Evidence map›Paper›PMID 29547617›Full record

ArticlePLoS biology2018

A population genetic interpretation of GWAS findings for human quantitative traits.

Yuval B Simons, Kevin Bullaughey, Richard R Hudson, Guy Sella

Abstract read
In one paragraph

Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.

0numbers the graph read from it
0cells of the map it votes in
119citing 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

119 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Genetic architectures of brain-related traits are shaped by strong selective constraints.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Principled measures and estimates of trait polygenicity.American journal of human genetics · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Chromosome-specific drift under stabilizing selection generates polygenic barriers to sex chromosome turnover.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  15. Background selection in recombining genomes and its consequences for the maintenance of variation in complex traits.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  16. Article
  17. Review
  18. Parameterizing the genetic architecture under stabilizing selection.bioRxiv : the preprint server for biology · 2026
    Article
  19. Article
  20. Quantitative system drift.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Yuval B SimonsDepartment of Biological Sciences, Columbia University, New York, New York, United States of America.ORCID 0000-0002-0037-4673
Kevin BullaugheyDepartment of Ecology & Evolution, University of Chicago, Chicago, Illinois, United States of America.
Richard R HudsonDepartment of Ecology & Evolution, University of Chicago, Chicago, Illinois, United States of America.
Guy SellaDepartment of Biological Sciences, Columbia University, New York, New York, United States of America.

Funding

The population genetics of disease risk and other quantitative traitsR01GM115889 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI SELLA, GUY · 2015 to 2025
$2.9M
NIGMS NIH HHS R01 GM115889
6 · The paper itself

Abstract

Human genome-wide association studies (GWASs) are revealing the genetic architecture of anthropomorphic and biomedical traits, i.e., the frequencies and effect sizes of variants that contribute to heritable variation in a trait. To interpret these findings, we need to understand how genetic architecture is shaped by basic population genetics processes-notably, by mutation, natural selection, and genetic drift. Because many quantitative traits are subject to stabilizing selection and because genetic variation that affects one trait often affects many others, we model the genetic architecture of a focal trait that arises under stabilizing selection in a multidimensional trait space. We solve the model for the phenotypic distribution and allelic dynamics at steady state and derive robust, closed-form solutions for summary statistics of the genetic architecture. Our results provide a simple interpretation for missing heritability and why it varies among traits. They predict that the distribution of variances contributed by loci identified in GWASs is well approximated by a simple functional form that depends on a single parameter: the expected contribution to genetic variance of a strongly selected site affecting the trait. We test this prediction against the results of GWASs for height and body mass index (BMI) and find that it fits the data well, allowing us to make inferences about the degree of pleiotropy and mutational target size for these traits. Our findings help to explain why the GWAS for height explains more of the heritable variance than the similarly sized GWAS for BMI and to predict the increase in explained heritability with study sample size. Considering the demographic history of European populations, in which these GWASs were performed, we further find that most of the associations they identified likely involve mutations that arose shortly before or during the Out-of-Africa bottleneck at sites with selection coefficients around s = 10-3.

Indexed as

Body Mass IndexGenome-Wide Association StudyModels, GeneticQuantitative Trait LociBody HeightGenetic DriftGenetics, PopulationGenetic VariationHumansPhenotypeSelection, Genetic

Identifiers

PMID29547617
PMCPMC5871013

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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.