Pubdate: Sat, 23 Nov 2002
Source: British Medical Journal, The (UK)
Copyright: 2002 The BMJ
Contact:  http://www.bmj.com/
Details: http://www.mapinc.org/media/60
Note: LTEs regarding published articles should be submitted via the 
website's 'rapid response' facility (box at top right of the article in 
question) or may be emailed to contact address above but must include a 
subheading to article
Authors: Louise Arseneault, Mary Cannon, Richie Poulton, Robin Murray,
Avshalom Caspi, and Terrie E Moffitt

CANNABIS USE IN ADOLESCENCE AND RISK FOR ADULT PSYCHOSIS: LONGITUDINAL
PROSPECTIVE STUDY

Papers pp 1195, 1199 Louise Arseneault, lecturer a, Mary Cannon,
Wellcome Trust advanced fellow b, Richie Poulton, director, Dunedin
multidisciplinary health and development study c, Robin Murray,
professor b, Avshalom Caspi, professor a, Terrie E Moffitt, professor
a.

a SGDP Research Centre, King's College, London SE5 8AF, b Division of
Psychological Medicine, King's College, c Dunedin Multidisciplinary
Health and Development Research Unit, University of Otago, Dunedin,
New Zealand

Correspondence to: T E Moffitt The strongest evidence that cannabis use may be a risk factor for
later psychosis comes from a Swedish cohort study which found that
heavy cannabis use at age 18 increased the risk of later schizophrenia
sixfold. 1 2 This study could not establish whether adolescent
cannabis use was a consequence of pre-existing psychotic symptoms
rather than a cause. We present the first prospective longitudinal
study of adolescent cannabis use as a risk factor for adult
schizophreniform disorder, taking into account childhood psychotic
symptoms3 antedating cannabis use.

View this table:  Association between cannabis use in adolescence and
schizophrenia and depressive symptoms and disorders at age 26
(n=3D759), controlling for childhood psychotic symptoms and use of
other drugs in adolescence

Methods And Results

The Dunedin multidisciplinary health and development study (a study of
a general population birth cohort of 1037 individuals born in Dunedin,
New Zealand, in 1972-3)4 has a 96% follow up rate at age 26. It
obtained information on psychotic symptoms at age 11 and drug use at
ages 15 and 18 from self reports and assessed psychiatric symptoms at
age 26 with a standardised interview schedule to obtain DSM-IV
(diagnostic and statistical manual of mental disorders, 4th edition)
diagnoses. We analysed data from a representative group of 759 (74%)
living study members who had complete data on adult psychiatric
outcomes, adolescent use of illicit substances, and childhood
psychotic symptoms.

We divided the sample into three groups based on cannabis use at ages
15 and 18. The 494 controls (65.1% of the sample) had reported using
cannabis "never" or "once or twice" at both ages; cannabis users by
age 18 (236; 31.1%) first reported using cannabis "three times or
more" at age 18; and cannabis users by age 15 (29; 3.8%) had reported
using cannabis "three times or more" at age 15 (all of whom continued
to use cannabis at age 18).

Psychiatric outcomes at age 26 were symptoms of schizophrenia and
depression and diagnoses of schizophreniform disorder and depression.

Multiple linear regression analyses showed that cannabis users by age
15 and by age 18 had more schizophrenia symptoms than controls at age
26 (table). These results remained significant after psychotic
symptoms at age 11 were controlled for. The effect was stronger with
earlier use.

Logistic regression analyses showed that people who used cannabis by
age 15 were four times as likely to have a diagnosis of
schizophreniform disorder at age 26 than controls. After psychotic
symptoms at age 11 were controlled for, the risk for adult
schizophreniform disorder remained higher among those who used
cannabis at age 15; however, this risk was reduced by 31% and was no
longer significant.

Cannabis use by age 15 did not predict depressive outcomes at age 26.
Use of other drugs in adolescence did not predict schizophrenia
outcomes over and above the effect of cannabis use.

Comment

Using cannabis in adolescence increases the likelihood of experiencing
symptoms of schizophrenia in adulthood. Our findings agree with those
of the Swedish study1 and add three new pieces of evidence. Firstly,
cannabis use is associated with an increased risk of experiencing
schizophrenia symptoms, even after psychotic symptoms preceding the
onset of cannabis use are controlled for, indicating that cannabis use
is not secondary to a pre-existing psychosis. Secondly, early cannabis
use (by age 15) confers greater risk for schizophrenia outcomes than
later cannabis use (by age 18). The youngest cannabis users may be
most at risk because their cannabis use becomes longstanding.5
Thirdly, risk was specific to cannabis use, as opposed to use of other
drugs, and early cannabis use did not predict later depression. Our
findings now require replication in large population studies with
detailed measures of cannabis use and schizophrenia.

Although most young people use cannabis in adolescence without harm, a
vulnerable minority experience harmful outcomes. A tenth of the
cannabis users by age 15 in our sample (3/29) developed
schizophreniform disorder by age 26 compared with 3% of the remaining
cohort (22/730). Our findings suggest that cannabis use among
psychologically vulnerable adolescents should be strongly discouraged
by parents, teachers, and health practitioners. Policy makers and law
makers should concentrate on delaying onset of cannabis use.

Acknowledgments

We thank the Dunedin study members, data managers HonaLee Harrington
and Barry Milne, study founder Phil Silva, and Air New Zealand.
Helpful comments on earlier drafts were provided by Griffith Edwards.

Contributors: LA participated in the study design, analysed and interpreted
the data, and wrote the first draft of the paper. MC and RP participated in
the study design and assisted with the analysis and interpretation of the
data and the writing of the paper. RM, AC, and TEM participated in the
study design and assisted with the interpretation of the data and writing
of the paper. RP, AC, and TEM coordinated the collection of the data. LA,
RP, and TEM are guarantors of the study.

Footnotes

Editorial by Rey and Tennant

Funding: The Dunedin Multidisciplinary Health and Development Research Unit
and RP are supported by the New Zealand Health Research Council. This
research received support from the Schizophrenia Research Fund, London (MC,
AC, TEM), the UK Medical Research Council, the EJLB Foundation (MC) and
from US-NIMH grants MH45070 (TEM) and MH49414 (AC). LA is supported by the
Canadian Institute of Health Research. TEM is a Royal Society-Wolfson Merit
Award holder.

Competing interests: None declared.

References

1.  Andreasson S, Allebeck P, Engstrom A, Rydberg U. Cannabis and
schizophrenia: a longitudinal study of Swedish conscripts. Lancet 1987; ii:
1483-1485.
2.  Strang J, Witton J, Hall W. Improving the quality of the cannabis
debate: defining the different domains. BMJ 2000; 320: 108-110[Free Full
Text].
3.  Poulton R, Caspi A, Moffitt TE, Cannon M, Murray RM, Harrington H.
Children's self-reported psychotic symptoms and adult schizophreniform
disorder: a 15-year longitudinal study. Arch Gen Psychiatry 2000; 57:
1053-1058[ISI][Medline].
4.  Silva PA, Stanton WR, eds. From child to adult: the Dunedin
multidisciplinary health and development study. Auckland: Oxford University
Press, 1996.
5.  Fergusson DM, Horwood LJ. Early onset cannabis use and psychosocial
adjustment in young adults. Addiction 1997; 92: 279-296[ISI][Medline].
- ---
MAP posted-by: SHeath(DPFFlorida)