A large study of about half a million UK Biobank participants has linked both short and long sleep with faster biological ageing across several organs.
Researchers found the lowest signs of biological ageing among people who reported sleeping roughly six to eight hours a day.
The study used 23 ageing clocks across 17 organ systems, including the brain, heart, lungs and immune system.
The findings do not prove that sleep duration directly causes faster or slower ageing, but suggest sleep is closely tied to health across the body.
Too little sleep, and possibly too much, may be linked to faster ageing in the brain, heart, lungs, immune system and other parts of the body, according to a new study.
The research, published in the journal Nature on May 13, 2026, analysed data from about half a million adults in the UK Biobank. UK Biobank is the world’s most extensive repository of biological, health, and lifestyle data.
The researchers found that people who reported sleeping between about 6.4 and 7.8 hours a day had the lowest biological age gaps across a range of “ageing clocks”, according to a press statement by Columbia University. Those who slept fewer than six hours, or more than eight hours, tended to show signs of faster biological ageing, explained an article on the research in the journal.
The study does not prove that short or long sleep directly causes organs to age faster. Sleep duration was self-reported, and long sleep in particular may be a sign of existing illness, poor sleep quality, depression, pain or other health problems. But the findings add to evidence that sleep is closely tied to health throughout the body, not just the brain.
“Previous studies have found that sleep is largely linked to aging and the pathological burden of the brain,” said Junhao Wen, assistant professor of radiology at Columbia University Vagelos College of Physicians and Surgeons, who led the study. “Our study goes further and shows that too little and too much sleep are associated with faster aging in nearly every organ.”
Ageing clocks are tools that use biological data to estimate whether a person, or a part of the body, appears older or younger than their actual age. They can be built from blood proteins, metabolites, scans and other measurements.
Many ageing clocks look at the body as a whole. Wen’s team looked more closely at organs and systems. Using machine learning and data from the UK Biobank, the researchers studied 23 ageing clocks across 17 organ systems. These included clocks based on medical images, organ-specific proteins and molecules found in blood.
The idea was to ask whether sleep duration was linked to ageing in different parts of the body in similar or different ways.
Across the study population, a U-shaped pattern emerged. People at both ends of the sleep range, short sleepers and long sleepers, tended to have higher biological age gaps. The lowest gaps were seen among those sleeping roughly six to eight hours a day, though the exact range varied by organ and sex.
The researchers also found that abnormal sleep duration was associated with several diseases.
Short sleep was linked with depressive episodes and anxiety disorders. It was also associated with obesity, type 2 diabetes, hypertension, ischaemic heart disease and heart rhythm problems. Both short and long sleep were associated with chronic obstructive pulmonary disease, asthma and some digestive disorders, including gastritis and gastro-oesophageal reflux disease, according to the Columbia release.
The study also found associations between short and long sleep duration and higher risks of systemic disease and all-cause mortality when compared with normal sleep duration of six to eight hours.
Wen said the wider pattern matters because it suggests sleep is “a deeply embedded part of our entire physiology”, with effects or signals that reach across the body.
The team also examined late-life depression to see whether different biological pathways might be involved in short and long sleepers.
Using mediation analysis, they found that short sleep may be more directly linked with late-life depression burden, while long sleep may be connected through pathways involving brain and adipose, or fat-related, ageing clocks. The authors say this suggests that short and long sleep should not automatically be treated as the same problem, even when they are linked to the same condition.
“This has a strong implication for future sleep management and future therapeutics,” Wen said. “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.”
The findings should not be read as a simple instruction that everyone must sleep within one exact window. Sleep needs vary between people and across age groups. The study also cannot show that changing sleep duration by itself will slow ageing.
The article on the study noted that the results do not prove that the six-to-eight-hour range is optimal for every person, or that reaching it directly improves health. But it described the work as one of the most comprehensive looks so far at sleep and ageing across the body.
There is another caution: people who sleep for long hours may be sleeping more because of underlying health problems. In such cases, long sleep may be a marker of illness rather than the cause of it.
Still, researchers say the findings are useful because sleep is, at least partly, modifiable. Abigail Dove, a neuroepidemiologist at the Karolinska Institute in Stockholm who was not involved in the study, told Nature that sleep “affects every organ of the body” and may offer a practical way to reduce the risk of age-related disease.
For Wen, the next question is whether these clocks can help identify lifestyle factors early enough to protect health.
“Everyone is excited by these ageing clocks and their ability to predict disease and mortality risk,” he said. “But to me, the more exciting question is, can we link ageing clocks to a lifestyle factor that can be modified in time to slow ageing?”