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

• Published in: Development and psychopathology Vol. 30; no. 3; pp. 787 - 806
• Main Authors: Davis, Elysia Poggi, Hankin, Benjamin L., Swales, Danielle A., Hoffman, M. Camille
• Format: Journal Article
• Language: English
• Published: New York, USA Cambridge University Press 01.08.2018
• Subjects: Adult; Antidepressive Agents - adverse effects; Antidepressive Agents - therapeutic use; Brain - physiopathology; Child; Children & youth; Cognitive ability; Depressive Disorder - physiopathology; Depressive Disorder - psychology; Depressive Disorder - therapy; Design; Female; Fetal Development - physiology; Fetuses; Humans; Hypothalamo-Hypophyseal System - physiopathology; Hypothalamus; Infant; Infant, Newborn; Influence; Intervention; Life span; Male; Mental depression; Mental health; Offspring; Ontogeny; Pituitary; Pituitary-Adrenal System - physiopathology; Postpartum depression; Pregnancy; Pregnancy complications; Pregnancy Complications - physiopathology; Pregnancy Complications - psychology; Pregnancy Complications - therapy; Prenatal depression; Prenatal exposure; Prenatal Exposure Delayed Effects - physiopathology; Prenatal Exposure Delayed Effects - psychology; Prenatal Exposure Delayed Effects - therapy; Psychopathology; Psychotherapy; Risk Factors; Special Issue Articles; Stress, Psychological - complications; Stress, Psychological - therapy; Womens health
• ISSN: 0954-5794; 1469-2198; 1469-2198
• DOI: 10.1017/S0954579418000470

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.