Evidence map›Paper›PMID 25187623›Full record

ReviewReproduction (Cambridge, England)2014

Epigenetics and life-long consequences of an adverse nutritional and diabetic intrauterine environment.

Nady El Hajj, Eberhard Schneider, Harald Lehnen, Thomas Haaf

Abstract readReview
In one paragraph

Review in Reproduction (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

93 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Maternal glycaemia and child educational attainment at age 5 in the Born in Bradford cohort.Diabetic medicine : a journal of the British Diabetic Association · 2026
    Article
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  9. MicroRNAs in diabetes mellitus.Journal of diabetes and metabolic disorders · 2025
    Review
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33 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.

Nady El HajjInstitute of Human GeneticsJulius-Maximilians-Universität Würzburg, Biozentrum, Am Hubland, 97074 Würzburg, GermanyDepartment of Gynecology and ObstetricsStädtische Kliniken, 41239 Mönchengladbach, Germany.
Eberhard SchneiderInstitute of Human GeneticsJulius-Maximilians-Universität Würzburg, Biozentrum, Am Hubland, 97074 Würzburg, GermanyDepartment of Gynecology and ObstetricsStädtische Kliniken, 41239 Mönchengladbach, Germany.
Harald LehnenInstitute of Human GeneticsJulius-Maximilians-Universität Würzburg, Biozentrum, Am Hubland, 97074 Würzburg, GermanyDepartment of Gynecology and ObstetricsStädtische Kliniken, 41239 Mönchengladbach, Germany.
Thomas HaafInstitute of Human GeneticsJulius-Maximilians-Universität Würzburg, Biozentrum, Am Hubland, 97074 Würzburg, GermanyDepartment of Gynecology and ObstetricsStädtische Kliniken, 41239 Mönchengladbach, Germany thomas.haaf@uni-wuerzburg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The phenomenon that adverse environmental exposures in early life are associated with increased susceptibilities for many adult, particularly metabolic diseases, is now referred to as 'developmental origins of health and disease (DOHAD)' or 'Barker' hypothesis. Fetal overnutrition and undernutrition have similar long-lasting effects on the setting of the neuroendocrine control systems, energy homeostasis, and metabolism, leading to life-long increased morbidity. There are sensitive time windows during early development, where environmental cues can program persistent epigenetic modifications which are generally assumed to mediate these gene-environment interactions. Most of our current knowledge on fetal programing comes from animal models and epidemiological studies in humans, in particular the Dutch famine birth cohort. In industrialized countries, there is more concern about adverse long-term consequences of fetal overnutrition, i.e. by exposure to gestational diabetes mellitus and/or maternal obesity which affect 10-20% of pregnancies. Epigenetic changes due to maternal diabetes/obesity may predispose the offspring to develop metabolic disease later in life and, thus, transmit the adverse environmental exposure to the next generation. This vicious cycle could contribute significantly to the worldwide metabolic disease epidemics. In this review article, we focus on the epigenetics of an adverse intrauterine environment, in particular gestational diabetes, and its implications for the prevention of complex disease.

Indexed as

AnimalsDiabetes, GestationalDisease SusceptibilityEpigenesis, GeneticFemaleHumansMetabolic DiseasesMiceModels, AnimalPhenotypePregnancyPrenatal Exposure Delayed EffectsPrenatal Nutritional Physiological PhenomenaRisk Factors

Identifiers

PMID25187623
PMCPMC4241689

What OpenQuestion holds

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Registered trials

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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.