Evidence map›Paper›PMID 37726359›Full record

ArticleScientific reports2023

Recent natural selection conferred protection against schizophrenia by non-antagonistic pleiotropy.

Javier González-Peñas, Lucía de Hoyos, Covadonga M Díaz-Caneja, Álvaro Andreu-Bernabeu, Carol Stella, Xaquín Gurriarán, Lourdes Fañanás, Julio Bobes, Ana González-Pinto, Benedicto Crespo-Facorro and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.6field-weighted citation impact, top 14% of its field
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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

18 authors at 10 institutions in 2 countries.

Javier González-PeñasDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain. javier.gonzalez@iisgm.com.
Lucía de HoyosDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain.
Covadonga M Díaz-CanejaDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain.
Álvaro Andreu-BernabeuDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain.
Carol StellaDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain.
Xaquín GurriaránDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain.
Lourdes FañanásCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Julio BobesCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Ana González-PintoCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Benedicto Crespo-FacorroCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Lourdes MartorellCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Elisabet VilellaCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Gerard MuntanéCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
María Dolores MoltoCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Jose Carlos Gonzalez-PiquerasCIBERSAM, Centro Investigación Biomédica en Red Salud Mental, Madrid, Spain.
Mara ParelladaDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain.
Celso ArangoDepartment of Child and Adolescent Psychiatry, Institute of Psychiatry and Mental Health, Hospital General Universitario Gregorio Marañón, Calle Ibiza, 43, 28009, Madrid, Spain.
Javier CostasInstituto de Investigación Sanitaria (IDIS) de Santiago de Compostela, Complexo Hospitalario Universitario de Santiago de Compostela (CHUS), Servizo Galego de Saúde (SERGAS), Santiago de Compostela, Galicia, Spain.
Centro de Investigación Biomédica en Red de Salud Mental · ESHospital General Universitario Gregorio Marañón · ESHospital Universitario Virgen del Rocío · ESINCLIVA Health Research Institute · ESInstitut de Biologia Evolutiva · ESInstitut d'Investigació Sanitària Pere Virgili · ESInstituto de Investigación Sanitaria de Santiago · ESInstitut Pere Mata · ESUniversidad Complutense de Madrid · ESUniversity of the Basque Country · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia is a debilitating psychiatric disorder associated with a reduced fertility and decreased life expectancy, yet common predisposing variation substantially contributes to the onset of the disorder, which poses an evolutionary paradox. Previous research has suggested balanced selection, a mechanism by which schizophrenia risk alleles could also provide advantages under certain environments, as a reliable explanation. However, recent studies have shown strong evidence against a positive selection of predisposing loci. Furthermore, evolutionary pressures on schizophrenia risk alleles could have changed throughout human history as new environments emerged. Here in this study, we used 1000 Genomes Project data to explore the relationship between schizophrenia predisposing loci and recent natural selection (RNS) signatures after the human diaspora out of Africa around 100,000 years ago on a genome-wide scale. We found evidence for significant enrichment of RNS markers in derived alleles arisen during human evolution conferring protection to schizophrenia. Moreover, both partitioned heritability and gene set enrichment analyses of mapped genes from schizophrenia predisposing loci subject to RNS revealed a lower involvement in brain and neuronal related functions compared to those not subject to RNS. Taken together, our results suggest non-antagonistic pleiotropy as a likely mechanism behind RNS that could explain the persistence of schizophrenia common predisposing variation in human populations due to its association to other non-psychiatric phenotypes.

Indexed as

SchizophreniaAfricaAllelesBrainFertilityHumans

Identifiers

PMID37726359
PMCPMC10509162
OpenAlexW4386864815

What Socratic holds

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LicenceCC BY
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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 Socratic graph.