Depression and immune function: Central pathways to morbidity and mortality

• Published in: Journal of psychosomatic research 2002-10, Vol.53 (4), p.873-876
• Main Authors: Kiecolt-Glaser, Janice K, Glaser, Ronald
• Format: Article
• Language: English
• Subjects: Aging - immunology; C-Reactive Protein - biosynthesis; Cardiovascular Diseases - immunology; Chronic diseases; Depression; Depressive Disorder - epidemiology; Depressive Disorder - immunology; Depressive Disorder - mortality; Diabetes Mellitus - immunology; Health Behavior; Health Status Indicators; Humans; Immune response; Inflammation - immunology; Interleukin 6; Interleukin-6 - biosynthesis; Older people; Proinflammatory cytokines; Psychoneuroimmunology; Stress
• ISSN: 0022-3999; 1879-1360
• DOI: 10.1016/S0022-3999(02)00309-4

Objective: The increased morbidity and mortality associated with depression is substantial. In this paper, we review evidence suggesting that depression contributes to disease and death through immune dysregulation. Method: This review focuses on recent human studies addressing the impact of depression on immune function, and the health consequences of those changes. Results: There is growing evidence that depression can directly stimulate the production of proinflammatory cytokines that influence a spectrum of conditions associated with aging, including cardiovascular disease, osteoporosis, arthritis, type 2 diabetes, certain cancers, periodontal disease, frailty, and functional decline. Additionally, depression can down-regulate the cellular immune response; as a consequence, processes such as prolonged infection and delayed wound healing that fuel sustained proinflammatory cytokine production may be promoted by depression. Conclusions: These direct and indirect processes pose the greatest health risks for older adults who already show age-related increases in proinflammatory cytokine production. Thus, aging interacts with depression to enhance risks for morbidity and mortality.