Exposure to Adverse Childhood Experiences and Insulin Resistance in Otherwise Healthy Young Adults: Role of Reduced Sleep Efficiency

Introduction: Adverse Childhood Experiences (ACEs) are significant psychosocial stressors occurring within the first 18 years of life that are associated with a dose-dependent, lifelong increase in risk of cardiometabolic diseases such as type II diabetes. Recent evidence has suggested that ACE exposure may be associated with insulin resistance as well as with disturbed sleep prior to overt disease. Further, experimental studies demonstrate that reducing sleep quality impairs insulin sensitivity. Therefore, we hypothesized that sleep quality would mediate the relation of ACE exposure with insulin resistance. Purpose: To investigate the role of sleep quality in ACEs-related insulin resistance in apparently healthy young adults. Methods: A total of 56 other healthy young adults (mean ± SD; age = 25 ± 5 y, BMI = 25 ± 5 kg/m 2 ) completed this cross-sectional cohort study and had ACE exposure, sleep, and HOMA-IR data available. ACE exposure was quantified as the total number of affirmative responses to specific ACE exposures (e.g., abuse, witnessed violence, household dysfunction) with a possible range of 0–10. Sleep quality was characterized as reported habitual sleep efficiency (SE%) and calculated as total sleep duration relative to time-in-bed via the Pittsburgh Sleep Quality Index (PSQI). Insulin resistance was assessed by calculating the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) using fasting glucose and insulin concentrations. Associations of ACE exposure with HOMA-IR and SE% were assessed independently using multiple-linear regression while accounting for age, sex, BMI, and anxiety and depression symptoms. The mediating effect of SE% in the association of ACE exposure with HOMA-IR was then examined using the bootstrapped (1,000 replications) bias-corrected percentile confidence interval method. The variance accounted for (VAF) was calculated as the ratio of the indirect effect to total effect β-coefficients and a VAF of 20%–80% and >80% was interpreted qualitatively as partial and full mediation, respectively. Results: ACE exposure was independently associated with HOMA-IR (β =.37, p = 0.02) and SE% (β = -.30, p = 0.03). The indirect effect of ACE exposure on HOMA-IR mediated by SE% was not significant (β ab = 0.04 [95% CI: -0.03, 0.12]; p = 0.098), although the VAF by SE% was 27.2%. Conclusions: These findings support that ACE exposure is independently associated with increased insulin resistance and reduced self-reported habitual sleep efficiency. While there was evidence that sleep efficiency partially mediated the association of ACE exposure on HOMA-IR, this effect was not statistically significant likely due to limitations in statistical power. Future prospective studies will be necessary to understand the strength and nature of these associations to determine whether metabolic health can be improved by improving sleep in individuals with ACE exposure. Pilot grant from the Iowa Injury Prevention Research Center through the CDC (R49 CE003095; NDMJ), and funding from the NIH (R01HL167788, L30HL149066, and NCATS UL1TR002537). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.