Abstract

Abstract Introduction Poor sleep has been shown to negatively impact cardiometabolic health. Adverse Childhood Experiences (ACEs), potentially traumatic events occurring within the first 18 years of life, have been linked to both poor sleep and cardiometabolic disease in adulthood. Evidence is needed to understand whether poor sleep plays a mechanistic role in the link between ACE exposure and cardiometabolic risk. The purpose of this study was to examine associations of ACE exposure with self-reported sleep efficiency (SE%) and waist circumference (WC). Methods In 25 young adults (21F/4M; mean±SD, age=25±5 y), we assessed ACE exposure using the 10-item ACE Questionnaire and SE% as the reported average sleep duration relative to time-in-bed from the Pittsburgh Sleep Quality Index. We measured WC, a known cardiometabolic risk factor, as a surrogate of visceral adiposity. We used multiple linear regression analyses to examine associations between ACE exposure, SE%, and WC adjusted for sex. We then utilized ANCOVA analyses to examine the possible mechanistic effect of SE% on the relationship between ACE exposure and WC. For these analyses, participants with 0-1 ACEs were categorized as low-ACE exposure (ACE-low) and participants with 2+ ACEs were categorized as moderate-to-high ACE exposure (ACE-mh). Results Following adjustment for sex, ACE score predicted SE% (β=-0.53, p=0.009) and WC (β=0.52, p=0.01), and SE% predicted WC (β=-0.44, p=0.03). Similarly, ANCOVA analyses indicated that ACE-mh was associated with greater WC than ACE-low, adjusted for sex (adjusted means ± 95% CI, 0.86 ± 0.07 m vs. 0.78±0.06 m; p=0.049). However, the effect of ACE group on WC was no longer significant following inclusion of SE% as a covariate (0.84 ± 0.07 m vs. 0.80 ± 0.07 m; p=0.29). Conclusion Both ACEs and sleep efficiency are associated with visceral adiposity. Further, SE% may serve as a mechanistic biobehavioral link between ACE exposure and increased visceral adiposity in young adults. These preliminary findings warrant further investigation with implications for sleep interventions as a possible preventative approach to reduce cardiometabolic risk in individuals exposed to ACEs. Support (if any) Research reported in this publication was partly supported by the NCATS of the NIH (UL1TR002537) and by the Injury Prevention Research Center through the CDC (R49 CE003095).

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