Evidence map›Paper›PMID 38848516›Full record

ArticleSchizophrenia bulletin2024

Shared Genetic Architecture Between Schizophrenia and Anorexia Nervosa: A Cross-trait Genome-Wide Analysis.

Zheng-An Lu, Alexander Ploner, Andreas Birgegård, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Cynthia M Bulik, Sarah E Bergen

Abstract read
In one paragraph

Article in Schizophrenia bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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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

6 authors.

Zheng-An LuDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Alexander PlonerDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-5042-8326
Andreas BirgegårdDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Eating Disorders Working Group of the Psychiatric Genomics Consortium
Cynthia M BulikDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Sarah E BergenDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-5888-0034

Funding

Eating Disorders Genetics Initiative (EDGI)R01MH120170 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BULIK, CYNTHIA M · 2019 to 2023
$7.2M
1/7 PGC: Advancing Discovery and ImpactR01MH124871 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BULIK, CYNTHIA M, SULLIVAN, PATRICK F · 2021 to 2025
$3.5M
Predicting Binge and Purge Episodes from Passive and Active Apple Watch Data Using a Dynamical Systems ApproachR01MH119084 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BULIK, CYNTHIA M, BUTNER, JONATHAN · 2019 to 2022
$2.8M
Genetic Architecture of Avoidant/Restrictive Food Intake DisorderR56MH129437 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BULIK, CYNTHIA M, MICALI, NADIA · 2022 to 2023
$1.5M
Chinese Scholarship Council CSC202206010089Lundbeck Foundation R276-2018-4581NIMH NIH HHS R01 MH119084NIMH NIH HHS R01 MH120170NIMH NIH HHS R01 MH124871NIMH NIH HHS R56 MH129437NIMH NIH HHS R56MH129437Swedish Research CouncilVetenskapsrådet
6 · The paper itself

Abstract

background and hypothesisSchizophrenia (SCZ) and anorexia nervosa (AN) are 2 severe and highly heterogeneous disorders showing substantial familial co-aggregation. Genetic factors play a significant role in both disorders, but the shared genetic etiology between them is yet to be investigated. STUDY

designUsing summary statistics from recent large genome-wide association studies on SCZ (Ncases = 53 386) and AN (Ncases = 16 992), a 2-sample Mendelian randomization analysis was conducted to explore the causal relationship between SCZ and AN. MiXeR was employed to quantify their polygenic overlap. A conditional/conjunctional false discovery rate (condFDR/conjFDR) framework was adopted to identify loci jointly associated with both disorders. Functional annotation and enrichment analyses were performed on the shared loci. STUDY

resultsWe observed a cross-trait genetic enrichment, a suggestive bidirectional causal relationship, and a considerable polygenic overlap (Dice coefficient = 62.2%) between SCZ and AN. The proportion of variants with concordant effect directions among all shared variants was 69.9%. Leveraging overlapping genetic associations, we identified 6 novel loci for AN and 33 novel loci for SCZ at condFDR <0.01. At conjFDR <0.05, we identified 10 loci jointly associated with both disorders, implicating multiple genes highly expressed in the cerebellum and pituitary and involved in synapse organization. Particularly, high expression of the shared genes was observed in the hippocampus in adolescence and orbitofrontal cortex during infancy.

conclusionsThis study provides novel insights into the relationship between SCZ and AN by revealing a shared genetic component and offers a window into their complex etiology.

Indexed as

Anorexia NervosaGenome-Wide Association StudyMendelian Randomization AnalysisMultifactorial InheritanceSchizophreniaHumansanorexiaarchitecturegeneticGWASMendelian randomizationnervosapleiotropypolygenic overlapschizophrenia

Identifiers

PMID38848516
PMCPMC11349005

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.