Sleep debt

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Main health effects of sleep deprivation, indicating impairment of normal maintenance by sleep Effects of sleep deprivation.svg
Main health effects of sleep deprivation, 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, and can adversely affect one's mood, energy, and ability to think clearly.

Contents

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 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 § Scientific debate), and it is not considered to be a disorder.[ citation needed ]

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, 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. [2] 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. [2] 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. [2] [3] 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, [4] 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. [2]

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. [5] 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. [5] 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. [5] 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. [6] 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. [5]

Sleep debt and obesity

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. [3] 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[ clarification needed ] unhealthy, sedentary lifestyles and habits, as well as higher food consumption. [3] 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. [3] In comparison to adults, children exhibit a more consistent association between sleep debt and obesity. [3]

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. [7] 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. [7] Consistent weekday sleep debt exhibited a detrimental association with mortality and morbidity, but this effect was negated when compensated with long sleep during weekends. [7] [8] However, the harmful consequences of sleep debt over weekdays and weekends were not seen in individuals aged 65 years and older. [7]

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 [9] and Jim Horne. [10] A 1997 experiment conducted by psychiatrists at the 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. [11]

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. [12] [13]

Evaluation

Sleep debt has been tested in a number of studies through the use of a sleep onset latency test. [14] 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. [15]

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. [16]

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.[ clarification needed ] Inhibition of the Sik3 gene decreases phosphorylation and slow-wave activity in both normal and modified mice. [17]

See also

Related Research Articles

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<span class="mw-page-title-main">Sleep disorder</span> Medical disorder of a persons sleep patterns

A sleep disorder, or somnipathy, is a medical disorder of an individual's sleep patterns. Some sleep disorders are severe enough to interfere with normal physical, mental, social and emotional functioning. Sleep disorders are frequent and can have serious consequences on patients' health and quality of life. Polysomnography and actigraphy are tests commonly ordered for diagnosing sleep disorders.

<span class="mw-page-title-main">Insomnia</span> Disorder causing trouble with sleeping

Insomnia, also known as sleeplessness, is a sleep disorder where people have trouble sleeping. They may have difficulty falling asleep, or staying asleep for as long as desired. Insomnia is typically followed by daytime sleepiness, low energy, irritability, and a depressed mood. It may result in an increased risk of accidents of all kinds as well as problems focusing and learning. Insomnia can be short term, lasting for days or weeks, or long term, lasting more than a month. The concept of the word insomnia has two possibilities: insomnia disorder (ID) and insomnia symptoms, and many abstracts of randomized controlled trials and systematic reviews often underreport on which of these two possibilities the word insomnia refers to.

<span class="mw-page-title-main">Orexin</span> Neuropeptide that regulates arousal, wakefulness, and appetite.

Orexin, also known as hypocretin, is a neuropeptide that regulates arousal, wakefulness, and appetite. It exists in the forms of orexin-A and orexin-B. The most common form of narcolepsy, type 1, in which the individual experiences brief losses of muscle tone, is caused by a lack of orexin in the brain due to destruction of the cells that produce it.

Shift work is an employment practice designed to keep a service or production line operational at all times. The practice typically sees the day divided into shifts, set periods of time during which different groups of workers perform their duties. The term "shift work" includes both long-term night shifts and work schedules in which employees change or rotate shifts.

<span class="mw-page-title-main">Obstructive sleep apnea</span> Sleeping and breathing disorder

Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder and is characterized by recurrent episodes of complete or partial obstruction of the upper airway leading to reduced or absent breathing during sleep. These episodes are termed "apneas" with complete or near-complete cessation of breathing, or "hypopneas" when the reduction in breathing is partial. In either case, a fall in blood oxygen saturation, a disruption in sleep, or both, may result. A high frequency of apneas or hypopneas during sleep may interfere with the quality of sleep, which – in combination with disturbances in blood oxygenation – is thought to contribute to negative consequences to health and quality of life. The terms obstructive sleep apnea syndrome (OSAS) or obstructive sleep apnea–hypopnea syndrome (OSAHS) may be used to refer to OSA when it is associated with symptoms during the daytime.

Shift work sleep disorder (SWSD) is a circadian rhythm sleep disorder characterized by insomnia, excessive sleepiness, or both affecting people whose work hours overlap with the typical sleep period. Insomnia can be the difficulty to fall asleep or to wake up before the individual has slept enough. About 20% of the working population participates in shift work. SWSD commonly goes undiagnosed, so it's estimated that 10–40% of shift workers have SWSD. The excessive sleepiness appears when the individual has to be productive, awake and alert. Both symptoms are predominant in SWSD. There are numerous shift work schedules, and they may be permanent, intermittent, or rotating; consequently, the manifestations of SWSD are quite variable. Most people with different schedules than the ordinary one might have these symptoms but the difference is that SWSD is continual, long-term, and starts to interfere with the individual's life.

<span class="mw-page-title-main">Psychomotor vigilance task</span> A psychometric test of attention

A psychomotor vigilance task (PVT) is a sustained-attention, reaction-timed task that measures the consistency with which subjects respond to a visual stimulus. Research indicates increased sleep debt or sleep deficit correlates with deteriorated alertness, slower problem solving, declined psychomotor skills, and increased rate of false responses.

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<span class="mw-page-title-main">Sleep deprivation</span> Condition of not having enough sleep

Sleep deprivation, also known as sleep insufficiency or sleeplessness, is the condition of not having adequate duration and/or quality of sleep to support decent alertness, performance, and health. It can be either chronic or acute and may vary widely in severity. All known animals sleep or exhibit some form of sleep behavior, and the importance of sleep is self-evident for humans, as nearly a third of a person's life is spent sleeping.

<span class="mw-page-title-main">Narcolepsy</span> Human sleep disorder

Narcolepsy is a chronic neurological disorder that impairs the ability to regulate sleep–wake cycles, and specifically impacts REM sleep. The pentad symptoms of narcolepsy include excessive daytime sleepiness (EDS), sleep related hallucinations, sleep paralysis, disturbed nocturnal sleep (DNS) and cataplexy. There are two recognized forms of narcolepsy, narcolepsy type 1 and type 2. Narcolepsy type 1 (NT1) can be clinically characterized by symptoms of EDS and cataplexy, and/or will have CSF orexin levels of less than 110 pg/ml. Cataplexy are transient episodes of aberrant tone, most typically loss of tone, that can be associated with strong emotion. In pediatric onset narcolepsy, active motor phenomena are not uncommon. Cataplexy may be mistaken for syncope, tic disorder or seizures. Narcolepsy type 2 (NT2) does not have features of cataplexy and CSF orexin levels are normal. Sleep related hallucinations, also known as hypnogogic and hypnopompic are vivid hallucinations that can be auditory, visual or tactile and may occur independent of or in combination with an inability to move. People with narcolepsy tend to sleep about the same number of hours per day as people without it, but the quality of sleep is typically compromised. Narcolepsy is a clinical syndrome of hypothalamic disorder, but the exact cause of narcolepsy is unknown, with potentially several causes. A leading consideration for the cause of narcolepsy type 1 is that it is an autoimmune disorder. Proposed pathophysiology as an autoimmune disease suggest antigen presentation by DQ0602 to specific CD4+ T cells resulting in CD8+ T-cell activation and consequent injury to orexin producing neurons. Familial trends of narcolepsy are suggested to be higher than previously appreciated. Familial risk of narcolepsy among first degree relatives is high. Relative risk for narcolepsy in a first degree relative has been reported to be 361.8. However, it is important to note that there is a spectrum of symptoms found in this study, including asymptomatic abnormal sleep test findings to significantly symptomatic.

<span class="mw-page-title-main">Nap</span> Short period of sleep during typical waking hours

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<span class="mw-page-title-main">Suvorexant</span> Medication used to treat insomnia

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Sleep and weight is the association between the amount of sleep an individual obtains and the weight of that individual.

<span class="mw-page-title-main">Sleep and emotions</span>

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<span class="mw-page-title-main">Sleep deprivation in higher education</span> Health issue in students

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References

  1. ↑ Reference list is found on image page on Wikimedia Commons: Commons:File:Effects of sleep deprivation.svg#References.
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  4. ↑ "Sleep Deprivation and Deficiency - What Are Sleep Deprivation and Deficiency? | NHLBI, NIH". 24 March 2022.
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  12. ↑ 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.
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  15. ↑ "First Biomarker for Human Sleepiness Identified". Washington University in St. Louis. January 25, 2007.
  16. ↑ Kang JE, Lim MM, Bateman RJ, Lee JJ, Smyth LP, Cirrito JR, Fujiki N, Nishino S, Holtzman DM (November 2009). "Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle". Science. 326 (5955): 1005–7. Bibcode:2009Sci...326.1005K. doi:10.1126/science.1180962. PMC   2789838 . PMID   19779148.
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