View source for Effects of cannabis

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{{See also|Long-term effects of cannabis}}
{{Use dmy dates|date=May 2022}}[[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]], 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 | bibcode = 2016JNAtP..79..324A | 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 | url-access = subscription }}</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>

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== 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>

[[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>

==Chemistry ==
[[File:THC-skeletal.png|thumb|right|The [[structural formula]] of [[tetrahydrocannabinol]]]]
[[File:THV structure.png|thumb|right|[[Tetrahydrocannabivarin]]]]
[[File:Cannabidiol.png|thumb|right|[[Cannabidiol]]]]
[[File:CBN structure.png|thumb|right|[[Cannabinol]]]]
[[File:Cannabivarin.png|thumb|right|[[Cannabivarin]]]]
[[File:Cannabidivarin.png|thumb|right|[[Cannabidivarin]]]]

===Cannabinoids and cannabinoid receptors===
The most prevalent [[psychoactive]] substances in [[cannabis]] are [[cannabinoids]], particularly [[tetrahydrocannabinol|THC]]. Some varieties, having undergone careful selection and growing techniques, can yield as much as 34% THC.<ref>{{cite web|url=https://hightimes.com/grow/the-strongest-strains-on-earth-2017/|title=The Strongest Strains on Earth 2017|last=Escondido|first=Nico|name-list-style=vanc|website=[[High Times]]|access-date=30 June 2018|date=26 April 2017|archive-date=1 July 2018|archive-url=https://web.archive.org/web/20180701030500/https://hightimes.com/grow/the-strongest-strains-on-earth-2017/|url-status=live}}</ref> Another psychoactive cannabinoid present in ''Cannabis sativa'' is [[tetrahydrocannabivarin]] (THCV), but it is only found in small amounts and is a [[Cannabinoid receptor antagonist|cannabinoid antagonist]].<ref>{{cite journal | vauthors = Turner CE, Bouwsma OJ, Billets S, Elsohly MA | title = Constituents of Cannabis sativa L. XVIII--Electron voltage selected ion monitoring study of cannabinoids | journal = Biomedical Mass Spectrometry | volume = 7 | issue = 6 | pages = 247–56 | date = June 1980 | pmid = 7426688 | doi = 10.1002/bms.1200070605 }}</ref>

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 (chemistry)|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 [[Gasotransmitter|neurotransmitter]]) by upon metabolism of CBD.<ref>{{Cite journal|last1=Hopper|first1=Christopher P.|last2=Zambrana|first2=Paige N.|last3=Goebel|first3=Ulrich|last4=Wollborn|first4=Jakob|date=June 2021|title=A brief history of carbon monoxide and its therapeutic origins|url=https://linkinghub.elsevier.com/retrieve/pii/S1089860321000367|journal=Nitric Oxide|language=en|volume=111-112|pages=45–63|doi=10.1016/j.niox.2021.04.001|pmid=33838343|s2cid=233205099|access-date=23 April 2021|archive-date=25 May 2021|archive-url=https://web.archive.org/web/20210525202037/https://linkinghub.elsevier.com/retrieve/pii/S1089860321000367|url-status=live|url-access=subscription}}</ref> THC is converted rapidly to [[11-hydroxy-THC]], which is also pharmacologically active, so the euphoria outlasts measurable THC levels in blood.<ref name="Kalant">{{Cite book| title=Principles of Medical Pharmacology | edition=6th |author1=H.K. Kalant |author2=W.H.E. Roschlau | year=1998 | pages=373–375}}</ref>

===Biochemical mechanisms in the brain===
{{see also|Cannabis (drug)#Mechanism of action}}
Cannabinoids usually contain a 1,1'-di-methyl-pyran ring, a variedly derivatized [[aromatic ring]] and a variedly [[Saturated and unsaturated compounds|unsaturated]] [[Cyclohexane|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 biology|evolutionary history]] of 500 million years. The binding of cannabinoids to cannabinoid receptors decrease [[adenylyl cyclase]] activity, inhibit [[N-type calcium channel|calcium N channels]], and disinhibit [[potassium channel|K<sup>+</sup><sub>A</sub> channels]]. There are at least two types of cannabinoid receptors (CB1 and CB2).<ref>{{cite journal | vauthors = Pertwee RG | title = Pharmacology of cannabinoid CB1 and CB2 receptors | journal = Pharmacology & Therapeutics | volume = 74 | issue = 2 | pages = 129–80 | date = January 1997 | pmid = 9336020 | doi = 10.1016/S0163-7258(97)82001-3 }}</ref>

===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.{{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 tens to hundreds of 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>

[[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 ===
[[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&nbsp;mg/kg.<ref>{{cite journal | vauthors = Fitzgerald KT, Bronstein AC, Newquist KL | title = Marijuana poisoning | journal = Topics in Companion Animal Medicine | volume = 28 | issue = 1 | pages = 8–12 | date = February 2013 | pmid = 23796481 | doi = 10.1053/j.tcam.2013.03.004 }}</ref> According to ''[[The Merck Index]]'',<ref name=merck1996>1996. ''The Merck Index'', 12th ed., Merck & Co., Rahway, New Jersey</ref> the {{LD50}} of THC (the dose which causes the death of 50% of individuals) is 1270&nbsp;mg/kg for male rats and 730&nbsp;mg/kg for female rats from oral consumption in sesame oil, and 42&nbsp;mg/kg for rats from inhalation.<ref>{{cite web |title=Cannabis Chemistry |url=http://www.erowid.org/plants/cannabis/cannabis_chemistry.shtml |publisher=Erowid.org |access-date=29 July 2007 |archive-date=14 March 2007 |archive-url=https://web.archive.org/web/20070314000115/http://www.erowid.org/plants/cannabis/cannabis_chemistry.shtml |url-status=live }}</ref>
<!-- A typical marijuana "joint" contains less than 10&nbsp;mg of THC, and one would have to smoke thousands of those in a short period of time to approach toxic levels. According to a 2006 [[United Kingdom]] government report, using cannabis is much less dangerous than tobacco, prescription drugs, and alcohol in social harms, physical harm, and addiction.<ref name="UK government report">{{Cite news |url=http://news.bbc.co.uk/1/shared/bsp/hi/pdfs/31_07_06_drugsreport.pdf |title=UK government report|publisher=House of Commons Science and Technology Committee |date=18 July 2006 |via=[[BBC News]] |access-date=29 August 2006 |format=PDF}} The information is not in the report, but in evidence submitted to the committee. Needs correcting – can cite Lancet paper by David Nutt et al.</ref>-->

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.<ref>{{Cite journal|doi=10.2174/1389200217666151210142051 |pmid=26651971 |title=Cannabinoids and Cytochrome P450 Interactions |year=2016 |last1=Zendulka |first1=Ondřej |last2=Dovrtělová |first2=Gabriela |last3=Nosková |first3=Kristýna |last4=Turjap |first4=Miroslav |last5=Šulcová |first5=Alexandra |last6=Hanuš |first6=Lumír |last7=Juřica |first7=Jan |journal=Current Drug Metabolism |volume=17 |issue=3 |pages=206–226 }}</ref>

===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]]]]
As of 2025, no high-quality evidence has been found linking cannabis smoking to lung cancer, despite cannabis smoke having similar properties to tobacco smoke. Why this is the case remains unclear. Various studies have speculated that differences in patterns of use compared to tobacco could account for the difference, as well as the anti-inflammatory properties of certain cannabinoids. The health effects of cannabis smoke are an area of active study.

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 |bibcode=1982nap..book18942I |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 |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 |article-number=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 | 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 |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 |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>

=== Related to vaping ===
In 2019 and 2020, [[2019–20 vaping lung illness outbreak|severe lung illness from unregulated vapes]] was strongly linked to [[Tocopheryl acetate|vitamin E acetate]] by the [[United States Centers for Disease Control and Prevention]].<ref name="BoudiPatel2019">{{cite journal |last1=Boudi |first1=F Brian |last2=Patel |first2=Sonia |last3=Boudi |first3=Ava |last4=Chan |first4=Connie |year=2019 |title=Vitamin E Acetate as a Plausible Cause of Acute Vaping-related Illness |journal=Cureus |volume=11 |issue=12 |article-number=e6350 |doi=10.7759/cureus.6350 |issn=2168-8184 |pmc=6952050 |pmid=31938636 |doi-access=free}}{{CC-notice|cc=by3|url=https://www.cureus.com/articles/25498-vitamin-e-acetate-as-a-plausible-cause-of-acute-vaping-related-illness|author(s)=F Brian Boudi, Sonia Patel, Ava Boudi, Connie Chan}}</ref>

A common chemical found in e-cigarettes is [[ketene]]. When it enters the lungs after being inhaled, this chemical causes damage to the cellular structure of lung tissue causing the cells to not function at maximum capacity and not absorb gasses as readily. This can cause shortness of breath which can lead to other health conditions such as tachycardia and respiratory failure.<ref>{{Cite journal |last1=Virgili |first1=F. |last2=Nenna |first2=R. |last3=Ben David |first3=S. |last4=Mancino |first4=E. |last5=Di Mattia |first5=G. |last6=Matera |first6=L. |last7=Petrarca |first7=L. |last8=Midulla |first8=F. |title= E-cigarettes and youth: An unresolved Public Health concern |journal=Italian Journal of Pediatrics |date=2022 |volume=48 |issue=1 |page=97 |doi=10.1186/s13052-022-01286-7 |doi-access=free |pmid=35701844 |pmc=9194784 }}</ref>
==Short-term effects==
[[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
}}

]]

=== Onset and duration ===
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 |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 |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 |url=https://kclpure.kcl.ac.uk/portal/en/publications/e66d476c-bdc4-4eb8-9781-19848fff20ca }}</ref>

=== Psychological effects ===
The psychoactive effects of cannabis, known as a [[Substance intoxication|"high", or being "stoned"]], etc., 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]], 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 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}}</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 | page = 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 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 | 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 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 }}</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]]
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 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 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===
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 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> 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 | url-access = subscription }}</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=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-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 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===
{{main|Cannabis and memory}}
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 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 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}}
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}}</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 | article-number = 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 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 | 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 | date=3 May 2000 }}</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 | article-number = 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 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 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 |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 |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 }}</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 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
|publisher=www.hempfood.com
|access-date=22 June 2008
|archive-date=11 July 2011
|archive-url=https://web.archive.org/web/20110711162446/http://www.hempfood.com/IHA/iha01205.html
}}{{unreliable source?|date=July 2021}}</ref>

[[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) 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 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 | article-number = 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|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>

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 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|article-number=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 may 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==
{{Excerpt|Cannabis in pregnancy}}

==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.<ref name=":1">{{Cite journal|last1=Wong|first1=Kei U.|last2=Baum|first2=Carl R.|date=November 2019|title=Acute Cannabis Toxicity|journal=Pediatric Emergency Care|language=en-US|volume=35|issue=11|pages=799–804|doi=10.1097/PEC.0000000000001970|pmid=31688799|s2cid=207897219|issn=0749-5161}}</ref> These complications include encephalopathy, hypotension, respiratory depression severe enough to require ventilation, somnolence, coma, and in extreme cases, reports of death.<ref name=":1" /><ref>{{Cite journal|last1=Nappe|first1=Thomas M.|last2=Hoyte|first2=Christopher O.|date=16 March 2017|title=Pediatric Death Due to Myocarditis After Exposure to Cannabis|journal=Clinical Practice and Cases in Emergency Medicine|volume=1|issue=3|pages=166–170|doi=10.5811/cpcem.2017.1.33240|issn=2474-252X|pmc=5965161|pmid=29849306}}</ref><ref>{{Cite journal|last1=Claudet|first1=Isabelle|last2=Le Breton|first2=Mathilde|last3=Bréhin|first3=Camille|last4=Franchitto|first4=Nicolas|date=April 2017|title=A 10-year review of cannabis exposure in children under 3-years of age: do we need a more global approach?|journal=European Journal of Pediatrics|volume=176|issue=4|pages=553–556|doi=10.1007/s00431-017-2872-5|issn=1432-1076|pmid=28210835|s2cid=11639790}}</ref> 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.<ref>{{Cite journal|date=1 June 2014|title=Association of Unintentional Pediatric Exposures With Decriminalization of Marijuana in the United States|url=https://www.sciencedirect.com/science/article/abs/pii/S0196064414000791|journal=Annals of Emergency Medicine|language=en|volume=63|issue=6|pages=684–689|doi=10.1016/j.annemergmed.2014.01.017|issn=0196-0644|last1=Wang|first1=George S.|last2=Roosevelt|first2=Genie|last3=Le Lait|first3=Marie-Claire|last4=Martinez|first4=Erin M.|last5=Bucher-Bartelson|first5=Becki|last6=Bronstein|first6=Alvin C.|last7=Heard|first7=Kennon|pmid=24507243|access-date=29 July 2021|archive-date=29 July 2021|archive-url=https://web.archive.org/web/20210729171357/https://www.sciencedirect.com/science/article/abs/pii/S0196064414000791|url-status=live|url-access=subscription}}</ref>

==See also==
* [[Effects of legalized cannabis]]
* [[Cannabis smoking]]
* [[Psychoactive drug]]

==References==
{{reflist}}

==Further reading==
* {{Cite book|author1=National Academies of Sciences, Engineering, and Medicine|author-link1=National Academies of Sciences, Engineering, and Medicine|title=The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research|url=http://nationalacademies.org/hmd/reports/2017/health-effects-of-cannabis-and-cannabinoids.aspx|website=National Academies of Sciences, Engineering, and Medicine|publisher=The National Academies Press|location=Washington, DC|doi=10.17226/24625|pmid=28182367|date=2017|bibcode=2017nap..book24625N |isbn=978-0-309-45304-2}} {{open access}}

{{Cannabis|state=expanded}}
{{cannabinoids}}
{{Health effects of food, drink and lifestyle}}
{{Psychoactive substance use}}

{{DEFAULTSORT:Effects Of Cannabis}}
[[Category:Cannabis and health]]
[[Category:Cannabis smoking]]
[[Category:Effects of psychoactive drugs]]