Evidence map›Paper›PMID 30068416›Full record

Trial reportDevelopment and psychopathology2018

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

Elysia Poggi Davis, Benjamin L Hankin, Danielle A Swales, M Camille Hoffman

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Development and psychopathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 4 pooled it
6.7field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 4 syntheses or guidelines pooled it, 87 citations in OpenAlex.

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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 4 institutions in 1 country.

Elysia Poggi DavisUniversity of Denver.
Benjamin L HankinUniversity of Illinois.
Danielle A SwalesUniversity of Denver.
M Camille HoffmanUniversity of Colorado School of Medicine.
University of California, Irvine · USUniversity of Colorado Denver · USUniversity of Denver · USUniversity of Illinois System · US

Funding

Structural & Network-Function Correlates of Fragmented Early-Life Across SpeciesP50MH096889 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARAM, TALLIE Z. · 2013 to 2023
$25.4M
Reducing Fetal Exposure to Maternal Depression to Improve Infant Risk MechanismsR01MH109662 · NIMH · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI DAVIS, ELYSIA POGGI, HANKIN, BENJAMIN L · 2017 to 2021
$4.0M
NIMH NIH HHS P50 MH096889NIMH NIH HHS R01 MH109662
6 · The paper itself

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.

Indexed as

PsychotherapyAdultAntidepressive AgentsBrainChildDepressive DisorderFemaleFetal DevelopmentHumansHypothalamo-Hypophyseal SystemInfantInfant, NewbornMalePituitary-Adrenal SystemPregnancyPregnancy ComplicationsAntidepressive Agents

Identifiers

PMID30068416
PMCPMC7040571
OpenAlexW2887226274

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.