Evidence map›Paper›PMID 31335958›Full record

ArticleInternational journal of epidemiology2019

Using a two-sample Mendelian randomization design to investigate a possible causal effect of maternal lipid concentrations on offspring birth weight.

Liang-Dar Hwang, Deborah A Lawlor, Rachel M Freathy, David M Evans, Nicole M Warrington

Open access · hybridAbstract read
In one paragraph

Article in International journal of epidemiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
7.0field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  7. Genetic Susceptibility toLife (Basel, Switzerland) · 2026
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  10. Two-step Mendelian randomization reveals a lipid-driven protective effect of type 2 diabetes on ALS.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  15. Association between gut microbiota and male infertility: a two-sample Mendelian randomization study.International microbiology : the official journal of the Spanish Society for Microbiology · 2024
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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

5 authors at 3 institutions in 3 countries.

Liang-Dar HwangThe University of Queensland Diamantina Institute, The University of Queensland, Brisbane, Australia.
Deborah A LawlorMedical Research Council Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Rachel M FreathyInstitute of Biomedical and Clinical Science, College of Medicine and Health, University of Exeter, Exeter, UK.
David M EvansThe University of Queensland Diamantina Institute, The University of Queensland, Brisbane, Australia.
Nicole M WarringtonThe University of Queensland Diamantina Institute, The University of Queensland, Brisbane, Australia.
The University of Queensland · AUUniversity of Bristol · GBUniversity of Exeter · GB

Funding

British Heart Foundation AA/18/1/34219Department of Health NF-SI-0611–10196Medical Research Council MC_PC_17228Medical Research Council MC_QA137853Medical Research Council MC_UU_00011/6Medical Research Council MC_UU_12013/4Wellcome Trust 104150
6 · The paper itself

Abstract

backgroundThe intrauterine environment is critical for fetal growth and development. However, observational associations between maternal gestational lipid concentrations and offspring birth weight (BW) have been inconsistent and ascertaining causality is challenging.

methodsWe used a novel two-sample Mendelian randomization (MR) approach to estimate the causal effect of maternal gestational high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride concentrations on offspring BW. Single nucleotide polymorphisms (SNPs) associated with serum HDL-C, LDL-C and triglyceride concentrations identified in the Global Lipids Genetics Consortium genome-wide association study meta-analysis (n = 188 577 European-ancestry individuals; sample 1) were selected as instrumental variables. The effects of these SNPs on offspring BW were estimated using a structural equation model in the UK Biobank and Early Growth Genetics consortium (n = 230 069 European-ancestry individuals; sample 2) that enabled partitioning of the genetic associations into maternal- (intrauterine) and fetal-specific effects.

resultsWe found no evidence for a causal effect of maternal gestational HDL-C, LDL-C or triglyceride concentrations on offspring BW [standard deviation change in BW per standard deviation higher in HDL-C = -0.005 (95% confidence interval: -0.039, 0.029), LDL-C = 0.014 (-0.017, 0.045), and triglycerides = 0.014 (-0.025, 0.052)].

conclusionsOur findings suggest that maternal gestational HDL-C, LDL-C and triglyceride concentrations play a limited role in determining offspring BW. However, we cannot comment on the impact of these and other lipid fractions on fetal development more generally. Our study illustrates the power and flexibility of two-sample MR in assessing the causal effect of maternal environmental exposures on offspring outcomes.

Indexed as

Birth WeightCholesterol, HDLCholesterol, LDLDatabases, FactualFemaleGenome-Wide Association StudyHumansLipidsMaleMendelian Randomization AnalysisPolymorphism, Single NucleotidePregnancyPrenatal Exposure Delayed EffectsRisk FactorsTriglyceridesWhite PeopleCholesterol, HDLCholesterol, LDLLipidsTriglyceridesbirth weighthigh-density lipoprotein cholesterollow-density lipoprotein cholesterolmaternal effectMendelian randomizationtriglycerides

Identifiers

PMID31335958
PMCPMC6857765
OpenAlexW2963578359

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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.