Editing Sleep (section)

=== Process S ===
{{Main|Sleep debt}}
Generally speaking, the longer an organism is awake, the more it feels a need to sleep ("sleep debt"). This driver of sleep is referred to as '''Process S'''. The balance between sleeping and waking is regulated by a process called [[homeostasis]]. Induced or perceived lack of sleep is called [[sleep deprivation]].

Process S is driven by the depletion of [[glycogen]] and accumulation of [[adenosine]] in the forebrain that disinhibits the [[ventrolateral preoptic nucleus]], allowing for inhibition of the [[ascending reticular activating system]].<ref>{{cite journal | vauthors = Schwartz JR, Roth T | title = Neurophysiology of sleep and wakefulness: basic science and clinical implications | journal = Current Neuropharmacology | volume = 6 | issue = 4 | pages = 367–78 | date = December 2008 | pmid = 19587857 | pmc = 2701283 | doi = 10.2174/157015908787386050 }}</ref>

Sleep deprivation tends to cause slower brain waves in the [[frontal cortex]], shortened attention span, higher anxiety, impaired memory, and a grouchy [[Mood (psychology)|mood]]. Conversely, a well-rested organism tends to have improved memory and mood.<ref>[[#Brown|Brown]], pp. 1134–1138.</ref> Neurophysiological and functional [[imaging studies]] have demonstrated that frontal regions of the brain are particularly responsive to homeostatic sleep pressure.<ref>{{cite journal | vauthors = Gottselig JM, Adam M, Rétey JV, Khatami R, Achermann P, Landolt HP | title = Random number generation during sleep deprivation: effects of caffeine on response maintenance and stereotypy | journal = Journal of Sleep Research | volume = 15 | issue = 1 | pages = 31–40 | date = March 2006 | pmid = 16490000 | doi = 10.1111/j.1365-2869.2006.00497.x | s2cid = 10355305 }}</ref>

There is disagreement on how much sleep debt is possible to accumulate, and whether sleep debt is accumulated against an individual's average sleep or some other benchmark. It is also unclear whether the prevalence of sleep debt among adults has changed appreciably in the [[developed country|industrialized world]] in recent decades. Sleep debt does show some evidence of being cumulative. Subjectively, however, humans seem to reach maximum sleepiness 30 hours after waking.<ref name=DijkEdgar1999 /> It is likely that in [[Western world|Western societies]], children are sleeping less than they previously have.<ref>{{cite journal | vauthors = Iglowstein I, Jenni OG, Molinari L, Largo RH | title = Sleep duration from infancy to adolescence: reference values and generational trends | journal = Pediatrics | volume = 111 | issue = 2 | pages = 302–7 | date = February 2003 | pmid = 12563055 | doi = 10.1542/peds.111.2.302 | quote = Thus, the shift in the evening bedtime across cohorts accounted for the substantial decrease in sleep duration in younger children between the 1970s and the 1990s... [A] more liberal parental attitude toward evening bedtime in the past decades is most likely responsible for the bedtime shift and for the decline of sleep duration... | s2cid = 8727836 }}</ref>

One neurochemical indicator of sleep debt is [[adenosine]], a neurotransmitter that inhibits many of the bodily processes associated with wakefulness. Adenosine levels increase in the cortex and basal forebrain during prolonged wakefulness, and decrease during the sleep-recovery period, potentially acting as a homeostatic regulator of sleep.<ref name="pmid25175972">{{cite journal | vauthors = Huang ZL, Zhang Z, Qu WM | title = Roles of adenosine and its receptors in sleep-wake regulation | journal = International Review of Neurobiology | volume = 119 | pages = 349–71 | date = 2014 | pmid = 25175972 | doi = 10.1016/B978-0-12-801022-8.00014-3 | isbn = 978-0-12-801022-8 }}</ref><ref>{{cite web|url=https://thebrain.mcgill.ca/flash/a/a_11/a_11_m/a_11_m_cyc/a_11_m_cyc.html|title=The brain from top to bottom: Molecules that build up and make you sleep|publisher=McGill University, Montreal, Quebec, Canada|access-date=20 September 2012|archive-url=https://web.archive.org/web/20130207001251/https://thebrain.mcgill.ca/flash/a/a_11/a_11_m/a_11_m_cyc/a_11_m_cyc.html|archive-date=7 February 2013|url-status=live}}</ref> [[Coffee]], tea, and other sources of [[caffeine]] temporarily block the effect of adenosine, prolong sleep latency, and reduce total sleep time and quality.<ref>{{cite journal | vauthors = Clark I, Landolt HP | title = Coffee, caffeine, and sleep: A systematic review of epidemiological studies and randomized controlled trials | journal = Sleep Medicine Reviews | volume = 31 | pages = 70–78 | date = February 2017 | pmid = 26899133 | doi = 10.1016/j.smrv.2016.01.006 | url = https://www.zora.uzh.ch/id/eprint/127096/14/Clark_Landolt_Sleep%20Med%20Rev%20%282016%29.pdf | access-date = 19 November 2018 | url-status = live | archive-url = https://web.archive.org/web/20181104121236/https://www.zora.uzh.ch/id/eprint/127096/14/Clark_Landolt_Sleep%20Med%20Rev%20(2016).pdf | archive-date = 4 November 2018 | doi-access = free }}</ref>