ArticleJournal of epidemiology and global health2025
Associations Between Chronotype, Genetic Susceptibility and Risk of Colorectal Cancer in UK Biobank.
Article in Journal of epidemiology and global health, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
Abstract
backgroundSleep problems are common in the general population, with evidence suggesting a link between circadian rhythm disruptions and various health outcomes. However, the role of chronotype in influencing colorectal cancer (CRC) risk, particularly in conjunction with genetic predisposition, remains unclear and warrants further investigation.
methodsWe analyzed data from 295,729 UK Biobank participants, among whom 4305 developed colorectal cancer. Chronotype was self-reported as morning or evening type, and a polygenic risk score for chronotype was generated from 316 genome-wide significant SNPs using 23andMe effect sizes to reduce overlap bias. Colorectal cancer risk was estimated using Cox proportional hazards models adjusted for age, sex, smoking, alcohol consumption, and the Townsend index.
resultsLate chronotype and high polygenic risk were independently associated with an increased risk of CRC. Compared to participants with an early chronotype, those with a late chronotype exhibited a 6.5% increased risk of CRC [HR 1.065, P = 0.046]. Similarly, individuals in the high genetic risk group had a 11.0% increased risk compared with those in the low genetic risk group [HR, 1.110, P = 0.032]. Stratified analyses revealed that individuals with an intermediate genetic risk who had a late chronotype showed a 17.6% higher risk of CRC [OR, 1.176, P = 0.004], whereas those with a high genetic risk had a 25.3% increase [OR, 1.253, P = 0.001]. Through analyzing the combined effects of chronotype and PRS, we found that among individuals with an early chronotype, those with intermediate PRS had a 15.4% increased risk of CRC [HR, 1.154, P = 0.005], and those with high PRS had a 14.7% increased risk [HR, 1.147, P = 0.027].
conclusionsOur findings highlight the importance of considering circadian rhythm patterns and genetic predispositions when assessing CRC risk, suggesting that chronotype may be associated with CRC risk, but further studies are needed to integrate objective circadian measurements.
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