rexresearch.com
Cannabis & Health
(2003-2005)
Fred Gardner: "Smoking Pot Kills ... Not"; Anderson Valley Advertiser (CA) 24 Sep 2003.
BBC News (UK Web) 13 Oct 2003: "Marijuana Smoking Damages Sperm"
BBC News (UK Web) 13 Oct 2003: "Study -- Pot Compound Inhibits Tumor Cell Growth".
Anna Seward: "Cannabis May Help Relieve Bowel Disease"; The Telegraph (UK) 8-1-05.
Fred Gardner: "Study: Smoking Marijuana Does Not Cause Lung Cancer"; CounterPunch.com (2 July 2005).
Helen Pearson: "Innate Cannabis Chemical Erases Fears"; nature.com ( 1 August 2002 ).
NORML.org (4-5-04): "Cannabis Relieves Lou Gehrig's Symptoms -- New Study".
Emma Young: "Cannabis Smoking 'More Harmful' Than Tobacco"; NewScientist.com ( 11 November 2002 ).
NewScientist.com (25 March 03): "Marijuana Use in Pregnancy Damages Kids' Learning".
NORML ( 1-28-5 ): "Moderate Use Of Cannabis 'Safe' Study Says"; J. Current Opinion In Pharmacology.
CBC News ( 12-4-4 ):"Marijuana Use Boosts Risk of Psychosis -- Study".
Patricia Reaney: "Cannabis Compound Slows Artery Disease in Mice"; Reuters (6 April 2005).
Anderson Valley Advertiser (CA) 24 Sep 2003 ~
http://www.mapinc.org/media/2667
http://www.mapinc.org/drugnews/v03.n1466.a04.html"Smoking Pot Kills ... Not"
by Fred Gardner
For the health-conscious pothead who can't afford or can't get motivated to use a vaporizer, the mother of all questions has to be: does smoking cannabis lower life expectancy? A recent editorial in the British Medical Journal generated ominous headlines, attributing some 30,000 deaths annually in the UK to cannabis smoking. But you can relax a little, dear reader: the authors simply extrapolated from the number of deaths caused by cigarette smoking (120,000) and assumed that pot smoking was 1/4 as common and equally dangerous.
In the Sept. 20 BMJ, Stephen Sidney, MD -the associate director of clinical research for Kaiser Permanente, who has conducted the most relevant studies-explains how to approach the question scientifically:
"Firstly, we need to examine published data regarding use of cannabis and mortality. These data come from two large studies. The first study done in a cohort of 45,450 male Swedish conscripts, age 18-20 when interviewed about the use of cannabis, reported no increase in the 15-year mortality associated with the use of cannabis after social factors were taken into account.
BBC News (UK Web) 13 Oct 2003
http://www.mapinc.org/media/558
Continues: http://www.mapinc.org/drugnews/v03.n1581.a03.html"Marijuana Smoking Damages Sperm"
Men who smoke marijuana frequently damage their fertility in several different ways, research suggests. Scientists at Buffalo University found regular smokers had significantly less seminal fluid, and a lower sperm count. Their sperm were also more likely to swim too fast too early, leading to burn-out before they reach the egg. Dr Burkman conceded that many men who smoke marijuana have fathered children.
http://www.norml.org/index.cfm?Group_ID=5836"Study -- Pot Compound Inhibits Tumor Cell Growth"
NORML's Weekly Bulletin
http://www.mapinc.org/drugnews/v04.n064.a01.html"Study: Marijuana Buzz Linked to Runners' High"
by Paul Simao
The same family of chemicals that produces a buzz in marijuana smokers may be responsible for "runner's high," the euphoric feeling that some people get when they exercise, U.S. researchers say.
High levels of anandamide were found in young men who ran or cycled at a moderate rate for about an hour, according to a study made public this week by the Georgia Institute of Technology and the University of California, Irvine... (&c)
Source: Reuters (Wire), 9 Jan 2004
Proceedings of the National Academy of Sciences // NewScientist.com's news service (25 March 2003) ~ "Marijuana Use in Pregnancy Damages Kids' Learning"
Shaoni Bhattacharya
Children born to mothers who use marijuana during pregnancy may suffer a host of lasting mental defects, suggests a new study in rats. Marijuana is the most widely used illegal drug among women of reproductive age.The offspring of pregnant rats given a low dose of cannabinoid were found to perform poorly in learning tests throughout their lives, compared to rats that were not exposed.
The Italian research team found that long-term learning in the rats was damaged by the cannabinoids irreversibly disrupting chemical and electrical processes in the brain during gestation. The exposed rats were also more hyperactive as infants, although this effect wore off as the rats reached adulthood.
Vincenzo Cuomo, at the La Sapienza University in Rome, and colleagues suggest that similar brain effects could explain learning problems in children born to mothers who use the soft drug during pregnancy.
"This is absolutely relevant," says Peter Fried, a psychologist at Carleton University in Ottawa, Canada, who has done similar work in humans. "What they have found is very consistent with what we have found in humans."
Confounding Factors ~
The possible effects of maternal marijuana use on the unborn child and the child's later behaviour are controversial, say Cuomo and colleagues. They argue that rat studies can be very useful in assessing human effects, because studies of people can be hampered by complex confounding factors. These could include cigarette smoking, wealth or urban living.
In the study, pregnant rats were injected with a low dose of an artificial cannabinoid. Offspring exposed to the drug during gestation showed hyperactivity during infancy and adolescence, as measured by how many times they broke infrared beams crisscrossing their cages.
This stopped when they reached adulthood, but was replaced by problems with memory retention. The researchers showed reduced levels of a messenger chemical called glutamate in the hippocampus, part of the brain associated with learning and visual ability. They also found disruption of electrical processes associated with learning in this region.
Fried told New Scientist that as well as affecting memory and learning, exposure to marijuana during pregnancy has a strong effect on visual mapping and analysis in human children.
The Telegraph (UK) 8-1-5 ~
http://telegraph.co.uk/news/main.jhtml
?xml=/news/2005/08/01/ncann01.xml&sSheet
=/news/2005/08/01/ixhome.html"Cannabis May Help Relieve Bowel Disease"
By Anna Seward
Drugs derived from cannabis plants could help to relieve symptoms of inflammatory bowel disease, according to research published today.
Researchers examined anecdotal evidence that cannabis eases the unpleasant symptoms associated with the disease. Their findings, published in the journal Gastroenterology, will give hope for sufferers of Crohn's disease and ulcerative colitis, forms of IBD which affect up to 180,000 people in Britain.
The disease causes recurrent bouts of severe abdominal pain, diarrhoea, fever and weight loss, and puts sufferers at a greater risk of bowel cancer.
Patients are usually treated with steroids to reduce the inflammation and surgery is sometimes required to remove damaged parts of the intestine, but there is currently no cure for Crohn's disease or ulcerative colitis.
Dr Karen Wright, of the department of pharmacy and pharmacology at the University of Bath, who led the study, said that using cannabinoids, a cannabis extract, helped the body recover from some effects of the diseases and heal the gut lining.
Neurology (vol 64, p 488)
NewScientist.com news service (7 February 2005) ~"Marijuana Makes Blood Rush to the Head"
by Katharine Davis
Smoking marijuana can affect blood flow in the brain so much that it takes over a month to return to normal. And for heavy smokers, the effects could last much longer, a new study suggests.Regular marijuana use can harm memory and the ability to make decisions, according to Jean Cadet at the National Institute on Drug Abuse in Baltimore, Maryland, US. To find out why, he monitored the flow of blood through the brains of 54 marijuana smokers, among whom the heaviest user smoked 50 joints every day.
People who smoked cannabis had higher blood flow through their brains than non-users. Yet there was also greater resistance to the blood flow, suggesting that cannabis changes the blood vessels in the brain in a way which hinders oxygen in reaching the tissue effectively. In an attempt to compensate, extra blood is sent to that part of the brain, increasing resistance but probably failing to get enough oxygen through the vessels, Cadet suggests.
Cadet and his colleagues used an extremely sensitive non-invasive technique called transcranial Doppler sonography to "see" the blood flow through individual arteries from the head's surface.
After a month without cannabis - during which the volunteers agreed to remain in a clinic, with no access to marijuana -- Cadet repeated the sonography. The resistance to blood flow of light and moderate users - who usually smoked an average of 11 and 44 joints per week, respectively -- was starting to return to normal.
Neuropsychological problems ~
But there was no improvement observed in the heavy users, who smoked an average of 131 joints per week. "We were surprised because we'd expected that as marijuana cleared the system things would improve," says Cadet. He now wants to see if there is a link between the changes in the brain's blood flow and the extent of neuropsychological problems.
To eliminate the effect of tobacco in the joints, Cadet compared his results to those obtained from smokers, who showed normal blood flow. But, says William Notcutt of James Paget Hospital in Norfolk, UK, the longer-term effect on the brain may not have been caused by the same substance that produces the high.
"Somebody smoking 50 joints per day is getting a huge number of carcinogens from the marijuana plant," he notes. "We know the cardiovascular effect [of cannabis] is very complex and multi-factorial so it's not as simple as with other drugs. The group that needs to be studied now is people that use high quality medicinal extracts."
He adds that the results may also be different for people that only smoke marijuana occasionally, and so are exposed to lower doses of the toxic substances.
CounterPunch.com ( 2 Jul 2005 ) ~"Study: Smoking Marijuana Does Not Cause Lung Cancer"
by Fred Gardner
Marijuana smoking -- "even heavy longterm use"- does not cause cancer of the lung, upper airwaves, or esophagus, Donald Tashkin reported at this year's meeting of the International Cannabinoid Research Society. Coming from Tashkin, this conclusion had extra significance for the assembled drug-company and university-based scientists ( most of whom get funding from the U.S. National Institute on Drug Abuse ). Over the years, Tashkin's lab at UCLA has produced irrefutable evidence of the damage that marijuana smoke wreaks on bronchial tissue. With NIDA's support, Tashkin and colleagues have identified the potent carcinogens in marijuana smoke, biopsied and made photomicrographs of pre-malignant cells, and studied the molecular changes occurring within them. It is Tashkin's research that the Drug Czar's office cites in ads linking marijuana to lung cancer. Tashkin himself has long believed in a causal relationship, despite a study in which Stephen Sidney examined the files of 64,000 Kaiser patients and found that marijuana users didn't develop lung cancer at a higher rate or die earlier than non-users. Of five smaller studies on the question, only two -involving a total of about 300 patients- concluded that marijuana smoking causes lung cancer. Tashkin decided to settle the question by conducting a large, prospectively designed, population-based, case-controlled study. "Our major hypothesis," he told the ICRS, "was that heavy, longterm use of marijuana will increase the risk of lung and upper-airwaves cancers."The Los Angeles County Cancer Surveillance program provided Tashkin's team with the names of 1,209 L.A. residents aged 59 or younger with cancer ( 611 lung, 403 oral/pharyngeal, 90 laryngeal, 108 esophageal ). Interviewers collected extensive lifetime histories of marijuana, tobacco, alcohol and other drug use, and data on diet, occupational exposures, family history of cancer, and various "socio-demographic factors." Exposure to marijuana was measured in joint years ( joints per day x 365 ). Controls were found based on age, gender and neighborhood. Among them, 46% had never used marijuana, 31% had used less than one joint year, 12% had used 10-30 j-yrs, 2% had used 30-60 j-yrs, and 3% had used for more than 60 j-yrs. 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. "We found absolutely no suggestion of a dose response." The data on tobacco use, as expected, revealed "a very potent effect and a clear dose-response relationship -a 21-fold greater risk of developing lung cancer if you smoke more than two packs a day." Similarly high odds obtained for oral/pharyngeal cancer, laryngeal cancer and esophageal cancer. "So, in summary" Tashkin concluded, "we failed to observe a positive association of marijuana use and other potential confounders."
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."
Abrams had results of his own to report at the ICRS meeting. He and his colleagues at San Francisco General Hospital had conducted a randomized, placebo-controlled study involving 50 patients with HIV-related peripheral neuropathy. Over the course of five days, patients recorded their pain levels in a diary after smoking either NIDA-supplied marijuana cigarettes or cigarettes from which the THC had been extracted. About 25% didn't know or guessed wrong as to whether they were smoking the placebos, which suggests that the blinding worked. Abrams requested that his results not be described in detail prior to publication in a peer-reviewed medical journal, but we can generalize: they exceeded expectations, and show marijuana providing pain relief comparable to Gabapentin, the most widely used treatment for a condition that afflicts some 30% of patients with HIV.
To a questioner who bemoaned the difficulty of "separating the high from the clinical benefits," Abrams replied: "I'm an oncologist as well as an AIDS doctor and I don't think that a drug that creates euphoria in patients with terminal diseases is having an adverse effect." His study was funded by the University of California's Center for Medicinal Cannabis Research.
CounterPunch.com ( July 24 / 25, 2004 ) ~"The Politics of Pot -- The Year of the Antagonist"
by Fred Gardner
This is your preliminary warning about a weight -- loss drug called Rimonabant that works by blocking cannabinoid receptors in the brain. Scientists from Sanofi, France's biggest pharmaceutical company, announced favorable clinical -- trial results at this year's meeting of the International Cannabinoid Research Society and expect FDA approval to market Rimonabant within a year.
Cannabinoid receptors are proteins on the surface of certain cells to which certain compounds bind, setting off molecular cascades within the cells that produce effects in the body such as reduced inflammation, increased appetite, etc. Two kinds of cannabinoid receptors have been discovered -- CB1, highly concentrated in the brain and central nervous system, and CB2, found mainly in tissues associated with the immune system.
There are three different kinds of cannabinoids, or chemical "agonists" that activate the cannabinoid receptors. They are, in order of evolutionary appearance: compounds made in the body for purposes of neurotransmission, compounds unique to the cannabis plant (the most famous being delta-9 THC), and compounds made in the lab s-- synthetics -- developed in recent decades.
The cannabinoids made in the body are called "endocannabinoids" (just as the body's endogenous morphine--like chemicals are called "endorphins"). The first to be identified, by Raphael Mechoulam and William Devane in 1992, was named "anandamide" after the Sanskrit word for "bliss." It has since been learned that endocannabinoids help regulate the cardiovascular, digestive, endocrine, excretory, immunological, nervous, reproductive, and respiratory systems.
Rimonabant is an "antagonist" drug that engages the CB1 receptors so they can't be activated. Originally called SR-141716, it was developed by Sanofi in the early '90s as a research tool. If a given effect is blocked by SR-141716, that effect is said to be mediated by CB1 receptors. Rimonabant is SR-141716 redefined as a "therapeutic drug" that counteracts unwanted effects -- like overeating -- mediated by the cannabinoid receptor system.
In a talk at the ICRS meeting entitled "Clinical Results with Rimonabant in Obesity," Sanofi researcher Gerard Le Fur reported that the drug had done well in phase--three clinical trials involving 13,000 patients. The trials were conducted at numerous sites in the U.S. Obese patients were treated with Rimonabant for 52 weeks. "Over 72% of patients at 1 year showed a weight loss of greater than 5 percent, with over 44% showing a weight loss of greater than 10%," according to Le Fur. "There was also an increase in HDL-cholesterol values, a reduction in triglyceride values and reductions in glucose and insulin values... The general tolerance of the compound was excellent."
But the advent of Rimonabant troubles California doctors who have made a specialty of monitoring their patients' cannabis use, as well as some scientists who are studying the basic nature of the cannabinoid system. Jeffrey Hergenrather, MD, of Sebastopol -- one of the few clinicians to attend the ICRS meeting, which was held in Paestum, Italy, in late June -- says "We are only now be becoming aware of the modulating effects the cannabinoids have on the body and mind. The consequences of interfering with the cannabinoid receptor system have not been evaluated in normal human physiology."
Le Fur and other Sanofi researchers were asked how a drug could block the CB1 receptor system without adversely affecting mood, sleep, pain relief, and other CB1--mediated aspects of well -- being. The answers were vague -- other neurotransmitters may play compensatory roles. We were told that no pattern of adverse effects had been observed during the clinical trials, and that such effects are probably so rare that they won't be detectable until Rimonabant has been used by millions of people over a period of years.
The developer of another antagonist drug, a rival of Sanofi's, claimed that Rimonabant induced "food aversion" in five percent of the test subjects. Le Fur responded that obesity was such a widespread and serious health problem that five percent seems like an acceptable rate of anorexia. Other criticisms and misgivings were only whispered. A multiple sclerosis specialist told of a case in which Rimonabant apparently caused an immediate, extreme exacerbation. A physician wondered -- since the body's own cannabinoids have neuroprotectant and anti-oxidant functions -- if Rimonabant users would be at increased risk for stroke and cancer. But the negative remarks were anecdotal or speculative; the positive data belonged to Sanofi.
Le Fur and two colleagues accepted the ICRS's 2004 achievement award on behalf of their company. It was presented by Mechoulam, the grand old man of the field. who observed that Sanofi had shown great foresight in developing a weight -- loss drug in the late 1990s, because it has since swallowed up two much larger drug companies, Synthelabo and Aventis.
From the perspective of the scientists in the ICRS -- mainly employees of universities or pharmaceutical companies who get funding from the U.S. National Institute on Drug Abuse-- it's a win--win--win to honor Sanofi for developing CB-receptor antagonists as "new therapeutic drugs." NIDA is eager to sponsor research involving cannabinoid antagonists. A lot will be learned about the cannabinoid system, its mechanism of action, etc. And a therapeutic effect is a therapeutic effect, whether it's produced by activating or blocking the cannabinoid receptors.
But common sense and a few cautious clinicians say DANGER DANGER DANGER. CB1 receptors are concentrated in the cerebellum and the basal ganglia (responsible for motor control, which may help explain why marijuana eases muscle spasticity in disorders like multiple sclerosis), the hippocampus (responsible for storage of short-term memory), and the limbic system (emotional control).
Although other neurotransmitters may play compensatory roles when the cannabinoid receptors are blocked, the longterm impacts will not be known until years after Sanofi gets approval to market Rimonabant to the slimness-loving masses. Before marketing commences, says Hergenrather, "It would be ethical to design longitudinal studies to assess the consequences of interfering with the cannabinoid system."
Other uses for cannabinoid-antagonist drugs are being studied with active encouragement from NIDA. Walter Fratta of the University of Cagliari gave a paper in Paestum proposing antagonists "as therapeutic agents to prevent relapse to heroin abuse." Carl Lupica of NIDA discussed Rimonabant as a "potential treatment" for food, alcohol and nicotine cravings. "It is also clear that marijuana craving may be successfully treated by this drug," according to Lupica.
Alas, this was supposed to be the year that G.W. Pharmaceuticals won the ICRS achievement award. G.W. is the British firm that in 1998 got government approval to develop and test an extract of the cannabis plant which it formulated as an oral spray and dubbed "Sativex." Clinical trials of Sativex as a treatment for neuropathic pain, multiple sclerosis and other conditions were conducted and favorable results reported to the regulators. Bayer agreed to market Sativex in Europe when the approval came through. G.W. generously made Sativex and other plant extracts with different cannabinoid contents available to investigators who previously could experiment only with NIDA-weed or synthetics.
But the marketing approval that Guy said he expected by the end of 2003, and then by spring '04, has yet to be granted. So he and his associates had to walk a bit of a tightrope in Paestum, reassuring all concerned that Sativex certainly will get approved, while not risking any more misstatements about when.
Guy cited favorable data produced in recent trials of Sativex as a treatment for pain in rheumatoid arthritis and spasticity in multiple sclerosis. Unfortunately, in the U.K. as in the U.S., favorable trial results can count for less than the establishment connections of the doctors who conduct them. And so the British regulatory authorities continue to ponder G.W.'s dossier, while the banquet at this year's ICRS meeting was hosted by Sanofi.
nature.com ( 1 August 2002 )"Innate Cannabis Chemical Erases Fears"
Calming Brain Circuit Could Treat Anxieties
by Helen Pearson
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.
Phobics are often treated by gradually exposing them to the object of their fear in a safe environment, to erase the bad association. Lutz suggests that cannabinoid-enhancing drugs, taken at the same time as this exposure, might aid memory clearance.
A joint is unlikely to do the trick: smoking floods the brain with cannabis's active ingredient and produces other effects such as memory changes and pain relief. More effective would be a drug that raised levels of cannabinoids only in the brain's fear centre, the amygdala, says Lutz.
Shock Tactics ~
Lutz's team gave mice mild shocks while playing a loud tone, until the animals froze at the noise alone. When the shocks stopped, mice normally forgot the ordeal and stopped freezing in less than a week. Mice genetically engineered to lack the receptors that bind to cannabinoids were unable to forget within that time.
During memory erasure the amygdala is flooded with cannabinoids; these dampen the action of nerve cells.
Lutz is now giving normal mice cannabinoid boosters to see if they forget learnt fears more quickly.
Other brain chemicals are involved in erasing fear. Clinical trials are planned for compounds that activate NMDA receptors in the amygdala, which are also involved in erasing unpleasant memories.
NORML.org (4-5-04) -- http://norml.org/index.cfm?Group_ID=6012"Cannabis Relieves Lou Gehrigs Symptoms -- New Study
Patients with amyotrophic lateral sclerosis (ALS) experience symptom relief after smoking cannabis, according to a study published in the March/April issue of the American Journal of Palliative Care.According to the study's findings, based on an anonymous survey of ALS patients conducted by the MDA/ALS Center at the University of Washington, respondents found marijuana to be "moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling." Cannabis' depression-relieving effects lasted two to three hours, patients reported.
The survey is the first ever conducted regarding use of medicinal cannabis among patients with ALS. Also known as Lou Gehrig's disease, ALS is a chronic, often fatal condition marked by a gradual degeneration of the nerve cells in the central nervous system that control voluntary muscle movement.
Respondents said that cannabis was ineffective in reducing difficulties with speech and swallowing, and sexual dysfunction.
A previous clinical trial examining the effectiveness of Marinol (synthetic THC) on patients with ALS found it to improve appetite, sleep, and muscle tightness.
For more information, please contact Paul Armentano, NORML Senior Policy Analyst, at (202) 483-5500. Abstracts of the study, entitled "Survey of cannabis use in patients with amyotrophic lateral sclerosis," are available online at: http://www.pnpco.com/pn01035.html
NewScientist.com's news service ( 11 November 2002 ) ~"Cannabis Smoking 'More Harmful' Than Tobacco"
by
Emma Young
Smoking pure marijuana is at least as harmful to lungs as smoking tobacco, a report from the British Lung Foundation concludes. And in some key ways, it may be more dangerous.For example, the BLF's review of previous research highlights that just three marijuana joints a day causes the same damage to the lung's airways as 20 cigarettes, mainly because of the way joints are smoked.
Individually, cannabis and tobacco produce the same constituents and quantities of chemicals known to be toxic to respiratory tissue, other than nicotine, the report says. But when cannabis and tobacco are smoked together, the health effects are worse.
"These statistics will come as a surprise to many people, especially those who choose to smoke cannabis rather than tobacco in the belief it is safer for them," says Mark Britton, chairman of the BLF. A UK survey conducted earlier in 2002 found that 79 per cent of children believed cannabis to be 'safe'.
Deep Breath ~
A key finding highlighted by the review of 90 published papers is that the amount of smoke taken into the lungs is two thirds larger if cannabis is being smoked. The smoke is also taken one third deeper into the lungs -- and that smoke is held an average of four times longer before being exhaled.
"You inhale deeper and hold your breath with the smoke for longer before exhaling. This results in more poisonous carbon monoxide and tar entering into the lungs," says Helena Shovelton, BLF's chief executive.
Other points in the report include:
Tar from cannabis cigarettes contains up to 50 per cent higher concentrations of carcinogens benzathracenes and benzpyrenes than tobacco smoke;
THC, the primary psychoactive ingredient of cannabis, decreases the function of immune system cells that help protect the lungs from infection;
The average cannabis cigarette smoked in the 1960s contained about 10 milligrams of tetrahydrocanabinol (THC), the primary psychoactive ingredient. Today, it may contain 150 mg.
"This means that the modern cannabis smoker may be exposed to greater doses of THC than in the 1960s or 1970s," says the report. "This in turn means that studies investigating the long-term effects of smoking cannabis have to be interpreted cautiously."
Mouth Spray ~
Cannabis is the most widely consumed illegal drug in the UK. In 2000, almost 45 per cent of 16 to 29 year olds in the UK said they had used cannabis at some point.
"We are not making any policy recommendations. The aim of this report is to try to inform the public that if you do choose to smoke cannabis, be aware of the health risks," says a BLF spokeswoman.
Cannabis-based medicines could be prescribed for medical use in the UK as early as 2003, following the recent success of final-stage trials. But medicinal cannabis is supplied through a mouth spray or in tablet form.
"We have always been keen to find additional ways of administering cannabis as a medicine," says Nina Booth-Clibborn of the UK's Medicinal Cannabis Research Foundation. "It did seem that smoking would not be the best way."
Lyndon Pugh, editor of pro-cannabis magazine CC Newz, is not impressed by the report: "These allegations have been made before countless times. Lot of things are dangerous, like driving."
NewScientist.com news service (25 March 03) ~"Marijuana Use in Pregnancy Damages Kids' Learning"
Children born to mothers who use marijuana during pregnancy may suffer a host of lasting mental defects, suggests a new study in rats. Marijuana is the most widely used illegal drug among women of reproductive age.The offspring of pregnant rats given a low dose of cannabinoid were found to perform poorly in learning tests throughout their lives, compared to rats that were not exposed.
The Italian research team found that long-term learning in the rats was damaged by the cannabinoids irreversibly disrupting chemical and electrical processes in the brain during gestation. The exposed rats were also more hyperactive as infants, although this effect wore off as the rats reached adulthood.
Vincenzo Cuomo, at the La Sapienza University in Rome, and colleagues suggest that similar brain effects could explain learning problems in children born to mothers who use the soft drug during pregnancy.
"This is absolutely relevant," says Peter Fried, a psychologist at Carleton University in Ottawa, Canada, who has done similar work in humans. "What they have found is very consistent with what we have found in humans."
Confounding Factors ~
The possible effects of maternal marijuana use on the unborn child and the child's later behaviour are controversial, say Cuomo and colleagues. They argue that rat studies can be very useful in assessing human effects, because studies of people can be hampered by complex confounding factors. These could include cigarette smoking, wealth or urban living
Canadian Medical Association Journal (Vol. 166: 887); from NewScientist.com's news service (8 April 2002) ~
"Pot Luck"A little bit of what you fancy will not make you dull
by Alison Motluk
Smoking cannabis does not have a long-term effect on intelligence, say researchers in Canada who have followed volunteers from before birth to early adulthood.
Heavy pot smokers did experience a dip in their intelligence quotient (IQ). But people who had once smoked heavily and then given up were right back up to normal, the study found. Light smokers appeared no different to non-smokers.
What the researchers do not know is if decades of pot-smoking could have a more lasting impact. Looking at long-term users in their 30s and 40s could show different results, admits Peter Fried, at Carleton University in Ottowa, who led the study. "Perhaps the nervous system isn't as flexible then," he says.
"You can't argue with what they are saying," says William Campbell, President of the Canadian Society of Addiction Medicine. "It doesn't surprise me or disappoint me."
British Medical Journal (Vol. 325: 1195, 1199, 1212, 1183); from NewScientist.com's news service (21 November 2002) ~"Cannabis Link to Mental Illness Strengthened"
by Emma Young
The link between regular cannabis use and later depression and schizophrenia has been significantly strengthened by three new studies.The studies provide "little support" for an alternative explanation - that people with mental illnesses self-medicate with marijuana - according to Joseph Rey and Christopher Tennant of the University of Sydney, who have written an editorial on the papers in the British Medical Journal.
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 works also highlights potential risks associated with using cannabis as a medicine to ease the symptoms of muscular sclerosis, for example.
Pharmacological Effect ~
Patton's team followed over 1600 Australian school pupils aged 14 to 15 for seven years. Daily cannabis use was associated with a five-fold increased risk of depression at the age of 20. Weekly use was linked to a two-fold increase. The regular users were no more likely to have suffered from depression or anxiety at the start of the study.
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.
In separate research, a team led by Stanley Zammit at the University of Cardiff, UK, evaluated data on over 50,000 men who had been Swedish military conscripts in 1969 and1970. This group represents 97 per cent of men aged 18 to 20 in the population at that time.
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.
Genetic Factors ~
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.
"The overall weight of evidence is that occasional use of cannabis has few harmful effects overall," Zammit's team writes. "Nevertheless, our results indicate a potentially serious risk to the mental health of people who use cannabis. Such risks need to be considered in the current move to liberalise and possibly legalise the use of cannabis in the UK and other countries."
Journal Current Opinion In Pharmacology ~"Moderate Use Of Cannabis 'Safe' Study Says"
NORML
( 1-28-5 )
Oxford, United Kingdom -- Moderate cannabis use, even long-term, is "relatively safe" when compared to the health effects of other recreational intoxicants, according to a scientific review published in the February issue of the journal Current Opinion in Pharmacology. "A review of the literature suggests that the majority of cannabis users, who use the drug occasionally rather than on a daily basis, will not suffer any lasting physical or mental harm," writes the study's author, Dr. Leslie Iversen of the University of Oxford. "Overall, by comparison with other drugs used mainly for 'recreational' purposes, cannabis could be rated to be a relatively safe drug." The author concludes that there is little evidence that long-term cannabis use causes permanent cognitive impairment or has an adverse effect on global intelligence. Iversen does acknowledge, however, that smoking marijuana long-term may cause "the possibility of damage to the airways," though he admits that "little progress has been made in quantifying such risks." The author also notes that various longitudinal studies have found an association between the long-term, heavy use of cannabis and specific adverse psychosocial features, including lower educational achievement, though he acknowledges that there exists no "clear cause and effect relationship to explain the psychosocial associations." NORML Executive Director Allen St. Pierre praised the review, stating: "Marijuana is not a harmless substance, though its scientifically acknowledged harms are quite minimal compared to other legally regulated intoxicants, including alcohol and tobacco. By far the greatest danger to health posed by the responsible use of cannabis in the United States today stems from a criminal arrest or conviction." For more information, please contact Allen St. Pierre, NORML Executive Director, at (202) 483-5500.
http://www.cbc.ca/story/science/national/2004/12/02/pot-psychosis041202.html ~"Marijuana Use Boosts Risk of Psychosis - Study"
CBC News ( 12-4-4 )
Teens and young adults who frequently use marijuana are at higher risk of developing psychotic symptoms later in life, researchers say. Dutch scientists studied 2,437 young people aged 14-24 to identify their predisposition to psychosis. Participants were questioned about their use of cannabis and followed for up to four years. In the study, researchers used a broad definition of psychosis, ranging from occasionally hearing voices and paranoia to schizophrenia. Jim van Os of the University of Maastricht in the Netherlands and his team found 21 per cent of cannabis users had experienced psychotic symptoms compared with 15 per cent among non-users. The odds of experiencing symptoms were also higher among those who frequently smoked marijuana, after adjusting for other factors, such as social and economic status, use of other drugs, alcohol and tobacco. In the past, it has been difficult for scientists to figure out if cannabis triggers the psychotic symptoms or whether those with mental health problems are more likely to use the drug. Researchers on van Os's team found that the risk of developing symptoms was about four times higher in young people with a pre-existing susceptibility to mental instability. The study appears in this week's issue of BMJ Online First.
Department of the Environment, Transport and the Regions ~
by B F Sexton, TRL, et al.\ Executive Summary
Introduction ~
Results from the study of the "Incidence of alcohol and drugs in road accident fatalities" have consistently shown a large increase in the incidence of drugs in fatal road casualties (drivers, riders, passengers and pedestrians) since the last comparable study in the mid-1980s. The latest results show that among all road users traces of illicit drugs were present in 18% of fatalities. These figures represent a six-fold increase in presence of illicit drugs when compared with the previous study. Cannabis constitutes around two thirds of the illegal drugs found.Despite the increase in the incidence of drugs, it is not possible to say that drugs caused these deaths. There may be an association, but presence cannot be taken as evidence of causation - there is no way of telling how much was consumed and how long before the fatal accident. So far as cannabis is concerned, the prevalence in drivers was not significantly different from that of passengers, who can be taken as a (albeit imperfect) measure of the prevalence in the population as a whole. However, cannabis remains detectable in the body for up to four weeks after use - long after any impairment of driving.
In addition, in most surveys reported in Europe cannabis is the most frequently detected illicit drug. In a range of accident involved populations cannabis is found with an incidence between 2 and 12% with a mode incidence around 5-8%. This is certainly significantly above that of any other illicit drug.
Previous research studies on cannabis and driving have focussed largely on the effects of cannabinoids on driving performance. These studies have been almost exclusively experimental, involving laboratory tasks, driving simulator and on road 'real driving' experiments. A much smaller number of studies have attempted to gain broader sociological information about driving habits under the influence of cannabis and what factors influence the decision to drive. This research attempted to combine these two aspects, certainly for the first time in the UK, with a view to assessing the degree to which there may be a problem with cannabis in relation to driving. The research had three primary objectives:
The research attempted to address these objectives using experienced cannabis users carrying out a variety of laboratory-based tasks and driving in a simulator under four cannabis conditions: placebo; low THC; high THC; and cannabis resin. The placebo, low and high dose THC conditions used herbal cannabis ('grass') cigarettes supplied by the National Institute on Drug Abuse (NIDA), while the cannabis resin condition used cannabis supplied by Customs and Excise from seized supplies.To provide reliable data, under laboratory conditions, on the impairing effects of cannabis on driving. To determine the duration and extent of any impairment under different degrees of intoxication (using different levels of cannabis). To provide an overview of attitudes and habits of cannabis users in relation to driving and explore factors which may influence the decision to drive under its influence. In 1999 the DETR commissioned a review of the latest evidence of the impairment effects of cannabis. That report provided an overview of the effects of cannabis on driving and accident risk and identified key research questions for areas where current knowledge was deemed to be insufficient to guide road safety policy. These research questions have shaped and informed the current research project. In addition to the primary objectives outlined above, the research reported here sought to inform four key issues identified by the review.
These were: exposure; biological response; acute psychomotor response; and driving response.
Exposure ~
Prior to this research, few studies have attempted to gain broader sociological information about driving under the influence of cannabis. A comparison between the participants in the current study and a group of regular users in the West Midlands showed the trial group to be fairly typical. Both groups showed a reluctance to drive after consuming more than 4 units of alcohol, believing their driving to be significantly impaired. The majority of both groups again thought that cannabis impaired their driving, but only to a slight degree.
Biological Response ~
In considering the results of the present study, the biological response of the participants to the consumption of cannabis is of fundamental importance. Urine was screened on arrival to check for and exclude multiple drug use.
Blood and saliva measurements were taken immediately prior to dosing and at 10 and 30 minutes post dosing. The subjective reports given by the participants of the effects of smoking the various strengths of cannabis cigarettes showed an extremely good correlation between what participants thought they had smoked and the THC dosage in the cigarettes. The maximum amounts of THC administered were around 10mg for the low dose and 20 mg for the high and the majority of participants were able to distinguish between the effects of these doses and placebo. The subjective feelings of the "highs" experienced were also closely correlated with the participants "liking" of the smoking effect as stated in the mood questionnaire. Making allowance for the experimental situation, the majority of participants also found the experience of smoking cannabis similar to their normal experience.
Acute Psychomotor Response and Tests of Impairment ~
It is of the utmost importance to try to relate the observations derived from this experimental study to the situations likely to be encountered in real life drug driving cases. Part of the experimental procedures therefore included the formal sobriety testing of participants. Two registered medical practitioners (experienced Forensic Medical Examiners (FMEs)) examined the participants and carried out a comprehensive physical examination to see whether the suggested standard "impairment" tests currently used were effective in detecting impairment due to cannabis.
The results of the sobriety testing clearly show a strong correlation between cannabis dose received and whether impairment was judged to be present. In total, 56 assessments were performed on the 15 participants at the various dose levels. In 7 cases on high dose and 3 cases on low dose impairment was judged to be present, but no cases on placebo. In assessments where a condition was judged to be due to a drug 30 had received one of the three cannabis dose levels and only 2 were placebo conditions. On the basis of these observations, the general medical examination and standardised impairment testing applied by the FMEs were judged to be effective in determining both impairment and establishing condition due to a drug. There was also a strong relation between the FME's decision regarding the participant's impairment and the participant's subjective rating, which formed part of the mood questionnaire.
These results are important for two reasons. First, they offer strong support for the validity of the FME's decisions and for the effectiveness of the sobriety tests as detectors of impairment. Second, they offer further support for the view that, under the influence of cannabis, users are acutely aware of their impairment.
It is also interesting to note that, despite participants having smoked some form of cannabis before 42 of these examinations, on only 11 occasions did the FME consider the participant to be impaired. This finding could have implications for the number of cases that will be detected by the Field Impairment Testing recently launched in the UK by the police.
In addition to the general medical examination, pupil size was measured using a Pupillometer, supplied by Procyon Ltd. The Pupillometer showed a significant increase in pupil sizes 25-30 minutes after dosing. The difference was statistically significant for the placebo v high dose and the placebo v low dose. This suggests that this measure may be helpful in assessing if a person has recently smoked and may be impaired through cannabis, although this would require a baseline and an 'impaired condition' measure to be useful.
Driving Response ~
The final key objective of the study was to consider the effects of cannabis on driving response. Statistically significant results, which have been found for the simulator-derived measures, are given in the report. There was a reduction of average speed on the motorway when participants had the high or low doses of cannabis. This confirms the results from many previous studies. It strongly suggests that the participants as drivers are aware of their impairment, but attempt to compensate by driving more cautiously. Participants did not know what strength of cannabis they had received, but knew there was a likelihood of having had something 'active' and so were perhaps being more careful. A post trial survey of participants showed that they were very good at guessing when they had taken the placebo dose and most participants even managed to correctly guess if they had the low dose or high dose.
In the simulator trials, participants reacted more slowly to a pulling-out event when they had taken the low dose of cannabis, suggesting a similar compensatory action for the effects of cannabis impairment. However, when taking the high dose this effect was not significant. This is probably due to the variability in the response data.
Similarly, there was no significant difference between braking reaction times. The mean response times increased slightly, but there was too much variability in the data for this to be statistically significant. This variability in the results when considering the impairing effects of cannabis has been observed by other researchers. The variability of drug effects on individuals is well recognised and this seems to be even more in evidence with cannabis than with other drugs.
When considering the simulator tracking tasks, participants tended to drive less accurately on the left and right loops of the 'figure of eight' when they had been on the high cannabis dose. There was also a significant increase in their Standard Deviation of Lateral Position (SDLP) on the right loop when on the high dose as compared to the low dose of cannabis. This suggests that they were unable to control their steering as well when under the influence of the high cannabis dose. This again confirms previous observations that cannabis adversely affects drivers' tracking ability.
The mean time to move from stationary at a traffic light controlled junction once the lights had turned to red/amber on the driving simulator produced an interesting result. This was significantly reduced with high cannabis dose level, the reduction was in the order of ½ second between the placebo condition and high dose condition, and slightly less from the low dose to high dose. There are a number of possible explanations for this. It may suggest that in the "observational" conditions of the driving simulator participants were aware of missing the traffic light change and so reacted slightly more quickly. Alternatively, the effects on the participants' internal clocks might have made them feel that they had been at the lights longer than they actually had and therefore heightened their attention to the imminent change in lights. It has been suggested that cannabis, in a similar way to alcohol at low doses, can have a stimulant effect on dopamine that may account for more risky behaviour in some circumstances. Other explanations are possible, however, and further assessment of this observation will be required.
The hazard perception (HP) task did not produce any statistically significant results. Although reaction times were found to increase with dose level, there was too much variability in the data for statistical significance. An increase of 0.08 seconds between the placebo and low dose and an increase of 0.14 seconds between the placebo and high dose was observed. This suggests that there may be an effect on the reaction time of participants responding to hazards, but it is quite a small effect which would require a much larger sample to determine whether or not it was statistically significant. This would also seem to confirm earlier observations of the effects of cannabis on the various aspects of driver performance; the effect on reaction time being somewhat indeterminate.
The mean tracking accuracy on the Compensatory Tracking Task (CTT) decreased with increasing level of dose. The placebo tracking accuracy was higher than either the high dose or resin tracking accuracy. Thus tracking accuracy does change with dose. The proportion of correct trials also decreased with increasing dose level. All participants were still quite accurate, but the difference from 99.5% accuracy when on placebo was statistically significantly different from the 97.0% accuracy when on the high dose. The HP and CTT results are of particular interest because the HP test was taken at least 75 minutes post smoking the cannabis, and the CTT test at least 85 minutes post dosing. Some of the acute impairment effects may well have diminished by then.
In summary, the results of this study show a broad consistency with the effects of cannabis on driver performance observed by previous researchers. In addition, the habits and attitudes of cannabis users in relation to driving have been explored for the first time in the UK.
Conclusions ~
The research has demonstrated the practicability of assessing the influence of cannabis on driving performance in a controlled clinical trials experimental situation. Participants were recruited, medically screened and tested under conditions of a strict protocol that had local ethics committee approval.The maximum amounts of THC administered in the cannabis cigarettes were shown to be typical of that available with 'street' cannabis. Participants were generally able to distinguish between the effects of cannabis with active THC and placebo conditions. The subjective reports of smokers on the effects of smoking the various strengths of cannabis cigarettes showed an extremely good correlation between what participants thought they had smoked and the THC dosage in the cigarettes.
The feelings of the "highs" experienced were also closely correlated with participants' positive reactions as measured by a mood questionnaire. Given the controlled conditions of the experimental situation, the majority of participants also found the experience of smoking cannabis similar to their normal experience.
Previous studies have shown that simulated and actual driving and divided attention tasks which all require integrative mental processes are severely affected by alcohol. Simple attention / vigilance tasks are not so much affected and psychomotor skills, especially tracking, and simple reaction time tasks are only affected at relatively high blood alcohol levels. Alcohol may, therefore, be seen as first disturbing higher cognitive processes, especially those that require integrative performances. Compared to those effects, the losses in psychomotor skills and simple attentional processes are much smaller. In contrast, previous studies with cannabis show that it first seems to affect all tasks requiring psychomotor skills and continuous attention. Thus, tracking tasks, which are very sensitive to short term changes in attention, are very sensitive to cannabis impairment. On the other hand, integration processes and higher cognitive functions are not as time critical. A short attention lapse can be compensated for by increased activity later.
In the case of the overall driving task, it seems that the negative effects of these short-term distortions can be reduced by lowering the difficulty, and hence the time critical aspects, of the task. This would explain the frequently reported observation that drivers under the influence of cannabis drive at notably reduced speeds.
Results from the current study using the TRL driving simulator confirm the results from these previous studies. There was a reduction of average speed on simulated motorway driving when participants had the high or low doses of cannabis. This strongly suggests that the participants as drivers are aware of their impairment, but attempt to compensate by driving more cautiously.
When considering the simulator tracking tasks, participants tended to drive less accurately on the left and right loops of the 'figure of eight' when they had been on the high cannabis dose. This suggests that they were unable to control their steering as well when under the influence of the high cannabis dose. This again confirms previous observations that cannabis adversely affects drivers' tracking ability.
There is variability in the results when considering the impairing effects of cannabis that has been observed by other researchers. The variability of drug effects on individuals is well recognised and this seems to be even more in evidence with cannabis than with other drugs. The failure to produce significant results on various driving performance measurements when compared to alcohol may be explained by the more variable effects of cannabis on participants.
The results of the driving related laboratory tests conducted in general did not produce statistically significant results. Although reaction times were found to increase with dose level, there was too much variability in the data for statistical significance. This suggests that there may be an effect on the reaction time of participants responding to hazards, but it is quite a small effect which would require a much larger sample to determine whether or not it was statistically significant. This again confirms earlier observations of the effects of cannabis on the various aspects of driver performance; the effect on reaction time being somewhat difficult to predict.
The general medical examination and standardised impairment testing applied by the FMEs were judged to be effective in determining both impairment and establishing condition due to a drug. Preliminary conclusions were drawn by the FMEs on the number and combination of impairment test failures which would allow a conclusion that the driver was "impaired". Further refinement and calibration of these techniques in the field, for use by both police officers and FMEs, is however desirable and is planned.
Overall, it is possible to conclude that cannabis has a measurable effect on psychomotor performance, particularly tracking ability. Its effect on higher cognitive functions, for example divided attention tasks associated with driving, appear not to be as critical. Drivers under the influence of cannabis seem aware that they are impaired, and attempt to compensate by reducing the difficulty of the driving task, for example by driving more slowly.
In terms of road safety, it cannot be concluded that driving under the influence of cannabis is not a hazard, as the effects on various aspects of driver performance are unpredictable. However, in comparison with alcohol, the severe effects of alcohol on the higher cognitive processes of driving are likely to make this more of a hazard, particularly at higher blood alcohol levels.
A copy of the full TRL Report, TRL477 (price at publication £50), may be obtained from: TRL Publications Sales by telephone on 01344 770783 or by writing to: TRL Limited, Publication Sales, PO Box 303, Wokingham, Berkshire RG45 6YX.
Science News Online; Vol. 168, No. 16 -- 10-15-5 ~"Pot-Like Drug Multiplies Neurons In Brain Growth"
By Christen Brownlee
In the stoner stereotype, pot smokers and dying brain cells go hand in hand. However, new research suggests the situation may be more uplifting than that. A drug that functions as concentrated marijuana does may spur neurogenesis, the process by which the brain gives birth to new nerve cells. Previous research had suggested that neurogenesis happens only in select locations in the brain, such as the hippocampus, a region involved in learning and memory. Some studies have shown that this process is inhibited by most illicit drugs, such as cocaine, heroin, and methamphetamine. However, says Xia Zhang of the University of Saskatchewan in Saskatoon, marijuanas effect on neurogenesis has not been clear. He and his colleagues started investigating this mystery by searching cell surfaces in live, cultured slices of rat hippocampus for receptors that respond to marijuana and a few other similar drugs, called cannabinoids. They reasoned that if marijuana affected neurogenesis in the hippocampus, then cells in that area must have a way to recognize the drug. Sure enough, 95 percent of hippocampus cells responsible for neurogenesis showed evidence of cannabinoid 1 (CB1) receptors, one of two receptors that respond to cannabinoid drugs. Next, Zhangs team incubated samples of rat hippocampus with a solution containing HU210, a drug that stimulates CB1 receptors with a strength 100 times greater than that of pot. Other rat-hippocampus cells were incubated with the same solution minus the drug or with AM281, a drug that blocks CB1 receptors. After 2 days, the researchers found a significant increase in the number of new brain cells in the samples incubated with HU210, but no significant increase of such cells in the other samples. Finally, the researchers injected adult rats with various doses of HU210. A single high-dose injection seemed to make no significant difference in the number of new nerve cells. However, animals injected with high daily doses of the drug over the course of 2 weeks had about 30 percent more newborn nerve cells than did rats given AM281 or a solution without either drug. Animals given the 2-week course of HU210 also showed less anxiety and depressionlike behavior than did rats not given the drug. When the researchers irradiated the rats hippocampi with X rays, which kill off new neurons, animals given HU210 responded to these tests much as did animals that didnt receive the drug. These results suggest that, while these new neurons probably dont increase intelligence, they could be responsible for antianxiety and antidepressive effects, says Zhang. He and his team report their findings in the November Journal of Clinical Investigation. While data suggesting that cannabinoid drugs can accelerate neurogenesis are "interesting and potentially promising," its too early to tell whether high doses of marijuana over long periods have a similar effect on depression and anxiety in people, says Ron Duman, a neuroscientist at Yale University. "There is very little clinical evidence demonstrating that cannabinoid administration produces an antidepressant response," he says.
http://www.smh.com.au/text/articles/2004/08/04/1091557927241.html ~"Stressed IDF Soldiers To Be Treated With Pot"
( 8-5-4 )
(AFP) -- Israeli soldiers suffering from combat stress after tours of duty in the Palestinian territories could soon be treated with cannabis to relieve their symptoms, the Ma'ariv daily reported.
The mental health department of the Medical Corps is set to to begin tests in the next few days on volunteers suffering from post-traumatic stress disorder after reserve duty, the paper said. A scientist who will help conduct the experiment heads a research team, which discovered that cannabis helped mice that had suffered physical stress and even reduced the risk of stroke. Hundreds of Israelis have been treated for combat stress after performing their mandatory national service in the West Bank and Gaza Strip. There was no immediate comment on the report from the Israeli military.
Reuters (6 April 2005) ~
"Cannabis Compound Slows Artery Disease in Mice"by Patricia Reaney
LONDON (Reuters) - An active ingredient in cannabis can ease inflammation and slow the progression of coronary artery disease in mice, and possibly humans, researchers said on Wednesday.Daily low doses of the ingredient, THC, prevented atherosclerosis, a primary cause of heart disease and stroke in western countries, without producing the associated high.
"We have proven that very low doses of cannabis therapy will have an anti-inflammatory effect that will slow the progression of atherosclerosis in mice," said Dr Francois Mach, of Geneva University Hospital in Switzerland.
He and his team do not know whether TCH, or delta-9-tetrahydrocannabinol, will have the same effect in humans. But they believe the discovery will help find compounds that produce the same effect in humans without side effects such as raised blood pressure or euphoria.
"The goal now is to find new molecules, new compounds, that will act only on this anti-inflammatory effect," Mach told Reuters. Atherosclerosis is a common disorder of the arteries. Fatty materials build up and eventually block the arteries and interfere with blood flow.
THC and similar molecules are known as cannabinoids. Cannabis, which contains more than 60 different cannabinoids, and hashish have been used for centuries for medicinal purposes.
Mach and his team gave mice which were genetically engineered to be prone to atherosclerosis very low oral doses of THC with food each day. The dose was about 10 times less than that from smoking cannabis.
"It is the first study showing any beneficial effect of cannabis therapy on atherosclerosis," said Mach.
Cannabis creates a high when it binds to receptors called CB1 on the surface of cells in the brain. In the mouse study, another receptor, CB2, which is found on immune system cells and has nothing to do with euphoria, was affected. The dose given to the mice was too low to create a sense of euphoria.
Mice given THC had a slower progression of the disease than other mice not given the compound. The scientists are now studying whether THC can prevent the illness in the rodents.
"We are planning to look in more detail into how cannabis interferes with inflammation," said Mach. Continued ...