Evidence map›Paper›PMID 25942577›Full record

ArticlePLoS genetics2015

Genomic heritability: what is it?

Gustavo de Los Campos, Daniel Sorensen, Daniel Gianola

Abstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
189citing papers in PubMed, 5 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

189 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
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  18. Quantitative genetics of microbiome-mediated traits.Evolution; international journal of organic evolution · 2025
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129 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

3 authors.

Gustavo de Los CamposDepartments of Epidemiology & Biostatistics, and Statistics, Michigan State University, United States of America.
Daniel SorensenDepartment of Molecular Biology and Genetics, Aarhus University, Tjele, Denmark.
Daniel GianolaDepartments of Animal Science, Dairy Science and Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.

Funding

Statistical Tools for Whole-Genome Prediction of Complex Traits and DiseasesR01GM101219 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DE LOS CAMPOS, GUSTAVO · 2012 to 2017
$1.6M
Factors Affecting Prediction Accuracy of Complex Human Traits and DiseasesR01GM099992 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DE LOS CAMPOS, GUSTAVO · 2012 to 2015
$1.0M
NIGMS NIH HHS R01 GM099992NIGMS NIH HHS R01 GM101219
6 · The paper itself

Abstract

Whole-genome regression methods are being increasingly used for the analysis and prediction of complex traits and diseases. In human genetics, these methods are commonly used for inferences about genetic parameters, such as the amount of genetic variance among individuals or the proportion of phenotypic variance that can be explained by regression on molecular markers. This is so even though some of the assumptions commonly adopted for data analysis are at odds with important quantitative genetic concepts. In this article we develop theory that leads to a precise definition of parameters arising in high dimensional genomic regressions; we focus on the so-called genomic heritability: the proportion of variance of a trait that can be explained (in the population) by a linear regression on a set of markers. We propose a definition of this parameter that is framed within the classical quantitative genetics theory and show that the genomic heritability and the trait heritability parameters are equal only when all causal variants are typed. Further, we discuss how the genomic variance and genomic heritability, defined as quantitative genetic parameters, relate to parameters of statistical models commonly used for inferences, and indicate potential inferential problems that are assessed further using simulations. When a large proportion of the markers used in the analysis are in LE with QTL the likelihood function can be misspecified. This can induce a sizable finite-sample bias and, possibly, lack of consistency of likelihood (or Bayesian) estimates. This situation can be encountered if the individuals in the sample are distantly related and linkage disequilibrium spans over short regions. This bias does not negate the use of whole-genome regression models as predictive machines; however, our results indicate that caution is needed when using marker-based regressions for inferences about population parameters such as the genomic heritability.

Indexed as

Models, GeneticQuantitative Trait, HeritableBayes TheoremGenetic MarkersGenomicsHumansLikelihood FunctionsLinear ModelsLinkage DisequilibriumModels, StatisticalQuantitative Trait LociGenetic Markers

Identifiers

PMID25942577
PMCPMC4420472

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.