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Insufficient sleep: Definition, epidemiology, and adverse outcomes

Insufficient sleep: Definition, epidemiology, and adverse outcomes
Literature review current through: May 2024.
This topic last updated: Mar 13, 2024.

INTRODUCTION — Chronic sleep insufficiency is common in modern society and may result from a variety of factors, including work demands, social and family responsibilities, medical conditions, and sleep disorders. As sleep debt accumulates, individuals may experience reduced performance, increased risk for accidents and death, and detrimental effects on both psychological and physical health.

Sleep has two dimensions: duration (quantity) and depth (quality). When individuals fail to obtain adequate duration or quality of sleep, daytime alertness and function suffer. In response to sleep deprivation, sleep is often both longer and deeper. In many cases, however, sleep intensity can change without major changes in sleep duration. Sleep duration alone is therefore not a good indicator of how much sleep is needed to feel refreshed in the morning and function properly.

The definition, epidemiology, causes, and consequences of acute sleep deprivation and sleep insufficiency are reviewed here. The evaluation and management of insufficient sleep are reviewed separately. Insomnia, which is distinct from sleep deprivation, is also reviewed separately. (See "Insufficient sleep: Evaluation and management" and "Risk factors, comorbidities, and consequences of insomnia in adults" and "Evaluation and diagnosis of insomnia in adults".)

DEFINITIONS — Sleep insufficiency exists when sleep is insufficient to support adequate alertness, performance, and health, either because of reduced total sleep time (decreased quantity) or fragmentation of sleep by brief arousals (decreased quality) (table 1).

Acute sleep deprivation refers to no sleep or a reduction in the usual total sleep time, usually lasting one or two days. Chronic sleep insufficiency (also called sleep restriction) exists when an individual routinely sleeps less than the amount required for optimal functioning.

Chronic sleep insufficiency is sometimes confused with insomnia (table 2). Although both conditions may be characterized by decreased quantity of sleep and impaired daytime function, chronic sleep insufficiency is due to volitional partial sleep loss or insufficient opportunity to sleep. Sleep-deprived individuals will rapidly fall asleep if given the opportunity, whereas individuals with insomnia are unable to fall asleep, even though they feel fatigued during the day. (See "Evaluation and diagnosis of insomnia in adults".)

The International Classification of Sleep Disorders, Third Edition, Text Revision (ICSD-3-TR) recognizes insufficient sleep syndrome as a disorder characterized by excessive daytime sleepiness caused by curtailed sleep almost every day for at least three months (table 1) [1].

HOW MUCH SLEEP DO WE NEED? — It is difficult to determine what constitutes a normal quantity of sleep for a given individual (figure 1). One approach involves determining how long a patient would sleep if left to awaken spontaneously. An alternative approach involves determining how alert the patient feels after different durations of sleep. Alertness is normal if the patient wakes feeling refreshed and is capable of moving through the day feeling alert without effort, even when placed in boring or monotonous situations.

Sleep need varies significantly among individuals and across the lifespan [2]. While most adults report sleeping six to eight hours per night, some otherwise healthy individuals may be short sleepers, requiring less than six hours of sleep per night without the need for catch-up sleep to feel refreshed. Others may report the need for ten or more hours of sleep per night. Even in children and adolescents, there is surprisingly little scientific evidence to recommend a fixed amount of sleep hours [3].

To reflect this interindividual variability, the National Sleep Foundation has updated their recommendations for daily sleep amounts across the lifespan, clarifying that the average recommended amount of hours "may be appropriate," but varies significantly among subjects, and new ranges for each age group were given [4]. While the range of sleep for newborns narrowed, sleep for all age groups widened by one to two hours (figure 1). The American Academy of Sleep Medicine (AASM) and the Sleep Research Society recommend that adults sleep seven or more hours per night on a regular basis to promote optimal health [5]. The AASM recommendations for sleep in children vary slightly compared with those of the National Sleep Foundation. (See "Assessment of sleep disorders in children", section on 'Insufficient sleep'.)

EPIDEMIOLOGY — Approximately one-third of adults report sleeping less than seven hours per night on weekdays or workday nights [6-9].

In the United States, groups most likely to report insufficient nightly sleep include Hispanic Americans, non-Hispanic Black Americans, native Americans including Alaska natives, and younger adults (<65 years of age) [7,8,10-14]. Other studies have found that both short and long sleep duration are more prevalent among Black compared with White Americans and among those with low socioeconomic status [15,16].

Short sleep duration also varies by occupation and industry. Population-based studies of United States workers have found an increased prevalence of short sleep duration in those with long or extended work hours, rotating or shift work, and increased job-related stress [17-19]. Analysis of the American Time Use Survey (ATUS) found that sleep time was most often exchanged with paid work time and commuting to and from work [20].

The prevalence of short sleep duration may be increasing over time. In a study that utilized time diaries from eight population-based studies conducted between 1975 and 2006, the prevalence of short sleep (<6 hours per night) increased from 7.6 percent in 1975 to 9.3 percent in 2006 [21]. The odds of short sleep duration were increased in full-time workers, males, those with some college education, and African Americans. A meta-analysis that included over 690,000 children in 20 countries found that children’s sleep had decreased by 0.75 minutes per year over the last century; the rate of change was greatest on school days, for older children, and males [22].

CONTRIBUTING FACTORS — Sleep insufficiency may be a consequence of a reduced amount of sleep and/or poor quality sleep.

Insufficient quantity of sleep — A sleep deficit may arise acutely (if full nights of sleep are missed) or it may build up more gradually if sleep is partially restricted on multiple nights. Cumulative partial sleep deprivation can be equivalent to acute total sleep deprivation but may be much harder for the patient and clinician to recognize [23].

A nightly reduction in sleep below the normal quantity of sleep for an individual may not have clear effects on performance or subjective sleepiness if the total sleep is not six hours or less. Sensitive instruments like the psychomotor vigilance test may detect decrements, but individuals may otherwise appear to adapt to the sleep loss as long as the nightly sleep duration remains in the range of six to nine hours. Short naps may restore full alertness [24].

A return to normal sleep quotas after a period of sleep deprivation results in rebound sleep. This means that deep sleep and rapid eye movement (REM) sleep will appear in quantities higher than expected for several nights after normal sleep duration has resumed if these stages of sleep had been reduced below their usual quantities during sleep deprivation. It appears that deep sleep will rebound first and REM second, but this may be an artifact of experimental methods that did not allow sufficient time in bed.

Poor quality sleep — It is possible for an individual to sleep eight or more hours and still be sleep deprived. In such cases, the sleep deprivation is usually due to disturbances in the quality of sleep [25].

Sleep quality is determined by the number of arousals (or awakenings) from sleep during the night, as well as the percentage, duration, and type of sleep stages. As few as five arousals per hour of sleep can result in daytime sleepiness and/or performance deficits, even after a single night of disruption [26]. Patients are unaware of the arousals, in part because their duration is only seconds and then the individual returns to the same sleep stage that was interrupted. Arousals are usually due to sleep disorders (eg, sleep apnea, periodic leg movements), but they may also occur spontaneously.

In one study, performance deficits equivalent to 40 to 60 hours of total sleep deprivation developed after sleep was experimentally disrupted 60 times per hour for two consecutive days [27]. Even repetitive administration of acoustic tones that fail to result in electroencephalographic arousal will result in objectively measured increases in daytime sleepiness and measurable alterations in mood [26]. Such tones will also nullify the positive effects of sleep on the consolidation of some memory tasks [28]. Experimental manipulations of sleep quality suggest that sleep disorders such as sleep apnea, which cause significant sleep fragmentation, may result in severely sleep-deprived patients.

EFFECTS OF ACUTE SLEEP DEPRIVATION — In laboratory and real-world settings, acute and accumulated sleep deprivation result in measurable changes in cognitive performance, alertness, and neurobehavioral function. Susceptibility to such changes varies among individuals and based on circadian factors.

Cognitive effects — Cognitive impairment is the most prominent effect of total sleep deprivation as well as sleep restriction for several nights [29-32]. In laboratory settings, sleeping less than seven hours per night results in cumulative deficits in behavioral alertness and vigilant attention [33,34].

Sleep-deprived individuals tend to take longer to respond to stimuli, particularly when tasks are monotonous and associated with low cognitive demands. Tasks requiring sustained attention can be impaired by even a few hours of sleep loss. In a study involving 48 subjects who were randomly assigned to four, six, or eight hours of sleep per night for 14 days, or a three-night period without sleep, restriction of sleep to six hours or less per night produced cognitive performance deficits equivalent to two nights of total sleep deprivation [35]. For subjects in all groups, wakefulness in excess of 16 hours predicted performance lapses. Of note, subjects appeared to be largely unaware of these increasing cognitive deficits, based on their own assessments.

Tasks that rely on higher cognitive functions are also significantly affected, even after one single night of sleep deprivation, including: logical reasoning and parsing complex sentences, complex subtraction tasks, and tasks involving a flexible thinking style and the ability to focus on a large number of goals simultaneously. Functional neuroimaging demonstrates a corresponding decrease in brain activation in the frontoparietal attention network (prefrontal cortex and intraparietal sulcus) and in the salience network (insula and medial frontal cortex) [36]. Other data suggest that certain aspects of executive function, such as working memory, may be less vulnerable to sleep loss [37]. However, even when sleep-deprived subjects perform at a normal level, they often report the need for greater effort to maintain performance [38].

Studies in health care professionals support the potential consequences of sleep deprivation on cognition and work performance. As an example, medical interns make more frequent serious diagnostic errors when they work frequent shifts of 24 hours or more than when they work shorter shifts [39]. A subsequent study confirmed that work schedules with fewer (≤16) consecutive working hours increase sleep duration, but also found that this benefit did not result in a better work experience for clinicians due to increased workload and short between-shift intervals [40]. In another study involving performance of screening colonoscopies, the adenoma detection rate was lower when clinicians had performed emergent on-call procedures the night before [41].

The extent of cognitive impairment varies as a function of the amount of nightly sleep obtained prior to the sleep restriction period, with more prior sleep having a protective effect [42]. Chronic sleep restriction likely triggers long-term neural changes, so that a single night of recovery may not be sufficient to recover all neurobiological functions [43]. In sleep-restricted adolescents, catch-up sleep during the weekend, even when combined with napping, is not enough to maintain sustained attention at the levels afforded by a nine-hour sleep opportunity each night [44].

The effects of acute sleep deprivation can also be seen at the cellular level. Increasingly, data suggest that cognitive impairment seen after sleep deprivation and sleep restriction is not exclusively due to sleepiness but also to progressive cellular dysfunction in cortical and other circuits that have been awake too long, a veritable form of neuronal "tiredness" [45-47].

Mood and judgment — Sleep deprivation may result in a mental status that resembles depression or anxiety [48], with patients reporting poor mood, irritability, low energy, decreased libido, poor judgment, and other signs of psychologic dysfunction. These symptoms often disappear when normal sleep is restored.

Sleepiness and microsleeps — Sleep deprivation results in a powerful drive for sleep that is not always under the control of the individual. This drive allows for sleep to intrude into wakefulness for only a few seconds whenever there is a lack of physical activity, such as driving. Such lapses are referred to as microsleeps.

Even such brief periods of sleep can result in serious or catastrophic consequences [30]. A car driving 60 miles per hour will travel more than 250 feet during a three-second microsleep and, if the road curves or a car stops in front of the driver, a serious accident may occur. Microsleeps also make performance inconsistent and unreliable [49]. As an example, a sleepy driver will either respond normally to an emergency or not at all, due to rapid changes in vigilance state and the sudden intrusion of microsleeps during waking.

Attentional deficits caused by sleep loss can be studied in the laboratory using specific quantitative tests. The most validated of these is the psychomotor vigilance test (PVT), which records response times to visual stimuli that occur at random 2- to 10-second interstimulus intervals over a 6- to 10-minute period. Sleep deprivation causes an overall slowing of response times, a steady increase in the number of errors of omission (ie, lapses of attention, usually defined as response times ≥500 ms), and a more modest increase in the number of errors of commission (ie, responses without a stimulus). These effects are associated with changes in neural activity in distributed areas of the cerebral cortex and thalamus, and they can increase as time on task increases [29-31].

Respiratory physiology — Sleep deprivation has been reported to depress ventilatory responses to hypercapnia and hypoxia in otherwise normal subjects, suggesting that sleep deprivation could contribute to hypoventilation in hospitalized patients [50-52]. However, these findings have not been universal, suggesting that such results may be an artifact of uncontrolled factors or environmental influences [53]. A study in rats found that sleep fragmentation for 24 hours attenuates the hypercapnic (but not hypoxic) ventilatory response [54].

Respiratory muscle endurance can also be affected by sleep deprivation [55]. Specifically, inspiratory muscle endurance is significantly decreased, while end-tidal PCO2 is increased. Effects of sleep deprivation on cardiopulmonary functioning may be much greater in patients with existing disease, including those with chronic obstructive pulmonary disease (COPD) or neuromuscular disease [56]. (See "Sleep-related breathing disorders in COPD" and "The effect of sleep in patients with neuromuscular and chest wall disorders".)

Circadian factors — The effects of sleep restriction are strongly modulated by time of day. In studies using a forced desynchrony protocol, which teases apart the variance in neurobehavioral function due to the circadian clock relative to the sleep homeostatic drive, the effects of sleep restriction are more obvious at night or in the early morning and less obvious in the late afternoon and early evening [29]. The circadian phase of lowest performance tends to be quite consistent across tasks, coincides with the peak of subjective sleepiness, and occurs three to four hours after the nadir of core body temperature. The interaction of the circadian and homeostatic processes is nonlinear, however, and may vary among subjects.

During sleep deprivation (eg, due to shift work or jet lag), sleep and wakefulness may become disconnected from their proper body temperature associations. If this occurs, the body may be physiologically prepared for sleep during the daytime, when the individual should be alert and active. The individual may be unable to sleep at socially acceptable times and/or may have to arise before a biologically optimal time. This may result in a reduction of total sleep time until the sleep-wake rhythm is realigned with core body temperature. Such patients may be sleepy regardless of the prior quantity and quality of sleep [57]. (See "Sleep-wake disturbances in shift workers".)

Interindividual variation — The effects of sleep deprivation vary significantly among individuals, but are quite stable within individuals [58]. It seems that individuals more vulnerable to the adverse neurobehavioral effects of chronic sleep restriction are also more vulnerable to acute sleep deprivation [59,60].

The ability to predict who will or will not be able to tolerate partial or total sleep deprivation has many practical applications, including shift work and sustained military operations [58]. Vulnerability or resistance to sleep deprivation does not appear to depend on demographic factors, IQ, or sleep need; instead, it has been shown to have trait-like qualities, suggesting a genetic predisposition [61]. A few candidate genes that may predict vulnerability to sleep loss have been identified. However, it is still impossible to establish a direct link between phenotypic differential vulnerability to the neurobehavioral effects of sleep loss and genetic polymorphisms [59].

Studies using advanced magnetic resonance imaging (MRI) techniques suggest that differences in hippocampal morphology or the microstructure of white and gray matter can predict interindividual differences in the resistance to sleep loss [62-65].

CONSEQUENCES OF CHRONIC SLEEP INSUFFICIENCY — In addition to measurable effects on neurocognitive function and alertness, chronic sleep insufficiency has been associated with a variety of adverse outcomes in observational studies. Potential consequences include reduced performance, increased risk for accidents and death, and detrimental effects on both psychological and physical health.

Accidents and workplace errors — Acute and cumulative sleep deprivation are often work-related. Work-related situations that can result in sleep insufficiency include compressed work time to obtain more consecutive time off, early start times, long work days, night shifts, extended shifts, shift rotation, consecutive work periods, unpredictable work schedules, and unstable work schedules [66,67].

Excessive sleepiness is a common cause of car crashes and near misses and contributes to over half of all fatal truck crashes in the United States. Sleep deficiency due to sleep apnea or insufficient sleep duration is associated with increased risk of motor vehicle accidents even in people who do not report excessive sleepiness [68]. The impact of sleep deprivation on driving performance is exacerbated by coexisting obstructive sleep apnea [69] and alcohol consumption [70,71]. (See "Drowsy driving: Risks, evaluation, and management".)

Occupational errors are also more common among individuals with sleep insufficiency [39,72]. This was illustrated by a prospective cohort study of 4957 police officers, of whom 2003 (40 percent) screened positive for at least one sleep disorder (mostly obstructive sleep apnea) [73]. Individuals who screened positive for any sleep disorder were significantly more likely to make an administrative error at work (18 versus 13 percent), to fall asleep while driving (14 versus 9 percent), to commit an error or safety violation due to fatigue (24 versus 16 percent), to exhibit uncontrolled anger toward suspects (34 versus 29 percent), to be absent from work (26 versus 21 percent), and to fall asleep during meetings (14 versus 7 percent).

Quality of life — Individuals frequently report that their quality of life suffers as a result of chronic sleep insufficiency. They often cut back on activities they enjoy, claiming that they do not have enough energy to perform the activity. Inappropriate drowsiness and unplanned naps may be a source of embarrassment and friction, both at home and at work. Patients who fall asleep at work or whose productivity suffers due to sleepiness may be reprimanded, denied advancement, or fired. Falling asleep at home may cause resentment and marital discord.

Cardiovascular morbidity — Short sleep duration has been associated with a variety of adverse cardiovascular outcomes [74-80]. In scientific statements from the American Heart Association, sleep restriction is recognized as a risk factor for adverse cardiometabolic profiles and outcomes, and healthy sleep behavior is recommended to promote ideal cardiac health, along with efforts to address other established risk factors including blood pressure, cholesterol, diet, blood glucose, physical activity, weight, and smoking cessation [81,82].

Representative prospective studies demonstrating this association include the following:

In a prospective study of over 160,000 healthy, nonobese adults age 20 to 80 years, self-reported sleep duration <6 hours per day was independently associated with increased risk for development of multiple cardiometabolic risk factors over an 18-year follow-up period, including central obesity (hazard ratio [HR] 1.12), elevated fasting glucose (HR 1.06), hypertension (HR 1.08), low high-density lipoprotein (HR 1.07), hypertriglyceridemia (HR 1.09), and metabolic syndrome (HR 1.09) [83]. Approximately 19 percent of the cohort reported short sleep duration, and the presence or absence of insomnia symptoms did not modify the effects of sleep duration.

In the United Kingdom Biobank prospective cohort study of nearly 500,000 adults age 40 to 69 years and free of cardiovascular disease at baseline, habitual sleep duration <6 hours per day by self-report was associated with a 20 percent increase in the risk of incident myocardial infarction (MI) over a median follow-up of seven years [84]. Long sleep duration (>9 hours per night) was also identified as a risk factor (HR 1.34). A Mendelian randomization analysis supported a causal link and estimated that one additional hour of sleep per night would decrease the risk of MI by 20 percent.

Among healthy middle-aged adults, short sleep duration has been associated with a higher burden of subclinical noncoronary atherosclerosis. In one large cross-sectional study that included nearly 4000 adults 40 to 54 years of age without a history of CVD or obstructive sleep apnea, those with the shortest sleep duration on seven-day actigraphy (<6 hours per night) had increased atherosclerotic plaque burden as measured by carotid and femoral vascular ultrasound, independent of conventional CVD risk factors [85].

Inflammation is one plausible mechanism for the observed relationship between short sleep duration and CVD. In laboratory experiments, acute sleep loss is associated with the induction of several proinflammatory markers, including C-reactive protein (CRP) [86,87]. Even a relatively mild restriction of sleep (eg, from eight to six hours for eight days) increases the level of pro-inflammatory cytokines.

Poor quality and quantity of sleep may have arrhythmogenic effects on the heart as well, although the evidence is not entirely consistent. In a large retrospective cohort study of over 31,000 adults undergoing diagnostic polysomnography (PSG), a one-hour reduction in sleep duration during PSG (used as a proxy for chronic sleep insufficiency) was associated with increased odds of both prevalent (odds ratio [OR] 1.17) and incident (OR 1.09) atrial fibrillation, independent of age, sex, body mass index, hypertension, CHD, heart failure, and sleep apnea severity [88]. In a 2018 meta-analysis of 10 observational studies in over 14 million individuals, self-reported insomnia and frequent awakenings were risk factors for atrial fibrillation (OR 1.3 and 1.4, respectively), whereas the association between short sleep duration and atrial fibrillation was not statistically significant (OR 1.20, 95% CI 0.93-1.55) [89].

Immunosuppression — Chronic sleep loss is not only associated with an increase in inflammatory markers but also with immunodeficiency [90]. The immune response to vaccination against influenza virus decreases after six days of restricted sleep [91]. There is also evidence for an enhanced susceptibility to the common cold with poor sleep efficiency [92]. Similar signs of an impaired immune defense have been described in rats subjected to excessive sleep deprivation [93,94].

Obesity and metabolism — Sleep restriction may have negative metabolic consequences that contribute to risk of obesity, metabolic syndrome, and associated conditions such as type 2 diabetes. Multiple observational studies have demonstrated an association between short sleep duration and obesity. In one of the larger prospective cohort studies that included over 3000 older adults without metabolic syndrome at baseline, those with a sleep duration ≤6 hours per night had threefold greater odds of developing metabolic syndrome over a five-year follow-up period [95]. Although causality has not been established, these studies suggest that sleep duration could be a modifiable risk factor. (See "Type 2 diabetes mellitus: Prevalence and risk factors", section on 'Sleep duration' and "Obesity in adults: Etiologies and risk factors", section on 'Sleep patterns'.)

Small studies in healthy adults undergoing experimentally-imposed sleep restriction have suggested possible mechanisms whereby short sleep duration contributes to weight gain and diabetes risk through effects on appetite and hormones such as leptin and ghrelin. (See "Obesity in adults: Etiologies and risk factors", section on 'Sleep patterns'.)

All-cause mortality — A large body of observational evidence has demonstrated that both short and long sleep duration, whether measured objectively or by self-report, are associated with increased all-cause mortality in a variety of populations [96-99].

In a representative meta-analysis that included 67 prospective cohort studies in over 3.5 million individuals, a U-shaped association was demonstrated for multiple endpoints (all-cause mortality, total cardiovascular disease, coronary heart disease, and stroke), with relative risk increasing in a dose-dependent manner for self-reported hours of sleep both below and above a reference point of seven hours of sleep per night [99]. The pooled relative risk (RR) estimate for all-cause mortality was 1.06 per one-hour reduction below seven hours per night and 1.13 per one-hour increase above seven hours per night.

Other studies have used accelerometry data to calculate a sleep regularity index based on day-to-day variations in sleep-wake timing. Such studies have found that low sleep regularity correlates with worse outcomes, and that sleep regularity may be a stronger predictor of mortality risk than sleep duration alone [100].

Others — One large prospective study found that self-reported short sleep duration (<7 hours per night) was associated with an increased rate of decline in renal function over an 11-year follow-up period, independent of established risk factors for chronic kidney disease (eg, hypertension, diabetes, and cardiovascular disease) [101]. Other studies have found that patients with chronic kidney disease, especially those with end-stage kidney disease, are at increased risk for sleep insufficiency as well other sleep disorders, including restless legs syndrome/Willis-Ekbom disease, sleep apnea, and chronic insomnia. (See "Sleep disorders in end-stage kidney disease".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Insomnia in adults" and "Society guideline links: Parasomnias, hypersomnias, and circadian rhythm disorders".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Sleep insufficiency (The Basics)")

SUMMARY

Definition – Sleep insufficiency exists when sleep is insufficient to support adequate alertness, performance, and health, either because of reduced total sleep time (decreased quantity) or fragmentation of sleep by brief arousals (decreased quality). (See 'Definitions' above.)

Contributing factors – Sleep insufficiency may be a consequence of a reduced amount of sleep and/or poor quality sleep. The effects of sleep restriction are also influenced by circadian factors. (See 'Contributing factors' above.)

Acute effects – Acute and accumulated sleep deprivation result in measurable changes in cognitive performance, alertness, and neurobehavioral function. Susceptibility to such changes varies among individuals and based on circadian factors. (See 'Effects of acute sleep deprivation' above.)

Chronic effects – Chronic sleep insufficiency has been associated with a variety of adverse outcomes in observational studies. Potential consequences include reduced performance, increased risk for accidents and death, and detrimental effects on both psychological and physical health. (See 'Consequences of chronic sleep insufficiency' above.)

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Topic 7715 Version 46.0

References

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