Evidence map›Paper›PMID 36721200›Full record

ArticleBMC medicine2023

The effect of maternal BMI, smoking and alcohol on congenital heart diseases: a Mendelian randomisation study.

Kurt Taylor, Robyn E Wootton, Qian Yang, Sam Oddie, John Wright, Tiffany C Yang, Maria Magnus, Ole A Andreassen, Maria Carolina Borges, Massimo Caputo and 1 more

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
11.6field-weighted citation impact, top 1% 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

14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 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

11 authors at 5 institutions in 2 countries.

Kurt TaylorBristol Medical School, Population Health Science, Bristol, BS8 2BN, UK. kurt.taylor@bristol.ac.uk.ORCID 0000-0003-4690-063X
Robyn E WoottonBristol Medical School, Population Health Science, Bristol, BS8 2BN, UK.
Qian YangBristol Medical School, Population Health Science, Bristol, BS8 2BN, UK.
Sam OddieUniversity of York, Heslington, York, UK.
John WrightBradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK.
Tiffany C YangBradford Institute for Health Research, Bradford Teaching Hospitals NHS Foundation Trust, Bradford, UK.
Maria MagnusBristol Medical School, Population Health Science, Bristol, BS8 2BN, UK.
Ole A AndreassenDivision of Mental Health and Addiction, NORMENT Centre, Oslo University Hospital and Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Maria Carolina BorgesBristol Medical School, Population Health Science, Bristol, BS8 2BN, UK.
Massimo CaputoBristol Medical School, Translational Science, Bristol, UK.
Deborah A LawlorBristol Medical School, Population Health Science, Bristol, BS8 2BN, UK.
At Bristol · GBBradford Teaching Hospitals NHS Foundation Trust · GBNorwegian Institute of Public Health · NOOslo University Hospital · NOUniversity of York · GB

Funding

British Heart Foundation CH/17/1/32804British Heart Foundation CH/F/20/90003British Heart Foundation CS/16/4/32482British Heart Foundation FS/17/60/33474Medical Research Council G9815508Medical Research Council MC_PC_15018Medical Research Council MC_PC_19009Medical Research Council MC_PC_21038Medical Research Council MC_UU_00011/6Medical Research Council MR/N024397/1
6 · The paper itself

Abstract

backgroundCongenital heart diseases (CHDs) remain a significant cause of infant morbidity and mortality. Epidemiological studies have explored maternal risk factors for offspring CHDs, but few have used genetic epidemiology methods to improve causal inference.

methodsThree birth cohorts, including 65,510 mother/offspring pairs (N = 562 CHD cases) were included. We used Mendelian randomisation (MR) analyses to explore the effects of genetically predicted maternal body mass index (BMI), smoking and alcohol on offspring CHDs. We generated genetic risk scores (GRS) using summary data from large-scale genome-wide association studies (GWAS) and validated the strength and relevance of the genetic instrument for exposure levels during pregnancy. Logistic regression was used to estimate the odds ratio (OR) of CHD per 1 standard deviation (SD) higher GRS. Results for the three cohorts were combined using random-effects meta-analyses. We performed several sensitivity analyses including multivariable MR to check the robustness of our findings.

resultsThe GRSs associated with the exposures during pregnancy in all three cohorts. The associations of the GRS for maternal BMI with offspring CHD (pooled OR (95% confidence interval) per 1SD higher GRS: 0.95 (0.88, 1.03)), lifetime smoking (pooled OR: 1.01 (0.93, 1.09)) and alcoholic drinks per week (pooled OR: 1.06 (0.98, 1.15)) were close to the null. Sensitivity analyses yielded similar results.

conclusionsOur results do not provide robust evidence of an effect of maternal BMI, smoking or alcohol on offspring CHDs. However, results were imprecise. Our findings need to be replicated, and highlight the need for more and larger studies with maternal and offspring genotype and offspring CHD data.

Indexed as

Genome-Wide Association StudyHeart Defects, CongenitalSmokingBody Mass IndexEthanolFemaleHumansInfantMendelian Randomization AnalysisPregnancyEthanolALSPAC, BiBCongenital heart diseaseMendelian randomisationMoBaRisk factors

Identifiers

PMID36721200
PMCPMC9890815
OpenAlexW4318684535

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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.