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((short description|Overview of long-term effects of the consumption of cannabis))
((Cannabis sidebar))
The '''long-term effects of cannabis''' have been the subject of ongoing debate. Because [[Cannabis (drug)|cannabis]] is [[legality of cannabis|illegal in most countries]], clinical research presents a challenge and there is limited evidence from which to draw conclusions.<ref>((cite book|chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK425757/|title=The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research|chapter=Challenges and Barriers in Conducting Cannabis Research|date=2017|publisher=National Academies of Sciences, Engineering, and Medicine/National Academies Press|access-date=2021-04-11|archive-date=2021-02-26|archive-url=https://web.archive.org/web/20210226074532/https://www.ncbi.nlm.nih.gov/books/NBK425757/|url-status=live))</ref> In 2017, the U.S. National Academies of Sciences, Engineering, and Medicine issued a report summarizing much of the published literature on [[Effects of cannabis|health effects of cannabis]], into categories regarded as conclusive, substantial, moderate, limited and of no or insufficient evidence to support an association with a particular outcome.<ref name="National_Academies_2017" />

==Dependency==
((Main|Cannabis use disorder))

Cannabis is the most widely used illicit drug in the Western world.<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 | type = Review | s2cid = 29063282 | url = https://zenodo.org/record/1232874 | access-date = 2018-08-28 | archive-date = 2019-08-07 | archive-url = https://web.archive.org/web/20190807172632/https://zenodo.org/record/1232874 | url-status = live ))</ref> In the United States, 10-20% of those who begin the use of cannabis daily will later become dependent.<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 | s2cid = 8503107 | citeseerx = 10.1.1.1017.1935 ))</ref><ref name=DAgov >((cite web |title=Is marijuana addictive? |url=https://nida.nih.gov/publications/research-reports/marijuana/marijuana-addictive |website=National Institute on Drug Abuse |quote=Marijuana use can lead to the development of problem use, known as a marijuana use disorder, which takes the form of addiction in severe cases. ... Marijuana use disorder becomes addiction when the person cannot stop using the drug even though it interferes with many aspects of his or her life. |access-date=2022-10-24 |archive-date=2022-10-24 |archive-url=https://web.archive.org/web/20221024114249/https://nida.nih.gov/publications/research-reports/marijuana/marijuana-addictive |url-status=live ))</ref> Cannabis use can lead to addiction, which is defined as "when the person cannot stop using the drug even though it interferes with many aspects of his or her life."(( r | DAgov ))<ref name="Zehra2018"/><ref>((cite journal | vauthors = Wenger T, Moldrich G, Furst S | title = Neuromorphological background of cannabis addiction | journal = Brain Research Bulletin | volume = 61 | issue = 2 | pages = 125–8 | date = July 2003 | pmid = 12831997 | doi = 10.1016/S0361-9230(03)00081-9 | s2cid = 20302345 ))</ref><ref>((cite journal | vauthors = Maldonado R, Berrendero F, Ozaita A, Robledo P | title = Neurochemical basis of cannabis addiction | journal = Neuroscience | volume = 181 | pages = 1–17 | date = May 2011 | pmid = 21334423 | doi = 10.1016/j.neuroscience.2011.02.035 | s2cid = 6660057 ))</ref> 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" /> A 2012 review of cannabis use and dependency in the United States by Danovitch ''et al'' said that "42% of persons over age 12 have used cannabis at least once in their lifetime, 11.5% have used within the past year, and 1.8% have met diagnostic criteria for cannabis abuse or dependence within the past year. Among individuals who have ever used cannabis, conditional dependence (the proportion who go on to develop dependence) is 9%." Although no medication is known to be effective in combating dependency, combinations of psychotherapy such as [[cognitive behavioural therapy]] and [[motivational enhancement therapy]] have achieved some success.<ref name="Danovitch2012">((cite journal | vauthors = Danovitch I, Gorelick DA | title = State of the art treatments for cannabis dependence | journal = The Psychiatric Clinics of North America | volume = 35 | issue = 2 | pages = 309–26 | date = June 2012 | pmid = 22640758 | pmc = 3371269 | doi = 10.1016/j.psc.2012.03.003 | type = Review ))</ref>

Cannabis dependence develops in 9% of users, significantly less than that of heroin, cocaine, alcohol, and prescribed [[anxiolytics]],<ref name="Wilkie2016">((cite journal | vauthors = Wilkie G, Sakr B, Rizack T | title = Medical Marijuana Use in Oncology: A Review | journal = JAMA Oncology | volume = 2 | issue = 5 | pages = 670–675 | date = May 2016 | pmid = 26986677 | doi = 10.1001/jamaoncol.2016.0155 | doi-access = free ))</ref> but slightly higher than that for [[psilocybin]], [[mescaline]], or [[LSD]]. Dependence on cannabis tends to be less severe than that observed with cocaine, opiates, and alcohol.<ref>((cite journal | vauthors = Budney AJ, Roffman R, Stephens RS, Walker D | title = Marijuana dependence and its treatment | journal = Addiction Science & Clinical Practice | volume = 4 | issue = 1 | pages = 4–16 | date = December 2007 | pmid = 18292704 | pmc = 2797098 | doi = 10.1151/ASCP07414 | type = Review ))</ref> A 2018 academic review, published in partnership with [[Canopy Growth]], discussed the limitations of current studies of therapeutic and non-therapeutic cannabis use, and further stated that the nature of dependence formation among regular marijuana consumers has declined since 2002.<ref name="Walsh">((cite journal | vauthors = Walsh Z, Gonzalez R, Crosby K, S Thiessen M, Carroll C, Bonn-Miller MO | title = Medical cannabis and mental health: A guided systematic review | journal = Clinical Psychology Review | volume = 51 | pages = 15–29 | date = February 2017 | pmid = 27816801 | doi = 10.1016/j.cpr.2016.10.002 ))</ref>

[[University of Cambridge|Cambridge University]] published a study in 2015 that showed the surprising fact that in England and Wales, the use of cannabis had decreased. Although there was a reported decrease in use, the need for addiction treatment was surging. The study looked more in depth on how the potency of the cannabis affected someone's dependence on the drug. They tested three different levels of potency and found that the most potent cannabis had the highest amount of dependence. Researchers believe that this is because of the high that the participants felt after using. The lower potency strains did not give users the same high, which made them not desire or in turn depend on that strain as much.<ref>((cite journal | vauthors = Freeman TP, Winstock AR | title = Examining the profile of high-potency cannabis and its association with severity of cannabis dependence | journal = Psychological Medicine | volume = 45 | issue = 15 | pages = 3181–9 | date = November 2015 | pmid = 26213314 | pmc = 4611354 | doi = 10.1017/S0033291715001178 ))</ref>

==Memory and intelligence==
Acute cannabis intoxication has been shown to negatively affect attention, psychomotor task ability, and [[short-term memory]].<ref name="Andrade2016">((cite journal | vauthors = Andrade C | title = Cannabis and neuropsychiatry, 1: benefits and risks | journal = The Journal of Clinical Psychiatry | volume = 77 | issue = 5 | pages = e551-4 | date = May 2016 | pmid = 27249079 | doi = 10.4088/JCP.16f10841 | doi-access = free ))</ref><ref name="Sagie2013">((cite journal |last1=Sagie |first1=Shira |last2=Eliasi |first2=Yehuda |last3=Livneh |first3=Ido |last4=Bart |first4=Yosi |last5=Monovich |first5=Einat |title=השפעות קצרות וארוכות טווח של קנבינואידים על זיכרון, נפש קוגניציה ומחלות |trans-title=Short-and long-term effects of cannabinoids on memory, cognition and mental illness |language=he |journal=Harefuah |date=December 2013 |volume=152 |issue=12 |pages=737–741, 751 |pmid=24483000 |url=https://www.ima.org.il/medicinesite/Article.aspx?NewspaperArticleId=3323 |url-access=subscription |access-date=2022-10-24 |archive-date=2022-10-24 |archive-url=https://web.archive.org/web/20221024115904/https://www.ima.org.il/medicinesite/Article.aspx?NewspaperArticleId=3323 |url-status=live ))</ref> Studies of chronic cannabis users have demonstrated, although inconsistently, a long-lasting effect on the attention span, memory function, and cognitive abilities of moderate-dose, long-term users. Once cannabis use is discontinued for several months, these effects disappear, unless the user started consuming during adolescence. It is speculated that this is due to neurotoxic effects of cannabis interfering with critical brain development.<ref name="Dunedin Study">((cite journal | vauthors = Meier MH, Caspi A, Ambler A, Harrington H, Houts R, Keefe RS, McDonald K, Ward A, Poulton R, Moffitt TE | display-authors = 6 | title = Persistent cannabis users show neuropsychological decline from childhood to midlife | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 40 | pages = E2657-64 | date = October 2012 | pmid = 22927402 | pmc = 3479587 | doi = 10.1073/pnas.1206820109 | doi-access = free ))</ref><ref>((cite journal | vauthors = Schoeler T, Bhattacharyya S | title = The effect of cannabis use on memory function: an update | journal = Substance Abuse and Rehabilitation | volume = 4 | pages = 11–27 | date = 2013 | pmid = 24648785 | pmc = 3931635 | doi = 10.2147/SAR.S25869 | doi-access = free ))</ref>

Chronic use of cannabis during adolescence, a time when the brain is still developing, is correlated in the long term with lower IQ and cognitive deficits. It is not clear, though, if cannabis use causes the problems or if the causality is in the reverse. Recent studies have shown that IQ deficits existed in some subjects before chronic cannabis use, suggesting that lower IQ may instead be a risk factor for cannabis addiction.<ref>((cite journal | vauthors = Jackson NJ, Isen JD, Khoddam R, Irons D, Tuvblad C, Iacono WG, McGue M, Raine A, Baker LA | display-authors = 6 | title = Impact of adolescent marijuana use on intelligence: Results from two longitudinal twin studies | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 113 | issue = 5 | pages = E500-8 | date = February 2016 | pmid = 26787878 | pmc = 4747759 | doi = 10.1073/pnas.1516648113 | bibcode = 2016PNAS..113E.500J | doi-access = free ))</ref><ref name="Zehra2018">((cite journal | vauthors = Zehra A, Burns J, Liu CK, Manza P, Wiers CE, Volkow ND, Wang GJ | title = Cannabis Addiction and the Brain: a Review | journal = Journal of Neuroimmune Pharmacology | volume = 13 | issue = 4 | pages = 438–452 | date = December 2018 | pmid = 29556883 | pmc = 6223748 | doi = 10.1007/s11481-018-9782-9 ))</ref><ref>((cite journal | vauthors = Ross JM, Ellingson JM, Rhee SH, Hewitt JK, Corley RP, Lessem JM, Friedman NP | title = Investigating the causal effect of cannabis use on cognitive function with a quasi-experimental co-twin design | journal = Drug and Alcohol Dependence | volume = 206 | pages = 107712 | date = January 2020 | pmid = 31753729 | pmc = 7179798 | doi = 10.1016/j.drugalcdep.2019.107712 ))</ref>

A [[prospective cohort study]] that took place between 1972 and 2012 investigated the association between cannabis use and neuropsychological decline. Subjects were tested at various points in their life administering [[Wechsler Scales (disambiguation)|multiple]] [[Cambridge Neuropsychological Test Automated Battery|different]] [[neuropsychological tests]]. The authors concluded that:
* persistent cannabis users show neuropsychological decline from childhood to midlife.<ref name="Dunedin Study" />
* neuropsychological impact of cannabis use is global instead of restricted to specific cognitive domains
* its effects last for longer than a week
* the findings cannot be explained by [[comorbidity]] with dependence on other drugs.
* the findings cannot be explained by comorbidity with schizophrenia
* cannabis use is correlated with lower levels of education
* the negative effect on intelligence is greater than that attributable to the lack of education.
* ceasing consumption does not fully restore cognitive function on adolescents.<ref name="Dunedin Study" />
[[File:Herb-2915337 1280.jpeg|thumb|Cannabis]]
Cannabis intoxication was not only found to affect attention, psychomotor task ability, and short-term memory.<ref name="Andrade2016" /><ref name="Sagie2013" /> It was also found that intoxicated users were facing the difficulty of having false memories.<ref>((cite journal | vauthors = Kloft L, Otgaar H, Blokland A, Monds LA, Toennes SW, Loftus EF, Ramaekers JG | title = Cannabis increases susceptibility to false memory | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 117 | issue = 9 | pages = 4585–4589 | date = March 2020 | pmid = 32041881 | doi = 10.1073/pnas.1920162117 | pmc = 7060677 | bibcode = 2020PNAS..117.4585K | doi-access = free ))</ref>

The use of cannabis has been heavily shown to affect the working-memory network function. Using large amounts of cannabis at a time is associated with hyperactivity of the network during a [[working memory|working-memory]] task. Most of these findings are showing that people who use cannabis on a daily basis will need additional effort in order to perform certain tasks.<ref>((Cite journal |last1=Battistella |first1=Giovanni |last2=Fornari |first2=Eleonora |last3=Annoni |first3=Jean-Marie |last4=Chtioui |first4=Haithem |last5=Dao |first5=Kim |last6=Fabritius |first6=Marie |last7=Favrat |first7=Bernard |last8=Mall |first8=Jean-Frédéric |last9=Maeder |first9=Philippe |last10=Giroud |first10=Christian |date=August 2014 |title=Long-Term Effects of Cannabis on Brain Structure |journal=Neuropsychopharmacology |language=en |volume=39 |issue=9 |pages=2041–2048 |doi=10.1038/npp.2014.67 |issn=1740-634X |pmc=4104335 |pmid=24633558))</ref><ref>((Cite journal |last1=Cousijn |first1=Janna |last2=Wiers |first2=Reinout W. |last3=Ridderinkhof |first3=K. Richard |last4=van den Brink |first4=Wim |last5=Veltman |first5=Dick J. |last6=Goudriaan |first6=Anna E. |date=May 2014 |title=Effect of baseline cannabis use and working-memory network function on changes in cannabis use in heavy cannabis users: A prospective fMRI study: Working-Memory Network Function and Cannabis Use |journal=Human Brain Mapping |language=en |volume=35 |issue=5 |pages=2470–2482 |doi=10.1002/hbm.22342 |pmc=6869744 |pmid=24038570))</ref><ref>((Cite journal |last1=McClure |first1=Erin A. |last2=Lydiard |first2=Jessica B. |last3=Goddard |first3=Scott D. |last4=Gray |first4=Kevin M. |date=January 2015 |title=Objective and subjective memory ratings in cannabis-dependent adolescents: Memory in Cannabis-Dependent Adolescents |journal=The American Journal on Addictions |language=en |volume=24 |issue=1 |pages=47–52 |doi=10.1111/ajad.12171 |pmc=4389632 |pmid=25823635))</ref>

==Mental health==

Cannabis contains over 100 different [[Cannabinoid|cannabinoid compounds]], many of which have displayed [[Psychoactive drug|psychoactive effects]]. The most distinguished cannabinoids are  [[tetrahydrocannabinol]] (THC) and [[cannabidiol]] (CBD), with THC being the primary psychoactive agent.<ref>((cite journal | vauthors = Schier AR, Ribeiro NP, Silva AC, Hallak JE, Crippa JA, Nardi AE, Zuardi AW | title = Cannabidiol, a Cannabis sativa constituent, as an anxiolytic drug | journal = Revista Brasileira de Psiquiatria | volume = 34 | issue = Suppl 1 | pages = S104-10 | date = June 2012 | pmid = 22729452 | doi = 10.1590/s1516-44462012000500008 | doi-access = free ))</ref><ref name="Walsh"/> The effects of THC and CBD are salient regarding psychosis and anxiety.<ref>((cite journal | vauthors = Crippa JA, Zuardi AW, Martín-Santos R, Bhattacharyya S, Atakan Z, McGuire P, Fusar-Poli P | title = Cannabis and anxiety: a critical review of the evidence | journal = Human Psychopharmacology | volume = 24 | issue = 7 | pages = 515–23 | date = October 2009 | pmid = 19693792 | doi = 10.1002/hup.1048 | s2cid = 13544234 | doi-access = free ))</ref>

===Chronic psychosis and schizophrenia spectrum disorders===
According to the National Academies of Sciences, Engineering and Medicine, there is substantial evidence of a statistical association between cannabis use and the development of schizophrenia or other chronic psychoses, with the highest risk potentially among the most frequent users.<ref name="National_Academies_2017"/> A possible connection between [[psychosis]] and cannabis is controversial because observational studies suggest a correlation but do not establish any causative effect of cannabis on long-term psychiatric health.<ref name="Parakh2013">((cite journal | vauthors = Parakh P, Basu D | title = Cannabis and psychosis: have we found the missing links? | journal = Asian Journal of Psychiatry | volume = 6 | issue = 4 | pages = 281–7 | date = August 2013 | pmid = 23810133 | doi = 10.1016/j.ajp.2013.03.012 | type = Review ))</ref> Medical evidence strongly suggests that the long-term use of cannabis by people who begin use at an early age display a higher tendency towards mental health problems and other physical and development disorders, although a causal link could not be proven by the available data.<ref name="Hoch2015">((cite journal | vauthors = Hoch E, Bonnet U, Thomasius R, Ganzer F, Havemann-Reinecke U, Preuss UW | title = Risks associated with the non-medicinal use of cannabis | journal = Deutsches Ärzteblatt International | volume = 112 | issue = 16 | pages = 271–8 | date = April 2015 | pmid = 25939318 | pmc = 4442549 | doi = 10.3238/arztebl.2015.0271 | type = Review ))</ref> The risks appear to be most acute in adolescent users.<ref name="Hoch2015" />
In one 2013 review, the authors concluded long-term cannabis use "increases the risk of psychosis in people with certain genetic or environmental vulnerabilities", but does not cause psychosis. Important predisposing factors were genetic liability, childhood trauma and urban upbringing.<ref name="Parakh2013"/> Another review that same year concluded that cannabis use may cause permanent psychological disorders in some users such as cognitive impairment, anxiety, paranoia, and increased risks of psychosis. Key predisposing variables included age of first exposure, frequency of use, the potency of the cannabis used, and individual susceptibility.<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> Nevertheless, some researchers maintain there exists "a strong association between schizophrenia and cannabis use...", while cannabis use alone does not predict the transition to subsequent psychiatric illness. Many factors are involved, including genetics, environment, time period of initiation and duration of cannabis use, underlying psychiatric pathology that preceded drug use, and combined use of other psychoactive drugs.<ref name=Chadwick>((cite journal | vauthors = Chadwick B, Miller ML, Hurd YL | title = Cannabis Use during Adolescent Development: Susceptibility to Psychiatric Illness | journal = Frontiers in Psychiatry | volume = 4 | pages = 129 | date = October 2013 | pmid = 24133461 | pmc = 3796318 | doi = 10.3389/fpsyt.2013.00129 | doi-access = free ))</ref>

The temporal relationship between [[Cannabis (drug)|cannabis]] and [[psychosis]] was reviewed in 2014, and the authors proposed that "[b]ecause longitudinal work indicates that cannabis use precedes psychotic symptoms, it seems reasonable to assume a causal relationship" between cannabis and psychosis, but that "more work is needed to address the possibility of gene-environment correlation."<ref>((cite journal | vauthors = van Winkel R, Kuepper R | title = Epidemiological, neurobiological, and genetic clues to the mechanisms linking cannabis use to risk for nonaffective psychosis | journal = Annual Review of Clinical Psychology | volume = 10 | issue = 1 | pages = 767–91 | date = 28 March 2014 | pmid = 24471373 | doi = 10.1146/annurev-clinpsy-032813-153631 ))</ref>

In 2016 a meta-analysis was published on associations studies covering a range of dosing habits, again showing that cannabis use is associated with a significantly increased risk of psychosis, and alleged that a [[dose–response relationship]] exists between the level of cannabis use and risk of psychosis. The risk was increased 4-fold with daily use, though the analysis was not adequate to establish a causal link.<ref>((cite journal | vauthors = Marconi A, Di Forti M, Lewis CM, Murray RM, Vassos E | title = Meta-analysis of the Association Between the Level of Cannabis Use and Risk of Psychosis | journal = Schizophrenia Bulletin | volume = 42 | issue = 5 | pages = 1262–9 | date = September 2016 | pmid = 26884547 | pmc = 4988731 | doi = 10.1093/schbul/sbw003 ))</ref> Another 2016 meta-analysis found that cannabis use only predicted transition to psychosis among those who met the criteria for abuse of or dependence on the drug.<ref>((cite journal | vauthors = Kraan T, Velthorst E, Koenders L, Zwaart K, Ising HK, van den Berg D, de Haan L, van der Gaag M | display-authors = 6 | title = Cannabis use and transition to psychosis in individuals at ultra-high risk: review and meta-analysis | journal = Psychological Medicine | volume = 46 | issue = 4 | pages = 673–81 | date = March 2016 | pmid = 26568030 | doi = 10.1017/S0033291715002329 | s2cid = 619268 ))</ref>[[File:Trichomes.jpg|thumb|''[[Cannabis]]'' flower with visible [[trichomes]]]]Another 2016 review concluded that the existing evidence did not show that cannabis caused psychosis, but rather that early or heavy cannabis use were among many factors more likely to be found in those at risk of developing psychosis.<ref>((cite journal | vauthors = Ksir C, Hart CL | title = Cannabis and Psychosis: a Critical Overview of the Relationship | journal = Current Psychiatry Reports | volume = 18 | issue = 2 | pages = 12 | date = February 2016 | pmid = 26781550 | doi = 10.1007/s11920-015-0657-y | type = Review | s2cid = 36538598 | quote = our review of the evidence leads us to conclude that both early use of cannabis and heavy use of cannabis are more likely in individuals with a vulnerability to a variety of other problem behaviors, such as early or heavy use of cigarettes or alcohol, use of other illicit drugs, and poor school performance. ))</ref>  An opposing view was expressed by Suzanne Gage and coauthors reviewing the literature available in 2016, who regarded the epidemiologic evidence on cannabis use and psychosis strong enough "to warrant a public health message that cannabis use can increase the risk of psychotic disorders," but also cautioning that additional studies are needed to determine the size of the effect.<ref name=Gage,et_al>((cite journal |last1=Gage |first1=Suzanne H. |last2=Hickman |first2=Matthew |last3=Zammit |first3=Stanley |title=Association Between Cannabis and Psychosis: Epidemiologic Evidence |journal=Biological Psychiatry |date=April 2016 |volume=79 |issue=7 |pages=549–556 |doi=10.1016/j.biopsych.2015.08.001 |pmid=26386480 |hdl=1983/b8fb2d3b-5a55-4d07-97c0-1650b0ffc05d |s2cid=1055335 |url=https://research-information.bris.ac.uk/ws/files/54173362/Gage_accepteduncorrected.pdf |hdl-access=free |access-date=2021-09-08 |archive-date=2021-09-25 |archive-url=https://web.archive.org/web/20210925212720/https://research-information.bris.ac.uk/ws/files/54173362/Gage_accepteduncorrected.pdf |url-status=live ))</ref> Such a public health message was subsequently issued in August 2019 by the Surgeon General of the United States.<ref>((cite web |title=U.S. Surgeon General's Advisory: Marijuana Use and the Developing Brain |url=https://www.hhs.gov/surgeongeneral/reports-and-publications/addiction-and-substance-misuse/advisory-on-marijuana-use-and-developing-brain/index.html |website=[[United States Department of Health and Human Services]] |date=29 August 2019 |access-date=12 February 2020 |archive-date=11 February 2020 |archive-url=https://web.archive.org/web/20200211224857/https://www.hhs.gov/surgeongeneral/reports-and-publications/addiction-and-substance-misuse/advisory-on-marijuana-use-and-developing-brain/index.html |url-status=live ))</ref> The review by Gage et al. also stated "If the association between cannabis and schizophrenia is causal and of the magnitude estimated across studies to date, this would equate to a schizophrenia lifetime risk of approximately 2% in regular cannabis users (though risk for broader psychotic outcomes will be greater). This implies that about 98% of regular cannabis users will not develop schizophrenia...[and that] risk could be much greater in those at a higher genetic risk, or in those who use particularly potent strains of cannabis.(( r | Gage,et_al | p=11 )) Expressed in terms of [[odds ratio]], another study found that "Daily cannabis use was associated with increased odds of psychotic disorder compared with never users (adjusted odds ratio [OR] 3.2, 95% CI 2.2–4.1), increasing to nearly five-times increased odds for daily use of high-potency types of cannabis (4.8, 2.5–6.3)."<ref name="DiForti 2019">((cite journal | vauthors = Di Forti M, Quattrone D, Freeman TP, Tripoli G, Gayer-Anderson C, Quigley H, Rodriguez V, Jongsma HE, Ferraro L, La Cascia C, La Barbera D, Tarricone I, Berardi D, Szöke A, Arango C, Tortelli A, Velthorst E, Bernardo M, Del-Ben CM, Menezes PR, Selten JP, Jones PB, Kirkbride JB, Rutten BP, de Haan L, Sham PC, van Os J, Lewis CM, Lynskey M, Morgan C, Murray RM | display-authors = 6 | title = The contribution of cannabis use to variation in the incidence of psychotic disorder across Europe (EU-GEI): a multicentre case-control study | journal = The Lancet. Psychiatry | volume = 6 | issue = 5 | pages = 427–436 | date = May 2019 | pmid = 30902669 | pmc = 7646282 | doi = 10.1016/S2215-0366(19)30048-3 | doi-access = free ))</ref> To calculate what the increased odds ratio<ref name="DiForti 2019"/> means for schizophrenia specifically, a 2005 review placed the lifetime morbid risk of [[Diagnosis of schizophrenia|narrowly defined schizophrenia]] at 0.72%.<ref name="Saha 2005">((cite journal | vauthors = Saha S, Chant D, Welham J, McGrath J | title = A systematic review of the prevalence of schizophrenia | journal = PLOS Medicine | volume = 2 | issue = 5 | pages = e141 | date = May 2005 | pmid = 15916472 | pmc = 1140952 | doi = 10.1371/journal.pmed.0020141 | doi-access = free ))</ref> For some locations, this translates into a substantial [[Attributable fraction for the population|population attributable risk]], such that "assuming causality, if high-potency cannabis types were no longer available, then 12% of cases of first-episode psychosis could be prevented across Europe, rising to 30% in London and 50% in Amsterdam."<ref name="DiForti 2019" />

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 | vauthors = Murrie B, Lappin J, Large M, Sara G | title = Transition of Substance-Induced, Brief, and Atypical Psychoses to Schizophrenia: A Systematic Review and Meta-analysis | journal = Schizophrenia Bulletin | volume = 46 | issue = 3 | pages = 505–516 | date = April 2020 | pmid = 31618428 | pmc = 7147575 | doi = 10.1093/schbul/sbz102 | doi-access = free ))</ref>

However, a 2004 study noted that general population statistics show no increase in psychosis incidence rates in any developed country over the last 50 years, despite a five-fold increase in cannabis use rates. To quote Macleod et al. 2004: "Cannabis use appears to have increased substantially amongst young people over the past 30 years, from around 10% reporting ever use in 1969–70, to around 50% reporting ever use in 2001, in Britain and Sweden. If the relation between use and schizophrenia were truly causal and if the relative risk was around five-fold then the incidence of schizophrenia should have more than doubled since 1970. However population trends in schizophrenia incidence suggest that incidence has either been stable or slightly decreased over the relevant time period."<ref>((cite journal | vauthors = Macleod J, Oakes R, Copello A, Crome I, Egger M, Hickman M, Oppenkowski T, Stokes-Lampard H, Davey Smith G | display-authors = 6 | title = Psychological and social sequelae of cannabis and other illicit drug use by young people: a systematic review of longitudinal, general population studies | journal = Lancet | volume = 363 | issue = 9421 | pages = 1579–88 | date = May 2004 | pmid = 15145631 | doi = 10.1016/S0140-6736(04)16200-4 | s2cid = 3044549 ))</ref>

Of note, cannabis with a high THC to CBD ratio produces a higher incidence of psychological effects. CBD may show antipsychotic and neuroprotective properties, acting as an antagonist to some of the effects of THC. Studies examining this effect have used high ratios of CBD to THC, and it is unclear to what extent these laboratory studies translate to the types of cannabis used by real life users.<ref name="Niesink2013" /><ref name="Scuderi2009">((cite journal | vauthors = Scuderi C, Filippis DD, Iuvone T, Blasio A, Steardo A, Esposito G | title = Cannabidiol in medicine: a review of its therapeutic potential in CNS disorders | journal = Phytotherapy Research | volume = 23 | issue = 5 | pages = 597–602 | date = May 2009 | pmid = 18844286 | doi = 10.1002/ptr.2625 | type = Review | s2cid = 21836765 | url = https://zenodo.org/record/1067705 | access-date = 2020-05-25 | archive-date = 2021-04-11 | archive-url = https://web.archive.org/web/20210411045636/https://zenodo.org/record/1067705 | url-status = live ))</ref> Research has suggested that CBD can safely reduce some symptoms of psychosis in general.<ref>((cite journal | vauthors = Zuardi AW, Crippa JA, Hallak JE, Bhattacharyya S, Atakan Z, Martin-Santos R, McGuire PK, Guimarães FS | display-authors = 6 | title = A critical review of the antipsychotic effects of cannabidiol: 30 years of a translational investigation | journal = Current Pharmaceutical Design | volume = 18 | issue = 32 | pages = 5131–40 | date = 12 September 2012 | pmid = 22716160 | doi = 10.2174/138161212802884681 | s2cid = 13446596 ))</ref>

A 2014 review examined psychological therapy as add-on for people with schizophrenia who are using cannabis:
{| class="wikitable"
|+ Cannabis reduction: adjunct psychological therapy versus treatment as usual<ref name=McL2014>((cite journal | vauthors = McLoughlin BC, Pushpa-Rajah JA, Gillies D, Rathbone J, Variend H, Kalakouti E, Kyprianou K | title = Cannabis and schizophrenia | journal = The Cochrane Database of Systematic Reviews | issue = 10 | pages = CD004837 | date = October 2014 | volume = 2014 | pmid = 25314586 | doi = 10.1002/14651858.CD004837.pub3 | pmc = 10107010 | s2cid = 8434704 | url = https://pure.bond.edu.au/ws/files/32844195/Cannabis_and_schizophrenia.pdf | access-date = 2020-12-13 | archive-date = 2021-03-01 | archive-url = https://web.archive.org/web/20210301013009/https://pure.bond.edu.au/ws/files/32844195/Cannabis_and_schizophrenia.pdf | url-status = live ))</ref>
|-
! Summary of adjunct therapy for cannabis users with psychosis
|-
|Results are limited and inconclusive because of the small number and size of [[randomized controlled trial]]s available and quality of data reporting within these trials. More research is needed to explore the effects of adjunct psychological therapy that is specifically about cannabis and psychosis as currently there is no evidence for any novel intervention being better than standard treatment, for those that both use cannabis and have schizophrenia.<ref name=McL2014/>
|-
| style="padding:0;" |
{| class="wikitable collapsible collapsed" style="width:100%;"
|-
! scope="col" style="text-align: left; | Outcome
! scope="col" style="text-align: left; | Findings in words
! scope="col" style="text-align: left; | Findings in numbers
! scope="col" style="text-align: left; | Quality of evidence
|-
! colspan="4" style="text-align: left; | Behavior
|-
| Frequency of cannabis use<br>(group-based therapy)<br>Follow up: 1 year || People in the intervention groups scored a little lower compared to people receiving treatment as usual but there was no clear difference between the therapy groups and standard care. This finding is based on data of moderate quality. || [[Mean absolute difference|MD]] 0.1 lower (2.44 lower to 2.24 higher)* || [[The Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach|Moderate]]
|-
! colspan="4" style="text-align: left; | [[Mental health|Mental state]]
|-
| Average score ([[Positive and Negative Syndrome Scale|PANSS]]) - positive symptoms<br>Follow up: 12 months || On average, people receiving cannabis reduction therapy scored lower than people treated with treatment as usual but there was no clear difference between groups. This finding is based on data of moderate quality. || MD 0.3 lower (2.55 lower to 1.95 higher)* || Moderate
|-
! colspan="4" style="text-align: left; | [[Life skills|Quality of life]]
|-
| Average score (WHO QOL questionnaire)<br>Follow up: 1 years || On average, people receiving cannabis reduction therapy scored higher compared to people in the control group receiving treatment as usual. There was, however, no clear difference between the groups and these findings are based on data of moderate quality. || MD 0.9 higher (1.15 lower to 2.95 higher)* || Moderate
|-
| || No study reported any data on outcomes such as relapse, [[Adverse event|adverse effects]], leaving the study early and information relating to [[Patient satisfaction|satisfaction with treatment]]||  || 
|-
|  || * At present the meaning of these scores in day-to-day care is unclear. ||  || 
|-
|}
|}

===Transient psychosis===
As of 2017 there was clear 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 | 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 | date = March 2017 | pmid = 28245077 | doi = 10.1002/da.22596 | s2cid = 205737272 | doi-access = free ))</ref> but see previous section. 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 | vauthors = D'Souza DC, Perry E, MacDougall L, Ammerman Y, Cooper T, Wu YT, Braley G, Gueorguieva R, Krystal JH | display-authors = 6 | title = The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis | journal = Neuropsychopharmacology | volume = 29 | issue = 8 | pages = 1558–72 | date = August 2004 | pmid = 15173844 | doi = 10.1038/sj.npp.1300496 | s2cid = 12508404 | doi-access = free ))</ref><ref name="Morrison 2011">((cite journal | 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 | display-authors = 6 | title = Disruption of frontal θ coherence by Δ9-tetrahydrocannabinol is associated with positive psychotic symptoms | journal = Neuropsychopharmacology | volume = 36 | issue = 4 | pages = 827–36 | date = March 2011 | pmid = 21150914 | pmc = 3055738 | doi = 10.1038/npp.2010.222 ))</ref><ref name="Bhattacharyya 2012">((cite journal | 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 | display-authors = 6 | 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 | date = January 2012 | pmid = 22213786 | doi = 10.1001/archgenpsychiatry.2011.161 | doi-access =  ))</ref><ref name="Freeman 2015">((cite journal | 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 | display-authors = 6 | 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 | date = March 2015 | pmid = 25031222 | pmc = 4332941 | doi = 10.1093/schbul/sbu098 ))</ref>

=== Depersonalization/derealization symptoms ===
Cannabis use may precipitate new-onset panic attacks and depersonalization/derealization symptoms simultaneously. The association between cannabis use and [[Depersonalization disorder|depersonalisation/derealisation disorder]] has been studied. Depersonalization is defined as a dissociative symptom in which one feels like an outside observer with respect to one's thoughts, body, and sensations. While derealization is marked by feelings of unreality and detachment from one's surroundings, such that one's environment is experienced as remote or unfamiliar.<ref>((cite journal|vauthors=Madden SP, Einhorn PM|date=February 2018|title=Cannabis-Induced Depersonalization-Derealization Disorder|journal=American Journal of Psychiatry Residents' Journal|volume=13|issue=2|pages=3–6|doi=10.1176/appi.ajp-rj.2018.130202|doi-access=free))</ref>

Some individuals experiencing depersonalisation/derealisation symptoms prior to any cannabis use have reported the effects of cannabis to calm these symptoms and make the depersonalisation/derealisation disorder more manageable with regular use.<ref>''Diagnostic and statistical manual of mental disorders : DSM-5.'' (Fifth edition. ed.). American Psychiatric Association. 2013. p. 304.</ref>

===Depressive disorder ===
((Refimprove section|date=March 2023))
Less attention has been given to the association between cannabis use and [[Depression (mood)|depression]], though according to the [[Australian National Drug & Alcohol Research Centre]], it is possible this is because cannabis users who have depression are less likely to access treatment than those with psychosis.<ref name="Australia">((cite book | vauthors = Copeland J |title= Evidence-based Answers to Cannabis Questions: A Review of the Literature |date=2006 |publisher=Australian National Council on Drugs |isbn=978-1-877018-12-1 ))((page needed|date=February 2020))</ref> The findings on marijuana's relationship to depressive disorder are scattered, showing that cannabis use has benefits, but can also be detrimental to overall mental health. However, sufficient evidence exists showing reductions in cannabis use improve anxiety, depression, and sleep quality.<ref>((cite journal |last1=Hser |first1=Yih-Ing |last2=Mooney |first2=Larissa J. |last3=Huang |first3=David |last4=Zhu |first4=Yuhui |last5=Tomko |first5=Rachel L. |last6=McClure |first6=Erin |last7=Chou |first7=Chih-Ping |last8=Gray |first8=Kevin M. |title=Reductions in cannabis use are associated with improvements in anxiety, depression, and sleep quality, but not quality of life |journal=Journal of Substance Abuse Treatment |date=October 2017 |volume=81 |pages=53–58 |doi=10.1016/j.jsat.2017.07.012 |pmid=28847455 |pmc=5607644 ))</ref> A 2017 review suggests that cannabis has been shown to improve the mood of depression-diagnosed patients.<ref name="Walsh" /> This is indicative of a longitudinal relationship between cannabis reduction and improvements in anxiety and depression.

Anxiety and depression have been found to increase susceptibility to marijuana use.<ref>((cite journal |last1=Stapinski |first1=Lexine A. |last2=Montgomery |first2=Alan A. |last3=Araya |first3=Ricardo |title=Anxiety, depression and risk of cannabis use: Examining the internalising pathway to use among Chilean adolescents |journal=Drug and Alcohol Dependence |date=September 2016 |volume=166 |pages=109–115 |doi=10.1016/j.drugalcdep.2016.06.032 |pmid=27427415 ))</ref> This is due to a desire to alleviate the symptoms of these experiences through marijuana use. Chronic users who use for anxiolytic purposes will even develop dependencies on cannabis, making it difficult to cope with anxiety when the drug is absent.

Teenage cannabis users show no difference from the general population in incidence of [[major depressive disorder]] (MDD), but an association exists between early exposure coupled with continued use into adult life and increased incidence of MDD in adulthood.<ref name="Chadwick2013">((cite journal | vauthors = Chadwick B, Miller ML, Hurd YL | title = Cannabis Use during Adolescent Development: Susceptibility to Psychiatric Illness | journal = Frontiers in Psychiatry | volume = 4 | pages = 129 | date = October 2013 | pmid = 24133461 | pmc = 3796318 | doi = 10.3389/fpsyt.2013.00129 | type = Review | doi-access = free ))</ref> Among cannabis users of all ages, there may be an increased risk of developing depression, with heavy users seemingly having a higher risk.<ref name="Lev-Ran2013">((cite journal | vauthors = Lev-Ran S, Roerecke M, Le Foll B, George TP, McKenzie K, Rehm J | title = The association between cannabis use and depression: a systematic review and meta-analysis of longitudinal studies | journal = Psychological Medicine | volume = 44 | issue = 4 | pages = 797–810 | date = March 2014 | pmid = 23795762 | doi = 10.1017/S0033291713001438 | s2cid = 36763290 ))</ref> Heavy marijuana use in adolescence has also been associated with deficits in cognition. A recent study assessing changes in neuropsychological functioning resulting from long-term cannabis use followed a group of adolescents (ages 12 –15 at baseline) over a 14-year period. Researchers found that more days of use were correlated with decreases in inhibitory control, and visuospatial ability. Contrary to existing cross-sectional studies showing marijuana use in adolescence is associated with poor cognitive functioning, there were no associations between long-term cannabis use and memory and processing speed.<ref>((Cite journal |last1=Infante |first1=M. Alejandra |last2=Nguyen-Louie |first2=Tam T. |last3=Worley |first3=Matthew |last4=Courtney |first4=Kelly E. |last5=Coronado |first5=Clarisa |last6=Jacobus |first6=Joanna |date=May 2020 |title=Neuropsychological Trajectories Associated with Adolescent Alcohol and Cannabis Use: A Prospective 14-Year Study |journal=Journal of the International Neuropsychological Society |language=en |volume=26 |issue=5 |pages=480–491 |doi=10.1017/S1355617719001395 |issn=1355-6177 |pmc=7205577 |pmid=31822320))</ref> While this study showed no correlations between memory and cannabis use, others have found that there is. It is important to know that studies looking at associations between cannabis use and poor neurocognitive functioning have found that extended abstinence from marijuana leads to improvements in cognitive deficits. Decreases in cognition resulting from marijuana use are indeed reversible.

A February 2019 [[systematic review]] and [[meta-analysis]] found that cannabis consumption during adolescence was associated with an increased risk of developing depression and suicidal behavior later in life, while finding no effect on anxiety.<ref name="Gobbi">((cite journal|author1-link=Gabriella Gobbi | vauthors = Gobbi G, Atkin T, Zytynski T, Wang S, Askari S, Boruff J, Ware M, Marmorstein N, Cipriani A, Dendukuri N, Mayo N | display-authors = 6 | title = Association of Cannabis Use in Adolescence and Risk of Depression, Anxiety, and Suicidality in Young Adulthood: A Systematic Review and Meta-analysis | journal = JAMA Psychiatry | volume = 76 | issue = 4 | pages = 426–434 | date = April 2019 | pmid = 30758486 | pmc = 6450286 | doi = 10.1001/jamapsychiatry.2018.4500 ))</ref> In a longitudinal study assessing the associations between long term use and mental health in a group of individuals participating in a drug-based treatment for depression, researchers found that, compared to non-users, patients using both medically and non-medically experienced less improvement in depressive symptoms and an increase in suicidal ideation. Additionally, those who used non-medically, were less likely to visit the psychiatrist.<ref>((Cite journal |last1=Bahorik |first1=Amber L. |last2=Sterling |first2=Stacy A. |last3=Campbell |first3=Cynthia I. |last4=Weisner |first4=Constance |last5=Ramo |first5=Danielle |last6=Satre |first6=Derek D. |date=2018-12-01 |title=Medical and non-medical marijuana use in depression: Longitudinal associations with suicidal ideation, everyday functioning, and psychiatry service utilization |journal=Journal of Affective Disorders |language=en |volume=241 |pages=8–14 |doi=10.1016/j.jad.2018.05.065 |issn=0165-0327 |pmc=6455811 |pmid=30086434))</ref> Further research should investigate this finding to see whether non-medical marijuana use serves as a barrier to treatment seeking behavior.

===Mania symptoms===
Mania is a mental illness marked by periods of great excitement or euphoria, delusions, and overactivity.<ref>((cite news |title=Mania: What Is It, Causes, Triggers, Symptoms & Treatment |url=https://my.clevelandclinic.org/health/diseases/21603-mania |work=Cleveland Clinic |access-date=2022-10-24 |archive-date=2022-10-24 |archive-url=https://web.archive.org/web/20221024114249/https://my.clevelandclinic.org/health/diseases/21603-mania |url-status=live ))</ref> This is common in cannabis users when they hit a point of their high that could lead to paranoia, anxiety, increased heart rate. Some strains of the drug can have these effects on the individuals that use them, but no effects are guaranteed when used. A case review reported that an adult user had marijuana-induced mania even though they had no previous psychiatric history.<ref>((cite journal |last1=Iskandar |first1=Joseph W. |last2=Griffeth |first2=Benjamin |last3=Sharma |first3=Taral |title=Marijuana-induced mania in a healthy adolescent: a case report |journal=General Hospital Psychiatry |date=May 2011 |volume=33 |issue=6 |pages=640.e3–4 |doi=10.1016/j.genhosppsych.2011.04.007 |pmid=21749837 ))</ref> However, some participants that have been previously diagnosed with bipolar disorder, had a worsen occurrence with mania symptoms.<ref>((cite journal |last1=Gibbs |first1=Melanie |last2=Winsper |first2=Catherine |last3=Marwaha |first3=Steven |last4=Gilbert |first4=Eleanor |last5=Broome |first5=Matthew |last6=Singh |first6=Swaran P. |title=Cannabis use and mania symptoms: A systematic review and meta-analysis |journal=Journal of Affective Disorders |date=January 2015 |volume=171 |pages=39–47 |doi=10.1016/j.jad.2014.09.016 |pmid=25285897 |url=http://wrap.warwick.ac.uk/64733/1/WRAP_Cannabis%20Use%20and%20Mania%20Symptoms%20%281%29.pdf |access-date=2019-08-16 |archive-date=2019-12-29 |archive-url=https://web.archive.org/web/20191229214223/http://wrap.warwick.ac.uk/64733/1/WRAP_Cannabis%20Use%20and%20Mania%20Symptoms%20%281%29.pdf |url-status=live ))</ref> This showed that anyone, diagnosed or psychiatrically stable, can develop mania symptoms when under the influence of cannabis.

===Suicidal behavior===
Adolescent cannabis users show no difference from their peers in [[suicidal ideation]] or rate of suicide attempts, but those who continue to use cannabis into adult life exhibit an increased incidence of both, although multiple other contributory factors are also implicated.<ref name="Chadwick2013" />

In the general population a weak (indirect) association appears to exist between suicidal behaviour and cannabis consumption in both psychotic and non-psychotic users,<ref name="Serafini2012">((cite journal | vauthors = Serafini G, Pompili M, Innamorati M, Rihmer Z, Sher L, Girardi P | title = Can cannabis increase the suicide risk in psychosis? A critical review | journal = Current Pharmaceutical Design | volume = 18 | issue = 32 | pages = 5165–87 | year = 2012 | pmid = 22716157 | doi = 10.2174/138161212802884663 | hdl = 11567/775343 | type = Review | hdl-access = free ))</ref> although it remains unclear whether regular cannabis use increases the risk of suicide.<ref name="Calabria2010">((cite journal | vauthors = Calabria B, Degenhardt L, Hall W, Lynskey M | title = Does cannabis use increase the risk of death? Systematic review of epidemiological evidence on adverse effects of cannabis use | journal = Drug and Alcohol Review | volume = 29 | issue = 3 | pages = 318–30 | date = May 2010 | pmid = 20565525 | doi = 10.1111/j.1465-3362.2009.00149.x | type = Review ))</ref> Cannabis use is a risk factor in suicidality, but suicide attempts are characterized by many additional risk factors including mood disorders, alcohol use, stress, personal problems and poor support.<ref name="Serafini2012" />

==Gateway drug hypothesis==
((Main|Gateway drug theory#Cannabis))
The [[gateway drug]] hypothesis asserts that the use of soft drugs such as cannabis, tobacco or alcohol may ultimately lead to the use of [[Hard and soft drugs|harder drugs]]. The release of dopamine at CB1 receptors when cannabinoids enter the body can enforce drug seeking behavior. In addition to the gateway framework, there is also the peer clustering theory which says that friendships influence drug seeking behaviors. Friends who use can influence one another to take drugs that are more rewarding and have a higher potential for abuse.<ref>((Cite journal |last1=Otten |first1=Roy |last2=Mun |first2=Chung Jung |last3=Dishion |first3=Thomas J. |date=October 2017 |title=The social exigencies of the gateway progression to the use of illicit drugs from adolescence into adulthood |journal=Addictive Behaviors |language=en |volume=73 |pages=144–150 |doi=10.1016/j.addbeh.2017.05.011 |pmc=6946384 |pmid=28511099))</ref>

Large-scale [[Longitudinal study|longitudinal studies]] in the UK and New Zealand from 2015 and 2017 showed an association between cannabis use and an increased probability of later disorders in the use of other drugs.<ref name="pmid290571982">((cite journal | vauthors = Courtney KE, Mejia MH, Jacobus J | title = Longitudinal Studies on the Etiology of Cannabis Use Disorder: A Review | journal = Current Addiction Reports | volume = 4 | issue = 2 | pages = 43–52 | date = June 2017 | pmid = 29057198 | pmc = 5644349 | doi = 10.1007/s40429-017-0133-3 ))</ref><ref name="pmid257590892">((cite journal | vauthors = Badiani A, Boden JM, De Pirro S, Fergusson DM, Horwood LJ, Harold GT | title = Tobacco smoking and cannabis use in a longitudinal birth cohort: evidence of reciprocal causal relationships | journal = Drug and Alcohol Dependence | volume = 150 | pages = 69–76 | date = May 2015 | pmid = 25759089 | doi = 10.1016/j.drugalcdep.2015.02.015 | hdl-access = free | hdl = 10523/10359 ))</ref><ref name="pmid285924202">((cite journal | vauthors = Taylor M, Collin SM, Munafò MR, MacLeod J, Hickman M, Heron J | title = Patterns of cannabis use during adolescence and their association with harmful substance use behaviour: findings from a UK birth cohort | journal = Journal of Epidemiology and Community Health | volume = 71 | issue = 8 | pages = 764–770 | date = August 2017 | pmid = 28592420 | pmc = 5537531 | doi = 10.1136/jech-2016-208503 ))</ref>

Over time, the marijuana gateway hypothesis has been studied more and more. In one published study, the use of marijuana was shown not a reliable gateway cause of illicit drug use.<ref>((cite journal |last1=Jorgensen |first1=Cody |last2=Wells |first2=Jessica |title=Is marijuana really a gateway drug? A nationally representative test of the marijuana gateway hypothesis using a propensity score matching design |journal=Journal of Experimental Criminology |date=September 2022 |volume=18 |issue=3 |pages=497–514 |doi=10.1007/s11292-021-09464-z |s2cid=233599789 ))</ref>

However, social factors and environment influence drug use and abuse, making the gateway effects of cannabis different for those in differing social circumstances. A study looking at associations between drug injection and cannabis use in street-involved youth found that cannabis use was associated with slower time to injection initiation.<ref name=":0">((Cite journal |last1=Reddon |first1=Hudson |last2=DeBeck |first2=Kora |last3=Socias |first3=Maria Eugenia |last4=Dong |first4=Huiru |last5=Wood |first5=Evan |last6=Montaner |first6=Julio |last7=Kerr |first7=Thomas |last8=Milloy |first8=Michael-John |date=March 2018 |title=Cannabis use is associated with lower rates of initiation of injection drug use among street-involved youth: A longitudinal analysis: Cannabis use and injection initiation |journal=Drug and Alcohol Review |language=en |volume=37 |issue=3 |pages=421–428 |doi=10.1111/dar.12667 |pmc=6154786 |pmid=29430806))</ref> Injection initiation leads to further patterns of injection initiation which will eventually lead to addiction.<ref name=":0" />

==Physical health==

A 2013 literature review said that exposure to cannabis <!-- had biologically-based physical, mental, behavioral and social health consequences and --> was "associated with diseases of the liver (particularly with co-existing hepatitis C), lungs, heart, and vasculature". 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/>

Researchers are concerned that with the increase in legalization will lead towards an increase of use which will in turn call for new strategies as well as rehabilitation to minimize the harm that cannabis can do on someone's body.<ref>((cite journal |last1=Broyd |first1=Samantha J. |last2=van Hell |first2=Hendrika H. |last3=Beale |first3=Camilla |last4=Yücel |first4=Murat |last5=Solowij |first5=Nadia |title=Acute and Chronic Effects of Cannabinoids on Human Cognition—A Systematic Review |journal=Biological Psychiatry |date=April 2016 |volume=79 |issue=7 |pages=557–567 |doi=10.1016/j.biopsych.2015.12.002 |pmid=26858214 |s2cid=9858298 |url=https://ro.uow.edu.au/cgi/viewcontent.cgi?article=3163&context=sspapers |access-date=2021-08-23 |archive-date=2022-06-03 |archive-url=https://web.archive.org/web/20220603041811/https://ro.uow.edu.au/cgi/viewcontent.cgi?article=3163&context=sspapers |url-status=live ))</ref>

===Brain===
Studies conflict on whether long-term cannabis use causes persistent structural changes in humans. Twin studies have shown no significant difference between users and non-users in twin pairs,<ref name="NIDAReport">((cite journal |last1=NIDA |title=What are marijuana's long-term effects on the brain? |journal=National Institute on Drug Abuse |url=https://nida.nih.gov/publications/research-reports/marijuana/what-are-marijuanas-long-term-effects-brain |access-date=29 October 2022 |language=en |archive-date=21 October 2022 |archive-url=https://web.archive.org/web/20221021211259/https://nida.nih.gov/publications/research-reports/marijuana/what-are-marijuanas-long-term-effects-brain |url-status=live ))</ref> but other studies have demonstrated that chronic use affects white matter and [[hippocampus|hippocampal]] volume in the brains of healthy (non-psychotic) patients, which is where large amounts of cannabinoid-1 receptors are present.<ref>((cite journal |last1=Mandelbaum |first1=David E. |last2=de la Monte |first2=Suzanne M. |title=Adverse Structural and Functional Effects of Marijuana on the Brain: Evidence Reviewed |journal=Pediatric Neurology |date=January 2017 |volume=66 |pages=12–20 |doi=10.1016/j.pediatrneurol.2016.09.004 |pmid=27789118 |url=http://www.pedneur.com/article/S0887899416304787/pdf |access-date=2022-10-24 |archive-date=2023-04-21 |archive-url=https://web.archive.org/web/20230421021630/https://www.pedneur.com/article/S0887-8994(16)30478-7/pdf |url-status=live |pmc=9954727 ))</ref><ref>((cite journal | vauthors = Rocchetti M, Crescini A, Borgwardt S, Caverzasi E, Politi P, Atakan Z, Fusar-Poli P | title = Is cannabis neurotoxic for the healthy brain? A meta-analytical review of structural brain alterations in non-psychotic users | journal = Psychiatry and Clinical Neurosciences | volume = 67 | issue = 7 | pages = 483–92 | date = November 2013 | pmid = 24118193 | doi = 10.1111/pcn.12085 | s2cid = 8245635 | quote = Aims - Despite growing research in the field of cannabis imaging, mostly in those with a psychotic illness, the possible neurotoxic effects of smoked cannabis on the healthy brain have yet to be fully understood. There appears to be a need to evaluate the existing imaging data on the neuroanatomical effects of cannabis use on non‐psychotic populations. Conclusions - Our results suggest that in the healthy brain, chronic and long‐term cannabis exposure may exert significant effects in brain areas enriched with cannabinoid receptors, such as the hippocampus, which could be related to a neurotoxic action. | doi-access =  ))</ref>

=== Gastrointestinal tract ===
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.<ref>((Cite journal |last=Sullivan |first=Stephen |date=2010 |title=Cannabinoid Hyperemesis |journal=Canadian Journal of Gastroenterology |language=en |volume=24 |issue=5 |pages=284–285 |doi=10.1155/2010/481940 |issn=0835-7900 |pmc=2886568 |pmid=20485701 |doi-access=free ))</ref>

===Heart and circulation===
The acute effects of cannabis use in humans include a dose-dependent increase in heart rate, typically accompanied by a mild increase in blood pressure while lying down and [[postural hypotension]] - a drop in blood pressure when standing up. These effects may vary depending on the relative concentration of the many different [[cannabinoids]] that can affect the cardiovascular function, such as [[cannabigerol]]. Smoking cannabis decreases exercise tolerance.<ref>((cite journal | vauthors = Sidney S | title = Cardiovascular consequences of marijuana use | journal = Journal of Clinical Pharmacology | volume = 42 | issue = S1 | pages = 64S–70S | date = November 2002 | pmid = 12412838 | doi = 10.1002/j.1552-4604.2002.tb06005.x | s2cid = 27401560 ))</ref> Cardiovascular effects may not lead to serious health issues for the majority of young, healthy users; on the contrary, heart attack, that is [[myocardial infarction]], [[stroke]], and other adverse cardiovascular events, have occurred in association with its use. Cannabis use by people with cardiovascular disease poses a health risk because it can lead to increased cardiac work, increased catecholamine levels, and impaired blood oxygen carrying capacity due to the production of [[carboxyhemoglobin]].<ref>((cite journal | vauthors = Jones RT | title = Cardiovascular system effects of marijuana | journal = Journal of Clinical Pharmacology | volume = 42 | issue = S1 | pages = 58S–63S | date = November 2002 | pmid = 12412837 | doi = 10.1002/j.1552-4604.2002.tb06004.x | s2cid = 12193532 ))</ref>

===Cancer===
A 2012 review examining the relation of cancer and cannabis found little direct evidence that [[cannabinoids]] found in cannabis, including [[THC]], are carcinogenic. Cannabinoids are not [[mutagenic]] according to the [[Ames test]]. However, cannabis ''smoke'' has been found to be carcinogenic in rodents and mutagenic in the Ames test. Correlating cannabis use with the development of human cancers has been problematic due to difficulties in quantifying cannabis use, unmeasured [[confounders]], and cannabinoids' potential as cancer treatment.<ref name="Bowles2012">((cite journal|vauthors=Bowles DW, O'Bryant CL, Camidge DR, Jimeno A|date=July 2012|title=The intersection between cannabis and cancer in the United States|journal=Critical Reviews in Oncology/Hematology|volume=83|issue=1|pages=1–10|doi=10.1016/j.critrevonc.2011.09.008|pmid=22019199))</ref>

According to a 2013 literature review, cannabis could be carcinogenic, but there are methodological limitations in studies making it difficult to establish a link between cannabis use and cancer risk.<ref name=Gordon2013/> The authors say that bladder cancer does seem to be linked to habitual cannabis use, and that there may be a risk for cancers of the head and neck among long-term (more than 20 years) users.<ref name=Gordon2013/>  Gordon and colleagues said, "there does appear to be an increased risk of cancer (particularly head and neck, lung, and bladder cancer) for those who use marijuana over a period of time, although what length of time that this risk increases is uncertain."<ref name=Gordon2013/>

====Lung ====
There have been a  limited number of studies that have looked at the [[Cannabis-associated respiratory disease|effects of smoking cannabis]] on the respiratory system.<ref name="MaistoGalizio2014">((cite book |vauthors=Maisto S, Galizio M, Connors G |title=Drug Use and Abuse |url=https://books.google.com/books?id=5F08AwAAQBAJ&pg=PA278 |year=2014 |publisher=Cengage Learning |isbn=978-1-305-17759-8 |page=278 |access-date=2016-03-14 |archive-date=2023-01-13 |archive-url=https://web.archive.org/web/20230113004528/https://books.google.com/books?id=5F08AwAAQBAJ&pg=PA278 |url-status=live ))</ref>  Chronic heavy cannabis smoking is associated with coughing, production of sputum, wheezing, and other symptoms of chronic bronchitis.<ref>((cite journal | vauthors = Hall W, Solowij N | title = Adverse effects of cannabis | journal = Lancet | volume = 352 | issue = 9140 | pages = 1611–6 | date = November 1998 | pmid = 9843121 | doi = 10.1016/S0140-6736(98)05021-1 | s2cid = 16313727 ))</ref> Regular cannabis use has not been shown to cause significant abnormalities in lung function.<ref name="Tashkin2013">((cite journal | vauthors = Tashkin DP | title = Effects of marijuana smoking on the lung | journal = Annals of the American Thoracic Society | volume = 10 | issue = 3 | pages = 239–47 | date = June 2013 | pmid = 23802821 | doi = 10.1513/AnnalsATS.201212-127FR | s2cid = 20615545 ))</ref>

Regular cannabis smokers show pathological changes in lung cells similar to those that precede the development of lung cancer in tobacco smokers.<ref>((cite journal | vauthors = Hall W, Degenhardt L | title = Adverse health effects of non-medical cannabis use | journal = Lancet | volume = 374 | issue = 9698 | pages = 1383–91 | date = October 2009 | pmid = 19837255 | doi = 10.1016/S0140-6736(09)61037-0 | s2cid = 31616272 ))</ref> Gordon and colleagues in a 2013 literature review said: "Unfortunately, methodological limitations in many of the reviewed studies, including selection bias, small sample size, limited generalizability, and lack of adjustment for tobacco smoking, may limit the ability to attribute cancer risk solely to marijuana use."<ref name=Gordon2013/>  Reviewing studies adjusted for age and tobacco use, they said there was a risk of lung cancer even after adjusting for tobacco use, but that the period of time over which the risk increases is uncertain.<ref name=Gordon2013/>

A 2013 review which specifically examined the effects of cannabis on the lung concluded "[f]indings from a limited number of well-designed epidemiological studies do not suggest an increased risk for the development of either lung or upper airway cancer from light or moderate use, although evidence is mixed concerning possible carcinogenic risks of heavy, long-term use."<ref name="Tashkin2013" />

In 2013 the [[International Lung Cancer Consortium]] found no significant additional lung cancer risk in tobacco users who also smoked cannabis. Nor did they find an increased risk in cannabis smokers who did not use tobacco. They concluded that "[o]ur pooled results showed no significant association between the intensity, duration, or cumulative consumption of cannabis smoke and the risk of lung cancer overall or in never smokers." They cautioned that "[o]ur results cannot preclude the possibility that cannabis may exhibit an association with lung cancer risk at extremely high dosage." The same authors supported further study, and called attention to evolving means of cannabis consumption: "Specifically, respiratory risks may differ with the use of water pipes and vaporizers or with consuming oral preparations."<ref name=Zhang-2013-full>((cite journal | vauthors = Zhang LR, Morgenstern H, Greenland S, Chang SC, Lazarus P, Teare MD, Woll PJ, Orlow I, Cox B, Brhane Y, Liu G, Hung RJ | display-authors = 6 | title = Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium | journal = International Journal of Cancer | volume = 136 | issue = 4 | pages = 894–903 | date = February 2015 | pmid = 24947688 | pmc = 4262725 | doi = 10.1002/ijc.29036 ))</ref>

Cannabis smoke contains thousands of organic and inorganic chemicals, including many of the same [[carcinogen]]s as [[tobacco]] smoke.<ref>((cite journal | vauthors = Hashibe M, Ford DE, Zhang ZF | title = Marijuana smoking and head and neck cancer | journal = Journal of Clinical Pharmacology | volume = 42 | issue = S1 | pages = 103S–107S | date = November 2002 | pmid = 12412843 | doi = 10.1002/j.1552-4604.2002.tb06010.x | type = Review | s2cid = 20738940 ))</ref> A 2012 special report by the [[British Lung Foundation]] concluded that cannabis smoking was linked to many adverse effects, including bronchitis and lung cancer.<ref name="BLA2012">((cite book |date=2012 |title=The impact of cannabis on your lungs |url=https://www.lunguk.org/Resources/British%20Lung%20Foundation/Website/The%20impact%20of%20cannabis%20on%20your%20lungs%20-%20BLF%20report%202012.pdf |publisher=British Lung Association |access-date=2022-10-24 |archive-date=2022-10-24 |archive-url=https://web.archive.org/web/20221024114250/https://www.lunguk.org/Resources/British%20Lung%20Foundation/Website/The%20impact%20of%20cannabis%20on%20your%20lungs%20-%20BLF%20report%202012.pdf |url-status=live ))</ref> They identified cannabis smoke as a carcinogen and also said awareness of the danger was low compared with the high awareness of the dangers of smoking tobacco particularly among younger users. They said there was an increased risk from each cannabis cigarette due to drawing in large puffs of smoke and holding them.<ref name=BLA2012/>  Cannabis smoke has been listed on the [[California Proposition 65 (1986)|California Proposition 65]] warning list as a carcinogen since 2009, but leaves and pure THC are not.<ref>((cite web |title=The Proposition 65 List |url=https://oehha.ca.gov/proposition-65/proposition-65-list |website=[[California Office of Environmental Health Hazard Assessment]] |access-date=2022-10-24 |archive-date=2014-10-31 |archive-url=https://web.archive.org/web/20141031102829/http://www.oehha.ca.gov/prop65/prop65_list/files/P65single060614.pdf |url-status=live ))</ref>

====Head and neck====
A 2015 review found no association between head and neck cancer and lifetime cannabis smoking.<ref>((cite journal | vauthors = de Carvalho MF, Dourado MR, Fernandes IB, Araújo CT, Mesquita AT, Ramos-Jorge ML | title = Head and neck cancer among marijuana users: a meta-analysis of matched case-control studies | journal = Archives of Oral Biology | volume = 60 | issue = 12 | pages = 1750–5 | date = December 2015 | pmid = 26433192 | doi = 10.1016/j.archoralbio.2015.09.009 ))</ref>

===Respiratory effects===
((anchor|Respiratory issues))
[[File:Cannabissativadior.jpg|thumb|right|upright|''Cannabis sativa'' from [[Vienna Dioscurides]], 512 AD]]

A 2013 literature review by Gordon and colleagues concluded that inhaled cannabis is associated with lung disease,<ref name=Gordon2013/> although Tashkin's 2013 review has found "no clear link to [[chronic obstructive pulmonary disease]]".<ref name="Tashkin2013"/>

Smoking cannabis has been linked to adverse respiratory effects including: chronic coughing, wheezing, sputum production, and acute bronchitis.<ref name="BLA2012" /> It has been suggested that the common practice of inhaling cannabis smoke deeply and holding breath could lead to [[pneumothorax]]. In a few case reports involving immunocompromised patients, pulmonary infections such as [[aspergillosis]] have been attributed to smoking cannabis contaminated with fungi. The transmission of [[tuberculosis]] has been linked to cannabis inhalation techniques, such as sharing water pipes and '[[Cannabis smoking#Hotboxing|Hotboxing]]'.<ref>((cite journal|vauthors=Lutchmansingh D, Pawar L, Savici D|date=2014|title=Legalizing Cannabis: A physician's primer on the pulmonary effects of marijuana|journal=Current Respiratory Care Reports|volume=3|issue=4|pages=200–205|doi=10.1007/s13665-014-0093-1|pmc=4226845|pmid=25401045))</ref>

Of the various methods of cannabis consumption, smoking is considered the most harmful; the inhalation of smoke from [[organic compound|organic materials]] can cause various health problems (e.g., coughing and [[sputum]]). [[Isoprene]]s help to modulate and slow down reaction rates, contributing to the significantly differing qualities of partial combustion products from various sources.<ref>((primary source inline|date=December 2013)) ((update after|2013|12|21)) ((Cite journal | vauthors = Grotenhermen F | title = Harm Reduction Associated with Inhalation and Oral Administration of Cannabis and THC | doi = 10.1300/J175v01n03_09 | journal = Journal of Cannabis Therapeutics | volume = 1 | issue = 3–4 | pages = 133–152 | year = 2001 ))</ref><ref>((cite journal | vauthors = Tashkin DP | title = Smoked marijuana as a cause of lung injury | journal = Monaldi Archives for Chest Disease = Archivio Monaldi per le Malattie del Torace | volume = 63 | issue = 2 | pages = 93–100 | date = June 2005 | pmid = 16128224 | doi = 10.4081/monaldi.2005.645 | type = Review | doi-access = free ))</ref>

=== Reproductive and endocrine effects ===
((Main|Cannabis and male fertilty))
Male cannabis use has been associated with reduced fertility and decreased sperm counts.<ref>((cite journal |last1=Schrott |first1=Rose |last2=Rajavel |first2=Maya |last3=Acharya |first3=Kelly |last4=Huang |first4=Zhiqing |last5=Acharya |first5=Chaitanya |last6=Hawkey |first6=Andrew |last7=Pippen |first7=Erica |last8=Lyerly |first8=H. Kim |last9=Levin |first9=Edward D. |last10=Murphy |first10=Susan K. |title=Sperm DNA methylation altered by THC and nicotine: Vulnerability of neurodevelopmental genes with bivalent chromatin |journal=Scientific Reports |date=29 September 2020 |volume=10 |issue=1 |pages=16022 |doi=10.1038/s41598-020-72783-0 |pmid=32994467 |pmc=7525661 |bibcode=2020NatSR..1016022S ))</ref> Initial epigenetic studies have shown that male cannabis use causes widespread DNA methylation changes in sperm, resulting in lower rates of fertilization and higher rates of miscarriage.<ref>((cite journal |last1=Schrott |first1=Rose |last2=Murphy |first2=Susan K |last3=Modliszewski |first3=Jennifer L |last4=King |first4=Dillon E |last5=Hill |first5=Bendu |last6=Itchon-Ramos |first6=Nilda |last7=Raburn |first7=Douglas |last8=Price |first8=Thomas |last9=Levin |first9=Edward D |last10=Vandrey |first10=Ryan |last11=Corcoran |first11=David L |last12=Kollins |first12=Scott H |last13=Mitchell |first13=John T |title=Refraining from use diminishes cannabis-associated epigenetic changes in human sperm |journal=Environmental Epigenetics |date=21 September 2021 |volume=7 |issue=1 |pages=dvab009 |doi=10.1093/eep/dvab009 |pmid=34557312 |pmc=8455898 ))</ref> Sperm DNA methylation alterations from cannabis extract exposure are evident in the offspring of rats.<ref>((cite journal |last1=Schrott |first1=Rose |last2=Modliszewski |first2=Jennifer L. |last3=Hawkey |first3=Andrew B. |last4=Grenier |first4=Carole |last5=Holloway |first5=Zade |last6=Evans |first6=Janequia |last7=Pippen |first7=Erica |last8=Corcoran |first8=David L. |last9=Levin |first9=Edward D. |last10=Murphy |first10=Susan K. |title=Sperm DNA methylation alterations from cannabis extract exposure are evident in offspring |journal=Epigenetics & Chromatin |date=10 September 2022 |volume=15 |issue=1 |pages=33 |doi=10.1186/s13072-022-00466-3 |pmid=36085240 |pmc=9463823 |doi-access=free ))</ref>

((Main|Cannabis in pregnancy))
A study released by the [[National Academies of Sciences, Engineering, and Medicine]] cited significant evidence for a statistical link between mothers who smoke cannabis during pregnancy and lower birth weights of their babies.<ref name="National_Academies_2017">((cite book |doi=10.17226/24625 |doi-access=free |title=The Health Effects of Cannabis and Cannabinoids |year=2017 |pmid=28182367 |isbn=978-0-309-45304-2 |author1=National Academies of Sciences, Engineering, and Medicine |author2=Health and Medicine Division |author3=Board on Population Health and Public Health Practice |author4=Committee on the Health Effects of Marijuana: An Evidence Review and Research Agenda ))((page needed|date=October 2022))</ref> Cannabis consumption in pregnancy is associated with [[Intrauterine growth restriction|restrictions in growth of the fetus]], [[miscarriage]], and cognitive deficits in offspring.<ref name=Fonseca2013>((cite journal | vauthors = Fonseca BM, Correia-da-Silva G, Almada M, Costa MA, Teixeira NA | title = The Endocannabinoid System in the Postimplantation Period: A Role during Decidualization and Placentation | journal = International Journal of Endocrinology | volume = 2013 | pages = 510540 | year = 2013 | pmid = 24228028 | pmc = 3818851 | doi = 10.1155/2013/510540 | quote = In fact, maternal marijuana use has been associated with foetal growth restrictions, spontaneous miscarriage, and cognitive deficits in infancy and adolescence. | type = Review | doi-access = free ))</ref> Although the majority of research has concentrated on the adverse effects of alcohol, there is now evidence that prenatal exposure to cannabis has serious effects on the developing brain and is associated with "deficits in language, attention, areas of cognitive performance, and delinquent behavior in adolescence".<ref name=Irner2012>((cite journal | vauthors = Irner TB | title = Substance exposure in utero and developmental consequences in adolescence: a systematic review | journal = Child Neuropsychology | volume = 18 | issue = 6 | pages = 521–49 | year = 2012 | pmid = 22114955 | doi = 10.1080/09297049.2011.628309 | type = Review | s2cid = 25014303 ))</ref> A report prepared for the [[Australian National Council on Drugs]] concluded cannabis and other [[cannabinoid]]s are contraindicated in pregnancy as it may interact with the [[endocannabinoid system]].<ref name="Australia" />

=== Mortality ===
No fatal overdoses associated with cannabis use have ever been reported.<ref name="Calabria2010" /> Due to the small number of studies that have been conducted, the evidence is insufficient to show a long-term elevated risk of mortality from any cause. Motor vehicle accidents, suicide, and possible respiratory and brain cancers are all of interest to many researchers, but no studies have been able to show a consistent increase in mortality from these causes.<ref name="Calabria2010" />

== See also ==
* [[Cannabinoid hyperemesis syndrome]] (CHS)
* [[Effects of cannabis]]
* [[Medical cannabis]]

== References ==
((Reflist|35em))

((Cannabis|state=expanded))
((cannabinoids))
((drug use))

((DEFAULTSORT:Long-Term Effects Of Cannabis))
[[Category:Cannabis and health]]

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Module:Category handler/data (view source) (protected)
Module:Category handler/shared (view source) (protected)
Module:Check for unknown parameters (view source) (protected)
Module:Citation/CS1 (view source) (protected)
Module:Citation/CS1/COinS (view source) (protected)
Module:Citation/CS1/Configuration (view source) (protected)
Module:Citation/CS1/Date validation (view source) (protected)
Module:Citation/CS1/Identifiers (view source) (protected)
Module:Citation/CS1/Utilities (view source) (protected)
Module:Citation/CS1/Whitelist (view source) (protected)
Module:Citation/CS1/styles.css (view source) (protected)
Module:DecodeEncode (view source) (template editor protected)
Module:Delink (view source) (protected)
Module:Disambiguation/templates (view source) (protected)
Module:Format link (view source) (template editor protected)
Module:GetParameters (view source) (template editor protected)
Module:Hatnote (view source) (template editor protected)
Module:Hatnote/styles.css (view source) (template editor protected)
Module:Hatnote list (view source) (template editor protected)
Module:Icon (view source) (template editor protected)
Module:Icon/data (view source) (template editor protected)
Module:Labelled list hatnote (view source) (template editor protected)
Module:List (view source) (protected)
Module:Message box (view source) (protected)
Module:Message box/ambox.css (view source) (protected)
Module:Message box/configuration (view source) (protected)
Module:Namespace detect/config (view source) (protected)
Module:Namespace detect/data (view source) (protected)
Module:Navbar (view source) (protected)
Module:Navbar/configuration (view source) (protected)
Module:Navbar/styles.css (view source) (protected)
Module:Navbox (view source) (template editor protected)
Module:Navbox/configuration (view source) (template editor protected)
Module:Navbox/styles.css (view source) (template editor protected)
Module:Navbox with collapsible groups (view source) (template editor protected)
Module:Ns has subpages (view source) (protected)
Module:Pagetype (view source) (protected)
Module:Pagetype/config (view source) (protected)
Module:Pagetype/disambiguation (view source) (protected)
Module:Pagetype/setindex (view source) (protected)
Module:Pagetype/softredirect (view source) (protected)
Module:Plain text (view source) (template editor protected)
Module:Portal (view source) (template editor protected)
Module:Portal-inline (view source) (template editor protected)
Module:Portal/images/c (view source) (template editor protected)
Module:SDcat (view source) (protected)
Module:Sidebar (view source) (template editor protected)
Module:Sidebar/configuration (view source) (template editor protected)
Module:Sidebar/styles.css (view source) (template editor protected)
Module:String (view source) (protected)
Module:String2 (view source) (template editor protected)
Module:TableTools (view source) (protected)
Module:Unsubst (view source) (protected)
Module:Wikitext Parsing (view source) (protected)
Module:Yesno (view source) (protected)

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