Evidence map›Paper›PMID 39915864›Full record

ArticleClinical epigenetics2025

Longitudinal maternal glycemia during pregnancy and placental epigenetic age acceleration.

Tesfa Dejenie Habtewold, Prabhavi Wijesiriwardhana, Richard J Biedrzycki, Cuilin Zhang, Katherine L Grantz, Jagteshwar Grewal, Fasil Tekola-Ayele

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

  1. Pooled it
  2. Article
  3. Article
  4. Late-Onset Preeclampsia is characterised by Accelerated Placental Aging.bioRxiv : the preprint server for biology · 2025
    Article
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

7 authors.

Tesfa Dejenie HabtewoldEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Drive, Room 3204, Bethesda, MD, 20892-7004, USA.
Prabhavi WijesiriwardhanaEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Drive, Room 3204, Bethesda, MD, 20892-7004, USA.
Richard J BiedrzyckiGlotech, Inc., Contractor for Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Cuilin ZhangGlobal Centre for Asian Women's Health, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Katherine L GrantzEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Drive, Room 3204, Bethesda, MD, 20892-7004, USA.
Jagteshwar GrewalEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Drive, Room 3204, Bethesda, MD, 20892-7004, USA.
Fasil Tekola-AyeleEpidemiology Branch, Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Drive, Room 3204, Bethesda, MD, 20892-7004, USA. ayeleft@mail.nih.gov.

Funding

Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH); American Recovery and Reinvestment Act HHSN27500006Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH); American Recovery and Reinvestment Act HHSN27500008Division of Population Health Research, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH); American Recovery and Reinvestment Act HHSN275200800003ICNICHD NIH HHS HHSN275200800002CNICHD NIH HHS HHSN275200800002INICHD NIH HHS HHSN275200800003CNICHD NIH HHS HHSN275200800003INICHD NIH HHS HHSN275200800012CNICHD NIH HHS HHSN275200800013CNICHD NIH HHS HHSN275200800014CNICHD NIH HHS HHSN275200800028CNICHD NIH HHS HHSN275201000009C
6 · The paper itself

Abstract

backgroundDysregulation of maternal glucose homeostasis has been related to an increased risk of morbidity and mortality in mothers and fetuses, yet the mechanism remains unclear. This study investigated the association between maternal glycemic levels and placental epigenetic age acceleration (PAA) in a multiethnic cohort.

methodsIn a sample of 301 pregnant women (102 Hispanic, 77 White, 72 Black, and 50 Asian/Pacific Islander), the association of glycemic markers cumulative exposure with PAA was tested using linear regression adjusting for fetal sex, maternal age, educational status, and health insurance status. Models were applied in the full cohort and stratified by race/ethnicity. Further, sensitivity analyses were performed after excluding women with GDM or preeclampsia.

resultsAmong Black women, high glucose, HbA1c, and insulin cumulative exposure levels were associated with lower PAA compared to low cumulative exposure levels (β = - 0.75 weeks, 95% CI = - 1.41 to - 0.08); β = - 0.86, 95% CI = - 1.51 to - 0.21; and β = - 0.76, 95% CI = - 1.49 to - 0.03, respectively). Among Asian/Pacific Islander women, medium insulin cumulative exposure level was associated with lower PAA (β = - 0.94 weeks, 95% CI = - 1.74 to - 0.14). No significant association was observed among White and Hispanic women as well as in the full cohort.

conclusionsElevated glucose, HbA1c, and insulin cumulative levels throughout pregnancy were associated with lower PAA in Black and Asian/Pacific Islander women. Placental epigenetic aging may be altered by maternal elevated glycemia and may in part underlie early programming of health outcomes in pregnancy and childhood health outcomes.

Indexed as

Blood GlucoseEpigenesis, GeneticPlacentaAdultCohort StudiesDiabetes, GestationalDNA MethylationFemaleGlycated HemoglobinHumansInsulinLongitudinal StudiesPregnancyYoung AdultBlood GlucoseGlycated HemoglobinInsulinGlucoseGlycemic biomarkersHbA1cHyperglycemiaInsulinLongitudinal modelingPlacental age accelerationPlacental agingPregnancy

Identifiers

PMID39915864
PMCPMC11803985

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.