A New Look at the Neural Diathesis-Stress Model of Schizophrenia, by Jones and Fernyhough

Nevertheless, more than biopsychosocial models, which emphasize factor interdependence, it is the diathesis-stress model, according to which a stressor may trigger an initial illness episode in persons with a genetic predisposition (diathesis), which seems to have become the predominant framework for thinking about the condition (see Jones and Fernyhough 2007 for a discussion of the neural version of this model). In spite of the epigenetic turn and the awareness that culture matters, schizophrenia remains depicted primarily as a brain disease.

Vidal, Fernando and Ortega, Francisco. Being Brains: Making the Cerebral Subject (Forms of Living)....

Abstract

The neural diathesis-stress model of schizophrenia proposes that stress, through its effects on cortisol production, acts upon a preexisting vulnerability to trigger and/or worsen the symptoms of schizophrenia. In line with its focus on the neurobiology of stress response in schizophrenia, this model treats stressors as a homogeneous category. Recent research has shown that, in healthy individuals, cortisol is most strongly produced in response to stressors that result from perceived uncontrollable threats to important goals and/or social-evaluative threats. We hypothesize that it is specifically these stressors that trigger and/or worsen the symptoms of schizophrenia in those with a preexisting vulnerability. This hypothesis may provide a way of making sense of contradictory findings on the relations between stress and schizophrenia. We propose some empirical tests of this hypothesis and explore implications for the treatment and management of the disorder.

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