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Abstract
Extremes of sleep duration have been associated with adverse health outcomes. The
mechanism is unclear but may be related to increased inflammation. We sought to assess
the association between sleep duration and inflammatory biomarkers.
A total of 614 individuals from the Cleveland Family Study completed questionnaires
about sleep habits and underwent polysomnography. A morning fasting blood sample was
assayed for 5 inflammatory cytokines.
In this cohort, mean (SD) habitual sleep duration based on self-report was 7.6 (1.6)
h and mean sleep duration by polysomnography (PSG) on the night prior to blood sampling
was 6.2 (1.3) h. After adjusting for obesity and apnea severity, each additional hour
of habitual sleep duration was associated with an 8% increase in C-reactive protein
(CRP) levels (P=0.004) and 7% increase in interleukin-6 (IL-6) levels (P=0.0003).
These associations were independent of self-reported sleepiness. In contrast, PSG
sleep duration was inversely associated with tumor necrosis factor alpha (TNFa) levels.
For each hour reduction in sleep, TNFalpha levels increased by 8% on average (P=0.02).
Sleep duration was not associated with IL-1 or IL-10.
Increases in habitual sleep durations are associated with elevations in CRP and IL-6
while reduced PSG sleep duration is associated with elevated TNFa levels. Activation
of pro-inflammatory pathways may represent a mechanism by which extreme sleep habits
affect health.