The prenatal environment and later cardiovascular disease

    Research output: Contribution to journalArticle

    49 Citations (Scopus)

    Abstract

    Exposure of an embryo or fetus to a sub-optimal environment increases its risk of acquiring coronary disease and heart failure in adult life through a process known as programming. For example, stress experienced in utero and during early postnatal life imparts an increased vulnerability for adult onset cardiovascular disease. Programming is a change in gene expression pattern that occurs in response to a stressor and leads to altered growth of specific organs during their most critical times of development. Known stressors include improper nourishment, hypoxia and excess glucocorticoids. Programming becomes evident through a number of risk factors that are only now becoming understood, including growth patterns in childhood, structural and cellular changes to the heart and coronary vessels, impaired endothelial function, and altered lipid metabolism. Thus, adults most vulnerable for coronary artery disease may have experienced rapid weight gain in childhood and now have dyslipidemias and depressed endothelial function.

    Original languageEnglish (US)
    Pages (from-to)745-751
    Number of pages7
    JournalEarly Human Development
    Volume81
    Issue number9
    DOIs
    StatePublished - Sep 2005

    Fingerprint

    Cardiovascular Diseases
    Dyslipidemias
    Growth
    Lipid Metabolism
    Glucocorticoids
    Weight Gain
    Coronary Disease
    Coronary Artery Disease
    Coronary Vessels
    Fetus
    Embryonic Structures
    Heart Failure
    Gene Expression
    Hypoxia

    Keywords

    • Adult disease
    • Cardiovascular disease
    • Fetal programming

    ASJC Scopus subject areas

    • Pediatrics, Perinatology, and Child Health

    Cite this

    The prenatal environment and later cardiovascular disease. / Louey, Samantha; Thornburg, Kent.

    In: Early Human Development, Vol. 81, No. 9, 09.2005, p. 745-751.

    Research output: Contribution to journalArticle

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