Evidence map›Paper›PMID 35853381›Full record

ArticlePsychoneuroendocrinology2022

Prospective association between maternal allostatic load during pregnancy and child mitochondrial content and bioenergetic capacity.

L E Gyllenhammer, M Picard, M A McGill, K E Boyle, M P Vawter, J M Rasmussen, C Buss, S Entringer, P D Wadhwa

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Psychoneuroendocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

L E GyllenhammerDevelopment, Health and Disease Research Program, University of California, School of Medicine, Irvine, CA, USA; Department of Pediatrics, University of California, School of Medicine, Irvine, CA, USA. Electronic address: lgyllenh@uci.edu.
M PicardDepartment of Psychiatry, Division of Behavioral Medicine, Columbia University Irving Medical Center, New York, NY, USA; Department of Neurology, Merritt Center, Columbia Translational Neuroscience Initiative, Columbia University Irving Medical Center, New York, NY, USA; New York State Psychiatric Institute, New York, NY, USA.
M A McGillDepartment of Psychiatry, Division of Behavioral Medicine, Columbia University Irving Medical Center, New York, NY, USA.
K E BoyleDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA; Lifecourse Epidemiology of Adiposity and Diabetes Center, Aurora, CO, USA.
M P VawterDepartment of Psychiatry and Human Behavior, University of California, School of Medicine, Irvine, CA, USA.
J M RasmussenDevelopment, Health and Disease Research Program, University of California, School of Medicine, Irvine, CA, USA; Department of Pediatrics, University of California, School of Medicine, Irvine, CA, USA.
C BussDevelopment, Health and Disease Research Program, University of California, School of Medicine, Irvine, CA, USA; Department of Pediatrics, University of California, School of Medicine, Irvine, CA, USA; Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Institute of Medical Psychology, Berlin, Germany.
S EntringerDevelopment, Health and Disease Research Program, University of California, School of Medicine, Irvine, CA, USA; Department of Pediatrics, University of California, School of Medicine, Irvine, CA, USA; Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health (BIH), Institute of Medical Psychology, Berlin, Germany.
P D WadhwaDevelopment, Health and Disease Research Program, University of California, School of Medicine, Irvine, CA, USA; Department of Pediatrics, University of California, School of Medicine, Irvine, CA, USA; Department of Psychiatry and Human Behavior, University of California, School of Medicine, Irvine, CA, USA; Department of Obstetrics and Gynecology, University of California, School of Medicine, Irvine, CA, USA; Department of Epidemiology, University of California, School of Medicine, Irvine, CA, USA.
University of California, Irvine · USColumbia University Irving Medical Center · USUniversity of Colorado Anschutz Medical Campus · US

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
Pre- and Postnatal Exposure Periods for Child Health: Common Risks and Shared MechanismsUH3OD023349 · OD · UNIVERSITY OF ROCHESTER · PI Emily S Barrett, Richard Kermit Miller · 2018 to 2026
$15.9M
EMA Assessment of Biobehavioral Processes in Human PregnancyR01HD060628 · NICHD · UNIVERSITY OF CALIFORNIA-IRVINE · PI WADHWA, PATHIK D · 2010 to 2014
$3.4M
FETAL PROGRAMMING OF THE NEWBORN AND INFANT HUMAN BRAINR01MH091351 · NIMH · UNIVERSITY OF CALIFORNIA-IRVINE · PI BUSS, CLAUDIA, WADHWA, PATHIK D · 2011 to 2015
$3.3M
Prenatal stress biology, infant body composition and obesity riskR01HD065825 · NICHD · UNIVERSITY OF CALIFORNIA-IRVINE · PI ENTRINGER, SONJA, WADHWA, PATHIK D · 2010 to 2014
$2.2M
Synergistic effect of maternal insulin-resistance and cortisol in pregnancy on fetal programming of child mitochondrial function and obesity riskR00HD097302 · NICHD · UNIVERSITY OF CALIFORNIA-IRVINE · PI GYLLENHAMMER, LAUREN ELIZABETH · 2022 to 2024
$744k
Synergistic effect of maternal insulin-resistance and cortisol in pregnancy on fetal programming of child mitochondrial function and obesity riskK99HD097302 · NICHD · UNIVERSITY OF CALIFORNIA-IRVINE · PI GYLLENHAMMER, LAUREN ELIZABETH · 2019 to 2021
$272k
NCATS NIH HHS UL1 TR001414NICHD NIH HHS K99 HD097302NICHD NIH HHS R00 HD097302NICHD NIH HHS R01 HD060628NICHD NIH HHS R01 HD065825NIH HHS UH3 OD023349NIMH NIH HHS R01 MH091351
6 · The paper itself

Abstract

backgroundMitochondria are multifunctional energy-producing and signaling organelles that support life and contribute to stress adaptation. There is a growing understanding of the dynamic relationship between stress exposure and mitochondrial biology; however, the influence of stress on key domains of mitochondrial biology during early-life, particularly the earliest phases of intra-uterine/prenatal period remains largely unknown. Thus, the goal of this study was to examine the impact of fetal exposure to stress (modeled as the biological construct allostatic load) upon mitochondrial biology in early childhood.

methodsIn n = 30 children (range: 3.5-6 years, 53% male), we quantified mitochondrial content via citrate synthase (CS) activity and mtDNA copy number (mtDNAcn), and measured mitochondrial bioenergetic capacity via respiratory chain enzyme activities (complexes I (CI), II (CII), and IV (CIV)) in platelet-depleted peripheral blood mononuclear cells (PBMCs). In a cohort of healthy pregnant women, maternal allostatic load was operationalized as a latent variable (sum of z-scores) representing an aggregation of early-, mid- and late-gestation measures of neuroendocrine (cortisol), immune (interleukin-6, C-reactive protein), metabolic (homeostasis model assessment of insulin resistance, free fatty acids), and cardiovascular (aggregate systolic and diastolic blood pressure) systems, as well as an anthropometric indicator (pre-pregnancy body mass index [BMI]).

resultsAn interquartile increase in maternal allostatic load during pregnancy was associated with higher mitochondrial content (24% and 15% higher CS and mtDNAcn), and a higher mitochondrial bioenergetic capacity (16%, 23%, and 25% higher CI, CII and CIV enzymatic activities) in child leukocytes. The positive association between maternal allostatic load during pregnancy and child mitochondrial content and bioenergetic capacity remained significant after accounting for the effects of key pre- and post-natal maternal and child covariates (p's < 0.05, except CI p = 0.073).

conclusionWe report evidence that prenatal biological stress exposure, modeled as allostatic load, was associated with elevated child mitochondrial content and bioenergetic capacity in early childhood. This higher mitochondrial content and bioenergetic capacity (per leukocyte) may reflect increased energetic demands at the immune or organism level, and thus contribute to wear-and-tear and pathophysiology, and/or programmed pro-inflammatory phenotypes. These findings provide potential mechanistic insight into the cellular processes underlying developmental programming, and support the potential role that changes in mitochondrial content and bioenergetic functional capacity may play in altering life-long susceptibility for health and disease.

Indexed as

AllostasisDNA, MitochondrialEnergy MetabolismFemaleHumansLeukocytes, MononuclearMaleMitochondriaPregnancyDNA, MitochondrialEnzymatic activityFetal programmingMitochondriaMtDNAcnPregnancyStress

Identifiers

PMID35853381
PMCPMC9706402
OpenAlexW4285500027

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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.