LAUSR

Introduction: Adverse childhood experiences (ACEs) are severe psychosocial stressors during the first 18 years of life that promote substantial increases in lifetime risk of cardiovascular disease. ACEs are highly prevalent and associated with impaired vascular endothelial function (VEF) and poor sleep, established cardiovascular risk factors. The purpose of this study was to investigate the role of sleep efficiency (SE%) in the association of ACEs with impaired VEF in young adults. We hypothesized that SE% would mediate the association of ACEs with impaired VEF. μethods: In 22 young adults (75% Female; age = 26 ± 7 y), we assessed ACE exposure and anxiety and depressive symptoms using the Zung Self-Rating Anxiety and Center for Epidemiologic Studies Depression scales, respectively. We assessed SE% as the reported total sleep duration relative to the time-in-bed from the Pittsburgh Sleep Quality Index. We also measured VEF using the flow mediated dilation technique normalized to the shear rate area under the curve. Using zero-order correlations we examined relations among ACE exposure, anxiety and depression symptoms, SE%, VEF, and age. We then utilized multiple-linear regression to examine the effect of ACE exposure and SE% on VEF while accounting for anxiety and depression symptoms. Finally, to better understand the role of SE% in the association of ACE exposure with VEF, we conducted mediation analysis with SE% as the mediator using the bootstrapped bias-corrected percentile confidence interval method. Results: ACEs were highly prevalent (64% with ≥1 ACE; 32% with ≥3 ACEs) and variable (range = 0 – 8 ACEs) in our sample. ACE exposure was associated with anxiety (r=0.48, p=0.018) and depression symptoms (r=0.48, p=0.024), SE% (r=-0.46, p=0.03), and VEF (r=-0.63, p=0.002), but was not associated with age (p=0.96). SE% was associated with VEF (r=0.59, p=0.004), but not correlated with age, anxiety, or depressive symptoms (all p≥0.14). Multiple linear regression analyses indicated that ACE exposure (β=-0.54, p<0.01) and SE% (β=0.45, p=0.02) predicted VEF independently of anxiety and depression symptoms. Further, SE% mediated the association of ACE exposure with VEF (indirect path β-estimate = -0.08 [95% CI = -0.21 – -0.009). Conclusions: ACE exposure is negatively associated with endothelial function, while SE% is positively associated with endothelial function independently of anxiety or depression symptoms among young adults. Notably, SE% appears to be a mediator in the relation between ACE exposure and endothelial function. Larger studies will be needed to more precisely quantify the role of disturbed sleep in the association of ACE exposure with impaired VEF and to determine whether improving sleep causes improvements in vascular health among those with high ACE exposure. This project was supported, in part, by funding from a pilot grant from the Iowa Injury Prevention Research Center through the CDC (R49 CE003095; NDMJ), an Old Gold Summer Fellowship (University of Iowa; NDMJ), the National Center For Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR002537 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.