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Objective: To explore the relationship between sleep habits (sleep duration, sleep efficiency, sleep onset timing) and ischemic stroke, and whether there is an interaction between sleep habits and ischemic stroke susceptibility gene loci., Methods: A questionnaire survey, physical examination, blood biochemical testing and genotyping were conducted among rural residents in Beijing, and the gene loci of ischemic stroke suggested by previous genome-wide association studies (GWAS) were screened. Multivariable generalized linear model was used to analyze the correlation between sleep habits, sleep-gene interaction and ischemic stroke., Results: A total of 4 648 subjects with an average age of (58.5±8.7) years were enrolled, including 1 316 patients with ischemic stroke. Compared with non-stroke patients, stroke patients with sleep duration ≥9 hours, sleep efficiency < 80%, and sleep onset timing earlier than 22:00 accounted for a higher proportion ( P < 0.05). There was no significant association between sleep duration and risk of ischemic stroke ( OR =1.04, 95% CI : 0.99-1.10, P =0.085). Sleep efficiency was inversely associated with the risk of ischemic stroke ( OR =0.18, 95% CI : 0.06-0.53, P =0.002). The risk of ischemic stroke in the subjects with sleep efficiency < 80% was 1.47-fold (95% CI : 1.03-2.10, P =0.033) of that in the subjects with sleep efficiency ≥80%. Falling asleep earlier than 22:00 was associated with 1.26 times greater risk of stroke than falling asleep between 22:00 and 22:59 (95% CI : 1.04-1.52, P =0.017). Multifactorial adjustment model showed that rs579459 on ABO gene had an interaction with sleep time ( P for interaction =0.040). When there were two T alleles for rs579459 on the ABO gene, those who fell asleep before 22:00 had 1.56 times (95% CI : 1.20-2.04, P =0.001) the risk of stroke compared with those who fell asleep between 22:00 and 22:59, and there was no significant difference when the number of pathogenic alleles was 0 or 1. In the model adjusted only for gender, age and family structure, sleep duration and the number of T allele rs2634074 on PITX2 gene had an interaction with ischemic stroke ( P for interaction=0.033)., Conclusion: Decreased sleep efficiency is associated with increased risk of ischemic stroke, and falling asleep earlier than 22:00 is associated with higher risk of ischemic stroke. Sleep onset timing interacted with rs579459 in ABO gene and the risk of ischemic stroke. Sleep duration and PITX2 rs2634074 may have a potential interaction with ischemic stroke risk.

Objective: To understand the association between peripheral leukocytes telomere length (TL) and sleep in middle-aged and old adults. Methods: A total of 176 middle-aged and old adults were investigated by using the Pittsburgh Sleep Quality Index and questionnaire. TL was measured by fluorescence quantitative PCR. The correlation and regression analysis between sleep and telomere length was performed. Results: TL had a mean T/S ratio of 0.995±0.23. There was a negative correlation between TL and age ( r =-0.241, P =0.003). With increasing age, sleep quality became worse ( r =-0.230, P <0.01), the time to fall asleep became longer ( r =0.227, P <0.01), sleep duration was shorter ( r =-0.486, P <0.01), sleep efficiency became worse ( r =-0.226, P <0.01). After controlling for the effects of gender, age, marital status, income level, residence, smoking, drinking, physical exercise and disease status, multiple linear regression analysis indicated that sleep quality ( β =0.057, P <0.01), time to fall asleep ( β =-0.046, P <0.01), sleep duration ( β =0.086, P <0.01) were independent influencing factors of telomere length, suggesting that the people who had better sleep quality, the shorter time to fall asleep, the longer sleep time would have longer telomere length. Conclusions: Sleep is a relevant factor affecting TL in middle-aged and elderly population. Good sleep may delay aging by slowing TL. We encourage to conduct health education about the importance of sleep quality in community.