Evidence map›Paper›PMID 22672778›Full record

ReviewEnvironmental health perspectives2012

Predicting later-life outcomes of early-life exposures.

Kim Boekelheide, Bruce Blumberg, Robert E Chapin, Ila Cote, Joseph H Graziano, Amanda Janesick, Robert Lane, Karen Lillycrop, Leslie Myatt, J Christopher States and 3 more

Open access · diamondAbstract readReview
In one paragraph

Review in Environmental health perspectives, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
22.1field-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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 201 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 10 institutions in 2 countries.

Kim BoekelheideDepartment of Pathology and Laboratory Medicine, Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912, USA. kim_boekelheide@brown.edu
Bruce Blumberg
Robert E Chapin
Ila Cote
Joseph H Graziano
Amanda Janesick
Robert Lane
Karen Lillycrop
Leslie Myatt
J Christopher States
Kristina A Thayer
Michael P Waalkes
John M Rogers
Environmental Protection Agency · USNational Institutes of Health · USUniversity of California, Irvine · USBrown University · USColumbia University · USPfizer (United States) · USThe University of Texas Health Science Center at San Antonio · USUniversity of Louisville · USUniversity of Southampton · GBUniversity of Utah · US

Funding

Stem Cell ToxicologyZIAES102925 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI TOKAR, ERIK · 2010 to 2021
$25.3M
Xenotransplant CoreP20ES018169 · NIEHS · BROWN UNIVERSITY · PI GRUPPUSO, PHILIP A. · 2010 to 2012
$985k
NIEHS NIH HHS P20 ES018169NIEHS NIH HHS P20ES018169
6 · The paper itself

Abstract

backgroundIn utero exposure of the fetus to a stressor can lead to disease in later life. Epigenetic mechanisms are likely mediators of later-life expression of early-life events.

objectivesWe examined the current state of understanding of later-life diseases resulting from early-life exposures in order to identify in utero and postnatal indicators of later-life diseases, develop an agenda for future research, and consider the risk assessment implications of this emerging knowledge.

methodsThis review was developed based on our participation in a National Research Council workshop titled "Use of in Utero and Postnatal Indicators to Predict Health Outcomes Later in Life: State of the Science and Research Recommendations." We used a case study approach to highlight the later-life consequences of early-life malnutrition and arsenic exposure. DISCUSSION: The environmental sensitivity of the epigenome is viewed as an adaptive mechanism by which the developing organism adjusts its metabolic and homeostatic systems to suit the anticipated extrauterine environment. Inappropriate adaptation may produce a mismatch resulting in subsequent increased susceptibility to disease. A nutritional mismatch between the prenatal and postnatal environments, or early-life obesogen exposure, may explain at least some of the recent rapid increases in the rates of obesity, type 2 diabetes, and cardiovascular diseases. Early-life arsenic exposure is also associated with later-life diseases, including cardiovascular disease and cancer.

conclusionsWith mounting evidence connecting early-life exposures and later-life disease, new strategies are needed to incorporate this emerging knowledge into health protective practices.

Indexed as

Epigenesis, GeneticMaternal ExposureAnimalsArsenicCardiovascular DiseasesDiabetes Mellitus, Type 2Disease SusceptibilityEnvironmental MonitoringFemaleHumansMalnutritionMiceObesityPregnancyPrenatal Exposure Delayed EffectsRatsArsenic

Identifiers

PMID22672778
PMCPMC3491941
OpenAlexW2038211009

What OpenQuestion holds

Textmetadata
LicenceCC0
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.