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Scientists have found that people who regularly sleep for more than 11 hours or less than 4 hours are 2-3 times more likely to develop the incurable disease pulmonary fibrosis than people who sleep for 7 hours a day.

They attributed this association to the body clock.

The study also shows that targeting the circadian clock can reduce fibrosis in vitro, revealing a potential target for the incurable disease, which kills around 5,000 people in the UK every year, the same number as leukemia.

Research team members are based at the Universities of Manchester, Oxford, Newcastle, University College London and the University of Toronto, as well as the University of Manchester NHS Foundation Trust.

The study, published in the Proceedings of the National Academy of Sciences, was funded by the Medical Research Council and the Wellcome Trust.

Our internal clock regulates nearly every cell in the body, driving a 24-hour cycle during many processes including sleep, hormone secretion, and metabolism.

In the lungs, clocks are located primarily in the airways, the main air-carrying pathways.

However, the team found that in people with pulmonary fibrosis, these clock oscillations extend into small spaces called alveoli.

Studies in mice suggest that by altering clock mechanisms, it is possible to disrupt the fibrotic process, making animals more susceptible to lung fibrosis.

The researchers then used human data from the UK Biobank to show that pulmonary fibrosis is associated with sleep duration.

The link between sleep duration and pulmonary fibrosis is similar in strength to other known risk factors for the disease.

Compared with people who slept 7 hours a day, people who reported regular sleep of 4 hours or less per day had twice the chance of developing pulmonary fibrosis, while people who slept 11 hours or more per day had an increased chance of developing the disease.

three times.

People who stay up late at night or work shifts also see a smaller but still higher risk.

The researchers explained their findings by finding that the core clock protein alters the production of a key protein in lung fibrosis.

They say this is an exciting discovery because the compound can change the function of REVERB.

The authors were able to show that one of these REVERB compounds reduced collagen in lung slices from people with the disease.

Dr John Blakeley from the University of Manchester, who is leading the project, said: "Pulmonary fibrosis is a devastating disease that currently has no cure.

Therefore, the discovery that the circadian clock may be a key factor provides new ways to treat or prevent this disease.

Studying the relationship between pulmonary fibrosis and sleep duration will require more work to establish causality and reproducibility.

If these results are confirmed, sleeping at optimal times may lessen the impact of this devastating disease.

Dr Peter Cunningham, lead co-author of the paper, said: "Surprisingly, clock activity is increased in fibrotic diseases.

Previous research has shown that the clock also plays an important role in infections, cancer and diabetes.

The clock plays a role in fibrosis, suggesting that altering these oscillations could become an important therapeutic approach.

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