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More evidence establishes clear link between use of cannabis and psychiatric illness
In the 1990s the use of cannabis increased much
among young people so that it is now becoming more common than tobacco
smoking in some countries.1-2 The ready availability of
the drug, the increasing social disapproval of cigarette smoking, stern
drink driving laws, and perceptions that cannabis is safe or less
harmful than cigarettes or alcohol may explain these changes. The
increase in use is of concern because cannabis may be a gateway to
other drugs,3 and it may cause psychiatric illnesses. The
link between cannabis and psychosis is well established, and recent
studies have found a link between use of marijuana and
depression.4-7 Does cannabis cause these conditions, or
do patients use cannabis to relieve their distress?
The explanation most accepted is that cannabis triggers the onset or
relapse of schizophrenia in predisposed people and also exacerbates the
symptoms generally.
4 5
Establishing direction of
causality is difficult and is most appropriately assessed in non-clinical samples, but a low incidence of the illness and the fact
that most drug users take other drugs in addition to cannabis create
methodological problems and explain the dearth of reliable evidence.
The study often quoted in support of the causal hypothesis examined the
incidence of schizophrenia in more than 50 000 Swedish conscripts
followed up for 15 years.8 It showed that use of marijuana
during adolescence increased the risk of schizophrenia in a
dose-response relation. Questions have, however, remained about the
validity of the diagnosis, the possible causal role of other drugs, and
prodromal symptoms of schizophrenia that might have led to the use of
cannabis, rather than cannabis triggering the
psychosis.
4 5
A longer follow up and reanalysis of this cohort published in this
issue (p 1199) confirms the earlier findings and clarifies that
cannabis, and not other drugs, is associated with later schizophrenia and that this is not explained by prodromal symptoms.9 In
a similar vein, a three year follow up of a Dutch cohort of 4045 people
free of psychosis and 59 with a baseline diagnosis of psychotic disorder showed a strong association between use of cannabis and psychosis.10 Length of exposure to use of cannabis
predicted the severity of the psychosis, which likewise was not
explained by use of other drugs. Participants who showed psychotic
symptoms at baseline and used cannabis had a worse outcome, which also implies an additive effect. In a New Zealand cohort, individuals who
had used cannabis three times or more by age 15 or 18 were not more
likely to have schizophreniform disorder at age 26 (p 1212), although
they showed an increase in "schizophrenia symptoms" (but not
schizophrenia).11 The meaning of "schizophrenia
symptoms" requires clarification to interpret these results.
The evidence in relation to depression is growing. A 15 year follow up
of an adult community sample of 1920 participants in the United States
showed that use of cannabis increased the risk of major depression at
follow up fourfold.7 Use of cannabis was specifically
associated with an increase in suicidal ideation and anhedonia. Similar
findings in an Australian study reported in this issue (p 1195) show a
dose-effect relation between the use of cannabis and anxiety or
depression in a large cohort of 14-15 year olds followed for seven
years.12 This is reflected in higher rates of anxiety or
depression according to the frequency with which cannabis was used. The
link is stronger for young women than young men in this cohort,
although sex differences have not been found in other
studies.
6 7
Baseline depression did not predict later
marijuana use in either study and therefore does not support the self
medication hypothesis. The study in the New Zealand cohort did not find
an association between cannabis use at age 15 and depressive disorder
at age 26. The authors found, however, that young people who had used
cannabis three times or more by age 18 were more likely to have a
depressive disorder at age 26, even after use of other drugs was
controlled for.
Although the number of studies is small, these findings
strengthen the argument that use of cannabis increases the risk of schizophrenia and depression, and they provide little support for the
belief that the association between marijuana use and mental health
problems is largely due to self medication. Whether the use of cannabis
triggers the onset of schizophrenia or depression in otherwise
vulnerable people or whether it actually causes these conditions in
non-predisposed people is not yet resolved. Further, it cannot be
assumed that mechanisms are the same for both conditions (cannabinoids
have effects on a variety of neurotransmitter systems) or at different
developmental stages. For example, although evidence shows that mental
disorder leads to the use of cannabis among adolescents, the reverse
seems true in early adulthood.13
The shown dose-response relation for both schizophrenia and depression
highlights the importance of reducing the use of cannabis in people who
use it. It was estimated that lack of exposure to cannabis would have
reduced the incidence of psychosis requiring treatment by as much as
50% in the Dutch cohort,10 and is similarly reflected in
the Swedish cohort, showing that the use of cannabis increased the risk
of schizophrenia by 30%.9 This large effect is surprising
and not yet reflected in an increased incidence of schizophrenia in the
population. If true, the use of cannabis will contribute to more
episodes or new cases of the illness University of Sydney, Coral Tree Family Service, PO Box 142, North Ryde, NSW 1670, Australia (jrey{at}doh.health.nsw.gov.au) University of Sydney, Royal North Shore Hospital, St Leonard's,
NSW 2065, Australia (ctennant{at}doh.health.nsw.gov.au)
food for thought for both
clinicians and legislators.
Christopher C Tennant
Footnotes
Competing interests: None declared.
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