Zhi-Hao Li1, Pei-Dong Zhang1,2, Qing Chen1, Xiang Gao3, Vincent C H Chung4, Dong Shen1, Xi-Ru Zhang1, Wen-Fang Zhong1, Qing-Mei Huang1, Dan Liu1, Pei-Liang Chen1, Wei-Qi Song1, Xian-Bo Wu1, Virginia Byers Kraus5, Chen Mao1. 1. Department of Epidemiology, School of Public Health, Southern Medical University, Guangzhou, Guangdong, China. 2. The Laboratory for Precision Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. 3. Department of Nutritional Sciences, Pennsylvania State University, University Park, Pennsylvania, USA. 4. Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong, China. 5. Duke Molecular Physiology Institute and Division of Rheumatology, Department of Medicine, Duke University School of Medicine, Durham, North Carolina, USA.
Abstract
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.
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.