Cannabis research, medicine and use

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Cannabis research, medicine and use

Postby Penguin » Sun Apr 05, 2009 5:20 am

Okies here comes the first installment. Ill continue and improve this thread later, but Ill just ram the first ones in without organizing them too well.

Cannabis extract shrinks brain tumours
http://www.medicalnewstoday.com/articles/12088.php

Researchers in Spain have discovered that a cannabis extract makes brain tumors shrink by halting the growth of blood vessels that supply the tumors with life. Cannabis has chemicals called cannabinoids, these are the chemicals that could effectively starve tumors to death, say the researchers.

The study was carried out at the Complutense University, Madrid, Spain.

The team used mice to demonstrate that the cannabinoids block vessel growth.

You can read about this latest research in the journal Cancer Research.

Apparently, the procedure is also effective in humans.

The Spanish team, led by Dr Manuel Guzm�n, wanted to see whether they could prevent glioblastoma multiforme cancer from growing by cutting off its blood supply. Glioblastoma multiforme is one of the most difficult cancers to treat - it seldom responds to any medical intervention, such as radiotherapy, chemotherapy and surgery.

The scientists knew that cannabinoids will block the growth of blood vessels (to tumors) in mice - they wanted to find out whether the same thing would happen with humans.

The mice were given a cancer similar to the human brain cancer (glioblastoma multiforme). The mice were then given cannabinoids and the genes examined.

The genes associated with blood vessel growth in tumors through the production of a chemical called vascular endothelial growth factor (VEGF) had their activity reduced.

Cannabinoids halt VEGF production by producing Ceramide. Ceramide controls cell death.

Dr Guzm�n said: "As far as we know, this is the first report showing that ceramide depresses VEGF pathway by interfering with VEGF production."

They then wanted to see if this would also happen with humans.

They selected two patients who had glioblastoma multiforme and had not responded to chemotherapy, radiotherapy or surgery. The scientists took samples from them before and after treating them with a cannabinoids solution - this was administered directly into the tumor.

Amazingly, both patients experienced reduced VEGF levels in the tumor as a result of treatment with cannabinoids.

The researchers said that the results were encouraging. In order to be sure about their findings they need to carry out a larger study, they said.

Dr Guzm�n said "The present findings provide a novel pharmacological target for cannabinoid-based therapies."

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Cannabis receptor linked to colon cancer
http://www.medicinenet.com/script/main/ ... ekey=91511

Cannabis-Linked Cell Receptor Might Help Prevent Colon Cancer

FRIDAY, Aug. 1 (HealthDay News) — A cannabinoid receptor lying on the surface of cells may help suppress colorectal cancer, say U.S. researchers. When the receptor is turned off, tumor growth is switched on.

Cannabinoids are compounds related to the tetrahydrocannabinol (THC) found in the cannabis plant.

It's already known that the receptor, CB1, plays a role in relieving pain and nausea, elevating mood and stimulating appetite by serving as a docking station for the cannabinoid group of signaling molecules. This study suggests that CB1 may offer a new path for cancer prevention or treatment.

"We've found that CB1 expression is lost in most colorectal cancers, and when that happens, a cancer-promoting protein is free to inhibit cell death," senior author Dr. Raymond Dubois, provost and executive vice president of the University of Texas M.D. Anderson Cancer Center, said in a university news release.

In their study of human colorectal tumor specimens, the researchers also found that the drug decitabine can restore CB1 expression.

In addition, mice that are prone to developing intestinal tumors and also have functioning CB1 receptors developed fewer and smaller tumors when treated with a drug that mimics a cannabinoid receptor ligand, the researchers found. Ligands are molecules that function by binding to specific receptors.

"Potential application of cannabinoids as anti-tumor drugs is an exciting prospect, because cannabinoid agonists (synthetic molecules that mimic the action of natural molecules) are being evaluated now to treat the side effects of chemotherapy and radiation therapy," DuBois said. "Turning CB1 back on and than treating with a cannabinoid agonist could provide a new approach to colorectal cancer treatment or prevention."

The study was published in the Aug. 1 issue of the journal Cancer Research.
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Cannabis compound shows promise in fighting breast cancer
http://www.sciencedaily.com/releases/20 ... 211703.htm

A compound found in cannabis may prove to be effective at helping stop the spread of breast cancer cells throughout the body.

The study, by scientists at the California Pacific Medical Center Research Institute, is raising hope that CBD, a compound found in Cannabis sativa, could be the first non-toxic agent to show promise in treating metastatic forms of breast cancer.

“Right now we have a limited range of options in treating aggressive forms of cancer,” says Sean D. McAllister, Ph.D., a cancer researcher at CPMCRI and the lead author of the study. “Those treatments, such as chemotherapy, can be effective but they can also be extremely toxic and difficult for patients. This compound offers the hope of a non-toxic therapy that could achieve the same results without any of the painful side effects.”

The researchers used CBD to inhibit the activity of a gene called Id-1, which is believed to be responsible for the aggressive spread of cancer cells throughout the body, away from the original tumor site.

“We know that Id-1 is a key regulator of the spread of breast cancer,” says Pierre-Yves Desprez, Ph.D., a cancer researcher at CPMCRI and the senior author of the study. “We also know that Id-1 has also been found at higher levels in other forms of cancer. So what is exciting about this study is that if CBD can inhibit Id-1 in breast cancer cells, then it may also prove effective at stopping the spread of cancer cells in other forms of the disease, such as colon and brain or prostate cancer.”

However, the researchers point out that while their findings are promising they are not a recommendation for people with breast cancer to smoke marijuana. They say it is highly unlikely that effective concentrations of CBD could be reached by smoking cannabis. And while CBD is not psychoactive it is still considered a Schedule 1 drug.

This study was recently published in the journal Molecular Cancer Therapeutics.

The study was primarily funded by the California Breast Cancer Research Program.

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Cannabis compound slows lung cancer
http://www.scienceblog.com/cms/marijuan ... 18538.html

The active ingredient in marijuana cuts tumor growth in common lung cancer in half and significantly reduces the ability of the cancer to spread, say researchers at Harvard University who tested the chemical in both lab and mouse studies.

They say this is the first set of experiments to show that the compound, Delta-tetrahydrocannabinol (THC), inhibits EGF-induced growth and migration in epidermal growth factor receptor (EGFR) expressing non-small cell lung cancer cell lines. Lung cancers that over-express EGFR are usually highly aggressive and resistant to chemotherapy.

THC that targets cannabinoid receptors CB1 and CB2 is similar in function to endocannabinoids, which are cannabinoids that are naturally produced in the body and activate these receptors. The researchers suggest that THC or other designer agents that activate these receptors might be used in a targeted fashion to treat lung cancer.

"The beauty of this study is that we are showing that a substance of abuse, if used prudently, may offer a new road to therapy against lung cancer," said Anju Preet, Ph.D., a researcher in the Division of Experimental Medicine.

Acting through cannabinoid receptors CB1 and CB2, endocannabinoids (as well as THC) are thought to play a role in variety of biological functions, including pain and anxiety control, and inflammation. Although a medical derivative of THC, known as Marinol, has been approved for use as an appetite stimulant for cancer patients, and a small number of U.S. states allow use of medical marijuana to treat the same side effect, few studies have shown that THC might have anti-tumor activity, Preet says. The only clinical trial testing THC as a treatment against cancer growth was a recently completed British pilot study in human glioblastoma.

In the present study, the researchers first demonstrated that two different lung cancer cell lines as well as patient lung tumor samples express CB1 and CB2, and that non-toxic doses of THC inhibited growth and spread in the cell lines. "When the cells are pretreated with THC, they have less EGFR stimulated invasion as measured by various in-vitro assays," Preet said.

Then, for three weeks, researchers injected standard doses of THC into mice that had been implanted with human lung cancer cells, and found that tumors were reduced in size and weight by about 50 percent in treated animals compared to a control group. There was also about a 60 percent reduction in cancer lesions on the lungs in these mice as well as a significant reduction in protein markers associated with cancer progression, Preet says.

Although the researchers do not know why THC inhibits tumor growth, they say the substance could be activating molecules that arrest the cell cycle. They speculate that THC may also interfere with angiogenesis and vascularization, which promotes cancer growth.

Preet says much work is needed to clarify the pathway by which THC functions, and cautions that some animal studies have shown that THC can stimulate some cancers. "THC offers some promise, but we have a long way to go before we know what its potential is," she said.

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Marijuana Use and the Risk of Lung and Upper Aerodigestive Tract Cancers: Results of a Population-Based Case-Control Study
http://cebp.aacrjournals.org/cgi/conten ... type=HWCIT

Abstract:
Background: Despite several lines of evidence suggesting the biological plausibility of marijuana being carcinogenic, epidemiologic findings are inconsistent. We conducted a population-based case-control study of the association between marijuana use and the risk of lung and upper aerodigestive tract cancers in Los Angeles.

Methods: Our study included 1,212 incident cancer cases and 1,040 cancer-free controls matched to cases on age, gender, and neighborhood. Subjects were interviewed with a standardized questionnaire. The cumulative use of marijuana was expressed in joint-years, where 1 joint-year is equivalent to smoking one joint per day for 1 year.

Results: Although using marijuana for 30 joint-years was positively associated in the crude analyses with each cancer type (except pharyngeal cancer), no positive associations were observed when adjusting for several confounders including cigarette smoking. The adjusted odds ratio estimate (and 95% confidence limits) for 60 versus 0 joint-years was 1.1 (0.56, 2.1) for oral cancer, 0.84 (0.28, 2.5) for laryngeal cancer, and 0.62 (0.32, 1.2) for lung cancer; the adjusted odds ratio estimate for 30 versus 0 joint-years was 0.57 (0.20, 1.6) for pharyngeal cancer, and 0.53 (0.22, 1.3) for esophageal cancer. No association was consistently monotonic across exposure categories, and restriction to subjects who never smoked cigarettes yielded similar findings.

Conclusions: Our results may have been affected by selection bias or error in measuring lifetime exposure and confounder histories; but they suggest that the association of these cancers with marijuana, even long-term or heavy use, is not strong and may be below practically detectable limits. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1829–34)

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Cannabis May Help Combat Cancer-causing Herpes Viruses
http://www.sciencedaily.com/releases/20 ... 092627.htm

ScienceDaily (Sep. 24, 2004) — Tampa, FL (Sept. 22, 2004) -- The compound in marijuana that produces a high, delta-9 tetrahydrocannbinol or THC, may block the spread of several forms of cancer causing herpes viruses, University of South Florida College of Medicine scientists report.

The findings, published Sept. 15 in the online journal BMC Medicine, could lead to the creation of antiviral drugs based on nonpsychoactive derivatives of THC.

The gamma herpes viruses include Kaposi's Sarcoma Associated Herpes virus, which is associated with an increased risk of cancer that is particularly prevalent in AIDS sufferers. Another is Epstein-Barr virus, which predisposes infected individuals to cancers such as Burkitt's lymphoma and Hodgkin's disease.

Once a person is infected, these viruses can remain dormant for long periods within white blood cells before they burst out and begin replicating. This reactivation of the virus boosts the number of cells infected thereby increasing the chances that the cells will become cancerous.

The USF team, led by virologist Peter Medveczky, MD, found that this sudden reactivation was prevented if infected cells were grown in the presence of THC. While cells infected with a mouse gamma herpes virus normally died when the virus was reactivated, these same cells survived when cultured in the laboratory along with the cannabinoid compound – further evidence that THC prevents viral reactivation.

Furthermore, the researchers showed that THC acts specifically on gamma herpes viruses. The chemical had no effect on another related virus, herpes simplex-1, which causes cold sores and genital herpes.

Small concentrations of THC were more potent and selective against gamma herpes viruses than the commonly used antiviral drugs acyclovir, gancicyclovir and foscamet, said Dr. Medveczky, a professor in the Department of Medical Microbiology and Immunology.

The USF researchers suggest that THC selectively inhibits the spread of gamma herpes viruses by targeting a gene these viruses all share called ORF50.

Dr. Medveczky emphasized that more studies are needed. "We have not evaluated the effect of THC in an animal model yet so we do not recommend people start using pot to prevent or treat cancers."

In fact, Dr. Meveczky said, THC has also been shown to suppress the immune system so smoking marijuana could "do more harm than good" to patients whose immune systems are often already weakened.

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Cannabis Use, Effect And Potential Therapy For Alzheimer's, MS and Parkinson's
http://www.sciencedaily.com/releases/20 ... 163644.htm

Cannabis (marijuana) is the most widely produced plant-based illicit drug worldwide and the illegal drug most frequently used in Europe. Its use increased in almost all EU countries during the 1990s, in particular among young people, including school students. Cannabis use is highest among 15- to 24-year-olds, with lifetime prevalence ranging for most countries from 20--40% (EMCDDA 2006).

Recently there has been a new surge in the level of concern about potential social and health outcomes of cannabis use, although the available evidence still does not provide a clear-cut understanding of the issues. Intensive cannabis use is correlated with non-drug-specific mental problems, but the question of co-morbidity is intertwined with the questions of cause and effect (EMCDDA 2006). Prevention is of importance in adolescents, which is underlined by evidence that early-onset cannabis-users (pre- to mid-adolescence) have a significantly higher risk of developing drug problems, including dependence (Von Sydow et al., 2002; Chen et al., 2005).

The illegal status and wide-spread use of cannabis made basic and clinical cannabis research difficult in the past decades; on the other hand, it has stimulated efforts to identify the psychoactive constituents of cannabis. As a consequence, the endocannabinoid system was discovered, which was shown to be involved in most physiological systems -- the nervous, the cardiovascular, the reproductive, the immune system, to mention a few.

One of the main roles of endocannabinoids is neuroprotection, but over the last decade they have been found to affect a long list of processes, from anxiety, depression, cancer development, vasodilatation to bone formation and even pregnancy (Panikashvili et al., 2001; Pachter et al., 2006).

Cannabinoids and endocannabinoids are supposed to represent a medicinal treasure trove which waits to be discovered.

Raphael Mechoulam will tell the discovery story of the endocannabinoid system. His research has not only helped us to advance our understanding of cannabis use and its effects, but has also made key contributions with regard to understanding "neuroprotection," and has opened the door for the development of new drugs.

Endocannabinoid system

In the 1960s the constituent of the cannabis plant was discovered -- named tetrahydrocannabinol, or THC -- which causes the 'high' produced by it (Gaoni & Mechoulam, 1964). Thousands of publications have since appeared on THC. Today it is even used as a therapeutic drug against nausea and for enhancing appetite, and, surprisingly, has not become an illicit drug -- apparently cannabis users prefer the plant-based marijuana and hashish.

Two decades later it was found that THC binds to specific receptors in the brain and the periphery and this interaction initiates a cascade of biological processes leading to the well known marijuana effects. It was assumed that a cannabinoid receptor is not formed for the sake of a plant constituent (that by a strange quirk of nature binds to it), but for endogenous brain constituents and that these putative 'signaling' constituents together with the cannabinoid receptors are part of a new biochemical system in the human body, which may affect various physiological actions.

In trying to identify these unknown putative signaling molecules, our research group in the 1990s was successful in isolating 2 such endogenous 'cannabinoid' components -- one from the brain, named anandamide (from the word ´ananda, meaning ´supreme joy´ in Sanscrit), and another one from the intestines named 2-arachidonoyl glycerol (2-AG) (Devane et al., 1992; Mechoulam et al., 1995).

Neuroprotection

The major endocannabinoid (2-AG) has been identified both in the central nervous system and in the periphery. Stressful stimuli -- traumatic brain injury (TBI) for example -- enhance brain 2-AG levels in mice. 2-AG, both of endogenous and exogenous origin, has been shown to be neuroprotective in closed head injury, ischemia and excitotoxicity in mice. These effects may derive from the ability of cannabinoids to act through a variety of biochemical mechanisms. 2-AG also helps repair the blood brain barrier after TBI.

The endocannabinoids act via specific cannabinoid receptors, of which the CB1 receptors are most abundant in the central nervous system. Mice whose CB1 receptors are knocked out display slower functional recovery after TBI and do not respond to treatment with 2-AG. Over the last few years several groups have noted that CB2 receptors are also formed in the brain, particularly as a reaction to numerous neurological diseases, and are apparently activated by the endocannabinoids as a protective mechanism.

Through evolution the mammalian body has developed various systems to guard against damage that may be caused by external attacks. Thus, it has an immune system, whose main role is to protect against protein attacks (microbes, parasites for example) and to reduce the damage caused by them. Analogous biological protective systems have also been developed against non-protein attacks, although they are much less well known than the immune system. Over the last few years the research group of Esther Shohami in collaboration with our group showed that the endocannabinoid system, through various biological routes, lowers the damage caused by brain trauma. Thus, it helps to attenuate the brain edema and the neurological injuries caused by it (Panikashvili et al., 2001; Panikashvili et al., 2006).

Clinical importance

Furthermore it is assumed that the endocannabinoid system may be involved in the pathogenesis of hepatic encephalopathy, a neuropsychiatric syndrome induced by fulminant hepatic failure. Indeed in an animal model the brain levels of 2-AG were found to be elevated. Administration of 2-AG improved a neurological score, activity and cognitive function (Avraham et al., 2006). Activation of the CB2 receptor by a selective agonist also improved the neurological score. The authors concluded that the endocannabinoid system may play an important role in the pathogenesis of hepatic encephalopathy.

Modulation of this system either by exogenous agonists specific for the CB2 receptors or possibly also by antagonists to the CB1 receptors may have therapeutic potential. The endocannabinoid system generally is involved in the protective reaction of the mammalian body to a long list of neurological diseases such as multiple sclerosis, Alzheimer's and Parkinson's disease. Thus, there is hope for novel therapeutic opportunities.

Numerous additional endocannabinoids -- especially various fatty acid ethanolamides and glycerol esters -- are known today and regarded as members of a large ´endocannabinoid family´. Endogenous cannabinoids, the cannabinoid receptors and various enzymes that are involved in their syntheses and degradations comprise the endocannabinoid system.

The endocannabinoid system acts as a guardian against various attacks on the mammalian body.

Conclusion

The above described research concerning the endocannabinoid-system is of importance in both basic science and in therapeutics:
The discovery of the cannabis plant active constituent has helped advance our understanding of cannabis use and its effects.
The discovery of the endocannabinoids has been of central importance in establishing the existence of a new biochemical system and its physiological roles -- in particular in neuroprotection.
These discoveries have opened the door for the development of novel types of drugs, such as THC for the treatment of nausea and for enhancing appetite in cachectic patients.
The endocannabinoid system is involved in the protective reaction of the mammalian body to a long list of neurological diseases such as multiple sclerosis, Alzheimer's and Parkinson's disease which raises hope for novel therapeutic opportunities for these diseases.

References

Avraham Y, Israeli E, Gabbay E, et al. Endocannabinoids affect neurological and cognitive function in thioacetamide-induced hepatic encephalopathy in mice. Neurobiology of Disease 2006;21:237-245

Chen CY, O´Brien MS, Anthony JC. Who becomes cannabis dependent soon after onset of use" Epidemiological evidence from the United States: 2000-2001. Drug and alcohol dependence 2005;79:11-22

Devane WA, Hanus L, Breuer A, et al. Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 1992;258:1946-1949

[EMCDDA 2006] European Monitoring Centre for Drugs and Drug Addiction. The state of the drugs problem in Europe. Annual Report 2006 (http://www.emcdda.europa.eu)

Gaoni Y, Mechoulam R. Isolation, structure and partial synthesis of an active constituent of hashish. J Amer Chem Soc 1964;86:1646-1647

Journal Interview 85: Conversation with Raphael Mechoulam. Addiction 2007;102:887-893

Mechoulam R, Ben-Shabat S, Hanus L, et al. Identification of an endogenous 2-monoglyceride, present in canine gut, that binds to cannabinoid receptors. Biochem Pharmacol 1995;50:83-90

Mechoulam R, Panikashvili D, Shohami E. Cannabinoids and brain injury. Trends Mol Med 2002;8:58-61

Pachter P, Batkai S, Kunos G. The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacol Rev 2006;58:389-462

Panikashvili D, Simeonidou C, Ben-Shabat S, et al. An endogenous cannabinoid (2-AG) is neuroprotective after brain injury. Nature 2001;413:527-531

Panikashvili D, Shein NA, Mechoulam R, et al. The endocannabinoid 2-AG protects the blood brain barrier after closed head injury and inhibits mRNA expression of proinflammatory cytokines. Neurobiol Disease 2006;22:257-264

Von Sydow K, Lieb R, Pfister H, et al. What predicts incident use of cannabis and progression to abuse and dependence" A 4-year prospective examination of risk factors in a community sample of adolescents and young adults. Drug and alcohol dependence 2002;68:49-64

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http://www.guardian.co.uk/uk/2005/feb/2 ... on.science
Scientists at one of Spain's leading research centres claimed yesterday to have found evidence that cannabis helps prevent the memory loss experienced by people suffering from Alzheimer's.

The potential breakthrough in understanding a disease that affects nearly half a million people in Britain, and around nine million worldwide, was made by a team led by María de Ceballos at the Cajal Institute in Madrid.

Their study seems to show that THC, the main active ingredient in cannabis, inhibits the activity of cells that cause damage to neurons in the brain.

Although the study is preliminary, it was welcomed by patient groups.

"Right now, there are no good drugs for Alzheimer's. There are some that treat symptoms but nothing that halts the disease," said Susanne Sorensen, head of research at the Alzheimer's Society.

While the beneficial effects of cannabis looked promising, Dr Sorensen cautioned that people with Alzheimer's should not start using the drug to help their memories, because of side effects.

Memory loss in Alzheimer's patients is not fully understood, but part of the problem is thought to lie with cells called microglia that surround neurons in the brain. In Alzheimer's, the activity of microglia gets out of control, damaging neurons and killing off parts of the brain. Dr de Ceballos's team conducted two separate experiments using human brain tissue and rats which showed that THC inhibits the activity of microglia, thus reducing memory loss.


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A review of studies done on cannabidiole, CBD
http://blog.norml.org/tag/zuardi/

While the prohibition of cannabis is absurd, the ban on the plant’s non-psychoactive components is even more mind-boggling — particularly when it’s apparent that these compounds possess amazing therapeutic properties. Case in point: cannabidiol (CBD).

A just published scientific review by Sao Paulo University (Brazil) researcher Antonio Zuardi reports that there’s been an “explosive increase” of interest in CBD over the past five years. It’s apparent why.

“Studies have suggested a wide range of possible therapeutic effects of cannabidiol on several conditions, including Parkinson’s disease, Alzheimer’s disease, cerebral ischemia, diabetes, rheumatoid arthritis, other inflammatory diseases, nausea and cancer,” Zuardi writes. Let’s look at a few of these in detail, shall we?

1. Antiepileptic action
“In 1973, a Brazilian group reported that CBD was active in … blocking convulsions produced in experimental animals.”

2. Sedative action
“In humans with insomnia, high doses of CBD increased sleep duration compared to placebo.”

3. Anxiolytic action
“CBD induce[s] a clear anxiolytic effect and a pattern of cerebral activity compatible with an anxiolytic activity.”

4. Antipsychcotic action
“[C]linical studies suggest that CBD is an effective, safe and well-tolerated alternative treatment for schizophrenic patients.”

5. Antidystonic action
“CBD … had antidystonic effects in humans when administered along with standard medication to five patients with dystonia, in an open study.”

6. Antioxidative action
“[I]t was demonstrated that CBD can reduce hydroperoxide-induced oxidative damage as well as or better than other antioxidants. CBD was more protective against glutamate neurotoxicity than either ascorbate or a-tocopherol, indicating that this drug is a potent antioxidant.”

7. Neuroprotective action
“A marked reduction in the cell survival was observed following exposure of cultured rat pheochromocytoma PC12 cells to beta-A peptide. Treatment of the cells with CBD prior to beta-A exposure significantly elevated the cell survival.”

8. Antiinflammatory action
“CBD, administered i.p. or orally, has blocked the progression of arthritis.”

9. Cardioprotective action
“CBD induces a substantial cardioprotective effect.”

10. Action on diabetes
“CBD treatment of NOD (non-obese diabetic) mice before the development of the disease reduced its incidence from 86% in the non-treated control mice to 30% in CBD-treated mice. … It was also observed that administration of CBD to 11-14 week old female NOD mice, which were either in a latent diabetes stage or had initial symptoms of diabetes, ameliorated the manifestations of the disease.”

11. Antiemetic action
“The expression of this conditioned retching reaction was completely suppressed by CBD and delta9-THC, but not by ondansetron, [an] antagonist that interferes with acute vomiting.”

12. Anticancer action
“A study of the effect of different cannabinoids on eight tumor cell lines, in vitro, has clearly indicated that, of the five natural compounds tested, CBD was the most potent inhibitor of cancer cell growth.”

In sum, the past 45 years of scientific study on CBD has revealed the compound to be non-toxic, non-psychoactive, and to possess a multitude of therapeutic properties. Yet, to this day it remains illegal to possess or use (and nearly impossible to study in US clinical trials) simply because it is associated with marijuana.

What possible advancements in medical treatment may have been achieved over the past decades had US government officials chosen to advance — rather than inhibit — clinical research into CBD (which, under federal law, remains a Schedule I drug defined as having “no currently accepted medical use”)? Perhaps it’s time someone asks John Walters or the DEA?

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Cannabis and schizophrenia - is there a link?
Arch Gen Psychiatry. 2008 Nov;65(11):1269-74.

Familial predisposition for psychiatric disorder: comparison of subjects treated for cannabis-induced psychosis and schizophrenia.

Arendt M, Mortensen PB, Rosenberg R, Pedersen CB, Waltoft BL.

Centre for Psychiatric Research, Aarhus University Hospital, Skovagervej 2, Risskov, 8240 Risskov, Denmark. mca@psykiatri.aaa.dk

CONTEXT: Cannabis-induced psychosis is considered a distinct clinical entity in the existing psychiatric diagnostic systems. However, the validity of the diagnosis is uncertain. OBJECTIVES: To establish rate ratios of developing cannabis-induced psychosis associated with predisposition to psychosis and other psychiatric disorders in a first-degree relative and to compare them with the corresponding rate ratios for developing schizophrenia spectrum disorders. DESIGN: A population-based cohort was retrieved from the Danish Psychiatric Central Register and linked with the Danish Civil Registration System. History of treatment of psychiatric disorder in family members was used as an indicator of predisposition to psychiatric disorder. Rate ratios of cannabis-induced psychosis and schizophrenia associated with predisposition to psychiatric disorders were compared using competing risk analyses. SETTING: Nationwide population-based sample of all individuals born in Denmark between January 1,1955, and July 1, 1990 (N = 2,276,309). Patients During the 21.9 million person-years of follow-up between 1994 and 2005, 609 individuals received treatment of a cannabis-induced psychosis and 6476 received treatment of a schizophrenia spectrum disorder. RESULTS: In general, the rate ratios of developing cannabis-induced psychosis and schizophrenia spectrum disorder associated with predisposition to schizophrenia spectrum disorder, other psychoses, and other psychiatric disorders in first-degree relatives were of similar magnitude. However, children with a mother with schizophrenia were at a 5-fold increased risk of developing schizophrenia and a 2.5-fold increased risk of developing cannabis-induced psychosis. The risk of a schizophrenia spectrum disorder following a cannabis-induced psychosis and the timing of onset were unrelated to familial predisposition. CONCLUSIONS: Predisposition to both psychiatric disorders in general and psychotic disorders specifically contributes equally to the risk of later treatment because of schizophrenia and cannabis-induced psychoses. Cannabis-induced psychosis could be an early sign of schizophrenia rather than a distinct clinical entity.
PMID: 18981338 [PubMed - indexed for MEDLINE]

http://stash.norml.org/new-study-casts- ... zophrenia/


NEW YORK (Reuters Health) - People who have long-lasting psychotic episodes after smoking marijuana may be exhibiting early signs of schizophrenia, researchers reported Monday in the Archives of General Psychiatry.

“Cannabis-induced psychosis,” in which a person loses touch with reality and the symptoms persist for at least 48 hours, is an established psychiatric diagnosis, but it is controversial, Dr. Mikkel Arendt of Aarhus University in Risskov, Denmark, and colleagues note in their report.

In a previous study, Arendt and colleagues found that nearly half of people who had an episode of cannabis-induced psychosis went on to develop schizophrenia within the next six years. In the current study, the researchers looked at the genetic roots of both conditions by comparing the family histories of 609 people treated for cannabis-induced psychosis and 6,476 who had been treated for schizophrenia or a related psychiatric condition.

They found that individuals treated for post-pot smoking psychotic episodes had the same likelihood of having a mother, sister or other “first-degree” relative with schizophrenia as did the individuals who had actually been treated for schizophrenia themselves. This suggests that cannabis-induced psychosis and schizophrenia are one and the same, the researchers note. “These people would have developed schizophrenia whether or not they used cannabis,” Arendt explained in comments to Reuters Health.

Based on the findings, the researcher says, “cannabis-induced psychosis is probably not a valid diagnosis. It should be considered schizophrenia.”

Even as we’ve complained that no data show that cannabis use causes schizophrenia, we’ve been told that for those who are genetically predisposed to schizophrenia, there seems to be a correlation between cannabis use and onset of psychotic symptoms. So while it may not be psychologically dangerous for most of us, there is that 1% minority that would be harmed, so we have to ban it for everyone.

But this report counteracts even that claim. In the conclusion of the report, the study authors note, “The degree of hereditary predisposition in individuals who receive treatment of cannabis-induced psychosis closely mirrors that in those who develop schizophrenia with no history of cannabis induced psychosis.” This seems to tell us that when you take a look at a group of schizophrenics, whether they smoked pot of not, they still had the same genetic chances of becoming schizophrenics - the pot use didn’t matter!

Schizophrenia is rare and it comes on slowly for some. This “cannabis-induced psychosis” is really just people in the beginning stages of schizophrenia who happen to smoke pot, and the pot is getting blamed. It would be as valid to say the schizophrenic having an episode in a Krispy Kreme shop was suffering from “donut-induced psychosis”.
Last edited by Penguin on Sun Apr 05, 2009 5:29 am, edited 1 time in total.
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Cannabis and prion diseases (mad cow etc)

Postby Penguin » Sun Apr 05, 2009 5:22 am

http://www.jneurosci.org/cgi/content/ab ... 537?ck=nck

Neurobiology of Disease
Nonpsychoactive Cannabidiol Prevents Prion Accumulation and Protects Neurons against Prion Toxicity

Sevda Dirikoc,1 Suzette A. Priola,2 Mathieu Marella,3 Nicole Zsürger,1 and Joëlle Chabry1

1Institut de Pharmacologie Moléculaire et Cellulaire, Unité Mixte de Recherche 6097, Centre National de la Recherche Scientifique, 06560 Valbonne, France, 2Laboratory of Persistent Viral Diseases, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratories, Hamilton, Montana 59840, and 3Scripps Research Institute, La Jolla, California 92037

Correspondence should be addressed to Dr. Joëlle Chabry, Institut de Pharmacologie Moléculaire et Cellulaire, Unité Mixte de Recherche 6097, Université de Nice-Sophia Antipolis, Centre National de la Recherche Scientifique, 660, route des lucioles, 06560 Valbonne, France. Email: chabry@ipmc.cnrs.fr

Prion diseases are transmissible neurodegenerative disorders characterized by the accumulation in the CNS of the protease-resistant prion protein (PrPres), a structurally misfolded isoform of its physiological counterpart PrPsen. Both neuropathogenesis and prion infectivity are related to PrPres formation. Here, we report that the nonpsychoactive cannabis constituent cannabidiol (CBD) inhibited PrPres accumulation in both mouse and sheep scrapie-infected cells, whereas other structurally related cannabinoid analogs were either weak inhibitors or noninhibitory. Moreover, after intraperitoneal infection with murine scrapie, peripheral injection of CBD limited cerebral accumulation of PrPres and significantly increased the survival time of infected mice. Mechanistically, CBD did not appear to inhibit PrPres accumulation via direct interactions with PrP, destabilization of PrPres aggregates, or alteration of the expression level or subcellular localization of PrPsen. However, CBD did inhibit the neurotoxic effects of PrPres and affected PrPres-induced microglial cell migration in a concentration-dependent manner. Our results suggest that CBD may protect neurons against the multiple molecular and cellular factors involved in the different steps of the neurodegenerative process, which takes place during prion infection. When combined with its ability to target the brain and its lack of toxic side effects, CBD may represent a promising new anti-prion drug.


Key words: prion; cannabinoid; neuroprotection; scrapie-infected mice; cell-free conversion; microglia

Received Feb. 20, 2006; revised May 24, 2007; accepted June 13, 2007.


Correspondence should be addressed to Dr. Joëlle Chabry, Institut de Pharmacologie Moléculaire et Cellulaire, Unité Mixte de Recherche 6097, Université de Nice-Sophia Antipolis, Centre National de la Recherche Scientifique, 660, route des lucioles, 06560 Valbonne, France. Email: chabry@ipmc.cnrs.fr

--------------------

http://www.technologyreview.com/biotech/21366/

A New MRSA Defense

Marijuana extracts kill antibiotic-resistant MRSA without a high.

Substances harvested from cannabis plants could soon outshine conventional antibiotics in the escalating battle against drug-resistant bacteria. The compounds, called cannabinoids, appear to be unaffected by the mechanism that superbugs like MRSA use to evade existing antibiotics. Scientists from Italy and the United Kingdom, who published their research in the Journal of Natural Products last month, say that cannabis-based creams could also be developed to treat persistent skin infections.

Cannabis has long been known to have antibacterial properties and was studied in the 1950s as a treatment for tuberculosis and other diseases. But research into using cannabis as an antibiotic has been limited by poor knowledge of the plant's active ingredients and by the controversy surrounding its use as a recreational drug.

Now Giovanni Appendino of the Piemonte Orientale University, in Italy, and Simon Gibbons of the School of Pharmacy at the University of London, U.K., have revisited the antibiotic power of marijuana by systematically testing different cannabinoids' ability to kill MRSA.

MRSA, short for methicillin-resistant Staphylococcus aureus, is a bacterium that can cause difficult-to-treat infections since it does not respond to many antibiotics. Many healthy people carry S. aureus on their skin, but problems arise when multi-drug-resistant strains infect people with weak immune systems through an open wound. In the worst cases, the bug spreads throughout the body, causing a life-threatening infection.

To make matters worse, resistance to antibiotics is rapidly increasing, and some strains are now even immune to vancomycin, a powerful antibiotic that is normally used only as a last resort when other drugs fail.

But when Appendino, Gibbons, and their colleagues applied extracts from five major cannabinoids to bacterial cultures of six strains of MRSA, they discovered that the cannabinoids were as effective at killing the bugs as vancomycin and other antibiotics.

"The cannabinoids even showed exceptional activity against the MRSA strain that makes extra amounts of the proteins that give the bugs resistance against many antibiotics," says Gibbons. These proteins, he explains, allow the bacteria to "hoover up unwanted things from inside the cell and spit them out again."

Conveniently, of the five cannabinoids tested by the researchers, the two most effective ones also happen to be nonpsychoactive, meaning that they cannot cause a high. "What this means is, we could use fiber hemp plants that have no use as recreational drugs to cheaply and easily produce potent antibiotics," says Appendino.

In an attempt to discover how the cannabinoids kill MRSA, the team manipulated several chemical groups within the compounds. Most of the changes did not affect the antibiotic activity at all, and those that did seemed to influence only how well the cannabinoid is taken up by the bacterial cells.

"Everything points towards these compounds having been evolved by the plants as antimicrobial defenses that specifically target bacterial cells," says Gibbons. "But the actual mechanism by which they kill the bugs is still a mystery. We've tested whether the cannabinoids affect common antibiotic targets like fatty acid synthesis or the [DNA-bending enzyme] DNA gyrase, but they don't. I really cannot hazard a guess how they do it, but their high potency as antibiotics suggests there must be a very specific mechanism."

Appendino and Gibbons say that cannabinoids could quickly be developed as treatments for skin infections, provided the nonpsychoactive varieties are used. "The most practical application of cannabinoids would be as topical agents to treat ulcers and wounds in a hospital environment, decreasing the burden of antibiotics," says Appendino.

Whether the cannabinoids could also be delivered in the form of an injection or in pills is less clear, the pair says, because they may be inactivated by blood serum.

Frank Bowling of the University of Manchester, who has had success treating MRSA-infected wounds with maggots, says that "any alternative treatment that removes MRSA from the wound and prevents it from spreading into the body is fantastic and preferable to using antibiotics that have strong side effects and against which resistance is already developing." He cautions, however, that the researchers still need to show that the cannabinoids are safe to use.

This is not something that Appendino is too concerned about: "The topical use of cannabis preparations has a long tradition in European medicine, and no allergies have been reported."

Mark Rogerson of GW Pharmaceuticals, a U.K.-based company that develops cannabinoid-based drugs to treat severe pain caused by multiple sclerosis and cancer, says that the discovery that cannabinoids kill MRSA "really underlines the potentially great diversity of medical applications that cannabis-based medicine can have. You can almost think of the cannabis plant as a mini pharma industry in its own right." But Rogerson says that it is unlikely that existing cannabis-based medicines could be used to treat MRSA because the exact effect will depend on the correct combination and dosage of cannabinoids.

Meanwhile, Appendino and Gibbons hope that antibacterial effectiveness could also make cannabinoids suitable preservatives for cosmetics and toiletries. "The golden standards of preservatives are parabens and chlorinated phenols," says Appendino, but these compounds do not degrade well in the environment and are strongly suspected to be hormonal modifiers. He also argues that, since all major cannabinoids are similarly effective, complete purification of a single compound isn't necessary. So semipurified cannabinoid mixtures extracted from nonpsychoactive plants could make a cheap and easy alternative to conventional preservatives.

-----------------------

http://www.ncbi.nlm.nih.gov/pubmed/18681481

Antibacterial cannabinoids from Cannabis sativa: a structure-activity study.
Appendino G, Gibbons S, Giana A, Pagani A, Grassi G, Stavri M, Smith E, Rahman MM.

Dipartimento di Scienze Chimiche, Alimentari, Farmaceutiche e Farmacologiche, Università del Piemonte Orientale, 28100 Novara, Italy. appendino@pharm.unipmn.it

Marijuana (Cannabis sativa) has long been known to contain antibacterial cannabinoids, whose potential to address antibiotic resistance has not yet been investigated. All five major cannabinoids (cannabidiol (1b), cannabichromene (2), cannabigerol (3b), Delta (9)-tetrahydrocannabinol (4b), and cannabinol (5)) showed potent activity against a variety of methicillin-resistant Staphylococcus aureus (MRSA) strains of current clinical relevance. Activity was remarkably tolerant to the nature of the prenyl moiety, to its relative position compared to the n-pentyl moiety (abnormal cannabinoids), and to carboxylation of the resorcinyl moiety (pre-cannabinoids). Conversely, methylation and acetylation of the phenolic hydroxyls, esterification of the carboxylic group of pre-cannabinoids, and introduction of a second prenyl moiety were all detrimental for antibacterial activity. Taken together, these observations suggest that the prenyl moiety of cannabinoids serves mainly as a modulator of lipid affinity for the olivetol core, a per se poorly active antibacterial pharmacophore, while their high potency definitely suggests a specific, but yet elusive, mechanism of activity.

PMID: 18681481 [PubMed - indexed for MEDLINE]

-----------------------

Story of Ricky Simpson, Canadian man who cured himself of cancer using self-made high potency cannabis resin extract. Then gave this medicine to several other cancer, MS, pain and infection patients with good results.
He was convicted of drug trafficking and the court refused testimony from doctors whose patients Ricky had treated succesfully with cannabis extract.

He also shows how to make the extract yourself, and gives dosages he has used. Shows topical applications curing skin infections of MRSA. He has never charged money from anyone for the extract hes given.

http://www.youtube.com/watch?v=pjhT9282-Tw Part 1 of 7 on Youtube

http://www.phoenixtears.ca/ Simpsons own site, DVD quality version of the documentary available.

---------------------------

http://cannabis.net/oncology/anticancer.html

Cannabinoids: potential anticancer agents
by
Guzman M.
Department of Biochemistry and Molecular Biology I,
School of Biology, Complutense University,
28040 Madrid, Spain.
mgp@bbm1.ucm.es
Nat Rev Cancer. 2003 Oct;3(10):745-55

ABSTRACT
Cannabinoids - the active components of Cannabis sativa and their derivatives - exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite. In addition, these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually well tolerated, and do not produce the generalized toxic effects of conventional chemotherapies. So, could cannabinoids be used to develop new anticancer therapies?
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Postby Penguin » Sun Apr 05, 2009 5:27 am

Cannabis vaporization (ie. this device does not burn the herbs, only vaporizes in sub-pyrolizing temperatures) hence is the cleanest inhalation method available. For medical use this is a must. Added bonus is less wastage, as in burning stuff about 90% of it is incinerated into useless waste. Of course it will also work for any other inhalable substance that is normally smoked. I do not recommend industrial tobacco thou, its got too many nasty additives and you should remember that also 90% of tobaccos nicotine is normally destroyed by combustion, so overdosing on tobacco is a risk. Not recommended.

http://www.storz-bickel.com/

Volcano Vaporizer - Advanced Technology

The primary requirement of a vaporizer is the capacity to maintain the temperature just above the point of vaporization in order to obtain an optimum level of both efficiency and flavour, along with minimized production of harmful substances. Other important points are the greatest level of safety for the user, ease of operation and application which is separate from the vaporizing process.

The Volcano Vaporization System solves the problem of hot air generation by employing an astoundingly simple principle: the air is pumped through a heated aluminium block and thus inevitably assumes the desired temperature. A diaphragm pump ensures that the air flow remains constant, and volumetric flow fluctuations are thus ruled out. This means that the Volcano Vaporizers have the most accurate temperature control of all vaporizers.

However, the main distinguishing feature of the Volcano Vaporization System is the patented valve balloon into which the vapor generated is pumped. The valve balloon can be completely detached from the device after filling and the contents inhaled at the user's ease. This ensures that the application is absolutely safe, as vaporization occurs previously and the user does not come into contact with glass, heat or electricity during inhalation.


http://www.canorml.org/healthfacts/vaporizerstudy2.html

Cal NORML/MAPS Study Shows Vaporizer Can Drastically Reduce Toxins in Marijuana Smoke
(Click here for full report published in the Journal of Cannabis Therapeutics 4(1), 2004) . http://www.canorml.org/healthfacts/jcan ... rvapor.pdf

Harmful toxins in marijuana smoke can be effectively avoided by a vaporization device, according to a new study by California NORML and MAPS (Multidisciplinary Association for Psychedelic Studies) with support from a grant from the MPP (Marijuana Policy Project).

The study, conducted by Chemic Labs in Canton, Mass., tested vapors from cannabis heated in an herbal vaporizer known as the Volcano® ( manufactured by Storz & Bickel GmbH&Co. KG, Tuttlingen, Germany www.storz-bickel.com) and compared them to smoke produced by combusted marijuana. The Volcano® is designed to heat material to temperatures of 130° to 230° C (266° to 446° F) where medically active vapors are produced, but below the threshold of combustion where smoke is formed.

The vapors from the Volcano® were found to consist overwhelmingly of THC, the major active component in marijuana, whereas the combusted smoke contained over 100 other chemicals, including several polynuclear aromatic hydrocarbons (PAHs), carcinogenic toxins that are common in tobacco smoke. The respiratory hazards of marijuana and tobacco smoke are due to toxic byproducts of combustion, not the active ingredients in the plant, known as cannabinoids.

The study suggests that medical marijuana patients can avoid the respiratory hazards of smoking by using a vaporizer. In its 1999 report on medical marijuana, the Institute of Medicine recommended against long-term use of smoked marijuana because of the health risks of smoking. However, the IOM failed to take account of vaporizers.

Previous studies have found that vaporizers can reduce harmful toxins in cannabis smoke. However this is the first study to analyze the gas phase of the vapor for a wide range of toxins. A previous NORML/MAPS study conducted by Chemic Labs found that a vaporizer known as the M-1 Volatizer® (www.volatizer.com) completely eliminated three specific toxins (naphthalene, benzene and toluene) in. the solid phase of the vapor (D. Gieringer, "Cannabis Vaporization: A Promising Strategy for Smoke Harm Reduction," Journal of Cannabis Therapeutics Vol. 1#3-4: 153-70 (2001); www.canorml.org/healthfacts/vaporizerstudy1.html).

The new study used a gas chromatograph mass spectrometer (GCMS) to examine the gas components of the vapor. .The analysis showed that the Volcano® vapor was remarkably clean, consisting 95% of THC with traces of cannabinol (CBN), another cannabinoid. The remaining 5% consisted of small amounts of three other components: one suspected cannabinoid relative, one suspected PAH, and caryophyllene, a fragrant oil in cannabis and other plants. In contrast over 111 different components appeared in the gas of the combusted smoke, including a half dozen known PAHs. Non-cannabinoids accounted for as much as 88% of the total gas content of the smoke.

The study used standard NIDA cannabis with 4% THC content. A quantitative analysis found that the Volcano® delivered 46% of the THC into vapor following three 45-second exposures of the sample to the heat. This compares favorably with the typical efficiency of marijuana cigarettes as observed in other studies, which depending on conditions can fall below 25% due to loss of THC in sidestream smoke. An important feature of the Volcano® is that it uses a balloon to capture the vapor, thereby avoiding leakage to the air. It is possible that higher THC efficiencies could have been reached with the Volcano® by stirring the sample around and exposing it to more heat.

The combusted sample achieved a relatively high THC efficiency of 78% upon complete combustion. The high efficiency seems due to the fact that the sample was completely consumed by combustion, and that smoke leakage was effectively prevented by the laboratory setup. Similar conditions do not obtain under normal circumstances when a marijuana cigarette is smoked and much of the THC is lost to the air or left in the unburned "roach."

Two other cannabinoids , cannabidiol (CBD) and cannabinol (CBN), were detected in the NIDA cannabis in trace amounts of 0.1%. Both the Volcano® and combustion delivered an apparent increase in CBD and CBN, but the variance of the data was too high to reach statistically significant conclusions.

Sponsors believe that the study results lend support for wider use of vaporizers by medical marijuana patients and researchers. At present, the only FDA-approved method for administering marijuana to human research subjects is via smoking NIDA cigarettes. NORML and MAPS are supporting efforts to have vaporizers approved by the FDA. As a first step in this effort, Dr. Donald Abrams of the University of California, San Francisco, has submitted a grant proposal to the California Center for Medical Cannabis Research in San Diego to test the Volcano® in human subjects. If the protocol is funded and the Volcano® approved by the FDA for human research, it will be the first human study using a vaporizer. If the FDA requests additional laboratory data about the Volcano@, additional funding may be necessary.

For more information , see

www.maps.org/mmj/vaporizer.html

www.canorml.org/healthfacts/vaporizers.html

California NORML Release May, 2003
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Book: Advances in Hemp Research

Postby Penguin » Sun Apr 05, 2009 6:28 am

Recommended, try your university library, they may stock this...

http://www.amazon.com/Advances-Hemp-Res ... 1560228725

http://www.cababstractsplus.org/abstrac ... 9990706278

Title: Advances in hemp research.
Personal Authors:
Author Affiliation: Correspondence address: Istituto Sperimentale per le Colture Industriali, Via di Corticella 133, I-40129 Bologna, Italy.
Editors: Ranalli, P.
Document Title: Advances in hemp research.

Abstract:

This multiauthor book has eleven chapters, with the following titles: (1) Botany of the genus Cannabis; (2) The phytochemistry of Cannabis: its ecological and evolutionary implications; (3) Detecting and monitoring plant THC content: innovative and conventional methods; (4) Agronomical and physiological advances in hemp crops; (5) Crop physiology of Cannabis sativa L.: a simulation study of potential yield of hemp in Northwest Europe; (6) A survey of hemp diseases and pests; (7) Hemp germplasm resources; (8) Genetic improvement: conventional approaches; (9) Advances in biotechnological approaches for hemp breeding and industry; (10) Alkaline pulping of fibre hemp; (11) Hemp seed: a valuable food source.

Publisher: Food Products Press


A review of the book here: http://www.hemphasis.net/Books/books1.htm

This is the modern compilation for all your hemp questions, with the answers coming from years of hemp research done in Europe. If you don’t have a degree in agronomy or a heavy background in agriculture and terminology then this book may be a bit of a hard read, but it does cover all of the information that is needed to piece together the results of dozens of years of hemp farming in Europe.

Its contents include a detailed look at Cannabis genes, taxonoly and hemp breeding techniques, Biogenetic info, THC variations, crop rotation, methods of planting, seeding rates, growing conditions, nitrogen trials, study of the potential yield of hemp crops, a survey of the pest to hemp, plus genetic improvement, and advances in biotechnological approaches, pulping hemp fiber, and a look at hemp nutrition. Advances in Hemp Research is a valuable reference book for all hemp researchers. It’s like the official hemp science book. It is filled with great graphs and tables to help the readeer see the results. The info is based in Europe, which means that the information doesn’t directly correlate to American soil and conditions, but it gives us the best view of what to expect if we do ever get to grow hemp in America.

This is the book I was waiting for. I had trouble understanding all the technical issues, but I am better off for getting through it. It’s not reading for fun, but for knowledge. I used this book extensively in my hunt to find the facts!

Distributed by Haworth Press – 800 HAWORTH – getinfo@haworthpressinc.com


http://books.google.com/books?id=UEaTaD ... rch+review

Google books.
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Sativex entering market

Postby Penguin » Sun Apr 05, 2009 7:37 am

http://en.wikipedia.org/wiki/Sativex

Sativex is an oromucosal (mouth) spray developed by the UK company GW Pharmaceuticals for multiple sclerosis patients, who can use it to alleviate neuropathic pain and spasticity, also Sativex is being prescribed to alleviate pain due to cancer, research is being made on Sativex to cure cancer and other diseases that involve mutant cells. Sativex is distinct from all other pharmaceutically produced cannabinoids currently available because it is derived from botanical material, rather than a solely synthetic process. Sativex is a pharmaceutical product standardised in composition, formulation, and dose. Its principal active cannabinoid components are the cannabinoids: tetrahydrocannabinol (THC) and cannabidiol (CBD). The product is formulated as an oromucosal spray which is administered by spraying into the mouth. Each spray of Sativex delivers a fixed dose of 2.7mg THC and 2.5mg CBD.

Approved by Health Canada under a licence with conditions (NOC/c) for prescription use[1] in April 2005, Sativex is the world's first artificial pharmaceutical prescription medicine derived from the cannabis plant. The product is approved in Canada as adjunctive treatment for the symptomatic relief of neuropathic pain in multiple sclerosis,[1] and more recently for pain due to cancer.[1][2] It is available in the UK as an unlicensed medicine which enables UK doctors to prescribe the product to individual patients who they consider may benefit. It is also available in Catalonia, Spain, for 600 patients suffering from multiple sclerosis and a number of other conditions under a compassionate access programme (130 of the patients will be people with multiple sclerosis, a further 130 will be patients with neuropathic pain arising from a range of medical conditions, 40 will be suffering from anorexia and malnutrition caused by AIDS, and the remaining 300 will be cancer patients undergoing chemotherapy and suffering from nausea and vomiting).

In February 2007, GW and Otsuka Pharmaceutical announced an exclusive agreement for Otsuka to develop and market Sativex in the United States. Sativex has received permission from the US regulatory authority, the FDA, to enter directly into late stage Phase III trials in the US. The first large scale US trial in the US for cancer patients is expected to start in summer 2007. The 300-patient, double-blind, randomised, placebo-controlled study will evaluate the effect of Sativex in relieving average daily pain, reducing the use of breakthrough opioid medications, improving the quality of sleep and relevant aspects of quality of life among other outcome measures.

In December 2005, GW and the Spanish pharmaceutical company Almirall announced an exclusive agreement for Almirall to market Sativex in Europe (excluding the UK). In the UK and Canada, Bayer HealthCare have been appointed as exclusive distributors.

In clinical trials, Sativex has generally been well tolerated. Sativex is to be released for clinical trials in the U.S. in early 2008.[3][4][5]

Compare dronabinol (marketed as Marinol), a synthetic version of THC (that does not contain cannabidiol).

------------------------------

http://www.ft.com/cms/s/0/d90c5caa-0e5c ... ck_check=1

Shares in GW Pharmaceuticals jumped more than 40 per cent on Wednesday after positive trial results for Sativex, its cannabis-based medicine, which could pave the way for approval of the drug by UK and European regulators.

“This is the third study in the past six months that we have reported which have shown unequivocally positive results,” said Stephen Wright, director of research and development.

During the 16-week trial, each patient self-administered between eight and nine daily doses of Sativex, which is produced in an oral spray roughly the size of a lipstick. Sativex reduced spasticity by 48 per cent in patients.

“These are clear efficacy results,” said Paul Cuddon, a biotechnology analyst at KBC Peel Hunt.

“This is the sort of data that will convince patients and clinicians that Sativex is effective. The share price has quickly reacted to the good news, but with the results that have been achieved there could be more upside.”

GW said that it had amended the terms of its licensing deal with Almiral, which will market the drug in most of Europe if it is approved.


http://www.gwpharma.co.uk/sativex.asp
http://www.gwpharma.co.uk/sativex1.asp

http://www.hc-sc.gc.ca/dhp-mps/prodphar ... 89-eng.php
Approval of SATIVEX® with Conditions
Fact Sheet
What is SATIVEX®?

SATIVEX® is a cannabis based medicine containing Tetranabinex® and Nabidiolex® extracts of chemically and genetically characterised Cannabis sativa L. plants. The principal active components are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD).

Health Canada has approved SATIVEX® with conditions, under the Notice of Compliance with Conditions (NOC/c) policy. This authorisation reflects the promising nature of the clinical evidence which must be confirmed with further studies. Products approved under Health Canada's NOC/c policy, have demonstrated promising benefit, are of high quality and possess an acceptable safety profile based on a benefit/risk assessment for the approved use.


http://www.mssociety.org.uk/about_ms/tr ... tivex.html
How to get prescription in UK
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Postby Penguin » Sun Apr 05, 2009 7:48 am

http://www.qmul.ac.uk/news/newsrelease.php?news_id=175

Cannabis destroys cancer cells... reveals research at Barts and The London, Queen Mary's School of Medicine and Dentistry

01 March 2006

Researchers investigating the role of cannabis in cancer therapy reveal it has the potential to destroy leukaemia cells, in a paper published in the March 2006 edition of Letters in Drug Design & Discovery. Led by Dr Wai Man Liu, at Barts and the London, Queen Mary’s School of Medicine and Dentistry, the team has followed up on their findings of 2005 which showed that the main active ingredient in cannabis, tetrahydrocannabinol, or THC, has the potential to be used effectively against some forms of cancer. Dr Liu has since moved to the Institute of Cancer in Sutton where he continues his work into investigating the potential therapeutic benefit of new anti-cancer agents.

It has previously been acknowledged that cannabis-based medicines have merit in the treatment of cancer patients as a painkiller; appetite stimulant and in reducing nausea, but recently evidence has been growing of its potential as an anti-tumour agent. The widely reported psychoactive side effects and consequent legal status of cannabis have, however, complicated its use in this capacity. Although THC and its related compounds have been shown to attack cancer cells by interfering with important growth-processing pathways, it has not hitherto been established exactly how this is achieved.

Now Dr Liu and his colleagues, using highly sophisticated microarray technology – allowing them to simultaneously detect changes in more than 25,000 genes in cells treated with THC – have begun to uncover further the existence of crucial processes through which THC can kill cancer cells and potentially promote survival. Further, Dr Liu found that the mechanism of cannabis may be independent of the presence of receptors – proteins found on the surface of cells to which other signalling molecules bind. Binding of molecules to receptors elicits a response in the cell, be it growth or death. The finding that cannabis action may not require the presence of these receptors introduces the possibility that the drug may be used more widely as the cancer cell’s dependence on the cannabis receptor is removed.

Whilst leukaemia treatment is on the whole successful, some people cannot be treated with conventional therapy - 25 per cent of children with leukaemia fail to respond to traditional treatment leaving their prognosis outcome poor. Dr Liu’s research findings provide a crucial first step towards the development of new therapies that can eradicate a deadly disease which affects millions of children and adults worldwide.

Dr Liu said: “It is important to stress that these cannabis-like substances are far removed from the cannabis that is smoked. These novel compounds have been specifically designed to be free of the psychoactive features, whilst maintaining anti-cancer action. Ultimately, understanding the fundamental mechanisms of these compounds will provide us with insights into developing new drugs that can be used to effectively treat cancers.”
Ends-

For further information, please contact:

Alexandra Fernandes
Deputy Head of Communications
Queen Mary, University of London
Tel: +44 (0) 20 7882 7910
email: a.fernandes@qmul.ac.uk

http://bloodjournal.hematologylibrary.o ... 105/3/1214

Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway
Thomas Powles, Robert te Poele, Jonathan Shamash, Tracy Chaplin, David Propper, Simon Joel, Tim Oliver, and Wai Man Liu

From the New Drug Study Group, St Bartholomew's Hospital (SBH), London, United Kingdom; the Department of Medical Oncology, SBH, London, United Kingdom; the Centre for Cancer Therapeutics, Institute of Cancer Research, Surrey, United Kingdom; the Department of Medical Oncology, Charterhouse Square, London, United Kingdom; and the Barry Reed Oncology Laboratory, SBH, London, United Kingdom.


9-Tetrahydrocannabinol (THC) is the active metabolite of cannabis. THC causes cell death in vitro through the activation of complex signal transduction pathways. However, the role that the cannabinoid 1 and 2 receptors (CB1-R and CB2-R) play in this process is less clear. We therefore investigated the role of the CB-Rs in mediating apoptosis in 3 leukemic cell lines and performed microarray and immunoblot analyses to establish further the mechanism of cell death. We developed a novel flow cytometric technique of measuring the expression of functional receptors and used combinations of selective CB1-R and CB2-R antagonists and agonists to determine their individual roles in this process. We have shown that THC is a potent inducer of apoptosis, even at 1 x IC50 (inhibitory concentration 50%) concentrations and as early as 6 hours after exposure to the drug. These effects were seen in leukemic cell lines (CEM, HEL-92, and HL60) as well as in peripheral blood mononuclear cells. Additionally, THC did not appear to act synergistically with cytotoxic agents such as cisplatin. One of the most intriguing findings was that THC-induced cell death was preceded by significant changes in the expression of genes involved in the mitogen-activated protein kinase (MAPK) signal transduction pathways. Both apoptosis and gene expression changes were altered independent of p53 and the CB-Rs.
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Hempseed nutrition

Postby Penguin » Sun Apr 05, 2009 8:45 am

http://www.cababstractsplus.org/abstrac ... 0053039578

Title: Hempseed as a nutritional resource: an overview.
Personal Authors: Callaway, J. C.
Author Affiliation: Department of Pharmaceutical Chemistry, University of Kuopio, FIN-70211 Kuopio, Finland.
Editors: Mandolino, G., Ranalli, P.
Document Title: Euphytica

Abstract:

The seed of Cannabis sativa L. has been an important source of nutrition for thousands of years in Old World cultures. Non-drug varieties of Cannabis, commonly referred to as hemp, have not been studied extensively for their nutritional potential in recent years, nor has hempseed been utilized to any great extent by the industrial processes and food markets that have developed during the 20th century. Technically a nut, hempseed typically contains over 30% oil and about 25% protein, with considerable amounts of dietary fiber, vitamins and minerals. Hempseed oil is over 80% in polyunsaturated fatty acids (PUFAs), and is an exceptionally rich source of the two essential fatty acids (EFAs) linoleic acid (18:2 omega-6) and alpha-linolenic acid (18:3 omega-3). The omega-6 to omega-3 ratio (n6/n3) in hempseed oil is normally between 2:1 and 3:1, which is considered to be optimal for human health. In addition, the biological metabolites of the two EFAs, gamma-linolenic acid (18:3 omega-6; 'GLA') and stearidonic acid (18:4 omega-3; 'SDA'), are also present in hempseed oil. The two main proteins in hempseed are edestin and albumin. Both of these high-quality storage proteins are easily digested and contain nutritionally significant amounts of all essential amino acids. In addition, hempseed has exceptionally high levels of the amino acid arginine. Hempseed has been used to treat various disorders for thousands of years in traditional oriental medicine. Recent clinical trials have identified hempseed oil as a functional food, and animal feeding studies demonstrate the long-standing utility of hempseed as an important food resource.

Publisher: Kluwer Academic Publishers


http://www.hempfood.com/IHA/iha03208.html
Occurrence of "omega-3" stearidonic acid (cis-6,9,12,15-
octadecatetraenoic acid) in hemp (Cannabis sativa L.) seed

http://www.finola.com/HempseedNutrition.pdf
Hempseed as a nutritional resource: An overview, Callaway JC. Euphytica, 2004, volume 14, pages 65-72,

http://www.finola.com/FinolaOilandAtopy.pdf
"Efficacy of dietary hempseed oil in patients with atopic dermatitis", Callaway JC, Schwab U, Harvimaa I, Halonen P, Mykkänen O, Hyvönen P & Järvinen T. Journal of Dermatological Treatment. 2005, volume 16, pages 87-94,

Check out also the Finola homepage www.finola.com . Nutritional and farming information on the seed variety.

WE HAVE THE TOOLS, SO LET'S FEED THE WORLD (or at least the birds)!

Finola is another great weapon of mass production in the war on hunger, poverty and even ignorance. This plant is an excellent source of sustainable food, fiber and medicine. The exceptional fatty acid profile in Finola® oil offers a rich source of essential fatty acids (EFAs); polyunsaturated omega-3 and omega-6 fatty acids, including significant amounts of GLA and SDA. We can't make EFAs ourselves, so we have to get them from the daily diet. The EFAs are needed to produce many important things in our bodies, including optimal nerve functions throughout the brain and central nervous system. So at Finola, we're also fighting a guerrilla war on ignorance, at the neuronal level, one fatty acid at a time!


;)

http://www.ratical.org/renewables/hempseed1.html

Part One
by Lynn Osburn

Seeds of the plant cannabis sativa, hemp seed, contain all the essential amino acids and essential fatty acids necessary to maintain healthy human life. No other single plant source has the essential amino acids in such an easily digestible form, nor has the essential fatty acids in as perfect a ratio to meet human nutritional needs.

The importance of hemp seed nutrients to human health cannot be fully appreciated without some understanding of bio-chemistry in life. Unfortunately, any attempt to understand the flow of life leads into the realm of the most troublesome of the three infinities -- the infinitely complex.

Some deep thinkers believe life is a paradox not to be understood but experienced to the fullest. However, the Sages have said, "Know thyself." At any rate it is paradoxic to attempt simplifying the infinite complexity of flowing life. Yet, it is far better for the health and development of any thinking and feeling, uniquely individual human being, to pursue knowledge than to lounge in ignorance.

One out of two Americans win die from the effects of cardiovascular disease (CVD). One out of four Americans will die from cancer. Researchers believe cancers erupt when immune system response is weakened. Pioneers in the fields of biochemistry and human nutrition now believe CVD and most cancers are really diseases of fatty degeneration caused by the continued over-consumption of saturated fats and refined vegetable oils that turn essential fatty acids into carcinogenic killers. And if this is not scary enough, more Americans are succumbing to immune deficiency diseases than ever before. Sadly it is ignorance of human nutritional needs that will cause this overwhelming majority of Americans to die slowly from these afflictions -- the greatest killers in affluent nations.

HEMP SEED PROTEINS AND THE
BUILDING BLOCKS OF LIFE AND IMMUNITY

There are eight amino acids the human body cannot make and two more the body cannot make in sufficient quantity, so they are essential to life. A diet without any one of them will eventually cause disease and death. These essential amino acids, along with eleven others the body can make from them, are chained together in accordance to genetic guidelines, via RNA formats from DNA blueprints, into structural proteins that give body to life, and into enzymes (globular proteins) that carry out the mechanics of living.

Nearly three quarters of body solids are proteins. The body is literally constructed and maintained by an infinitely complex system that simply builds proteins from amino acid sub units. Every amino acid consists of an amine and a carboxyl bound to the same carbon atom. All but the smallest amino acid have one, more or less complex, carbon containing side chain connected to the carbon atom shared by the amine and carboxyl groups. The amine group, ND, is slightly basic; the carboxyl group, COOH, is a mild acid. The amine group of one amino acid unites with the carboxyl group of another forming a peptide link. Proteins are made of amino acid peptide chains in specific sequences. The number of possible amino acid peptide combinations is infinite.

Peptide chains can bend, twist and unite with other peptide chains by forming weak hydrogen bonds between nitrogen and oxygen atoms along the chain. Amino acids can also form bonds through side chain linkages. All three types of amino acid bonding methods contribute to the infinite possibility of protein shapes and reactivity potentials. Though each species builds proteins unique to itself, life can tailor new ones if challenged by the pressures of existence.

Hemp is not unique in having all the essential amino acids in its embryonic seed. Flax seeds also contain all the essential amino acids as do many other seeds in the plant kingdom. What is unique about hemp seed protein is that 65% of it is globulin edistin. That is the highest in the plant kingdom.

Globulins are one of seven classes of simple proteins. Simple proteins are constructed from amino acids and contain no non-protein substances. Globulins are in seeds and animal blood. Edistins are found in seeds; serum globulin is in blood. Edistins are plant globulins. And globulins along with albumins are classified as globular proteins. All enzymes, antibodies, many hormones, hemoglobin and fibrogin (the body converts fibrogin into non-soluble, fibrin, a blood clotting agent) are globular proteins. They carry out the main work of living.

Albumin, globulin and fibrogin are the three major types of plasma proteins. Plasma is the fluid portion of blood that supplies nutrients to tissues. And the three protein types: serum albumin, serum globulin and fibrogin, compose about 80% of plasma solids. These plasma proteins serve as a reservoir of rapidly available amino acids should any body tissues be in need.

Plant seeds contain albumin and globulin but no fibrogin. Albumin is the nutritive material that fills the space in the seed between the embryo and the seed coat. The embryo needs albumin to fuel its initial growth until photosynthesis begins. Globulin edistins within the embryo guarantee this new life has the enzymes necessary for metabolic activity.

Globulin is the third most abundant protein in the human body. Globulins perform many enzymatic (causing reactions to take place) functions within the plasma itself. More importantly, they are responsible for both the natural and acquired immunity a person has against invading organisms. The body uses globulin proteins to make antibodies which attack infecting agents (antigens) that invade the body. Globulins like gamma globulin are absolutely essential to maintain a healthy immune system. They neutralize alien microorganisms and toxins.

Globulins are divided into three classes: alpha, beta and gamma globulins. Alpha and beta globulins operate as transport vehicles by combining with other substances and carry protein from one part of the body to another. They haul the materials needed to build new and replace worn or damaged bodily structures. Gamma globulins are divided into five classes of antibodies called immunoglobulins. All are formed to combat specific cell invading antigens. They comprise the body's first line of defense against disease and infection. Immunoglobulins are produced by B lymphocyte (white blood cells) plasma cell clones located in lymph system nodes. Infecting antigens normally must pass through the lymph system before entering the blood stream.

Regarding human protein requirement: "Qualitively, it is considered desirable to secure amino acids similar to those of human tissues, both as to kinds and relative quantities of the various kinds." [Textbook of Anatomy and Physiology, Kimber, Gray, Stackpole, 1943]

During digestion proteins in food are broken down into amino acids. The amino acids are then taken into the body and reassembled into human proteins according to need and the availability of the amino acids necessary to make specific proteins.

The body needs the necessary kinds of amino acids in sufficient quantity in order to make proteins such as the globulins. Proper quantities of the right kinds may not be available to the body much of the time. So even though the body has enough essential amino acids available to prevent deficiency diseases, it may not have enough to build quantities of immunoglobulins necessary for the immune system to repel infection.

The best way to insure the body has enough amino acid material to make the globulins is to eat foods high in globulin proteins. Since hemp seed protein is 65% globulin edistin, and also includes quantities of albumin, its protein is readily available in a form quite similar to that found in blood plasma. Eating hemp seeds gives the body all the essential amino acids required to maintain health, and provides the necessary kinds and amounts of amino acids the body needs to make human serum albumin and serum globulins like the immune enhancing gamma globulins. Eating hemp seeds could aid, if not heal, people suffering from immune deficiency diseases. This conclusion is supported by the fact that hemp seed was used to treat nutritional deficiencies brought on by tuberculosis, a severe nutrition blocking disease that causes the body to waste away. [Czechoslovakia Tubercular Nutritional Study, 1955]

ANTIBODIES

Antibodies are globulin proteins programmed to destroy antigens (any substance eliciting a response from lymphocytes: bacteria, viruses, toxins, living and dead tissue, internal debris, etc.). Circulating in blood plasma like mines floating in a harbor antibodies await contact with the enemy, then initiate a cascade of corrosive enzymes that bore holes in the antigen surface causing it to break apart.

Antibodies are custom designed to neutralize or disintegrate one specific type of antigen. White blood cells called B cell lymphocytes seek out and lock-on to antigenic proteins or sugars on the invader's surface. The B cell then uses that lock and key pattern to make antibodies tailored to that antigen only. It also will make clones of itself called plasma cells. Most of the clones begin producing antibodies for that antigen. Others become memory cells which may spend years wandering through the blood stream looking for that specific antigen. If the body is exposed to it again the memory cells lock-on to one and begin producing plasma cell clones and a flood of antibodies that wipe out the invader. One lymphocyte can divide into hundreds of plasma cells in a few days. A mature plasma cell can make about 2000 antibodies every second for the few days it lives. This is how the body acquires immunity.

The body's ability to resist and recover from illness depends upon how rapidly it can produce massive amounts of antibodies to fend off the initial attack. If the globulin protein starting material is in short supply the army of antibodies may be too small to prevent the symptoms of sickness from setting in.

Hemp seed is the premier plant-seed provider of globulin starting material -- the highest in the plant kingdom. Eating hemp seeds will insure the immune system has the reservoir of immunoglobulin resources needed to make disease destroying antibodies.

Next issue: Part II, Hempseed Oils and the Flow of Life Force
here: http://www.ratical.org/renewables/hempseed2.html
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Postby Penguin » Mon Apr 13, 2009 1:59 am

edit - scrubbed the pic, was there for long enuff

(that was so filthy....)

:wink:
Last edited by Penguin on Sat Oct 31, 2009 4:28 am, edited 2 times in total.
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Postby OP ED » Tue Apr 14, 2009 2:47 am

i like filthy.
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Cannabis and cytokine system

Postby Penguin » Sat May 02, 2009 6:04 am

http://www.cannabis.net/cytokines/index.html

The cannabinoid system and cytokine network
by
Klein TW, Lane B, Newton CA, Friedman H
University of South Florida,
Tampa, Florida 33612, USA.
Proc Soc Exp Biol Med 2000 Oct;225(1):1-8

ABSTRACT
Many advances have been made in the last few years concerning our understanding of the receptors and ligands composing the cannabinoid system. Likewise, the science surrounding cytokine biology has advanced enabling us to measure these proteins more precisely as well as understand and interpret the meaning of changes in their levels. Scientists wishing to study the health consequences of smoking marijuana as well as understand the possible role of endogenous cannabimimetic ligands in immune regulation have continued to study the influence of these substances on the regulation and development of the cytokine network. Research has shown that two major cannabinoid receptor subtypes exist and that subtype 1 (CB1) is expressed primarily in the brain whereas subtype 2 (CB2) is expressed primarily in the periphery. A variety of ligands for these receptors based on the cannabinoid structure have been synthesized and studied as well as low affinity compounds, noncannabinoid ligands, and endogenous ligands derived from fatty acid eicosanoids. Highly selective receptor antagonists have also been introduced and studied. Synthetic, low affinity ligands such as (+)-HU-211 and DMH-11C have been shown to cause anti-inflammatory effects possibly through inhibiting the production and action of TNF-alpha and other acute phase cytokines. In addition, suppression of TNF and other cytokines such as GM-CSF, IL-6, IFNgamma, and IL-12 has also been seen following exposure to high affinity and psychoactive ligands such as marijuana and THC. However, some of these ligands have also been shown to increase rather than decrease interleukins such as IL-1, IL-4, IL-10, and IL-6, cytokines such as TNF-alpha, and chemokines such as IL-8, MIP-1, and RANTES. The endogenous ligand, anandamide, has been shown in culture to either suppress the proliferation response to prolactin or enhance the response to cytokines such as IL-3 and IL-6. This eicosanoid has also been shown to increase the production of interleukins and other cytokines. Cannabinoid receptors have been shown to be involved in some but not all of these effects. It is clear that psychoactive and nonpsychoactive compounds have demonstrated effects in vivo and in vitro on the production and function of a variety of cytokines. Depending upon the model system, these effects are often conflicting, and the involvement of cannabinoid receptors is unclear. However, enough evidence exists to suggest that the cannabinoid system significantly impacts the functioning of the cytokine network, and this association may provide clues to the mechanisms of certain immune diseases and form the basis for new immunotherapies.
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Postby OP ED » Sat May 02, 2009 3:02 pm

cannabimimetic


*adds to list of favorite words*
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Postby Penguin » Mon Jun 15, 2009 6:57 pm

http://www.reuters.com/article/rbssBiot ... 20?sp=true

UPDATE 3-GW Pharma files cannabis drug for MS in Europe

* Multiple sclerosis drug Sativex filed for European OK

* Firm posts maiden first-half profit of 4 mln pounds

* Plans to test new cannabinoid medicine for dyslipidaemia

* Shares up 8 percent


(Adds comments from R&D head, analyst, latest shares)

By Ben Deighton and Ben Hirschler

LONDON, May 20 (Reuters) - A pioneering cannabis-based medicine for multiple sclerosis from GW Pharmaceuticals (GWP.L) has been filed for approval in Europe, paving the way for its potential approval at the end of 2009 or early in 2010.

Following numerous delays, the submission to regulators in Britain and Spain is a landmark for the British drugmaker, which also announced on Wednesday it had made a maiden net profit of 4.0 million pounds ($6.2 million) in the six months to March 31 from a 4.2 million loss a year ago.

Shares in the company rose 7.6 percent to 85 pence by midday after touching a high of 89.5p.

Clinical trials have shown GW's drug Sativex, which is sprayed under the tongue, reduces spasticity in multiple sclerosis patients who do not respond adequately to existing therapies.

If it is approved, Sativex will be marketed in Britain by Germany's Bayer (BAYG.DE) and in the rest of Europe by Spain's Almirall (ALM.MC).

Following the filings in Britain and Spain, submissions for approval will made in other European countries during 2010.

Further clinical trials need to be completed before the medicine is ready for submission for approval in the United States, where GW's partner is Otsuka.

Sativex became the world's first cannabis medicine to win regulatory approval when it was approved in Canada in 2005.

The drug -- extracted from marijuana plants grown at secret locations in the English countryside -- has been hit by a string of delays in Europe, where GW originally hoped to win approval in 2003.

Despite past disappointments, analysts are hopeful that this time GW will win a green light.

"Since the pivotal trial was designed largely by the regulators we feel there is relatively low risk of a rejection," said KBC analyst Paul Cuddon.

The spray contains two active cannabinoids, CBD and THC. The latter substance is responsible for the euphoria associated with smoking cannabis.

GW also said it was planning a mid-stage Phase II clinical trial with a new cannabinoid medicine for the treatment of dyslipidaemia, or raised levels of fat in the blood, in type II diabetes patients.

Other potential use for cannabinoid medicines could include treatments for cancer and schizophrenia.

"We're looking at developing other products from the plant which are not psychoactive ... The plant has 60 or 70 of them, many of which have a very interesting pharmacology," R&D Director Stephen Wright told Reuters.

(Editing by John Stonestreet)


http://www.opposingviews.com/articles/r ... 1244508946

Marijuana Use Can Help Treat Drug Abuse

It is conventional wisdom that any substance use during drug treatment leads to lower rates of success. But a new study in the American Journal on Addictions suggests that’s not always so.

The study looked at patients in treatment for opiate dependence using a drug called naltrexone – a treatment whose effectiveness, the researchers write, “has been severely limited by poor adherence.” As part of a study designed to test two different support protocols intended to help patients stay on naltrexone treatment, researchers also looked at use of other substances by means of regular urine tests conducted during clinic visits.

Contrary to conventional wisdom, patients with “intermittent” marijuana use (defined as between 1% and 79% of urine tests coming back positive) stayed on treatment for nearly four times as long as those who abstained completely. Treatment adherence by “consistent” marijuana users (80% or more positive urine tests) was almost identical to that of the abstainers.

The researchers note that the beneficial effect was most apparent early in treatment, that marijuana use was not only associated with staying in treatment longer but also with more consistent pill-taking, and that during the study the patients tended to maintain or even increase their marijuana use. This, they write, is “consistent with a process of self-medication. These findings are of interest because they suggest the hypothesis that moderate cannabis use may be exerting a beneficial pharmacological effect improving the tolerability of naltrexone in the early weeks after induction.”


http://www.informaworld.com/smpp/conten ... a911211653

Intermittent Marijuana Use Is Associated with Improved Retention in Naltrexone Treatment for Opiate-Dependence
Authors: Wilfrid Noel Raby a; Kenneth M. Carpenter a; Jami Rothenberg a; Adam C. Brooks a; Huiping Jiang a; Maria Sullivan a; Adam Bisaga a; Sandra Comer a; Edward V. Nunes a Affiliation: a Division on Substance Abuse, Department of Psychiatry, Columbia University, New York State Psychiatric Institute, New York, New York

DOI: 10.1080/10550490902927785
Publication Frequency: 6 issues per year
Published in: American Journal on Addictions, Volume 18, Issue 4 July 2009 , pages 301 - 308
Subject: Addiction & Treatment;
Formats available: HTML (English) : PDF (English)


Abstract
Naltrexone is a theoretically promising alternative to agonist substitution treatment for opioid dependence, but its effectiveness has been severely limited by poor adherence. This study examined, in an independent sample, a previously observed association between moderate cannabis use and improved retention in naltrexone treatment. Opioid dependent patients (N = 63), admitted for inpatient detoxification and induction onto oral naltrexone, and randomized into a six-month trial of intensive behavioral therapy (Behavioral Naltrexone Therapy) versus a control behavioral therapy (Compliance Enhancement), were classified into three levels of cannabis use during treatment based on biweekly urine toxicology: abstinent (0% cannabis positive urine samples); intermittent use (1% to 79% cannabis positive samples); and consistent use (80% or greater cannabis positive samples). Intermittent cannabis users showed superior retention in naltrexone treatment (median days retained = 133; mean = 112.8, SE = 17.5), compared to abstinent (median = 35; mean = 47.3, SE = 9.2) or consistent users (median = 35; mean = 68.3, SE = 14.1) (log rank = 12.2, df = 2, p = .002). The effect remained significant in a Cox model after adjustment for baseline level of heroin use and during treatment level of cocaine use. Intermittent cannabis use was also associated with greater adherence to naltrexone pill-taking. Treatment interacted with cannabis use level, such that intensive behavioral therapy appeared to moderate the adverse prognosis in the consistent cannabis use group. The association between moderate cannabis use and improved retention on naltrexone treatment was replicated. Experimental studies are needed to directly test the hypothesis that cannabinoid agonists exert a beneficial pharmacological effect on naltrexone maintenance and to understand the mechanism.
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Postby Penguin » Mon Jun 15, 2009 7:06 pm

http://journals.lww.com/psychopharmacol ... ol.10.aspx

Synthetic [DELTA]-9-Tetrahydrocannabinol (Dronabinol) Can Improve the Symptoms of Schizophrenia
Schwarcz, Glenn MD; Karajgi, Basawaraj MD; McCarthy, Richard MD, PhD

Abstract

We are reporting improvement of symptoms of schizophrenia in a small group of patients who received the cannabinoid agonist dronabinol (synthetic Δ-9-tetrahydrocannabinol). Before this report, cannabinoids had usually been associated with worsening of psychotic symptoms. In a heuristic, compassionate use study, we found that 4 of 6 treatment-refractory patients with severe chronic schizophrenia but who had a self-reported history of improving with marijuana abuse improved with dronabinol. This improvement seems to have been a reduction of core psychotic symptoms in 3 of the 4 responders and not just nonspecific calming. There were no clinically significant adverse effects. These results complement the recent finding that the cannabinoid blocker rimonabant does not improve schizophrenic symptoms and suggest that the role of cannabinoids in psychosis may be more complex than previously thought. They open a possible new role for cannabinoids in the treatment of schizophrenia.
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Postby Penguin » Mon Jun 15, 2009 7:57 pm

http://norml.org/index.cfm?Group_ID=6812

Cannabis and the Brain: A User's Guide

by Paul Armentano


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

Cannabinoids & Neurogenesis

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

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

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

Cannabis & Neuroprotection

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

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

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

Cannabinoids & Glioma

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

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

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

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

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

Cannabinoids & Neurodegeneration

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

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

Cannabis & Cognition

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

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

Finally, a 2001 study published in the journal Archives of General Psychiatry found that long-term cannabis smokers who abstained from the drug for one week "showed virtually no significant differences from control subjects (those who had smoked marijuana less than 50 times in their lives) on a battery of 10 neuropsychological tests." Investigators further added, "Former heavy users, who had consumed little or no cannabis in the three months before testing, [also] showed no significant differences from control subjects on any of these tests on any of the testing days."

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


Some of the studies cited:

http://www.jci.org/articles/view/25509/version/1
Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects

Wen Jiang1,2, Yun Zhang1, Lan Xiao1, Jamie Van Cleemput1, Shao-Ping Ji1, Guang Bai3 and Xia Zhang1


http://jpet.aspetjournals.org/cgi/content/abstract/314/2/780?maxtoshow=&HITS=&hits=&RESULTFORMAT=&fulltext=cannabidiol%2Bantioxidants%2Bdiuretics%2Bneurotoxicity&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
Comparison of Cannabidiol, Antioxidants, and Diuretics in Reversing Binge Ethanol-Induced Neurotoxicity
Carol Hamelink1, Aidan Hampson1, David A. Wink, Lee E. Eiden, and Robert L. Eskay


http://stroke.ahajournals.org/cgi/content/abstract/36/5/1071
Cannabidiol Prevents Cerebral Infarction Via a Serotonergic 5-Hydroxytryptamine1A Receptor–Dependent Mechanism
Kenichi Mishima, PhD; Kazuhide Hayakawa; Kohji Abe, PhD; Tomoaki Ikeda, PhD, MD; Nobuaki Egashira, PhD; Katsunori Iwasaki, PhD Michihiro Fujiwara, PhD


http://www.ncbi.nlm.nih.gov/pubmed/12850548?dopt=Citation
Post-ischemic treatment with cannabidiol prevents electroencephalographic flattening, hyperlocomotion and neuronal injury in gerbils.

Braida D, Pegorini S, Arcidiacono MV, Consalez GG, Croci L, Sala M.


http://www.jneurosci.org/cgi/content/full/21/17/6475
Neuroprotection by 9-Tetrahydrocannabinol, the Main Active Compound in Marijuana, against Ouabain-Induced In Vivo Excitotoxicity
M. van der Stelt1, W. B. Veldhuis2, 3, P. R. Bär3, G. A. Veldink1, J. F. G. Vliegenthart1, and K. Nicolay2


http://www.pnas.org/content/95/14/8268.full

(FULL TEXT at link)

Cannabidiol and (−)Δ9-tetrahydrocannabinol are neuroprotective antioxidants
A. J. Hampson*,†, M. Grimaldi‡, J. Axelrod*, and D. Wink§

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Author Affiliations
*Laboratory of Cellular and Molecular Regulation, National Institutes of Mental Health, Bethesda, MD 20892; ‡Laboratory of Adaptive Systems, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892; and §Radiology and Biology Branch, National Cancer Institute, Bethesda, MD 20892

Contributed by Julius Axelrod

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Abstract

The neuroprotective actions of cannabidiol and other cannabinoids were examined in rat cortical neuron cultures exposed to toxic levels of the excitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both cannabidiol, a nonpsychoactive constituent of marijuana, and the psychotropic cannabinoid (−)Δ9-tetrahydrocannabinol (THC). Cannabinoids protected equally well against neurotoxicity mediated by N-methyl-d-aspartate receptors, 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid receptors, or kainate receptors. N-methyl-d-aspartate receptor-induced toxicity has been shown to be calcium dependent; this study demonstrates that 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid/kainate receptor-type neurotoxicity is also calcium-dependent, partly mediated by voltage sensitive calcium channels. The neuroprotection observed with cannabidiol and THC was unaffected by cannabinoid receptor antagonist, indicating it to be cannabinoid receptor independent. Previous studies have shown that glutamate toxicity may be prevented by antioxidants. Cannabidiol, THC and several synthetic cannabinoids all were demonstrated to be antioxidants by cyclic voltametry. Cannabidiol and THC also were shown to prevent hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures. Cannabidiol was more protective against glutamate neurotoxicity than either ascorbate or α-tocopherol, indicating it to be a potent antioxidant. These data also suggest that the naturally occurring, nonpsychotropic cannabinoid, cannabidiol, may be a potentially useful therapeutic agent for the treatment of oxidative neurological disorders such as cerebral ischemia.

Cannabinoid components of marijuana are known to exert behavioral and psychotropic effects but also to possess therapeutic properties including analgesia (1), ocular hypotension (2), and antiemesis (3). This report examines another potential therapeutic role for cannabinoids as neuroprotectants and describes their mechanism of action in rat cortical neuronal cultures.

During an ischemic episode, large quantities of the excitatory neurotransmitter glutamate are released. This event causes neuronal death by over-stimulating N-methyl-d-aspartate receptors (NMDAr) and 2-amino-3-(4-butyl-3-hydroxyisoxazol-5-yl)propionic acid (AMPA) and kainate-type receptors and results in metabolic stress and accumulation of toxic levels of intracellular calcium (4). In vitro and in vivo studies (4, 5, 6) have demonstrated that such neurotoxicity can be reduced by antioxidants or antagonists to NMDAr and AMPA/kainate receptors. Antioxidants such as α-tocopherol (5, 6) are effective neuroprotectants because of their ability to reduce the toxic reactive oxygen species (ROS) formed during ischemic metabolism. Cannabinoids like (−)Δ9-tetrahydrocannabinol (THC) and its psychoactive analogues also have been reported to be neuroprotective against glutamate toxicity in vitro (7). Cannabinoids have been suggested to prevent glutamate neurotoxicity by activating cannabinoid receptors (7, 8), which can reduce calcium influx through voltage sensitive calcium channels (8, 9). A synthetic cannabinoid (HU-211) also has been demonstrated to be neuroprotective even though it does not activate cannabinoid receptors. This compound is an atypical cannabinoid, however, in that it, unlike other cannabinoids, directly antagonizes NMDAr (10) and possesses some antioxidant properties (11). The present study examines classical cannabinoids as neuroprotectants in vitro but focuses on the nonpsychoactive cannabinoid cannabidiol. Like THC, cannabidiol is a natural component of the marijuana plant, Cannabis sativa, although unlike THC, cannabidiol does not activate cannabinoid receptors and so is devoid of psychoactive effects (12). This study reports that cannabidiol and other cannabinoids such as THC are potent antioxidants that protect neurons from glutamate-induced death without cannabinoid receptor activation.
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Postby beeline » Thu Jul 09, 2009 2:54 pm

http://www.philly.com/philly/wires/ap/news/nation_world/50211172.html
Posted on Wed, Jul. 8, 2009


Pro-marijuana ad pushes pot as Calif. budget fixMARCUS WOHLSEN

The Associated Press

SAN FRANCISCO - A pro-marijuana group is launching another television bid to legalize pot in California , this time with the pitch that legalizing and taxing the drug could help solve the state's massive budget deficit.

The 30-second spot, airing Wednesday and paid for by the Marijuana Policy Project, features a retired 58-year-old state worker who says state leaders "are ignoring millions of Californians who want to pay taxes."

"We're marijuana consumers," says Nadene Herndon of Fair Oaks, who says she began using marijuana after suffering multiple strokes three years ago. "Instead of being treated like criminals for using a substance safer than alcohol, we want to pay our fair share."

State lawmakers are bitterly debating how to close a $26.3 billion budget deficit that likely means cuts to state services.

In February, Assemblyman Tom Ammiano, D-San Francisco, introduced a bill to tax and regulate marijuana like alcohol. Bill supporters estimate the state's pot industry could bring in more than $1 billion in taxes.

The ad will air on several cable news channels and network broadcast affiliates in Los Angeles, Sacramento and the San Francisco Bay area, according to the Marijuana Policy Project.

The group said in a statement that three California stations , KABC-TV in Los Angeles, KGO-TV of San Francisco and KNTV-TV in San Jose , refused to air the ad.

Representatives from the three stations did not immediately return calls from The Associated Press seeking comment.

In an e-mail to the group, a KNTV account executive said the station's standards department had rejected the ad.

Marijuana Policy Project spokesman Bruce Mirken said the ad was meant to promote conversation about the issues, not to encourage pot use.

"It was consciously unsensational," Mirken said. "It's time to talk about this, and we feel very frustrated that some of these stations have taken it upon themselves to stifle the discussion."

In a phone interview, Herndon said that before filming the ad, she had not told very many people about her marijuana use. But she said her concern over the state's fiscal crisis and her support of medical marijuana led her to go public.

"I came out of the closet with this ad," she said.

Herndon said she worked as a policy analyst for several state social services departments during a 38-year career.

She said she was approached to star in the ad while her husband was taking classes at Oaksterdam University, an Oakland trade school that trains students to grow medical marijuana.

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