4.6 Article

Association of sleep and circadian patterns and genetic risk with incident type 2 diabetes: a large prospective population-based cohort study

期刊

EUROPEAN JOURNAL OF ENDOCRINOLOGY
卷 185, 期 5, 页码 765-774

出版社

BIOSCIENTIFICA LTD
DOI: 10.1530/EJE-21-0314

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资金

  1. National Natural Sciences Foundation of China [81973109]
  2. Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (2019)
  3. Construction of High-level University of Guangdong [G619339521, G618339167, G621339832]
  4. National Institutes of Health/National Institute on Aging of USA [P30-AG028716]

向作者/读者索取更多资源

This study found that unfavorable sleep and circadian patterns, high genetic risk, and incident type 2 diabetes risk are associated independently. Adhering to a healthy sleep and circadian pattern can reduce the risk of developing diabetes, which provides important implications for public health strategies.
Objective: To examine the association of incident type 2 diabetes (T2D) risk with sleep factors, genetic risk, and their combination effects. Design: Large prospective population-based cohort study. Methods: This population-based prospective cohort study included 360 403 (mean (S.D.) age: 56.6 (8.0) years) participants without T2D at baseline from the UK Biobank. Genetic risk was categorised as high (highest quintile), intermediate (quintiles: 2-4), and low (lowest quintile) based on a polygenic risk score for T2D. Sleep scores, including long or short sleep duration, insomnia, snoring, late chronotype, and excessive daytime sleepiness, were categorized as an unfavourable, intermediate, or favourable sleep and circadian pattern. Results: During a median follow-up of 9.0 years, 13 120 incident T2D cases were recorded. Among the participants with an unfavourable sleep and circadian pattern, 6.96% (95% CI: 6.68-7.24%) developed T2D vs 2.37% (95% CI: 2.28-2.46%) of participants with a favourable sleep and circadian pattern (adjusted hazard ratio (HR): 1.53, 95% CI: 1.45-1.62). Of participants with a high genetic risk, 5.53% (95% CI: 5.36-5.69%) developed T2D vs 2.01% (95% CI: 1.91-2.11%) of participants with a low genetic risk (adjusted HR: 2.89, 95% CI: 2.72-3.07). The association with sleep and circadian patterns was independent of genetic risk strata. Participants in the lowest quintile with an unfavourable sleep and circadian pattern were 3.97-fold more likely to develop T2D than those in the lowest quintile with a favourable sleep and circadian pattern. Conclusions: Sleep and circadian patterns and genetic risk were independently associated with incident T2D. These results indicate the benefits of adhering to a healthy sleep and circadian pattern in entire populations, independent of genetic risk.

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