Allostatic load in patients with post-traumatic stress disorder (PTSD): Stress and blood pressure regulation

Introduction: Post-traumatic stress disorder (PTSD) may increase the risk of cardiovascular disease (CVD). Greater levels of daily stress and exaggerated cardiovascular responses to stress with PTSD may contribute to high allostatic load, or the cumulative physiological effects accompanying chronic stress, and subsequently lead to elevated blood pressure and CVD. The purpose of this study was to compare levels of daily stress, systolic blood pressure (SBP) responses during acute stress, and 24-hour SBP values in PTSD and control (CON) subjects, and the relationships between these variables. We hypothesized greater levels of daily stress, SBP responses during acute stress and 24-hour SBP values in PTSD, as well as positive relationships between SBP responses during acute mental and physical stressors, levels of daily stress, and 24-hour SBP values. Methods: In PTSD ( n = 4, 31±8 yrs) and CON subjects ( n = 8, 34±7 yrs), we measured SBP changes (Δ; Finapres) during separate 3-minutes of mental arithmetic (MA) and static handgrip exercise (SHG) at 40% of their maximal voluntary contraction. Over 7-days, subjects kept a daily log of stressful events (DLSE). Last, subjects underwent ambulatory blood pressure monitoring (ABPM) for 24 hours. Group differences were assessed using unpaired t -tests and simple linear regression was performed to explore relationships between variables. Results: Peak ΔSBP was greater in PTSD compared to CON during MA (18±7 vs. 10±4, mmHg, P =0.03) and SHG (51±9 vs. 31±11 mmHg, P =0.01). In PTSD, compared to CON, there was a greater number of stressors/day (5±2 vs. 2±1, no., P <0.01), mean stressor severity (3±1 vs. 2±0, 1-5 scale, P <0.01), and sum stressor severity (SSS) over 7 days (104±37 vs. 31±16, a.u., P =0.01). 24-hr SBP and awake SBP were not different between groups (125±14 vs. 113±7, mmHg, P =0.06 and 125±13 vs. 118±8, mmHg; P =0.21, respectively), although asleep SBP was greater in PTSD compared to CON (112±10 vs. 101±7 mmHg, P =0.04). Amongst all subjects, no significant relationships existed between the peak ΔSBP during MA and ABPM or DLSE variables. No significant relationships existed between ΔSBP during SHG and ABPM variables. Significant relationships were noted between peak ΔSBP during SHG and SSS (R=0.60, P =0.05) and between SSS and 24-hr SBP (R=0.62, P =0.05) Conclusion: These data indicate peak ΔSBP during acute mental and physical stressors are exaggerated in PTSD. Along with greater levels of stress over a 7-day period, those with PTSD may experience higher SBP, particularly while asleep. Although a relationship existed between peak ΔSBP during SHG and SSS, as well as 24-hr SBP and SSS, these data do not clearly indicate significant relationships between ΔSBP during acute stress, DLSE and ABPM variables. In all, exaggerated ΔSBP during acute stress and elevated levels of daily stress may be important factors contributing to increased allostatic load and CVD risk, though further investigation is needed to clearly define these relationships. This project was funded by the National Institutes of Health (HL118313, D.W.W.) and the U.S. Department of Veterans Affairs (I01RX001311, D.W.W.; IK2RX003670, to K.B.). 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.