In anticipation of the 23rd European conference on psychosis and pharmacology, scientists discussed new models examining the combined role of genes and the environment.
According to the experts, the incidence of psychotic disorders varies greatly across places and demographic groups, as do symptoms, course, and treatment response across individuals.
Scientists note that high rates of schizophrenia in large cities, and among immigrants, cannabis users, and traumatized individuals reflect the influence of environmental exposures.
This, in combination with progress in the area of molecular genetics, has generated interest in more complicated models of schizophrenia that point to the role of gene-environment interactions.
Undoubtedly, schizophrenia and related psychotic disorders have a complex origin.
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.
Conceptualized 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.
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.
Given the evidence for detrimental effects of big cities on mental health and a wide range of somatic disorders, the impact of the increasing urbanisation and other environmental risk factors in European countries (e.g. migration) should be prioritized in scientific research.
Since genetic factors impact on a rather common, transitory expression of psychosis during development, poor prognosis in terms of clinical need can be predicted by environmental exposure interacting with genetic risk.
The current development of tools allowing the actual measurement of vulnerability caused by gene-environment interaction will enable clinicians to monitor, and possibly modify, vulnerability at the behavioural level.
Until recently, researchers found it difficult to unveil the causes of schizophrenia and related psychotic disorders.
100 years after the modern definition of schizophrenia, research is beginning to understand the biological mechanisms underlying the symptoms of this most mysterious of mental disorders and the psychosocial factors that moderate their expression.
Recent research findings in psychiatry indicate that genes are likely to influence disorder mostly indirectly, via their impact upon physiological pathways, and work by increasing the likelihood of developing a psychiatric disorder, rather than as direct causes of disorder per se (Van Os et al., 2008).
A significant proportion of psychotic disorders may be understood as the rare poor outcome of a common developmental phenotype characterized by persistence of detectable subclinical psychotic experiences.
The current model of gene-environment interaction is nurturing promising approaches to understand the symptoms of schizophrenia and related psychotic disorders and improve treatment.