Evidence map›Paper›PMID 41523971›Full record

ArticleAlpha psychiatry2025

Exploring Causal Associations Between Plasma Metabolites and Autism Spectrum Disorder.

Shangyun Shi, Ancha Baranova, Hongbao Cao, Fuquan Zhang

Abstract read
In one paragraph

Article in Alpha psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Shangyun ShiDepartment of Psychiatry, The Affiliated Brain Hospital of Nanjing Medical University, 210029 Nanjing, Jiangsu, China.ORCID https://orcid.org/0009-0006-7510-7250
Ancha BaranovaSchool of Systems Biology, George Mason University, Fairfax, VA 22030, USA.ORCID https://orcid.org/0000-0001-6810-5982
Hongbao CaoSchool of Systems Biology, George Mason University, Fairfax, VA 22030, USA.ORCID https://orcid.org/0000-0001-6591-9518
Fuquan ZhangDepartment of Psychiatry, The Affiliated Brain Hospital of Nanjing Medical University, 210029 Nanjing, Jiangsu, China.ORCID https://orcid.org/0000-0003-3204-8191

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: In autism spectrum disorder (ASD), the human plasma metabolome is altered but the causal relationship between the levels of metabolites and ASD is unclear. We aimed to assess bidirectional causal associations between plasma metabolites and ASD. Methods: We investigated potential causal associations between the genetic variation contributing to the levels of metabolites and ASD via Mendelian randomization (MR) analyses. Genome-wide association study (GWAS) summary datasets were used in the study, including ASD (n = 46,350) and 871 plasma metabolite (n = 8299) datasets. We used druggability analysis to prioritize metabolites with therapeutic potential. Results: Our MR analysis identified 32 plasma metabolites whose levels were protective against the risk of ASD, including 5 alpha-androstan-3 alpha, 17 beta-diol disulfate (odds ratio (OR): 0.94, 95% CI: 0.90-0.97) and 11beta-hydroxyetiocholanolone glucuronide (OR: 0.95, 95% CI: 0.92-0.98). Additionally, 12 metabolites were found to be positively associated with the risk of ASD, including indoleacetylglutamine (OR: 1.04, 95% CI: 1.01-1.08) and sphingomyelin (d18:1/24:1, d18:2/24:0) (OR: 1.06, 95% CI: 1.01-1.11). Some metabolites may be regulated through drug intervention, including sphingomyelin, chiro-inositol, carotene diol (1)/(2), and glycerol. Genetic variation contributing to ASD may increase the abundance of five metabolites, including deoxycholic acid glucuronide (OR: 1.18, 95% CI: 1.03-1.34); meanwhile, the abundance of 27 metabolites, including stearoyl choline (OR: 0.80, 95% CI: 0.69-0.92) may be causally reduced. Conclusions: Our MR analysis uncovered bidirectional causal associations between certain plasma metabolites and ASD, suggesting that these metabolites could be biomarkers for ASD and paving the way for novel therapeutic targets in ASD phenotypes.

Indexed as

autism spectrum disordercausal associationMendelian randomizationplasma metabolite

Identifiers

PMID41523971
PMCPMC12781214

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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.