Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation.

TitleSleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation.
Publication TypeJournal Article
Year of Publication2016
AuthorsIrwin MR, Olmstead R, Carroll JE
JournalBiol Psychiatry
Volume80
Issue1
Pagination40-52
Date Published2016 Jul 1
ISSN1873-2402
Abstract

BACKGROUND: Sleep disturbance is associated with inflammatory disease risk and all-cause mortality. Here, we assess global evidence linking sleep disturbance, sleep duration, and inflammation in adult humans.

METHODS: A systematic search of English language publications was performed, with inclusion of primary research articles that characterized sleep disturbance and/or sleep duration or performed experimental sleep deprivation and assessed inflammation by levels of circulating markers. Effect sizes (ES) and 95% confidence intervals (CI) were extracted and pooled using a random effect model.

RESULTS: A total of 72 studies (n > 50,000) were analyzed with assessment of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor α (TNFα). Sleep disturbance was associated with higher levels of CRP (ES .12; 95% CI = .05-.19) and IL-6 (ES .20; 95% CI = .08-.31). Shorter sleep duration, but not the extreme of short sleep, was associated with higher levels of CRP (ES .09; 95% CI = .01-.17) but not IL-6 (ES .03; 95% CI: -.09 to .14). The extreme of long sleep duration was associated with higher levels of CRP (ES .17; 95% CI = .01-.34) and IL-6 (ES .11; 95% CI = .02-20). Neither sleep disturbances nor sleep duration was associated with TNFα. Neither experimental sleep deprivation nor sleep restriction was associated with CRP, IL-6, or TNFα. Some heterogeneity among studies was found, but there was no evidence of publication bias.

CONCLUSIONS: Sleep disturbance and long sleep duration, but not short sleep duration, are associated with increases in markers of systemic inflammation.

DOI10.1016/j.biopsych.2015.05.014
Alternate JournalBiol. Psychiatry
PubMed ID26140821
PubMed Central IDPMC4666828
Grant ListK01 AG044462 / AG / NIA NIH HHS / United States
R01 AG026364 / AG / NIA NIH HHS / United States
R01 AG034588 / AG / NIA NIH HHS / United States
R01 CA160245 / CA / NCI NIH HHS / United States