Scientists have discovered that people who regularly sleep for more than 11 hours or less than 4 hours are 2-3 times more likely to have the incurable disease, pulmonary fibrosis, compared to those that sleep for 7 hours in a day. They attribute this association to the body clock.

The study also reveals that targeting the body clock reduces fibrosis in vitro, revealing a potential target for this incurable disease that kills about 5,000 people, a year in the U.K.,the same number as leukaemia.

The research team members are based at the Universities of Manchester, Oxford, Newcastle, University College London, and Toronto, as well as 91Ö±²¥ University NHS Foundation Trust.

The study is published in and is funded by the Medical Research Council, and the Wellcome Trust.

Our internal body clocks regulate nearly every cell in the human body, driving 24-hour cycles in many processes such as sleeping, hormone secretion and metabolism.

In the lungs, the clock is mainly located in the main air carrying passages – the airways. However, the team discovered that in people with lung fibrosis, these clock oscillations extend out to the small air spaces, called alveoli.

Studies in mice revealed that by altering the clock mechanism it was possible to disrupt the fibrotic process making the animals more likely to develop pulmonary fibrosis.

The researchers then showed, that pulmonary fibrosis is associated with short and long sleep duration using human data from the UK Biobank.

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

People who report they regularly sleep 4 hours or less in a day doubled their chance of having pulmonary fibrosis while those sleeping 11 hours or longer in a day tripled their chance of having the disease, compared to those sleeping 7 hours per day.

Smaller, but still elevated, risks were also seen in people who like to stay up late at night or those who do shift work.

The researchers explain their findings by the discovery that a core clock protein (REVERBα) which alters the production of a key protein in lung fibrosis (collagen).

This is an exciting finding, they say, because chemical compounds can alter the function of REVERBα.

The authors were able to show that one of these REVERBα compounds can reduce collagen in lung slices from people with this disease.

Dr John Blaikley from The University of Manchester, who led the project said: “Pulmonary fibrosis is a devastating condition which is incurable at present. Therefore, the discovery that the body clock is potentially a key player potentially opens new ways to treat or prevent the condition. More work will need to be done around studying the association between pulmonary fibrosis and sleep duration to establish both causation and reproducibility. If these results are confirmed, then sleeping for the optimal time may reduce the impact of this devastating disease.”

Dr Peter Cunningham, joint lead author on the paper, said: “It is fascinating to think that clock activity is increased in fibrotic disease. Previous studies have shown that the clock also plays an important role in infection, cancer and diabetes. The discovery that the clock plays a role in fibrosis suggests that altering these oscillations could become an important therapeutic approach.”

Patients with some of the most common lung diseases are substantially more likely to suffer a heart attack and develop other major heart problems according to new research.

The team of heart and lung doctors from the University of Manchester and Aston Medical School found people with asthma, chronic obstructive pulmonary disease (COPD) and lung fibrosis, were more likely to develop, and die from, heart disease and heart failure.

The study of nearly 100,000 people with lung disease in the North West of England who were followed up for up to 14 years is published in the .

The increased risk was in addition to the risk posed by other common conditions such as diabetes and high blood pressure.

However, despite the association, the team found that patients with lung disease were less likely to receive heart bypass surgery or angioplasty.

First author Dr Paul Carter, part of the ACALM 91Ö±²¥ Unit, Aston Medical School said: “The most striking findings were that the risk of coronary heart disease was increased by 50% in patients with asthma, 60% in patients with lung fibrosis and 70% in patients with COPD. Furthermore, having COPD more than doubled the risk of developing heart failure.”

Dr Rahul Potluri, founder of the ACALM 91Ö±²¥ Unit, Aston Medical School, said: “Despite the increased risk of heart disease, patients with lung diseases were less likely to receive heart treatments. Potential reasons include difficulties in diagnosis due to similar symptoms, and heart treatments having higher rates of complications in patients with lung diseases. Further work is required to understand this finding in more detail and how it could be addressed.“

Dr Chris Miller, senior author of the study from The University of Manchester said; “Research into why lung disease is associated with heart disease and the underlying disease mechanisms, is urgently required. If we could understand that, then we could potentially develop treatments that target these disease pathways.”