Abstract
A medical model seems inescapable when considering the biological factors that may contribute to schizophrenia. The question is which medical model is most appropriate. An interactive developmental model provides, we believe, a broad conception of disease that is most adequate for integrating the available facts relevant to the etiologies of schizophrenia. However, genetic and biochemical hypotheses have often been presented within a narrower biomedical model of illness. Such a model has stated or implied that deviations in brain physiology are sufficient to account for schizophrenia without the need to implicate environmental factors. In such a view, psychology and sociology are recognized as relevant to the expression of illness, of course, but etiology is viewed solely in biomedical terms. The presumed brain dysfunction could be conceptualized as structural or functional. In either case, etiology might originate within the brain (e.g., in abnormal limbic system anatomy or function), or the brain could be viewed as the organ of response (e.g., to an abnormal metabolite formed in the gut or liver).
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Strauss, J.S., Carpenter, W.T. (1981). Etiologies of Schizophrenia. In: Schizophrenia. Critical Issues in Psychiatry. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0327-3_7
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