背景:健康的睡眠对于维持最佳的身心健康至关重要。越来越多的证据表明,睡眠损失和干扰在生物衰老过程中起着重要作用。疾病的早期发作,减少寿命。虽然许多研究探索了生物衰老与其驱动因素之间的关联,只有少数研究检查了它与睡眠质量的关系。在这项研究中,我们使用692名韩国成年人的全血样本调查了睡眠质量与表观遗传年龄加速之间的关系.使用经过验证的匹兹堡睡眠质量指数(PSQI)评估每位参与者的睡眠质量,其中包括七个领域:主观睡眠质量,睡眠潜伏期,睡眠持续时间,习惯性睡眠效率,睡眠障碍,使用睡眠药物,和白天功能障碍。四个表观遗传年龄加速(HorvathAgeAccel,HannumAgeAccel,PhenoAgeAccel,和GrimAgeAccel)和衰老的步伐,DunedinPACE,进行了表观遗传衰老估计调查。
结果:在692名参与者中(睡眠良好[n=441,63.7%];睡眠不良[n=251,36.3%]),睡眠不良者DunedinPACE与PSQI评分呈正相关(γ=0.18,p<0.01)。GrimAgeAccel(β=0.18,p=0.02)和DunedinPACE(β=0.01,p<0.01)仅在睡眠不良的患者中显示出与PSQI得分的统计学显着关联。此外,PSQI每增加1分,睡眠不良者的代谢综合征(MetS)风险增加15%(OR=1.15,95%CI=1.03~1.29,p=0.011).在MetS组件中,PSQI评分与空腹血糖呈正相关(γ=0.19,p<0.01)。
结论:这项研究表明,睡眠质量恶化,尤其是在睡眠不佳的人中,与具有代谢综合征风险的GrimAgeAccel和DundinePACE的加速表观遗传衰老相关。这一发现可能成为未来预防与年龄有关的疾病的有希望的策略。
BACKGROUND: Healthy sleep is vital for maintaining optimal mental and physical health. Accumulating evidence suggests that sleep loss and disturbances play a significant role in the biological aging process, early onset of disease, and reduced lifespan. While numerous studies have explored the association between biological aging and its drivers, only a few studies have examined its relationship with sleep quality. In this study, we investigated the associations between sleep quality and epigenetic age acceleration using whole blood samples from a cohort of 692 Korean adults. Sleep quality of each participant was assessed using the validated Pittsburgh Sleep Quality Index (
PSQI), which encompassed seven domains: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbance, use of sleep medication, and daytime dysfunction. Four epigenetic age accelerations (HorvathAgeAccel, HannumAgeAccel, PhenoAgeAccel, and GrimAgeAccel) and the pace of aging, DunedinPACE, were investigated for epigenetic aging estimates.
RESULTS: Among the 692 participants (good sleepers [n = 441, 63.7%]; poor sleepers [n = 251, 36.3%]), DunedinPACE was positively correlated with
PSQI scores in poor sleepers ( γ =0.18, p < 0.01). GrimAgeAccel ( β =0.18, p = 0.02) and DunedinPACE ( β =0.01, p < 0.01) showed a statistically significant association with
PSQI scores only in poor sleepers by multiple linear regression. In addition, every one-point increase in
PSQI was associated with a 15% increase in the risk of metabolic syndrome (MetS) among poor sleepers (OR = 1.15, 95% CI = 1.03-1.29, p = 0.011). In MetS components, a positive correlation was observed between
PSQI score and fasting glucose ( γ = 0.19, p < 0.01).
CONCLUSIONS: This study suggests that worsening sleep quality, especially in poor sleepers, is associated with accelerated epigenetic aging for GrimAgeAccel and DundinePACE with risk of metabolic syndrome. This finding could potentially serve as a promising strategy for preventing age-related diseases in the future.