Sleeping fewer than six hours or more than eight hours a night is linked to faster biological aging in the brain, heart, lungs, liver, immune system and other organs, according to a major study published in the journal Nature on May 13.
The research, led by Junhao Wen, assistant professor of radiology at Columbia University Vagelos College of Physicians and Surgeons, drew on data from approximately 500,000 adults in the UK Biobank — one of the world’s largest health and biological data repositories — and used 23 biological aging clocks spanning 17 organ systems.
The findings do not prove that sleep duration directly causes organs to age faster. But they add substantial weight to the view that sleep is a body-wide process, with consequences that reach far beyond the brain.
The researchers measured biological age gaps — the difference between a person’s chronological age and the biological age of their organs — using aging clocks built from medical images, organ-specific blood proteins, and metabolites.
Across the entire study population, a consistent U-shaped pattern emerged. People who reported sleeping between 6.4 and 7.8 hours showed the lowest biological age gaps. Those at either extreme — short sleepers and long sleepers — showed signs of faster aging across multiple organ systems.
The optimal range varied slightly by organ and by sex, but the broad pattern held across brain, lung, liver, immune, skin, endocrine, adipose, and pancreatic systems.
“Previous studies have found that sleep is largely linked to aging and the pathological burden of the brain,” said Wen. “Our study goes further and shows that too little and too much sleep are associated with faster aging in nearly every organ.”
What Are Aging Clocks?
Aging clocks are machine-learning tools that use biological data — blood proteins, metabolites, or medical scan measurements — to estimate whether a person’s organs appear older or younger than their actual age.
Most aging clocks assess the body as a whole. Wen’s team built clocks for individual organs, allowing them to examine whether sleep affected aging differently across specific systems. In the liver, for example, the team used three separate clocks — one from protein data, one from metabolic data, and one from imaging data.
“Everyone is excited by these aging clocks and their ability to predict disease and mortality risk,” Wen said. “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?”
Sleep and Disease Risk
The study also found associations between abnormal sleep duration and a wide range of diseases.
Short sleep — under six hours — was significantly associated with depressive episodes, anxiety disorders, obesity, type 2 diabetes, hypertension, ischaemic heart disease, and heart arrhythmias. Both short and long sleep were linked to chronic obstructive pulmonary disease, asthma, and digestive disorders including gastritis and gastro-oesophageal reflux disease.
People with short or long sleep duration also showed higher risks of death from any cause compared with those sleeping six to eight hours.
The team examined late-life depression separately, using a technique called mediation analysis to ask whether aging clocks sat in the pathway between sleep and depression.
The results suggested that short sleep may act more directly on depression burden, while long sleep appeared to work through an indirect route — particularly through brain and adipose, or fat-related, aging clocks.
The distinction matters clinically. Long sleep, the researchers suggest, may be less a cause of harm and more a signal of underlying illness — a marker rather than a driver.
“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,” Wen said.
What This Does Not Mean
The study carries important caveats. Sleep duration was self-reported, not measured by sleep trackers or laboratory monitoring, which limits precision. The study population was predominantly of European ancestry, which limits how widely the findings apply.
Causality remains unproven. People who sleep long hours may do so because of existing illness, pain, depression, or poor sleep quality — meaning long sleep may reflect disease rather than cause it.
Abigail Dove, a neuroepidemiologist at the Karolinska Institute in Stockholm who was not involved in the research, told Nature that sleep “affects every organ of the body” and may offer a practical way to reduce the risk of age-related disease.
The researchers are clear that the six-to-eight-hour window is not a rigid prescription. Sleep needs vary between individuals and across age groups. No study has shown that changing sleep duration alone, without addressing underlying health, reverses biological aging.
Sleep is modifiable. That is the core argument behind this line of research — and why the findings carry practical weight even without proof of direct causation.
If the biological age of your organs tracks with how long you sleep, and sleep can be changed, then sleep becomes one of the few lifestyle factors that aging clocks might one day flag early enough to act on.
For Wen, that is the question worth asking. The organs, it turns out, may be keeping score.
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