Just as psychotic disorders, their symptoms,course, and treatment response vary between individuals, they differ across places and demographic groups too.
This, in combination with progress in the area of molecular genetics, has generated interest in more complicated models of schizophrenia aetiology that explicitly posit gene-environment interactions.
According to twin and family studies more than half of the vulnerability for schizophrenia is of genetic origin. However, attempts to discover genes that relate directly to psychotic disorder have been frustrating, mainly due to the phenomenon of gene-environment interaction, which is defined as genetic control of sensitivity to the environment.
Exciting findings in other areas of psychiatry have motivated researchers to turn their attention to better understanding the complex ways in which genetic factors interact with non-genetic factors to produce psychosis.
Conceptualised in a model, gene-environment interaction proposes that genes influencing risk for schizophrenia may not do so directly (the dominant model until recently), but indirectly by making individuals more sensitive to the effects of causal environmental risk factors.
Gene-environment interaction approach is particularly suitable 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 this approach, research is focussing on subclinical symptoms that can be traced to prior persistence of clinically relevant symptoms.
According to the model of psychosis proneness - persistence - impairment, genetic background factors impact on a broadly distributed and transitory population expression of psychosis during development. Hence, poor prognosis, in terms of persistence and clinical need, can be predicted by environmental exposure interacting with genetic risk.
