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.

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

November 5, 2009 – The debate over its risks has split political and scientific opinion. But Picture 6American mother Marie Myung-Ok Lee says cannabis isn’t only safe enough for her autistic son – it’s dramatically improved his condition.

My son, J, has autism. He’s also had two serious operations for a spinal cord tumour and has an inflammatory bowel condition, all of which may be causing him pain, if he could tell us. He can say words, but many of them – “duck in the water, duck in the water”, for instance – don’t convey what he means. For a time, anti-inflammatory medication seemed to control his pain. But in the last year, it stopped working. He began to bite and to smack the glasses off my face. If you were in that much pain, you’d probably want to hit someone, too.

J’s school called my husband and me in for a meeting about J’s tantrums, which were affecting his ability to learn. The teachers were wearing Tae Kwon Do arm pads to protect themselves against his biting. Their solution was to hand us a list of child psychiatrists. As autistic children can’t exactly do talk therapy, this meant using sedating, antipsychotic drugs like Risperdal.

Last year, Risperdal was prescribed for more than 389,000 children in the US – 240,000 of them under the age of 12 – for bipolar disorder, ADHD, autism and other disorders. Yet the drug has never been tested for long-term safety in children and carries a severe warning of side-effects. From 2000 to 2004, Risperdal, or one of five other popular drugs also classified as “atypical antipsychotics”, was the “primary suspect” in 45 paediatric deaths, according to a review of US Food and Drug Administration (FDA) data by USA Today. When I canvassed parents of autistic children who take Risperdal, I didn’t hear a single story of an improvement that seemed worth the risks. A 2002 study on the use of Risperdal for autism, in The New England Journal of Medicine, showed moderate improvements in “autistic irritation” – but the study followed only 49 children over eight weeks, which limits the inferences that can be drawn from it.

We met with J’s doctor, who’d read the studies and agreed: No Risperdal or its kin. The school called us in again. What were we going to do, they asked. As an occasional health writer and blogger, I was intrigued when a homeopath suggested medical marijuana. Cannabis has long-documented effects as an analgesic and an anxiety modulator. Best of all, it is safe. The homeopath referred me to a publication by the Autism Research Institute describing cases of reduced aggression, with no permanent side- effects. Rats given 40 times the psychoactive level merely fall sleep. Dr Lester Grinspoon, an emeritus professor of psychiatry at Harvard Medical School who has been researching cannabis for 40 years, says he has yet to encounter a case of marijuana causing a death, even from lung cancer.

A prescription drug called Marinol, which contains a synthetic cannabinoid, seemed mainstream enough to bring up with J’s doctor. I cannot say that with a few little pills everything turned around. But after about a week of fiddling with the dosage, J began garnering a few glowing school reports: “J was a pleasure have in speech class,” instead of “J had 300 aggressions today.”

But J tends to build tolerance to synthetics, and in a few months we could see the aggressive behaviour coming back. One night, I went to the meeting of a medical marijuana patient advocacy group on the campus of the college where I teach. The patients told me that Marinol couldn’t compare to marijuana, the plant, which has at least 60 cannabinoids to Marinol’s one.

***

Rhode Island, where we live, is one of 13 states where the use of medical marijuana is legal. But I was resistant. My late father was an anaesthesiologist, and compared with the precise drugs he worked with, I know he would think marijuana to be ridiculously imprecise and unscientific. I looked at my son’s tie-dye socks (his avowed favourite). At his school, I was already the weirdo mom who packed lunches with organic kale and kimchi and wouldn’t let him eat any “fun” foods with artificial dyes. Now, I’d be the mom who shunned the standard operating procedure and gave her kid pot instead.

I thought back to when J was 18 months old. We were vacationing on the Cape, and, although he just had the slightest hitch in his gait, I was sure there was something wrong. His paediatrician laughed. I called back repeatedly until a different doctor agreed to see us. J was taken in for emergency surgery, to remove a tumour that was on the verge of inflicting irreparable damage. Sometimes, you just have to go with your gut.

And yet, I still hesitated. The Marinol had been disorienting enough – no protocol to follow, just trying varying numbers of pills and hoping for the best. Now we were dealing with an illegal drug, one for which few evidence-based scientific studies existed, precisely because it is an illegal drug. But when I sent J’s doctor the physician’s form that is mandatory for medical marijuana licensing, it came back signed. We underwent a background check with the Rhode Island Bureau of Criminal Identification, and J became the state’s youngest licensee.

Having a licence, however, is different from having access to marijuana. While California has a network of “compassion centres,” basically pharmacy-like storefronts that provide quality product from registered growers, Rhode Island’s Republican governor has consistently vetoed that idea, despite the local stories of frail patients being mugged in downtown Providence as they go in search of pot. We weren’t about to purchase street marijuana, which could be contaminated with other drugs, so we looked into growing the pot ourselves. But by law, medical marijuana must be grown indoors, and it requires a separate room with a complex system of hydroponics, fans and precise lighting schedules. (This made me wonder how much THC, the main psychoactive substance found in cannabis, was actually in the spindly plants the high school goofballs I knew grew in their closets).

The coordinator of our patient group introduced us to a licensed grower. A recent horticulture school graduate, he’d figured out how to cultivate marijuana using a custom organic soil mix. His e-mail signature even quoted Rudolf Steiner. The grower arrived at our house with a knapsack containing jars of herbs. We opened the jars to sniff the different strains of “bud” – Blueberry, which did smell fleetingly of wild blueberries, and Sour Diesel, which had a rich, winey scent. The grower had also cured some leaves for tea, and he brought a glycerine tincture, a marijuana distillate in olive oil (yes, organic), cookies (ditto), and a strange machine that looked, fittingly, like a lava lamp. Basically an almost-bong, this vaporiser heated the cannabis without producing carcinogenic smoke.

For most adults, the vaporiser is the delivery method of choice, as it allows the patient to feel the effects immediately and adjust the dose precisely. J gamely put his mouth on the valve and let us squeeze a little smoke into him. It shot right back out of his nose. He looked like Puff the Magic Dragon. The grower left us with a month’s worth of marijuana tea, glycerine, and olive oil – and a cookie recipe. No buds. We paid $80 (£50).

We made the cookies with the marijuana olive oil, starting J off with half a small cookie, eaten after dinner. J normally goes to bed around 7.30pm; by 6.30 he declared he was tired and conked out. We checked on him hourly. As we anxiously peeked in, half-expecting some red-eyed ogre from Reefer Madness to come leaping out at us, we saw instead that he was sleeping peacefully. Usually, his sleep is shallow and restless. J also woke up happy.

But in a few days, J decided he didn’t like the cookie anymore and smashed it with his fist. We brewed him the tea, which smelled funky and grassy. He slurped it down, but it didn’t seem to do much. Many of the psychoactive compounds in marijuana are fat soluble, so I added a dropperful of the oil that we used in the cookies. That made him sleepy-looking but still aggressive. It became clear that when J ingested pot orally, it took two hours to see the results, and by then there wasn’t much we could do to dial the dose up or down. The grower visited us again to give J another try at the bong, but with little success.

Perhaps J needed a little time to get off the Marinol. After two weeks, we noticed a slight but consistent lessening of aggression. And he wasn’t nervously chewing holes in his shirts.

***

A month or so into the treatment, it was still too early to know if we could find a dose and mode of delivery that would give us consistent results. Even if J could learn to use the vaporiser, it costs $600 and would leave the house reeking of pot. And we didn’t want to get too dependent, because of the inherent limitations. Though we’d love to calm J with pot so that he can visit his grandmother in Minnesota, bringing a controlled substance on the plane isn’t the best idea.

But since we started him on his “special tea,” J’s little face, which is sometimes a mask of pain, has softened. He’s smiled more. For most of the last year, his individual education plan at his special-needs school was full of blanks, recording “no progress” because he spent his whole day an irritated, frustrated mess. But soon after starting on the tea, his reports began to show real progress, including “two community outings with the absence of aggressions”.

My husband and I are both academics and writers (me, novelist and essayist; he, historian), given to close observation and note taking. It was these habits that finally helped us see our son’s allergic sensitivity to certain foods and seek advice from a gastroenterologist for his behaviours – aggression and chronic diarrhoea – instead of the recommended psychiatrist. (Gut pain and digestive problems, coined as “autistic entercolitis”, are now considered a common biological affliction of many autistic children).

At first we weren’t sure if we were seeing results from the cannabis, but after about three months, which included weekly consultations with our grower as we experimented with different strains, we observed a much happier and outgoing child – who did not act or appear “stoned” in any way. Four months in, J came home from school and I noticed something different. Pre-pot, J ate the collars of his shirts, teasing his clothes apart and swallowing the threads. There’s a name for this disorder – pica (pregnant women sometimes chew on chalk). It got so bad he ate his pyjamas and we had to start dressing him in organic cotton shirts. Then one day he came home from school wearing a whole shirt.

J’s school reports improved too. At one parent meeting, his teacher produced the latest “aggression” chart, showing attempts or instances of hitting, kicking biting or pinching other people. For a year he had scored an average of 30 to 50 aggressions a day, with a high of 300. The latest data showed days, sometimes consecutive, with zero aggressions. And on the school bus, J has transformed from a child who has hit the driver in the face and bitten people into a sparkly eyed boy who says hi and quietly takes his seat.

***

There’s a twist to this happy story, though. The aggression has eased but J’s autism has become more distinct. His vocal outbursts – screams, barks, yips of happiness – still happen and while our home is no longer full of thrown food, broken dishes and scratched faces, we still see people in the local area react to a family that remains different – and not always to their liking. There’s a father on the next street who stops playing ball with his son when we approach. A mother won’t make eye contact and ignored a party invitation. Most people responded well to J but sometimes we feel we’re being shunned.

Marijuana isn’t a miracle cure for autism. But in our son’s case it eases his pain and inflammation so dramatically that he can participate in life and learning again. It also protects him from the sometimes dangerous side-effects of pharmaceutical drugs. We have settled on a good strain (White Russian, a favourite pain-reliever for end-stage cancer patients) and a good dose. And now he’s not in pain, J can go to school instead of a children’s psychiatric hospital, where all too many of his peers end up as a result of violent behaviour.

When I think of the embarrassment I may feel if my colleagues see this article, or teachers or parents at J’s school, or his less open-minded doctors, I pause. Although I occasionally smoked pot as a teenager (believe me, in northern Minnesota, there was not much else to do), now that I’m a law-abiding adult, all the scary anti-drug messages are flashing in my brain. But when I researched cannabis the way I did conventional drugs, it seemed clear that marijuana wouldn’t harm J, and might help. It’s strange that the virtues of such a useful and harmless botanical have been so clouded by stigma. Even the limited studies that have been done suggest marijuana’s potential as an adjunctive therapy for cancer. Marijuana, you need some re-branding. Maybe a cool new name.

One of the biggest tests for J through this journey was a visit from Grandma. The last time she came, over Christmas, J hit her during a tantrum. This time, we gave him his tea, mixing it with goji berries to mask any odour, although it occurs to me that my mother, a Korean immigrant, probably doesn’t even know what pot smells like (it actually smells a lot like ssuk, a Korean medicinal herb). She remarked that J seemed calmer. As we were preparing for a trip to the park, J disappeared, and we wondered if he was going to throw one of his tantrums. Instead, he returned with Grandma’s shoes, laying them in front of her, even carefully adjusting them so that they were parallel and easy to step into. He looked into her face, and smiled.

What are the downsides to this experiment?

By Jeremy Laurance, Health Editor

The first reaction of most parents to Marie Myung-Ok Lee’s story is likely to be one of surprise, shock, even horror. What is she doing turning her nine-year-old son into a pot-head? Has she not heard of the dangers of cannabis smoking to the mental health of adolescents, never mind the disorienting effects of an intoxicating substance on one so young?

Possibly this will be their second and third reactions, too. Ms Myung-Ok Lee was giving her son, J, cannabis to relieve pain (from his spinal tumour and inflamed gut), not just to treat his autism. Even so, the stigma that surrounds illegal drugs is so deeply entrenched, just because they are illegal, that many people are simply not prepared to weigh up their benefits and harms.

We have seen in the row this week over the sacking of the UK Government’s chief drugs adviser, Professor David Nutt, how the debate over drugs is driven more by fear, emotion and political calculation than by scientific evidence. The Labour Government, facing possible annihilation at the next election, is anxious to be seen to be tough on drugs – so the outspoken Professor Nutt had to go.

As an academic, Ms Myung-Ok Lee is perhaps better placed than many to resist the voices of unreason and take a cool look at the evidence. Cannabis, as she points out, is already prescribed as a pain killer, as an anti-nausea agent for cancer sufferers and as a treatment for multiple sclerosis. In all these areas it has been shown to be effective, though there is debate about just how effective. In the UK, it is available as Sativex, a spray taken under the tongue, which contains a cannabis extract. More than 1,200 patients in the UK have received it for relief of symptoms associated with multiple sclerosis. It is not, however, prescribed to nine-year-olds (or anyone under 18).

Ms Myung-Ok Lee started her son on medicinal cannabis, and then went a step further by giving him the herbal kind, as a tincture or baked in a cookie. This, too, is not without precedent – among adults. There have been frequent reports of patients smoking cannabis and gaining relief from pain or the spasticity associated with multiple sclerosis, and in the UK when they have been prosecuted for possession of a controlled drug, the courts have shown leniency.

But in trying herbal cannabis on her son, Ms Myung-Ok Lee and her doctor have stepped beyond even the anecdotal evidence, into the unknown. J became Rhode Island’s youngest ever patient licensed to use marijuana for medical reasons.

She acknowledges it is an experiment, but she reasons that as cannabis has low toxicity and is safer than most other drugs, the risks are low. Any parent, confronted with a screaming, suffering child who is so distressed that he smashes things, hits people and tears at his clothing with his teeth, must feel sympathy for her. In that situation, which of us would not try anything to ease our child’s pain? Moreover, the experiment appears to have worked – at least for the first few months.

The difficult questions are: will the effect last? Will there be a downside to using the drug in one so young? Is the effect real? The last question is the trickiest. Children grow and change and those with autism are no different from the rest. The changes his parents have noticed in J might have happened anyway, as part of his natural development. The cannabis could turn out to be a coincidental factor, with zero impact on his condition. It was coincidence that led to the scare over MMR and autism – because the first symptoms of the condition typically occur around 14 months which is the age at which babies receive their first MMR jab.

It would be a disaster if cannabis came to be seen as a panacea for children in the same situation, on the basis of this anecdotal report. As always in science, we need more evidence.

October 27, 2009 – Last week, the Justice Department ordered its staff to back off prosecution of people who use marijuana for medical purposes in the 14 states in which such use is legal. The directive reopened a med_mary_4question that has been part of the debate on U.S. drug policy for decades.

To understand more about the drug’s medical properties, we turned to Daniele Piomelli, who since 1998 has led a program, funded by the National Institutes of Health, to study the impact of marijuana and other psychoactive drugs on the brain. He is a professor of pharmacology and biological chemistry at the University of California at Irvine as well as and director of the center for Drug Discovery and Development at the Italian Institute of Technology in Genoa.

What medical benefits does marijuana offer? Have these benefits been demonstrated in rigorous scientific studies?

Several controlled clinical trials have been carried out in the last few years, using either smoked marijuana or a mouth spray that contains an extract of the marijuana plant. The results are quite consistent. They show that marijuana improves the well-being of patients with multiple sclerosis and alleviates chronic pain in patients with damage or dysfunction of nerve fibers (so-called neuropathic pain). Other work has shown that marijuana and its active ingredient THC (delta-9-tetrahydrocannabinol) reduce the nausea that accompanies chemotherapy, stimulate appetite in AIDS wasting syndrome and lessen tics in Tourette’s syndrome. By and large, the use of marijuana in these trials was associated with few and mild side effects (for example, dry mouth and memory lapses).

What are the risks of medical use of marijuana? Could it become addictive or lead to use of other, more dangerous drugs?
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Marijuana can produce dependence, though less aggressively than, say, tobacco or the so-called opiate painkillers. Frequent use is risky, however, particularly during adolescence when the neural circuits in the brain are still maturing. It turns out that the brain employs its own marijuana-like substances, called endocannabinoids, to send signals from one neural cell to another, and that THC mimics these substances. The endocannabinoids seem to be very important in brain development, so messing with them before the nervous system becomes fully mature is not a smart thing to do.

There is little hard evidence that using marijuana leads to the subsequent use of other addictive drugs. On the other hand, it is becoming increasingly clear that stressful life events (particularly in critical periods such as adolescence) can encourage drug use and facilitate the development of addictions.

How would a marijuana user be sure to get the correct dose of the active ingredient?

It is difficult to say, because the various types of marijuana now available contain widely different concentrations of THC. Standardized marijuana preparations that contain a fixed amount of THC are not currently sold to the public, though the National Institute on Drug Abuse does provide them to investigators for use in clinical trials.

Is there an alternative way to get the same ingredient in some other form?

A clinical form of THC was approved by the Food and Drug Administration many years ago. It is marketed under the name of Marinol and is used to treat nausea in cancer patients undergoing chemotherapy as well as loss of appetite in AIDS patients. It comes in capsules and is taken orally. Many medical marijuana users say the fixed dose of oral THC creates a problem; they say they prefer smoked marijuana because its dosage can be adjusted simply by changing the length and intensity of the puffs. They may be right, but the burning of a marijuana joint creates tars and other toxic chemicals that can be harmful with prolonged exposure. An alternative is to use so-called smokeless delivery systems such as vaporizers and sprays. Source.

October 19, 2009 – The Justice Department announced today that federal drug agents will no longer arrest or prosecute people who are legally using, selling or supplying medical marijuana in the states that allow it.

“It will not be a priority to use federal resources to prosecute patients with serious illnesses or their caregivers who are complying with state laws on medical marijuana,” Attorney General Eric Holder said in a statement when he released the new guidelines. But, Mr. Holder said, “we will not tolerate drug traffickers who hide behind claims of compliance with state law to mask activities that are clearly illegal.”

How significant is the change in federal drug policy? What will the new guidelines mean for local and state law enforcement?

A Muddier Federal Role
Picture 29Tom Riley-Tom Riley was associate director of the White House Office of National Drug Control Policy from 2001 to 2009.

The new policy announced on medical marijuana can be broken down into two parts. The first of these is not really “new” and the second is not really “policy.”

First, Attorney General Holder announced that it would no longer be a “priority” for the federalPicture 31 government to prosecute patients with serious illnesses. But that has never been a priority of federal law enforcement, which has been focused on people engaged in the cultivation and trafficking of significant quantities of illegal drugs. Let’s not be conned here: The average quantity of marijuana that someone is in federal prison for marijuana possession is over 100 lbs.

That is not “personal use,” nor is it Granny getting locked in the slammer for puffing a few joints for “medical” purposes. Leaving aside the wisdom of determining medical policy by ballot measure rather than by science, keeping the federal law enforcement focus on drug trafficking is nothing new — it is a continuation of the Bush and Clinton administration policies.

Second, the memo itself is internally conflicted to the point of incoherence. While ostensibly encouraging prosecutors to defer to state and local laws on marijuana, it also recognizes that federal “interest” can still allow the feds, at their discretion, to step in and prosecute. In fact, federal law remains completely unchanged.

The memo specifically states that the new policy should not be interpreted to mean that medical marijuana has been legalized, and that it does not provide a legal defense against federal prosecution. Moreover, it states that even if an individual scrupulously complies with state laws, they still may be subject to federal prosecution.

The gap between the headlines and the reality can only lead to further confusion. California municipalities are struggling with an explosion of store-front pot shops and grow operations. The new federal “guidelines” make the federal role muddier, and may send a green light to cultivators and traffickers who have been cynically using the “medical” label.

A Victory for Common Sense
Picture 30Richard N. Van Wickler-Richard N. Van Wickler is the Cheshire County superintendent of New Hampshire Department of Corrections and a member of Law Enforcement Against Prohibition.

The announcement by the Obama administration to not use limited resources to target states that allow the use of medicinal marijuana, and the citizens who use them, is a significant victory for common sense.

One case in point is California, which has built 21 new penitentiaries in a five-year period. Picture 32
The state should get some relief from the no fewer than 200 raids by federal officers on state-approved medicinal marijuana cooperatives — a significant acknowledgment of compassion for the sick and respect for the autonomy of our individual states. The change shines a new light on the horribly failed drug war.

Citing limited federal resources as a principal reason not to pursue state-approved medicinal marijuana cooperatives is only one of many excellent reasons why our country must change course. Considering that 83 percent of property crimes and as much as 40 percent of violent crimes are unsolved in our country, it seems that what resources we do have could be much better utilized. If preventing crime, reducing disease and addiction rates, and reducing violence and needless death are goals of this administration with respect to the drug war, then an exit strategy is urgently needed on this failed war.

But Is It Effective?
Picture 34Henry I. Miller-Henry I. Miller, a medical doctor, is a senior fellow at the Hoover Institution. He was an official at the Food and Drug Administration from 1979 to 1994.

As an “exercise of investigative and prosecutorial discretion,” in the words of the Department of Justice, this decision is understandable — and even welcome — but it is not altogether satisfactory. Arguably, if marijuana has therapeutic potential, it should be required to pass scientific and regulatory muster like any other medicine.

We have considerable experience with making drugs from the opium poppy, for example, butPicture 33 we don’t authorize patients to smoke opium for medical purposes; rather, we require that opiate products, including morphine for analgesia and paregoric for diarrhea, be standardized and quality-controlled by composition and dose, fully tested, delivered in an appropriate manner, and shown to be safe and effective. Why should marijuana be any different?

A promising and rational alternative to smoked marijuana is a marijuana-derived drug called Sativex, formulated as a mouth spray, which has been approved in Canada for the treatment of neuropathic pain associated with multiple sclerosis and is in advanced clinical trials for muscle spasticity, intractable pain and other uses. Unlike crude marijuana, its purity and potency can be standardized.

Patients who are genuinely in need deserve safe and effective medicines, and rigorous testing and oversight are the best ways to provide them.

Hypocritical Foolishness
Picture 36Joseph McNamara-Joseph D. McNamara, a retired deputy inspector of the New York Police Department and former police chief of San Jose, Calif., is a research fellow at the Hoover Institution, Stanford University.

I never smoked a cigarette in my life, let alone a reefer. It’s not that I was a puritan. Like the overwhelming majority of my fellow cops, I thought it manly and cool to consume my share of beer and booze.

But as a veteran of more than 30 years in law enforcement, I always thought it hypocritical Picture 35foolishness to bust 700,000 to 800,000 Americans a year for pot, and especially ridiculous to get excited about sick people smoking marijuana because they believed accurately or mistakenly, that it helped ease their pain.

I’m not inclined to enter the endless debates between crusading zealots against marijuana and those who cite contrary evidence that marijuana is a relatively harmless drug. I am convinced, however, that if you must be a heavy drug user, you’re far better off smoking pot than, say, playing the dangerous, insane drinking games common among our high school and college kids, and excessive alcohol consumption by older heavy boozers.

In my mind, the question should focus on the societal costs of arresting someone for using certain substances we disapprove of, and consequently giving them a criminal record that can damage their lives and turn them into career criminals. If Misters Clinton, Bush, or Obama, and countless other successful people had been busted for their youthful flirtation with drugs most would have been stigmatized and suffered irreparable career harm. The learning moment here is that there is a terrible human cost to arresting someone, which must be balanced against the harm it supposedly prevents.

Additional costs of the violence, corruption, and other crimes associated with prohibition never seem to be included in estimated costs of drug war policies. For example, the use of scarce police, court, and correctional resources, and the disproportional mischief that aggressive arrest tactics impose on minorities tilt the already out of balance price tag for our irrational policy of unnecessarily criminalizing widespread conduct. Why is a free society so terrified of trusting adults to make responsible decisions?

Source.

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