Depression and immune function: central pathways to morbidity and mortality.
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.


METHODS
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.
Kiecolt-Glaser
Janice K
JK
Department of Psychiatry, The Ohio State University College of Medicine, 1670 Upham Drive, Columbus, OH 43210, USA. kiecolt-glaser.l@osu.edu
Glaser
Ronald
R
D000375:Aging / Q000276:immunology*; D002097:C-Reactive Protein / Q000096:biosynthesis; D002318:Cardiovascular Diseases / Q000276:immunology; D003866:Depressive Disorder / Q000453:epidemiology / Q000276:immunology* / Q000401:mortality; D003920:Diabetes Mellitus / Q000276:immunology; D015438:Health Behavior; D006305:Health Status Indicators; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D015850:Interleukin-6 / Q000096:biosynthesis
D015850:Interleukin-6; D002097:C-Reactive Protein