Evidence map›Paper›PMID 36322199›Full record

ArticleBehavior genetics2023

Using Genomic Structural Equation Modeling to Partition the Genetic Covariance Between Birthweight and Cardiometabolic Risk Factors into Maternal and Offspring Components in the Norwegian HUNT Study.

Gunn-Helen Moen, Michel Nivard, Laxmi Bhatta, Nicole M Warrington, Cristen Willer, Bjørn Olav Åsvold, Ben Brumpton, David M Evans

Open access · hybridAbstract read
In one paragraph

Article in Behavior genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

8 citing papers in PubMed, 6 citations in OpenAlex.

  1. Promotion of long-term health in early life.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

8 authors at 5 institutions in 5 countries.

Gunn-Helen MoenInstitute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway. g.h.moen@medisin.uio.no.ORCID 0000-0002-8768-0904
Michel NivardDepartment of Biological Psychology, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Laxmi BhattaDepartment of Public Health and Nursing, K.G. Jebsen Center for Genetic Epidemiology, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Nicole M WarringtonInstitute of Molecular Biosciences, The University of Queensland, Brisbane, Australia.
Cristen WillerDepartment of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, USA.
Bjørn Olav ÅsvoldDepartment of Public Health and Nursing, K.G. Jebsen Center for Genetic Epidemiology, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
Ben BrumptonDepartment of Public Health and Nursing, K.G. Jebsen Center for Genetic Epidemiology, NTNU, Norwegian University of Science and Technology, Trondheim, Norway.
David M EvansInstitute of Molecular Biosciences, The University of Queensland, Brisbane, Australia. d.evans1@uq.edu.au.
Norwegian University of Science and Technology · NOThe University of Queensland · AUAmsterdam University Medical Centers · NLTranslational Research Institute · AUUniversity of Michigan · US

Funding

Australian National Health and Medical Research Council (NHMRC) 1137714Australian Research Council DE220101226National Health and Medical Research Council 2008723NHMRC GNT1157714NHMRC GNT1183074Research Council of Norway 287198Research Council of Norway 325640
6 · The paper itself

Abstract

The Barker Hypothesis posits that adverse intrauterine environments result in fetal growth restriction and increased risk of cardiometabolic disease through developmental compensations. Here we introduce a new statistical model using the genomic SEM software that is capable of simultaneously partitioning the genetic covariation between birthweight and cardiometabolic traits into maternally mediated and offspring mediated contributions. We model the covariance between birthweight and later life outcomes, such as blood pressure, non-fasting glucose, blood lipids and body mass index in the Norwegian HUNT study, consisting of 15,261 mother-eldest offspring pairs with genetic and phenotypic data. Application of this model showed some evidence for maternally mediated effects of systolic blood pressure on offspring birthweight, and pleiotropy between birthweight and non-fasting glucose mediated through the offspring genome. This underscores the importance of genetic links between birthweight and cardiometabolic phenotypes and offer alternative explanations to environmentally based hypotheses for the phenotypic correlation between these variables.

Indexed as

Cardiometabolic Risk FactorsCardiovascular DiseasesBirth WeightGenomicsHumansLatent Class AnalysisRisk FactorsBirthweightDevelopmental Origin of Health and DiseaseGenomic SEMMaternal genetic effectOffspring genetic effect

Identifiers

PMID36322199
PMCPMC9823066
OpenAlexW4307971801

What OpenQuestion holds

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LicenceCC BY
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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.