Cannabis use and psychotic disorders: an update

Cannabis use and psychotic disorders: an update

WAYNE HALL1, LOUISA DEGENHARDT

2& MAREE TEESSON

2

1Office of Public Policy and Ethics, Institute for Molecular Bioscience, University of Queensland, Australia and 2National

Drug and Alcohol Research Centre, University of New South Wales, Australia

AbstractThis paper evaluates three hypotheses about the relationship between cannabis use and psychosis in the light of recent evidencefrom prospective epidemiological studies. These are that: (1) cannabis use causes a psychotic disorder that would not haveoccurred in the absence of cannabis use; (2) that cannabis use may precipitate schizophrenia or exacerbate its symptoms; and (3)that cannabis use may exacerbate the symptoms of psychosis. There is limited support for the first hypothesis. As a consequence ofrecent prospective studies, there is now stronger support for the second hypothesis. Four recent prospective studies in three countrieshave found relationships between the frequency with which cannabis had been used and the risk of receiving a diagnosis ofschizophrenia or of reporting psychotic symptoms. These relationships are stronger in people with a history of psychotic symptomsand they have persisted after adjustment for potentially confounding variables. The absence of any change in the incidence ofschizophrenia during the three decades in which cannabis use in Australia has increased makes it unlikely that cannabis use canproduce psychoses that would not have occurred in its absence. It seems more likely that cannabis use can precipitate schizophreniain vulnerable individuals. There is also reasonable evidence for the third hypothesis that cannabis use exacerbates psychosis. [HallW, Degenhardt L, Teeson M. Cannabis use and psychotic disorders: an update. Drug Alcohol Rev 2004;23:433 – 443]

Key words: cannabis, psychosis.

Introduction

There is abundant epidemiological evidence of an

association between cannabis use and psychotic symp-

toms and disorders (e.g. [1,2]) but the reasons for the

association have been controversial. Thornicroft [3]

examined the evidence supporting an association

between cannabis and psychosis but was unable to

draw strong conclusions about causality. Nearly a

decade later, Hall [1] came to a similar conclusion.

Both authors argued that prospective longitudinal

population-based cohort studies were required to

elucidate any causal role that cannabis use may play

in psychosis. We reconsider the question in the light of

four prospective epidemiological studies that have

recently been published.

The nature of any relationship between cannabis use

and psychosis remains an important issue. Cannabis

has been used by most young Australians in late

adolescence and early adulthood, the peak risk period

for the onset of psychoses. These disorders can be

disabling and they carry an elevated risk of premature

death by suicide [4]. The continuing debate about the

legal status of recreational cannabis in Australia and

other developed societies ensures that the evidence on

this issue carries special policy weight. It is accordingly

important to review the evidence carefully and critically

but without setting standards for proof unreasonably

high and thereby precluding sensible policy recom-

mendations.

Possible types of relationship between cannabis

use and psychoses

It is useful to begin by distinguishing three possible

types of hypotheses about relationships between can-

nabis use and psychosis [1]. The strongest hypothesis is

that heavy cannabis use causes a unique ‘cannabis

psychosis’. This hypothesis assumes (a) that the

psychosis would not occur in the absence of cannabis

use, and (b) that the causal role of cannabis can be

inferred from the type of psychotic symptoms reported,

Received 13 September 2004; accepted for publication 13 September 2004.

Wayne Hall PhD, Office of Public Policy and Ethics, Institute for Molecular Bioscience, University of Queensland, Australia, Louisa DegenhardtPhD, National Drug and Alcohol Research Centre, University of New South Wales, Australia, and Maree Teesson PhD, National Drug andAlcohol Research Centre, University of New South Wales, Australia. Correspondence to Wayne Hall 8PhD, Director, Office of Public Policy andEthics, Institute for Molecular Bioscience, University of Queensland, St Lucia, Qld, 4072, Australia. Tel: 07 3346 2150; Fax: 07 3346 2159;E-mail: [email protected]

Drug and Alcohol Review (December 2004), 23, 433 – 443

ISSN 0959-5236 print/ISSN 1465-3362 online/04/040433–11 # Australian Professional Society on Alcohol and Other Drugs

DOI: 10.1080/09595230412331324554

and the fact that these symptoms are preceded by heavy

cannabis use and remit swiftly after abstinence from

cannabis.

A second 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 may act together to precipitate

schizophrenia. It does not assume that a causal role for

cannabis can be inferred from the symptoms of the

disorder, or that the disorder will necessarily remit

when cannabis use ceases. It does not assume that

cannabis use is either a necessary or a sufficient cause of

schizophrenia.

Thirdly, cannabis use may exacerbate the symptoms

of schizophrenia. If cannabis use can precipitate

schizophrenia, it is also likely to exacerbate its

symptoms. However, cannabis use may exacerbate

symptoms of schizophrenia (even if it is not a

precipitant of the disorder) by reducing compliance

with treatment, or interfering with the effects of the

neuroleptic drugs that are used to treat it.

Making causal inferences

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 cannabis use preceded the psychosis;

and that plausible alternative explanations of the

association can be excluded [5].

Association requires that cannabis use and psychosis

occur together. This means that cannabis users should

have higher rates of psychosis and that cannabis use

should occur more frequently among people with

psychoses. As indicated above, the fact of an association

is not in doubt; it is its interpretation that is contested.

Associations between cannabis use and psychosis may

occur because psychosis leads to cannabis use. To rule

out this possibility, cannabis use needs to be shown to

precede the onset of psychosis. An association between

cannabis use and psychosis also has to be shown to arise

from cannabis use and not from some uncontrolled

factors that are associated with cannabis use and

psychosis (such as for example other drug use, or a

genetic predisposition to develop schizophrenia and use

cannabis).

We first review the evidence for the strongest causal

hypothesis, that heavy cannabis use causes a unique

‘cannabis psychosis’.

A ‘cannabis psychosis’

There are case reports of ‘cannabis psychoses’ [6 – 9]

that describe individuals who develop psychotic dis-

orders after using cannabis. Chopra & Smith [7]

reported one of the largest, a series of 200 patients

who were admitted to a psychiatric hospital in Calcutta

between 1963 and 1968 with psychotic symptoms that

followed the use of cannabis. The most common

symptoms ‘were sudden onset of confusion, generally

associated with delusions, hallucinations (usually vi-

sual) and emotional lability. . . amnesia, disorientation,

depersonalisation and paranoid symptoms’ (p. 24).

Most psychoses were preceded by using large amounts

of cannabis and those who used the most potent

cannabis developed psychoses after the shortest periods

of use.

The findings of Chopra & Smith have been

supported by case series which suggest that large doses

of potent cannabis products can produce a ‘toxic’

psychotic disorder with ‘organic’ features of amnesia

and confusion. These disorders have been reported in

the Caribbean [10], New Zealand [11], Scotland [9],

South Africa [8], Sweden [6] and the United Kingdom

[12].

These disorders have been attributed to cannabis

use for combinations of the following reasons: the

onset of the disorders followed the use of large

quantities of cannabis; the affected individuals were

confused, disorientated and amnesic; some had no

personal or family history of psychosis; their symp-

toms remitted within days to weeks of enforced

abstinence from cannabis use; recovery was complete,

with the person having no residual psychotic symp-

toms such as those seen in schizophrenia; and if the

disorder recurred, it was only after the individual

resumed cannabis use [1].

Some commentators [3,13] have criticized the poor

information on cannabis use and its relationship to the

onset of psychosis, the person’s premorbid adjustment

and their family history of psychosis. They also

emphasize the varied clinical picture of ‘cannabis

psychoses’ as reported by different observers.

A number of controlled studies have been

conducted over the past 20 years [14 – 19]. Studies

have either compared people with ‘cannabis psy-

choses’ with people who have schizophrenia, or

compared psychoses occurring in people who have

and have not used cannabis prior to presenting for

treatment. Their results have been mixed, in part

because of the small sample sizes and variations in

research methods [1].

Summary

The evidence for there being a distinct ‘cannabis

psychosis’ is weak. The lack of support for ‘a

cannabis psychosis’ does not, however, rule out the

hypothesis that cannabis use may precipitate an

episode of schizophrenia. The evidence for this is

reviewed below.

434 Wayne Hall et al.

Association between cannabis use and psychosis

Several studies have examined the relationship between

cannabis use and psychotic symptoms in the general

population. Tien & Anthony [20] used data from the

Epidemiologic Catchment Area study to examine

correlates of reporting one or more ‘psychotic experi-

ences’ (four types of hallucinations and seven types of

delusional belief). They compared 477 cases who

reported one or more of these symptoms in a 1-year

follow-up with 1818 controls who did not. Cases and

controls were matched for age and social and demo-

graphic 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 [21] 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 experi-

ences such as hearing voices or becoming convinced

that someone is trying to harm you or that you are being

persecuted’ after using cannabis.

The National Survey of Mental Health and Well-

being (NSMHWB) conducted in Australia in 1997

included a screening questionnaire for psychotic

symptoms [1]. Among those under 50 years of age

who screened positive for a psychotic disorder, 7.8%

(n=27) met International Classification of Diseases

(ICD)- 10 criteria for cannabis dependence in the past

12 months. This was 17.2% of all persons diagnosed

with cannabis dependence. A diagnosis of cannabis

dependence increased the chances of reporting psycho-

tic symptoms 1.71 times, after adjusting for age,

affective and anxiety disorders, smoking status and

alcohol dependence [2].

Association between schizophrenia and cannabis

use

In case – control studies [22,23], patients with schizo-

phrenia are more likely to use cannabis than other

psychiatric patients or normal controls [24]. The

prevalence of use in schizophrenia patients has varied

between studies but it is generally higher than rates in

the general population [24]. These variations are

probably due to differences in the sampling of patients,

with younger cases reporting higher rates than older

people with chronic disorders. Generally, cannabis is

the most commonly used drug after alcohol and

tobacco, and it is often used with alcohol [25,26].

The controlled clinical studies provide conflicting

evidence on the correlates of substance abuse in

schizophrenia, apart from the consistent finding that

young males are over-represented among cannabis

users [1], as they are in the general community [27].

In some studies, cannabis users have had an earlier

onset of psychotic symptoms, a better premorbid

adjustment, more episodes of illness and more hallu-

cinations [26,28,29]. Other controlled studies have

failed to replicate some of these findings [30 – 32].

A recent clinical study has adopted a novel approach

to studying the relationship between cannabis use and

psychosis [33]. In this study, 100 young people (49%

male with an average age of 19.3 years) were identified

as being at ‘ultra high’ risk of psychosis on the basis of

one or more of the following: schizophrenia in a first

degree relative; the presence of attenuated psychotic

symptoms; or a brief limited psychosis. Cannabis was

the most commonly used drug in the 12 months

preceding assessment (35%), with 18% meeting criteria

for cannabis dependence in the previous year. Cannabis

use, however, did not predict an increased risk of

developing an acute psychosis during the follow-up

period, regardless of whether cannabis use was defined

as any use, frequent use or dependent use in the past

year. The rate of cannabis use was low by comparison

with the other studies and this, in combination with the

small number of cases, may explain the absence of an

association.

Community surveys of psychiatric disorders, such as

the ECA, have also reported higher rates of substance

use disorders among persons with schizophrenia [34].

Nearly half the patients identified as having schizo-

phrenia in the ECA study had a diagnosis of substance

abuse or dependence (34% for an alcohol disorder and

28% for another drug disorder) [35]. These rates were

higher than the rates in general population, namely,

14% for alcohol disorders [36] and 6% for drug abuse

[34]. The most common patterns of substance use

among 231 cases of schizophrenia in the ECA study

were: alcohol (37%) and cannabis (23%), followed by

stimulants and hallucinogens (13%), narcotics (10%)

and sedatives (8%). The most common combination of

drugs was alcohol and cannabis use (31%) [31]. These

findings were replicated in Edmonton, Alberta [37].

In the Australian NSMHWB, 11.5% of those who

reported that they had been diagnosed with schizo-

phrenia, met ICD-10 criteria for a cannabis use

disorder in the past 12 months and 21.2% met criteria

for an alcohol use disorder. After adjusting for

confounding variables, those who met criteria for

cannabis dependence were 2.9 times more likely to

report that they had been diagnosed with schizophrenia

than those who did not.

The important questions in explaining the elevated

rates of cannabis use among people with schizophrenia

are: does cannabis use usually precede psychosis? Can

we rule out the possibility of other causes that may

explain the association? The best evidence for answer-

ing these questions comes from longitudinal popula-

Cannabis use and psychotic disorders 435

tion-based studies that have assessed cannabis use

before the onset of psychotic symptoms, followed the

cohort over a substantial period and used statistical

methods to assess the contribution of factors other than

cannabis use.

Explanations of the association

One explanation of the association is that cannabis use

precipitates schizophrenia in vulnerable people. This is

consistent with the earlier age of onset of psychosis

among cannabis users (with their drug use typically

preceding symptoms), and the fact that cannabis users

who develop schizophrenia often have better premorbid

adjustment, fewer negative symptoms and better treat-

ment outcome [38].

Another possibility is that the association between

cannabis use and an early onset and good prognosis are

spurious. Arndt et al. [29] argue that individuals with

schizophrenia with a better premorbid personality are

more likely to be offered cannabis by peers than people

with schizophrenia who are socially withdrawn. There is

also evidence [39] that people 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 especially withdrawn people whose illness has an

insidious onset.

A third possibility is that cannabis use is a con-

sequence (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 [29].

The Swedish conscript study

Until very recently, the most convincing evidence that

cannabis use precipitates schizophrenia came from a

15-year prospective study of cannabis use and schizo-

phrenia in 50 465 Swedish conscripts [40]. This study

investigated the relationship between self-reported

cannabis use at age 18 and the risk of being diagnosed

with schizophrenia in the Swedish psychiatric case

register during the next 15 years.

Andreasson et al. [40] found that those who had tried

cannabis by age 18 were 2.4 times more likely to receive

a diagnosis of schizophrenia than those who had not.

The risk of a diagnosis of schizophrenia was related to

cannabis use in a dose – response manner to the

number of times cannabis had been used by age 18.

Compared with those who had not used cannabis, the

risk of developing schizophrenia was 1.3 times higher

for those who had used cannabis one to 10 times, three

times higher for those who had used cannabis between

one and 50 times, and six times higher for those who

had used cannabis more than 50 times.

These risks were reduced substantially after statistical

adjustment for variables that were related to the risk of

developing schizophrenia. These included having a

psychiatric diagnosis at age 18, and having parents who

had divorced (as an indicator of parental psychiatric

disorder). Nevertheless, these relationships remained

statistically significant after adjustment. Compared with

those who had never used cannabis, the those who had

used cannabis one to 10 times were 1.5 times more

likely, and those who had used 10 or more times were

2.3 times more likely to receive a diagnosis of

schizophrenia. Andreasson et al. [40] argued that this

means that cannabis use precipitates schizophrenia in

vulnerable individuals.

Other authors offered a number of alternative

explanations of the Swedish finding. 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 [41]. The diagnosis of

schizophrenia was based upon a case register, so there

was no data on how many individuals used cannabis up

until the time that their schizophrenia was diagnosed.

Andreasson et al. argued that cannabis use persisted

because cannabis use at age 18 was also related strongly

to the risk of attracting a diagnosis of drug abuse.

A second possibility was that schizophrenia had been

misdiagnosed. On this hypothesis, the higher rate of

‘schizophrenia’ among heavy cannabis users reflected

cannabis-induced psychoses which were diagnosed

mistakenly as schizophrenia [41]. Andreasson et al.

[40] examined 21 cases of schizophrenia among con-

scripts in the case register (eight 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 6 months,

thereby excluding the diagnoses of transient drug-

induced psychotic symptoms.

A third hypothesis was that the relationship between

cannabis use and schizophrenia was due to the use of

amphetamines. People who use cannabis in adoles-

cence are at higher risk of later using amphetamines

[42], which can produce an acute paranoid psychosis

[43]. Amphetamines were the major illicit drugs of

abuse in Sweden during the study period [44]. The

evidence that psychotic symptoms persisted beyond 6

months [40] also makes this an unlikely hypothesis.

A fourth hypothesis was that cannabis use at age 18

was a symptom of emerging schizophrenia. Andreasson

et al. [40] 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. Moreover, there was still a dose –

response relationship between cannabis use and schizo-


phrenia among those who had no history of psychiatric

disorder. The persuasiveness of this evidence depends

upon how confident we can be that a failure to identify a

psychiatric disorder at conscription meant that no

disorder was present.

A fifth hypothesis depended upon the validity of the

self-reported cannabis use at conscription. Andreasson

et al. [40] acknowledged that cannabis use was probably

under-reported because this information was not

collected anonymously. They argued, however, that

this would underestimate the relationship between

cannabis use and schizophrenia. This is true if the

schizophrenia and non-schizophrenia conscripts were

equally likely to under-report. If, for example, pre-

schizophrenia subjects were more candid about their

drug use, then the apparent relationship between

cannabis use and schizophrenia could be due to

response bias [41]. This seems unlikely in view of the

strong dose – response relationship between the fre-

quency of cannabis use by age 18, and the large

unadjusted relative risk of schizophrenia among heavy

users.

Zammit et al. [45] has recently reported a follow-up

of the Swedish cohort study, reporting on risk over a

27-year follow-up that covers most of the risk period for

the onset of psychotic disorders in a cohort that was

first studied when 18 – 20 years old. This study

improved on the earlier study in a number of ways.

The psychiatric register provided more complete cover-

age of all cases diagnosed with schizophrenia; there was

better statistical control of a larger number of potential

confounding variables, including other drug use, IQ,

known risk factors for schizophrenia and social integra-

tion; the study distinguished between cases that

occurred in the first 5 years of the study period and

those that occurred more than 5 years afterwards in

order to look at the possible role of a prodrome; and the

study undertook a separate analyses in those who only

reported using cannabis at the initial assessment.

Zammit et al. [45] found, as did Andreasen et al.

[40], that cannabis use at baseline predicted an

increased risk of schizophrenia during the follow-up

period. They also found a dose – response relationship

between frequency of cannabis use at baseline and risk

of schizophrenia during the follow-up. They demon-

strated that the relationship between cannabis use and

schizophrenia persisted when they controlled statisti-

cally for the effects of other drug use and other potential

confounding factors, including a history of psychiatric

symptoms at baseline. They estimated that 13% of

cases of schizophrenia could be averted if all cannabis

use were prevented (i.e. the attributable risk of cannabis

to schizophrenia was 13%). The same relationships

were observed in the subset of the sample who reported

cannabis use only at baseline and among cases

diagnosed in the first 5 years after assessment and for

the 22 years afterwards. The relationship was a little

stronger in cases observed in the first 5 years, probably

reflecting the decline in cannabis use that occurs with

age.

The NEMESIS study

Zammit et al.’s [45] findings have been supported by a

study conducted by Van Os and colleagues [46]. This

was a 3-year longitudinal study of the relationship

between self-reported cannabis use and psychosis in a

community sample of 4848 people in the Netherlands.

Subjects were assessed at baseline on cannabis and

other drug use. Psychotic symptoms were assessed

using a computerized diagnostic interview. A diagnosis

of psychosis was validated in positive cases by a

diagnostic telephone interview with a psychiatrist or

psychologist. A consensus clinical judgement was made

on the basis of the interview material as to whether

individuals had a psychotic disorder for which they

were in need of psychiatric care.

Van Os et al. [46] substantially replicated the findings

of the Swedish cohort and extended them in a number

of important ways. First, cannabis use at baseline

predicted an increased risk of psychotic symptoms

during the follow-up period in individuals who had not

reported psychiatric symptoms at baseline. Secondly,

there was a dose – response relationship between

frequency of cannabis use at baseline and risk of

psychotic symptoms during the follow up period.

Thirdly, the relationship between cannabis use and

psychotic symptoms persisted when they controlled

statistically for the effects of other drug use. Fourthly,

the relationship between cannabis use and psychotic

symptoms was stronger for cases with more severe

psychotic symptoms that were adjudged to need

psychiatric care. Van Os et al. [46] estimated the

attributable risk of cannabis to psychosis was 13% for

psychotic symptoms and 50% for cases with psychotic

disorders adjudged to need psychiatric treatment.

Fifthly, those who reported any psychotic symptoms

at baseline were more likely to develop schizophrenia if

they used cannabis than were individuals who were not

so vulnerable. They estimated that cannabis use

accounted for 80% of the increased risk of developing

a psychotic disorder that warranted treatment among

vulnerable individuals.

The Dunedin study

Arsenault et al. [47] reported a prospective study of the

relationship between adolescent cannabis use and

psychosis in young adults in a New Zealand birth

cohort (n=759) whose members had been assessed

intensively on risk factors for psychotic symptoms and

disorders since birth. Psychotic disorders were assessed


conservatively according to DSM-IV diagnostic criter-

ia, with corroborative reports from family members or

friends on social adjustment. They assessed psychotic

symptoms at age 11 before the onset of cannabis use and

distinguished between early and late onset of cannabis

use. They also examined the specificity of the associa-

tion between cannabis use and psychosis by conducting

analyses of the effects of: (i) other drug use on psychotic

symptoms and disorders; and (ii) cannabis use on

depressive disorders.

Arsenault et al. [47] found a relationship between

cannabis use by age 15 and an increased risk of

psychotic symptoms by age 26. The relationship did

not change when they controlled for other drug use, but

it was no longer statistically significant after adjustment

for reporting psychotic symptoms at age 11. The latter

probably reflected the small number of psychotic

disorders observed in the sample. The small number

of cases also limited the ability of the study to examine

predictors of psychotic disorders at age 26. The

measurement of cannabis and other drug use was

crude (namely: none, one, two or three or more times)

although this was more likely to work against finding

relationships. An interesting result was the specificity of

the effects of cannabis on psychotic symptoms: there

was no relationship between other drug use and

psychotic disorders and no relationship between

cannabis use and depression. There was also an

interaction between psychosis risk and age of onset of

cannabis use, with earlier onset being more strongly

related to psychosis. There was also the suggestion of

an interaction between cannabis use and vulnerability,

with a higher risk of psychosis among cannabis users

who reported psychotic symptoms at age 11.

The Christchurch Health and Development study

Fergusson, Horwood & Swain-Campbell [48] have

reported a longitudinal study of the relationship

between cannabis dependence at age 18 and the

number of psychotic symptoms reported at age 21 in

the Christchurch birth cohort in New Zealand. They

assessed cannabis dependence using DSM-IV criteria,

and psychotic symptoms were assessed by 10 items

from the SCL-90. Because this was a birth cohort

that had been assessed throughout childhood and

adolescence, Fergusson et al. were able to adjust for a

large number of potential confounding variables,

including self-reported psychotic symptoms at the

previous assessment, other drug use and other

psychiatric disorders. They found that cannabis

dependence at age 18 predicted an increased risk of

psychotic symptoms at age 21 years [relative risk

(RR) of 2.3]. This association was smaller but still

significant after adjustment for potential confounders

(RR of 1.8).

Limitations of the longitudinal studies

The longitudinal studies find consistent associations

between cannabis use in adolescence and the occur-

rence of psychotic symptoms in early adult life but all

share a weakness: there is uncertainty about the

temporal relationship between cannabis use and the

timing of the onset of psychotic symptoms. Subjects in

these studies have usually been assessed once a year or

less often, and asked to report retrospectively on their

cannabis use during the preceding number of years.

Moreover, cannabis use has often been crudely assessed

by the number of times that cannabis was used or the

number of times it was used per week or month.

A recent French study improves upon these limita-

tions by providing greater detail on the temporal

relationship between cannabis use and psychotic

symptoms by using an experience sampling method to

study the relationship [49]. These investigators asked

79 college students to report on their drug use and

experience of psychotic symptoms at randomly selected

time-points, several times each day over 7 consecutive

days. The ratings were prompted by randomly pro-

grammed signals sent to a portable electronic device

that the students carried. The students were a stratified

sample from a larger group in which high cannabis

users (n=41) and students identified as vulnerable to

psychosis (n=16) were over-represented. Vulnerability

to psychosis was indicated by reporting one or more

psychotic symptoms in the past month during a

personal interview.

Verdoux et al. [49] found a positive association

between self-reported cannabis use and unusual per-

ceptions and a negative association between cannabis

use and hostility. That is, in time-periods when

cannabis was used, users reported more unusual

perceptions and less hostility. These relationships

depended upon vulnerability to psychosis: in vulnerable

individuals, cannabis use was more strongly associated

with strange impressions and unusual perceptions and

its use did not decrease feelings of hostility in the way

that it did in individuals who lacked this vulnerability.

They also found a relationship between self-reported

use of psychostimulant drugs and unusual perceptions

and thought influence but these relationships were

independent of those between cannabis use and

psychotic experiences. There was no temporal relation-

ship between reporting unusual experiences and using

cannabis use, as would be expected if some form of self-

medication were involved.

Exacerbation of schizophrenia

The final relationship examined in this paper is whether

cannabis use exacerbates the symptoms of schizophre-

nia. Clinical reports clearly suggest that patients with


schizophrenia who continue to use cannabis have more

psychotic symptoms [50], respond poorly to neurolep-

tic drugs [51] and have a worse clinical course than

those patients who do not [52]. These reports have

been supported by a small number of controlled

studies.

Negrete et al. [53] conducted a retrospective study of

the relationship between self-reported cannabis use and

symptoms using clinical records in 137 schizophrenic

patients who had a disorder for at least 6 months. They

compared the rates of hallucinations, delusions and

hospitalizations among cannabis users with those

among patients who had previously used cannabis and

those who had never used cannabis. There were higher

rates of hallucinations and delusions and more hospi-

talizations among current cannabis users, and these

relationships persisted after statistical adjustment for

age and sex differences between the groups.

Cleghorn et al. [54] compared the symptom profiles

of schizophrenic patients with histories of substance

abuse, among whom cannabis was the most heavily

used drug. Drug users had a higher prevalence of

hallucinations, delusions and positive symptoms than

those who did not use drugs.

Jablensky et al. [55] reported a 2-year follow-up of

1202 first-episode schizophrenic patients in a 10-

country 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 hospitalization. Martinez-

Arevalo et al. [56] also reported that continued use of

cannabis during a 1-year follow-up of 62 DSM-

diagnosed schizophrenia patients predicted a higher

rate of relapse and poorer compliance with anti-

psychotic drug treatment.

Linszen et al. [57] reported a prospective study of 93

psychotic patients whose symptoms were assessed

monthly over a year. Twenty-four of their patients

were cannabis users (11 were less than daily users and

13 were daily cannabis users). Despite the small

samples, they found that the cannabis users 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: daily users relapsed 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

statistical correction for premorbid adjustment, and

alcohol and other drug use during the follow-up period.

The major cause of uncertainty about this relation-

ship is the contribution of confounding factors, such as

differences between patients who do and do not use

cannabis in premorbid personality, family history and

other characteristics. This is unlikely in the WHO

schizophrenia study [55] and the Linszen et al. study

[57], both of which used statistical methods to adjust

for many of these confounders. The other difficulty is

separating the contributions that cannabis and alcohol

make to the exacerbation of schizophrenic symptoms.

The concurrent use of alcohol is common, and the

heavier the cannabis use the more likely they are to use

psychostimulants and hallucinogens [25]. Only the

Linszen et al. 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 replica-

tions of the Linszen et al. finding which would greatly

clarify the contribution that cannabis makes to the

exacerbation of psychoses.

Intervention studies

If we were able to reduce cannabis use among patients

with schizophrenia who used cannabis, then we could

discover whether their disorders improved and their

risk of relapse was reduced. The major difficulty with

this strategy is that it presupposes that we can

successfully treat cannabis use disorders in persons

with schizophrenia. Dependence on alcohol and other

drugs is difficult to treat [58], and many people with

schizophrenia have characteristics that predict a poor

outcome, namely, they lack social support, may be

cognitively impaired, unemployed, and do not comply

with treatment [25,59].

There are very few controlled outcome studies of

substance abuse treatment in schizophrenia [60]. A

recent Cochrane review identified only six relevant

studies, four of which were small [61]. The few that

have been large enough [52] have not reported results

separately by diagnosis. The Cochrane review found no

clear evidence that supported any type of substance

abuse treatment in schizophrenia over standard care.

Self-medication

The self-medication hypothesis is superficially plausible

but the evidence in its favour is not very compelling

[63]. The reasons that most people with schizophrenia

give for using alcohol, cannabis and other illicit drugs

are similar to those given by people who do not have

schizophrenia, namely, to relieve boredom, to provide

stimulation, to feel good and to socialize with peers

(e.g. [25,64]). The drugs that are most often used by

patients with schizophrenia are also those that are used

by their peers, namely, tobacco, alcohol and cannabis.

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. [22,28,65]). Dixon et

al. [28], 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.

Hamera et al. [66] examined correlations over 84

consecutive days between self-reported psychotic symp-

toms, licit and illicit drug use and medication com-

pliance in 17 persons with schizophrenia. They found

relationships only between nicotine and prodromal

psychotic symptoms and between caffeine use and

symptoms of anxiety and depression, but no relation-

ships were found between psychotic symptoms and

alcohol or cannabis use. Their negative results have

recently been supported by Verdoux et al. [49] who

found that cannabis use predicted psychotic symptoms

in the following few hours but not vice versa.

The issue of cannabis potency

Cohen [67] claimed that research undertaken in the

1970s and early 1980s underestimated the adverse

health effects of cannabis because it was based upon the

use of less potent cannabis (0.5 – 1.0% THC) than was

used in the United States in the late 1980s (3.5% THC

in 1985 – 86). This claim has been repeated in the

scientific media (e.g. [59,66]) and in Australia claims

have been made that there has been a ‘thirty-fold’

increase in the THC content of cannabis [70].

The United States is the only country that has

analysed the THC content of cannabis products over

the past few decades. This shows an increase from the

early 1970s to the mid-1980s but critics have argued

that samples studied in the 1970s were unrepresentative

of cannabis at that time. They cite data from cannabis

tested in the same period by independent laboratories

which show much higher THC levels. More recent US

data have shown that the THC content of seizures

increased from 3.3% in 1980 to 4.4% in 1998 [71,72].

A more important factor in determining exposure to

THC may have been changes in patterns of cannabis

use between 1970 and 2000. Survey data in Australia

[73] and the United States [74] indicate that young

people initiate cannabis use at an earlier age than was

the case in the 1980s. Earlier initiation of use increases

the risks of cannabis dependence and adverse health

effects of use [75]. Regular cannabis use also makes

users tolerant to the effects of THC, encouraging the

use of more potent cannabis preparations [70]. Over

the past two decades a large-scale illicit cannabis

industry has developed in many countries, which aims

to meet the demand for cannabis from daily users who

prefer more potent forms of cannabis [70]. These

changes in patterns of use—earlier initiation of use and

more regular use of more potent cannabis products—

have probably increased the amount of THC consumed

by regular cannabis users [70]. In so far as this has

happened, young cannabis users who initiate at an early

age and subsequently use cannabis regularly are

probably exposing themselves to an increased risk of

experiencing psychotic symptoms. This may explain the

relationship between age of initiation and risk of

psychosis reported in the Dunedin birth cohort.

Summary

The evidence in favour of the hypothesis that there is a

‘cannabis psychosis’ is weak. In its favour are case series

and the small number of controlled studies. Critics of

the hypothesis emphasize the fallibility of clinical

judgments 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’ [76]. It is a

plausible hypothesis that high doses of cannabis can

produce psychotic symptoms but the evidence for a

specific ‘cannabis psychoses’ is less compelling because

the clinical symptoms reported by different observers

have been so mixed.

There is reasonable epidemiological evidence that

cannabis use exacerbates the symptoms of schizophre-

nia. This is supported by the findings of a number of

retrospective and prospective studies that have con-

trolled 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 [77,78]. Cannabinoids such as THC

increase dopamine release in the nucleus acumbens

[79].

There is now consistent evidence from prospective

epidemiological studies that cannabis use precipitates

schizophrenia in people who are vulnerable because of a

personal or family history of schizophrenia. This

hypothesis is consistent with the stress – diathesis model

of schizophrenia [39,80] in which the likelihood of

developing schizophrenia is the product of stress acting

upon a genetic ‘diathesis’ to develop schizophrenia.

There is also evidence that a genetic vulnerability to

psychosis increases the risk that cannabis users will

develop psychosis [17,47,49].

The most contentious issue is whether cannabis use

can cause schizophrenia that would not have occurred

in its absence. The estimated attributable risk in early

studies was 7% [40] but higher estimates (13%) have

been produced in more recent studies and one study

has estimated that cannabis use is a contributory cause

of 50% of cases in need of treatment [46]. The puzzle is

that the treated incidence of schizophrenia, and parti-

cularly early onset, acute cases has not obviously

increased during the 1970s and 1980s [81] when there

have been substantial increases in cannabis use among

young adults in Australia and North America [82,83].


Although there are complications in interpreting such

trends [84], a large reduction in treated incidence has

been observed in a number of countries which have a

high prevalence of cannabis use and in which the

reduction is unlikely to be a diagnostic artefact [85].

Debate has not been about whether incidence has

increased, but about whether it has declined or

remained stationary [86].

Australia has high rates of cannabis use among

adolescents and young adults. While the majority of

cannabis users will not experience psychosis as a

consequence of their use, a vulnerable minority appear

to be at increased risk of experiencing harmful out-

comes. The epidemiological evidence now suggests that

cannabis use among this vulnerable group should be

discouraged where they can be identified. The Dunedin

study suggests that younger age of initiation to cannabis

use may increase the risk substantially.

The major challenge will be in communicating with

young people about the probable psychotogenic risks of

cannabis use. This task will be complicated by the

conflicting interpretations of the evidence on either side

of the policy debate about the legal status of cannabis.

We can expect those who defend current policy to

support a strong causal interpretation of the evidence

and proponents of cannabis liberalization to dismiss the

evidence as the latest version of ‘reefer madness’. These

contrasting responses may amplify scepticism among

young people about messages about the mental health

risks of cannabis use.

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Cannabis use and psychotic disorders: an update

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