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The journal Nature has recently published a paper about the study.
"We've identified a mechanism," says senior study author Filip K. Swirski, Ph.D.,
who is an associate professor at MGH and Harvard Medical School, also in Boston,
"by which a brain hormone controls production of inflammatory cells in the bone
marrow in a way that helps protect the blood vessels from damage."
Sleep, health, and atherosclerosis
"Sleep is integral to life," note the authors, and yet insufficient or disturbed
sleep is a significant public health issue that affects millions of people.
The Centers for Disease Control and Prevention (CDC) estimate that 35
percent of adults in the United States were regularly sleeping less than 7
hours per 24-hour period in 2014.
So, Dr. Swirski and his colleagues decided to investigate how sleep might help to
protect cardiovascular health by focusing on the development of atherosclerosis.
The plaques that arise in atherosclerosis can take years to form and consist
of calcium, fat molecules, cholesterol, and other substances. As they accumulate,
they lessen the flow of nutrient- and oxygen-rich blood.
Comparing them with the mice that slept well, the team found that the
disrupted-sleep mice developed arterial plaques that were up to one third
larger.
The sleep-disrupted mice also produced twice the amount of a certain type of
inflammatory white blood cell in their bone marrow, and "the lateral
hypothalamus" of their brains produced less hypocretin.
The authors note that hypocretin controls blood cell production in bone
marrow by regulating CSF1, which is a type of signaling protein.
They conclude that the rise in white blood cells and acceleration of
atherosclerosis in the sleep-disturbed mice were due to the reduction of
hypocretin and increase in CSF1.
The National Heart, Lung, and Blood Institute (NHLBI), which is part of the
National Institutes of Health (NIH), funded the research.