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The short-term effects of cannabis are caused by many chemical compounds in the cannabis plant, including 113^{[clarification needed]} different cannabinoids, such as tetrahydrocannabinol (THC), and 120 terpenes,^[1] which allow its drug to have various psychological and physiological effects on the human body. Different plants of the genus Cannabis contain different and often unpredictable concentrations of THC and other cannabinoids and hundreds of other molecules that have a pharmacological effect,^[2]^[3] so the final net effect cannot reliably be foreseen. Acute effects while under the influence can sometimes include euphoria or anxiety.^[4]^[5] Although some assert that cannabidiol (CBD), another cannabinoid found in cannabis in varying amounts, may alleviate the adverse effects of THC that some users experience,^[6] little is known about CBD's effects on humans.^[7]^[8] Cannabinoid receptor antagonists have previously been tested as antidotes for cannabis intoxication with success, reducing or eliminating the physiological and psychological effects of intoxication.^[9] Some of these products are currently in development as cannabis antidotes.

Background and chronic use

In the United States, medical cannabis research is limited by federal restrictions.^[10]

Cannabis use disorder is defined as a medical diagnosis in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).^[11]

Chemistry

The structural formula of tetrahydrocannabinol

Cannabinoids and cannabinoid receptors

The most prevalent psychoactive substances in cannabis are cannabinoids, particularly THC. Some varieties, having undergone careful selection and growing techniques, can yield as much as 34% THC.^[12] Another psychoactive cannabinoid present in Cannabis sativa is tetrahydrocannabivarin (THCV), but it is only found in small amounts and is a cannabinoid antagonist.^[13]

There are similar compounds in cannabis that do not exhibit psychoactive response but are obligatory for functionality: cannabidiol (CBD), an isomer of THC; cannabivarin (CBV), an analog of cannabinol (CBN) with a different side chain, cannabidivarin (CBDV), an analog of CBD with a different side chain, and cannabinolic acid. CBD is believed to regulate the metabolism of THC by inactivating cytochrome P450 enzymes that metabolize drugs; one such mechanism is via generation of carbon monoxide (a pharmacologically active neurotransmitter) by upon metabolism of CBD.^[14] THC is converted rapidly to 11-hydroxy-THC, which is also pharmacologically active, so the euphoria outlasts measurable THC levels in blood.^[15]

Biochemical mechanisms in the brain

Cannabinoids usually contain a 1,1'-di-methyl-pyran ring, a variedly derivatized aromatic ring and a variedly unsaturated cyclohexyl ring and their immediate chemical precursors, constituting 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, the electrochemical system of sending signals through neurons for a biological response. 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 cannabinoid receptors decrease adenylyl cyclase activity, inhibit calcium N channels, and disinhibit K⁺_A channels. There are at least two types of cannabinoid receptors (CB1 and CB2).^[16]

Sustainability in the body

Most cannabinoids are lipophilic (fat soluble) compounds that are easily stored in fat, thus yielding a long elimination half-life relative to other recreational drugs. The THC molecule, and related compounds, are usually detectable in drug tests from 3 days up to 10 days.^{[citation needed]} Long-term users can produce positive tests for two to three months after ceasing cannabis use (see drug test).^[17]

Toxicities

When cannabis is smoked, blood levels of THC peak rapidly after a few minutes and then decline, although the psychotropic effects persist for longer. Edible forms of cannabis often contain several hundred milligrams of THC, much more than the 32 mg of a typical cannabis cigarette.^{[citation needed]} The rise of edible cannabis products has been responsible for a large increase of poisoning of children and young people.^{[citation needed]} Symptoms in children can include lethargy, sedation and seizure.^[18]

Synthetic cannabis is suspected of being a potential contributory factor or direct cause of sudden death, due to the strain it can place on the cardiovascular system, or because of cannabinoid hyperemesis syndrome.^[19]

Related to cannabinoids

THC, the principal psychoactive constituent of the cannabis plant, has an extremely low toxicity and the amount that can enter the body through the consumption of cannabis plants poses no threat of death. In dogs, the minimum lethal dose of THC is over 3000 mg/kg.^[20] According to The Merck Index,^[21] the LD₅₀ of THC (the dose which causes the death of 50% of individuals) is 1270 mg/kg for male rats and 730 mg/kg for female rats from oral consumption in sesame oil, and 42 mg/kg for rats from inhalation.^[22]

Cannabinoids and other molecules present in cannabis can alter the metabolism of other drugs, especially due to competition for clearing metabolic pathways such as cytochromes CYP450, thus leading to drug toxicities by medications that the person consuming cannabis may be taking.^[23]

Related to smoking

A 2007 study found that while tobacco and cannabis smoke are quite similar, cannabis smoke contained higher amounts of ammonia, hydrogen cyanide, and nitrogen oxides, but lower levels of carcinogenic polycyclic aromatic hydrocarbons (PAHs).^[24] This study found that directly inhaled cannabis smoke contained as much as 20 times as much ammonia and 5 times as much hydrogen cyanide as tobacco smoke and compared the properties of both mainstream and sidestream (smoke emitted from a smouldering 'joint' or 'cone') smoke.^[24] Mainstream cannabis smoke was found to contain higher concentrations of selected polycyclic aromatic hydrocarbons (PAHs) than sidestream tobacco smoke.^[24] However, other studies have found much lower disparities in ammonia and hydrogen cyanide between cannabis and tobacco, and that some other constituents (such as polonium-210, lead, arsenic, nicotine, and tobacco-specific nitrosamines) are either lower or non-existent in cannabis smoke.^[25]^[26] A 2021 longitudinal study conducted among populations of HIV-positive and HIV-negative adults found that smoke-related carcinogenic toxicants and biomarkers detected in tobacco smokers were also detected in exclusive cannabis smokers, including carbon monoxide (CO), polycyclic aromatic hydrocarbons (PAHs), aldehydes (such as acrolein), acrylonitrile and acrylamide metabolites, but exposures are lower compared with tobacco or dual smokers.^[27] Increased levels of acrolein exposure by tobacco smoking but not exclusive cannabis smoking were detected both in HIV-positive and HIV-negative adults, and contribute to increased diagnoses of cardiovascular diseases and respiratory diseases among tobacco smokers.^[27]

Cannabis smoke contains thousands of organic and inorganic chemical compounds. This tar is chemically similar to that found in tobacco smoke or cigars.^[28] Over fifty known carcinogens have been identified in cannabis smoke.^[29] These include nitrosamines, reactive aldehydes, and polycylic hydrocarbons, including benz[a]pyrene.^[30] Cannabis smoke was listed as a cancer agent in California in 2009.^[31] A study by the British Lung Foundation published in 2012 identifies cannabis smoke as a carcinogen and also finds awareness of the danger is low compared with the high awareness of the dangers of smoking tobacco particularly among younger users. Other observations include possible increased risk from each cigarette; lack of research on the effect of cannabis smoke alone; low rate of addiction compared to tobacco; and episodic nature of cannabis use compared to steady frequent smoking of tobacco.^[32]^{[unreliable medical source?]} Professor David Nutt, a UK drug expert, points out that the study cited by the British Lung Foundation has been accused of both "false reasoning" and "incorrect methodology". Further, he notes that other studies have failed to connect cannabis with lung cancer, and accuses the BLF of "scaremongering over cannabis".^[33]

Short-term effects

Onset and duration

When smoked, the short-term effects of cannabis manifest within seconds and are fully apparent within a few minutes,^[34] typically lasting 1–3 hours, varying by the person and the strain of cannabis.^[35] With oral ingestion, however, the onset of effect is delayed, taking 30 minutes to 2 hours, but the duration is prolonged due to continued slow absorption.^[34] The duration of noticeable effects has been observed to diminish after prolonged, repeated use leading to the development of increased tolerance to cannabinoids.^[36]

Psychological effects

The psychoactive effects of cannabis, known as a "high", are subjective and vary among persons and the method of use.

When THC enters the blood stream and reaches the brain, it binds to cannabinoid receptors. The endogenous ligand of these receptors is anandamide, the effects of which THC emulates. This agonism of the cannabinoid receptors results in changes in the levels of various neurotransmitters, especially dopamine and norepinephrine, which are closely associated with the acute effects of cannabis ingestion, such as euphoria and anxiety. Some effects may include a general altered state of consciousness, euphoria, relaxation or stress reduction, increased appreciation of the arts, including humor and music, joviality, metacognition and introspection, enhanced recollection (episodic memory), and increased sensuality, sensory awareness, libido, and creativity.^[37] Abstract or philosophical thinking, disruption of linear memory and paranoia or anxiety are also typical. Anxiety is cannabis's most commonly reported adverse side effect. Up to 30 percent of recreational users experience intense anxiety and/or panic attacks after smoking cannabis. Some report anxiety only after not smoking cannabis for a prolonged period of time.^[38] Inexperience and use in an unfamiliar environment are major contributing factors to this anxiety. Cannabidiol (CBD), another cannabinoid found in cannabis, has been shown to mitigate THC's adverse effects, including anxiety.^[39]

Cannabis produces many other subjective effects, including increased enjoyment of food taste and aroma, and marked distortions in the perception of time. At higher doses, effects can include altered body image, auditory or visual illusions, pseudohallucinations, and ataxia from selective impairment of polysynaptic reflexes.^{[citation needed]} In some cases, cannabis can lead to acute psychosis and dissociative states such as depersonalization^[40]^[41] and derealization.^[42]

Furthermore, even in those with no family history of psychosis, the administration of pure THC in clinical settings has been demonstrated to elicit transient psychotic symptoms.^[43]^[44]^[45]^[46] Any episode of acute psychosis that accompanies cannabis use usually abates after six hours, but in rare instances, users may find the symptoms continuing for many days.^[47]

While psychoactive drugs are typically categorized as stimulants, depressants, or hallucinogens, cannabis exhibits a mix of all of these effects. Scientific studies have suggested that other cannabinoids like CBD may also play a significant role in its psychoactive effects.^[48]^[49]^[50]

Somatic effects

Cannabis use can decrease blood pressure, which increases the risk of fainting.^[51] Combining alcohol with cannabis greatly increases the level of impairment and the risk of injury or death from accidents.^[52]

Some of the short-term physical effects of cannabis use include increased heart rate, dry mouth, reddening of the eyes (congestion of the conjunctival blood vessels), a reduction in intra-ocular pressure, muscle relaxation, and a sensation of cold or hot hands and feet.^[53]

Electroencephalography (EEG) shows somewhat more persistent alpha waves of slightly lower frequency than usual.^[54] Cannabinoids produce a marked depression of motor activity via activation of receptors of cannabinoid receptor type 1.^[55]

Duration

Peak levels of cannabis-associated intoxication occur about 20 minutes after smoking it and last several hours.^[56] The total short-term duration of cannabis use when smoked depends on the potency, method of smoking – e.g. whether pure or in conjunction with tobacco – and quantity. Peak levels of intoxication typically last an average of three to four hours.^[56] When taken orally (in the form of capsules, food, or drink), the psychoactive effects take longer to manifest and generally last longer, typically an average of four to six hours after consumption.^[57]^{[unreliable medical source?]} Oral ingestion use eliminates the need to inhale toxic combustion products created by smoking and therefore negates the risk of respiratory harm associated with cannabis smoking.

Appetite

Increased appetite after cannabis use has been documented for hundreds of years^[58] and is known colloquially as the "munchies". Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food.^[59]^[60] A 2015 study suggests that cannabis triggers uncharacteristic behaviour in proopiomelanocortin (POMC) neurons, which are usually associated with decreasing hunger.^[61]^[62]

Endogenous cannabinoids, more commonly known as endocannabinoids, exist in cow and human milk.^[63]^[64]^[65]^[66]^[67]^[68]^[69] It is widely accepted that the neonatal survival of many species is largely dependent upon their suckling behavior, and research has identified the endogenous cannabinoid system as the first neural system to display complete control over milk ingestion and neonatal survival.^[70]^[69]

Cardiovascular effects

Short-term (one to two hours) effects on the cardiovascular system can include increased heart rate, dilation of blood vessels, and fluctuations in blood pressure.^[71]^[72]^[73] There are medical reports of occasional heart attacks or myocardial infarction, stroke, and other cardiovascular side effects.^[74] Cannabis's cardiovascular effects are not associated with serious health problems for most young, healthy users.^[74] Researchers reported in the International Journal of Cardiology, "Marijuana use by older people, particularly those with some degree of coronary artery or cerebrovascular disease, poses greater risks due to the resulting increase in catecholamines, cardiac workload, and carboxyhemoglobin levels, and concurrent episodes of profound postural hypotension. Indeed, marijuana may be a much more common cause of myocardial infarction than is generally recognized. In day-to-day practice, a history of marijuana use is often not sought by many practitioners, and even when sought, the patient's response is not always truthful".^[75]

A 2013 analysis of 3,886 myocardial infarction survivors over an 18-year period showed "no statistically significant association between marijuana use and mortality".^[76]

A 2008 study by the National Institutes of Health Biomedical Research Centre in Baltimore found that heavy, chronic smoking of marijuana (138 joints per week) changed blood proteins associated with heart disease and stroke.^[77]

A 2000 study by researchers at Boston's Beth Israel Deaconess Medical Center, Massachusetts General Hospital, and Harvard School of Public Health found that a middle-aged person's risk of heart attack rises nearly fivefold in the first hour after smoking cannabis, "roughly the same risk seen within an hour of sexual activity".^[78]^[79]

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.^[80]

Memory and learning

Studies on cannabis and memory are hindered by small sample sizes, confounding drug use, and other factors.^[81] The strongest evidence regarding cannabis and memory focuses on its temporary negative effects on short-term and working memory.^[81]

In a 2001 study of neuropsychological performance in long-term cannabis users, researchers found "some cognitive deficits appear detectable at least 7 days after heavy cannabis use but appear reversible and related to recent cannabis exposure rather than irreversible and related to cumulative lifetime use".^[82] Of his studies on cannabis use, lead researcher and Harvard professor Harrison Pope said he found it is not dangerous over the long term, but there are short-term effects. From neuropsychological tests, Pope found that chronic cannabis users showed difficulty with verbal memory in particular for "at least a week or two" after they stopped smoking. Within 28 days, memory problems vanished and the subjects "were no longer distinguishable from the comparison group".^[83] Researchers at the University of California, San Diego School of Medicine failed to show substantial, systemic neurological effects from long-term cannabis use. Their findings were published in the July 2003 issue of the Journal of the International Neuropsychological Society.^[84] The research team, headed by Igor Grant, found that cannabis use affects perception but does not cause permanent brain damage. Researchers looked at data from 15 previously published controlled studies involving 704 long-term cannabis users and 484 nonusers. The results showed long-term cannabis use was only marginally harmful on memory and learning. Other functions such as reaction time, attention, language, reasoning ability, and perceptual and motor skills were unaffected. The observed effects on memory and learning, they said, showed long-term cannabis use caused "selective memory defects", but "of a very small magnitude".^[85] A study by Johns Hopkins University School of Medicine found that heavy cannabis use is associated with decrements in neurocognitive performance even after 28 days of abstinence.^[86]

Effects on driving

Several studies have shown increased risk associated with cannabis use by drivers, but others have found no increased risk.^[87] Cannabis usage has been shown in some studies to have an adverse effect on driving ability.^[88] The British Medical Journal 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".^[89]

In Cannabis and driving: a review of the literature and commentary, the United Kingdom's Department for Transport reviewed data on cannabis and driving, finding that, although impaired, "subjects under cannabis treatment appear to perceive that they are indeed impaired. Where they can compensate, they do".^[90] In a review of driving simulator studies, researchers found that "even in those who learn to compensate for a drug's impairing effects, substantial impairment in performance can still be observed under conditions of general task performance (i.e. when no contingencies are present to maintain compensated performance)."^[91]

A 2012 meta-analysis found that acute cannabis use increased the risk of an automobile crash.^[92] An extensive 2013 review of 66 studies of crash risk and drug use found that cannabis is associated with slightly but not statistically significantly increased odds of injury or fatal accident.^[93]

In the largest and most precisely controlled study of its kind, carried out by the U.S. Department of Transportation's National Highway Traffic Safety Administration, it was found that other "studies that measure the presence of THC in the drivers' blood or oral fluid, rather than relying on self-report tend to have much lower (or no) elevated crash risk estimates. Likewise better controlled studies have found lower (or no) elevated crash risk estimates".^[87] The study found that "after adjusting for age, gender, race and alcohol use, drivers who tested positive for marijuana were no more likely to crash than those who had not used any drugs or alcohol prior to driving".^[94] A 2018 study found that fatal crashes involving cannabis increased in Colorado, Washington, and Massachusetts after recreational cannabis legalization or decriminalization.^[95]

Combination with other drugs

A confounding factor in cannabis research is the prevalent usage of other recreational drugs, especially alcohol and nicotine.^[96] Such complications demonstrate the need for studies with stronger controls, and investigations into alleged symptoms of cannabis use that may also be caused by tobacco. Some critics question whether agencies doing the research make an honest effort to present an unbiased summary of the evidence without "cherry-picking" data to please funding sources such as the tobacco industry or governments dependent on cigarette tax revenue; others caution that the raw data, and not the final conclusions, are what should be examined.^[97]

The Australian National Household Survey of 2001^[98] found that cannabis is rarely used in Australia without other drugs. 95% of cannabis users also drank alcohol; 26% took amphetamines; 19% took ecstasy and only 2.7% reported not having used any other drug with cannabis.^[99] While there has been research on the combined effects of alcohol and cannabis on performing certain tasks, little has been done on the reasons this combination is so popular. Evidence from a controlled experimental study by Lukas and Orozco^[100] suggests that alcohol causes THC to be absorbed more rapidly into the user's blood plasma. Data from the Australian National Survey of Mental Health and Wellbeing^[101] found that three-quarters of recent cannabis users reported using alcohol when cannabis was not available, suggesting that the two have similar effects.^[102]

Pathogens and microtoxins

Most microorganisms found in cannabis affect only plants, not humans, but some, especially those that proliferate when the herb is not correctly dried and stored, can be harmful to humans. Some users store cannabis in an airtight bag or jar in a refrigerator to prevent fungal and bacterial growth.^[103]

The fungi Aspergillus flavus,^[104] Aspergillus fumigatus,^[104] Aspergillus niger,^[104] Aspergillus parasiticus, Aspergillus tamarii, Aspergillus sulphureus, Aspergillus repens, Mucor hiemalis (not a human pathogen), Penicillium chrysogenum, Penicillium italicum, and Rhizopus nigricans have been found in moldy cannabis.^[103] Aspergillus mold species can infect the lungs via smoking or handling of infected cannabis and cause opportunistic and sometimes deadly aspergillosis.^[105] Some of the microorganisms found create aflatoxins, which are toxic and carcinogenic. Mold is also found in smoke from mold-infected cannabis,^[103]^[104] and the lungs and nasal passages are a major means of contracting fungal infections. Levitz and Diamond (1991) suggest baking cannabis in home ovens at 150 °C [302 °F], for five minutes before smoking. Oven treatment killed conidia of A. fumigatus, A. flavus and A. niger, and did not lower THC levels.^[103] Cannabis contaminated with Salmonella muenchen was correlated with dozens of cases of salmonellosis in 1981.^[106] Thermophilic actinomycetes were also found in cannabis.^[104]

Long-term effects

Exposure to cannabis may have biologically based physical, mental, behavioral, and social health consequences and is "associated with diseases of the liver (particularly with co-existing hepatitis C), lungs, heart, eyesight, and vasculature" according to a 2013 literature review by Gordon and colleagues. The association with these diseases has only been reported in cases where people have smoked cannabis. The authors cautioned that "evidence is needed, and further research should be considered, to prove causal associations of cannabis with many physical health conditions".^[107]

Cannabis use disorder is defined in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) as a condition requiring treatment.^[107] Several drugs have been investigated in an attempt to ameliorate the symptoms of stopping cannabis use. Such drugs include bupropion, divalproex, nefazodone, lofexidine, and dronabinol. Of these, dronabinol (a trade name for THC) has proven the most effective.^[108] The drugs buspirone and rimonabant have shown some success in helping maintain cannabis abstinence.^[109]

There is evidence that long-term use of cannabis increases the risk of psychosis, regardless of confounding factors, and particularly for people who have genetic risk factors.^[110] A 2019 meta-analysis found that 34% of people with cannabis-induced psychosis transitioned to schizophrenia. This was found to be comparatively higher than hallucinogens (26%) and amphetamines (22%).^[111]

Long-term cannabis users are at risk for developing cannabinoid hyperemesis syndrome (CHS), characterized by recurrent bouts of intense vomiting and abdominal cramping during or within 48 hours of heavy cannabis use.^[112] The mechanism behind CHS is poorly understood and is contrary to the antiemetic properties of cannabis and cannabinoids. Of those who went to the emergency department (ED) with recurrent vomiting in one institution in the United States from 2005 to 2010, about 6% had the condition.^[113]^[114] The condition is usually not responsive to traditionally used antiemetics and the primary treatment is cessation from cannabis use.^[112]

Smoking cannabis can potentially cause cancer, due to carcinogens present in smoke.^[115]^[116]^[117]

Effects in pregnancy

Cannabis consumption in pregnancy might be associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits in offspring based on animal studies, although there is limited evidence for this in humans at this time.^[118] A 2012 systematic review found although it was difficult to draw firm conclusions, there was some evidence that prenatal exposure to cannabis was associated with "deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence".^[119] A report prepared for the Australian National Council on Drugs concluded cannabis and other cannabinoids are contraindicated in pregnancy as it may interact with the endocannabinoid system.^[120]

Effects in pediatrics

Children can become exposed to cannabis, typically through accidental exposure which can lead to very high doses, especially in the case of edibles. Unlike in adults, these levels of exposure can lead to major complications in children.^[121] These complications include encephalopathy, hypotension, respiratory depression severe enough to require ventilation, somnolence, coma, and in extreme cases, reports of death.^[121]^[122]^[123] Pediatric exposure to edibles is of increasing concern because these products are typically sweets (gummies, cookies, etc.), and their prevalence is increasing as cannabis is legalized or decriminalized in many territories.^[124]

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@@ Line 1: / Line 1: @@
-{{Short description|Effects resulting from the use of cannabis}}
+{{Short description|none}}
-{{Use dmy dates|date=May 2022}}
+{{Use dmy dates|date=May 2022}}{{See also|Long-term effects of cannabis}}
+[[File:Marijuana-Cannabis-Weed-Bud-Gram.jpg|thumb|right|A dried cannabis flower]]The '''short-term''' '''effects of cannabis''' are caused by many [[chemical compound]]s in the [[Cannabis|cannabis plant]], including 113{{clarify|reason=if there are 113 cannaboids why do we then say there are 120 terpenes?|date=April 2022}} different [[cannabinoid]]s, such as [[tetrahydrocannabinol]] (THC), and 120 [[terpenes]],<ref name=":0">{{cite journal | vauthors = Aizpurua-Olaizola O, Soydaner U, Öztürk E, Schibano D, Simsir Y, Navarro P, Etxebarria N, Usobiaga A | title = Evolution of the Cannabinoid and Terpene Content during the Growth of Cannabis sativa Plants from Different Chemotypes | journal = Journal of Natural Products | volume = 79 | issue = 2 | pages = 324–31 | date = February 2016 | pmid = 26836472 | doi = 10.1021/acs.jnatprod.5b00949 | url = https://figshare.com/articles/journal_contribution/5028338 | access-date = 24 November 2022 | archive-date = 5 January 2023 | archive-url = https://web.archive.org/web/20230105025827/https://figshare.com/articles/journal_contribution/Evolution_of_the_Cannabinoid_and_Terpene_Content_during_the_Growth_of_Cannabis_sativa_Plants_from_Different_Chemotypes/5028338 | url-status = live }}</ref> which allow [[Cannabis (drug)|its drug]] to have various [[psychology|psychological]] and [[physiology|physiological]] effects on the human body. Different plants of the genus [[Cannabis]] contain different and often unpredictable concentrations of THC and other cannabinoids and hundreds of other molecules that have a [[pharmacological]] effect,<ref>{{cite web|url=http://www.medicinalgenomics.com/wp-content/uploads/2011/12/Chemical-constituents-of-cannabis.pdf|title=Chemistry and Analysis of Phytocannabinoids and Other Cannabis Constituents|author=Rudolf Brenneisen|website=Medicinalgenomics.com|access-date=9 April 2018|archive-date=7 April 2018|archive-url=https://web.archive.org/web/20180407144421/https://www.medicinalgenomics.com/wp-content/uploads/2011/12/Chemical-constituents-of-cannabis.pdf|url-status=live}}</ref><ref>{{cite journal | vauthors = Atakan Z | title = Cannabis, a complex plant: different compounds and different effects on individuals | journal = Therapeutic Advances in Psychopharmacology | volume = 2 | issue = 6 | pages = 241–54 | date = December 2012 | pmid = 23983983 | pmc = 3736954 | doi = 10.1177/2045125312457586 }}</ref> so the final net effect cannot reliably be foreseen.
-[[File:Marijuana-Cannabis-Weed-Bud-Gram.jpg|thumb|right|A dried cannabis flower]]
-The '''effects of cannabis''' are caused by [[chemical compound]]s in the [[Cannabis|cannabis plant]], including 113{{clarify|reason=if there are 113 cannaboids why do we then say there are 120 terpenes?|date=April 2022}} different [[cannabinoid]]s such as [[tetrahydrocannabinol]] (THC) and 120 [[terpenes]],<ref name=":0">{{cite journal | vauthors = Aizpurua-Olaizola O, Soydaner U, Öztürk E, Schibano D, Simsir Y, Navarro P, Etxebarria N, Usobiaga A | title = Evolution of the Cannabinoid and Terpene Content during the Growth of Cannabis sativa Plants from Different Chemotypes | journal = Journal of Natural Products | volume = 79 | issue = 2 | pages = 324–31 | date = February 2016 | pmid = 26836472 | doi = 10.1021/acs.jnatprod.5b00949 | url = https://figshare.com/articles/journal_contribution/5028338 | access-date = 24 November 2022 | archive-date = 5 January 2023 | archive-url = https://web.archive.org/web/20230105025827/https://figshare.com/articles/journal_contribution/Evolution_of_the_Cannabinoid_and_Terpene_Content_during_the_Growth_of_Cannabis_sativa_Plants_from_Different_Chemotypes/5028338 | url-status = live }}</ref> which allow [[Cannabis (drug)|its drug]] to have various [[psychology|psychological]] and [[physiology|physiological]] effects on the human body. Different plants of the genus Cannabis contain different and often unpredictable concentrations of THC and other cannabinoids and hundreds of other molecules that have a pharmacological effect,<ref>{{cite web|url=http://www.medicinalgenomics.com/wp-content/uploads/2011/12/Chemical-constituents-of-cannabis.pdf|title=Chemistry and Analysis of Phytocannabinoids and Other Cannabis Constituents|author=Rudolf Brenneisen|website=Medicinalgenomics.com|access-date=9 April 2018|archive-date=7 April 2018|archive-url=https://web.archive.org/web/20180407144421/https://www.medicinalgenomics.com/wp-content/uploads/2011/12/Chemical-constituents-of-cannabis.pdf|url-status=live}}</ref><ref>{{cite journal | vauthors = Atakan Z | title = Cannabis, a complex plant: different compounds and different effects on individuals | journal = Therapeutic Advances in Psychopharmacology | volume = 2 | issue = 6 | pages = 241–54 | date = December 2012 | pmid = 23983983 | pmc = 3736954 | doi = 10.1177/2045125312457586 }}</ref> so the final net effect cannot reliably be foreseen.
-Acute effects while under the influence can sometimes include [[euphoria]] or [[anxiety]].<ref name=osborne2008>{{cite journal | vauthors = Osborne GB, Fogel C | title = Understanding the motivations for recreational marijuana use among adult Canadians | journal = Substance Use & Misuse | volume = 43 | issue = 3–4 | pages = 539–72; discussion 573–9, 585–7 | year = 2008 | pmid = 18365950 | doi = 10.1080/10826080701884911 | s2cid = 31053594 }}</ref><ref name=acutememory>{{cite journal | vauthors = Ranganathan M, D'Souza DC | title = The acute effects of cannabinoids on memory in humans: a review | journal = Psychopharmacology | volume = 188 | issue = 4 | pages = 425–44 | date = November 2006 | pmid = 17019571 | doi = 10.1007/s00213-006-0508-y | s2cid = 10328820 }}</ref> Although some assert that [[cannabidiol]] (CBD), another cannabinoid found in cannabis in varying amounts, may alleviate the adverse effects of THC that some users experience,<ref name="Grotenhermen2003">{{cite journal | vauthors = Grotenhermen F | title = Pharmacokinetics and pharmacodynamics of cannabinoids | journal = Clinical Pharmacokinetics | volume = 42 | issue = 4 | pages = 327–60 | year = 2003 | pmid = 12648025 | doi = 10.2165/00003088-200342040-00003 | s2cid = 25623600 }}</ref> little is known about CBD effects on humans.<ref>{{cite journal | vauthors = White CM | title = A Review of Human Studies Assessing Cannabidiol's (CBD) Therapeutic Actions and Potential | journal = Journal of Clinical Pharmacology | volume = 59 | issue = 7 | pages = 923–934 | date = July 2019 | pmid = 30730563 | doi = 10.1002/jcph.1387 | s2cid = 73452711 }}</ref><ref>{{cite journal | vauthors = Haney M, Malcolm RJ, Babalonis S, Nuzzo PA, Cooper ZD, Bedi G, Gray KM, McRae-Clark A, Lofwall MR, Sparenborg S, Walsh SL | display-authors = 6 | title = Oral Cannabidiol does not Alter the Subjective, Reinforcing or Cardiovascular Effects of Smoked Cannabis | journal = Neuropsychopharmacology | volume = 41 | issue = 8 | pages = 1974–82 | date = July 2016 | pmid = 26708108 | pmc = 4908634 | doi = 10.1038/npp.2015.367 }}</ref> [[Cannabinoid receptor antagonist]]s have previously been tested as antidotes for cannabis intoxication with success, reducing or eliminating the physiological and psychological effects of intoxication.<ref>{{Cite journal|last1=Sabioni|first1=Pamela|last2=Le Foll|first2=Bernard|date=2018|title=Psychosocial and pharmacological interventions for the treatment of cannabis use disorder|journal=F1000Research|volume=7|page=173|doi=10.12688/f1000research.11191.1|issn=2046-1402|pmc=5811668|pmid=29497498 |doi-access=free }}</ref> Some of these products are currently in development as cannabis antidotes.
+Acute effects while under the influence can sometimes include [[euphoria]] or [[anxiety]].<ref name="osborne2008">{{cite journal | vauthors = Osborne GB, Fogel C | title = Understanding the motivations for recreational marijuana use among adult Canadians | journal = Substance Use & Misuse | volume = 43 | issue = 3–4 | pages = 539–72; discussion 573–9, 585–7 | year = 2008 | pmid = 18365950 | doi = 10.1080/10826080701884911 | s2cid = 31053594 }}</ref><ref name="acutememory">{{cite journal | vauthors = Ranganathan M, D'Souza DC | title = The acute effects of cannabinoids on memory in humans: a review | journal = Psychopharmacology | volume = 188 | issue = 4 | pages = 425–44 | date = November 2006 | pmid = 17019571 | doi = 10.1007/s00213-006-0508-y | s2cid = 10328820 }}</ref> Although some assert that [[cannabidiol]] (CBD), another cannabinoid found in cannabis in varying amounts, may alleviate the adverse effects of THC that some users experience,<ref name="Grotenhermen2003">{{cite journal | vauthors = Grotenhermen F | title = Pharmacokinetics and pharmacodynamics of cannabinoids | journal = Clinical Pharmacokinetics | volume = 42 | issue = 4 | pages = 327–60 | year = 2003 | pmid = 12648025 | doi = 10.2165/00003088-200342040-00003 | s2cid = 25623600 }}</ref> little is known about CBD's effects on humans.<ref>{{cite journal | vauthors = White CM | title = A Review of Human Studies Assessing Cannabidiol's (CBD) Therapeutic Actions and Potential | journal = Journal of Clinical Pharmacology | volume = 59 | issue = 7 | pages = 923–934 | date = July 2019 | pmid = 30730563 | doi = 10.1002/jcph.1387 | s2cid = 73452711 }}</ref><ref>{{cite journal | vauthors = Haney M, Malcolm RJ, Babalonis S, Nuzzo PA, Cooper ZD, Bedi G, Gray KM, McRae-Clark A, Lofwall MR, Sparenborg S, Walsh SL | display-authors = 6 | title = Oral Cannabidiol does not Alter the Subjective, Reinforcing or Cardiovascular Effects of Smoked Cannabis | journal = Neuropsychopharmacology | volume = 41 | issue = 8 | pages = 1974–82 | date = July 2016 | pmid = 26708108 | pmc = 4908634 | doi = 10.1038/npp.2015.367 }}</ref> [[Cannabinoid receptor antagonist]]s have previously been tested as [[Antidote|antidotes]] for cannabis intoxication with success, reducing or eliminating the physiological and psychological effects of intoxication.<ref>{{Cite journal|last1=Sabioni|first1=Pamela|last2=Le Foll|first2=Bernard|date=2018|title=Psychosocial and pharmacological interventions for the treatment of cannabis use disorder|journal=F1000Research|volume=7|page=173|doi=10.12688/f1000research.11191.1|issn=2046-1402|pmc=5811668|pmid=29497498 |doi-access=free }}</ref> Some of these products are currently in development as cannabis antidotes.{{TOC limit|3}}
+== Background and chronic use ==
-In the [[United States]], [[medical cannabis]] research is limited by federal restrictions.<ref name=Borgelt2013>{{cite journal | vauthors = Borgelt LM, Franson KL, Nussbaum AM, Wang GS | title = The pharmacologic and clinical effects of medical cannabis | journal = Pharmacotherapy | volume = 33 | issue = 2 | pages = 195–209 | date = February 2013 | pmid = 23386598 | doi = 10.1002/phar.1187 | type = Review | citeseerx = 10.1.1.1017.1935 | s2cid = 8503107 }}</ref> Smoking any substance could possibly carry similar risks as smoking tobacco due to carcinogens present in all smoke,<ref>{{cite web
+In the [[United States]], [[medical cannabis]] research is limited by federal restrictions.<ref name=Borgelt2013>{{cite journal | vauthors = Borgelt LM, Franson KL, Nussbaum AM, Wang GS | title = The pharmacologic and clinical effects of medical cannabis | journal = Pharmacotherapy | volume = 33 | issue = 2 | pages = 195–209 | date = February 2013 | pmid = 23386598 | doi = 10.1002/phar.1187 | type = Review | citeseerx = 10.1.1.1017.1935 | s2cid = 8503107 }}</ref>
-| url = http://oehha.ca.gov/prop65/hazard_ident/pdf_zip/FinalMJsmokeHID.pdf
-| last = Tomar
-| first = Rajpal C.
-| author2 = Beaumont and Hsieh
-| date = August 2009
-| title = Evidence on the carcinogenicity of marijuana smoke
-| publisher = Reproductive and Cancer Hazard Assessment Branch Office of Environmental Health Hazard Assessment, California Environmental Protection Agency
-| access-date = 29 November 2018
-| archive-date = 24 July 2012
-| archive-url = https://web.archive.org/web/20120724183619/http://oehha.ca.gov/prop65/hazard_ident/pdf_zip/FinalMJsmokeHID.pdf
-| url-status = live
-}}</ref><ref name=mentaldisorders>
-{{cite journal | vauthors = Leweke FM, Koethe D | title = Cannabis and psychiatric disorders: it is not only addiction | journal = Addiction Biology | volume = 13 | issue = 2 | pages = 264–75 | date = June 2008 | pmid = 18482435 | doi = 10.1111/j.1369-1600.2008.00106.x | s2cid = 205400285 }}</ref><ref name=adolescenceschizo>{{cite journal | vauthors = Rubino T, Parolaro D | title = Long lasting consequences of cannabis exposure in adolescence | journal = Molecular and Cellular Endocrinology | volume = 286 | issue = 1–2 Suppl 1 | pages = S108-13 | date = April 2008 | pmid = 18358595 | doi = 10.1016/j.mce.2008.02.003 | s2cid = 39245784 | url = https://hal.archives-ouvertes.fr/hal-00531997 | type = Submitted manuscript | access-date = 28 August 2018 | archive-date = 29 November 2018 | archive-url = https://web.archive.org/web/20181129225219/https://hal.archives-ouvertes.fr/hal-00531997 | url-status = live }}</ref> and the ultimate conclusions on these factors are disputed.<ref>{{cite web |author=Michael Slezak |url=http://www.abc.net.au/science/articles/2009/09/01/2673334.htm |title=Doubt cast on cannabis, schizophrenia link |publisher=Abc.net.au |date=1 September 2009 |access-date=8 January 2013 |archive-date=5 May 2019 |archive-url=https://web.archive.org/web/20190505161029/http://www.abc.net.au/science/articles/2009/09/01/2673334.htm |url-status=live }}</ref><ref>{{cite web |url=http://norml.org/pdf_files/brief_bank/AFFIDAVIT_OF_LESTER_GRINSPOON_MD.pdf |title=Boston Municipal Courtcentral Division. Docket # 0701CR7229 |year=2008 |access-date=8 January 2013 |archive-date=29 August 2017 |archive-url=https://web.archive.org/web/20170829230438/http://norml.org/pdf_files/brief_bank/AFFIDAVIT_OF_LESTER_GRINSPOON_MD.pdf |url-status=live }}</ref><ref name=DeLisi2008>{{cite journal | vauthors = DeLisi LE | title = The effect of cannabis on the brain: can it cause brain anomalies that lead to increased risk for schizophrenia? | journal = Current Opinion in Psychiatry | volume = 21 | issue = 2 | pages = 140–50 | date = March 2008 | pmid = 18332661 | pmc = 4337025 | doi = 10.1097/YCO.0b013e3282f51266 }}</ref><ref name="decreased depression">{{cite journal | vauthors = Denson TF, Earleywine M | title = Decreased depression in marijuana users | journal = Addictive Behaviors | volume = 31 | issue = 4 | pages = 738–42 | date = April 2006 | pmid = 15964704 | doi = 10.1016/j.addbeh.2005.05.052 }}</ref>
 [[Cannabis use disorder]] is defined as a medical diagnosis in the fifth revision of the [[Diagnostic and Statistical Manual of Mental Disorders]] ([[DSM-5]]).<ref>Grohol, John M. (21 May 2013) [http://pro.psychcentral.com/dsm-5-changes-addiction-substance-related-disorders-alcoholism/004370.html# Psy.D:DSM-5 Changes: Addiction, Substance-Related Disorders & Alcoholism] {{Webarchive|url=https://web.archive.org/web/20171211194042/https://pro.psychcentral.com/dsm-5-changes-addiction-substance-related-disorders-alcoholism/004370.html |date=11 December 2017 }}. Pro.psychcentral.com. Retrieved on 19 December 2016.</ref>
-{{TOC limit|3}}
 ==Chemistry ==
 [[File:THC-skeletal.png|thumb|right|The [[structural formula]] of [[tetrahydrocannabinol]]]]
@@ Line 43: / Line 28: @@
 ===Sustainability in the body===
 {{main|Cannabis drug testing}}
-Most [[cannabinoids]] are [[lipophilic]] (fat soluble) compounds that are easily stored in fat, thus yielding a long [[elimination half-life]] relative to other [[recreational drug use|recreational drug]]s. The THC molecule, and related compounds, are usually detectable in drug tests from 3 days up to 10 days according to Redwood Laboratories.{{citation needed|date=April 2022}} Long-term users can produce positive tests for two to three months after ceasing cannabis use (see [[drug test]]).<ref>{{cite web | url=http://www.nhs.uk/chq/Pages/2287.aspx?CategoryID=53 | title=How long does cannabis stay in the body after smoking? | website=NHS | access-date=4 August 2015 | archive-date=16 July 2015 | archive-url=https://web.archive.org/web/20150716065232/http://www.nhs.uk/chq/Pages/2287.aspx?CategoryID=53 | url-status=live }}{{failed verification|date=April 2020}}<!-- IF this is a NHS website, why does it link to https://www.talktofrank.com/contact-frank ? --></ref>
+Most [[cannabinoids]] are [[lipophilic]] (fat soluble) compounds that are easily stored in fat, thus yielding a long [[elimination half-life]] relative to other [[recreational drug use|recreational drug]]s. The THC molecule, and related compounds, are usually detectable in drug tests from 3 days up to 10 days.{{citation needed|date=April 2022}} Long-term users can produce positive tests for two to three months after ceasing cannabis use (see [[drug test]]).<ref>{{cite web | url=http://www.nhs.uk/chq/Pages/2287.aspx?CategoryID=53 | title=How long does cannabis stay in the body after smoking? | website=NHS | access-date=4 August 2015 | archive-date=16 July 2015 | archive-url=https://web.archive.org/web/20150716065232/http://www.nhs.uk/chq/Pages/2287.aspx?CategoryID=53 | url-status=live }}{{failed verification|date=April 2020}}<!-- IF this is a NHS website, why does it link to https://www.talktofrank.com/contact-frank ? --></ref>
 ==Toxicities==
-When cannabis is smoked, blood levels of THC peak rapidly after a few minutes and then decline, although the [[psychotropic]] effects persist for longer. Edible forms of cannabis often contain several hundred milligrams of THC, much more than the 32&nbsp;mg of a typical [[cannabis cigarette]].{{citation needed|date=March 2024}} The rise of [[Edible cannabis|edible cannabis products]] has been responsible for a large increase of poisoning of children and young people: in American states which have legalized cannabis, emergency room admissions of such cases have typically doubled. Symptoms in children can include [[lethargy]], sedation and [[seizure]].<ref name=blohm>{{cite journal |vauthors=Blohm E, Sell P, Neavyn M |title=Cannabinoid toxicity in pediatrics |journal=Curr Opin Pediatr |volume=31 |issue=2 |pages=256–261 |date=April 2019 |pmid=30694824 |doi=10.1097/MOP.0000000000000739 |s2cid=59410966 |url=}}</ref>
+When cannabis is smoked, blood levels of THC peak rapidly after a few minutes and then decline, although the [[psychotropic]] effects persist for longer. Edible forms of cannabis often contain several hundred milligrams of THC, much more than the 32&nbsp;mg of a typical [[cannabis cigarette]].{{citation needed|date=March 2024}} The rise of [[Edible cannabis|edible cannabis products]] has been responsible for a large increase of poisoning of children and young people.{{citation needed|date=March 2024}} Symptoms in children can include [[lethargy]], sedation and [[seizure]].<ref name=blohm>{{cite journal |vauthors=Blohm E, Sell P, Neavyn M |title=Cannabinoid toxicity in pediatrics |journal=Curr Opin Pediatr |volume=31 |issue=2 |pages=256–261 |date=April 2019 |pmid=30694824 |doi=10.1097/MOP.0000000000000739 |s2cid=59410966 |url=}}</ref>
-Cannabis is suspected of being a potential contributory factor or direct cause of sudden death, due to the strain it can place on the [[cardiovascular system]], or because of [[cannabinoid hyperemesis syndrome]].<ref name=drummer>{{cite journal |vauthors=Drummer OH, Gerostamoulos D, Woodford NW |title=Cannabis as a cause of death: A review |journal=Forensic Sci Int |volume=298 |issue= |pages=298–306 |date=May 2019 |pmid=30925348 |doi=10.1016/j.forsciint.2019.03.007 |s2cid=87511682 |url=}}</ref>
+[[Synthetic cannabinoids|Synthetic cannabis]] is suspected of being a potential contributory factor or direct cause of sudden death, due to the strain it can place on the [[cardiovascular system]], or because of [[cannabinoid hyperemesis syndrome]].<ref name=drummer>{{cite journal |vauthors=Drummer OH, Gerostamoulos D, Woodford NW |title=Cannabis as a cause of death: A review |journal=Forensic Sci Int |volume=298 |issue= |pages=298–306 |date=May 2019 |pmid=30925348 |doi=10.1016/j.forsciint.2019.03.007 |s2cid=87511682 |url=}}</ref>
 ===Related to cannabinoids===
@@ Line 57: / Line 42: @@
 ===Related to smoking===
+[[File:Ganja Smoking - Gangasagar Fair Transit Camp - Kolkata 2013-01-12 2646.JPG|thumb|right|250px|A man smoking cannabis in [[Kolkata, India]]]]
-A 2007 study found that while [[tobacco smoking|tobacco]] and cannabis smoke are quite similar, cannabis smoke contained higher amounts of [[ammonia]], [[hydrogen cyanide]], and [[nitrogen oxides]], but lower levels of [[carcinogenic]] [[polycyclic aromatic hydrocarbon]]s (PAHs).<ref name=MoirRickert>{{cite journal | vauthors = Moir D, Rickert WS, Levasseur G, Larose Y, Maertens R, White P, Desjardins S | title = A comparison of mainstream and sidestream marijuana and tobacco cigarette smoke produced under two machine smoking conditions | journal = Chemical Research in Toxicology | volume = 21 | issue = 2 | pages = 494–502 | date = February 2008 | pmid = 18062674 | doi = 10.1021/tx700275p | doi-access = free }}</ref> This study found that directly inhaled cannabis smoke contained as much as 20 times as much ammonia and 5 times as much hydrogen cyanide as tobacco smoke and compared the properties of both mainstream and sidestream (smoke emitted from a smouldering 'joint' or 'cone') smoke.<ref name=MoirRickert/> Mainstream cannabis smoke was found to contain higher concentrations of selected polycyclic aromatic hydrocarbons (PAHs) than sidestream tobacco smoke.<ref name=MoirRickert/> However, other studies have found much lower disparities in ammonia and hydrogen cyanide between cannabis and tobacco, and that some other constituents (such as polonium-210, lead, arsenic, nicotine, and tobacco-specific nitrosamines) are either lower or non-existent in cannabis smoke.<ref>{{cite book |last=Institute of Medicine |date=1982 |title=Marijuana and Health |url=https://archive.org/details/marijuanahealthr0000inst |location=Washington, D.C. |publisher=The National Academies Press |doi=10.17226/18942 |isbn=978-0-309-03236-0 |url-access=registration }}</ref><ref>{{cite web |url=http://www.acsa2000.net/HealthAlert/radioactive_tobacco.html |title=Radioactive Tobacco |author=Malmo-Levine, David |date=2 January 2002 |website=acsa2000.net |url-status=dead |archive-url=https://web.archive.org/web/20130112032208/http://www.acsa2000.net/HealthAlert/radioactive_tobacco.html |archive-date=12 January 2013 }}</ref> A 2021 [[longitudinal study]] conducted among populations of [[HIV-positive people|HIV-positive]] and [[HIV-negative]] adults found that smoke-related [[carcinogenic]] [[toxicant]]s and [[biomarker]]s detected in tobacco smokers were also detected in exclusive marijuana smokers, including [[carbon monoxide]] (CO), [[polycyclic aromatic hydrocarbons]] (PAHs), [[aldehydes]] (such as [[acrolein]]), [[acrylonitrile]] and [[acrylamide]] [[metabolites]], but exposures are lower compared with tobacco or dual smokers.<ref name="EClinicalMedicine">{{cite journal |last1=Lorenz |first1=David R. |last2=Misra |first2=Vika |last3=Chettimada |first3=Sukrutha |last4=Uno |first4=Hajime |last5=Wang |first5=Lanqing |last6=Blount |first6=Benjamin C. |last7=De Jesus |first7=Victor R. |last8=Gelman |first8=Benjamin B. |last9=Morgello |first9=Susan |last10=Wolinsky |first10=Steven M. |last11=Gabuzda |first11=Dana |date=January 2021 |title=Acrolein and other toxicant exposures in relation to cardiovascular disease among marijuana and tobacco smokers in a longitudinal cohort of HIV-positive and negative adults |url=https://www.thelancet.com/action/showPdf?pii=S2589-5370%2820%2930441-7 |format=PDF |journal=eClinicalMedicine |publisher=[[Elsevier]] |volume=31 |issue=100697 |page=100697 |doi=10.1016/j.eclinm.2020.100697 |doi-access=free |pmc=7846668 |pmid=33554087 |s2cid=231802821 |access-date=7 September 2021 |archive-date=20 April 2023 |archive-url=https://web.archive.org/web/20230420131252/https://www.thelancet.com/action/showPdf?pii=S2589-5370%2820%2930441-7 |url-status=live }}</ref> Increased levels of acrolein exposure by tobacco smoking but not exclusive marijuana smoking were detected both in HIV-positive and HIV-negative adults, and contribute to increased diagnoses of [[cardiovascular diseases]] and [[respiratory diseases]] among tobacco smokers.<ref name="EClinicalMedicine"/>
+A 2007 study found that while [[tobacco smoking|tobacco]] and cannabis smoke are quite similar, cannabis smoke contained higher amounts of [[ammonia]], [[hydrogen cyanide]], and [[nitrogen oxides]], but lower levels of [[carcinogenic]] [[polycyclic aromatic hydrocarbon]]s (PAHs).<ref name="MoirRickert">{{cite journal | vauthors = Moir D, Rickert WS, Levasseur G, Larose Y, Maertens R, White P, Desjardins S | title = A comparison of mainstream and sidestream marijuana and tobacco cigarette smoke produced under two machine smoking conditions | journal = Chemical Research in Toxicology | volume = 21 | issue = 2 | pages = 494–502 | date = February 2008 | pmid = 18062674 | doi = 10.1021/tx700275p | doi-access = free }}</ref> This study found that directly inhaled cannabis smoke contained as much as 20 times as much ammonia and 5 times as much hydrogen cyanide as tobacco smoke and compared the properties of both mainstream and sidestream (smoke emitted from a smouldering 'joint' or 'cone') smoke.<ref name="MoirRickert" /> Mainstream cannabis smoke was found to contain higher concentrations of selected polycyclic aromatic hydrocarbons (PAHs) than sidestream tobacco smoke.<ref name="MoirRickert" /> However, other studies have found much lower disparities in ammonia and hydrogen cyanide between cannabis and tobacco, and that some other constituents (such as polonium-210, lead, arsenic, nicotine, and tobacco-specific nitrosamines) are either lower or non-existent in cannabis smoke.<ref>{{cite book |last=Institute of Medicine |date=1982 |title=Marijuana and Health |url=https://archive.org/details/marijuanahealthr0000inst |location=Washington, D.C. |publisher=The National Academies Press |doi=10.17226/18942 |isbn=978-0-309-03236-0 |url-access=registration }}</ref><ref>{{cite web |url=http://www.acsa2000.net/HealthAlert/radioactive_tobacco.html |title=Radioactive Tobacco |author=Malmo-Levine, David |date=2 January 2002 |website=acsa2000.net |url-status=dead |archive-url=https://web.archive.org/web/20130112032208/http://www.acsa2000.net/HealthAlert/radioactive_tobacco.html |archive-date=12 January 2013 }}</ref> A 2021 [[longitudinal study]] conducted among populations of [[HIV-positive people|HIV-positive]] and [[HIV-negative]] adults found that smoke-related [[carcinogenic]] [[toxicant]]s and [[biomarker]]s detected in tobacco smokers were also detected in exclusive cannabis smokers, including [[carbon monoxide]] (CO), [[polycyclic aromatic hydrocarbons]] (PAHs), [[aldehydes]] (such as [[acrolein]]), [[acrylonitrile]] and [[acrylamide]] [[metabolites]], but exposures are lower compared with tobacco or dual smokers.<ref name="EClinicalMedicine">{{cite journal |last1=Lorenz |first1=David R. |last2=Misra |first2=Vika |last3=Chettimada |first3=Sukrutha |last4=Uno |first4=Hajime |last5=Wang |first5=Lanqing |last6=Blount |first6=Benjamin C. |last7=De Jesus |first7=Victor R. |last8=Gelman |first8=Benjamin B. |last9=Morgello |first9=Susan |last10=Wolinsky |first10=Steven M. |last11=Gabuzda |first11=Dana |date=January 2021 |title=Acrolein and other toxicant exposures in relation to cardiovascular disease among marijuana and tobacco smokers in a longitudinal cohort of HIV-positive and negative adults |url=https://www.thelancet.com/action/showPdf?pii=S2589-5370%2820%2930441-7 |format=PDF |journal=eClinicalMedicine |publisher=[[Elsevier]] |volume=31 |issue=100697 |page=100697 |doi=10.1016/j.eclinm.2020.100697 |doi-access=free |pmc=7846668 |pmid=33554087 |s2cid=231802821 |access-date=7 September 2021 |archive-date=20 April 2023 |archive-url=https://web.archive.org/web/20230420131252/https://www.thelancet.com/action/showPdf?pii=S2589-5370%2820%2930441-7 |url-status=live }}</ref> Increased levels of acrolein exposure by tobacco smoking but not exclusive cannabis smoking were detected both in HIV-positive and HIV-negative adults, and contribute to increased diagnoses of [[cardiovascular diseases]] and [[respiratory diseases]] among tobacco smokers.<ref name="EClinicalMedicine" />
-Cannabis smoke contains thousands of organic and inorganic chemical compounds. This [[Tar (tobacco residue)|tar]] is chemically similar to that found in tobacco smoke or cigars.<ref>{{cite journal | vauthors = Hashibe M, Straif K, Tashkin DP, Morgenstern H, Greenland S, Zhang ZF | title = Epidemiologic review of marijuana use and cancer risk | journal = Alcohol | volume = 35 | issue = 3 | pages = 265–75 | date = April 2005 | pmid = 16054989 | doi = 10.1016/j.alcohol.2005.04.008 }}</ref> Over fifty known [[carcinogen]]s have been identified in cannabis smoke.<ref>{{Cite journal | title = Does smoking cannabis cause cancer? | publisher = Cancer Research UK | date = 20 September 2010 | url = http://cancerhelp.cancerresearchuk.org/about-cancer/cancer-questions/does-smoking-cannabis-cause-cancer | access-date = 23 June 2012 | url-status=dead | archive-url = https://web.archive.org/web/20120729115046/http://cancerhelp.cancerresearchuk.org/about-cancer/cancer-questions/does-smoking-cannabis-cause-cancer | archive-date = 29 July 2012 }}</ref> These include nitrosamines, reactive aldehydes, and polycylic hydrocarbons, including benz[a]pyrene.<ref>{{Cite journal |last=Tashkin |first=Donald |name-list-style=vanc |date=March 1997 |title=Effects of marijuana on the lung and its immune defenses |publisher=UCLA School of Medicine |url=http://www.ukcia.org/research/EffectsOfMarijuanaOnLungAndImmuneDefenses.php |access-date=23 June 2012 |archive-date=23 June 2012 |archive-url=https://web.archive.org/web/20120623140306/http://www.ukcia.org/research/EffectsOfMarijuanaOnLungAndImmuneDefenses.php |url-status=live }}</ref>  Marijuana smoke was listed as a cancer agent in California in 2009.<ref>{{cite web |url=http://oehha.ca.gov/prop65/prop65_list/files/p65single072012.pdf |title=Chemicals known to the state to cause cancer or reproductive toxicity |publisher=ca.gov |date=20 July 2012 |access-date=8 January 2013 |url-status=dead |archive-url=https://web.archive.org/web/20130120030810/http://oehha.ca.gov/prop65/prop65_list/files/p65single072012.pdf |archive-date=20 January 2013 }}</ref>  A study by the [[British Lung Foundation]] published in 2012 identifies cannabis smoke as a carcinogen and also finds awareness of the danger is low compared with the high awareness of the dangers of smoking tobacco particularly among younger users. Other observations include possible increased risk from each cigarette; lack of research on the effect of cannabis smoke alone; low rate of addiction compared to tobacco; and episodic nature of cannabis use compared to steady frequent smoking of tobacco.<ref name=BLA2012>{{Cite journal |url=http://www.blf.org.uk/Files/8ec171b2-9b7e-49d9-b3b1-a07e00f11c05/ |title=The impact of cannabis on your lung |publisher=British Lung Association |date=June 2012 |access-date=8 January 2013 |url-status=dead |archive-url=https://web.archive.org/web/20130927183248/http://www.blf.org.uk/Files/8ec171b2-9b7e-49d9-b3b1-a07e00f11c05/ |archive-date=27 September 2013 }}</ref>{{unreliable medical source|date=November 2019}}<!-- Should this study and the complaints about it all be removed and just replaced with a reliable study?--> Professor [[David Nutt]], a UK drug expert, points out that the study cited by the British Lung Foundation has been accused of both "false reasoning" and "incorrect methodology". Further, he notes that other studies have failed to connect cannabis with lung cancer, and accuses the BLF of "scaremongering over cannabis".<ref>{{Cite journal |last=Le |first=Bryan |name-list-style=vanc |url=http://www.thefix.com/content/david-nutt-cannabis-carcinogenic90225 |title=Drug prof slams pot lung-danger claims |publisher=The Fix |date=8 June 2012 |access-date=9 January 2013 |archive-date=30 December 2012 |archive-url=https://web.archive.org/web/20121230000132/http://www.thefix.com/content/david-nutt-cannabis-carcinogenic90225 |url-status=live }}</ref>
+Cannabis smoke contains thousands of organic and inorganic chemical compounds. This [[Tar (tobacco residue)|tar]] is chemically similar to that found in tobacco smoke or cigars.<ref>{{cite journal | vauthors = Hashibe M, Straif K, Tashkin DP, Morgenstern H, Greenland S, Zhang ZF | title = Epidemiologic review of marijuana use and cancer risk | journal = Alcohol | volume = 35 | issue = 3 | pages = 265–75 | date = April 2005 | pmid = 16054989 | doi = 10.1016/j.alcohol.2005.04.008 }}</ref> Over fifty known [[carcinogen]]s have been identified in cannabis smoke.<ref>{{Cite journal | title = Does smoking cannabis cause cancer? | publisher = Cancer Research UK | date = 20 September 2010 | url = http://cancerhelp.cancerresearchuk.org/about-cancer/cancer-questions/does-smoking-cannabis-cause-cancer | access-date = 23 June 2012 | url-status=dead | archive-url = https://web.archive.org/web/20120729115046/http://cancerhelp.cancerresearchuk.org/about-cancer/cancer-questions/does-smoking-cannabis-cause-cancer | archive-date = 29 July 2012 }}</ref> These include nitrosamines, reactive aldehydes, and polycylic hydrocarbons, including benz[a]pyrene.<ref>{{Cite journal |last=Tashkin |first=Donald |name-list-style=vanc |date=March 1997 |title=Effects of marijuana on the lung and its immune defenses |publisher=UCLA School of Medicine |url=http://www.ukcia.org/research/EffectsOfMarijuanaOnLungAndImmuneDefenses.php |access-date=23 June 2012 |archive-date=23 June 2012 |archive-url=https://web.archive.org/web/20120623140306/http://www.ukcia.org/research/EffectsOfMarijuanaOnLungAndImmuneDefenses.php |url-status=live }}</ref>  Cannabis smoke was listed as a cancer agent in California in 2009.<ref>{{cite web |url=http://oehha.ca.gov/prop65/prop65_list/files/p65single072012.pdf |title=Chemicals known to the state to cause cancer or reproductive toxicity |publisher=ca.gov |date=20 July 2012 |access-date=8 January 2013 |url-status=dead |archive-url=https://web.archive.org/web/20130120030810/http://oehha.ca.gov/prop65/prop65_list/files/p65single072012.pdf |archive-date=20 January 2013 }}</ref>  A study by the [[British Lung Foundation]] published in 2012 identifies cannabis smoke as a carcinogen and also finds awareness of the danger is low compared with the high awareness of the dangers of smoking tobacco particularly among younger users. Other observations include possible increased risk from each cigarette; lack of research on the effect of cannabis smoke alone; low rate of addiction compared to tobacco; and episodic nature of cannabis use compared to steady frequent smoking of tobacco.<ref name="BLA2012">{{Cite journal |url=http://www.blf.org.uk/Files/8ec171b2-9b7e-49d9-b3b1-a07e00f11c05/ |title=The impact of cannabis on your lung |publisher=British Lung Association |date=June 2012 |access-date=8 January 2013 |url-status=dead |archive-url=https://web.archive.org/web/20130927183248/http://www.blf.org.uk/Files/8ec171b2-9b7e-49d9-b3b1-a07e00f11c05/ |archive-date=27 September 2013 }}</ref>{{unreliable medical source|date=November 2019}}<!-- Should this study and the complaints about it all be removed and just replaced with a reliable study?--> Professor [[David Nutt]], a UK drug expert, points out that the study cited by the British Lung Foundation has been accused of both "false reasoning" and "incorrect methodology". Further, he notes that other studies have failed to connect cannabis with lung cancer, and accuses the BLF of "scaremongering over cannabis".<ref>{{Cite journal |last=Le |first=Bryan |name-list-style=vanc |url=http://www.thefix.com/content/david-nutt-cannabis-carcinogenic90225 |title=Drug prof slams pot lung-danger claims |publisher=The Fix |date=8 June 2012 |access-date=9 January 2013 |archive-date=30 December 2012 |archive-url=https://web.archive.org/web/20121230000132/http://www.thefix.com/content/david-nutt-cannabis-carcinogenic90225 |url-status=live }}</ref>
 ==Short-term effects==
-[[File:Cannabinoid Receptors With THC-2.svg|thumb|Difference between natural cannabinoids and THC A) THC B) CB-1 receptor C) Neurotransmitters D) Postsynaptic Receptors E) Cannabinoid]]
+[[File:Cannabinoid Receptors With THC-2.svg|thumb|Difference between natural cannabinoids and THC:
+{{ordered list|list-style-type=upper-alpha
+| THC
+| CB-1 receptor
+| Neurotransmitters
+| Postsynaptic Receptors
+| Cannabinoid
+}}
-When smoked, the short-term effects of cannabis manifest within seconds and are fully apparent within a few minutes,<ref name=bjp-ashton>{{cite journal | vauthors = Ashton CH | title = Pharmacology and effects of cannabis: a brief review | journal = The British Journal of Psychiatry | volume = 178 | issue = 2 | pages = 101–6 | date = February 2001 | pmid = 11157422 | doi = 10.1192/bjp.178.2.101 | doi-access = free }}</ref> typically lasting for 1–3 hours, varying by the person and the strain of cannabis.<ref name="sagov">{{cite web|url=http://www.dasc.sa.gov.au/site/page.cfm?u=128 |title=Cannabis |publisher=Dasc.sa.gov.au |access-date=20 April 2011 |url-status=dead |archive-url=https://web.archive.org/web/20110327053822/http://www.dasc.sa.gov.au/site/page.cfm?u=128 |archive-date=27 March 2011 }}</ref> After oral ingestion of cannabis, the onset of effect is delayed relative to smoking, taking 30 minutes to 2 hours, but the duration is prolonged due to continued slow absorption.<ref name=bjp-ashton /> The duration of noticeable effects has been observed to diminish after prolonged, repeated use and the development of increased tolerance to cannabinoids.<ref>{{Cite journal |last1=Colizzi |first1=Marco |last2=Bhattacharyya |first2=Sagnik |date=October 2018 |title=Cannabis use and the development of tolerance: a systematic review of human evidence |url=https://pubmed.ncbi.nlm.nih.gov/30056176/ |journal=Neuroscience and Biobehavioral Reviews |volume=93 |pages=1–25 |doi=10.1016/j.neubiorev.2018.07.014 |issn=1873-7528 |pmid=30056176 |s2cid=51718458 |access-date=20 December 2022 |archive-date=20 December 2022 |archive-url=https://web.archive.org/web/20221220003736/https://pubmed.ncbi.nlm.nih.gov/30056176/ |url-status=live }}</ref>
+]]
-Cannabis use can decrease blood pressure, which increases the risk of [[syncope (medicine)|fainting]].<ref>{{Cite web |last=Canada |first=Health |date=2018-03-02 |title=Health effects of cannabis |url=https://www.canada.ca/en/health-canada/services/drugs-medication/cannabis/health-effects/effects.html |access-date=2022-11-17 |website=www.canada.ca |archive-date=17 November 2022 |archive-url=https://web.archive.org/web/20221117173810/https://www.canada.ca/en/health-canada/services/drugs-medication/cannabis/health-effects/effects.html |url-status=live }}</ref> Combining alcohol with cannabis greatly increases the level of impairment and the risk of injury or death from accidents.<ref>{{Cite web |title=Health effects of cannabis |url=https://www.canada.ca/content/dam/hc-sc/documents/services/campaigns/27-16-1808-Factsheet-Health-Effects-eng-web.pdf |access-date=17 November 2022 |archive-date=17 November 2022 |archive-url=https://web.archive.org/web/20221117173817/https://www.canada.ca/content/dam/hc-sc/documents/services/campaigns/27-16-1808-Factsheet-Health-Effects-eng-web.pdf |url-status=live }}</ref>
+=== Onset and duration ===
-===Psychological effects===
+When smoked, the short-term effects of cannabis manifest within seconds and are fully apparent within a few minutes,<ref name="bjp-ashton">{{cite journal | vauthors = Ashton CH | title = Pharmacology and effects of cannabis: a brief review | journal = The British Journal of Psychiatry | volume = 178 | issue = 2 | pages = 101–6 | date = February 2001 | pmid = 11157422 | doi = 10.1192/bjp.178.2.101 | doi-access = free }}</ref> typically lasting 1–3 hours, varying by the person and the [[Cannabis strain|strain of cannabis]].<ref name="sagov">{{cite web|url=http://www.dasc.sa.gov.au/site/page.cfm?u=128 |title=Cannabis |publisher=Dasc.sa.gov.au |access-date=20 April 2011 |url-status=dead |archive-url=https://web.archive.org/web/20110327053822/http://www.dasc.sa.gov.au/site/page.cfm?u=128 |archive-date=27 March 2011 }}</ref> With oral ingestion, however, the onset of effect is delayed, taking 30 minutes to 2 hours, but the duration is prolonged due to continued slow absorption.<ref name="bjp-ashton" /> The duration of noticeable effects has been observed to diminish after prolonged, repeated use leading to the development of increased tolerance to cannabinoids.<ref>{{Cite journal |last1=Colizzi |first1=Marco |last2=Bhattacharyya |first2=Sagnik |date=October 2018 |title=Cannabis use and the development of tolerance: a systematic review of human evidence |url=https://pubmed.ncbi.nlm.nih.gov/30056176/ |journal=Neuroscience and Biobehavioral Reviews |volume=93 |pages=1–25 |doi=10.1016/j.neubiorev.2018.07.014 |issn=1873-7528 |pmid=30056176 |s2cid=51718458 |access-date=20 December 2022 |archive-date=20 December 2022 |archive-url=https://web.archive.org/web/20221220003736/https://pubmed.ncbi.nlm.nih.gov/30056176/ |url-status=live }}</ref>
-[[File:Ganja Smoking - Gangasagar Fair Transit Camp - Kolkata 2013-01-12 2646.JPG|thumb|right|250px|A man smoking cannabis in [[Kolkata, India]]]]
+=== Psychological effects ===
 The psychoactive effects of cannabis, known as a "[[Substance intoxication|high]]", are subjective and vary among persons and the method of use.
-When THC enters the blood stream and reaches the brain, it binds to [[cannabinoid receptor]]s. The [[Ligand (biochemistry)|endogenous ligand]] of these receptors is [[anandamide]], the effects of which THC emulates. This [[agonist|agonism]] of the cannabinoid receptors results in changes in the levels of various neurotransmitters, especially [[dopamine]] and [[norepinephrine]]; neurotransmitters which are closely associated with the acute effects of cannabis ingestion, such as [[euphoria]] and [[anxiety]].
+When THC enters the blood stream and reaches the brain, it binds to [[cannabinoid receptor]]s. The [[Ligand (biochemistry)|endogenous ligand]] of these receptors is [[anandamide]], the effects of which THC emulates. This [[agonist|agonism]] of the cannabinoid receptors results in changes in the levels of various neurotransmitters, especially [[dopamine]] and [[norepinephrine]], which are closely associated with the acute effects of cannabis ingestion, such as [[euphoria]] and [[anxiety]].
-Some effects may include a general [[altered state of consciousness]], [[euphoria]], relaxation or stress reduction, increased appreciation of the arts, including humor and music, joviality, [[metacognition]] and [[introspection]], enhanced recollection ([[episodic memory]]), and increased sensuality, sensory awareness, [[libido]], and creativity.<ref>{{cite journal|vauthors=Osborne GB, Fogel C|year=2009|title=Understanding the motivations for recreational marijuana use among adult Canadians|url=http://cannabislink.ca/info/MotivationsforCannabisUsebyCanadianAdults-2008.pdf|url-status=live|journal=Substance Use & Misuse|volume=43|issue=3–4|pages=539–72; discussion 573–9, 585–7|doi=10.1080/10826080701884911|pmid=18365950|archive-url=https://web.archive.org/web/20160303204835/http://cannabislink.ca/info/MotivationsforCannabisUsebyCanadianAdults-2008.pdf|archive-date=3 March 2016|s2cid=31053594}}</ref> Abstract or philosophical thinking, disruption of linear memory and [[paranoia]] or [[anxiety]] are also typical. [[Anxiety]] is the most commonly reported negative side effect of smoking marijuana. Up to 30 percent of recreational users experience intense anxiety and/or [[panic attack]]s after smoking cannabis. Some report anxiety only after not smoking cannabis for a prolonged period of time.<ref>{{Cite journal|title=Medical Marijuana and the Mind|journal=Harvard Mental Health Letter|date=April 2010|url=http://www.health.harvard.edu/newsletters/Harvard_Mental_Health_Letter/2010/April/medical-marijuana-and-the-mind|access-date=25 April 2011|archive-date=16 January 2015|archive-url=https://web.archive.org/web/20150116150214/http://www.health.harvard.edu/newsletters/Harvard_Mental_Health_Letter/2010/April/medical-marijuana-and-the-mind|url-status=dead}}</ref> Inexperience and use in an unfamiliar environment are major contributing factors to this anxiety. [[Cannabidiol]] (CBD), another cannabinoid found in cannabis, has been shown to improve the adverse effects of THC, including anxiety.<ref name="Niesink2013">{{cite journal | vauthors = Niesink RJ, van Laar MW | title = Does Cannabidiol Protect Against Adverse Psychological Effects of THC? | journal = Frontiers in Psychiatry | volume = 4 | pages = 130 | date = October 2013 | pmid = 24137134 | pmc = 3797438 | doi = 10.3389/fpsyt.2013.00130 | type = Review | doi-access = free }}</ref>
+Some effects may include a general [[altered state of consciousness]], [[euphoria]], relaxation or stress reduction, increased appreciation of the arts, including humor and music, joviality, [[metacognition]] and [[introspection]], enhanced recollection ([[episodic memory]]), and increased sensuality, sensory awareness, [[libido]], and creativity.<ref>{{cite journal|vauthors=Osborne GB, Fogel C|year=2009|title=Understanding the motivations for recreational marijuana use among adult Canadians|url=http://cannabislink.ca/info/MotivationsforCannabisUsebyCanadianAdults-2008.pdf|url-status=live|journal=Substance Use & Misuse|volume=43|issue=3–4|pages=539–72; discussion 573–9, 585–7|doi=10.1080/10826080701884911|pmid=18365950|archive-url=https://web.archive.org/web/20160303204835/http://cannabislink.ca/info/MotivationsforCannabisUsebyCanadianAdults-2008.pdf|archive-date=3 March 2016|s2cid=31053594}}</ref> Abstract or philosophical thinking, disruption of linear memory and paranoia or anxiety are also typical. Anxiety is cannabis's most commonly reported adverse side effect. Up to 30 percent of recreational users experience intense anxiety and/or [[panic attack]]s after smoking cannabis. Some report anxiety only after not smoking cannabis for a prolonged period of time.<ref>{{Cite journal|title=Medical Marijuana and the Mind|journal=Harvard Mental Health Letter|date=April 2010|url=http://www.health.harvard.edu/newsletters/Harvard_Mental_Health_Letter/2010/April/medical-marijuana-and-the-mind|access-date=25 April 2011|archive-date=16 January 2015|archive-url=https://web.archive.org/web/20150116150214/http://www.health.harvard.edu/newsletters/Harvard_Mental_Health_Letter/2010/April/medical-marijuana-and-the-mind|url-status=dead}}</ref> Inexperience and use in an unfamiliar environment are major contributing factors to this anxiety. [[Cannabidiol]] (CBD), another cannabinoid found in cannabis, has been shown to mitigate THC's adverse effects, including anxiety.<ref name="Niesink2013">{{cite journal | vauthors = Niesink RJ, van Laar MW | title = Does Cannabidiol Protect Against Adverse Psychological Effects of THC? | journal = Frontiers in Psychiatry | volume = 4 | pages = 130 | date = October 2013 | pmid = 24137134 | pmc = 3797438 | doi = 10.3389/fpsyt.2013.00130 | type = Review | doi-access = free }}</ref>
-Cannabis produces many other subjective effects, including an increased enjoyment of food taste and aroma, and marked [[Cannabis and time perception|distortions in the perception of time]]. At higher doses, effects can include altered [[body image]], auditory and/or visual [[illusion]]s, [[pseudohallucination]]s, and [[ataxia]] from selective impairment of polysynaptic reflexes.{{Citation needed|date=June 2020}} In some cases, cannabis can lead to [[Stimulant psychosis|acute psychosis]] and [[dissociation (psychology)|dissociative]] states such as [[depersonalization]]<ref name="medscape1">{{cite web|url=http://www.medscape.com/viewarticle/468728_3|title=Medication-Associated Depersonalization Symptoms|website=Medscape|access-date=2 April 2009|archive-date=14 February 2015|archive-url=https://web.archive.org/web/20150214055436/http://www.medscape.com/viewarticle/468728_3|url-status=live}}</ref><ref name="pmid15889607">{{cite journal | vauthors = Shufman E, Lerner A, Witztum E | title = [Depersonalization after withdrawal from cannabis usage] | language = he | journal = Harefuah | volume = 144 | issue = 4 | pages = 249–51, 303 | date = April 2005 | pmid = 15889607 | url = http://www.ima.org.il/Ima/FormStorage/Type3/05-04-07.pdf | archive-url = https://web.archive.org/web/20110304142926/http://www.ima.org.il/Ima/FormStorage/Type3/05-04-07.pdf | url-status=dead | archive-date = 4 March 2011 }}</ref> and [[derealization]].<ref name="Johnson1990">{{cite journal | vauthors = Johnson BA | title = Psychopharmacological effects of cannabis | journal = British Journal of Hospital Medicine | volume = 43 | issue = 2 | pages = 114–6, 118–20, 122 | date = February 1990 | pmid = 2178712 }}</ref>
+Cannabis produces many other subjective effects, including increased enjoyment of food taste and aroma, and marked [[Cannabis and time perception|distortions in the perception of time]]. At higher doses, effects can include altered [[body image]], auditory or visual illusions, [[pseudohallucination]]s, and [[ataxia]] from selective impairment of polysynaptic reflexes.{{Citation needed|date=June 2020}} In some cases, cannabis can lead to [[Stimulant psychosis|acute psychosis]] and [[dissociation (psychology)|dissociative]] states such as [[depersonalization]]<ref name="medscape1">{{cite web|url=http://www.medscape.com/viewarticle/468728_3|title=Medication-Associated Depersonalization Symptoms|website=Medscape|access-date=2 April 2009|archive-date=14 February 2015|archive-url=https://web.archive.org/web/20150214055436/http://www.medscape.com/viewarticle/468728_3|url-status=live}}</ref><ref name="pmid15889607">{{cite journal | vauthors = Shufman E, Lerner A, Witztum E | title = [Depersonalization after withdrawal from cannabis usage] | language = he | journal = Harefuah | volume = 144 | issue = 4 | pages = 249–51, 303 | date = April 2005 | pmid = 15889607 | url = http://www.ima.org.il/Ima/FormStorage/Type3/05-04-07.pdf | archive-url = https://web.archive.org/web/20110304142926/http://www.ima.org.il/Ima/FormStorage/Type3/05-04-07.pdf | url-status=dead | archive-date = 4 March 2011 }}</ref> and [[derealization]].<ref name="Johnson1990">{{cite journal | vauthors = Johnson BA | title = Psychopharmacological effects of cannabis | journal = British Journal of Hospital Medicine | volume = 43 | issue = 2 | pages = 114–6, 118–20, 122 | date = February 1990 | pmid = 2178712 }}</ref>
-Furthermore, even in those with no family history of psychosis, the administration of pure THC in clinical settings has been demonstrated to elicit transient psychotic symptoms.<ref name="D'Souza 2004">{{cite journal|display-authors=6|vauthors=D'Souza DC, Perry E, MacDougall L, Ammerman Y, Cooper T, Wu YT, Braley G, Gueorguieva R, Krystal JH|date=August 2004|title=The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis|journal=Neuropsychopharmacology|volume=29|issue=8|pages=1558–72|doi=10.1038/sj.npp.1300496|pmid=15173844|doi-access=free|s2cid=12508404}}</ref><ref name="Morrison 2011">{{cite journal|display-authors=6|vauthors=Morrison PD, Nottage J, Stone JM, Bhattacharyya S, Tunstall N, Brenneisen R, Holt D, Wilson D, Sumich A, McGuire P, Murray RM, Kapur S, Ffytche DH|date=March 2011|title=Disruption of frontal θ coherence by Δ9-tetrahydrocannabinol is associated with positive psychotic symptoms|journal=Neuropsychopharmacology|volume=36|issue=4|pages=827–36|doi=10.1038/npp.2010.222|pmc=3055738|pmid=21150914}}</ref><ref name="Bhattacharyya 2012">{{cite journal|display-authors=6|vauthors=Bhattacharyya S, Crippa JA, Allen P, Martin-Santos R, Borgwardt S, Fusar-Poli P, Rubia K, Kambeitz J, O'Carroll C, Seal ML, Giampietro V, Brammer M, Zuardi AW, Atakan Z, McGuire PK|date=January 2012|title=Induction of psychosis by Δ9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing|journal=Archives of General Psychiatry|volume=69|issue=1|pages=27–36|doi=10.1001/archgenpsychiatry.2011.161|pmid=22213786|doi-access=}}</ref><ref name="Freeman 2015">{{cite journal|display-authors=6|vauthors=Freeman D, Dunn G, Murray RM, Evans N, Lister R, Antley A, Slater M, Godlewska B, Cornish R, Williams J, Di Simplicio M, Igoumenou A, Brenneisen R, Tunbridge EM, Harrison PJ, Harmer CJ, Cowen P, Morrison PD|date=March 2015|title=How cannabis causes paranoia: using the intravenous administration of ∆9-tetrahydrocannabinol (THC) to identify key cognitive mechanisms leading to paranoia|journal=Schizophrenia Bulletin|volume=41|issue=2|pages=391–9|doi=10.1093/schbul/sbu098|pmc=4332941|pmid=25031222}}</ref> Any episode of acute psychosis that accompanies cannabis use usually abates after six hours, but in rare instances, heavy users may find the symptoms continuing for many days.<ref name=barceloux>{{cite book|first=Donald G|last=Barceloux| name-list-style = vanc |title=Medical Toxicology of Drug Abuse: Synthesized Chemicals and Psychoactive Plants|chapter=Chapter 60: Marijuana (''Cannabis sativa'' L.) and synthetic cannabinoids|chapter-url=https://books.google.com/books?id=OWFiVaDZnkQC&pg=PA915|date=20 March 2012|publisher=John Wiley & Sons|isbn=978-0-471-72760-6|page=915}}</ref>
+Furthermore, even in those with no [[Family medical history|family history]] of [[psychosis]], the administration of pure THC in clinical settings has been demonstrated to elicit transient psychotic symptoms.<ref name="D'Souza 2004">{{cite journal|display-authors=6|vauthors=D'Souza DC, Perry E, MacDougall L, Ammerman Y, Cooper T, Wu YT, Braley G, Gueorguieva R, Krystal JH|date=August 2004|title=The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis|journal=Neuropsychopharmacology|volume=29|issue=8|pages=1558–72|doi=10.1038/sj.npp.1300496|pmid=15173844|doi-access=free|s2cid=12508404}}</ref><ref name="Morrison 2011">{{cite journal|display-authors=6|vauthors=Morrison PD, Nottage J, Stone JM, Bhattacharyya S, Tunstall N, Brenneisen R, Holt D, Wilson D, Sumich A, McGuire P, Murray RM, Kapur S, Ffytche DH|date=March 2011|title=Disruption of frontal θ coherence by Δ9-tetrahydrocannabinol is associated with positive psychotic symptoms|journal=Neuropsychopharmacology|volume=36|issue=4|pages=827–36|doi=10.1038/npp.2010.222|pmc=3055738|pmid=21150914}}</ref><ref name="Bhattacharyya 2012">{{cite journal|display-authors=6|vauthors=Bhattacharyya S, Crippa JA, Allen P, Martin-Santos R, Borgwardt S, Fusar-Poli P, Rubia K, Kambeitz J, O'Carroll C, Seal ML, Giampietro V, Brammer M, Zuardi AW, Atakan Z, McGuire PK|date=January 2012|title=Induction of psychosis by Δ9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing|journal=Archives of General Psychiatry|volume=69|issue=1|pages=27–36|doi=10.1001/archgenpsychiatry.2011.161|pmid=22213786|doi-access=}}</ref><ref name="Freeman 2015">{{cite journal|display-authors=6|vauthors=Freeman D, Dunn G, Murray RM, Evans N, Lister R, Antley A, Slater M, Godlewska B, Cornish R, Williams J, Di Simplicio M, Igoumenou A, Brenneisen R, Tunbridge EM, Harrison PJ, Harmer CJ, Cowen P, Morrison PD|date=March 2015|title=How cannabis causes paranoia: using the intravenous administration of ∆9-tetrahydrocannabinol (THC) to identify key cognitive mechanisms leading to paranoia|journal=Schizophrenia Bulletin|volume=41|issue=2|pages=391–9|doi=10.1093/schbul/sbu098|pmc=4332941|pmid=25031222}}</ref> Any episode of acute psychosis that accompanies cannabis use usually abates after six hours, but in rare instances, users may find the symptoms continuing for many days.<ref name=barceloux>{{cite book|first=Donald G|last=Barceloux| name-list-style = vanc |title=Medical Toxicology of Drug Abuse: Synthesized Chemicals and Psychoactive Plants|chapter=Chapter 60: Marijuana (''Cannabis sativa'' L.) and synthetic cannabinoids|chapter-url=https://books.google.com/books?id=OWFiVaDZnkQC&pg=PA915|date=20 March 2012|publisher=John Wiley & Sons|isbn=978-0-471-72760-6|page=915}}</ref>
 While psychoactive drugs are typically categorized as [[stimulant]]s, [[depressant]]s, or [[hallucinogen]]s, cannabis exhibits a mix of all of these effects. Scientific studies have suggested that other cannabinoids like CBD may also play a significant role in its psychoactive effects.<ref>{{cite book |author=Stafford, Peter |title=Psychedelics Encyclopedia |year=1992 |isbn=978-0-914171-51-5 |publisher=Ronin Publishing, Inc |location=Berkeley, California, United States}}</ref><ref>{{cite book |author=McKim, William A |title=Drugs and Behavior: An Introduction to Behavioral Pharmacology |publisher=Prentice Hall |year=2002 |edition=5 |isbn=978-0-13-048118-4 |page=[https://archive.org/details/drugsbehaviori00mcki/page/400 400] |url=https://archive.org/details/drugsbehaviori00mcki/page/400 }}</ref><ref>{{cite web |title=Information on Drugs of Abuse |website=Commonly Abused Drug Chart |url=http://www.nida.nih.gov/DrugPages/DrugsofAbuse.html |publisher=nih.gov |date=2 July 2018 |access-date=2 December 2013 |archive-date=29 December 2011 |archive-url=https://web.archive.org/web/20111229075616/http://www.nida.nih.gov/DrugPages/DrugsofAbuse.html |url-status=live }}</ref>
 ===Somatic effects===
+Cannabis use can decrease [[blood pressure]], which increases the risk of [[syncope (medicine)|fainting]].<ref>{{Cite web |last=Canada |first=Health |date=2018-03-02 |title=Health effects of cannabis |url=https://www.canada.ca/en/health-canada/services/drugs-medication/cannabis/health-effects/effects.html |url-status=live |archive-url=https://web.archive.org/web/20221117173810/https://www.canada.ca/en/health-canada/services/drugs-medication/cannabis/health-effects/effects.html |archive-date=17 November 2022 |access-date=2022-11-17 |website=www.canada.ca}}</ref> Combining alcohol with cannabis greatly increases the level of impairment and the risk of injury or death from accidents.<ref>{{Cite web |title=Health effects of cannabis |url=https://www.canada.ca/content/dam/hc-sc/documents/services/campaigns/27-16-1808-Factsheet-Health-Effects-eng-web.pdf |url-status=live |archive-url=https://web.archive.org/web/20221117173817/https://www.canada.ca/content/dam/hc-sc/documents/services/campaigns/27-16-1808-Factsheet-Health-Effects-eng-web.pdf |archive-date=17 November 2022 |access-date=17 November 2022}}</ref>[[File:Bloodshot EyeBall.jpg|thumb|right|Bloodshot eye]]
-[[File:Bloodshot EyeBall.jpg|thumb|right|Bloodshot eye]]
-Some of the short-term physical effects of cannabis use include increased [[heart rate]], [[xerostomia|dry mouth]], reddening of the eyes (congestion of the [[conjunctiva]]l [[blood vessel]]s), a reduction in [[intra-ocular pressure]], muscle relaxation and a sensation of cold or hot hands and feet.<ref>{{cite web |url=http://web4health.info/en/answers/add-cannabis-physical.htm |title=How does Marijuana Affect Your Body? What are the Marijuana Physical Effects? |first=Wendy |last=Moelker |name-list-style=vanc |date=19 September 2008 |access-date=22 January 2009 |archive-date=7 February 2009 |archive-url=https://web.archive.org/web/20090207012048/http://web4health.info/en/answers/add-cannabis-physical.htm |url-status=live }}</ref>
+Some of the short-term physical effects of cannabis use include increased [[heart rate]], [[xerostomia|dry mouth]], reddening of the eyes (congestion of the [[conjunctiva]]l [[blood vessel]]s), a reduction in [[intra-ocular pressure]], muscle relaxation, and a sensation of cold or hot hands and feet.<ref>{{cite web |url=http://web4health.info/en/answers/add-cannabis-physical.htm |title=How does Marijuana Affect Your Body? What are the Marijuana Physical Effects? |first=Wendy |last=Moelker |name-list-style=vanc |date=19 September 2008 |access-date=22 January 2009 |archive-date=7 February 2009 |archive-url=https://web.archive.org/web/20090207012048/http://web4health.info/en/answers/add-cannabis-physical.htm |url-status=live }}</ref>
-[[Electroencephalography]] (EEG) shows somewhat more persistent [[alpha wave]]s of slightly lower [[frequency]] than usual.<ref name=autogenerated2>{{cite book| title=Principles of Medical Pharmacology | edition=6th |author1=Kalant, H.K. |author2=Roschlau, W.H.E. | year=1998 | pages=373–375}}</ref> Cannabinoids produce a marked depression of motor activity via activation of neuronal [[cannabinoid]] receptors belonging to the [[Cannabinoid receptor type 1]].<ref>{{cite journal | vauthors = Andersson M, Usiello A, Borgkvist A, Pozzi L, Dominguez C, Fienberg AA, Svenningsson P, Fredholm BB, Borrelli E, Greengard P, Fisone G | title = Cannabinoid action depends on phosphorylation of dopamine- and cAMP-regulated phosphoprotein of 32 kDa at the protein kinase A site in striatal projection neurons | journal = The Journal of Neuroscience | volume = 25 | issue = 37 | pages = 8432–8 | date = September 2005 | pmid = 16162925 | pmc = 6725667 | doi = 10.1523/JNEUROSCI.1289-05.2005 }}</ref>
+[[Electroencephalography]] (EEG) shows somewhat more persistent [[alpha wave]]s of slightly lower [[frequency]] than usual.<ref name=autogenerated2>{{cite book| title=Principles of Medical Pharmacology | edition=6th |author1=Kalant, H.K. |author2=Roschlau, W.H.E. | year=1998 | pages=373–375}}</ref> Cannabinoids produce a marked depression of motor activity via activation of receptors of [[cannabinoid receptor type 1]].<ref>{{cite journal | vauthors = Andersson M, Usiello A, Borgkvist A, Pozzi L, Dominguez C, Fienberg AA, Svenningsson P, Fredholm BB, Borrelli E, Greengard P, Fisone G | title = Cannabinoid action depends on phosphorylation of dopamine- and cAMP-regulated phosphoprotein of 32 kDa at the protein kinase A site in striatal projection neurons | journal = The Journal of Neuroscience | volume = 25 | issue = 37 | pages = 8432–8 | date = September 2005 | pmid = 16162925 | pmc = 6725667 | doi = 10.1523/JNEUROSCI.1289-05.2005 }}</ref>
 ===Duration===
-Peak levels of cannabis-associated intoxication occur approximately 20 minutes after smoking it and last for several hours.<ref name="ReferenceA">{{cite journal | vauthors = Crean RD, Crane NA, Mason BJ | title = An evidence based review of acute and long-term effects of cannabis use on executive cognitive functions | journal = Journal of Addiction Medicine | volume = 5 | issue = 1 | pages = 1–8 | date = March 2011 | pmid = 21321675 | pmc = 3037578 | doi = 10.1097/ADM.0b013e31820c23fa }}</ref> The total short-term duration of cannabis use when smoked depends on the potency, method of smoking – e.g. whether pure or in conjunction with tobacco – and how much is smoked. Peak levels of intoxication typically last an average of three to four hours.<ref name="ReferenceA"/> When taken orally (in the form of capsules, food, or drink), the psychoactive effects take longer to manifest and generally last longer, typically lasting for an average of four to six hours after consumption.<ref name="erowid.org">{{cite web|url=http://www.erowid.org/plants/cannabis/cannabis_effects.shtml|title=Erowid Cannabis (Marijuana) Vault : Effects|website=Erowid.org|access-date=9 April 2018|archive-date=19 August 2016|archive-url=https://web.archive.org/web/20160819023850/https://www.erowid.org/plants/cannabis/cannabis_effects.shtml|url-status=live}}</ref>{{Unreliable medical source|date=February 2011}} Oral ingestion use eliminates the need to inhale toxic combustion products created by smoking and therefore negates the risk of respiratory harm associated with cannabis smoking.
+Peak levels of cannabis-associated intoxication occur about 20 minutes after smoking it and last several hours.<ref name="ReferenceA">{{cite journal | vauthors = Crean RD, Crane NA, Mason BJ | title = An evidence based review of acute and long-term effects of cannabis use on executive cognitive functions | journal = Journal of Addiction Medicine | volume = 5 | issue = 1 | pages = 1–8 | date = March 2011 | pmid = 21321675 | pmc = 3037578 | doi = 10.1097/ADM.0b013e31820c23fa }}</ref> The total short-term duration of cannabis use when smoked depends on the potency, method of smoking – e.g. whether pure or in conjunction with tobacco – and quantity. Peak levels of intoxication typically last an average of three to four hours.<ref name="ReferenceA"/> When taken orally (in the form of capsules, food, or drink), the psychoactive effects take longer to manifest and generally last longer, typically an average of four to six hours after consumption.<ref name="erowid.org">{{cite web|url=http://www.erowid.org/plants/cannabis/cannabis_effects.shtml|title=Erowid Cannabis (Marijuana) Vault : Effects|website=Erowid.org|access-date=9 April 2018|archive-date=19 August 2016|archive-url=https://web.archive.org/web/20160819023850/https://www.erowid.org/plants/cannabis/cannabis_effects.shtml|url-status=live}}</ref>{{Unreliable medical source|date=February 2011}} Oral ingestion use eliminates the need to inhale toxic combustion products created by smoking and therefore negates the risk of respiratory harm associated with cannabis smoking.
 ===Appetite===
-The feeling of increased appetite following the use of [[cannabis]] has been documented for hundreds of years,<ref>{{cite book |vauthors = Mechoulam R |year=1984 |title=Cannabinoids as therapeutic agents |location=Boca Raton, FL |publisher=CRC Press |isbn=978-0-8493-5772-5}}{{Page needed|date=February 2011}}</ref> and is known colloquially as the "munchies". Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food.<ref>{{cite web | author = Ad Hoc Group of Experts | url = http://www.nih.gov/news/medmarijuana/MedicalMarijuana.htm | title = Workshop on the Medical Utility of Marijuana | work = Report to the Director, [[Institute of Medicine]] | publisher = U.S. National Institutes of Health | archive-url =   https://web.archive.org/web/20071103221831/http://www.nih.gov/news/medmarijuana/MedicalMarijuana.htm | archive-date = 3 November 2007 }}</ref><ref name=Bonsor>Bonsor, Kevin. "[http://health.howstuffworks.com/marijuana4.htm How Marijauan Works: Other Physiological Effects] {{Webarchive|url=https://web.archive.org/web/20070811061603/http://health.howstuffworks.com/marijuana4.htm |date=11 August 2007 }}". [[HowStuffWorks]]. Retrieved on 3 November 2007</ref> A 2015 study suggests that cannabis triggers uncharacteristic behaviour in [[proopiomelanocortin]] (POMC) neurons, which are usually associated with decreasing hunger.<ref>{{Cite news|url=https://www.theguardian.com/science/2015/feb/18/study-on-why-cannabis-kicks-in-urge-to-eat-could-help-create-new-drugs-to-control-appetite|title=Cannabis 'munchies' explained by new research|last=Devlin|first=Hannah|name-list-style=vanc|date=18 February 2015|newspaper=The Guardian|access-date=18 October 2018|archive-date=18 October 2018|archive-url=https://web.archive.org/web/20181018201630/https://www.theguardian.com/science/2015/feb/18/study-on-why-cannabis-kicks-in-urge-to-eat-could-help-create-new-drugs-to-control-appetite|url-status=live}}</ref><ref>{{cite journal | vauthors = Koch M, Varela L, Kim JG, Kim JD, Hernández-Nuño F, Simonds SE, Castorena CM, Vianna CR, Elmquist JK, Morozov YM, Rakic P, Bechmann I, Cowley MA, Szigeti-Buck K, Dietrich MO, Gao XB, Diano S, Horvath TL | title = Hypothalamic POMC neurons promote cannabinoid-induced feeding | journal = Nature | volume = 519 | issue = 7541 | pages = 45–50 | date = March 2015 | pmid = 25707796 | pmc = 4496586 | doi = 10.1038/nature14260 | bibcode = 2015Natur.519...45K }}</ref>
+Increased appetite after cannabis use has been documented for hundreds of years<ref>{{cite book |vauthors = Mechoulam R |year=1984 |title=Cannabinoids as therapeutic agents |location=Boca Raton, FL |publisher=CRC Press |isbn=978-0-8493-5772-5}}{{Page needed|date=February 2011}}</ref> and is known colloquially as the "munchies". Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food.<ref>{{cite web | author = Ad Hoc Group of Experts | url = http://www.nih.gov/news/medmarijuana/MedicalMarijuana.htm | title = Workshop on the Medical Utility of Marijuana | work = Report to the Director, [[Institute of Medicine]] | publisher = U.S. National Institutes of Health | archive-url =   https://web.archive.org/web/20071103221831/http://www.nih.gov/news/medmarijuana/MedicalMarijuana.htm | archive-date = 3 November 2007 }}</ref><ref name=Bonsor>Bonsor, Kevin. "[http://health.howstuffworks.com/marijuana4.htm How Marijauan Works: Other Physiological Effects] {{Webarchive|url=https://web.archive.org/web/20070811061603/http://health.howstuffworks.com/marijuana4.htm |date=11 August 2007 }}". [[HowStuffWorks]]. Retrieved on 3 November 2007</ref> A 2015 study suggests that cannabis triggers uncharacteristic behaviour in [[proopiomelanocortin]] (POMC) neurons, which are usually associated with decreasing hunger.<ref>{{Cite news|url=https://www.theguardian.com/science/2015/feb/18/study-on-why-cannabis-kicks-in-urge-to-eat-could-help-create-new-drugs-to-control-appetite|title=Cannabis 'munchies' explained by new research|last=Devlin|first=Hannah|name-list-style=vanc|date=18 February 2015|newspaper=The Guardian|access-date=18 October 2018|archive-date=18 October 2018|archive-url=https://web.archive.org/web/20181018201630/https://www.theguardian.com/science/2015/feb/18/study-on-why-cannabis-kicks-in-urge-to-eat-could-help-create-new-drugs-to-control-appetite|url-status=live}}</ref><ref>{{cite journal | vauthors = Koch M, Varela L, Kim JG, Kim JD, Hernández-Nuño F, Simonds SE, Castorena CM, Vianna CR, Elmquist JK, Morozov YM, Rakic P, Bechmann I, Cowley MA, Szigeti-Buck K, Dietrich MO, Gao XB, Diano S, Horvath TL | title = Hypothalamic POMC neurons promote cannabinoid-induced feeding | journal = Nature | volume = 519 | issue = 7541 | pages = 45–50 | date = March 2015 | pmid = 25707796 | pmc = 4496586 | doi = 10.1038/nature14260 | bibcode = 2015Natur.519...45K }}</ref>
-Endogenous cannabinoids, more commonly known as [[endocannabinoids]], exist in cow and human milk.<ref>{{cite journal | vauthors = Di Marzo V, Sepe N, De Petrocellis L, Berger A, Crozier G, Fride E, Mechoulam R | title = Trick or treat from food endocannabinoids? | journal = Nature | volume = 396 | issue = 6712 | pages = 636–7 | date = December 1998 | pmid = 9872309 | doi = 10.1038/25267 | bibcode = 1998Natur.396..636D | s2cid = 4425760 | url = https://escholarship.org/uc/item/1qh5k290 | access-date = 27 August 2020 | archive-date = 20 April 2023 | archive-url = https://web.archive.org/web/20230420131323/https://escholarship.org/uc/item/1qh5k290 | url-status = live | doi-access = free }}</ref><ref>{{cite journal | vauthors = di Tomaso E, Beltramo M, Piomelli D | title = Brain cannabinoids in chocolate | journal = Nature | volume = 382 | issue = 6593 | pages = 677–8 | date = August 1996 | pmid = 8751435 | doi = 10.1038/382677a0 | url = http://www.escholarship.org/uc/item/2kk1604c | type = Submitted manuscript | bibcode = 1996Natur.382..677D | s2cid = 4325706 | access-date = 28 August 2018 | archive-date = 19 October 2018 | archive-url = https://web.archive.org/web/20181019001636/https://escholarship.org/uc/item/2kk1604c | url-status = live }}</ref><ref>{{cite journal | vauthors = Fride E, Bregman T, Kirkham TC | title = Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood | journal = Experimental Biology and Medicine | volume = 230 | issue = 4 | pages = 225–34 | date = April 2005 | pmid = 15792943 | doi = 10.1177/153537020523000401 | s2cid = 25430588 | url = http://www.ebmonline.org/cgi/reprint/230/4/225.pdf | access-date = 20 June 2017 | archive-date = 2 August 2009 | archive-url = https://web.archive.org/web/20090802181308/http://www.ebmonline.org/cgi/reprint/230/4/225.pdf | url-status = live }}</ref><ref>[http://www.nel.edu/pdf_/25_12/NEL251204A01_Fride_.pdf The Endocannabinoid-CB Receptor System: Importance for development and in pediatric disease] {{Webarchive|url=https://web.archive.org/web/20160402083340/http://www.nel.edu/pdf_/25_12/NEL251204A01_Fride_.pdf |date=2 April 2016 }} Neuroendocrinology Letters Nos.1/2, Feb-Apr Vol.25, 2004.</ref><ref>[http://www.cannabis-med.org/data/pdf/2002-03-04-3.pdf Cannabinoids and Feeding: The Role of the Endogenous Cannabinoid System as a Trigger for Newborn Suckling] {{Webarchive|url=https://web.archive.org/web/20201001042840/http://www.cannabis-med.org/data/pdf/2002-03-04-3.pdf |date=1 October 2020 }} Women and Cannabis: Medicine, Science, and Sociology, 2002 The Haworth Press, Inc.</ref><ref name=Wu2016>{{cite journal | vauthors = Wu J, Gouveia-Figueira S, Domellöf M, Zivkovic AM, Nording ML | title = Oxylipins, endocannabinoids, and related compounds in human milk: Levels and effects of storage conditions | journal = Prostaglandins & Other Lipid Mediators | volume = 122 | pages = 28–36 | date = January 2016 | pmid = 26656029 | doi = 10.1016/j.prostaglandins.2015.11.002 }}</ref><ref name="ReferenceB">{{cite journal | vauthors = Fride E | title = The endocannabinoid-CB(1) receptor system in pre- and postnatal life | journal = European Journal of Pharmacology | volume = 500 | issue = 1–3 | pages = 289–97 | date = October 2004 | pmid = 15464041 | doi = 10.1016/j.ejphar.2004.07.033 }}</ref> It is widely accepted that the neonatal survival of many species is largely dependent upon their suckling behavior and research has identified the endogenous cannabinoid system to be the first neural system to display complete control over milk ingestion and neonatal survival.<ref name="ncpic.org.au">{{cite web|url=http://ncpic.org.au/ncpic/publications/research-briefs/?page=1 |title=NCPIC Research Briefs • NCPIC |publisher=Ncpic.org.au |date=11 March 2011 |access-date=20 April 2011 |url-status=usurped |archive-url=https://web.archive.org/web/20110706125755/http://ncpic.org.au/ncpic/publications/research-briefs/?page=1 |archive-date=6 July 2011 }}</ref><ref name="ReferenceB"/>
+Endogenous cannabinoids, more commonly known as [[endocannabinoids]], exist in cow and human milk.<ref>{{cite journal | vauthors = Di Marzo V, Sepe N, De Petrocellis L, Berger A, Crozier G, Fride E, Mechoulam R | title = Trick or treat from food endocannabinoids? | journal = Nature | volume = 396 | issue = 6712 | pages = 636–7 | date = December 1998 | pmid = 9872309 | doi = 10.1038/25267 | bibcode = 1998Natur.396..636D | s2cid = 4425760 | url = https://escholarship.org/uc/item/1qh5k290 | access-date = 27 August 2020 | archive-date = 20 April 2023 | archive-url = https://web.archive.org/web/20230420131323/https://escholarship.org/uc/item/1qh5k290 | url-status = live | doi-access = free }}</ref><ref>{{cite journal | vauthors = di Tomaso E, Beltramo M, Piomelli D | title = Brain cannabinoids in chocolate | journal = Nature | volume = 382 | issue = 6593 | pages = 677–8 | date = August 1996 | pmid = 8751435 | doi = 10.1038/382677a0 | url = http://www.escholarship.org/uc/item/2kk1604c | type = Submitted manuscript | bibcode = 1996Natur.382..677D | s2cid = 4325706 | access-date = 28 August 2018 | archive-date = 19 October 2018 | archive-url = https://web.archive.org/web/20181019001636/https://escholarship.org/uc/item/2kk1604c | url-status = live }}</ref><ref>{{cite journal | vauthors = Fride E, Bregman T, Kirkham TC | title = Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood | journal = Experimental Biology and Medicine | volume = 230 | issue = 4 | pages = 225–34 | date = April 2005 | pmid = 15792943 | doi = 10.1177/153537020523000401 | s2cid = 25430588 | url = http://www.ebmonline.org/cgi/reprint/230/4/225.pdf | access-date = 20 June 2017 | archive-date = 2 August 2009 | archive-url = https://web.archive.org/web/20090802181308/http://www.ebmonline.org/cgi/reprint/230/4/225.pdf | url-status = live }}</ref><ref>[http://www.nel.edu/pdf_/25_12/NEL251204A01_Fride_.pdf The Endocannabinoid-CB Receptor System: Importance for development and in pediatric disease] {{Webarchive|url=https://web.archive.org/web/20160402083340/http://www.nel.edu/pdf_/25_12/NEL251204A01_Fride_.pdf |date=2 April 2016 }} Neuroendocrinology Letters Nos.1/2, Feb-Apr Vol.25, 2004.</ref><ref>[http://www.cannabis-med.org/data/pdf/2002-03-04-3.pdf Cannabinoids and Feeding: The Role of the Endogenous Cannabinoid System as a Trigger for Newborn Suckling] {{Webarchive|url=https://web.archive.org/web/20201001042840/http://www.cannabis-med.org/data/pdf/2002-03-04-3.pdf |date=1 October 2020 }} Women and Cannabis: Medicine, Science, and Sociology, 2002 The Haworth Press, Inc.</ref><ref name=Wu2016>{{cite journal | vauthors = Wu J, Gouveia-Figueira S, Domellöf M, Zivkovic AM, Nording ML | title = Oxylipins, endocannabinoids, and related compounds in human milk: Levels and effects of storage conditions | journal = Prostaglandins & Other Lipid Mediators | volume = 122 | pages = 28–36 | date = January 2016 | pmid = 26656029 | doi = 10.1016/j.prostaglandins.2015.11.002 }}</ref><ref name="ReferenceB">{{cite journal | vauthors = Fride E | title = The endocannabinoid-CB(1) receptor system in pre- and postnatal life | journal = European Journal of Pharmacology | volume = 500 | issue = 1–3 | pages = 289–97 | date = October 2004 | pmid = 15464041 | doi = 10.1016/j.ejphar.2004.07.033 }}</ref> It is widely accepted that the neonatal survival of many species is largely dependent upon their suckling behavior, and research has identified the endogenous cannabinoid system as the first neural system to display complete control over milk ingestion and neonatal survival.<ref name="ncpic.org.au">{{cite web|url=http://ncpic.org.au/ncpic/publications/research-briefs/?page=1 |title=NCPIC Research Briefs • NCPIC |publisher=Ncpic.org.au |date=11 March 2011 |access-date=20 April 2011 |url-status=usurped |archive-url=https://web.archive.org/web/20110706125755/http://ncpic.org.au/ncpic/publications/research-briefs/?page=1 |archive-date=6 July 2011 }}</ref><ref name="ReferenceB"/>
 ===Cardiovascular effects===
-Short-term (one to two hours) effects on the cardiovascular system can include increased heart rate, dilation of blood vessels, and fluctuations in blood pressure.<ref>{{cite book | last = Falvo | first = D R | title = Medical and psychosocial aspects of chronic illness and disability | publisher = Jones & Bartlett Learning | edition = Third | year = 2005 | page = 217 | isbn = 978-0-7637-3166-3 }}</ref><ref>{{cite book | last = Ghodse | first = Hamid | title = Ghodse's Drugs and Addictive Behaviour | publisher = Cambridge University Press | year = 2010 | page = 97 | isbn = 978-1-139-48567-8 }}</ref><ref>{{cite journal|vauthors=Jones RT|date=November 2002|title=Cardiovascular system effects of marijuana|journal=Journal of Clinical Pharmacology|volume=42|issue=S1|pages=58S–63S|doi=10.1002/j.1552-4604.2002.tb06004.x|pmid=12412837|s2cid=12193532}}<!--| access-date =19 October 2013--></ref>  There are medical reports of occasional heart attacks or [[myocardial infarction]], [[stroke]] and other cardiovascular side effects.<ref name="Jones2002">{{cite journal|vauthors=Jones RT|date=November 2002|title=Cardiovascular system effects of marijuana|journal=Journal of Clinical Pharmacology|volume=42|issue=S1|pages=58S–63S|doi=10.1002/j.1552-4604.2002.tb06004.x|pmid=12412837|s2cid=12193532}}<!--| access-date =31 January 2013--></ref> Marijuana's cardiovascular effects are not associated with serious health problems for most young, healthy users.<ref name="Jones2002"/> Researchers reported in the ''[[International Journal of Cardiology]]'', "Marijuana use by older people, particularly those with some degree of [[coronary artery disease|coronary artery]] or [[cerebrovascular disease]], poses greater risks due to the resulting increase in [[catecholamine]]s, [[cardiac physiology|cardiac workload]], and [[carboxyhemoglobin]] levels, and concurrent episodes of profound postural [[hypotension]]. Indeed, marijuana may be a much more common cause of [[myocardial infarction]] than is generally recognized. In day-to-day practice, a history of marijuana use is often not sought by many practitioners, and even when sought, the patient's response is not always truthful".<ref>{{cite journal | vauthors = Aryana A, Williams MA | title = Marijuana as a trigger of cardiovascular events: speculation or scientific certainty? | journal = International Journal of Cardiology | volume = 118 | issue = 2 | pages = 141–4 | date = May 2007 | pmid = 17005273 | doi = 10.1016/j.ijcard.2006.08.001 | url = http://www.internationaljournalofcardiology.com/article/S0167-5273(06)00778-9/abstract | access-date = 6 April 2013 | archive-date = 17 April 2018 | archive-url = https://web.archive.org/web/20180417051017/http://www.internationaljournalofcardiology.com/article/S0167-5273%2806%2900778-9/abstract | url-status = live }}</ref>
+Short-term (one to two hours) effects on the cardiovascular system can include increased heart rate, dilation of blood vessels, and fluctuations in blood pressure.<ref>{{cite book | last = Falvo | first = D R | title = Medical and psychosocial aspects of chronic illness and disability | publisher = Jones & Bartlett Learning | edition = Third | year = 2005 | page = 217 | isbn = 978-0-7637-3166-3 }}</ref><ref>{{cite book | last = Ghodse | first = Hamid | title = Ghodse's Drugs and Addictive Behaviour | publisher = Cambridge University Press | year = 2010 | page = 97 | isbn = 978-1-139-48567-8 }}</ref><ref>{{cite journal|vauthors=Jones RT|date=November 2002|title=Cardiovascular system effects of marijuana|journal=Journal of Clinical Pharmacology|volume=42|issue=S1|pages=58S–63S|doi=10.1002/j.1552-4604.2002.tb06004.x|pmid=12412837|s2cid=12193532}}<!--| access-date =19 October 2013--></ref> There are medical reports of occasional heart attacks or [[myocardial infarction]], [[stroke]], and other cardiovascular side effects.<ref name="Jones2002">{{cite journal|vauthors=Jones RT|date=November 2002|title=Cardiovascular system effects of marijuana|journal=Journal of Clinical Pharmacology|volume=42|issue=S1|pages=58S–63S|doi=10.1002/j.1552-4604.2002.tb06004.x|pmid=12412837|s2cid=12193532}}<!--| access-date =31 January 2013--></ref> Cannabis's cardiovascular effects are not associated with serious health problems for most young, healthy users.<ref name="Jones2002"/> Researchers reported in the ''[[International Journal of Cardiology]]'', "Marijuana use by older people, particularly those with some degree of [[coronary artery disease|coronary artery]] or [[cerebrovascular disease]], poses greater risks due to the resulting increase in [[catecholamine]]s, [[cardiac physiology|cardiac workload]], and [[carboxyhemoglobin]] levels, and concurrent episodes of profound postural [[hypotension]]. Indeed, marijuana may be a much more common cause of [[myocardial infarction]] than is generally recognized. In day-to-day practice, a history of marijuana use is often not sought by many practitioners, and even when sought, the patient's response is not always truthful".<ref>{{cite journal | vauthors = Aryana A, Williams MA | title = Marijuana as a trigger of cardiovascular events: speculation or scientific certainty? | journal = International Journal of Cardiology | volume = 118 | issue = 2 | pages = 141–4 | date = May 2007 | pmid = 17005273 | doi = 10.1016/j.ijcard.2006.08.001 | url = http://www.internationaljournalofcardiology.com/article/S0167-5273(06)00778-9/abstract | access-date = 6 April 2013 | archive-date = 17 April 2018 | archive-url = https://web.archive.org/web/20180417051017/http://www.internationaljournalofcardiology.com/article/S0167-5273%2806%2900778-9/abstract | url-status = live }}</ref>
 A 2013 analysis of 3,886 myocardial infarction survivors over an 18-year period showed "no statistically significant association between marijuana use and mortality".<ref>{{cite journal | vauthors = Frost L, Mostofsky E, Rosenbloom JI, Mukamal KJ, Mittleman MA | title = Marijuana use and long-term mortality among survivors of acute myocardial infarction | journal = American Heart Journal | volume = 165 | issue = 2 | pages = 170–5 | date = February 2013 | pmid = 23351819 | pmc = 3558923 | doi = 10.1016/j.ahj.2012.11.007 }}</ref>
-A 2008 study by the [[National Institutes of Health]] Biomedical Research Centre in Baltimore found that heavy, chronic smoking of marijuana (138 joints per week) changed [[blood proteins]] associated with [[heart disease]] and [[stroke]].<ref>{{cite news |url=http://www.cbc.ca/news/health/story/2008/05/13/pot-stroke.html |title=Heavy pot smoking could raise risk of heart attack, stroke |publisher=CBC |access-date=17 April 2009 |date=13 May 2008 |archive-date=10 November 2012 |archive-url=https://web.archive.org/web/20121110102914/http://www.cbc.ca/news/health/story/2008/05/13/pot-stroke.html |url-status=live }}</ref>
+A 2008 study by the [[National Institutes of Health]] Biomedical Research Centre in Baltimore found that heavy, chronic smoking of marijuana (138 joints per week) changed [[blood proteins]] associated with heart disease and stroke.<ref>{{cite news |url=https://www.cbc.ca/news/science/heavy-pot-smoking-could-raise-risk-of-heart-attack-stroke-1.738372 |title=Heavy pot smoking could raise risk of heart attack, stroke |publisher=CBC |access-date=17 April 2009 |date=13 May 2008 |archive-date=10 November 2012 |archive-url=https://web.archive.org/web/20121110102914/http://www.cbc.ca/news/health/story/2008/05/13/pot-stroke.html |url-status=live }}</ref>
-A 2000 study by researchers at Boston's [[Beth Israel Deaconess Medical Center]], [[Massachusetts General Hospital]] and [[Harvard School of Public Health]] found that a middle age person's risk of heart attack rises nearly fivefold in the first hour after smoking marijuana, "roughly the same risk seen within an hour of sexual activity".<ref>{{cite magazine | url=http://healthland.time.com/2013/02/08/marijuana-linked-to-increased-stroke-risk/#ixzz2TmRWjqKa | magazine=[[Time (magazine)|Time]] | title=Marijuana Linked to Increased Stroke Risk | date=8 February 2013 | access-date=19 May 2013 | archive-date=20 April 2023 | archive-url=https://web.archive.org/web/20230420141333/https://healthland.time.com/2013/02/08/marijuana-linked-to-increased-stroke-risk/#ixzz2TmRWjqKa | url-status=live }}</ref><ref name="NYT 2000">{{cite news |url=https://www.nytimes.com/2000/03/03/us/report-links-heart-attacks-to-marijuana.html |title=Report Links Heart Attacks To Marijuana |last=Noble |first=Holcomb B. |name-list-style=vanc |date=3 March 2000 |work=[[The New York Times]] |access-date=26 April 2009 |archive-date=7 August 2009 |archive-url=https://web.archive.org/web/20090807140810/http://www.nytimes.com/2000/03/03/us/report-links-heart-attacks-to-marijuana.html |url-status=live }}</ref>
+A 2000 study by researchers at Boston's [[Beth Israel Deaconess Medical Center]], [[Massachusetts General Hospital]], and [[Harvard School of Public Health]] found that a middle-aged person's risk of heart attack rises nearly fivefold in the first hour after smoking cannabis, "roughly the same risk seen within an hour of sexual activity".<ref>{{cite magazine | url=https://healthland.time.com/2013/02/08/marijuana-linked-to-increased-stroke-risk/#ixzz2TmRWjqKa | magazine=[[Time (magazine)|Time]] | title=Marijuana Linked to Increased Stroke Risk | date=8 February 2013 | access-date=19 May 2013 | archive-date=20 April 2023 | archive-url=https://web.archive.org/web/20230420141333/https://healthland.time.com/2013/02/08/marijuana-linked-to-increased-stroke-risk/#ixzz2TmRWjqKa | url-status=live }}</ref><ref name="NYT 2000">{{cite news |url=https://www.nytimes.com/2000/03/03/us/report-links-heart-attacks-to-marijuana.html |title=Report Links Heart Attacks To Marijuana |last=Noble |first=Holcomb B. |name-list-style=vanc |date=3 March 2000 |work=[[The New York Times]] |access-date=26 April 2009 |archive-date=7 August 2009 |archive-url=https://web.archive.org/web/20090807140810/http://www.nytimes.com/2000/03/03/us/report-links-heart-attacks-to-marijuana.html |url-status=live }}</ref>
-[[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 of which occurred in Europe.<ref>{{cite journal | vauthors = Peyrot I, Garsaud AM, Saint-Cyr I, Quitman O, Sanchez B, Quist D | title = Cannabis arteritis: a new case report and a review of literature | journal = Journal of the European Academy of Dermatology and Venereology | volume = 21 | issue = 3 | pages = 388–91 | date = March 2007 | pmid = 17309465 | doi = 10.1111/j.1468-3083.2006.01947.x | s2cid = 43529847 | quote = Amputation of the right second toe and of the left leg finally became necessary. }}</ref>
+[[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.<ref>{{cite journal | vauthors = Peyrot I, Garsaud AM, Saint-Cyr I, Quitman O, Sanchez B, Quist D | title = Cannabis arteritis: a new case report and a review of literature | journal = Journal of the European Academy of Dermatology and Venereology | volume = 21 | issue = 3 | pages = 388–91 | date = March 2007 | pmid = 17309465 | doi = 10.1111/j.1468-3083.2006.01947.x | s2cid = 43529847 | quote = Amputation of the right second toe and of the left leg finally became necessary. }}</ref>
 ===Memory and learning===
@@ Line 109: / Line 103: @@
 Studies on cannabis and memory are hindered by small sample sizes, confounding drug use, and other factors.<ref name= "memory_hindered" >{{cite book | vauthors = Riedel G, Davies SN | chapter = Cannabinoid function in learning, memory and plasticity | volume = 168 | issue = 168 | pages = 445–77 | year = 2005 | pmid = 16596784 | doi = 10.1007/3-540-26573-2_15 | isbn = 978-3-540-22565-2 | series = Handbook of Experimental Pharmacology | title = Cannabinoids }}</ref> The strongest evidence regarding cannabis and memory focuses on its temporary negative effects on short-term and working memory.<ref name= "memory_hindered" />
-In a 2001 study looking at neuropsychological performance in long-term cannabis users, researchers found "some cognitive deficits appear detectable at least 7 days after heavy cannabis use but appear reversible and related to recent cannabis exposure rather than irreversible and related to cumulative lifetime use".<ref>{{cite journal | vauthors = Pope HG, Gruber AJ, Hudson JI, Huestis MA, Yurgelun-Todd D | title = Neuropsychological performance in long-term cannabis users | journal = Archives of General Psychiatry | volume = 58 | issue = 10 | pages = 909–15 | date = October 2001 | pmid = 11576028 | doi = 10.1001/archpsyc.58.10.909 | doi-access =  }}</ref> On his studies regarding cannabis use, lead researcher and Harvard professor [[Harrison Pope]] said he found marijuana is not dangerous over the long term, but there are short-term effects. From neuropsychological tests, Pope found that chronic cannabis users showed difficulties, with verbal memory in particular, for "at least a week or two" after they stopped smoking. Within 28 days, memory problems vanished and the subjects "were no longer distinguishable from the comparison group".<ref>Lyons, Casey (October 2012) [http://www.bostonmagazine.com/2012/09/medical-marijuana-in-massachusetts/5 "Lost in the Weeds: Legalizing Medical Marijuana in Massachusetts"] {{Webarchive|url=https://web.archive.org/web/20141024181655/http://www.bostonmagazine.com/2012/09/medical-marijuana-in-massachusetts/5 |date=24 October 2014 }}. ''[[Boston (magazine)|Boston]]''.</ref>
+In a 2001 study of neuropsychological performance in long-term cannabis users, researchers found "some cognitive deficits appear detectable at least 7 days after heavy cannabis use but appear reversible and related to recent cannabis exposure rather than irreversible and related to cumulative lifetime use".<ref>{{cite journal | vauthors = Pope HG, Gruber AJ, Hudson JI, Huestis MA, Yurgelun-Todd D | title = Neuropsychological performance in long-term cannabis users | journal = Archives of General Psychiatry | volume = 58 | issue = 10 | pages = 909–15 | date = October 2001 | pmid = 11576028 | doi = 10.1001/archpsyc.58.10.909 | doi-access =  }}</ref> Of his studies on cannabis use, lead researcher and Harvard professor [[Harrison Pope]] said he found it is not dangerous over the long term, but there are short-term effects. From neuropsychological tests, Pope found that chronic cannabis users showed difficulty with verbal memory in particular for "at least a week or two" after they stopped smoking. Within 28 days, memory problems vanished and the subjects "were no longer distinguishable from the comparison group".<ref>Lyons, Casey (October 2012) [http://www.bostonmagazine.com/2012/09/medical-marijuana-in-massachusetts/5 "Lost in the Weeds: Legalizing Medical Marijuana in Massachusetts"] {{Webarchive|url=https://web.archive.org/web/20141024181655/http://www.bostonmagazine.com/2012/09/medical-marijuana-in-massachusetts/5 |date=24 October 2014 }}. ''[[Boston (magazine)|Boston]]''.</ref>
-Researchers from the [[University of California, San Diego School of Medicine]] failed to show substantial, systemic neurological effects from long-term recreational use of cannabis. Their findings were published in the July 2003 issue of the ''Journal of the International Neuropsychological Society''.<ref>[https://web.archive.org/web/20130314031728/http://health.ucsd.edu/news/2003/06_27_Grant.html Minimal Long-Term Effects of Marijuana Use Found]. ''Journal of the International Neuropsychological Society'' (27 June 2003)</ref> The research team, headed by Dr. Igor Grant, found that cannabis use did affect perception, but did not cause permanent [[brain damage]]. Researchers looked at data from 15 previously published controlled studies involving 704 long-term cannabis users and 484 nonusers. The results showed long-term cannabis use was only marginally harmful on memory and learning. Other functions such as reaction time, attention, language, reasoning ability, perceptual and motor skills were unaffected. The observed effects on memory and learning, they said, showed long-term cannabis use caused "selective memory defects", but that the impact was "of a very small magnitude".<ref>Beasley, Deena (27 June 2003) [https://web.archive.org/web/20150306045312/http://www.cmcr.ucsd.edu/images/pdfs/Reuters_062703.pdf Study – Pot doesn't cause permanent brain damage]. ''Reuters Health E-Line''</ref>  A study by [[Johns Hopkins University School of Medicine]] showed that heavy use of marijuana is associated with decrements in neurocognitive performance even after 28 days of abstinence.<ref>{{cite journal | vauthors = Bolla KI, Brown K, Eldreth D, Tate K, Cadet JL | s2cid = 11525660 | title = Dose-related neurocognitive effects of marijuana use | journal = Neurology | volume = 59 | issue = 9 | pages = 1337–43 | date = November 2002 | pmid = 12427880 | doi = 10.1212/01.WNL.0000031422.66442.49 }}</ref>
+Researchers at the [[University of California, San Diego School of Medicine]] failed to show substantial, systemic neurological effects from long-term cannabis use. Their findings were published in the July 2003 issue of the ''Journal of the International Neuropsychological Society''.<ref>[https://web.archive.org/web/20130314031728/http://health.ucsd.edu/news/2003/06_27_Grant.html Minimal Long-Term Effects of Marijuana Use Found]. ''Journal of the International Neuropsychological Society'' (27 June 2003)</ref> The research team, headed by Igor Grant, found that cannabis use affects perception but does not cause permanent [[brain damage]]. Researchers looked at data from 15 previously published controlled studies involving 704 long-term cannabis users and 484 nonusers. The results showed long-term cannabis use was only marginally harmful on memory and learning. Other functions such as reaction time, attention, language, reasoning ability, and perceptual and motor skills were unaffected. The observed effects on memory and learning, they said, showed long-term cannabis use caused "selective memory defects", but "of a very small magnitude".<ref>Beasley, Deena (27 June 2003) [https://web.archive.org/web/20150306045312/http://www.cmcr.ucsd.edu/images/pdfs/Reuters_062703.pdf Study – Pot doesn't cause permanent brain damage]. ''Reuters Health E-Line''</ref> A study by [[Johns Hopkins University School of Medicine]] found that heavy cannabis use is associated with decrements in neurocognitive performance even after 28 days of abstinence.<ref>{{cite journal | vauthors = Bolla KI, Brown K, Eldreth D, Tate K, Cadet JL | s2cid = 11525660 | title = Dose-related neurocognitive effects of marijuana use | journal = Neurology | volume = 59 | issue = 9 | pages = 1337–43 | date = November 2002 | pmid = 12427880 | doi = 10.1212/01.WNL.0000031422.66442.49 }}</ref>
 ===Effects on driving===
 {{Main|Cannabis and impaired driving}}
-While several studies have shown increased risk associated with cannabis use by drivers, other studies have not found increased risk.<ref name="Compton-2015">{{cite journal|vauthors=Compton R, Berning A|title=Drug and Alcohol Crash Risk|journal=Traffic Safety Facts|date=February 2015|url=http://www.nhtsa.gov/staticfiles/nti/pdf/812117-Drug_and_Alcohol_Crash_Risk.pdf|access-date=13 February 2015|archive-date=9 August 2018|archive-url=https://web.archive.org/web/20180809021403/https://www.nhtsa.gov/staticfiles/nti/pdf/812117-Drug_and_Alcohol_Crash_Risk.pdf|url-status=dead}}</ref> Cannabis usage has been shown in some studies to have a negative effect on driving ability.<ref>{{cite journal | vauthors = Li MC, Brady JE, DiMaggio CJ, Lusardi AR, Tzong KY, Li G | title = Marijuana use and motor vehicle crashes | journal = Epidemiologic Reviews | volume = 34 | issue = 1 | pages = 65–72 | year = 2012 | pmid = 21976636 | pmc = 3276316 | doi = 10.1093/epirev/mxr017 }}</ref>
+Several studies have shown increased risk associated with cannabis use by drivers, but others have found no increased risk.<ref name="Compton-2015">{{cite journal|vauthors=Compton R, Berning A|title=Drug and Alcohol Crash Risk|journal=Traffic Safety Facts|date=February 2015|url=http://www.nhtsa.gov/staticfiles/nti/pdf/812117-Drug_and_Alcohol_Crash_Risk.pdf|access-date=13 February 2015|archive-date=9 August 2018|archive-url=https://web.archive.org/web/20180809021403/https://www.nhtsa.gov/staticfiles/nti/pdf/812117-Drug_and_Alcohol_Crash_Risk.pdf|url-status=dead}}</ref> Cannabis usage has been shown in some studies to have an adverse effect on driving ability.<ref>{{cite journal | vauthors = Li MC, Brady JE, DiMaggio CJ, Lusardi AR, Tzong KY, Li G | title = Marijuana use and motor vehicle crashes | journal = Epidemiologic Reviews | volume = 34 | issue = 1 | pages = 65–72 | year = 2012 | pmid = 21976636 | pmc = 3276316 | doi = 10.1093/epirev/mxr017 }}</ref>
 The British Medical Journal 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".<ref>{{cite journal | vauthors = Asbridge M, Hayden JA, Cartwright JL | title = Acute cannabis consumption and motor vehicle collision risk: systematic review of observational studies and meta-analysis | journal = BMJ | volume = 344 | pages = e536 | date = February 2012 | pmid = 22323502 | pmc = 3277079 | doi = 10.1136/bmj.e536 }}</ref>
-In ''Cannabis and driving: a review of the literature and commentary'', the United Kingdom's [[Department for Transport]] reviewed data on cannabis and driving, finding although impaired, "subjects under cannabis treatment appear to perceive that they are indeed impaired. Where they can compensate, they do".<ref>{{cite journal | url = http://www.dft.gov.uk/pgr/roadsafety/research/rsrr/theme3/cannabisanddrivingareviewoft4764?page=12 | archive-url = http://webarchive.nationalarchives.gov.uk/20100209042022/http:/www.dft.gov.uk/pgr/roadsafety/research/rsrr/theme3/cannabisanddrivingareviewoft4764?page=12 | url-status=dead | archive-date = 9 February 2010 | title = Cannabis and driving: a review of the literature and commentary (No.12) | journal = Department of Transport | publisher = UK Government | access-date = 19 December 2016 | last1 = Department For Transport | first1 = Great Minster House }}</ref> In a review of driving simulator studies, researchers note that "even in those who learn to compensate for a drug's impairing effects, substantial impairment in performance can still be observed under conditions of general task performance (i.e. when no contingencies are present to maintain compensated performance)."<ref name=EMCDDA>{{cite book |editor1-first=Sharon Rödner |editor1-last=Sznitman |editor2-first=Börje |editor2-last=Olsson |editor3-first=Robin |editor3-last=Room |name-list-style=vanc |date=June 2008 |title=A cannabis reader: global issues and local experiences |volume=2 |location=Lisbon |publisher=[[European Monitoring Centre for Drugs and Drug Addiction]] |doi=10.2810/13807 |isbn=978-92-9168-312-3 |url=https://archive.org/details/CannabisMonograph8Vol1 |url-access=registration |author1=European Monitoring Centre for Drugs Drug Addiction }}{{Page needed|date=February 2011}}</ref>
+In ''Cannabis and driving: a review of the literature and commentary'', the United Kingdom's [[Department for Transport]] reviewed data on cannabis and driving, finding that, although impaired, "subjects under cannabis treatment appear to perceive that they are indeed impaired. Where they can compensate, they do".<ref>{{cite journal | url = http://www.dft.gov.uk/pgr/roadsafety/research/rsrr/theme3/cannabisanddrivingareviewoft4764?page=12 | archive-url = http://webarchive.nationalarchives.gov.uk/20100209042022/http:/www.dft.gov.uk/pgr/roadsafety/research/rsrr/theme3/cannabisanddrivingareviewoft4764?page=12 | url-status=dead | archive-date = 9 February 2010 | title = Cannabis and driving: a review of the literature and commentary (No.12) | journal = Department of Transport | publisher = UK Government | access-date = 19 December 2016 | last1 = Department For Transport | first1 = Great Minster House }}</ref> In a review of driving simulator studies, researchers found that "even in those who learn to compensate for a drug's impairing effects, substantial impairment in performance can still be observed under conditions of general task performance (i.e. when no contingencies are present to maintain compensated performance)."<ref name=EMCDDA>{{cite book |editor1-first=Sharon Rödner |editor1-last=Sznitman |editor2-first=Börje |editor2-last=Olsson |editor3-first=Robin |editor3-last=Room |name-list-style=vanc |date=June 2008 |title=A cannabis reader: global issues and local experiences |volume=2 |location=Lisbon |publisher=[[European Monitoring Centre for Drugs and Drug Addiction]] |doi=10.2810/13807 |isbn=978-92-9168-312-3 |url=https://archive.org/details/CannabisMonograph8Vol1 |url-access=registration |author1=European Monitoring Centre for Drugs Drug Addiction }}{{Page needed|date=February 2011}}</ref>
-A 2012 meta-analysis found that acute cannabis use increased the risk of an automobile crash.<ref>{{cite journal | vauthors = Asbridge M, Hayden JA, Cartwright JL | title = Acute cannabis consumption and motor vehicle collision risk: systematic review of observational studies and meta-analysis | journal = BMJ | volume = 344 | issue = feb09 2 | pages = e536 | date = February 2012 | pmid = 22323502 | pmc = 3277079 | doi = 10.1136/bmj.e536 }}</ref> An extensive 2013 review of 66 studies regarding crash risk and drug use found that cannabis was associated with minor, but not statistically significant increased odds of injury or fatal accident.<ref>{{cite journal | vauthors = Elvik R | title = Risk of road accident associated with the use of drugs: a systematic review and meta-analysis of evidence from epidemiological studies | journal = Accident Analysis and Prevention | volume = 60 | pages = 254–67 | date = November 2013 | pmid = 22785089 | doi = 10.1016/j.aap.2012.06.017 }}</ref>
+A 2012 meta-analysis found that acute cannabis use increased the risk of an automobile crash.<ref>{{cite journal | vauthors = Asbridge M, Hayden JA, Cartwright JL | title = Acute cannabis consumption and motor vehicle collision risk: systematic review of observational studies and meta-analysis | journal = BMJ | volume = 344 | issue = feb09 2 | pages = e536 | date = February 2012 | pmid = 22323502 | pmc = 3277079 | doi = 10.1136/bmj.e536 }}</ref> An extensive 2013 review of 66 studies of crash risk and drug use found that cannabis is associated with slightly but not statistically significantly increased odds of injury or fatal accident.<ref>{{cite journal | vauthors = Elvik R | title = Risk of road accident associated with the use of drugs: a systematic review and meta-analysis of evidence from epidemiological studies | journal = Accident Analysis and Prevention | volume = 60 | pages = 254–67 | date = November 2013 | pmid = 22785089 | doi = 10.1016/j.aap.2012.06.017 }}</ref>
-In the largest and most precisely controlled study of its kind carried out by the U.S. Department of Transportation's [[National Highway Traffic Safety Administration]], it was found that other "studies that measure the presence of THC in the drivers' blood or oral fluid, rather than relying on self-report tend to have much lower (or no) elevated crash risk estimates. Likewise better controlled studies have found lower (or no) elevated crash risk estimates".<ref name=Compton-2015 /> The study found that "after adjusting for age, gender, race and alcohol use, drivers who tested positive for marijuana  were no more likely to crash than those who had not used any drugs or alcohol prior to driving".<ref name=Ingraham-2015>{{cite news|last1=Ingraham|first1=C|title=Stoned drivers are a lot safer than drunk ones, new federal data show|url=https://www.washingtonpost.com/blogs/wonkblog/wp/2015/02/09/stoned-drivers-are-a-lot-safer-than-drunk-ones-new-federal-data-show/?tid=rssfeed|access-date=13 February 2015|newspaper=Washington Post|date=9 February 2015|archive-date=13 February 2015|archive-url=https://web.archive.org/web/20150213203953/http://www.washingtonpost.com/blogs/wonkblog/wp/2015/02/09/stoned-drivers-are-a-lot-safer-than-drunk-ones-new-federal-data-show/?tid=rssfeed|url-status=live}}</ref> A 2018 study indicated that the number of fatal crashes involving marijuana after the recreational marijuana legalization or decriminalization increased in Colorado, Washington, and Massachusetts.<ref>{{Cite journal| vauthors = Lee J, Abdel-Aty A, Park J |date=May 2018|title=Investigation of associations between marijuana law changes and marijuana-involved fatal traffic crashes: A state-level analysis|journal=Journal of Transport & Health|volume=10|pages=194–202|doi=10.1016/j.jth.2018.05.017 |s2cid=159774424 }}</ref>
+In the largest and most precisely controlled study of its kind, carried out by the U.S. Department of Transportation's [[National Highway Traffic Safety Administration]], it was found that other "studies that measure the presence of THC in the drivers' blood or oral fluid, rather than relying on self-report tend to have much lower (or no) elevated crash risk estimates. Likewise better controlled studies have found lower (or no) elevated crash risk estimates".<ref name=Compton-2015 /> The study found that "after adjusting for age, gender, race and alcohol use, drivers who tested positive for marijuana were no more likely to crash than those who had not used any drugs or alcohol prior to driving".<ref name=Ingraham-2015>{{cite news|last1=Ingraham|first1=C|title=Stoned drivers are a lot safer than drunk ones, new federal data show|url=https://www.washingtonpost.com/blogs/wonkblog/wp/2015/02/09/stoned-drivers-are-a-lot-safer-than-drunk-ones-new-federal-data-show/?tid=rssfeed|access-date=13 February 2015|newspaper=Washington Post|date=9 February 2015|archive-date=13 February 2015|archive-url=https://web.archive.org/web/20150213203953/http://www.washingtonpost.com/blogs/wonkblog/wp/2015/02/09/stoned-drivers-are-a-lot-safer-than-drunk-ones-new-federal-data-show/?tid=rssfeed|url-status=live}}</ref> A 2018 study found that fatal crashes involving cannabis increased in Colorado, Washington, and Massachusetts after recreational cannabis legalization or decriminalization.<ref>{{Cite journal| vauthors = Lee J, Abdel-Aty A, Park J |date=May 2018|title=Investigation of associations between marijuana law changes and marijuana-involved fatal traffic crashes: A state-level analysis|journal=Journal of Transport & Health|volume=10|pages=194–202|doi=10.1016/j.jth.2018.05.017 |bibcode=2018JTHea..10..194L |s2cid=159774424 }}</ref>
 ===Combination with other drugs===
-A confounding factor in cannabis research is the prevalent usage of other recreational drugs, especially [[alcohol (drug)|alcohol]] and nicotine.<ref name=zhang1999>{{cite journal | vauthors = Zhang ZF, Morgenstern H, Spitz MR, Tashkin DP, Yu GP, Marshall JR, Hsu TC, Schantz SP | title = Marijuana use and increased risk of squamous cell carcinoma of the head and neck | journal = Cancer Epidemiology, Biomarkers & Prevention | volume = 8 | issue = 12 | pages = 1071–8 | date = December 1999 | pmid = 10613339 | url = http://cebp.aacrjournals.org/cgi/pmidlookup?view=long&pmid=10613339 | access-date = 27 January 2011 | archive-date = 23 February 2013 | archive-url = https://archive.today/20130223075049/http://cebp.aacrjournals.org/cgi/pmidlookup?view=long&pmid=10613339 | url-status = live }}</ref> Such complications demonstrate the need for studies on cannabis that have stronger controls, and investigations into alleged symptoms of cannabis use that may also be caused by tobacco. Some critics question whether agencies doing the research make an honest effort to present an accurate, unbiased summary of the evidence, or whether they "cherry-pick" their data to please funding sources which may include the tobacco industry or governments dependent on cigarette tax revenue; others caution that the raw data, and not the final conclusions, are what should be examined.<ref name=wiki4weed>{{cite web | url = http://wiki4weed.com/archive/public-opinion-drugs-drug-policy/ | title = Public opinion on drugs and drug policy | archive-url = https://web.archive.org/web/20140715031443/http://wiki4weed.com/archive/public-opinion-drugs-drug-policy/ | archive-date= 15 July 2014 | work = Fact Research Guide | quote = Data is notoriously easy to cherry pick or spin to support a particular agenda or position. Often the raw data will conceal all sorts of interesting facts that the headlines have missed. | publisher = Transform Drug Policy Foundation | location = Easton Business Centre, Felix Rd., Bristol, UK. | access-date = 24 March 2007 }}</ref>
+A confounding factor in cannabis research is the prevalent usage of other recreational drugs, especially [[alcohol (drug)|alcohol]] and nicotine.<ref name=zhang1999>{{cite journal | vauthors = Zhang ZF, Morgenstern H, Spitz MR, Tashkin DP, Yu GP, Marshall JR, Hsu TC, Schantz SP | title = Marijuana use and increased risk of squamous cell carcinoma of the head and neck | journal = Cancer Epidemiology, Biomarkers & Prevention | volume = 8 | issue = 12 | pages = 1071–8 | date = December 1999 | pmid = 10613339 | url = http://cebp.aacrjournals.org/cgi/pmidlookup?view=long&pmid=10613339 | access-date = 27 January 2011 | archive-date = 23 February 2013 | archive-url = https://archive.today/20130223075049/http://cebp.aacrjournals.org/cgi/pmidlookup?view=long&pmid=10613339 | url-status = live }}</ref> Such complications demonstrate the need for studies with stronger controls, and investigations into alleged symptoms of cannabis use that may also be caused by tobacco. Some critics question whether agencies doing the research make an honest effort to present an unbiased summary of the evidence without "cherry-picking" data to please funding sources such as the tobacco industry or governments dependent on cigarette tax revenue; others caution that the raw data, and not the final conclusions, are what should be examined.<ref name=wiki4weed>{{cite web | url = http://wiki4weed.com/archive/public-opinion-drugs-drug-policy/ | title = Public opinion on drugs and drug policy | archive-url = https://web.archive.org/web/20140715031443/http://wiki4weed.com/archive/public-opinion-drugs-drug-policy/ | archive-date= 15 July 2014 | work = Fact Research Guide | quote = Data is notoriously easy to cherry pick or spin to support a particular agenda or position. Often the raw data will conceal all sorts of interesting facts that the headlines have missed. | publisher = Transform Drug Policy Foundation | location = Easton Business Centre, Felix Rd., Bristol, UK. | access-date = 24 March 2007 }}</ref>
-The Australian National Household Survey of 2001<ref>{{cite web |url=http://www.aihw.gov.au/publications/index.cfm/title/8227 |title=2001 National Drug Strategy Household Survey: detailed findings |publisher=[[Australian Institute of Health and Welfare]] |date=19 December 2002 |access-date=1 February 2011 |url-status=dead |archive-url=https://web.archive.org/web/20110221033932/http://www.aihw.gov.au/publications/index.cfm/title/8227 |archive-date=21 February 2011 }} AIHW cat no. PHE 41.</ref> showed that cannabis in Australia is rarely used without other drugs. 95% of cannabis users also drank alcohol; 26% took amphetamines; 19% took ecstasy and only 2.7% reported not having used any other drug with cannabis.<ref>{{cite web |url=http://www.aihw.gov.au/publications/index.cfm/title/7553 |title=2001 National Drug Steategy Household Survey: first results |publisher=[[Australian Institute of Health and Welfare]] |date=20 May 2002 |access-date=1 February 2011 |url-status=dead |archive-url=https://web.archive.org/web/20110221034225/http://www.aihw.gov.au/publications/index.cfm/title/7553 |archive-date=21 February 2011 }} AIHW cat no. PHE 35.</ref> While research has been undertaken on the combined effects of alcohol and cannabis on performing certain tasks, little research has been conducted on the reasons why this combination is so popular. Evidence from a controlled experimental study undertaken by Lukas and Orozco<ref>{{cite journal | vauthors = Lukas SE, Orozco S | title = Ethanol increases plasma Delta(9)-tetrahydrocannabinol (THC) levels and subjective effects after marihuana smoking in human volunteers | journal = Drug and Alcohol Dependence | volume = 64 | issue = 2 | pages = 143–9 | date = October 2001 | pmid = 11543984 | doi = 10.1016/S0376-8716(01)00118-1 }}</ref> suggests that alcohol causes THC to be absorbed more rapidly into the blood plasma of the user. Data from the Australian National Survey of Mental Health and Wellbeing<ref>{{cite book |first1=Carol |last1=Kee |date=August 1998 |title=National Survey of Mental Health and Wellbeing of Adults 1997 |publisher=ACT Department of Health and Community Care |url=http://www.health.act.gov.au/c/health?a=sendfile&ft=p&fid=1075349689&sid= |access-date=1 February 2011 |archive-url=https://web.archive.org/web/20110314073334/http://www.health.act.gov.au/c/health?a=sendfile&ft=p&fid=1075349689&sid= |archive-date=14 March 2011 |url-status=dead }}</ref> found that three-quarters of recent cannabis users reported using alcohol when cannabis was not available, this suggests that the two are substitutes.<ref>{{cite journal | vauthors = Degenhardt L, Hall W | title = The relationship between tobacco use, substance-use disorders and mental health: results from the National Survey of Mental Health and Well-being | journal = Nicotine & Tobacco Research | volume = 3 | issue = 3 | pages = 225–34 | date = August 2001 | pmid = 11506766 | doi = 10.1080/14622200110050457 }}</ref>
+The Australian National Household Survey of 2001<ref>{{cite web |url=http://www.aihw.gov.au/publications/index.cfm/title/8227 |title=2001 National Drug Strategy Household Survey: detailed findings |publisher=[[Australian Institute of Health and Welfare]] |date=19 December 2002 |access-date=1 February 2011 |url-status=dead |archive-url=https://web.archive.org/web/20110221033932/http://www.aihw.gov.au/publications/index.cfm/title/8227 |archive-date=21 February 2011 }} AIHW cat no. PHE 41.</ref> found that cannabis is rarely used in Australia without other drugs. 95% of cannabis users also drank alcohol; 26% took amphetamines; 19% took ecstasy and only 2.7% reported not having used any other drug with cannabis.<ref>{{cite web |url=http://www.aihw.gov.au/publications/index.cfm/title/7553 |title=2001 National Drug Steategy Household Survey: first results |publisher=[[Australian Institute of Health and Welfare]] |date=20 May 2002 |access-date=1 February 2011 |url-status=dead |archive-url=https://web.archive.org/web/20110221034225/http://www.aihw.gov.au/publications/index.cfm/title/7553 |archive-date=21 February 2011 }} AIHW cat no. PHE 35.</ref> While there has been research on the combined effects of alcohol and cannabis on performing certain tasks, little has been done on the reasons this combination is so popular. Evidence from a controlled experimental study by Lukas and Orozco<ref>{{cite journal | vauthors = Lukas SE, Orozco S | title = Ethanol increases plasma Delta(9)-tetrahydrocannabinol (THC) levels and subjective effects after marihuana smoking in human volunteers | journal = Drug and Alcohol Dependence | volume = 64 | issue = 2 | pages = 143–9 | date = October 2001 | pmid = 11543984 | doi = 10.1016/S0376-8716(01)00118-1 }}</ref> suggests that alcohol causes THC to be absorbed more rapidly into the user's blood plasma. Data from the Australian National Survey of Mental Health and Wellbeing<ref>{{cite book |first1=Carol |last1=Kee |date=August 1998 |title=National Survey of Mental Health and Wellbeing of Adults 1997 |publisher=ACT Department of Health and Community Care |url=http://www.health.act.gov.au/c/health?a=sendfile&ft=p&fid=1075349689&sid= |access-date=1 February 2011 |archive-url=https://web.archive.org/web/20110314073334/http://www.health.act.gov.au/c/health?a=sendfile&ft=p&fid=1075349689&sid= |archive-date=14 March 2011 |url-status=dead }}</ref> found that three-quarters of recent cannabis users reported using alcohol when cannabis was not available, suggesting that the two have similar effects.<ref>{{cite journal | vauthors = Degenhardt L, Hall W | title = The relationship between tobacco use, substance-use disorders and mental health: results from the National Survey of Mental Health and Well-being | journal = Nicotine & Tobacco Research | volume = 3 | issue = 3 | pages = 225–34 | date = August 2001 | pmid = 11506766 | doi = 10.1080/14622200110050457 }}</ref>
 ===Pathogens and microtoxins===
-Most [[microorganism]]s found in cannabis only affect plants and not humans, but some microorganisms, especially those that proliferate when the herb is not correctly dried and stored, can be harmful to humans. Some users may store marijuana in an airtight bag or jar in a [[refrigerator]] to prevent fungal and bacterial growth.<ref name="mojo">{{cite web
+Most [[microorganism]]s found in cannabis affect only plants, not humans, but some, especially those that proliferate when the herb is not correctly dried and stored, can be harmful to humans. Some users store cannabis in an airtight bag or jar in a refrigerator to prevent fungal and bacterial growth.<ref name="mojo">{{cite web
 |url=http://www.hempfood.com/IHA/iha01205.html
 |title=Microbiological contaminants of marijuana
@@ Line 141: / Line 135: @@
 [[File:Aspergillus.jpg|thumb|right|''[[Aspergillus fumigatus]]'']]
-The fungi ''[[Aspergillus flavus]]'',<ref name="mj">{{cite journal | vauthors = Kagen SL, Kurup VP, Sohnle PG, Fink JN | title = Marijuana smoking and fungal sensitization | journal = The Journal of Allergy and Clinical Immunology | volume = 71 | issue = 4 | pages = 389–93 | date = April 1983 | pmid = 6833678 | doi = 10.1016/0091-6749(83)90067-2 }}</ref> ''[[Aspergillus fumigatus]]'',<ref name="mj"/> ''[[Aspergillus niger]]'',<ref name="mj"/> ''[[Aspergillus parasiticus]]'', ''[[Aspergillus tamarii]]'', ''[[Aspergillus sulphureus]]'', ''[[Aspergillus repens]]'', ''[[Mucor hiemalis]]'' (not a human pathogen), ''[[Penicillium chrysogenum]]'', ''[[Penicillium italicum]]'' and ''[[Rhizopus nigricans]]'' have been found in moldy cannabis.<ref name="mojo"/> ''[[Aspergillus]]'' mold species can infect the lungs via smoking or handling of infected cannabis and cause opportunistic and sometimes deadly [[aspergillosis]].<ref>{{cite journal | vauthors = Remington TL, Fuller J, Chiu I | title = Chronic necrotizing pulmonary aspergillosis in a patient with diabetes and marijuana use | journal = CMAJ | volume = 187 | issue = 17 | pages = 1305–8 | date = November 2015 | pmid = 26100839 | pmc = 4646751 | doi = 10.1503/cmaj.141412 }}</ref> Some of the microorganisms found create [[aflatoxin]]s, which are [[toxic]] and [[carcinogenic]]. Mold is also found in smoke from mold-infected cannabis,<ref name="mojo"/><ref name="mj"/> and the lungs and nasal passages are a major means of contracting fungal infections. Levitz and Diamond (1991) suggested baking marijuana in home ovens at 150&nbsp;°C [302&nbsp;°F], for five minutes before smoking. Oven treatment killed [[conidia]] of ''A. fumigatus'', ''A. flavus'' and ''A. niger'', and did not lower THC levels.<ref name="mojo"/> Cannabis contaminated with ''Salmonella muenchen'' was correlated with dozens of cases of [[salmonellosis]] in 1981.<ref>{{cite journal | vauthors = Taylor DN, Wachsmuth IK, Shangkuan YH, Schmidt EV, Barrett TJ, Schrader JS, Scherach CS, McGee HB, Feldman RA, Brenner DJ | title = Salmonellosis associated with marijuana: a multistate outbreak traced by plasmid fingerprinting | journal = The New England Journal of Medicine | volume = 306 | issue = 21 | pages = 1249–53 | date = May 1982 | pmid = 7070444 | doi = 10.1056/NEJM198205273062101 }}</ref> Thermophilic [[actinomycete]]s were also found in cannabis.<ref name="mj"/>
+The fungi ''[[Aspergillus flavus]]'',<ref name="mj">{{cite journal | vauthors = Kagen SL, Kurup VP, Sohnle PG, Fink JN | title = Marijuana smoking and fungal sensitization | journal = The Journal of Allergy and Clinical Immunology | volume = 71 | issue = 4 | pages = 389–93 | date = April 1983 | pmid = 6833678 | doi = 10.1016/0091-6749(83)90067-2 }}</ref> ''[[Aspergillus fumigatus]]'',<ref name="mj"/> ''[[Aspergillus niger]]'',<ref name="mj"/> ''[[Aspergillus parasiticus]]'', ''[[Aspergillus tamarii]]'', ''[[Aspergillus sulphureus]]'', ''[[Aspergillus repens]]'', ''[[Mucor hiemalis]]'' (not a human pathogen), ''[[Penicillium chrysogenum]]'', ''[[Penicillium italicum]]'', and ''[[Rhizopus nigricans]]'' have been found in moldy cannabis.<ref name="mojo"/> ''[[Aspergillus]]'' mold species can infect the lungs via smoking or handling of infected cannabis and cause opportunistic and sometimes deadly [[aspergillosis]].<ref>{{cite journal | vauthors = Remington TL, Fuller J, Chiu I | title = Chronic necrotizing pulmonary aspergillosis in a patient with diabetes and marijuana use | journal = CMAJ | volume = 187 | issue = 17 | pages = 1305–8 | date = November 2015 | pmid = 26100839 | pmc = 4646751 | doi = 10.1503/cmaj.141412 }}</ref> Some of the microorganisms found create [[aflatoxin]]s, which are toxic and carcinogenic. Mold is also found in smoke from mold-infected cannabis,<ref name="mojo"/><ref name="mj"/> and the lungs and nasal passages are a major means of contracting fungal infections. Levitz and Diamond (1991) suggest baking cannabis in home ovens at 150&nbsp;°C [302&nbsp;°F], for five minutes before smoking. Oven treatment killed [[conidia]] of ''A. fumigatus'', ''A. flavus'' and ''A. niger'', and did not lower THC levels.<ref name="mojo"/> Cannabis contaminated with ''Salmonella muenchen'' was correlated with dozens of cases of [[salmonellosis]] in 1981.<ref>{{cite journal | vauthors = Taylor DN, Wachsmuth IK, Shangkuan YH, Schmidt EV, Barrett TJ, Schrader JS, Scherach CS, McGee HB, Feldman RA, Brenner DJ | title = Salmonellosis associated with marijuana: a multistate outbreak traced by plasmid fingerprinting | journal = The New England Journal of Medicine | volume = 306 | issue = 21 | pages = 1249–53 | date = May 1982 | pmid = 7070444 | doi = 10.1056/NEJM198205273062101 }}</ref> Thermophilic [[actinomycete]]s were also found in cannabis.<ref name="mj"/>
 ==Long-term effects==
 {{Main|Long-term effects of cannabis|Cannabis dependence}}
-Exposure to marijuana may have biologically based physical, mental, behavioral, and social health consequences and is "associated with diseases of the liver (particularly with co-existing hepatitis C), lungs, heart, eyesight, and vasculature" according to a 2013 literature review by Gordon and colleagues. The association with these diseases has only been reported in cases where people have smoked cannabis. The authors cautioned that "evidence is needed, and further research should be considered, to prove causal associations of marijuana with many physical health conditions".<ref name=Gordon2013>{{cite journal | vauthors = Gordon AJ, Conley JW, Gordon JM | title = Medical consequences of marijuana use: a review of current literature | journal = Current Psychiatry Reports | volume = 15 | issue = 12 | pages = 419 | date = December 2013 | pmid = 24234874 | doi = 10.1007/s11920-013-0419-7 | s2cid = 29063282 | url = https://zenodo.org/record/1232874 | type = Submitted manuscript | access-date = 28 August 2018 | archive-date = 7 August 2019 | archive-url = https://web.archive.org/web/20190807172632/https://zenodo.org/record/1232874 | url-status = live }}</ref>
+Exposure to cannabis may have biologically based physical, mental, behavioral, and social health consequences and is "associated with diseases of the liver (particularly with co-existing hepatitis C), lungs, heart, eyesight, and vasculature" according to a 2013 literature review by Gordon and colleagues. The association with these diseases has only been reported in cases where people have smoked cannabis. The authors cautioned that "evidence is needed, and further research should be considered, to prove causal associations of cannabis with many physical health conditions".<ref name=Gordon2013>{{cite journal | vauthors = Gordon AJ, Conley JW, Gordon JM | title = Medical consequences of marijuana use: a review of current literature | journal = Current Psychiatry Reports | volume = 15 | issue = 12 | pages = 419 | date = December 2013 | pmid = 24234874 | doi = 10.1007/s11920-013-0419-7 | s2cid = 29063282 | url = https://zenodo.org/record/1232874 | type = Submitted manuscript | access-date = 28 August 2018 | archive-date = 7 August 2019 | archive-url = https://web.archive.org/web/20190807172632/https://zenodo.org/record/1232874 | url-status = live }}</ref>
 [[Cannabis dependence|Cannabis use disorder]] is defined in the fifth revision of the ''[[Diagnostic and Statistical Manual of Mental Disorders]]'' ([[DSM-5]]) as a condition requiring treatment.<ref name=Gordon2013/> Several drugs have been investigated in an attempt to ameliorate the symptoms of stopping cannabis use. Such drugs include [[bupropion]], [[divalproex]], [[nefazodone]], [[lofexidine]], and [[dronabinol]]. Of these, dronabinol (a trade name for THC) has proven the most effective.<ref name="Vandrey">{{cite journal | vauthors = Vandrey R, Haney M | title = Pharmacotherapy for cannabis dependence: how close are we? | journal = CNS Drugs | volume = 23 | issue = 7 | pages = 543–53 | year = 2009 | pmid = 19552483 | pmc = 2729499 | doi = 10.2165/00023210-200923070-00001 | type = Review }}</ref> The drugs [[buspirone]] and [[rimonabant]] have shown some success in helping maintain cannabis abstinence.<ref>{{Cite journal|last1=Benyamina|first1=Amine|last2=Lecacheux|first2=Marie|last3=Blecha|first3=Lisa|last4=Reynaud|first4=Michel|last5=Lukasiewcz|first5=Michael|date=1 March 2008|title=Pharmacotherapy and psychotherapy in cannabis withdrawal and dependence|url=https://doi.org/10.1586/14737175.8.3.479|journal=Expert Review of Neurotherapeutics|volume=8|issue=3|pages=479–491|doi=10.1586/14737175.8.3.479|pmid=18345976|s2cid=207194905|issn=1473-7175}}</ref>
@@ Line 151: / Line 145: @@
 There is evidence that long-term use of cannabis increases the risk of psychosis, regardless of [[confounding]] factors, and particularly for people who have genetic risk factors.<ref name="Steenkamp2017">{{cite journal|vauthors=Steenkamp MM, Blessing EM, Galatzer-Levy IR, Hollahan LC, Anderson WT|date=March 2017|title=Marijuana and other cannabinoids as a treatment for posttraumatic stress disorder: A literature review|journal=Depression and Anxiety|volume=34|issue=3|pages=207–216|doi=10.1002/da.22596|pmid=28245077|s2cid=205737272|doi-access=free}}</ref> A 2019 meta-analysis found that 34% of people with cannabis-induced psychosis transitioned to schizophrenia. This was found to be comparatively higher than hallucinogens (26%) and amphetamines (22%).<ref>{{cite journal |last1=Murrie |first1=Benjamin |last2=Lappin |first2=Julia |last3=Large |first3=Matthew |last4=Sara |first4=Grant |title=Transition of Substance-Induced, Brief, and Atypical Psychoses to Schizophrenia: A Systematic Review and Meta-analysis |journal=Schizophrenia Bulletin |date=16 October 2019 |volume=46 |issue=3 |pages=505–516 |doi=10.1093/schbul/sbz102 |pmid=31618428 |pmc=7147575 |doi-access=free }}</ref>
-Long-term cannabis users are at risk for developing [[cannabinoid hyperemesis syndrome]] (CHS), characterized by recurrent bouts of intense vomiting. The mechanism behind CHS is poorly understood and is contrary to the antiemetic properties of cannabis and cannabinoids. Of those who went to the emergency department (ED) with recurrent vomiting in one institution in the United States from 2005 to 2010, about 6% had the condition.<ref>{{Cite journal|last1=Simonetto|first1=Douglas A.|last2=Oxentenko|first2=Amy S.|last3=Herman|first3=Margot L.|last4=Szostek|first4=Jason H.|date=2012|title=Cannabinoid Hyperemesis: A Case Series of 98 Patients|journal=Mayo Clinic Proceedings|volume=87|issue=2|pages=114–119|doi=10.1016/j.mayocp.2011.10.005|issn=0025-6196|pmc=3538402|pmid=22305024}}</ref><ref>{{Cite journal|last1=Chocron|first1=Yaniv|last2=Zuber|first2=Jean-Philippe|last3=Vaucher|first3=Julien|date=2019|title=Cannabinoid hyperemesis syndrome|journal=BMJ|language=en|volume=366|pages=l4336|doi=10.1136/bmj.l4336|issn=0959-8138|pmid=31324702|s2cid=198133206}}</ref>
+Long-term cannabis users are at risk for developing [[cannabinoid hyperemesis syndrome]] (CHS), characterized by recurrent bouts of intense vomiting and abdominal cramping during or within 48 hours of heavy cannabis use.<ref name="Gorelick 2023">{{cite journal |last1=Gorelick |first1=David A. |title=Cannabis-Related Disorders and Toxic Effects |journal=New England Journal of Medicine |date=14 December 2023 |volume=389 |issue=24 |pages=2267–2275 |doi=10.1056/NEJMra2212152|pmid=38091532 }}</ref> The mechanism behind CHS is poorly understood and is contrary to the antiemetic properties of cannabis and cannabinoids. Of those who went to the emergency department (ED) with recurrent vomiting in one institution in the United States from 2005 to 2010, about 6% had the condition.<ref>{{Cite journal|last1=Simonetto|first1=Douglas A.|last2=Oxentenko|first2=Amy S.|last3=Herman|first3=Margot L.|last4=Szostek|first4=Jason H.|date=2012|title=Cannabinoid Hyperemesis: A Case Series of 98 Patients|journal=Mayo Clinic Proceedings|volume=87|issue=2|pages=114–119|doi=10.1016/j.mayocp.2011.10.005|issn=0025-6196|pmc=3538402|pmid=22305024}}</ref><ref>{{Cite journal|last1=Chocron|first1=Yaniv|last2=Zuber|first2=Jean-Philippe|last3=Vaucher|first3=Julien|date=2019|title=Cannabinoid hyperemesis syndrome|journal=BMJ|language=en|volume=366|pages=l4336|doi=10.1136/bmj.l4336|issn=0959-8138|pmid=31324702|s2cid=198133206}}</ref> The condition is usually not responsive to traditionally used [[antiemetics]] and the primary treatment is cessation from cannabis use.<ref name="Gorelick 2023" />
+Smoking cannabis can potentially cause cancer, due to carcinogens present in smoke.<ref>{{cite web
+| url = http://oehha.ca.gov/prop65/hazard_ident/pdf_zip/FinalMJsmokeHID.pdf
+| last = Tomar
+| first = Rajpal C.
+| author2 = Beaumont and Hsieh
+| date = August 2009
+| title = Evidence on the carcinogenicity of marijuana smoke
+| publisher = Reproductive and Cancer Hazard Assessment Branch Office of Environmental Health Hazard Assessment, California Environmental Protection Agency
+| access-date = 29 November 2018
+| archive-date = 24 July 2012
+| archive-url = https://web.archive.org/web/20120724183619/http://oehha.ca.gov/prop65/hazard_ident/pdf_zip/FinalMJsmokeHID.pdf
+| url-status = live
+}}</ref><ref name=mentaldisorders>
+{{cite journal | vauthors = Leweke FM, Koethe D | title = Cannabis and psychiatric disorders: it is not only addiction | journal = Addiction Biology | volume = 13 | issue = 2 | pages = 264–75 | date = June 2008 | pmid = 18482435 | doi = 10.1111/j.1369-1600.2008.00106.x | s2cid = 205400285 }}</ref><ref name=adolescenceschizo>{{cite journal | vauthors = Rubino T, Parolaro D | title = Long lasting consequences of cannabis exposure in adolescence | journal = Molecular and Cellular Endocrinology | volume = 286 | issue = 1–2 Suppl 1 | pages = S108-13 | date = April 2008 | pmid = 18358595 | doi = 10.1016/j.mce.2008.02.003 | s2cid = 39245784 | url = https://hal.archives-ouvertes.fr/hal-00531997 | type = Submitted manuscript | access-date = 28 August 2018 | archive-date = 29 November 2018 | archive-url = https://web.archive.org/web/20181129225219/https://hal.archives-ouvertes.fr/hal-00531997 | url-status = live }}</ref>
 ==Effects in pregnancy==

v t e Health effects of food, drink, and use of natural substances
Food	Chocolate Dairy Honey Red meat Salt Saturated fat Trans fat Sugar Fructose Ultra-processed food
Drink	Alcohol Coffee Tea Wine
Phytochemicals	Caffeine Natural phenols and polyphenols (including tannins)
Other	Cannabis Noise pollution Pesticide exposure Sawdust exposure Sun exposure Tobacco Electromagnetic radiation Ionizing radiation Microplastics