Evidence map›Paper›PMID 29180423›Full record

SynthesisProceedings of the National Academy of Sciences of the United States of America2017

Prenatal stress accelerates offspring growth to compensate for reduced maternal investment across mammals.

Andreas Berghänel, Michael Heistermann, Oliver Schülke, Julia Ostner

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
13.4field-weighted citation impact, top 1% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
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  12. Conceptual and analytical approaches for modelling the developmental origins of inequality.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Article
  13. Mechanisms of equality and inequality in mammalian societies.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Article
  14. Metronidazole Potentiation by Panax Ginseng andAntibiotics (Basel, Switzerland) · 2023
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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 3 institutions in 2 countries.

Andreas BerghänelDepartment of Anthropology, University of New Mexico, Albuquerque, NM 87131; abergha@gwdg.de.
Michael HeistermannEndocrinology Laboratory, German Primate Center - Leibniz Institute for Primate Research, 37077 Göttingen, Germany.
Oliver SchülkeDepartment of Behavioral Ecology, University of Göttingen, 37077 Göttingen, Germany.
Julia OstnerDepartment of Behavioral Ecology, University of Göttingen, 37077 Göttingen, Germany.
University of Göttingen · DEGerman Primate Center · DEUniversity of New Mexico · US

Funding

Cumulative Life Course Effects on Aging and Health in a Long-Lived Primate ModelR37AG049395 · NIA · UNIVERSITY OF NEW MEXICO · PI Elizabeth Vinson Lonsdorf, Melissa Emery Thompson · 2022 to 2026
$3.2M
Biodemography of Aging in Wild ChimpanzeesR01AG049395 · NIA · UNIVERSITY OF NEW MEXICO · PI MITANI, JOHN CARY, ROSATI, ALEXANDRA G · 2015 to 2019
$2.9M
NIA NIH HHS R01 AG049395NIA NIH HHS R37 AG049395
6 · The paper itself

Abstract

Across mammals, prenatal maternal stress (PREMS) affects many aspects of offspring development, including offspring growth. However, how PREMS translates to offspring growth is inconsistent, even within species. To explain the full range of reported effects of prenatal adversity on offspring growth, we propose an integrative hypothesis: developmental constraints and a counteracting adaptive growth plasticity work in opposition to drive PREMS effects on growth. Mothers experiencing adversity reduce maternal investment leading to stunted growth (developmental constraints). Concomitantly, the pace of offspring life history is recalibrated to partly compensate for these developmental constraints (adaptive growth plasticity). Moreover, the relative importance of each process changes across ontogeny with increasing offspring independence. Thus, offspring exposed to PREMS may grow at the same rate as controls during gestation and lactation, but faster after weaning when direct maternal investment has ceased. We tested these predictions with a comparative analysis on the outcomes of 719 studies across 21 mammal species. First, the observed growth changes in response to PREMS varied across offspring developmental periods as predicted. We argue that the observed growth acceleration after weaning is not "catch-up growth," because offspring that were small for age grew slower. Second, only PREMS exposure early during gestation produced adaptive growth plasticity. Our results suggest that PREMS effects benefit the mother's future reproduction and at the same time accelerate offspring growth and possibly maturation and reproductive rate. In this sense, PREMS effects on offspring growth allow mother and offspring to make the best of a bad start.

Indexed as

Adaptation, PhysiologicalBody SizeAnimalsFemaleMammalsPregnancyPrenatal Exposure Delayed EffectsStress, Psychologicalcatch-up growthdevelopmental constraintsdevelopmental plasticitygrowth plasticityphenotypic plasticity

Identifiers

PMID29180423
PMCPMC5740685
OpenAlexW2770424707

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.