Developmental origins of cardiovascular disease: Impact of early life stress in humans and rodents
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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.
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Emerging epidemiologic evidence strongly supports that ELS/CT is an independent albeit silent risk factor of future chronic cardiovascular risk through various systemic and molecular mechanisms.
“Emerging epidemiologic evidence strongly supports that ELS/CT is an independent albeit silent risk factor of future chronic cardiovascular risk through various systemic and molecular mechanisms (267–272)”
From Developmental Trajectories of Early Life Stress and Trauma: A Narrative Review on Neurobiological Aspects Beyond Stress System Dysregulation (2019) · cites this paper as [272]
The Introduction and Summary describe early-life stress as an independent predictor of later cardiovascular disease, and the inflammatory-system section discusses a possible pathway. The copy does not establish that this risk is clinically silent, and it presents the molecular mechanisms as proposed and in need of further investigation rather than established routes of causation. The supplied passages have section labels but no page numbers. (LLM, conf=0.83)
Experimental — accuracy not yet measuredChildhood trauma is associated with increased risk of cardiovascular disease, autoimmune disease, gastrointestinal symptoms, poor dental health, obesity, and type 2 diabetes.
“Physically, childhood trauma has been associated with increased risk of cardiovascular disease (6), autoimmune disease (7), gastrointestinal symptoms (8), poor dental health (9), obesity, and type 2 diabetes (10).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [6]
Childhood stress raises the risk of adult health conditions, including pregnancy complications such as preterm birth.
“There is growing evidence that childhood stress also increases risk for health conditions in adulthood (Murphy et al., 2017; Nusslock and Miller, 2016), including complications of pregnancy such as PTB (Blackmore et al., 2016; Christiaens et al., 2015; Hillis et al., 2004; Smith et al., 2016).”
From Childhood stress and birth timing among African American women: cortisol as biological mediator (2017) · cites this paper as Murphy et al., 2017
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Sex differences in heart failure
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“Physically, childhood trauma has been associated with increased risk of cardiovascular disease (6), autoimmune disease (7), gastrointestinal symptoms (8), poor dental health (9), obesity, and type 2 diabetes (10).”
BackgroundSex Differences in Heart Failure
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- Authors
- Murphy, M. O., Cohn, D. M., & Loria, A. S.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Loria, A.S.
- ORCID
- Loria, A.S.
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2017-03
- Volume
- 74
- Issue
- Pt B
- Pages
- 453-465
- ISSN
- 0149-7634 (ISSN-L)
- PMC
- PMC5250589
- OpenAlex
- W2486428594
- Cited by
- 117
- References
- 192
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 11 · 2023: 12 · 2022: 18 · 2021: 17 · 2020: 20 · 2019: 10 · 2018: 10 · 2017: 5 · 2016: 2
- FWCI
- 1.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- ScholarWorks @ UTRGV (The University of Texas Rio Grande Valley) (submittedVersion)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by-nc-nd)
- Funders
- NIH National Heart, Lung, and Blood Institute (R00 HL 111354)
- Topics
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- developmental origins of health and disease, early life stress, cardiovascular disease, adverse childhood experiences, maternal separation, hypertension, postpartum stress, molecular mechanisms, animal models, personalized treatment
- MeSH terms
- Animals, Cardiovascular Diseases, Humans, Maternal Deprivation, Risk Factors, Rodentia, Stress, Psychological
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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