Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Aug;30(3):807-824.
doi: 10.1017/S0954579418000469.

Incorporating epigenetic mechanisms to advance fetal programming theories

Affiliations
Review

Incorporating epigenetic mechanisms to advance fetal programming theories

Elisabeth Conradt et al. Dev Psychopathol. 2018 Aug.

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.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest: The authors report no conflict of interest.

References

    1. Adkins DE, Khachane AN, McClay JL, Åberg K, Bukszár J, Sullivan PF, van den Oord EJCG. SNP-based analysis of neuroactive ligand–receptor interaction pathways implicates PGE2 as a novel mediator of antipsychotic treatment response: Data from the CATIE study. Schizophrenia Research. 2012;135(1–3):200–201. doi: 10.1016/j.schres.2011.11.002. - DOI - PMC - PubMed
    1. Ahnert L, Gunnar MR, Lamb ME, Barthel M. Transition to Child Care: Associations With Infant-Mother Attachment, Infant Negative Emotion, and Cortisol Elevations. Child Development. 2004;75(3):639–650. doi: 10.1111/j.1467-8624.2004.00698.x. - DOI - PubMed
    1. Aiken CE, Ozanne SE. Transgenerational developmental programming. Human Reproduction Update. 2014;20(1):63–75. doi: 10.1093/humupd/dmt043. - DOI - PubMed
    1. Aiken CE, Tarry-Adkins JL, Ozanne SE. Transgenerational effects of maternal diet on metabolic and reproductive ageing. Mammalian Genome. 2016;27(7–8):430–439. doi: 10.1007/s00335-016-9631-1. - DOI - PMC - PubMed
    1. Bagot RC, van Hasselt FN, Champagne DL, Meaney MJ, Krugers HJ, Joëls M. Maternal care determines rapid effects of stress mediators on synaptic plasticity in adult rat hippocampal dentate gyrus. Neurobiology of Learning and Memory. 2009;92(3):292–300. doi: 10.1016/j.nlm.2009.03.004. - DOI - PubMed

Publication types