Evidence map›Paper›PMID 33631142›Full record

ArticleMetabolism: clinical and experimental2021

Impact of body composition on COVID-19 susceptibility and severity: A two-sample multivariable Mendelian randomization study.

Dennis Freuer, Jakob Linseisen, Christa Meisinger

Open access · bronzeAbstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 4 pooled it
9.4field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 4 syntheses or guidelines pooled it, 129 citations in OpenAlex.

  1. Pooled it
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  4. Mendelian Randomization Analysis Reveals No Causal Relationship Between Nonalcoholic Fatty Liver Disease and Severe COVID-19.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2022
    Pooled it
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  20. The impact of obesity: a narrative review.Singapore medical journal · 2023
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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

3 authors at 2 institutions in 1 country.

Dennis FreuerChair of Epidemiology at UNIKA-T Augsburg, Ludwig-Maximilians-Universität München, 86156 Augsburg, Germany; Independent Research Group Clinical Epidemiology, Helmholtz Zentrum München, German Research Centre for Environmental Health, 85764, Neuherberg, Germany. Electronic address: d.freuer@unika-t.de.
Jakob LinseisenChair of Epidemiology at UNIKA-T Augsburg, Ludwig-Maximilians-Universität München, 86156 Augsburg, Germany; Independent Research Group Clinical Epidemiology, Helmholtz Zentrum München, German Research Centre for Environmental Health, 85764, Neuherberg, Germany.
Christa MeisingerChair of Epidemiology at UNIKA-T Augsburg, Ludwig-Maximilians-Universität München, 86156 Augsburg, Germany; Independent Research Group Clinical Epidemiology, Helmholtz Zentrum München, German Research Centre for Environmental Health, 85764, Neuherberg, Germany.
University of Augsburg · DEHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRecent studies suggested obesity to be a possible risk factor for COVID-19 disease in the wake of the coronavirus (SARS-CoV-2) infection. However, the causality and especially the role of body fat distribution in this context is still unclear. Thus, using a univariable as well as multivariable two-sample Mendelian randomization (MR) approach, we investigated for the first time the causal impact of body composition on the susceptibility and severity of COVID-19.

methodsAs indicators of overall and abdominal obesity we considered the measures body mass index (BMI), waist circumference (WC), and trunk fat ratio (TFR). Summary statistics of genome-wide association studies (GWASs) for these body composition measures were drawn from the GIANT consortium and UK Biobank, while for susceptibility and severity due to COVID-19 disease data from the COVID-19 Host Genetics Initiative was used. For the COVID-19 cohort neither age nor gender was available. Total and direct causal effect estimates were calculated using Single Nucleotide Polymorphisms (SNPs), sensitivity analyses were done applying several robust MR techniques and mediation effects of type 2 diabetes (T2D) and cardiovascular diseases (CVD) were investigated within multivariable MR analyses.

resultsGenetically predicted BMI was strongly associated with both, susceptibility (OR = 1.31 per 1 SD increase; 95% CI: 1.15-1.50; P-value = 7.3·10

conclusionsThis study provides strong evidence for a causal impact of overall obesity on the susceptibility and severity of COVID-19 disease. The impact of abdominal obesity was weaker and disappeared after adjustment for BMI. Therefore, obese people should be regarded as a high-risk group. Future research is necessary to investigate the underlying mechanisms linking obesity with COVID-19.

Indexed as

Body CompositionSARS-CoV-2Body Mass IndexCOVID-19Disease SusceptibilityGenome-Wide Association StudyHumansMendelian Randomization AnalysisObesityPolymorphism, Single NucleotideSeverity of Illness IndexBody compositionBody fat distributionCOVID-19Mendelian randomizationObesitySARS-CoV-2

Identifiers

PMID33631142
PMCPMC7900753
OpenAlexW3130906542

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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.