Long-term effects of cannabis
||This article's lead section may not adequately summarize its contents. (December 2013)|
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.
Memory and intelligenceEdit
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.
Use of cannabis negatively impacts driving skills and leads to an increased risk of crashing.
Cannabis is the most widely used illicit drug in the Western world, and in the US 10 to 20% of consumers who use cannabis daily become dependent. 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 US by Danovitch et al said that in the US, "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.
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.
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.
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.
In 2014, a review was published in Frontiers in Psychiatry which concluded that "The relationship between cannabis and schizophrenia fulfills many but not all of the standard criteria for causality, including temporality, biological gradient, biological plausibility, experimental evidence, consistency, and coherence," and that this potential relationship "warrants serious consideration from the point of view of public health policy." A 2014 review said that "Because 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:
|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|
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 with psychosis.
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.
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.
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 hypothesisEdit
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 conditions".
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 circulationEdit
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 on 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. Using Marijuana for people with cardiovascular disease constitutes a health risk because it can lead to increased cardiac work, increased catecholamine levels, 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 uncertain."
In 2012 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 uncertain.
A 2013 review which specifically examined the effects of cannabis on the lung concluded "Findings 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 "Our 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 "Our 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 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 THC are not.
Head and neckEdit
A 2011 review of studies in the US 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.
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 pulmonary disease".
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 various sources.
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 effectsEdit
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 endocannabinoid system.
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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