Answers are grounded in this paper and cite their sources.
Objective/background Unhealthy sleep may be associated with metabolic and inflammatory dysregulation. We aimed to describe longitudinal patterns of sleep duration and sleep efficiency from childhood through adolescence and to examine their associations with metabolic and inflammatory biomarkers at 18 years of age among participants of the 2004 Pelotas Birth Cohort. Methods A total of 2,344 participants were included. Sleep duration and efficiency were assessed using ActiGraph accelerometers from ages 6, 11, and 15; a semi-parametric group-based approach was used to identify different sleep trajectories. Biochemical markers (glucose, total cholesterol, HDL cholesterol, albumin, creatinine, uric acid, triglyceride, and C-reactive protein; CRP) were measured in serum samples collected at age 18. Multiple linear regression models examined the associations between exposures and outcomes. Results Four trajectories of sleep duration and three trajectories of sleep efficiency were identified. The “Maintenance and Decline” trajectory was associated with higher CRP levels (ratio of geometric means = 1.68; 95% CI: 1.15–2.46), while the “Decline and Slight Increase” group showed higher uric acid levels (β = 0.31; 95% CI: 0.10–0.53). Participants with “Lower Efficiency” had higher CRP and creatinine concentrations (ratio of geometric means = 1.30; 95% CI: 1.00–1.68) (β = 0.04; 95% CI: 0.00- 0.07) and those with “Intermediate Efficiency” had lower HDL cholesterol concentration (β = −1.23; 95% CI: −2.42 to −0.03). Conclusion These findings suggest that sleep patterns across childhood and early adolescence were associated with inflammatory and lipid biomarkers at age 18, supporting the relevance of sleep in studies of cardiometabolic health during development.
No takes yet. Share an insight, caveat, or question.
Maciel et al. (2026) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: