ArticlemedRxiv : the preprint server for health sciences2025
Shared genetic architecture between anorexia nervosa and metabolomic biomarkers suggest underlying causal pathways.
Article in medRxiv : the preprint server for health sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Metabolic regulation of synaptic plasticity in anorexia nervosa.Frontiers in synaptic neuroscience · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Background: Anorexia Nervosa (AN) has a high mortality rate and often a chronic illness course, yet few existing treatments are effective. AN is heritable and shares genetic architecture with cardiometabolic traits, while the relationship to metabolomic markers is unknown. Methods: We analyzed genome-wide association studies (GWAS) of 249 circulating plasma metabolomic biomarkers and AN to map their shared genetic architecture and compare with related mental health, anthropometric and cardiometabolic traits. We leveraged multiple methods to estimate genetic overlap, including global genetic correlations with linkage disequilibrium score regression, conjunctional false discovery rate, and bivariate Gaussian mixture modeling. We mapped shared genetic variants to genes and biological pathways, as well as gene expression enrichment across body and brain tissue. We also explored causal relationships between AN, body mass index (BMI), and metabolomic biomarkers. Results: Significant genetic correlations were found between AN and 142 circulating metabolomic biomarkers, which were opposite in direction to metabolic traits such as BMI and type 2 diabetes (r Conclusions: Our findings point to strong associations between AN and metabolomic markers, opposite in direction to anthropometric and cardiometabolic traits. Our results suggest a mediating role for BMI and implicate developmental and lipid-based biological processes with a bidirectional causal relationship. The findings offer a novel perspective on the etiology of AN and suggest opportunities for targeting specific metabolomic biomarkers in weight restoration approaches.
Identifiers
What Socratic holds
Registered trials
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.