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Poor sleep increases atherosclerosis

23.02.2019

Atherosclerotic plaques that appear on the inner walls of blood vessels are not only composed of lipids. Connective tissue proteins, vascular wall cells, and, most importantly, immune cells are involved in the formation of plaques - they try to absorb excess lipids and various cellular debris, but they cannot cope with this task, and eventually begin to secrete inflammatory signals. And inflammation, in turn, stimulates the further growth of the plaque.

Medical statistics show that atherosclerosis is exacerbated by poor sleep - even if you take into account factors such as obesity, diabetes, etc., you can still see a connection between the way a person sleeps and the development of atherosclerosis. The immune system, like much else in our body, is subject to sleep-wake cycles, so it can be assumed that poor sleep is associated with atherosclerosis precisely through the immune system.

Scientists at the Massachusetts General Hospital experimented with mice: the animals were kept awake by regularly pushing them with a stick that moved over the floor of the cage - the mice constantly had to wake up and step over it. Although all of the experimental mice were initially predisposed to atherosclerosis, those who had to sleep in snatches, things were worse with blood vessels than those who slept normally. At the same time, they more actively formed leukocytes in the bone marrow, and in the blood there were especially a lot of two types of leukocytes - monocytes and neutrophils.

It turned out that in mice that were not allowed to sleep, little of the protein hypocretin (or orexin) was produced in the hypothalamus. Hypocretin regulates, firstly, appetite and energy balance, and secondly, sleep: it makes you eat more and helps you stay awake. If little hypocretin is synthesized in the hypothalamus, then the brain begins to sleep; it is known that malfunctions with hypocretin often lead to narcolepsy.

Further experiments showed that if hypocretin synthesis was turned off in mice, they would also have many white blood cells and atherosclerosis would increase - like those mice that were not allowed to sleep. But why did animals that were not allowed to sleep have low levels of hypocretin? Because the neurons that synthesized it could not cope with such a regime and, due to overload, stopped synthesizing it. Stem cells in the bone marrow, from which leukocytes should be obtained, felt that there was not enough hypocretin (these cells have special receptors for it), and in response they began to actively produce neutrophils with monocytes. And those, in turn, having entered the bloodstream, were included in the atherosclerotic process: the more leukocytes in the blood became, the more actively atherosclerotic plaques grew.

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