December 5, 2009 – Cannabis, otherwise known as marijuana (or marihuana), has been a topic of debate for many years, not only in Canada, but also in several other countries including the U.S. and the U.K. However, while marijuana for recreational use has not been legalized in Canada, medical marijuana use can be granted for medicinal needs.

The Definition of Chronic Pain

Although “chronic pain” seems all encompassing and thus easily used as a reason for medical marijuana use, the organization of Health Canada very clearly defines what can be considered severe enough pain for medical marijuana. With that said, there are many suffering from chronic pain – due to a variety of reasons – with grants for the medical use of cannabis.

Arthritis, headaches and back pain are the most common, but fibromyalgia, carpal tunnel syndrome, neuropathy and phantom limb pain are also common reason for chronic pain. Continuing pain can also be caused by debilitating illnesses such as MS (multiple sclerosis), scoliosis, osteoporosis and others.

Original Treatments for Chronic Pain

For many, medical marijuana use is a “last resort”, used only after several pharmacologic treatments fail. Typically, the first treatments include pain relievers such as aspirin or ibuprofen. Unfortunately, long-term use can cause serious side effects; even if there is pain relief, it can only be in short periods due to the need for short-term use of the “first line” of treatments.

Should the first treatments fail, narcotic opioids such as codeine, morphine and oxycodone are generally prescribed. Although often highly affective, the concern for these types of narcotics is that they have a high possibility for addiction and abuse. As well, their use is also limited, due to possible side effects in higher doses. The withdrawal symptoms for addictive pharmaceuticals can be mild to painfully severe.

Medical Marijuana for Chronic Pain

For those that don’t respond to the first or second line of treatments, medical marijuana may be prescribed. As well, there are those who prefer not to use man-made pharmaceuticals that have a high rate of addiction or serious side effects.

According to Health Canada, “Dependence is unlikely to be problematic when cannabis is used therapeutically, although withdrawal affects may be uncomfortable. These include restlessness, anxiety, mild agitation, irritability, tremor, insomnia and EEG/ sleep disturbance, nausea, diarrhea and cramping.”

Relief from chronic pain, however, far outweighs the possibility of addiction for many:

– Migraines – Severe, incredibly painful and often lasting as long as 72 hours, migraines can cause serious debilitating issues such as nausea, vision changes, vomiting and a high sensitivity to light and sound. Many of the pharmaceuticals used to either stop or lessen the amount of migraines cause the same issues as the onset of the migraines themselves. Often, sufferers stop treatment because it doesn’t work or because the side effects are too severe.

Medical marijuana, on the other hand, has been a well-documented treatment for many years – even throughout the nineteenth century. Cannabinoids have often demonstrated anti-inflammatory effects, as well as dopamine blocking. It is believed by some that one of the causes of migraines is the lack of natural endocannabinoids in the body, which might explain why cannabis works to decrease the pain as well as the symptoms.

– Multiple sclerosis (MS) – MS is a degenerative disease that attacks myelin in the brain and spinal cord. If you imagine nerves to be like electrical wires, myelin is the insulating, protective sheath around the nerves. The autoimmune system treats myelin as a foreign invader, destroying patches of it and leaving nerve fibers exposed, interrupting their normal function. It is debilitating and painful, causing such symptoms as tingling and numbness, painful muscle spasms, tremors, paralysis and more.

Prescribed pharmaceuticals can cause severe, debilitating medical issues such as seizures, abdominal cramps, dizziness, mental disturbances and other problems. Many MS sufferers prefer to self-medicate with marijuana, and have noticed that cannabis helps them control tremors, spasms and bladder control. Tests have also shown that THC helps reduce pain intensity and sleep disturbance significantly.

Although these two illnesses are common for the use of medical marijuana in relieving chronic pain sufferers, the same can be said for rheumatoid arthritis, spinal cord injuries and even phantom limb pain. While more studies need to be performed to explain exactly how cannabinoids and medical marijuana work, the fact that they do work is clear. Source.

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

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

September 9, 2009 – LONDON – Chemicals in cannabis have been found to stop prostate cancer cells from growing in the laboratory, suggesting that cannabis-based medicines could one day help fight the disease, scientists said Wednesday.
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After working initially with human cancer cell lines, Ines Diaz-Laviada and colleagues from the University of Alcala in Madrid also tested one compound on mice and discovered it produced a significant reduction in tumor growth.

Their research, published in the British Journal of Cancer, underlines the growing interest in the medical use of active chemicals called cannabinoids, which are found in marijuana.

Experts, however, stressed that the research was still exploratory and many more years of testing would be needed to work out how to apply the findings to the treatment of cancer in humans.

“This is interesting research which opens a new avenue to explore potential drug targets but it is at a very early stage,” said Lesley Walker, director of cancer information at Cancer Research UK, which owns the journal.

“It absolutely isn’t the case that men might be able to fight prostate cancer by smoking cannabis,” she added

The cannabinoids tested by the Spanish team are thought to work against prostate cancer because they block a receptor, or molecular doorway, on the surface of tumour cells. This stops them from dividing.

In effect, the cancer cell receptors can recognize and “talk to” chemicals found in cannabis, said Diaz-Laviada.

“These chemicals can stop the division and growth of prostate cancer cells and could become a target for new research into potential drugs to treat prostate cancer,” she said.

Her team’s work with two cannabinoids — called methanandamide and JWH-015 — is the first demonstration that such cannabis chemicals prevent cancer cells from multiplying.

Some drug companies are already exploring the possibilities of cannabinoids in cancer, including British-based cannabis medicine specialist GW Pharmaceuticals.

It is collaborating with Japan’s Otsuka on early-stage research into using cannabis extracts to tackle prostate cancer — the most commonly diagnosed cancer in men — as well as breast and brain cancer.

GW has already developed an under-the-tongue spray called Sativex for the relief of some of the symptoms of multiple sclerosis, which it plans to market in Europe with Bayer and Almirall.

Other attempts to exploit the cannibinoid system have met with mixed success. Sanofi-Aventis was forced to withdraw its weight-loss drug Acomplia from the market last year because of links to mental disorders. Source.

August 16, 2009 – Editor’s note: There are millions of regular pot smokers in America and millions more infrequent smokers. Smoking pot clearly has far top-ten-goldfewer dangerous and hazardous effects on society than legal drugs such as alcohol. Here is High Times’s top 10 reasons that marijuana should be legal, part of its 420 Campaign legalization strategy.

10. Prohibition has failed to control the use and domestic production of marijuana. The government has tried to use criminal penalties to prevent marijuana use for over 75 years and yet: marijuana is now used by over 25 million people annually, cannabis is currently the largest cash crop in the United States, and marijuana is grown all over the planet. Claims that marijuana prohibition is a successful policy are ludicrous and unsupported by the facts, and the idea that marijuana will soon be eliminated from America and the rest of the world is a ridiculous fantasy.

9. Arrests for marijuana possession disproportionately affect blacks and Hispanics and reinforce the perception that law enforcement is biased and prejudiced against minorities. African-Americans account for approximately 13% of the population of the United States and about 13.5% of annual marijuana users, however, blacks also account for 26% of all marijuana arrests. Recent studies have demonstrated that blacks and Hispanics account for the majority of marijuana possession arrests in New York City, primarily for smoking marijuana in public view. Law enforcement has failed to demonstrate that marijuana laws can be enforced fairly without regard to race; far too often minorities are arrested for marijuana use while white/non-Hispanic Americans face a much lower risk of arrest.

8. A regulated, legal market in marijuana would reduce marijuana sales and use among teenagers, as well as reduce their exposure to other drugs in the illegal market. The illegality of marijuana makes it more valuable than if it were legal, providing opportunities for teenagers to make easy money selling it to their friends. If the excessive profits for marijuana sales were ended through legalization there would be less incentive for teens to sell it to one another. Teenage use of alcohol and tobacco remain serious public health problems even though those drugs are legal for adults, however, the availability of alcohol and tobacco is not made even more widespread by providing kids with economic incentives to sell either one to their friends and peers.

7. Legalized marijuana would reduce the flow of money from the American economy to international criminal gangs. Marijuana’s illegality makes foreign cultivation and smuggling to the United States extremely profitable, sending billions of dollars overseas in an underground economy while diverting funds from productive economic development.

6. Marijuana’s legalization would simplify the development of hemp as a valuable and diverse agricultural crop in the United States, including its development as a new bio-fuel to reduce carbon emissions. Canada and European countries have managed to support legal hemp cultivation without legalizing marijuana, but in the United States opposition to legal marijuana remains the biggest obstacle to development of industrial hemp as a valuable agricultural commodity. As US energy policy continues to embrace and promote the development of bio-fuels as an alternative to oil dependency and a way to reduce carbon emissions, it is all the more important to develop industrial hemp as a bio-fuel source – especially since use of hemp stalks as a fuel source will not increase demand and prices for food, such as corn. Legalization of marijuana will greatly simplify the regulatory burden on prospective hemp cultivation in the United States.

5. Prohibition is based on lies and disinformation. Justification of marijuana’s illegality increasingly requires distortions and selective uses of the scientific record, causing harm to the credibility of teachers, law enforcement officials, and scientists throughout the country. The dangers of marijuana use have been exaggerated for almost a century and the modern scientific record does not support the reefer madness predictions of the past and present. Many claims of marijuana’s danger are based on old 20th century prejudices that originated in a time when science was uncertain how marijuana produced its characteristic effects. Since the cannabinoid receptor system was discovered in the late 1980s these hysterical concerns about marijuana’s dangerousness have not been confirmed with modern research. Everyone agrees that marijuana, or any other drug use such as alcohol or tobacco use, is not for children. Nonetheless, adults have demonstrated over the last several decades that marijuana can be used moderately without harmful impacts to the individual or society.

4. Marijuana is not a lethal drug and is safer than alcohol. It is established scientific fact that marijuana is not toxic to humans; marijuana overdoses are nearly impossible, and marijuana is not nearly as addictive as alcohol or tobacco. It is unfair and unjust to treat marijuana users more harshly under the law than the users of alcohol or tobacco.

3. Marijuana is too expensive for our justice system and should instead be taxed to support beneficial government programs. Law enforcement has more important responsibilities than arresting 750,000 individuals a year for marijuana possession, especially given the additional justice costs of disposing of each of these cases. Marijuana arrests make justice more expensive and less efficient in the United States, wasting jail space, clogging up court systems, and diverting time of police, attorneys, judges, and corrections officials away from violent crime, the sexual abuse of children, and terrorism. Furthermore, taxation of marijuana can provide needed and generous funding of many important criminal justice and social programs.

2. Marijuana use has positive attributes, such as its medical value and use as a recreational drug with relatively mild side effects. Many people use marijuana because they have made an informed decision that it is good for them, especially Americans suffering from a variety of serious ailments. Marijuana provides relief from pain, nausea, spasticity, and other symptoms for many individuals who have not been treated successfully with conventional medications. Many American adults prefer marijuana to the use of alcohol as a mild and moderate way to relax. Americans use marijuana because they choose to, and one of the reasons for that choice is their personal observation that the drug has a relatively low dependence liability and easy-to-manage side effects. Most marijuana users develop tolerance to many of marijuana’s side effects, and those who do not, choose to stop using the drug. Marijuana use is the result of informed consent in which individuals have decided that the benefits of use outweigh the risks, especially since, for most Americans, the greatest risk of using marijuana is the relatively low risk of arrest.

1. Marijuana users are determined to stand up to the injustice of marijuana probation and accomplish legalization, no matter how long or what it takes to succeed. Despite the threat of arrests and a variety of other punishments and sanctions marijuana users have persisted in their support for legalization for over a generation. They refuse to give up their long quest for justice because they believe in the fundamental values of American society. Prohibition has failed to silence marijuana users despite its best attempts over the last generation. The issue of marijuana’s legalization is a persistent issue that, like marijuana, will simply not go away. Marijuana will be legalized because marijuana users will continue to fight for it until they succeed.

Source.

July 8, 2009 – Like many medical marijuana users, Kristin Redeen needed additional prescription medications for her severe chronic pain. For seven years she had been treated at a private pain clinic in the Central Valley, painmanagementwhere a doctor maintained her on Percocet, a semi-synthetic opioid. One day Kristin was unexpectedly asked to submit a urine sample.

“They already knew about my medical marijuana use,” says Kristin, who contacted California NORML. “I didn’t think I was doing anything wrong.”

When the test came back, Kristin was informed that the clinic would no longer renew her prescription because she had tested positive for an illegal controlled substance. Her doctor at the clinic cited legal concerns, claiming –falsely– that DEA regulations forbid giving prescription narcotics to users of marijuana or other illegal drugs.

Kristin was cut off from her Percocet and began suffering seizures. She finally found a physician who was willing to prescribe her another opioid, Vicodin, but only at low doses insufficient to relieve her constant pain.

Kristin is one of a growing number of medical marijuana patients discriminated against by pain clinics. “I must have heard of 25 cases this year,” says Doug Hiatt, an attorney in Washington state. “It’s Jim Crow medicine.”

NORML has received a surge of complaints within the last six months. Many medical marijuana users report that they can’t find a clinic willing to take them on. Others, like Kristin, have been abandoned by clinics that suddenly adopted aggressive drug-screening policies.

Clinics say they are legally compelled to drug-test chronic pain patients so as to avoid liability for overdoses and diversion of prescription drugs, particularly opioids such as oxycontin –which have nothing to do with cannabis.

Chronic pain patients have good reason to object to being denied medical access to cannabis. Chronic pain is the leading indication for medical cannabis use, accounting for 90% of the patients in Oregon’s medical marijuana program. More than 60 studies have shown cannabinoids to be effective in pain relief, according to a compilation by the International Association of Cannabis Medicine which includes four controlled studies of smoked marijuana by California’s Center for Medicinal Cannabis Research.

Studies indicate that cannabis interacts synergistically with opioids in such a way as to improve pain relief [1, 2]. California medical cannabis specialists consistently report that patients are able to reduce use of opioids –typically by 50%– when they add cannabis to their regimen. Cannabis can therefore be seen as a gateway drug leading away from opioid addiction. Nevertheless, patients are being pressured to stop using cannabis if they want to get prescription opioids.

To their dismay, patients have to pay for the drug tests at their own (or their insurers’) expense. Carol, a chronic pain patient who had been treated for seven years by the same clinic without any testing, reports that she was billed $325 for a urine screen. The balance of the bill, which totaled $1,601, was paid by her insurer.

Carol says her doctor told her that “the DEA requires him to drug test all his clients, that he has no choice, it is the law.”

In fact, there is no law requiring clinics to drug screen patients for marijuana. “It’s BS,” says Hiatt. Not a single case is known in which pain doctors have been sued or prosecuted for allowing medical marijuana use along with opiates.

Prosecutors have argued that marijuana might be obtained on the illicit market in trade for prescription drugs, though such a scenario seems implausible in medical cannabis states. “It’s unwarranted paranoia,” says Gregory Carter, MD, one of the few practicing pain experts who recommend marijuana in Washington.

Given that cannabis is notably less toxic and addictive than other prescription narcotics, it seems highly ironic that pain clinics are discouraging its use. The prejudice against marijuana has nothing to do with medical science, but rather with political and legal pressures to crack down on prescription drug use. Non-medical use of prescription drugs has recently emerged as the nation’s number-one drug problem du jour.

A new government report, ominously entitled the “National Prescription Drug Threat Assessment,” reported 8,500 deaths in 2005 from prescription pain relievers (mainly opioids), more than double the 2001 total. “Diversion and abuse of prescription drugs are a threat to our public health and safety – similar to the threat posed by illicit drugs such as heroin and cocaine,” warned Drug Czar Gil Kerlikowske.

The Pain Specialists’ Meeting

The 2009 American Pain Society Convention in San Diego included a panel on “Cannabinoids in Pain Management,” chaired by Dr. Mark Ware of McGill University. Dr. Andrea Hohmann, an expert on stress-level analgesia from the University of Georgia, presented evidence from rodent studies which showed that cannabinoids suppress nociceptive processing through both the CB1 and CB2 receptors, and that endocannabinoids, including 2-AG and anandamide, help suppress pain.

Donald Abrams, MD, of the University of California at San Francisco, discussed his studies showing that inhaled marijuana significantly reduced neuropathic pain experienced by HIV patients. Cannabinoids and opioids interact synergistically on separate but parallel pain receptors, Abrams said. He is conducting another study on combined use of cannabinoids and opioids, preliminary results of which appear promising.

Dr. Ware discussed studies involving the variety of cannabinoid medicines available in Canada, which include dronabinol, Sativex, Nabilone, and herbal THC. All of them have demonstrated efficacy in pain relief. Cannabis is now recognized as a “third line” agent for neuropathic pain in Canada. Noting that that its adverse effects are mild to moderate, Ware concluded that “cannabinoid analgesia is the real thing.”

During the question session, your correspondent asked why it was that, in light of evidence that cannabis was so useful in pain therapy, there appeared to be an upsurge in drug testing to prevent its use. The panelists could offer no explanation.

We moved on to the exhibition hall, where drug testing companies were conspicuously displaying their wares. Their exhibits showed how well their products could monitor usage of opiates. The exhibitors seemed surprised when we told them that their products were being used against medical marijuana.

One of the more sophisticated exhibitors was Ameritox, which boasted panels for distinguishing a dozen different opioids plus numerous sedatives, tricyclic anti-depressants, barbiturates, and stimulants as well as “drugs of abuse,” among them marijuana. Their saleswoman seemed surprised to hear that the Ameritox test was being used to screen out medical marijuana patients. She said that clinics could easily order the screens without the marijuana if they wanted. Another company boasted how their test could be administered at the doctor’s office, thereby allowing the doctor rather than the lab to collect the bill.

Finally, we spoke to a legal expert on pain medication, Ms. Jennifer Bolen, a former prosecutor turned defense attorney, who has a useful website devoted to the subject: www.legalsideofpain.com.

Ms Bolen pointed to three recent developments that have increased the pressure to conduct drug screening of pain patients. First, pain doctors have suffered a string of stinging legal judgments for over-prescribing opioids to patients who subsequently overdosed. One notable example involved Dr. Thomas Merrill of Florida, whose life sentence was sustained by the Eleventh Circuit Court of Appeals last year.

This February, a prestigious panel of the American Pain Society issued “New Guidelines for Prescribing Opioid Pain Drugs” which counsels that “diligent monitoring of patients is essential. “ The report specifically recommends periodic drug screens for chronic opioid patients at risk for aberrant drug behavior, though it doesn’t mention cannabis.

Lastly, under legislation that took effect this year, the FDA has new authority to require pharmaceutical companies to implement “risk management” programs to prevent consumer drug misuse.

Medical cannabis patients have no easy remedy to the current drug testing onslaught. In the absence of dire bodily harm, malpractice suits are of no avail. In general, pain clinics have no legal obligation to treat anyone. They commonly require patients to sign contracts allowing them to conduct drug screening at will. Nonetheless, patients may have good grounds to complain to their state medical boards. This is particularly the case where they have been abandoned by their doctors after being made dependent on prescription narcotics.

The ultimate recourse is to educate doctors, many of whom remain woefully ignorant of the literature on medical marijuana and chronic pain. At the APS convention we encountered a distinguished pain specialist from San Diego, who joked about having enjoyed the marijuana muchies with his son, but averred that he wouldn’t let his patients use it, on the grounds that it wouldn’t be useful, and anyway smoked medicine is bad for the lungs. Like most convention attendees, he had missed the panel on medical cannabis, where Dr. Abrams had discussed the use of smokeless vaporizers.

Still, good physicians should be open to persuasion from patients. Cynthia, a severe chronic pain patient. had frequented the same clinic for 10 years when she was confronted with a surprise urine test. In addition to prescription opiates, she had been using medical marijuana, though her recommendation was four years out of date. The test cost her $100 and her insurer $500 more.

On finding her positive for marijuana, her doctor informed her that she would have to reduce her cannabinoid level to zero. After a heart-to-heart talk, in which she explained to him how she had been able to reduce her opiate use to minimal levels thanks to medical cannabis, her doctor relented. “I feel really lucky,’ says Cynthia, “You have to feel out the doctor. We have a special relationship. I don’t think he plans to do this with all his patients.”

REFERENCES

[1] Lynch and Clark, “Cannabis reduces opioid dose in the treatment of chronic non-cancer pain,” Journal Pain Symptom Management, (2003) 25(6) 496-8.

[2[ Narang et al., 2008 Efficacy of dronabinol as an adjuvant treatment for chronic pain patients on opioid therapy, J Pain. Mar;9(3):254-64.

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