A process model for the development of schizophrenia.

Less than two decades ago scientists interested in the etiology of schizophrenia were still vigorously debating the nature-nurture controversy, with many adhering to the view that the illness grew either out of a constitutional deficit or a pathological family environment. Today, virtually all researchers adopt interactional models that include both constitutional and environmental factors. Interactional models are most often expressed in diathesis-stress terms: Development of schizophrenia requires both a biological vulnerability (diathesis) and stressful life circumstances that facilitate expression of the illness. Modern debate within the field now primarily focuses on understanding the characteristics of the biological diathesis, the stressful environment, and their interaction. Scientists using diathesis-stress theories have employed several research strategies (Rosenthal 1970): (1) consanguinity studies exploring the distribution of illness among the relatives of schizophrenics, (2) twin studies comparing the concordance of schizophrenic illness in monozygotic and dizygotic twin pairs reared together or apart, (3) retrospective studies examining the premorbid behavior and development of schizophrenic parents, and (4) prospective studies of children at high risk for schizophrenia. The population most frequently followed in prospective high-risk studies has been offspring of schizophrenics. Biological offspring of schizophrenics who are reared by their parents are at extremely high risk for becoming schizophrenic themselves, approximately ten times greater risk than the general population. The present paper will make use of the Israeli High-Risk Study to test a diathesis-stress model for the transmission of schizophrenia. The goodness of fit of this model to the data will be explored using a simple decision tree data analytic approach.