Atherosclerosis refers to the thickening or stiffening of blood vessels, which supply oxygen and nutrients to the heart. This is usually caused by unhealthy diets and other risk factors, which induce the buildup of plaque. Plaques are composed of various substances like cholesterol and fats. When these accumulate along the walls of blood vessels, they restrict blood flow to the heart. Plaques can burst and trigger a blot clot, which can cause heart attack and permanent heart damage. Although atherosclerosis is often associated with heart disease, it can happen anywhere in the body. Atherosclerosis is both treatable and preventable.
Numerous studies link insufficient sleep to the development of chronic diseases, such as obesity, Type 2 diabetes, cardiovascular disease, and depression. However, not much is known about the mechanisms underlying the effects of sleep. This led the researchers to investigate how sleep influences heart health, particularly how it affects the development of atherosclerosis.
For their experiment, they used mice genetically engineered to become prone to atherosclerosis and divided them into two groups. They allowed the first group to sleep well, while they disturbed the sleep of the second group. Upon comparison, the researchers found that the mice in the second group developed larger plaques in their arteries than the mice in the first group. (Related: Poor Sleep and Lack of Sleep Can Cause Elevated Blood Pressure in Adolescents.)
The mice that had their sleep disturbed also produced twice as much inflammatory white blood cells in their bone marrows as the mice that slept well, but they produced less hypocretin in their hypothalamus. Hypocretin is a neuropeptide involved in the regulation of sleep and arousal states. It also regulates a protein called CSF1 to control blood cell production in the bone marrow.
When the researchers supplemented sleep-disrupted mice with hypocretin, they observed that atherosclerosis developed at a much slower rate in those animals than it did in those who did not receive supplementation. The hypocretin-supplemented mice also produced less white blood cells. This suggested that the decrease in hypocretin and the increase in CSF1 induced by insufficient sleep were responsible for the increase in white blood cells and the accelerated development of atherosclerosis in sleep-disturbed mice.
Based on these findings, the researchers concluded that good-quality sleep can protect the blood vessels from atherosclerosis by regulating the concentration of hypocretin in the hypothalamus.
"We've identified a mechanism 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," said Filip Swirski, one of the authors of the study.
"This anti-inflammatory mechanism is regulated by sleep, and it breaks down when you frequently disrupt sleep or experience poor sleep quality."
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