Cited by 60Birth, Development, and HealthMaternal Mental Health During Pregnancy and PostpartumEpigenetics and DNA Methylation

Incorporating epigenetic mechanisms to advance fetal programming theories

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Conradt, Elisabeth, Adkins, Daniel E., Crowell, Sheila E., Raby, K. Lee, Diamond, Lisa M., Ellis, Bruce·2018·Development and Psychopathology

Abstract

Decades of fetal programming research indicates that we may be able to map the origins of many physical, psychological, and medical variations and morbidities before the birth of the child. While great strides have been made in identifying associations between prenatal insults, such as undernutrition or psychosocial stress, and negative developmental outcomes, far less is known about how adaptive responses to adversity regulate the developing phenotype to match stressful conditions. As the application of epigenetic methods to human behavior has exploded in the last decade, research has begun to shed light on the role of epigenetic mechanisms in explaining how prenatal conditions shape later susceptibilities to mental and physical health problems. In this review, we describe and attempt to integrate two dominant fetal programming models: the cumulative stress model (a disease-focused approach) and the match–mismatch model (an evolutionary–developmental approach). In conjunction with biological sensitivity to context theory, we employ these two models to generate new hypotheses regarding epigenetic mechanisms through which prenatal and postnatal experiences program child stress reactivity and, in turn, promote development of adaptive versus maladaptive phenotypic outcomes. We conclude by outlining priority questions and future directions for the fetal programming field.

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  • Other factors, such as epimutations, fetal reprogramming, and gut microbiome transfer, may induce intergenerational phenotypic changes.

    “Importantly, in addition to epigenetic modifications, other factors, such as epimutations (an mutation occur at the epigenetic level), fetal reprogramming (266), and even gut microbiome transfer (267) may induce intergenerational phenotypic changes.”

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Research works printed but not linked: 2

  1. Chisholm JS 1999 Death, hope and sex: steps to an evolutionary ecology of mind and morality Cambridge University Press
  2. Ellis BJ Del Giudice M Shirtcliff EA 2017 The adaptive calibration model of stress responsivity: concepts, findings, and implications for developmental psychopathology Child and adolescent psychopathology 3 237 276 New York Wiley & Sons

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Authors
Conradt, E., Adkins, D. E., Crowell, S. E., Raby, K. L., Diamond, L. M., & Ellis, B.
Affiliations
University of Utah (US)
Corresponding author
Conradt, Elisabeth
Venue
Development and Psychopathology
Published
2018-08
Volume
30
Issue
3
Pages
807-824
ISSN
  • 0954-5794 (ISSN-L)
  • 1469-2198
OpenAlex
W2886796995
Cited by
60
References
155
Citations by year
2026: 4 · 2025: 4 · 2024: 4 · 2023: 5 · 2022: 13 · 2021: 8 · 2020: 11 · 2019: 8 · 2018: 3
FWCI
1.43
Type
journal article
Language
en
Open access
Locations
  • Development and Psychopathology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • University of Utah
  • National Institutes of Health
  • National Institute of Mental Health (R21MH109777)
  • National Institute on Drug Abuse (K08DA038959)
Topics
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Maternal Mental Health During Pregnancy and Postpartum
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords
fetal programming, epigenetics, prenatal stress, stress reactivity, developmental origins of health and disease, psychosocial stress, malnutrition
MeSH terms
Child, Child, Preschool, Female, Humans, Infant, Infant, Newborn, Male, Models, Genetic, Phenotype, Pregnancy, Prenatal Exposure Delayed Effects, Genetic Predisposition to Disease, Epigenesis, Genetic, Fetal Development

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