The incidence of psychotic disorders varies greatly across places and demographic groups, as do symptoms, course, and treatment response across individuals. High rates of schizophrenia in large cities, and among immigrants, cannabis users, and traumatised individuals reflect the causal influence of environmental exposures. 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.
Unravelling the causes of psychotic disorders
Schizophrenia and related psychotic disorders have a complex aetiology. Research has attempted to determine the role of specific biological variables, such as genetic and biochemical factors and subtle changes in brain morphology. Genetic vulnerability in schizophrenia is shared in part with bipolar disorder and recent molecular genetic findings also indicate an overlap with developmental disorders such as autism (Van Os & Kapur, 2009). 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 and often disappointing, and despite enormous investments, the identification of actual molecular genetic variants underlying schizophrenia liability has proven extremely difficult. This difficulty is 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. Biological vulnerability factors with a genetic background interact with complex physical, psychological and environmental vulnerability factors. Conceptualised in a model, gene-e
|Contact: Sonja Mak|
European College of Neuropsychopharmacology