Editing Sleep (section)

== Timing ==
Sleep timing is controlled by the [[circadian clock]] (Process C), sleep-wake [[homeostasis]] (Process S), and to some extent by the individual will.

=== Circadian clock ===
{{Main|Circadian rhythm}}
{{further|Circadian rhythm sleep disorder}}
[[image:Biological clock human.svg|402px|thumb|The human "[[Circadian rhythm|biological clock]]"]]

Sleep timing depends greatly on [[hormone|hormonal]] signals from the circadian clock, or Process C, a complex neurochemical system which uses signals from an organism's environment to recreate an internal day–night rhythm. Process C counteracts the homeostatic drive for sleep during the day (in [[diurnality|diurnal]] animals) and augments it at night.<ref name=FullerEtAl2006>{{cite journal | vauthors = Fuller PM, Gooley JJ, Saper CB | title = Neurobiology of the sleep-wake cycle: sleep architecture, circadian regulation, and regulatory feedback | journal = Journal of Biological Rhythms | volume = 21 | issue = 6 | pages = 482–93 | date = December 2006 | pmid = 17107938 | doi = 10.1177/0748730406294627 | s2cid = 36572447 }}</ref><ref name=WaterhouseEtAl2012 /> The [[suprachiasmatic nucleus]] (SCN), a brain area directly above the [[optic chiasm]], is presently considered the most important nexus for this process; however, secondary clock systems have been found throughout the body.

An organism whose circadian clock exhibits a regular rhythm corresponding to outside signals is said to be ''[[Entrainment (chronobiology)|entrained]]''; an entrained rhythm persists even if the outside signals suddenly disappear. If an entrained human is isolated in a bunker with constant light or darkness, he or she will continue to experience rhythmic increases and decreases of body temperature and melatonin, on a period that slightly exceeds 24 hours. Scientists refer to such conditions as [[Free-running sleep|free-running]] of the circadian rhythm. Under natural conditions, light signals regularly adjust this period downward, so that it corresponds better with the exact 24 hours of an Earth day.<ref name=RonnenbergEtAl2007 /><ref>{{cite book | author-link1 = Phyllis C. Zee | vauthors = Zee PC, Turek FW | date = 1999 | chapter = Introduction to Sleep and Circadian Rhythms | veditors = Zee PC, Turek FW | title = Regulation of Sleep and Circadian Rhythms | pages = 1–17 }}</ref><ref name=DijkEdgar1999>{{cite book | vauthors = Derk-Jan D, Edgar DM | date = 1999 | chapter = Circadian and Homeostatic Control of Wakefulness and Sleep | veditors = Zee PC, Turek FW | title = Regulation of Sleep and Circadian Rhythms | pages = 111–147 }}</ref>

The circadian clock exerts constant influence on the body, affecting [[Sine wave|sinusoidal]] oscillation of [[thermoregulation|body temperature]] between roughly 36.2&nbsp;°C and 37.2&nbsp;°C.<ref name=DijkEdgar1999 /><ref name=CzeislerWright1999>{{cite book | vauthors = Czeisler CA, Wright Jr KP | date = 1999 | chapter = Influence of Light on Circadian Rhythmicity in Humans | veditors = Zee PC, Turek FW | title = Regulation of Sleep and Circadian Rhythms | pages = 149–180 }}</ref> The suprachiasmatic nucleus itself shows conspicuous oscillation activity, which intensifies during subjective day (i.e., the part of the rhythm corresponding with daytime, whether accurately or not) and drops to almost nothing during subjective night.<ref name=ZlomanczukSchwartz1999>{{cite book | vauthors = Zlomanczuk P, Schwartz WJ | date = 1999 | chapter = Cellular and Molecular Mechanisms of Circadian Rhythms in Mammals | veditors = Zee PC, Turek FW | title = Regulation of Sleep and Circadian Rhythms | pages = 309–342 }}</ref> The circadian pacemaker in the suprachiasmatic nucleus has a direct neural connection to the [[pineal gland]], which releases the hormone [[melatonin]] at night.<ref name=ZlomanczukSchwartz1999 /> [[Cortisol]] levels typically rise throughout the night, [[Cortisol awakening response|peak in the awakening hours]], and diminish during the day.<ref name="VanCauterSpiegel1999"/><ref name=Wehr1999>{{cite book | vauthors = Wehr TA | date = 1999 | chapter = The Impact of Changes in Nightlength (Scotoperiod) on Human Sleep | veditors = Zee PC, Turek FW | title = Regulation of Sleep and Circadian Rhythms | pages = 263–285 }}</ref> Circadian [[prolactin]] secretion begins in the late afternoon, especially in women, and is subsequently augmented by sleep-induced secretion, to peak in the middle of the night. Circadian rhythm exerts some influence on the nighttime secretion of growth hormone.<ref name=VanCauterSpiegel1999 />

The circadian rhythm influences the ideal timing of a restorative sleep episode.<ref name=RonnenbergEtAl2007 /><ref name=Wyatt1999>{{cite journal | vauthors = Wyatt JK, Ritz-De Cecco A, Czeisler CA, Dijk DJ | title = Circadian temperature and melatonin rhythms, sleep, and neurobehavioral function in humans living on a 20-h day | journal = The American Journal of Physiology | volume = 277 | issue = 4 Pt 2 | pages = R1152-63 | date = October 1999 | pmid = 10516257 | doi = 10.1152/ajpregu.1999.277.4.r1152 | s2cid = 4474347 | quote = ... significant homeostatic and circadian modulation of sleep structure, with the highest sleep efficiency occurring in sleep episodes bracketing the melatonin maximum and core body temperature minimum <!-- the quote is only relevant to one time that this ref is used --> }}</ref> Sleepiness increases during the night. REM sleep occurs more during body temperature minimum within the circadian cycle, whereas [[slow-wave sleep]] can occur more independently of circadian time.<ref name=DijkEdgar1999 />

The internal circadian clock is profoundly influenced by changes in light, since these are its main clues about what time it is. Exposure to even small amounts of light during the night can suppress melatonin secretion, and increase body temperature and wakefulness. Short pulses of light, at [[phase response curve|the right moment]] in the circadian cycle, can significantly 'reset' the internal clock.<ref name=CzeislerWright1999 /> Blue light, in particular, exerts the strongest effect,<ref name=WaterhouseEtAl2012 /> leading to concerns that [[Electronic media and sleep|use of a screen]] before bed may interfere with sleep.<ref name="ChangAM">{{cite journal | vauthors = Chang AM, Aeschbach D, Duffy JF, Czeisler CA | title = Evening use of light-emitting eReaders negatively affects sleep, circadian timing, and next-morning alertness | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 112 | issue = 4 | pages = 1232–7 | date = January 2015 | pmid = 25535358 | pmc = 4313820 | doi = 10.1073/pnas.1418490112 | bibcode = 2015PNAS..112.1232C | doi-access = free }}</ref>

Modern humans often find themselves desynchronized from their internal circadian clock, due to the requirements of work (especially [[Shift work|night shifts]]), long-distance travel, and the influence of universal indoor lighting.<ref name=DijkEdgar1999 /> Even if they have sleep debt, or feel sleepy, people can have difficulty staying asleep at the peak of their circadian cycle. Conversely, they can have difficulty waking up in the trough of the cycle.<ref name=AkerstedtEtAl2002 /> A healthy young adult entrained to the sun will (during most of the year) fall asleep a few hours after sunset, experience body temperature minimum at 6 a.m., and wake up a few hours after sunrise.<ref name=DijkEdgar1999 />

=== 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>

=== Social timing ===
Humans are also influenced by aspects of ''social time'', such as the hours when other people are awake, the hours when work is required, the time on clocks, etc. [[Time zone]]s, standard times used to unify the timing for people in the same area, correspond only approximately to the natural rising and setting of the sun. An extreme example of the approximate nature of time zones is China, a country which used to span five time zones and now [[Time in China|officially uses only one]] (UTC+8).<ref name=RonnenbergEtAl2007 />

=== Distribution ===
In [[polyphasic sleep]], an organism sleeps several times in a 24-hour cycle, whereas in monophasic sleep this occurs all at once. Under experimental conditions, humans tend to alternate more frequently between sleep and wakefulness (i.e., exhibit more polyphasic sleep) if they have nothing better to do.<ref name=DijkEdgar1999 /> Given a 14-hour period of darkness in experimental conditions, humans tended towards bimodal sleep, with two sleep periods concentrated at the beginning and at the end of the dark time. Bimodal sleep in humans was more common before the [[Industrial Revolution]].<ref name=Wehr1999 />

Different characteristic sleep patterns, such as the familiarly so-called "[[Lark (person)|early bird]]" and "[[Night owl (person)|night owl]]", are called ''[[chronotype]]s''. Genetics and sex have some influence on chronotype, but so do habits. Chronotype is also liable to change over the course of a person's lifetime. Seven-year-olds are better disposed to wake up early in the morning than are fifteen-year-olds.<ref name=WaterhouseEtAl2012 /><ref name=RonnenbergEtAl2007 /> Chronotypes far outside the normal range are called circadian rhythm sleep disorders.<ref>{{cite journal | vauthors = Dagan Y | title = Circadian rhythm sleep disorders (CRSD) | journal = Sleep Medicine Reviews | volume = 6 | issue = 1 | pages = 45–54 | date = February 2002 | pmid = 12531141 | doi = 10.1053/smrv.2001.0190 | url = https://www.neurosono.com.br/arquivos/1155473343.pdf | access-date = 5 June 2016 | url-status = dead | quote = Early onset of CRSD, the ease of diagnosis, the high frequency of misdiagnosis and erroneous treatment, the potentially harmful psychological and adjustment consequences, and the availability of promising treatments, all indicate the importance of greater awareness of these disorders. | format = PDF: full text | archive-url = https://web.archive.org/web/20080227161654/https://www.neurosono.com.br/arquivos/1155473343.pdf | archive-date = 27 February 2008 }}</ref>

====Naps====
{{main|Nap}}Naps are short periods of sleep that one might take during the daytime, often in order to get the necessary amount of rest. Napping is often associated with childhood, but around one-third of American adults partake in it daily. The optimal nap duration is around 10–20 minutes, as researchers have proven that it takes at least 30 minutes to enter slow-wave sleep, the deepest period of sleep.<ref name=":0">Fry, A. (9 October 2020). ''Napping: Health Benefits & Tips for your best nap''. Sleep Foundation. Retrieved 14 November 2021, from https://www.sleepfoundation.org/sleep-hygiene/napping .</ref> Napping too long and entering the slow wave cycles can make it difficult to awake from the nap and leave one feeling unrested. This period of drowsiness is called [[sleep inertia]].

[[File:Hombre echando una siesta en San Cristóbal, Cusco, Perú, 2015-07-31, DD 49.JPG|thumb|Man napping in San Cristobal, [[Peru]]]]
The [[siesta]] habit has recently been associated with a 37% lower coronary mortality, possibly due to reduced cardiovascular stress mediated by daytime sleep.<ref name=Naska>{{cite journal | vauthors = Naska A, Oikonomou E, Trichopoulou A, Psaltopoulou T, Trichopoulos D | title = Siesta in healthy adults and coronary mortality in the general population | journal = Archives of Internal Medicine | volume = 167 | issue = 3 | pages = 296–301 | date = February 2007 | pmid = 17296887 | doi = 10.1001/archinte.167.3.296 | doi-access = free }}</ref> Short naps at mid-day and mild evening exercise were found to be effective for improved sleep, cognitive tasks, and mental health in elderly people.<ref>{{cite journal | vauthors = Tanaka H, Tamura N | title = Sleep education with self-help treatment and sleep health promotion for mental and physical wellness in Japan | journal = Sleep and Biological Rhythms | volume = 14 | issue = S1 | pages = 89–99 | date = January 2016 | pmid = 26855610 | pmc = 4732678 | doi = 10.1007/s41105-015-0018-6 }}</ref>

=== Genetics ===
Monozygotic (identical) but not dizygotic (fraternal) twins tend to have similar sleep habits. Neurotransmitters, molecules whose production can be traced to specific genes, are one genetic influence on sleep that can be analyzed. The circadian clock has its own set of genes.<ref>[[#Brown|Brown]], pp. 1138–1102.</ref> Genes which may influence sleep include [[ABCC9]], [[DEC2]], [[Dopamine receptor D2]]<ref name="The Molecular Genetics of Human Sleep">{{cite journal | vauthors = Zhang L, Fu YH | title = The molecular genetics of human sleep | journal = The European Journal of Neuroscience | volume = 51 | issue = 1 | pages = 422–428 | date = January 2020 | pmid = 30144347 | pmc = 6389443 | doi = 10.1111/ejn.14132 }}</ref> and variants near [[PAX8|PAX 8]] and [[VRK2]].<ref name=pmid27494321>{{cite journal | vauthors = Jones SE, Tyrrell J, Wood AR, Beaumont RN, Ruth KS, Tuke MA, Yaghootkar H, Hu Y, Teder-Laving M, Hayward C, Roenneberg T, Wilson JF, Del Greco F, Hicks AA, Shin C, Yun CH, Lee SK, Metspalu A, Byrne EM, Gehrman PR, Tiemeier H, Allebrandt KV, Freathy RM, Murray A, Hinds DA, Frayling TM, Weedon MN | display-authors = 6 | title = Genome-Wide Association Analyses in 128,266 Individuals Identifies New Morningness and Sleep Duration Loci | journal = PLOS Genetics | volume = 12 | issue = 8 | pages = e1006125 | date = August 2016 | pmid = 27494321 | pmc = 4975467 | doi = 10.1371/journal.pgen.1006125 | doi-access = free }}</ref> While the latter have been found in a [[Genome-wide association study|GWAS study]] that primarily detects correlations (but not necessarily causation), other genes have been shown to have a more direct effect. For instance, mice lacking [[Dihydropyrimidine dehydrogenase (NADP+)|dihydropyrimidine dehydrogenase]] (Dpyd) had 78.4 min less sleep during the lights-off period than wild-type mice. Dpyd encodes the rate-limiting [[enzyme]] in the metabolic pathway that catabolizes [[uracil]] and [[thymidine]] to β-[[alanine]], an inhibitory [[neurotransmitter]]. This also supports the role of β-alanine as a neurotransmitter that promotes sleep in mice.<ref>{{cite journal | vauthors = Keenan BT, Galante RJ, Lian J, Zhang L, Guo X, Veatch OJ, Chesler EJ, O'Brien WT, Svenson KL, Churchill GA, Pack AI | display-authors = 6 | title = The dihydropyrimidine dehydrogenase gene contributes to heritable differences in sleep in mice | journal = Current Biology | volume = 31 | issue = 23 | pages = 5238–5248.e7 | date = December 2021 | pmid = 34653361 | pmc = 8665053 | doi = 10.1016/j.cub.2021.09.049 | bibcode = 2021CBio...31E5238K | s2cid = 238754563 }}</ref>

==== Genes for short sleep duration ====
{{Excerpt|Familial natural short sleep}} The genes [[DEC2]], [[ADRB1]], [[NPSR1]] and [[GRM1]] are implicated in enabling short sleep.<ref>{{cite journal |last1=Zheng |first1=Liubin |last2=Zhang |first2=Luoying |title=The molecular mechanism of natural short sleep: A path towards understanding why we need to sleep |journal=Brain Science Advances |date=September 2022 |volume=8 |issue=3 |pages=165–172 |doi=10.26599/BSA.2022.9050003 |s2cid=250363367 |language=en |issn=2096-5958}}</ref>

=== Quality ===
The quality of sleep may be evaluated from an objective and a subjective point of view. Objective sleep quality refers to how difficult it is for a person to fall asleep and remain in a sleeping state, and how many times they wake up during a single night. Poor sleep quality disrupts the cycle of transition between the different stages of sleep.<ref>{{cite journal | vauthors = Barnes CM, Lucianetti L, Bhave DP, Christian MS |year=2015 |title=You wouldn't like me when I'm sleepy: Leaders' sleep, daily abusive supervision, and work unit engagement |journal=Academy of Management Journal |volume=58 |issue=5 |pages=1419–1437 |doi=10.5465/amj.2013.1063 |s2cid=145056840 |url=https://ink.library.smu.edu.sg/lkcsb_research/4353 }}</ref> Subjective sleep quality in turn refers to a sense of being rested and regenerated after awaking from sleep. A study by A. Harvey et al. (2002) found that insomniacs were more demanding in their evaluations of sleep quality than individuals who had no sleep problems.<ref>{{cite journal | vauthors = Harvey AG, Payne S | title = The management of unwanted pre-sleep thoughts in insomnia: distraction with imagery versus general distraction | journal = Behaviour Research and Therapy | volume = 40 | issue = 3 | pages = 267–77 | date = March 2002 | pmid = 11863237 | doi = 10.1016/s0005-7967(01)00012-2 | s2cid = 16647017 }}</ref>

Homeostatic sleep propensity (the need for sleep as a function of the amount of time elapsed since the last adequate sleep episode) must be balanced against the circadian element for satisfactory sleep.<ref name="Zisapel">{{cite journal | vauthors = Zisapel N | title = Sleep and sleep disturbances: biological basis and clinical implications | journal = Cellular and Molecular Life Sciences | volume = 64 | issue = 10 | pages = 1174–86 | date = May 2007 | pmid = 17364142 | doi = 10.1007/s00018-007-6529-9 | s2cid = 2003308 | pmc = 11136060 }}</ref><ref>{{cite journal | vauthors = Dijk DJ, Lockley SW | title = Integration of human sleep-wake regulation and circadian rhythmicity | journal = Journal of Applied Physiology | volume = 92 | issue = 2 | pages = 852–62 | date = February 2002 | pmid = 11796701 | doi = 10.1152/japplphysiol.00924.2001 | quote = Consolidation of sleep for 8 h or more is only observed when sleep is initiated ~6–8 h before the temperature nadir. | s2cid = 2502686 }}</ref> Along with corresponding messages from the circadian clock, this tells the body it needs to sleep.<ref name="autogenerated1">{{cite web|url=https://www.helpguide.org/life/sleeping.htm |title=Understanding Sleep: Sleep Needs, Cycles, and Stages |access-date=25 January 2008 | vauthors = de Benedictis T, Larson H, Kemp G, Barston S, Segal R |year=2007 |publisher=Helpguide.org |url-status=dead |archive-url=https://web.archive.org/web/20080124000744/https://www.helpguide.org/life/sleeping.htm |archive-date=24 January 2008 }}</ref> The timing is correct when the following two circadian markers occur after the middle of the sleep episode and before awakening:<ref name=Wyatt1999 /> maximum concentration of the hormone melatonin, and minimum core body temperature.