Cannabis Freedom Activist Network's Guide To
Cannabis Research

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OTHER CANNABIS RELATED
Cannabis Freedom Activist Network

Cannabis Research Organizations & Websites

CannabisMD
Cannabis.net
Cannabis Research Institute
Coalition for Rescheduling Cannabis
Drug Reform Coordination Network
DrugScience.org
Drugtext Foundation
ElectricEmperor.com
Erowid
International Cannabinoid Research Society
Lycaeum
Marijuana Policy Project
New Scientist
North American Industrial Hemp Council
Olsen Marijuana Archive
OnlinePot
Partnership for Responsible Drug Information
Schaffer Library of Drug Policy
Science of Medical Marijuana
UK Cannabis Internet Activists
Web Station #19

Accidents

Also see Safety

2005: "All major studies show that marijuana consumption has little or no effect on driving ability, and may actually reduce accidents." claims Dana Larsen from "Stoned drivers are safe drivers", Cannabis Culture, Jan 11 2005.

2004: "No increased risk for road trauma was found for drivers exposed to cannabis." claims KL Movig, MP Mathijssen, PH Nagel, T van Egmond, JJ de Gier, HG Leufkens, AC Egberts from "Psychoactive substance use and the risk of motor vehicle accidents", PubMed, National Library of Medicine, July 2004.

2003: "Although the levels were low, subjects generally correctly identified if they were truly dosed or not. Their task was to drive through city streets while responding to traffic controls, crossing intersections and making turns at intersections. Using driving instructors' performance scores, Lamers and Ramaekers found essentially no differences between the dosed and non-dosed conditions. However, they also found that drivers under the THC-only condition evaluated their performance as significantly worse than under the placebo, the alcohol and the alcohol+THC condition. Thus, the study confirmed the hypothesis that, unlike alcohol, marijuana actually enhances rather than mitigates the perception of impairment. The only negative behavioral effect of THC was a slight reduction in the frequency of intersections searched for cross traffic (based on the drivers' eye movement records). Although statistically significant, the drop was negligible: from a mean frequency of 85% of the intersections in the placebo condition, to a mean frequency of 82% in the combined alcohol+THC condition." – "State of Knowledge of Drug-Impaired Driving", DOT HS 809 642, Sept 2003.

2002: "When Doctor Yesavage was funded by the federal government to repeat the study with the simple controls that others and I [Dr John Morgan] had suggested, they were unable to show any impact of marijuana use after four hours in a similar group of people. Therefore, I believe that the truth is that marijuana use will impact airplane and driving simulators and to some degree driving performance for three hours to four hours after use; however there is no sustained impact. Any impact is relatively minor. ... The study findings show that cannabis alone does not increase the likelihood of responsibility in an accident. However, most of the studies used a measurement of THC-COOH, an inactive metabolite that can remain in urine for several days. When the authors separated out THC alone, the risk ratio was slightly higher, even though it did not reach the required level of significance. In addition, as the concentration of THC increases, the more the ratio increases, once again suggesting a dose-response relationship. Furthermore, the cannabis and alcohol combination significantly increases risk. Without being able to draw any definite conclusions, there are some signs that their effects are in synergy and not merely additive. Studies on injured drivers (Terhune (1982) and Hunter (1998)) have ratios somewhat higher than in the other studies on fatal accidents. According to Bates and Blakely (1999), the apparent reduction in the risk of a fatal accident stems from the fact that drivers under the influence of cannabis drive less dangerously, for example by reducing their speed." – "Cannabis: Our Position for a Canadian Public Policy", Vol 1, Chap 8, Sept 2002.

2000: "In conclusion, cannabis impairs driving behaviour. However, this impairment is mediated in that subjects under cannabis treatment appear to perceive that they are indeed impaired. Where they can compensate, they do, for example, by not overtaking, by slowing down and by focusing their attention when they know a response will be required. However, such compensation is not possible where events are unexpected or where continuous attention is required. Effects of driving behaviour are present up to an hour after smoking but do not continue for extended periods." – "Cannabis and driving: a review of the literature and commentary (No 12)", Chap 11, Department of Transport, Great Britain

2000: "... [United Kingdom] government-funded research ... shows that driving under the influence of drugs makes motorists more cautious and has a limited impact on their risk of crashing. In the study, conducted by the Transport Research Laboratory, grade A cannabis specially imported from America was given to 15 regular users. ... drivers were then put through four weeks of tests on driving simulators to gauge reaction times and awareness. Regular smokers were used because previous tests in America using first-timers resulted in the volunteers falling over and feeling ill. The laboratory found its guinea pigs through what it described as a 'snowballing technique' - one known user was asked to find another after being promised anonymity and exemption from prosecution agreed with the Home Office. Instead of proving that drug-taking while driving increased the risk of accidents, researchers found that the mellowing effects of cannabis made drivers more cautious and so less likely to drive dangerously. Although the cannabis affected reaction time in regular users, its effects appear to be substantially less dangerous than fatigue or drinking. Research by the Australian Drugs Foundation found that cannabis was the only drug tested that decreased the relative risk of having an accident. The findings will embarrass ministers at the Department of the Environment, Transport and the Regions (DETR) who commissioned the study after pressure from motoring organisations and anti-drug campaigners. Lord Whitty, the transport minister, will receive the report later this month. Last week police revealed details of new drug-driving tests to be administered by the roadside, which were received with some amusement. They require suspected drug-drivers to stand on one leg, lean back and touch their nose with their eyes closed, and to count to 30 silently with their eyes shut. This is apparently difficult for those on a drug trip. ... if the findings are less than frightening on the effects of marijuana, they may convince [UK] ministers to put more money into raising driver awareness of fatigue. Tiredness is now blamed for causing 10% of all fatal accidents, compared with 6% for alcohol and 3% for drugs. The report's surprising conclusions will not sway organisations such as the RAC, which believes there is incontrovertible evidence that drug-driving is a growing menace. DETR statistics published in January showed a six-fold increase in the number of people found to be driving with drugs in their system after fatal road accidents. The figure jumped from 3% in 1989 to 18%. Dr Rob Tunbridge, the report's author, refused to reveal his findings before they were published but said: 'If you were to ask me to rank them in order of priority, fatigue is the worst killer, followed by alcohol, and drugs follow way behind in third.' Tunbridge admitted that the effect of drugs differed with the individual, the amount taken, the environment they were taken in and the point at which you tested reactions." claims Jonathan Carr-Brown from "Cannabis may make you a safer driver", Times United Kingdom, Aug 13 2000.
mapinc.org/newscc/v00/n1161/a02.html, ~~the-times.co.uk/news/pages/sti/2000/08/13/stinwenws03043.html~~ (2005)

1999: "Recent research into impairment and traffic accident reports from several countries shows that marijuana taken alone in moderate amounts does not significantly increase a driver's risk of causing an accident -- unlike alcohol ... While smoking marijuana does impair driving ability, it does not share alcohol's effect on judgment. Drivers on marijuana remain aware of their impairment, prompting them to slow down and drive more cautiously to compensate ..." claims Alison Smiley, Univ of Toronto researcher, from "Marijuana Not a Factor in Driving Accidents", Mar 29 1999.

1998: "The largest study ever done linking road accidents with drugs and alcohol has found drivers with cannabis in their blood were no more at risk than those who were drug-free. In fact, the findings by a pharmacology team from the University of Adelaide and Transport SA showed drivers who had smoked marijuana were marginally less likely to have an accident than those who were drug-free. ... the difference was not great enough to be statistically significant but could be explained by anecdotal evidence that marijuana smokers were more cautious and drove more slowly because of altered time perception." claims Dr Jason White from "Cannabis and driving", Oct 21 1998.

1996: "Compared to alcohol, which makes people take more risks on the road, marijuana made drivers slow down and drive more carefully.... Cannabis is good for driving skills, as people tend to overcompensate for a perceived impairment." claims Professor Olaf Drummer, forensic scientist, Royal College of Surgeons in Melbourne, Australia.

1995: "In high doses marijuana probably produces driving impairment in most people. However, there is no evidence that marijuana, in current consumption patterns, contributes substantially to the rate of vehicular accidents in America." claims "Claim #12 : Marijuana is a Major Cause of Highway Accidents", Exposing Marijuana Myths, by Lynn Zimmer, Associate Professor of Sociology, Queens College, and John P Morgan, Professor of Pharmacology, City University of New York Medical School, published by Lindesmith Center.
druglibrary.org/schaffer/hemp/general/mjmyth/Exposing_11_1095.html, erowid.org/plants/cannabis/cannabis_myth12.shtml, pdxnorml.org/Exposing_11_1095.html, drugtext.org/library/articles/marijuan.html

1994: "The Incidence and Role of Drugs in Fatally Injured Drivers" by K W Terhune, et al, published by Department of Transportation.

1994: "Testing Reckless Drivers for Cocaine and Marijuana" by D Brookoff, et al, New England Journal of Medicine #331, pgs 518-522.

1993: "This program of research has shown that marijuana, when taken alone, produces a moderate degree of driving impairment which is related to the consumed THC dose. The impairment manifests itself mainly in the ability to maintain a steady lateral position on the road, but its magnitude is not exceptional in comparison with changes produced by many medicinal drugs and alcohol. Drivers under the influence of marijuana retain insight in their performance and will compensate, where they can, for example, by slowing down or increasing effort. As a consequence, THC's adverse effects on driving performance appear relatively small. THC's effects on road-tracking after doses up to 300 g/kg never exceeded alcohol's at bacs of 0.08 %; and, were in no way unusual compared to many medicinal drugs' (Robbe, 1994; Robbe and O'Hanlon, 1995; O'Hanlon et al., 1995). Yet, THC's effects differ qualitatively from many other drugs, especially alcohol. Evidence from the present and previous studies strongly suggests that alcohol encourages risky driving whereas THC encourages greater caution, at least in experiments. Another way THC seems to differ qualitatively from many other drugs is that the former's users seem better able to compensate for its adverse effects while driving under the influence. Although THC's adverse effects on driving performance appeared relatively small in the tests employed in this program, one can still easily imagine situations where the influence of marijuana smoking might have a dangerous effect; i.e., emergency situations which put high demands on the driver's information processing capacity, prolonged monotonous driving, and after THC has been taken with other drugs, especially alcohol. Because these possibilities are real, the results of the present studies should not be considered as the final word. They should, however, serve as the point of departure for subsequent studies that will ultimately complete the picture of THC's effects on driving performance." claims Marijuana and Actual Driving Performance (DOT HS 808 078, Final Report, Nov 1993), National Highway Traffic Safety Administration. Also published in Journal of the International Hemp Association, vol 1, pgs 44-48.
nhtsa.gov, paston.co.uk/users/webbooks/driving.html#usdot, erowid.org/plants/cannabis/cannabis_driving4.shtml

1992: "The report concluded that alcohol was by far the 'dominant problem' in drug-related accidents. A responsibility analysis showed that alcohol-using drivers were conspicuously culpable in fatal accidents, especially at high blood concentrations or in combination with other drugs, including marijuana. However, those who used marijuana alone were found to be if anything less culpable than non-drug-users. The report concluded, "there was no indication that marijuana by itself was a cause of fatal accidents." reports Dale Gieringer from "The Incidence and Role of Drugs in Fatally Injured Drivers" by K W Terhune et al, Calspan Corp Accident Research Group, Buffalo, NY, Oct 1992.

1987: In January, 16 persons die and 170 are injured after an engineer drunk on alcohol passes out and crashes his Amtrak passenger train into three locomotives. The engineer had also been smoking cannabis. Many cannabis prohibitionists point to this incident when arguing that cannabis use is not a victimless act.

1983: A simulator study of the combined effects of alcohol and marijuana on driving behavior, A C Stein, et al, DOT HS 806 405, US Department of Transportation.

1980: "Marijuana and Driving", A J McBay and S M Owens, Problems of Drug Dependence 1980, editted by L S Harris, published by US Government Printing Office, pgs 257-263.

1977: "Effects of Marijuana on Human Reaction Time and Motor Control", T O Kv'alseth, Perceptual and Motor Skills, vol 45, pgs 935-939.

1976: "Effects of Cannabis and Alcohol on Automobile Driving and Psychomotor Tracking", R W Hansteen, et al, Annals of New York Academy of Science, vol 282, pgs 240-56.

1976: " Marijuana: Effects on Simulated Driving Performance", H Moskowitz, et al, Accident Analysis and Prevention, vol 8, pgs 45-50.

1976: "Visual Search Behaviour While Viewing Driving Scenes Under the Influence of Alcohol and Marijuana", H Moskowitz, et al, Human Factors, vol 18, pgs 417-431.

Cannabis and Road Safety, research studies to examine the effects of cannabis on driving skills and on actual driving performance by Dr. G.B.Chesher, Dept of Pharmacology University of Sydney and National Drug and Alcohol Research Centre University of New South Wales, Australia.
shug.co.uk/research/driving2.htm

"Simulated driving scores for subjects experiencing a normal social 'high' and the same subjects under control conditions are not significantly different. However, there are significantly more errors for alcohol intoxicated than for control subjects" claims Crancer Study, Washington Department of Motor Vehicles.
csuchico.edu/pot/driving.html, druglibrary.org/schaffer/Library/studies/ledain/nonmed3.htm

National Organization for the Reform of Marijuana Laws' "Driving and Marijuana"
norml.org/index.cfm?Group_ID=5448

Acquired Immune Deficiency Syndrome

Also see AIDS medicine, AIDS safety

AIDS medicine

Also see AIDS safety, Appetite, Immune System, Nausea, Weight

2005: "Controlled studies have revealed therapeutic utility of cannabinoids in the treatment of ... AIDS wasting syndrome ... THC itself is approved in the U.S. by the FDA, and it is used in many other countries ... for appetite enhancement. We, and many others, have found that not only THC does that, but also the endocannabinoids. This is one of the main reasons for high endocannabinoid levels during hunger and so on. Now, THC can be used, and is being used, for these two things." claims Dr Raphael Mechoulam, as reported by David Jay Brown, "The New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael Mechoulam".

2000: "A study by researchers from the University of California, San Francisco has found that patients with HIV infection taking protease inhibitors do not experience short-term adverse virologic effects from using cannabinoids. ... All three groups gained weight. Part of that was due to regularly scheduled meals and snacks being readily available. However, the placebo arm averaged a gain of 1.30 kilograms while the subjects who took oral dronabinol gained an average of 3.18 kilograms. Those who smoked marijuana gained an average of 3.51 kilograms. Caloric intake reflected the same order." claims Dr Donald Abrams, Professor of Clinical Medicine, University of California at San Francisco from "Marijuana Does Not Appear To Alter Viral Loads of HIV Patients Taking Protease Inhibitors", July 13 2000.
also at cannabismd.org/reports/abrams1.php, marijuananews.com/news.php3?sid=253

1997: Australian AIDS patients who use cannabis have a better quality of life and patients with AIDS for more than 10 years find cannabis to be critical. One patient believes cannabis to be his "savior", claims "Dope Use Improves Lives of Patients: Research", Canberra Times, Jan 15, 1997.

1989: "One study of marijuana use suggests that daily use for 9 weeks restored initially low numbers of T lymphocytes to normal." claims Multicenter AIDS Cohort Study in its report "No evidence for a Role of Alcohol or Other Psychoactive Drugs in Accelerating Immunodeficiency in HIV-1 Positive Individuals", Journal of the American Medical Association, June 16, 1989.

AIDS safety

Also see Immune System safety

2004: "Short-term cannabis use does not seem to adversely affect CD4+ cell counts or viral loads in HIV -infected patients, according to a report published in the August 19th issue of the Annals of Internal Medicine. In HIV-infected patients, marijuana has been used as an appetite stimulant and as a treatment for the nausea associated with some antiretroviral agents. However, concern has been raised that such therapy could have a harmful effect on disease status, because in theory, cannabinoid use could increase HIV levels by impairing the immune response or by interfering with the activity of protease inhibitors. Previously it was shown that short-term marijuana use did not influence nelfinavir metabolism. Although marijuana use did produce a drop in indinavir levels, this fall was small and unlikely to be clinically meaningful. However, it still remained unclear whether cannabinoid use had an effect on viral load or CD+ cell counts. To investigate, Dr. Donald I. Abrams, from the University of California at San Francisco, and colleagues assessed the outcomes of 67 HIV-infected patients who were randomly assigned to use marijuana cigarettes, cannabinoid capsules, or sugar pills (placebo) three times daily for 21 days. All of the patients had been receiving the same antiretroviral regimen, which included indinavir or nelfinavir, for at least 8 weeks before the study began. More than half of the subjects in each group had undetectable viral loads throughout the study, the researchers note. Although not statistically significant, marijuana and cannabinoid use were actually associated with a slight drop in viral load compared with placebo use. Marijuana and cannabinoid use did not produce a drop in CD4+ or CD8+ cell counts. In fact, compared with placebo use, treatment with these agents was actually associated with a slight increase in cell counts. The results suggest that short-term cannabinoid use is not unsafe for patients with HIV infection, the authors note. 'Further studies investigating the therapeutic potential of marijuana and other cannabinoids in patients with HIV infection and other populations are ongoing and should provide additional safety information over longer exposure periods,' they write."
420times.com/forums/showthread.php?s=f6455a74d8fdae687b3a38344f18f516&t=34497, paktribune.com/news/index.php?id=88101

2003: "These findings suggest no major, short-term harmful effects and possibly some beneficial effects of cannabinoids in HIV-infected patients taking protease inhibitors." claims D I Abrams, J F Hilton, R J Leiser, et al, from "Does Marijuana Affect Viral Loads in People with HIV?", Annals of Internal Medicine, Aug 2003, vol 139, pgs 258-266.
annals.org/cgi/content/summary/139/4/..., jointogether.org/sa/news/summaries/reader/0,1854,566530,00.html

2003: "The study noted that marijuana smokers with AIDS ... mortality was virtually the same as it was for AIDS patients who didn’t smoke marijuana.” from "Marijuana Smoking Doesn't Lead to Higher Death Rate", O'Shaughnessy's Jouurnal of the California Cannabis Research Medical Group, Summer 2003.

"Studies on certain species of rats using high doses of THC showed observable suppression of the immune system and the actions of 'tumoricidal' cells. This evidence suggests that the wonderful auto-immune-disease-curative powers of THC measured in 1989 ... has a negative side to it - perhaps THC allows cancer and opportunistic infections to spread more easily? A report by the National Toxicology Program failed to support this notion. As described in AIDS Treatment News, the research project tested rats for two years with a steady dose of either THC or placebo. The THC dose was extremely high. The rats on THC lived longer and developed fewer tumors than those on the placebo. This report was not released on schedule and people have suggested it was deliberately suppressed because the results were too shocking." claims Los Angeles Cannabis Resource Center from "Cannabinoids in the Immune System".

Addiction

Also see Alcoholism, Habituation, Tolerance, Withdrawal

2006: "Now, marijuana's addictiveness is supported by clinical and epidemiological studies based on the American Psychiatric Association's diagnostic manual. But marijuana for some time has been widely used as a countercultural recreational drug, and drug policy reformers in particular refuse to apply the addictive label to this substance. Political conservatives, on the other hand, insist on the harmfulness of marijuana as a tenet of their drug policy. The grounds are thus set for perpetual conflict around the drug, conflict that cannot be resolved by clinical designations or epidemiological research. ... The addictiveness of caffeine, for example in coffee, is periodically rediscovered (see Juliano & Griffiths, 2004), but ignored because people mainly don't care about addiction to this popular, legal, accepted drug (unless, occasionally, someone is trying to quit). Moreover, caffeine dependence is not considered in the American Psychiatric Association's diagnostic manual, DSM-IV ... In recent years, however, middle-class whites have discovered that marijuana is a relatively safe experience. Although we still get sporadic, alarmist reports on one or another harmful aspect of marijuana, respected organs of society are now calling for the decriminalization of the drug. We are near the end of a process of cultural acceptance of marijuana. Students and young professionals, many of whom lead very staid lives, have become comfortable with it, while still feeling sure that people who take heroin become addicted. ... The two most widely used substances that are thought of as addictive are cigarettes and alcohol. These are legal, and there is no serious effort in place to proscribe them. These are joined by pain killers, which are also widely recognized as addictive (such as, most recently, Oxycontin; Peele, 2004). Obviously, we are prepared to accept addictive drugs in our legal pharmacopoeia. ... What is the correct attitude towards marijuana's addictive potential? We need to recognize that addiction is not so much bound up in the characteristics of drugs (aside from their ability to modify mood quickly and predictably), as it is in the situations of users. ... But a spate of recent studies have identified a marijuana dependence syndrome in about 10 percent of current users. ... For the most part, the debate over marijuana's addictiveness is all flash and no substance. Certainly, marijuana is addictive - as are coffee, antidepressants, and tranquilizers. This, in itself, has no weight in policy decisions about marijuana." claims internationally recognized addiction expert Stanton Peele from "Marijuana Is Addictive - So What?", Jan 18 2006.

2004: "All patients reported benefit, indicating that for at least a subset of alcoholics, cannabis use is associated with reduced drinking. ... There are ample references, however, to the use of cannabis as a substitute for opiates (Birch 1889) and as a treatment for delirium tremens (Clendinning 1843; Moreau 1845), which were among the first uses by European physicians. ... At the turn of the 19th century in the United States, cannabis was listed as a treatment for delirium tremens in standard medical texts (Edes 1887; Potter 1895) and manuals (Lilly 1898; Merck 1899; Parke Davis 1909). Since delirium tremens is associated with advanced alcoholism, we can adduce that patients who were prescribed cannabis and used it on a long term basis were making a successful substitution. ... The patient had observed that when she smoked marijuana socially on weekends she decreased her alcoholic intake. She was instructed to substitute cannabis any time she felt the urge to drink. This regimen helped her to reduce her alcohol intake to zero. ... Even if use is daily, cannabis replacing alcohol (or other addictive, toxic drugs) reduces harm because of its relatively benign side-effect profile. Cannabis-only usage is not associated with car crashes; it does not damage the liver, the esophagus, the spleen or the digestive tract. The chronic alcohol-inebriation-withdrawal cycle ceases with successful cannabis substitution. Sleep and appetite are restored, ability to focus and concentrate is enhanced, energy and activity levels are improved, and pain and muscle spasms are relieved. Family and social relationships can be sustained as pursuit of long-term goals ends the cycle of crisis and apology. ... Treating alcoholism by cannabis substitution creates a different doctor-patient relationship. Patients seek out the physician to confer legitimacy on what they are doing or are about to do. My most important service is to end their criminal status, Aeschalapian protection from the criminal justice system, which often brings an expression of relief. An alliance is created that promotes candor and trust. The physician is permitted to act as a coach or an enabler in a positive sense." claims Tod Hiro Mikuriya from "Cannabis as a Substitute for Alcohol: A Harm-Reduction Approach", Journal of Cannabis Therapeutics, Vol 4(1) 2004.

2003: "The reportedly successful use of cannabis as an alternative to alcohol, SSRI antidepressants, and stimulants (in the treatment of ADHD) warrants serious, large-scale investigation. A necessary first step is for the doctors who are monitoring patients using cannabis for these purposes to agree on basic definitions, diagnostic criteria, etc., and to adopt uniform record-keeping methods. Hergenrather’s observation that half his cannabis-using patients have been able to stop taking pharmaceutical drugs – and others have reduced their intake – suggests a line of inquiry that belongs on a common interview form." claims Fred Gardner from "Which Conditions are Californians Actually Treating With Cannabis?", O'Shaughnessy's Journal of the California Cannabis Research Medical Group, Summer 2003.

1990: "To rank today's commonly used drugs by their addictiveness, we asked experts to consider two questions: How easy is it to get hooked on these substances and how hard is it to stop using them? Although a person's vulnerability to drug also depends on individual traits – physiology, psychology, and social and economic pressures – these rankings reflect only the addictive potential inherent in the drug. The numbers below are relative rankings, based on the experts' scores for each substance:"

100 nicotine (tobacco)
99 methamphetamine, smoked (ice, glass)
98 cocaine, smoked (crack)
92 methamphetamine, injected (crystal meth)
85 diazepam (Valium)
82 methaqualone (Quaalude)
80 secobarbital (Seconal)
80 ethanol (alcohol)
79 heroin
78 methamphetamine, snorted (crank)
72 cocaine, snorted
70 caffeine (coffee)
60 phencyclidine (PCP)
20 cannabis (marijuana)
19 methylenedioxymethamphetamine (MDMA, ecstasy)
17 psilocybin (mushrooms)
17 lysergic acid diethylamide (LSD)
17 mescaline (peyote)

– reports John Hastings, In Health, Nov/Dec 1990

1970: "Cannabis Substitution: An Adjunctive Therapeutic Tool in the Treatment of Alcoholism" by Dr Tod Hiro Mikuriya, MD, Medical Times, vol 98 no 4, Apr 1970, pgs 187-191.

Aggression

Also see Amotivation, Progression

2004: "NDTS 2003 data indicate, however, that a relatively small percentage (4.6%) of state and local law enforcement agencies nationwide identify marijuana as the drug most contributing to violent crime in their areas." claims US National Drug Intelligence Center from National Drug Threat Assessment 2004: Marijuana, Apr 2004.

2003: "Cannabis reduces likelihood of violence during intoxication, but mounting evidence associates withdrawal with aggressivity. ... While cannabis has historically been excoriated for being a social 'menace' and for inducing homicidal rages (Julien, 1992), more contemporary research indicates cannabis-intoxicated individuals are in fact less likely to act aggressively. However, a developing literature demonstrates an authentic cannabis withdrawal syndrome, one symptom of which may be increased likelihood of interpersonal aggression. ... the effects of tetrahydrocannabinol (THC) (the primary psychoactive component of cannabis) on aggressive behavior have been studied at length, with the preponderance of studies focusing on the acute effects of THC intoxication. The results of these studies suggest that while low doses of THC may slightly increase aggression, moderate and high doses can suppress or even eliminate aggressive behavior (Myerscough & Taylor, 1986; Taylor, 1976). ... The animal literature also largely fails to support the cannabis–violence relationship; cannabis administration tends to foster submissive behaviors and suppress attack behaviors (Miczek, 1978; Sieber, Frischknect, & Waser, 1980). ... According to legislators, one of the reasons drugs are made illegal and the cost of policing and legislating justifiable is to curb the threat of violence. There are two ironies to this. First, the drug we know to be most likely to induce aggressive behavior [alcohol] is not only readily and legally available, it is often sold by the state for profit. Second, the greatest amount of drug-related violence may be due to the means of regulating an illegal and highly profitable industry (Fagin & Chin, 1990)." claims Peter NS Hoakena, Sherry H Stewart from "Drugs of abuse and the elicitation of human aggressive behavior", Addictive Behaviors, vol 28, pgs 1533-1554.

1968: "The evidence of a link with violent crime is far stronger with alcohol than with the smoking of cannabis." claims British Advisory Committee on Drug Dependence in Wootten Report: Advisory Committee on Drug Dependence.

Alcoholism

Also see Addiction, Alcohol, Comparative Pharmacology of Cannabis v Alcohol, Habituation, Tolerance, Withdrawal

2003: "All patients reported benefit, indicating that for at least a subset of alcoholics, cannabis use is associated with reduced drinking. The cost of alcoholism to individual patients and society-at-large warrants testing of the cannabis-substitution approach and study of the drug-of-choice phenomenon. ... As could be expected among patients seeking physician approval to treat alcoholism with cannabis, all reported that they’d found it 'very effective' (41) or 'effective' (38). Efficacy was inferred from other responses on seven questionnaires. ... Nine patients reported that they practiced total abstinence from alcohol and attributed their success to cannabis. Their years in sobriety: 19, 18, 16, 10, 7, 6, 4 (2), and 2. Twenty-nine patients reported a return of symptoms when cannabis was discontinued. Typical comments: 'I quit using cannabis while I was in the army and my drinking doubled. I was also involved in several violent incidents due to alcohol.' ” reports Dr Tod Hiro Mikuriya, MD from "Cannabis as a Substitute for Alcohol", O'Shaughnessy's Jouurnal of the California Cannabis Research Medical Group, Summer 2003.

2003: "The reportedly successful use of cannabis as an alternative to alcohol, SSRI antidepressants, and stimulants (in the treatment of ADHD) warrants serious, large-scale investigation. A necessary first step is for the doctors who are monitoring patients using cannabis for these purposes to agree on basic definitions, diagnostic criteria, etc., and to adopt uniform record-keeping methods. Hergenrather’s observation that half his cannabis-using patients have been able to stop taking pharmaceutical drugs – and others have reduced their intake – suggests a line of inquiry that belongs on a common interview form." claims Fred Gardner from "Which Conditions are Californians Actually Treating With Cannabis?", O'Shaughnessy's Jouurnal of the California Cannabis Research Medical Group, Summer 2003.

1970: "Cannabis Substitution: An Adjunctive Therapeutic Tool in the Treatment of Alcoholism" by Dr Tod Hiro Mikuriya, MD, Medical Times, vol 98 no 4, Apr 1970, pgs 187-191.

Alzheimer's

Also see Brain, Parkinson's

2006: "We have demonstrated that THC competitively inhibits AChE and, furthermore, binds to the AChE PAS and diminishes [amyloid-beta-peptide] aggregation. In contrast to previous studies aimed at utilizing cannabinoids in Alzheimer's disease therapy, our results provide a mechanism whereby the THC molecule can directly impact Alzheimer's disease pathology. We note that while THC provides an interesting Alzheimer's disease drug lead, it is a psychoactive compound with strong affinity for endogenous cannabinoid receptors. It is noteworthy that THC is a considerably more effective inhibitor of AChE-induced [amyloid-beta-peptide] deposition than the approved drugs for Alzheimer's disease treatment, donepezil and tacrine, which reduced [amyloid-beta-peptide] aggregation by only 22% and 7%, respectively, at twice the concentration used in our studies. Therefore, AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer's disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing [amyloid-beta-peptide] aggregation, thereby simultaneously treating both the symptoms and progression of Alzheimer's disease." reports Lisa M Eubanks, Claude J Rogers, Albert E Beuscher IV, George F Koob, Arthur J Olson, Tobin J Dickerson, Kim D Janda from "A Molecular Link between the Active Component of Marijuana and Alzheimer's Disease Pathology", Molecular Pharmaceutics, Aug 9 2006

2005: "The active ingredient in marijuana may stall decline from Alzheimer's disease, research suggests. Scientists showed a synthetic version of the compound may reduce inflammation associated with Alzheimer's and thus help to prevent mental decline. They hope the cannanbinoid may be used to developed new drug therapies. The research, by Madrid's Complutense University and the Cajal Institute, is published in the Journal of Neuroscience. The scientists first compared the brain tissue of patients who died from Alzheimer's disease with that of healthy people who had died at a similar age. They looked closely at brain cell receptors to which cannabinoids bind, allowing their effects to be felt. They also studied structures called microglia, which activate the brain's immune response. Microglia collect near the plaque deposits associated with Alzheimer's disease and, when active, cause inflammation. The researchers found a dramatically reduced functioning of cannabinoid receptors in diseased brain tissue. This was an indication that patients had lost the capacity to experience cannabinoids' protective effects. The next step was to test the effect of cannabinoids on rats injected with the amyloid protein that forms Alzheimer's plaques. Those animals who were also given a dose of a cannabinoid performed much better in tests of their mental functioning. The researchers found that the presence of amyloid protein in the rats' brains activated immune cells. However, rats that also received the cannabinoid showed no sign of microglia activation. Using cell cultures, the researchers confirmed that cannabinoids counteracted the activation of microglia and thus reduced inflammation. ... Researcher Dr Maria de Ceballos said: 'These findings that cannabinoids work both to prevent inflammation and to protect the brain may set the stage for their use as a therapeutic approach for Alzheimer's disease.' Dr Susanne Sorensen, head of research at the Alzheimer's Society, said: 'This is important research because it provides another piece of the jigsaw puzzle on the workings of the brain. There is no cure for Alzheimer's disease, so the identification of another target for drug development is extremely welcome. The Alzheimer's Society looks forward to seeing further research being carried out on cannabinoid receptors as drug targets for Alzheimer's disease but would warn the public against taking marijuana as a way of preventing Alzheimer's. It is now generally recognised that as well as providing a 'high', long-term use of marijuana can also lead to depression in many individuals.' ... Harriet Millward, of the Alzheimer's Research Trust, said there were two main types of cannabinoid receptor, CR1 and CR2. 'It is CR1 that produces most of the effects of marijuana, including the harmful ones. If it is possible to make drugs that act only on CR2, as suggested by the authors of this study, they might mimic the positive effects of cannabinoids without the damaging ones of marijuana. However, this is a fairly new field of research and producing such selective drugs is not an easy task. There is also no evidence yet that cannabinoid-based drugs can slow the decline in human Alzheimer's patients." – "Marijuana may block Alzheimer's", BBC News, Feb 22 2005.

"Another very intriguing link between natural cannabinoids and memory was found in the brains of people who died of Alzheimer's disease. The researchers discovered that the brains of people died of Alzheimer's showed substantially less cannabinoid binding than shown by the brains of the control group. The abnormal absences of cannabinoid receptors weren't located in regions correleated with the damage done by Alzhemier's disease itself, so the researchers did not believe that the Alzheimer's disease caused the disappearance of CB1 receptors. The difference between the Alzheimer's and control CB1 levels was the highest in the hippocampus, the same region of the brain where cannabinoids help regulate short-term memory. The Alzheimer's brains showed binding to the test cannabinoid that was reduced by 49% compared to the binding observed in the control brains. There is not yet an explanation for this difference. Research showed that in rats, cannabinoid receptors and the ability to respond to anandamide (and THC) develop gradually from birth until adulthood, and then remain fairly constant as the animals age." claims Los Angeles Cannabis Resource Center from "Cannabinoids in the brain".

Amyotrophic Lateral Sclerosis (ALS)

aka Lou Gehrig's Disease
also see Neurological Disorders

2004: "Cannabis (marijuana) has been proposed as treatment for a widening spectrum of medical conditions and has many properties that may be applicable to the management of amyotrophic lateral sclerosis (ALS). This study is the first, anonymous survey of persons with ALS regarding the use of cannabis. There were 131 respondents, 13 of whom reported using cannabis in the last 12 months. Although the small number of people with ALS that reported using cannabis limits the interpretation of the survey findings, the results indicate that cannabis may be moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling. Cannabis was reported ineffective in reducing difficulties with speech and swallowing, and sexual dysfunction. The longest relief was reported for depression (approximately two to three hours)." – Abstract of "Survey of cannabis use in patients with amyotrophic lateral sclerosis" by Dagmar Amtmann, Patrick Weydt, Kurt L Johnson, Mark P Jensen, Gregory T Carter, American Journal of Hospice & Palliative Medicine, Mar-Apr 2004, pgs 95-104. norml.org/index.cfm?Group_ID=6012

2002: "The neuroprotective effect of cannabinoids may have potential clinical relevance for the treatment of neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson.s disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and Patrick Weydt from "Cannabis: Old medicine with new promise for neurological disorders"

"Marijuana is a substance with many properties that may be applicable to the management of amyotrophic lateral sclerosis (ALS). These include analgesia, muscle relaxation, bronchodilation, saliva reduction, appetite stimulation, and sleep induction. In addition, marijuana has now been shown to have strong antioxidative and neuroprotective effects, which may prolong neuronal cell survival. In areas where it is legal to do so, marijuana should be considered in the pharmacological management of ALS. Further investigation into the usefulness of marijuana in this setting is warranted." claim Gregory Carter, MD and Bill S Rosen, MD from "Marijuana In The Management of Amyotrophic Lateral Sclerosis"

Amotivation

Includes "Amotivational Syndrome" and "Pacifist Syndrome"
Also see Aggression

1995: "... it is doubtful that cannabis use produces a well defined amotivational syndrome. ... [The value of studies which support the] adult amotivation [theory are] limited by their small sample sizes..." claims W Hall, R Room, S Bondy, World Health Organization Project on Health Implications of Cannabis Use: A Comparative Appraisal of the Health and Psychological Consequences of Alcohol, Cannabis, Nicotine and Opiate Use, Aug 28 1995.

1978: "Federally funded studies of long-tern users of high-potency marijuana in three foreign countries showed no difference between the health, ability to work, and brain function of users and non-users, a number of researchers said ... Dr Sidney Cohen of the University of California at Los Angeles, former head of drug research at the National Institute of Mental Health, added that studies of marijuana users at UCLA and University of California at Berkeley disputed the notion that smoking pot killed a student's motivation to work. But Dr Glen D Mellinger, in his studies of Berkeley students, concluded that the dropouts were poorly motivated even before they began using marijuana and the poor motivation may have led to drug use instead of the other way around." reports Stuart Auerbach in "Studies See No Health Effect of Pot Smoking, Researchers Say", Washington Post, Jan 28, 1978.

Anorexia

Also see Appetite

Anxiety

also see Depression

2005: "We show that 1 month after chronic HU210 [a potent synthetic cannabinoid] treatment, rats display increased newborn neurons in the hippocampal dentate gyrus and significantly reduced measures of anxiety- and depression-like behavior. Thus, cannabinoids appear to be the only illicit drug whose capacity to produce increased hippocampal newborn neurons is positively correlated with its anxiolytic- [anti-anxiety] and antidepressant-like effects. ... To determine the relationship between hippocampal neurogenesis and anxiolytic- and antidepressant-like effects produced by chronic HU210, we examined the effects of a selective destruction of the hippocampal neural stem cells on the behavioral effects of chronic HU210. During the course of receiving chronic HU210 injections, 1 group of Long-Evans rats received two 5-Gy doses of x-rays confined to a limited brain region including the hippocampus ... Because two 5-Gy doses of x-rays were not found to alter the morphology and function of mature neurons in the hippocampus, hypothalamus, and amygdala, our results together suggest that chronic HU210 treatment reduced anxiety and depression, likely via promoting hippocampal neurogenesis. It has been shown that acute, high doses of CB1 agonists or cannabinoids produced anxiety-like effects in ratsor depression-like effects in mice. We observed here that chronic administration of high, but not low, doses of HU210 exerts anxiolytic- and antidepressant-like effects. To make things more complicated, acute, low doses of cannabinoids have been found to induce anxiolytic-like effects in rodents. These complicated effects of high and low doses of acute and chronic exposure to cannabinoids may explain the seemingly conflicting results observed in clinical studies regarding the effects of cannabinoid on anxiety and depression. In summary, since adult hippocampal neurogenesis is suppressed following chronic administration of opiates, alcohol, nicotine, and cocaine, the present study suggests that cannabinoids are the only illicit drug that can promote adult hippocampal neurogenesis following chronic administration. Increased hippocampal neurogenesis appears to underlie the mechanism of anxiolytic- and antidepressant-like effects produced by a high dose of chronic HU210 treatment. The opposing effects of high doses of acute and chronic cannabinoids, together with the anxiolytic-like effects caused by a low dose of cannabinoids, may finally explain discrepancies in the clinical study literature regarding the effects of cannabinoid on anxiety and depression." claims Wen Jiang, Yun Zhang, Lan Xiao, Jamie Van Cleemput, Shao-Ping Ji, Guang Bai, Xia Zhang, "Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects", Journal of Clinical Investigation, Nov 1 2005. PDF

2002: "Brain chemicals similar to those in cannabis wipe out bad memories - and could point to new drugs for severe anxiety. The chemicals are called cannabinoids. Mice with faulty cannabinoids can't forget traumatic events, Beat Lutz of the Max Planck Institute of Psychiatry in Munich, Germany and his colleagues have found. They suggest that the chemicals wipe fearful memories from the brain. Drugs that boost cannabinoids could help people who suffer post-traumatic stress disorder, phobias and panic attacks, say the researchers. Its 'a great new idea,' says neuroscientist Pankaj Sah of the Australian National University in Canberra: 'It introduces a whole new target,' for such therapies, he says." reports Helen Pearson from "Innate cannabis chemical erases fears: Calming brain circuit could treat anxieties", Nature, Aug 1 2002.

Appetite

Also see Anorexia, Nausea, Weight Loss

2005: "THC itself is approved in the U.S. by the FDA, and it is used in many other countries for the prevention of vomiting during cancer chemotherapy, and for appetite enhancement. We, and many others, have found that not only THC does that, but also the endocannabinoids. This is one of the main reasons for high endocannabinoid levels during hunger and so on. Now, THC can be used, and is being used, for these two things. ... Sanofi-Synthélabo Recherché in France is doing some interesting work. They have a compound, which is an antagonist of the cannabinoid system, and they have tested it in about eight thousand obese people. They have found that it is extremely useful. Their appetite goes down slowly, as it should, and they lose weight. They plan to introduce the compound in twelve months time, I think. They're doing a lot of work in the field, and they expect huge sales." claims Dr Raphael Mechoulam, as reported by David Jay Brown, "The New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael Mechoulam".

1988: "Effects of Smoked Marijuana on Food Intake and Body Weight of Humans Living in a Residential Laboratory" by R W Foltin, et al, Appetite, vol 11, pgs 1-14.

1986: "I started feeling the changes pretty much right away. Smoking marijuana also felt ten times better than taking Marinol pill. It helped reduce my nausea and I could hold down food better." claims Jim Kerns, cancer and chemotherapy patient.

1986: "Behavioral analysis of marijuana effects on food intake in humans" by R W Foltin, J V Brady and M W Fischman, Pharmacology, Biochemistry and Behavior, vol 25, pgs 577-582.

1976: "Effects of Marijuana use on Body Weight and Caloric Intake in Humans" by Greenberg, et al, Psychopharmacology, vot 49, pgs 79-84.

"I was diagnosed with secondary-progressive multiple sclerosis in 1986 ... My neurologist prescribed the drugs Compazine and Antivert. They had little affect on the nausea and no affect on the appetite, even after the dosage was doubled. After a couple of weeks of feeling sick and not eating, I had lost 15 pounds and no medication was helping. ... I decided to try smoking Cannabis/Marijuana. At first I felt worse, but after the effects of the smoke were gone I began to relax and get an appetite. I could finally eat again. Since that time, I have used cannabis to maintain a healthy body weight and a decent standard of living. For years I left my prescription drugs setting on the counter, as Cannabis was more effective." claims John E Precup from "Patient Testimonials"

Arthritis

Also see Pain

2005: "Controlled studies have revealed therapeutic utility of cannabinoids in the treatment of ... rheumatoid arthritis ... many years ago we elucidated the structure of a compound called cannabidiol, which is present in very large amounts in cannabis. It's more than THC, and it is anti-inflammatory. It is excellent against rheumatoid arthritis, at least in animals. We worked together with a London group–real top of the field people in rheumatoid arthritis–and they have never seen anything as good as that. So chances are that this particular compound, cannabidiol, can be used in rheumatoid arthritis. And it has no psychotropic effects, as a matter of fact, because it does not bind to the receptors. Maybe it has something to do with the metabolism of anandamide. Maybe it blocks the anandamide breakdown. Maybe. This is something we saw, but whether it's relevant to its activity, frankly I don't know. So this compound possibly will be used for rheumatoid arthritis. A company is already working on that ..." claims Dr Raphael Mechoulam, as reported by David Jay Brown, "The New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael Mechoulam".

2004: "A drug made from an extract of cannabis has helped to reduce the pain caused by rheumatoid arthritis. The drug, Sativex, has been developed by GW Pharmaceuticals, which is assessing the medical benefits of cannabis under a UK government licence. Tests of a spray form of the drug on 58 arthritis patients showed it helped reduce pain, and improve quality of sleep. Few people showed signs of side effects, the company said. ... Arthritis Research Campaign ... spokeswoman said: 'It's not going to cure the disease, but it will do a lot to allieviate the pain and suffering of people with rheumatoid arthritis. Cannabis is probably less harmful than other available painkillers. This idea that people with rheumatoid arthritis will be sitting around smoking joints and getting high is quite wrong; cannabis-based pain killers should be taken very seriously.' " – from "Cannabis drug cuts arthritis pain", BBC News, June 9 2004. Also see news.bbc.co.uk/1/hi/health/3790227.stm, Arthritis Research Campaign.

Asthma

Also see Spasticity

2005: "Controlled studies have revealed therapeutic utility of cannabinoids in the treatment of ... asthma" claims Dr Raphael Mechoulam, as reported by David Jay Brown, "The New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael Mechoulam".

Botany

2005: "AS POLICE and dope smokers know, there are two types of cannabis. Cannabis sativa sativa is mainly used to make hemp, while the indica subspecies is prized for its tetrahydrocannabinol (THC) content, which produces the 'high'. But now Australian researchers have discovered a third type of cannabis, called rasta. Simon Gilmore of the Canberra Institute of Technology catagorised 196 sample plants according to the DNA in their mitochondria and chloroplasts. The samples included plants grown for drugs and hemp as well as wild varieties from Europe, Asia, Africa, Mexico and Jamaica. The results showed three distinct 'races' of cannabis. In central Asia the THC-rich indica predominated, while in western Europe sativa was more common. In India, south-east Asia, Africa, Mexico and Jamaica the rasta variant predominated. It looks similar to the sativa subspecies, but generally contains higher levels of THC." – "Rasta lends its name to a third type of cannabis", New Scientist, Sept 20 2005, pg 12.
(Editor's note: "Rasta" is actually a fourth strain of cannabis. The third strain is called "Ruderalis" and is native to Russia.)

Erowid Cannabis Vault: Cultivation
erowid.org/plants/cannabis/cannabis_cultivation.shtml

How to Grow Medical Marijuana by Todd McCormick
drugsense.org/mcwilliams/www.growmedicine.com/pdf/How2grow.pdf

Brain

Also see Alzheimer's, Cerebral Palsy, Headache, Neurological Disorders, Pain, Parkinson's, Stroke

2007: "Smoking pot won't make you crazy, but trying to find the truth behind the recent rash of headlines regarding a supposed link between cannabis and mental illness might. According to the Associated Press and other news sources, a new study in the British medical journal The Lancet reports that smoking cannabis – even occasionally – can increase one's risk of becoming psychotic. It sounds alarming at first, but a closer look at the evidence reveals that there's less here than the headlines imply. First, there is no new study. The paper published in The Lancet is a meta-analysis – a summary of seven studies that previously appeared in other journals, including some that were published decades ago. Second, the touted association between cannabis and mental illness is small–about the same size as the link between head injury and psychosis. Finally, despite what some new sources suggest, this association is hardly proof of a cause-and-effect relationship between cannabis and psychosis ... In fact, investigators actually reported that cannabis use was associated with a slight increase in psychotic outcomes. However, the authors emphasized (even if many in the media did not) that this small association does not reflect a causal relationship. Cannabis use can correlate with mental illness for many reasons. People often turn to cannabis to alleviate the symptoms of distress. A recent study performed in Germany showed that cannabis offsets certain cognitive declines in schizophrenic patients. Another study shows that psychotic symptoms predict later use of cannabis, suggesting that people might turn to the plant for help rather than become ill after use. Perhaps the most impressive evidence against the cause-and-effect relationship concerns the unvarying rate of psychoses across different eras and different countries. People are no more likely to be psychotic in Canada or the United States (two nations where large percentages of citizens use cannabis) than they are in Sweden or Japan (where self-reported marijuana use is extremely low). Even after the enormous popularity of cannabis in the 1960s and 1970s, rates of psychotic disorders haven't increased." from "Interpreting Hazy Warnings About Pot and Mental Illness" by Paul Armentano, Mitch Earleywine, Aug 7 2007.

2007: "There was an increased risk of any psychotic outcome in individuals who had ever used cannabis. Findings were consistent with a dose-response effect, with greater risk in people who used cannabis most frequently. Results of analyses restricted to studies of more clinically relevant psychotic disorders were similar. Depression, suicidal thoughts, and anxiety outcomes were examined separately. Findings for these outcomes were less consistent, and fewer attempts were made to address non-causal explanations, than for psychosis. A substantial confounding eff ect was present for both psychotic and affective outcomes. Interpretation: The evidence is consistent with the view that cannabis increases risk of psychotic outcomes independently of confounding and transient intoxication effects, although evidence for aff ective outcomes is less strong. The uncertainty about whether cannabis causes psychosis is unlikely to be resolved by further longitudinal studies such as those reviewed here. However, we conclude that there is now suffi cient evidence to warn young people that using cannabis could increase their risk of developing a psychotic illness later in life." from "Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review", by Theresa H M Moore, Stanley Zammit, Anne Lingford-Hughes, Thomas R E Barnes, Peter B Jones, Margaret Burke, Glyn Lewis, The Lancet, 370: pgs 319-328, 2007.

2006: "U.S. scientists have discovered the active ingredient in marijuana interferes with synchronized activity between neurons in the hippocampus of rats. The authors suggest action of tetrahydrocannabinol, or THC, might explain why marijuana impairs memory. Gyorgy Buzsaki and colleagues at Rutgers University recorded the activity of multiple neurons in the hippocampus of rats. Normally neurons in that region form groups that fire action potentials, or nerve impulses, together at about 4-10 times per second. But when the authors injected THC, or a related synthetic drug, into the hippocampus, that synchrony was disrupted. The researchers said the drugs did not change the total number of action potentials produced, just their tendency to occur at the same time. Animals with less synchronized neural activity under the drug performed less well in a standard test of memory, suggesting synchronized neural firing is important for normal hippocampal function." from "Study: Marijuana may affect neuron firing", Nov 29 2006

2006: "Cannabinoids impair hippocampus-dependent memory in both humans and animals, but the network mechanisms responsible for this effect are unknown. Here we show that the cannabinoids 9-tetrahydrocannabinol and CP55940 decreased the power of theta, gamma and ripple oscillations in the hippocampus of head-restrained and freely moving rats. These effects were blocked by a CB1 antagonist. The decrease in theta power correlated with memory impairment in a hippocampus-dependent task. By simultaneously recording from large populations of single units, we found that CP55940 severely disrupted the temporal coordination of cell assemblies in short time windows (<100 ms) yet only marginally affected population firing rates of pyramidal cells and interneurons. The decreased power of local field potential oscillations correlated with reduced temporal synchrony but not with firing rate changes. We hypothesize that reduced spike timing coordination and the associated impairment of physiological oscillations are responsible for cannabinoid-induced memory deficits." claims David Robbe, Sean M Montgomery, Alexander Thome, Pavel E Rueda-Orozco, Bruce L McNaughton, György Buzsaki, "Cannabinoids reveal importance of spike timing coordination in hippocampal function", Nov 19 2006

2006: "Although differences were observed between subjects who used cannabis during adolescence and those who did not, no finding indicated pathological change. Regions of higher ADC, putative evidence of atrophy, were not present, although regions of significantly lower ADC were. While low FA would be indicative of less white matter integrity, particularly with respect to fiber direction, all FA differences in this study were higher values in cannabis users than non-users. ... Thus, these data lead to the likely conclusion that cannabis use, in at least moderate amounts, during adolescence does not appear to be neurotoxic ..." claims Lynn E DeLisi, Hilary C Bertisch, Kamila U Szulc, Magda Majcher, Kyle Brown, Arthika Bappal, Babak A Ardekani, "A preliminary DTI study showing no brain structural change associated with adolescent cannabis use", Harm Reduction Journal, May 9 2008

2005: "A recent study in the Journal of Clinical Investigation suggests that smoking pot can make the brain grow. Though most drugs inhibit the growth of new brain cells, injections of a synthetic cannibinoid have had the opposite effect in mice in a study performed at the University of Saskatchewan. ... Many drugs – heroin, cocaine, and the more common alcohol and nicotine – inhibit the growth of these new cells. It was thought that marijuana did the same thing, but this new research suggests otherwise. ... The researchers found that rats treated with HU-210 [a potent synthetic cannabinoid] on a regular basis showed neurogenesis – the growth of new brain cells in the hippocampus. A current hypothesis suggests depression may be triggered when the hippocampus grows insufficient numbers of new brain cells. If true, HU-210 could offer a treatment for such mood disorders by stimulating this growth." reports Juanita King from "science: Study shows marijuana increases brain cell growth", The Peak, Oct 31 2005. Study Text, PDF

2005: "The relentless influx of emails, cellphone calls and instant messages received by modern workers can reduce their IQ by more than smoking marijuana, suggests UK research. ... says Glenn Wilson, a psychiatrist at the University of London, UK, who carried out the study, sponsored by Hewlett-Packard." reports Will Knight from "'Info-mania' dents IQ more than marijuana", New Scientist, Apr 22 2005

2004: "After studying more than 2000 users and non-users aged between 14 and 24, Jim van Los of the University of Maastricht in the Netherlands concludes ... 21 per cent of cannabis users in his sample had psychotic symptoms, compared with 15 per cent of non-users. The more often people used cannabis, the stronger the effect. The risk appears greatest for those with a predisposition to psychosis. In people with mild signs of psychosis at the start of the study, 51 per cent of users developed symptoms compared with 26 per cent of non-users. However, several other reviews have come to a different conclusion. In 1998, a French government study found that cannabis was the least dangerous of all potentially addictive drugs." – "Cannabis use linked to psychotic experiences", New Scientist, Dec 4 2004, pg 5.

2004: "A cannabis-like substance produced by the brain may dampen delusional or psychotic experiences, rather than trigger them. Heavy cannabis use has been linked to psychosis in the past, leading researchers to look for a connection between the brain's natural cannabinoid system and schizophrenia. Sure enough, when Markus Leweke of the University of Cologne, Germany, and Andrea Giuffrida and Danielle Piomelli of the University of California, Irvine, looked at levels of the natural cannabis-like substance anandamide, they were higher in people with schizophrenia than in healthy controls. The team measured levels of anandamide in the cerebrospinal fluid (CSF) of 47 people suffering their first bout of schizophrenia, but who had not yet taken any drugs for it, and 26 people who had symptoms of psychosis and have a high risk of schizophrenia. Compared with 84 healthy volunteers, levels were six times as high in people with symptoms of psychosis and eight times as high in those with schizophrenia. 'This is a massive increase in anandamide levels,' Leweke told the National Cannabis and Mental Illness Conference in Melbourne, Australia, last week. And that is just in the CSF. Levels could be a hundred times higher in the synapses, where nerve signalling is taking place, he says. ... But were the high anandamide levels triggering the psychotic symptoms or a response to them? Leweke and his colleagues found, to their surprise, that the more severe people's schizophrenia was the lower their anandamide levels. The team's theory is that rather than triggering psychosis, the substance is released in response to psychotic symptoms to help control them. People with the worst symptoms might be unable to produce sufficient anandamide to prevent them. At some point in their lives, between 5 and 30 per cent of healthy people have had symptoms such as delusions or hallucinations, which can be triggered by something as simple as sleep deprivation. 'All of us are potentially psychotic,' says David Castle of the University of Melbourne. So for the body to have a system that prevents these experiences getting out of hand makes sense, he says. ... The new findings suggest antipsychotic drugs could be developed that target the anandamide system, but it will not be simple. The active ingredient in cannabis, THC, binds to anandamide receptors. But people with schizophrenia who use cannabis actually have more severe and frequent psychotic episodes than those who do not. This may be because THC makes anandamide receptors less sensitive. Leweke's team also found anandamide levels lowest in people with schizophrenia who used cannabis more frequently, suggesting it may disrupt the system in other ways too. Up to 60 per cent of people with schizophrenia use cannabis. A study by Castle, also reported at the Melbourne meeting, has found that people use the drug to get rid of unpleasant emotions associated with the disease such as anxiety and depression." reports Rachel Nowak from "Brain may produce its own antipsychotic drug", New Scientist, Aug 30 2004.

2003: "Smoking marijuana will certainly affect perception, but it does not cause permanent brain damage, researchers from the University of California at San Diego said Friday in a study. 'The findings were kind of a surprise. One might have expected to see more impairment of higher mental function,' said Dr. Igor Grant, a UCSD professor of psychiatry and the study's lead author. Other illegal drugs, or even alcohol, can cause brain damage. His team analyzed data from 15 previously published, controlled studies into the impact of long-term, recreational cannabis use on the neurocognitive ability of adults. The studies tested the mental functions of routine pot smokers, but not while they were actually high, Grant said. The results, published in the July issue of the Journal of the International Neuropsychological Society, show that marijuana has only a marginally harmful long-term effect on learning and memory. No effect at all was seen on other functions, including reaction time, attention, language, reasoning ability, and perceptual and motor skills. ... The UCSD analysis of studies involving 704 long-term cannabis users and 484 nonusers was sponsored by a state-supported program that oversees research into the use of cannabis to treat certain diseases. ... The UCSD research team said the problems observed in learning and forgetting suggest that long-term marijuana use results in selective memory defects, but said the impact was of a very small magnitude. 'If we barely find this tiny effect in long-term heavy users of cannabis, then we are unlikely to see deleterious side effects in individuals who receive cannabis for a short time in a medical setting,' Grant said." reports Walter Cronkite, "Pot Doesn't Harm Brain, Study Shows", June 30 2003

2002: "The link between regular cannabis use and later depression and schizophrenia has been significantly strengthened by three new studies. ... One of the key conclusions of the research is that people who start smoking cannabis as adolescents are at the greatest risk of later developing mental health problems. Another team calculates that eliminating cannabis use in the UK population could reduce cases of schizophrenia by 13 per cent. Until now, say Rey and Tennant, there was 'a dearth of reliable evidence' to support the idea that cannabis use could cause schizophrenia or depression. That lack of good evidence 'has handicapped the development of rational public health policies,' according to one of the research groups, led by George Patton at the Murdoch Children's Research Institute in Melbourne, Australia. The reason for the link is unclear. Social consequences of frequent cannabis use include educational failure and unemployment, which could increase the risk of depression. "However, because the risk seems confined largely to daily users, the question about a direct pharmacological effect remains," says Patton. ... The new analysis revealed a dose-dependant relationship between the frequency of cannabis use and schizophrenia. This held true in men with no psychotic symptoms before they started using cannabis, suggesting they were not self-medicating. Finally, researchers led by Terrie Moffitt at King's College London, UK, analysed comprehensive data on over 1000 people born in Dunedin, New Zealand in 1972 and 1973. They found that people who used cannabis by age 15 were four times as likely to have a diagnosis of schizophreniform disorder (a milder version of schizophrenia) at age 26 than non-users. But when the number of psychotic symptoms at age 11 was controlled for, this increased risk dropped to become non-significant. This suggests that people already at greater risk of later developing mental health problems are also more likely to smoke cannabis. The total number of high quality studies on cannabis use and mental health disorders remains small, stress Rey and Tennant. And it is still not clear whether cannabis can cause these conditions in people not predisposed by genetic factors, for example, to develop them." claims Emma Young from "Cannabis link to mental illness strengthened", New Scientist news service, Nov 21 2002.

2002: "Current marijuana use had a negative effect on global IQ score only in subjects who smoked 5 or more joints per week. A negative effect was not observed among subjects who had previously been heavy users but were no longer using the substance. We conclude that marijuana does not have a long-term negative impact on global intelligence. Whether the absence of a residual marijuana effect would also be evident in more specific cognitive domains such as memory and attention remains to be ascertained. ... For comparison, an IQ decrement of 5 points has been observed in children exposed prenatally to 3 alcoholic drinks per day, of 3.75 points in offspring exposed prenatally to cocaine and of 2.6 points after low lead exposure. ... Although the heavy current users experienced a decrease in IQ score, their scores were still above average at the young adult assessment (mean 105.1). If we had not assessed preteen IQ, these subjects would have appeared to be functioning normally. Only with knowledge of the change in IQ score does the negative impact of current heavy use become apparent." claims Peter Fried, Barbara Watkinson, Deborah James, and Robert Gray, "Current and former marijuana use: preliminary findings of a longitudinal study of effects on IQ in young adults," Canadian Medical Association Journal, Apr 2 2002, 166(7), pg 887, 890.

2002: "Do decades of dope-smoking wreck cannabis users' memory and concentration? Or is this just another anti-marijuana myth? This long-running debate reopened this week with the publication of a US government-funded study which claims that smoking cannabis daily for 20 years or more impairs memory and attention. Its findings are contradicted by others that have revealed no long-term effects. The latest research involved 102 cannabis smokers in Seattle, Farmington in Connecticut and Miami. Half had smoked for an average of 24 years. The other half, described as 'short-term'users, had smoked for 10 years on average. Both groups reported smoking about two joints a day. In tests such as memorising a list of 15 words, the long-term users recalled 8.5 words on average, 2.5 fewer than both the short-term users and 31 non-users. The long-term users were also slower at mental arithmetic. But in in other tasks, such as sorting cards, they were just as quick. claims Kurt Kleiner from "The war on weed: Controversy still rages over whether cannabis damages the brain", New Scientist news service, Mar 9 2002.

2002: "The neuroprotective effect of cannabinoids may have potential clinical relevance for the treatment of neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson's disease, cerebrovascular ischemia and stroke." claims Gregory T Carter and Patrick Weydt from "Cannabis: Old medicine with new promise for neurological disorders"

2001: "I am the mother of a 21-year-old male who was diagnosed with a serious mental illness at 17 years. He had suffered with this illness since 5th grade, a thought disorder that he is unable to control which includes suicidal thoughts. ... After three different facilities and uncountable medications, different opinions, no has really said they had treated this condition. [This condition] usually comes into view when the person is on death row. ... He has been on medications that caused him to be unable to read due to loss of vision, medications that made him more paranoid, to be incontinent, to be unable to function. ... Out of desperation to be free of the prison his mind creates at times, he smoked marijuana and says it is the only time he is totally free of these thoughts. ... He seriously uses this with a couple of other meds daily with good results. He doesn't stumble around or look dazed. He is clear-eyed and plain spoken.... There has not to my knowledge ever been a death recorded from this drug, but alcohol and cigarettes have killed many. ...If this one plant that God created for us can be used, let's not withhold it causing undue stress and paranoid feelings for these people." claims anonymous mother from "Patient Story - Mental Illness", June 26 2001.

1999: "There were no significant differences in cognitive decline between heavy users, light users, and nonusers of cannabis. There were also no male-female differences in cognitive decline in relation to cannabis use. The authors conclude that over long time periods, in persons under age 65 years, cognitive decline occurs in all age groups. This decline is closely associated with aging and educational level but does not appear to be associated with cannabis use." claims Constantine G Lyketsos, Elizabeth Garrett, Kung-Yee Liang, and James C Anthony, "Cannabis Use And Cognitive Decline In Persons Under 65 Years Of Age", American Journal of Epidemiology, vol 149, no 9, pgs 794-800.

1998: "The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid delta-9-tetrahydrocannabinol (THC). Cannabinoids protected equally well against neurotoxicity mediated by N-methyl-D-aspartate receptors, 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid receptors, or kainate receptors. N-methyl-D-aspartate receptor-induced toxicity has been shown to be calcium dependent; this study demonstrates that 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid/kainate receptor-type neurotoxicity is also calcium-dependent, partly mediated by voltage sensitive calcium channels. The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid receptor independent. Previous studies have shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants by cyclic voltametry. Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was more protective against glutamate neurotoxicity than either ascorbate or -tocopherol, indicating it to be a potent antioxidant. These data also suggest that the naturally occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially useful therapeutic agent for the treatment of oxidative neurological disorders such as cerebral ischemia." reports AJ Hampson, M Grimaldi, J Axelrod, D Wink from "Cannabidiol and delta-9-tetrahydrocannabinol are neuroprotective antioxidants", Proceedings of the National Academy of Sciences (PNAS), vol 95, no 14, July 7 1998.

1996: "Myth: Marijuana causes brain damage. The truth: This claim is bases on a 20-year-old study in which two rhesus monkeys were exposed to continuous massive doses of THC – up to 200 times the psychoactive dose for humans. It has never been replicated, and there is no evidence anywhere that marijuana users suffer brain damage." claims Ira Glasser, Exec. Dir., American Civil Liberties Union, from "More Reefer Madness" by Glasser, Visions of Liberty #8, Aug. 25, 1996.

1992: A study by Gordon T. Pryor and Charles Rebert at SRI International in Menlo Park, California failed to find any evidence of brain damage in rhesus monkeys exposed to cannabis. Article: "Chronic Marijuana Smoke Exposure in the Rhesus Monkey II: Effects on Progressive Ratio and Conditioned Position Responding", by Merle Paule, et al, Journal of Pharmacology and Experimental Therapeutics, #260, 1992, pgs. 213-222.

1991: Dr. David Blum of UCLA claims a Partnership for a Drug Free America (PDFA) Public Service Announcement (PSA) that shows a near-flatline brainwave electroencephalogram (EEG) of a cannabis user is not accurate. Dr. Blum is one of several doctors to complain that the brainwaves in the PDFA PSA were not those of a cannabis user. The producer of the PDFA PSA admits the EEG is actually that of a person in a coma or unconscious, but claims that, in a drug war, the "ends justify the means".

1991: Experimental exposure to cannabis smoke "does not compromise the general health of the rhesus monkey." concludes a study headed by Dr. William Slikker, Jr. at the National Center for Toxicological Research in Arkansas. The study failed to find any evidence of brain damage in rhesus monkeys exposed to cannabis. "Chronic Marijuana Smoke Exposure in the Rhesus Monkey", by William Slikker, Jr, et al, Fundamental and Applied Toxicology, #17, 1991, pgs. 321-322.

1989: "Whether the drug causes brain or other physical damage is much debated." claims American Medical Association Home Medical Encyclopedia, published by Reader's Digest, 1989.

1987: "... there are several reports of damaged brain cells and changes in brainwave readings in monkeys smoking marijuana, but neurological and neuropsychological tests in Greece, Jamiaca, and Costa Rica found no evidence of functional brain damage." claims Lester A Grinspoon, M.D., "Marijuana", The Harvard Medical School Mental Health Letter, Nov. 1987, pg. 3.

1978: "Federally funded studies of long-tern users of high-potency marijuana in three foreign countries showed no difference between the health, ability to work, and brain function of users and non-users, a number of researchers said ... Dr Max Fink of department of psychiatry of the State University of New York at Stoney Brook ... and ... Dr Alfred M Freedman, insisted all the results clearly showed that there is no brain damage from long-term marijuana smoking. ... Drs Paul Satz and Jack M Fletcher of the University of Florida and Louis W Sutker of University of Victoria found after giving 17 psychological and brain function tests to 41 users that ' chronic marijuana use is not associated with permanent or irreversible impairment in high brain functions or intelligence.' " reports Stuart Auerbach in "Studies See No Health Effect of Pot Smoking, Researchers Say", Washington Post, Jan 28 1978.

"For THC, the cannabinoid synthesized by cannabis sativa and indica, and andandamide, the cannabinoid synthesized in the central nervous systems of most animals on Earth, the receptor antagonist is called SR141716. SR141716 is like 'anti-marijuana' – it enhances the same memory functions that the natural brain cannabinoid anandamide and THC inhibit through the cannabinoid receptor. SR141716 improves short term memory in rodents by blocking the CB1 cannabinoid receptor from binding to andandamide, not just THC. But anandamide is made by the brain naturally. Why would the brain be making a chemical – andandamide – that seems to inhibit short-term memory? This question is partly answered by the effect of SR141716 on the sleep cycles of rats. SR141716 administered to rats interrupts their sleep cycles, causing a deficit in both short-wave and REM sleep. This research indicates that cannabinoids are important in the brain's regulation of the sleeping process. The cost of improving short-term memory by blocking cannabinoids from the brain is deficient and delayed slow-wave and REM sleep. In studying marijuana, we have learned something important about the brain. Inhibition of short-term memory-related processes occurring ion the hippocampus might be necessary for a healthy sleep cycle." claims Los Angeles Cannabis Resource Center from "Cannabinoids in the brain".

Cannabis.net
Cannabis, Cannabinoids and the Brain cannabis.net/refs/index.html

Cancer

Includes Leukemia, Lymphoma

Cancer medicine

Also see Appetite, Cancer safety, Chemotherapy, Nausea

2006: "delta-9-tetrahydrocannabinol (THC) exhibits anti-tumor effects on various cancer cell types, but its use in chemotherapy is limited by its psychotropic activity. We investigated the anti-tumor activities of other plant cannabinoids, i.e. cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid and THC-acid, and assessed whether there is any advantage in using Cannabis extracts (enriched in either cannabidiol or THC) over pure cannabinoids. Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC₅₀ between 6.0 and 10.6 µM), with significantly lower potency in noncancer cells. The cannabidiol-rich extract was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed in the rank of potency. Both cannabidiol and the cannabidiol-rich extract inhibited the growth of xenograft tumors obtained by subcutaneous injection into athymic mice of human MDA-MB-231 breast carcinoma or rat v-K-ras-transformed thyroid epithelial cells, and reduced lung metastases deriving from intra-paw injection of MDA-MB-231 cells. Judging from several experiments on its possible cellular and molecular mechanisms of action, we propose that cannabidiol lacks a unique mode of action in the cell lines investigated. At least for MDA-MB-231 cells, however, our experiments indicate that cannabidiol effect is due to its capability of inducing apoptosis via: 1) direct or indirect activation of cannabinoid CB₂ [cannabinoid receptor type-2] and vanilloid TRPV1 [transient receptor potential vanilloid type-1] receptors; and 2) cannabinoid/vanilloid receptor-independent elevation of intracellular Ca²⁺ and reactive oxygen species. Our data support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer. ... In conclusion, our data indicate that cannabidiol, and possibly Cannabis extracts enriched in this natural cannabinoid, represent a promising non-psychoactive antineoplastic strategy. In particular, for a highly malignant human breast carcinoma cell line we have shown here that cannabidiol and a cannabidiol-rich extract counteract cell growth both in vivo and in vitro as well as tumor metastasis in vivo. Cannabidiol exerts its effects on these cells through a combination of mechanisms that include either direct or indirect activation of CB₂ and TRPV1 receptors, and induction of oxidative stress, all contributing to induce apoptosis. Additional investigations are required to understand the mechanism of the growth inhibitory action of cannabidiol in the other cancer cell lines studied here." claim Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco, Vincenzo Di Marzo, "Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma", Endocannabinoid Research Group, Istituto di Chimica Biomolecolare, CNR Pozzuoli, Italy, May 25 2006.

2005: "Controlled studies have revealed therapeutic utility of cannabinoids ... tumor retardation have also been shown. ... There are several groups that have found it effective in reducing tumor growth. This is probably due to the same mechanism as before with the neuroprotection. It's probably not only neuroprotective; it's probably a protective agent in general. So, to a certain extent, the endocannabinoid system can be compared with the immune system. Now, the immune system obviously guards us against protein effects, viruses, and microbes, but not all damages. So just as our body protects itself with the immune system against microbes or viruses, it also tries to protect itself with other systems–and the endocannabinoid system is one of them. So I believe that it certainly acts against cancer cells. There is a very important group in Spain that has done some excellent work on that, and they're actually going into human work now with some cancers found in the brain. We have also done a little bit on that, and there is an Italian group that has done a lot of work on that. So, basically, it seems that this is one of the routes that our body uses to try and protect itself with–by acting on cancers using several different mechanisms, not just one." claims Dr Raphael Mechoulam, as reported by David Jay Brown, "The New Science of Cannabinoid-Based Medicine: An Interview with Dr. Raphael Mechoulam".

2005: "Tashkin controlled for tobacco use and calculated the relative risk of marijuana use resulting in lung and upper airwaves cancers. All the odds ratios turned out to be less than one (one being equal to the control group's chances)! Compared with subjects who had used less than one joint year, the estimated odds ratios for lung cancer were .78; for 1-10 j-yrs, .74; for 10-30 j-yrs, .85 for 30-60 j-yrs; and 0.81 for more than 60 j-yrs. The estimated odds ratios for oral/pharyngeal cancers were 0.92 for 1-10 j-yrs; 0.89 for 10-30 j-yrs; 0.81 for 30-60 j-yrs; and 1.0 for more than 60 j-yrs. 'Similar, though less precise results were obtained for the other cancer sites,' Tashkin reported. ... There was time for only one question, said the moderator, and San Francisco oncologist Donald Abrams, M.D., was already at the microphone: 'You don't see any positive correlation, but in at least one category [marijuana-only smokers and lung cancer], it almost looked like there was a negative correlation, i.e., a protective effect. Could you comment on that?' 'Yes,' said Tashkin. 'The odds ratios are less than one almost consistently, and in one category that relationship was significant, but I think that it would be difficult to extract from these data the conclusion that marijuana is protective against lung cancer. But that is not an unreasonable hypothesis.' " reports Fred Gardner from "Study: Smoking Marijuana Does Not Cause Lung Cancer", CounterPunch, July 2-4 2005.

2004: "Clinical research touted by the journal of the American Association for Cancer Research that shows marijuana's components can inhibit the growth of cancerous brain tumors is the latest in a long line of studies demonstrating the drug's potential as an anti-cancer agent. ... researchers at Madrid's Complutense University that found cannabis restricts the blood supply to glioblastoma multiforme tumors, an aggressive brain tumor ... the first experiment documenting pot's anti-tumor effects took place in 1974 at the Medical College of Virginia at the behest of the US government. The results of that study, reported in an Aug. 18, 1974, Washington Post newspaper feature, were that marijuana's psychoactive component, THC, 'slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent.' ... secret - clinical trial in the mid-1990s. That study, conducted by the US National Toxicology Program to the tune of $2 million concluded that mice and rats administered high doses of THC over long periods had greater protection against malignant tumors than untreated controls. However, rather than publicize their findings, government researchers shelved the results, which only became public after a draft copy of its findings were leaked in 1997 to a medical journal which in turn forwarded the story to the national media. ... In 1998, a research team at Complutense's Department of Biochemistry and Molecular Biology discovered that THC can selectively induce program cell death in brain tumor cells without negatively impacting the surrounding healthy cells. Then in 2000, they reported in the journal Nature Medicine that injections of synthetic THC eradicated malignant gliomas (brain tumors) in one-third of treated rats, and prolonged life in another third by six weeks. Last year, researchers at the University of Milan in Naples, Italy, reported in the Journal of Pharmacology and Experimental Therapeutics that non-psychoactive compounds in marijuana inhibited the growth of glioma cells in a dose dependent manner, and selectively targeted and killed malignant cells through a process known as apoptosis. And finally, this month, researchers reported that marijuana's constituents inhibited the spread of brain cancer in human tumor biopsies from patients who had failed standard cancer therapies." reports Paul Armentano from "Report Supressed That Marijuana Components Can Inhibit Cancer Growth", Coastal Post, Oct 26 2004.

2004: "Cannabinoids inhibit tumor angiogenesis in mice, but the mechanism of their antiangiogenic action is still unknown. Because t

Cannabis Freedom Activist Network's Guide To Cannabis Research