The long-term effects of cannabis have been the subject of ongoing
debate. Because cannabis is illegal in most countries, research
presents a challenge; as such, there remains much to be concluded.
1 Memory and intelligence
3 Mental health
3.1 Acute psychosis
3.3 Depersonalization/derealization symptoms
3.4 Chronic psychosis
3.5 Depressive disorder
3.6 Mania symptoms
3.7 Suicidal behaviour
Gateway drug hypothesis
5 Physical health
5.2 Heart and circulation
5.3.3 Head and neck
5.4 Respiratory effects
5.5 Reproductive and endocrine effects
6 See also
Memory and intelligence
Acute cannabis intoxication has been shown to negatively affect
attention, psychomotor task ability, and short-term memory. A
2016 review found that chronic use of cannabis during adolescence, a
time when the brain is still developing, was correlated in the long
term with lower IQ and chronic cognitive deficits, but it was not
clear if chronic use caused the problems or if "persons who have
poorer cognitive functioning may be more vulnerable to cannabis use
and abuse." A 2013 review had similar findings. A recent large
longitudinal twin study found little evidence that adolescent cannabis
use causes IQ decline. Previous findings of a detrimental effect were
likely due to confounding factors that influence both substance
initiation and IQ.
Cannabis use disorder
Cannabis is the most widely used illicit drug in the Western world,
and although in the United States 10 to 20% of consumers who use
cannabis daily become dependent, it is different from addiction.
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. 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
Cannabis dependence develops in 9% users, significantly less than that
of heroin, cocaine, alcohol, and prescribed anxiolytics, 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.
Historically, the possible connection between psychosis and cannabis
has been long-debated. Recent 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 the causal link is not
yet definitively established. These risks appear to be most acute
in adolescent users.
Cannabis alone is not believed to cause psychosis, although it may be
a contributory factor, particularly when combined with an existing
Although there has been an association noted between cases of acute
psychosis and long-term cannabis use, the precise nature of the
relationship is controversial; evidence suggests that cannabis use may
worsen psychotic symptoms and increase the risk of relapse.
A 2014 meta-analysis found an association between cannabis use and
Cannabis use may precipitate new-onset panic attacks and
depersonalization/derealization symptoms simultaneously.
According to one 2013 review, 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 include genetic liability, childhood trauma and urban
upbringing. Another 2013 review 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 include age of first exposure,
frequency of use, the potency of the cannabis used, and individual
susceptibility. A 2013 review stated that there exists "a strong
association between schizophrenia and cannabis use...". The authors
found that 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.
A 2014 review said 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." In the same year, a review examined psychological
therapy as add-on for people with schizophrenia who are using
Cannabis reduction: adjunct psychological therapy versus treatment as
Results are limited and inconclusive because of the small number and
size of randomized controlled trials 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.
Findings in words
Findings in numbers
Quality of evidence
Frequency of cannabis use
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.
MD 0.1 lower (2.44 lower to 2.24 higher)*
Average score (PANSS) - positive symptoms
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
MD 0.3 lower (2.55 lower to 1.95 higher)*
Quality of life
Average score (WHO QOL questionnaire)
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)*
No study reported any data on outcomes such as relapse, adverse
effects, leaving the study early and information relating to
satisfaction with treatment
* At present the meaning of these scores in day-to-day care is
A 2016 meta-analysis found that cannabis use increases the risk of
psychosis, and that a dose-response relationship exists between the
level of cannabis use and risk of psychosis. The analysis was not able
to establish a causal link. 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.
A 2016 review found that the epidemiologic evidence regarding cannabis
use and psychosis was strong enough "to warrant a public health
message that cannabis use can increase the risk of psychotic
disorders," but also cautioned that additional studies are needed to
determine the size of the effect. A 2016 review said 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.
There is substantial evidence of a statistical association between
cannabis use and the development of schizophrenia or other psychoses,
with the highest risk among the most frequent users.
Use of cannabis in adolescence or earlier is correlated with
developing schizoaffective disorders in adult life, although the
proportion of these cases is small. Susceptibility is most often found
in users with at least one copy of the polymorphic COMT gene.
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. Research has shown
that CBD can safely prevent psychosis in general.
Less attention has been given to the association between cannabis use
and depression, though according to the Australian National Drug &
Alcohol Research Center, it is possible this is because cannabis users
who have depression are less likely to access treatment than those
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. Among cannabis
users of all ages, there may be an increased risk of developing
depression, with heavy users seemingly having a higher risk.
Among those who have been previously diagnosed with bipolar disorder,
cannabis may worsen the occurrence of manic symptoms.
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
In the general population a weak (indirect) association appears to
exist between suicidal behaviour and cannabis consumption in both
psychotic and non-psychotic users, although it remains unclear
whether regular cannabis use increases the risk of suicide.
Cannabis use is a risk factor in suicidality, but suicide attempts are
characterized by many additional risk factors including mood
disorders, stress, personal problems and poor support.
Gateway drug hypothesis
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 harder
A 2013 literature review said that exposure to marijuana 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
Imaging studies suggest that long-term exposure does not lead to
decreases in white matter or grey matter volume, but may lead to
reductions in hippocampal volume. Variations in the methodologies used
lend some uncertainty to this conclusion.
Heart and circulation
The acute effects of marijuana 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
marijuana decreases exercise tolerance. 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.
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
that cannabinoids may have anti-cancer effects.
According to a 2013 literature review, marijuana could be
carcinogenic, but there are methodological limitations in studies
making it difficult to establish a link between marijuana use and
cancer risk. The authors say that bladder cancer does seem to be
linked to habitual marijuana use, and that there may be a risk for
cancers of the head and neck among long-term (more than 20 years)
users. 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
WebMD said that a number of studies had suggested a link
between cannabis use and an increased risk of testicular cancer, but
that the overall risk remained small and that more research is needed
to confirm the findings. According to Gordon and colleagues,
"several recent studies suggest an association between marijuana use
and testicular germ cell tumors".
There have been a limited number of studies that have looked at the
effects of smoking cannabis on the respiratory system. Chronic
heavy marijuana smoking is associated with coughing, production of
sputum, wheezing, and other symptoms of chronic bronchitis.
Regular cannabis use has not been shown to cause significant
abnormalities in lung function.
Regular cannabis smokers show pathological changes in lung cells
similar to those that precede the development of lung cancer in
tobacco smokers. 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." 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
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."
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."
Cannabis smoke contains thousands of organic and inorganic chemicals,
including many of the same carcinogens as tobacco smoke. A 2012
special report by the
British Lung Foundation
British Lung Foundation concluded that cannabis
smoking was linked to many adverse effects, including bronchitis and
lung cancer. 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.
Marijuana smoke has been listed on the California Proposition 65
warning list as a carcinogen since 2009, but leaves and pure
Head and neck
A 2011 review of studies in the United States found that although some
supported the hypothesis that cannabis use increased the risk of
getting head and neck cancer, when other factors are accounted for the
majority did not. Gordon and colleagues (2013) said there was a
risk of these cancers associated with marijuana use over a long period
of time. A 2015 review found no association with lifetime cannabis
use and the development of head and neck cancer.
Cannabis sativa from Vienna Dioscurides, 512 AD
A 2013 literature review by Gordon and colleagues concluded that
inhaled marijuana is associated with lung disease, although
Tashkin's 2013 review has found "no clear link to chronic obstructive
Of the various methods of cannabis consumption, smoking is considered
the most harmful; the inhalation of smoke from organic materials can
cause various health problems (e.g., coughing and sputum). Isoprenes
help to modulate and slow down reaction rates, contributing to the
significantly differing qualities of partial combustion products from
Smoking cannabis has been linked to adverse respiratory effects
including: chronic coughing, wheezing, sputum production, and acute
bronchitis. 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 'Hotboxing'.
Reproductive and endocrine effects
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 marijuana during pregnancy and lower birth weights
of their babies.
Cannabis consumption in pregnancy is associated
with restrictions in growth of the fetus, miscarriage, and cognitive
deficits in offspring. 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". A report prepared for the Australian National
Council on Drugs concluded cannabis and other cannabinoids are
contraindicated in pregnancy as it may interact with the
No fatal overdoses associated with cannabis use have been
reported. 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.
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consequences in adolescence: a systematic review". Child Neuropsychol
(Review). 18 (6): 521–49. doi:10.1080/09297049.2011.628309.
Recreational and medical applications
Difference between C. indica and C. sativa
Etymology (cannabis, marijuana)
Religious and spiritual use
List of hemp diseases
List of hemp products
List of hemp products (
Hempcrete • Jewelry • Milk
• Oil • Paper)
Hemp for Victory
Hemp Industries Association
The Emperor Wears No Clothes
Extracts by potency
Cannabis in pregnancy
Effects of cannabis
Adult lifetime use by country
Annual use by country
Bootleggers and Baptists
Legality by country
Legal and medical status
Legal history in the United States
Marijuana Anonymous (MA)
Marijuana Control, Regulation, and Education Act
Marihuana Tax Act of 1937
UK: Return to class B
Uruguay: Law No. 19172
Decriminalization of non-medical use
Rescheduling per the Controlled Substances Act
Cannabis political parties
List of British politicians who have acknowledged cannabis use
List of US politicians who have acknowledged cannabis use
Gonzales v. Raich
Ker v. California
Kyllo v. United States
Kyllo v. United States (thermal imaging)
Leary v. United States
Active metabolites: 8,11-DiOH-THC
Arachidonoyl ethanolamide (AEA; anandamide)
2-Arachidonyl glyceryl ether
2-Arachidonyl glyceryl ether (2-AGE; noladin ether)
N-Arachidonoyl dopamine (NADA)
2-Arachidonoyl lysophosphatidylinositol (2-ALPI)
Arachidonoyl serotonin (AA-5-HT)
O-Arachidonoyl ethanolamine (O-AEA; virodhamine)
Levonantradol (CP 50,5561)
AB-FUBINACA 2-fluorobenzyl isomer
Allosteric CBR ligands
Cannabinoid receptor modulators (cannabinoids by
List of: AM cannabinoids
Designer drugs § Synthetic cannabimimetics
Recreational drug use
nail polish remover
Psilocybin / Psilocin
Atropine and Scopolamine
Legal history of cannabis in the United States
Legality of cannabis
Marijuana Policy Project
Cannabis and religion
Counterculture of the 1960s
Party and play
Poly drug use
Religion and drugs
Sex and drugs
Coca production in Colombia
Opium production in Afghanistan
Rolling meth lab
Illegal drug trade
Date rape drug
Effects of cannabis
Opioid replacement therapy
Fetal alcohol spectrum disorder
Long-term effects of cannabis
of tobacco or other substances
1961 Narcotic Drugs
1971 Psychotropic Substances
1988 Drug Trafficking
Council of the European Union decisions on designer drugs
Drug Policy Alliance
Law Enforcement Action Partnership
Students for Sensible Drug Policy
Transform Drug Policy Foundation
Just Say No
Office of National Drug Control Policy
School district drug policies
Arguments for and against drug prohibition
Capital punishment for drug trafficking
Politics of drug abuse
War on Drugs
Mexican Drug War
Philippine Drug War
Anabolic steroid legality
Psilocybin mushrooms legali