannabis per se is not a hazard to society but driving it further underground may well be.

Cannabis, Mental Health and Context: The Case For Regulation


by Paul Armentano


Recent warning published in the United Kingdom and in America this week suggesting that cannabis' primary psychoactive compound THC may trigger mental illness, including psychosis and schizophrenia, warrant a serious reply.

According to news from the Associated Press and others, investigators at London's Kings College reported that the administration of doses of synthetic THC temporarily interfered with activity in the inferior frontal cortex, a region of the brain associated with paranoia, while administration of the non-psychoactive compound cannabidiol (CBD) stimulated relaxation. The reports go on to suggest that chronic use of cannabis may precipitate various types of mental illness and cite a separate unpublished study indicating that cannabis use may exacerbate symptoms of schizophrenia.

Such clinical findings and suggestions are not new. Scientists have known for decades that THC is psychoactive and that peak blood levels of its primary active metabolite 11-OH-THC are occasionally associated with temporary feelings of dysphoria, paranoia, and even panic attacks. (These events, when documented, typically occur in cannabis naïve users.)

Conversely, scientists have also been long aware of CBD's anxiolytic and anti-psychotic effects. In fact, many experts speculate that it is the lack of CBD in Marinol (the synthetic THC oral prescription pill) that is responsible for the drug's enhanced psychoactivity. By contrast, CBD occurs naturally in whole-plant cannabis, and is believed to modify and/or diminish some of the psychoactivity associated with THC when cannabis is inhaled.

Fears that chronic cannabis use may be positively associated with various mental illnesses, particularly schizophrenia, are also long-standing. However, a recent meta-analysis investigating the use of cannabis use and its impact on mental health reported that those who use cannabis in moderation, even long-term "will not suffer any lasting physical or mental harm. ... Overall, by comparison with other drugs used mainly for 'recreational' purposes, cannabis could be rated to be a relatively safe drug."

Cannabis In Context

The phrase "relatively safe" is appropriate in any discussion regarding cannabis and mental health. No substance is harmless and in many cases, the relative dangers of a drug may be increased or decreased depending on set and setting. Cannabis is no different.

There is limited data suggesting an association, albiet a minor one,between chronic cannabis (primarily among adolescents and/or those predisposed to mental illness) and increased symptoms of depression, psychotic symptoms, and/or schizophrenia.
However, interpretation of this data is troublesome and, to date, this observation association is not well understood.
Identified as well as unidentified confounding factors (such as poverty, family history, polydrug use, etc.) make it difficult, if not impossible, for researchers to adequately determine whether any cause-and-effect relationship exists between cannabis use and mental illness. Also, many experts point out that this association may be due to patients' self-medicating with cannabis,
as survey data and anecdotal reports of individuals finding therapeutic relief from both clinical depression and schizotypal behavior are common within medical lore, and clinical testing on the use of cannabinoids to treat certain symptoms of mental illness has been recommended.

Most recently, a large-scale study by investigators at London's Institute of Psychiatry reported that those patients diagnosed with schizophrenia who had previously used cannabis did not demonstrate exacerbated symptoms of the illness compared to age-adjusted controls who had not used cannabis. "This [finding] argues against a distinct schizophrenia-like psychosis caused by cannabis," they concluded.

Investigators in the study did not address whether cannabis consumers had greater odds of contracting schizophrenia when compared to otherwise matched controls who did not have a history of cannabis use. However, a 2006 review by Britain's Advisory Council on the Misuse of Drugs (ACMD) previously concluded, "For individuals, the current evidence suggests, at worst, that using cannabis increases lifetime risk of developing schizophrenia by one percent."

Nevertheless, until this association is better understood, there may be some merit to various government warnings that adolescents (particularly pre and early teens) and/or adults with pre-existing symptoms of mental illness refrain from using cannabis (and/or other psychoactive substances), particularly in large quantities. This statement, however, is hardly an indictment of cannabis' relative safety when used in moderation by adults or an endorsement of the federal government's efforts to criminally prohibit its use for all Americans. If anything, just the opposite is true.

Health Risks Call For Regulation, Not Prohibition

Health risks connected with drug use -- when scientifically documented -- should not be seen as legitimate reasons for criminal prohibition, but instead, as reasons for legal regulation. Specific to cannabis, if studies demonstrate that those "who first used marijuana before age 12 [are] twice as likely as adults who first used marijuana at age 18 or older to be classified as having serious mental illness,"

then this is an argument in favor of legally regulating cannabis in a manner similar to alcohol, so that better safeguards may be enacted restricting adolescents from legal access to it.These concerns, however, do not support criminally prohibiting the responsible use of the cannabis by adults any more than fears regarding the abuse of alcohol by a minority of teenagers support a blanket prohibition on the use of beer by adults.

In addition, if as some suggest, "as many as one in four people may have a genetic profile that makes marijuana five times more likely to trigger psychotic disorders,"this claim is yet another argument in favor of regulation. If there does exist a minority population of citizens who may be genetically prone to potential harms from cannabis (such as, possibly, those predisposed to schizophrenia), then a regulated system would best identify and educate this sub-population to pot's potential risks so that they may refrain from its use, if they so choose.

To draw a real world comparison, millions of Americans safely use ibuprofen as an effective pain reliever. However, among a minority of the population who suffer from liver and kidney problems, ibuprofen presents a legitimate and substantial health risk. However, this fact no more calls for the criminalization of ibuprofen among adults than do these latest allegations, even if true, call for the current prohibition of cannabis.

Finally, there lies the fact that cannabis prohibition has forever undermined the federal government's ability to educate its citizens, particularly young people, to the potential risks of marijuana when and where they present themselves. Ending prohibition and enacting a legal, regulated cannabis market would likely restore this lost credibility, as evidenced by the fact that science-based, federal education campaigns regarding the health risks of tobacco and drunk driving have greatly reduced smoking and driving under the influence among teenagers. Conversely, similar rhetorically-based campaigns regarding teen pot use have fostered increased levels of illicit drug use among their target audience.

As concluded by the Netherlands Drug Policy Foundation, cannabis' "health risks are remarkably limited, but cannabis is not completely harmless." As a result, the Foundation determined: "There ought to be a special legal regulatory system for cannabis because its use definitely does entail health risks. If cannabis was completely harmless, the same rules could be applied as to tea. Cannabis should not be made freely available, but the rules on cannabis can be very general and lenient." Placed in this context, the administration's latest anti-pot campaign does little to advance the government's position in favor of tightening prohibition, and provides ample ammunition to wage for its repeal.

Cannabis Smoke and Cancer: Assessing the Risk


Presumptions regarding cannabis use as a risk factor for the development of certain types of cancer, particularly lung cancer, warrant critical examination. Epidemiologic studies over the past several decades have established causation between alcohol consumption and cancers of the oral cavity, pharynx, larynx, esophagus, liver, colon and rectum, among others. Tobacco use, particularly cigarette smoking, has also been determined to cause similar upper aerodigestive tract (UAT) cancers, as well as cancers of the pancreas, kidneys and bladder, and is implicated with cancers of the stomach and liver, among others.

To date, similar epidemiologic and/or clinical studies on the use of cannabis and cancer are few and not definitive. However, the public and policy-makers should interpret the ambiguity of these results with caution – neither construing them at this time as an endorsement of cannabis’ safety nor as an indictment of its potential health hazards.

(References: Alcohol and cancer. The Lancet. 2006. | Tobacco use and cancer: an epidemiological perspective for geneticists. Oncogene. 2002)

Cannabis Smoke Versus Tobacco Smoke

Cannabis smoke contains many of the same carcinogens as tobacco smoke, including greater concentrations of certain aromatic hydrocarbons such as benzopyrene, prompting fears that chronic marijuana inhalation may be a risk factor for tobacco-use related cancers. However, marijuana smoke also contains cannabinoids such as THC (delta-9-tetrahydrocannabinol) and CBD (cannabidiol), which are non-carcinogenic and demonstrate anti-cancer properties in vivo and in vitro. By contrast, nicotine promotes the development of cancer cells and their blood supply. In addition, cannabinoids stimulate other biological activities and responses that may mitigate the carcinogenic effects of smoke, such as down-regulating the inflammatory arm of the immune system that is responsible for producing potentially carcinogenic free radicals (unstable atoms that are believed to accelerate the progression of cancer).

Cannabis smoke – unlike tobacco smoke – has not been definitively linked to cancer in humans, including those cancers associated with tobacco use. However, certain cellular abnormalities in the lungs have been identified more frequently in long-term smokers of cannabis compared to non-smokers. Chronic exposure to cannabis smoke has also been associated with the development of pre-cancerous changes in bronchial and epithelium cells in similar rates to tobacco smokers. Cellular abnormalities were most present in individuals who smoked both tobacco and marijuana, implying that cannabis and tobacco smoke may have an additive adverse effect on airway tissue. The results suggest that long-term exposure to cannabis smoke, particularly when combined with tobacco smoking, is capable of damaging the bronchial system in ways that could one day lead to respiratory cancers. However, to date, no epidemiologic studies of cannabis-only smokers have yet to reveal such a finding. Larger, better-controlled studies are warranted.

Cannabis consumers who desire the rapid onset of action associated with inhalation but who are concerned about the potential harms of noxious smoke can dramatically cut down on their intake of carcinogenic compounds by engaging in vaporization rather than smoking. Cannabis vaporization limits respiratory toxins by heating cannabis to a temperature where cannabinoid vapors form (typically around 180-190 degrees Celsius), but below the point of combustion where noxious smoke and associated toxins (i.e., carcinogenic hydrocarbons) are produced (near 230 degrees Celsius). Because vaporization can deliver doses of cannabinoids while reducing the users intake of carcinogenic smoke, it is considered to be a preferred and likely safer method of cannabis administration than smoking marijuana cigarettes or inhaling from a water pipe. According to the findings of a recent clinical trial, use of the Volcano vaporizing device delivered set doses of THC to subjects in a reproducible manner while suppressing the intake of respiratory toxins.

"Our results show that with the Volcano, a safe and effective cannabinoid delivery system seems to be available to patients," investigators at Leiden University's Institute of Biology (the Netherlands) concluded.

"The final pulmonal uptake of THC is comparable to the smoking of cannabis, while avoiding the respiratory disadvantages of smoking."

(References: On the carcinogenicity of marijuana smoke. Recent Advances in Phytochemistry. 1975. **Author’s Note: More recent studies on higher potency marijuana and/or sinsemilla have not been conducted and could potentially yield different results. | Cannabinoids and cancer: causation, remediation, and palliation. Lancet Oncology. 2005 | Cannabinoids: potential anticancer agents. Nature Reviews Cancer. 2003. | Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer. Journal of Clinical Investigation. 2003 | Cannabis and tobacco smoke are not equally carcinogenic. Harm Reduction Journal. 2005 | Ibid. | National Academy of Sciences, Institute of Medicine. Marijuana and Medicine: Assessing the Science Base. National Academy Press. 1999 | Tracheobronchial histopathology in habitual smokers of cocaine, marijuana and/or tobacco. Chest. 1997 | Histopathologic and molecular alterations in bronchial epithelium in habitual smokers of marijuana, cocaine and/or tobacco. Journal of the National Cancer Institute. 1998 | See footnotes 10 and 11 | Cannabis vaporizer combines efficient delivery of THC with effective suppression of pyrolytic compounds. Journal of Cannabis Therapeutics. 2004 | Hazekamp et al. 2006. Evaluation of a vaporizing device (Volcano) for pulmonary administration of tetrahydrocannabinol. Journal of Pharmaceutical Sciences 95: 1308-1317.) | Vaporization as a smokeless cannabis delivery system: a pilot study.
Clinical Pharmacology & Therapeutics. 2007.

Head, Neck and Lung Cancers

While a handful of anecdotal reports and one small case-control study associate heavy marijuana use among younger adults with increased incidents of head, neck and lung cancers, no large scale population studies have replicated these results. Investigators at John Hopkins University in Baltimore reported that neither "lifetime use" nor "ever use" of cannabis were associated with head, neck or lung cancer in younger adults in a large, hospital-based case-control study of 164 oral cancer patients and 526 controls. Researchers concluded, "The balance of evidence from this, the largest case-control study addressing marijuana use and cancer to date, does not favor the idea that marijuana as commonly used in the community is a major causal factor for head, neck or lung cancer in young adults."

More recently, the results of a 2004 population-based case-control study of 407 individuals diagnosed with oral squamous cell carcinoma and 615 healthy controls found "no association" between cannabis use and incidents of oral cancer, regardless of how long, how much or how often individuals had used it. A second 2004 case-control study of 116 oral cancer patients and 207 matched controls also failed to identify any association between self-reported cannabis use and oral cancers in adults age 45 years old or younger, although only 10 percent of patients in the study identified themselves as heavy users of cannabis.

A 1997 retrospective cohort study examining the relationship of marijuana use to cancer incidence in 65,171 men and women 15 to 49 years of age in California found that cannabis use was not associated with increased risks of developing tobacco-use related cancers of the lung and upper aerodigestive tract, and in fact, no cases of lung cancer were identified among men and women who used marijuana but did not smoke tobacco. Critics charge that volunteers in the study were relatively young and that the follow up period was fairly short, arguing that "such a study could not have been expected to detect any relationship between marijuana and lung cancer if the lag period were comparable to that seen with tobacco," which typically occurs after at least 20 years of smoking cigarettes and/or among adults over age 60. The study’s author responds: "n contrast to users of tobacco and alcohol, most cannabis users generally quit using cannabis relatively early in their adult lives. … Therefore, even diseases that might be related to long-term use of cannabis (e.g. lung cancer) are unlikely to have a sizeable public health impact because most people who try cannabis do not become long-term users."

Government reviews investigating a possible link between cannabis use and lung cancer have also failed to find a definitive causal connection between the two. A 1998 report by the British House of Lords Science and Technology Committee concluded, "There is as yet no epidemiological evidence for an increase risk of lung cancer" in cannabis smokers, though authors did concede that studies have revealed cellular changes in the airways of cannabis smokers that could potentially be pre-cancerous. An 18-month study by the US National Academy of Science Institute of Medicine also concluded, "There is no conclusive evidence that marijuana causes cancer in humans, including cancers generally related to tobacco use," but added that cellular studies and a handful of poorly controlled case studies suggest that cannabis smoke may be "an important risk factor" for the development of upper aerodigestive or lung cancers. A 2002 Canadian Senate review further commented that among the small number of case studies present in the literature: "[N]one compare the prevalence of cancer with a control group or evaluates the use of cannabis in a standardized way. Interpretation is also limited by the fact the patients smoked tobacco and drank alcohol."

More recent reviews of the subject published in the journals Alcohol and Lancet Oncology reach similar conclusions. A review of two cohort studies and 14 case-control studies assessing the association of marijuana and cancer risk by Hashibe and colleagues concluded, "[R]esults of cohort studies have not revealed an increased risk of tobacco related cancers among marijuana smokers." Authors did highlight a pair of African case control studies citing marijuana use as a possible elevated risk factor for lung cancer, though they added that investigators failed to assess either the durations of cannabis use or quantify the amount of tobacco used by subjects in conjunction with marijuana. A second 2005 review by Hall and colleagues conclude, "There is a conspicuous lack of evidence on the association between cannabis smoking and lung cancers," and recommends the subject receive additional study.

A large US case-control study funded by the US National Institutes of Health assessing the effects of marijuana smoking on the risks of lung cancer and upper aerodigestive tract cancers among 2,400 Los Angeles County residents less than 60 years of age is ongoing. Preliminary data from the study, presented by investigators at the 2005 annual conference of the International Cannabinoid Research Society (ICRS), report that those who self-reported using moderate levels of cannabis had no greater odds of suffering from lung or UAT cancers than controls.

(References: Marijuana use and increased risk of squamous cell carcinoma of the head and neck. Cancer Epidemiology Biomarkers & Prevention. 1999 | Marijuana use is not associated with head, neck or lung cancer in adults younger than 55 years: Results of a case cohort study. In: National Institute on Drug Abuse (Eds) Workshop on Clinical Consequences of Marijuana: Program Book. National Institutes of Health. 2001 | Marijuana use and risk of squamous cell carcinoma. Cancer Research. 2004 | An analysis of risk factors for oral cancer in young people: a case-control study. Oral Oncology. 2004 | Marijuana use and cancer incidence. Cancer, Causes & Controls. 1997 | Leslie Iversen. The Science of Marijuana. Oxford University Press. 2000 | Comparing cannabis with tobacco – again. British Medical Journal. 2003 | House of Lords Science and Technology Committee. Ninth Report. 1998 | National Academy of Sciences, Institute of Medicine. Marijuana and Medicine: Assessing the Science Base. National Academy Press. 1999 | Report of the Special Senate Committee on Illegal Drugs. Cannabis: Our Position for a Canadian Public Policy. 2002 | Epidemiologic review of marijuana use and cancer risk. Alcohol. 2005 | Cannabinoids and cancer: causation, remediation, and palliation. Lancet Oncology. 2005 | Ongoing case-control study of marijuana use and cancer. In: National Institute on Drug Abuse (Eds) Workshop on Clinical Consequences of Marijuana: Program Book. National Institutes of Health. 2001 | Marijuana Use and the Risk of Lung and Upper Aerodigestive Tract Cancers: Results of a Population-Based Case-Control Study. Cancer Epidemiology Biomarkers & Prevention. 2006.

Childhood Cancers

Acute myeloid leukemia (AML) comprises approximately 16 percent of leukemias diagnosed in individuals younger than 15 years of age. A 1989 study suggested that prenatal exposure to marijuana increased the risk of childhood leukemia. However, a more recent 2006 study – the largest epidemiological study of childhood AML to date in the US – rebuts this premise.

"Overall, no positive associations between parental marijuana use and childhood AML were observed," investigators at the University of North Carolina at Chapel Hill found. They concluded:

"The previously reported positive association between maternal marijuana use before or during pregnancy and childhood AML was not confirmed in this study. Parental marijuana use is unlikely as a strong risk factor for childhood AML."

Investigators also noted evidence of an "inverse association" between cannabis use and a decreased risk of childhood AML, though they suggested that this result was likely due to "recall bias" (e.g., case mothers may have been less likely than control mothers to report having used marijuana before or during pregnancy) rather than any potential protective effects of cannabis. At least one prior large, population-based case-control study also reports an inverse association between marijuana use and a reduced risk of cancer. That study, published in the American Journal of Epidemiology in 1999, reported that lifetime use of cannabis was associated with a reduced risk of adult, non-Hodgkin’s lymphoma. "Marijuana was the only recreational drug that remained associated with a reduced risk for non-Hodgkin’s lymphoma after adjusting for potential cofounding factors, investigators determined. (A second study on marijuana use and non-Hodgkin’s lymphoma found no association between cannabis use and onset of the disease.)

A review of the literature reveals two additional case-control studies suggesting an increased risk of certain childhood cancers in offspring of mothers who reported using cannabis. However, neither study was a planned investigation of the potential association between maternal cannabis use and childhood cancers; rather, marijuana use was one of several possible confounding variables measured, making it impossible for investigators to ascribe causation. To date, neither of these findings has been replicated.

(References: Maternal drug use and risk of childhood nonlymphoblastic leukemia among offspring. 1989. Cancer | Parental marijuana use and risk of childhood acute myeloid leukemia: a report from the Children’s Cancer Group. Paediatric and Perinatal Epidemiology. 2006 | Case-Control study of non-Hodgkin’s Lymphoma among women and heterosexual men in the San Francisco Bay area, California. American Journal of Epidemiology. 1999 | Alcohol, tobacco and recreational drug use and the risk of non-Hodgkin’s lymphoma. British Journal of Cancer. 1997 | Parents’ use of cocaine and marijuana and increased risk of rhabdomyosarcoma in their children. Cancer Causes and Control. 1993 | Gestational and familial risks factors for childhood astrocytoma: results of a case-control study. Cancer Research. 1990)

Other Cancers

Sidney and colleagues, in their 1997 retrospective cohort study of 65,171 men and women, determined that "ever" and "current use" of cannabis was not associated with an increased risk of tobacco-use related cancers or cancers of the colon, lung, skin, prostate, breast and cervix. "Compared with nonusers/experimenters (lifetime use of less than seven times), … marijuana use [was] not associated with increased risk of cancer … in analyses adjusted for sociodemographic factors, cigarette smoking, and alcohol use," investigators determined. A 2005 review of case studies by Hashibe and colleagues also failed to note evidence of a strong association between cannabis use and either anal or penile cancer.

A second cohort study by University of Hawaii researchers investigating the risk for malignant primary onset glioma (brain cancer) associated with cigarette smoking and other lifestyle behaviors did report an increased incidence risk for individuals who smoked cannabis at least once per month, after adjustment for sex, race, education, smoking status, alcohol consumption, and coffee intake. However, no dose-response relation was observed -- by contrast, drinkers of >7 cups of coffee per day had a 70 percent increased risk for glioma – and cannabis was only incidentally assessed as a potential confounding factor

The above finding is curious in light of several recent preclinical studies demonstrating that the administration of cannabinoids selectively inhibit the growth of glioma cells in a dose dependent manner. Among these, an Italian research team, writing in the 2004 issue of the Journal of Pharmacology and Experimental Therapeutics demonstrated that the administration of the non-psychoactive cannabinoid cannabidiol (CBD) to nude mice significantly inhibited the growth of subcutaneously implanted U87 human glioma cells. Authors wrote, "In conclusion, … CBD was able to produce a significant antitumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent (an agent that inhibits the growth of malignant cells.)" More recently, investigators at the California Pacific Medical Center Research Institute reported that the administration of THC on human glioblastoma multiforme cell lines decreased the proliferation of malignant cells and induced apoptosis (programmed cell death) more rapidly than did the administration of an alternative synthetic cannabis receptor agonist.

Finally, a team of investigators from Stanford University and the Medical College of Georgia recently reported an association between marijuana exposure and bladder cancer in a pilot study of Vietnam-era veterans aged less than 60 years old. However, 77 percent of the cancer patients in the study reported smoking both tobacco and marijuana, and only six subjects (11 percent) admitted to having used marijuana and not tobacco. A 2006 case report published in the journal Urology also suggests heavy cannabis use (up to five cigarettes daily for more than 30 years) as a potential risk factor in a 45-year-old man with transitional cell carcinoma. Follow-up, large-scale epidemiological studies may be warranted in this area.

(References: Marijuana use and cancer incidence. Cancer, Causes & Controls. 1997 | Epidemiologic review of marijuana use and cancer risk. Alcohol. 2005 | The risk for malignant primary adult-onset glioma in a large, multiethnic, managed-care cohort: cigarette smoking and other lifestyle behaviors. Journal of Neurooncology. 2004 | Anti-tumor effects of cannabidiol, a non-psychotropic cannabinoid, on human glioma cell lines. Journal of Pharmacology and Experimental Therapeutics. 2003 | Cannabinoids selectively inhibit proliferation and induce cell death of cultured human glioblastoma multiforme cells. Journal of Neurooncology. 2005 | Association between marijuana use and transitional cell carcinoma. Urology. 2006 | Transitional cell carcinoma associated with marijuana: case report and review of the literature. Urology. 2006.)

Cannabis and the Brain: A User's Guide


Preclinical data recently published in the Journal of Clinical Investigation demonstrating that cannabinoids may spur brain cell growth has reignited the international debate regarding the impact of marijuana on the brain. However, unlike previous pseudo-scientific campaigns that attempted to link pot smoking with a litany of cognitive abnormalities, modern research suggests what many cannabis enthusiasts have speculated all along: ganja is good for you.

Cannabinoids & Neurogenesis

"Study turns pot wisdom on its head," pronounced the Globe and Mail in October. News wires throughout North America and the world touted similar headlines -- all of which were met with a monumental silence from federal officials and law enforcement. Why all the fuss? Researchers at the University of Saskatchewan in Saskatoon found that the administration of synthetic cannabinoids in rats stimulated the proliferation of newborn neurons (nerve cells) in the hippocampus region of the brain and significantly reduced measures of anxiety and depression-like behavior. The results shocked researchers -- who noted that almost all other so-called "drugs of abuse," including alcohol and tobacco, decrease neurogenesis in adults -- and left the "pot kills brain cells" crowd with a platter of long-overdue egg on their faces.

While it would be premature to extrapolate the study's findings to humans, at a minimum, the data reinforce the notion that cannabinoids are unusually non-toxic to the brain and that even long-term use of marijuana likely represents little risk to brain function. The findings also offer further evidence that cannabinoids can play a role in the alleviation of depression and anxiety, and that cannabis-based medicines may one day offer a safer alternative to conventional anti-depressant pharmaceuticals such as Paxil and Prozac.

(Reference: Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic and depressant-like effects. The Journal of Clinical Investigation. 2005)

Cannabis & Neuroprotection

Not only has modern science refuted the notion that marijuana is neurotoxic, recent scientific discoveries have indicated that cannabinoids are, in fact, neuroprotective, particularly against alcohol-induced brain damage. In a recent preclinical study -- the irony of which is obvious to anyone who reads it -- researchers at the US National Institutes of Mental Health (NIMH) reported that the administration of the non-psychoactive cannabinoid cannabidiol (CBD) reduced ethanol-induced cell death in the brain by up to 60 percent. "This study provides the first demonstration of CBD as an in vivo neuroprotectant ... in preventing binge ethanol-induced brain injury," the study's authors wrote in the May 2005 issue of the Journal of Pharmacology and Experimental Therapeutics. Alcohol poisoning is linked to hundreds of preventable deaths each year in the United States, according to the Centers for Disease Control, while cannabis cannot cause death by overdose.

Of course, many US neurologists have known about cannabis' neuroprotective prowess for years. NIMH scientists in 1998 first touted the ability of natural cannabinoids to stave off the brain-damaging effects of stroke and acute head trauma. Similar findings were then replicated by investigators in the Netherlands and Italy and, most recently, by a Japanese research in 2005. However, attempts to measure the potential neuroprotective effects of synthetic cannabinoid-derived medications in humans have so far been inconclusive.

(References: Comparison of cannabidiol, antioxidants and diuretics in reversing binge ethanol-induced neurotoxicity. Journal of Pharmacology and Experimental Therapeutics. 2005 | Cannabidiol prevents cerebral infarction. Stroke. 2005 | Post-ischemic treatment with cannabidiol prevents electroencephalographic flattening, hyperlocomotion and neuronal injury in gerbils. Neuroscience Letters. 2003 | Neuroprotection by Delta9-tetrahydrocannabinol, the main active compound in marijuana, against ouabain-induced in vivo excitotoxicity. Journal of Neuroscience. 2001 | Cannabidiol and Delta9-tetrahydrocannabinol are neuroprotective antioxidants. Proceedings of the National Academy of Sciences. 1998)

Cannabinoids & Glioma

Of all cancers, few are as aggressive and deadly as glioma. Glioma tumors quickly invade healthy brain tissue and are typically unresponsive to surgery and standard medical treatments. One agent they do respond to is cannabis.

Writing in the August 2005 issue of the Journal of Neurooncology, investigators at the California Pacific Medical Center Research Institute reported that the administration of THC on human glioblastoma multiforme cell lines decreased the proliferation of malignant cells and induced apoptosis (programmed cell death) more rapidly than did the administration of the synthetic cannabis receptor agonist, WIN-55,212-2. Researchers also noted that THC selectively targeted malignant cells while ignoring healthy ones in a more profound manner than the synthetic alternative. Patients diagnosed with glioblastoma multiforme typically die within three months without therapy.

Previous research conducted in Italy has also demonstrated the capacity of CBD to inhibit the growth of glioma cells both in vitro (e.g., a petri dish) and in animals in a dose dependent manner. As a result, a Spanish research team is currently investigating whether the intracranial administration of cannabinoids can prolong the lives of patients diagnosed with inoperable brain cancer.

Most recently, a scientific analysis in the October issue of the journal Mini-Reviews in Medicinal Chemistry noted that, in addition to THC and CBD's brain cancer-fighting ability, studies have also shown cannabinoids to halt the progression of lung carcinoma, leukemia, skin carcinoma, colectoral cancer, prostate cancer and breast cancer.

(References: Cannabinoids selectively inhibit proliferation and induce cell death of cultured human glioblastoma multiforme cells. Journal of Neurooncology. 2005 | Cannabinoids and cancer. Mini-Reviews in Medicinal Chemistry. 2005 | Anti-tumor effects of cannabidiol, a non-psychotropic cannabinoid, on human glioma cell lines. Journal of Pharmacology and Experimental Therapeutics. 2003)

Cannabinoids & Neurodegeneration

Emerging evidence also indicates that cannabinoids may play a role in slowing the progression of certain neurodegenerative diseases, such as Multiple Sclerosis, Parkinson's disease, Alzheimer's, and Amyotrophic Lateral Sclerosis (a.k.a. Lou Gehrig's Disease). Recent animal studies have shown cannabinoids to delay disease progression and inhibit neurodegeneration in mouse models of ALS, Parkinson's, and MS. As a result, the Journal of Neurological Sciences recently pronounced, "There is accumulating evidence ... to support the hypothesis that the cannabinoid system can limit the neurodegenerative processes that drive progressive disease," and patient trials investigating whether the use of oral THC and cannabis extracts may slow the progression of MS are now underway in the United Kingdom.

(References: Cannabinoids and neuroprotection in CNS inflammatory disease. Journal of the Neurological Sciences. 2005. Amyotrophic lateral sclerosis: delayed disease progression in mice by treatment with a cannabinoid. Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders. 2004 | Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. Brain. 2003)

Cannabis & Cognition

But what about claims of cannabis' damaging effect of cognition? A review of the scientific literature indicates that rumors regarding the "stoner stupid" stereotype are unfounded. According to clinical trial data published this past spring in the American Journal of Addictions, cannabis use -- including heavy, long-term use of the drug -- has, at most, only a negligible impact on cognition and memory. Researchers at Harvard Medical School performed magnetic resonance imaging on the brains of 22 long-term cannabis users (reporting a mean of 20,100 lifetime episodes of smoking) and 26 controls (subjects with no history of cannabis use). Imaging displayed "no significant differences" between heavy cannabis smokers compared to controls, the study found.

Previous trials tell a similar tale. An October 2004 study published in the journal Psychological Medicine examining the potential long-term residual effects of cannabis on cognition in monozygotic male twins reported "an absence of marked long-term residual effects of marijuana use on cognitive abilities." A 2003 meta-analysis published in the Journal of the International Neuropsychological Society also "failed to reveal a substantial, systematic effect of long-term, regular cannabis consumption on the neurocognitive functioning of users who were not acutely intoxicated," and a 2002 clinical trial published in the Canadian Medical Association Journal determined, "Marijuana does not have a long-term negative impact on global intelligence."

Finally, a 2001 study published in the journal Archives of General Psychiatry found that long-term cannabis smokers 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." Investigators further added, "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."

(References: Lack of hippocampal volume change in long-term heavy cannabis users. American Journal of Addictions. 2005 | Neuropsychological consequences of regular marijuana use: a twin study. Psychological Medicine. 2004 | Non-acute (residual) neurocognitive effects of cannabis use: A meta-analytic study. Journal of the International Neuropsychological Society. 2003 | Current and former marijuana use: preliminary findings of a longitudinal study of effects on IQ in young adults. Canadian Medical Association Journal. 2002 | Neuropsychological Performance in Long-term Cannabis Users. Archives of General Psychiatry. 2001)

Complete with references to respected medical establishments.

Are we done with the weak arguement that weed is bad for you? Even if it was, so is McDonalds, Budweiser, Pepsi and about half of the Rx's available to you.

i do know that it depends on the person...i even said some people are fine on it.

It's all good, I just read the posts about how it causes cancer, makes you crazy, Etc. Easily proven to be false, difference is, my rebuttal posts comes complete with reference material.

End the War on Drugs

Ron Paul
Prisonplanet.com
Tuesday, March 31, 2009

We have recently heard many shocking stories of brutal killings and ruthless violence related to drug cartels warring with Mexican and US officials. It is approaching the fever pitch of a full-blown crisis. Unfortunately, the administration is not likely to waste this opportunity to further expand government. Hopefully, we can take a deep breath and look at history for the optimal way to deal with this dangerous situation, which is not unprecedented.

Alcohol prohibition in the 1920’s brought similar violence, gangs, lawlessness, corruption and brutality. The reason for the violence was not that making and selling alcohol was inherently dangerous. The violence came about because of the creation of a brutal black market which also drove profits through the roof. These profits enabled criminals like Al Capone to become incredibly wealthy, and militantly defensive of that wealth. Al Capone saw the repeal of Prohibition as a great threat, and indeed smuggling operations and gangland violence fell apart after repeal. Today, picking up a bottle of wine for dinner is a relatively benign transaction, and beer trucks travel openly and peacefully along their distribution routes.

Similarly today, the best way to fight violent drug cartels would be to pull the rug out from under their profits by bringing these transactions out into the sunlight. People who, unwisely, buy drugs would hardly opt for the back alley criminal dealer as a source, if a coffeehouse-style dispensary was an option. Moreover, a law-abiding dispensary is likely to check ID’s and refuse sale to minors, as bars and ABC stores tend to do very diligently. Think of all the time and resources law enforcement could save if they could instead focus on violent crimes, instead of this impossible nanny-state mandate of saving people from themselves!

If these reasons don’t convince the drug warriors, I would urge them to go back to the Constitution and consider where there is any authority to prohibit private personal choices like this. All of our freedoms – the freedom of religion and assembly, the freedom of speech, the right to bear arms, the right to be free from unnecessary government searches and seizures – stem from the precept that you own yourself and are responsible for your own choices. Prohibition laws negate self-ownership and are an absolute affront to the principles of freedom. I disagree vehemently with the recreational use of drugs, but at the same time, if people are only free to make good decisions, they are not truly free. In any case, states should decide for themselves how to handle these issues and the federal government should respect their choices.

My great concern is that instead of dealing deliberatively with the actual problems, Congress will be pressed again to act quickly without much thought or debate. I can’t think of a single problem we haven’t made worse that way. The panic generated by the looming crisis in Mexico should not be redirected into curtailing more rights, especially our second amendment rights, as seems to be in the works. Certainly, more gun laws in response to this violence will only serve to disarm lawful citizens. This is something to watch out for and stand up against. We have escalated the drug war enough to see it only escalates the violence and profits associated with drugs. It is time to try freedom instead.

like i said...it is just like alcohol...some can handle it...some can't and neither are good in large amounts. my sister and I have tried it for pain before because of our blood disease (which is often misdiagnosed). she hallucinated and got paranoid...my muscles tensed so bad i couldn't move for a time. the neighbor kid went crazy when he started smoking ALOT (pretty much all day long) and he stalked my niece. she had to change her number and finally moved in with her grandmother. this is why i said it's something people have observed...not all in statistics.

http://www.nida.nih.gov/ResearchReports/Marijuana/Marijuana3.html

is another site as well. I believe IF they make it legal...it needs to have the same laws as alcohol

War,

That's not true. It does affect the lungs. Look at these sites: NIDA, CDC, AMA (American Medical Association). The facts are there.

I agree!

Great information warmachine!

hey now...do I look like war to you??? i know I'm sick but I don't look like a man

I agree!

Great information warmachine!


hey now...do I look like war to you??? i know I'm sick but I don't look like a man


Sorry trying to save space

Nope. Never be legal. Too high a potential for law suits. Just look at all the hoops for the legal drugs the manufacturers have to jump through prior to marketing.

That's a good point. I never thought about that. There's the FDA to go through.

Yes and you're talking about a substance without a measurable dose whose effects vary greatly by strain. Conceivably, there would be absolutely no way to regulate it. At least with alcohol you have blood-alcohol content at a certain percentage. With marijuana it's all or nothing.

And...if it does have to go through that scrutiny (most likely will), can you imagine how much it would cost to purchase then?