Getting enough sleep reduces the risk of cardiovascular disease
Researchers from Massachusetts General Hospital (MGH) have found that getting enough sleep protects against atherosclerosis, the buildup of arterial plaques. As the study’s authors describe in Nature, not getting adequate sleep can increase the production of inflammatory white blood cells that play into atherosclerosis.
“We have discovered that sleep helps to regulate the production in the bone marrow of inflammatory cells and the health of blood vessels and that, conversely, sleep disruption breaks down control of inflammatory cell production, leading to more inflammation and more heart disease,” said senior author Filip Swirski, PhD, of the MGH Center for Systems Biology. “We also have identified how a hormone in the brain known to control wakefulness controls processes in the bone marrow and protects against cardiovascular disease.”
To test their theory, researchers subjected atherosclerosis-prone mice to multiple interruptions during sleep. These mice ultimately developed larger arterial plaques and had higher levels of monocytes and neutrophils — the inflammatory cells that contribute to atherosclerosis — within their blood vessels. Furthermore, the sleep-deprived mice had double the amount of stem cells that contribute to the production of white blood cells in their bone marrow.
Researchers also found that hypocretin, a sleep regulation-contributing hormone produced in the brain’s hypothalamus, also plays a role in the controlling the production of white blood cells. Compared to healthy mice and humans who produce high levels of hypocretin when awake, the sleep-deprived mice showed an overall reduced level of hypocretin.
Hypocretin interacts with neutrophil progenitors in the bone marrow, which induces monocyte production via release of a factor called CSF-1. Investigators found through experiments on mice lacking hypocretin that CSF-1 expression, monocyte production and the development of arterial plaques. And in sleep-deprived mice, the drop in hypocretin led to increased CSF-1 production by neutrophils, elevated monocyte production and accelerated atherosclerosis.
“This is a direct demonstration that hypocretin is also an important inflammatory mediator,” Swirski said. “We now need to study this pathway in humans, explore additional mechanisms by which proper sleep maintains vascular health and further explore this newly identified neuro-immune axis.”