TY - JOUR
T1 - An experimental test of the fetal programming hypothesis
T2 - Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression?
AU - Davis, Elysia Poggi
AU - Hankin, Benjamin L.
AU - Swales, Danielle A.
AU - Hoffman, M. Camille
N1 - Funding Information:
Doyle Colleen Cicchetti Dante Editors Davis Elysia Poggi a b Hankin Benjamin L. c Swales Danielle A. a Hoffman M. Camille d a University of Denver b University of California , Irvine c University of Illinois d University of Colorado School of Medicine Supported by the National Institutes of Health Grants R01 MH109662 and P50 MH096889. 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 . 02 08 2018 08 2018 30 3
PY - 2018/8/1
Y1 - 2018/8/1
N2 - 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.
AB - 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.
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U2 - 10.1017/S0954579418000470
DO - 10.1017/S0954579418000470
M3 - Article
C2 - 30068416
AN - SCOPUS:85051007147
VL - 30
SP - 787
EP - 806
JO - Development and Psychopathology
JF - Development and Psychopathology
SN - 0954-5794
IS - 3
ER -