Evidence map›Paper›PMID 26791940›Full record

ArticleJournal of translational medicine2016

Mitochondrial DNA variants correlate with symptoms in myalgic encephalomyelitis/chronic fatigue syndrome.

Paul Billing-Ross, Arnaud Germain, Kaixiong Ye, Alon Keinan, Zhenglong Gu, Maureen R Hanson

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 4 pooled it
5.8field-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

37 citing papers in PubMed, 4 syntheses or guidelines pooled it, 62 citations in OpenAlex.

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  18. Redox imbalance links COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2021
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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 1 institution in 1 country.

Paul Billing-RossDivision of Nutritional Sciences, Cornell University, Ithaca, NY, 14853, USA. pdb87@cornell.edu.
Arnaud GermainDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA. ag297@cornell.edu.
Kaixiong YeDepartment of Biological Statistics and Computational Biology, Cornell University, Ithaca, NY, 14853, USA. ky297@cornell.edu.
Alon KeinanDepartment of Biological Statistics and Computational Biology, Cornell University, Ithaca, NY, 14853, USA. ak735@cornell.edu.
Zhenglong GuDivision of Nutritional Sciences, Cornell University, Ithaca, NY, 14853, USA. zg27@cornell.edu.
Maureen R HansonDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY, 14853, USA. mrh5@cornell.edu.
Cornell University · US

Funding

The X-factor of complex disease: From population genetics to GWAS of Chromosome XR01HG006849 · NHGRI · CORNELL UNIVERSITY · PI CLARK, ANDREW G · 2013 to 2020
$2.3M
NHGRI NIH HHS R01 HG006849
6 · The paper itself

Abstract

backgroundMitochondrial dysfunction has been hypothesized to occur in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), a disease characterized by fatigue, cognitive difficulties, pain, malaise, and exercise intolerance. We investigated whether haplogroup, single nucleotide polymorphisms (SNPs), or heteroplasmy of mitochondrial DNA (mtDNA) were associated with health status and/or symptoms.

methodsIllumina sequencing of PCR-amplified mtDNA was performed to analyze sequence and extent of heteroplasmy of mtDNAs of 193 cases and 196 age- and gender-matched controls from DNA samples collected by the Chronic Fatigue Initiative. Association testing was carried out to examine possible correlations of mitochondrial sequences with case/control status and symptom constellation and severity as reported by subjects on Short Form-36 and DePaul Symptom Questionnaires.

resultsNo ME/CFS subject exhibited known disease-causing mtDNA mutations. Extent of heteroplasmy was low in all subjects. Although no association between mtDNA SNPs and ME/CFS vs. healthy status was observed, haplogroups J, U and H as well as eight SNPs in ME/CFS cases were significantly associated with individual symptoms, symptom clusters, or symptom severity.

conclusionsAnalysis of mitochondrial genomes in ME/CFS cases indicates that individuals of a certain haplogroup or carrying specific SNPs are more likely to exhibit certain neurological, inflammatory, and/or gastrointestinal symptoms. No increase in susceptibility to ME/CFS of individuals carrying particular mitochondrial genomes or SNPs was observed.

Indexed as

AdultAgedAllelesCohort StudiesDNA, MitochondrialFatigue Syndrome, ChronicFemaleGenetic Association StudiesGenetic MarkersGenetic Predisposition to DiseaseHaplotypesHumansMaleMiddle AgedMutationPolymorphism, Single NucleotideDNA, MitochondrialGenetic Markers

Identifiers

PMID26791940
PMCPMC4719218
OpenAlexW2285758361

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.