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睡眠延迟和生物年龄:晚睡与端粒长度较短有关。

Delayed sleep-onset and biological age: late sleep-onset is associated with shorter telomere length.

机构信息

PsyQ Expertise Center Adult ADHD, The Hague, The Netherlands.

Department of Psychiatry, Amsterdam Public Health Research Institute, VU University Medical Center, Amsterdam, The Netherlands.

出版信息

Sleep. 2019 Oct 9;42(10). doi: 10.1093/sleep/zsz139.

DOI:10.1093/sleep/zsz139
PMID:31270544
Abstract

STUDY OBJECTIVES

We evaluated the relationship between leukocyte telomere length (LTL) and sleep duration, insomnia symptoms, and circadian rhythm, to test whether sleep and chronobiological dysregulations are associated with cellular aging.

METHODS

Data from the Netherlands Study of Depression and Anxiety (N = 2,936) were used at two waves 6 years apart, to measure LTL. Telomeres shorten during the life span and are important biomarkers for cellular aging. LTL was assessed by qualitative polymerase chain reaction and converted into base pair number. Sleep parameters were: sleep duration and insomnia symptoms from the Insomnia Rating Scale. Circadian rhythm variables were: indication of Delayed Sleep Phase Syndrome (DSPS), mid-sleep corrected for sleep debt on free days (MSFsc), sleep-onset time, and self-reported chronotype, from the Munich Chronotype Questionnaire. Generalized estimating equations analyzed the associations between LTL, sleep, and chronobiological factors, adjusted for baseline age, sex, North European ancestry, and additionally for current smoking, depression severity, obesity, and childhood trauma.

RESULTS

Indicators of delayed circadian rhythm showed a strong and consistent effect on LTL, after adjustment for sociodemographic and health indicators. Late MSFsc (B = -49.9, p = .004), late sleep-onset time (B = -32.4, p = .001), indication of DSPS (B = -73.8, p = .036), and moderately late chronotype in adulthood (B = -71.6, p = .003) were associated with significantly shorter LTL across both waves; whereas sleep duration and insomnia symptoms were not. Extremely early chronotype showed significantly less LTL shortening than intermediate chronotype (B = 161.40, p = .037). No predictors showed accelerated LTL attrition over 6 years.

CONCLUSIONS

Individuals with delayed circadian rhythm have significantly shorter LTL, but not faster LTL attrition rates.

摘要

研究目的

我们评估了白细胞端粒长度(LTL)与睡眠时长、失眠症状和昼夜节律之间的关系,以检验睡眠和生物节律紊乱是否与细胞衰老有关。

方法

使用荷兰抑郁和焦虑研究(N=2936)的数据,该研究在 6 年的两个时间点进行测量,通过定性聚合酶链反应测量 LTL。端粒在生命过程中会缩短,是细胞衰老的重要生物标志物。LTL 通过定量聚合酶链反应进行测量,并转换为碱基对数量。睡眠参数包括:来自失眠评定量表的睡眠时长和失眠症状。昼夜节律变量包括:延迟睡眠相位综合征(DSPS)的迹象、睡眠债务修正后的自由日中间睡眠时间(MSFsc)、入睡时间和来自慕尼黑昼夜类型问卷的自我报告的昼夜类型。广义估计方程分析了 LTL、睡眠和昼夜生物学因素之间的关联,调整了基线年龄、性别、北欧血统以及当前吸烟、抑郁严重程度、肥胖和儿童创伤等因素。

结果

调整社会人口学和健康指标后,延迟昼夜节律的指标对 LTL 有很强的一致影响。晚 MSFsc(B=-49.9,p=0.004)、晚入睡时间(B=-32.4,p=0.001)、DSPS 迹象(B=-73.8,p=0.036)和成人中期的昼夜类型(B=-71.6,p=0.003)与两个时间点的 LTL 显著缩短相关;而睡眠时长和失眠症状则没有。非常早的昼夜类型与中间昼夜类型相比,LTL 缩短的程度明显较小(B=161.40,p=0.037)。没有预测指标显示在 6 年内 LTL 损耗加速。

结论

昼夜节律延迟的个体的 LTL 明显缩短,但 LTL 损耗率没有加快。

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