Evidence map›Paper›PMID 27428752›Full record

ArticleNature genetics2016

Evaluating the contribution of genetics and familial shared environment to common disease using the UK Biobank.

María Muñoz, Ricardo Pong-Wong, Oriol Canela-Xandri, Konrad Rawlik, Chris S Haley, Albert Tenesa

Abstract readEvaluation Study
In one paragraph

Article in Nature genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 7 pooled it
–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

67 citing papers in PubMed, 7 syntheses or guidelines pooled it.

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7 more citing papers are in PubMed but not listed here.

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.

María MuñozRoslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.
Ricardo Pong-WongRoslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.
Oriol Canela-XandriRoslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.ORCID 0000-0003-4601-6289
Konrad RawlikRoslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.
Chris S HaleyRoslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.
Albert TenesaRoslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Midlothian, UK.

Funding

Biotechnology and Biological Sciences Research Council BB/J004235/1Biotechnology and Biological Sciences Research Council BBS/E/D/20211553Medical Research Council MC_PC_U127592696Medical Research Council MC_QA137853Medical Research Council MR/K014781/1Medical Research Council MR/N003179/1
6 · The paper itself

Abstract

Genome-wide association studies have detected many loci underlying susceptibility to disease, but most of the genetic factors that contribute to disease susceptibility remain unknown. Here we provide evidence that part of the 'missing heritability' can be explained by an overestimation of heritability. We estimated the heritability of 12 complex human diseases using family history of disease in 1,555,906 individuals of white ancestry from the UK Biobank. Estimates using simple family-based statistical models were inflated on average by ∼47% when compared with those from structural equation modeling (SEM), which specifically accounted for shared familial environmental factors. In addition, heritabilities estimated using SNP data explained an average of 44.2% of the simple family-based estimates across diseases and an average of 57.3% of the SEM-estimated heritabilities, accounting for almost all of the SEM heritability for hypertension. Our results show that both genetics and familial environment make substantial contributions to familial clustering of disease.

Indexed as

Biological Specimen BanksGene-Environment InteractionGenetic Predisposition to DiseaseQuantitative Trait, HeritableDiseaseFemaleGenome-Wide Association StudyHumansMaleModels, GeneticPhenotypePolymorphism, Single NucleotideUnited Kingdom

Identifiers

PMID27428752
PMCPMC5989924

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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.