Plants - Drugs Mind - Spirit Freedom - Law Arts - Culture Library  
Erowid References Database
Fergusson DM, Horwood LJ, Ridder EM. 
“Tests of causal linkages between cannabis use and psychotic symptoms”. 
Addiction. 2005 Mar;100(3):354-66.
AIMS: To examine possible causal linkages between cannabis use and psychosis using data gathered over the course of a 25-year longitudinal study.

DESIGN: A 25-year longitudinal study of the health, development and adjustment of a birth cohort of 1265 New Zealand children (635 males, 630 females).

SETTING: The Christchurch Health and Development Study, a general community sample.

PARTICIPANTS:A total of 1055 participants from the Christchurch Health and Development Study (CHDS) cohort for whom data on cannabis use and psychotic symptoms were available on at least one occasion from 18, 21 and 25 years.

MEASUREMENTS: As part of this study, data were gathered on frequency of cannabis use and psychotic symptoms at ages 18, 21 and 25 years.

FINDINGS: Regression models adjusting for observed and non-observed confounding suggested that daily users of cannabis had rates of psychotic symptoms that were between 1.6 and 1.8 times higher (P < 0.001) than non-users of cannabis. Structural equation modelling suggested that these associations reflected the effects of cannabis use on symptom levels rather than the effects of symptom levels on cannabis use.

CONCLUSIONS: The results of the present study add to a growing body of evidence suggesting that regular cannabis use may increase risks of psychosis. The present study suggests that: (a) the association between cannabis use and psychotic symptoms is unlikely to be due to confounding factors; and (b) the direction of causality is from cannabis use to psychotic symptoms.
Comments and Responses to this Article
Apr 17, 2011 1:59
Study Fails to Resolve Causation Issue #

A handful of issues come up around this and similar studies. Recently, this topic has been receiving wide media attention, including such lurid quotes as, 'Smoking cannabis almost doubles the risk of psychotic mental illness...' [Evening Standard, March 1, 2005]

The evidence that cannabis use may be increasing 'psychotic' mental symptoms is growing steadily. The Fergusson et al. paper and other studies make it clear that the question of causation needs to be addressed seriously.

However, I remain skeptical that this report resolves any of the problems regarding the theory that cannabis use actually causes psychosis rather than increasing risk factors for those with a relatively high propensity for psychotic symptoms. The correlation between cannabis use and psychosis (or schizotypal symptoms) is a hot topic, and has led to an increase in funding to address the concern, in concert with increased media coverage over the last 5 years. Indeed, several related articles have been published. However, noteworthy problems in trying to prove a casual linkage between psychosis and cannabis use remain, including:

1) Lack of epidemiological evidence. The assertion that cannabis use directly causes psychosis has not been determined through epidemiological studies. The use of cannabis in the United States and other countries starting in the 1950s and ending around 1980 increased substantially. For instance, the percentage of cannabis use went from (rough estimates) 1-5% of the population to 50% of 20-25 year olds.Clear data about the prevalence of cannabis use before 1970 is sparse, but estimates generally put the number well below 5% of the U.S. population before 1960.

'The earliest survey data on marijuana use in the U.S. was obtained through a Gallup Poll in the spring of 1967. The nationally-based telephone poll of college students found a 5% lifetime prevalence of marijuana use. Two years later, this proportion jumped to 22%. A Gallup Poll of the adult population in the summer of 1969 found a 4% lifetime prevalence...[Harrison et al 1995]

If there were a causal connection between cannabis use and psychosis, a commensurate increase in the rates of psychosis would likely manifest. The fact that psychosis rates did not increase in conjunction with the increase in cannabis use suggests causation is unlikely (cf. Degenhardt et al, Degenhardt & Hall 2002).

2) Confounding factors. The authors (Fergusson, Horwood, Ridder 2005) admit that there are many confounding factors when trying to establish causation between behavior and psychophysiological symptoms. A large part of their paper is dedicated to listing confounds and describing how they attempted to work around them. Although they do try to control for many with the study design (longitudinal, exclusion criteria, statistical model, etc.), factors not recognized or considered could account for the apparent connection. Perhaps the main confound that the authors attempt to address is the possibility that people who experience psychotic symptoms self-medicate or are more likely to use cannabis because of the symptoms. Although there may be cases where this is true, several studies, including this one, have begun to foreclose on the possibility that the correlation between psychotic symptoms and cannabis can be explained by psychosis causing an increase in cannabis use. Unfortunately, it will be some time before definitive answers can be given on this and other confounds.

3) Measures of psychosis. Fergusson et al provide very little raw data and only a few tables of highly derived statistics, so one is left making assumptions about their findings. The psychosis measured was based on self reports using an instrument (set of questions in survey form) called the Symptom Checklist 90 (SCL-90), rather than DSM-IV diagnosis criteria. The researchers selected 10 questions they determined represented psychotic symptoms.

The questions they chose present serious problems for measuring psychosis in this population of highly studied birth-cohort in New Zealand who were part of a 25 year longitudinal health study that asked questions about cannabis use and mental health that were used as the data for this paper. The self-reported symptom survey questions include:

'...having ideas and beliefs that others do not share; ... feeling other people cannot be trusted; feeling that you are watched or talked about by others.'

The list of symptoms chosen to identify psychosis may ostensibly bias the outcome measures to fit their hypothesis that psychosis is caused by cannabis use. There are two major points to be made here:

a) Cannabis is a strong psychoactive plant and is well known to cause paranoid ideation. The researchers do not specify whether they asked the participants to exclude from their answers the periods during which they were intoxicated. Asking someone who smoked pot if they have felt paranoid recently does not give indication that the person is psychotic. In other words, paranoia associated with cannabis inebriation is ephemeral.

b) Cannabis use is illegal. It is almost a tautology to say that cannabis users in societies where its use is strongly prohibited 'have ideas and beliefs that others do not share' and that they 'feel other people cannot be trusted'. Those who use cannabis are at risk of losing personal freedoms if arrested for possession, which is enough to make users careful about selecting those they can trust with their usage. I see no indication that the authors of this survey were aware of the possible confound that the illegal and subculture nature of the use of cannabis could be a factor in the outcome of the study.

4) Medicinal Interactions. Although no indication is given as to whether diagnosed psychotics were identified in the study and their data considered separately, there is the possibility that people who are undergoing treatment for mental health problems may experience a negative interaction between their medication and the cannabis itself, increasing the frequency of psychotic symptoms (see below)

This is a fairly minor point, because diagnosed psychotics should only represent a small portion of the study sample. However, it needs to be taken into consideration when evaluating a study design that looks at symptoms and relapse rates for psychosis sufferers. Some anti-psychotics -- especially haloperidol-type drugs -- are considered to be very unpleasant to take if one uses cannabis (Marchese et al. 2003; Green et al. 2004). If there is a substantial increase in side effects caused by an interaction between medications and cannabis, it is important to separate those from the more general effect of cannabis on the population. In other words, these examples suggest that cannabis use 'worsens symptoms for psychosis sufferers' rather than causes psychosis.

Although the authors of this article and the media reports about it suggest they have resolved many of the confounding issues, it seems obvious this is unfounded. It is widely accepted that cannabis use can worsen symptoms in psychotics and schizophrenics, but this study does not prove that cannabis causes psychosis in otherwise healthy people.

It is imperative that future studies address these issues in order to inform accurately the public and scientific community about the association between cannabis use and psychotic symptoms.

- - - - - - - - - - - -

References Cited:

* BBC. Drug 'doubles mental health risk'. March 1, 2005.

* Degenhard L, Hall W. 'Cannabis and Psychosis'. Current Psychiatry Reports 2002, 4:191-196. June 2002.


* Evening Standard, March 1, 2005. 'Cannabis doubles the risk of psychosis'

* Green AI, Tohen MF, Hamer RM, Strakowski SM, Lieberman JA, Glick I, Clark WS. 'First episode schizophrenia-related psychosis and substance use disorders: acute response to olanzapine and haloperidol.' Schizophr Res. 2004 Feb 1;66(2-3):125-35.

* Harrison LD, Backenheimer M, Inciardi JA. 'Cannabis use in the United States: Implications for policy.' In: Peter Cohen & Arjan Sas (Eds)(1996), Cannabisbeleid in Duitsland, Frankrijk en de Verenigde Staten. Amsterdam, Centrum voor Drugsonderzoek, Universiteit van Amsterdam. pp. 206-230. 1995.

* Marchese G, Casti P, Ruiu S, Saba P, Sanna A, Casu G, Pani L. 'Haloperidol, but not clozapine, produces dramatic catalepsy in delta9-THC-treated rats: possible clinical implications.' Br J Pharmacol. 2003 Oct;140(3):520-6. Epub 2003 Aug 26.
Submit Comment
[ Cite HTML ]