Psychobiological Determinants of Stress Reactivity in Schizophrenia
Schizophrenia is a debilitating illness, characterized by significant impairment in functioning across the social, emotional, and cognitive domains. Although there is strong evidence to suggest that life stressors precede symptom exacerbation in schizophrenia, important gaps in the research literature still remain. First, the biological mechanisms through which stress may contribute to the onset and expression of clinical symptoms have not been well defined. Second, there is considerable variability across schizophrenia patients in terms of their susceptibility to an elevation in symptoms following life stress.
According to the neural-diathesis stress model of schizophrenia, cortisol interacts with a biological vulnerability for heightened dopamine neurotransmission to influence illness expression. Utilizing this framework, the present investigation sought to clarify whether the specific stressor and patient characteristics that lead to heightened cortisol release also place patients at greater risk for stress-induced relapse. Furthermore, this study was designed so as to elucidate whether cortisol serves as one of the biological mechanisms through which life stress gets "under the skin" to influence symptom expression in schizophrenia.
Drawing upon data obtained from 125 schizophrenia patients and 95 healthy individuals, results indicated that clinical symptoms were most closely linked to acute and chronic stressors characterized by social evaluative content. Specific individual difference factors, including low trait positive affect, a reduced use of adaptive coping styles, early life adversity, and the Met allele of the catechol-O-methyltransferase Val158Met (COMT) polymorphism, placed patients with schizophrenia at greater risk for symptom exacerbation following the experience of social evaluative stress. In healthy individuals, low trait positive affect and maladaptive coping styles moderated the relationship between life stress and depressive symptoms. Results also indicated that the specific individual characteristics moderating the relationships between social evaluative episodic stress and clinical symptoms also influenced the magnitude of the cortisol response to a laboratory psychosocial stressor, the Trier Social Stress Test. These findings have implications for not only furthering our understanding of the psychobiological determinants of stress reactivity in schizophrenia, but can contribute significantly to the development of specific treatment and management strategies aimed at resolving stress in the lives of individuals with this debilitating condition.