Sleep is a naturally recurring state of mind and body characterized by altered consciousness, relatively inhibited sensory activity, inhibition of nearly all voluntary muscles, and reduced interactions with surroundings. It is distinguished from wakefulness by a decreased ability to react to stimuli, but is more easily reversed than the state of hibernation or of being comatose. Mammalian sleep occurs in repeating periods, in which the body alternates between two highly distinct modes known as non-REM and REM sleep. REM stands for "rapid eye movement" but involves many other aspects including virtual paralysis of the body.
During sleep, most systems in an animal are in an anabolic state, building up the immune, nervous, skeletal, and muscular systems. Sleep in non-human animals is observed in mammals, birds, reptiles, amphibians, and some fish, and, in some form, in insects and even in simpler animals such as nematodes. The internal circadian clock promotes sleep daily at night in diurnal organisms (such as humans) and in the day in nocturnal organisms (such as rodents). However, sleep patterns vary among individual humans and even more widely among other species. In the last century, artificial light has in many areas of the world substantially altered sleep timing among both humans and many other species.
The diverse purposes and mechanisms of sleep are the subject of substantial ongoing research. Sleep seems to assist animals with improvements in the body and mind. A well-known feature of sleep in humans is the dream, an experience typically recounted in narrative form, which resembles waking life while in progress, but which usually can later be distinguished as fantasy. Sleep is sometimes confused with unconsciousness, but is quite different in terms of thought process.
Humans may suffer from a number of sleep disorders. These include dyssomnias (such as insomnia, hypersomnia, and sleep apnea), parasomnias (such as sleepwalking and REM behavior disorder), bruxism, and the circadian rhythm sleep disorders.
- 1 Physiology
- 1.1 Stages
- 1.2 Circadian timing
- 1.3 Sleep homeostasis, deprivation and optimization
- 1.4 Functions
- 1.5 Dreaming
- 1.6 Evolution
- 1.7 Genetics
- 1.8 Non-human animals
- 2 Disorders
- 3 Effect of food and drugs on sleep
- 4 Impact on Culture
- 5 See also
- 6 References
- 7 External links
In mammals and birds, sleep is divided into two broad types: rapid eye movement (REM sleep) and non-rapid eye movement (NREM or non-REM sleep). Each type has a distinct set of physiological and neurological features associated with it. REM sleep is associated with dreaming, desynchronized and faster brain waves, loss of muscle tone, and suspension of homeostasis. REM and non-REM sleep are so different that physiologists classify them as distinct behavioral states. In this view, REM, non-REM, and waking represent the three major modes of consciousness, neural activity, and physiological regulation. According to the Hobson & McCarley activation-synthesis hypothesis, proposed in 1975–1977, the alternation between REM and non-REM can be explained in terms of cycling, reciprocally influential neurotransmitter systems.
Especially during non-REM sleep, the brain uses significantly less energy during sleep than it does in waking. In areas with reduced activity, the brain restores its supply of adenosine triphosphate (ATP), the molecule used for short-term storage and transport of energy. (Since in quiet waking the brain is responsible for 20% of the body's energy use, this reduction has an independently noticeable impact on overall energy consumption.) During slow-wave sleep, humans secrete bursts of growth hormone. All sleep, even during the day, is associated with secretion of prolactin.
Sleep increases an organism's sensory threshold. In other words, a sleeping creature perceives fewer stimuli. However, it can generally still respond to loud noises and other salient sensory events.
Key physiological indicators in sleep include EEG of brain waves, electrooculography (EOG) of eye movements, and electromyography (EMG) of skeletal muscle activity. Simultaneous collection of these measurements is called polysomnography and can be performed in a specialized sleep laboratory.
Human sleep occurs in periods of approximately 90 minutes, which include increasing proportions of paradoxical (REM) sleep as they repeat. This rhythm is called the ultradian sleep cycle. Sleep proceeds in cycles of NREM and REM, normally in that order and usually four or five of them per night. The American Academy of Sleep Medicine (AASM) divides NREM into three stages: N1, N2, and N3, the last of which is also called delta sleep or slow-wave sleep. The whole period normally proceeds in the order: N1 → N2 → N3 → N2 → REM. In other animals the subdivision between phases of non-REM sleep is not typically used, although animal non-REM sleep can be described as lighter or deeper. There is a greater amount of deep sleep (stage N3) earlier in the night, while the proportion of REM sleep increases in the two cycles just before natural awakening.
Each stage may have a distinct physiological function and this can result in sleep that exhibits loss of consciousness but does not fulfill its physiological functions (i.e., one may still feel tired after apparently sufficient sleep).
As an awake organism falls asleep, the activity of its body slows down. Body temperature, heart rate, breathing rate, and energy use all decrease. Brain waves get slower and bigger. The excitatory neurotransmitter acetylcholine becomes less available in the brain. The organism will maneuver, as best it can, to create a thermally friendly environment—for example, by curling up into a ball if the organism is cold. Reflexes remain fairly active. These characteristics apply to some degree during all non-REM sleep, which constitutes ~80% of all sleep in humans.
NREM Stage 1 (N1 – light sleep, somnolence, drowsy sleep – 5–10% of total sleep in adults): This is a stage of sleep that usually occurs between sleep and wakefulness, and sometimes occurs between periods of deeper sleep and periods of REM. The muscles are active, and the eyes roll slowly, opening and closing moderately. The brain transitions from alpha waves having a frequency of 8–13 Hz (common in the awake state) to theta waves having a frequency of 4–7 Hz. Sudden twitches and hypnic jerks, also known as positive myoclonus, may be associated with the onset of sleep during N1. Some people may also experience hypnagogic hallucinations during this stage. During Non-REM1, the organism loses some muscle tone and most conscious awareness of the external environment.
NREM Stage 2 (N2 – 45–55% of total sleep in adults): In this stage, theta activity is observed and sleepers become gradually harder to awaken; the alpha waves of the previous stage are interrupted by abrupt activity called sleep spindles (or thalamocortical spindles) and K-complexes. Sleep spindles range from 11 to 16 Hz (most commonly 12–14 Hz). During this stage, muscular activity as measured by EMG decreases, and conscious awareness of the external environment disappears.
NREM Stage 3 (N3 – deep sleep, slow-wave sleep – 15–25% of total sleep in adults): Formerly divided into stages 3 and 4, this stage is called slow-wave sleep (SWS) or deep sleep. SWS is initiated in the preoptic area and consists of delta activity, high amplitude waves at less than 3.5 Hz. The sleeper is less responsive to the environment; many environmental stimuli no longer produce any reactions. Slow-wave sleep is thought to be the most restful form of sleep, the phase which most relieves subjective feelings of sleepiness and restores the body.
This stage is characterized by the presence of a minimum of 20% delta waves ranging from 0.5–2 Hz and having a peak-to-peak amplitude >75 μV. (EEG standards define delta waves to be from 0 to 4 Hz, but sleep standards in both the original R&K, as well as the new 2007 AASM guidelines have a range of 0.5–2 Hz.) This is the stage in which parasomnias such as night terrors, nocturnal enuresis, sleepwalking, and somniloquy occur. Many illustrations and descriptions still show a stage N3 with 20–50% delta waves and a stage N4 with greater than 50% delta waves; these have been combined as stage N3.
REM Stage (REM Sleep – 20–25% of total sleep in adults): Entering rapid eye movement (REM) sleep where most muscles are paralyzed, and heart rate, breathing and body temperature become unregulated, the sleeper may dream. REM sleep is turned on by acetylcholine secretion and is inhibited by neurons that secrete monoamines including serotonin. This level is also referred to as paradoxical sleep because the sleeper, although exhibiting high-frequency EEG waves similar to a waking state, is harder to arouse than at any other sleep stage. Vital signs indicate arousal and oxygen consumption by the brain is higher than when the sleeper is awake. An adult reaches REM approximately every 90 minutes, and remains in REM sleep for longer during latter half of sleep. REM sleep occurs as a person returns to stage 2 or 1 from a deep sleep.
The function of REM sleep is uncertain but a lack of it impairs the ability to learn complex tasks. Functional paralysis from muscular atonia in REM may be necessary to protect organisms from self-damage through physically acting out scenes from the often-vivid dreams that occur during this stage.
A newborn baby spends almost 9 hours a day just in REM sleep. By the age of five or so, only slightly over two hours is spent in REM.
One approach to understanding the role of sleep is to study the deprivation of it. The study of REM deprivation began with William C. Dement more than fifty years ago. He conducted a sleep and dream research project on eight subjects, all male. For a span of up to 7 days, he deprived the participants of REM sleep by waking them each time they started to enter the stage. He monitored this with small electrodes attached to their scalp and temples. As the study went on, he noticed that the more he deprived the men of REM sleep, the more often he had to wake them. Afterwards, they showed more REM sleep than usual, later named REM rebound.
Awakening can mean the end of sleep, or simply a moment to survey the environment and readjust body position before falling back asleep. Sleepers typically awaken from slow-wave sleep, soon after the end of a REM phase or sometimes in the middle of REM. Internal circadian indicators, along with successful reduction of homeostatic sleep need, typically bring about awakening and the end of the sleep episode.
Today, many humans wake up with an alarm clock. (Some people, however, can reliably wake themselves up at a specific time with no need for an alarm.) Many sleep quite differently on workdays versus days off, a pattern which can lead to chronic circadian desynchronization. Many people regularly look at television and other screens before going to bed, a factor which may exacerbate this mass circadian disruption.
Awakening involves heightened electrical activation in the brain, beginning with the thalamus and spreading throughout the cortex.
During a night's sleep, a small portion is usually spent in a waking state. As measured by electroencephalography, young females are awake for 0–1% of the larger sleeping period; young males are awake for 0–2%. In adults, wakefulness increases, especially in later cycles. One study found 3% awake time in the first ninety-minute sleep cycle, 8% in the second, 10% in the third, 12% in the fourth, and 13–14% in the fifth. Most of this awake time occurred shortly after REM sleep.
Scientific studies on sleep have shown that sleep stage at awakening is an important factor in amplifying sleep inertia. Alarm clocks involving sleep stage monitoring appeared on the market in 2005. Using sensing technologies such as EEG electrodes or accelerometers, these alarm clocks are supposed to wake people only from light sleep.
Historical development of the stages model
The stages of sleep were first described in 1937 by Alfred Lee Loomis and his coworkers, who separated the different electroencephalography (EEG) features of sleep into five levels (A to E), representing the spectrum from wakefulness to deep sleep. In 1953, REM sleep was discovered as distinct, and thus William C. Dement and Nathaniel Kleitman reclassified sleep into four NREM stages and REM. The staging criteria were standardized in 1968 by Allan Rechtschaffen and Anthony Kales in the "R&K sleep scoring manual."
In the R&K standard, NREM sleep was divided into four stages, with slow-wave sleep comprising stages 3 and 4. In stage 3, delta waves made up less than 50% of the total wave patterns, while they made up more than 50% in stage 4. Furthermore, REM sleep was sometimes referred to as stage 5. In 2004, the AASM commissioned the AASM Visual Scoring Task Force to review the R&K scoring system. The review resulted in several changes, the most significant being the combination of stages 3 and 4 into Stage N3. The revised scoring was published in 2007 as The AASM Manual for the Scoring of Sleep and Associated Events. Arousals, respiratory, cardiac, and movement events were also added.
Sleep timing is controlled by the circadian clock, sleep-wake homeostasis, and in humans, within certain bounds, willed behavior. The circadian clock—an inner timekeeping, temperature-fluctuating, enzyme-controlling device—works in tandem with these other mechanisms. Circadian timing, known as process C, is cyclical, based on the time of day; sleep-wake homeostasis, or process S, operates on a more absolute scale. The circadian process is thought to counteract the homeostatic drive for sleep during the day (in diurnal animals) and to enable it at night.
Humans are also influenced by aspects of social time: the hours when other people are awake, the hours when work is required, the time on the clock, etc. Time zones, standard times used to unify the timing for people in the same area, correspond only approximately to the natural rising and setting of the sun. The approximate nature of the timezone can be shown with China, a country which used to span five time zones and now uses only one (UTC +8).
Biologically, the most important human circadian clock currently known to science is a dense cluster of neurons in the suprachiasmatic nucleus (SCN), a part of the brain directly above the optic chiasm, where the optic nerves cross on their paths from the two eyes to the visual cortex. This clock measures the time of day, primarily based on input from outside light signals. An organism whose circadian clock exhibits a regular rhythm corresponding to outside signals is said to be entrained; the rhythm so established persists even if the outside signals suddenly disappear. If you take an entrained human and put them in a bunker with constant light (or darkness), they will continue to experience rhythmic increases and decreases of body temperature and melatonin, on a period which slightly exceeds 24 hours. Scientists refer to such conditions as free-running of the circadian rhythm. (Under natural conditions, light signals regularly adjust this period downward, so that it corresponds better with the exact 24 hours of an Earth day.) 
The clock exerts constant influence on the body, effecting continuous sinusoidal oscillation of body temperature between roughly 36.2 °C and 37.2 °C. The suprachiasmatic nucleus itself shows conspicuous oscillation activity, which intensifies during subjective day (i.e., the part of the rhythm corresponding with daytime, whether accurately or not) and drops to almost nothing during subjective night. The circadian pacemaker in the suprachiasmatic nucleus has a direct neural connection to the pineal gland, which releases the hormone melatonin at night. Melatonin is an important circadian indicator but its mechanisms of action are not well understood. Nocturnal mammals, which tend to stay awake at night, have higher melatonin at night just like diurnal mammals do. And, although removing the pineal gland in many animals abolishes melatonin rhythms, it does not stop circadian rhythms altogether—though it may alter them and weaken their responsiveness to light cues. Cortisol levels in diurnal animals typically rise throughout the night, peak in the awakening hours, and diminish during the day. Circadian prolactin secretion begins in the late afternoon, especially in women, and is subsequently augmented by sleep-induced secretion, to peak in the middle of the night. Circadian rhythm exerts some influence on the nighttime secretion of growth hormone.
The circadian rhythm influences the ideal timing of a restorative sleep episode. In diurnal animals, sleepiness increases during the night. REM sleep occurs more during the low part (i.e., near body temperature minimum) of the circadian cycle, whereas slow-wave sleep occurs relatively independently of circadian time.
The internal circadian clock is profoundly influenced by changes in light, since these are its main clues about what time it is. Exposure to even small amounts of light during the night can suppress melatonin secretion, increase body temperature, and increase cognitive ability. Short pulses of light, at the right moment in the circadian cycle, can significantly 'reset' the internal clock. Blue light, in particular, exerts the strongest effect, leading to concerns that electronic media use before bed may interfere with sleep.
Modern humans often find themselves desynchronized from their internal circadian clock, due to the requirements of work (especially night shifts), long-distance travel, and the influence of widespread indoor lighting. Even if they have sleep debt, or feel sleepy, people can have difficulty staying asleep at the peak of their circadian cycle. Conversely they can have difficulty waking up in the trough of the cycle. A healthy young adult entrained to the sun will (during most of the year) fall asleep a few hours after sunset, experience body temperature minimum at 6AM, and wake up a few hours after sunrise.
Nocturnal animals have higher body temperatures, greater activity, rising serotonin, and diminishing cortisol during the night—the inverse of diurnal animals. Nocturnal and diurnal animals both have increased electrical activity in the suprachiasmatic nucleus, and corresponding secretion of melatonin from the pineal gland, at night.
In polyphasic sleep, an organism sleeps at multiple times during a 24-hour cycle. Monophasic sleep occurs all at once. Under experimental conditions, humans tend to alternate more frequently between sleep and wakefulness (i.e., exhibit more polyphasic sleep) if they have nothing better to do. Given a 14-hour period of darkness in experimental conditions, humans tended towards bimodal sleep, with two sleep periods concentrated at the beginning and at the end of the dark time. Bimodal sleep in humans was more common before the industrial revolution.
Different characteristic sleep patterns, such as the familiarly so-called "early bird" and "night owl", are called chronotypes. Genetics and sex have some influence on chronotype, but so do habits. Chronotype is also liable to change over the course of a person's lifetime. Seven-year-olds are better disposed to wake up early in the morning than are fifteen-year-olds. Chronotypes far outside the normal range are called circadian rhythm sleep disorders.
The siesta habit has recently been associated with a 37% reduction in coronary mortality, possibly due to reduced cardiovascular stress mediated by daytime sleep. Nevertheless, epidemiological studies on the relations between cardiovascular health and siestas have led to conflicting conclusions, possibly because of poor control of moderator variables, such as physical activity. It is possible that people who take siestas have different physical activity habits, e.g., waking earlier and scheduling more activity during the morning. Such differences in physical activity may mediate different 24-hour profiles in cardiovascular function. Even if such effects of physical activity can be discounted for explaining the relationship between siestas and cardiovascular health, it is still unknown whether it is the daytime nap itself, a supine posture, or the expectancy of a nap that is the most important factor. It was recently suggested that a short nap can reduce stress and blood pressure (BP), with the main changes in BP occurring between the time of lights off and the onset of stage 1.
Sleep duration in long-term experienced meditators is lower than in non-meditators and general population norms, with no apparent decrements in vigilance.
The quality of sleep may be evaluated from an objective and a subjective point of view. Objective sleep quality refers to how difficult it is for a person to fall asleep and remain in a sleeping state, and how many times they wake up during a single night. Poor sleep quality disrupts the cycle of transition between the different stages of sleep. Subjective sleep quality in turn refers to a sense of being rested and regenerated after awaking from sleep. A study by A. Harvey et al. (2002) found that insomniacs were more demanding in their evaluations of sleep quality than individuals who had no sleep problems.
Sleep homeostasis, deprivation and optimization
Generally speaking, the longer an organism is awake, the more it feels a need to sleep. The balance between sleeping and waking is called homeostasis. Induced or perceived lack of sleep is commonly called sleep deprivation.
Sleep deprivation tends to cause slower brain waves in the frontal cortex, shortened attention span, higher anxiety, impaired memory, and a grouchy mood. Conversely, a well-rested organism tends to have improved memory and mood.
In rats, sleep deprivation causes weight loss and reduced body temperature. If prevented from sleeping for several weeks, rats die. In humans, sleep deprivation has been studied up to 11 days, during which subjects are more likely to gain weight.
Homeostatic sleep propensity (the need for sleep as a function of the amount of time elapsed since the last adequate sleep episode) 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. Sleep offset (awakening) is primarily determined by circadian rhythm. A person who regularly awakens at an early hour will generally not be able to sleep much later than his or her normal waking time, even if moderately sleep-deprived.
Sleep duration is affected by the gene DEC2. People with a certain DEC2 mutation sleep two hours less than normal. The gene also affects the sleep patterns of mice, and likely does so for all mammals.
Sleep debt is the effect of not getting enough sleep; a large debt causes mental, emotional and physical fatigue.
Sleep debt results in diminished abilities to perform high-level cognitive functions. Neurophysiological and functional imaging studies have demonstrated that frontal regions of the brain are particularly responsive to homeostatic sleep pressure.
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. Sleep debt does show some evidence of being cumulative. Subjectively, however, humans seem to reach maximum sleepiness after 30 hours of waking.
One neurochemical indicator of sleep debt is adenosine, a neurotransmitter that inhibits many of the bodily processes associated with wakefulness. Adenosine is an ingredient in adenosine triphosphate (ATP) and also a product of ATP metabolism. Thus as the brain uses stored energy in the form of ATP, adenosine builds up—and subjective sleepiness increases. Caffeine and theophylline temporarily block the effect of adenosine, thus allowing it to build up further before the need for sleep reasserts itself.
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; one should be asleep at least six hours before the lowest body temperature. The timing is correct when the following two circadian markers occur after the middle of the sleep episode and before awakening: maximum concentration of the hormone melatonin, and minimum core body temperature.
Human sleep needs vary by age and amongst individuals, and sleep is considered to be adequate when there is no daytime sleepiness or dysfunction. Moreover, self-reported sleep duration is only moderately correlated with actual sleep time as measured by actigraphy, and those affected with sleep state misperception may typically report having slept only four hours despite having slept a full eight hours.
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. Another study of sleep duration and mortality risk in women showed similar results. Other studies[which?] 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 socioeconomic status, which would correlate statistically.
Researchers at 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 be associated with a doubling of the risk of death, though not primarily from cardiovascular disease.
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 seven hours per night is optimal for health, and a sustained reduction may predispose to ill health."[clarification needed]
Furthermore, sleep difficulties are closely associated with psychiatric disorders such as depression, alcoholism, and bipolar disorder. Up to 90% of adults with depression are found to have sleep difficulties. Dysregulation found on EEG includes disturbances in sleep continuity, decreased delta sleep and altered REM patterns with regard to latency, distribution across the night and density of eye movements.
By the time infants reach the age of two, their brain size has reached 90 percent of an adult-sized brain; a majority of this brain growth has occurred during the period of life with the highest rate of sleep. The hours that children spend asleep influence their ability to perform on cognitive tasks. Children who sleep through the night and have few night waking episodes have higher cognitive attainments and easier temperaments than other children.
Sleep also influences language development. To test this, researchers taught infants a faux language and observed their recollection of the rules for that language. Infants who slept within four hours of learning the language could remember the language rules better, while infants who stayed awake longer did not recall those rules as well. There is also a relationship between infants' vocabulary and sleeping: infants who sleep longer at night at 12 months have better vocabularies at 26 months.
Children need many hours of sleep per day in order to develop and function properly: up to 18 hours for newborn babies, with a declining rate as a child ages. Early in 2015, after a two-year study, the National Sleep Foundation in the US announced newly revised recommendations as shown in the table below.
|Age and condition||Sleep Needs|
|Newborns (0–3 months)||14 to 17 hours|
|Infants (4–11 months)||12 to 15 hours|
|Toddlers (1–2 years)||11 to 14 hours|
|Preschoolers (3–4 years)||10 to 13 hours|
|School-age children (5–12 years)||9 to 11 hours|
|Teenagers (13–17 years)||8 to 10 hours|
|Adults (18–64 years)||7 to 9 hours|
|Older Adults (65 years and over)||7 to 8 hours|
The multiple hypotheses proposed to explain the function of sleep reflect the incomplete understanding of the subject. (When asked, after 50 years of research, what he knew about the reason people sleep, William C. Dement, founder of Stanford University's Sleep Research Center, answered, "As far as I know, the only reason we need to sleep that is really, really solid is because we get sleepy.") It is likely that sleep evolved to fulfill some primeval function and took on multiple functions over time (analogous to the larynx, which controls the passage of food and air, but descended over time to develop speech capabilities).
If sleep were not essential, one would expect to find:
- Animal species that do not sleep at all
- Animals that do not need recovery sleep after staying awake longer than usual
- Animals that suffer no serious consequences as a result of lack of sleep
Outside of a few basal animals that have no brain or a very simple one, no animals have been found to date that satisfy any of these criteria. While some varieties of shark, such as great whites and hammerheads, must remain in motion at all times to move oxygenated water over their gills, it is possible they still sleep one cerebral hemisphere at a time as marine mammals do. However it remains to be shown definitively whether any fish is capable of unihemispheric sleep.
Sleep is sometimes thought to help conserve energy, though this theory is not fully adequate as it only decreases metabolism by about 5–10%. Additionally it is observed that mammals require sleep even during the hypometabolic state of hibernation, in which circumstance it is actually a net loss of energy as the animal returns from hypothermia to euthermia in order to sleep.
Some of the many proposed functions of sleep are as follows:
Increased waste clearance of brain
A publication by L. Xie and colleagues in 2013 explored the efficiency of the glymphatic system during sleep and provided the first direct evidence that the clearance of interstitial waste products increases during the resting state. Using a combination of diffusion ionophoresis techniques pioneered by Nicholson and colleagues, in vivo 2-photon imaging, and electroencephalography to confirm the wake and sleep states, Xia and Nedergaard demonstrated that the changes in efficiency of CSF–ISF exchange between the awake and sleeping brain were caused by expansion and contraction of the extracellular space, which increased by ≈60% in the sleeping brain to promote clearance of interstitial wastes such as amyloid beta. On the basis of these findings, they hypothesized that the restorative properties of sleep may be linked to increased glymphatic clearance of metabolic waste products produced by neural activity in the awake brain.
It has been shown that sleep deprivation affects the immune system. When compared with a control group, sleep-deprived rats' blood tests indicated a 20% decrease in white blood cell count, a significant change in the immune system. It is now possible to state that "sleep loss impairs immune function and immune challenge alters sleep," and it has been suggested that mammalian species which invest in longer sleep times are investing in the immune system, as species with the longer sleep times have higher white blood cell counts. A 2014 study found that depriving mice of sleep increased cancer growth and dampened the immune system's ability to control cancers. The researchers found higher levels of M2 tumor-associated macrophages and TLR4 molecules in the sleep deprived mice and proposed this as the mechanism for increased susceptibility of the mice to cancer growth. M2 cells suppress the immune system and encourage tumour growth. TRL4 molecules are signalling molecules in the activation of the immune system. Sleep has also been theorized to effectively combat the accumulation of free radicals in the brain, by increasing the efficiency of endogenous antioxidant mechanisms.
The effect of sleep duration on somatic growth is not completely known. One study 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 is well established that slow-wave sleep affects growth hormone levels in adult men. During eight hours' sleep, Van Cauter, Leproult, and Plat 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 is some supporting evidence of the restorative function of sleep. The sleeping brain has been shown to remove metabolic waste products at a faster rate than during an awake state. While awake, metabolism generates reactive oxygen species, which are damaging to cells. In sleep, metabolic rates decrease and reactive oxygen species generation is reduced allowing restorative processes to take over. It is theorized that sleep helps facilitate the synthesis of molecules that help repair and protect the brain from these harmful elements generated during waking. The metabolic phase during sleep is anabolic; anabolic hormones such as growth hormones (as mentioned above) are secreted preferentially during sleep. The duration of sleep among species is, broadly speaking, inversely related to animal size and directly related to basal metabolic rate (BMR). Rats, which have a high BMR, sleep for up to 14 hours a day, whereas elephants and giraffes, which have 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 nonsleeping animal is more likely to survive predators, while still preserving energy. Sleep, therefore, seems to serve another purpose, or other purposes, than simply conserving energy; for example, hibernating animals waking 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. Rats kept awake indefinitely develop skin lesions, hyperphagia, loss of body mass, hypothermia, and, eventually, fatal sepsis.
Another potential purpose for sleep could be to restore signal strength in synapses that are activated while awake to a "baseline" level, weakening unnecessary connections to better facilitate learning and memory functions again the next day.
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. 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, and an abnormal amount of neuronal cell death.
REM sleep appears to be important for development of the brain. REM sleep occupies the majority of time of sleep of infants, who 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 that may get the infant in trouble. Additionally, REM deprivation results in developmental abnormalities later in life.
Scientists have shown numerous ways in which sleep is related to memory. In a study conducted by Turner, Drummond, Salamat, and Brown (2007), 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. The study allowed 18 women and 22 men to sleep only 26 minutes per night over a four-day period. Subjects were given initial cognitive tests while well-rested, and then were tested again twice a day during the four 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.
The relation between working memory and sleep can also be explored by testing how working memory works during sleep. Daltrozzo, Claude, Tillmann, Bastuji, and Perrin, using Event-Related Potentials to the perception of sentences during sleep showed that working memory for linguistic information is partially preserved during sleep with a smaller capacity compared to wake.
Memory seems to be affected differently by certain stages of sleep such as REM and slow-wave sleep (SWS). In one study, multiple groups of human subjects were used: wake control groups and sleep test groups. Sleep and wake groups were taught a task and were 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, which entails more time spent in REM, test group performed 25% better on the procedural memory test than the control group. This suggests that procedural memory benefits from late, REM-rich sleep, whereas declarative memory benefits from early, slow wave-rich sleep.
A study conducted by Datta indirectly supports these results. A box was constructed wherein 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 five-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 five-second delay to move to the other end of the box and avoid the shock entirely. The length of the shock never exceeded five 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 six hours of polygraphic recordings. This process was repeated for three consecutive days. During the posttrial sleep recording session, rats spent 25.47% more time in REM sleep after learning trials than after control trials.
An 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 study shows that after spatial exploration activity, patterns of hippocampal place cells are reactivated during SWS following the experiment. 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. The mean firing rates of hippocampal place cells during prebehavior SWS (PRE) and three ten-minute intervals in postbehavior SWS (POST) were calculated by averaging across 22 track-running sessions from seven rats. The results showed that ten minutes after the trial RUN session, there was a 12% increase in the mean firing rate of hippocampal place cells from the PRE level. 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 slow-wave sleep in Datta's study, as it also dealt with a form of spatial exploration.
A study has also been done involving direct current stimulation to the prefrontal cortex to increase the amount of slow oscillations during SWS. The direct current stimulation greatly enhanced word-pair retention the following day, giving evidence that SWS plays a large role in the consolidation of episodic memories.
The different studies suggest that there is a correlation between sleep and the complex functions of memory. Harvard sleep researchers Saper and Stickgold point out that an essential part of memory and learning consists of nerve cell dendrites' sending of 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 it is suggested that this may be why it is during sleep that memories and knowledge are solidified and organized.
Recent studies examining gene expression and evolutionary increases in brain size offer complimentary support for the role of sleep in the mammalian memory consolidation theory. Evolutionary advances in the size of the mammalian amygdala, (a brain structure active during sleep and involved in memory processing), are also associated with increases in NREM sleep durations. Likewise, nighttime gene expression differs from daytime expression and specifically targets genes thought to be involved in memory consolidation and brain plasticity.
The "Preservation and Protection" theory holds that sleep serves an adaptive function. It protects the animal 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.
This theory fails to explain why the brain disengages from the external environment during normal sleep. However, the brain consumes a large proportion of the body's energy at any one time and preservation of energy could only occur by limiting its sensory inputs. 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 needs to explain why carnivores like lions, which are on top of the food chain and thus have little to fear, sleep the most. It has been suggested that they need to minimize energy expenditure when not hunting.
Preservation also does not explain why aquatic mammals sleep while moving. Quiescence during these vulnerable hours would do the same and would be more advantageous, because the animal would still be able to respond to environmental challenges like predators, etc. Sleep rebound that occurs after a sleepless night will be maladaptive, but obviously must occur for a reason. A zebra falling asleep the day after it spent the sleeping time running from a lion is more, not less, vulnerable to predation.
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Some research shows sleep clears negative emotions.
During sleep, especially REM sleep, people tend to have dreams: elusive first-person experiences, which, despite their frequently bizarre qualities, seem realistic while in progress. Dreams can seamlessly incorporate elements within a person's mind that would not normally go together. They can include apparent sensations of all types, especially vision and movement.
Dreams can also be suppressed or encouraged; using anti-depressants, acetaminophen, ibuprofen, or alcoholic beverages is thought to potentially suppress dreams, whereas melatonin may have the ability to encourage them.
People have proposed many hypotheses about the functions of dreaming. Sigmund Freud postulated that dreams are the symbolic expression of frustrated desires that have been relegated to the unconscious mind, and he used dream interpretation in the form of psychoanalysis in attempting to uncover these desires.
Freud's work concerns the psychological role of dreams, which does not exclude any physiological role they may have. Recent research claims that sleep has the overall role of consolidation and organization of synaptic connections formed during learning and experience. As such, Freud's work is not ruled out. Nevertheless, Freud's research has been expanded on, especially with regard to the organization and consolidation of recent memory.
While penile erections during sleep are commonly believed to indicate dreams with sexual content, they are not more frequent during sexual dreams than they are during nonsexual dreams. The parasympathetic nervous system experiences increased activity during REM sleep which may cause erection of the penis or clitoris. In males, 80% to 95% of REM sleep is normally accompanied by partial to full penile erection, while only about 12% of men's dreams contain sexual content.
John Allan Hobson and Robert McCarley propose that dreams are caused by the random firing of neurons in the cerebral cortex during the REM period. Neatly, this theory helps explain the irrationality of the mind during REM periods, as, according to this theory, the forebrain then creates a story in an attempt to reconcile and make sense of the nonsensical sensory information presented to it. Ergo, the odd nature of many dreams.
According to Tsoukalas (2012), REM sleep is an evolutionary transformation of a well-known defensive mechanism, the tonic immobility reflex. This reflex, also known as animal hypnosis or death feigning, functions as the last line of defense against an attacking predator and consists of the total immobilization of the animal: the animal appears dead (cf. "playing possum"). The neurophysiology and phenomenology of this reaction show striking similarities to REM sleep, a fact which betrays a deep evolutionary kinship. For example, both reactions exhibit brainstem control, paralysis, sympathetic activation, and thermoregulatory changes. This theory integrates many earlier findings into a unified, and evolutionary well informed, framework.
Mammals, birds and reptiles evolved from amniotic ancestors, the first vertebrates with life cycles independent of water. The fact that birds and mammals are the only known animals to exhibit REM and NREM sleep indicates a common trait before divergence. Reptiles are therefore the most logical group to investigate the origins of sleep. Daytime activity in reptiles alternates between basking and short bouts of active behavior, which has significant neurological and physiological similarities to sleep states in mammals. It is proposed that REM sleep evolved from short bouts of motor activity in reptiles while SWS evolved from their basking state which shows similar slow wave EEG patterns.
Early mammals engaged in polyphasic sleep, dividing sleep into multiple bouts per day. Higher daily sleep quotas and shorter sleep cycles in polyphasic species as compared to monophasic species, suggest that polyphasic sleep may be a less efficient means of attaining sleep’s benefits. Small species with higher BMR may therefore have less efficient sleep patterns. It follows that the evolution of monophasic sleep may hitherto be an unknown advantage of evolving larger mammalian body sizes and therefore lower BMR.
The evolution of different types of sleep patterns is influenced by a number of selective pressures, including body size, relative metabolic rate, predation, type and location of food sources, and immune function.
It is hypothesized that a considerable amount of sleep-related behavior, such as when and how long a person needs to sleep, is regulated by genetics. Researchers have discovered some evidence that seems to support this assumption. Monozygotic (identical) but not dizygotic (fraternal) twins tend to have similar sleep habits. Neurotransmitters, molecules whose production can be traced to specific genes, are one genetic influence on sleep which can be analyzed. And the circadian clock has its own set of genes. ABCC9 is one gene found which influences the duration of human sleep.
Neurological sleep states can be difficult to detect in some animals. In these cases, sleep may be 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 or deeper rebound 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.
Unicellular organisms do not necessarily "sleep", although many of them have pronounced circadian rhythms. Insects go through circadian rhythms of activity and passivity but some do not seem to have a homeostatic sleep need. Drosophila does seem to have a behavioral state analogous to mammalian sleep, but it is not well-understood. Insects do not seem to exhibit REM sleep. Fish are similar, exhibiting periods of inactivity but showing no significant reactions to deprivation of this condition. Amphibians have periods of inactivity but show high vigilance (receptivity to potentially threatening stimuli) in this state. Reptiles have quiescent periods more similar to mammalian sleep, but do not exhibit REM or muscle atonia. Birds do have a REM phase; they may not accumulate sleep debt; but sleep deprivation may affect their normal waking condition.
Mammals have wide diversity in sleep phenomena. Generally, they go through periods of alternating non-REM and REM sleep, but these manifest differently. In the monotreme, REM electrical activation occurs in the brain stem, as it does in humans, but does not extend at all to the forebrain—suggesting that platypi do not dream. Inversely to humans and rats, male armadillos get erections during non-REM sleep.
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. 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 extent that most mammals do.
Many mammals sleep for a large proportion of each 24-hour period when they are very young. However, killer whales and some other dolphins do not sleep during the first month of life. Instead, young dolphins and whales frequently take rests by pressing their body next to their mother’s while she swims. As the mother swims she is keeping her offspring afloat to prevent them from drowning. This allows young dolphins and whales to rest, which will help keep their immune system healthy; in turn, protecting them from illnesses. During this period, mothers often sacrifice sleep for the protection of their young from predators. However, unlike other mammals, adult dolphins and whales are able to go without sleep for a month.
The consequences of falling into a deep sleep for marine mammalian species can be suffocation and drowning, or becoming easy prey for predators. Thus, dolphins, whales, and pinnipeds (seals) engage in unihemispheric sleep while swimming, which allows one brain hemisphere to remain fully functional, while the other goes to sleep. The hemisphere that is asleep, alternates so that both hemispheres can be fully rested. Just like terrestrial mammals, pinnipeds that sleep on land fall into a deep sleep and both hemispheres of their brain shut down and are in full sleep mode.
Insomnia, a dyssomnia, is a general term describing difficulty falling asleep and staying asleep. Insomnia is the most common sleep problem, with many adults reporting occasional insomnia, and 10–15% reporting a chronic condition. Insomnia can have many different causes, including psychological stress, a poor sleep environment, an inconsistent sleep schedule, or excessive mental or physical stimulation in the hours before bedtime. Insomnia is often treated through behavioral changes like keeping a regular sleep schedule, avoiding stimulating or stressful activities before bedtime, and cutting down on stimulants such as caffeine. The sleep environment may be improved by installing heavy drapes to shut out all sunlight, and keeping computers, televisions and work materials out of the sleeping area.
A 2010 review of published scientific research suggested that exercise generally improves sleep for most people, and helps sleep disorders such as insomnia. The optimum time to exercise may be 4 to 8 hours before bedtime, though exercise at any time of day is beneficial, with the exception of heavy exercise taken shortly before bedtime, which may disturb sleep. However, there is insufficient evidence to draw detailed conclusions about the relationship between exercise and sleep. Sleeping medications such as Ambien and Lunesta are an increasingly popular treatment for insomnia. Although these nonbenzodiazepine medications are generally believed to be better and safer than earlier generations of sedatives, they have still generated some controversy and discussion regarding side-effects. White noise appears to be a promising treatment for insomnia.
Obstructive sleep apnea
Obstructive sleep apnea is a condition in which major pauses in breathing occur during sleep, disrupting the normal progression of sleep and often causing other more severe health problems. Apneas occur when the muscles around the patient's airway relax during sleep, causing the airway to collapse and block the intake of oxygen. Obstructive sleep apnea is more common than central sleep apnea. As oxygen levels in the blood drop, the patient then comes out of deep sleep in order to resume breathing. When several of these episodes occur per hour, sleep apnea rises to a level of seriousness that may require treatment.
Diagnosing sleep apnea usually requires a professional sleep study performed in a sleep clinic, because the episodes of wakefulness caused by the disorder are extremely brief and patients usually do not remember experiencing them. Instead, many patients simply feel tired after getting several hours of sleep and have no idea why. Major risk factors for sleep apnea include chronic fatigue, old age, obesity and snoring.
Sleep disorders include narcolepsy, periodic limb movement disorder (PLMD), restless leg syndrome (RLS), upper airway resistance syndrome (UARS), and the circadian rhythm sleep disorders. Fatal familial insomnia, or FFI, an extremely rare genetic disease with no known treatment or cure, is characterized by increasing insomnia as one of its symptoms; ultimately sufferers of the disease stop sleeping entirely, before dying of the disease.
Somnambulism, known as sleep walking, is also a common sleeping disorder, especially among children. In somnambulism the individual gets up from his/her sleep and wanders around while still sleeping.
Effect of food and drugs on sleep
- Nonbenzodiazepine hypnotics such as eszopiclone (Lunesta), zaleplon (Sonata), and zolpidem (Ambien) are commonly used as sleep aids prescribed by doctors to treat forms of insomnia. Nonbenzodiazepines are the most commonly prescribed and over-the-counter sleep aids used worldwide and have been greatly growing in use since the 1990s. They target the GABAA receptor.
- Benzodiazepines target the GABAA receptor also, and as such, they are commonly used sleep aids as well, though benzodiazepines have been found to decrease REM sleep.
- Antihistamines, such as diphenhydramine (Benadryl) and doxylamine (found in various OTC medicines, such as NyQuil)
- Alcohol (ethanol) – Often, people start drinking alcohol in order to get to sleep (alcohol is initially a sedative and will cause somnolence, encouraging sleep). 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 forms of insomnia. Alcohol also reduces REM sleep.
- Barbiturates cause drowsiness and have actions similar to alcohol in that they have a rebound effect and inhibit REM sleep, so they are not used as a long-term sleep aid.
- 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).
- Siesta and the "post-lunch dip" – Many people have a temporary drop in alertness in the early afternoon, commonly known as the "post-lunch dip." While a large meal can make a person feel sleepy, the post-lunch dip is mostly an effect of the circadian clock. People naturally feel most sleepy at two times of the day about 12 hours apart—for example, at 2:00 a.m. and 2:00 p.m. At those two times, the body clock "kicks in." At about 2 p.m. (14:00), it overrides the homeostatic buildup 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.
- Tryptophan – The amino acid tryptophan is a building block of proteins. It has been claimed to contribute to sleepiness, since it is a precursor of the neurotransmitter serotonin, involved in sleep regulation. However, no solid data have ever linked modest dietary changes in tryptophan to changes in sleep.
- Cannabis – Some people use cannabis to induce sleepiness. Users often report relaxation and drowsiness. It has been shown that tetrahydrocannabinol (THC), the principal psychoactive constituent in cannabis, reduces the amount of REM sleep. Frequent users often report being unable to recall their dreams.
- Amphetamine (dextroamphetamine, and a related, slightly more powerful drug methamphetamine, etc.) are used to treat narcolepsy. Their most common effects are anxiety, insomnia, stimulation, increased alertness, and decreased hunger.
- Caffeine is a stimulant that works by slowing the action of the hormones in the brain that cause somnolence, particularly by acting as an antagonist at adenosine receptors. Effective dosage is individual, in part dependent on prior usage. It can cause a rapid reduction in alertness as it wears off.
- Cocaine and crack cocaine – Studies on cocaine have shown its effects to be mediated through the circadian rhythm system. This may be related to the onset of hypersomnia (oversleeping) in regard to "cocaine-induced sleep disorder."
- MDMA, including similar drugs like MDA, MMDA, or bk-MDMA – The class of drugs called empathogen-entactogens keep users awake with intense euphoria.
- Methylphenidate – Commonly known by the brand names Ritalin and Concerta, methylphenidate is similar in action to amphetamine and cocaine; its chemical composition more closely resembles that of cocaine.
- Other analeptic drugs like Modafinil and Armodafinil are prescribed to treat narcolepsy, idiopathic hypersomnia, shift work sleep disorder, and other conditions causing excessive daytime sleepiness. The precise mechanism of these central nervous system (CNS) stimulants is not known, but they have been shown to increase both the release of monoamines and levels of hypothalamic histamine, thereby promoting wakefulness.
Nutritional effects on sleep
Dietary and nutritional choices affect sleep duration and quality. Research is being conducted in an attempt to discover what kinds of nutritional choices result in better sleep quality.
A study in the Western Journal of Nursing Research in 2011 compared how sleep quality was affected by four different diets: a high-protein diet, a high-fat diet, a high-carbohydrate diet, and a control diet. Results indicated that the diets high in protein resulted in fewer wakeful episodes during night-time sleep. The high carbohydrate diet was linked to much shorter periods of quiescent or restful sleep. These results suggest that ingested nutrients do play a role in determining sleep quality. Another investigation published in Nutrition Research in 2012 examined the effects of various combinations of dietary choices in regard to sleep. Although it is difficult to determine one perfect diet for sleep enhancement, this study indicated that a variety of micro and macro nutrients are needed to maintain levels of healthful and restful sleep. A varied diet containing fresh fruits and vegetables, low-fat proteins, and whole grains can be the best nutritional option for individuals seeking to improve the quality of their sleep.
Impact on Culture
Research suggests that sleep patterns vary significantly across cultures. The most striking differences are between societies that have plentiful sources of artificial light and ones that do not. The primary difference appears to be that pre-light cultures have more broken-up sleep patterns. For example, people without artificial light might go to sleep far sooner after the sun sets, but then wake up several times throughout the night, punctuating their sleep with periods of wakefulness, perhaps lasting several hours.
The boundaries between sleeping and waking are blurred in these societies. Some observers believe that nighttime sleep in these societies is most often split into two main periods, the first characterized primarily by deep sleep and the second by REM sleep.
Some societies display a fragmented sleep pattern in which people sleep at all times of the day and night for shorter periods. In many nomadic or hunter-gatherer societies, people will sleep on and off throughout the day or night depending on what is happening. Plentiful artificial light has been available in the industrialized West since at least the mid-19th century, and sleep patterns have changed significantly everywhere that lighting has been introduced. In general, people sleep in a more concentrated burst through the night, going to sleep much later, although this is not always true.
Historian Roger Ekirch thinks that the traditional pattern of "segmented sleep," as it is called, began to disappear among the urban upper class in Europe in the late 17th century and the change spread over the next 200 years; by the 1920s "the idea of a first and second sleep had receded entirely from our social consciousness." Ekirch attributes the change to increases in "street lighting, domestic lighting and a surge in coffee houses," which slowly made nighttime a legitimate time for activity, decreasing the time available for rest. Today in most societies people sleep during the night, but in very hot climates they may sleep during the day. During Ramadan, many Muslims sleep during the day rather than at night.
In some societies, people sleep with at least one other person (sometimes many) or with animals. In other cultures, people rarely sleep with anyone except for an intimate partner. In almost all societies, sleeping partners are strongly regulated by social standards. For example, a person might only sleep with the immediate family, the extended family, a spouse or romantic partner, children, children of a certain age, children of specific gender, peers of a certain gender, friends, peers of equal social rank, or with no one at all. Sleep may be an actively social time, depending on the sleep groupings, with no constraints on noise or activity.
People sleep in a variety of locations. Some sleep directly on the ground; others on a skin or blanket; others sleep on platforms or beds. Some sleep with blankets, some with pillows, some with simple headrests, some with no head support. These choices are shaped by a variety of factors, such as climate, protection from predators, housing type, technology, personal preference, and the incidence of pests.
Zwei schlafende Mädchen auf der Ofenbank, Albert Anker, 1895
Lullaby, William-Adolphe Bouguereau, 1875
Flaming June by Frederic Lord Leighton, ~1895
Sleeping Jaguar, Paul Klimsch
Chrapek (Snorer), Wrocław's dwarfs
The Sleep of Reason Produces Monsters by Goya, 1799
Positions, practices, and rituals
- Macmillan Dictionary for Students Macmillan, Pan Ltd. (1981), p. 936. Retrieved 1 October 2009.
- Randall, David K. (19 September 2012). "Book excerpt: How the lightbulb disrupted our sleeping patterns and changed the world". National Post. Retrieved 31 August 2016.
"... the sudden introduction of bright nights during hours when it should be dark threw a wrench into a finely choreographed system of life.
- Bingham, Roger; Sejnowski, Terrence; Siegel, Jerry; Dyken, Mark Eric; Czeisler, Charles (February 2007). "Waking Up To Sleep" (Several conference videos). The Science Network. Retrieved 25 January 2008.
- "Brain Basics: Understanding Sleep". nih.gov.
- J. Alan Hobson, Edward F. Pace-Scott, & Robert Stickgold (2000), "Dreaming and the brain: Toward a cognitive neuroscience of conscious states", Behavioral and Brain Sciences 23.
- Hobson J. Alan; McCarley Robert W. (1977). "The Brain as a Dream-State Generator: An Activation-Synthesis Hypothesis of the Dream Process". American Journal of Psychiatry. 134 (12): 1335–1348. doi:10.1176/ajp.134.12.1335. PMID 21570.
- Brown et al. (2012), "Control of Sleep and Wakefulness", p. 1118–1119. "Compared with wakefulness, sleep reduces brain energy demands, as suggested by the 44% reduction in the cerebral metabolic rate (CMR) of glucose (791) and a 25% reduction in the CMR of O2 (774) during sleep."
- Siegel Jerome M (2008). "Do all animals sleep?". Trends in Neurosciences. 31 (4): 208–13. doi:10.1016/j.tins.2008.02.001.
- Eve Van Cauter & Karine Spiegel (1999). "Circadian and Sleep Control of Hormonal Secretions", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms, pp. 397–425.
- Brown et al. (2012), "Control of Sleep and Wakefulness", p. 1087.
- Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, p. 9–11.
- Silber MH, Ancoli-Israel S, Bonnet MH, Chokroverty S, Grigg-Damberger MM, Hirshkowitz M, Kapen S, Keenan SA, Kryger MH, Penzel T, Pressman MR, Iber C (March 2007). "The visual scoring of sleep in adults" (PDF). Journal of Clinical Sleep Medicine. 3 (2): 121–31. PMID 17557422.
- Brown et al. (2012), "Control of Sleep and Wakefulness", pp. 1108–1109.
- Brown et al. (2012), "Control of Sleep and Wakefulness", pp. 1100–1102.
- Parmeggiani (2011), Systemic Homeostasis and Poikilostasis in Sleep, passim.
- Fuller Patrick M.; Gooley Joshua J.; Saper Clifford B. (2006). "Neurobiology of the Sleep-Wake Cycle: Sleep Architecture, Circadian Regulation, and Regulatory Feedback". Journal of Biological Rhythms. 21: 6.
- Schacter, Daniel L.; Gilbert, Daniel T. and Wegner, Daniel M. (2009) Psychology, Worth Publishers, ISBN 1429206152
- Waterhouse Jim; Fukuda Yumi; Morita Takeshi (2012). "Daily rhythms of the sleep-wake cycle". Journal of Physiological Anthropology. 31 (5).
- David G. Myers (22 September 2003). Psychology, Seventh Edition, in Modules (High School Version). Macmillan. pp. 268–. ISBN 978-0-7167-8595-8. Retrieved 22 August 2012.
- Saladin, Kenneth S. (2012). Anatomy and Physiology: The Unity of Form and Function, 6th Edition. McGraw-Hill. p. 537. ISBN 978-0-07-337825-1.
- Siegel, Jerome M (1999). "Sleep". Encarta Encyclopedia. Microsoft. Archived from the original on 14 December 2007. Retrieved 25 January 2008.
- Carlson NR, Miller HL, Heth DS, Donahoe JW, Martin GN (2010). Psychology The Science of Behavior, Books a La Carte Edition. Pearson College Div. ISBN 0205762239.
- Hock, R. R. (2013). To sleep, no doubt to dream… In Forty Studies That Changed Psychology (7th ed., pp. 42–49). Upper Saddle River, NJ: Pearson Education. ISBN 0205918395.
- William Dement, "The Effect of Dream Deprivation: The need for a certain amount of dreaming each night is suggested by recent experiments." Science 131.3415, 10 June 1960.
- Åkerstedt Torbjorn; Billiard Michel; Bonnet Michael; Ficca Gianluca; Garma Lucile; Mariotti Maurizio; Salzarulo Piero; Schulz Hartmut (2002). "Awakening from Sleep". Sleep Medicine Reviews. 6 (4): 267–286. doi:10.1053/smrv.2001.0202.
- Roenneberga Till; Kuehnlea Tim; Judaa Myriam; Kantermanna Thomas; Allebrandta Karla; Gordijnb Marijke; Merrow Martha (2007). "Epidemiology of the human circadian clock". Sleep Medicine Reviews. 11: 429–438. doi:10.1016/j.smrv.2007.07.005. PMID 17936039.
- Basner Mathias; Dinges David F (2009). "Dubious Bargain: Trading Sleep for Leno and Letterman". Sleep. 32: 6.
- "Sleep inertia.". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 20 April 2016.
- Fenton, Reuven (29 August 2007). "Bio-alarm clocks set for perfect wake-up". Reuters. Retrieved 9 June 2008.
- Loomis AL, Harvey EN, Hobart GA (1937). "III Cerebral states during sleep, as studied by human brain potentials". J Exp Psychol. 21 (2): 127–44. doi:10.1037/h0057431.
- Dement W, Kleitman N (1957). "Cyclic variations in EEG during sleep and their relation to eye movements, body motility and dreaming". Electroencephalogr Clin Neurophysiol. 9 (4): 673–90. doi:10.1016/0013-4694(57)90088-3. PMID 13480240.
- Rechtschaffen A, Kales A, editors. (1968). A Manual of Standardized Terminology, Techniques and Scoring System for Sleep Stages of Human Subjects. (PDF). Washington: Public Health Service, US Government Printing Office.
- Iber, C; Ancoli-Israel, S; Chesson, A; Quan, SF for the American Academy of Sleep Medicine (2007). The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester: American Academy of Sleep Medicine.
- Psychology World (1998). "Stages of Sleep" (PDF). Retrieved 15 June 2008.
(includes illustrations of "sleep spindles" and "K-complexes")
- Schulz H (April 2008). "Rethinking sleep analysis". Journal of Clinical Sleep Medicine. 4 (2): 99–103. PMC . PMID 18468306.
- Phyllis C. Zee & Fred W. Turek (1999), "Introduction to Sleep and Circadian Rhythms", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms, pp. 1–17.
- Derk-Jan Dijk & Dale M. Edgar (1999), "Circadian and Homeostatic Control of Wakefulness and Sleep", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms', pp. 111–147'
- Charles A. Czeisler & Kenneth P. Wright, Jr. (1999), "Influence of Light on Circadian Rhythmicity in Humans", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms, pp. 149–180.
- Piotr Zlomanczuk & William J. Schwartz (1999). "Cellular and Molecular Mechanisms of Circadian Rhythms in Mammals", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms, pp. 309–342.
- Fred W. Turek & Charles A. Czeisler (1999). "Role of Melatonin in the Regulation of Sleep", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms, pp. 181–195.
- David R. Weaver (1999), "Melatonin and Circadian Rhythmicity in Vertebrates: Physiological Roles and Pharmacological Effects", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms, pp. 197–262.
- Thomas A. Wehr (1999). "The Impact of Changes in Nightlength (Scotoperiod) on Human Sleep", in Turek & Zee (eds.), Regulation of Sleep and Circadian Rhythms, pp. 263–285.
- Wyatt JK, Ritz-De Cecco A, Czeisler CA, Dijk DJ (1 October 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.
- Challet Etienne (2007). "Minireview: Entrainment of the Suprachiasmatic Clockwork in Diurnal and Nocturnal Mammals". Endocrinology. 148: 12.
- Dagan Y (2002). "Circadian rhythm sleep disorders (CRSD)" (PDF: full text). Sleep Med Rev. 6 (1): 45–54. doi:10.1053/smrv.2001.0190. PMID 12531141. Retrieved 2016-06-05.
Early onset of CRSD, the ease of diagnosis, the high frequency of misdiagnosis and erroneous treatment, the potentially harmful psychological and adjustment consequences, and the availability of promising treatments, all indicate the importance of greater awareness of these disorders.
- Naska A, Oikonomou E, Trichopoulou A, Psaltopoulou T, Trichopoulos D (2007). "Siesta in healthy adults and coronary mortality in the general population". Archives of Internal Medicine. 167 (3): 296–301. doi:10.1001/archinte.167.3.296. PMID 17296887.
- Zaregarizi M, Edwards B, George K, Harrison Y, Jones H, Atkinson G (2007). "Acute changes in cardiovascular function during the onset period of daytime sleep: comparison to lying awake and standing". Journal of Applied Physiology (Bethesda, Md. : 1985). 103 (4): 1332–8. doi:10.1152/japplphysiol.00474.2007. PMID 17641220.
- MohammadReza Zaregarizi. Effects of Exercise & Daytime Sleep on Human Haemodynamics: With Focus on Changes in Cardiovascular Function during Daytime Sleep Onset. ISBN 978-3-8484-1726-1.. Dr. Zaregarizi and his team have concluded that the acute time of falling asleep was when beneficial cardiovascular changes take place. This study has indicated that a large decline in BP occurs during the daytime sleep-onset period only when sleep is expected. However, when subjects rest in a supine position, the same reduction in BP is not observed. This BP reduction may be associated with the lower coronary mortality rates seen in Mediterranean and Latin American populations in which siestas are common. Dr. Zaregarizi assessed cardiovascular function (BP, heart rate, and measurements of blood vessel dilation) while nine healthy volunteers, 34 years of age on average, spent an hour standing quietly, reclining at rest but not sleeping, or reclining to nap. All participants were restricted to 4 hours of sleep on the night prior to each of the sleep laboratory tests. During the three phases of daytime sleep, he noted significant reductions in BP and heart rate. By contrast, they did not observe changes in cardiovascular function while the participants were standing or reclining at rest. These findings also show that the greatest decline in BP occurs between lights-off and onset of daytime sleep itself. During this sleep period, which lasted 9.7 minutes on average, BP decreased, while blood vessel dilation increased by more than 9 percent. "There is little change in blood pressure once a subject is actually asleep," Dr. Zaregarizi noted, and he found minor changes in blood vessel dilation during sleep.
- Kaul P, Passafiume J, Sargent CR, O'Hara BF (2010). "Meditation acutely improves psychomotor vigilance, and may decrease sleep need". Behav Brain Funct. 6: 47. doi:10.1186/1744-9081-6-47 (inactive 2 February 2015). PMC . PMID 20670413.
- Barnes, C. M.; Lucianetti, L.; Bhave, D. P.; Christian, M. S. (2015). "You wouldn't like me when I'm sleepy: Leaders' sleep, daily abusive supervision, and work unit engagement". Academy of Management Journal. 58 (5): 1419–1437.
- Harvey, A. G.; Payne, S. (2002). "The management of unwanted pre-sleep thoughts in insomnia: Distraction with imagery versus general distraction". Behaviour Research and Therapy. 40 (3): 267–277. PMID 11863237.
- Brown et al. (2012), "Control of Sleep and Wakefulness", pp. 1134–1138.
- Zisapel N (2007). "Sleep and sleep disturbances: biological basis and clinical implications". Cell Mol Life Sci. 64 (10): 1174–86. doi:10.1007/s00018-007-6529-9. PMID 17364142.
- de Benedictis, Tina; Larson, Heather; Kemp, Gina; Barston, Suzanne; Segal, Robert (2007). "Understanding Sleep: Sleep Needs, Cycles, and Stages". Helpguide.org. Archived from the original on 24 January 2008. Retrieved 25 January 2008.
- "Gene Cuts Need for Sleep - Sleep Disorders Including, Sleep Apnea, Narcolepsy, Insomnia, Snoring and Nightmares on MedicineNet.com". Archived from the original on 14 July 2011. Retrieved 11 June 2010.
- He Y, Jones CR, Fujiki N, Xu Y, Guo B, Holder JL, Rossner MJ, Nishino S, Fu YH (2009). "The transcriptional repressor DEC2 regulates sleep length in mammals". Science. 325 (5942): 866–70. doi:10.1126/science.1174443. PMC . PMID 19679812.
- Gottselig JM, Adam M, Rétey JV, Khatami R, Achermann P, Landolt HP (March 2006). "Random number generation during sleep deprivation: effects of caffeine on response maintenance and stereotypy". Journal of Sleep Research. 15 (1): 31–40. doi:10.1111/j.1365-2869.2006.00497.x. PMID 16490000.
- Iglowstein I, Jenni OG, Molinari L, Largo RH (February 2003). "Sleep duration from infancy to adolescence: reference values and generational trends". Pediatrics. 111 (2): 302–7. 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...
- Molecules that build up and make you sleep. thebrain.mcgill.ca
- Brown et al. (2012), "Control of Sleep and Wakefulness", pp. 1113–1114. "Adenosine levels correlate with time spent awake. Endogenous, extracellular adenosine levels in the BF (102, 591, 843, 1017, 1018) and cortex (591, 1017) increase in proportion with time spent awake. Thus adenosine induces sleep and adenosine levels track sleep need, fulfilling the criteria for adenosine being a homeostatic sleep factor."
- Reference list is found on image page in Commons: Commons:File:Effects of sleep deprivation.svg#References
- Dijk DJ, Lockley SW (February 2002). "Functional Genomics of Sleep and Circadian Rhythm Invited Review: Integration of human sleep-wake regulation and circadian rhythmicity". J Appl Physiol. 92 (2): 852–62. doi:10.1152/japplphysiol.00924.2001 (inactive 2 February 2015). PMID 11796701.
Consolidation of sleep for 8 h or more is only observed when sleep is initiated ~6–8 h before the temperature nadir.
- Wyatt JK, Ritz-De Cecco A, Czeisler CA, Dijk DJ (1 October 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.
... 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
- Lauderdale DS, Knutson KL, Yan LL, Liu K, Rathouz PJ (2008). "Self-Reported and Measured Sleep Duration: How Similar Are They?". Epidemiology. 19 (6): 838–45. doi:10.1097/EDE.0b013e318187a7b0. PMC . PMID 18854708.
- Insomnia Causes. Healthcommunities.com. Original Publication: 1 December 2000, Updated: 1 December 2007.
- Rhonda Rowland (15 February 2002). "Experts challenge study linking sleep, life span". CNN. Retrieved 29 October 2013.
- Patel SR, Ayas NT, Malhotra MR, White DP, Schernhammer ES, Speizer FE, Stampfer MJ, Hu FB (May 2004). "A prospective study of sleep duration and mortality risk in women". Sleep. 27 (3): 440–4. PMID 15164896.
- Patel SR, Malhotra A, Gottlieb DJ, White DP, Hu FB (July 2006). "Correlates of long sleep duration". Sleep. 29 (7): 881–9. PMC . PMID 16895254.; cf. Irwin MR, Ziegler M (February 2005). "Sleep deprivation potentiates activation of cardiovascular and catecholamine responses in abstinent alcoholics". Hypertension. 45 (2): 252–7. doi:10.1161/01.HYP.0000153517.44295.07. PMID 15642774.
- Ferrie JE, Shipley MJ, Cappuccio FP, Brunner E, Miller MA, Kumari M, Marmot MG (December 2007). "A prospective study of change in sleep duration: associations with mortality in the Whitehall II cohort". Sleep. 30 (12): 1659–66. PMC . PMID 18246975. Lay summary – University of Warwick.
- Thase ME (2006). "Depression and sleep: pathophysiology and treatment" (Free full text). Dialogues in clinical neuroscience. 8 (2): 217–226. ISSN 1294-8322. PMC . PMID 16889107.
- Mann, Joseph John; David J. Kupfer (1993). Biology of Depressive Disorders: Subtypes of depression and comorbid disorders, Part 2 (Google books). Springer. p. 49. ISBN 0-306-44296-5. Retrieved 24 July 2009.
- Dahl RE (2009). "The regulation of sleep and arousal: Development and psychopathology". Development and Psychopathology. 8 (01): 3–27. doi:10.1017/S0954579400006945.
- Jenni OG, Dahl RE (2008). "Sleep, cognition, and neuron, and emotion: A developmental review.". In Nelson CA, Luciana M. Handbook of developmental cognitive neuroscience (2nd ed.). Cambridge, Mass.: MIT Press. pp. 807–817. ISBN 0262141043.
- Scher A (2005). "Infant sleep at 10 months of age as a window to cognitive development". Early Human Development. 81 (3): 289–92. doi:10.1016/j.earlhumdev.2004.07.005. PMID 15814211.
- Spruyt K, Aitken RJ, So K, Charlton M, Adamson TM, Horne RS (2008). "Relationship between sleep/wake patterns, temperament and overall development in term infants over the first year of life". Early Human Development. 84 (5): 289–96. doi:10.1016/j.earlhumdev.2007.07.002. PMID 17707119.
- Bernier A, Carlson SM, Bordeleau S, Carrier J (2010). "Relations between physiological and cognitive regulatory systems: infant sleep regulation and subsequent executive functioning". Child Development. 81 (6): 1739–52. doi:10.1111/j.1467-8624.2010.01507.x. PMID 21077861.
- Hupbach A, Gomez RL, Bootzin RR, Nadel L (2009). "Nap-dependent learning in infants". Developmental Science. 12 (6): 1007–12. doi:10.1111/j.1467-7687.2009.00837.x. PMID 19840054.
- Hirshkowitz, Max; Whiton, Kaitlyn; et al. (14 January 2015). "National Sleep Foundation's sleep time duration recommendations: methodology and results summary". Sleep Health: Journal of the National Sleep Foundation. Elsevier Inc. 1: 40–43. doi:10.1016/j.sleh.2014.12.010. Retrieved 4 February 2015.
- "Backgrounder: Later School Start Times". National Sleep Foundation. n.d. Retrieved 2 October 2009.
Teens are among those least likely to get enough sleep; while they need on average 9 1⁄4 hours of sleep per night...
- "How Much Sleep Is Enough?". National Heart, Lung and Blood Institute. Retrieved 25 July 2015.
- Max, D. T. The Secrets of Sleep National Geographic Magazine, May 2010.
- Cirelli C, Tononi G (26 August 2008). "Is Sleep Essential?". PLoS Biol. Public Library of Science. 6 (8): e216. doi:10.1371/journal.pbio.0060216. PMC . PMID 18752355.
... it would seem that searching for a core function of sleep, particularly at the cellular level, remains a worthwhile exercise
- "Sleep Syllabus. B. The Phylogeny of Sleep". Sleep Research Society, Education Committee. Archived from the original on 2005-03-18. Retrieved 26 September 2010.
- "Function of Sleep.". Scribd.com. Retrieved on 1 December 2011.
- Daan S, Barnes BM, Strijkstra AM (1991). "Warming up for sleep? Ground squirrels sleep during arousals from hibernation". Neurosci. Lett. 128 (2): 265–8. doi:10.1016/0304-3940(91)90276-Y. PMID 1945046.
- Lulu Xie, Hongyi Kang1, Qiwu Xu, Michael J. Chen, Yonghong Liao, Meenakshisundaram Thiyagarajan, John O'Donne, Daniel J. Christensen, Charles Nicholson, Jeffrey J. Iliff, Takahiro Takano, Rashid Deane, Maiken Nedergaard (2013). "Sleep Drives Metabolite Clearance from the Adult Brain". Science. 342 (6156): 373–377. doi:10.1126/science.1241224. PMID 24136970. Retrieved 18 October 2013.
- Gümüştekín K, Seven B, Karabulut N, Aktaş O, Gürsan N, Aslan S, Keleş M, Varoglu E, Dane S (2004). "Effects of sleep deprivation, nicotine, and selenium on wound healing in rats". Int J Neurosci. 114 (11): 1433–42. doi:10.1080/00207450490509168. PMID 15636354.
- Zager A, Andersen ML, Ruiz FS, Antunes IB, Tufik S (2007). "Effects of acute and chronic sleep loss on immune modulation of rats". American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. 293 (1): R504–9. doi:10.1152/ajpregu.00105.2007. PMID 17409265.
- Opp MR (January 2009). "Sleeping to fuel the immune system: mammalian sleep and resistance to parasites" (Full text, Creative Commons Attribution License). BMC Evolutionary Biology. BioMed Central Ltd. 9: 1471–2148. doi:10.1186/1471-2148-9-8. PMC . PMID 19134176.
- Peres, Judy (14 March 2012) A good reason to get your zzz's Chicago Tribune Health, retrieved 26 March 2014
- Reimund E (October 1994). "The free radical flux theory of sleep". Medical Hypotheses. 45 (4): 231–3. doi:10.1016/0306-9877(94)90071-X. PMID 7838006.
- Jenni OG, Molinari L, Caflisch JA, Largo RH (2007). "Sleep duration from ages 1 to 10 years: Variability and stability in comparison with growth". Pediatrics. 120 (4): e769–e776. doi:10.1542/peds.2006-3300. PMID 17908734.
- 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". Journal of the American Medical Association. 284 (7): 861–868. doi:10.1001/jama.284.7.861. PMID 10938176.
- "Brain may flush out toxins during sleep". National Institutes of Health. Retrieved 25 October 2013.
- Siegel JM (2005). "Clues to the functions of mammalian sleep". Nature. 437 (7063): 1264–1271. Bibcode:2005Natur.437.1264S. doi:10.1038/nature04285. PMID 16251951.
- 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. p. 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).
- Guilio Tononi and Chiara Cirelli. "Perchance to Prune" Scientific American. August 2013. Pgs 34–39. Print.
- Marks GA, Shaffery JP, Oksenberg A, Speciale SG, Roffwarg HP (1995). "A functional role for REM sleep in brain maturation". Behavioural Brain Research. 69 (1–2): 1–11. doi:10.1016/0166-4328(95)00018-o. PMID 7546299.
- Mirmiran M, Scholtens J, van de Poll NE, Uylings HB, van der Gugten J, Boer GJ (April 1983). "Effects of experimental suppression of active (REM) sleep during early development upon adult brain and behavior in the rat". Brain Research. 283 (2–3): 277–86. doi:10.1016/0165-3806(83)90184-0. PMID 6850353.
- Morrissey MJ, Duntley SP, Anch AM, Nonneman R (2004). "Active sleep and its role in the prevention of apoptosis in the developing brain". Medical Hypotheses. 62 (6): 876–9. doi:10.1016/j.mehy.2004.01.014. PMID 15142640.
- Amanda Schaffer (27 May 2007). "Why do we Sleep?". Slate.com. Retrieved 23 August 2008.
- Turner TH, Drummond SP, Salamat JS, Brown GG (2007). "Effects of 42 hr sleep deprivation on component processes of verbal working memory". Neuropsychology. 21 (6): 787–795. doi:10.1037/0894-4184.108.40.2067. PMID 17983292.
- Daltrozzo J, Claude L, Tillmann B, Bastuji H, Perrin F (2012). Zang, Yu-Feng, ed. "Working Memory Is Partially Preserved during Sleep". PLoS ONE. 7 (12): e50997. doi:10.1371/journal.pone.0050997. PMC . PMID 23236418.
- Cited in Born J, Rasch B, Gais S (2006). "Sleep to remember". Neuroscientist. 12 (5): 410–24. doi:10.1177/1073858406292647. PMID 16957003.
- Datta S (2000). "Avoidance task training potentiates phasic pontine-wave density in the rat: A mechanism for sleep-dependent plasticity". The Journal of Neuroscience. 20 (22): 8607–8613. PMID 11069969.
- Kudrimoti HS, Barnes CA, McNaughton BL (1999). "Reactivation of hippocampal cell assemblies: Effects of behavioral state, experience, and EEG dynamics". The Journal of Neuroscience. 19 (10): 4090–4101. PMID 10234037.
- Marshall et al., 2006, as cited in Walker MP (2009). "The role of sleep in cognition and emotion". Annals of the New York Academy of Sciences. 1156: 168–97. doi:10.1111/j.1749-6632.2009.04416.x. PMID 19338508.
- Saper CB, Scammell TE, Lu J (2005). "Hypothalamic regulation of sleep and circadian rhythms". Nature. 437 (7063): 1257–63. doi:10.1038/nature04284. PMID 16251950.
- Stickgold R (2005). "Sleep-dependent memory consolidation". Nature. 437 (7063): 1272–8. doi:10.1038/nature04286. PMID 16251952.
- Capellini I, McNamara P, Preston BT, Nunn CL, Barton RA (2009). Sporns, Olaf, ed. "Does sleep play a role in memory consolidation? A comparative test". PLoS ONE. 4 (2): 4609. Bibcode:2009PLoSO...4.4609C. doi:10.1371/journal.pone.0004609. PMC . PMID 19240803.
- Cirelli C, Gutierrez CM, Tononi G (2004). "Extensive and divergent effects of sleep and wakefulness on brain gene expression". Neuron. 41 (1): 35–43. doi:10.1016/S0896-6273(03)00814-6. PMID 14715133.
- Choi, Charles Q. (25 August 2009) New Theory Questions Why We Sleep, LiveScience.com.
- "BPS Research Digest: An afternoon nap tunes out negative emotions, tunes in positive ones". bps.org.uk.
- Naiman, Rubin (2007). "How To Interpret Your Dreams". Allure. 17 (5): n/a.
- See Freud: The Interpretation of Dreams.
- Connor, Steve (3 April 2009). "Revealed: why we need a good night's sleep". The Independent. Archived from the original on 2009-04-05. Retrieved 2 December 2010.
- Pinel, John P. J. (2011). Biopsychology, 8th Edition. Pearson Education, Inc. p. 359. ISBN 978-0-205-83256-9.
- Tsoukalas, Ioannis (2012). "The origin of REM sleep: A hypothesis". Dreaming. 22 (4): 253–283. doi:10.1037/a0030790.
- Vitelli, R. (2013). Exploring the Mystery of REM Sleep. Psychology Today, On-line blog, 25 March
- Low PS, Shank SS, Sejnowski TJ, Margoliash D (2008). "Mammalian-like features of sleep structure in zebra finches". Proceedings of the National Academy of Sciences of the United States of America. 105 (26): 9081–9086. Bibcode:2008PNAS..105.9081L. doi:10.1073/pnas.0703452105. PMC . PMID 18579776.
- Rial RV, Akaârir M, Gamundí A, Nicolau C, Garau C, Aparicio S, Tejada S, Gené L, González J, De Vera LM, Coenen AM, Barceló P, Esteban S (2010). "Evolution of wakefulness, sleep and hibernation: From reptiles to mammals". Neuroscience and Biobehavioral Reviews. 34 (8): 1144–1160. doi:10.1016/j.neubiorev.2010.01.008. PMID 20109487.
- Capellini I, Nunn CL, McNamara P, Preston BT, Barton RA (2008). "Energetic constraints, not predation, influence the evolution of sleep patterning in mammals". Functional Ecology. 22 (5): 847–853. doi:10.1111/j.1365-2435.2008.01449.x. PMC . PMID 20428321.
- McNamara, P., R. A. Barton, and C. L. Nunn. 2010, Evolution of sleep: Phylogenetic and functional perspectives. Cambridge University Press, Cambridge.
- Capellini, I., C. L. Nunn, P. McNamara, B. T. Preston, and R. A. Barton. 2008. Energetic constraints, not predation, influence the evolution of sleep patterning in mammals. Functional Ecology 22:847-853.
- Acerbi, A., P. McNamara, and C. L. Nunn. 2008. To sleep or not to sleep: The ecology of sleep in artificial organisms. BMC Ecology 8:10.
- Preston, B. T., I. Capellini, P. McNamara, R. A. Barton, and C. L. Nunn. 2009. Parasite resistance and the adaptive significance of sleep. Bmc Evolutionary Biology 9.
- He Y, Jones CR, Fujiki N, Xu Y, Guo B, Holder JL, Rossner MJ, Nishino S, Fu YH (2009). "The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals". Science. 325 (5942): 866–70. doi:10.1126/science.1174443. PMC . PMID 19679812.
- Brown et al. (2012), "Control of Sleep and Wakefulness", pp. 1138–1102.
- "The ABCC9 of Sleep: A Genetic Factor Regulates How Long We Sleep". Science Daily. Retrieved 21 August 2012.
- Mukhametov LM, Supin AY, Polyakova IG (14 October 1977). "Interhemispheric asymmetry of the electroencephalographic sleep patterns in dolphins". Brain Research. 134 (3): 581–584. doi:10.1016/0006-8993(77)90835-6. PMID 902119.
- Faraco, Juliette (1 August 2000). "Re: Are there animals who don't sleep or that sleep very little?". MadSci Network: Zoology. Retrieved 25 January 2008.
- The giraffe only sleeps 2 hours a day in about 5–15 minute sessions. Koalas are the longest sleeping-mammals, about 20–22 hours a day.Insomnia Mania: Newborn Mammals Don't Sleep for a Month. LiveScience.com
- Hecker, Bruce (2 February 1998). "How do Whales and Dolphins Sleep without Drowning?". Scientific American. mirror
- Britt, Robert (29 June 2005). "Insomnia Mania: Newborn Mammals Don't Sleep for a Month". Live Science.
- "Seals Sleep with Only Half of Their Brain at a Time". Oceana.org. 12 March 2013.
- Lapierre JL, Kosenko PO, Lyamin OI, Kodama T, Mukhametov LM, Siegel JM (2007). "Cortical Acetylcholine Release Is Lateralized during Asymmetrical Slow-Wave Sleep in Northern Fur Seals". The Journal of Neuroscience. 27 (44): 11999–12006. doi:10.1523/JNEUROSCI.2968-07.2007. PMID 17978041.
- "Study Seals Sleep with Half Their Brain". upi.com. 19 February 2013.
- Brown et al. (2012), "Control of Sleep and Wakefulness", pp. 1146–1147.
- Buman, M.P. and King, A.C.: "Exercise as a Treatment to Enhance Sleep", American Journal of Lifestyle Medicine, Nov–Dec 2010.
- López HH, Bracha AS, Bracha HS (2002). "Evidence based complementary intervention for insomnia" (PDF). Hawaii Med J. 61 (9): 192, 213. PMID 12422383.
- "What is Sleep Apnoea? (Sleep Apnea)". britishsnoring.co.uk.
- Dugdale, David, C. (22 May 2011). Sleepwalking. US National institutes of health.
- How Aging Changes Sleep Patterns by Allison Aubrey. Morning Edition, 3 August 2009.
- Lee-chiong, Teofilo (24 April 2008). Sleep Medicine: Essentials and Review. Oxford University Press, USA. p. 52. ISBN 0-19-530659-7.
- Alcohol and Sleep. Alcoholism.about.com (10 January 2011). Retrieved on 1 December 2011.
- Marijuana, Sleep and Dreams. psychologytoday.com. Retrieved on 10 February 2012.
- Abarca C, Albrecht U, Spanagel R (June 2002). "Cocaine sensitization and reward are under the influence of circadian genes and rhythm". Proceedings of the National Academy of Sciences of the United States of America. 99 (13): 9026–30. doi:10.1073/pnas.142039099. PMC . PMID 12084940.
- Primary hypersomnia: Diagnostic Features. mindsite.com
- Lindseth, Gelinda, Paul Lindseth, and Mark Thompson. "Nutritional Effects on Sleep." Western Journal of Nursing Research (2011): n. pag. Web.
- Peuhkuri Katri; Sihvola Nora; Korpela Riitta (2012). "Diet Promotes Sleep Duration and Quality". Nutrition Research. 32 (5): 309–19. doi:10.1016/j.nutres.2012.03.009.
- Carol M. Worthman; Melissa K. Melby. "6. Toward a comparative developmental ecology of human sleep" (PDF). A comparative developmental ecology (PDF). Emory University.
- Slumber's Unexplored Landscape. Science News Online (25 September 1999). Retrieved on 1 December 2011.
- Hegarty, Stephanie (22 February 2012). "The myth of the eight-hour sleep". BBC News. Retrieved 22 February 2012.
- Ellsworth Huntington, Civilization and Climate – Page 126
- Dilara Hafiz; Imran Hafiz; Yasmine Hafiz (2009). The American Muslim Teenager's Handbook. ISBN 978-1416986997.
- Brown Ritchie E.; Basheer Radhika; McKenna James T.; Strecker Robert E.; McCarley Robert W. (2012). "Control of Sleep and Wakefulness". Physiological Review. 92: 1087–1187. doi:10.1152/physrev.00032.2011. PMC . PMID 22811426.
- Parmeggiani, Pier Luigi (2011). Systemic Homeostasis and Poikilostasis in Sleep: Is REM Sleep a Physiological Paradox? London: Imperial College Press. ISBN 978-1-94916-572-2
- Turek, Fred W. & Phyllis C. Zee, eds. (1999). Regulation of Sleep and Circadian Rhythms. New York: Marcel Dekker, Inc. ISBN 0-8247-0231-X
|Wikimedia Commons has media related to Sleep.|
|Look up sleep in Wiktionary, the free dictionary.|
- nih.gov, National Center on Sleep Disorders Research
- National Sleep Foundation, information on School Start Time and Sleep at National Sleep Foundation
- HealthySleep.med.harvard.edu, from the Division of Sleep Medicine at Harvard Medical School and WGBH Educational Foundation
- PLOSjournals.org, Is Sleep Essential? by Chiara Cirelli and Giulio Tononi, from the Public Library of Science, Biology
- New York Times, 2012; "Rethinking Sleep"
- Sleep.com, an informational database offering sleep-related articles and resources.