Article about the mental health effects of cannabis use.
- Patterns of cannabis use
- Acute psychological effects of cannabis use
- Chronic psychological effects of cannabis use
- Cannabis dependence
- Cannabis psychosis
- Cannabis and schizophrenia
- Other disorders
- Cognitive impairment
- An amotivational syndrome
- Behavioural effects in adolescence
Cannabis the drug
Cannabis is derived from the female plant of Cannabis sativa. Its primary psychoactive constituent is delta-9-tetrahydrocannabinol (THC). (1) The THC content is highest in the flowering tops of the plant. Marijuana (THC content 0.5–5 per cent) is prepared from the dried flowering tops and leaves of the plant. Hashish (THC content 2–20 per cent) consists of dried cannabis resin and compressed flowers. (1)
Cannabis is usually smoked in a ‘joint', like a tobacco cigarette, or in a water pipe, often mixed with tobacco. Although marijuana and hashish may be eaten, cannabis is usually smoked because this is the most efficient way to achieve the desired level of intoxication. (2)
THC acts on a widely distributed specific receptor in those brain regions involved in cognition, memory, reward, pain perception, and motor coordination. (1) These receptors respond to an endogenous ligand, anandamide, which is considerably less potent and has a shorter duration of action than THC. (1)
Patterns of cannabis use
Cannabis has been tried by many young adults in Europe, the United States, and Australia. (3) Most cannabis users in the United States stop in their middle to late twenties, and very few engage in daily cannabis use over a period of years. (3,4) In the United States and Australian surveys, about 10 per cent of those who ever use cannabis become daily users, and another 20 to 30 per cent use weekly. (3) This pattern of use in developed countries differs from that in traditional cannabis-using countries, such as Egypt and India, where recreational cannabis use is uncommon and heavy cannabis use is confined to small and marginalized groups in the population. (3)
Because of uncertainties about THC content, ‘heavy' cannabis use is usually defined as daily or near-daily use. (5) This pattern of use over years places users at the greatest risk of experiencing adverse psychological consequences. Daily cannabis users are more likely to use alcohol and tobacco regularly and to use amphetamines, hallucinogens, psychostimulants, sedatives, and opioids. (2,3)
Acute psychological effects of cannabis use
Cannabis produces euphoria and relaxation, perceptual alterations (including time distortion, and impaired short-term memory and attention), and intensification of ordinary sensory experiences, such as eating and listening to music. (2) The most common unpleasant psychological effects are anxiety and panic reactions. (2) These may be reported by naive users and they are a common reason for discontinuing use. (2)
Cannabis produces dose-related impairments in cognitive and behavioural functions that may potentially impair driving an automobile or operating machinery. (6)
Chronic psychological effects of cannabis use
For much of the 1970s cannabis was not regarded as a drug of dependence because of the apparent absence of tolerance and withdrawal symptoms, and a lack of persons seeking help to stop their cannabis use. There is now evidence that animals and humans develop tolerance to the effects of THC, (1) with some heavy users experiencing withdrawal symptoms on the abrupt cessation of cannabis use. (7) During the 1980s and 1990s there was an increase in the number of persons in the United States, Australia, and Europe seeking help to stop their cannabis use. (2)
There is clinical and epidemiological evidence that a cannabis-dependence syndrome occurs in heavy chronic users of cannabis who report problems in controlling their cannabis use, but who continue despite experiencing adverse personal and social consequences. (8)
The lifetime prevalence of cannabis abuse and dependence (as defined in DSM-IIIR) in the United States has been estimated at 4.4 per cent of adults. (9) Similar estimates have been obtained in New Zealand and Australia. (2) The risk of becoming dependent on cannabis seems to have more similarities with that for alcohol than with that for nicotine or the opioids, with around 10 per cent of those who ever use cannabis meeting criteria for dependence at some point in their lives. (2,9)
It is not clear how cannabis dependence is best managed. Stephens and Roffman (10) have reported controlled trials of cognitive-behavioural relapse prevention and social support. They found rates of abstinence at 12 months of around only 30 per cent, but the rates of use had substantially declined among those who continued to use cannabis.
High doses of THC have been reported to produce visual and auditory hallucinations, delusional ideas, and thought disorder in normal volunteers. (2) In traditional cannabis-using cultures, such as India, a ‘cannabis psychosis' has been reported in which the symptoms are preceded by heavy cannabis use and remit after abstinence. (11,12)
The existence of a ‘cannabis psychosis' in Western cultures is still a matter for debate. In its favour are case series of ‘cannabis psychoses', and a small number of controlled studies that compare the characteristics of ‘cannabis psychoses' with those of psychoses in individuals who were not using cannabis at the time of hospital admission. (13) Critics of the hypothesis emphasize the fallibility of clinical judgements about aetiology, the poorly specified criteria used in diagnosing these psychoses, the dearth of controlled studies, and the striking variations in the clinical features of ‘cannabis psychoses'. (14)
Cannabis and schizophrenia
There is good clinical and epidemiological evidence of an association between schizophrenia and cannabis use, which suggests that cannabis use can precipitate schizophrenia or exacerbate its symptoms. But this is not the only explanation of the association. Persons with schizophrenia may use cannabis as a form of self-medication, or there may be other variables that explain both; for example, cannabis use is a marker of other psychotogenic drug use, or of vulnerability to schizophrenia. (2)
There is clinical and epidemiological evidence that cannabis use exacerbates the symptoms of schizophrenia in affected individuals. This includes the findings of a number of prospective studies that have controlled for confounding variables. (12) It is also a biologically plausible relationship. Psychotic disorders involve disturbances in the dopamine neurotransmitter systems, since drugs that increase do pamine release produce psychotic symptoms when given in large doses, and neuroleptic drugs that reduce psychotic symptoms also reduce dopamine levels. (12) Cannabinoids, such as THC, increase dopamine release. (1)
There is good prospective evidence from a Swedish conscript study that cannabis use precipitates schizophrenia in persons who are vulnerable because of a personal or family history of this disorder. (15) This hypothesis is consistent with the stress–diathesis model of schizophrenia, (16) in which the likelihood of its developing is the product of stress acting upon a genetic ‘diathesis' to develop schizophrenia.
Although plausible, there is very little direct evidence that genetic vulnerability increases the risk that cannabis users will develop psychosis. McGuire et al. (17) reported that persons with a history of heavy cannabis use who developed a psychosis were 10 times more likely to have a family history of schizophrenia than persons with a psychosis who had not used cannabis. It is difficult to identify a genetic diathesis in the majority of cases of schizophrenia since 81 per cent of persons with schizophrenia will not have a first-degree relative with the disorder, and 63 per cent will not have an affected first- or second-degree relative. (16)
The most contentious issue is whether cannabis use can cause schizophrenia that would not otherwise have occurred. This possibility cannot be excluded, but it is unlikely to account for more than a minority of cases. Most of the 274 Swedish conscripts who developed schizophrenia had not used cannabis, and only 7 per cent, at most, of schizophrenia cases could be attributed to cannabis use. Moreover, the treated incidence of schizophrenia, and particularly of early-onset acute cases, declined (or remained stable) during the 1970s and 1980s (12) when cannabis use increased among young adults in Australia and North America. (3) Although there are complications in interpreting such trends, a large reduction in treated incidence has been observed in a number of countries, while cannabis use has increased. (12)
The fact that cannabis use acutely impairs cognitive functioning has raised the reasonable concern that chronic use may produce chronic cognitive impairment. The available evidence, however, suggests that even the long-term heavy use of cannabis does not produce any severe or grossly debilitating impairment of cognitive function. (18) There is no evidence, for example, that it produces anything comparable to the cognitive impairments found in chronic heavy alcohol drinkers; if it did, it should have been detected by research to date. (2)
However, there is some clinical and experimental evidence that the long-term use of cannabis may produce more subtle cognitive impairment in the higher cognitive functions of memory, attention and organization, and the integration of complex information. (18) The evidence suggests that the longer the period of heavy cannabis use, the more pronounced is the cognitive impairment. (18) None the less, the impairments in performance are subtle, and so it remains to be determined how significant they are for everyday functioning. It is also remains to be investigated whether these impairments can be reversed after an extended period of abstinence from cannabis.
A suspicion that chronic heavy cannabis use may cause gross structural brain damage was raised by a single poorly controlled study using an outmoded method of investigation, which reported that cannabis users had enlarged cerebral ventricles. (19) Since then, a number of better controlled studies using more sophisticated methods of investigation have consistently failed to demonstrate evidence of structural change in the brains of heavy long-term cannabis users. (18) These negative results are consistent with the evidence that any cognitive effects of chronic cannabis use are subtle, and are unlikely to be manifest as gross structural changes in the brain. (18)
An amotivational syndrome
Anecdotal reports that chronic heavy cannabis use impairs motivation and social performance have been described in societies with a long history of cannabis use, such as Egypt, the Caribbean, and elsewhere. (2) Among young American adults who were heavy cannabis users in the early 1970s, there were clinical reports (2) of individuals who became apathetic, withdrawn, lethargic, and unmotivated, apparently as a result of chronic heavy cannabis use. This constellation of symptoms was described as an ‘amotivational syndrome'. As these reports were uncontrolled it was not possible to disentangle the effects of chronic cannabis use from those of pre-existing personality and other psychiatric disorders. (2)
Field studies of chronic heavy cannabis users in societies with a tradition of such use, for example Costa Rica and Jamaica, (2) have produced evidence that has usually been interpreted as failing to demonstrate the existence of the amotivational syndrome. Critics have argued that these studies are unconvincing because the chronic users studied have come from socially marginal groups, so that the cognitive and motivational demands of their everyday lives were insufficient to detect any impairment caused by chronic cannabis use. (20)
The status of the amotivational syndrome remains contentious. Many clinicians find the cases of ‘amotivational syndrome' compelling, while many researchers are more impressed by the largely negative findings of the field and epidemiological studies. However, the possibility has been kept alive by reports that regular cannabis users experience a loss of ambition and impaired school and occupational performance. (2) Some former cannabis users report that impaired occupational performance was a reason for their stopping. (2) Although heavy users who request assistance to give up report impaired motivation as a symptom of cannabis use, a well-defined amotivational syndrome has not been documented. It may be more parsimonious to explain impaired motivation as a symptom of chronic cannabis intoxication. (2)
There are a small number of case reports of cannabis ‘flashbacks', i.e. experiencing symptoms of cannabis intoxication days or weeks after the individual last used cannabis. (21) Because of their rarity and the fact that many affected individuals have also used other drugs, it is difficult to draw any conclusions about the relationship between these symptoms and cannabis use. It is often difficult to decide whether these are rare events that are coincidental with cannabis use, the effects of other drugs that are often taken together with cannabis, rare consequences of cannabis use that only occur at much higher doses than those used recreationally or that require unusual forms of personal vulnerability, or the results of interactions between cannabis and other drugs.
Behavioural effects in adolescence
There has been understandable societal concern about the effects of adolescent cannabis use on school performance, mental health and adjustment, and the use of other more hazardous drugs.
There is a strong cross-sectional association between heavy cannabis use in adolescence and the risk of discontinuing a high-school education and experiencing job instability in young adulthood. (22) However, the strength of this association is reduced in longitudinal studies when adjustments are made for the fact that heavy cannabis users have lower academic aspirations and poorer high-school performance prior to using cannabis than their peers. (22,23)
There is some evidence that heavy cannabis use has adverse effects upon family formation, mental health, and involvement in drug-related crime. (22) In each case, the strong associations in cross-sectional studies are more modest in longitudinal studies after statistically controlling for associations between cannabis use and other pre-existing characteristics which independently predict these adverse outcomes. (23)
A consistent finding in the United States (4,22) has been the regular sequence of initiation into drug use, in which cannabis use has typically preceded involvement with ‘harder' illicit drugs such as stimulants and opioids. The interpretation of this sequence of events remains controversial. The least compelling hypothesis is that cannabis use directly increases the use of later drugs in the sequence. There is better support for two other hypotheses:
- there is a selective recruitment into cannabis use of non-conforming adolescents who have a propensity to use other illicit drugs;
- once recruited to cannabis use, it is the social interaction with drug-using peers and greater access to illicit drug markets that increases the likelihood of using other illicit drugs. (2,23)
The major adverse acute psychological effects of cannabis use are as follows:
- anxiety, dysphoria, panic, and paranoia, especially in naive users
- impairment of attention and memory, psychomotor impairment while intoxicated
- probably an increased risk of accident if an intoxicated person attempts to drive a motor vehicle.
The major psychological effects of daily heavy cannabis use over many years remain uncertain, but probably include the following: (24)
- a cannabis-dependence syndrome that is characterized by an inability to abstain from or control cannabis use
- subtle forms of cognitive impairment that affect attention and memory and which persist while the user remains chronically intoxicated, and may or may not be reversible after prolonged abstinence from cannabis
- impaired educational achievement in adolescents with a history of poor school performance, whose achievement may be limited by the cognitive impairments produced by chronic intoxication with cannabis
- among those who initiate cannabis use in the early teens, a higher risk of progressing to heavy cannabis and other illicit drug use, and becoming dependent on cannabis.
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