Long-term effects of cannabis
The long term effects of cannabis has 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. Studies have investigated both the detrimental and beneficial effects of long-term use of cannabis. The vast majority of this research focuses on those who use cannabis at least once a day. Recent research has investigated whether its long-term effects on adolescents differ from those on adults.
A 2013 literature review said that exposure to marijuana 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".
Data supporting negative effects of cannabis alone are weak.[medical citation needed] Discerning between correlation and causation is an important consideration. Studies exist showing both negative and positive effects, and much is conflicting.[medical citation needed] For instance, studies have associated heavy cannabis use with the development of various mental disorders, while other science points to both an ameliorative effect[medical citation needed] and no relationship whatsoever.[medical citation needed]
- 1 Memory and intelligence
- 2 Reproductive and endocrine effects
- 3 Cannabis dependency
- 4 Mental health
- 5 Behavioral effects
- 6 Cancer
- 7 Gateway drug hypothesis
- 8 Respiratory effects
- 9 See also
- 10 References
Memory and intelligence
|This section may be confusing or unclear to readers. (December 2013)|
Most scientific research leans toward cognitive deficits during intoxication and a residual effect for heavy users. A 2013 literature review said that changes in "attention, psychomotor task ability, and short-term memory" were associated with very recent (12 to 24 hours) marijuana use, available date does not evidence any long-term central nervous system effects. "Any long-term effects of residual drug on the CNS could be influenced by the acute effects of the drug, the susceptibility of the user, or any pre-existing psychiatric disorder."
The strongest evidence regarding cannabis and memory focuses on its non-acute negative effects on short-term and working memory. Evidence also suggests that long-term effects exist, but these appear to be reversible except possibly in very heavy users.
Reproductive and endocrine effects
Cannabis consumption in pregnancy is associated with restrictions in growth of the fetus, miscarriage, and cognitive deficits in offspring. A 2012 systematic review found although it was difficult to draw firm conclusions, there was some evidence that prenatal exposure to certain substances, especially marijuana and cocaine, was 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.
Cannabis is the most widely used illicit drug in the Western world. Marijuana use disorder is defined in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) as a condition requiring treatment. According to a NIDA ranking of the addictiveness 6 substances (cannabis, caffeine, cocaine, alcohol, heroin and nicotine), cannabis ranked least addictive, with caffeine being the second least addictive and nicotine being the most addictive.
Several studies correlate cannabis use with the development of anxiety, psychosis, and depression. Some researchers at least partially attribute the correlation between cannabis use and mental illness to self-medication.[medical citation needed] Indeed, as much as 60% of the mentally ill are suspected to be substance abusers, and many seem to prefer cannabis and alcohol. The suggested increase in psychotic episodes and the development of psychosis is relatively modest, and these occurrences are rare to begin with.[medical citation needed]
A 2007 review of available data by Moore, Zammit and colleagues found a dose-dependent correlation between cannabis use and psychotic illness. They concluded that the heaviest cannabis users are 40% more likely than non-users to suffer a psychotic illness.
The BEACH study (Bettering the Evaluation and Care of Health) conducted by the Australian General Practice Statistics and Classification Centre suggested that "cannabis smokers are more likely to suffer depression, anxiety and psychosis". The report continues that of the number of patients who mentioned cannabis use to their general practitioner, 48% had a psychological condition, including 19% with depression, 9% with psychosis and 6% with anxiety.[unreliable medical source?] The study states that few cannabis users tell their doctors of their use, which could potentially bias the results of the study.[medical citation needed][original research?]
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 2005 meta analysis of available data which evaluated several hypotheses regarding the correlation of cannabis and psychosis found that there is no support for the hypothesis that cannabis can cause cases of psychosis which would not have occurred otherwise, however further study is needed to explore the correlation between cannabis and other types of psychosis patients. Studies have shown that a risk does exist in some individuals with a predisposition to mental illness to develop symptoms of psychosis. The risk was found to be directly related to high dosage and frequency of use, early age of introduction to the drug, and was especially pronounced for those with a predisposition for mental illness. These results have been questioned as being biased by failing to account for medicinal versus recreational usage — critics contend it could be a causal relationship, or it could be that people who are susceptible to mental problems tend to smoke cannabis, or it could be connected to the criminalization of cannabis. Another important question is whether the observed symptoms of mental illness are actually connected to development of a permanent mental disorder; cannabis may trigger latent conditions, or be part of a complex coordination of causes of mental illness, referred to in psychology as the diathesis-stress model. People with developed psychological disorders are known to self-medicate their symptoms with cannabis as well, although one study has claimed that those with a predisposition for psychosis did not show a statistically significant increase in likelihood of cannabis use four years later.
Research based on the Dunedin Multidisciplinary Health and Development Study has found that those who begin regular use of cannabis in early adolescence (from age 15, median 25 days per year by age 18) and also fit a certain genetic profile (specifically, the Val/Val variant of the COMT gene) are five times more likely to develop psychotic illnesses than individuals with differing genotypes, or those who do not use cannabis.
A 2011 paper said that after alcohol and nicotine, cannabis was the substance most abused by people with schizophrenia; whether the condition generally precedes, or postdates substance use is however uncertain, since evidence from studies is limited.
A 2008 Cochrane review said there was insufficient evidence "to say whether using cannabis causes an improvement or a deterioration of the mental health of people with schizophrenia".
A 2009 review said cannabis use during adolescence increases the risk of developing schizophrenia in adulthood due to interference with brain development. In adults with a genetic risk cannabis abuse can cause psychosis or may worsen the progress of schizophrenia. Cannabis use does not appear to be causally related to the incidence of schizophrenia.
As early as 2006, it was hypothesized based on a variety of animal and clinical evidence that cannabidiol (CBD), a cannabinoid present in cannabis, may be an effective atypical antipsychotic in treating schizophrenia and bipolar disorder.
Depressive disorder – Unipolar
Less attention has been given to the association between cannabis use and depression, though it is possible this is because cannabis users who suffer from depression are less likely to access treatment than those suffering from psychosis. Chen and colleagues (2002) re-analyzed the US National Comorbidity Survey (NCS) to examine the relationship between cannabis use and a major depressive episode and discovered that the risk of first Major Depressive Episode was moderately associated with the number of occasions of cannabis use and with more advanced stages of cannabis use. Relative to newer users, non-dependent cannabis users had 1.6 times greater risk of MDE. Cannabis dependence was associated with a 3.4 time greater risk of major depression. Grant (1995), using data from the US Longitudinal Alcohol Epidemiologic Survey, showed that a diagnosis of cannabis abuse or dependence within the past year was associated with a 6.4 fold chance of also receiving a diagnosis for major depression in that time.
Depressive disorder – Bipolar
A 2005 literature review of the use of cannabis in mental health patients found that the drug can have very different effects on different patients. Although "no controlled trials of THC have been done in bipolar disorder", there is anecdotal evidence that "for some people marijuana is beneficial" as a treatment for bipolar disorder. The reviewers suggested that randomized studies and standardized administration techniques would be required to create conclusive evidence.[medical citation needed]
The question of suicide and cannabis use is considered by Borges, Walters, and Kessler who examined whether cannabis use heightens the risk of suicide or attempted suicide. Cross-sectional data from the US National Comorbidity Survey indicated that cannabis-dependent individuals were 2.4 times more likely to report a suicide attempt than non-cannabis-dependent individuals, after controlling for socio-demographic factors, psychiatric disorders and other drug use. Beautrais et al. (1999) examined 302 hospitalized cases of suicide attempts and found that 16% screened positive for cannabis abuse or dependence, compared with 2% of a random community sample. After controlling for depression and social disadvantage the study found this translated to a twofold suicide attempt risk for those who used cannabis.
Researchers from Cardiff University School of Medicine analyzed over 30 years' worth of death records on more than 50,000 Swedish military recruits and found cannabis was unlikely to increase a person's suicide risk later on. Dr. Stanley Zammit of the department of psychological medicine stated, "we can pretty much rule out a strong effect of cannabis on long-term risk of suicide whether it's through depression or whatever".
Effects on cognitive decline
Cannabinoids are strong antioxidants and therefore defends cells from β-amyloid, the peptide that causes Alzheimer's disease. Some studies have found that cannabis has no effect on ageing-related cognitive decline while others suggest that it slows cognitive decline through its antioxidant effect. The cannabinoids present in cannabis have been reliably shown to lessen cell damage and death from ischemia, likely due to their antioxidant properties.
Government studies often point to statistical data accumulated by methods like the National Household Survey on Drug Abuse (NHSDA), the Monitoring the Future (MTF) study, and the Arrestee Drug Abuse Monitoring (ADAM) program, which claim lower school averages and higher dropout rates among users than non-users. However, these surveys are usually self-administered and may be anonymous, which greatly reduces their reliability. Additionally, while they establish a relationship between cannabis use and academic underperformance they do not determine whether the former causes the latter. The ADAM study is conducted anonymously, but only seeks information from a sample of people who have been arrested for drug-related offenses. Socially deviant behavior may be found more frequently in individuals of the criminal justice system compared to those in the general population, including non-users. In response, independent studies of college students have shown that there was no difference in grade point average, and achievement, between cannabis users and non-users. However, the users surveyed had slightly more difficulty deciding on career goals, and a smaller number were seeking advanced professional degrees.
Psychology studies have been conducted to test differences in motivation between users and non-users. A study in which volunteers completed operant tasks for a wage representing a working world model found no difference between users and non-users.
A longitudinal study of heavy cannabis users from ages 14 to 25 in a Christchurch, New Zealand birth cohort concluded, "The results of the present study suggest that increasing cannabis use in late adolescence and early adulthood is associated with a range of adverse outcomes in later life. High levels of cannabis use are related to poorer educational outcomes, lower income, greater welfare dependence and unemployment and lower relationship and life satisfaction. The findings add to a growing body of knowledge regarding the adverse consequences of heavy cannabis use." However, this study primarily established correlation rather than causality.
A study published in the American Journal of Epidemiology in 2011, concluded that the prevalence of obesity is lower in cannabis users than in nonusers. A 2013 study confirmed this correlation and also found that cannabis users had better insulin resistance, lower insulin levels, and higher high-density lipoprotein ("good cholesterol") levels.
A 2008 study published in the British Journal of Psychiatry showed significant differences in Oxford-Liverpool Inventory of Feelings and Experiences scores between three groups: The first consisted of non-cannabis users, the second of users who tested positive for THC only, and the third consisted of users who tested positive for both THC and CBD. The Δ9-THC only subset scored significantly higher for unusual experiences, while users of both THC and CBD had much lower introvertive anhedonia scores. This suggests that CBD prevents some of the negative behavioral effects of THC.
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".
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.
Cannabis smoke contains thousands of organic and inorganic chemicals, including many of the same carcinogens as tobacco smoke.[unreliable medical source?] A 2012 report by the British Lung Foundation suggested that the risk of developing lung cancer is nearly 20 times higher from smoking typical cannabis cigarettes than from smoking tobacco cigarettes, due to deeper, longer inhalation and the lack of filters. The disparity between cannabis' carcinogen content and its cancer risk is likely due to the antitumor effects of its cannabinoids.[medical citation needed]
Head and neck cancer
Gordon and colleagues (2013) said there was a risk of head and neck cancer associated with marijuana use over a long period of time.
Gateway drug hypothesis
The gateway drug hypothesis asserts that the use of cannabis may ultimately lead to the use of harder drugs. For the most part, it was commonly thought that cannabis gateways to other drugs because of social factors. For example, the criminalization of cannabis in many countries associates its users with organized crime promoting the illegal drug trade.
A study of twins by researchers at Virginia Commonwealth University showed that cannabis use in adolescence strongly predicted later use of multiple drugs. The main causation was tied to shared environmental and genetic vulnerability, but there was some evidence for a causal role of cannabis. A July 2006 study by Ellgren et al. strictly tested lab rats for the biological mechanism of the gateway drug effect. The study administered 6 "teenage" (28 and 49 days old) rats delta-9-tetrahydrocannabinol, and 6 were the control. One week after the first part was completed, catheters were inserted in the jugular vein of all of the adult rats and they were able to self-administer themselves heroin by pushing a lever. The study found that initially both groups behaved the same and began to self-administer heroin frequently, but then stabilized at different levels. The rats that had previously been administered THC consumed about 1.5 times more heroin than those that had not. Because many THC receptors interact with the opioid system, the study surmised that adolescent cannabis use overstimulates and alters the pleasure and reward structures of the brain, thus increasing the already high risk of addiction for people who start to use heroin. However, the rats took up self-administration at the same rate regardless of adolescent THC exposure, and observed levels of "drug-seeking behavior" were also the same. Psychopharmacologist Ian Stolerman, from King's College London, finds the biological cannabis gateway drug effect "somewhat preliminary", and states "it's too early to say there's a consensus, but a small number of studies like this suggest that there is a physiological basis for this effect." Other drugs, he notes, such as cocaine and amphetamines are involved in another brain pathway called the dopaminergic system. Cells in that system also interact with THC receptors and could be modified by cannabis exposure. Cannabinoid receptors are 10 times more prevalent in the brain than opioid receptors. According to Dr. Hurd, one of the study leaders, two other drugs that also stimulate opioid cells, and could therefore also feasibly cause a gateway effect, are nicotine and alcohol.
However, a December 2006 study by the American Psychiatric Association challenges these findings. A 12 year study on 214 boys from ages 10–12 showed that adolescents who used cannabis prior to using other drugs, including alcohol and tobacco, were no more likely to develop a substance abuse disorder than other subjects in the study. "This evidence supports what's known as the common liability model… states the likelihood that someone will transition to the use of illegal drugs is determined not by the preceding use of a particular drug, but instead by the user's individual tendencies and environmental circumstances", investigators stated in a press release. They added, "The emphasis on the drugs themselves, rather than other, more important factors that shape a person's behavior, has been detrimental to drug policy and prevention programs."
Models used in a 2002 study by RAND cast doubt on the gateway effect and show "that the marijuana gateway effect is not the best explanation for the link between marijuana use and the use of harder drugs", as noted by Andrew Morral, associate director of RAND's Public Safety and Justice unit and lead author of the study.
According to a 2013 literature review by Gordon and colleagues, inhaled marijuana is associated with lung 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.
A 2012 literature review by the British Lung Foundation identified cannabis smoke as a carcinogen and also found awareness of the danger was low compared with the high awareness of the dangers of smoking tobacco particularly among younger users. Other observations include increased risk from each cigarette due to drawing in large puffs of smoke and holding them; lack of research on the effect of cannabis smoke alone due to common mixing of cannabis and tobacco and frequent cigarette smoking by cannabis users; low rate of addiction compared to tobacco; and episodic nature of cannabis use compared to steady frequent smoking of tobacco.
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