Evidence map›Paper›PMID 25422463›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2014

Measuring missing heritability: inferring the contribution of common variants.

David Golan, Eric S Lander, Saharon Rosset

Registry-linked trialAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04331535 (Pragmatic Randomized Trial of Polygenic Risk Scoring for Common Diseases in Primary Care), which is not on this map. Cited by 177 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
177citing papers in PubMed, 8 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.

NCT04331535 naunknown statusnot on this mapstarted 2020, after this paper: background citation

Pragmatic Randomized Trial of Polygenic Risk Scoring for Common Diseases in Primary Care

TypeinterventionalSponsorBoston VA Research Institute, Inc.Ran2020 to 2025Enrolled1,076ConditionsCoronary Artery Disease, Atrial Fibrillation, Type 2 Diabetes, Colorectal CancerArmsPolygenic risk score (PRS)
3 · Its place in the literature

Who cites it

177 citing papers in PubMed, 8 syntheses or guidelines pooled it.

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  4. Systematic Review of Polygenic Risk Scores for Type 1 and Type 2 Diabetes.International journal of molecular sciences · 2020
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  18. Dissecting Alzheimer's disease heritability across populations.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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117 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

David GolanDepartment of Statistics and Operations Research, School of Mathematical Sciences, Tel-Aviv University, Tel-Aviv, Israel 69978;
Eric S LanderBroad Institute of MIT and Harvard, Cambridge, MA 02142; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139; and Department of Systems Biology, Harvard Medical School, Boston, MA 02155 lander@broadinstitute.org saharon@post.tau.ac.il.
Saharon RossetDepartment of Statistics and Operations Research, School of Mathematical Sciences, Tel-Aviv University, Tel-Aviv, Israel 69978; lander@broadinstitute.org saharon@post.tau.ac.il.

Funding

Large Scale Sequencing and Analysis of GenomesU54HG003067 · NHGRI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GABRIEL, STACEY, LANDER, ERIC S · 2004 to 2015
$568.6M
NHGRI NIH HHS NIH HG003067NHGRI NIH HHS U54 HG003067
6 · The paper itself

Abstract

Genome-wide association studies (GWASs), also called common variant association studies (CVASs), have uncovered thousands of genetic variants associated with hundreds of diseases. However, the variants that reach statistical significance typically explain only a small fraction of the heritability. One explanation for the "missing heritability" is that there are many additional disease-associated common variants whose effects are too small to detect with current sample sizes. It therefore is useful to have methods to quantify the heritability due to common variation, without having to identify all causal variants. Recent studies applied restricted maximum likelihood (REML) estimation to case-control studies for diseases. Here, we show that REML considerably underestimates the fraction of heritability due to common variation in this setting. The degree of underestimation increases with the rarity of disease, the heritability of the disease, and the size of the sample. Instead, we develop a general framework for heritability estimation, called phenotype correlation-genotype correlation (PCGC) regression, which generalizes the well-known Haseman-Elston regression method. We show that PCGC regression yields unbiased estimates. Applying PCGC regression to six diseases, we estimate the proportion of the phenotypic variance due to common variants to range from 25% to 56% and the proportion of heritability due to common variants from 41% to 68% (mean 60%). These results suggest that common variants may explain at least half the heritability for many diseases. PCGC regression also is readily applicable to other settings, including analyzing extreme-phenotype studies and adjusting for covariates such as sex, age, and population structure.

Indexed as

Genetic VariationResearch DesignAllelesCase-Control StudiesComputer SimulationGene FrequencyGenetic Association StudiesGenetic Diseases, InbornGenome-Wide Association StudyGenomicsGenotypeHumansModels, GeneticModels, StatisticalPhenotypePolymorphism, Single Nucleotidegenome-wide association studiesheritability estimationstatistical genetics

Identifiers

PMID25422463
PMCPMC4267399

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Registered trials

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.