Blunted rest-activity rhythm is associated with increased white blood-cell-based inflammatory markers in adults: an analysis from NHANES 2011-2014

ABSTRACT

Circadian rhythm disruption is associated with immune system disturbance and has been observed in many health problems where chronic-inflammation acts as a major contributor. We aim to examine whether rest-activity circadian rhythm is associated with chronic inflammation using white blood-cell-based inflammatory indices including white blood cell (WBC) count, neutrophil count, neutrophil-to-lymphocyte ratio (NLR) and systemic immune-inflammation index (SII). We analyzed the data from 8089 adults (age≥20) with at least 4 days of validated accelerometer recordings and a valid WBC count from the National Health and Nutrition Examination Survey (NHANES) 2011–2014. Non-parametric rest-activity circadian rhythm parameters were derived from the accelerometer recordings. In the models adjusting multiple covariates, a one-quantile increase in relative amplitude (i.e. more robust circadian rhythm) was associated with 1 × 10⁸ cells/L decrease in WBC number (95% CI: 5 × 10⁷ to 1.5 × 10⁸, P < .001), 7 × 10⁷ cells/L decrease in neutrophils (95% CI: 3 × 10⁷ to 1.1 × 10⁸, P = .003) and 15.2 × 10⁹ /L decrease in SII (95% CI: 6 × 10⁹ /L to 20 × 10⁹/L, P = .019). Consistent results were also observed for the association of M10 value and L5 value with these inflammatory indices. Our results indicated that blunted rest-activity circadian rhythm is associated with increased white blood-cell-based inflammatory indices in adults, suggesting interventions aiming at enhancing circadian rhythm by lifestyle programs may be a novel approach to improve the general health.

KEYWORDS:

• Rest-activity rhythm
• circadian rhythm
• WBC count
• inflammation

Acknowledgements

X. W. receives funding from NIH DK117365 and AHA SFRN863620 and S. S. receives funds from NIH HL143440 and MD013307.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Supplementary material

Supplemental data for this article can be accessed on the publisher’s website.

Additional information

Funding

This work was supported by the American Heart Association [SFRN863620]; National Institutes of Health [DK117365,HL143440,MD013307].