Mental health practitioners used to think in terms of ‘visible’ environmental risks in relation to onset and persistence of psychiatric disorders. Stressful life events, obstetric complications and dysfunctional parental interactions are but a few examples. Traditional psychiatric epidemiology was concerned mainly with such environmental risks. Conversely, clinical genetics was until recently almost exclusively concerned with Mendelian syndromes, for which single-gene defects could be mapped by positional cloning. Over the past decades, however, there has been increasing awareness that, for common psychiatric disorders, ‘hidden’ genetic factors can have a substantial influence on the effect of environmental exposures or even pose as risk factors. As genes can be considered as a conventional epidemiological risk factor in association studies (Sham, 1996), and epidemiological theory can be readily applied to genetically sensitive datasets (Susser and Susser, 1989; Ottman, 1990), epidemiologists and human geneticists have been gradually integrating their respective fields of research into a new discipline called genetic epidemiology (Khoury et al., 1993). Within genetic epidemiology, the term ecogenetics refers to the study of specific gene-environment relationships, the application of which to schizophrenia is relevant though still in the initial stages (van Os and Marcelis, 1998; Malaspina et al., 1999).

The interplay of genes and environment

The models of gene-environment relationships presented below all assume that genetic and environmental factors increase the risk for schizophrenia rather than reducing it.