Editing Sleep debt

{{short description|Cumulative effect of not getting enough sleep}}
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[[File:Effects of sleep deprivation.svg|thumb|300px|Main health effects of [[sleep deprivation]],<ref>Reference list is found on image page on [[Wikimedia Commons]]: [[:Commons:File:Effects of sleep deprivation.svg#References]].</ref> indicating impairment of normal maintenance by sleep]]
'''Sleep debt''' or '''sleep deficit''' is the cumulative effect of not getting enough [[sleep]]. A large sleep debt may lead to mental or physical [[fatigue (medical)|fatigue]], and can adversely affect one's [[Mood (psychology)|mood]], energy, and ability to [[Thought|think]] clearly.

There are two kinds of sleep debt: the result of partial [[sleep deprivation]], and of total sleep deprivation. Partial sleep deprivation occurs when a person or a [[animal testing|lab animal]] sleeps too little for several days or weeks. Total sleep deprivation, on the other hand, occurs when the subject is kept awake for at least 24 hours. There is debate in the scientific community over the specifics of sleep debt (see {{Slink||Scientific debate}}), and it is not considered to be a [[Mental disorder|disorder]].{{citation needed|date=May 2016}}

== Physiological effects of sleep debt ==

The effects of chronic sleep debt on the human body's metabolic and endocrine processes are significant, particularly for those individuals who are overweight. An analysis of the physiological impacts of sleep debt, published in ''[[The Lancet]]'', investigated the physiological effects of sleep debt by assessing the sympathovagal balance (an indicator of the [[sympathetic nervous system]] activity), thyrotropic function, [[Hypothalamic–pituitary–adrenal axis|HPA axis]] activity, as well as the carbohydrate metabolism of 11 young adult males whose sleep period for six nights was either restricted to four hours per night or extended to 12 hours in bed per night.<ref name=":0">{{cite journal | vauthors = Spiegel K, Leproult R, Van Cauter E | title = Impact of sleep debt on metabolic and endocrine function | language = English | journal = Lancet | volume = 354 | issue = 9188 | pages = 1435–9 | date = October 1999 | pmid = 10543671 | doi = 10.1016/S0140-6736(99)01376-8 | s2cid = 3854642 | url = https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(99)01376-8/abstract | url-access = subscription }}</ref> Results revealed that in the sleep-debt condition, thyrotropin concentrations were decreased, while lowered glucose and insulin responses indicated a clear impairment of carbohydrate tolerance, a 30% decrease than in the well-rested sleep condition.<ref name=":0" /> Males who were sleep-restricted also showed significantly elevated concentrations of evening cortisol (the "stress" hormone) and elevated sympathetic nervous system activity in comparison to those who enjoyed a full sleep, throughout 6 nights.<ref name=":0" /><ref name=":2">{{cite journal | vauthors = Bayon V, Leger D, Gomez-Merino D, Vecchierini MF, Chennaoui M | title = Sleep debt and obesity | journal = Annals of Medicine | volume = 46 | issue = 5 | pages = 264–72 | date = August 2014 | pmid = 25012962 | doi = 10.3109/07853890.2014.931103 | s2cid = 36653608 | doi-access = free }}</ref> Losing so much sleep could lead to many chronic health problems that could include: heart disease, kidney disease, high blood pressure, diabetes, stroke, obesity, and depression. As stated by the [[National Institutes of Health]],<ref>{{cite web | url=https://www.nhlbi.nih.gov/health/sleep-deprivation | title=Sleep Deprivation and Deficiency - What Are Sleep Deprivation and Deficiency? &#124; NHLBI, NIH | date=24 March 2022 }}</ref> chronic sleep debt has a detrimental impact on human neurophysiological functioning and can disrupt immune, endocrine, and metabolic function, while increasing the severity of cardiovascular and age-related illnesses over a period of time.<ref name=":0" />

== Neuropsychological effects of sleep debt on emotions ==

Accumulated and continuous short-term sleep deficit has been shown to increase and intensify psychophysiological reactions in humans to emotional stimuli.<ref name="Motomura_2013">{{cite journal | vauthors = Motomura Y, Kitamura S, Oba K, Terasawa Y, Enomoto M, Katayose Y, Hida A, Moriguchi Y, Higuchi S, Mishima K | title = Sleep debt elicits negative emotional reaction through diminished amygdala-anterior cingulate functional connectivity | journal = PLOS ONE | volume = 8 | issue = 2 | pages = e56578 | date = 2013 | pmid = 23418586 | pmc = 3572063 | doi = 10.1371/journal.pone.0056578 | bibcode = 2013PLoSO...856578M | doi-access = free }}</ref> The [[amygdala]] plays a strong functional role in the expression of negative emotions such as fear, and, through its anatomical connections with the [[medial prefrontal cortex]] (mPFC), has an important function in the subjective suppression of and the reframing and reappraisal of negative emotions.<ref name="Motomura_2013" /> A study assessing sleep deficit in young Japanese men over a 5-day period (during which they slept only 4 hours per day) showed that there was greater left amygdala activation to fearful faces but not happy faces, and an overall subjective mood deterioration.<ref name="Motomura_2013" /> As a result, even short-term continuous sleep debt, or deprivation, has been shown to reduce this functional relationship between the amygdala and mPFC, inducing negative mood changes through increased fear and anxiety to unpleasant emotional stimuli and events.<ref>{{cite journal | vauthors = Minkel JD, Banks S, Htaik O, Moreta MC, Jones CW, McGlinchey EL, Simpson NS, Dinges DF | title = Sleep deprivation and stressors: evidence for elevated negative affect in response to mild stressors when sleep deprived | journal = Emotion | volume = 12 | issue = 5 | pages = 1015–20 | date = October 2012 | pmid = 22309720 | pmc = 3964364 | doi = 10.1037/a0026871 }}</ref> Thus, a full and uninterrupted 7-hour sleep is crucial for the proper functioning of the amygdala in modulating an individual's mood states—by reducing negative emotional intensities and increasing reactivity to positive emotional stimuli.<ref name="Motomura_2013" />

== Sleep debt and obesity ==
{{Main|Sleep and weight}}
Epidemiological research has solidified the association between sleep debt or deprivation and [[obesity]] as a result of an elevated [[body mass index]] (BMI) through various ways, such as disruptions in the hormones [[leptin]] and [[ghrelin]] that regulate appetite, higher food consumption and poor diets, and a decrease in overall calorie burning.<ref name=":2" /> However, in recent years, multimedia usages such as Internet and television consumption that play an active role in sleep deficit have also been linked to obesity by provoking{{clarify|date=August 2023|reason=need a better word here}} unhealthy, sedentary lifestyles and habits, as well as higher food consumption.<ref name=":2" /> Moreover, work-related behaviors such as long working and commuting hours and irregular work timings such as during shift work also function as contributing factors to being overweight or obese as a result of shorter sleeping periods.<ref name=":2" /> In comparison to adults, children exhibit a more consistent association between sleep debt and obesity.<ref name=":2" />

== Sleep debt and mortality ==

Several studies have shown that sleep duration, specifically sleep deficit or shorter sleep duration, predicts mortality, whether it be on weekdays or weekends.<ref name=":1" /> In people aged 65 years and younger, daily sleep duration of 5 hours or less (amounting to a sleep deficit of 2 hours per day) during weekends correlated with a 52% higher mortality rate—as compared to a control group who slept for 7 hours.<ref name=":1">{{cite journal | vauthors = Åkerstedt T, Ghilotti F, Grotta A, Zhao H, Adami HO, Trolle-Lagerros Y, Bellocco R | title = Sleep duration and mortality - Does weekend sleep matter? | journal = Journal of Sleep Research | volume = 28 | issue = 1 | pages = e12712 | date = February 2019 | pmid = 29790200 | doi = 10.1111/jsr.12712 | pmc = 7003477 | doi-access = free }}</ref> Consistent weekday sleep debt exhibited a detrimental association with mortality and morbidity, but this effect was negated when compensated with long sleep during weekends.<ref name=":1" /><ref>{{Cite journal|last1=Grandner|first1=Michael A.|last2=Hale|first2=Lauren|last3=Moore|first3=Melisa|last4=Patel|first4=Nirav P.|date=June 2010|title=Mortality associated with short sleep duration: The evidence, the possible mechanisms, and the future|journal=Sleep Medicine Reviews|language=en|volume=14|issue=3|pages=191–203|doi=10.1016/j.smrv.2009.07.006|pmc=2856739|pmid=19932976}}</ref> However, the harmful consequences of sleep debt over weekdays and weekends were not seen in individuals aged 65 years and older.<ref name=":1" />

==Scientific debate==

There is debate among researchers as to whether the concept of sleep debt describes a measurable phenomenon. The September 2004 issue of the journal ''Sleep'' contains dueling editorials from two leading sleep researchers, [[David F. Dinges]]<ref>{{cite journal | vauthors = Dinges DF | title = Sleep debt and scientific evidence | journal = Sleep | volume = 27 | issue = 6 | pages = 1050–2 | date = September 2004 | pmid = 15532196 | authorlink1 = David F. Dinges }}</ref> and [[Jim Horne (neuroscientist)|Jim Horne]].<ref>{{cite journal | vauthors = Horne J | title = Is there a sleep debt? | journal = Sleep | volume = 27 | issue = 6 | pages = 1047–9 | date = September 2004 | pmid = 15532195 }}</ref> A 1997 experiment conducted by psychiatrists at the [[Perelman School of Medicine at the University of Pennsylvania|University of Pennsylvania School of Medicine]] suggested that cumulative nocturnal sleep debt affects daytime sleepiness, particularly on the first, second, sixth, and seventh days of sleep restriction.<ref>{{cite journal | vauthors = Dinges DF, Pack F, Williams K, Gillen KA, Powell JW, Ott GE, Aptowicz C, Pack AI | title = Cumulative sleepiness, mood disturbance, and psychomotor vigilance performance decrements during a week of sleep restricted to 4-5 hours per night | journal = Sleep | volume = 20 | issue = 4 | pages = 267–77 | date = April 1997 | pmid = 9231952 }}</ref>

In one study, subjects were tested using the [[psychomotor vigilance task]] (PVT). Different groups of people were tested with different sleep times for two weeks: 8 hours, 6 hours, 4 hours, and total [[sleep deprivation]]. Each day, they were tested for the number of lapses on the PVT. The results showed that, as time went by, each group's performance worsened, with no sign of any stopping point. Moderate sleep deprivation was found to be detrimental; people who slept 6 hours a night for 10 days had similar results to those who were completely sleep deprived for 1 day.<ref>Walker, M.P. (2009, October 21). *Sleep Deprivation III: Brain consequences – Attention, concentration and real life.* Lecture given in Psychology 133 at the University of California, Berkeley, CA.</ref><ref>{{cite journal | vauthors = Knutson KL, Spiegel K, Penev P, Van Cauter E | title = The metabolic consequences of sleep deprivation | journal = Sleep Medicine Reviews | volume = 11 | issue = 3 | pages = 163–78 | date = June 2007 | pmid = 17442599 | pmc = 1991337 | doi = 10.1016/j.smrv.2007.01.002 | authorlink1 = Kristen L Knutson }}</ref>

==Evaluation==

Sleep debt has been tested in a number of studies through the use of a [[sleep onset latency]] test.<ref>{{cite journal | vauthors = Klerman EB, Dijk DJ | title = Interindividual variation in sleep duration and its association with sleep debt in young adults | journal = Sleep | volume = 28 | issue = 10 | pages = 1253–9 | date = October 2005 | pmid = 16295210 | pmc = 1351048 | doi = 10.1093/sleep/28.10.1253 }}</ref> This test attempts to measure how easily a person can fall asleep. When this test is done several times during the day, it is called a [[multiple sleep latency test]] (MSLT). The subject is told to go to sleep and is awakened after determining the amount of time it took to fall asleep. The [[Epworth Sleepiness Scale]] (ESS), an eight-item questionnaire with scores ranging from 0 to 24, is another tool used to screen for potential sleep debt.

A January 2007 study from [[Washington University in St. Louis]] suggests that saliva tests of the enzyme [[amylase]] could be used to indicate sleep debt, as the enzyme increases its activity in correlation with the length of time a subject has been deprived of sleep.<ref>{{cite web |date=January 25, 2007 |title=First Biomarker for Human Sleepiness Identified |url=https://record.wustl.edu/news/page/normal/8539.html |publisher=[[Washington University in St. Louis]]}}</ref>

The control of wakefulness has been found to be strongly influenced by the protein [[orexin]]. A 2009 study from Washington University in St. Louis has illuminated important connections between sleep debt, orexin, and [[amyloid beta]], with the suggestion that the development of [[Alzheimer's disease]] could hypothetically be a result of chronic sleep debt or excessive periods of wakefulness.<ref name="kang">{{cite journal | vauthors = Kang JE, Lim MM, Bateman RJ, Lee JJ, Smyth LP, Cirrito JR, Fujiki N, Nishino S, Holtzman DM | title = Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle | journal = Science | volume = 326 | issue = 5955 | pages = 1005–7 | date = November 2009 | pmid = 19779148 | pmc = 2789838 | doi = 10.1126/science.1180962 | bibcode = 2009Sci...326.1005K }}</ref>

==Phosphorylation of proteins==

In mice, there are 80 proteins in the brain, called "sleep need index phosphoproteins" (SNIPPs), which become more and more [[phosphorylated]] during waking hours, and are dephosphorylated during sleep. The phosphorylation is aided by the gene Sik3. A type of [[laboratory mouse]] (named Sleepy) possesses an altered version of this protein, which is called SLEEPY, where the protein is more active than the regular version. This results in the mice showing more [[slow-wave sleep]] activity during non-REM sleep—a reliable indicator that more sleep is met.{{Clarify|date=December 2023}} Inhibition of the Sik3 gene decreases phosphorylation and slow-wave activity in both normal and modified mice.<ref>{{cite journal | vauthors = Wang Z, Ma J, Miyoshi C, Li Y, Sato M, Ogawa Y, Lou T, Ma C, Gao X, Lee C, Fujiyama T, Yang X, Zhou S, Hotta-Hirashima N, Klewe-Nebenius D, Ikkyu A, Kakizaki M, Kanno S, Cao L, Takahashi S, Peng J, Yu Y, Funato H, Yanagisawa M, Liu Q | title = Quantitative phosphoproteomic analysis of the molecular substrates of sleep need | journal = Nature | volume = 558 | issue = 7710 | pages = 435–439 | date = June 2018 | pmid = 29899451 | pmc = 6350790 | doi = 10.1038/s41586-018-0218-8 | bibcode = 2018Natur.558..435W }}</ref>

== See also ==

*[[Excessive daytime sleepiness]]
*[[Hypersomnia]]
*[[Insomnia]]

== References ==

{{Reflist}}

== Further reading ==
* {{cite book | last = Dement | first = William C. | title = The Promise of Sleep | publisher = Delacorte Press, Random House Inc. | location = New York | date = 1999 }}

== External links ==

* [https://web.archive.org/web/20051025003046/http://www.harvardmagazine.com/on-line/070587.html ''Harvard Magazine'' article, "Deep into Sleep"]
* [https://www.livescience.com/health/lost-sleep-catch-up-100113.html Lost Sleep Can't Be Made Up, Study Suggests] – [[LiveScience]]

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[[Category:Sleeplessness and sleep deprivation]]
[[Category:Sleep physiology]]
[[Category:Sleep medicine]]
[[Category:Sleep disorders]]