Linking the hemodynamic consequences of adverse childhood experiences to an altered HPA axis and acute stress response.

Autor: Dempster KS; Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, Canada; Brock-Niagara Centre for Health and Well-Being, Brock University, Canada., O'Leary DD; Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, Canada; Brock-Niagara Centre for Health and Well-Being, Brock University, Canada. Electronic address: doleary@brocku.ca., MacNeil AJ; Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, Canada., Hodges GJ; Department of Kinesiology, Faculty of Applied Health Sciences, Brock University, Canada., Wade TJ; Department of Health Sciences, Faculty of Applied Health Sciences, Brock University, Canada; Brock-Niagara Centre for Health and Well-Being, Brock University, Canada.
Jazyk: angličtina
Zdroj: Brain, behavior, and immunity [Brain Behav Immun] 2021 Mar; Vol. 93, pp. 254-263. Date of Electronic Publication: 2020 Dec 21.
DOI: 10.1016/j.bbi.2020.12.018
Abstrakt: Adverse childhood experiences (ACEs), such as maltreatment and severe household dysfunction, represent a significant threat to public health as ACEs are associated with increased prevalence of several chronic diseases. Biological embedding, believed to be rooted in dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, is the prevailing theory by which chronic diseases become imprinted in individuals following childhood adversity. A shift towards HPA axis hypoactivity occurs in response to ACEs exposure and is proposed to contribute towards altered cortisol secretion, chronic low-grade inflammation, and dysregulated hemodynamic and autonomic function. This shift in HPA axis activity may be a long-term effect of glucocorticoid receptor methylation with downstream effects on hemodynamic and autonomic function. Emerging evidence suggests syncopal tendencies are increased among those with ACEs and coincides with altered neuroimmune function. Similarly, chronic low-grade inflammation may contribute towards arterial baroreceptor desensitization through increased arterial stiffness, negatively impacting autonomic regulation following posture change and increasing rates of syncope in later life, as has been previously highlighted in the literature. Although speculative, baroreceptor desensitization may be secondary to increased arterial stiffness and changes in expression of glucocorticoid receptors and arginine vasopressin, which are chronically altered by ACEs. Several research gaps and opportunities exist in this field and represent prospective areas for future investigation. Here, we synthesize current findings in the areas of acute psychosocial stress reactivity pertaining to HPA axis function, inflammation, and hemodynamic function while suggesting ideas for future research emphasizing systemic interactions and postural stress assessments among those with ACEs. This review aims to identify specific pathways which may contribute towards orthostatic intolerance in populations with history of childhood adversity.
(Copyright © 2020 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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