ReviewMammalian genome : official journal of the International Mammalian Genome Society2025
Utilising genomic association data for causal inference in anorexia nervosa.
Review in Mammalian genome : official journal of the International Mammalian Genome Society, 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
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.
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.
Who cites it
1 citing paper in PubMed.
- Integrated multi-omics and functional analyses reveal a GDCA-TGR5-mediated immunometabolic signature in anorexia nervosa.European archives of psychiatry and clinical neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anorexia nervosa (AN) is a prevalent psychiatric disorder with high rates of mortality and limited treatment options. AN is a complex disorder, for which common variation contributes to disorder risk. To dissect the genetic architecture of AN, a variety of statistical methods can be applied. Many of these utilise genome-wide association study (GWAS) datasets to investigate biological mechanisms within disease progression in addition to broader associations between complex traits. GWAS for AN have revealed important biological insights, however, these have not translated into new pharmacotherapies. Here, we review the application of statistical methods that use GWAS, to investigate the relationship between genetic variation, biochemical compounds and complex traits to identify potential relationships which could advance our understanding of disease biology. We discuss genetic variant association data for AN, the application of gene-based and complex trait level correlation methods and approaches for establishing evidence of causality between complex traits and AN. These methods all contribute to the growing literature regarding the genetic influences of AN risk and demonstrate that statistical analysis utilising genetic data is a valuable tool to progress our understanding of this disease.
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Registered trials
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