Abstract

Abstract Introduction Psychosocial stress exposure during the first 18 years of life promotes adverse sleep and cardiometabolic health effects. The purpose of the study was to investigate the relationships between childhood stress (CS), sleep efficiency (SE), and fasting glucose levels (FG) in young adulthood. Methods In 24 adults between the ages of 18 and 35 years (83% Female; mean±SD, age = 24±5 y), CS was assessed using a retrospective childhood stress assessment and averaged across reference ages of 5, 10, and 15 years old. FG concentrations were obtained from whole blood samples and SE was assessed using an actigraphy device (ActTrust2) worn on the wrist for 7 days, yielding ≥6 days of sleep data. Zero-order correlations were used to investigate the relationships among CS, SE, and FG. Multiple linear regression analyses were used to examine the effect of CS and SE on FG controlling for sex. To explore preliminary indications of a mechanistic effect of SE on the link between CS and FG, ANCOVA analysis was used. Participants were grouped as either low CS (CS-low) or high CS (CS-high), and analyses were completed with sex as the only covariate and sex and SE as covariates, with FG as the outcome. Results CS was associated with FG (r=0.50, p=0.01) and SE (r=-0.41, p=0.47), and SE with FG (r=-0.45, p=0.03). The association of CS with FG (β=0.51, p=0.016) and SE (β=-0.43, p=0.046) remained with adjustment for sex. ANCOVA analyses confirmed the effect of CS on FG, where FG was higher in CS-high than CS-low with adjustment for sex (92.4±4.8 vs. 83.6±5.4 mg/dL; p=0.008). Additional adjustment for SE reduced the difference between CS-high and CS-low, but this difference remained significant (91.6±5.0 vs. 84.5±5.5 mg/dL; p=0.044). Conclusion CS is linked with elevated FG and low SE in young adults. Our preliminary data suggest that SE warrants further examination as a potential mechanism by which CS relates to FG, but larger sample sizes will be necessary to draw definitive conclusions. Support (if any) Research reported in this publication was supported in part by the NCATS of the NIH (UL1TR002537) and by the Injury Prevention Research Center through the CDC (R49 CE003095).

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