ArticleBiological psychiatry global open science2026
Associations of Mechanistically Partitioned Type 2 Diabetes Polygenic Risk With Psychiatric and Related Phenotypes in UK Biobank.
Article in Biological psychiatry global open science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Type 2 diabetes (T2D) and psychiatric disorders frequently co-occur; however, it remains unclear whether this overlap is generalized or defined by particular T2D mechanisms and psychiatric phenotypes. We investigated whether genetically defined T2D pathways show distinct associations with psychiatric and related phenotypes. Methods: We calculated polygenic risk scores (PRSs) for 8 mechanistic T2D clusters and tested associations with psychiatric and sleep phenotypes and chronic pain in the UK Biobank. The study included 408,063 White British participants (54.1% female) and 50,214 non-overlapping White European participants (56.2% female). Models incorporated demographic, socioeconomic, lifestyle, anthropometric, and medication factors, with false discovery rate (FDR) correction across all tests. Results: Adiposity PRS showed the broadest associations. Body-fat distribution PRS was associated with atypical major depressive disorder across all models, whereas obesity-mediated insulin-resistance PRS was associated only in the minimally adjusted model. Neither PRS was associated with nonatypical depression after FDR correction. Body-fat PRS was associated with generalized anxiety disorder, mood instability, long sleep duration, and chronic pain in all models. Associations for the other pathways were more selective and were concentrated in sleep duration and chronotype; metabolic-syndrome PRS was consistently associated with neuroticism. Cross-sample support was strongest for the association between obesity-mediated insulin-resistance PRS and morning chronotype. Conclusions: The overlap between T2D and psychiatric phenotypes was heterogeneous, with the strongest evidence for adiposity PRS and atypical depression and with more selective associations across other pathways. Considering heterogeneity in both T2D biology and psychiatric presentation may help clarify shared mechanisms.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.