Abstract
The Developmental Origins of Health and Disease (DOHaD) hypothesizes that environmental insults during childhood programs the individual to develop chronic disease in adulthood. Emerging epidemiological data strongly supports that early life stress (ELS) given by the exposure to adverse childhood experiences is regarded as an independent risk factor capable of predicting future risk of cardiovascular disease. Experimental animal models utilizing chronic behavioral stress during postnatal life, specifically maternal separation (MatSep) provides a suitable tool to elucidate molecular mechanisms by which ELS increases the risk to develop cardiovascular disease, including hypertension. The purpose of this review is to highlight current epidemiological studies linking ELS to the development of cardiovascular disease and to discuss the potential molecular mechanisms identified from animal studies. Overall, this review reveals the need for future investigations to further clarify the molecular mechanisms of ELS in order to develop more personalized therapeutics to mitigate the long-term consequences of chronic behavioral stress including cardiovascular and heart disease in adulthood.
Document Type
Article
Publication Date
3-2017
Digital Object Identifier (DOI)
https://doi.org/10.1016/j.neubiorev.2016.07.018
Funding Information
This study was supported by grants from the NIH National Heart, Lung, and Blood Institute (A. S. Loria: K99 HL111354).
Repository Citation
Murphy, Margaret O.; Cohn, Dianne M.; and Loria, Analia S., "Developmental Origins of Cardiovascular Disease: Impact of Early Life Stress in Humans and Rodents" (2017). Pharmacology and Nutritional Sciences Faculty Publications. 87.
https://uknowledge.uky.edu/pharmacol_facpub/87
Included in
Behavior and Behavior Mechanisms Commons, Cardiovascular Diseases Commons, Pharmacology, Toxicology and Environmental Health Commons
Notes/Citation Information
Published in Neuroscience & Biobehavioral Reviews, v. 74, part B, p. 453-465.
© 2016 Elsevier Ltd. All rights reserved.
This manuscript version is made available under the CC‐BY‐NC‐ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/.
The document available for download is the author's post-peer-review final draft of the article.