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Depression and the risk of autoimmune disease: a nationally representative, prospective longitudinal study

  • N. W. Andersson (a1) (a2) (a3), L. N. Gustafsson (a1), N. Okkels (a1) (a4), F. Taha (a3), S. W. Cole (a5), P. Munk-Jørgensen (a1) and R. D. Goodwin (a3) (a6)...
Abstract
Background.

Autoimmune diseases are associated with substantial morbidity and mortality, yet the etiology remains unclear. Depression has been implicated as a risk factor for various immune-related disorders but little is known about the risk of autoimmune disease. This study examined the association between depression and the risk of autoimmune disease, and investigated the temporal and dose-response nature of these relationships.

Method.

A prospective population-based study including approximately 1.1 million people was conducted using linked Danish registries. Depression and autoimmune diseases were diagnosed by physicians and documented in medical records. In total, 145 217 individuals with depression were identified between 1995 and 2012. Survival analyses were used to estimate the relative risk of autoimmune disease among those with, compared to without, depression. Analyses were adjusted for gender, age, and co-morbid mental disorders.

Results.

Depression was associated with a significantly increased risk of autoimmune disease [incidence rate ratio (IRR) 1.25, 95% CI 1.19–1.31], compared to those without a history of depression. Results suggest a general increased risk of autoimmune diseases following the onset of depression during first year (IRR 1.29, 95% CI 1.05–1.58), which remained elevated for the ensuing 11 years and beyond (IRR 1.53, 95% CI 1.34–1.76). Findings did not support a dose-response relationship.

Conclusions.

Depression appears to be associated with an increased risk of a range of autoimmune diseases. Depression may play a role in the etiology of certain autoimmune conditions. If replicated, findings could highlight additional clinical implications in the treatment and management of depression. Future studies are needed to investigate the possible social, genetic, and neurobiological underpinnings of these relationships.

Copyright
Corresponding author
* Address for correspondence: R. D. Goodwin, PhD, MPH, Department of Psychology, Queens College and The Graduate Center, City University of New York, 65-30 Kissena Bvld, Queens, NY 11367, USA. (Email: renee.goodwin@qc.cuny.edu)
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