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Cannabis use & Psychosis :-

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Cannabis is a genus of flowering plant that includes one or more species. The plant is believed to have originated in the mountainous regions just north-west of the Himalayas in India. Cannabis sativa male plants show evidence of selection for traits that enhance fiber production and seed-oil (for fuel) but the female plant produce seeds (for food) and flower buds that can be used as a psychoactive substance because it has higher levels of the psychoactive delta-9-tetrahydrocannabinol (THC), whereas Cannabis indica was primarily selected for drug production and has relatively higher levels of cannabidiol (CBD) and Cannabinol (CBN) than THC.

David Blunkett announced in 2001 that cannabis would be transferred from Class B of the Act to Class C, removing the threat of arrest for possession. This action was supported at the time by David Cameron, who is now leader of the Conservative Party. Arrest would still be possible for distribution, however[.The change was designed to enable police forces to concentrate resources on other (more serious) offences, including those involving 'harder drugs'. The Government has argued that the reclassification of cannabis has had the desired effect, with arrests for cannabis possession falling by one third in the first year since reclassification, saving an estimated 199,000 police hours. The Serious Organised Crime and Police Act 2005, which was enacted on 1 January 2006, abolished the concept of an 'Arrestable Offence' by making all offences arrestable. This has meant that people may once again be arrested for possession of cannabis in the United Kingdom.

•I n 1998, 11% of 11-15 year olds in England had used drugs in the last year. The prevalence of drug use increased sharply with age: only 1% of 11 year olds had used drugs in the last year compared with over a quarter (28%) of 15 year olds.

• Among 11-15 year olds, cannabis was the most frequently reported illicit drug used in the last year, used by one in ten (10%). Two percent had used amphetamines, 2% poppers, 1% cocaine, fewer than 0.5% had used crack or heroin in the last year.

• 7% of 11-15 year olds in England had used drugs in the last month.

• In 1999, 12% of 11-15 year olds had used drugs in the last year, compared with 11% in 1998, although this difference is not statistically significant.

• In 1998, among those aged 16-24 years, in England and Wales, 29% had used drugs in the last year and 19% in the last month.

• Among those aged 16-24 years, 27% had used cannabis in the last year, 10% amphetamines, 5% ecstasy, 5% poppers, 3% cocaine and fewer than 0.5% crack or heroin.

• The proportion among those aged 16-24 who had used drugs in the last year was at the same level in 1994, 1996 and 1998 (29%). Between 1994 and 1998 the only drug to show a significant increase in misuse was cocaine; this increased from 1% in 1994 to 3% in 1998 for use in the last year.

A US organisation,, defines the problems of cannabis as follows:

“ … if cannabis controls our lives and our thinking, and if our desires centre around marijuana - scoring it, dealing it, and finding ways to stay high so that we lose interest in all else.”

Traditional herbal cannabis contains between 1 and 15 per cent of the main psycho-active ingredient, THC. Some of the newer strains, including skunk, contain up to 20 per cent, so can be 3 times as strong as traditional cannabis. It works more quickly, and can produce hallucinations with profound relaxation and elation – along with nervousness, anxiety attacks, projectile vomiting and a strong desire to eat. They may be used by some as a substitute for Ecstasy or LSD.

Legally, these strains remain calssified Class C drugs. While there is little research so far, it is likely that these stronger strains carry a higher risk of causing mental illness. A major study currently underway, has already reported problems with concentration and short-term memory in users of stronger types of cannabis.

Recent research in Europe, and in the UK, has suggested that people who have a family background of mental illness – so probably have a genetic vulnerability anyway - are more likely to develop schizophrenia if they use cannabis as well.

Recent research in Denmark suggests that yes, there is. It is a short-lived psychotic disorder that seems to be brought on by cannabis use but which subsides fairly quickly once the individual has stopped using it. It's quite unusual though – in the whole of Denmark they found only around 100 new cases per year.

However, they also found that:

• Three quarters had a different psychotic disorder diagnosed within the next year

• Nearly half still had a psychotic disorder 3 years later.

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So, it also seems probable that nearly half of those diagnosed as having cannabis psychosis are actually showing the first signs of a more long-lasting psychotic disorder, such as schizophrenia. It may be this group of people who are particularly vulnerable to the effects of cannabis, and so should probably avoid it in the future.

Three major studies followed large numbers of people over several years, and showed that those people who use cannabis have a higher than average risk of developing schizophrenia. If you start smoking it before the age of 15, you are 4 times more likely to develop a psychotic disorder by the time you are 26. They found no evidence of self-medication. It seemed that, the more cannabis someone used, the more likely they were to develop symptoms.

Why should teenagers be particularly vulnerable to the use of cannabis? No one knows for certain, but it may be something to do with brain development. The brain is still developing in the teenage years – up to the age of around 20, in fact. A massive process of ‘neural pruning’ is going on. This is rather like streamlining a tangled jumble of circuits so they can work more effectively. Any experience, or substance, that affects this process has the potential to produce long-term psychological effects.

A study following 1600 Australian school-children, aged 14 to 15 for seven years, found that while children who use cannabis regularly have a significantly higher risk of depression, the opposite was not the case - children who already suffered from depression were not more likely than anyone else to use cannabis. However, adolescents who used cannabis daily were five times more likely to develop depression and anxiety in later life.

There is growing evidence that people with serious mental illness, including depression and psychosis, are more likely to use cannabis or have used it for long periods of time in the past. Regular use of the drug has appeared to double the risk of developing a psychotic episode or long-term schizophrenia. However, does cannabis cause depression and schizophrenia or do people with these disorders use it as a medication?

There are about 60 compounds and 400 chemicals in an average cannabis plant. The four main compounds are called delta-9-tetrahydrocannabinol (delta-9-THC), cannabidiol, delta-8-tetrahydrocannabinol and cannabinol. Apart from cannabidiol (CBD), these compounds are psychoactive, the strongest one being delta-9-tetrahydrocannabinol. The stronger varieties of the plant contain little cannabidiol (CBD), whilst the delta-9-THC content is a lot higher.

When cannabis is smoked, its compounds rapidly enters the bloodstream and are transported directly to the brain and other parts of the body. The feeling of being ‘stoned’ or ‘high’ is caused mainly by the delta-9-THC binding to cannabinoid receptors in the brain. A receptor is a site on brain cell where certain substances can stick or “bind” for a while. If this happens, it has an effect on the cell and the nerve impulses it produces. Curiously, there are also cannabis-like substances produced naturally by the brain itself – these are called endocannabinoids.

Two million people in the UK smoke cannabis. Half of all 16 to 29 year olds have tried it at least once. In spite of government warnings about health risks, many people see it as a harmless substance that helps you to relax and ‘chill’ – a drug that, unlike alcohol and cigarettes, might even be good for your physical and mental health. On the other hand, recent research has suggested that it can be a major cause of psychotic illnesses in those who are genetically vulnerable.

Two million people in the UK smoke cannabis. Half of all 16 to 29 year olds have tried it at least once. In spite of government warnings about health risks, many people see it as a harmless substance that helps you to relax and ‘chill’ – a drug that, unlike alcohol and cigarettes, might even be good for your physical and mental health. On the other hand, recent research has suggested that it can be a major cause of psychotic illnesses in those who are genetically vulnerable.

Biochemical Effects :-

The most prevalent psychoactive substance in cannabis is delta-9-tetrahydrocannabinol (commonly called [ch916]9-THC, or simply THC). In the past two decades, the average content of THC in marijuana sold in North America has increased from about 1% to 3-4% or more. Carefully selected and cloned plants can yield as much as 15% THC. [2] Another psychoactive cannabinoid present in Cannabis sativa is Tetrahydrocannabivarin (THCV), but it is only found in small amounts.

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One of the primary effects of marijuana in humans is the disruption of short-term memory, which is consistent with the abundance of CB1 receptors on the hippocampus. The effects of THC at these receptor sites produce what is called a 'temporary hippocampal lesion.' [3] As a result of this lesion, several neurotransmitters like acetylcholine, norepinephrine, and glutamate, are released that trigger a major decrease in neuronal activity in the hippocampus and its inputs. The total duration of cannabis intoxication when smoked is about 1 to 4 hours.

Preliminary research, published in the April 2006 issue of the Journal of Consulting and Clinical Psychology, indicates that cannabis addiction can be offset by a combination of cognitive-behavioral therapy and motivational incentives. Participants in the study (previously diagnosed with marijuana dependence) received either vouchers as incentives to stay drug free, cognitive-behavioral therapy, or both over a 14-week period. At the end of 3 months, 43 percent of those who received both treatments were no longer using marijuana, compared with 40 percent of the voucher group, and 30 percent of the therapy group. At the end of a 12-month follow-up, 37 percent of those who got both treatments remained abstinent, compared with 17 percent of the voucher group, and 23 percent of the therapy group. [8]

Behavioral effects

It is sometimes observed, and generally stereotyped, that systematic changes in a person’s lifestyle, ambitions, motivation, and personality happen when a young person starts smoking marijuana. In fact, in many situations when people are asked to describe the personality traits of a marijuana user, they will most likely portray a person of apathy or loss of effectiveness: a person with diminished capacity or willingness to carry out complex long-term plans, endure frustration, concentrate for long periods, follow routines, or even successfully master new material. [16]

The term 'amotivational syndrome' is often applied to young individuals who have changed from clean, assertive, upwardly mobile achievers into the sort of person just described, with marijuana as the culprit. The syndrome, like other correlational phenomena, raises a chicken-and-egg type problem; marijuana use can just as easily be seen as the result of such a personality shift as it can be the cause of it. Regardless, studies to raise this and other questions, like the prevalence of such 'syndrome' in the population, and proving a biological or psychological connection of the 'syndrome' to substance use, have not happened. Instead, a political tug of war has ensued with each point of view claiming their own scientific research as evidence.

Government studies often point to statistical data accumulated by methods like the National Household Survey on Drug Abuse (NHSDA), the Monitoring the Future study (MTF), and the Arrestee Drug Abuse Monitoring (ADAM) program, which claim lower school averages and higher dropout rates among users than nonusers, even though these differences are very small and may be exaggerated by the stigma attached to students who use the drug. However, the major contributor to a lack of credibility in these studies, is that in many cases, like with NHSDA and MTF, these surveys are usually self-administered and may or may not be anonymous. The likeliness of over or under representing data definitely undermines the effectiveness of these instruments. [4] The MTF study is conducted anonymously, but only seeks information from a sample of people who have been arrested for drug-related offenses. Clearly, the case can easily be made that socially deviant behavior will 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 marijuana users and nonusers, but the users had a little more difficulty deciding on career goals, and a smaller number were seeking advanced professional degrees. [17] Laboratory studies of the relationship between motivation and marijuana outside of the classroom, where volunteers worked on operant tasks for a wage representing a working world model, also fail to distinguish a noticeable difference between users and non users. [18]

Co-occurrence of mental illness

Scientific studies have correlated a change in mental health with cannabis use for young people. Particularly, studies have shown that a risk does exist in some individuals to develop symptoms of psychosis [22] and anxiety [23]. 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: [24] It could be a causal relationship,

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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 as the diathesis-stress model in psychology. People with developed psychological disorders often tend to self-medicate their symptoms with cannabis as well, although one study has claimed that those with a predisposition for psychosis did not show an increase in likelihood of cannabis use four years later. There has not currently been enough scientific study of the drug's effects to come to a definite conclusion.

Similarity of symptoms

There is a classification of psychosis within the DSM-IV called 'cannabis psychosis' which is very rare. In susceptible individuals, ingestion of sufficient quantities of the drug can trigger an acute psychotic event. It should be noted that the extent of a subject's experience with cannabis is a strong factor determining susceptibility.

A Yale research study notes that subjects administered pure delta-9-THC induced transient symptoms which resemble those of schizophrenia 'ranging from suspiciousness and delusions to impairments in memory and attention'. There were no side effects in the study participants one, three, and six months after the study.

Correlation studies

Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It might be a component cause, part of a complex constellation of factors leading to psychosis, or it might be a correlation without forward causality at all. Similar correlations can be drawn between cannabis usage and cancer, for instance, because those who suffer from cancer may be more likely to use cannabis due to the pain relief it provides.

A review of the evidence by Louise Arsenault, et al in 2004 reports that on an individual level, cannabis use confers an overall twofold increase in the relative risk of later schizophrenia. This same research also states that 'There is little dispute that cannabis intoxication can lead to acute transient psychotic episodes in some individuals'. The study synthesizes the results of several studies into a statistical model. [26]

A landmark study, in 1987, of 50,000 Swedish Army conscripts, found that those who admitted at age 18 to having taken cannabis on more than 50 occasions, were six times more likely to develop schizophrenia in the following 15 years. In fact, psychosis cases were restricted to patients requiring a hospital admission. These findings have not been replicated in another population based sample. [27] As the study did not control for symptoms preexisting onset of cannabis use, the study does not resolve the correlation versus causality question but has fueled a major debate within the scientific community.

A 2005 study found that 'the onset of schizotypal symptoms generally precedes the onset of cannabis use. The findings do not support a causal link between cannabis use and schizotypal traits'. [28] It should be noted that a schizotypal personality disorder is a personality disorder different from schizophrenia, which is a mood disorder.

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. [29] [30] The study was noted for it having controlled for preexisting symptoms, but is open to the criticism that it cannot control for late adolescent onset of psychotic illness. Also, the study was on a cohort population, so there is no way to correlate a change in the rate of adolescent use with a change in the rate of incidence of schizophenia in the study population. These points undermine its value in resolving the correlation versus causality question.

This report reviews evidence on two hypotheses about the relationship between cannabis use and psychosis. The first hypothesis is that heavy cannabis use may cause a 'cannabis psychosis' - a psychosis that would not occur in the absence of cannabis use, the symptoms of which are preceded by heavy cannabis use and remit after abstinence. The second hypothesis is that cannabis use may precipitate schizophrenia, or exacerbate its symptoms.

Evaluation of these hypotheses requires evidence of an association between cannabis use and psychosis, that is unlikely to be due to chance, in which cannabis use precedes psychosis, and in which we can exclude the hypothesis that the relationship is due to other factors, such a

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Evaluation of these hypotheses requires evidence of an association between cannabis use and psychosis, that is unlikely to be due to chance, in which cannabis use precedes psychosis, and in which we can exclude the hypothesis that the relationship is due to other factors, such as, other drug use, or a personal vulnerability to psychosis.

There is some clinical support for the first hypothesis. If these disorders exist they seem to be rare, because they require very high doses of THC, the prolonged use of highly potent forms of cannabis, or a pre-existing (but as yet unspecified) vulnerability. There is more support for the second hypothesis in that a large prospective study has shown a linear relationship between the frequency with which cannabis had been used by age 18 and the risks over the subsequent 15 years of a diagnosis of schizophrenia. It is still unclear whether this means that cannabis use precipitates schizophrenia, whether it is a form of 'self-medication', or whether the association is due to the use of other drugs, such as amphetamines, which heavy cannabis users are more likely to use. There is better evidence that cannabis use can exacerbate the symptoms of schizophrenia. Mental health services should identify patients with schizophrenia who use alcohol, cannabis and other drugs and advise them to abstain or to greatly reduce their drug use.



There are good reasons to be concerned about the possibility that cannabis use may be a cause of psychotic disorders. Psychoses are serious and disabling disorders [1]. Cannabis is widely used by young Australians during late adolescence[2], and high doses of tetrahydrocannabinol -the psychoactive substance in cannabis - have been reported to produce psychotic symptoms, such as, visual and auditory hallucinations, delusional ideas, and thought disorder, in normal volunteers [3).

There are a number of hypotheses about the relationship between cannabis use and psychosis that need to be distinguished [4]. The strongest hypothesis is that heavy cannabis use causes a specific 'cannabis psychosis'. This assumes that these psychoses would not occur in the absence of cannabis use, and that the causal role of cannabis use can be inferred from the symptoms and their relationship to cannabis us; e.g. they are preceded by heavy cannabis use and remit after abstinence.

A weaker type of hypothesis is that cannabis use may precipitate an episode of schizophrenia. This hypothesis assumes that cannabis use is one factor among many others (including genetic predisposition and other unknown causes) that bring about schizophrenia It does not assume that the role of cannabis can be inferred from the symptoms of the disorder, or that it will remit when cannabis use ceases.

Finally, if cannabis use can precipitate schizophrenia it is also likely that it can exacerbate the symptoms of the disorder. It may exacerbate symptoms of schizophrenia (even if it is not a precipitant of the disorder) if it reduces compliance with treatment, or interferes with the effects of the drugs used to treat it.


In order to infer that cannabis use is a cause of psychosis in any of these ways we need evidence: that there is an association between cannabis use and psychosis; that chance is an unlikely explanation of the association; that cannabis use preceded the psychosis; and that plausible alternative explanations of the association can be excluded [5).

Evidence that cannabis use and psychosis are associated and that chance is an unlikely explanation of the association are readily available. There are a smaller number of prospective studies that show cannabis use precedes psychoses. The most difficult task is excluding the hypothesis that the relationship between cannabis use and psychosis is due to other factors (e.g. other drug use, or a genetic predisposition to develop schizophrenia and use cannabis).

Since ethical reasons preclude experimental humans studies and there are no suitable animal models, epidemiological methods must be used to rule out common causal hypotheses. These estimate the relationship between cannabis use and the risk of developing a psychosis after adjusting for variables that may affect the risk (e.g. personal characteristics prior to using cannabis, family history of psychotic illness, and other drug use). If the relationship persists after statistical adjustment, then we can be confident that it is not due to the variables for which statistical adjustment has been made.

'A Cannabis Psychosis'

There are a substantial number of case reports of cannabis psychoses [6-18]. These describe individuals who develop psychotic symptoms or disorders after using cannabis.

Chopra and Smith [9], for example, described 200 patients who were admitted to a psychiatric hospital in Calcutta between 1963 and 1968 with psychotic symptoms following the use of cannabis. The most common symptoms 'w

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Chopra and Smith [9], for example, described 200 patients who were admitted to a psychiatric hospital in Calcutta between 1963 and 1968 with psychotic symptoms following the use of cannabis. The most common symptoms 'were sudden onset of confusion, generally associated with delusions, hallucinations (usually visual) and emotional lability... amnesia, disorientation, depersonalisation and paranoid symptoms' (p 24). Most psychoses were preceded by the ingestion of a large dose of cannabis and there was amnesia for the period between ingestion and hospitalisation. They argued that it was unlikely that excessive cannabis use was a sign of pre-existing psychopathology because a third of their cases had no prior psychiatric history, the symptoms were remarkably uniform regardless of prior psychiatric history, and those who used the most potent cannabis preparations experienced psychotic reactions after the shortest period of use.

The findings of Chopra and Smith [9] have received some support from other case series which suggest that large doses of potent cannabis products can be followed by a 'toxic' psychotic disorder with 'organic' features of amnesia and confusion. These disorders have been reported from a variety of different places including: the Caribbean [19-20], India [9], New Zealand [11], Scotland [18], South Africa [14], Sweden [8, 17, 21], the United Kingdom [6-7, 13] and the United States [15-16].

These disorders have been attributed to cannabis use for combinations of the following reasons: the onset of the symptoms followed closely upon ingestion of large quantities of cannabis; the affected individuals often exhibited 'organic' symptoms, such as, confusion, disorientation and amnesia; some had no reported personal or family history of psychoses prior to using cannabis; their symptoms rapidly remitted after a period of enforced abstinence from cannabis use, usually within several days to several weeks; recovery was usually complete with the person having no residual psychotic symptoms of the type often seen in persons with schizophrenia; and if the disorder recurred it was after the individual starting using cannabis.

Some commentators have been critical of this evidence [4, 22-25]. They criticise the poor quality of information on cannabis use and its relationship to the onset of psychosis, and the person's premorbid adjustment and their family history of psychosis. They also emphasise the wide variety of clinical pictures of 'cannabis psychoses' reported by different observers. These weaknesses impair the evidential value of these case series.

Controlled Studies

A small number of controlled studies have been conducted over the past 20 years. Some case-control studies have either compared persons with 'cannabis psychoses' with persons who have schizophrenia, or compared psychoses occurring in persons who do and do not have biochemical evidence of cannabis use prior to presenting for treatment. Their results have been mixed.

Thacore and Shuckla [26], for example, reported a case control study that compared 25 cases who had a 'cannabis psychosis' with 25 controls who were diagnosed as having paranoid schizophrenia with no history of cannabis use. Their cases had a paranoid psychosis resembling schizophrenia in which there was a clear temporal relationship between the prolonged use of cannabis and the development of psychosis on more than two occasions. Patients with the 'cannabis psychosis' displayed more odd and bizarre behaviour, violence, panic, and insight, and less evidence of thought disorder, than those with schizophrenia. They also responded swiftly to neuroleptic drugs and recovered completely.

Rottanburg et at [27] conducted a similar study in which 20 psychotic patients with cannabinoids in their urine were compared with 20 psychotic patients who did not have cannabinoids in their urine. Psychotic patients with cannabinoids in their urine had more symptoms of hypomania and agitation, and less auditory hallucinations, flattening of affect, incoherent speech and hysteria than controls. They also showed marked improvements in symptoms by the end of a week, whereas there was no change in the patients whose urine did not contain cannabinoids.

Chaudry et al [28] reported a comparison of 15 psychotic 'bhang' users with 10 bhang users without psychosis. They found that their cases were more likely to have a history of chronic cannabis use and past psychotic episodes. They also were more likely to be uncooperative and to have symptoms of excitement, hostility, grandiosity, hallucinations, disorientation and unusual thought content

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All cases remitted within 5 days and had no residual psychotic symptoms.

Mathers et al [29] reported a study of patients presenting to two London hospitals whose urine was analysed for the presence of cannabinoids. They found a relationship between the presence of cannabinoids in urine and having a psychotic diagnosis. Rolfe et al [30] reported a similar association between urinary cannabinoids and psychosis in 234 patients admitted to a Gambian psychiatric unit.

In contrast to these positive findings, a number of controlled studies have not found such a clear association. Imade and Ebie [31], compared the symptoms of 70 patients with cannabis-induced functional psychoses, 163 patients with schizophrenia, and 39 patients with mania. They reported that there were no symptoms that were unique to cannabis psychosis, and none that enabled them to distinguish a 'cannabis psychosis' from schizophrenia.

Thornicroft et al [32] compared 45 cases who had a psychosis and a urine positive for cannabinoids with 45 controls who had a psychosis but either had a urine negative for cannabinoids or reported no cannabis use. They found very few demographic or clinical differences between the groups.

McGuire et al [33-34] compared 23 cases of psychoses occurring in persons whose urines were positive for cannabinoids with 46 psychotic patients whose urines were negative for cannabinoids or who reported no cannabis use. The two groups did not differ in their psychiatric histories or symptoms profile, as assessed by 'blind' ratings of clinical files using the PSE (McGuire et al [33]). The cases, however, were more likely to have a family history of schizophrenia.

Two studies have examined the relationship between cannabis use and psychotic symptoms in the general population. Tien and Anthony [35] used data from the Epidemiologic Catchment Area study to compare the drug use of individuals who reported 'psychotic experiences' during a twelve month period. These psychotic experiences comprised 4 types of hallucinations and seven types of delusional belief. They compared 477 cases who reported one or more psychotic symptoms in the one year follow-up with 1818 controls who did not. Cases and controls were matched for age and social and demographic characteristics. Daily cannabis use was found to double the risk of reporting psychotic symptoms (after statistical adjustment for alcohol use and psychiatric diagnoses at baseline).

Thomas [36] reported the prevalence of psychotic symptoms among cannabis users in a random sample of people drawn from the electoral role of a large city in the North Island of New Zealand. One in seven (14%) cannabis users reported 'strange, unpleasant experiences such as hearing voices or becoming convinced that someone is trying to harm you or that you are being persecuted' after using cannabis.

Two studies have reported no difference in the prevalence of psychotic disorders in chronic cannabis users and controls. Beaubruhn and Knight [37] compared the rate of psychoses in 30 chronic daily Jamaican cannabis users with that in 30 non-cannabis using controls. Stefanis et al [38] reported a study of 47 chronic cannabis users in Greece and 40 controls. The small number of cases and the low prevalence of psychosis in the population make these negative findings unconvincing.

Overall Evaluation

The existence of a 'cannabis psychosis' 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 (e.g. [39]). Critics of the hypothesis emphasise 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' [24).

It is a plausible hypothesis that high doses of cannabis can produce psychotic symptoms. There is no compelling evidence, however, that there is a specific clinical syndrome that is identifiable as a 'cannabis psychosis'. The clinical symptoms reported by different observers have been mixed. These symptoms seem to rapidly remit, with full recovery, after abstinence from cannabis.

If cannabis-induced psychoses exist, they are rare or they only rarely receive medical intervention in Western societies (e.g. [40-41]). The total number of cases of putative 'cannabis psychoses' in the 12 case series reviewed was 397 and 200 of these came from a single series (Chopra and Smith [9]) collected over 6 years from a large geographic area in which heavy cannabis use was endemic (e-g. [9]).

There are a number of likely reasons for the rarity of 'cannabis psychoses' in Western societies. One is that they occur after the use of large doses of THC, or long periods of sustained heavy use. Although lifetime use of cannabis has incre

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One is that they occur after the use of large doses of THC, or long periods of sustained heavy use. Although lifetime use of cannabis has increased in Western societies, the pattern of heavy cannabis use remains rare [2]. A second possibility (discussed below) is that cannabis psychoses only occur in persons who have a pre-existing vulnerability to psychotic disorder A third possibility is that heavy sustained use and vulnerability are both required.



Clinical studies

In case-control studies of cannabis and other psychoactive drug use among schizophrenic patients [42-43], schizophrenic patients are more likely to have used psychotomimetic drugs such as amphetamines, cocaine, and hallucinogens than other psychiatric patients [42, 44-45] or normal controls [46, 30]. The prevalence of substance use in schizophrenic patients varies between studies but it is generally higher than comparable figures in the general population [47). Rates of alcohol and stimulant use among schizophrenic patients also appear to have increased over the past several decades [48]. These variations are probably due to differences in the sampling of patients, with younger samples of newly incident cases reporting higher rates than older samples of chronic cases. Studies have also differed in the criteria for diagnosing schizophrenia and in way that substance use has been assessed [49].

Alcohol use abuse and dependence are probably more common in the schizophrenic population than in the general population [42,48-49]. The findings on cannabis use have been more mixed (e.g. [29, 42, 44, 49, 50]. Generally, cannabis is the next most commonly used drug after alcohol and tobacco, although it is usually used with alcohol [49, 52].

Correlates of cannabis use in schizophrenia

The controlled clinical studies disagree about the correlates of substance abuse in schizophrenia. Most have found that young males are over-represented among cannabis users (e.g. [49, 53-54]), as in the general community [55]. In some studies, substance abusers have been reported to have an earlier onset of psychotic symptoms, a better premorbid adjustment, more episodes of illness, and more hallucinations (e.g. [44, 46, 50, 54, 56]). But other well controlled studies have failed to replicate some or all of these findings [53, 57-58].

Population studies

Surveys of psychiatric disorders in the community have reported higher rates of substance abuse disorders among persons with schizophrenia The ECA study found an association between schizophrenia and alcohol and drug abuse and dependence [55]. Nearly half of the patients identified as schizophrenic in the ECA study had a diagnosis of substance abuse or dependence (34% for an alcohol disorder and 28% for another drug disorder) [59]. These rates were higher than the rates in general population, namely, 14% for alcohol disorders [60] and 6% for drug abuse [55]. The ECA findings have also been replicated in Edmonton, Alberta [61].

More recently, Cuffel et al [53] have reported on patterns of substance abuse among 231 cases of schizophrenia identified in the ECA study. They found that the most commonly used substances were: alcohol (37%) and cannabis (23%), followed by stimulants and hallucinogens (13%), narcotics (10%) and sedatives (8%). Multiple drug use was common and the most common combinations of drugs was alcohol and cannabis (31%).

Explanations of the Association

One possible explanation of the association is that cannabis use precipitates schizophrenic disorders in vulnerable persons (e.g. [62]). Proponents of this hypothesis cite the earlier age of onset of psychotic symptoms among cannabis users (with their drug use typically preceding the onset of symptoms), their better premorbid adjustment their fewer negative symptoms, and their better treatment response (e.g. [42, 44, 63]).

Another suggestion is that the associations between cannabis use and an early onset and good prognosis are spurious. Arndt et al [56] argue that schizophrenics with a better premorbid personality are more likely to be exposed to illicit drug use among peers than persons with schizophrenia who are socially withdrawn. There is also evidence (e.g. [1, 64]) that persons with acute onset psychoses usually have a better premorbid adjustment and a better prognosis. They also have greater opportunities to use cannabis and other illicit drugs than persons who have an insidious onset and are socially withdrawn.

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A third possibility is that cannabis use is a consequence (rather than a cause) of schizophrenia. For example, cannabis and other drugs may be used to medicate the unpleasant symptoms of schizophrenia, such as, depression, anxiety, lethargy, and anhedonia, or the unpleasant side effects of the neuroleptic drugs that are often used to treat the disorder [44].

Precipitation of Schizophrenia

The most convincing evidence that cannabis use may precipitate schizophrenia comes from a 15-year prospective study of cannabis use and schizophrenia in 50,465 Swedish conscripts [65]. This study investigated the relationship between self-reported cannabis use at age 18 and the risk of receiving a diagnosis of schizophrenia in the subsequent 15 years, as indicated by inclusion in the Swedish psychiatric case register.

Andreasson et al [67] found that the relative risk of receiving a diagnosis of schizophrenia was 2.4 times higher among those who had tried cannabis by age 18 compared to those who had not. There was also a dose-response relationship between a diagnosis of schizophrenia and the number of times that cannabis had been used by age 18. Compared to those who had not used cannabis, the risk of developing schizophrenia was 1.3 times higher for those who had used cannabis one to ten times, 3 times higher for those who had used cannabis between one and fifty times, and 6 times higher for those who had used cannabis more than fifty times.

These risks were substantially reduced after statistical adjustment for variables that were independently related to the risk of developing schizophrenia, namely, having a psychiatric diagnosis at conscription, and having parents who had divorced (as a proxy for parental psychiatric disorder). Nevertheless, after adjustment, the dose response relationship remained statistically significant The adjusted relative risk of a diagnosis of schizophrenia for those who had smoked cannabis from one to ten times was 1.5 times, and that for those who had used ten or more times was 2.3 times, the risk for those who had never used cannabis. Andreasson et al [65] and Allebeck [62] have concluded that cannabis use precipitates schizophrenia in vulnerable individuals.

A number of alternative explanations of the Swedish finding have been offered by other authors. First, there was a large temporal gap between self-reported cannabis use at age 18 and the development of schizophrenia over the next 15 years or so [66-67]. Because the diagnosis of schizophrenia was based upon a case register there was no data on how many individuals used cannabis up until the time that their schizophrenia was diagnosed. Andreasson et al [65] argued that cannabis use persisted because cannabis use at age 18 was also strongly related to the risk of attracting a diagnosis of drug abuse.

A second possibility is that schizophrenia was misdiagnosed. On this hypothesis, the excess rate of 'schizophrenia' among the heavy cannabis users was due to cannabis-induced psychoses which were mistakenly diagnosed as schizophrenia [66, 67-8] examined 21 cases of schizophrenia among conscripts in the case register (8 of whom had used cannabis and 13 of whom had not). They found that 80% of these cases met the DSM-III requirement that the symptoms had been present for at least six months, thereby excluding the diagnoses of transient drug-induced psychotic symptoms.

A third hypothesis is that the relationship between cannabis use and schizophrenia is due to the use of other drugs. Longitudinal studies of illicit drag use indicate that persons who had used cannabis a large number of times by late adolescence were at increased risk of subsequently using other illicit drugs, such as, amphetamine [66, 69]. Amphetamines which can produce an acute paranoid psychosis [70-72] were the major illicit drugs of abuse in Sweden during the study period [73-75]. On this hypothesis, amphetamine-induced psychoses may explain the spurious association between cannabis use and schizophrenia. The evidence that psychotic symptoms persisted beyond 6 months [68] would also seem to exclude this hypothesis.

A fourth hypothesis is that cannabis use at age 18 was a symptom of emerging schizophrenia. Andreasson et al [68] rejected this hypothesis, noting that the cannabis users who developed schizophrenia had better premorbid personalities, a more abrupt onset, and more positive symptoms than the non-users who developed schizophrenia [68]. Moreover, although 58% of the heavy cannabis users had a psychiatric diagnosis at the time of conscription, there was still a dose-response relationship between cannabis use and schizophrenia among those who had no such history. The persuasiveness of this evidence depends upon how confident we can be that a failure to identity a psychiatric disorder at conscription meant that no disorder was present.

A fifth hypothesis depends upon the validity of the self-reported cannabis use at conscription. Andreasson et al [66] acknowledge

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acknowledged that there probably was under-reporting of cannabis use because this information was not collected anonymously. They argued, however, that this would produce an under-estimate of the relationship between cannabis use and the risk of schizophrenia. This will be true if the schizophrenic and non-schizophrenics conscripts were equally likely to under-report. If, for example, pre-schizophrenic subjects were more candid about their drug use, then the apparent relationship between cannabis use and schizophrenia could be due to response bias [67]. This seems unlikely in view of the strong dose-response relationship between the frequency of cannabis use by age 18, and the large unadjusted relative risk of schizophrenia among heavy users.

Exacerbation of Schizophrenia

Clinical reports suggest that schizophrenic patients who continue to use cannabis experience more psychotic symptoms [76], respond poorly to neuroleptic drugs [77], and have a worse clinical course than those patients who do not [78-80]. These reports have been supported by controlled studies.

Negrete et al [81] conducted a retrospective study of the relationship between self-reported cannabis use and symptoms. They used clinical records of symptoms and treatment seeking among 137 schizophrenic patients who had a disorder of at least six months duration, and who had made three visits to their psychiatric service during the previous six months. Negrete et al [81] compared the prevalence of hallucinations, delusions and hospitalisations among the active cannabis users with that in patients who had previously used cannabis, and those who had never used cannabis. There were higher rates of continuous hallucinations and delusions, and more hospitalisations among active cannabis users. These relationships persisted after statistical adjustment for age and sex differences between the user groups.

Negrete et al [81] argued that cannabis use exacerbated schizophrenic symptoms. They rejected the alternative hypothesis that patients with a poorer prognosis were more likely to use cannabis because those who no longer used cannabis experienced fewer symptoms, and reported a high rate of adverse effects when they did use it. They also discounted the possibility that these were toxic psychoses because the minimum duration of symptoms had been six months.

Cleghorn et al [82] compared the symptom profiles of schizophrenic patients with histories of substance abuse, among whom cannabis was the most heavily used drug. Drug abusers had a higher prevalence of hallucinations, delusions and positive symptoms than those who did not abuse drugs.

Jablensky et al [64] reported a two year follow-up of 1202 first episode schizophrenic patients enrolled in 10 countries as part of a WHO Collaborative study. They found that the use of 'street drugs', including cannabis and cocaine, during the follow up period predicted more psychotic symptoms and periods of hospitalisation. Martinez-Arevalo et al [83] also reported that continued use of cannabis during a one year follow up of 62 DSM-diagnosed schizophrenic patients predicted a higher rate of relapse and poorer compliance with anti-psychotic drug treatment.

Linszen et al [84] recently reported a prospective study of outcome in 93 psychotic patients whose symptoms were assessed monthly over a year. Twenty four of their patients were cannabis abusers (11 were less than daily users and 13 were daily cannabis users). Despite the small sample sizes, they found that the cannabis users as a whole relapsed to psychotic symptoms sooner, and had more frequent relapses. in the year of follow up, than the patients who had not used cannabis. There was also a dose response relationship, with the daily users relapsing earlier, and more often, than the less than daily users who, in turn, relapsed sooner, and more often, than the patients who did not use cannabis. These relationships persisted after multivariate adjustment for premorbid adjustment, and alcohol and other drug use during the follow up period.

Most but not all studies [58], indicate that cannabis use exacerbates psychotic symptoms in patients with schizophrenia. The major cause of uncertainty about this relationship is assessing the contribution of confounding factors. It may be, for example, that the difference in psychotic symptoms between schizophrenia patients who do and do not use cannabis is due to differences in premorbid personality, family history, and other characteristics [52]. This is unlikely in the WHO schizophrenia study [64] and the recent study of Linzen [84], both of which used multivariate statistical methods to adjust for many of these confounders.

The other difficulty is separating the contributions that cannabis and alcohol make to exacerbations of schizophrenic symptoms. It is rare for a schizophrenic patient to only use cannabis [49]. The concurrent use of alcohol is common, and the heavier their cannabis use, the more likely they are to use

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The concurrent use of alcohol is common, and the heavier their cannabis use, the more likely they are to use psychostimulants and hallucinogens. Only the Linszen et al [84] study statistically adjusted for the effects of concurrent alcohol and drug use and found that the relationship persisted. Our confidence that the effect is attributable to cannabis would be increased by replications of the Linszen et al [84] finding.

Intervention Studies

If we could reduce cannabis use among patients with schizophrenia who use cannabis, then we could discover whether their disorders improved and whether the risks of relapse were substantially reduced. The major difficulty with this strategy is that it presupposes that we can successfully treat substance abuse in persons with schizophrenia. Alcohol and other substance abuse are difficult to treat [85], and many persons with schizophrenia have characteristics that predict a poor treatment outcome, namely, they lack social support, they may be cognitively impaired, they are unemployed, and they do not comply with treatment [49, 52].

There are very few controlled outcome studies of substance abuse treatment in schizophrenia [86]. Few of these have produced large enough benefits of treatment, or treated a large enough number of patients, to provide an adequate chance of detecting any positive impacts of abstinence on the course of disorders [49, 52]. The few that have been large enough [87] have not reported results separately by diagnosis.


The reasons that most persons with schizophrenia give for using alcohol, cannabis and other illicit drugs are similar to those given by persons who do not have schizophrenia, namely, to relieve boredom, to provide stimulation, to feel good and to socialise with peers (e.g. [49, 88-90]). The drugs that are most often used by schizophrenic patients are also those that are most readily available [48-49].

In favour of the self-medication hypothesis, is the evidence that some schizophrenic patients report using cannabis because its euphoric effects relieve negative symptoms and depression (e.g. [42, 44, 91]). Dixon et al [44], for example; surveyed 83 patients with schizophrenia who reported that cannabis reduced anxiety and depression, and increased a sense of calm but at the cost of increased suspiciousness.

More recently, Hamera et at [90] have reported a time series study that examined correlations over 84 consecutive days between self-reported: psychotic symptoms, licit and illicit drug use, and medication compliance in 17 persons with schizophrenia. They only found relationships between nicotine and prodromal psychotic symptoms and between caffeine use and symptoms of anxiety and depression. No relationships were found between psychotic symptoms and alcohol or cannabis use.

This study does have limitations. The difficulty of the self-monitoring task probably selected patients who were more compliant and less disordered than a representative sample of schizophrenics. There were also relatively low rates of heavy drug use. The time period of 84 days may have been too short to examine the relationship between drug use and major exacerbations of the illness, and the task of self-monitoring may have had reactive effects on drug use.

An Overall Evaluation

The epidemiological evidence is strongest that cannabis use exacerbates the symptoms of schizophrenia in affected individuals. This is supported by the findings of a number of retrospective and prospective studies which have controlled for confounding variables. It is also biologically plausible. Psychotic disorders involve disturbances in the dopamine neurotransmitter systems since drugs that increase dopamine release produce psychotic symptoms when given in large doses, and neuroleptic drugs that reduce psychotic symptoms also reduce dopamine levels [93]. Cannabinoids, such as THC, increase dopamine release [92].

It is also likely that cannabis use precipitates schizophrenia in persons who are vulnerable because of a personal or family history of schizophrenia (e.g. [22, 39, 41]). This hypothesis is consistent with the stress-diathesis model of schizophrenia [39, 95] in which the likelihood of developing schizophrenia 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 [34] 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 also difficult to identify a genetic diathesis in the majority of cases of schizophrenia. Having a first degree relative (parent or sibling) who has schizophrenia increases the risks of developing the disorder between 9 and 18 times [95]. But, according to Gottesman [95], 81% of persons wit

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81% of persons with schizophrenia will not have a first degree relative with the disorder, and 63% will not have an affected first or second degree relative.

The most contentious issue is whether cannabis use can cause schizophrenia that would not have occurred in its absence. One cannot rule it out but it is unlikely to account for more than a minority of cases. Most of the 274 conscripts who developed schizophrenia had not used cannabis, and only 21 were heavy cannabis users and at most 7% of cases of schizophrenia could be attributed to cannabis use. The treated incidence of schizophrenia, and particularly early onset, acute cases, has declined (or remained stable) during the 1970s and 1980s [94] when cannabis use increased among young adults in Australia and North America [2]. Although there are complications in interpreting such trends [97-99] a large reduction in treated incidence has been observed in a number of countries and it cannot be explained as a diagnostic artefact [100].



Mental health services should identify patients with schizophrenia who use alcohol, cannabis and other drugs, and discuss its impact on their disorder with them. Although this paper has primarily focused on cannabis we, the role alcohol should not be neglected. Cannabis is most often used with alcohol and heavy alcohol use is a stronger predictor of psychotic symptoms (OR = 7.9) than regular cannabis use (OR = 2.0) [35].

Patients whose drug use may be exacerbating their symptoms should be advised to trial abstinence. Advice to abstain or to substantially reduce use may be better received if accompanied by alternative suggestions about how to deal with the negative symptoms and depression [52, 49]. if they are not prepared to abstain, they may be prepared to reduce the frequency and quantity of drug use [52]. A positive effect on well-being and social functioning may motivate patients to consider longer term abstinence or a sustained reduction in use.

In assisting patients who wish to become abstinent, we may need to notify some traditional treatment methods [49, 52]. Alcoholics Anonymous and Narcotics Anonymous group based approaches [52] may pose difficulties for many patients with schizophrenia who find social interaction difficult. These groups may also be opposed to using anti-psychotic medication.



[1] Bromet EJ, Dew A, Eaton W. Epidemiology of psychosis with special reference to schizophrenia. In Tsuang MT, Tohen M, Zalmer GEP, eds. Textbook in Psychiatric Epidemiology. John Wiley and Sons, New York, 1995.

[2] Donnelly N, Hall W. Patterns of Cannabis Use in Australia. National Drug Strategy Monograph Series No. 27. Australian Government Publication Service, Canberra, 1994.

[3] Hall W, Solowij N, Lemon J. The Health and Psychological Effects of Cannabis Use. National Drug Strategy Monograph Series No.25. Australian Government Publication Service, Canberra, 1994.

[4] Thornicroft G. (1990) Cannabis and psychosis: Is there epidemiological evidence for association. British Journal of Psychiatry, 1990;157:25-33.

[5] Hall W. A simplified logic of causal inference. Australian arid New Zealand Journal of Psychiatry, 1987; 21:507-513.

[6] Carney MWP, Bacelle L, Robinson B. Psychosis after cannabis use. British Medical Journal, 1984;288: 1047.

[7] Drummond L. Cannabis psychosis: a case report. British Journal of Addiction, 1986;81:139-140.

[8] Bernardson G, Gunne LM. Forty-six cases of psychosis in cannabis abusers. International Journal of Addictions, 1972;7: 9-16.

[9] Chopra GS, Smith JW. Psychotic reactions following cannabis use in East Indians. Archives of General Psychiatry, 1974;30:24-27.

[10] Cohen S, Johnson K. Psychosis from alcohol or drug abuse. British Medical [10] Cohen S, Johnson K. Psychosis from alcohol or drug abuse. British Medical Journal, 1988;297:1270-1271.

[11] Eva J. Cannabis psychosis. Psychiatric Bulletin, 1992;16:310-311.

[12] Kolansky H, Moore RT. Effects of marihuana on adolescents and young adults. Journal of the American Medical Association, 1971;216(3):486-492.

[13] Onyango RS. Cannabis psychosis in young psychiatric inpatients. British Journal of Addiction, 1986;8l :419-423.

[14] Solomons K, Neppe VM, Kuyl JM. Toxic cannabis psychosis is a valid entity. South African Medical Journal, 1990;78:476-481.

[15] Talbott JA, Teague JW. Marihuana psychosis: Acute toxic psychosis associated with the use of cannabis derivatives. Journal of the American Medical Association, 1969;210:299- 302.

[16] Tennant FS, Groesbeek CJ. Psychiatric effects of hashish. Archives of General Psychiatry, 1972;27: 133-136.

[17] Tunving K. Psychiatric aspects of cannabis use in adolescents and young adults. Pediatrician, 1987; 14:83-91.

[18] Wylie AS, Scott RTA, Burnett SJ. Psychosis due to 'skunk'. British Medical Journal, 1995;311:125.

[19] Harding T, Knight F. Marijuan

Share this post

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[19] Harding T, Knight F. Marijuana-modified mania. Archives of General Psychiatry, 1973;29:635-637.

[20] Spencer DJ. Cannabis-induced psychosis. International Journal of the Addictions, 1971;6:323-326.

[21] Paisson A, Thulin SO, Tunviung K. Cannabis psychoses in South Sweden. Acta Psychiatrica Scandinavica, 1982; 66:311-321.

[22] Lewis A. A review of the international clinical literature. In Report of the Advisory Committee on Drug Dependence. Cannabis. Her Majesty's Stationary Office, London, 1968.

[23] Gruber AJ, Pope HG. Cannabis psychotic disorder. Does it exist? American Journal of the Addictions, 1994;3:72-83.

[24] Poole R, Brabbins C. Drug induced psychosis. British Journal of Psychiatry, 1996;168:135-138.

[25] Schuckit MA. Can marijuana cause a long-lasting psychosis? Drug Abuse and Alcoholism Newsletter, 1994;23:1-4.

[26] Thacore VR, Shuckla SRP. Cannabis psychosis and paranoid schizophrenia. Archives of General Psychiatry, 1976;33:383-386.

[27] Rottanburg D, Robins AH, Ben-Arie O, Teggin A, Elk R. Cannabis-associated psychosis with hypomanic features. Lancet, 1982;2:1364-1366.

[28] Chaudry HR, Moss HB, Bashir A, Suliman T. Cannabis psychosis following bhang ingestion. British Journal of Addiction, 1991 ;86: 1075-1081.

[29] Mathers DC, Ghodse H, Caan AW, Scott SA. Cannabis use in a large sample of acute psychiatric admissions. British Journal of Addiction, 1991;86:779-784.

[30] Rolfe M, Tang CM, Sabally S, Todd JE, Sam EB, Hatib N'Jie AB. (1993) Psychosis and cannabis abuse in The Gambia: A case-control study. British Journal of Psychiatry, 1993;163:789-801.

[31] Imade AGT, Ebie JC. A retrospective study of symptom patterns of cannabis-induced psychosis. Acta Psychiatrica Scandinavica, 1991;8:134-136.

[32] Thornicroft G, Meadows G, Politi P. Is 'cannabis psychosis' a distinct category? European Psychiatry, 1992;7:277-282.

[33] McGuire P, Jones R, Harvey I, Bebbington P, Toone B, Lewis S, Murray, R. Cannabis and acute psychosis. Schizophrenia Research, 1994;13:161-168.

[34] McGuire P, Jones R, Harvey I, Williams M, McGuffin P, Murray R Morbid risk of schizophrenia for relatives of patients with cannabis associated psychosis. Schizophrenia Research, 1995; 15:277-281.

[35] Tien AY, Anthony JC. Epidemiological analysis of alcohol and drug use as risk factors for psychotic experiences. Journal of Nervous and Mental Disease, 1990;178:473-480.

[36] Thomas H. A community survey of adverse effects of cannabis use. Drug and Alcohol Dependence, 1996;42:201-207.

[37] Beaubruhn M, Knight F. Psychiatric assessment of 30 chronic users of cannabis and 30 matched controls. American Journal of Psychiatry, 1973;130:309-311.

[38] Stefanis C, Boulougouris J, Liakos A. Clinical and psychophysiological effects of cannabis in long-term users. In Braude MC, Szara S, eds. The Pharmacology of Marihuana. Raven Press, New York, 1976.

[39] Boutros NN, Bowers MB. Chronic substance-induced psychotic disorders: state of the literature. Journal of Neuropsychiatry and Clinical Neurosciences, 1996;8:262-269.

[40] American Psychiatric Association. Diagnostic and Statistical Manual Forth Edition (DSM-IV). Washington, DC: American Psychiatric Association, 1994.

[41] Lishman WA. Organic Psychiatry: The Psychological Consequences of Cerebral Disorder. Second Edition. Blackwell Scientific Publications, Oxford, 1987.

[42] Schneier FR, Siris SG. A review of psychoactive substance use and abuse in schizophrenia: patterns of drug choice. Journal of Nervous and Mental Disorders, 1987;175:641-652.

[43] Smith J, Hucker S. Schizophrenia and substance abuse. British Journal of Psychiatry, 1994;165:13-21.

[44] Dixon L, Haas G, Wedien PJ, Sweeney J, Frances AJ. Acute effects of drug abuse in schizophrenic patients: clinical observations and patients' self-reports. Schizophrenia Bulletin, 1990; 16:69-79.

[45] Weller MPI, Ang PC, Latimer-Sayer DT, Zachary A. Drug abuse and mental illness. Lancet, 1988; 1:977.

[46] Breakey WR, Goodell H, Lorenz PC, McHugh PR. Hallucinogenic drugs as precipitants of schizophrenia. Psychological Medicine, 1974;4:255-261.

[47] Warner R, Taylor D, Wright J, Sloat A, Springen G, Arnold S, Weinberg H. Substance use among the mentally ill: prevalence, reasons for use and effects on illness. American Journal of Orthopsychiatry, 1994;74:30-39.

[48] Cuffel BJ. Prevalence estimates of substance abuse in schizophrenia and their correlates. Journal of Nervous and Mental Disease, 1992;l80:589-592.

[49] Mueser KT, Beflack AS, Blanchard JJ. Comorbidity and substance abuse: Implications for treatment. Journal of Consulting and Clinical Psychology, 1992;60:845-856.

[50] Hambrecht M, Hafner H. Substance abuse and the onset of schizophrenia. Biological Psychiatry, 1996;40:l155-1163.

[51] Mueser KT, Yamold PR, Levinson DF, Singh H, Bellack AS, Kee K, Morrison RL, Yadalam KG. Prevalence of substance abuse in schizophrenia: demographic and clinical correlates. Schizophrenia Bulletin, 1990; 16:31-56.

[52] Kava

Share this post

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[52] Kavanagh DJ. An intervention for substance abuse in schizophrenia. Behaviour Change, 1995; 12:20-30.

[53] Cuffel BJ, Heithoff KA, Lawson W. Correlates of patterns of substance abuse among patients with schizophrenia. Hospital and Community Psychiatry, 1993;44:247-251.

[54] Drake RE,Wallach MA. Substance abuse among the chronic mentally ill. Hospital and Community Psychiatry, 1989;4:1041-1046.

[55] Anthony JC, Helzer JE. Syndromes of drug abuse and dependence. In Robins LN, Regier DA, eds. Psychiatric Disorders in America. Free Press, MacMillan, New York, 1991.

[56] Arndt S, Tyrrell G, Flaum M, Andreasen NC. Comorbidity of substance abuse and schizophrenia: the role of premorbid adjustment. Psychological Medicine, 1992;22:379- 388.

[57] Kovasznay B, Bromet E, Schwartz JE, Ram R, Lavelle J, Brandon L. Substance abuse and onset of psychotic illness. Hospital and Community Psychiatry, 1993;44:567-571.

[58] Zisook S, Heaton R, Moranville J, Kuck J, Jernigan T, Braff D. Past substance abuse and clinical course of schizophrenia. American Journal of Psychiatry, 1992;149:552-553.

[59] Regier DA, Farmer ME, Rae DS, Locke BZ, Keith SJ, Judd LL, Goodwin FK (1990) Comorbidity of mental disorders with alcohol and other drug abuse: results from the Epidemiologic Catchment Area (ECA) Study. Journal of the American Medical Association, 1990;264:2511-2518.

[60] Helzer JE, Burnam A, McEvoy LT. Alcohol abuse and dependence. In Robins LN, Regier DA, eds. Psychiatric Disorders in America: the Epidemiologic Catchment Area Study. The Free Press, New York, 1991.

[61] Bland RC, Newman SC, Orn H. Schizophrenia: lifetime co-morbidity in a community sample. Acta Psychiatrica Scandinavica, 1987;75:383-391.

[62] Allebeck P. Cannabis and schizophrenia: is there a causal association? In Nahas GG, Latour C, eds. Physiopathology of Illicit Drugs: Cannabis, Cocaine, Opiates Pergamon Press, Oxford, 1991.

[63] Allebeck P, Adamsson C, Engstrom, Rydberg U. Cannabis and schizophrenia: a longitudinal study of cases treated in Stockholm county. Acta Psychiatrica Scandinavica, 1993;88: 21-24.

[64] Jablensky A, Sartorius N, Ernberg G, Anker M, Korten A, Cooper JE, Day R, Bertelsen A. Schizophrenia: manifestations, incidence and course in different cultures. A World Health Organization Ten-Country Study. Psychological Medicine Monograph Supplement No. 20, 1991.

[65] Andreasson S, Allebeck P, Engstrom A, Rydberg U. Cannabis and schizophrenia: A longitudinal study of Swedish conscripts. Lancet, 1987;2:1483-1486. [66] Johnson BA, Sinith BL, Taylor P. Cannabis and schizophrenia Lancet, 1988;l :592-593. [ 67] Negrete JC. Cannabis and schizophrenia. British Journal of Addiction, 1989; 84:349-351.

[68] Andreasson S, Allebeck P, Rydberg U. Schizophrenia in users and nonusers of cannabis. Acta Psychiatrica Scandinavica, 1989;79:505-510.

[69] Kandel D, Faust R. Sequence and stages in patterns of adolescent drug use. Archives of General Psychiatry, 1975;32:923-932.

[70] Bell D. The experimental reproduction of amphetamine psychosis. Archives of General Psychiatry, 1973;29:35-40.

[71] Connell PH. Amphetamine Psychosis. Maudlsey Monograph Number 5, Institute of Psychiatry, Oxford University Press, London, 1959.

[72] Gawin PH, Ellinwood EH. Cocaine arid other stimulants: Actions, abuse and treatment New England Journal of Medicine, 1988;3 18:1173-1182.

[73] Inghe G. The present state of abuse and addiction to stimulant drugs in Sweden. In Sjoqvist F, Tottie M, eds. Abuse of Central Stimulants. Raven Press, New York, 1969.

[74] Goldberg L. Drug abuse in Sweden. Part I. Bulletin On Narcotics, 1968a;20:(1) 1-31(a). [75] Goldberg L. Drug abuse in Sweden. Part II. Bulletin On Narcotics, 1968b;20:(2) 9-36(B).

[76] Weil A. Adverse reactions to marihuana. New England Journal of Medicine, l970;282:997-1000.

[77] Bowers MB, Mazure CM, Nelson JC, Jatlow PI. Psychotogenic drug use and neuroleptic response. Schizophrenia Bulletin, 1990; 16:81-85.

[78] Knudsen P, Vilmar T. Cannabis and neuroleptic agents in schizophrenia. Acta Psychiatrica Scandinavica, 1984;69: 162-174.

[79] Perkins KA, Simpson JC, Tsuang MT. Ten-year follow-up of drug abusers with acute or chronic psychosis. Hospital and Community Psychiatry, 1986;37:481-484.

[80] Turner WM, Tsuang MT. Impact of substance abuse on the course and outcome of schizophrenia. Schizophrenia Bulletin, 1990; 16:87-372.

[81] Negrete JC, Knapp WP, Douglas D, Smith WB. Cannabis affects the severity of schizophrenic symptoms: results of a clinical survey. Psychological Medicine, 1986;16:515-520.

[82] Cleghom JM, Kaplan RD, Szechtman B, Szechtman H, Brown GM, Franco S. Substance abuse and schizophrenia: effect on symptoms but not on neurocognitive function. Journal of Clinical Psychiatry, 1991;52:26-30.

[83] Martinez-Arevalo MJ, Calcedo-Ordonez A, Varo-Prieto JR. Cannabis consumption as a prognostic factor in schizophrenia. British Journal of Psychiatry, 1994;.164:679-681.

[84] Linszen DH, Dingemans PM, Len

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[84] Linszen DH, Dingemans PM, Lenior ME. Cannabis abuse and the course of recent-onset schizophrenic disorders. Archives of General Psychiatry, l 994;51:273-279.

[85] Heather N, Tebbutt J, eds. The Effectiveness of Treatment for Drug and Alcohol Problems: An Overview. National Campaign Against Drug Abuse Monograph Series Number 11. Australian Government Publishing Service, Canberra, 1989.

[86] Lehman AF, Herron JD, Schwartz RP, Myers CP. Rehabilitation for adults with severe mental illness and substance use disorders: A clinical trial. Journal of Nervous and Mental Disease, 1993;18l:86-90.

[87] Jerrell J, Ridgely MS. Comparative effectiveness of three approaches to serving people with severe mental illness and substance abuse disorders. Journal of Nervous and Mental Disease, 1995;183:566-576.

[88] Bergman HC, Harris M. Substance abuse among young adult chronic patients. Psychosocial Rehabilitation Journal, 1985;9:49-54.

[89] Noordsy DL, Drake RE, Teague GB, Osher PC, Hulbut SC, Beaudett MS, Parkus TS. Subjective experiences related to alcohol use among schizophrenics. Journal of Nervous and Mental Disease, 1991,179:411-414.

[90] Test MA, Wallisch LS, Aliness DJ, Tripp K. Substance use in young adults with schizophrenic disorders. Schizophrenia Bulletin, 1989;15:465-476.

[91] Peralta V, Cuesta MJ. Influence of cannabis abuse on schizophrenic psychopathology. Acta Psychiatrica Scandinavica 1992;85:127-30.

[92] Hamera E, Schneider JK, Deviney S. Alcohol, cannabis, nicotine and caffeine use and symptom distress in schizophrenia. Journal of Nervous and Mental Disease, 1995;183:559-565.

[93] Stahl SM. Essential Psychopharmacology. Cambridge University Press, Cambridge, 1996.

[94] Adams IB, Martin BR. Cannabis: pharmacology and toxicology in animals and humans. Addiction, 1996;91 :1585-14.

[95] Gottesman II. Schizophrenia Genesis: The origins of madness. W.H. Freeman and Co, New York, 1991.

[96] Der G, Gupta S, Murray RM. Is schizophrenia disappearing? Lancet, 1990;l:513-516.

[97] Jablensky A. The epidemiology of schizophrenia. Current Opinion in Psychiatry, 1993;6:43-52.

[98] Kendell RB, Malcolm DE, Adams W. The problem of detecting changes in the incidence of schizophrenia. British Journal of Psychiatry, 1993; 1 62:212-218.

[99] Warner R, de Girolamo G. Schizophrenia. World Health Organization, Geneva, 1995.

[100] Joyce PR. Changing trends in first admissions and readmissions for mania and schizophrenia in New Zealand. Australian and New Zealand Journal of Psychiatry, 1987;21 :82-86.

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Sorry for the Loooooooooooooooooong Post ! I was confused about the whole business & I have tried to understand it. I am no expert, just an unabashed plagiaser of many an expert !

I feel with the new varieties of serious skunk, it is time we tell our patients that cannabis is harmful in plain language.(without suffixes and prefixes & riders).

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Hi maryam ,this is information overdose thanks :)

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