Scientific Research


December 4, 2009 – Cancer patients, glaucoma patients and others can benefit from medical marijuana, and now a new analysis shows that it can help multiple sclerosis (MS) patients find relief from the muscle spasms that are the hallmark of the debilitating autoimmune disease.

“The therapeutic potential of cannabinoids in MS appears to be comprehensive, and should be given considerable attention,” said lead researcher Dr. Shaheen Lakhan, executive director of the Global Neuroscience Initiative Foundation.

“Spasticity, an involuntary increase in muscle tone or rapid muscle contractions, is one of the more common and distressing symptoms of MS,” the researchers noted in their review. “Medicinal treatment may reduce spasticity, but may also be ineffective, difficult to obtain or associated with intolerable side effects,” they added.

“We found evidence that cannabis plant extracts may provide therapeutic benefit for MS spasticity symptoms,” Lakhan said.

Although some objective measures showed improvement, there were no significant changes in after-treatment assessments, Lakhan said. “However, subjective assessment of symptom relief did often show significant improvement post-treatment,” he added.

For the study, Lakhan and his colleague Marie Rowland reviewed six studies where marijuana was used by MS patients. Five of the trials showed that marijuana reduced spasms and improved mobility, according to the report published Dec. 3 in the online journal BMC Neurology.

Specifically, the studies evaluated the cannabis extracts delta9-tetrahydrocannabinol (THC) and cannabidiol (CBD). These studies found that both THC and CBD extracts may provide therapeutic benefit for MS spasticity symptoms, Lakhan said.

Although there was a benefit from using marijuana there were also side effects, such as intoxication. This varied depending on the amount of marijuana needed to effectively limit spasms, but side effects were also seen in the placebo groups, Lakhan and Rowland noted.

The careful monitoring of symptom relief and side effects is critical in reaching an individual’s optimal dose, Lakhan said. “Moreover, there is evidence that cannabinoids may provide neuroprotective and anti-inflammatory benefits in MS,” he added.

“Considering the distress and limitations spasticity brings to individuals with MS, it would be important to carefully weigh the potential for side effects with the potential for symptom relief, especially in view of the relief reported in subjective assessment,” Lakhan said.

Dr. Moses Rodriguez, a professor of neurology and immunology at the Mayo Clinic, said that “the idea of using cannabis to treat MS has been around for a long time.”

Rodriguez noted that the effects of using marijuana have been mixed. “It has been difficult to know whether the effect has been just a general well-being or whether it has a direct effect on muscle fibers and spasticity,” he said.

If drugs could be developed that take away the intoxicating effects of marijuana, it could have a direct effect on spasms without the high, Rodriguez said.

The Obama administration announced in October that it will no longer prosecute medical marijuana users or suppliers, provided they obey the laws of states that allow use of the drug for medicinal purposes.

Rodriguez said he is often asked by his MS patients about whether there is a benefit to using marijuana.

“What I tell my patients,” he said, “is if they want to try it they should try it. They should understand that there is a potential for it to be habit-forming and there may be a potential that they are fooling themselves.”

Patricia A. O’Looney, vice president of biomedical research at the National Multiple Sclerosis Society, said the society has studied this issue and does not think enough is known to recommend that MS patients use marijuana.

“Because the studies to date do not demonstrate a clear benefit compared to existing therapy, and issues of side effects and long-term effects are not clear, the recommendation is that it should not be recommended at this time,” she said.

Another expert, Dr. William Sheremata, director of the Multiple Sclerosis Center at the University of Miami School of Medicine, also doesn’t think MS patients necessarily benefit from marijuana use.

Sheremata noted that the objective measures in the study did not show any benefit from marijuana. “Those are the only valid measures. Subjective responses are subjective; they really don’t have much in the way of validity,” he said. “I am not convinced that the use of marijuana benefits patients as a whole.” Source.

For more information on multiple sclerosis, visit the National Multiple Sclerosis Society.

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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

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 16, 2009 – Medicinal use of cannabis is being discussed more actively than ever. Although prior to its prohibition in 1937 cannabis was used widely in conditionsmap_340pharmacies, there was little debate about its usefulness to treat various symptoms such as inflammatory pain. Cannabis remedies were well known, publicly advertised and widely prescribed.

“Marijuana,” on the other hand, was virtually unknown Mexican jargon before becoming the “assassin of youth” in propaganda films. Such depictions led to an unceremonious vote by Congress to effectively criminalize Cannabis sativa in all of its forms. The strongest opposition came not from the public (which did not equate the new “scourge” with cannabis remedies) but from the American Medical Association, whose congressional liaison decried the legislation as speciously motivated by “indirect hearsay evidence.”

Over the next 72 years, the image of the American cannabis user morphed from the immigrant madman and criminal deviant of the ’40s, to the counter-culture crowd of the ’60s to the unmotivated slacker of the ’80s. In the ’90s, a “new” image arose: the medical marijuana patient, who is driven not to get high but to get well. It is linguistically ironic that “medical marijuana” may usher in a new chapter in the ancient relationship between human society and the cannabis plant.

Now the American Medical Association has turned heads by again weighing in on cannabis policy. After extensive review of scientific and clinical evidence regarding the harms and benefits of cannabinoids (molecules found in cannabis) as well as recent legal precedence regarding medical marijuana, the AMA announced that the federal Schedule I status of marijuana (most prohibited) should be reconsidered in order to advance clinical research with botanical cannabinoid medicines. The AMA report furthermore expresses that “physicians who comply with their ethical obligations to ‘first do no harm’ and to ‘relieve pain and suffering’ should be protected in their endeavors, including advising and counseling their patients on the use of cannabis for therapeutic purposes.”

The emphasis on research is important. There is a future for botanical cannabis-based medicines, but patients and physicians should be empowered to base health care decisions on real evidence rather than hyperbolic claims of marijuana’s dangers or virtues. Not surprisingly, the AMA does not support legalizing medical marijuana through state ballot initiatives, such as the one Floridians could vote on next year if a petition by the group People United for Medical Marijuana gains traction. Cannabis is a plant and modern standards for purity, packaging and delivery of drugs play an important part in assuring reliable predictability. Also at play is the arena of pharmaceutical development — new drugs are being pioneered to enhance the body’s THC-like “endocannabinoid system,” intended to achieve therapeutic effect with improved specificity and minimal psychoactivity. Research is clearly needed to ensure efficacy and safety of these new drugs.

Nonetheless, the perceived promise of such drugs highlights a need for greater maturity in social discussion of medical use for cannabis and/or its constituent molecules. Whatever else might be said about the apparent sea change of public opinion about cannabis, the oft-repeated claims by federal drug czars that medical marijuana is a “smoke screen” or lacks even a “shred of evidence” must be laid to rest as a relic of socially juvenile, 20th century reefer madness. Public policy should be based on sound scientific evidence — not a roadblock to it. Cannabis has been used safely as a folkloric remedy for thousands of years, but in modern America inappropriate Schedule I listing of marijuana has obstructed research to find promising therapies for debilitating human conditions. This is a paramount reason why the scheduling should be changed. By Gregory L. Gerdeman and Juan Sanchez-Ramos. Source.

Gregory L. Gerdeman, Ph.D., is an assistant professor of biology at Eckerd College in St. Petersburg. Juan Sanchez-Ramos, Ph.D./M.D., is the Helen Ellis Professor of Neurology and chair for Parkinson’s Disease Research at the University of South Florida College of Medicine in Tampa.

Sanchez-Ramos was a physician involved in the “Compassionate Use Protocol for Marijuana” sponsored by the National Institute on Drug Abuse and approved by the Food and Drug Administration and the Drug Enforcement Administration. In this study, marijuana was prepared and shipped by NIDA to patients with various medical conditions. His patient suffered from muscle spasms and pain caused by a rare disease, successfully treated with cannabis.

Professor at Hebrew University in Jerusalem, Dr. Mechoulam describes the role of Cannabinoids as anti-inflammatory for arthritis, as neuroprotectant for brain injury and as a possible treatment for PTSD. Dr. Mechoulam first isolated THC in 1964. Conference hosted by Patients Out of Time. DVDs are available. http://MedicalCannabis.com

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

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