The effects of cannabis are caused by chemical compounds in the plant, including cannabinoids, such as tetrahydrocannabinol (THC), which is just one of more than 100 cannabinoids present in the plant. Marijuana has various psychological and physiological effects on the human body.
Different plants of the genus Cannabis contain different and often unpredictable THC and cannabinoids concentrations and hundreds of other molecules that have pharmacological effects, so the final net effect is unpredictable.
The acute effects of being under the influence may include euphoria and anxiety. Cannabidiol (CBD), another cannabinoid found in cannabis in varying amounts, has been shown to reduce the adverse effects of THC experienced by some consumers. When ingested orally, THC can produce a stronger psychotropic effect than when inhaled. At doses exceeding the psychotropic threshold, users may experience adverse side effects such as anxiety and panic attacks that can result in increased heart rate and blood pressure changes.
Research on the medical benefits of marijuana has been obstructed by US federal law. Smoking any substance will carry the same risk as tobacco smoking because of carcinogens in all the smoke, and the final conclusion on these factors is debatable.
Disorders of cannabis use are defined as medical diagnoses in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorder (DSM-5).
Video Effects of cannabis
Efficacies
Cannabinoids and cannabinoid receptors
The most common psychoactive substances in cannabis are cannabinoids, especially THC. Some varieties, after a careful selection and growing technique, can produce as much as 29% THC. Another psychoactive cannabinoid present in Cannabis sativa is tetrahydrocannabivarin (THCV), but is found only in small amounts and is a cannabinoid antagonist.
There are also similar compounds contained in cannabis that do not exhibit psychoactive responses but are mandatory for functionality: cannabidiol (CBD), an isomer of THC; cannabivarin (CBV), analogue cannabinol (CBN) with different side chains, cannabidivarin (CBDV), CBD analogs with different side chains, and cannabinolic acid. How these other compounds interact with THC is not fully understood. Several clinical studies have suggested that CBD acts as a counterweight force to regulate THC psychoactive agent strength. The CBD is also believed to regulate THC body metabolism by inactivating cytochrome P450, an important class of enzymes that metabolize drugs. Experiments in which mice treated with CBD followed by THC showed that CBD treatment was associated with a substantial increase in THC brain concentrations and its major metabolites, most likely due to a decrease in the THC clearance rate from the body. The cannabis cofactor compound has also been linked to lower body temperature, modulate immune function, and cell protection. The essential oil of marijuana contains many terpenoids that can synergize with cannabinoids to produce their unique effects. THC is rapidly converted to 11-hydroxy-THC, which is also pharmacologically active, so its drug effects exceed THC levels measured in the blood.
THC and cannabidiol are also neuroprotective antioxidants. Studies in mice have shown that THC prevents oxidative damage induced by hydroperoxide as well as or better than other antioxidants in chemical systems (Fenton reactions) and neuronal cultures. Cannabidiol is significantly more protective than vitamin E or vitamin C.
The cannabinoid receptors are distinctive members of the largest known receptor family called the protein-coupled G protein. The signatures of this type of receptor are different patterns of how the receptor molecule stretches the cell membrane seven times. The location of the cannabinoid receptors is in the cell membrane, and both outside (extracellular) and inside (intracellular) cell membranes. The CB1 receptor, which is bigger than both, is amazingly abundant in the brain: 10 times more than the -opioid receptor, the receptor responsible for the effects of morphine. The CB2 receptor is structurally different (the similarity sequence between the two receptor subtypes is 44%), found only in immune system cells, and appears to function similarly to its CB1 counterpart. CB2 receptors are most common in B cells, natural killer cells, and monocytes, but can also be found in polymorphonuclear neutrophil cells, T8 cells, and T4 cells. In the tonsils of CB2 receptors appear to be confined to the enriched B-lymphocyte region.
THC and its endogenous anandamide also interact with glycine receptors.
Biochemical mechanisms in the brain
Cannabinoids typically contain 1.1'-di-methyl-pyran rings, varying derivative aromatic rings and varied unsaturated cyclohexyl rings and their direct chemical precursors, are a family of about 60 bi-cyclic and tri-cyclic compounds. Like most other neurological processes, the effects of cannabis on the brain follow the standard protocol of signal transduction, electrochemical systems of sending signals through neurons for biological responses. It is now understood that cannabinoid receptors appear in similar forms in most vertebrates and invertebrates and have a long evolutionary history of 500 million years. The binding of cannabinoids to the cannabinoid receptors decreases the activity of adenylyl cyclase, inhibits the calcium N channel, and removes the channel K A . There are at least two types of cannabinoid receptors (CB1 and CB2).
The CB1 receptors are found primarily in the brain and mediate the psychological effects of THC. CB2 receptors are most commonly found in immune system cells. Cannabinoids act as immunomodulators at CB2 receptors, which means they increase some immune responses and reduce others. For example, nonpsychotropic cannabinoids can be used as highly effective anti-inflammatory agents. The affinity of kanabinoid to bind both receptors is almost the same, with only a slight increase observed with CBD-derived compounds from plants that bind to CB2 receptors more frequently. Cannabinoids may have a role in brain control of movement and memory, as well as modulation of natural pain. It is clear that cannabinoids can affect the transmission of pain and, in particular, cannabinoids that interact with endogenous brain opioid systems and may affect the transmission of dopamine.
Sustainability in body
Most cannabinoids are lipophilic compounds (fat soluble) easily stored in fat, resulting in long elimination half-life relative to other recreational drugs. THC molecules, and related compounds, are usually detected in drug tests from 3 days to 10 days according to Redwood Laboratories; long-term users can produce positive tests for two to three months after stopping marijuana use (see drug test).
Maps Effects of cannabis
Toxicities
Associated with cannabinoids
No fatal overdose with cannabis use has been reported in 2006. A review published in the British Journal of Psychiatry in February 2008 says that "no direct deaths due to acute use of kanabis have been reported".
THC, the main psychoactive constituent of cannabis plants, has very low toxicity and the amount that can enter the body through the consumption of cannabis plants does not pose a threat of death. In dogs, the lethal minimum thc dose is more than 3 g/kg.
According to Merck Index, LD 50 of THC (dose causing 50% mortality from individuals) is 1270 mg/kg for male rats and 730 mg/kg for mice females of oral consumption in sesame oil, and 42 mg/kg for inhaled mice.
The ratio of cannabis needed to produce a fatal overdose with the amount required to saturate cannabinoid receptors and cause poisoning is around 40.000: 1.
It is important to note that the cannabinoids and other molecules present in cannabis can alter the metabolism of other drugs, especially because of the competition to clear metabolic pathways such as CYP450 cytochrome, thus causing drug toxicity by drugs that people consuming marijuana may take.
Related to smoking
A 2007 study found that although tobacco smoke and marijuana are very similar, cannabis smoke contains higher amounts of ammonia, hydrogen cyanide, and nitrogen oxide, but lower levels of carcinogenic polycyclic aromatic hydrocarbons (PAHs). The study found that directly inhaled smoke contains 20 times as much ammonia and 5 times as much hydrogen cyanide as tobacco smoke and compares mainstream and sidestream properties (smoke emitted from the burning 'joints' or 'cones' ) smoking. Mainstream marijuana smoke is found to contain higher concentrations of selected polycyclic aromatic hydrocarbons (PAHs) than sidestream tobacco smoke. However, other studies have found far lower differences in ammonia and hydrogen cyanide between cannabis and tobacco, and that some other constituents (such as polonium-210, lead, arsenic, nicotine, and specific tobacco nitrosamines) are either lower or absent in marijuana smoke.
Marijuan smoke contains thousands of organic and inorganic chemicals. This tar is chemically similar to that found in tobacco smoke or cigars. More than fifty known carcinogens have been identified in cannabis smoke. These include nitrosamines, reactive aldehydes, and polyclic hydrocarbons, including benz [a] pyrene. Marijuana smoke was listed as a cancer agent in California in 2009. A study by the British Lung Foundation published in 2012 identified cannabis smoke as a carcinogen and also found an awareness of low hazards compared to a high awareness of the dangers of tobacco cigarettes in particular. among younger users. Other observations include the possibility of an increased risk of each cigarette; lack of research on the effects of cannabis smoke alone; low addiction rate compared to tobacco; and the nature of episodic marijuana use compared to the prevalent smoking habit. Professor David Nutt, a British pharmacist, pointed out that the study cited by the British Lung Foundation has been accused of being "the wrong reason" and "incorrect methodology". Furthermore, he notes that other studies have failed to connect marijuana with lung cancer, and accused BLF of "embezzling marijuana".
Short-term effects
When smoking, short-term effects of marijuana manifest in seconds and are apparent within minutes, usually lasting 1-3 hours, varying by the person and strain of marijuana. After oral administration of marijuana, the onset of delayed effects relative to smoking, taking 30 minutes to 2 hours, but prolonged duration due to continued slow absorption. The observed effect duration has been observed to be reduced due to prolonged and repeated use and development of tolerance to cannabinoids.
Psychological effects
The psychoactive effects of cannabis, known as "high", are subjective and may vary based on the person and method of use.
When THC enters the bloodstream and reaches the brain, THC binds to the cannabinoid receptors. The endogenous ligand of this receptor is anandamide, a THC imitating effect. This cannabinoid receptor agonist produces changes at the level of various neurotransmitters, especially dopamine and norepinephrine; neurotransmitters are closely related to the acute effects of cannabis consumption, such as euphoria and anxiety. Some effects may include general changes of conscious perception, euphoria, feelings of well-being, relaxation or stress reduction, increased appreciation of art, including humor and music (especially differentiating different components/instruments), cheerful, metacognition and introspection, enhanced memory (episodic memory) , increased sensuality, increased awareness of sensation, increased libido, and creativity. Abstract or philosophical thought, linear memory disorder and paranoia or anxiety are also typical. Anxiety is the most commonly reported smoking side effect. Between 20 and 30 percent of recreational users experience intense anxiety and/or panic attacks after smoking marijuana, however, some report anxiety only after not smoking cannabis for long periods of time. Experience and usage in unfamiliar surroundings is a major factor contributing to this anxiety. Cannabidiol (CBD), another cannabinoid found in cannabis in varying amounts, has been shown to improve the adverse effects of THC, including anxiety, which some consumers experience.
Cannabis also produces many subjective and highly visible effects, such as greater enjoyment of food flavor and aroma, increased musical and comedic pleasure, and marked distortions in perceptions of time and space (where experiencing a "rush" of ideas from long-term memory banks can creating a subjective impression of a long time gone by, while in reality only a short time has passed). At higher doses, effects may include changes in body image, auditory and/or visual illusions, pseudohalucination, and ataxia from selective polysynaptic reflective disorders. In some cases, cannabis can cause dissociative states such as depersonalization and derealization.
Each episode of acute psychosis that accompanies the use of marijuana usually subsides after 6 hours, but in rare cases, heavy users may find symptoms that persist for several days. If the episode is accompanied by aggression or sedation, physical control may be necessary.
While many psychoactive drugs clearly fall into the categories of either stimulants, depressants, or hallucinogens, marijuana exhibits a mixture of all traits, perhaps most geared toward hallucinogenic or psychedelic properties, although with other effects quite self-explanatory as well. THC is usually considered to be the main active component of cannabis plants; various scientific studies have shown that certain other cannabinoids such as CBD can also play an important role in their psychoactive effects.
Somatic effects
Some of the short-term physical effects of cannabis use include increased heart rate, dry mouth, redness of the eyes (conjunctival vascular congestion), decreased intra-ocular pressure, muscle relaxation and cold or hot hand sensation. and feet and/or face flushed.
Electroencephalography or EEG shows a rather persistent alpha wave with a slightly lower frequency than usual. Cannabinoids produce "signs of depression of motor activity" through activation of neuronal cannabinoid receptors belonging to the CB1 subtype.
Duration
The peak level of cannabis-related intoxication occurs about 30 minutes after sucking and lasts for several hours.
Smoked and Vaporized
The total duration of short-term use of cannabis when smoked is based on potential, smoking or evaporation methods - eg. whether pure or with tobacco - and how many are smoked or evaporated. The peak level of intoxication usually lasts several hours.
Oral
When taken orally (in capsule, food or drink), psychoactive effects take longer to manifest and generally last longer, usually lasting 4-10 hours after consumption. Very high doses can last longer. In addition, the use of oral ingestion eliminates the need to inhale toxic burning products created by smoking and therefore negates the risk of respiratory distress associated with smoking marijuana.
Neurological effects
The area of ​​the brain where cannabinoid receptors are most often found is consistent with the behavioral effects produced by cannabinoids. The area of ​​the brain in which the abundant cannabinoid receptor is the basal ganglia, which is associated with motion control; cerebellum, associated with the coordination of body movement; hippocampus, associated with learning, memory, and stress control; cerebral cortex, associated with higher cognitive function; and the nucleus accumbens, which is considered the center of the brain's reward. Another area where the concentrated cannabinoid receptor is the hypothalamus, which regulates homeostatic function; the amygdala, which is associated with an emotional and fear response; spinal cord, associated with peripheral sensations such as pain; brain stem, associated with sleep, arousal, and motor control; and the nucleus of the solitary canal, is associated with visceral sensations such as nausea and vomiting.
Experiments on animals and human tissue have shown a short-term memory formation disorder, which is consistent with the large number of C receptors in the hippocampus, the region of the brain most closely related to memory. Cannabinoids inhibit the release of several neurotransmitters in the hippocampus such as acetylcholine, norepinephrine, and glutamate, resulting in a large decrease in neuronal activity in the region. This decrease in activity resembles "temporary hippocampal lesions."
In-vitro THC experiments at very high concentrations, which can not be achieved with the usual dose consumed, lead to competitive inhibition of the AChE enzyme and inhibition of aggregation of the peptide-amyloid, which is involved in the development of Alzheimer's. disease. Compared with currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a very superior inhibitor of aggregation A, and this study provides a previously unknown molecular mechanism through which the cannabinoid molecule can have an impact on the development of this debilitating disease.
Effects while driving
While some studies have shown an increased risk associated with the use of kanabis by drivers, other studies have found no increased risk. The use of marijuana has been shown in several studies to have a negative effect on driving ability. The British Medical Journal points out that "drivers who consumed marijuana in three hours were driving almost twice as likely to cause a vehicle collision as those who were not under the influence of drugs or alcohol."
In marijuana and driving: a review of literature and commentaries, the UK Department of Transportation reviewed data on marijuana and driving, finding despite the disruption, â € subjects under marijuana care seem to perceive that they are indeed disturbed.. Where they can compensate, they... "In a study review driving simulator, the researchers noted that" even in those who learn to compensate for the damaging effects of drugs, a substantial decrease in performance can still be observed under general task performance conditions (ie when none exist contingencies present to maintain compensation performance). "
A meta-analysis 2012 found that the use of acute kanabis increases the risk of car accidents. A broad review of 2013 of 66 studies on accident risk and drug use found that marijuana was associated with a minor, but not a statistically significant increase in the likelihood of a fatal injury or accident.
In the largest and most appropriate controlled study of its kind carried out by the National Highway Traffic Safety Administration of the US Department of Transportation, it was found that "other studies that measure the presence of THC in the blood of drivers or oral fluids, rather than relying on self-reports tend to have lower (or none) an increase in the estimated risk of accidents, as well as better controlled studies have found a lower (or not) increased risk estimate of accidents ". The study found that "after adjusting for age, sex, race and alcohol use, the drivers tested positive for marijuana were no more likely to have accidents than those who did not use drugs or alcohol before driving."
Cardiovascular effects
Short-term effects (one to two hours) in the cardiovascular system may include increased heart rate, dilation of blood vessels, and blood pressure fluctuations. There are medical reports about occasional heart attacks or myocardial infarction, stroke and other cardiovascular side effects. Cardiovascular effects of marijuana are not associated with serious health problems for most healthy young users. The researchers report in the International Journal of Cardiology, "The use of marijuana by older people, especially those with multiple levels of coronary artery or cerebrovascular disease, poses a greater risk due to increased catecholamines, heart workload, and carboxyhemoglobin levels, and concurrent episodes of deep postural hypotension. True, marijuana may be a more common cause of myocardial infarction than is generally recognized. In everyday practice, the history of marijuana use is often not sought by many practitioners, and even when sought, not always true ".
A 2013 analysis of 3,886 victims of myocardial infarction during the 18-year period showed "no statistically significant relationship between marijuana use and mortality".
A 2008 study by the National Institutes of Health Biomedical Research Center in Baltimore found that heavy and chronic cannabis smoking (138 joints per week) altered blood proteins associated with heart disease and stroke.
A 2000 study by researchers at the Beth Israel Deaconess Medical Center in Boston, Massachusetts General Hospital and Harvard Public Health School found that the risk of a person suffering from a heart attack increased almost fivefold in the first hour after smoking marijuana, "roughly risk the same is seen in an hour of sexual activity ".
Cannabis arteritis is a very rare peripheral vascular disease similar to Buerger's disease. There were about 50 confirmed cases from 1960 to 2008, all in Europe.
Combination with other drugs
The confounding factor in marijuana research is the use of other recreational drugs, especially alcohol and nicotine. Such complications indicate the need for research on potentially more controlled marijuana, and investigation of possible alleged cannabis use symptoms that may also be caused by tobacco. Some critics question whether the agency conducting the study makes a genuine effort to present an accurate and unbiased summary of the evidence, or whether they "cherry" their data for possible funding sources including the tobacco industry or government dependent on tax revenues cigarette. ; others remind that the raw data, rather than the final conclusion, is what should be examined.
The 2001 National Household Survey of Australia showed that marijuana in Australia is rarely used without other drugs. 95% of cannabis users also drink alcohol; 26% take amphetamines; 19% took ecstasy and only 2.7% reported not taking other drugs with marijuana. While research has been done on the combined effect of alcohol and hashish on performing certain tasks, little research has been done on the reasons why this combination is so popular. Evidence from a controlled experimental study conducted by Luke and Orozco shows that alcohol causes THC to be absorbed more rapidly into the user's blood plasma. Data from the Australian National Mental Health and Welfare Survey found that three quarters of marijuana users recently reported using alcohol when marijuana was not available, indicating that both are substitutes.
Memory and learning
The study of marijuana and memory is hindered by small sample sizes, confusing drug use, and other factors. The strongest evidence of marijuana and memory focuses on negative effects while on short-term memory and work.
In a 2001 study that looked at neuropsychological performance in long-term marijuana users, the researchers found "some cognitive deficits appear detected at least 7 days after heavy cannabis use but appear reversible and associated with recent marijuana exposure rather than irreversible and associated with age use cumulative life ". In his study of cannabis use, lead researcher and Harvard professor Harrison Pope said he found marijuana harmless in the long run, but there were short-term effects. From a neuropsychological test, the Pope found that chronic cannabis users showed difficulty, with particularly verbal memory, to "at least a week or two" after they quit smoking. In 28 days, memory problems disappear and the subject "is no longer distinguishable from the comparison group". Researchers from the University of California, San Diego School of Medicine have failed to show substantial systemic neurological effects of long-term use of cannabis use. Their findings were published in the July 2003 issue of the Journal of the International Neuropsychological Society. The research team, led by Dr Igor Grant, found that the use of cannabis influences perception, but does not cause permanent brain damage. The researchers looked at data from 15 previously controlled controlled studies involving 704 users of marijuana in the long run and 484 non-users. The results show that long-term use of cannabis is only slightly damaging to memory and learning. Other functions such as reaction time, attention, language, reasoning ability, perceptual and motor skills are not affected. The observed effects on memory and learning, they said, suggest long-term use of marijuana causes "selective memory damage", but the impact is "very small". A study at Johns Hopkins University School of Medicine showed that the very heavy use of marijuana was associated with a decrease in neurocognitive performance even after 28 days of abstinence.
Appetite
The growing appetite feeling after the use of marijuana has been documented for hundreds of years, and is known as everyday language as a "snack" in the English-speaking world. Clinical studies and survey data have found that marijuana increases the enjoyment of food and interest in food. Scientists have claimed to be able to explain what causes increased appetite, concluding that "endocannabinoids in the hypothalamus activate cannabinoid receptors responsible for maintaining food intake". Rarely, chronic users experience severe vomiting disorder, cannabinoid hyperemesis syndrome, after smoking and find relief with a hot shower.
Endogenous cannabinoids ("endocannabinoids") are found in cow's milk and soft cheeses. Endocannabinoids are also found in human milk. It has been widely accepted that the neonatal survival of many species "depends heavily on their breastfeeding behavior, or appetite for breast milk" and recent research has identified endogenous kanabinoid systems into the first nervous system that shows complete control over breast milk and neonatal consumption. survive. It is possible that "cannabinoid receptors in our body interact with cannabinoids in milk to stimulate the breastfeeding response in newborns to prevent growth failure".
Pathogen and mikrotoxin
Most of the microorganisms found in cannabis affect only plants and not humans, but some microorganisms, especially those that proliferate when herbs are not dried and stored properly, can be harmful to humans. Some users can store marijuana in airtight pockets or jars in the refrigerator to prevent the growth of mold and bacteria.
Mushroom
Mushrooms Aspergillus flavus Aspergillus flavus Aspergillus fumigatus Aspergillus niger Aspergillus parasiticus Aspergillus tamarii Aspergillus flavus Aspergillus flavus , Aspergillus fumigatus Aspergillus sulphureus, Aspergillus repens, Mucor hiemalis (not human pathogens), Penicillium chrysogenum , Penicillium italicum and Rhizopus nigrans have been found in moldy marijuana. Aspergillus fungal species can infect the lungs through smoking or handling infected marijuana and causing opportunistic and sometimes lethal aspergillosis. Some of the microorganisms that are found create aflatoxin, which is toxic and carcinogenic. The researchers argue that moldy marijuana should be discarded to avoid this serious risk.
Fungi are also found in the smoke from marijuana infected mushrooms, and the lungs and nasal passages are the primary means of contracting fungal infections. Levitz and Diamond (1991) suggested baking marijuana in a home oven at a temperature of 150 ° C [302 ° F], for five minutes before smoking. Oven treatment kills conidia from A. fumigatus , A. flavus and A. niger , and does not decrease the active component of marijuana, tetrahydrocannabinol (THC). "
Bacteria
Cannabis contaminated with Salmonella muenchen was positively correlated with dozens of cases of salmonellosis in 1981. "Thermophilic actinomisetes" was also found in cannabis.
src: cbd-international.net
Long-term effects
Exposure to marijuana may have biological, physical, mental, behavioral and social health consequences and is associated with liver disease (especially with existing hepatitis C), lung, heart, and blood vessels "according to a review of the 2013 literature by Gordon and colleagues work. The relationship with the disease is only reported in cases where people smoke cannabis. The authors warn that "evidence is needed, and further research should be considered, to prove causal associations of cannabis with many physical health conditions".
The cannabis use disorder was defined in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorder (DSM-5) as a condition requiring treatment. Several drugs have been studied in an attempt to improve the symptoms of discontinuing the use of cannabis. They include bupropion, divalproex, nefazodone, lofexidine, and dronabinol. Of these, dronabinol has proven most effective.
src: www.mentalhealth.com
Effect on pregnancy
The consumption of marijuana in pregnancy may be related to fetal growth restriction, miscarriage, and cognitive deficits in offspring based on animal studies, although there is limited evidence for this in humans today. A systematic review of 2012 found that although it is difficult to draw strong conclusions, there is some evidence that prenatal exposure to marijuana is associated with "deficits in language, attention, cognitive performance areas, and misbehavior in adolescence." A report prepared for the Australian National Drug Board concluded that other cannabis and cannabinoids are contraindicated in pregnancy as they interact with the endocannabinoid system.
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See also
- Smoking marijuana
- Psychoactive drugs
src: mychronicrelief.com
References
src: stopsmokingweedplan.com
Further reading
- National Academy of Sciences, Engineering, and Medicine (2017). "The Health Effects of Cannabis and Cannabinoids: Current Conditions of Evidence and Recommendations for Research". National Academy of Science, Engineering, and Medicine . Washington, DC: The National Academies Press. doi: 10.17226/24625. Ã, CS1 maint: Many names : list of authors (links)
src: redeyesonline.net
External links
- The Use of Cannabis and Psychosis from the National Center for Drug and Alcohol Research, Australia
- Cannabis and Other Compounds For Scientific Research Recommendation from National Institute on National Advisory Council on Drug Abuse
- Scientific American Magazine (December 2004 Edition) The Brain's Own Marijuana
- RamstrÃÆ'¶m, J. (2003), Health Consequences of Cannabis Disorders, Scientific Study Survey Published and including Autumn 2003, National Institute of Public Health, Sweden, Stockholm.
- Hall, W., Solowij, N., Lemon, J., Health and Psychological Consequences of Cannabis Usage. Canberra: Australian Government Publishing Service; 1994.
- World Health Organization, GAWAT ABUSE PROGRAM, Ganja: health perspective and research agenda, 1997.
- National Cannabis Prevention and Information Center (Australia)
- EU Research Papers on potential Cannabis (2004)
- Marian Spreads and Mental Health information from the mental health charity Royal College of Psychiatrists
Source of the article : Wikipedia
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