Epigenetic basis for fetal origins of age-related disease

Reid F. Thompson, Francine H. Einstein

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The current concept of fetal origins of adult diseases describes in utero programming, or adaptation to a spectrum of adverse environmental conditions that ultimately leads to increased susceptibility to age-related diseases (e.g., type 2 diabetes and cardiovascular disease) later in life. Although the precise mechanism of this biological memory remains unclear, mounting evidence suggests an epigenetic basis. The increased susceptibility to chronic disease and involvement of multiple organ systems that is observed is analogous to the decline in resistance to disease that is typical of normal aging. Although the cumulative environment over the course of a lifetime can induce increasing epigenetic dysregulation, we propose that adverse events that occur during early development can induce significant additional dysregulation of the epigenome. Here, we describe the current evidence for fetal origins of adult disease and the associated role of epigenetic dysregulation. In addition, we present a new perspective on the induction of epigenetic alterations in utero, which subsequently lead to an aging phenotype marked by increased susceptibility to age-related diseases.

Original languageEnglish (US)
Pages (from-to)581-587
Number of pages7
JournalJournal of Women's Health
Volume19
Issue number3
DOIs
StatePublished - Mar 1 2010

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Epigenomics
Gestational Age
Disease Resistance
Type 2 Diabetes Mellitus
Cardiovascular Diseases
Phenotype

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Epigenetic basis for fetal origins of age-related disease. / Thompson, Reid F.; Einstein, Francine H.

In: Journal of Women's Health, Vol. 19, No. 3, 01.03.2010, p. 581-587.

Research output: Contribution to journalArticle

Thompson, Reid F. ; Einstein, Francine H. / Epigenetic basis for fetal origins of age-related disease. In: Journal of Women's Health. 2010 ; Vol. 19, No. 3. pp. 581-587.
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