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Stress precipitates depression. Depression, in turn, generates and exacerbates life stress.  Chronic stress and depression share common physiologic processes, including perturbations of the hypothalamic pituitary-adrenal (HPA) axis and potential disruption of the normal circadian rhythm of cortisol secretion.  Despite evidence  to suggest that stress-induced dysregulation of HPA axis plays a key role in the etiology and course of depression, the specific relationships among stress, depression, and HPA function over time have yet to be fully elucidated.  The proposed study will explore stress-depression relationships in a sample of depressed patients at high risk for chronic life stress, i.e., depressed mothers of psychiatrically ill children.  Thirty depressed mothers taking part in a psychosocial treatment trial will be recruited to provide salivary cortisol samples over a two-day period, and to complete an acute stress reactivity task and assessments of depression, anxiety, past and current life stress, perceived stress and perceived social support at two time points:  baseline and post-treatment (16 weeks later)  This project will pilot the inclusion of a psychophysiologic stress assessment battery within the context of our outpatient depression prevention clinic.  We hypothesize that depressed patients reporting both childhood trauma and recent life stress will display the greatest basal and acute cortisol release.  We also hypothesize that patients receiving active interpersonal psychotherapy will report a greater reduction in perceived stress and a greater increase in perceived social support as compared with patients receiving treatment as usual, and that these indicators will be associated with cortisol outcomes at the post-treatment assessment.  This project will provide pilot data needed to support an RO1 application developed to characterize the interplay of stress, depression, and HPA function among chronically-burdened, depressed outpatients with treatment and over time.
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  12/7/2005  tc

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