Schizophrenia: genes and environment

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Abstract

The historical and genetic foundations of our current understanding of schizophrenia are reviewed, as are the present and future directions for research. Genetic epidemiological investigations, including family, twin, and adoption studies have confirmed the contributions of genetic and environmental determinants of schizophrenia. For example, identical twins show average concordance rates of only 50%; rates of 100% would be expected on the basis of genetic equivalence alone. Genetic factors may cause errors in brain development and synaptic connections. A broad range of environmental components may further damage the brain. Biological components may include pregnancy and delivery complications, such as intrauterine fetal hypoxia, infections, and malnutrition. Primarily nonbiological components may include psychosocial stressors, such as residence in an urban area and dysfunctional family communication. It is likely that the environmental factors interact with the genetic liability in a negative manner to produce disorders in the schizophrenic spectrum. Genetic and environmental components of the disorder are examined, as well as their interactions in producing either neurodevelopmental syndromes or schizophrenia itself. The implication of these findings for prevention and treatment are considered.

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Is schizophrenia a progressive neurodevelopmental disorder? Toward a unitary pathogenetic mechanism.

H B Woods (1998)

The author 1) reassesses the case against a neuronal degeneration hypothesis for schizophrenia; 2) demonstrates that the hypothesis that schizophrenia is a disorder caused by early (i.e., pre- or perinatal) and static (i.e., fixed, nonprogressive) damage to the brain is unsatisfactory because it cannot readily account for brain imaging results from schizophrenic patients and lacks both satisfactory clinical examples and experimental models of early, static developmental disorders resulting in the late spontaneous functional deterioration that characterizes schizophrenia; and 3) offers an alternative pathogenetic hypothesis for schizophrenia that is consistent with the available imaging and neuropathological data. Published data on schizophrenia and relevant clinical and experimental studies of neurodevelopment and its disorders are reviewed. The neuropathological studies provide strong evidence against a classic neurodegenerative pathogenesis of schizophrenia and moderate support for prenatal developmental abnormalities. The imaging data provide strong evidence that excessive brain volume loss occurs after maximum brain volume expansion and equivocal evidence that it continues after onset of overt illness. The available clinical and experimental models of late deterioration after static, early brain lesions are unconvincing. A progressive developmental mechanism can reconcile the neuropathological and imaging data, while being compatible with both early onset and late deterioration. It matters whether the pathogenetic agent in schizophrenia is static or progressive, since if it is the latter it is worthwhile to search not only for means of prevention but also for interventions that will arrest progression as early as possible.

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Urbanization and psychosis: a study of 1942-1978 birth cohorts in The Netherlands.

Leo F. M. Marcelis, F Mesa Navarro, C Meurs … (1998)

Urban birth is associated with later schizophrenia. This study examined whether this finding is diagnosis-specific and which individuals are most at risk. All live births recorded between 1942 and 1978 in any of the 646 Dutch municipalities were followed-up through the National Psychiatric Case Register for first psychiatric admission for psychosis between 1970 and 1992 (N = 42115). Urban birth was linearly associated with later schizophrenia (incidence rate ratio linear trend (IRR), 1.39; 95% confidence interval (95% CI), 1.36-1.42), affective psychosis (IRR, 1.18; 95% CI, 1.15-1.21) and other psychosis (IRR, 1.27; 95% CI, 1.24-1.30). Individuals born in the highest category of the three-level urban exposure were around twice as likely to develop schizophrenia. Associations were stronger for men and for individuals with early age of onset. The effect of urban birth was also stronger in the more recent birth cohorts. There are quantitative differences between diagnostic categories in the strength of the association between urban birth and later psychiatric disorder. High rates of psychosis in urban areas may be the result of environmental factors associated with urbanization, the effect of which appears to be increasing over successive generations.