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After a week of too little sleep, I slept about 12 hours last night to "catch up". It made me wonder: what is happening physically that signals that I'm done sleeping, or conversely, that I need to sleep. I read this question and its answers, which explain how brain waves indicate different sleep stages: Why sleep? No, actually, why wake?

But what causes the changes in these brain waves? I'm curious about the mechanism by which my body determines that it needs sleep, and not just a set amount, but a specific amount based on my previous week's lack of sleep. is it something in my brain or is it a hormone or something else?

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During sleep the cerebrospinal fluid clears out the waste products of brains cells. Sleep fragmentation or sleep deprivation can prevent this process, or reduce its efficiency. So I think the accumulation of waste products cause that you have to sleep more after sleep deprivation and extreme sleep deprivation (e.g. by fatal insomnia) can cause death. Low quality sleep and sleep deprivation can cause or worsen both neural (e.g. Alzheimer's disease), and metabolic diseases (e.g. diabetes mellitus, etc...), so you should avoid it, if you can (I cannot :D).

Daily sleep is regulated by the circadian clock. Many hormones can affect that clock, e.g. melatonin (dependent on blue light), insulin, etc...

The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.

According to the traditional understanding of cerebrospinal fluid (CSF) physiology, the majority of CSF is produced by the choroid plexus, circulates through the ventricles, the cisterns, and the subarachnoid space to be absorbed into the blood by the arachnoid villi. This review surveys key developments leading to the traditional concept. Challenging this concept are novel insights utilizing molecular and cellular biology as well as neuroimaging, which indicate that CSF physiology may be much more complex than previously believed. The CSF circulation comprises not only a directed flow of CSF, but in addition a pulsatile to and fro movement throughout the entire brain with local fluid exchange between blood, interstitial fluid, and CSF. Astrocytes, aquaporins, and other membrane transporters are key elements in brain water and CSF homeostasis. A continuous bidirectional fluid exchange at the blood brain barrier produces flow rates, which exceed the choroidal CSF production rate by far. The CSF circulation around blood vessels penetrating from the subarachnoid space into the Virchow Robin spaces provides both a drainage pathway for the clearance of waste molecules from the brain and a site for the interaction of the systemic immune system with that of the brain. Important physiological functions, for example the regeneration of the brain during sleep, may depend on CSF circulation.

Sleep fragmentation is present in numerous sleep pathologies and constitutes a major feature of patients with obstructive sleep apnea. A prevalence of metabolic syndrome, diabetes and obesity has been shown to be associated to obstructive sleep apnea. While sleep fragmentation has been shown to impact sleep homeostasis, its specific effects on metabolic variables are only beginning to emerge. In this context, it is important to develop realistic animal models that would account for chronic metabolic effects of sleep fragmentation. We developed a 14-day model of instrumental sleep fragmentation in mice, and show an impact on both brain-specific and general metabolism. We first report that sleep fragmentation increases food intake without affecting body weight. This imbalance was accompanied by the inability to adequately decrease brain temperature during fragmented sleep. In addition, we report that sleep-fragmented mice develop glucose intolerance. We also observe that sleep fragmentation slightly increases the circadian peak level of glucocorticoids, a factor that may be involved in the observed metabolic effects. Our results confirm that poor-quality sleep with sustained sleep fragmentation has similar effects on general metabolism as actual sleep loss. Altogether, these results strongly suggest that sleep fragmentation is an aggravating factor for the development of metabolic dysfunctions that may be relevant for sleep disorders such as obstructive sleep apnea.

Inadequate sleep simultaneously modulates the levels of multiple hormones that govern metabolism, In general, with sleep deprivation, the following hormones are decreased: insulin, growth hormone (GH), growth hormone releasing hormone (GHRH), and leptin levels. In contrast, ghrelin and somatostatin are increased. Essentially, hormones that signal that the body has plenty of energy are decreased, while those that signal energy need are increased. Experiments utilizing knockout animals as well as pharmacological agonists, antagonists, and immunodepletion of the proteins, illustrate that these hormones affect sleep regulation. Diabetic rats have decreased sleep time and consolidation while replacement of insulin increases increases slow-wave sleep.

In humans, melatonin is produced by the pineal gland, a small endocrine gland[26] located in the center of the brain but outside the blood–brain barrier. The melatonin signal forms part of the system that regulates the sleep–wake cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system (specifically the suprachiasmatic nuclei, or SCN)[26] that controls the daily cycle in most components of the paracrine and endocrine systems[27][28] rather than the melatonin signal (as was once postulated).

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    $\begingroup$ Maybe some explanation about the downvote? :D I guess I have a fan... $\endgroup$ – inf3rno Oct 27 '14 at 8:24

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