Depression and Immune Function: Central Pathways to Morbidity and Mortality

J Psychosom Res. 2002 Oct;53(4):873-6. doi: 10.1016/s0022-3999(02)00309-4.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Aging / immunology*
  • C-Reactive Protein / biosynthesis
  • Cardiovascular Diseases / immunology
  • Depressive Disorder / epidemiology
  • Depressive Disorder / immunology*
  • Depressive Disorder / mortality
  • Diabetes Mellitus / immunology
  • Health Behavior
  • Health Status Indicators
  • Humans
  • Inflammation / immunology*
  • Interleukin-6 / biosynthesis

Substances

  • Interleukin-6
  • C-Reactive Protein