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Sleep is a natural state of bodily rest observed throughout the animal kingdom. It is common to all mammals and birds, and is also seen in many reptiles, amphibians and fish. In humans, other mammals, and a substantial majority of other animals which have been studied — such as fish, birds, ants, and fruit-flies — regular sleep is essential for survival.^[1] However, its purposes are only partly clear and are the subject of intense research.^[2]

Physiology

In mammals and birds the measurement of eye movement during sleep is used to divide sleep into the two broad types of Rapid Eye Movement (REM) and Non-Rapid Eye Movement (NREM) or "Non-REM" sleep. Each type has a distinct set of associated physiological, neurological and psychological features.

Sleep proceeds in cycles of REM and the four stages of NREM, the order normally being:

stages 1 -> 2 -> 3 -> 4 -> 3 -> 2 -> REM.

In humans this cycle is on average 90 to 110 minutes,^[3] with a greater amount of stages 3 and 4 early in the night and more REM later in the night. Each phase may have a distinct physiological function. Drugs such as sleeping pills and alcoholic beverages can suppress certain stages of sleep (see Sleep deprivation). This can result in a sleep that exhibits loss of consciousness but does not fulfill its physiological functions.

Allan Rechtschaffen and Anthony Kales originally outlined the criteria for identifying the stages of sleep in 1968. The American Academy of Sleep Medicine (AASM) updated the staging rules in 2007.

Stages of sleep

Criteria for REM sleep include not only rapid eye movements but also a rapid low voltage electroencephalogram EEG. In mammals, at least, low muscle tone is also seen. Most memorable dreaming occurs in this stage. NREM accounts for 75–80% of total sleep time in normal human adults. In NREM sleep, there is relatively little dreaming. Non-REM encompasses four stages; stages 1 and 2 are considered 'light sleep', and 3 and 4 'deep sleep' or slow-wave sleep, SWS. They are differentiated solely by using EEG, unlike REM sleep which is characterized by observable rapid eye movements and relative absence of muscle tone. In non-REM sleep there are often limb movements, and parasomnias such as sleepwalking may occur. A cyclical alternating pattern may sometimes be observed during a stage.

NREM consists of four stages according to the 2007 AASM standards:

During Stage N1 the brain transitions from alpha waves (having a frequency of 8 to 13 Hz, common to people who are awake) to theta waves (with a frequency of 4 to 7 Hz). This stage is sometimes referred to as somnolence, or "drowsy sleep". Associated with the onset of sleep during N1 may be sudden twitches and hypnic jerks also known as positive myoclonus. Some people may also experience hypnagogic hallucinations during this stage, which can be troublesome to them. During N1 the subject loses some muscle tone and most conscious awareness of the external environment.
Stage N2, is characterized by "sleep spindles" (12 to 16 Hz) and "K-complexes." During this stage, muscular activity as measured by electromyography (EMG) decreases and conscious awareness of the external environment disappears. This stage occupies 45 to 55% of total sleep.
In Stage N3, the delta waves (0.5 to 4 Hz), also called delta rhythms, make up less than 50% of the total wave-patterns. This is considered part of deep or slow-wave sleep (SWS) and appears to function primarily as a transition into stage N4. This is the stage in which night terrors, bedwetting, sleepwalking and sleep-talking occur.
In Stage N4, delta-waves make up more than 50% of the wave-patterns. Stages N3 and N4 are the deepest forms of sleep; N4 is effectively a deeper version of N3, in which the deep-sleep characteristics, such as delta-waves, are more pronounced. As of new AASM guidelines, the distinction between stage 3 and stage 4 sleep is inconsequential; both may be considered delta sleep or slow wave sleep. Therefore, in order to make the scoring guidelines more precise, a recent ruling by the AASM discontinued stage four sleep (N4) and left only stage N3 to describe delta sleep.^[4]

Both REM sleep and NREM sleep stages 3 and 4 are homeostatically driven; that is, a person or animal selectively deprived of one of these stages will rebound once uninhibited sleep is allowed. This finding suggests that both types of sleep are essential.

Sleep timing

Sleep timing is controlled by the circadian clock, by homeostasis and, in humans, by willed behavior. The circadian clock, an inner time-keeping, temperature-fluctuating, enzyme-controlling device, works in tandem with adenosine, a neurotransmitter which inhibits many of the bodily processes that are associated with wakefulness. Adenosine is created over the course of the day; high levels of adenosine lead to sleepiness. In diurnal animals, sleepiness occurs as the circadian element causes the release of the hormone melatonin and a gradual decrease in core body temperature. The timing is affected by one's chronotype. It is the circadian rhythm which determines the ideal timing of a correctly structured and restorative sleep episode.^[5]

Homeostatic sleep propensity, the need for sleep as a function of the amount of time elapsed since the last adequate sleep episode, is also important and must be balanced against the circadian element for satisfactory sleep. Along with corresponding messages from the circadian clock, this tells the body it needs to sleep.^[6] Sleep offset, awakening, is primarily determined by circadian rhythm. A normal person who regularly awakens at an early hour will generally not be able to sleep much later than the person's normal waking time, even if moderately sleep deprived.

Optimal amount in humans

Adults

The optimal amount of sleep is not a meaningful concept unless the timing of that sleep is seen in relation to an individual's circadian rhythms. A person's major sleep episode is relatively inefficient and inadequate when it occurs at the "wrong" time of day. The timing is correct when the following two circadian markers occur after the middle of the sleep episode but before awakening:^[7]

maximum concentration of the hormone melatonin, and
minimum core body temperature.

The National Sleep Foundation in the United States maintains that eight to nine hours of sleep for adult humans is optimal and that sufficient sleep benefits alertness, memory and problem solving, and overall health, as well as reducing the risk of accidents.^[8] A widely publicized 2003 study^[9] performed at the University of Pennsylvania School of Medicine demonstrated that cognitive performance declines with fewer than eight hours of sleep.

However, a University of California, San Diego psychiatry study of more than one million adults found that people who live the longest self-report sleeping for six to seven hours each night.^[10] Another study of sleep duration and mortality risk in women showed similar results.^[11] Other studies show that "sleeping more than 7 to 8 hours per day has been consistently associated with increased mortality", though this study suggests the cause is probably other factors such as depression and socio-economic status which would correlate statistically. ^[12] It has been suggested that the correlation between lower sleep hours and reduced morbidity only occurs with those who wake after less sleep naturally, rather than those who use an alarm.

Causal links are currently speculative: the available data may only reflect comorbid depression, socioeconomic status, or even alcohol use, for example.^[13] These studies cannot be used to determine optimal sleep habits, only correlation — and empirically observed correlation is a necessary but not sufficient condition for causality. A need for nine or ten hours of sleep a day, or only five to six, may or may not have the same cause as the shortened life span. In other words, long or short sleep duration itself has not been shown to be a cause of early death.

Researchers from the University of Warwick and University College London have found that lack of sleep can more than double the risk of death from cardiovascular disease, but that too much sleep can also double the risk of death.^[14]^[15] Professor Francesco Cappuccio said: “Short sleep has been shown to be a risk factor for weight gain, hypertension and Type 2 diabetes sometimes leading to mortality but in contrast to the short sleep-mortality association it appears that no potential mechanisms by which long sleep could be associated with increased mortality have yet been investigated. Some candidate causes for this include depression, low socioeconomic status and cancer-related fatigue. [...] In terms of prevention, our findings indicate that consistently sleeping around 7 hours per night is optimal for health and a sustained reduction may predispose to ill-health.”

Furthermore, sleep difficulties are closely associated with psychiatric disorders such as depression, alcoholism and bipolar disorder. Up to 90% of patients with depression are found to have sleep difficulties.^{[citation needed]}

Hours by age

Children need a greater amount of sleep per day than adults to develop and function properly: up to 18 hours for newborn babies, with a declining rate as a child ages.^[8]^[6] A newborn baby spends almost half of its sleep time in REM-sleep. By the age of five or so, only a bit over two hours are spent in REM.^[16]

Age	Average amount of sleep per day
Newborn	up to 18 hours
1–12 months	14–18 hours
1–3 years	12–15 hours
3–5 years	11–13 hours
5–12 years	9–11 hours
Adolescents	9–10 hours
Adults, including elderly	7–8 (+) hours
Pregnant women	8 (+) hours

Sleep debt

Sleep debt is the effect of not getting quite enough rest and sleep; a large debt causes mental, emotional and physical fatigue. It is unclear why a lack of sleep causes irritability; however theories are emerging that suggest if the body produces insufficient cortisol during stage 3 and 4 sleep it can have negative effects on our alertness and emotions during the day.^{[citation needed]}

Scientists do not agree on how much sleep debt it is possible to accumulate, whether it is accumulated against an individual's average sleep or some other benchmark, nor on whether the prevalence of sleep debt among adults has changed appreciably in the industrialized world in recent decades. It is likely that children are sleeping less than previously in western societies.^[17]

Functions

The multiple theories proposed to explain the function of sleep reflect the as yet incomplete understanding of the subject.

It is likely that sleep evolved to fulfill some primeval function, but has taken over multiple functions over time as organisms have evolved as with the larynx which today performs multiple functions such as controlling the passage of food and air, phonation for communicating, and social purposes.

Some of the many proposed functions of sleep are as follows.

Restoration

Wound healing has been shown to be affected by sleep. A study conducted by Gumustekin et al.^[18] in 2004 shows sleep deprivation hindering the healing of burns on rats.

It has also been shown that sleep deprivation affects the immune system and metabolism. In a study by Zager et al in 2007,^[19] rats were deprived of sleep for 24 hours. When compared with a control group, the sleep-deprived rats' blood tests indicated a 20% decrease in white blood cell count, a significant change in the immune system.

A study by Bonnet and Arand^[20] in 2003 indicates that sleep affects metabolism, is indeed a metabolic phase—anabolism. Comparing normal human sleepers and sleepers with sleep state misperception insomnia, where patients complain of poor sleep but have normal sleep by electroencephalographic (EEG) criteria, the researchers found significantly greater metabolism values for the normal sleepers.

It has yet to be clearly proven that sleep duration affects somatic growth. One study by Jenni et al^[21] in 2007 recorded growth, height and weight, as correlated to parent-reported time-in-bed in 305 children over a period of nine years (age 1–10). It was found that "the variation of sleep duration among children does not seem to have an effect on growth". It has been shown that sleep, more specifically slow-wave sleep (SWS), does affect growth hormone levels in adult men. During eight hours sleep, Van Cauter, Leproult, and Plat^[22] found that the men with a high percentage of SWS (average 24%) also had high growth hormone secretion, while subjects with a low percentage of SWS (average 9%) had low growth hormone secretion.

There are multiple arguments supporting the restorative function of sleep. We are rested after sleeping and it is natural to assume that this is a basic purpose of sleep. The metabolic phase during sleep is anabolic; anabolic hormones such as growth hormones as mentioned above are secreted preferentially during sleep. Sleep among species is, in general, inversely related to the animal size and basal metabolic rate. Rats with a very high basal metabolic rate sleep for up to 14 hours a day whereas elephants and giraffes with lower BMRs sleep only 3–4 hours per day.

Energy conservation could as well have been accomplished by resting quiescent without shutting off the organism from the environment, potentially a dangerous situation. A sedentary non-sleeping animal is more likely to survive predators, while still preserving energy. Sleep therefore does something else other than conserving energy. Most interestingly, hibernating animals that wake up from hibernation go into rebound sleep because of lack of sleep during the hibernation period. They are definitely well rested and are conserving energy during hibernation, but need sleep for something else.^[23] Rats kept awake indefinitely develop skin lesions, hyperphagia, loss of body mass, hypothermia, and eventually septicemia and death.^[24]

Anabolic/catabolic

Non-REM sleep may be an anabolic state marked by physiological processes of growth and rejuvenation of the organism's immune, nervous, muscular, and skeletal systems (with some exceptions). Wakefulness may perhaps be viewed as a cyclical, temporary, hyperactive catabolic state during which the organism acquires nourishment and reproduces.

Ontogenesis

According to the ontogenetic hypothesis of REM sleep, the activity occurring during neonatal REM sleep (or active sleep) seems to be particularly important to the developing organism (Marks et al., 1995). Studies investigating the effects of deprivation of active sleep have shown that deprivation early in life can result in behavioral problems, permanent sleep disruption, decreased brain mass (Mirmiran et al. 1983), and an abnormal amount of neuronal cell death (Morrissey, Duntley & Anch, 2004).

REM sleep appears to be important for development of the brain. REM sleep occupies the majority of time of sleep of infants, which spend most of their time sleeping. Among different species, the more immature the baby is born, the more time it spends in REM sleep. Proponents also suggest that REM-induced muscle inhibition in the presence of brain activation exists to allow for brain development by activating the synapses yet without any motor consequences which may get the infant in trouble. Additionally, REM deprivation results in developmental abnormalities later in life.

However, this does not explain why older adults still need REM sleep. Aquatic mammal infants do not have REM sleep in infancy ^[25] REM sleep in those animals increases as they age.

Memory processing

Scientists have shown numerous ways in which sleep is related to memory. In a study conducted by Turner, Drummond, Salamat, and Brown^[26] working memory was shown to be affected by sleep deprivation. Working memory is important because it keeps information active for further processing and supports higher-level cognitive functions such as decision making, reasoning, and episodic memory. Turner et al. allowed 18 women and 22 men to sleep only 26 minutes per night over a 4-day period. Subjects were given initial cognitive tests while well rested and then tested again twice a day during the 4 days of sleep deprivation. On the final test the average working memory span of the sleep deprived group had dropped by 38% in comparison to the control group.

Memory also seems to be affected differently by certain stages of sleep such as REM and slow-wave sleep (SWS). In one study cited in Born, Rasch, and Gais^[27] multiple groups of human subjects were used: wake control groups and sleep test groups. Sleep and wake groups were taught a task and then tested on it both on early and late nights, with the order of nights balanced across participants. When the subjects' brains were scanned during sleep, hypnograms revealed that SWS was the dominant sleep stage during the early night representing around 23% on average for sleep stage activity. The early night test group performed 16% better on the declarative memory test than the control group. During late night sleep, REM became the most active sleep stage at about 24%, and the late night test group performed 25% better on the procedural memory test than the control group. This indicates that procedural memory benefits from late REM-rich sleep whereas declarative memory benefits from early SWS-rich sleep.

Another study conducted by Datta^[28] indirectly supports these results. The subjects chosen were 22 male rats. A box was constructed where a single rat could move freely from one end to the other. The bottom of the box was made of a steel grate. A light would shine in the box accompanied by a sound. After a 5 second delay an electrical shock would be applied. Once the shock commenced the rat could move to the other end of the box, ending the shock immediately. The rat could also use the 5-second delay to move to the other end of the box and avoid the shock entirely. The length of the shock never exceeded 5 seconds. This was repeated 30 times for half the rats. The other half, the control group, was placed in the same trial but the rats were shocked regardless of their reaction. After each of the training sessions the rat would be placed in a recording cage for 6 hours of polygraphic recordings. This process was repeated for 3 consecutive days. This study found that during the post-trial sleep recording session rats spent 25.47% more time in REM sleep after learning trials than after control trials. These trials support the results of the Born et al. study, indicating an obvious correlation between REM sleep and procedural knowledge.

Another interesting observation of the Datta study is that the learning group spent 180% more time in SWS than did the control group during the post-trial sleep-recording session. This phenomenon is supported by a study performed by Kudrimoti, Barnes, and McNaughton.^[29] This study shows that after spatial exploration activity, patterns of hippocampal place cells are reactivated during SWS following the experiment. In a study by Kudrimoti et al. seven rats were run through a linear track using rewards on either end. The rats would then be placed in the track for 30 minutes to allow them to adjust (PRE), then they ran the track with reward based training for 30 minutes (RUN), and then they were allowed to rest for 30 minutes. During each of these three periods EEG data were collected for information on the rats' sleep stages. Kudrimoti et al. computed the mean firing rates of hippocampal place cells during pre-behavior SWS (PRE) and three 10-minute intervals in post-behavior SWS (POST) by averaging across 22 track-running sessions from seven rats. The results showed that 10 minutes after the trial RUN session there was a 12% increase in the mean firing rate of hippocampal place cells from the PRE level, however after 20 minutes the mean firing rate returned rapidly toward the PRE level. The elevated firing of hippocampal place cells during SWS after spatial exploration could explain why there were elevated levels of SWS sleep in Datta's study as it also dealt with a form of spatial exploration.

The different studies all suggest that there is a correlation between sleep and the many complex functions of memory. Harvard sleep researchers Saper and Stickgold^[30] point out that an essential part of memory and learning consists of nerve cell dendrites sending information to the cell body to be organized into new neuronal connections. This process demands that no external information is presented to these dendrites, and they suggest that this may be why it is during sleep that we solidify memories and organize knowledge.

Preservation

The "Preservation and Protection" theory holds that sleep serves an adaptive function. It protects the person during that portion of the 24-hour day in which being awake, and hence roaming around, would place the individual at greatest risk. Organisms do not require 24 hours to feed themselves and meet other necessities. From this perspective of adaptation, organisms are safer by staying out of harm's way where potentially they could be prey to other, stronger organisms. They sleep at times that maximize their safety, given their physical capacities and their habitats. (Allison & Cicchetti, 1976; Webb, 1982).

However, this theory fails to explain why the brain disengages from the external environment during normal sleep. Another argument against the theory is that sleep is not simply a passive consequence of removing the animal from the environment, but is a "drive": animals alter their behaviors in order to obtain sleep. Therefore, circadian regulation is more than sufficient to explain periods of activity and quiescence that are adaptive to an organism, but the more peculiar specializations of sleep probably serve different and unknown functions.

Moreover, the preservation theory does not explain why carnivores like lions, which are on top of the food chain, sleep the most. By the preservation logic, these top carnivores should not need any sleep at all. Preservation does not explain why aquatic mammals sleep while moving. Lethargy during these vulnerable hours would do the same, and will be more advantageous because the animal will be quiescent but still be able to respond to environmental challenges like predators etc. Sleep rebound that occurs after a sleepless night will be maladaptive, but still occurs for a reason. For example, a zebra falling asleep the day after it spent the sleeping time running from a lion is more and not less vulnerable to predation.

Dreaming

Dreaming is the perception of sensory images and sounds during sleep, in a sequence which the sleeper/dreamer usually perceives more as an apparent participant than an observer. Dreaming is stimulated by the pons and mostly occurs during the REM phase of sleep.

People have proposed many hypotheses about the functions of dreaming. Sigmund Freud postulated that dreams are the symbolic expression of frustrated desires that had been relegated to the subconscious, and he used dream interpretation in the form of psychoanalysis to uncover these desires. Scientists have become skeptical about the Freudian interpretation, and place more emphasis on dreaming as a requirement for organization and consolidation of recent memory and experience. See Freud: The Interpretation of Dreams

Rosalind Cartwright stated that

One Function of dreams may be to restore our sense of competence.... it is also probable that in many times of stress, dreams have more work to do in resolving our problems and are thus more salient and memorable.^[31]
— Rosalind Cartwright, The Sunday Observer

J. Allan Hobson's and Robert McCarley's activation synthesis theory proposes that dreams are caused by the random firing of neurons in the cerebral cortex during the REM period. According to the theory, the forebrain then creates a story in an attempt to reconcile and make sense of the nonsensical sensory information presented to it; hence the odd nature of many dreams.^[32]

Effect of food and drink on sleep

Depressants

Tryptophan

The amino acid tryptophan is a building block of the protein found in foods. It contributes to sleepiness. Carbohydrates make tryptophan more available to the brain, which is why carbohydrate-heavy meals containing tryptophan tend to cause drowsiness. Tryptophan is a precursor to the neurotransmitter serotonin, which is a precursor to the neurohormone melatonin (see below).

Melatonin

Melatonin is a naturally occurring hormone that regulates sleepiness. It is made in the brain where tryptophan is converted into serotonin and then into melatonin, which is released at night by the pineal gland to induce and maintain sleep. Melatonin supplementation may be used as a sleep aid, both as a hypnotic and as a chronobiotic (see phase response curve, PRC).

The "Post-Lunch Dip"

Many people have a temporary drop in alertness in early afternoon, commonly known as the post-lunch dip. While a large meal, rich in carbohydrates, can make a person feel sleepy, the post-lunch dip is mostly an effect of the biological clock. People naturally feel most sleepy (have the greatest "drive for sleep") at two times of the day about 12 hours apart, for example at 2:00 AM and 2:00 PM. At those two times, the body clock "kicks in". At about 2 p.m. (14:00), it overrides the homeostatic build-up of sleep debt, allowing several more hours of wakefulness. At about 2 a.m. (02:00), with the daily sleep debt paid off, it "kicks in" again to ensure a few more hours of sleep.

Alcohol

Often people start drinking alcohol in order to get to sleep (alcohol is initially a sedative and will make you get to sleep faster). However, being addicted to alcohol can lead to disrupted sleep because alcohol has a rebound effect later in the night. As a result there is strong evidence linking alcoholism and insomnia.^{[citation needed]}

Barbiturates

Barbiturates when taken cause drowsiness and have actions similar to ethanol (drinking alcohol).

Anti-Depressants

5-hydroxy-tryptophan (5-HTP)

5-HTP, the precursor to serotonin (5-HT) can cause drowsiness when ingested.

Stimulants

Caffeine

Caffeine is a stimulant that works by slowing the action of the hormones in the brain that cause sleepiness. Effective dosage is individual, in part dependent on prior usage. It can cause a rapid reduction in alertness as it wears off.

Energy Drinks

The stimulating effects of energy drinks comes from natural stimulants such as caffeine, sugars, and essential amino acids, and eventually will create a rapid reduction in alertness similar to that of caffeine.

Amphetamines

Amphetamines (amphetamine, dextroamphetamine, methamphetamine, etc) are often used to treat narcolepsy and ADHD disorders. The most common effects are decreased appetite, stimulation and insomnia, and increased alertness.

Cocaine and Crack Cocaine

Similar in action to the amphetamines.

MDMA

Commonly known as ecstacy, users are kept awake similar to amphetamines with intense euphoria, includes other similar drugs like MDA, MMDA, or bk-MDMA.

Methylphenidate

Commonly known as Ritalin, similar in action to amphetamines and cocaine.

Causes of difficulty in sleeping

There are a great many possible reasons for sleeping poorly. Following sleep hygienic principles may solve problems of physical or emotional discomfort.^[33] When pain, illness, drugs, or stress are the culprit, the cause must be treated. Sleep disorders, including the sleep apneas, narcolepsy, primary insomnia, periodic limb movement disorder (PLMD), restless leg syndrome (RLS) and the circadian rhythm sleep disorders, are treatable.

Elderly people may to some degree lose the ability to consolidate sleep. They need the same amount per day as they've always needed but may need to take some of their sleep as daytime naps.

Anthropology of sleep

Recent research suggests that sleep patterns vary significantly across human cultures.^[34]^[35] The most striking differences are between societies that have plentiful artificial light and those that do not. Cultures without artificial light have more broken-up sleep patterns. This is called polyphasic sleep or segmented sleep and has led to expressions such as "first sleep," "watch," and "second sleep" which appear in literature from all over the world.

Some cultures have fragmented sleep patterns in which people sleep at all times of the day and for shorter periods at night. For example, many Mediterranean and Latin American cultures have a siesta, in which people sleep for a period in the afternoon. In many nomadic or hunter-gatherer societies people sleep off and on throughout the day or night depending on what is happening.^{[citation needed]}

Sleep in non-humans

Horses and other herbivorous ungulates can sleep while standing, but must necessarily lie down for REM sleep (which causes muscular atony) for short periods - giraffes, for example, only need to lie down for REM sleep for a few minutes at a time. Bats sleep while hanging upside down. Some aquatic mammals and some birds can sleep with one half of the brain, while the other half is awake, so called unihemispheric slow-wave sleep.^[36] Birds and mammals have cycles of non-REM and REM sleep as described above for humans, though birds’ cycles are much shorter and they do not lose muscle tone (go limp) to the same extent that most mammals do.

Many animals sleep, but neurological sleep states are difficult to define in lower order animals. In these animals, sleep is defined using behavioral characteristics such as minimal movement, postures typical for the species and reduced responsiveness to external stimulation. Sleep is quickly reversible, as opposed to hibernation or coma, and sleep deprivation is followed by longer and/or deeper sleep. Herbivores, who require a long waking period to gather and consume their diet, typically sleep less each day than similarly sized carnivores who might well consume several days supply of meat in a sitting.

Many species of mammals sleep for a large proportion of each 24-hour period when they are very young.^[37] However, killer whales and some dolphins do not sleep during the first month of life.^[38] Such differences may be explained by the ability of land mammal newborns to be easily protected by parents while sleeping, while marine animals must, even while very young, be more continuously vigilant for predators.

William C Dement in his book "The Promise of Sleep". states that the dolphin, originally a land mammal that has returned to the sea, maintains a number of terrestrial traits including bearing their offspring alive and, unlike fish, breathing air. When terrestrial mammals breathe, they do so through an involuntary process similar to the one that causes our hearts to beat continuously. In dolphins the breathing process is under voluntary control throughout the day --- a process that, seemingly, would preclude sleep. In order to accomplish what seems to be an impossible task, dolphins allow one half of their brain to go to sleep while the other half remains awake. This is accomplished in two-hour cycles where one half of the brain is awake while the other half sleeps until the dolphin's day's sleep need has been fulfilled.

References

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^ Bonnet, M. H. & Arand, D. L. (2003). Insomnia, metabolic rate and sleep restoration [Electronic version]. Journal of Internal Medicine, 254, 23–31.
^ Jenni, O. G., Molinari, L., Caflisch, J. A., & Largo, R. H. (2007). Sleep duration from ages 1 to 10 years: Variability and stability in comparison with growth [Electronic version]. Pediatrics, 120, e769-e776.
^ Van Cauter, E., Leproult, R., & Plat, L. (2000). Age-related changes in slow-wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men [Electronic version]. Journal of the American Medical Association, 284, 861-868.
^ Daan S, Barnes BM, Strijkstra AM (1991). "Warming up for sleep? Ground squirrels sleep during arousals from hibernation". Neurosci. Lett. 128 (2): 581. doi:10.1016/0304-3940(91)90276-Y. PMID 1945046.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Guidelines for the Care and Use of Mammals in Neuroscience and Behavioral Research. Institute for Laboratory Animal Research (ILAR), National Research Council. The National Academies Press. 2003. pp. pg 121. ISBN 978-0-309-08903-6. Sleep deprivation of over 7 days with the disk-over-water system results in the development of ulcerative skin lesions, hyperphagia, loss of body mass, hypothermia, and eventually septicemia and death in rats (Everson, 1995; Rechtschaffen et al., 1983). {{cite book}}: |pages= has extra text (help); Cite has empty unknown parameters: |accessyear=, |origmonth=, |accessmonth=, |chapterurl=, |month=, |origdate=, and |coauthors= (help)CS1 maint: others (link)
^ Amanda Schaffer (Mai 27, 2007). "Why do we Sleep?". Slate.com. Retrieved 2008-08-23. {{cite web}}: Check date values in: |date= (help)
^ Turner, T. H., Drummond, S. P. A., Salamat, J. S., & Brown, G. G. (2007). Effects of 42 hr sleep deprivation on component processes of verbal working memory [Electronic version]. Neuropsychology, 21, 787-795.
^ Born, J., Rasch, J., & Gais, S. (2006). Sleep to remember [Electronic version]. Neuroscientist, 12, 410.
^ Datta, S. (2000). Avoidance task training potentiates phasic pontine-wave density in the rat: A mechanism for sleep-dependent plasticity [Electronic version]. The Journal of Neuroscience, 20, 8607-8613.
^ Kudrimoti, H. S., Barnes, C. A., & McNaughton, B. L. (1999). Reactivation of hippocampal cell assemblies: Effects of behavioral state, experience, and EEG dynamics [Electronic version]. The Journal of Neuroscience, 19, 4090-4101.
^ "Nature, 10/05
^ Nanayakkara, Anushka. "Dream your dreams away". The Sunday Observer. Retrieved 2008-07-09.
^ Hobson, J. A., & McCarley, R. (1977). The brain as a dream state generator: An activation-synthesis hypothesis of the dream process. American Journal of Psychiatry, 134, 1335–1348.
^ Little, Nan (2007-01-01). "What Causes Sleep Difficulty?". Insight Journal. Retrieved 2008-01-25.
^ Carol M. Worthman and Melissa K. Melby. "6. Toward a comparative developmental ecology of human sleep". A comparative developmental ecology. Emory University. {{cite book}}: |format= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
^ Slumber's Unexplored Landscape, Science News Online (9/25/99)
^ Mukhametova LM (1977-10-14). "Interhemispheric asymmetry of the electroencephalographic sleep patterns in dolphins". Brain Research. 134 (3): pp. 581–584. doi:10.1016/0006-8993(77)90835-6. PMID 902119. {{cite journal}}: |pages= has extra text (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
^ Faraco, Juliette (2000-08-01). "Re: Are there animals who don't sleep or that sleep very little?". MadSci Network: Zoology. Retrieved 2008-01-25. {{cite web}}: Cite has empty unknown parameter: |coauthors= (help)
^ Insomnia Mania: Newborn Mammals Don't Sleep for a Month | LiveScience

External links

[1] Guidelines for the Care and Use of Mammals in Neuroscience and Behavioral Research. Institute for Laboratory Animal Research (ILAR), National Research Council. The National Academies Press. 2003. pp. pg 121. ISBN 978-0-309-08903-6. Sleep deprivation of over 7 days with the disk-over-water system results in the development of ulcerative skin lesions, hyperphagia, loss of body mass, hypothermia, and eventually septicemia and death in rats (Everson, 1995; Rechtschaffen et al., 1983). {{cite book}}: |pages= has extra text (help); Cite has empty unknown parameters: |accessyear=, |origmonth=, |accessmonth=, |chapterurl=, |month=, |origdate=, and |coauthors= (help)CS1 maint: others (link)

[2] Bingham, Roger (2007). "Waking Up To Sleep" (Several conference videos). The Science Network. Retrieved 2008-01-25. {{cite web}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

[3] Swierzewski, Stanley J., M.D. (01 December 2000, reviewed 04 December 2007). "Sleep Stages. Overview, Waking, Non-REM, REM, Sleep Cycle, Factors, Age". Sleep Channel, Healthcommunities.com. Retrieved 2008-02-10. {{cite web}}: Check date values in: |date= (help)CS1 maint: multiple names: authors list (link)

[Pinel,_J.P.J.-4] Psychology World (1998). "Stages of Sleep" (PDF). Retrieved 2008-06-15. {{cite web}}: Cite has empty unknown parameter: |coauthors= (help)

[5] Wyatt, James K. (1999). "Circadian temperature and melatonin rhythms, sleep, and neurobehavioral function in humans living on a 20-h day". Am J Physiol. 277 (4): R1152–R1163. Fulltext. PMID 10516257. Retrieved 2007-11-25. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

[autogenerated1-6] Benedictis, Tina, Ph.D. (2007). "Understanding Sleep: Sleep Needs, Cycles, and Stages". Helpguide.org. Retrieved 2008-01-25. {{cite web}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: multiple names: authors list (link)

[7] Wyatt, James K. (1999). "Circadian temperature and melatonin rhythms, sleep, and neurobehavioral function in humans living on a 20-h day". Am J Physiol. 277 (4): R1152–R1163. PMID 10516257. Retrieved 2007-11-25. ... significant homeostatic and circadian modulation of sleep structure, with the highest sleep efficiency occurring in sleep episodes bracketing the melatonin maximum and core body temperature minimum {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

[let_sleep_work_for_you-8] ""Let Sleep Work for You" provided by the National Sleep Foundation".

[9] Van Dongen HP, Maislin G, Mullington JM, Dinges DF. The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation. Sleep. 2003 Mar 15;26(2):117–26.

[10] Rhonda Rowland (2002-02-15). "Experts challenge study linking sleep, life span". Retrieved 2007-04-22.

[11] Patel SR, Ayas NT, Malhotra MR et al (2004) A prospective study of sleep duration and mortality risk in women Sleep 1;27(3):440-4

[12] Patel SR, Malhotra A, Gottlieb DJ et al (2006) Correlates of long sleep duration Sleep 29(7):881-889

[13] Irwin MR, Ziegler M (2005) Sleep deprivation potentiates activation of cardiovascular and catecholamine responses in abstinent alcoholics Hypertension 45(2):252-7

[14] ""Researchers say lack of sleep doubles risk of death… but so can too much sleep"".

[15] Jane E. Ferrie, Martin J. Shipley, Francesco P. Cappuccio, Eric Brunner, Michelle A. Miller, Meena Kumari, and Michael G. Marmot. “A prospective study of change in sleep duration; associations with mortality in the Whitehall II cohort”. SLEEP Journal.

[16] Siegel, Jerome M. (1999). "Sleep". Encarta Encyclopedia. Microsoft. Retrieved 2008-01-25.

[17] Iglowstein, Ivo (2003). "Sleep Duration From Infancy to Adolescence: Reference Values and Generational Trends". Pediatrics. 111 (2): pp. 302-307. doi:10.1542/peds.111.2.302. PMID 12563055. Thus, the shift in the evening bedtime across cohorts accounted for the substantial decrease in sleep duration in younger children between the 1970s and the 1990s. ... [A] more liberal parental attitude toward evening bedtime in the past decades is most likely responsible for the bedtime shift and for the decline of sleep duration... {{cite journal}}: |pages= has extra text (help); Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)

[18] Gumustekin, K. (2004). "Effects of sleep deprivation, nicotine, and selenium on wound healing in rats" (Abstract). Int J Neurosci 2004;114(11): 1433-42. {{cite web}}: Cite has empty unknown parameter: |month= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)

[19] Zager, A., Andersen, M. L., Ruiz, F. S., Antunes, I. B., & Tufik, S. (2007). Effects of acute and chronic sleep loss on immune modulation of rats [Electronic version]. Regulatory, Integrative and Comparative Physiology, 293, R504-R509.

[20] Bonnet, M. H. & Arand, D. L. (2003). Insomnia, metabolic rate and sleep restoration [Electronic version]. Journal of Internal Medicine, 254, 23–31.

[21] Jenni, O. G., Molinari, L., Caflisch, J. A., & Largo, R. H. (2007). Sleep duration from ages 1 to 10 years: Variability and stability in comparison with growth [Electronic version]. Pediatrics, 120, e769-e776.

[22] Van Cauter, E., Leproult, R., & Plat, L. (2000). Age-related changes in slow-wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men [Electronic version]. Journal of the American Medical Association, 284, 861-868.

[pmid1945046-23] Daan S, Barnes BM, Strijkstra AM (1991). "Warming up for sleep? Ground squirrels sleep during arousals from hibernation". Neurosci. Lett. 128 (2): 581. doi:10.1016/0304-3940(91)90276-Y. PMID 1945046.{{cite journal}}: CS1 maint: multiple names: authors list (link)

[24] Guidelines for the Care and Use of Mammals in Neuroscience and Behavioral Research. Institute for Laboratory Animal Research (ILAR), National Research Council. The National Academies Press. 2003. pp. pg 121. ISBN 978-0-309-08903-6. Sleep deprivation of over 7 days with the disk-over-water system results in the development of ulcerative skin lesions, hyperphagia, loss of body mass, hypothermia, and eventually septicemia and death in rats (Everson, 1995; Rechtschaffen et al., 1983). {{cite book}}: |pages= has extra text (help); Cite has empty unknown parameters: |accessyear=, |origmonth=, |accessmonth=, |chapterurl=, |month=, |origdate=, and |coauthors= (help)CS1 maint: others (link)

[25] Amanda Schaffer (Mai 27, 2007). "Why do we Sleep?". Slate.com. Retrieved 2008-08-23. {{cite web}}: Check date values in: |date= (help)

[26] Turner, T. H., Drummond, S. P. A., Salamat, J. S., & Brown, G. G. (2007). Effects of 42 hr sleep deprivation on component processes of verbal working memory [Electronic version]. Neuropsychology, 21, 787-795.

[27] Born, J., Rasch, J., & Gais, S. (2006). Sleep to remember [Electronic version]. Neuroscientist, 12, 410.

[28] Datta, S. (2000). Avoidance task training potentiates phasic pontine-wave density in the rat: A mechanism for sleep-dependent plasticity [Electronic version]. The Journal of Neuroscience, 20, 8607-8613.

[29] Kudrimoti, H. S., Barnes, C. A., & McNaughton, B. L. (1999). Reactivation of hippocampal cell assemblies: Effects of behavioral state, experience, and EEG dynamics [Electronic version]. The Journal of Neuroscience, 19, 4090-4101.

[30] "Nature, 10/05

[31] Nanayakkara, Anushka. "Dream your dreams away". The Sunday Observer. Retrieved 2008-07-09.

[32] Hobson, J. A., & McCarley, R. (1977). The brain as a dream state generator: An activation-synthesis hypothesis of the dream process. American Journal of Psychiatry, 134, 1335–1348.

[33] Little, Nan (2007-01-01). "What Causes Sleep Difficulty?". Insight Journal. Retrieved 2008-01-25.

[34] Carol M. Worthman and Melissa K. Melby. "6. Toward a comparative developmental ecology of human sleep". A comparative developmental ecology. Emory University. {{cite book}}: |format= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)

[35] Slumber's Unexplored Landscape, Science News Online (9/25/99)

[36] Mukhametova LM (1977-10-14). "Interhemispheric asymmetry of the electroencephalographic sleep patterns in dolphins". Brain Research. 134 (3): pp. 581–584. doi:10.1016/0006-8993(77)90835-6. PMID 902119. {{cite journal}}: |pages= has extra text (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)

[37] Faraco, Juliette (2000-08-01). "Re: Are there animals who don't sleep or that sleep very little?". MadSci Network: Zoology. Retrieved 2008-01-25. {{cite web}}: Cite has empty unknown parameter: |coauthors= (help)

[38] Insomnia Mania: Newborn Mammals Don't Sleep for a Month | LiveScience

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