Evidence map›Paper›PMID 28957414›Full record

ArticlePloS one2017

Red blood cell distribution width: Genetic evidence for aging pathways in 116,666 volunteers.

Luke C Pilling, Janice L Atkins, Michael O Duff, Robin N Beaumont, Samuel E Jones, Jessica Tyrrell, Chia-Ling Kuo, Katherine S Ruth, Marcus A Tuke, Hanieh Yaghootkar and 8 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Genetic Variation and Hot Flashes: A Systematic Review.The Journal of clinical endocrinology and metabolism · 2020
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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

18 authors at 4 institutions in 2 countries.

Luke C PillingEpidemiology and Public Health Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0002-3332-8454
Janice L AtkinsEpidemiology and Public Health Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0003-4919-9068
Michael O DuffDepartment of Genetics and Genome Sciences, Institute for Systems Genomics, University of Connecticut Health Center, Farmington, Connecticut, United States of America.
Robin N BeaumontGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0003-0750-8248
Samuel E JonesGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0003-0153-922X
Jessica TyrrellGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0002-9256-6065
Chia-Ling KuoDepartment of Community Medicine and Health Care, Connecticut Institute for Clinical and Translational Science, Institute for Systems Genomics, University of Connecticut Health Center, Farmington, Connecticut, United States of America.
Katherine S RuthGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0003-4966-9170
Marcus A TukeGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.
Hanieh YaghootkarGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.
Andrew R WoodGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.
Anna MurrayGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0002-2351-2522
Michael N WeedonGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.
Lorna W HarriesInstitute of Biomedical and Clinical Sciences, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, United Kingdom.ORCID http://orcid.org/0000-0001-7791-8061
George A KuchelCenter on Aging, University of Connecticut, Farmington, CT, United States of America.ORCID http://orcid.org/0000-0001-8387-7040
Luigi FerrucciNational Institute on Aging, Baltimore, MD, United States.
Timothy M FraylingGenetics of Complex Traits Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.ORCID http://orcid.org/0000-0001-8362-2603
David MelzerEpidemiology and Public Health Group, University of Exeter Medical School, RILD Level 3, Royal Devon & Exeter Hospital, Exeter, EX2 5DW, United Kingdom.
University of Exeter · GBUConn Health · USUniversity of Connecticut · USNational Institute on Aging · US

Funding

Medical Research Council MC_QA137853Medical Research Council MR/M005070/1Medical Research Council MR/M023095/1Wellcome Trust
6 · The paper itself

Abstract

introductionVariability in red blood cell volumes (distribution width, RDW) increases with age and is strongly predictive of mortality, incident coronary heart disease and cancer. We investigated inherited genetic variation associated with RDW in 116,666 UK Biobank human volunteers.

resultsA large proportion RDW is explained by genetic variants (29%), especially in the older group (60+ year olds, 33.8%, <50 year olds, 28.4%). RDW was associated with 194 independent genetic signals; 71 are known for conditions including autoimmune disease, certain cancers, BMI, Alzheimer's disease, longevity, age at menopause, bone density, myositis, Parkinson's disease, and age-related macular degeneration. Exclusion of anemic participants did not affect the overall findings. Pathways analysis showed enrichment for telomere maintenance, ribosomal RNA, and apoptosis. The majority of RDW-associated signals were intronic (119 of 194), including SNP rs6602909 located in an intron of oncogene GAS6, an eQTL in whole blood.

conclusionsAlthough increased RDW is predictive of cardiovascular outcomes, this was not explained by known CVD or related lipid genetic risks, and a RDW genetic score was not predictive of incident disease. The predictive value of RDW for a range of negative health outcomes may in part be due to variants influencing fundamental pathways of aging.

Indexed as

AdultAgedAgingBiological Specimen BanksErythrocyte IndicesFemaleGene OntologyGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyGenotypeHealthy VolunteersHumansMaleMiddle AgedSignal Transduction

Identifiers

PMID28957414
PMCPMC5619771
OpenAlexW2952861350

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.