Psychological Medicine

Original Article

Does normal developmental expression of psychosis combine with environmental risk to cause persistence of psychosis? A psychosis proneness–persistence model

a1 INSERM U 657, University Victor Segalen Bordeaux 2, IFR99 of Public Health, Bordeaux, France
a2 Department of Psychiatry and Neuropsychology, South Limburg Mental Health Research and Teaching Network, EURON, Maastricht University, Maastricht, The Netherlands
a3 Netherlands Institute of Mental Health and Addiction (Trimbos Institute), Utrecht, The Netherlands
a4 Max Planck Institute of Psychiatry, Clinical Psychology and Epidemiology Unit, Munich, Germany
a5 Institute of Clinical Psychology and Psychotherapy, Technical University Dresden, Dresden, Germany
a6 Division of Psychological Medicine, Institute of Psychiatry, London, UK

Article author query
cougnard a   [PubMed][Google Scholar] 
marcelis m   [PubMed][Google Scholar] 
myin-germeys i   [PubMed][Google Scholar] 
de graaf r   [PubMed][Google Scholar] 
vollebergh w   [PubMed][Google Scholar] 
krabbendam l   [PubMed][Google Scholar] 
lieb r   [PubMed][Google Scholar] 
wittchen hu   [PubMed][Google Scholar] 
henquet c   [PubMed][Google Scholar] 
spauwen j   [PubMed][Google Scholar] 
van os j   [PubMed][Google Scholar] 


Background. Research suggests that low-grade psychotic experiences in the general population are a common but transitory developmental phenomenon. Using two independent general population samples, the hypothesis was examined that common, non-clinical developmental expression of psychosis may become abnormally persistent when synergistically combined with developmental exposures that may impact on behavioural and neurotransmitter sensitization such as cannabis, trauma and urbanicity.

Method. The amount of synergism was estimated from the additive statistical interaction between baseline cannabis use, childhood trauma and urbanicity on the one hand, and baseline psychotic experiences on the other, in predicting 3-year follow-up psychotic experiences, using data from two large, longitudinal, random population samples from the Netherlands [The Netherlands Mental Health Survey and Incidence Study (NEMESIS)] and Germany [The Early Developmental Stages of Psychopathology (EDSP) study].

Results. The 3-year persistence rates of psychotic experiences were low at 26% in NEMESIS and 31% in EDSP. However, persistence rates were progressively higher with greater baseline number of environmental exposures in predicting follow-up psychotic experiences (χ2=6·9, df=1, p=0·009 in NEMESIS and χ2=4·2, df=1, p=0·04 in EDSP). Between 21% and 83% (NEMESIS) and 29% and 51% (EDSP) of the subjects exposed to both environmental exposures and psychotic experiences at baseline had persistence of psychotic experiences at follow-up because of the synergistic action of the two factors.

Conclusion. The findings suggest that environmental risks for psychosis act additively, and that the level of environmental risk combines synergistically with non-clinical developmental expression of psychosis to cause abnormal persistence and, eventually, need for care.

c1 Department of Psychiatry and Neuropsychology, Maastricht University, PO Box 616 (DRT 10), 6200 MD Maastricht, The Netherlands. (Email: