People who say they sleep too little or too much tend to have organs that look older than their years, according to a large study published in the journal Nature on 13 May 20261. The researchers compared self-reported sleep with 23 different “aging clocks”, lab-based estimates of how old a body part looks, and found the same U-shaped pattern across the body: the oldest-looking readings came at the short and long ends of sleep, and the youngest in the middle2.
The lowest aging readings came between about 6.4 and 7.8 hours of sleep a night, with the exact sweet spot varying by organ and by sex1. The study is observational, which means it spotted patterns in existing health data. It did not ask anyone to change their sleep, and the team said it is hard to conclude that sleep length directly causes organs to age3.
What the researchers did
The paper, titled “Sleep chart of biological ageing clocks in middle and late life”, comes from a group called the MULTI Consortium, with 26 listed authors2. DongA Science reported that the work was led by a team at Columbia University Irving Medical Center3. The authors call their approach “Sleep Chart”, a way to map how reported sleep length lines up with biological age across many parts of the body1.
The data came from the UK Biobank, a large British health database whose volunteers in this analysis were aged 37 to 841. According to DongA Science, the clocks were built using health information from roughly 500,000 UK Biobank participants3.
What an aging clock is
An aging clock is a computer model, trained with machine learning, that reads biological data such as blood tests or medical scans and estimates whether a person’s organs look older or younger than their actual age3. The gap between the two is called the “biological age gap”. In this study the clocks drew on three kinds of data: body scans, the mix of proteins in blood plasma, and the mix of small chemicals (metabolites) in blood1.
Many earlier clocks treated the whole body as one unit, but organs age at different rates, so the team built separate clocks for separate body systems3. For the liver, for example, they made three versions: one from proteins, one from metabolites and one from imaging3. The paper’s summary describes the clocks as covering nine brain and body systems2, while DongA Science described 23 clocks across 17 organ systems3. The sources do not explain the difference, which may come down to how systems were grouped.
What the study found
Across the body systems and all three types of data, the researchers saw what they called a “systemic, U-shaped pattern” between sleep length and biological age gaps2. As sleep fell below six hours or rose above eight, the aging readings went up, and the pattern was not limited to one organ: it showed up from the brain to the heart, lungs and immune system3.
The team also looked at disease and death. Compared with a “normal” 6 to 8 hours, both short sleep (under 6 hours) and long sleep (over 8 hours) were linked to a higher risk of diseases beyond the brain, such as depression and diabetes, and to a higher risk of dying from any cause1. This rested on two kinds of analysis: genetic correlations, which look at whether the same inherited variants are tied to both traits, and predictions of who went on to develop a disease over time2.
DongA Science reported more detail on the disease links. Short sleep was tied to depression and anxiety, and to obesity, type 2 diabetes, high blood pressure, heart disease caused by narrowed arteries, and irregular heartbeat3. Both short and long sleep were linked to digestive and lung conditions, including COPD (a long-term lung disease), asthma, gastritis and acid reflux3.
Different routes to depression in later life
In a closer look at depression in older age, the team found that short and long sleep seemed to be connected to it in different ways1. For long sleep, the aging clocks may partly explain the link, meaning long sleepers’ older-looking organs could sit on the path toward depression2. DongA Science reported that this indirect route ran through the aging of the brain and of fat tissue3. Short sleep showed a more direct link to depression1.
Junhao Wen, an assistant professor and one of the authors, told DongA Science:
“Sleep duration is deeply involved in the entire brain-body integrated network, including metabolic balance and the immune system. Short sleepers and long sleepers may develop the same disease through different mechanisms, so they should not be treated in the same way.”
That quote is attributed to Wen in the DongA Science report3.
What it does not show yet
The biggest limit is cause and effect. The research team said very short or very long sleep often goes along with poor overall health, so unusual sleep may be a sign that health is already slipping rather than the reason organs age faster3. A person who is already ill, for example, may sleep more.
The authors also used Mendelian randomization, a method that uses inherited genetic differences as a kind of natural experiment to test which way cause and effect might run. It did not give strong evidence that disease changes sleep, but the authors wrote that it “cannot completely exclude such reverse causality”1.
Other points to keep in mind:
- Sleep was self-reported. The analysis used how long people said they slept, not measurements from a sleep lab or a wearable1.
- Aging clocks are estimates. They are models that compare a person’s data with patterns in a population3. A higher reading is a statistical signal, not a diagnosis.
- One population. All the data came from the UK Biobank, among adults aged 37 to 841. The sources do not show whether the same pattern holds elsewhere.
- The ideal range was not fixed. The lowest readings fell somewhere between 6.4 and 7.8 hours depending on organ and sex, rather than at one number for everyone2.
The authors’ own conclusion points to “the potential of sleep optimization to promote healthy ageing, lower disease risk and extend longevity”1. That is a hope about future work. The study itself did not test whether changing sleep changes any of these measures.
Who is behind it
The study was published under the MULTI Consortium name2. The UK Biobank lists it under application 647044, titled “MULTI: modeling human aging and disease via multi-organ and multi-omics biomedical data”1. Christos Davatzikos and Junhao Wen are the final listed authors, and the author list also includes Luigi Ferrucci, Daniel W. Belsky and Susan M. Resnick among others1. The sources read for this article do not describe who funded the work or any conflicts of interest.
How it fits the field
The finding sits within a wider push to measure aging organ by organ rather than as one number for the whole body. DongA Science noted that organs age at different rates, citing how women’s ovaries age faster than other organs, as the reason the team built organ-specific clocks3. By running sleep against many clocks at once, the study suggests the sleep pattern is body-wide rather than confined to the brain2.
The study also adds a twist to how sleep is usually discussed. Long sleep, not only short sleep, tracked with older-looking organs, and the two ends appeared to connect to depression by different routes1. Wen’s point that short and long sleepers “should not be treated in the same way” reflects that split3.
What to watch next
- Studies that measure sleep directly, with devices or in sleep labs, to check whether the U-shape holds without relying on people’s memories.
- Work in other countries and age groups, since this analysis drew only on UK Biobank volunteers aged 37 to 841.
- Trials that change people’s sleep and then re-measure aging clocks, which would be needed to test whether sleep length drives organ aging or simply reflects health that is already changing3.
Biohack will follow this thread as new research on sleep and biological aging appears. This article is news, not medical advice.
