A very well built documentary about cannabis and drug prohibition by Producer Adam Scorgie a non-cannabis user. Does the drug prohibition work? Have a look and think for yourself.
see also an interview with Producer Adam Scorgie
Monday, August 31, 2009
SMOKING CANNABIS DOES NOT CAUSE LUNG CANCER
United States
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New Research Shows Here Seems to Be Something in Pot That Actually Undermines Cancer, Instead of Causing It. -- And the Media Are Doing Their Best to Ignore It.
One in three Americans will be afflicted with cancer, we are told by the government ( as if it's our immutable fate and somehow acceptable ). Cancer is the second-leading cause of death in the U.S. and lung cancer the leading killer among cancers.
You'd think it would have been very big news in June 2005 when UCLA medical school professor Donald Tashkin reported that components of marijuana smoke -- although they damage cells in respiratory tissue - -- somehow prevent them from becoming malignant. In other words, something in marijuana exerts an anti-cancer effect!
Tashkin has special credibility. He was the lead investigator on studies dating back to the 1970s that identified the components in marijuana smoke that are toxic. It was Tashkin et al. who published photomicrographs showing that marijuana smoke damages cells lining the upper airways. It was the Tashkin lab's finding that benzpyrene - -- a component of tobacco smoke that plays a role in most lung cancers -- is especially prevalent in marijuana smoke. It was Tashkin's data showing that marijuana smokers are more likely than non-smokers to cough, wheeze, and produce sputum.
Tashkin reviewed his findings in April 2008, at a conference organized by "Patients Out of Time," a reform group devoted to educating doctors and the public ( as opposed to lobbying politicians ). Some 30 MDs and nurses got continuing medical education credits for attending the event, which was held at Asilomar, on the Monterey Peninsula.
The National Institute on Drug Abuse, which supported Tashkin's marijuana-related research over the decades, readily gave him a grant in 2002 to conduct a large, population-based, case-controlled study that would prove definitively that heavy, long-term marijuana use increases the risk of lung and upper-airways cancers.
What Tashkin and his colleagues found, however, disproved their hypothesis. ( Tashkin is to marijuana as a cause of lung cancer what Hans Blix was to Iraq's weapons of mass destruction -- an honest investigator who set out to find something, concluded that it wasn't there, and reported his results. )
Tashkin's team interviewed 1,212 cancer patients from the Los Angeles County Cancer Surveillance program, matched for age, gender, and neighborhood with 1,040 cancer-free controls. Marijuana use was measured in "joint years" ( number of years smoked times number of joints per day ).
It turned out that increased marijuana use did not result in higher rates of lung and pharyngeal cancer, whereas tobacco smokers were at greater risk the more they smoked. Tobacco smokers who also smoked marijuana were at slightly lower risk of getting lung cancer than tobacco-only smokers.
These findings were not deemed worthy of publication in "NIDA Notes." Tashkin reported them at the 2005 meeting of the International Cannabinoid Research Society. They were published in the October 2006 issue of Cancer Epidemiology Biomarkers & Prevention.
Without a press release from NIDA calling attention to its significance, the assignment editors of America had no idea that "Marijuana Use and the Risk of Lung and Upper Aerodigestive Tract Cancers: Results of a Population-Based Case-Control Study" by Mia Hashibe1, Hal Morgenstern, Yan Cui, Donald P. Tashkin, Zuo-Feng Zhang, Wendy Cozen, Thomas M. Mack and Sander Greenland was a blockbuster story.
I suggested to Eric Bailey of the L.A. Times that he write up Tashkin's findings -- UCLA provided the local angle if the anti-cancer effect wasn't enough. Bailey said his editors wouldn't be interested for some time because he had just filed a marijuana-related piece. The Tashkin scoop is still there for the taking!
Tashkin Defends His Findings
Investigators from New Zealand recently got widespread media attention for a study contradicting Tashkin's results. "Heavy cannabis users may be at greater risk of chronic lung disease - -including cancer- compared to tobacco smokers," is how BBC News summed up the New Zealanders' findings.
The very small size of the study -79 smokers took part, 21 of whom smoked cannabis only- was not held against the authors. In fact, the small New Zealand study was given much more coverage by the corporate press than the large UCLA study that preceded it.
The New Zealand study was portrayed as the latest word on this important subject. As if scientific inquiry were some kind of tennis match and the truth just gets truthier with every volley.
Tashkin criticized the New Zealanders' methodology in his talk at Asilomar: "There's some cognitive dissonance associated with the interpretation of their findings. I think this has to do with the belief model among the investigators and -I wish they were here to defend themselves- the integrity of the investigators... They actually published another paper in which they mimicked the design that we used for looking at lung function."
Tashkin spoke from the stage of an airy redwood chapel designed by Julia Morgan. He is pink-cheeked, 70ish, wears wire-rimmed spectacles. "For tobacco they found what you'd expect: a higher risk for lung cancer and a clear dose-response relationship. A 24-fold increase in the people who smoked the most... What about marijuana? If they smoked a small or moderate amount there was no increased risk, in fact slightly less than one. But if they were in the upper third of the group, then their risk was six-fold... A rather surprising finding, and one has to be cautious about interpreting the results because of the very small number of cases -- fourteen-- and controls -- four."
Tashkin said the New Zealanders employed "statistical sleight of hand." He deemed it "completely implausible that smokers of only 365 joints of marijuana have a risk for developing lung cancer similar to that of smokers of 7,000 tobacco cigarettes... Their small sample size led to vastly inflated estimates... They had said 'it's ideal to do the study in New Zealand because we have a much higher prevalence of marijuana smoking.' But 88 percent of their controls had never smoked marijuana, whereas 36% of our controls ( in Los Angeles ) had never smoked marijuana. Why did so few of the controls smoke marijuana? Something fishy about that!"
Strong words for a UCLA School of Medicine professor!
As to the highly promising implication of his own study -that something in marijuana stops damaged cells from becoming malignant-- Tashkin noted that an anti-proliferative effect of THC has been observed in cell-culture systems and animal models of brain, breast, prostate, and lung cancer. THC has been shown to promote apoptosis ( damaged cells die instead of reproducing ) and to counter angiogenesis ( the process by which blood vessels are formed --a requirement of tumor growth ). Other antioxidants in cannabis may also be involved in countering malignancy, said Tashkin.
COPD
Much of Tashkin's talk was devoted to Chronic Obstructive Pulmonary Disease, another condition prevalent among tobacco smokers. Chronic bronchitis and emphysema are two forms of COPD, which is the fourth-leading cause of death in the United States. Air pollution and tobacco smoke are known culprits. Inhaled pathogens cause an inflammatory response, resulting in diminished lung function. COPD patients have increasing difficulty clearing the airways as they get older.
Tashkin and colleagues at UCLA conducted a major study in which they measured lung function of various cohorts over eight years and found that tobacco-only smokers had an accelerated rate of decline, but marijuana smokers -even if they smoked tobacco as well- experienced the same rate of decline as non-smokers.
"The more tobacco smoked, the greater the rate of decline," said Tashkin. "In contrast, no matter how much marijuana was smoked, the rate of decline was similar to normal."
Tashkin concluded that his and other studies "do not support the concept that regular smoking of marijuana leads to COPD."
Breathe easier, everybody.
[sidebar]
Editor's Note: There is a groundswell of attention in the news to marijuana's role in causing and preventing various types of cancers. Last week, AlterNet published an article from the Marijuana Policy Project about a new study finding that pot smokers have a lower risk of head and neck cancers than people who don't smoke pot. Earlier this year, the corporate media pounced on a study suggesting that men who had been using marijuana at least once per week and who had started smoking pot prior to age 18 had an elevated risk of testicular cancer known as nonseminoma, which makes up fewer than half of one percent of all cancer cases among men.
Head, neck and testicular cancers are of course quite serious ailments to deal with, but what about cancer of the most obvious organ at risk with pot smoking, the lungs? Where's the science on that? The article below by Fred Gardner, editor of the medical marijuana research quarterly journal O'Shaughnessy's, shares the results of a major medical study the media completely ignored, and his conclusions are quite blunt on the matter: Smoking pot doesn't cause lung cancer. In fact, the study found that cigarette smokers who also smoked marijuana were at a lower risk of contracting lung cancer than tobacco-only smokers.
Source: NORML- http://www.mapinc.org/norml/v09/n820/a09.htm
Sunday, August 30, 2009
Human Brains Make Their Own 'Marijuana'
U.S. and Brazilian scientists have discovered that the brain manufactures proteins that act like marijuana at specific receptors in the brain itself. This discovery may lead to new marijuana-like drugs for managing pain, stimulating appetite, and preventing marijuana abuse.
"Ideally, this development will lead to drugs that bind to and activate the THC receptor, but are devoid of the side effects that limit the usefulness of marijuana," said Lakshmi A. Devi of the Department of Pharmacology and Systems Therapeutics at Mount Sinai School of Medicine in New York and one of the senior researchers involved in the study. "It would be helpful to have a drug that activated or blocked the THC receptor, and our findings raise the possibility that this will lead to effective drugs with fewer side effects."
Scientists made their discovery by first extracting several small proteins, called peptides, from the brains of mice and determining their amino acid sequence. The extracted proteins were then compared with another peptide previously known to bind to, but not activate, the receptor (THC) affected by marijuana. Out of the extracted proteins, several not only bound to the brain's THC receptors, but activated them as well.
"The War on Drugs has hit very close to home," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Last year, scientists found that our skin makes its own marijuana-like substance. Now, we see that our brain has been making proteins that act directly on the marijuana receptors in our head. The next step is for scientists to come up with new medicines that eliminate the nasty side of pot—a better joint, so to speak."
--------------------------------------------------------------------------------
Journal reference:
1.Ivone Gomes, Julia S. Grushko, Urszula Golebiewska, Sascha Hoogendoorn, Achla Gupta, Andrea S. Heimann, Emer S. Ferro, Suzanne Scarlata, Lloyd D. Fricker, and Lakshmi A. Devi. Novel endogenous peptide agonists of cannabinoid receptors. FASEB J, DOI: 10.1096/fj.09-132142
Adapted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.
http://www.sciencedaily.com/releases/2009/04/090420151240.htm
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"Ideally, this development will lead to drugs that bind to and activate the THC receptor, but are devoid of the side effects that limit the usefulness of marijuana," said Lakshmi A. Devi of the Department of Pharmacology and Systems Therapeutics at Mount Sinai School of Medicine in New York and one of the senior researchers involved in the study. "It would be helpful to have a drug that activated or blocked the THC receptor, and our findings raise the possibility that this will lead to effective drugs with fewer side effects."
Scientists made their discovery by first extracting several small proteins, called peptides, from the brains of mice and determining their amino acid sequence. The extracted proteins were then compared with another peptide previously known to bind to, but not activate, the receptor (THC) affected by marijuana. Out of the extracted proteins, several not only bound to the brain's THC receptors, but activated them as well.
"The War on Drugs has hit very close to home," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Last year, scientists found that our skin makes its own marijuana-like substance. Now, we see that our brain has been making proteins that act directly on the marijuana receptors in our head. The next step is for scientists to come up with new medicines that eliminate the nasty side of pot—a better joint, so to speak."
--------------------------------------------------------------------------------
Journal reference:
1.Ivone Gomes, Julia S. Grushko, Urszula Golebiewska, Sascha Hoogendoorn, Achla Gupta, Andrea S. Heimann, Emer S. Ferro, Suzanne Scarlata, Lloyd D. Fricker, and Lakshmi A. Devi. Novel endogenous peptide agonists of cannabinoid receptors. FASEB J, DOI: 10.1096/fj.09-132142
Adapted from materials provided by Federation of American Societies for Experimental Biology, via EurekAlert!, a service of AAAS.
http://www.sciencedaily.com/releases/2009/04/090420151240.htm
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Marijuana-inspired Painkiller? New Chemical Pathway Discovered
Marijuana can be an effective painkiller, but social issues and unhealthy smoke inhalation complicate its use. As a result, researchers have focused great attention on understanding the biochemical system involved so they might manipulate it by other means. Toward that end, scientists have definitively identified a chemical pathway that, in mice, imitates marijuana's painkilling effect. The work could enable the development of new pain treatments.
Marijuana kills pain by activating a set of proteins known as cannabinoid receptors, which can also regulate appetite, inflammation, and memory. The body also has chemicals known as endocannabinoids that naturally activate these same receptors, namely N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).
These natural components of the cannabinoid system remain the focus of intense efforts to develop new treatments not only for chronic pain, but also for obesity, anxiety, and depression. However, until the new paper (citation below) specific methods to study 2-AG signaling have been lacking.
AEA's activity has been well understood for years. In past research, Cravatt and his team identified an enzyme called fatty acid amide hydrolase, or FAAH, that breaks down AEA, effectively reducing its pain killing activity. A number of compounds are now in clinical development that target and breakdown FAAH, allowing AEA to build up, reducing pain. However, FAAH does not control 2-AG metabolism in vivo, and therefore, the potential biological functions and therapeutic potential of this second endocannabinoid have remained largely unknown.
Teasing out 2-AG's specific impacts have proven challenging. Comparable to FAAH, an enzyme called monoacylglycerol lipase (MAGL) breaks down 2-AG. But, despite numerous attempts, no group had been able to develop a chemical that inhibits MAGL specifically.
"The tools—selective and efficacious MAGL inhibitors—just weren't there, " says Jonathan Long, a graduate student of the Scripps Research Kellogg School of Science and Technology who is a member of the Cravatt lab and a first author of the new paper.
But now, a MAGL-specific inhibitor is finally available, thanks to the lab's new work. Key to this success was Activity-Based Protein Profiling, a unique chemical technique the group devised and has used fruitfully in other inhibitor hunts. This system enables the rapid engineering and testing of chemical compounds against many members of enzyme families, in hope of finding effective and selective inhibitors.
For this project, the group developed about 200 compounds and found that one was a highly effective block for MAGL. The scientists dubbed the compound JZL184, named after Long's initials and the order in the series of potential inhibitors tested. JZL184 effectively blocks only MAGL among more than 40 related brain enzymes, which opened the door for the first definitive study of 2-AG's activity.
A New View of 2-AG
Unlike increased AEA, which causes only reduced pain sensation, the team found that MAGL inhibition using JZL184, and the resulting increase in 2-AG concentration, not only reduced pain in mice, but also induced other effects associated with the cannabinoid receptors, namely hypothermia and decreased movement.
"This really does suggest a sort of segregation of labor, if you will," says Cravatt of the differential effects of elevating AEA versus 2-AG as part of the overall function of the cannabinoid system. "That, I think, is a truly unique result."
While treatments based on inhibiting FAAH show great promise for controlling pain, manipulating MAGL levels could also be a boon for treatment development, especially if 2-AG's other effects, such as hypothermia, can be managed.
"There are so many different types of pain," Cravatt says, "that it's possible some types could be more effectively treated with one treatment than another."
This research was supported by the National Institutes of Health, the Helen L. Dorris Child and Adolescent Neuro-Psychiatric Disorder Institute, and the Skaggs Institute for Chemical Biology.
Journal reference:
1. Long et al. Selective blockade of 2-arachidonoylglycerol hydrolysis produces cannabinoid behavioral effects. Nature Chemical Biology, Online November 24, 2008; DOI: 10.1038/nchembio.129
Adapted from materials provided by Scripps Research Institute, via EurekAlert!, a service of AAAS.
Marijuana-inspired Painkiller? New Chemical Pathway Discovered
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Marijuana kills pain by activating a set of proteins known as cannabinoid receptors, which can also regulate appetite, inflammation, and memory. The body also has chemicals known as endocannabinoids that naturally activate these same receptors, namely N-arachidonoyl ethanolamine (AEA) and 2-arachidonoylglycerol (2-AG).
These natural components of the cannabinoid system remain the focus of intense efforts to develop new treatments not only for chronic pain, but also for obesity, anxiety, and depression. However, until the new paper (citation below) specific methods to study 2-AG signaling have been lacking.
AEA's activity has been well understood for years. In past research, Cravatt and his team identified an enzyme called fatty acid amide hydrolase, or FAAH, that breaks down AEA, effectively reducing its pain killing activity. A number of compounds are now in clinical development that target and breakdown FAAH, allowing AEA to build up, reducing pain. However, FAAH does not control 2-AG metabolism in vivo, and therefore, the potential biological functions and therapeutic potential of this second endocannabinoid have remained largely unknown.
Teasing out 2-AG's specific impacts have proven challenging. Comparable to FAAH, an enzyme called monoacylglycerol lipase (MAGL) breaks down 2-AG. But, despite numerous attempts, no group had been able to develop a chemical that inhibits MAGL specifically.
"The tools—selective and efficacious MAGL inhibitors—just weren't there, " says Jonathan Long, a graduate student of the Scripps Research Kellogg School of Science and Technology who is a member of the Cravatt lab and a first author of the new paper.
But now, a MAGL-specific inhibitor is finally available, thanks to the lab's new work. Key to this success was Activity-Based Protein Profiling, a unique chemical technique the group devised and has used fruitfully in other inhibitor hunts. This system enables the rapid engineering and testing of chemical compounds against many members of enzyme families, in hope of finding effective and selective inhibitors.
For this project, the group developed about 200 compounds and found that one was a highly effective block for MAGL. The scientists dubbed the compound JZL184, named after Long's initials and the order in the series of potential inhibitors tested. JZL184 effectively blocks only MAGL among more than 40 related brain enzymes, which opened the door for the first definitive study of 2-AG's activity.
A New View of 2-AG
Unlike increased AEA, which causes only reduced pain sensation, the team found that MAGL inhibition using JZL184, and the resulting increase in 2-AG concentration, not only reduced pain in mice, but also induced other effects associated with the cannabinoid receptors, namely hypothermia and decreased movement.
"This really does suggest a sort of segregation of labor, if you will," says Cravatt of the differential effects of elevating AEA versus 2-AG as part of the overall function of the cannabinoid system. "That, I think, is a truly unique result."
While treatments based on inhibiting FAAH show great promise for controlling pain, manipulating MAGL levels could also be a boon for treatment development, especially if 2-AG's other effects, such as hypothermia, can be managed.
"There are so many different types of pain," Cravatt says, "that it's possible some types could be more effectively treated with one treatment than another."
This research was supported by the National Institutes of Health, the Helen L. Dorris Child and Adolescent Neuro-Psychiatric Disorder Institute, and the Skaggs Institute for Chemical Biology.
Journal reference:
1. Long et al. Selective blockade of 2-arachidonoylglycerol hydrolysis produces cannabinoid behavioral effects. Nature Chemical Biology, Online November 24, 2008; DOI: 10.1038/nchembio.129
Adapted from materials provided by Scripps Research Institute, via EurekAlert!, a service of AAAS.
Marijuana-inspired Painkiller? New Chemical Pathway Discovered
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Saturday, August 29, 2009
Cannabinoids in bipolar affective disorder: a review and discussion of their therapeutic potential
Department of Psychiatry, University of Newcastle upon Tyne, Royal Victoria Infirmary, Newcastle upon Tyne, UK
Bipolar affective disorder is often poorly controlled by prescribed drugs. Cannabis use is common in patients with this disorder and anecdotal reports suggest that some patients take it to alleviate symptoms of both mania and depression. We undertook a literature review of cannabis use by patients with bipolar disorder and of the neuropharmacological properties of cannabinoids suggesting possible therapeutic effects in this condition. No systematic studies of cannabinoids in bipolar disorder were found to exist, although some patients claim that cannabisrelieves symptoms of mania and/or depression. The cannabinoids Dgr9-tetrahydrocannabinol (THC) and cannabidiol (CBD) may exert sedative, hypnotic, anxiolytic, antidepressant, antipsychotic and anticonvulsant effects. Pure synthetic cannabinoids, such as dronabinol and nabilone and specific plant extracts containing THC, CBD, or amixture of the two in known concentrations, are available and can be delivered sublingually. Controlled trials of these cannabinoids as adjunctive medication in bipolar disorder are now indicated.
C. H. Ashton, P. B. Moore, P. Gallagher, A. H. Young
http://www.uccs.edu/~rmelamed/Evolutionism/medical_uses_of_cannabinoid_2/mental_disorders/bipolar_disorder.html
doctorbob@cannabuzz.net
Bipolar affective disorder is often poorly controlled by prescribed drugs. Cannabis use is common in patients with this disorder and anecdotal reports suggest that some patients take it to alleviate symptoms of both mania and depression. We undertook a literature review of cannabis use by patients with bipolar disorder and of the neuropharmacological properties of cannabinoids suggesting possible therapeutic effects in this condition. No systematic studies of cannabinoids in bipolar disorder were found to exist, although some patients claim that cannabisrelieves symptoms of mania and/or depression. The cannabinoids Dgr9-tetrahydrocannabinol (THC) and cannabidiol (CBD) may exert sedative, hypnotic, anxiolytic, antidepressant, antipsychotic and anticonvulsant effects. Pure synthetic cannabinoids, such as dronabinol and nabilone and specific plant extracts containing THC, CBD, or amixture of the two in known concentrations, are available and can be delivered sublingually. Controlled trials of these cannabinoids as adjunctive medication in bipolar disorder are now indicated.
C. H. Ashton, P. B. Moore, P. Gallagher, A. H. Young
http://www.uccs.edu/~rmelamed/Evolutionism/medical_uses_of_cannabinoid_2/mental_disorders/bipolar_disorder.html
doctorbob@cannabuzz.net
Friday, August 28, 2009
Schizophrenia link to cannabis denied
A STUDY by North Staffordshire academics has rejected a link between smoking cannabis and an increase in mental illness.
The research found there were no rises in cases of schizophrenia or psychoses diagnosed in the UK over nine years, during which the use of the drug had grown substantially.
Pro-cannabis campaigners seized on the results as supporting the legalising of cannabis, and claimed the report had been suppressed.
But the leading expert behind the study said it could be too low-key to re-ignite the debate on whether restrictions should be removed from soft drugs.
From their base at the Harplands Psychiatric Hospital in Hartshill, the four experts reviewed the notes of hundreds of thousands of patients at 183 GP practices throughout the country to look for any changing rate in cases of schizophrenia.
The work had been set up to see if earlier forecasts from other experts had been borne out, that the mental disorder would soar through the growing popularity of cannabis.
Published in the Schizophrenia Research journal, a paper on the study said: "A recent review concluded that cannabis use increases the risk of psychotic outcomes.
"Furthermore an accepted model of the association between cannabis and schizophrenia indicated its incidence would increase from 1990 onwards.
"We examined trends in the annual psychosis incidence and prevalence as measured by diagnosed cases from 1996 to 2005 and found it to be either stable or declining.
"The casual models linking cannabis with schizophrenia and other psychoses are therefore not supported by our study."
The research was conducted by Drs Martin Frisher and Orsolina Martino, from the department of medicines management at Keele University; psychiatrist Professor Ilana Crome, from the Harplands academic unit, who specialises in addiction; and diseases expert Professor Peter Croft, pictured below, from the university's primary care research centre.
Its findings come shortly after the Government reclassified cannabis from Class C to Class B, which invokes heavier penalties.
Yet Dr Frisher revealed last night that the study had been partly commissioned by the Government's advisory committee on the misuse of drugs.
He said: "We concentrated on looking into the incidence of schizophrenia during those years and not specifically at cannabis use.
"It was relatively low-key research so I don't believe it will re-ignite the debate on whether the drug should be legalised."
Hartshill-based Dilys Wood, national co-ordinator of the Legalise Cannabis Alliance, said that so far the report had been published in medical journals and would have a far-reaching reaction if it surfaced more widely.
She added: "I believe that if it had found a causal link between cannabis and schizophrenia it would have been all over the press.
"The public needs to know the truth about drugs; not more Government-led propaganda."
And Alliance press officer Don Barnard said: "It is hard to believe the then Home Secretary Jacqui Smith did not know of this very important research when deciding to upgrade cannabis to Class B."
The team said a number of alternative explanations for the stabilising of schizophrenia had been considered and while they could not be wholly discounted, they did not appear to be plausible.
www.thisisstaffordshire.co.uk/news/
Thursday, August 27, 2009, 09:20
The research found there were no rises in cases of schizophrenia or psychoses diagnosed in the UK over nine years, during which the use of the drug had grown substantially.
Pro-cannabis campaigners seized on the results as supporting the legalising of cannabis, and claimed the report had been suppressed.
But the leading expert behind the study said it could be too low-key to re-ignite the debate on whether restrictions should be removed from soft drugs.
From their base at the Harplands Psychiatric Hospital in Hartshill, the four experts reviewed the notes of hundreds of thousands of patients at 183 GP practices throughout the country to look for any changing rate in cases of schizophrenia.
The work had been set up to see if earlier forecasts from other experts had been borne out, that the mental disorder would soar through the growing popularity of cannabis.
Published in the Schizophrenia Research journal, a paper on the study said: "A recent review concluded that cannabis use increases the risk of psychotic outcomes.
"Furthermore an accepted model of the association between cannabis and schizophrenia indicated its incidence would increase from 1990 onwards.
"We examined trends in the annual psychosis incidence and prevalence as measured by diagnosed cases from 1996 to 2005 and found it to be either stable or declining.
"The casual models linking cannabis with schizophrenia and other psychoses are therefore not supported by our study."
The research was conducted by Drs Martin Frisher and Orsolina Martino, from the department of medicines management at Keele University; psychiatrist Professor Ilana Crome, from the Harplands academic unit, who specialises in addiction; and diseases expert Professor Peter Croft, pictured below, from the university's primary care research centre.
Its findings come shortly after the Government reclassified cannabis from Class C to Class B, which invokes heavier penalties.
Yet Dr Frisher revealed last night that the study had been partly commissioned by the Government's advisory committee on the misuse of drugs.
He said: "We concentrated on looking into the incidence of schizophrenia during those years and not specifically at cannabis use.
"It was relatively low-key research so I don't believe it will re-ignite the debate on whether the drug should be legalised."
Hartshill-based Dilys Wood, national co-ordinator of the Legalise Cannabis Alliance, said that so far the report had been published in medical journals and would have a far-reaching reaction if it surfaced more widely.
She added: "I believe that if it had found a causal link between cannabis and schizophrenia it would have been all over the press.
"The public needs to know the truth about drugs; not more Government-led propaganda."
And Alliance press officer Don Barnard said: "It is hard to believe the then Home Secretary Jacqui Smith did not know of this very important research when deciding to upgrade cannabis to Class B."
The team said a number of alternative explanations for the stabilising of schizophrenia had been considered and while they could not be wholly discounted, they did not appear to be plausible.
www.thisisstaffordshire.co.uk/news/
Thursday, August 27, 2009, 09:20
BIG JOINT to blow in on NCPIC Powerhouse Conference.
To confirm the arrangements which will govern the protest activity planned by your organisation (Nimbin Hemp Embassy) to take place on Monday and Tuesday, 7th and 8th of September 2009 in the Sydney CBD
Timings: Assemble 8am outside the Power House Museum, Harris Street, Ultimo and hold a rally in relation to raising issues concerning the regulating of cannabis for medical use. Pamphlets to be handed out. Disperse by 6pm each day.
Agreed Conditions:
It is anticipated the number of participants will not exceed 50 persons at each assembly point.
from within that number the organisation “Nimbin Hemp Embassy ” are to nominate marshalls to guide and maintain a level of control over the gathering
all marshalls are to be readily identifiable to police
all participants are to obey the lawful directions of police
The assembly are not to encroach upon the roadway.
participants are not to block footpaths, stairs or entry or exit points so as to obstruct the free movement of other pedestrians or traffic.
participants are not to block the entrance to any building at any time
participants are not to engage in criminal or anti social behaviour
reasonable use of a small, portable public address system is permitted
reasonable use of hand held megaphones by marshalls is also permitted
use of an inflatable `Big Joint’ is permitted, however, must not block pedestrian traffic or encroach on the roadway.
The assembly will disperse by 6.00pm.
Small banners are to be used only and are not to contain offensive language or obscene slogans or pictures during the event/rally.
The NSW Police Force considers the burning of any article, flag or effigy a public safety hazard. The Police Force reserves the right to take any such action/s as may be necessary to ensure the safety of participants. The general public and police officers, should such activity occur.
The event/rally organiser is to ensure that no damage is occasioned to public or private property. Should such damage occur, the organizer to the best of his/her ability is to assist police in identifying those responsible for such damage.
The organiser is to assist Police identify any persons responsible for commission of any offence.
Notification of the protest activity to the Power House Museum must be completed prior to the activity by contacting them by phone or email.
The Duty Officer for that date, working from City Central Police station will contact you a short time prior to the protest activity commencing.
----------
Reprinted information from NSW Police in the interest of public safety. Nimbin HEMP Embassy.
hempembassy.net
NimbinMardiGrass.com
BIGJOINT.org
Thursday, August 27, 2009
Please don’t smoke the walls
It is absolutely amazing the diversity of materials we are using these days as building materials for our homes and business. As we move further into a world looking for sustainability and ways not to damage the environment around us the ideas are coming hot and heavy about even newer materials. Considering that in the US buildings account for thirty-eight percent of the CO2 emissions the demand for carbon neutral and/or zero footprint building the demand for building materials to meet these needs will only increase.
One new (to the United States) material that is getting a lot of attention is from a UK-based business, Lhoist Group, and their Tradical® Hemcrete® concrete substitute. This a product made from mixing hemp, lime and water and is 7x as strong as normal concrete as well as being carbon negative.
source: http://current.com/1hgam4c
Wednesday, August 26, 2009
The International Cannabinoid Research Society
The ICRS is a non-political and non-religious organization dedicated to scientific research in all fields of the cannabinoids, ranging from biochemical, chemical and physiological studies of the endogenous cannabinoid system to studies of the abuse potential of recreational cannabis. In addition to acting as a source for impartial information on cannabis and the cannabinoids, the main role of the ICRS is to provide an open forum for researchers to meet and discuss their results.
The ICRS is a scientific association with over 400 members, all active researchers in the field of endogenous, plant-derived and synthetic cannabinoids and related bioactive lipids.
Mission Statement:
ICRS History:
http://www.cannabinoidsociety.org/
The ICRS is a scientific association with over 400 members, all active researchers in the field of endogenous, plant-derived and synthetic cannabinoids and related bioactive lipids.
Mission Statement:
The mission of the ICRS is to: foster cannabinoid research, to promote exchange of information and ideas about cannabis and the cannabinoids through the organization of scientific meetings; to encourage financial support from funding agencies and industries; to facilitate liasons between funding agencies, industry and the academic community, and to serve as a source of reliable information on the chemistry, pharmacology, toxicology and the behavioral, psychological and social effects of cannabis and the cannabinoids (ICRS By-Laws, adopted June 1992).
ICRS History:
The ICRS was formally incorporated as a scientific research society in 1991. Prior to that, Symposia were organized by various researchers in the field since 1970. Membership in the Society has risen from about 50 members, in its first year, to 458 in 2008.
http://www.cannabinoidsociety.org/
Dr Bob Melamede
Dr Robert Melamede is paving the way in cannabis research and cannabis medicines
http://www.uccs.edu/~rmelamed/
"Throughout my life I have been fascinated and amazed by life, always wondering what it is and how it works. Modern molecular biology and far from equilibrium thermodynamics have provided me with answers that I find very satisfying. Simply and simplistically put, it is natural for the flow of energy and matter to act "creatively". This fact of physics serves as the central theme for all courses that I teach. It provides a scientific basis for understanding life and death, health and disease. I hope you will enjoy and benefit from this approach."Read more from Dr Melamede
http://www.uccs.edu/~rmelamed/
Cannabis and ADD / ADHD
What is ADD / ADHD?
Individuals with ADHD essentially have problems with self-regulation and self-motivation, predominantly due to problems with distractibility, procrastination, organization, and prioritization. It is a chronic condition, beginning in early childhood and persisting throughout a person’s lifetime. It is estimated that up to 70% of children with ADHD will continue to have significant ADHD-related symptoms persisting into adulthood, resulting in a significant impact on education, employment, interpersonal relationships, and in social settings.
In layman’s terms, ADHD is a condition in which the brain can not efficiently “ignore” unimporant stimuli. Essentially, a person not suffering from ADHD will have an easier time remaining focused on a specific project and ignore distractions while an ADHD brain is more prone to distraction due to its inability to ignore stimuli.
Current research has shown that certain strains of marijuana can provide focus to people with ADHD and many people have successfully used marijuana as a replacement to other medications (such as Ritalin or Methylphenidate).
Marijuana Facts and Resources:
- The potential role of phytotherapy for ADHD – Phytotherapy Review & Commentary
Very lengthy and heavily cited article discussing the use of plants to treat ADHD. - References on Cannabinoids Science and ADHD
Large list of references and studies showing the interaction of cannabinoids, cannabinoid receptors in the brain, and their relationship with ADHD. - How Cannabinoids Improve ADHD?
List of symptoms of ADHD which can be treated or improved with the use of marijuana. Includes citations and studies. - Videos on Marijuana and ADHD
Nice compiled list of videos ranging from doctors and experts to technical explanations of the inner-workings of ADHD and the relationship to cannabinoid receptors. - Marijuana and ADD Therapeutic uses of Medical Marijuana in the treatment of ADD
Well-cited research paper supporting the use of medical marijuana to treat ADD. - Cannabis ‘Scrips to Calm Kids?
Article from FOX News examining the success of marijuana as an ADHD medication rather than the use of synthetic drugs which come with their own risks. - Cannabis effective in animal model of hyperactivity disorder
Short snippet of research about the use of marijuana and hyperactive rats. - THC normalized impaired psychomotor performance and mood
Article discussing research that showed marijuana–specifically THC–improved the driving ability of persons with ADHD. Another source locate here. - Moderate cannabis use has a positive effect on treatment for cocaine dependence in patients with comorbid ADHD and cocaine dependence
Article discussing research showing improved results for cocaine dependent ADHD patients using marijuana. It is worth noting that Ritalin is very similar to cocaine. - Cannabis improves symptoms of ADHD
Case report showing how cannabis can improve the symptoms of ADHD patients. Link to original PDF here.
Anecdotal:
- ADHD by Ryan P
A very detailed account of how marijuana helped one ADHD man. - Testimonies from Doctors and Patients
A large list of testimonies from patients as well as physicians in support of the use of marijuana for ADHD. - Recipe For Trouble
48 Hours Special on a mother who prefers to treat her ADHD child with marijuana rather than synthetic drugs. - Posts from users at Marijuana.com regarding ADD/ADHD:
-ADHD Medicine
-ADHD and Medical Marijuana
-ADHD Strains
-My Life with ADD/ADHD – Success Story
-Marijuana and ADHD – Success Story
Will Kevin Rudd seriously consider Cannabis Reform
Lobbyists to ambush Rudd with giant joint
August 23, 2009 07:24pm
IF Prime Minister Kevin Rudd can't stop giggling, feels paranoid or overly hungry when he visits Lismore hospital, he'll know exactly what's to blame.
It could be the subliminal influence of a 10-metre inflatable joint, which drug legalisation lobbyists will use to try to get the prime minister's attention during his visit tomorrow.
Members of the Nimbin Hemp Embassy will gather outside the hospital with their trusty mascot, hoping to talk to Mr Rudd about what they say is a health issue - legalising cannabis in Australia.
The group's president Michael Balderstone says he hopes to appeal to Mr Rudd's Christian sense of compassion.
"I think he is a compassionate man and he is a Christian and what would Jesus say – we're talking about the best pain-relieving herbs on the planet," he said.
Mr Balderstone said young people in Nimbin are constantly targeted in police raids and suffer permanent consequences. Nimbin has become a centre for alternative culture after a new generation of people decided to settle there following the Aquarius Festival in 1973.
"I live and work in Nimbin and we've become this big backpacker place and ... (police) are busting a lot of young people," he said.
"And it's making no difference and they're just all getting criminal records for life.
"Politicians are quite sheltered in a way and what's going on out here in the street is a huge culture of people who have lost respect for the system, because these laws have criminalised them and made something that makes them feel good into an illicit act."
Mr Rudd has previously said he has never smoked marijuana and takes a tough line on drugs.
Mainstream Media Finally Does Its Job (Sort Of)
Well, that only took a month.
Earlier today Reuters News Wire finally took the time to report that lifetime marijuana use is associated with a reduced risk of head and neck cancer. That’s according to the findings of a population-based case control study of some 1,000 subjects, published in the journal Cancer Prevention Research.
But you already know this because NORML initially posted the news in July.
To review, here is what the study found:
Authors reported, “After adjusting for potential confounders (including smoking and alcohol drinking), 10 to 20 years of marijuana use was associated with a significantly reduced risk of head and neck squamous cell carcinoma … [as was] moderate weekly use.”
Subjects who smoked marijuana and consumed alcohol and tobacco (two known high risk factors for head and neck cancers) also experienced a reduced risk of cancer, the study found.
“This association was consistent across different measures of marijuana use (marijuana use status, duration, and frequency of use). … Further, we observed that marijuana use modified the interaction between alcohol and cigarette smoking, resulting in a decreased HNSCC risk among moderate smokers and light drinkers, and attenuated risk among the heaviest smokers and drinkers.“
Notably, Reuters‘ writers took a much more skeptical view of the study’s findings, as evident by the headline:
Could smoking pot cut risk of head, neck cancer?
via Reuters Health
Strange that Reuters would frame their headline in the form of a question. After all, the study’s authors expressed no such reservations, concluding in the final line of their abstract, “Our study suggests that moderate marijuana use is associated with reduced risk of HNSCC (head and neck cancer).”
Reuters skepticism continues:
It’s unclear why marijuana would prevent cancer, if in fact the study is borne out by others, but the authors note that chemicals in pot called cannabinoids have been shown to have potential antitumor effects. Other studies have linked marijuana use to a reduced risk of some cancers, such as cancer of the prostate, and now head and neck cancer.
… Overall, however, research on the effects of marijuana on human health is mixed. Some studies have suggested the drug can increase a person’s risk of heart attack or stroke and cause some cancers such as lung cancer.
Let’s take things one at a time, shall we. First, it’s hardly ‘unclear’ as to why marijuana would be cancer-preventive. To quote the scientific journal Nature Reviews Cancer from 2003:
Cannabinoids: potential anticancer agents
via Nature Reviews CancerCannabinoids inhibit tumor growth in laboratory animals. They do so by modulating key cell-signaling pathways, thereby inducing direct growth arrest and death of tumor cells, as well as by inhibiting tumor angiogenesis and metastasis. Cannabinoids are selective anti-tumor compounds, as they can kill tumor cells without affecting their non-transformed counterparts.
Reuters unnamed author(s) further add the caveat: “if in fact the study is borne out by others.” News flash: this study was performed precisely because pot’s cancer preventive effects had been “borne out in others,” such as this:
Study finds no cancer-marijuana connection
via The Washington PostThe largest study of its kind has unexpectedly concluded that smoking marijuana, even regularly and heavily, does not lead to lung cancer. … “We hypothesized that there would be a positive association between marijuana use and lung cancer, and that the association would be more positive with heavier use,” he said. “What we found instead was no association at all, and even a suggestion of some protective effect.”
Reuters further states: “Other studies have linked marijuana use to a reduced risk of some cancers, such as cancer of the prostate, and now head and neck cancer.” Notably, the wire service failed to include that cannabinoids also have documented anti-cancer fighting abilities in the treatment of: brain cancer, breast cancer, lung cancer, skin cancer, and pancreatic cancer — just to name a few.
And finally, Reuters obligatorily adds that pot’s effects on health are ‘mixed,’ alleging that “some studies have suggested the drug can increase a person’s risk of heart attack or stroke and cause some cancers such as lung cancer.” Ah yes, the ever elusive “some studies.”
Well, as for cannabis smoking and lung cancer, that claim was rebutted by the largest study of its kind, profiled above. As for the alleged risk of “heart attack or stroke,” a large-scale population study by Kaiser Permanente reported “no association of marijuana use with cardiovascular disease hospitalization or mortality.”
That said, I’m all for the media espousing skepticism regarding claims about cannabis. Of course, were the MSM to apply this same attitude to the federal government’s claims about marijuana and pot prohibition, we wouldn’t have to suffer through stories like these, now would we?
Mainstream Media Finally Does Its Job (Sort Of) — It Only Took Four Weeks!
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