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Volume 62, Issue 2, Pages 198-202 (February 2004)


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Daily hassles, cortisol, and the pathogenesis of depression

Leo SherCorresponding Author Informationemail address

Received 28 January 2003; accepted 9 October 2003.

Abstract 

Daily hassles and/or ongoing stress are associated with increased cortisol secretion in healthy individuals. Hassles are also associated with increased cortisol levels in depressed patients. Considerable evidence suggests that hypercortisolism is involved in the pathogenesis of depressive disorders. Over the past decade, there has been a shift from viewing excessive hypothalamic–pituitary–adrenal (HPA) activity in depression as an epiphenomenon to its having specific effects on symptom formation. The author suggests that increased cortisol secretion caused by daily hassles and/or ongoing stress contributes to the development of depressive disorders. Minor stressful events may lead to depression in vulnerable individuals. Genetic factors interact with environmental factors to influence the vulnerability to stress and mood disorders. The author also proposes that elevated cortisol levels associated with stressful daily events may worsen the condition of depressed patients. The author notes that one of the goals of prevention of stress-related disorders is to help individuals be more competent in managing their behavior and emotions in reaction to negative aspects of their environment, and briefly discusses stress management methods and techniques.

The risk of developing depression is determined by a complex interplay between genetic susceptibility, environmental exposures, and aging. These influences also account for long term changes in the regulation of HPA function. Further studies of HPA function may not only advance our understanding of the role of the HPA system in the etiology and pathogenesis of psychiatric disorders, but also be useful in refining conceptions of psychiatric disorders themselves and possible approaches to the treatment of these conditions.

Division of Neuroscience, Department of Psychiatry, Columbia University, 1051 Riverside Drive, Suite 2917, P.O. Box 42, New York, NY 10032, USA

Corresponding Author InformationTel.: +1-212-543-6240; fax: +1-212-543-6017

PII: S0306-9877(03)00320-7

doi:10.1016/S0306-9877(03)00320-7


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