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Psychoneuroendocrinology. 2019 Jul;105:123-137. doi: 10.1016/j.psyneuen.2018.12.011. Epub 2018 Dec 12.

Translating basic research knowledge on the biological embedding of early-life stress into novel approaches for the developmental programming of lifelong health.

Author information

1
Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Institute of Medical Psychology, Berlin, Germany; Department of Biobehavioral Health, College of Health & Human Development, The Pennsylvania State University, University Park, PA, USA. Electronic address: christine.heim@charite.d.
2
Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Institute of Medical Psychology, Berlin, Germany; Development, Health, and Disease Research Program, University of California Irvine, Orange, CA, USA. Electronic address: sonja.entringer@charite.de.
3
Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Institute of Medical Psychology, Berlin, Germany; Development, Health, and Disease Research Program, University of California Irvine, Orange, CA, USA. Electronic address: claudia.buss@charite.de.

Abstract

This review integrates scientific knowledge obtained over the past few decades on the biological mechanisms that contribute to the profound association between exposure to early adversity, including childhood trauma and prenatal stress, and the lifelong elevated risk to develop a broad range of diseases. We further discuss insights into gene-environment interactions moderating the association between early adversity and disease manifestation and we discuss the role of epigenetic and other molecular processes in the biological embedding of early adversity. Based on these findings, we propose potential mechanisms that may contribute to the intergenerational transmission of risk related to early adversity from the mother to the fetus. Finally, we argue that basic research knowledge on the biological embedding of early adversity must now be translated into novel intervention strategies that are mechanism-driven and sensitive to developmental timing. Indeed, to date, there are no diagnostic biomarkers of risk or mechanism-informed interventions that we can offer to victims of early adversity in order to efficiently prevent or reverse adverse health outcomes. Such translational efforts can be expected to have significant impact on both clinical practice and the public health system, and will promote precision medicine in pediatrics and across the lifespan.

KEYWORDS:

Developmental programming; Early life stress; Intergenerational transmission; Prenatal stress; Targeted intervention

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