|Minor periorbital dark circles, in addition to a hint of eye bags - a combination suggestive of minor sleep deprivation.|
A chronic sleep-restricted state can cause fatigue, daytime sleepiness, clumsiness and increased appetite leading to weight gain. It adversely affects the brain and cognitive function. However, in a subset of cases sleep deprivation can, paradoxically, lead to increased energy and alertness and enhanced mood; although its long-term consequences have never been evaluated, it has even been used as a treatment for depression.
Few studies have compared the effects of acute total sleep deprivation and chronic partial sleep restriction. Complete absence of sleep over long periods is not frequent in humans (unless they suffer from fatal familial insomnia or specific issues caused by surgery); it appears that brief microsleeps cannot be avoided. Long-term total sleep deprivation has caused death in lab animals.
- 1 Physiological effects
- 2 Uses
- 3 Causes
- 4 Treatment
- 5 Changes in American sleep habits
- 6 Longest periods without sleep
- 7 See also
- 8 References
Generally, sleep deprivation may result in:
- aching muscles
- confusion, memory lapses or loss
- development of false memory
- hypnagogic and hypnopompic hallucinations during falling asleep and waking, which are entirely normal
- hand tremor
- periorbital puffiness, commonly known as "bags under eyes" or eye bags
- increased blood pressure
- increased stress hormone levels
- increased risk of Type 2 diabetes
- lowering of immunity, increased susceptibility to illness
- increased risk of fibromyalgia
- nystagmus (rapid involuntary rhythmic eye movement)
- temper tantrums in children
- violent behavior
- Sleep Inertia
- symptoms similar to:
Type 2 DiabetesEdit
It has been suggested that people experiencing short-term sleep restrictions process glucose more slowly than individuals receiving a full 8 hours of sleep, increasing the likelihood of developing type 2 diabetes. In 2005, a study of over 1400 participants showed that participants who habitually slept few hours were more likely to have associations with type 2 diabetes. However, because this study was merely correlational, the direction of cause and effect between little sleep and diabetes is uncertain. The authors point to an earlier study which showed that experimental rather than habitual restriction of sleep resulted in impaired glucose tolerance (IGT).
On the brainEdit
Sleep deprivation can adversely affect the brain and cognitive function. A 2000 study, by the University of California, San Diego School of Medicine and the Veterans Affairs Healthcare System in San Diego, used functional magnetic resonance imaging (fMRI) technology to monitor activity in the brains of sleep-deprived subjects performing simple verbal learning tasks. The study showed that regions of the brain's prefrontal cortex, an area that supports mental faculties such as working memory and logical and practical ("means-ends") reasoning, displayed more activity in sleepier subjects. Researchers interpreted this result as indicating that the brain of the average sleep-deprived subject had to work harder than that of the average non-sleep-deprived subject to accomplish a given task. They therefore concluded that the brains of sleep-deprived subjects were attempting to compensate for adverse effects caused by sleep deprivation.
The temporal lobe, a brain region involved in language processing, was activated during verbal learning in rested subjects but not in sleep-deprived subjects. The parietal lobe, not activated in rested subjects during the verbal exercise, was more active when the subjects were deprived of sleep. Getting less than the required number of hours needed to function leads to a decline in memory and judgement, this change in brain chemicals often leads to depression. Although memory performance was less efficient with sleep deprivation, greater activity in the parietal region was associated with better short term memory.
A link between sleep deprivation and psychosis was documented in 2007 through a study at Harvard Medical School and the University of California at Berkeley. The study revealed, using MRI scans, that sleep deprivation causes the brain to become incapable of putting an emotional event into the proper perspective and incapable of making a controlled, suitable response to the event.
The negative effects of sleep deprivation on alertness and cognitive performance suggest decreases in brain activity and function. These changes primarily occur in two regions: the thalamus, a structure involved in alertness and attention; and the prefrontal cortex, a region sub-serving alertness, attention, and higher-order cognitive processes. This was the finding of an American study in 2000. Seventeen men in their 20s were tested. Sleep deprivation was progressive with measurements of glucose (absolute regional CMRglu), cognitive performance, alertness, mood, and subjective experiences collected after 0, 24, 48, and 72 hours of sleep deprivation. Additional measures of alertness, cognitive performance, and mood were collected at fixed intervals. PET scans were used and attention was paid to the circadian rhythm of cognitive performance.
A noted 2002 University of California animal study indicated that non-rapid eye movement sleep (NREM) is necessary for turning off neurotransmitters and allowing their receptors to "rest" and regain sensitivity which allows monoamines (norepinephrine, serotonin and histamine) to be effective at naturally produced levels. This leads to improved regulation of mood and increased learning ability. The study also found that rapid eye movement sleep (REM) deprivation may alleviate clinical depression because it mimics selective serotonin reuptake inhibitors (SSRIs). This is because the natural decrease in monoamines during REM is not allowed to occur, which causes the concentration of neurotransmitters in the brain, that are depleted in clinically depressed persons, to increase. Sleep outside of the REM phase may allow enzymes to repair brain cell damage caused by free radicals. High metabolic activity while awake damages the enzymes themselves preventing efficient repair. This study observed the first evidence of brain damage in rats as a direct result of sleep deprivation.
Animal studies suggest that sleep deprivation increases levels of stress hormones, which may reduce new cell production in adult brains.
A 1999 study found that sleep deprivation resulted in reduced cortisol secretion the next day, driven by increased subsequent slow-wave sleep. Sleep deprivation was found to enhance activity on the hypothalamic-pituitary-adrenal axis (which controls reactions to stress and regulates body functions such as digestion, the immune system, mood, sex, or energy usage) while suppressing growth hormones. The results supported previous studies, which observed adrenal insufficiency in idiopathic hypersomnia.
On the healing processEdit
A study conducted in 2005 showed that a group of rats, which were deprived of REM sleep for five days, experienced no significant changes in their ability to heal wounds, compared to a group of rats not deprived of "dream" sleep. The rats were allowed deep (NREM) sleep. However, another study conducted by Gumustekin et al. in 2004 showed sleep deprivation hindering the healing of burns on rats. A prime reason for this could be the fact that extended periods without sleep have a genuine impact on the body's immune system.
On attention and working memoryEdit
Among the possible physical consequences of sleep deprivation, deficits in attention and working memory are perhaps the most important; such lapses in mundane routines can lead to unfortunate results, from forgetting ingredients while cooking to missing a sentence while taking notes. Performing tasks that require attention appears to be correlated with number of hours of sleep received each night, declining as a function of hours of sleep deprivation. Working memory is tested by such methods as choice-reaction time tasks.
The attentional lapses also extend into more critical domains in which the consequences can be life-or-death; car crashes and industrial disasters can result from inattentiveness attributable to sleep deprivation. To empirically measure the magnitude of attention deficits, researchers typically employ the psychomotor vigilance task (PVT) which requires the subject to press a button in response to a light at random intervals. Failure to press the button in response to the stimulus (light) is recorded as an error, attributable to the microsleeps that occur as a product of sleep deprivation.
Crucially, individuals' subjective evaluations of their fatigue often do not predict actual performance on the PVT. While totally sleep-deprived individuals are usually aware of the degree of their impairment, lapses from chronic (lesser) sleep deprivation can build up over time so that they are equal in number and severity to the lapses occurring from total (acute) sleep deprivation. Chronically sleep-deprived people, however, continue to rate themselves considerably less impaired than totally sleep-deprived participants. Since people usually evaluate their capability on tasks like driving subjectively, their evaluations may lead them to the false conclusion that they can perform tasks that require constant attention when their abilities are in fact impaired.
On driving abilityEdit
The dangers of sleep deprivation are apparent on the road; the American Academy of Sleep Medicine (AASM) reports that one in every five serious motor vehicle injuries is related to driver fatigue, with 80,000 drivers falling asleep behind the wheel every day and 250,000 accidents every year related to sleep, though the National Highway Traffic Safety Administration suggests the figure for traffic accidents may be closer to 100,000. The AASM recommends pulling off the road and taking a 15- or 20-minute nap to alleviate drowsiness.
According to a 2000 study published in the British Medical Journal, researchers in Australia and New Zealand reported that sleep deprivation can have some of the same hazardous effects as being drunk. People who drove after being awake for 17–19 hours performed worse than those with a blood alcohol level of 0.05 percent, which is the legal limit for drunk driving in most western European countries and Australia. Another study suggested that performance begins to degrade after 16 hours awake, and 21 hours awake was equivalent to a blood alcohol content of 0.08 percent, which is the blood alcohol limit for drunk driving in Canada, the U.S., and the U.K.
Fatigue of drivers of goods trucks and passenger vehicles have come to the attention of authorities in many countries, where specific laws have been introduced with the aim of reducing the risk of traffic accidents due to driver fatigue. Rules concerning minimum break lengths, maximum shift lengths and minimum time between shifts are common in the driving regulations used in different countries and regions, such as the drivers' working hours regulations in the European Union and hours of service regulations in the United States.
The Exxon Valdez Oil Spill was the second largest oil spill in the United States. This accident occurred when an Exxon oil tanker struck a reef at the Prince William Sound in Alaska. Approximately 10.8 million gallons of oil spilled into the sea. The accident caused great environmental damage including the death of hundreds of thousands of birds and sea creatures. Fatigue and sleep deprivation were the major contributors to the accident. The captain of the ship was asleep after a night of heavy drinking; he was severely fatigued and had been awake for 18 hours. The entire crew was suffering from fatigue and inadequate sleep. 
On sleep transitionEdit
Sleep propensity (SP) can be defined as the readiness to transit from wakefulness to sleep, or the ability to stay asleep if already sleeping. Sleep deprivation increases this propensity, who can be measured by polysomnography (PSG) as a reduction in sleep latency (the time needed to fall asleep). An indicator of sleep propensity can also be seen in the shortening of transition from light stages of non-REM sleep to deeper slow-waves oscillations can also be measured as indicator of sleep propensity.
In average, the latency in healthy adults decreases by a few minutes after a night without sleep, and the latency from sleep onset to slow-wave sleep is halved. Sleep latency is generally measured with the multiple sleep latency test (MSLT). In contrast, the maintenance of wakefulness test (MWT) also uses sleep latency, but this time as a measure of the capacity of the participants to stay awake (when asked to) instead of falling asleep.
On sleep-wake cycleEdit
Research studying sleep deprivation show its impact on mood, cognitive and motor functioning, due to dysregulation of the sleep-wake cycle and augmented sleep propensity. Multiple studies that identified the role of hypothalamus and multiple neural systems controlling circadian rhythms and homeostasis have been helpful to understand sleep deprivation better. To describe the temporal course of the sleep-wake cycle, the two-process model of sleep regulation can be mentioned.
This model proposes a homeostatic process (process S) and a circadian process (Process C) that interact to define the time and intensity of sleep. Process S represents the drive for sleep, increasing during wakefulness and decreasing during sleep, until a defined threshold level, while process C is the oscillator responsible for these levels. When being sleep deprived, homeostatic pressure accumulates to the point that waking functions will be degraded even at the highest circadian drive for wakefulness.
In addition, as a result of continuous muscular activity without proper rest time, effects such as cramping are much more frequent in sleep-deprived individuals. Extreme cases of sleep deprivation have been reported to be associated with hernias, muscle fascia tears, and other such problems commonly associated with physical overexertion.
A 2006 study has shown that while total sleep deprivation for one night caused many errors, the errors were not significant until after the second night of total sleep deprivation. However, combining alcohol with acute sleep deprivation results in a tripled rate of driving off the road when using a simulator.
The National Sleep Foundation identifies several warning signs that a driver is dangerously fatigued. These include rolling down the window, turning up the radio, trouble keeping eyes open, head-nodding, drifting out of their lane, and daydreaming. At particular risk are lone drivers between midnight and 6:00am.
Sleep deprivation can negatively impact overall performance, and has led to major fatal accidents. Due largely to the February 2009 crash of Colgan Air Flight 3407, which killed 50 people and was partially attributed to pilot fatigue, the FAA reviewed its procedures to ensure that pilots are sufficiently rested. Air traffic controllers were under scrutiny when in 2010 there were 10 incidents of controllers falling asleep while on shift. The common practice of turn-around shifts caused sleep deprivation and was a contributing factor to all air traffic control incidents. The FAA reviewed its practices of shift changes and the findings saw that controllers were not well rested. A 2004 study also found medical residents with less than four hours of sleep a night made more than twice as many errors as the 11% of surveyed residents who slept for more than seven hours a night.
Twenty-four hours of continuous sleep deprivation results in the choice of less difficult math tasks without decreases in subjective reports of effort applied to the task. Naturally caused sleep loss affects the choice of everyday tasks such that low effort tasks are mostly commonly selected. Adolescents who experience less sleep show a decreased willingness to engage in sports activities that require effort through fine motor coordination and attention to detail.
Great sleep deprivation mimics psychosis: distorted perceptions can lead to inappropriate emotional and behavioral responses.
Astronauts have reported performance errors and decreased cognitive ability during periods of extended working hours and wakefulness as well as due to sleep loss caused by circadian rhythm disruption and environmental factors.
Microsleeps occur when a person has a significant sleep deprivation. Microsleeps usually last for a few seconds and happen most frequently when a person is trying to stay awake when they are feeling sleepy. The person usually falls into microsleep while doing a monotonous task like driving, reading a book, or staring at a computer. Microsleeps are similar to blackouts and a person experiencing them is not consciously aware that they are occurring.
An even lighter type of sleep has been seen in rats that have been kept awake for long periods of time. In a process known as local sleep, specific localized brain regions went into periods of short (~80 ms) but frequent (~40/min) NREM-like states. Despite the on and off periods where neurons shut off, the rats appeared to be awake, although they performed poorly at tests.
In rats, prolonged, complete sleep deprivation increased both food intake and energy expenditure with a net effect of weight loss and ultimately death. This study hypothesizes that the moderate chronic sleep debt associated with habitual short sleep is associated with increased appetite and energy expenditure with the equation tipped towards food intake rather than expenditure in societies where high-calorie food is freely available.
Several large studies using nationally representative samples suggest that one of the causes of high obesity rates in the United States might be a corresponding decrease in the average number of hours that people are sleeping. The findings suggest that this might be happening because sleep deprivation could be disrupting hormones that regulate glucose metabolism and appetite. Leptin is one of the hormones that communicate with one's brain to indicate that the body is full. When one becomes sleep deprived, leptin levels decrease, resulting in a more aggressive appetite.
The association between sleep deprivation and obesity appears to be strongest in young and middle-age adults. Other scientists hold that the physical discomfort of obesity and related problems, such as sleep apnea, reduce an individual's chances of getting a good night's sleep.[by whom?]
Sleep loss is currently[timeframe?] proposed to disturb endocrine regulation of energy homeostasis leading to weight gain and obesity. For instance, laboratory sleep deprivation studies in young men have demonstrated that one night of wakefulness (typically found in shift workers) exerts significant effects on the energy balance the next morning, including reduced energy expenditure, enhanced hedonic stimulus processing in the brain underlying the drive to consume food, and overeating that goes beyond satiety. Further recent studies have shown that a reduction of sleep duration to four hours for two consecutive nights has been shown to decrease circulating leptin levels and to increase ghrelin levels, as well as self-reported hunger. Similar endocrine alterations have been shown to occur even after a single night of sleep restriction.
In a balanced order, nine healthy normal-weight men spent three nights in a sleep laboratory separated by at least two weeks: one night with a total sleep time of seven hours, one night with a total sleep time of 4.5 hours, and one night with total sleep deprivation (SD). On a standard symptom-rating scale, subjects rated markedly stronger feelings of hunger after total SD than after seven hours of sleep (3.9 ± 0.7 versus 1.7 ± 0.3; P = 0.020) or 4.5 hours sleep (2.2 ± 0.5; P = 0.041). Plasma ghrelin levels were 22 ± 10% higher after total SD than after seven hours of sleep (0.85 ± 0.06 versus 0.72 ± 0.04 ng mL(−1); P = 0.048) with intermediate levels of the hormone after 4.5 hours sleep (0.77 ± 0.04 ng mL(−1)). Feelings of hunger as well as plasma ghrelin levels are already elevated after one night of SD, whereas morning serum leptin concentrations remain unaffected. Thus, the results provide further evidence for a disturbing influence of sleep loss on endocrine regulation of energy homeostasis, which in the long run may result in weight gain and obesity.
Scientific study of laboratory animalsEdit
In science, sleep deprivation (of rodents, e.g.) is used in order to study the function(s) of sleep and the biological mechanisms underlying the effects of sleep deprivation.
Some sleep deprivation techniques are:
- Gentle handling: during the sleep deprivation period, the animal and its polysomnograph record are continuously observed; when the animal displays sleep electrophysiological signals or assumes a sleep posture, it is given objects to play with and activated by acoustic and, if necessary, tactile stimuli. Although subjective, this technique is used for total sleep deprivation as well as REM or NREM sleep deprivation. This technique often requires polysomnography.
- Single platform: during the sleep deprivation period, the animal is placed on an inverted flower pot, the bottom diameter of which is small relative to the animal's size (usually 7 cm for adult rats). The pot is placed in a large tub filled with water to within 1 cm of the flower pot bottom. The animal is able to rest on the pot and is even able to get NREM sleep, but at the onset of REM sleep, with its ensuing muscular relaxation, it will either fall into the water and clamber back to its pot or will get its nose wet enough to awaken it. Thus, this technique is only useful for studying REM sleep deprivation. This was one of the first scientific methods developed (see Jouvet, 1964 for cats and for rodents).
- Multiple platform: in an effort to reduce the elevated stress response induced by the single platform method, researchers developed the "multiple platform" technique of REM sleep deprivation. In this configuration, the animal is placed within a large tank containing multiple platforms, thereby eliminating the movement restriction in the earlier setup.
- Modified multiple platform: modification of the multiple platform method where several animals together experience sleep deprivation (Nunes and Tufik, 1994).
- Pendulum: animals are prevented from entering into REM sleep by allowing them to sleep for only brief periods of time. This is accomplished by an apparatus that moves the animals' cages backwards and forwards in a pendular motion. At the extremes of the motion, the animals experience postural imbalance, forcing them to walk back and forth to retain their balance.
To help facilitate abusive controlEdit
Under one interrogation technique, a subject might be kept awake for several days and when finally allowed to fall asleep, suddenly awakened and questioned. Menachem Begin, the Prime Minister of Israel from 1977 to 1983, described his experience of sleep deprivation as a prisoner of the NKVD in Russia as follows:
In the head of the interrogated prisoner, a haze begins to form. His spirit is wearied to death, his legs are unsteady, and he has one sole desire: to sleep... Anyone who has experienced this desire knows that not even hunger and thirst are comparable with it.
Sleep deprivation was one of the five techniques used by the British government in the 1970s. The European Court of Human Rights ruled that the five techniques "did not occasion suffering of the particular intensity and cruelty implied by the word torture ... [but] amounted to a practice of inhuman and degrading treatment", in breach of the European Convention on Human Rights.
The United States Justice Department released four memos in August 2002 describing interrogation techniques used by the Central Intelligence Agency. They first described 10 techniques used in the interrogation of Abu Zubaydah, described as a terrorist logistics specialist, including sleep deprivation. Memos signed by Steven G. Bradbury in May 2005 claimed that forced sleep deprivation for up to 180 hours (7 1⁄2 days) by shackling a diapered prisoner to the ceiling did not constitute torture, nor did the combination of multiple interrogation methods (including sleep deprivation) constitute torture under United States law. These memoranda were repudiated and withdrawn during the first months of the Obama administration.
The question of extreme use of sleep deprivation as torture has advocates on both sides of the issue. In 2006, Australian Federal Attorney-General Philip Ruddock argued that sleep deprivation does not constitute torture. Nicole Bieske, a spokeswoman for Amnesty International Australia, has stated the opinion of her organization thus: "At the very least, sleep deprivation is cruel, inhumane and degrading. If used for prolonged periods of time it is torture."
Studies show that sleep restriction has some potential in the treatment of depression. Those who suffer from depression tend to have earlier occurrences of REM sleep with an increased number of rapid eye movements; therefore, monitoring patients' EEG and awakening them during occurrences of REM sleep appears to have a therapeutic effect, alleviating depressive symptoms. This kind of treatment is known as wake therapy. As many as 60% of patients, when sleep-deprived, show immediate recovery, although most relapse the following night. The effect has been shown to be linked to increases in the brain-derived neurotrophic factor (BDNF). It has been shown that chronotype is related to the effect of sleep deprivation on mood in normal people: those with morningness preference become more depressed following sleep deprivation while those with eveningness preference show an improvement in mood. A comprehensive evaluation of the human metabolome in sleep deprivation in 2014 found that 27 metabolites are increased after 24 waking hours and suggested serotonin, tryptophan, and taurine may contribute to the antidepressive effect.
The incidence of relapse can be decreased by combining sleep deprivation with medication or a combination of light therapy and phase advance (going to bed substantially earlier than ones normal time). Many tricyclic antidepressants suppress REM sleep, providing additional evidence for a link between mood and sleep. Similarly, tranylcypromine has been shown to completely suppress REM sleep at adequate doses.
Sleep deprivation can be implemented for a short period of time in the treatment of insomnia. Some common sleep disorders have been shown to respond to cognitive behavioral therapy for insomnia. One of the components is a controlled regime of "sleep restriction" in order to restore the homeostatic drive to sleep and encourage normal "sleep efficiency". The main goal of stimulus control and sleep restriction therapy is to create an association between bed and sleep. Taken on its own, sleep restriction therapy measures have not yet proven to show efficacy. Sleep restriction therapy does show efficacy when applied as an element of cognitive-behavioral therapy.
Insomnia, one of the six types of dyssomnia, affects 21%-37% of the adult population. Many of its symptoms are easily recognizable, including excessive daytime sleepiness; frustration or worry about sleep; problems with attention, concentration, or memory; extreme mood changes or irritability; lack of energy or motivation; poor performance at school or work; and tension headaches or stomach aches.
Primary insomnia is a sleep disorder not attributable to a medical, psychiatric, or environmental cause. There are three main types of primary insomnia. These include: psychophysiological, idiopathic insomnia, and sleep state misperception (paradoxical insomnia). Psychophysiological insomnia is anxiety-induced. Idiopathic insomnia generally begins in childhood and lasts the rest of a person’s life. It’s suggested that idiopathic insomnia is a neurochemical problem in a part of the brain that controls the sleep-wake cycle, resulting in either under-active sleep signals or over-active wake signals. Sleep state misperception is diagnosed when people get enough sleep but inaccurately perceive that their sleep is insufficient.
Secondary insomnia, or comorbid insomnia, occurs concurrently with other medical, neurological, psychological and psychiatric conditions. Causation is not necessarily implied.
Sleep is known to be cumulative. This means that the fatigue and sleep one lost as a result, for example, staying awake all night, would be carried over to the following day. Not getting enough sleep a couple days cumulatively builds up a deficiency and that's when all the symptoms of sleep deprivation come in. When one is well rested and healthy, the body naturally spends not as much time in the REM stage of sleep. The more time one's body spends in REM sleep, causes one to be exhausted, less time in that stage will promote more energy when awakened.
Sleep deprivation can sometimes be self-imposed due to a lack of desire to sleep or the habitual use of stimulant drugs. Sleep deprivation is also self-imposed to achieve personal fame in the context of record-breaking stunts.
Obstructive sleep apnea is often caused by collapse of the upper airway during sleep, which reduces airflow to the lungs. It has many serious health outcomes if untreated. Positive airway pressure therapy using a CPAP (Continuous positive airway pressure), APAP or BPAP devices is considered to be the first line treatment option for sleep apnea. Mandibular displacement devices in some cases can reposition the jaw and tongue to prevent the airway from collapsing. For some patients supplemental oxygen therapy may be indicated. Nasal problems such as a deviated septum will shut down the airway and increase swelling in the mucus lining and nasal turbinates. Corrective surgery (septoplasty) in some cases may be an appropriate choice of treatment.
Central Sleep apnea is caused by a failure of the central nervous system to signal the body to breathe during sleep. Treatments similar to obstructive sleep apnea may be used as well as other treatments such as Adaptive Servo Ventilation and certain medications. Some medications such as opioids may contribute to or cause central sleep apnea.
The specific causal relationships between sleep loss and effects on psychiatric disorders have been most extensively studied in patients with mood disorders. Shifts into mania in bipolar patients are often preceded by periods of insomnia, and sleep deprivation has been shown to induce a manic state in susceptible individuals. Sleep deprivation may represent a final common pathway in the genesis of mania, and sleep loss is both a precipitating and reinforcing factor for the manic state.
The National Sleep Foundation cites a 1996 paper showing that college/university-aged students got an average of less than 6 hours of sleep each night. A 2018 study highlights the need for a good night's sleep for students finding that college students who averaged eight hours of sleep for the five nights of finals week scored higher on their final exams than those who didn’t.
In the study, 70.6% of students reported obtaining less than 8 hours of sleep, and up to 27% of students may be at risk for at least one sleep disorder. Sleep deprivation is common in first year college students as they adjust to the stress and social activities of college life.
There is not enough evidence to determine potential benefits or adverse effects related to later school times for adolescents. In 1997, University of Minnesota research compared students who started school at 7:15 am with those who started at 8:40 am. They found that students who started at 8:40 got higher grades and more sleep on weekday nights than those who started earlier. One in four U.S. high school students admits to falling asleep in class at least once a week.
It is known that during human adolescence, circadian rhythms and therefore sleep patterns typically undergo marked changes. Electroencephalogram (EEG) studies indicate a 50% reduction of deep (stage 4) sleep and a 75% reduction in the peak amplitude of delta waves during NREM sleep in adolescence. School schedules are often incompatible with a corresponding delay in sleep offset, leading to a less than optimal amount of sleep for the majority of adolescents.
A study performed nationwide in the Netherlands found that general ward patients staying at the hospital experienced shorter total sleep (83 min. less), more night-time awakenings, and earlier awakenings compared to sleeping at home. Over 70% experienced being woken up by external causes, such as hospital staff (35.8%). Sleep disturbing factors included noise of other patients, medical devices, pain, and toilet visits. Sleep deprivation is even more severe in ICU patients, where the naturally occurring nocturnal peak of melatonin secretion was found to be absent, possibly causing the disruption in the normal sleep-wake cycle. However, as the personal characteristics and the clinical picture of hospital patients are so diverse, the possible solutions to improve sleep and circadian rhythmicity should be tailored to the individual and within the possibilities of the hospital ward. Multiple interventions could be considered to aid patient characteristics, improve hospital routines, or the hospital environment.
Study published in the Journal of Economic Behavior and Organisation found out that the broadband internet connection caused sleep deprivation. The study concluded that the people with a broadband connection tend to sleep 25 minutes less than those without the broadband connection, hence they are less likely to get the scientifically recommended 7–9 hours of sleep.
Sleep deprivation is not a disease but rather a symptom of illnesses such as insomnia. Several strategies are common in attempting to increase alertness and counteract the effects of sleep deprivation. Caffeine is often used over short periods to boost wakefulness when acute sleep deprivation is experienced; however, caffeine is less effective if taken routinely. Other strategies recommended by the American Academy of Sleep Medicine include prophylactic sleep before deprivation, naps, other stimulants, and combinations thereof. However, the only sure and safe way to combat sleep deprivation is to increase nightly sleep time.
Recovery of cognitive function is accomplished more rapidly after acute total sleep deprivation than after chronic partial sleep restriction. Chronic deprivation is the more common in everyday life. Just one night of recovery sleep can reverse adverse effects of total sleep deprivation. Recovery sleep is more efficient than normal sleep with shorter sleep latency and increased amounts of deep and REM sleep.
For long term involuntary sleep deprivation, cognitive behavioral therapy for Insomnia (CBT-i) is now commonly recommended as a first-line treatment, after exclusion of physical diagnosis (f.e. sleep apnea). CBT-i contains five different components: cognitive therapy, stimulus control, sleep restriction, sleep hygiene, and relaxation. These components together have shown to be effective in adults, with clinical meaningful effect sizes As this approach has minimal adverse adverse effects, and long-term benefits, it is often preferred to (chronic) drug therapy.
Changes in American sleep habitsEdit
The examples and perspective in this section may not represent a worldwide view of the subject. (December 2010) (Learn how and when to remove this template message)
National Geographic Magazine has reported that the demands of work, social activities, and the availability of 24-hour home entertainment and Internet access have caused people to sleep less now than in premodern times. USA Today reported in 2007 that most adults in the USA get about an hour less than the average sleep time 40 years ago.
Other researchers have questioned these claims. A 2004 editorial in the journal Sleep stated that according to the available data, the average number of hours of sleep in a 24-hour period has not changed significantly in recent decades among adults. Furthermore, the editorial suggests that there is a range of normal sleep time required by healthy adults, and many indicators used to suggest chronic sleepiness among the population as a whole do not stand up to scientific scrutiny.
A comparison of data collected from the Bureau of Labor Statistics' American Time Use Survey from 1965–1985 and 1998–2001 has been used to show that the median amount of sleep, napping, and resting done by the average adult American has changed by less than 0.7%, from a median of 482 minutes per day from 1965 through 1985, to 479 minutes per day from 1998 through 2001.
Longest periods without sleepEdit
Randy Gardner holds the scientifically documented record for the longest period of time a human being has intentionally gone without sleep not using stimulants of any kind. Gardner stayed awake for 264 hours (11 days), breaking the previous record of 260 hours held by Tom Rounds of Honolulu. LCDR John J. Ross of the U.S. Navy Medical Neuropsychiatric Research Unit later published an account of this event, which became well-known among sleep-deprivation researchers.
Claims of total sleep deprivation lasting years have been made several times, but none are scientifically verified. Claims of partial sleep deprivation are better documented. For example, Rhett Lamb of St. Petersburg, Florida was initially reported to not sleep at all, but actually had a rare condition permitting him to sleep only one to two hours per day in the first three years of his life. He had a rare abnormality called an Arnold-Chiari malformation where brain tissue protrudes into the spinal canal and the skull puts pressure on the protruding part of the brain. The boy was operated on at All Children's Hospital in St. Petersburg in May 2008. Two days after surgery he slept through the night.
French sleep expert Michel Jouvet and his team reported the case of a patient who was quasi-sleep-deprived for four months, as confirmed by repeated polygraphic recordings showing less than 30 minutes (of stage-1 sleep) per night, a condition they named "agrypnia". The 27-year-old man was suffering from Morvan's fibrillary chorea, a rare disease that leads to involuntary movements, and in this particular case, extreme insomnia. The researchers found that treatment with 5-HTP restored almost normal sleep stages. However some months after this recovery the patient died during a relapse which was unresponsive to 5-HTP. Despite the extreme insomnia, psychological investigation showed no sign of cognitive deficits, except for some hallucinations.
Fatal familial insomnia is a neurodegenerative disease eventually resulting in a complete inability to go past stage 1 of NREM sleep. In addition to insomnia, patients may experience panic attacks, paranoia, phobias, hallucinations, rapid weight loss, and dementia. Death usually occurs between 7 and 36 months from onset.
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