December 3, 2009 – Marijuana is a complex substance containing over 60 different forms of cannabinoids, the active ingredients. Cannabinoids are now known to have the capacity for neuromodulation, via direct receptor-based mechanisms at numerous levels within the nervous system. These have therapeutic properties that may be applicable to the treatment of neurological disorders; including anti-oxidative, neuroprotective, analgesic and anti-inflammatory actions; immunomodulation, modulation of glial cells and tumor growth regulation. This article reviews the emerging research on the physiological mechanisms of endogenous and exogenous cannabinoids in the context of neurological disease.

Introduction
Over the past few decades, there has been widening interest in the viable medicinal uses of cannabis. The National Institutes of Health, the Institute of Medicine, and the Food and Drug Administration have all issued statements calling for further investigation. The discovery of an endogenous cannabinoid system with specific receptors and ligands has led the progression of our understanding of the actions of cannabis from folklore to valid science. It now appears that the cannabinoid system evolved with our species and is intricately involved in normal human physiology, specifically in the control of movement, pain, memory and appetite, among others. The detection of widespread cannabinoid receptors in the brain and peripheral tissues suggests that the cannabinoid system represents a previously unrecognized ubiquitous network in the nervous system. Dense receptor concentrations have been found in the cerebellum, basal ganglia and hippocampus, accounting for the effects on motor tome, coordination and mood state. Low concentrations are found in the brainstem, accounting the remarkably low toxicity. Lethal doses in humans has not been described.

The Chemistry of Cannabis
Marijuana is a complex plant, with several subtypes of cannabis, each containing over 400 chemicals. Approximately 60 are chemically classified as cannabinoids. The cannabinoids are 21 carbon terpenes, biosynthesized predominantly via a recently discovered deoxyxylulose phosphate pathway. The cannabinoids are lipophilic and not soluble in water. Among the most psychoactive is D9-tetrahydrocannabinol (THC), the active ingredient in dronabinol (Unimed Pharmaceuticals Inc). Other major cannabinoids include cannabidiol (CBD) and cannabinol (CBN), both of which may modify the pharmacology of THC or have distinct effects of their own. CBD is not psychoactive but has significant anticonvulsant, sedative and other pharmacological activity likely to interact with THC. In mice, pretreatment with CBD increased brain levels of THC nearly 3-fold and there is strong evidence that cannabinoids can increase the brain concentrations and pharmacological actions of other drugs.

Two endogenous lipids, anandamide (AEA) and 2-aracidonylglycerol (2-AG), have been identified as cannabinoids, although there are likely to be more. The physiological roles of these endocannabinoids have been only partially clarified but available evidence suggests they function as diffusible and short-lived intercellular messengers that modulate synaptic transmission. Recent studies have provided strong experimental evidence that endogenous cannabinoids mediate signals retrogradely from depolarized post synaptic neurons to presynaptic terminals to suppress subsequent neurotransmitter release, driving the synapse into an altered state. In hippocampal neurons, depolarization of postsynaptic neurons and the resultant elevation of calcium lead to transient suppression of inhibitory transmitter release. Depolarized hippocampal neurons rapidly release both AEA and 2-AG in a calcium-dependent manner. In the hippocampus, cannabinoid receptors are expressed mainly by GABA-mediated inhibitory interneurons. Synthetic cannabinoid agonists depress GABAA release from hippocampal slices. However, in cerebellar Purkinje cells, depolarization-induced elevation of calcium causes transient suppression of excitatory transmitter release. Thus endogenous cannabinoids released by depolarized hippocampal neurons may function to downregulate GABA release. Further, signaling by the endocannabinoid system appears to represent a mechanism enabling neurons to communicate backwards across synapses in order to modulate their inputs.

There are two known cannabinoid receptor subtypes; subtype 1 (CB1) is expressed primarily in the brain, whereas subtype 2 (CB2) is expressed primarily in the periphery. Cannabinoid receptors constitute a major family of G protein-coupled, 7-helix transmembrane nucleotides, similar to the receptors of other neurotransmitters such as dopamine, serotonin and norepinephrine. Activation of protein kinases may be responsible for some of the cellular responses elicited by the CB1 receptor.

Neuromodulation and neuroprotection
As we are developing an increased cognizance of the physiological function of endogenous and exogenous cannabinoids it is becoming evident that they may be involved in the pathology of certain diseases, particularly neurological disorders. Cannabinoids may induce proliferation, growth arrest or apoptosis in a number of cells, including neurons, lymphocytes and various transformed neural and non-neural cells. In the CNS, most of the experimental evidence indicates that cannabinoids may protect neurons from toxic insults such as glutamatergic overstimulation, ischemia and oxidative damage. The neuroprotective effect of cannabinoids may have potential clinical relevance for the treatment of neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson.s disease, cerebrovascular ischemia and stroke. Both endogenous and exogenous cannabinoids apear to have neuroprotective and antioxidant effects. Recent studies have demonstrated the neuroprotective effects of synthetic, non-psychotropic cannabinoids, which appear to protect neurons from chemically-induced excitotoxicity. Direct measurement of oxidative stress reveals that cannabinoids prevent cell death by antioxidation. The antioxidative property of cannabinoids is confirmed by their ability to antagonize oxidative stress and consequent cell death induced by the powerful oxidant, retinoid anhydroretinol. Cannabinoids also modulate cell survival and the growth of B-lymphocytes and fibroblasts.

The neuroprotective actions of cannabidiol and other cannabinoids have been examined in rat cortical neuron cultures exposed to toxic levels of the exitatory neurotransmitter glutamate. Glutamate toxicity was reduced by both CBD (non-psychoactive) and THC. The neuroprotection observed with CBD and THC was unaffected by a cannabinoid receptor antagonist, indicating it to be cannabinoid receptor-independent. CBD was more protective against glutamate neurotoxicity than either ascorbate (vitamin C) or a-tocopherol (vitamin E).

Cannabinoids have demonstrated efficacy as immune modulators in animal models of neurological conditions such as MS and neuritis. Current data suggests that the naturally occurring, non-psychotropic cannabinoid, CBD, may have a potential role as a therapeutic agent for neurodegenerative disorders produced by excessive cellular oxidation, such as ALS, a disease characterized by excess glutamate activity in the spinal cord.

It is not yet known how glutamatergic insults affect in vivo endocannabinoid homeostasis, including AEA, 2-AG, as well as other constituents of their lipid families, N-acylethanolamines (NAEs) and 2-monoacylglycerols (2-MAGs). Hansen et al used three in vivo neonatal rat models characterized by widespread neurodegeneration as a consequence of altered glutamatergic neurotransmission and assessed changes in endocannabinoid homeostasis. A 46-fold increase in cortical NAE concentration and a 13-fold increase in AEA was noted 24 h after intracerebral NMDA injection, while less severe insults triggered by mild concussive head trauma or NDMA receptor blockade produced a less pronounced NAE accumulation. In contrast, levels of 2-AG and other 2-MAGs were unaffected by the insults employed, rendering it likely that key enzymes in biosynthetic pathways of the two different endocannabinoid structures are not equally associated with intracellular events that cause neuronal damage in vivo. Analysis of cannabinoid CB1 receptor mRNA expression and binding capacity revealed that cortical subfields exhibited an upregulation of these parameters following mild concussive head trauma and exposure to NMDA receptor blockade. This suggests that mild-to-moderate brain activity via concomitant increase of anandamide levels, but not 2-AG, and CB1 receptor density. Panikashvili et al demonstrated that 2-AG has an important neuroprotective role. After closed head injury (CHI) in mice, the level of endogenous 2-AG was significantly elevated. After administering synthetic 2-AG to mice following CHI, a significant reduction of brain edema, better clinical recovery, reduced infarct volume and reduced hippocampal cell death compared with controls occurred. When 2-AG was administered together with additional inactive 2-acyl-glycerols that are normally present in the brain, functional recovery was significantly enhanced. The beneficial effect of 2-AG was dose-dependently attenuated by SR-141716A (Sanofi-Synthélabo), an antagonist of the CB1 receptor [30]. Ferraro et al looked at the effects of the cannabinoid receptor agonist WIN-55212-2 (Sanofi Winthrop Inc) on endogenous extracellular GABA levels in the cerebral cortex of the awake rat using microdialysis. Win-55212-2 was associated with a concentration-dependent decrease in dialysate GABA levels. Win-55212-2 induces inhibition was counteracted by the CB1 receptor antagonist SR-141716A, which by itself was without effect on cortical GABA levels. These findings suggest that cannabinoids decrease cortical GABA levels in vivo.

Sinor has shown that AEA and 2-AG increase cell viability in cerebral cortical neuron cultures subjected to 8 h of hypoxia and glucose deprivation. This effect was observed at nanomolar concentrations, was reproduced by a non-hydrolyzable analog of anandamide, and was unaltered by CB1 or CB2 receptor antagonists. In the immune system, low doses of cannabinoids may enhance cell proliferation, whereas high doses of cannabinoids usually induce growth arrests or apoptosis.

In addition, cannabinoids produce analgesia by modulating rostral ventromedial medulla neuronal activity in a manner similar to, but pharmacologically distinct from, that of morphine. Cannabinoids have been shown to produce an anti-inflammatory effect by inhibiting the production and action of tumor necrosis factor (TNF) and other acute phase cytokines. These areas are discussed in great detail in a recent paper by Rice.
Glia as the cellular targets of cannabinoids

There is now accumulating in vitro evidence that glia (astrocytes and microglia in particular) have cannabinoid signaling systems. This provides further insight into the understanding of the therapeutic effects of cannabinoid compounds. Glial cells are the non-neuronal cells of the CNS. In humans they outnumber neurons by a factor of about 10:1. Because of their smaller average size they make up about 50% of the cellular volume of the brain. Glial cells of the CNS fall into three general categories: astrocytes, oligodendrocytes and microglia. Schwann cells and the less well-recognized enteric glia are their counterparts in the peripheral nervous system. Glia are ubiquitous in the nervous system and are critical in maintaining the extracellular environment, supporting neurons, myelinating axons and immune surveillance of the brain. Glia are involved, actively or passively, in virtually all disorders or insults involving the brain. This makes them logical targets for therapeutic pharmacological interventions in the CNS. Astrocytes are the most abundant cell type of the CNS. They express CB1 receptors, and take up and degrade the endogenous cannabinoid anandamide. The expression of CB2 receptors in this population appears to be limited to gliomas and may be an indicator of tumor malignancy. Two recent studies suggest that some of the anti-inflammatory effects of cannabinoids, such as the inhibition of nitric oxide (NO) and TNF release are mediated by CB1 receptors on astrocytes.

The most recent therapeutic role for cannabinoids in the CNS evolved from the discovery that cannabinoids selectively induce apoptosis in glioma cells in vitro and that THC and other cannabinoids lead to a spectacular regression of malignant gliomas in immune-compromised rats in vivo. The mechanism underlying this is not yet clear but it appears to involve both CB1 and CB2 receptor activation. A recent study comparing the antiproliferative effects of cannabinoids on C6 glioma cells suggests the involvement of vanilloid receptors.

Microglia are the tissue macrophages of the brain. In variance from other immune tissue but in accordance with their place in the CNS microglia appear to lack CB2 receptors on protein and RNA levels. Similar to their effect on peripheral macrophages, cannabinoids inhibit the release of NO and the production of various inflammatory cytokines in microglia. Interestingly, the inhibition of NO release seems to be CB1 receptor- mediated, whereas the differential inhibition of cytokines is not mediated by either CB1 or CB2 receptors, suggesting as yet unidentified receptors or a receptor independent mechanism. Irrespective, the potential of cannabinoids on inflammatory processes such as a mouse model of MS or future experiments on brain tumors in immunocompetent animal.

Nothing is known of the effects of cannabinoids on oligodendroglia. In the light of the clinical and experimental evidence suggesting the beneficial effects of cannabinoids in MS, investigations in this direction appear promising.

Future trends

A growing number of strategies for separating the sought-after therapeutic effects of cannabinoid receptor agonists from the unwanted consequences of CB1 receptor activation are now emerging. However, further improvements in the development of selective agonists and antagonists for CB1 and CB2 receptors are needed. This would allow for the refinement of cannabinoids with good therapeutic potential and would facilitate the design of effective therapeutic drugs from the cannabinoid family. Customized delivery systems are also needed; as the cannabinoids are volatile, they will vaporize at a temperature much lower than actual combustion. Thus heated air can be drawn through marijuana and the active compounds will vaporize and can easily be inhaled. Theoretically this removes most of the wealth hazards of smoking, although this has not been well studied. Recently, pharmacologically active, aerosolized forms of THC have been developed. This form of administration is achieved via a small particle nebulizer that generates an aerosol which penetrates deeply into the lungs.

From a regulatory perspective, the scientific process should be allowed to evaluate the potential therapeutic effects of cannabis, dissociated from the societal debate over the potentially harmful effects of non-medical marijuana use. This class of compounds not only holds tremendous therapeutic potential for neurological disease but is also confirmed as having remarkably low toxicity. Source.

Benefits of Cannabis Use

Advertisements

November 26, 2009 – Alberta Canada is going green, but not in the way some might think. Just outside the town of Vegreville, the Alberta Research Council is working to add hemp farming to Alberta’s list of lucrative industries.

The Vegreville nursery is home to the largest research and production facility of hemp in North America. Industrial hemp grown in Alberta can be used in a number of products ranging anywhere from textiles to fibreglass. Products made from hemp have less environmental impact than those made from glass or plastics, and in many cases are more energy efficient.

Jan Slaski, breeder and plant physiologist at the Vegreville facility, explained why this is the case.

“Bio composites produced from hemp are more environmentally friendly. Replacing glass fibre with bio-fibre produces a much lighter product. A lighter product means that your car, boat, or airplane is lighter and uses less fuel. High-end European car manufacturers, particularly German manufacturers, use bio-composites in their panels,” he said.

Historically, hemp has been grown in Canada for hundreds of years, but was banned in 1938 due to the associations hemp has with marijuana. This ban was later lifted in 1998. Industrial hemp, unlike marijuana, does not contain high levels of THC, the compound in marijuana that causes intoxication.

According to Slaski, Canada has very strict guidelines for hemp farmers.

“Cultivating hemp in Canada is regulated by Health Canada,” he stated. “The hemp that can be grown in Canada is strictly industrial hemp, and can only contain less than 0.3 per cent THC.”

This amount of THC is not enough to associate industrial hemp with narcotics. Such a low amount of chemical in industrial hemp should take the negative drug associations out of the industry.

The varieties of hemp currently grown in Alberta have mostly European origins. Researchers at the ARC have adapted European varieties to thrive in Alberta’s climate. Researchers have tested about 80 different cultivars (or plant varieties) from different regions to distinguish which varieties grow best in Alberta soil. The ARC has identified a Polish cultivar, also known as the Silesia variety, which has a 20–40 per cent higher crop yield than the cultivars presently allowed for cultivation in Canada. The group owns the sole rights to this variety of hemp in North America, and covers all aspects of hemp from development to processing to production, which is a benefit to the Alberta economy.

“ARC is offering solutions from seeds to the final product. This means we work with hemp to develop new cultivars and new agricultural practices. The new cultivars have a high yield and are adapted to our Alberta climate conditions,” Slaski said “We then take the hemp stock to our facilities in Millwoods, and soon we will have a processing facility in Vegreville, and process it.

The ARC oversees the hemp from seed to the final product. This means that all research, farming, and processing of the fibres is done locally keeping jobs and revenue within Alberta.

Slaski argued that this is a huge benefit to Alberta farmers and the overall economy. It’s also a benefit to individual farmers because hemp is a very lucrative crop.

“Farmers here in the province look for cash crops. They want something they can finally start making money on and hemp provides that opportunity,” Slaski said. Because industrial hemp is relatively new to Alberta, bio-composites are a bit more expensive, but the ARC is setting industry standards.

“At this point, it is a niche market,” Slaski said. “Working with mainstream industry, working with auto industries, buildings, textiles, it means we can get a much larger volume of materials produced and we can re-establish hemp as a valuable crop to Alberta.” By Krista Allan. Source.

November 24, 2009 – Marijuana. It’s a small word that generates a large reaction (for better or for worse). People are polarized on the topic. Yes, there is a definite social stigma surrounding this infamous, leafy plant. Consequently, the potential for cannabis-based drugs has been greatly hindered by legal and political considerations – obstacles that researchers and pharmaceutical companies do not normally find themselves battling. After all, it’s not everyday that research and development teams are looking to create novel drugs from a Schedule I substance – a substance that by definition is not considered to have a legitimate medical use. However, with the recent recommendation by the American Medical Association (AMA) that marijuana’s Schedule I drug classification be reconsidered in order to facilitate research and development of cannabinoid-based medications, could this be the dawn of a new era?

I believe that the AMA’s recommendation is right on the mark. From the limited number of clinical trials conducted on smoked cannabis, the description conferred by a Schedule I classification – namely, that there is no legitimate medical use – no longer appears to apply. According to the executive summary of the Council on Science and Public Health’s (CSAPH) report accompanying the new recommendation, trials have suggested that smoked cannabis can reduce neuropathic pain, improve caloric intake and appetite in patients with reduced muscle mass, and possibly reduce pain and improve spasticity in patients with multiple sclerosis. Thus, it seems plausible that cannabis-based medicines could be developed. The re-classification of marijuana from its current Schedule I status is a necessary step to take if we hope to further explore and take advantage of the ameliorating properties of cannabis.

The question then becomes, should pharmaceutical companies dedicate some of their research and development budgets to cannabis-based drugs? From a scientific perspective, the answer is a resounding yes. Scientists steer their investigations based on preliminary experiments and promising results, and as articulated in the CSAPH report, preliminary trials suggest a variety of medicinal uses for cannabis. Furthermore, assuming that there are legitimate medicinal applications for cannabis, the development of cannabis-based medicines (in the form of pills, for example) would work to neutralize much of the stigma associated with medicinal marijuana (only 13 states even allow the use of marijuana for medicinal purposes). Cannabis-based drugs, a few steps removed from the plant itself, would allow patients access to the therapeutic effects of cannabis, while distancing the treatment from the contentious issue of smoked marijuana. This is, of course, in addition to the obvious advantage that an efficacious cannabis-based pill or other medication medium is much safer than toxic, unrefined smoke.

So what is the greatest obstacle threatening to hinder the development of cannabis-based drugs? Ironically, it is the same thing that I just mentioned above: medicinal marijuana. While the current guidelines regarding medicinal marijuana leave much to be desired – and in fact invite the development of safer, easier-to-regulate cannabis-based treatments – the fact of the matter is, pharmaceutical companies are looking to make a profit. Nobody is going to invest the funds necessary to get a drug on the market unless there is a foreseeable fortune to be made on that product. Drug companies are in the business of “blockbusters,” after all. As long as the raw marijuana plant is legal in some states for medicinal purposes, there really isn’t a market for other cannabis-based treatments. (At least, not the financially-fruitful market for which drug companies are always on the lookout.) A consequence of the legalization of marijuana for medicinal purposes is the creation of numerous, often poorly-regulated marijuana shops and boutiques (just look at the 800+ dispensaries in California). Given the diversity of outlets from which to purchase the plant, as well as the wide variety of plant strains and price range for medicinal marijuana, patients in need could no doubt find a cheaper alternative to expensive pills. Thus, if cannabis-based drugs are ever to be developed, not only does the federal classification of marijuana need to be changed, the availability of the raw plant for medicinal purposes needs to be restricted. It’s a game of supply and demand – and that’s a game that pharmaceutical companies are looking to win. Source.

November 17, 2009 – The active ingredient in marijuana may stall decline from Alzheimer’s disease, research suggests.

Scientists showed a synthetic version of the compound may reduce inflammation associated with Alzheimer’s and thus help to prevent mental decline.

They hope the cannabinoid may be used to developed new drug therapies.

The research, by Madrid’s Complutense University and the Cajal Institute, is published in the Journal of Neuroscience.

The scientists first compared the brain tissue of patients who died from Alzheimer’s disease with that of healthy people who had died at a similar age.

They looked closely at brain cell receptors to which cannabinoids bind, allowing their effects to be felt.

They also studied structures called microglia, which activate the brain’s immune response.

Microglia collect near the plaque deposits associated with Alzheimer’s disease and, when active, cause inflammation.

The researchers found a dramatically reduced functioning of cannabinoid receptors in diseased brain tissue.

This was an indication that patients had lost the capacity to experience cannabinoids’ protective effects.

The next step was to test the effect of cannabinoids on rats injected with the amyloid protein that forms Alzheimer’s plaques.

Those animals who were also given a dose of a cannabinoid performed much better in tests of their mental functioning.

The researchers found that the presence of amyloid protein in the rats’ brains activated immune cells.

However, rats that also received the cannabinoid showed no sign of microglia activation.

Using cell cultures, the researchers confirmed that cannabinoids counteracted the activation of microglia and thus reduced inflammation. Video:

November 10, 2009 – The American Medical Assn. changes its policy to promote clinical amaresearch and development of cannabis-based medicines and alternative delivery methods.

The American Medical Assn. on Tuesday urged the federal government to reconsider its classification of marijuana as a dangerous drug with no accepted medical use, a significant shift that puts the prestigious group behind calls for more research.

The nation’s largest physicians organization, with about 250,000 member doctors, the AMA has maintained since 1997 that marijuana should remain a Schedule I controlled substance, the most restrictive category, which also includes heroin and LSD.

In changing its policy, the group said its goal was to clear the way for clinical research, develop cannabis-based medicines and devise alternative ways to deliver the drug.

“Despite more than 30 years of clinical research, only a small number of randomized, controlled trials have been conducted on smoked cannabis,” said Dr. Edward Langston, an AMA board member, noting that the limited number of studies was “insufficient to satisfy the current standards for a prescription drug product.”

The decision by the organization’s delegates at a meeting in Houston marks another step in the evolving view of marijuana, which an AMA report notes was once linked by the federal government to homicidal mania. Since California voters approved the use of medical marijuana in 1996, marijuana has moved steadily into the cultural mainstream spurred by the growing awareness that it has some beneficial effects for chronically ill people.

This year, the Obama administration sped up that drift when it ordered federal narcotics agents not to arrest medical marijuana users and providers who follow state laws. Polls show broadening support for marijuana legalization.

Thirteen states allow the use of medical marijuana and about a dozen more have considered it this year.

The AMA, however, also adopted as part of its new policy a sentence that admonishes: “This should not be viewed as an endorsement of state-based medical cannabis programs, the legalization of marijuana, or that scientific evidence on the therapeutic use of cannabis meets the current standards for a prescription drug product.”

The association also rejected a proposal to issue a more forceful call for marijuana to be rescheduled.

Nevertheless, marijuana advocates welcomed the development. “They’re clearly taking an open-minded stance and acknowledging that the evidence warrants a review. That is very big,” said Bruce Mirken, a spokesman for the Marijuana Policy Project. “It’s not surprising that they are moving cautiously and one step at a time, but this is still a very significant change.”

Advocates also noted that the AMA rejected an amendment that they said would undercut the medical marijuana movement. The measure would have made it AMA’s policy that “smoking is an inherently unsafe delivery method for any therapeutic agent, and therefore smoked marijuana should not be recommended for medical use.”

Dr. Michael M. Miller, a psychiatrist who practices addiction medicine, proposed the amendment. “Smoking is a bad delivery system because you’re combusting something and inhaling it,” he said.

Reaction from the federal government was muted.

Dawn Dearden, a spokeswoman for the Drug Enforcement Administration, said, “At this point, it’s still a Schedule I drug, and we’re going to treat it as such.” The Food and Drug Administration declined to comment.

In a statement, the office of the White House drug czar reiterated the administration’s opposition to legalization and said that it would defer to “the FDA’s judgment that the raw marijuana plant cannot meet the standards for identity, strength, quality, purity, packaging and labeling required of medicine.”

The DEA classifies drugs into five schedules, with the fifth being the least restrictive. Schedule II drugs, such as cocaine and morphine, are considered to have a high potential for abuse, but also to have accepted medical uses.

Several petitions have been filed to reschedule marijuana. The first, filed in 1972, bounced back and forth between the DEA and the courts until it died in 1994. A petition filed in 2002 is under consideration.

Kris Hermes, a spokesman for Americans for Safe Access, said that advocates hoped the petition would receive more attention. “Given the change of heart by the AMA, there is every opportunity for the Obama administration to do just that,” he said.

In a report released with its new policy, the AMA notes that the organization was “virtually alone” in opposing the first federal restrictions on marijuana, which were adopted in 1937. Cannabis had been used in various medicinal products for years, but fell in to disuse in the early 20th century.

Sunil Aggarwal, a medical student at the University of Washington, helped spark the AMA’s reconsideration after he researched marijuana’s effect on 186 chronically ill patients. “I had reason to believe that there was medical good that could come from these products, and I wanted to see AMA policy reflect that,” he said.

The AMA is not the only major doctors organization to rethink marijuana. In 2008, the American College of Physicians, the second-largest physician group, called for “rigorous scientific evaluation of the potential therapeutic benefits of medical marijuana” and an “evidence-based review of marijuana’s status as a Schedule I controlled substance.”

Last month, the California Medical Assn. passed resolutions that declared the criminalization of marijuana “a failed public health policy” and called on the organization to take part in the debate on changing current policy. By John Hoeffel. Source.

November 7, 2009 – The use of marijuana (cannabinoids) may be helpful in treating patients who have post-traumatic stress disorder, according to a new study released by the University of Haifa’sptsd Department of Psychology. Post-traumatic stress disorder is especially a concern among war veterans.

Post-traumatic stress disorder:
Nearly 7.7 million Americans have post-traumatic stress disorder (PTSD) at any given time, according to the National Institute of Mental Health, which also notes that about 30 percent of men and women who have spent time in war zones experience the disorder. PTSD is a debilitating condition that often follows a horrifying emotional or physical event, which causes the individual to have persistent, terrifying memories and thoughts, or flashbacks, of the situation. PTSD was once referred to as “shell shock” or “battle fatigue” because of its high prevalence among war veterans.

For people who have PTSD, the most prominent symptoms include reawakened trauma, avoiding anything that could recall the trauma, and psychological and physiological disturbances. It is difficult to treat PTSD patients because they are frequently exposed to additional stress, which hinders their efforts to overcome the trauma.

Marijuana and PTSD study
In the study from the University of Haifa, the researchers examined the efficiency of cannabinoids as a medical treatment for coping with the symptoms of PTSD. The researchers used a synthetic form of marijuana that has properties similar to those in the natural plant, and chose a rat model.

During the first stage of the experiment, the researchers noted how long it took for rats to overcome a traumatic experience without any intervention. Briefly, the experiment involved placing some rats in a cell colored white on one side and black on the other. The rats were placed in the white area, but when they moved to the black area, which they prefer, they received a light electric shock. The researchers brought the rats to the white area over a series of days. Immediately after the rats were exposed to the shock, they stopped moving to the black area voluntarily. However, after a few days of not receiving further electric shocks in the black area, they moved there without hesitation.

During the second phase of the experiment, a second group of rats were placed on a platform after receiving the electric shock, which added stress to the traumatic situation. The rats avoided the black area for a much longer time, which showed that exposure to additional stress hinders the process of overcoming trauma.

The third phase of the experiment involved another group of rats that were exposed to the electric shock and additional stress, but before they were placed on the platform they received an injection of synthetic marijuana in the amygdala area of the brain, which is connected to emotional memory. These rats returned to the black area after the same amount of time as the first group, which indicated that the marijuana eliminated the symptoms of stress. Even when the researchers administered marijuana injections at different times to additional groups of rats, the stress symptoms did not return. When the researchers examined hormone levels in the rats during the experiment, they found that synthetic marijuana prevented the release of the hormone produced by the body during times of stress.

The University of Haifa investigators believe their results indicate that marijuana can have an important role in treating stress-related conditions such as post-traumatic stress disorder. Individuals who worry that using marijuana for PTSD may encourage illicit drug use can turn to another study in which researchers examined the relation between PTSD symptom severity and motives for marijuana use among 103 young adult marijuana users. After considering other variables, including cigarette and alcohol use, the investigators found PTSD symptom severity was significantly related to marijuana use coping motives but no other motives for its use. Source.

SOURCES:
Bonn-Miller MO et al. Journal of Traumatic Stress 2007 Aug; 20(4): 577-86
University of Haifa news release

November 6, 2009 – The symptoms and side effects of reefer madness are now clearer than ever.IB_MPCP_Hemp_Slaski_590_0

Politicians, even those who never inhaled, suffer paranoid delusions. Over the past century, Canada’s ludicrous and draconian marijuana policies wasted billions in criminal-justice resources.

Crime gangs got rich and recreational marijuana users–about as dangerous as contented cats–were fined and jailed by the thousands.

But that’s only half of it. What we now know is that the government’s marijuana paranoia cost this country a cash crop of boundless potential.

I don’t mean marijuana, though some of us wish pot was grown and taxed by government so the windfall could enrich society instead of gangsters.

I refer instead to hemp, a benign super-plant and casualty of Canada’s war on drugs.

Fortunately, hemp is finally making a comeback, in part because of the work of the Alberta Research Council.

ARC plant physiologist Jan Slaski is as keen on hemp as he is tired of reefer jokes.

Slaski isn’t laughing, he says, because the jokes only perpetuate a bad myth.

Hemp, or industrial hemp as Slaski calls it, is not marijuana. Two different plants.

Slaski says the hardy hemp plant has been cultivated for more than 8,000 years. Its plant fibres were used in everything from clothes to shoes to rope. Its seed oil is rich in health Omega-3 and Omega-6 fatty acids.

When Ukrainian settlers came to Canada, they brought hemp seeds. One record in the archives talked about pioneers using hemp to create a soothing tea.

But while industrial hemp has some of the psycho-active THC found in marijuana, the amounts are far less intoxicating than all-ages, de-alcoholized beer.

Slaski says THC concentrations in hemp are a fraction–one per cent or less–of that in marijuana. You’d die of smoke inhalation trying to get high.

Still, one of the research council’s aims is to breed a hemp plant with no detectable THC. Why? Because of marijuana paranoia.

In 1998, 60 years after the feds prohibited the growing of hemp as part of its war on drugs, controlled plots were again allowed.

Modern hemp growers had to jump through high hoops, including a criminal record check and detailed license application to Health Canada.

The lingering hemp hysteria is summed up nicely by one of Health Canada’s rules: No hemp can be grown within one kilometre of a school.

So why is the research council working so hard to redeem hemp? Well, because of its potential to not only give Alberta farmers an economic edge, but also help save the environment.

Hemp literally grows like a weed. It can reach or exceed three metres in height during our short growing season.

It produces biomass–usable plant material–like nothing else.

Researchers have yet to identify a pest threat to hemp. It’s early season vigour allows it to out-compete weeds. So unlike cereal crops, hemp is organic, requiring no pesticide applications.

“It truly is a super crop,” Slaski says.

Forget hemp’s healthy food-oil potential for a moment. That may come if people can get over the fear of taking a trip on hemp-fried foods.

But the fibre from hemp could be used in everything from pulp-and-paper to textiles. Alberta is only one of many jurisdictions in the world that clear-cuts forests for pulp.

Forest companies must travel further and further from the pulp mill to retrieve feed stock, which then takes at least 60 years to regrow.

Put enough hemp in production and you’d get an annual, renewable fibre supply for paper production.

Hemp could also replace cotton, which requires large applications of pesticides. Hemp could also replace glass fibre, which is used in the making of composite materials, like plastics for the automotive industry.

Glass fibre requires high heat and energy in its industrial production. Hemp? Rain and sun. Glass fibres aren’t biodegradable like hemp. Hemp fibres are lighter. Lighter cars require less fuel.

The use of hemp in composite plastics is being studied in earnest by the ARC. Slaski has talked to automakers who say they’ll sign contracts if hemp composites meet strict requirements. And if production levels can be guaranteed.

The first requirement is being met ARC labs. But we’re a long way from widespread hemp farming, largely because of its undeserved reputation.

But then again, marijuana also has an undeserved reputation. It’s obvious to anyone who looks objectively at the facts that marijuana causes less harm than alcohol, both to the individual and society.

Is marijuana safe? Any psychoactive substance can be abused. But marijuana doesn’t kill brain cells or inspire violence like alcohol does.

So when you consider how this society promotes and celebrates the use of a more dangerous drug, alcohol, our marijuana policies appear silly.

But even sillier is that industrial hemp got caught up in the madness.

In case you’re wondering, the answer is no. I don’t smoke pot. I tried it as a teenager but I found it made me paranoid. By Scott McKeen. Source.