睡眠不足と過剰睡眠が老化を加速(Too Little Sleep and Too Much Associated With Faster Aging)

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2026-05-13 コロンビア大学

コロンビア大学アーヴィング医療センターの研究チームは、睡眠時間が短すぎる場合だけでなく、長すぎる場合も生物学的老化の加速と関連することを明らかにした。研究では、多数の参加者データを用いて睡眠時間と生物学的年齢指標との関係を解析した結果、適切な睡眠時間から外れるほど老化関連指標が悪化する傾向が確認された。特に極端な短時間睡眠や長時間睡眠では、炎症反応や代謝異常、身体機能低下と関連する可能性が示唆された。研究者らは、睡眠が細胞修復や免疫調節、脳機能維持に重要な役割を果たすため、不適切な睡眠習慣が加齢関連疾患リスクを高める可能性があると指摘している。また、睡眠時間だけでなく睡眠の質や生活習慣全体を考慮した健康管理の重要性も強調された。本研究は、健康寿命延伸や予防医療戦略における睡眠管理の重要性を裏付ける成果とされる。

睡眠不足と過剰睡眠が老化を加速(Too Little Sleep and Too Much Associated With Faster Aging)
For many organs, sleep duration betwen 6.4 and 7.8 hours was associated with less aging as measured by organ-specific biological clocks. The clocks in this image are created from protein data specific to each organ. Blue lines represent males; red lines represent females. Image from The MULTI Consortium et al. Nature (2026)

<関連情報>

中年期および老年期における生物学的老化時計の睡眠チャート Sleep chart of biological ageing clocks in middle and late life

The MULTI Consortium,Cliodhna Kate O’Toole,Zhiyuan Song,Filippos Anagnostakis,Zhijian Yang,Ye Ella Tian,Michael R. Duggan,Chunrui Zou,Yue Leng,Yi Cai,Wenjia Bai,Cynthia H. Y. Fu,Michael S. Rafii,Paul Aisen,Gao Wang,Philip L. De Jager,Jian Zeng,Hamilton Se-Hwee Oh,Xia Zhou,Keenan A. Walker,Daniel W. Belsky,Andrew Zalesky,Eleanor M. Simonsick,Susan M. Resnick,… Junhao Wen
Nature  Published:13 May 2026
DOI:https://doi.org/10.1038/s41586-026-10524-5

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 7.8 h of sleep duration, varying by organ and sex in the UK Biobank (aged 37–84 years). Furthermore, short (<6 h) and long (>8 h) sleep duration, compared with a normal sleep duration (6–8 h), 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.

医療・健康
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