TY - JOUR
T1 - Association of sleep and circadian patterns and genetic risk with incident type 2 diabetes
T2 - a large prospective population-based cohort study
AU - Li, Zhi Hao
AU - Zhang, Pei Dong
AU - Chen, Qing
AU - Gao, Xiang
AU - Chung, Vincent C.H.
AU - Shen, Dong
AU - Zhang, Xi Ru
AU - Zhong, Wen Fang
AU - Huang, Qing Mei
AU - Liu, Dan
AU - Chen, Pei Liang
AU - Song, Wei Qi
AU - Wu, Xian Bo
AU - Byers Kraus, Virginia
AU - Mao, Chen
PY - 2021/10/19
Y1 - 2021/10/19
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85119458136&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85119458136&partnerID=8YFLogxK
U2 - 10.1530/EJE-21-0314
DO - 10.1530/EJE-21-0314
M3 - Article
C2 - 34524977
AN - SCOPUS:85119458136
SN - 0804-4643
VL - 185
SP - 765
EP - 774
JO - European Journal of Endocrinology
JF - European Journal of Endocrinology
IS - 5
ER -