Summary and conclusions

After nearly a century of epidemiological research, many essential questions about the nature and causes of schizophrenia still await answers. Two major conclusions stand out.

First, the clinical syndrome of schizophrenia is robust and can be identified reliably in diverse populations, regardless of wide-ranging demographic, ecological, and cultural differences among them. This suggests that a common pathophysiology is likely to underlie the characteristic symptoms of schizophrenia. On balance, the evidence suggests that no major differences in incidence and disease risk can be found across populations at the level of large population aggregates. However, the study of 'atypical' populations such as genetic isolates or minority groups may be capable of detecting unusual variations in the incidence of schizophrenia that could provide novel clues to the aetiology and pathogenesis of disorder.

The second conclusion is that no single environmental risk factor of major effect on the incidence of schizophrenia has yet been discovered. Further studies using large samples are required to evaluate potential risk factors, antecedents, and predictors for which the present evidence is inconclusive. Assuming that the methodological pitfalls of risk-factor epidemiology (such as the 'ecological fallacy') can be avoided and that a number of variables will eventually be identified as risk factors of small to moderate effect, the results will complement those of genetic research which also implicate multiple genes. All this suggests that the key to understanding schizophrenia is likely to be found in gene-environment interactions.

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