Evidence map›Paper›PMID 41073879›Full record

ArticleGenetics2025

Mutation-selection-drift balance models of complex diseases.

Jeremy J Berg, Xinyi Li, Kellen Riall, Laura K Hayward, Guy Sella

Erratum issuedAbstract read
In one paragraph

Article in Genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. 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
  4. Article
  5. Principled measures and estimates of trait polygenicity.American journal of human genetics · 2026
    Article
  6. 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
  7. Article
  8. Article
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Jeremy J BergDepartment of Human Genetics, The University of Chicago, Chicago, IL 60637, United States.ORCID 0000-0001-5411-6840
Xinyi LiCommittee on Genetics, Genomics and Systems Biology, The University of Chicago, Chicago, IL 60637, United States.
Kellen RiallCommittee on Genetics, Genomics and Systems Biology, The University of Chicago, Chicago, IL 60637, United States.
Laura K HaywardInstitute of Science and Technology Austria  Klosterneuburg 3400, Lower Austria, Austria.
Guy SellaDepartment of Biological Sciences, Columbia University, New York, NY 10027, United States.

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
Refining mutation rates and measures of purifying selection with an application to understanding the impact of non-coding variation on neuropsychiatric diseasesR01HG010773 · NHGRI · UNIVERSITY OF CHICAGO · PI HE, XIN, NOVEMBRE, JOHN · 2020 to 2023
$1.7M
Population genetic modeling of genetic variation for complex traits and diseasesR35GM151257 · NIGMS · UNIVERSITY OF CHICAGO · PI Jeremy Jackson Berg · 2023 to 2026
$1.6M
Population genetic modeling of the genetic architecture of complex diseaseF32GM126787 · NIGMS · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI BERG, JEREMY JACKSON · 2018 to 2018
$55k
NHGRI NIH HHS R01 HG010773NIGMS NIH HHS F32 GM126787NIGMS NIH HHS R01 GM115889NIGMS NIH HHS R35 GM151257NIH HHS GM115889NIH HHS GM126787NIH HHS GM151257
6 · The paper itself

Abstract

Genetic variation that influences complex disease susceptibility is introduced into the population by mutation and removed by natural selection and genetic drift. This mutation-selection-drift balance (MSDB) shapes the prevalence of a disease and its genetic architecture. To date, however, MSDB has been modeled only for monogenic (Mendelian) diseases. Here, we develop an MSDB model for complex disease susceptibility: we assume that genotype relates to disease risk according to the canonical liability threshold model and that the selection on variants affecting risk stems from the fitness cost of the disease. We focus on diseases that are highly polygenic, entail a substantial fitness cost, and are neither extremely common in the population nor exceedingly rare. The comparison of model predictions with genome-wide association studies and other observations in humans indicates that common genetic variation affecting complex disease susceptibility is little affected by directional selection and instead shaped by pleiotropic stabilizing selection on other traits. In turn, directional selection may exert a more substantial effect on rare, large-effect variants. Our results also suggest that current estimates of disease heritability are likely biased. The model thus provides a better understanding of the evolutionary processes that shape the architecture and prevalence of complex diseases.

Indexed as

Genetic DriftModels, GeneticMutationSelection, GeneticGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansMultifactorial Inheritancecomplex diseasegenetic driftmutationselection

Identifiers

PMID41073879
PMCPMC12693578

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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.