Sufficient sleep cuts cardiovascular disease risk

Getting eugh sleep can help protect against cardiovascular disease by preventing buildup of plaques in arteries, a study has found.

research. published in journal Nature, describes mechanism by which insufficient sleep increases production of inflammatory white blood cells kwn to be major contributors to arosclerosis.

"We have discovered that sleep helps to regulate production in bone marrow of inflammatory cells and health of blood vessels and that, conversely, sleep disruption breaks down control of inflammatory cell production, leing to more inflammation and more heart disease," said Filip Swirski, from Massachusetts General Hospital (MGH) in US.

"We also have identified how a hormone in brain kwn to control wakefulness controls processes in bone marrow and protects against cardiovascular disease," said Swirski.

To investigate how insufficient sleep increases arosclerosis, Swirski's team subjected mice genetically programmed to develop aroslcerosis to repeated interruptions of ir sleep, similar to experience of someone constantly waking up because of ise or discomfort.

While re were changes in weight, cholesterol levels or glucose tolerance in sleep-deprived mice, compared to animals from same strain allowed to sleep rmally, those subjected to sleep fragmentation developed larger arterial plaques and h higher levels of mocytes and neutrophils -- inflammatory cells that contribute to arosclerosis -- in ir blood vessels.

Furr experiments revealed that sleep-deprived mice h a nearly two-fold increase in production in ir bone marrow of stem cells that give rise to white blood cells.

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A hormone called hypocretin, produced in brain structure called hypothalamus and kwn to have a role in regulation of sleep, was found to play an unexpected role in controlling white blood cell production.

While rmally produced at high levels when animals -- including humans -- are awake, hypocretin levels were significantly reduced in sleep-deprived mice.

team found that hypocretin regulates production of white blood cells through interaction with neutrophil progenitors in bone marrow.

Neutrophils, y discovered, induce mocyte production through release of a factor called CSF-1, and experiments with mice lacking gene for hypocretin revealed that hormone controls CSF-1 expression, mocyte production and development of arterial plaques. 

In sleep-deprived animals, drop in hypocretin led to increased CSF-1 production by neutrophils, elevated mocyte production and accelerated arosclerosis.

"This is a direct demonstration that hypocretin is also an important inflammatory mediator," said Swirski.

"We w need to study this pathway in humans, explore ditional mechanisms by which proper sleep maintains vascular health and furr explore this newly identified neuro-immune axis," he said. 

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