Evidence map›Paper›PMID 24498077›Full record

ArticlePloS one2014

BMI-associated alleles do not constitute risk alleles for polycystic ovary syndrome independently of BMI: a case-control study.

Yvonne V Louwers, Nigel W Rayner, Blanca M Herrera, Lisette Stolk, Christopher J Groves, Thomas M Barber, Andre G Uitterlinden, Stephen Franks, Joop S E Laven, Mark I McCarthy

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Observational
  6. Article
  7. Review
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

10 authors at 5 institutions in 2 countries.

Yvonne V LouwersDepartment of Obstetrics and Gynecology, Subdivision of Reproductive Medicine, Erasmus MC University Medical Center, Rotterdam, the Netherlands.
Nigel W RaynerWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom ; Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
Blanca M HerreraWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom.
Lisette StolkDepartment of Internal Medicine, Erasmus MC University Medical Center, Rotterdam, the Netherlands.
Christopher J GrovesWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom ; Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
Thomas M BarberOxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
Andre G UitterlindenDepartment of Internal Medicine, Erasmus MC University Medical Center, Rotterdam, the Netherlands ; Department of Epidemiology, Erasmus MC University Medical Center, Rotterdam, the Netherlands.
Stephen FranksInstitute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Hospital, London, United Kingdom.
Joop S E LavenDepartment of Obstetrics and Gynecology, Subdivision of Reproductive Medicine, Erasmus MC University Medical Center, Rotterdam, the Netherlands.
Mark I McCarthyWellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom ; Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, United Kingdom.
Erasmus MC · NLUniversity of Oxford · GBCentre for Human Genetics · GBHammersmith Hospital · GBOxford Centre for Diabetes, Endocrinology and Metabolism · GB

Funding

Medical Research Council G0802782Wellcome Trust 090532
6 · The paper itself

Abstract

introductionPolycystic Ovary Syndrome (PCOS) has a strong genetic background and the majority of patients with PCOS have elevated BMI levels. The aim of this study was to determine to which extent BMI-increasing alleles contribute to risk of PCOS when contemporaneous BMI is taken into consideration.

methodsPatients with PCOS and controls were recruited from the United Kingdom (563 cases and 791 controls) and The Netherlands (510 cases and 2720 controls). Cases and controls were of similar BMI. SNPs mapping to 12 BMI-associated loci which have been extensively replicated across different ethnicities, i.e., BDNF, FAIM2, ETV5, FTO, GNPDA2, KCTD15, MC4R, MTCH2, NEGR1, SEC16B, SH2B1, and TMEM18, were studied in association with PCOS within each cohort using the additive genetic model followed by a combined analysis. A genetic allelic count risk score model was used to determine the risk of PCOS for individuals carrying increasing numbers of BMI-increasing alleles.

resultsNone of the genetic variants, including FTO and MC4R, was associated with PCOS independently of BMI in the meta-analysis. Moreover, no differences were observed between cases and controls in the number of BMI-risk alleles present and no overall trend across the risk score groups was observed.

conclusionIn this combined analysis of over 4,000 BMI-matched individuals from the United Kingdom and the Netherlands, we observed no association of BMI risk alleles with PCOS independent of BMI.

Indexed as

Body Mass IndexPolymorphism, Single NucleotideAllelesBody WeightCase-Control StudiesFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHumansNetherlandsObesityOverweightPolycystic Ovary SyndromeRisk AssessmentRisk Factors

Identifiers

PMID24498077
PMCPMC3909077
OpenAlexW2067910476

What OpenQuestion holds

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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.