Evidence map›Paper›PMID 34057592›Full record

ArticleHuman genetics2021

Phenome-wide screening of GWAS data reveals the complex causal architecture of obesity.

Luis M García-Marín, Adrián I Campos, Pik-Fang Kho, Nicholas G Martin, Gabriel Cuéllar-Partida, Miguel E Rentería

Abstract read
PubMed Publisher
In one paragraph

Article in Human genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
5.5field-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, 1 synthesis or guideline pooled it, 19 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

6 authors at 3 institutions in 2 countries.

Luis M García-MarínDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0003-4731-6558
Adrián I CamposDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0003-3468-8619
Pik-Fang KhoDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0001-7831-6062
Nicholas G MartinDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0003-4069-8020
Gabriel Cuéllar-PartidaUniversity of Queensland Diamantina Institute, The University of Queensland, Brisbane, QLD, Australia. g.cuellarpartida@uq.edu.au.ORCID http://orcid.org/0000-0001-7648-4097
Miguel E RenteríaDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. miguel.renteria@qimrberghofer.edu.au.ORCID http://orcid.org/0000-0003-4626-7248
The University of Queensland · AUQueensland University of Technology · AUQIMR Berghofer Medical Research Institute · AU

Funding

National Health and Medical Research Council GNT1102821
6 · The paper itself

Abstract

objectiveIn the present study, we sought to identify causal relationships between obesity and other complex traits and conditions using a data-driven hypothesis-free approach that uses genetic data to infer causal associations.

methodsWe leveraged available summary-based genetic data from genome-wide association studies on 1498 phenotypes and applied the latent causal variable method (LCV) between obesity and all traits.

resultsWe identified 110 traits causally associated with obesity. Of those, 109 were causal outcomes of obesity, while only leg pain in calves was a causal determinant of obesity. Causal outcomes of obesity included 26 phenotypes associated with cardiovascular diseases, 22 anthropometric measurements, nine with the musculoskeletal system, nine with behavioural or lifestyle factors including loneliness or isolation, six with respiratory diseases, five with body bioelectric impedances, four with psychiatric phenotypes, four related to the nervous system, four with disabilities or long-standing illness, three with the gastrointestinal system, three with use of analgesics, two with metabolic diseases, one with inflammatory response and one with the neurodevelopmental disorder ADHD, among others. In particular, some causal outcomes of obesity included hypertension, stroke, ever having a period of extreme irritability, low forced vital capacity and forced expiratory volume, diseases of the musculoskeletal system, diabetes, carpal tunnel syndrome, loneliness or isolation, high leukocyte count, and ADHD.

conclusionsOur results indicate that obesity causally affects a wide range of traits and comorbid diseases, thus providing an overview of the metabolic, physiological, and neuropsychiatric impact of obesity on human health.

Indexed as

Body Mass IndexCardiovascular DiseasesFemaleGastrointestinal DiseasesGenetic Association StudiesGenome-Wide Association StudyGenotypeHumansLonelinessLung DiseasesMaleMental DisordersMetabolic DiseasesMultifactorial InheritanceMusculoskeletal DiseasesObesity

Identifiers

PMID34057592
OpenAlexW3165576023

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.