Adverse childhood experiences (ACEs), stressful or traumatic events occurring prior to the age of 18 (e.g. abuse, neglect, household dysfunction, or community adversity), are highly prevalent and independently associated with cardiometabolic disease risk. Altered postprandial hemodynamic adjustments may signify subclinical cardiometabolic risk and could represent an important early pathophysiological link between ACEs and poor cardiometabolic health outcomes. Purpose: To determine whether meal-induced changes in arterial dynamics are related to ACE exposure among healthy young adults. We hypothesized that ACE exposure would be associated with blunted meal-induced reductions in augmentation index (AIx). Methods: Twenty-four healthy young adults (9M/15F; 22±3 y; 24.7±3.1 kg/m 2 ) with normal HbA1c (4.6±0.5%) completed the Maltreatment and Abuse Chronology of Exposure (MACE) questionnaire and then an oral mixed meal tolerance test. ACE exposure was quantified using a multiplicity score representing the total exposure to ten categories of maltreatment during childhood (0-18 years). Eleven participants were classified as having low (0–1 ACE; ACELOW), while thirteen were classified as having moderate-to-high (≥2 ACEs; ACEM-H) ACE exposure. Heart rate-adjusted augmentation index (AIx75) was assessed via pulse wave analysis before, and every 15 minutes for one hour after ingestion of a liquid mixed meal (62% carbohydrate, 22% fat) providing energy equivalent to 20% of basal metabolic rate (321±42 mL; 101 kcal/100 mL). Mixed-effects repeated measures ANOVAs were used to examine the effects of ACE exposure (ACELOW vs ACEM-H) on meal-induced changes in AIx75. Results: There was a significant ACE exposure ´ time interaction (F = 2.8; p = 0.032). AIx75 decreased from baseline to 15 (-10% -3, -17, p < 0.01), 30 (-9% -2, -16, p = 0.02), and 45 (-10% 0, -20, p = 0.04) minutes postprandial in ACELOW, but did not change in ACEM-H participants (all p ≥ 0.29). Thus, while preprandial AIx75 was not different in ACELOW versus ACEM-H, postprandial AIx75 was lower in ACELOW than ACEM-H at 15 (-14 -3, -25, p = 0.015), 45 (-10 -1, -19, p = 0.03), and 60 min (-9 -1, -18, p = 0.03) after meal consumption. Conclusion: Oral consumption of a mixed meal caused significant reductions in AIx75 in ACELOW participants likely owing to decreases in peripheral vascular resistance caused by meal-induced vasodilation. However, no such effects were observed in ACEM-H. Thus, our findings suggest that prior ACE exposure is associated with blunted postprandial arterial responses in apparently healthy young adults, which could serve as a possible link between early life stress and risk of cardiometabolic diseases later in life. Future studies will be necessary to specifically probe whether these effects are due to impaired metabolic hormone-related signaling in the endothelium. Funding: This project was supported by from PI discretionary funds and funding from the NIH (L30HL149066 and NCATS UL1TR002537). This abstract was presented at the American Physiology Summit 2026 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.
Flores et al. (Fri,) studied this question.