How Stress Kills:  New Perspectives on Stress and Inflammation

Proinflammatory cytokines influence the onset and course of a spectrum of conditions associated with aging.  The production of proinflammatory cytokines can be substantially enhanced by stress and depression.  Furthermore, stress and depression also contribute to greater risk for infection, prolonged infectious episodes, and delayed wound healing, all processes that indirectly fuel sustained proinflammatory cytokine production. Compounding the risks, health behaviors including poor sleep are commonplace consequences of stress and depression; poor sleep enhances proinflammatory cytokine production. In addition to these pathways, stress and depression can permanently alter the responsiveness of the immune system; stressors can effectively prime the inflammatory response, promoting larger proinflammatory cytokine increases in response to subsequent stressors and/or minor infectious challenges.  Through these pathways stress and depression may influence the incidence and progression of age-related diseases. Interventions that diminish stress or depression or inflammation may enhance health through their positive impact on immune and endocrine regulation.