What is medical marijuana? A brief history.
The Colorado Constitution provides for access to medical marijuana for Colorado State residents over the age of 18.
Cannabis, also known as marijuana (from the Mexican Spanish marihuana) and by other names,a[›] is a preparation of the Cannabis plant intended for use as a psychoactive drug and as medicine. Chemically, the major psychoactive compound in cannabis is delta-9-tetrahydrocannabinol (?9-THC); it is one of 400 compounds in the plant, including other cannabinoids, such as cannabidiol (CBD), cannabinol (CBN), and tetrahydrocannabivarin (THCV), which can produce sensory effects unlike the psychoactive effects of THC.
Contemporary uses of cannabis are as a recreational drug, as religious or spiritual rites, or as medicine; the earliest recorded uses date from the 3rd millennium BC. In 2004, the United Nations estimated that global consumption of cannabis indicated that approximately 4.0 percent of the adult world population (162 million people) used cannabis annually, and that approximately 0.6 percent (22.5 million) of people used cannabis daily. Since the early 20th century cannabis has been subject to legal restrictions with the possession, use, and sale of cannabis preparations containing psychoactive cannabinoids currently illegal in most countries of the world; the United Nations has said that cannabis is the most used illicit drug in the world.
MEDICAL MARIJUANA & CANNABIS
Cannabis indica fluid extract, American Druggists Syndicate, pre-1937.
Medical cannabis refers to the parts of the herb cannabis used as a physician-recommended form of medicine or herbal therapy, or to synthetic forms of specific cannabinoids such as THC as a physician-recommended form of medicine. The Cannabis plant has a long history of use as medicine, with historical evidence dating back to 2737 BCE. Cannabis is one of the 50 “fundamental” herbs of traditional Chinese medicine, and is prescribed to for a broad range of indications.
Supporters of medical cannabis argue that cannabis does have several well-documented beneficial effects. Among these are: the amelioration of nausea and vomiting, stimulation of hunger in chemotherapy and AIDS patients, lowered intraocular eye pressure (shown to be effective for treating glaucoma), as well as gastrointestinal illness. Its effectiveness as an analgesic has been suggested—and disputed—as well.
There are several methods for administration of dosage, including vaporizing or smoking dried buds, drinking, or eating extracts, and taking capsules. The comparable efficiency of these methods was the subject of an investigative study conducted by the National Institutes of Health.
“Victoria”, the United States’ first legal medical marijuana plant grown by The Wo/Men’s Alliance for Medical Marijuana.
A 2002 review of medical literature by Franjo Grotenhermen states that medical cannabis has established effects in the treatment of nausea, vomiting, premenstrual syndrome, unintentional weight loss, insomnia, and lack of appetite. Other “relatively well-confirmed” effects were in the treatment of “spasticity, painful conditions, especially neurogenic pain, movement disorders, asthma, [and] glaucoma”.
Preliminary findings indicate that cannabis-based drugs could prove useful in treating inflammatory bowel disease, migraines, fibromyalgia, and related conditions.
Medical cannabis has also been found to relieve certain symptoms of multiple sclerosis and spinal cord injuries by exhibiting antispasmodic and muscle-relaxant properties as well as stimulating appetite.
Other studies state that cannabis or cannabinoids may be useful in treating alcohol abuse, amyotrophic lateral sclerosis, collagen-induced arthritis, asthma, atherosclerosis, bipolar disorder, colorectal cancer, HIV-Associated Sensory Neuropathy depression, dystonia, epilepsy, digestive diseases, gliomas, hepatitis C, Huntington’s disease, leukemia, skin tumors, methicillin-resistant Staphylococcus aureus (MRSA), Parkinson’s disease, pruritus, posttraumatic stress disorder (PTSD), psoriasis, sickle-cell disease, sleep apnea, and anorexia nervosa. Controlled research on treating Tourette syndrome with a synthetic version of tetrahydrocannabinol, (brand name Marinol) (the main psychoactive chemical found in cannabis), showed the patients taking Marinol had a beneficial response without serious adverse effects; other studies have shown that cannabis “has no effects on tics and increases the individuals inner tension”. Case reports found that cannabis helped reduce tics, but validation of these results requires longer, controlled studies on larger samples.
A study done by Craig Reinarman surveyed among why people in California used cannabis and it found many reasons why people had used cannabis. It was used to relieve pain, muscle spasms, headaches, anxiety, nausea, vomiting, depression, cramps, panic attacks, diarrhea, and itching. Others used cannabis to improve sleep, relaxation, appetite, concentration or focus, and energy. Some patients used it to prevent medication side effects, anger, involuntary movements, and seizures, while others used it as a substitute for other prescription medications and alcohol.
Safety of cannabis
Various strains of medical marijuana in front of a vaporizer
Cannabis smoke contains thousands of organic and inorganic chemical compounds. This tar is chemically similar to that found in cigarette smoke and includes many of the same carcinogens.
A statement from a source in the US Department of Justice in 1988 said, “Nearly all medicines have toxic, potentially lethal effects. But cannabis is not such a substance. There is no record in the extensive medical literature describing a proven, documented cannabis-induced fatality. In practical terms, cannabis cannot induce a lethal response as a result of drug-related toxicity.”
From January 1997 to June 2005, the U.S. Food and Drug Administration (FDA) reported zero deaths caused by the primary use of cannabis. In contrast, common FDA-approved drugs which are often prescribed in lieu of cannabis (such as anti-emetics and anti-psychotics), were the primary cause of 10,008 deaths. The cannabinoid THC has an extremely low toxicity and the amount that can enter the body through the consumption of cannabis plants poses no threat of death.
Cannabis smoke contains substances that can damage DNA and increase the risk of cancer just like tobacco smoke, though no definitive link between cannabis and cancer has been found. Cancer causing chemicals in cannabis smoke have been found in amounts 50% higher than those found in tobacco smoke. According to the British Lung Foundation, smoking three to four joints (cannabis cigarettes) a day has been found to be associated with the same degree of damage to tissue in the airways of the lung as 20 or more tobacco cigarettes a day.
The Journal of the American Medical Association released findings from a 20-year study that bolstered evidence that cannabis doesn’t do the kind of damage tobacco does. Analysis of over 5,000 smokers showed that cannabis did not appear to harm lung function, although cigarettes did. Cigarette smokers’ scores worsened steadily over the course of the study. Participants who smoked up to 1 joint daily for 7 years, or 1 joint weekly for 20 years, were not linked with worse scores. Dr Donald Tashkin suggested the reason for this might be that cannabis helps fight inflammation and may counteract the effects of irritating chemicals in the drug. The study concluded: “Occasional and low cumulative marijuana use was not associated with adverse effects on pulmonary function”.
Cannabis usage has been shown to negatively affect the ability to drive safely. The British Medical Journal recently indicated that “Drivers who consume cannabis within three hours of driving are nearly twice as likely to cause a vehicle collision as those who are not under the influence of drugs or alcohol”
In glaucoma, cannabis and THC have been shown to reduce intra-ocular pressure (IOP) by an average of 24% in people with normal IOP who have visual-field changes. In studies of healthy adults and glaucoma patients, IOP was reduced by an average of 25% after smoking a cannabis “cigarette” that contained approximately 2% THC—a reduction as good as that observed with most other medications available today, according to a review by the Institute of Medicine.
In a separate study, the use of cannabis and glaucoma was tested and found that the duration of smoked or ingested cannabis or other cannabinoids is very short, averaging 3 to 3.5 hours. Their results showed that for cannabis to be a viable therapy, the patient would have to take in cannabis in some form every 3 hours. They said that for ideal glaucoma treatment it would take two times a day at most for compliance purposes from patients.
Spasticity in multiple sclerosis
A review of six randomized controlled trials of a combination of THC and CBD extracts for the treatment of multiple sclerosis (MS) related muscle spasticity reported, “Although there was variation in the outcome measures reported in these studies, a trend of reduced spasticity in treated patients was noted.” The authors postulated that “cannabinoids may provide neuroprotective and anti-inflammatory benefits in MS.” A small study done on whether or not cannabis could be used to control tremors of MS patients was conducted. The study found that there was no noticeable difference of the tremors in the patients. Although there was no difference in the tremors the patients felt as if their symptoms had lessened and their quality of life had improved. The researchers concluded that the mood enhancing or cognitive effects that cannabis has on the brain could have given the patients the effect that their tremors were getting better.
Research done by the Scripps Research Institute in California shows that the active ingredient in marijuana, THC, prevents the formation of deposits in the brain associated with Alzheimer’s disease. THC was found to prevent an enzyme called acetylcholinesterase from accelerating the formation of “Alzheimer plaques” in the brain more effectively than commercially marketed drugs. THC is also more effective at blocking clumps of protein that can inhibit memory and cognition in Alzheimer’s patients, as reported in Molecular Pharmaceutics. Cannabinoids can also potentially prevent or slow the progression of Alzheimer’s disease by reducing tau protein phosphorylation, oxidative stress, and neuroinflammation.
According to a 2007 study at the California Pacific Medical Center Research Institute, cannabidiol (CBD) may stop breast cancer from spreading throughout the body. These researchers believe their discovery may provide a non-toxic alternative to chemotherapy while achieving the same results minus the painful and unpleasant side effects. The research team says that CBD works by blocking the activity of a gene called Id-1, which is believed to be responsible for a process called metastasis, which is the aggressive spread of cancer cells away from the original tumor site.
Investigators at Columbia University published clinical trial data in 2007 showing that HIV/AIDS patients who inhaled cannabis four times daily experienced substantial increases in food intake with little evidence of discomfort and no impairment of cognitive performance. They concluded that smoked cannabis has a clear medical benefit in HIV-positive patients. In another study in 2008, researchers at the University of California, San Diego School of Medicine found that marijuana significantly reduces HIV-related neuropathic pain when added to a patient’s already-prescribed pain management regimen and may be an “effective option for pain relief” in those whose pain is not controlled with current medications. Mood disturbance, physical disability, and quality of life all improved significantly during study treatment. Despite management with opioids and other pain modifying therapies, neuropathic pain continues to reduce the quality of life and daily functioning in HIV-infected individuals. Cannabinoid receptors in the central and peripheral nervous systems have been shown to modulate pain perception. No serious adverse effects were reported, according to the study published by the American Academy of Neurology. A study examining the effectiveness of different drugs for HIV associated neuropathic pain found that smoked Cannabis was one of only three drugs that showed evidence of efficacy.
A study by Complutense University of Madrid found the chemicals in cannabis promote the death of brain cancer cells by essentially helping them feed upon themselves in a process called autophagy. The research team discovered that cannabinoids such as THC had anticancer effects in mice with human brain cancer cells and in people with brain tumors. When mice with the human brain cancer cells received the THC, the tumor shrank. Using electron microscopes to analyze brain tissue taken both before and after a 26- to 30-day THC treatment regimen, the researchers found that THC eliminated cancer cells while leaving healthy cells intact. The patients did not have any toxic effects from the treatment; previous studies of THC for the treatment of cancer have also found the therapy to be well tolerated. However, the mechanisms which promote THC’s tumor cell–killing action are unknown.
Injections of THC eliminate dependence on opiates in stressed rats, according to a research team at the Laboratory for Physiopathology of Diseases of the Central Nervous System (France) in the journal Neuropsychopharmacology. Deprived of their mothers at birth, rats become hypersensitive to the rewarding effect of morphine and heroin (substances belonging to the opiate family), and rapidly become dependent. When these rats were administered THC, they no longer developed typical morphine-dependent behavior. In the striatum, a region of the brain involved in drug dependence, the production of endogenous enkephalins was restored under THC, whereas it diminished in rats stressed from birth which had not received THC. Researchers believe the findings could lead to therapeutic alternatives to existing substitution treatments.
In humans, drug treatment subjects who use cannabis intermittently are found to be more likely to adhere to treatment for opioid dependence. Historically, similar findings were reported by Edward Birch, who, in 1889, reported success in treating opiate and chloral addiction with cannabis.
Controlling ALS symptoms
Recent research has been conducted on if the use of cannabis could control some of the symptoms of ALS or Lou Gehrig’s Disease. A survey was conducted on 131 people who suffered from ALS. The survey asked if the subjects had used cannabis in the last 12 months to control some of their symptoms. The survey resulted in 13 people who had used the drug in some form to control symptoms. The survey results found that cannabis was moderately effective in reducing symptoms of appetite loss, depression, pain, spasticity, drooling and weakness and the longest relief reported was for depression. The pattern of symptom relief was consistent with those reported by people with other conditions, including multiple sclerosis (Amtmann et al. 2004).
Cannabis contains 483 compounds. At least 80 of these are cannabinoids, which are the basis for medical and scientific use of cannabis. This presents the research problem of isolating the effect of specific compounds and taking account of the interaction of these compounds. Cannabinoids can serve as appetite stimulants, antiemetics, antispasmodics, and have some analgesic effects. Six important cannabinoids found in the cannabis plant are tetrahydrocannabinol, tetrahydrocannabinolic acid, cannabidiol, cannabinol, ß-caryophyllene, and cannabigerol.
Main article: Tetrahydrocannabinol
Chemical structure of tetrahydrocannabinol (THC)
Tetrahydrocannabinol (THC) is the primary compound responsible for the psychoactive effects of cannabis. The compound is a mild analgesic, and cellular research has shown the compound has antioxidant activity. THC is believed to interact with parts of the brain normally controlled by the endogenous cannabinoid neurotransmitter, anandamide. Anandamide is believed to play a role in pain sensation, memory, and sleep.
Cannabidiol has been shown to relieve convulsions, inflammation, anxiety, cough, congestion and nausea, and it inhibits cancer cell growth.
Cannabidiol (CBD) is a major constituent of medical cannabis. CBD represents up to 40% of extracts of medical cannabis. Cannabidiol has been shown to relieve convulsion, inflammation, anxiety, cough, congestion and nausea, and it inhibits cancer cell growth. Recent studies have shown cannabidiol to be as effective as atypical antipsychotics in treating schizophrenia. Because cannabidiol relieves the aforementioned symptoms, cannabis strains with a high amount of CBD may benefit people with multiple sclerosis, frequent anxiety attacks and Tourette syndrome.
Structure of Cannabinol
Cannabinol (CBN) is a therapeutic cannabinoid found in Cannabis sativa and Cannabis indica. It is also produced as a metabolite, or a breakdown product, of tetrahydrocannabinol (THC). CBN acts as a weak agonist of the CB1 and CB2 receptors, with lower affinity in comparison to THC.
Chemical structure of ß-caryophyllene
Part of the mechanism by which medical cannabis has been shown to reduce tissue inflammation is via the compound ß-caryophyllene. A cannabinoid receptor called CB2 plays a vital part in reducing inflammation in humans and other animals. ß-Caryophyllene has been shown to be a selective activator of the CB2 receptor. ß-Caryophyllene is especially concentrated in cannabis essential oil, which contains about 12–35% ß-caryophyllene.
Like cannabidiol, cannabigerol is not psychoactive. Cannabigerol has been shown to relieve intraoccular pressure, which may be of benefit in the treatment of glaucoma.
Pharmacologic THC and THC derivatives
In the USA, the FDA has approved several cannabinoids for use as medical therapies: dronabinol (Marinol) and nabilone. These medicines are taken orally.
These medications are usually used when first line treatments for nausea and vomiting associated with cancer chemotherapy fail to work. In extremely high doses and in rare cases “psychotomimetic” side effects are possible. The other commonly used antiemetic drugs are not associated with these side effects.
Canasol is a cannabis-based medication for glaucoma that relieves intraocular pressure symptoms associated with late-stage glaucoma.
It was created by an ophthalmologist, Dr. Albert Lockhart and Dr. Manley E. West, and began distribution in 1987. As of 2003, it was still being distributed in the United Kingdom, several US states, and several Caribbean nations.
It is notable for being one of the first cannabis-containing pharmaceuticals to be developed for the modern pharmaceutical market and being one of the few such pharmaceuticals to have ever been legally marketed in the United States.
The prescription drug Sativex, an extract of cannabis administered as a sublingual spray, has been approved in Canada for the adjunctive treatment (use along side other medicines) of both multiple sclerosis and cancer related pain. Sativex has also been approved in the United Kingdom, New Zealand, and the Czech Republic, and is expected to gain approval in other European countries. William Notcutt is one of the chief researchers that has developed Sativex, and he has been working with GW and founder Geoffrey Guy since the company’s inception in 1998. Notcutt states that the use of MS as the disease to study “had everything to do with politics.”
Cannabis sativa, Cannabis indica, and Cannabis ruderalis
A Cannabis indica plant may have a CBD/THC ratio 4–5 times that of Cannabis sativa. Marijuana and Medicine: Assessing the Science Base (1999) states that “There are numerous anecdotal reports claiming that marijuana with relatively higher ratios of THC:CBD is less likely to induce anxiety in the user than marijuana with low THC:CBD ratios; but, taken together, the results published thus far are inconclusive.” (Page 36) Indica has more cannabidiol and sativa has more THC. This might partially be due to CBD’s antagonist effects at the cannabinoid receptor, compared to THC’s partial agonist effect. The relatively large amount of CBD contained in Cannabis indica, means, compared to an Cannabis sativa, the effects are modulated significantly. The effects of sativa are well known for its cerebral high, hence used daytime as medical cannabis, while indica is well known for its sedative effects and preferred night time as medical cannabis. Indica plants are normally shorter and stockier plants than sativas. They have wide, deeply serrated leaves and a compact and dense flower cluster. The effects of indicas are predominantly physical and sedative. Due to the relaxing nature of indicas, they are best used for non-active times of the day, and before bed. Indica strains generally have higher levels of C.B.D and C.B.N and lower levels of T.H.C.
One of the major criticisms of cannabis as medicine is opposition to smoking as a method of consumption. However, smoking is no longer necessary due to the development of healthier methods. Today, medicinal cannabis patients can use vaporizers, where the essential cannabis compounds are extracted and inhaled. In addition, edible cannabis, which is produced in various baked goods, is also available, and has demonstrated longer lasting effects.
The United States Food and Drug Administration (FDA) issued an advisory against smoked medical cannabis stating that, “marijuana has a high potential for abuse, has no currently accepted medical use in treatment in the United States, and has a lack of accepted safety for use under medical supervision. The National Institute on Drug Abuse NIDA state that “Marijuana itself is an unlikely medication candidate for several reasons: (1) it is an unpurified plant containing numerous chemicals with unknown health effects; (2) it is typically consumed by smoking further contributing to potential adverse effects; and (3) its cognitive impairing effects may limit its utility”.
The Institute of Medicine, run by the United States National Academy of Sciences, conducted a comprehensive study in 1999 to assess the potential health benefits of cannabis and its constituent cannabinoids. The study concluded that smoking cannabis is not recommended for the treatment of any disease condition, but did conclude that nausea, appetite loss, pain and anxiety can all be mitigated by marijuana. While the study expressed reservations about smoked cannabis due to the health risks associated with smoking, the study team concluded that until another mode of ingestion was perfected that could provide the same relief as smoked cannabis, there was no alternative. In addition, the study pointed out the inherent difficulty in marketing a non-patentable herb. Pharmaceutical companies will not substantially profit unless there is a patent. For those reasons, the Institute of Medicine concluded that there is little future in smoked cannabis as a medically approved medication. The report also concluded that for certain patients, such as the terminally ill or those with debilitating symptoms, the long-term risks are not of great concern.
Marinol was less effective than the steroid megestrol in helping cancer patients regain lost appetites. A phase III study found no difference in effects of an oral cannabis extract or THC on appetite and quality of life (QOL) in patients with cancer-related anorexia-cachexia syndrome (CACS) to placebo. “Citing the dangers of cannabis and the lack of clinical research supporting its medicinal value” the American Society of Addiction Medicine in March 2011 issued a white paper recommending a halt to using marijuana as a medicine in U.S. states where it has been declared legal.
A study of 50,000 Swedish soldiers who had smoked at least once were twice as likely to develop schizophrenia as those who had not smoked. The study concluded that either smoking caused a higher rate of schizophrenia, or that those with schizophrenia were more likely to be drawn to cannabis.
A study by Keele University commissioned by the British government found that between 1996 and 2005 there had been significant reductions in the incidence and prevalence of schizophrenia. From 2000 onwards there were also significant reductions in the prevalence of psychoses.
The authors say this data is “not consistent with the hypothesis that increasing cannabis use in earlier decades is associated with increasing schizophrenia or psychoses from the mid-1990s onwards”.
A 10 year study on 1923 individuals from the general population in Germany, aged 14–24, concluded that cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder.
Lung cancer and chronic obstructive pulmonary disease
The evidence to date is conflicting as to whether smoking cannabis increases the risk of developing lung cancer or chronic obstructive pulmonary disease (COPD) among people who do not smoke tobacco. In 2006 a study by Hashibe, Morgenstern, Cui, Tashkin, et al. suggested that smoking cannabis does not, by itself, increase the risk of lung cancer. Many studies did report a strongly synergistic effect, however, between tobacco use and smoking cannabis such that tobacco smokers who also smoked cannabis dramatically increased their already very high risk of developing lung cancer or chronic obstructive pulmonary disease by as much as 300%. Some of these research results follow below:
In 2006, Hashibe, Morgenstern, Cui, Tashkin, et al. presented the results from a study involving 2,240 subjects that showed non-tobacco users who smoked marijuana did not exhibit an increased incidence of lung cancer or head-and-neck malignancies. These results were supported even among very long-term, very heavy users of marijuana. Tashkin, a pulmonologist who has studied cannabis for 30 years, commenting in news reports in the lay media on the results of the study he co-authored, suggested, “It’s possible that tetrahydrocannabinol (THC) in cannabis smoke may encourage apoptosis, or programmed cell death, causing cells to die off before they have a chance to undergo malignant transformation”. He summarized the results found by his study, saying “We hypothesized that there would be a positive association between cannabis use and lung cancer, and that the association would be more positive with heavier use. What we found instead was no association at all, and even a suggestion of some protective effect.”
A case-control study of lung cancer in adults 55 years of age and younger found that the risk of lung cancer increased 8% (95% confidence interval (CI) 2–15) for each joint-year of cannabis smoking, after adjustment for confounding variables including cigarette smoking, and 7% (95% CI 5–9) for each pack-year of cigarette smoking, after adjustment for confounding variables including cannabis smoking.
A 2008 study by Hii, Tam, Thompson, and Naughton found that cannabis smoking leads to asymmetrical bullous disease, often in the setting of normal CXR and lung function. In subjects who smoke cannabis, these pathological changes occur at a younger age (approximately 20 years earlier) than in tobacco smokers.
Researchers from the University of British Columbia presented a study at the American Thoracic Society 2007 International Conference showing that smoking cannabis and tobacco together more than tripled the risk of developing COPD over just smoking tobacco alone.[unreliable medical source?] Similar findings were released in April 2009 by the Vancouver Burden of Obstructive Lung Disease Research Group. The study reported that smoking both tobacco and cannabis synergistically increased the risk of respiratory symptoms and COPD. Smoking only cannabis, however, was not associated with an increased risk of respiratory symptoms of COPD. In a related commentary, pulmonary researcher Donald Tashkin wrote, “…we can be close to concluding that cannabis smoking by itself does not lead to COPD”.
The harm caused by smoking can be minimized or eliminated by the use of a vaporizer or ingesting the drug in an edible form. Vaporizers are devices that heat the active constituents to a temperature below the ignition point of the cannabis, so that their vapors can be inhaled. Combustion of plant material is avoided, thus preventing the formation of carcinogens such as polyaromatic hydrocarbons, benzene and carbon monoxide. A pilot study led by Donald Abrams of UC San Francisco showed that vaporizers eliminate the release of irritants and toxic compounds, while delivering equivalent amounts of THC into the bloodstream. According to Matthew Seamon and his co-authors “Vaporizers are the optimal route of administration because they allow for rapid and complete absorption with minimal combustible byproducts, often considered the major health risk associated with smoking tobacco.”
In order to kill microorganisms, especially the molds A. fumigatus, A. flavus and A. niger, Levitz and Diamond suggested baking marijuana at 150 °C (302 °F) for five minutes. They also found that tetrahydrocannabinol (THC) was not degraded by this process.
A number of medical organizations have endorsed reclassification of marijuana to allow for further study. These include, but are not limited to:
The American Medical Association
The American College of Physicians – America’s second largest physicians group
Leukemia & Lymphoma Society – America’s second largest cancer charity
American Academy of Family Physicians opposes the use of marijuana except under medical supervision
Other medical organizations recommend a halt to using marijuana as a medicine in U.S.
The American Society of Addiction Medicine
Ancient China and Taiwan
The use of cannabis, at least as fiber, has been shown to go back at least 10,000 years in Taiwan. “Dà má” (Pinyin pronunciation) is the Chinese expression for cannabis, the first character meaning “big” and the second character meaning “hemp.”
Cannabis, called má ? (meaning “hemp; cannabis; numbness”) or dàmá ?? (with “big; great”) in Chinese, was used in Taiwan for fiber starting about 10,000 years ago. The botanist Li Hui-Lin wrote that in China, “The use of Cannabis in medicine was probably a very early development. Since ancient humans used hemp seed as food, it was quite natural for them to also discover the medicinal properties of the plant.” The oldest Chinese pharmacopeia, the (ca. 100 CE) Shennong Bencaojing ????? (“Shennong’s Materia Medica Classic”), describes dama “cannabis”.
The flowers when they burst (when the pollen is scattered) are called ?? [mafen] or ?? [mabo]. The best time for gathering is the 7th day of the 7th month. The seeds are gathered in the 9th month. The seeds which have entered the soil are injurious to man. It grows in [Taishan] (in [Shandong] …). The flowers, the fruit (seed) and the leaves are officinal. The leaves and the fruit are said to be poisonous, but not the flowers and the kernels of the seeds.
In the early 3rd century CE, Hua Tuo was the first person known to use cannabis as an anesthetic. He reduced the plant to powder and mixed it with wine for administration. In China, the era of Han Western, the iii th century the great surgeon Hua Tuo conducts operations under anesthesia using Indian hemp. The Chinese term for anesthesia (??: má zui ) is also composed of the ideogram which means hemp, followed by means of intoxication. Elizabeth Wayland Barber says the Chinese evidence “proves a knowledge of the narcotic properties of Cannabis at least from the 1st millennium B.C.” when ma was already used in a secondary meaning of “numbness; senseless.” “Such a strong drug, however, suggests that the Chinese pharmacists had now obtained from far to the southwest not THC-bearing Cannabis sativa but Cannabis indica, so strong it knocks you out cold.
Cannabis is one of the 50 “fundamental” herbs in traditional Chinese medicine, and is prescribed to treat diverse indications.
Every part of the hemp plant is used in medicine; the dried flowers (?), the achenia (?), the seeds (??), the oil (??), the leaves, the stalk, the root, and the juice. The flowers are recommended in the 120 different forms of (? feng) disease, in menstrual disorders, and in wounds. The achenia, which are considered to be poisonous, stimulate the nervous system, and if used in excess, will produce hallucinations and staggering gait. They are prescribed in nervous disorders, especially those marked by local anaesthesia. The seeds, by which is meant the white kernels of the achenia, are used for a great variety of affections, and are considered to be tonic, demulcent, alterative, laxative, emmenagogue, diuretic, anthelmintic, and corrective. They are made into a congee by boiling with water, mixed with wine by a particular process, made into pills, and beaten into a paste. A very common mode of exhibition, however, is by simply eating the kernels. It is said that their continued use renders the flesh firm and prevents old age. They are prescribed internally in fluxes, post-partum difficulties, aconite poisoning, vermillion poisoning, constipation, and obstinate vomiting. Externally they are used for eruptions, ulcers, favus, wounds, and falling of the hair. The oil is used for falling hair, sulfur poisoning, and dryness of the throat. The leaves are considered to be poisonous, and the freshly expressed juice is used as an anthelmintic, in scorpion stings, to stop the hair from falling out and to prevent it from turning grey. They are especially thought to have antiperiodic properties. The stalk, or its bark, is considered to be diuretic, and is used with other drugs in gravel. The juice of the root is used for similar purposes, and is also thought to have a beneficial action in retained placenta and post-partum hemorrhage. An infusion of hemp (for the preparation of which no directions are given) is used as a demulcent drink for quenching thirst and relieving fluxes.
“Medical use of cannabis included, rheumatism, intestinal constipation, female reproductive system disorders, malaria, and other uses” (Zuardi, 2006, 4).
The Ebers Papyrus (ca. 1550 BCE) from Ancient Egypt has a prescription for medical marijuana applied directly for inflammation
The Ebers Papyrus (ca. 1550 BCE) from Ancient Egypt describes medical cannabis. Other ancient Egyptian papyri that mention medical cannabis are the Ramesseum III Papyrus (1700 BC), the Berlin Papyrus (1300 BC) and the Chester Beatty Medical Papyrus VI (1300 BC). The ancient Egyptians even used hemp (cannabis) in suppositories for relieving the pain of hemorrhoids. Around 2,000 B.C., the ancient Egyptians used cannabis to treat sore eyes. The egyptologist Lise Manniche notes the reference to “plant medical cannabis” in several Egyptian texts, one of which dates back to the eighteenth century BCE.
Surviving texts from ancient India confirm that cannabis’ psychoactive properties were recognized, and doctors used it for treating a variety of illnesses and ailments. These included insomnia, headaches, a whole host of gastrointestinal disorders, and pain: cannabis was frequently used to relieve the pain of childbirth.
In India, the use of cannabis was widely disseminated, both as a medicine and as a recreational drug. Such a broad use may be due to the fact that cannabis maintained a straight association with religion, which assigned sacred virtues to the plant” (Zuardi, 2006, 3).
The Ancient Greeks used cannabis not only for human medicine, but also in veterinary medicine to dress wounds and sores on their horses.
The Ancient Greeks used cannabis to dress wounds and sores on their horses.
In humans, dried leaves of cannabis were used to treat nose bleeds, and cannabis seeds were used to expel tapeworms. The most frequently described use of cannabis in humans was to steep green seeds of cannabis in either water or wine, later taking the seeds out and using the warm extract to treat inflammation and pain resulting from obstruction of the ear.
In the 5th century BCE Herodotus, a Greek historian, described how the Scythians of the Middle East used cannabis in steam baths.
South East Asia
Patani from Asia are primary natural producers of the diuretic, antiemetic, antiepileptic, anti-inflammatory, pain killing and antipyretic properties of Cannabis sativa, and used it extensively for ‘Kopi Kapuganja’ and ‘Pecel Ganja’, as recreation food, drinks and relaxing medication for centuries.
Medieval Islamic world
In the medieval Islamic world, Arabic physicians made use of the diuretic, antiemetic, antiepileptic, anti-inflammatory, pain killing and antipyretic properties of Cannabis sativa, and used it extensively as medication from the 8th to 18th centuries.
Medical cannabis ad from Sweden (1800)
An Irish physician, William Brooke O’Shaughnessy, is credited with introducing the therapeutic use of cannabis to Western medicine. He was Assistant-Surgeon and Professor of Chemistry at the Medical College of Calcutta, and conducted a cannabis experiment in the 1830s, first testing his preparations on animals, then administering them to patients in order to help treat muscle spasms, stomach cramps or general pain.
Cannabis as a medicine became common throughout much of the Western world by the 19th century. It was used as the primary pain reliever until the invention of aspirin. Modern medical and scientific inquiry began with doctors like O’Shaughnessy and Moreau de Tours, who used it to treat melancholia and migraines, and as a sleeping aid, analgesic and anticonvulsant. At the local level authorities introduced various laws that required the mixtures that contained cannabis, that was not sold on prescription, must be marked with warning labels under the so-called poison laws.
A Swedish lexicon printed in 1912 describes cannabis drug and cannabis extract as a now with us deserted method for medical treatment.
There were at least 2000 cannabis medicines prior to 1937 with over 280 manufacturers.
Later in the century, researchers investigating methods of detecting cannabis intoxication discovered that smoking the drug reduced intraocular pressure. In 1955 the antibacterial effects were described at the Palacký University of Olomouc. Since 1971 Lumír Ondrej Hanuš was growing cannabis for his scientific research on two large fields in authority of the University. The marijuana extracts were then used at the University hospital as a cure for aphthae and haze. In 1973 physician Tod H. Mikuriya reignited the debate concerning cannabis as medicine when he published “Marijuana Medical Papers”. High intraocular pressure causes blindness in glaucoma patients, so he hypothesized that using the drug could prevent blindness in patients. Many Vietnam War veterans also found that the drug prevented muscle spasms caused by spinal injuries suffered in battle. Later medical use focused primarily on its role in preventing the wasting syndromes and chronic loss of appetite associated with chemotherapy and AIDS, along with a variety of rare muscular and skeletal disorders.
In 1964, Dr. Albert Lockhart and Manley West began studying the health effects of traditional cannabis use in Jamaican communities. They discovered that Rastafarians had unusually low glaucoma rates and local fishermen were washing their eyes with cannibis extract in the belief that it would improve their sight. Lockhart and West developed, and in 1987 gained permission to market, the pharmaceutical Canasol: one of the first to cannabis extracts. They continued to work with cannabis throughout the years, developing more pharmaceuticals and eventually receiving the Jamaican Order of Merit for their work.
Later, in the 1970s, a synthetic version of THC was produced and approved for use in the United States as the drug Marinol. It was delivered as a capsule, to be swallowed. Patients complained that the violent nausea associated with chemotherapy made swallowing capsules difficult. Further, along with ingested cannabis, capsules are harder to dose-titrate accurately than smoked cannabis because their onset of action is so much slower. Smoking has remained the route of choice for many patients because its onset of action provides almost immediate relief from symptoms and because that fast onset greatly simplifies titration. For these reasons, and because of the difficulties arising from the way cannabinoids are metabolized after being ingested, oral dosing is probably the least satisfactory route for cannabis administration. Relatedly, some studies have indicated that at least some of the beneficial effects that cannabis can provide may derive from synergy among the multiplicity of cannabinoids and other chemicals present in the dried plant material. Such synergy is, by definition, impossible with respect to the use of single-cannabinoid drugs like Marinol.
During the 1970s and 1980s, six U.S. states’ health departments performed studies on the use of medical cannabis. These are widely considered some of the most useful and pioneering studies on the subject. Voters in eight states showed their support for cannabis prescriptions or recommendations given by physicians between 1996 and 1999, including Alaska, Arizona, California, Colorado, Maine, Michigan, Nevada, Oregon, and Washington, going against policies of the federal government.
Cannabis female flowers closeup with trichomes (white). These plant parts contain the highest concentration of medicinal compounds.
In May 2001, “The Chronic Cannabis Use in the Compassionate Investigational New Drug Program: An Examination of Benefits and Adverse Effects of Legal Clinical Cannabis” (Russo, Mathre, Byrne et al.) was completed. This three-day examination of major body functions of four of the five living US federal cannabis patients found “mild pulmonary changes” in two patients.
Medical Marijuana Dispensary
In the United States federal level of government, cannabis per se has been made criminal by implementation of the Controlled Substances Act which classifies cannabis as a Schedule I drug, the strictest classification on par with heroin, LSD and ecstasy, and the Supreme Court ruled in 2005 that the Commerce Clause of the U.S. Constitution allowed the government to ban the use of cannabis, including medical use. The United States Food and Drug Administration states “marijuana has a high potential for abuse, has no currently accepted medical use in treatment in the United States, and has a lack of accepted safety for use under medical supervision”.
Only one American (for-profit) Company, Cannabis Science Inc., is working towards getting FDA approval for cannabis based medicines (including smoked cannabis). They want to have medical cannabis approved by the FDA so anyone, regardless of state, will have access to the medicine . Also, there is one non-profit organization, the Multidisciplinary Association for Psychedelic Studies (MAPS) working towards getting Cannabis approved by the FDA for PTSD.
Nineteen states have legalized medical cannabis or effectively decriminalized it: Alaska, Arizona, California, Colorado, Connecticut,  Delaware, Hawaii, Maine, Michigan, Montana, Nevada, New Jersey, New Mexico, Oregon, Rhode Island, Vermont, Virginia, Washington; and Washington D.C. Maryland allows for reduced or no penalties if cannabis use has a medical basis. Despite its legality in Washington, and Michigan, an employee can still be fired if they test positive on a drug test, despite having a doctor’s recommendation. California, Colorado, New Mexico, Maine, Rhode Island, Montana, and Michigan are currently the only states to utilize dispensaries to sell medical cannabis. Connecticut will be the eighth but has yet to issue any licenses. California’s medical cannabis industry took in about $2 billion a year and generated $100 million in state sales taxes during 2008 with an estimated 2,100 dispensaries, co-operatives, wellness clinics and taxi delivery services in the sector colloquially known as “cannabusiness”.
On 19 October 2009 the US Deputy Attorney General issued a US Department of Justice memorandum to “All United States Attorneys” providing clarification and guidance to federal prosecutors in US States that have enacted laws authorizing the medical use of marijuana. The document is intended solely as “a guide to the exercise of investigative and prosecutorial discretion and as guidance on resource allocation and federal priorities.” The US Deputy Attorney General David W. Ogden provided seven criteria, the application of which acts as a guideline to prosecutors and federal agents to ascertain whether a patients use, or their caregivers provision, of medical cannabis “represents part of a recommended treatment regiment consistent with applicable state law”, and recommends against prosecuting patients using medical cannabis products according to state laws. Not applying those criteria, the Dep. Attorney General Ogden concludes, would likely be “an inefficient use of limited federal resources”. The memorandum does not change any laws. Sale of cannabis remains illegal under federal law. The U.S. Food and Drug Administration’s position, that marijuana has no accepted value in the treatment of any disease in the United States, has also remained the same.
The Health and Human Services Division of the Federal government of the United States holds a patent US 6630507 for medical cannabis.
The Health and Human Services Division of the federal government holds a patent US 6630507 for medical cannabis. The patent, “Cannabinoids as antioxidants and neuroprotectants”, issued October 2003 reads:
Cannabinoids have been found to have antioxidant properties, unrelated to NMDA receptor antagonism. This new found property makes cannabinoids useful in the treatment and prophylaxis of wide variety of oxidation associated diseases, such as ischemic, age-related, inflammatory and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia… .
1.^ Mohamed Ben Amar (2006). “Cannabinoids in medicine: A review of their therapeutic potential”. Journal of Ethnopharmacology 105 (1–2): 1–25. doi:10.1016/j.jep.2006.02.001. PMID 16540272. Retrieved 8 April 2010.
2.^ a b Wong, Ming (1976). La Médecine chinoise par les plantes. Paris: Tchou. OCLC 2646789.[page needed]
3.^ Aggarwal SK, Carter GT, Sullivan MD, ZumBrunnen C, Morrill R, Mayer JD (2009). “Medicinal use of cannabis in the United States: historical perspectives, current trends, and future directions”. J Opioid Manag 5 (3): 153–68. PMID 19662925. Lay summary – SF Weekly (15 September 2009).
4.^ “IACM 5th Conference on Cannabinoids in Medicine” (PDF). International Association for Cannabis as Medicine. Retrieved 2011-07-28.
5.^ Joy, Janet E.; Watson, Stanley J.; Benson, John A., eds. (1999). Marijuana and Medicine: Assessing the Science Base. Washington, D.C.: National Academies Press. p. 13. ISBN 978-0-309-07155-0. OCLC 246585475.
6.^ a b “Workshop on the Medical Utility of Marijuana”. National Institutes of Health. 1997. Retrieved 26 April 2009.
7.^ Grotenhermen, Franjo (2002). “Review of Therapeutic Effects”. Cannabis and Cannabinoids: Pharmacology, Toxicology and Therapeutic Potential. New York City: Haworth Press. p. 124. ISBN 978-0-7890-1508-2.
8.^ Russo EB (2004). “Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions?”. Neuro Endocrinology Letters 25 (1–2): 31–9. PMID 15159679.
9.^ Zajicek J; Fox P; Sanders H; Wright, David; Vickery, Jane; Nunn, Andrew; Thompson, Alan; Uk Ms Research, Group (2003). “Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial”. Lancet 362 (9395): 1517–26. doi:10.1016/S0140-6736(03)14738-1. PMID 14615106.
10.^ “Spinal Cord Injury and Disease”. Therapeutic Uses of Marijuana. Medical Marijuana Information Resource Centre. Retrieved 9 August 2009.
11.^ Maurer M, Henn V, Dittrich A, Hofmann A (1990). “Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial”. European Archives of Psychiatry and Clinical Neuroscience 240 (1): 1–4. doi:10.1007/BF02190083. PMID 2175265.
12.^ Kogel RW, Johnson PB, Chintam R, Robinson CJ, Nemchausky BA (1995). “Treatment of Spasticity in Spinal Cord Injury with Dronabinol, a Tetrahydrocannabinol Derivative”. American Journal of Therapeutics 2 (10): 799–805. doi:10.1097/00045391-199510000-00012. PMID 11854790.
13.^ Thanos PK, Dimitrakakis ES, Rice O, Gifford A, Volkow ND (2005). “Ethanol self-administration and ethanol conditioned place preference are reduced in mice lacking cannabinoid CB1 receptors”. Behavioural Brain Research 164 (2): 206–13. doi:10.1016/j.bbr.2005.06.021. PMID 16140402.
14.^ Carter GT, Rosen BS (2001). “Marijuana in the management of amyotrophic lateral sclerosis”. The American Journal of Hospice & Palliative Care 18 (4): 264–70. doi:10.1177/104990910101800411. PMID 11467101.
15.^ Weydt P, Hong S, Witting A, Möller T, Stella N, Kliot M (2005). “Cannabinol delays symptom onset in SOD1 (G93A) transgenic mice without affecting survival”. Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders 6 (3): 182–4. doi:10.1080/14660820510030149. PMID 16183560.
16.^ Malfait AM; Gallily R; Sumariwalla PF; Malik, AS; Andreakos, E; Mechoulam, R; Feldmann, M (2000). “The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis” (Free full text). Proceedings of the National Academy of Sciences of the United States of America 97 (17): 9561–6. doi:10.1073/pnas.160105897. PMC 16904. PMID 10920191.
17.^ Tashkin DP, Shapiro BJ, Lee YE, Harper CE (1975). “Effects of smoked marijuana in experimentally induced asthma”. The American Review of Respiratory Disease 112 (3): 377–86. PMID 1099949.
18.^ Steffens S; Veillard NR; Arnaud C; Pelli, Graziano; Burger, Fabienne; Staub, Christian; Zimmer, Andreas; Frossard, Jean-Louis et al. (16 April 2005). “Cannabis may help keep arteries clear”. Nature 434 (7034): 782–6. doi:10.1038/nature03389. PMID 15815632. Lay summary – New Scientist.
19.^ Grinspoon L, Bakalar JB (1998). “The use of cannabis as a mood stabilizer in bipolar disorder: anecdotal evidence and the need for clinical research”. Journal of Psychoactive Drugs 30 (2): 171–7. doi:10.1080/02791072.1998.10399687. PMID 9692379.
20.^ Ashton CH, Moore PB, Gallagher P, Young AH (2005). “Cannabinoids in bipolar affective disorder: a review and discussion of their therapeutic potential”. Journal of Psychopharmacology 19 (3): 293–300. doi:10.1177/0269881105051541. PMID 15888515.
21.^ Patsos HA; Hicks DJ; Dobson RR; Greenhough, A; Woodman, N; Lane, JD; Williams, AC; Paraskeva, C (2005). “The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase 2”. Gut 54 (12): 1741–50. doi:10.1136/gut.2005.073403. PMC 1774787. PMID 16099783.
22.^ Abrams, D.I., MD; Jay, C.A., MD (2007). “Cannabis in painful HIV-Associated Sensory Neuropathy”. Neurology 68 (7): 515–521. doi:10.1212/01.wnl.0000253187.66183.9c. PMID 17296917. Retrieved 2/3/2011.
23.^ Bambico FR, Katz N, Debonnel G, Gobbi G (2007). “Cannabinoids elicit antidepressant-like behavior and activate serotonergic neurons through the medial prefrontal cortex” (Free full text). The Journal of Neuroscience 27 (43): 11700–11. doi:10.1523/JNEUROSCI.1636-07.2007. PMID 17959812. Lay summary – Fox News Channel (25 October 2007).
24.^ Denson TF, Earleywine M (2006). “Decreased depression in marijuana users”. Addictive Behaviors 31 (4): 738–42. doi:10.1016/j.addbeh.2005.05.052. PMID 15964704.
25.^ Jiang W; Zhang Y; Xiao L; Van Cleemput, J; Ji, SP; Bai, G; Zhang, X (2005). “Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects” (Free full text). The Journal of Clinical Investigation 115 (11): 3104–16. doi:10.1172/JCI25509. PMC 1253627. PMID 16224541.
26.^ El-Remessy AB, Al-Shabrawey M, Khalifa Y, Tsai NT, Caldwell RB, Liou GI (2006). “Neuroprotective and Blood-Retinal Barrier-Preserving Effects of Cannabidiol in Experimental Diabetes” (Free full text). The American Journal of Pathology 168 (1): 235–44. doi:10.2353/ajpath.2006.050500. PMC 1592672. PMID 16400026.
27.^ Fox SH, Kellett M, Moore AP, Crossman AR, Brotchie JM (2002). “Randomised, double-blind, placebo-controlled trial to assess the potential of cannabinoid receptor stimulation in the treatment of dystonia”. Movement Disorders 17 (1): 145–9. doi:10.1002/mds.1280. PMID 11835452.
28.^ “Cannabis could be used to treat epilepsy”. Telegraph. 2011-04-10. Retrieved 2011-04-20.
29.^ Marsicano G; Goodenough S; Monory K; Zieglgänsberger, H; Di Marzo, M; Behl, A; Lutz, SC; Cascio, MG et al. (2003). “CB1 cannabinoid receptors and on-demand defense against excitotoxicity”. Science 302 (5642): 84–8. doi:10.1126/science.1088208. PMID 14526074.
30.^ Bacci A, Huguenard JR, Prince DA (2004). “Long-lasting self-inhibition of neocortical interneurons mediated by endocannabinoids”. Nature 431 (7006): 312–6. doi:10.1038/nature02913. PMID 15372034. Lay summary – Science Daily (16 September 2004).
31.^ Di Carlo G, Izzo AA (2003). “Cannabinoids for gastrointestinal diseases: potential therapeutic applications”. Expert Opinion on Investigational Drugs 12 (1): 39–49. doi:10.1517/13543718.104.22.168. PMID 12517253.
32.^ Lorente M; Carracedo A; Torres S; Natali, Francesco; Egia, Ainara; Hernández-Tiedra, Sonia; Salazar, María; Blázquez, Cristina et al. (2009). “Amphiregulin is a factor for resistance of glioma cells to cannabinoid-induced apoptosis”. Glia 57 (13): 1374–85. doi:10.1002/glia.20856. PMID 19229996.
33.^ Ramer R, Hinz B (2008). “Inhibition of cancer cell invasion by cannabinoids via increased expression of tissue inhibitor of matrix metalloproteinases-1” (Free full text). Journal of the National Cancer Institute 100 (1): 59–69. doi:10.1093/jnci/djm268. PMID 18159069.
34.^ Sylvestre DL, Clements BJ, Malibu Y (2006). “Cannabis use improves retention and virological outcomes in patients treated for hepatitis C”. European Journal of Gastroenterology & Hepatology 18 (10): 1057–63. doi:10.1097/01.meg.0000216934.22114.51. PMID 16957511.
35.^ Iuvone, T.; Esposito, G.; De Filippis, D.; Scuderi, C.; Steardo, L. (2009). “Cannabidiol: A Promising Drug for Neurodegenerative Disorders?”. CNS Neuroscience & Therapeutics 15 (1): 65–75. doi:10.1111/j.1755-5949.2008.00065.x. PMID 19228180. edit
36.^ Powles T; te Poele R; Shamash J; Chaplin, T; Propper, D; Joel, S; Oliver, T; Liu, WM (2005). “Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway” (Free full text). Blood 105 (3): 1214–21. doi:10.1182/blood-2004-03-1182. PMID 15454482.
37.^ Casanova ML; Blázquez C; Martínez-Palacio J; Villanueva, Concepción; Fernández-Aceñero, M. Jesús; Huffman, John W.; Jorcano, José L.; Guzmán, Manuel (2003). “Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors” (Free full text). The Journal of Clinical Investigation 111 (1): 43–50. doi:10.1172/JCI16116. PMC 151833. PMID 12511587.
38.^ Appendino G, Gibbons S, Giana A, Pagani A, Grassi G, Stavri M, Smith E, Rahman MM (2008). “Antibacterial Cannabinoids from Cannabis sativa: A Structure—Activity Study” (PDF). J Nat Prod 71 (8): 1427–30. doi:10.1021/np8002673. PMID 18681481. Retrieved 6 November 2010. Lay summary – WebMD (4 September 2008).
39.^ Kreitzer AC, Malenka RC (2005). “Endocannabinoid-mediated rescue of striatal LTD and motor deficits in Parkinson’s disease models”. Nature 445 (7128): 643–7. doi:10.1038/nature05506. PMID 17287809. Lay summary – Stanford University School of Medicine (7 February 2007).
40.^ Szepietowski JC, Szepietowski T, Reich A (2005). “Efficacy and tolerance of the cream containing structured physiological lipids with endocannabinoids in the treatment of uremic pruritus: a preliminary study”. Acta Dermatovenerologica Croatica 13 (2): 97–103. PMID 16324422.
41.^ Bergasa NV (2005). “The pruritus of cholestasis”. Journal of Hepatology 43 (6): 1078–88. doi:10.1016/j.jhep.2005.09.004. PMID 16253381.
42.^ Ganon-Elazar E, Akirav I (2009). “Cannabinoid receptor activation in the basolateral amygdala blocks the effects of stress on the conditioning and extinction of inhibitory avoidance”. J. Neurosci 29 (36): 11078–88. doi:10.1523/JNEUROSCI.1223-09.2009. PMID 19741114. Lay summary – PsychCentral (5 November 2009).
43.^ Wilkinson, J. D.; Williamson, E. M. (2007). “Cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis”. Journal of Dermatological Science 45 (2): 87–92. doi:10.1016/j.jdermsci.2006.10.009. PMID 17157480. edit
44.^ Howard, J.; Anie, K. A.; Holdcroft, A.; Korn, S.; Davies, S. C. (2005). “Cannabis use in sickle cell disease: A questionnaire study”. British Journal of Haematology 131 (1): 123–128. doi:10.1111/j.1365-2141.2005.05723.x. PMID 16173972. edit
45.^ Carley DW, Paviovic S, Janelidze M, Radulovacki M (2002). “Functional role for cannabinoids in respiratory stability during sleep” (Free full text). Sleep 25 (4): 391–8. PMID 12071539.
46.^ Grotenhermen, Russo. Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. New York: The Hawthorn Integrative Healing Press, 2002,. Grotenhermen, “Review of Therapeutic Effects.” Chapter 11, p. 128
47.^ Singer HS (2005). “Tourette’s syndrome: from behaviour to biology”. Lancet Neurol 4 (3): 149–59. doi:10.1016/S1474-4422(05)01012-4. PMID 15721825.
48.^ Singer HS (2005). “Tourette’s syndrome: from behaviour to biology”. The Lancet Neurology 4 (3): 149–59. doi:10.1016/S1474-4422(05)01012-4. PMID 15721825.
49.^ Robertson MM (2000). “Tourette syndrome, associated conditions and the complexities of treatment”. Brain: a journal of neurology 123 (3): 425–62. doi:10.1093/brain/123.3.425. PMID 10686169.
50.^ Sandyk R, Awerbuch G (1988). “Marijuana and Tourette’s syndrome”. Journal of Clinical Psychopharmacology 8 (6): 444–5. doi:10.1097/00004714-198812000-00021. PMID 3235704.
51.^ Müller-Vahl KR, Kolbe H, Dengler R (1997). “Gilles de la Tourette syndrome. Effect of nicotine, alcohol and marihuana on clinical symptoms”. Der Nervenarzt 68 (12): 985–9. PMID 9465342.
52.^ Reinarman, C; Nunberg, H; Lanthier, F; Heddleston, T (2011). “Who Are Medical Marijuana Patients? Population Characteristics from Nine California Assessment Clinics”. Journal of Psychoactive Drugs 43 (2): 128–135. doi:10.1080/02791072.2011.587700. PMID 21858958.
53.^ Tomar, Rajpal C.; Beaumont and Hsieh (August 2009) (PDF), Evidence on the carcinogenicity of marijuana smoke, Reproductive and Cancer Hazard Assessment Branch Office of Environmental Health Hazard Assessment, California Environmental Protection Agency, retrieved 23 June 2012
54.^ “In the Matter of Marijuana Rescheduling Petition” (Docket #86-22)”. US Department of Justice to the Drug Enforcement Administration. September 6, 1988. pp. 56–57. Retrieved 2011-08-12.
55.^ Sprague, Elizabeth (July 15, 2009). “Pot No Longer Focus of Anti-Drug Campaigns”. CBS News. Retrieved 2011-08-12.
56.^ “Safe Use of Cannabis”. Safety.
57.^ a b Tanner, Lindsey, Marijuana and lungs: Study finds drug doesn’t do same kind of damage as tobacco, Huffingtonpost.com, retrieved 2012-06-10
58.^ Cannabis and the Lungs, British Lung Foundation, retrieved 6 June 2012
59.^ Mark J. Pletcher, et al. (2012-01-11), “Association between marijuana exposure and pulmonary function over 20 years”, Journal of the American Medical Association 307 (2): 173-181, doi:10.1001/jama.2011.1961, retrieved 2012-06-10
60.^ Li MC, Brady JE, DiMaggio CJ, Lusardi AR, Tzong KY, Li G. (2012), Marijuana use and motor vehicle crashes., Epidemiol Rev. 2012 Jan;34(1):65-72., PMID 21976636
61.^ Ashbridge, Mark (2012), Acute cannabis consumption and motor vehicle collision risk, British Medical Journal, retrieved 14 june, 2012
62.^ Joy, Janet E.; Watson, Stanley J.; Benson, John A., eds. (1999). Marijuana and Medicine: Assessing the Science Base. Washington, D.C.: National Academies Press. ISBN 978-0-309-07155-0. OCLC 246585475.
63.^ Kaufman, Paul. (1998). “Marijuana and Glaucoma”. Archives of Ophthalmology 116 (11): 1512–13. doi:10.1001/archopht.116.11.1512.
64.^ a b Lakhan SE, Rowland M (2009). “Whole plant cannabis extracts in the treatment of spasticity in multiple sclerosis: a systematic review”. BMC Neurology 9: 59. doi:10.1186/1471-2377-9-59. PMC 2793241. PMID 19961570.
65.^ a b De-Vries, Kay; Anita J Green (17). “Cannabis use in palliative care – an examination of the evidence and the implications for nurses”. Journal of Clinical Nursing 19 (17–18): 2454–2462. doi:10.1111/j.1365-2702.2010.03274.x. PMID 20920073.
66.^ a b AMA meeting: Delegates support review of marijuana’s schedule I status; A change could make it easier for researchers to test potential medical uses and develop a drug delivery form safer than smoking. By Kevin B. O’Reilly, American Medical News. Nov 30, 2009
67.^ Eubanks LM; Rogers CJ; Beuscher AE; Koob, George F.; Olson, Arthur J.; Dickerson, Tobin J.; Janda, Kim D. (2006). “A Molecular Link Between the Active Component of Marijuana and Alzheimer’s Disease Pathology” (Free full text). Molecular Pharmaceutics 3 (6): 773–7. doi:10.1021/mp060066m. PMC 2562334. PMID 17140265.
68.^ Campbell, VA; Gowran, A (2007 Nov). “Alzheimer’s disease; taking the edge off with cannabinoids?”. British Journal of Pharmacology 152 (5): 655–62. doi:10.1038/sj.bjp.0707446. PMC 2190031. PMID 17828287.
69.^ a b McAllister SD, Christian RT, Horowitz MP, Garcia A, Desprez PY (2007). “Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells” (Free full text). Molecular Cancer Therapeutics 6 (11): 2921–7. doi:10.1158/1535-7163.MCT-07-0371. PMID 18025276. Lay summary – BBC News (19 November 2007).
70.^ Haney M; Gunderson EW; Rabkin J; Hart, Carl L; Vosburg, Suzanne K; Comer, Sandra D; Foltin, Richard W (2007). “Dronabinol and marijuana in HIV-positive marijuana smokers. Caloric intake, mood, and sleep”. Journal of Acquired Immune Deficiency Syndromes 45 (5): 545–54. doi:10.1097/QAI.0b013e31811ed205. PMID 17589370.
71.^ Abrams DI; Hilton JF; Leiser RJ; Bacchetti, SB; Mccune, TA; Schambelan, FT; Benowitz, NL; Bredt, BM et al. (2003). “Short-term effects of cannabinoids in patients with HIV-1 infection: a randomized, placebo-controlled clinical trial”. Annals of Internal Medicine 139 (4): 258–66. PMID 12965981.
72.^ Ellis RJ; Toperoff W; Vaida F; Van Den Brande, Geoffrey; Gonzales, James; Gouaux, Ben; Bentley, Heather; Atkinson, J Hampton (2009). “Smoked Medicinal Cannabis for Neuropathic Pain in HIV: A Randomized, Crossover Clinical Trial”. Neuropsychopharmacology 34 (3): 672–80. doi:10.1038/npp.2008.120. PMC 3066045. PMID 18688212.
73.^ Abrams DI; Jay CA; Shade SB; Vizoso, H.; Reda, H.; Press, S.; Kelly, M. E.; Rowbotham, M. C. et al. (2007). “Cannabis in painful HIV-associated sensory neuropathy: a randomized placebo-controlled trial”. Neurology 68 (7): 515–21. doi:10.1212/01.wnl.0000253187.66183.9c. PMID 17296917.
74.^ Phillips TJ, Cherry CL, Cox S, Marshall SJ, Rice AS (2010). Pai, Nitika Pant. ed. “Pharmacological Treatment of Painful HIV-Associated Sensory Neuropathy: A Systematic Review and Meta-Analysis of Randomised Controlled Trials”. PLoS ONE 5 (12): e14433. doi:10.1371/journal.pone.0014433. PMC 3010990. PMID 21203440.
75.^ a b Salazar M; Carracedo A; Salanueva IJ; Cecconi, Sonia; Pandolfi, Mar; González-Feria, Ainara; Iovanna, Patricia; Guzmán, Cristina et al. (2009). “Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells”. The Journal of Clinical Investigation 119 (5): 1359–72. doi:10.1172/JCI37948. PMC 2673842. PMID 19425170. Lay summary – HealthDay (1 April 2009).
76.^ a b Morel LJ, Giros B, Daugé V (2009). “Adolescent Exposure to Chronic Delta-9-Tetrahydrocannabinol Blocks Opiate Dependence in Maternally Deprived Rats”. Neuropsychopharmacology 34 (11): 2469–76. doi:10.1038/npp.2009.70. PMID 19553915. Lay summary – PhysOrg.com (7 July 2009).
77.^ Raby, Wilfrid Noel; Carpenter, Kenneth M.; Rothenberg, Jami; Brooks, Adam C.; Jiang, Huiping; Sullivan, Maria; Bisaga, Adam; Comer, Sandra et al. (2009). “Intermittent Marijuana Use Is Associated with Improved Retention in Naltrexone Treatment for Opiate-Dependence”. The American Journal on Addictions 18 (4): 301–8. doi:10.1080/10550490902927785. PMC 2753886. PMID 19444734.
78.^ Mikuriya TH (1969). “Marijuana in medicine: past, present and future”. California Medicine 110 (1): 34–40. PMC 1503422. PMID 4883504.
79.^ Downer EJ, Campbell VA (2010). “Phytocannabinoids, CNS cells and development: A dead issue?”. Drug and Alcohol Review 29 (1): 91–98. doi:10.1111/j.1465-3362.2009.00102.x. PMID 20078688.
80.^ Burns TL, Ineck JR (2006). “Cannabinoid analgesia as a potential new therapeutic option in the treatment of chronic pain”. The Annals of Pharmacotherapy 40 (2): 251–260. doi:10.1345/aph.1G217. PMID 16449552.
81.^ “Medical Cannabis Information”. Medical Cannabis Information.
82.^ Kohn, David (5 November 2004). “Researchers buzzing about marijuana-derived medicines”. San Francisco Chronicle. Retrieved 26 April 2009.
83.^ Ben Amar M (2006). “Cannabinoids in medicine: A review of their therapeutic potential”. Journal of Ethnopharmacology 105 (1–2): 1–25. doi:10.1016/j.jep.2006.02.001. PMID 16540272.
84.^ Hampson AJ, Grimaldi M, Axelrod J, Wink D. (July 1998). “Cannabidiol and (-)?9-tetrahydrocannabinol are neuroprotective antioxidants”. PNAS 95 (14): 8268–73. Bibcode 1998PNAS…95.8268H. doi:10.1073/pnas.95.14.8268. PMC 20965. PMID 9653176. Retrieved 15 May 2011.
85.^ Devane WA, Hanus L, Breuer A, Pertwee RG, Stevenson LA, Griffin G, Gibson D, Mandelbaum A, Etinger A, Mechoulam R (1992). “Isolation and structure of a brain constituent that binds to the cannabinoid receptor”. Science 258 (5090): 1946–1949. doi:10.1126/science.1470919. PMID 1470919.
86.^ Mechoulam R, Fride E (1995). “The unpaved road to the endogenous brain cannabinoid ligands, the anandamides”. In Pertwee RG. Cannabinoid receptors. Boston: Academic Press. pp. 233–258. ISBN 0-12-551460-3.
87.^ a b c Mechoulam R, Peters M, Murillo-Rodriguez E, Hanus LO (2007). “Cannabidiol—recent advances”. Chemistry & Biodiversity 4 (8): 1678–92. doi:10.1002/cbdv.200790147. PMID 17712814.
88.^ Grlie, L (1976). “A comparative study on some chemical and biological characteristics of various samples of cannabis resin”. Bulletin on Narcotics 14: 37–46.
89.^ Zuardi AW, Crippa JA, Hallak JE, Moreira FA, Guimarães FS (2006). “Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug”. Brazilian Journal of Medical and Biological Research 39 (4): 421–9. doi:10.1590/S0100-879X2006000400001. PMID 16612464.
90.^ Sandyk, R.; Awerbuch, G. (1988). “Marijuana and Tourette’s syndrome”. Journal of Clinical Psychopharmacology 8 (6): 444–445. doi:10.1097/00004714-198812000-00021. PMID 3235704. edit
91.^ Karniol IG, Shirakawa I, Takahashi RN, Knobel E, Musty RE (1975). “Effects of delta9-tetrahydrocannabinol and cannabinol in man”. Pharmacology 13 (6): 502–12. doi:10.1159/000136944. PMID 1221432.
92.^ McCallum ND, Yagen B, Levy S, Mechoulam R (1975). “Cannabinol: a rapidly formed metabolite of delta-1- and delta-6-tetrahydrocannabinol”. Experientia 31 (5): 520–1. PMID 1140243.
93.^ Mahadevan A, Siegel C, Martin BR, Abood ME, Beletskaya I, Razdan RK (2000). “Novel cannabinol probes for CB1 and CB2 cannabinoid receptors”. Journal of Medicinal Chemistry 43 (20): 3778–85. doi:10.1021/jm0001572. PMID 11020293.
94.^ Petitet F, Jeantaud B, Reibaud M, Imperato A, Dubroeucq MC (1998). “Complex pharmacology of natural cannabinoids: evidence for partial agonist activity of delta9-tetrahydrocannabinol and antagonist activity of cannabidiol on rat brain cannabinoid receptors”. Life Sciences 63 (1): PL1–6. doi:10.1016/S0024-3205(98)00238-0. PMID 9667767.
95.^ a b c d Gertsch J; Leonti M; Raduner S; Racz, I.; Chen, J.-Z.; Xie, X.-Q.; Altmann, K.-H.; Karsak, M. et al. (2008). “Beta-caryophyllene is a dietary cannabinoid” (Free full text). Proceedings of the National Academy of Sciences of the United States of America 105 (26): 9099–104. doi:10.1073/pnas.0803601105. PMC 2449371. PMID 18574142.
96.^ Colasanti, B. (1990). “A comparison of the ocular and central effects of delta 9-tetrahydrocannabinol and cannabigerol”. Journal of ocular pharmacology 6 (4): 259–269. PMID 1965836. edit
97.^ Colasanti, B.; Craig, C.; Allara, R. (1984). “Intraocular pressure, ocular toxicity and neurotoxicity after administration of cannabinol or cannabigerol”. Experimental eye research 39 (3): 251–259. PMID 6499952. edit
98.^ West, M. E.; Homi, J. (1996). “Cannabis as a medicine”. Br. J. Anaesth 76 (1): 167. doi:10.1093/bja/76.1.167-a.
99.^ a b c Dr Farid F. Youssef. “Cannibis Unmasked: What it is and why it does what it does”. UWIToday: June 2010. http://sta.uwi.edu/uwitoday/archive/june_2010/article9.asp
100.^ Evans, T. “Ganja-based eyedrops a hot sell.” Jamaica Gleaner: August 24, 2003.
101.^ Eulalee Thompson. “Seeing through ganja”. The Jamaica Gleaner: January 29, 2001
102.^ Koch, Wendy (23 June 2005). “Spray alternative to pot on the market in Canada”. USA Today. Retrieved 16 August 2009.
103.^ “Sativex – Investigational Cannabis-Based Treatment for Pain and Multiple Sclerosis Drug Development Technology”. SPG Media. Retrieved 2008-08-08.
104.^ Cooper, Rachel.”GW Pharmaceuticals launches world’s first prescription cannabis drug in Britain” The Telegraph. 21 June 2010. Retrieved 15 May 2011.
105.^ “Sativex Approved in New Zealand” GW Pharmaceuticals. 3 Nov.2010. Retrieved 15 May 2011.
106.^ “Sativex Approved in the Czech Republic” GW Pharmaceuticals. 15 April 2011. Retrieved 15 May 2011.
107.^ Greenberg, Gary (2005). “Respectable Reefer”. Mother Jones. Retrieved 15 August 2009.
108.^ Skrabek RQ, Galimova L, Ethans K, Perry D (2008). “Nabilone for the treatment of pain in fibromyalgia”. The Journal of Pain 9 (2): 164–73. doi:10.1016/j.jpain.2007.09.002. PMID 17974490. Lay summary – News-Medical.Net (17 February 2008).
109.^ “ALL PRICES FOR: Marinol – Brand Version: 10 mg”. PharmacyChecker.com. Retrieved 2009-08-15.
110.^ “FDA approves new indication for Dronabinol” (Press release). Food and Drug Administration. 23 December 1992. Archived from [http://www.fda.gov/bbs/topics/ANSWERS/ANS00457.html the original] on 6 May 1997. Retrieved 15 August 2009.
111.^ “Sativex: CEDAC Final Recommendation on Reconsideration and Reasons for Recommendation”. Canadian Agency for Drugs and Technologies in Health. 27 September 2007. Retrieved 16 August 2009.
112.^ Marijuana and Medicine: Assessing the Science Base (1999), Page 36 at link. Retrieved on 2012-06-10.
113.^ Amsterdam Coffeeshop Directory. www.coffeeshop.freeuk.com. Retrieved on 2012-05-19.
114.^ J.E. Joy, S. J. Watson, Jr., and J.A. Benson, Jr, (1999). Marijuana and Medicine: Assessing The Science Base. Washington D.C: National Academy of Sciences Press. ISBN 0-585-05800-8.
115.^ “Medical Cannabis Information”. Indica.
117.^ “Nida: Marijuana, An update from the National Institute on Drug Abuse”. Nida.nih.gov. February 2011. Retrieved 2011-08-23.
118.^ “Medical Marijuana Passes House Civil Justice Committee Without Dissent” (Press release). Minnesotans for Compassionate Care. 11 March 2009. Retrieved 10 August 2009.
119.^ Joy, Janet E.; Watson, Stanley J.; Benson, John A., eds. (1999). Marijuana and Medicine: Assessing the Science Base. Washington, D.C.: National Academies Press. ISBN 978-0-309-07155-0. OCLC 246585475.
120.^ Jatoi A; Windschitl HE; Loprinzi CL; Sloan, JA; Dakhil, SR; Mailliard, JA; Pundaleeka, S; Kardinal, CG et al. (2002). “Dronabinol versus megestrol acetate versus combination therapy for cancer-associated anorexia: a North Central Cancer Treatment Group study” (PDF). Journal of Clinical Oncology (Alexandria, VA: American Society of Clinical Oncology) 20 (2): 567–73. doi:10.1200/JCO.20.2.567. PMID 11786587. Lay summary – Medscape (30 January 2002).
121.^ Strasser, F; Strasser, F; Luftner, D; Possinger, K; Ernst, G; Ruhstaller, T; Meissner, W; Ko, YD et al. (20 July 2006). “Comparison of Orally Administered Cannabis Extract and Delta-9-Tetrahydrocannabinol in Treating Patients With Cancer-Related Anorexia-Cachexia Syndrome: A Multicenter, Phase III, Randomized, Double-Blind, Placebo-Controlled Clinical Trial From the Cannabis-In-Cachexia-Study-Group”. Journal of Clinical Oncology (Alexandria, VA: American Society of Clinical Oncology) 24 (21): 3394–3400. doi:10.1200/JCO.2005.05.1847. PMID 16849753.
122.^ a b “American Society of Addiction Medicine Rejects Use of ‘Medical Marijuana,’ Citing Dangers and Failure To Meet Standards of Patient Care, March 23, 2011”. Maryland: Prnewswire.com. Retrieved 2011-04-20.
123.^ a b “Medical Marijuana, American Society of Addiction Medicine, 2010”. Asam.org. 2010-04-01. Retrieved 2011-04-20.
124.^ Anon (2010). “Medical marijuana and the mind”. Harvard Mental Health Letter 26 (10): 1–3. PMID 20499454.
125.^ “Frisher, M., et al., Assessing the impact of cannabis use on trends in diagnosed schizophrenia in the United Kingdom from 1996 to 2005, Schizophr. Res. (2009)”. Keele University. 2009. doi:10.1016/j.schres.2009.05.031. Retrieved 30 May 2009.
126.^ Kuepper, R.; Van Os, J.; Lieb, R.; Wittchen, H.-U.; Hofler, M.; Henquet, C. (2011). “Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study”. BMJ (BMJ) 342: d738. doi:10.1136/bmj.d738. PMC 3047001. PMID 21363868.
127.^ Hashibe M; Morgenstern H; Cui Y; Tashkin D; Zhang, Z.-F.; Cozen, W.; Mack, T. M.; Greenland, S. (2006). “Marijuana use and the risk of lung and upper aerodigestive tract cancers: results of a population-based case-control study”. Cancer Epidemiol. Biomarkers Prev. 15 (10): 1829–34. doi:10.1158/1055-9965.EPI-06-0330. PMID 17035389. Lay summary.
128.^ Osterweil, Neil (24 May 2006). “ATS: Marijuana Smoking Found Non-Carcinogenic”. MedPage Today. Retrieved 12 August 2009.
129.^ Kaufman, Marc (26 May 2006). “Study Finds No Cancer-Marijuana Connection”. The Washington Post. Retrieved 12 August 2009.
130.^ Aldington S; Harwood M; Cox B; Weatherall, M.; Beckert, L.; Hansell, A.; Pritchard, A.; Robinson, G. et al. (2008). “Cannabis use and risk of lung cancer: a case-control study”. European Respiratory Journal 31 (1): 280–6. doi:10.1183/09031936.00065707. PMC 2516340. PMID 18238947.
131.^ Hii SW, Tam JD, Thompson BR, Naughton MT (2008). “Bullous lung disease due to marijuana”. Respirology 13 (1): 122–7. doi:10.1111/j.1440-1843.2007.01186.x. PMID 18197922. Lay summary.
132.^ [unreliable medical source?]”Marijuana Worsens COPD Symptoms in Current Cigarette Smokers” (Press release). American Thoracic Society. 21 May 2007. Retrieved 11 August 2009.
133.^ Tan, WC; Lo, C; Jong, A; Xing, L; Fitzgerald, MJ; Vollmer, WM; Buist, SA; Sin, DD et al. (14 April 2009). “Marijuana and chronic obstructive lung disease: a population-based study” (PDF). CMAJ (Toronto: Canadian Medical Association) 180 (8): 814–20. doi:10.1503/cmaj.081040. PMC 2665947. PMID 19364790. Retrieved 15 August 2009. Lay summary (13 April 2009).
134.^ Tashkin, Donald P. (14 April 2009). “Does smoking marijuana increase the risk of chronic obstructive pulmonary disease?” (PDF). CMAJ (Toronto: Canadian Medical Association) 180 (8): 797–8. doi:10.1503/cmaj.090142. PMC 2665954. PMID 19364782. Retrieved 16 August 2009.
135.^ “MAPS/CaNORML vaporizer and waterpipe studies”. Maps.org. Retrieved 2009-11-14.
136.^ Abrams DI, Vizoso HP, Shade SB, Jay C, Kelly ME, Benowitz NL (2007). “Vaporization as a smokeless cannabis delivery system: a pilot study”. Clinical Pharmacology and Therapeutics 82 (5): 572–8. doi:10.1038/sj.clpt.6100200. PMID 17429350.
137.^ Seamon, Matthew; Jennifer Fass, Maria Maniscalo-Feichtl, and Nada Abu-Sharie (15 May 2007). “Medical Marijuana and the developing role of the Pharmacist”. American Journal of Health-System Pharmacy 64 (10): 1037–1044. doi:10.2146/ajhp060471. PMID 17494903.
138.^ Levitz SM, Diamond RD (1991). “Aspergillosis and marijuana”. Annals of Internal Medicine 115 (7): 578–9. PMID 1652910.
139.^ “AMA Urges Reclassifying Marijuana”. Americans for Safe Access. Retrieved 10 January 2010.
140.^ “Use of Cannabis for Medicinal Purposes”. Report 3 of the Council on Science and Public Health (I-09). American Medical Assn. Retrieved 10 January 2010.
141.^ “Supporting Research into the Therapeutic Role of Marijuana” (PDF). The American College of Physicians. 2008. Retrieved 15 August 2009.
142.^ “Medical Marijuana Endorsements and Statements of Support”. Marijuana Policy Project. 2007. Archived from the original on 14 March 2008. Retrieved 29 January 2008.
143.^ “Marijuana: Policy & Advocacy”. American Academy of Family Physicians. 2009. Retrieved 6 October 2009.
144.^ Abel, Ernest L. (1980). “Cannabis in the Ancient World”. Marihuana: the first twelve thousand years. New York City: Plenum Publishers. ISBN 978-0-306-40496-2.[page needed]
145.^ Li, Hui-Lin (1974). “An Archaeological and Historical Account of Cannabis in China”, Economic Botany 28.4:437–448, p. 444.
146.^ Bretschneider, Emil (1895). Botanicon Sinicum: Notes on Chinese Botany from Native and Western Sources. Part III, Botanical Investigations in the Materia Medica of the Ancient Chinese. Kelly & Walsh. p. 378.
147.^ de Crespigny, Rafe (2007). A Biographical Dictionary of Later Han to the Three Kingdoms (23–220 CE). Leiden: Brill Publishers. p. 332. ISBN 978-90-04-15605-0. OCLC 71779118.
148.^ Barber, Elizabeth Wayland. (1992). Prehistoric Textiles: The Development of Cloth in the Neolithic and Bronze Ages with Special Reference to the Aegean. Princeton University Press. p. 38.
149.^ Smith, Frederick Porter (1911). Chinese Materia Medica: Vegetable Kingdom. Shanghai: American Presbyterian Mission Press. pp. 90–91.
150.^ “The Ebers Papyrus The Oldest (confirmed) Written Prescriptions For Medical Marihuana era 1,550 BC”. www.onlinepot.org. Retrieved 2008-06-10.
151.^ “History of Cannabis”. www.reefermadnessmuseum.org. Archived from the original on 2008-05-25. Retrieved 2008-07-09.
152.^ Pain, Stephanie (2007-12-15). “The Pharaoh’s pharmacists”. New Scientist (Reed Business Information Ltd.).
153.^ (Webley, Kayla. “Brief History: Medical Marijuana.” Time June 21, 2010.)
154.^ Lise Manniche, An Ancient Egyptian Herbal, University of Texas Press, 1989, ISBN 978-0-292-70415-2[page needed]
155.^ Touw M (1981). “The religious and medicinal uses of Cannabis in China, India and Tibet”. Journal of Psychoactive Drugs 13 (1): 23–34. doi:10.1080/02791072.1981.10471447. PMID 7024492.
156.^ a b c d e “The Haworth Press Online Catalog: Article Abstract”. www.haworthpress.com. Retrieved 2009-01-18.
157.^ Lozano, Indalecio (2001). “The Therapeutic Use of Cannabis sativa (L.) in Arabic Medicine”. Journal of Cannabis Therapeutics 1 (1): 63–70. doi:10.1300/J175v01n01_05.
158.^ Mack, Allyson; Janet Elizabeth Joy (2001). Marijuana as Medicine?: The Science Beyond the Controversy. National Academy Press.
159.^ “History of Cannabis”. BBC News. 2 November 2001. Retrieved 17 August 2011.
160.^ Anon (1886). Chemist & druggist (London, New York City, Melbourne: Benn Brothers) 28: 68,330. http://books.google.com/books?id=qiPOAAAAMAAJ.
161.^ “Hasjisj in Nordisk Famijebok 1912” (in sv). Runeberg.org. Retrieved 2012-01-15.
162.^ The Antique Cannabis Book. antiquecannabisbook.com (2012-03-16). Retrieved on 2012-05-19.
163.^ “Golden Guide”. www.zauberpilz.com.
164.^ (Czech) “Nad lécivými jointy s Lumírem Hanušem”. blisty.cz. Retrieved 2011-05-03.
165.^ Zimmerman, Bill; Nancy Crumpacker and Rick Bayer (1998). Is Marijuana the Right Medicine for You?: A Factual Guide to Medical Uses of Marijuana. Keats Publishing. ISBN 0-87983-906-6.[page needed]
166.^ Baker, D.; Pryce, G., Giovannoni, G., Thompson, A.J. (2003). “The therapeutic potential of cannabis”. Lancet Neurology 2 (5): 291–98. doi:10.1016/S1474-4422(03)00381-8. PMID 12849183. Retrieved 15 August 2009.
167.^ McPartland, John M.; Russo, Ethan B.. “Cannabis and Cannabis Extracts: Greater Than the Sum of Their Parts?”. Journal of Cannabis Therapeutics. International Association for Cannabis as Medicine.
168.^ Mack,Alison ; Joy, Janet (2001). Marijuana As Medicine. National Academy Press. ISBN 0-309-06531-3.[page needed]
169.^ Russo, Ethan; Mathre, Mary Lynn; Byrne, Al; Velin, Robert; Bach, Paul J; Sanchez-ramos, Juan; Kirlin, Kristin A (2002). “Chronic Cannabis Use in the Compassionate Investigational New Drug Program: An Examination of Benefits and Adverse Effects of Legal Clinical Cannabis” (PDF). Journal of Cannabis Therapeutics (The Haworth Press) 2 (1): 3. doi:10.1300/J175v02n01_02.
170.^ a b “Single Convention on Narcotic Drugs, 1961 As amended by the 1972 Protocol” (PDF). International Narcotics Control Board. United Nations. 13 March 1961. pp. 2–3. Retrieved 17 August 2009.
171.^ (German) “Verordnung der Bundesministerin für Arbeit, Gesundheit und Soziales über den Verkehr und die Gebarung mit Suchtgiften – SV”. Bundesministerium für Arbeit, Gesundheit und Soziales. 2011. Retrieved 25 March 2011.
172.^ (German) Valenta, Claudia (2005). “Magistrale Problem-Rezepturen”. Österreichische Apothekerzeitung (Vienna: Österreichische Apotheker-Verlagsges.m.b.H.) (5). Retrieved 30 July 2009.
173.^ a b (German) ABDA – Bundesvereinigung Deutscher Apothekerverbände (21 April 2008). “Rezepturhinweise: Dronabinol- und Cannabis-Zubereitungen” (PDF). Pharmazeutische Zeitung (Eschborn: Govi-Verlag Pharmazeutischer Verlag GmbH). Retrieved 30 July 2009.
174.^ “AFP: Austria allows cannabis for medical purposes”. afp.google.com. Retrieved 21 July 2008.
175.^ (German) Anon (19 December 2008). “Änderung des Suchtmittelgesetzes – SMG” (PDF). Bundesgesetzblatt für die Republik Österreich (Vienna: Österreichischer Bundesverlag). Retrieved 30 July 2009.
176.^ “MMAR FAQ”. MMAR FAQ.
177.^ “Frequently Asked Questions – Medical Use of Marihuana”. Health Canada. 13 June 2005. Retrieved 23 September 2009.
178.^ “More pot, please: Demand booming for Prairie Plant’s marijuana”. CBC News. 23 October 2006. Retrieved 23 September 2009.
179.^ Capler, Rielle (2007). “A Review of the Cannabis Cultivation Contract between Health Canada and Prairie Plant Systems”. British Columbia Compassion Club Society. Retrieved 23 September 2009.
180.^ Kari, Shannon (June 1, 2009). “Court challenge aims to legalize all cannabis use; Advocates say previous rule a ‘mockery’.”. National Post (Toronto): p. A.6. ProQuest Newsstand, Document ID: 1739130721.
181.^ Collet, J.P; Shapiro, S., Tongtong, W., & Ware, M. A. (2008). “Adverse effects of medical cannabinoids: a systematic review”. Canadian Medical Association Journal 178 (13): 1669–1678. doi:10.1503/cmaj.071178. PMC 2413308. PMID 18559804.
182.^ Germany: First Patients to Receive cannabis from the pharmacy, IACM-Bulletin of 15 February 2009. www.cannabis-med.org (2003-10-01). Retrieved on 2012-05-19.
183.^ Grotenhermen, Franjo (2002). “The Medical Use of Cannabis in Germany”. Journal of Drug Issues 32 (2): 607–34. doi:10.1177/002204260203200218.
184.^ (German) “Gesetz über den Verkehr mit Betäubungsmitteln (Betäubungsmittelgesetz – BtMG)” (PDF). Bundesministerium der Justiz. 19 January 2009. Retrieved 30 July 2009.
185.^ News: ISRAELVALLEY SANTE – Les vertus du cannabis – En Israël, le « fournisseur médical » de marijuana du Ministère de la santé, Tikun Olam, prône les bienfaits de la plante controversée pour le traitement du cancer. Israelvalley.com – Site officiel de la Cambre de Commerce France-Israël, CCFI (2010-11-22). Retrieved on 2012-05-19.
186.^ Hidalgo, Susana. “El debate sobre el cannabis no espabila.” Público.es 
187.^ a b Pérez-Lanzac C. El cannabis pelea por un espacio legal. El País. September 12, 2008. 
188.^ “Drug Offences Definitive Guideline”. Sentencing Council.
189.^ a b The Committee Office, House of Lords. “House of Lords – Science and Technology – Ninth Report”. Parliament.the-stationery-office.co.uk. Retrieved 2010-10-20.
190.^ “Inter-Agency Advisory Regarding Claims That Smoked Marijuana Is a Medicine” (Press release). Food and Drug Administration. 20 April 2006. Retrieved 9 August 2009.
191.^ “The DEA Position On Marijuana”. Drug Enforcement Administration. 2006. Archived from the original on 28 August 2010. Retrieved 11 August 2009.
193.^ “Marijuana Registry”. Alaska Health and Social Services. Retrieved 2009-10-08.
194.^ “Arizona Becomes 15th State to Approve Medical Marijuana”. The New York Times. Associated Press. 2010-11-14. Retrieved 2010-11-15.
195.^ “Medical Marijuana Program”. California Department of Public Health. Retrieved 2009-10-08.
196.^ “Colorado Medical Marijuana Registry”. Colorado Department of Public Health and Environment. Retrieved 2009-10-08.
197.^ Zalaznick, Matt. “Connecticut Docs Can Prescribe Medical Marijuana”. The Norwalk Daily Voice. Retrieved 26 July 2012.
198.^ “Connecticut Senate Passes Medical Marijuana Bill”. ABC News. Retrieved 2012-05-05.
199.^ “Delaware Medical Marijuana Patient Laws”. Chronic Resource for Delaware Marijuana. Retrieved 2012-01-20.
200.^ “Delaware legalizes medical marijuana”. Reuters. 2011-05-13. Retrieved 2012-01-20.
201.^ “Narcotics Enforcement Division”. Hawaii Department of Public Safety. Retrieved 2009-10-08.
202.^ Nemitz, Bill (2009-02-26). “Maine’s cannabis contradiction”. Portland Press Herald. Archived from the original on 2009-05-02. Retrieved 2009-10-08.
203.^ “Michigan Medical Marijuana Program”. Michigan Department of Community Health. Retrieved 2009-10-08.
204.^ “Montana Medical Marijuana Program”. Montana Department of Public Health and Human Services. Retrieved 2009-10-08.
205.^ “Medical Marijuana”. Nevada Department of Health and Human Services. Retrieved 2009-10-08.
206.^ Kocieniewski, David (11-01-2010). “New Jersey Lawmakers Pass Medical Marijuana Bill”. nytimes.com. Retrieved 15 May 2010.
207.^ “Medical Cannabis Program”. New Mexico Department of Health. Retrieved 2009-10-08.
208.^ “Oregon Medical Marijuana Program (OMMP)”. State of Oregon – Department of Human Services. Retrieved 2009-10-07.
209.^ “Medical Marijuana Program (MMP)”. Rhode Island Department of Health. Retrieved 2009-10-08.
210.^ “Vermont Marijuana Registry: A Guide for Patients and Physicians”. Vermont Criminal Information Center. Retrieved 2009-10-08.
211.^ “§ 18.2–251.1. Possession or distribution of marijuana for medical purposes permitted”. Virginia Department of Health. Retrieved 2010-08-30.
212.^ “Medical Marijuana Frequently Asked Questions”. Washington State Department of Health. Retrieved 2009-10-08.
213.^ “Medical marijuana now legal”. The Washington Post.
214.^ “US medical cannabis policy eased”. BBC News. 20 October 2009. Retrieved 30 October 2009.
215.^ NORML – “Maryland Medical Marijuana”.
216.^ “BILL INFO-2011 Regular Session-SB 308”.
217.^ “Employers now able to fire medical marijuana users legally in Washington”. MedicalMarijuanaBill.com. 2011-06-13. Retrieved 2011-07-31.
218.^ Mitchell, Dan (31 May 2008). “Legitimizing Marijuana”. The New York Times. Retrieved 11 August 2009.
219.^ The Times – California dreaming of full marijuana legalisation, The Times, September 28, 2009
220.^ “19 October 2009; Office of the Deputy Attorney General, US Dept. of Justice, Washington D.C. 20530. Memorandum for Selected United States Attorneys. Subject: Investigations and Prosecutions in States Authorizing the Medical Use of Marijuana” (PDF). Retrieved 2010-10-20.
221.^ US patent 6630507, Hampson, Aidan J.; Axelrod, Julius; Grimaldi, Maurizio, “Cannabinoids as antioxidants and neuroprotectants”, issued 2003-10-07
222.^ Billy, Michael (7 July 2008). “Opinion: US Government Holds Patent For Medical Marijuana, Shows Hipocrisy”. DigitalJournal.com. Retrieved 11 August 2009.