近日，美国哥伦比亚大学Junhao Wen及其研究团队揭示了中老年生物衰老时钟睡眠图。该项研究成果发表在2026年5月13日出版的《自然》上。

在这里，小组提出了睡眠图表来评估自我报告的睡眠时间与23个生物衰老时钟之间的关系，这些生物钟来自体内成像、血浆蛋白质组学和代谢组学。首先，在九个大脑和身体系统以及三种组学技术中，睡眠时间和生物年龄差距之间出现了一个系统性的U型模式。在英国生物银行（年龄范围为37-84岁）中，样本特定的最低生物年龄差距出现在6.4至7.8小时的睡眠时长之间，且因器官和性别的不同而有所变化。

此外，与正常睡眠时长（6-8小时）相比，睡眠时间过短（<6小时）和过长（>8小时）均与脑部以外全身性疾病风险和全因死亡率的增加相关，遗传相关性和事件生存时间预测（如抑郁症和糖尿病）证明了这一点。最后，长睡眠时间和短睡眠时间与晚年抑郁相关的途径不同：衰老的生物钟可能部分调节长睡眠时间的途径，而短睡眠时间则表现出更直接的联系。虽然孟德尔随机化并没有提供强有力的证据表明疾病会直接影响睡眠，但它不能完全排除这种反向因果关系。他们的研究结果表明，睡眠时间与生物衰老时钟之间存在跨器官、多组学的U型关系，强调了优化睡眠在促进健康老龄化、降低疾病风险和延长寿命方面的潜力。

据悉，最佳睡眠对于促进健康衰老和延长寿命至关重要。

附：英文原文

Title: Sleep chart of biological ageing clocks in middle and late life

Author: OToole, Cliodhna Kate, Song, Zhiyuan, Anagnostakis, Filippos, Yang, Zhijian, Tian, Ye Ella, Duggan, Michael R., Zou, Chunrui, Leng, Yue, Cai, Yi, Bai, Wenjia, Fu, Cynthia H. Y., Rafii, Michael S., Aisen, Paul, Wang, Gao, De Jager, Philip L., Zeng, Jian, Oh, Hamilton Se-Hwee, Zhou, Xia, Walker, Keenan A., Belsky, Daniel W., Zalesky, Andrew, Simonsick, Eleanor M., Resnick, Susan M., Ferrucci, Luigi, Davatzikos, Christos, Wen, Junhao

Issue&Volume: 2026-05-13

Abstract: Optimal sleep has a vital role in promoting healthy ageing and enhancing longevity. Here we propose Sleep Chart to assess the relationship between self-reported sleep duration and 23 biological ageing clocks derived from in vivo imaging1, plasma proteomics2 and metabolomics3. First, a systemic, U-shaped pattern emerges between sleep duration and biological age gaps across nine brain and body systems and three omics technologies. The sample-specific lowest biological age gaps are achieved between 6.4 and 7.8h of sleep duration, varying by organ and sex in the UK Biobank (aged 37–84years). Furthermore, short (<6h) and long (>8h) sleep duration, compared with a normal sleep duration (6–8h), are associated with increased risk of systemic diseases beyond the brain and all-cause mortality, with evidence from genetic correlations and time-to-incident survival predictions, such as depression and diabetes. Finally, the pathways by which long and short sleep duration are associated with late-life depression differ: ageing clocks may partially mediate the pathway for long sleep duration, while short sleep duration shows a more direct link. Although Mendelian randomization does not provide strong evidence that disease causally affects sleep, it cannot completely exclude such reverse causality. Our findings suggest a cross-organ, multi-omics U-shaped relationship between sleep duration and biological ageing clocks, highlighting the potential of sleep optimization to promote healthy ageing, lower disease risk and extend longevity.

DOI: 10.1038/s41586-026-10524-5

Source: https://www.nature.com/articles/s41586-026-10524-5