Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study

The abstract of an article published in the March 1st edition of the British Medical Journal:

By Rebecca Kuepper, research psychologist (1), Jim van Os, professor (1), visiting professor (2), Roselind Lieb, professor (3,4), Hans-Ulrich Wittchen, professor (4,5), Michael Höfler, research statistician (5), Cécile Henquet, lecturer (1)

1. Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Center, Maastricht, Netherlands
2. King’s College London, King’s Health Partners, Department of Psychosis Studies, Institute of Psychiatry, London, UK
3. Department of Psychology, Division of Epidemiology and Health Psychology, University of Basel, Switzerland
4. Max Planck Institute of Psychiatry, Munich, Germany
5. Institute of Clinical Psychology and Psychotherapy, Technical University Dresden, Germany
   

Objective

To determine whether use of cannabis in adolescence increases the risk for psychotic outcomes by affecting the incidence and persistence of subclinical expression of psychosis in the general population (that is, expression of psychosis below the level required for a clinical diagnosis).


Design

Analysis of data from a prospective population based cohort study in Germany (early developmental stages of psychopathology study).


Setting

Population based cohort study in Germany.


Participants

1923 individuals from the general population, aged 14-24 at baseline.


Main outcome measure

Incidence and persistence of subthreshold psychotic symptoms after use of cannabis in adolescence. Cannabis use and psychotic symptoms were assessed at three time points (baseline, T2 (3.5 years), T3 (8.4 years)) over a 10 year follow-up period with the Munich version of the composite international diagnostic interview (M-CIDI).


Results

In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021). Furthermore, continued use of cannabis increased the risk of persistent psychotic symptoms over the period from T2 to T3 (2.2, 1.2 to 4.2; P=0.016). The incidence rate of psychotic symptoms over the period from baseline to T2 was 31% (152) in exposed individuals versus 20% (284) in non-exposed individuals; over the period from T2 to T3 these rates were 14% (108) and 8% (49), respectively.


Conclusion

Cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms.

Posting of this abstract is for the purposes of research into psychosis.

Also see:

Cannabis use 'raises psychosis risk' - study

Cannabis use 'doubles risk of psychosis for teenagers'

Marijuana Use Linked to Risk of Psychotic Symptoms

Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study


Image credit

Evidence That Familial Liability for Psychosis Is Expressed as Differential Sensitivity to Cannabis

The abstract of a paper posted online on October 4th by the journal Archives of General Psychiatry:

An Analysis of Patient-Sibling and Sibling-Control Pairs

By Genetic Risk and Outcome in Psychosis (GROUP) Investigators

Context

Individual differences in cannabis sensitivity may be associated with genetic risk for psychotic disorder.

Objectives

To demonstrate and replicate, using 2 conceptually different genetic epidemiological designs, that (familial) liability to psychosis is associated with sensitivity to cannabis.

Design, Setting, and Participants

Sibling-control and cross-sibling comparisons using samples of patients with a psychotic disorder (n = 1120), their siblings (n = 1057), and community controls (n = 590) in the Netherlands and Flanders.

Main Outcome Measures

Positive and negative schizotypy using the Structured Interview for Schizotypy–Revised (for siblings and controls) and self-reported positive and negative psychotic experiences using the Community Assessment of Psychic Experiences (for siblings and patients). Cannabis use was assessed as current use (by urinalysis) and lifetime frequency of use (by Composite International Diagnostic Interview).

Results

In the sibling-control comparison, siblings displayed more than 15 times greater sensitivity to positive schizotypy associated with particularly current cannabis use by urinalysis (adjusted B = 0.197, P < .001) than controls (adjusted B = 0.013, P = .86) (P interaction = .04) and a similar difference in sensitivity to its effect on negative schizotypy (siblings: adjusted B = 0.120, P < .001; controls: B = –0.008, P = .87; P interaction = .03). Similarly, siblings exposed to cannabis resembled their patient relative nearly 10 times more closely in the positive psychotic dimension of the Community Assessment of Psychic Experiences (adjusted B = 0.278, P < .001) compared with nonexposed siblings (adjusted B = 0.025, P = .12) (P interaction < .001). No significant effect was apparent for the Community Assessment of Psychic Experiences negative domain, although the association was directionally similar (2 times more resemblance; P interaction = .17). Cross-sibling, cross-trait analyses suggested that the mechanism underlying these findings was moderation (familial risk increasing sensitivity to cannabis) rather than mediation (familial risk increasing use of cannabis).

Conclusions

Genetic risk for psychotic disorder may be expressed in part as sensitivity to the psychotomimetic effect of cannabis. Cannabis use may synergistically combine with preexisting psychosis liability to cause positive and negative symptoms of psychosis.

Author Affiliations:

René S. Kahn MD, PhD, Department of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, the Netherlands; Don H.Linszen MD, PhD, Department of Psychiatry, Academic Medical Centre, University of Amsterdam, Amsterdam, the Netherlands; Jim van Os MD, PhD, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Centre, Maastricht, the Netherlands, and King's College London, King's Health Partners, Department of Psychosis Studies, Institute of Psychiatry, London, United Kingdom; Durk Wiersma PhD, Department of Psychiatry, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; Richard Bruggeman MD, PhD, Department of Psychiatry, University Medical Center Groningen, University of Groningen; Wiepke Cahn MD, PhD, Department of Psychiatry, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht; Lieuwe de Haan MD, PhD, Department of Psychiatry, Academic Medical Centre, University of Amsterdam; Lydia Krabbendam PhD, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Centre; and Inez Myin-Germeys PhD, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University Medical Centre.

Posting of this abstract is for the purposes of research into psychosis and schizophrenia.

Largest effort to find gene-environment interactions underlying schizophrenia risk

An article posted on July 16th by news-medical.net:

At the 23rd ECNP Congress 2010 in Amsterdam, Professor Dr. Jim van Os, Chairman of the Department of Psychiatry and Neuropsychology at Maastricht University Medical Centre, The Netherlands, will present the EU-GEI project, involving more than 7,500 patients and their families, which brings together a multidisciplinary research team from 15 countries in the largest effort to date to find gene-environment interactions underlying schizophrenia risk. In particular, he will explain the development of tools that will make it possible to monitor, and possibly modify, vulnerability at the behavioural level, thus preventing transition to overt illness.

Schizophrenia and related psychotic disorders are the most mysterious and costliest of mental disorders in terms of human suffering and societal expenditure, representing a major challenge to scientists. Until recently, researchers had relatively few starting points in trying to unravel the causes of psychosis and to identify better treatments. While epidemiological research has characterised powerful environmental effects on schizophrenia risk, twin and family studies have established that more than half of the vulnerability for schizophrenia is of genetic origin. However, despite enormous investments, it has proven extremely difficult to identify molecular genetic variants underlying schizophrenia liability. According to the model of gene-environment interaction, genes influencing schizophrenia risk may do so indirectly by making individuals more sensitive to the effects of causal environmental risk factors (e.g. urbanisation, migration, cannabis use, childhood trauma). Now, for the first time, a focused scientific collaboration has been organised in Europe in order to elucidate the causes of schizophrenia, focussing on both genes and environments in the same research project.

Image credit

A salience dysregulation syndrome

The abstract of an editorial published in the February 2009 edition of The British Journal of Psychiatry:

By Jim van Os, MRCPsych (pictured}

Department of Psychiatry and Neuropsychology
Maastricht University Medical Centre
PO BOX 616 (DRT10) Maastricht
The Netherlands



Revisions of DSM and ICD are forthcoming. Should the old categories of psychotic disorder, in particular the construct of schizophrenia, be retained or is a new system of representation of psychosis in order? It is argued that both scientific and societal developments point to a system of classification combining categorical and dimensional representations of psychosis in DSM and ICD. Furthermore, it is proposed to introduce, analogous to the functional descriptive term `metabolic syndrome', the diagnosis of salience dysregulation syndrome. Within this syndrome, three sub-categories may be identified, based on scientific evidence of relatively valid and specific contrasts: with affective expression; with developmental expression; and not otherwise specified.

Posting of this abstract is for the purposes of research into schizophrenia and psychosis.