Evidence map›Paper›PMID 26469178›Full record

ArticlePloS one2015

In Search for the Genetic Basis of Quality of Life in Healthy Swedish Women--A GWAS Study Using the iCOGS Custom Genotyping Array.

Dounya Schoormans, Hatef Darabi, Jingmei Li, Yvonne Brandberg, Mikael Eriksson, Koos H Zwinderman, Mirjam A G Sprangers, Per Hall

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
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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

8 authors.

Dounya SchoormansDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Medical Psychology, Academic Medical Center, Amsterdam, The Netherlands; Department of Medical and Clinical Psychology, Tilburg University, Tilburg, The Netherlands.
Hatef DarabiDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Jingmei LiDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Human Genetics, Genome Institute of Singapore, Singapore, Singapore.
Yvonne BrandbergDepartment of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden.
Mikael ErikssonDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Koos H ZwindermanDepartment of Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam, The Netherlands.
Mirjam A G SprangersDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Medical Psychology, Academic Medical Center, Amsterdam, The Netherlands.
Per HallDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundQuality of life (QoL) is increasingly measured in both research and clinical practice. QoL-assessments are built on a long, empirically-based, and stringent approach. There is ample evidence that QoL is, in part, heritable. We therefore performed a GWAS relating genetic variation to QoL in healthy females.

methodsIn 5,142 healthy females, background characteristics (e.g. demographic, clinical, lifestyle and psychological factors) and QoL by means of the EORTC QLQ-C30 were measured. Moreover, women were genotyped using a custom array including ~210,000 single nucleotide polymorphisms (SNPs). Initially, SNPs were related to each QoL-domain, by means of partially adjusted (controlling for age and population stratification) and fully adjusted (controlling for age, population stratification, and background characteristics) regression analyses. Additionally, gene-based analyses were performed relating the combined effect of SNPs within each gene to QoL using the statistical software package VEGAS.

resultsNone of the associations between QoL and genetic variation (i.e. individual SNPs and genes) reached the bonferroni corrected significance level.

conclusionReasons for a lack of association between genetic markers and QoL could be low variation in QoL-scores; selecting genetic markers not tagging QoL; or that the genetic effect that impacts one's QoL is mediated through biological pathways rather than the effect of single SNPs or genes. Therefore, we opt for a pathway-based or system biology approach as a complementary and powerful approach to analyze the combined effect of genes and their biological implications in future studies focusing on QoL-issues.

Indexed as

Quality of LifeAdultAgedFemaleGenome-Wide Association StudyGenotypeHealthy VolunteersHumansMiddle AgedOligonucleotide Array Sequence AnalysisPolymorphism, Single NucleotideSwedenWhite People

Identifiers

PMID26469178
PMCPMC4607154

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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.