DOI
https://doi.org/10.25772/0VAC-EH14
Author ORCID Identifier
https://orcid.org/0000-0002-0428-6910
Defense Date
2025
Document Type
Dissertation
Degree Name
Doctor of Philosophy
Department
Rehabilitation and Movement Science
First Advisor
Ryan S. Garten, PhD
Second Advisor
Jody Greaney, PhD
Third Advisor
Danielle Kirkman, PhD
Fourth Advisor
Paula Rodriguez-Miguelez, PhD
Abstract
Posttraumatic stress disorder (PTSD) is a complex mental health condition with profound physiological implications, particularly affecting cardiovascular health. While extensive research has been conducted on its psychological effects, growing evidence links PTSD to significant disruptions in autonomic regulation, often characterized by an overactive sympathetic nervous system and diminished parasympathetic function. These autonomic disturbances raise the likelihood of CVD, such as hypertension and heart disease. The elevated CVD risk is further amplified by increased oxidative stress (OXS) in individuals with PTSD, as their chronic activation of the body’s stress response leads to excessive production of reactive oxygen species (ROS). This excess production of ROS damages cellular structures, promotes inflammation, and impairs vascular function, thereby compounding the physiological burden imposed by PTSD and contributing to further deterioration in cardiovascular health. The main objective of this study is to enhance our understanding of how PTSD influences cardiovascular health, particularly examining its relationship with autonomic and vascular function, and exploring the distinct role of oxidative stress. Despite the well-documented link between PTSD and CVD, the precise mechanisms by which the mental health disorder leads to cardiovascular dysfunction are still unclear, particularly with regard to the role of oxidative stress in driving the observed autonomic dysfunction. We adopted a multifaceted approach which minimized confounding factors such as negative lifestyle behaviors and aging, by selecting a young cohort of adults with PTSD and comparing them to an age- and sex-matched control group to assess these gaps. This approach enables us to isolate the independent physiological effects of PTSD. To investigate the potential role of oxidative stress in these physiological processes, we introduced antioxidant supplementation and studied its effects on key autonomic and cardiovascular measures. By comparing responses under placebo and antioxidant conditions across the PTSD and CTRL groups, we aimed to unveil the intricate dynamics at play between cardiovascular regulation, autonomic function, and oxidative stress in the context of PTSD. The major findings of the study indicate that, compared to healthy controls, young adults with PTSD exhibited a baseline autonomic dysregulation, characterized by elevated heart rate and blood pressure, which was unaffected by antioxidant supplementation. This suggests that any maladaptations observed in PTSD may not be directly driven by oxidative stress. Additionally, alterations in baroreflex sensitivity and vascular function highlight a complex interaction between PTSD and cardiovascular mechanisms. These findings imply that PTSD may disrupt normal cardiovascular responses, leading to a range of adaptive and potentially maladaptive changes in heart rate control and vascular regulation. This study contributes to a growing body of research on the physiological impacts of PTSD, providing new insights into how autonomic and vascular function are altered in this population. This opens avenues for further research into potential therapeutic interventions targeting specific pathways to mitigate CVD risk in those with PTSD.
Rights
© Jennifer B. Weggen
Is Part Of
VCU University Archives
Is Part Of
VCU Theses and Dissertations
Date of Submission
4-29-2025