Why broken sleep makes you tired and promotes cardiovascular disease

Chris Burns - Feb 20, 2019, 1:04 pm CST
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Why broken sleep makes you tired and promotes cardiovascular disease

Research was just released which suggests insufficient or disrupted sleep has several significant negative effects on the human body. Though the first of these might seem obvious to those that’ve experienced wakefulness and/or insomnia, it’s now clear that sleep fragmentation does, indeed, make it more difficult for you to wake up. It’s the science behind the situation that we’re most excited about here – now we know WHY it happens.

The study run by Cameron S. McAlpine et. all suggested that “insufficient or disrupted sleep” can lead to several pathological conditions, (one of which is cardiovascular disease,) and sought to find out the reasons why. By way of lab testing with lab mice, this study sought out the cellular and molecular mechanisms by which sleep maintains cardiovascular health.

The test had a bunch of mice in a tank sleeping in a pile and a swiping mechanism that swept under the mice to wake them up every 2 minutes. These mice were tested vs mice that’d had uninterrupted sleep, and several consistent results appeared.

The study showed how these mice that’d had fragmented sleep produced more Ly-6Chigh monocytes, develop larger atherosclerotic lesions and produce less hypocretin2 in the lateral hypothalamus.6

Keys to this tower:
• 1. Neuropeptide: Molecule used for communication by neurons.
• 2. Hypocretin: Wake-promoting neuropeptide, restricts CSF1 production wake-producing.
• 3. CSF1: Protein, separates HCSs into groups.
• 4. HSCs: Hematopoietic stem cells that promote blood cell production.
• 5. Hematopoiesis: Process by which blood cells are formed.
• 6. Lateral hypothalamus: A part of your brain (on the side of the forebrain) that’s largely responsible for telling your body how to feel.
• 7. Myelopoiesis: Process by which bone marrow is formed.

Hypocretin2 is a neuropeptide1 that’s important for the average late sleeper because it is both stimulatory and wake-promoting. As your sleep cycle is repeatedly interrupted, your body produces less hypocretin than it would with uninterrupted sleep. Less hypocretin results in difficulty for the test subject in waking up in the morning – or whenever it’s your normal time to pop out of bed.

Hypocretin also regulates appetite. As such, making sure you get a full night’s sleep allows you to take better care of your food-based health in the daytime.

Another important element at play here is the fact that hypocretin restricts production of CSF13 “by hypocretin-receptor-expressing pre-neutrophils in the bone marrow.” CSF1 is a cytokine protein that separates hematopoietic stem cells (HSCs)4 into groups. Restricting production of CSF1 in turn controls myelopoiesis.7

Hematopoietic stem cells (HSCs) form blood cells. Hematopoiesis is the process by which blood cells are formed. As the study outlines, “Whereas hypocretin-null and haematopoietic hypocretin-receptor-null mice develop monocytosis and accelerated atherosclerosis, sleep-fragmented mice with either haematopoietic CSF1 deficiency or hypocretin supplementation have reduced numbers of circulating monocytes and smaller atherosclerotic lesions.”

So go home tonight and get some sleep. Get lots of sleep – all at one time! Sleep is inextricably tied to haematopoiesis and atherosclerosis, making chopping up your sleep time a non-starter.

If you’d like to learn more about this subject, head over to the paper “Sleep modulates haematopoiesis and protects against atherosclerosis” authored by Cameron S. McAlpine, Máté G. Kiss, Sara Rattik, Shun He, Anne Vassalli, Colin Valet, Atsushi Anzai, Christopher T. Chan, John E. Mindur, Florian Kahles, Wolfram C. Poller, Vanessa Frodermann, Ashley M. Fenn, Annemijn F. Gregory, Lennard Halle, Yoshiko Iwamoto, Friedrich F. Hoyer, Christoph J. Binder, Peter Libby, Mehdi Tafti, Thomas E. Scammell, Matthias Nahrendorf, and Filip K. Swirski. This paper was published with DOI:10.1038/s41586-019-0948-2 on the 13th of February 2019 in the scientific publication Nature.


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