Authors: Abbas Smiley, Stephen Wolter, Dana Nissan.
There is a U-shaped association between sleep duration and risk of metabolic syndrome. The related mechanisms can be grouped into two categories: I. Too little slow-wave sleep; II. Too much REM sleep.
Too little slow-wave sleep. 1) Stage 3 is the most crucial sleep stage because growth hormone (GH) and GH releasing hormone (GHRH) are released during this stage. They induce fat burning, bone building, and general repair and regeneration. The greater the volume of GH and GHRH released, the more restorative the sleep. The longest part of stage 3 in sleep takes place before midnight. Delayed sleep onset until midnight or later, would suppress the largest GH pulse. 2) Sleep restriction induces high levels of ghrelin and low levels of leptin. Ghrelin stimulates appetite whereas leptin does the reverse. 3) Advanced glycation end products (AGEs) are significantly increased in chronic sleep insufficiency and are also associated with insulin resistance in males with chronic sleep insufficiency. 4) Sleep insufficiency increases sympathetic activity and pro-inflammatory cytokines, both of which increase insulin resistance. 5) Accumulations of extracellular β amyloid protein plaques and intracellular tau neurofibrillary tangles in brain tissues start immediately after one night of sleep insufficiency. These plaques and tangles are neurotoxins that potentiate each other’s destructive effects on the structures and functions of brain cells and cause neuronal death. The consequence is a global decrease in cognition and decision making, manifested in increased consumption of fatty foods and unhealthy snacks in late sleepers. 6) High levels of β amyloid and proteins might lead to sleep fragmentation, worsening of sleep quality and daytime somnolence. Concentration will be more difficult, and performance will be reduced. 7) Astrocytes are special giant cells in brain interstitial fluids that play a major role in β amyloid and tau cleanup. Their activity is increased by growth hormone. As a result, slow-wave sleep insufficiency may lead to impaired peripheral clearance of β amyloid and tau proteins predisposing the brain to Alzheimer’s disease.
Too much REM sleep. 1) The REM stage is the dreaming stage. The level of cortisol starts to rise in the middle of night based on circadian rhythm, and peaks in the morning. Cortisol is the fight or flight hormone, equipping the individual both to meet the demands of daily life and to handle stressful situations. It stimulates the release of epinephrine and norepinephrine. These hormones increase heart rate and blood pressure as they prepare the body to initiate activity quickly. These reactions occur on top of heart rate variability and a rise in blood pressure induced by REM sleep. If the individual wakes up early in the morning, he will use the cortisol properly to prepare for the new day. If instead he or she remains asleep, there will be no physical activity, and the cortisol levels that are normal for a person who is awake will be high levels for the one who is asleep. Then, the sleeper may experience higher blood sugar, heart rate, and blood pressure. 2) A simulation of fight or flight reactions may be reflected in dreams. The prevalence of bizarre dreams in the morning is double of that at the beginning of the night. Moreover, emotionally charged dreams are significantly more frequent in the morning than early in the night. Bad dreams bring negative physical effects such as accelerated heartbeat, blood vessel spasms, increased blood pressure, and so on. Acute exacerbations of many chronic disorders occur in early morning sleep. 3) Waking up during the REM stage can make an individual feel more sleepy or tired during the day than waking up during stages 1-2.
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