The course and outcome of schizophrenia: toward a new social biology of psychosis

Abstract

In recent decades, those searching for the causes of schizophrenia have not been especially interested in the social and cultural environment of their subjects. To some extent this is understandable: the prospect of models of risk in which causal agents are embedded in the social environment, operating at micro-, mezzo-, and macro levels, with untold complexities of interaction, has not seemed overly attractive. Moreover, because much of the earlier research into the role of family and social factors in the genesis of schizophrenia was so seriously flawed and of poor methodological quality, we focused on ‘harder’ and more easily measured biological mechanisms. The emphasis shifted to schizophrenia as a ‘brain disease’ with arguments appearing to rest on the proposition that if a disease is biological in character, it follows that it is biological in causation. The need for scientific respectability, the seductions of emerging new technologies, and the skilful and highly resourced advocacy roles of pharmaceutical companies, all played their part in ensuring that theory development in schizophrenia largely ignored social models of causation. As a result, our conceptual approach to the social environment became relatively crude and dualistic, with a tendency to dismiss associations between the schizophrenia phenotype and its environment as ‘fall out’ from what is happening in the brain.