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Cannabis Research

Here is some research regarding cannabis.

Aggarwal, S. K., G. T. Carter, M. D. Sullivan, C. ZumBrunnen, R. Morrill and J. D. Mayer (2009). “Medicinal use of cannabis in the United States: historical perspectives, current trends, and future directions.” J Opioid Manag 5(3): 153-168. (ISSN)1551-7489 (Print) 1551-7489 (Linking)

Cannabis (marijuana) has been used for medicinal purposes for millennia, said to be first noted by the Chinese in c. 2737 BCE. Medicinal cannabis arrived in the United States much later, burdened with a remarkably checkered, yet colorful, history. Despite early robust use, after the advent of opioids and aspirin, medicinal cannabis use faded. Cannabis was criminalized in the United States in 1937, against the advice of the American Medical Association submitted on record to Congress. The past few decades have seen renewed interest in medicinal cannabis, with the National Institutes of Health, the Institute of Medicine, and the American College of Physicians, all issuing statements of support for further research and development. The recently discovered endocannabinoid system has greatly increased our understanding of the actions of exogenous cannabis. Endocannabinoids appear to control pain, muscle tone, mood state, appetite, and inflammation, among other effects. Cannabis contains more than 100 different cannabinoids and has the capacity for analgesia through neuromodulation in ascending and descending pain pathways, neuroprotection, and anti-inflammatory mechanisms. This article reviews the current and emerging research on the physiological mechanisms of cannabinoids and their applications in managing chronic pain, muscle spasticity, cachexia, and other debilitating problems.

Aggarwal, S. K., G. T. Carter, M. D. Sullivan, C. ZumBrunnen, R. Morrill and J. D. Mayer (2009). “Medicinal use of cannabis in the United States: historical perspectives, current trends, and future directions.” J Opioid Manag 5(3): 153-168. (ISSN)1551-7489 (Print)

1551-7489 (Linking)

Cannabis (marijuana) has been used for medicinal purposes for millennia, said to be first noted by the Chinese in c. 2737 BCE. Medicinal cannabis arrived in the United States much later, burdened with a remarkably checkered, yet colorful, history. Despite early robust use, after the advent of opioids and aspirin, medicinal cannabis use faded. Cannabis was criminalized in the United States in 1937, against the advice of the American Medical Association submitted on record to Congress. The past few decades have seen renewed interest in medicinal cannabis, with the National Institutes of Health, the Institute of Medicine, and the American College of Physicians, all issuing statements of support for further research and development. The recently discovered endocannabinoid system has greatly increased our understanding of the actions of exogenous cannabis. Endocannabinoids appear to control pain, muscle tone, mood state, appetite, and inflammation, among other effects. Cannabis contains more than 100 different cannabinoids and has the capacity for analgesia through neuromodulation in ascending and descending pain pathways, neuroprotection, and anti-inflammatory mechanisms. This article reviews the current and emerging research on the physiological mechanisms of cannabinoids and their applications in managing chronic pain, muscle spasticity, cachexia, and other debilitating problems.

 

Amtmann, D., P. Weydt, K. L. Johnson, M. P. Jensen and G. T. Carter (2004). “Survey of cannabis use in patients with amyotrophic lateral sclerosis.” Am J Hosp Palliat Care 21(2): 95-104. (ISSN)1049-9091 (Print) 1049-9091 (Linking)

Cannabis (marijuana) has been proposed as treatment for a widening spectrum of medical conditions and has many properties that may be applicable to the management of amyotrophic lateral sclerosis (ALS). This study is the first, anonymous survey of persons with ALS regarding the use of cannabis. There were 131 respondents, 13 of whom reported using cannabis in the last 12 months. Although the small number of people with ALS that reported using cannabis limits the interpretation of the survey findings, the results indicate that cannabis may be moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling. Cannabis was reported ineffective in reducing difficulties with speech and swallowing, and sexual dysfunction. The longest relief was reported for depression (approximately two to three hours).

 

Ben Amar, M. (2006). “Cannabinoids in medicine: A review of their therapeutic potential.” J Ethnopharmacol 105(1-2): 1-25. (ISSN)0378-8741 (Print)

In order to assess the current knowledge on the therapeutic potential of cannabinoids, a meta-analysis was performed through Medline and PubMed up to July 1, 2005. The key words used were cannabis, marijuana, marihuana, hashish, hashich, haschich, cannabinoids, tetrahydrocannabinol, THC, dronabinol, nabilone, levonantradol, randomised, randomized, double-blind, simple blind, placebo-controlled, and human. The research also included the reports and reviews published in English, French and Spanish. For the final selection, only properly controlled clinical trials were retained, thus open-label studies were excluded. Seventy-two controlled studies evaluating the therapeutic effects of cannabinoids were identified. For each clinical trial, the country where the project was held, the number of patients assessed, the type of study and comparisons done, the products and the dosages used, their efficacy and their adverse effects are described. Cannabinoids present an interesting therapeutic potential as antiemetics, appetite stimulants in debilitating diseases (cancer and AIDS), analgesics, and in the treatment of multiple sclerosis, spinal cord injuries, Tourette’s syndrome, epilepsy and glaucoma.

 

Bogdanoski, T. (2010). “Accommodating the medical use of marijuana: surveying the differing legal approaches in Australia, the United States and Canada.” J Law Med 17(4): 508-531. (ISSN)1320-159X (Print) 1320-159X (Linking)

While the scientific and medical communities continue to be divided on the therapeutic benefits and risks of cannabis use, anecdotal evidence from medical users themselves suggests that using cannabis is indeed improving their quality of life by alleviating their pain and discomfort. Notwithstanding the benefits anecdotally claimed by these medical users and the existence of some scientific studies confirming their claims, criminal drug laws in all Australian and most United States jurisdictions continue to prohibit the possession, cultivation and supply of cannabis even for medical purposes. However, in contrast to Australia and most parts of the United States, the medical use of cannabis has been legal in Canada for about a decade. This article reviews these differing legal and regulatory approaches to accommodating the medical use of cannabis (namely, marijuana) as well as some of the challenges involved in legalising it for medical purposes.

Bonfa, L., R. C. Vinagre and N. V. de Figueiredo (2008). “Cannabinoids in chronic pain and palliative care.” Rev Bras Anestesiol 58(3): 267-279. (ISSN)0034-7094 (Print) 0034-7094 (Linking)

BACKGROUND AND OBJECTIVES: Several studies have focused on Cannabis sativa (Cs) due to its analgesic potential and its ability to alleviate symptoms of disorders of the central nervous system. However, since marijuana, one of its popular names, is the most common illicit drug throughout the world, it breeds prejudice both among lay people and health care professionals. The objective of this study was to determine the current level of knowledge about this drug and the perspectives for its use, to better understand its actions and effects, both in experimental studies and clinical use, in patients with degenerative neurological disorders or in those who do not have the possibility of cure and are being followed by palliative care programs. CONTENTS: The therapeutic use of Cannabis sativa is not recent. The present study presents the historical background and pharmacology of Cs, the development of its therapeutic use through synthetic cannabinoids, the current scientific knowledge, and its organic and psychological consequences, demonstrating the options for its clinical use and future perspectives. CONCLUSIONS: Pure delta-9-tetrahydrocannabinol (Delta9-THC) and its analogues have clinical applicability, being beneficial in selected individuals. The development of pure synthetic substances, in an attempt to attenuate undesirable psychoactive effects, indicates that perspectives for its use in the future are favorable. More detailed studies should be undertaken. Ample debates will be necessary to create standards for its formulation and clinical availability, since it is a substance that generates prejudice, due to its illegal commercialization and use, and also because its use has been attributed to mysticism.

Bostwick, J. M. (2012). “Blurred boundaries: the therapeutics and politics of medical marijuana.” Mayo Clin Proc 87(2): 172-186. (ISSN)1942-5546 (Electronic) 0025-6196 (Linking)

For 5 millennia, Cannabis sativa has been used throughout the world medically, recreationally, and spiritually. From the mid-19th century to the 1930s, American physicians prescribed it for a plethora of indications, until the federal government started imposing restrictions on its use, culminating in 1970 with the US Congress classifying it as a Schedule I substance, illegal, and without medical value. Simultaneous with this prohibition, marijuana became the United States’ most widely used illicit recreational drug, a substance generally regarded as pleasurable and relaxing without the addictive dangers of opioids or stimulants. Meanwhile, cannabis never lost its cachet in alternative medicine circles, going mainstream in 1995 when California became the first of 16 states to date to legalize its medical use, despite the federal ban. Little about cannabis is straightforward. Its main active ingredient, delta-9-tetrahydrocannabinol, was not isolated until 1964, and not until the 1990s were the far-reaching modulatory activities of the endocannabinoid system in the human body appreciated. This system’s elucidation raises the possibility of many promising pharmaceutical applications, even as draconian federal restrictions that hamstring research show no signs of softening. Recreational use continues unabated, despite growing evidence of marijuana’s addictive potential, particularly in the young, and its propensity for inducing and exacerbating psychotic illness in the susceptible. Public approval drives medical marijuana legalization efforts without the scientific data normally required to justify a new medication’s introduction. This article explores each of these controversies, with the intent of educating physicians to decide for themselves whether marijuana is panacea, scourge, or both. PubMed searches were conducted using the following keywords: medical marijuana, medical cannabis, endocannabinoid system, CB1 receptors, CB2 receptors, THC, cannabidiol, nabilone, dronabinol, nabiximols, rimonabant, marijuana legislation, marijuana abuse, marijuana dependence, and marijuana and schizophrenia. Bibliographies were hand searched for additional references relevant to clarifying the relationships between medical and recreational marijuana use and abuse.

Cohen, P. J. (2009). “Medical marijuana: the conflict between scientific evidence and political ideology. Part one of two.” J Pain Palliat Care Pharmacother 23(1): 4-25. (ISSN)1536-0539 (Electronic) 1536-0288 (Linking)

Whether “medical marijuana” (Cannabis sativa used to treat a wide variety of pathologic states) should be accorded the status of a legitimate pharmaceutical agent has long been a contentious issue. Is it a truly effective drug that is arbitrarily stigmatized by many and criminalized by the federal government? Or is it without any medical utility, its advocates hiding behind a screen of misplaced (or deliberately misleading) compassion for the ill? Should Congress repeal its declaration that smoked marijuana is without “current medical benefit”? Should cannabis be approved for medical use by a vote of the people as already has been done in 13 states? Or should medical marijuana be scientifically evaluated for safety and efficacy as any other new investigational drug? How do the competing–and sometimes antagonistic–roles of science, politics and prejudice affect society’s attempts to answer this question? This article examines the legal, political, policy, and ethical problems raised by the recognition of medical marijuana by over one-fourth of our states although its use remains illegal under federal law. Although draconian punishment can be imposed for the “recreational” use of marijuana, I will not address the contentious question of whether to legalize or decriminalize the use of marijuana solely for its psychotropic effects, a fascinating and important area of law and policy that is outside the scope of this paper. Instead, the specific focus of this article will be on the conflict between the development of policies based on evidence obtained through the use of scientific methods and those grounded on ideological and political considerations that have repeatedly entered the longstanding debate regarding the legal status of medical marijuana. I will address a basic question: Should the approval of medical marijuana be governed by the same statute that applies to all other drugs or pharmaceutical agents, the Food, Drug, and Cosmetic Act (FD&C Act), after the appropriate regulatory agency, the Food and Drug Administration (FDA), has evaluated its safety and efficacy? If not, should medical marijuana be exempted from scientific review and, instead, be evaluated by the Congress, state legislatures, or popular vote? I will argue that advocacy is a poor substitute for dispassionate analysis, and that popular votes should not be allowed to trump scientific evidence in deciding whether or not marijuana is an appropriate pharmaceutical agent to use in modern medical practice.

Cohen, P. J. (2009). “Medical marijuana: the conflict between scientific evidence and political ideology. Part two of two.” J Pain Palliat Care Pharmacother 23(2): 120-140. (ISSN)1536-0539 (Electronic) 1536-0288 (Linking)

In Part I of this article, I examined the role of the Food and Drug Administration (FDA) in drug approval and then detailed the known risks of medical marijuana (any form of Cannabis sativa used–usually by smoking–to treat a wide variety of pathologic states and diseases). Part II of the article will begin by reviewing the benefits of Cannabis sativa as documented by well designed scientific studies that have been published in the peer-reviewed literature. I will then propose that ability of scientists to conduct impartial studies designed to answer the question of marijuana’s role in medical therapy has been greatly hampered by political considerations. I will posit that in spite of the considerable efforts of policymakers, it is becoming apparent that marijuana’s benefits should be weighed against its well-described risks. I will conclude that political advocacy is a poor substitute for dispassionate analysis and that neither popular votes nor congressional “findings” should be permitted to trump scientific evidence in deciding whether or not marijuana is an appropriate pharmaceutical agent to use in modern medical practice. Whether or not marijuana is accepted as a legitimate medical therapy should remain in the hands of the usual drug-approval process and that the statutory role of the Food and Drug Administration should be dispositive.

 

Crean, R. D., N. A. Crane and B. J. Mason (2011). “An evidence based review of acute and long-term effects of cannabis use on executive cognitive functions.” J Addict Med 5(1): 1-8. (ISSN)1932-0620 (Print) 1932-0620 (Linking)

Cannabis use has been shown to impair cognitive functions on a number of levels-from basic motor coordination to more complex executive function tasks, such as the ability to plan, organize, solve problems, make decisions, remember, and control emotions and behavior. These deficits differ in severity depending on the quantity, recency, age of onset and duration of marijuana use. Understanding how cannabis use impairs executive function is important. Individuals with cannabis-related impairment in executive functions have been found to have trouble learning and applying the skills required for successful recovery, putting them at increased risk for relapse to cannabis use. Here we review the research on the acute, residual, and long-term effects of cannabis use on executive functions, and discuss the implications for treatment.

 

Curran, H. V., C. Brignell, S. Fletcher, P. Middleton and J. Henry (2002). “Cognitive and subjective dose-response effects of acute oral Delta 9-tetrahydrocannabinol (THC) in infrequent cannabis users.” Psychopharmacology (Berl) 164(1): 61-70. (ISSN)0033-3158 (Print) 0033-3158 (Linking)

RATIONALE: Although some aspects of memory functions are known to be acutely impaired by delta(9)-tetrahydrocannabinol (delta(9)-THC; the main active constituent of marijuana), effects on other aspects of memory are not known and the time course of functional impairments is unclear. OBJECTIVE: The present study aimed to detail the acute and residual cognitive effects of delta(9)-THC in infrequent cannabis users. METHODS: A balanced, double-blind cross-over design was used to compare the effects of 7.5 mg and 15 mg delta(9)-THC with matched placebo in 15 male volunteers. Participants were assessed pre and 1, 2, 4, 6, 8, 24 and 48 h post-drug. RESULTS: Delta(9)-THC 15 mg impaired performance on two explicit memory tasks at the time of peak plasma concentration (2 h post-drug). At the same time point, performance on an implicit memory task was preserved intact. The higher dose of delta(9)-THC resulted in no learning whatsoever occurring over a three-trial selective reminding task at 2 h. Working memory was generally unaffected by delta(9)-THC. In several tasks, delta(9)-THC increased both speed and error rates, reflecting “riskier” speed-accuracy trade-offs. Subjective effects were also most marked at 2 h but often persisted longer, with participants rating themselves as “stoned” for 8 h. Participants experienced a strong drug effect, liked this effect and, until 4 h, wanted more oral delta(9)-THC. No effects of delta(9)-THC were found 24 or 48 h following ingestion indicating that the residual effects of oral delta(9)-THC are minimal. CONCLUSIONS: These data demonstrate that oral delta(9)-THC impairs episodic memory and learning in a dose-dependent manner whilst sparing perceptual priming and working memory.

Evins, A. E., A. I. Green, J. M. Kane and R. M. Murray, Sr. (2013). “Does using marijuana increase the risk for developing schizophrenia?” J Clin Psychiatry 74(4): e08. (ISSN)1555-2101 (Electronic) 0160-6689 (Linking)

As more US states and other countries consider legalizing marijuana, clinicians need to know the possible effects of this drug. Research has shown a connection between marijuana use and an increased risk for schizophrenia in young people who are vulnerable to developing psychosis. An international panel of experts addresses topics such as risk factors for schizophrenia, the potency and effects of cannabis use on adolescents, the effects of concurrent drug use with cannabis on schizophrenia risk, and current attitudes toward marijuana.

Galli, J. A., R. A. Sawaya and F. K. Friedenberg (2011). “Cannabinoid hyperemesis syndrome.” Curr Drug Abuse Rev 4(4): 241-249. (ISSN)1874-4745 (Electronic) 1874-4737 (Linking)

Coinciding with the increasing rates of cannabis abuse has been the recognition of a new clinical condition known as Cannabinoid Hyperemesis Syndrome. Cannabinoid Hyperemesis Syndrome is characterized by chronic cannabis use, cyclic episodes of nausea and vomiting, and frequent hot bathing. Cannabinoid Hyperemesis Syndrome occurs by an unknown mechanism. Despite the well-established anti-emetic properties of marijuana, there is increasing evidence of its paradoxical effects on the gastrointestinal tract and CNS. Tetrahydrocannabinol, cannabidiol, and cannabigerol are three cannabinoids found in the cannabis plant with opposing effects on the emesis response. The clinical course of Cannabinoid Hyperemesis Syndrome may be divided into three phases: prodromal, hyperemetic, and recovery phase. The hyperemetic phase usually ceases within 48 hours, and treatment involves supportive therapy with fluid resuscitation and anti-emetic medications. Patients often demonstrate the learned behavior of frequent hot bathing, which produces temporary cessation of nausea, vomiting, and abdominal pain. The broad differential diagnosis of nausea and vomiting often leads to delay in the diagnosis of Cannabinoid Hyperemesis Syndrome. Cyclic Vomiting Syndrome shares several similarities with CHS and the two conditions are often confused. Knowledge of the epidemiology, pathophysiology, and natural course of Cannabinoid Hyperemesis Syndrome is limited and requires further investigation.

Gilman, J. M., J. K. Kuster, S. Lee, M. J. Lee, B. W. Kim, N. Makris, A. van der Kouwe, A. J. Blood and H. C. Breiter (2014). “Cannabis use is quantitatively associated with nucleus accumbens and amygdala abnormalities in young adult recreational users.” J Neurosci 34(16): 5529-5538. (ISSN)1529-2401 (Electronic) 0270-6474 (Linking)

Marijuana is the most commonly used illicit drug in the United States, but little is known about its effects on the human brain, particularly on reward/aversion regions implicated in addiction, such as the nucleus accumbens and amygdala. Animal studies show structural changes in brain regions such as the nucleus accumbens after exposure to Delta9-tetrahydrocannabinol, but less is known about cannabis use and brain morphometry in these regions in humans. We collected high-resolution MRI scans on young adult recreational marijuana users and nonusing controls and conducted three independent analyses of morphometry in these structures: (1) gray matter density using voxel-based morphometry, (2) volume (total brain and regional volumes), and (3) shape (surface morphometry). Gray matter density analyses revealed greater gray matter density in marijuana users than in control participants in the left nucleus accumbens extending to subcallosal cortex, hypothalamus, sublenticular extended amygdala, and left amygdala, even after controlling for age, sex, alcohol use, and cigarette smoking. Trend-level effects were observed for a volume increase in the left nucleus accumbens only. Significant shape differences were detected in the left nucleus accumbens and right amygdala. The left nucleus accumbens showed salient exposure-dependent alterations across all three measures and an altered multimodal relationship across measures in the marijuana group. These data suggest that marijuana exposure, even in young recreational users, is associated with exposure-dependent alterations of the neural matrix of core reward structures and is consistent with animal studies of changes in dendritic arborization.

 

Hall, W. and L. Degenhardt (2009). “Adverse health effects of non-medical cannabis use.” Lancet 374(9698): 1383-1391. (ISSN)1474-547X (Electronic) 0140-6736 (Linking)

For over two decades, cannabis, commonly known as marijuana, has been the most widely used illicit drug by young people in high-income countries, and has recently become popular on a global scale. Epidemiological research during the past 10 years suggests that regular use of cannabis during adolescence and into adulthood can have adverse effects. Epidemiological, clinical, and laboratory studies have established an association between cannabis use and adverse outcomes. We focus on adverse health effects of greatest potential public health interest-that is, those that are most likely to occur and to affect a large number of cannabis users. The most probable adverse effects include a dependence syndrome, increased risk of motor vehicle crashes, impaired respiratory function, cardiovascular disease, and adverse effects of regular use on adolescent psychosocial development and mental health.

Hegde, M., C. Santos-Sanchez, C. P. Hess, A. A. Kabir and P. A. Garcia (2012). “Seizure exacerbation in two patients with focal epilepsy following marijuana cessation.” Epilepsy Behav 25(4): 563-566. (ISSN)1525-5069 (Electronic) 1525-5050 (Linking)

While animal models of epilepsy suggest that exogenous cannabinoids may have anticonvulsant properties, scant evidence exists for these compounds’ efficacy in humans. Here, we report on two patients whose focal epilepsy was nearly controlled through regular outpatient marijuana use. Both stopped marijuana upon admission to our epilepsy monitoring unit (EMU) and developed a dramatic increase in seizure frequency documented by video-EEG telemetry. These seizures occurred in the absence of other provocative procedures, including changes to anticonvulsant medications. We review these cases and discuss mechanisms for the potentially anticonvulsant properties of cannabis, based on a review of the literature.

 

Kogan, N. M. and R. Mechoulam (2007). “Cannabinoids in health and disease.” Dialogues Clin Neurosci 9(4): 413-430. (ISSN)1294-8322 (Print) 1294-8322 (Linking)

Cannabis sativa L. preparations have been used in medicine for millenia. However, concern over the dangers of abuse led to the banning of the medicinal use of marijuana in most countries in the 1930s. Only recently, marijuana and individual natural and synthetic cannabinoid receptor agonists and antagonists, as well as chemically related compounds, whose mechanism of action is still obscure, have come back to being considered of therapeutic value. However, their use is highly restricted. Despite the mild addiction to cannabis and the possible enhancement of addiction to other substances of abuse, when combined with cannabis, the therapeutic value of cannabinoids is too high to be put aside. Numerous diseases, such as anorexia, emesis, pain, inflammation, multiple sclerosis, neurodegenerative disorders (Parkinson’s disease, Huntington’s disease, Tourette’s syndrome, Alzheimer’s disease), epilepsy, glaucoma, osteoporosis, schizophrenia, cardiovascular disorders, cancer, obesity, and metabolic syndrome-related disorders, to name just a few, are being treated or have the potential to be treated by cannabinoid agonists/antagonists/cannabinoid-related compounds. In view of the very low toxicity and the generally benign side effects of this group of compounds, neglecting or denying their clinical potential is unacceptable–instead, we need to work on the development of more selective cannabinoid receptor agonists/antagonists and related compounds, as well as on novel drugs of this family with better selectivity, distribution patterns, and pharmacokinetics, and–in cases where it is impossible to separate the desired clinical action and the psychoactivity–just to monitor these side effects carefully.

 

Leung, L. (2011). “Cannabis and its derivatives: review of medical use.” J Am Board Fam Med 24(4): 452-462. (ISSN)1557-2625 (Print) 1557-2625 (Linking)

BACKGROUND: Use of cannabis is often an under-reported activity in our society. Despite legal restriction, cannabis is often used to relieve chronic and neuropathic pain, and it carries psychotropic and physical adverse effects with a propensity for addiction. This article aims to update the current knowledge and evidence of using cannabis and its derivatives with a view to the sociolegal context and perspectives for future research.

METHODS: Cannabis use can be traced back to ancient cultures and still continues in our present society despite legal curtailment. The active ingredient, Delta9-tetrahydrocannabinol, accounts for both the physical and psychotropic effects of cannabis. Though clinical trials demonstrate benefits in alleviating chronic and neuropathic pain, there is also significant potential physical and psychotropic side-effects of cannabis. Recent laboratory data highlight synergistic interactions between cannabinoid and opioid receptors, with potential reduction of drug-seeking behavior and opiate sparing effects. Legal rulings also have changed in certain American states, which may lead to wider use of cannabis among eligible persons.

CONCLUSIONS: Family physicians need to be cognizant of such changing landscapes with a practical knowledge on the pros and cons of medical marijuana, the legal implications of its use, and possible developments in the future.

 

 

Lucas, P. G. (2008). “Regulating compassion: an overview of Canada’s federal medical cannabis policy and practice.” Harm Reduct J 5: 5. (ISSN)1477-7517 (Electronic) 1477-7517 (Linking)

BACKGROUND: In response to a number of court challenges brought forth by Canadian patients who demonstrated that they benefited from the use of medicinal cannabis but remained vulnerable to arrest and persecution as a result of its status as a controlled substance, in 1999 Canada became the second nation in the world to initiate a centralized medicinal cannabis program. Over its six years of existence, this controversial program has been found unconstitutional by a number of courts, and has faced criticism from the medical establishment, law enforcement, as well as the patient/participants themselves. METHODS: This critical policy analysis is an evidence-based review of court decisions, government records, relevant studies and Access to Information Act data related to the three main facets of Health Canada’s medicinal cannabis policy–the Marihuana Medical Access Division (MMAD); the Canadians Institute of Health Research Medical Marijuana Research Program; and the federal cannabis production and distribution program. This analysis also examines Canada’s network of unregulated community-based dispensaries.

RESULTS: There is a growing body of evidence that Health Canada’s program is not meeting the needs of the nation’s medical cannabis patient community and that the policies of the Marihuana Medical Access Division may be significantly limiting the potential individual and public health benefits achievable though the therapeutic use of cannabis. Canada’s community-based dispensaries supply medical cannabis to a far greater number of patients than the MMAD, but their work is currently unregulated by any level of government, leaving these organizations and their clients vulnerable to arrest and prosecution.

CONCLUSION: Any future success will depend on the government’s ability to better assess and address the needs and legitimate concerns of end-users of this program, to promote and fund an expanded clinical research agenda, and to work in cooperation with community-based medical cannabis dispensaries in order to address the ongoing issue of safe and timely access to this herbal medicine.

 

Manzanares, J., L. Uriguen, G. Rubio and T. Palomo (2004). “Role of endocannabinoid system in mental diseases.” Neurotox Res 6(3): 213-224. (ISSN)1029-8428 (Print) 1029-8428 (Linking)

In the last decade, a large number of studies using Delta9-tetrahydrocannabinol (THC), the main active principle derivative of the marijuana plant, or cannabinoid synthetic derivatives have substantially contributed to advance the understanding of the pharmacology and neurobiological mechanisms produced by cannabinoid receptor activation. Cannabis has been historically used to relieve some of the symptoms associated with central nervous system disorders. Nowadays, there are anecdotal evidences for the use of cannabis in many patients suffering from multiple sclerosis or chronic pain. Following the historical reports of the use of cannabis for medicinal purposes, recent research has highlighted the potential of cannabinoids to treat a wide variety of clinical disorders. Some of these disorders that are being investigated are pain, motor dysfunctions or psychiatric illness. On the other hand, cannabis abuse has been related to several psychiatric disorders such as dependence, anxiety, depression, cognitive impairment, and psychosis. Considering that cannabis or cannabinoid pharmaceutical preparations may no longer be exclusively recreational drugs but may also present potential therapeutic uses, it has become of great interest to analyze the neurobiological and behavioral consequences of their administration. This review attempts to link current understanding of the basic neurobiology of the endocannabinoid system to novel opportunities for therapeutic intervention and its effects on the central nervous system.

 

Martin-Santos, R., A. B. Fagundo, J. A. Crippa, Z. Atakan, S. Bhattacharyya, P. Allen, P. Fusar-Poli, S. Borgwardt, M. Seal, G. F. Busatto, et al. (2010). “Neuroimaging in cannabis use: a systematic review of the literature.” Psychol Med 40(3): 383-398. (ISSN)1469-8978 (Electronic) 0033-2917 (Linking)

BACKGROUND: We conducted a systematic review to assess the evidence for specific effects of cannabis on brain structure and function. The review focuses on the cognitive changes associated with acute and chronic use of the drug. METHOD: We reviewed literature reporting neuroimaging studies of chronic or acute cannabis use published up until January 2009. The search was conducted using Medline, EMBASE, LILACS and PsycLIT indexing services using the following key words: cannabis, marijuana, delta-9-tetrahydrocannabinol, THC, cannabidiol, CBD, neuroimaging, brain imaging, computerized tomography, CT, magnetic resonance, MRI, single photon emission tomography, SPECT, functional magnetic resonance, fMRI, positron emission tomography, PET, diffusion tensor MRI, DTI-MRI, MRS and spectroscopy. RESULTS: Sixty-six studies were identified, of which 41 met the inclusion criteria. Thirty-three were functional (SPECT/PET/fMRI) and eight structural (volumetric/DTI) imaging studies. The high degree of heterogeneity across studies precluded a meta-analysis. The functional studies suggest that resting global and prefrontal blood flow are lower in cannabis users than in controls. The results from the activation studies using a cognitive task are inconsistent because of the heterogeneity of the methods used. Studies of acute administration of THC or marijuana report increased resting activity and activation of the frontal and anterior cingulate cortex during cognitive tasks. Only three of the structural imaging studies found differences between users and controls. CONCLUSIONS: Functional neuroimaging studies suggest a modulation of global and prefrontal metabolism both during the resting state and after the administration of THC/marijuana cigarettes. Minimal evidence of major effects of cannabis on brain structure has been reported.

 

McCarberg, B. H. and R. L. Barkin (2007). “The future of cannabinoids as analgesic agents: a pharmacologic, pharmacokinetic, and pharmacodynamic overview.” Am J Ther 14(5): 475-483. (ISSN)1075-2765 (Print) 1075-2765 (Linking)

For thousands of years, physicians and their patients employed cannabis as a therapeutic agent. Despite this extensive historical usage, in the Western world, cannabis fell into disfavor among medical professionals because the technology available in the 1800s and early 1900s did not permit reliable, standardized preparations to be developed. However, since the discovery and cloning of cannabinoid receptors (CB1 and CB2) in the 1990s, scientific interest in the area has burgeoned, and the complexities of this fascinating receptor system, and its endogenous ligands, have been actively explored. Recent studies reveal that cannabinoids have a rich pharmacology and may interact with a number of other receptor systems-as well as with other cannabinoids-to produce potential synergies. Cannabinoids-endocannabinoids, phytocannabinoids, and synthetic cannabinoids-affect numerous bodily functions and have indicated efficacy of varying degrees in a number of serious medical conditions. Nevertheless, despite promising preclinical and early clinical data, particularly in the areas of inflammation and nociception, development challenges abound. Tetrahydrocannabinol (THC) and other CB1 receptor agonists can have an undesirable CNS impact, and, in many cases, dose optimization may not be realizable before onset of excessive side effects. In addition, complex botanically derived cannabinoid products must satisfy the demanding criteria of the U.S. Food and Drug Association’s approval process. Recent agency guidance suggests that these obstacles are not insurmountable, although cannabis herbal material (“medical marijuana”) may present fatal uncertainties of quality control and dosage standardization. Therefore, formulation, composition, and delivery system issues will affect the extent to which a particular cannabinoid product may have a desirable risk-benefit profile and acceptable abuse liability potential. Cannabinoid receptor agonists and/or molecules that affect the modulation of endocannabinoid synthesis, metabolism, and transport may, in the future, offer extremely valuable tools for the treatment of a number of currently intractable disorders. Further research is warranted to explore the therapeutic potential of this area.

McGuinness, T. M. (2009). “Update on marijuana.” J Psychosoc Nurs Ment Health Serv 47(10): 19-22. (ISSN)0279-3695 (Print) 0279-3695 (Linking)

Marijuana, the illicit drug most widely used by adolescents, is not a benign substance. Inhalation of marijuana smoke is more harmful than tobacco smoke; cannabis smoke delivers 50% to 70% more carcinogens. Other physiological effects include decreased immune function, higher rates of cardiac arrhythmias, and documented cases of cerebellar infarction. Mood and cognitive effects of marijuana include exacerbation of depression and anxiety (including panic attacks), as well as memory problems that may persist for a month after last use. Cannabis abuse is a risk factor for psychosis in genetically predisposed people and may lead to a worse outcome of schizophrenia. The cumulative respiratory, cardiovascular, metabolic, and mental health risks of marijuana are significant and should be emphasized by nurses who work with adolescents.

 

Nickerson, L. D., C. Ravichandran, L. H. Lundahl, J. Rodolico, S. Dunlap, G. H. Trksak and S. E. Lukas (2011). “Cue reactivity in cannabis-dependent adolescents.” Psychol Addict Behav 25(1): 168-173. (ISSN)1939-1501 (Electronic) 0893-164X (Linking)

The authors measured event-related potentials with a craving manipulation to investigate the neural correlates of drug cue reactivity in 13 adolescents who are cannabis dependent (CD; ages 14-17). The P300 responses to marijuana (MJ) pictures (MJ-P300) and control pictures (C-P300) were assessed after handling neutral objects and again after handling MJ paraphernalia (MJP). Self-reported drug craving and heart rates also were measured. MJ-P300 were larger than C-P300 (p < .001), and both the MJ-P300 and craving increased significantly after handling MJP (p = .002 and p = .003, respectively), with no association between the magnitude of craving and MJ-P300. Heart rates were not affected by handling MJP. The results showed that adolescents who are CD have an attentional bias to MJ stimuli that increases after handling marijuana paraphernalia. Generally, the results are consistent with what has been reported for adult heavy chronic cannabis smokers, although there were some differences that require further investigation.

Rahn, E. J. and A. G. Hohmann (2009). “Cannabinoids as pharmacotherapies for neuropathic pain: from the bench to the bedside.” Neurotherapeutics 6(4): 713-737. (ISSN)1878-7479 (Electronic) 1878-7479 (Linking)

Neuropathic pain is a debilitating form of chronic pain resulting from nerve injury, disease states, or toxic insults. Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics. Cannabinoids, drugs that share the same target as Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need. Here, we review studies evaluating cannabinoids for neuropathic pain management in the clinical and preclinical literature. Neuropathic pain associated with nerve injury, diabetes, chemotherapeutic treatment, human immunodeficiency virus, multiple sclerosis, and herpes zoster infection is considered. In animals, cannabinoids attenuate neuropathic nociception produced by traumatic nerve injury, disease, and toxic insults. Effects of mixed cannabinoid CB(1)/CB(2) agonists, CB(2) selective agonists, and modulators of the endocannabinoid system (i.e., inhibitors of transport or degradation) are compared. Effects of genetic disruption of cannabinoid receptors or enzymes controlling endocannabinoid degradation on neuropathic nociception are described. Specific forms of allodynia and hyperalgesia modulated by cannabinoids are also considered. In humans, effects of smoked marijuana, synthetic Delta(9)-THC analogs (e.g., Marinol, Cesamet) and medicinal cannabis preparations containing both Delta(9)-THC and cannabidiol (e.g., Sativex, Cannador) in neuropathic pain states are reviewed. Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment. Subjective (i.e., rating scales) and objective (i.e., stimulus-evoked) measures of pain and quality of life are considered. Finally, limitations of cannabinoid pharmacotherapies are discussed together with directions for future research.

 

Rahn, E. J. and A. G. Hohmann (2009). “Cannabinoids as pharmacotherapies for neuropathic pain: from the bench to the bedside.” Neurotherapeutics 6(4): 713-737. (ISSN)1878-7479 (Electronic) 1878-7479 (Linking)

Neuropathic pain is a debilitating form of chronic pain resulting from nerve injury, disease states, or toxic insults. Neuropathic pain is often refractory to conventional pharmacotherapies, necessitating validation of novel analgesics. Cannabinoids, drugs that share the same target as Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the psychoactive ingredient in cannabis, have the potential to address this unmet need. Here, we review studies evaluating cannabinoids for neuropathic pain management in the clinical and preclinical literature. Neuropathic pain associated with nerve injury, diabetes, chemotherapeutic treatment, human immunodeficiency virus, multiple sclerosis, and herpes zoster infection is considered. In animals, cannabinoids attenuate neuropathic nociception produced by traumatic nerve injury, disease, and toxic insults. Effects of mixed cannabinoid CB(1)/CB(2) agonists, CB(2) selective agonists, and modulators of the endocannabinoid system (i.e., inhibitors of transport or degradation) are compared. Effects of genetic disruption of cannabinoid receptors or enzymes controlling endocannabinoid degradation on neuropathic nociception are described. Specific forms of allodynia and hyperalgesia modulated by cannabinoids are also considered. In humans, effects of smoked marijuana, synthetic Delta(9)-THC analogs (e.g., Marinol, Cesamet) and medicinal cannabis preparations containing both Delta(9)-THC and cannabidiol (e.g., Sativex, Cannador) in neuropathic pain states are reviewed. Clinical studies largely affirm that neuropathic pain patients derive benefits from cannabinoid treatment. Subjective (i.e., rating scales) and objective (i.e., stimulus-evoked) measures of pain and quality of life are considered. Finally, limitations of cannabinoid pharmacotherapies are discussed together with directions for future research.

Sofuoglu, M., D. E. Sugarman and K. M. Carroll (2010). “Cognitive function as an emerging treatment target for marijuana addiction.” Exp Clin Psychopharmacol 18(2): 109-119. (ISSN)1936-2293 (Electronic) 1064-1297 (Linking)

Cannabis is the most widely used illicit substance in the world, and demand for effective treatment is increasing. However, abstinence rates following behavioral therapies have been modest, and there are no effective pharmacotherapies for the treatment of cannabis addiction. We propose a novel research agenda and a potential treatment strategy, based on observations that both acute and chronic exposure to cannabis are associated with dose-related cognitive impairments, most consistently in attention, working memory, verbal learning, and memory functions. These impairments are not completely reversible upon cessation of marijuana use, and moreover may interfere with the treatment of marijuana addiction. Therefore, targeting cognitive impairment associated with chronic marijuana use may be a promising novel strategy for the treatment of marijuana addiction. Preclinical studies suggest that medications enhancing the cholinergic transmission may attenuate cannabis-induced cognitive impairments, but these cognitive enhancing medications have not been examined in controlled human studies. Preliminary evidence from individuals addicted to other drugs suggests that computerized cognitive rehabilitation may also have utility to improve cognitive function in marijuana users. Future clinical studies optimally designed to measure cognitive function as well as drug use behavior would be needed to test the efficacy of these treatments for marijuana addiction.

 

Ste-Marie, P. A., M. A. Fitzcharles, A. Gamsa, M. A. Ware and Y. Shir (2012). “Association of herbal cannabis use with negative psychosocial parameters in patients with fibromyalgia.” Arthritis Care Res (Hoboken) 64(8): 1202-1208. (ISSN)2151-4658 (Electronic) 2151-464X (Linking)

OBJECTIVE: Patients with chronic pain, including fibromyalgia (FM), may seek treatments outside of mainstream medicine. Medicinal cannabinoids are popularly advocated for pain relief but with limited evidence for efficacy in FM. The extent of use of cannabinoids in FM is unknown. METHODS: We have documented the self-reported prevalence of cannabinoid use in 457 patients with the diagnosis of FM and referred to a tertiary care pain center. We validated the diagnosis of FM and examined the associations of cannabinoid use in these patients. RESULTS: Cannabinoids were being used by 13% of all patients, of whom 80% used herbal cannabis (marijuana), 24% used prescription cannabinoids, and 3% used both herbal cannabis and prescription cannabinoids. One-third of all men used cannabinoids. Current unstable mental illness (36% versus 23%; P = 0.002), opioid drug-seeking behavior (17% versus 4%; P = 0.002), and male sex (26% versus 7%; P = 0.0002) were all associated with herbal cannabis use. There was a trend for cannabinoid users to be unemployed and receiving disability payments. The diagnosis of FM was validated in 302 patients, with 155 assigned another primary diagnosis. When the FM group was analyzed separately, significant associations were lost, but trends remained. CONCLUSION: Cannabinoids were used by 13% of patients referred with a diagnosis of FM. The association of herbal cannabis use with negative psychosocial parameters raises questions regarding the motive for this self-medication practice. Although cannabinoids may offer some therapeutic effect, caution regarding any recommendation should be exercised pending clarification of general health and psychosocial problems, especially for those self-medicating.

 

Taylor, H. G. (1998). “Analysis of the medical use of marijuana and its societal implications.” J Am Pharm Assoc (Wash) 38(2): 220-227. (ISSN)1086-5802 (Print) 1086-5802 (Linking)

OBJECTIVE: To review the pharmacology, therapeutics, adverse effects, and societal implications of the medical use of marijuana. DATA SOURCES: MEDLINE and manual searches of English-language marijuana literature, supplemented with interviews of scientists currently conducting cannabinoid research. Search terms included pain OR palliative care AND cannabis or ALL marijuana; cachexia OR appetite OR appetite stimulants; muscle spasticity OR spasm; immune system and cannabis; nausea and vomiting and cancer and cannabis. MEDLINE search terms: cannabis OR marijuana smoking OR marijuana abuse; all glaucoma; multiple sclerosis AND cannabis OR marijuana smoking OR marijuana abuse. STUDY SELECTION: Studies on pharmacology, risks, and medical potential of marijuana. DATA EXTRACTION: Not applicable. DATA SYNTHESIS: The most prominent effects of marijuana are mediated by receptors in the brain. Acute intoxication is characterized by euphoria, loss of short-term memory, stimulation of the senses, and impaired linear thinking. Depersonalization and panic attacks are adverse effects. Increased heart rate and reddened conjunctivae are common physical effects. Chronic, high doses may cause subtle impairment of cognitive abilities that are appear to be long-term, but of unknown duration. Marijuana may be a risk factor for individuals with underlying mental illness. It causes dependence, but compared with cocaine, alcohol, heroin, and nicotine, marijuana has little addictive power and produces only mild withdrawal symptoms. Marijuana shows clinical promise for glaucoma, nausea and vomiting, analgesia, spasticity, multiple sclerosis, and AIDS wasting syndrome. CONCLUSION: As a recreational drug, marijuana poses dangers, particularly to social and emotional development during adolescence and young adulthood. As a medical drug, marijuana should be available for patients who do not adequately respond to currently available therapies.

Ware, M. A. (2011). “Clearing the smoke around medical marijuana.” Clin Pharmacol Ther 90(6): 769-771. (ISSN)1532-6535 (Electronic) 0009-9236 (Linking)

The hazy world of “medical marijuana” continues to cry out for clear data on which to base medical decision making and rational policy design. In this issue of Clinical Pharmacology & Therapeutics, Abrams and colleagues report that vaporized cannabis does not meaningfully affect opioid plasma levels and may even augment the efficacy of oxycodone and morphine in patients with chronic non-cancer pain. This Commentary considers the implications of this work for clinical practice and further research initiatives.

Wilsey, B., T. Marcotte, A. Tsodikov, J. Millman, H. Bentley, B. Gouaux and S. Fishman (2008). “A randomized, placebo-controlled, crossover trial of cannabis cigarettes in neuropathic pain.” J Pain 9(6): 506-521. (ISSN)1526-5900 (Print)

The Food and Drug Administration (FDA), Substance Abuse and Mental Health Services Administration (SAMHSA), and the National Institute for Drug Abuse (NIDA) report that no sound scientific studies support the medicinal use of cannabis. Despite this lack of scientific validation, many patients routinely use “medical marijuana,” and in many cases this use is for pain related to nerve injury. We conducted a double-blinded, placebo-controlled, crossover study evaluating the analgesic efficacy of smoking cannabis for neuropathic pain. Thirty-eight patients with central and peripheral neuropathic pain underwent a standardized procedure for smoking either high-dose (7%), low-dose (3.5%), or placebo cannabis. In addition to the primary outcome of pain intensity, secondary outcome measures included evoked pain using heat-pain threshold, sensitivity to light touch, psychoactive side effects, and neuropsychological performance. A mixed linear model demonstrated an analgesic response to smoking cannabis. No effect on evoked pain was seen. Psychoactive effects were minimal and well-tolerated, with some acute cognitive effects, particularly with memory, at higher doses. PERSPECTIVE: This study adds to a growing body of evidence that cannabis may be effective at ameliorating neuropathic pain, and may be an alternative for patients who do not respond to, or cannot tolerate, other drugs. However, the use of marijuana as medicine may be limited by its method of administration (smoking) and modest acute cognitive effects, particularly at higher doses.

 

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