ArticleSchizophrenia bulletin open2022
Evidence for Shared Genetic Aetiology Between Schizophrenia, Cardiometabolic, and Inflammation-Related Traits: Genetic Correlation and Colocalization Analyses.
Article in Schizophrenia bulletin open, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled 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.
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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.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Lipidomics and genomics in mental health: insights into major depressive disorder, bipolar disorder, schizophrenia, and obsessive-compulsive disorder.Lipids in health and disease · 2025Pooled it
- Genetic factor analysis for characterizing phenome-wide patterns of genetic pleiotropy.Nature genetics · 2026Article
- Associations between lifestyle, genetic liability for severe mental illness and risk of incident somatic illnesses.Translational psychiatry · 2026Article
- Multi-Level Latent Variable Models for Coheritability Analysis in Electronic Health Records.Statistics in medicine · 2026Article
- Psychosis as a multisystem disorder of aberrant aging.npj aging · 2026Review
- Stress-related multisystem dysregulation during adolescence predicts mental health symptoms in young adulthood.Psychological medicine · 2025Article
- Polygenic risk for psychotic disorders in relation to cardiac autonomic dysfunction in unmedicated patients with schizophrenia.European archives of psychiatry and clinical neuroscience · 2025Article
- Article
- Neuronal Synaptic Communication and Mitochondrial Energetics in Human Health and Disease.Advances in experimental medicine and biology · 2025Review
- Electroretinographic dysfunction, insulin resistance, and childhood trauma in early-course psychosis: A case-control exploratory study.Biomarkers in neuropsychiatry · 2024Article
- A network of transcriptomic signatures identifies novel comorbidity mechanisms between schizophrenia and somatic disorders.Discover mental health · 2024Article
- Genomic insights into the comorbidity between type 2 diabetes and schizophrenia.Schizophrenia (Heidelberg, Germany) · 2024Article
- Genomic insights into the comorbidity between type 2 diabetes and schizophrenia.medRxiv : the preprint server for health sciences · 2023Article
- Analysis of common genetic variation across targets of microRNAs dysregulated both in ASD and epilepsy reveals negative correlation.Frontiers in genetics · 2023Article
- Evidence that the pituitary gland connects type 2 diabetes mellitus and schizophrenia based on large-scale trans-ethnic genetic analyses.Journal of translational medicine · 2022Article
- The emerging role of furin in neurodegenerative and neuropsychiatric diseases.Translational neurodegeneration · 2022Review
- Crosstalk between Schizophrenia and Metabolic Syndrome: The Role of Oxytocinergic Dysfunction.International journal of molecular sciences · 2022Review
- Schizophrenia in Translation: Why the Eye?Schizophrenia bulletin · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSchizophrenia commonly co-occurs with cardiometabolic and inflammation-related traits. It is unclear to what extent the comorbidity could be explained by shared genetic aetiology.
methodsWe used GWAS data to estimate shared genetic aetiology between schizophrenia, cardiometabolic, and inflammation-related traits: fasting insulin (FI), fasting glucose, glycated haemoglobin, glucose tolerance, type 2 diabetes (T2D), lipids, body mass index (BMI), coronary artery disease (CAD), and C-reactive protein (CRP). We examined genome-wide correlation using linkage disequilibrium score regression (LDSC); stratified by minor-allele frequency using genetic covariance analyzer (GNOVA); then refined to locus-level using heritability estimation from summary statistics (ρ-HESS). Regions with local correlation were used in hypothesis prioritization multi-trait colocalization to examine for colocalisation, implying common genetic aetiology.
resultsWe found evidence for weak genome-wide negative correlation of schizophrenia with T2D (r
conclusionsLDSC may lead to downwardly-biased genetic correlation estimates between schizophrenia, cardiometabolic, and inflammation-related traits. Common genetic aetiology for these traits could be confined to lower-frequency common variants and involve opposing mechanisms. Genes related to BDNF and glucose transport amongst others may partly explain the comorbidity between schizophrenia and cardiometabolic disorders.
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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.