Sleep, immunity and atherosclerosis
Why poor Sleep increases Atherosclerosis
Kirill Stasevich, "Science and Life"
Atherosclerotic plaques that appear on the inner walls of blood vessels consist not only of lipids. Connective tissue proteins, vascular wall cells, and, most importantly, immune cells participate 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 emit inflammatory signals. And inflammation, in turn, stimulates further plaque proliferation.
On the other hand, medical statistics show that atherosclerosis is aggravated due to poor sleep - even if you take into account factors such as obesity, diabetes, etc., you can still see a link between how a person sleeps and the development of atherosclerosis. Immunity, like many other things in our body, is subject to sleep and wakefulness cycles, so it can be assumed that poor sleep is associated with atherosclerosis just through immunity. In an article in Nature (McAlpine et al., Sleep modulates haematopoiesis and protects against atherosclerosis), researchers from the Massachusetts General Hospital write that this is exactly what it is.
Filip K. Swirski and his colleagues experimented with mice: the animals were not allowed to sleep 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 the experimental mice were initially predisposed to atherosclerosis, those who had to sleep fitfully had worse vascular problems than those who slept normally. At the same time, leukocytes were formed more actively in their bone marrow, and there were especially many two types of leukocytes in their blood – monocytes and neutrophils.
It turned out that in mice that were not allowed to sleep, little protein hypocretin (or orexin) is formed in the hypothalamus. Hypocretin regulates, firstly, appetite and energy balance, and secondly, sleep: it makes you eat more and helps you stay awake. If hypocretin is not synthesized enough in the hypothalamus, then the brain begins to feel sleepy; it is known that problems with hypocretin often lead to narcolepsy.
Further experiments showed that if the synthesis of hypocretin is turned off in mice, they will also have a lot of white blood cells and atherosclerosis will increase – as in those mice who were not allowed to sleep. But why did animals that were not allowed to sleep have little hypocretin? Because the neurons that synthesized it could not cope with such a regime and stopped synthesizing it due to overload. Stem cells in the bone marrow, from which leukocytes should be obtained, felt that hypocretin was becoming scarce (these cells have special receptors for it), and in response began to actively produce neutrophils with monocytes. And those, in turn, entering the bloodstream, were involved in the atherosclerotic process: the more white blood cells in the blood, the more actively atherosclerotic plaques grew.
Most likely, this is not the only mechanism that links sleep, immunity and atherosclerosis. Some of the results obtained by the researchers suggest that there are some other metabolic reactions involved (let's not forget that hypocretin also controls the energy balance) with the participation of other hormones. At the same time, some proteins from bone marrow cells can directly affect the condition of blood vessels and those already mature immune cells that are located in the vascular wall. But in any case, if we think about some new anti-atherosclerotic drugs, then such drugs should probably somehow take into account the immune link between poor sleep and atherosclerosis.
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