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An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression?

Published online by Cambridge University Press:  02 August 2018

Elysia Poggi Davis ,
Benjamin L. Hankin ,
Danielle A. Swales  and
M. Camille Hoffman
Elysia Poggi Davis*
Affiliation:
University of Denver University of California, Irvine
Benjamin L. Hankin
Affiliation:
University of Illinois
Danielle A. Swales
Affiliation:
University of Denver
M. Camille Hoffman
Affiliation:
University of Colorado School of Medicine
*
Address correspondence and reprint requests to: Elysia Poggi Davis, Department of Psychology, 2155 South Race Street, University of Denver, Denver, CO 80208-3500; E-mail: Elysia.Davis@du.edu.
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Abstract

Maternal depression is one of the most common prenatal complications, and prenatal maternal depression predicts many child psychopathologies. Here, we apply the fetal programming hypothesis as an organizational framework to address the possibility that fetal exposure to maternal depressive symptoms during pregnancy affects fetal development of vulnerabilities and risk mechanisms, which enhance risk for subsequent psychopathology. We consider four candidate pathways through which maternal prenatal depression may affect the propensity of offspring to develop later psychopathology across the life span: brain development, physiological stress regulation (hypothalamic–pituitary–adrenocortical axis), negative emotionality, and cognitive (effortful) control. The majority of past research has been correlational, so potential causal conclusions have been limited. We describe an ongoing experimental test of the fetal programming influence of prenatal maternal depressive symptoms using a randomized controlled trial design. In this randomized controlled trial, interpersonal psychotherapy is compared to enhanced usual care among distressed pregnant women to evaluate whether reducing prenatal maternal depressive symptoms has a salutary impact on child ontogenetic vulnerabilities and thereby reduces offspring's risk for emergence of later psychopathology.

Type
Special Issue Articles
Information
Development and Psychopathology , Volume 30 , Special Issue 3: Developmental Origins of Psychopathology: Mechanisms, Processes, and Pathways Linking the Prenatal Environment to Postnatal Outcomes , August 2018 , pp. 787 - 806
Copyright
Copyright © Cambridge University Press 2018 

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Footnotes

Supported by the National Institutes of Health Grants R01 MH109662 and P50 MH096889.

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