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Influence of circadian alignment and sleep timing variability on sex-specific inflammatory markers in healthy adults.

Brooke M. Shafer,Kathryn Mcauliffe,Sophia A Kogan,M. R. Roberts Davis,Steven A. Shea,Ryan Olson,Andrew W. McHill

Published 2025 in American Journal of Physiology. Heart and Circulatory Physiology

ABSTRACT

Sleep and circadian disruption affect inflammatory mechanisms; however, the extent which to sex plays a role in the relationship between the circadian timing of behaviors and markers of inflammation is unclear. We investigated sex-specific associations between circadian alignment, variability in sleep timing, and inflammatory markers in healthy adults. Forty-two volunteers (23 female) underwent an evening in-laboratory dim-light melatonin onset (DLMO) assessment. Plasma C-reactive protein (CRP; all participants) and tumor necrosis factor-α (TNF-α; subset n=27 [13 female]) were assayed. Circadian alignment (i.e., phase angle) was determined as the time difference between DLMO and average sleep onset for up to 14-days. Participants were categorized into narrow/wide phase angle groups based on median phase angle split. Variability in sleep timing was defined as the standard deviation (SD) of self-reported sleep onset and offset times. Within sex differences in inflammatory markers were compared between phase angle groups. Linear models were used to test the interaction between sex, circadian alignment, and sleep timing variability on markers of inflammation. Females in the narrow phase angle group had higher CRP, while males with narrow phase angles had higher TNF-α (p<0.01). Increased CRP was associated with a narrower phase angle (B(SE)=-0.69(0.25), p=0.01) and greater sleep offset timing variability (B(SE)=2.00(0.68, p<0.01) in females, whereas TNF-α was associated with a narrower phase angle (B(SE)=-0.11(0.05), p=0.04) in males. Circadian disruptions and more variable sleep patterns could contribute to inflammatory-related CVD pathology, particularly as it pertains to sex. These data may have implications for sex-specific disease risk assessment and risk reduction strategies.

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