The 'genotype x environmental interaction' approach differs from the linear gene-phenotype approach by positing a causal role not for either genes or environment in isolation but for their synergistic co-participation in the cause of psychosis where the effect of one is conditional on the other (Van Os et al., 2008). Gene-environment interaction seems a particularly suitable approach for understanding the development of psychosis because this phenotype is known to be associated with environmentally mediated risks, yet people display considerable heterogeneity in their response to those environmental exposures.
In the framework of gene-environment interaction, research is focussing on subclinical symptoms that can be traced to prior persistence of clinically relevant symptoms. For example, in a substantial proportion of patients with bipolar disorder, onset of illness may be seen as the poor outcome of a developmentally common and usually transitory non-clinical bipolar phenotype (Tijssen et al., 2010).
In schizophrenia and related psychotic disorders, the median prevalence of subclinical psychotic experiences is reported to be around 5% and the median incidence rate to be around 3%. The difference between prevalence and incidence rates, together with data from follow-up studies, indicates that approximately 75% of developmental psychotic experiences are transitory and disappear over time. There is evidence, however, that transitory developmental expression of psychosis ('psychosis proneness') may become abnormally persistent ('persistence') and subsequently clinically relevant ('impairment'), depending on the degree of environmental risk the person is additionally exposed to (Van Os et al.,
|Contact: Sonja Mak|
European College of Neuropsychopharmacology