Summary: A comprehensive analysis of biological clocks across the human body reveals that both insufficient and excessive sleep are associated with accelerated aging in nearly every organ system.
The study demonstrates a coordinated “U-shaped” relationship between sleep duration and biological age. The findings suggest that sleep is not just a brain-centered activity but a critical factor in maintaining a coordinated brain-body network, influencing metabolic balance and immune health across 17 organ systems.
Key Research Findings
- The U-Shaped Pattern: Both short sleep (fewer than 6 hours) and long sleep (greater than 8 hours) correlate with faster biological aging. The “sweet spot” for minimal aging was found to be between 6.4 and 7.8 hours of sleep per day.
- Organ-Specific Aging Clocks: Using machine learning and data from the UK Biobank, researchers built 23 specialized clocks for 17 organs using medical imaging, proteins, and molecular data. This revealed that organs age at different rates and are uniquely sensitive to sleep patterns.
- Brain-Body Network: Short sleep was significantly linked to mental health disorders (depression, anxiety) as well as systemic physical conditions including obesity, type 2 diabetes, hypertension, and heart arrhythmias.
- Respiratory and Digestive Impact: Both short and long sleep durations were associated with chronic obstructive pulmonary disease (COPD), asthma, and digestive issues like gastritis and GERD.
- Late-Life Depression Pathways: Mediation analysis suggests that short sleep may act directly on the disease burden of late-life depression, whereas long sleep may influence depression through pathways involving the brain and adipose (fat) tissue clocks.
Source: Columbia University
An analysis of biological clocks throughout the human body suggests that too few hours of sleep—and too many—may speed aging in the brain, heart, lung, and immune system and is associated with a wide range of diseases.
“Previous studies have found that sleep is largely linked to aging and the pathological burden of the brain. Our study goes further and shows that too little and too much sleep are associated with faster aging in nearly every organ, supporting the idea that sleep is important in maintaining organ health within a coordinated brain-body network, including metabolic balance and a healthy immune system,” says study leader Junhao Wen, assistant professor of radiology at Columbia University Vagelos College of Physicians and Surgeons.
The research was published May 13 in Nature.
The power of aging clocks
Aging clocks are increasingly popular for digitizing how many years a person ages faster or slower than their chronological age using machine learning, based on the biological data (e.g., proteins from a minimally invasive blood test) from the person.
Though most aging clocks measure aging across the whole body, organs age at different rates—a fact well-known to women facing ticking biological clocks due to fast-aging ovaries.
Wen’s group has been at the forefront of constructing aging clocks for specific organs in the body that could provide more specific and personalized information to patients.
“Everyone is excited by these aging clocks and their ability to predict disease and mortality risk,” Wen says. “But to me, the more exciting question is, can we link aging clocks to a lifestyle factor that can be modified in time to slow aging?”
The U-shaped pattern between aging clocks and sleep
Sleep was the perfect test case, as sleep is increasingly thought to be an important factor in health. “I’m also a light sleeper and was getting worried about the effects on myself,” says Wen.
To build his aging clocks, Wen used data collected from half a million participants in the UK Biobank and used machine learning to determine signatures for an aging organ. Wen used a wide variety of data sources to create aging clocks based on structural data from medical images, organ-specific proteins, and molecules found in blood in each organ.
“In the liver, for example, we have an aging clock built with protein data, an aging clock of metabolic data, and an aging clock of imaging data,” Wen says. “This allows us to see whether sleep is distinctively associated with aging clocks derived from multiple omics and molecular layers.”
He then assessed the relationship between a person’s sleep duration (as reported by each Biobank participant) and their biological ages from 23 aging clocks across 17 organ systems.
Across the entire body, a coordinated U-shaped pattern emerged: In the UK Biobank population, both short sleep (fewer than 6 hours) and long sleep (greater than 8 hours) were associated with faster aging, while the least amount of aging occurred in people who reported between 6.4 and 7.8 hours of sleep per day.
This does not mean that sleep duration alone causes organs to age faster or slower, but it suggests that both insufficient and excessive sleep may be markers of poorer overall health across the body.
Sleep’s body-wide connection to disease
The relationship between sleep and disease suggests that there exists a connection between the brain and the body that extends beyond merely influencing the brain itself.
Among brain-related disorders, short sleep was significantly associated with depressive episodes and anxiety disorders, as seen in other studies of sleep and mental health. Short sleep was also associated with obesity, type 2 diabetes, hypertension, ischemic heart disease, and heart arrhythmias.
Short and long sleep were associated with chronic obstructive pulmonary disease, asthma, and a cluster of digestive disorders, including gastritis and gastroesophageal reflux disease.
Wen says, “The broad brain-body pattern is important because it tells us that sleep duration is a deeply embedded part of our entire physiology, with far-reaching implications across the body.”
A deeper look at late-life depression and sleep
Beyond predicting disease, the organ-specific aging clocks are also valuable for determining how sleep is related to specific conditions, as exemplified by Wen’s examination of late-life depression.
Although the study could not definitively determine if sleep duration caused late-life depression or if late-life depression impacted sleep duration, Wen’s group applied “mediation analysis” to late-life depression, asking whether aging clocks mediate the relationship between both short and long sleep and late-life depression.
The analyses suggest that short sleep may act directly on the disease burden of late-life depression, while long sleep may impact late-life depression via a mediation pathway underlying the brain and adipose clocks.
“This has a strong implication for future sleep management and future therapeutics,” Wen says. “Our study suggests there may be different biological pathways between long and short sleepers that lead to the same outcome, late-life depression, and we shouldn’t treat them the same way.”
Key Questions Answered:
A: While this study focuses on reported daily duration, the findings emphasize that sleep is a “deeply embedded” part of our physiology. Consistency within the 6.4 to 7.8-hour window is likely more effective for maintaining organ health than sporadic long-duration sleep, which itself is linked to faster aging.
A: The study suggests excessive sleep may be a marker of poorer overall health rather than a direct cause of aging. Long sleep was specifically linked to different biological pathways, such as the adipose (fat) clock, which can influence systemic inflammation and disease.
A: They use aging clocks powered by machine learning. By analyzing specific proteins from a blood test or structural data from medical images, these models digitize how much faster or slower your internal organs are wearing down compared to the years you’ve been alive.
Editorial Notes:
- This article was edited by a Neuroscience News editor.
- Journal paper reviewed in full.
- Additional context added by our staff.
About this sleep and aging research news
Author: Helen Garey
Source: Columbia University
Contact: Helen Garey – Columbia University
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Sleep chart of biological aging clocks in middle and late life” by 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, Luigi Ferrucci, Christos Davatzikos & Junhao Wen. Nature
DOI:10.1038/s41586-026-10524-5
Abstract
Sleep chart of biological aging clocks in middle and late life
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 imaging, plasma proteomics and metabolomics.
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.
