Sleep, Dreaming, and Circadian Rhythms How Much Do You Need to Sleep?
14.1 Stages of Sleep
14.2 Why Do We Sleep, and Why Do We Sleep When We Do?
14.3 Effects of Sleep Deprivation
14.4 Circadian Sleep Cycles
14.5 Four Areas of the Brain Involved in Sleep
14.6 Drugs That Affect Sleep
14.7 Sleep Disorders
14.8 Effects of Long-Term Sleep Reduction
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Even though she is now retired she is still busy in the community, helping sick friends whenever requested. She is an active painter and . . . writer. Although she becomes tired physically, when she needs to sit down to rest her legs, she does not ever report feeling sleepy. During the night she sits on her bed . . . reading, writing, crocheting or painting. At about 2:00 A.M. she falls asleep without any preceding drowsiness often while still holding a book in her hands. When she wakes about an hour later, she feels as wide awake as ever. . . .
We invited her along to the laboratory. She came will- ingly but on the first evening we hit our first snag. She an- nounced that she did not sleep at all if she had interesting things to do, and by her reckoning a visit to a university sleep laboratory counted as very interesting. Moreover, for the first time in years, she had someone to talk to for the whole of the night. So we talked.
In the morning we broke into shifts so that some could sleep while at least one person stayed with her and entertained her during the next day. The second night was a repeat performance of the first night. . . .
In the end we prevailed upon her to allow us to apply EEG electrodes and to leave her sitting comfortably on the bed in the bedroom. She had promised that she would co-operate by not resisting sleep although she claimed not to be especially tired. . . . At approximately 1:30 A.M., the EEG record showed the first signs of sleep even though . . . she was still sitting with the book in her hands. . . .
The only substantial difference between her sleep and what we might have expected. . . was that it was of short duration. . . . [After 99 minutes], she had no further inter- est in sleep and asked to . . . join our company again.
(“The Case of the Woman Who Wouldn’t Sleep,” from The Sleep Instinct by R. Meddis. Copyright © 1977, Routledge & Kegan Paul, London, pp. 42–44. Reprinted by permission of the Taylor & Francis Group.)
14.1 Stages of Sleep
Many changes occur in the body during sleep. This section introduces you to the major ones.
Three Standard Psychophysiological Measures of Sleep There are major changes in the human EEG during the course of a night’s sleep. Although the EEG waves that ac- company sleep are generally high-voltage and slow, there are periods throughout the night that are dominated by low- voltage, fast waves similar to those in nonsleeping individuals. In the 1950s, it was discovered that rapid eye movements (REMs) occur under the closed eyelids of sleepers during these periods of low-voltage, fast EEG activity. And in 1962,
Most of us have a fondness for eating and sex—the two highly esteemed motivated behaviorsdiscussed in Chapter 12 and 13. But the amount of time devoted to these behaviors by even the most amorous gourmands pales in comparison to the amount of time spent sleeping: Most of us will sleep for well over 175,000 hours in our lifetimes. This extraordinary com- mitment of time implies that sleep fulfills a critical biolog- ical function. But what is it? And what about dreaming: Why do we spend so much time dreaming? And why do we tend to get sleepy at about the same time every day? Answers to these questions await you in this chapter.
Almost every time I lecture about sleep, somebody asks “How much sleep do we need?” Each time, I provide the same unsatisfying answer: I explain that there are two fun-
damentally different answers to this question, but neither has emerged a clear winner.
One answer stresses the presumed health-promoting and recuperative powers of sleep and suggests that people need as much sleep as they can comfortably get—the usual prescription being at least 8 hours per night. The other answer is that many of us sleep more than we need to and are consequently sleeping part of our life away. Just think how your life could change if you slept 5 hours per night instead of 8. You would have an extra 21 waking hours each week, a mind-boggling 10,952 hours each decade.
As I prepared to write this chapter, I began to think of the personal implications of the idea that we get more sleep than we need. That is when I decided to do some-
thing a bit unconventional. I am going to participate in a sleep-reduction experiment—by trying to get no more
than 5 hours of sleep per night—11:00 P.M. to 4:00 A.M.— until this chapter is written. As I begin, I am excited by the prospect of having more time to write, but a little worried that this extra time might cost me too dearly.
It is now the next day—4:50 Saturday morning to be exact—and I am just sitting down to write. There was a party last night, and I didn’t make it to bed by 11:00; but considering that I slept for only 3 hours and 35 minutes, I feel quite good. I wonder what I will feel like later in the day. In any case, I will report my experiences to you at the end of the chapter.
The following case study challenges several common beliefs about sleep. Ponder its implications before pro- ceeding to the body of the chapter.
The Case of the Woman Who Wouldn’t Sleep Miss M . . . is a busy lady who finds her ration of twenty- three hours of wakefulness still insufficient for her needs.
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Berger and Oswald discovered that there is also a loss of elec- tromyographic activity in the neck muscles during these same sleep periods. Subsequently, the electroencephalo- gram (EEG), the electrooculogram (EOG), and the neck electromyogram (EMG) became the three standard psy- chophysiological bases for defining stages of sleep.
Figure 14.1 depicts a volunteer participating in a sleep experiment. A participant’s first night of sleep in a labo- ratory is often fitful. That’s why the usual practice is to have each participant sleep several nights in the labora- tory before commencing a sleep study. The disturbance of sleep observed during the first night in a sleep laboratory is called the first-night phenomenon. It is well known to graders of introductory psychology examinations because of the creative definitions of it that are offered by students who forget that it is a sleep-related, rather than a sex-related, phenomenon.
Four Stages of Sleep EEG There are four stages of sleep EEG: stage 1, stage 2, stage 3, and stage 4. Examples of these are presented in Figure 14.2.
After the eyes are shut and a person prepares to go to sleep, alpha waves—waxing and wan- ing bursts of 8- to 12-Hz EEG waves—begin to punctuate the low-voltage, high-frequency waves of alert wakefulness. Then, as the person falls asleep, there is a sud- den transition to a period of stage 1 sleep EEG. The stage 1 sleep EEG is a low-voltage, high- frequency signal that is similar to, but slower than, that of alert wakefulness.
There is a gradual increase in EEG voltage and a decrease in EEG frequency as the person pro- gresses from stage 1 sleep through stages 2, 3, and 4. Accordingly, the stage 2 sleep EEG has a slightly
35714.1 ■ Stages of Sleep
Alert wakefulness
Just before sleep
Stage 1
Stage 2
Stage 3
Stage 4
K complexSleep spindle
Alpha waves
FIGURE 14.1 A participant in a sleep experiment.
FIGURE 14.2 The EEG of alert wakefulness, the EEG that precedes sleep onset, and the four stages of sleep EEG. Each trace is about 10 seconds long.
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higher amplitude and a lower frequency than the stage 1 EEG; in addition, it is punctuated by two characteristic wave forms: K complexes and sleep spindles. Each K com-
plex is a single large negative wave (upward deflection) fol- lowed immediately by a single
large positive wave (downward deflection)—see Cash and colleagues (2009). Each sleep spindle is a 1- to 2-second waxing and waning burst of 12- to 14-Hz waves. The stage 3 sleep EEG is defined by the occasional presence of delta waves—the largest and slowest EEG waves, with a fre- quency of 1 to 2 Hz—whereas the stage 4 sleep EEG is de- fined by a predominance of delta waves.
Once sleepers reach stage 4 EEG sleep, they stay there for a time, and then they retreat back through the stages of sleep to stage 1. However, when they return to stage 1, things are not at all the same as they were the first time through. The first period of stage 1 EEG during a night’s sleep (initial stage 1 EEG) is not marked by any striking electromyographic or electrooculographic changes, whereas subsequent periods of stage 1 sleep EEG (emergent stage 1 EEG) are accompanied by REMs and by a loss of tone in the muscles of the body core.
After the first cycle of sleep EEG—from initial stage 1 to stage 4 and back to emergent stage 1—the rest of the night is spent going back and forth through the stages. Figure 14.3 illustrates the EEG cycles of a typical night’s sleep and the close relation between emergent stage 1 sleep, REMs, and the loss of tone in core muscles. Notice that each cycle tends to be about 90 minutes long and that, as the night progresses, more and more time is spent in emergent stage 1 sleep, and less and less time is spent in the other stages, particularly stage 4. Notice also that there are brief periods during the night when the person is awake, although he or she usually does not remember these periods of wakefulness in the morning.
Let’s pause here to get some sleep-stage terms straight. The sleep associated with emergent stage 1 EEG is usually called REM sleep (pronounced “rehm”), after the associated rapid eye movements; whereas all other stages of sleep together are called NREM sleep (non-REM sleep). Stages 3 and 4 together are referred to as slow-wave sleep (SWS), after the delta waves that characterize them.
REMs, loss of core-muscle tone, and a low-amplitude, high-frequency EEG are not the only physiological corre- lates of REM sleep. Cerebral activity (e.g., oxygen con- sumption, blood flow, and neural firing) increases to waking levels in many brain structures, and there is a gen- eral increase in the variability of autonomic nervous sys- tem activity (e.g., in blood pressure, pulse, and respiration). Also, the muscles of the extremities occasionally twitch, and there is often some degree of penile erection in males.
REM Sleep and Dreaming Nathaniel Kleitman’s laboratory was an exciting place in 1953. REM sleep had just been discovered, and Kleitman and his students were driven by the fascinating implica- tion of the discovery. With the exception of the loss of tone in the core muscles, all of the other measures sug- gested that REM sleep episodes were emotion-charged. Could REM sleep be the physiological correlate of dream- ing? Could it provide researchers with a window into the subjective inner world of dreams? The researchers began by waking a few sleepers in the middle of REM episodes:
The vivid recall that could be elicited in the middle of the night when a subject was awakened while his eyes were moving rapidly was nothing short of miraculous. It [seemed to open] . . . an exciting new world to the subjects whose only previous dream memories had been the vague morning-after recall. Now, instead of perhaps some fleet- ing glimpse into the dream world each night, the subjects could be tuned into the middle of as many as ten or twelve dreams every night. (From Some Must Watch While Some Must Sleep by William C. Dement, Portable Stanford Books, Stanford Alumni Association, Stanford University, 1978, p. 37. Used by permission of William C. Dement.)
Strong support for the theory that REM sleep is the phys- iological correlate of dreaming came from the observation that 80% of awakenings from REM sleep but only 7% of awakenings from NREM (non-REM) sleep led to dream recall. The dreams recalled from NREM sleep tended to
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Stage 4
1 2 3 4
Hours
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Stage 3
Stage 2
Stage 1
Awake Periods of REM Lack of core-muscle tone
S le
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FIGURE 14.3 The course of EEG stages during a typical night’s sleep and the relation of emergent stage 1 EEG to REMs and lack of tone in core muscles.
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be isolated experiences (e.g., “I was falling”), while those associated with REM sleep tended to take the form of sto- ries, or narratives. The phenomenon of dreaming, which
for centuries had been the subject of wild speculation, was finally rendered accessi-
ble to scientific investigation.
Testing Common Beliefs about Dreaming The high correlation between REM sleep and dream re- call provided an opportunity to test some common be- liefs about dreaming. The following five beliefs were among the first to be addressed:
● Many people believe that external stimuli can become incorporated into their dreams. Dement and Wolpert (1958) sprayed water on sleeping volunteeers after
they had been in REM sleep for a few minutes, and then awakened them
a few seconds later. In 14 of 33 cases, the water was in- corporated into the dream report. The following narra- tive was reported by one participant who had been dreaming that he was acting in a play:
I was walking behind the leading lady when she sud- denly collapsed and water was dripping on her. I ran over to her and water was dripping on my back and head. The roof was leaking. . . . I looked up and there was a hole in the roof. I dragged her over to the side of the stage and began pulling the curtains. Then I woke up. (p. 550)
● Some people believe that dreams last only an instant, but research suggests that dreams run on “real time.” In one study (Dement & Kleitman, 1957), volunteers were awakened 5 or 15 minutes after the beginning of a REM episode and asked to decide on the basis of the duration of the events in their dreams whether they had been dreaming for 5 or 15 minutes. They were correct in 92 of 111 cases.
● Some people claim that they do not dream. However, these people have just as much REM sleep as normal dreamers. Moreover, they report dreams if they are awakened during REM episodes (Goodenough et al., 1959), although they do so less frequently than do normal dreamers.
● Penile erections are commonly assumed to be indica- tive of dreams with sexual content. However, erections are no more complete during dreams with frank sexual content than during those without it (Karacan et al., 1966). Even babies have REM-related penile erections.
● Many people believe that sleeptalking (somniloquy) and sleepwalking (somnambulism) occur only during dream- ing. This is not so (see Dyken, Yamada, & Lin-Dyken, 2001). Sleeptalking has no special association with REM sleep—it can occur during any stage but often occurs
during a transition to wakefulness. Sleepwalking usually occurs during stage 3 or 4 sleep, and it never occurs during dreaming, when core muscles tend to be totally relaxed (Usui et al., 2007). There is no proven treat- ment for sleepwalking (Harris & Grunstein, 2008).
Interpretation of Dreams Sigmund Freud believed that dreams are triggered by un- acceptable repressed wishes, often of a sexual nature. He ar- gued that because dreams represent unacceptable wishes, the dreams we experience (our manifest dreams) are merely disguised versions of our real dreams (our latent dreams): He hypothesized an unconscious censor that disguises and subtracts information from our real dreams so that we can endure them. Freud thus concluded that one of the keys to understanding people and dealing with their psychological problems is to expose the meaning of their latent dreams through the interpretation of their manifest dreams.
There is no convincing evidence for the Freudian the- ory of dreams; indeed, the brain science of the 1890s, which served as its foundation, is now obsolete. Yet many people accept the notion that dreams bubble up from a troubled subconscious and that they represent repressed thoughts and wishes.
The modern alternative to the Freudian theory of dreams is Hobson’s (1989) activation-synthesis theory (see Eiser, 2005). It is based on the observation that, dur- ing REM sleep, many brain-stem circuits become active and bombard the cerebral cortex with neural signals. The essence of the activation-synthesis theory is that the in- formation supplied to the cortex during REM sleep is largely random and that the resulting dream is the cor- tex’s effort to make sense of these random signals.
14.2 Why Do We Sleep, and Why Do We Sleep When We Do?
Now that you have been introduced to the properties of sleep and its various stages, the focus of this chapter shifts to a consideration of two fundamental questions about sleep: Why do we sleep? And why do we sleep when we do?
Two kinds of theories for sleep have been proposed: recuperation theories and adaptation theories. The differ- ences between these two theoretical approaches are re- vealed by the answers they offer to the two fundamental questions about sleep.
The essence of recuperation theories of sleep is that being awake disrupts the homeostasis (internal physio- logical stability) of the body in some way and sleep is re- quired to restore it. Various recuperation theories differ in terms of the particular physiological disruption they
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propose as the trigger for sleep—for example, it is com- monly believed that the function of sleep is to restore en- ergy levels. However, regardless of the particular function postulated by restoration theories of sleep, they all imply that sleepiness is triggered by a deviation from home- ostasis caused by wakefulness and that sleep is termi- nated by a return to homeostasis.
The essence of adaptation theories of sleep is that sleep is not a reaction to the disruptive effects of being awake but the result of an internal 24-hour timing mechanism—that is, we humans are programmed to sleep at night regardless of what happens to us during the day. According to these theories, we have evolved to sleep at night because sleep protects us from accident and pre- dation during the night. (Remember that humans evolved long before the advent of artificial lighting.)
Adaptation theories of sleep focus more on when we sleep than on the function of sleep. Some of these theo- ries even propose that sleep plays no role in the efficient physiological functioning of the body. According to these theories, early humans had enough time to get their eat-
ing, drinking, and reproducing out of the way during the daytime, and their strong motivation to sleep at night evolved to
conserve their energy resources and to make them less susceptible to mishap (e.g., predation) in the dark (Rattenborg, Martinez-Gonzales, & Lesku, 2009; Siegel, 2009). Adaptation theories suggest that sleep is like repro- ductive behavior in the sense that we are highly motivated to engage in it, but we don’t need it to stay healthy.
Comparative Analysis of Sleep Sleep has been studied in only a small number of species, but the evidence so far suggests that most mammals and birds sleep. Furthermore, the sleep of mammals and birds, like ours, is characterized by high-amplitude, low- frequency EEG waves punctuated by periods of low- amplitude, high-frequency waves (see Siegel, 2008). The
evidence for sleep in amphibians, reptiles, fish, and insects is less clear: Some display periods of inactivity and unresponsive-
ness, but the relation of these periods to mammalian sleep has not been established (see Siegel, 2008; Zimmerman et al., 2008). Table 14.1 gives the average number of hours per day that various mammalian species spend sleeping.
The comparative investigation of sleep has led to several important conclusions. Let’s consider four of these.
First, the fact that most mammals and birds sleep sug- gests that sleep serves some important physiological function, rather than merely protecting animals from mishap and conserving energy. The evidence is strongest in species that are at increased risk of predation when they sleep (e.g., antelopes) and in species that have evolved complex mechanisms that enable them to sleep.
For example, some marine mammals, such as dolphins, sleep with only half of their brain at a time so that the other half can control resurfacing for air (see Rattenborg, Amlaner, & Lima, 2000). It is against the logic of natural selection for some animals to risk predation while sleep- ing and for others to have evolved complex mechanisms to permit them to sleep, unless sleep itself serves some critical function.
Second, the fact that most mammals and birds sleep suggests that the primary function of sleep is not some special, higher-order human function. For example, sug- gestions that sleep helps humans reprogram our complex brains or that it permits some kind of emotional release to maintain our mental health are improbable in view of the comparative evidence.
Third, the large between-species differences in sleep time suggest that although sleep may be essential for sur- vival, it is not necessarily needed in large quantities (refer to Table 14.1). Horses and many other animals get by quite nicely on 2 or 3 hours of sleep per day. Moreover, it is important to realize that the sleep patterns of mammals and birds in their natural environments can vary substan- tially from their patterns in captivity, which is where they are typically studied (see Horne, 2009). For example, some animals that sleep a great deal in captivity sleep lit- tle in the wild when food is in short supply or during pe- riods of migration (Siegel, 2008).
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Evolutiona Evolutionary Perspective Perspective
Evolutiona Evolutionary Perspective Perspective
Evolutiona Evolutionary Perspective Perspective
TABLE 14.1 Average Number of Hours Slept per Day by Various Mammalian Species
Hours of Sleep Mammalian Species per Day
Giant sloth 20
Opossum, brown bat 19
Giant armadillo 18
Owl monkey, nine-banded armadillo 17
Arctic ground squirrel 16
Tree shrew 15
Cat, golden hamster 14
Mouse, rat, gray wolf, ground squirrel 13
Arctic fox, chinchilla, gorilla, raccoon 12
Mountain beaver 11
Jaguar, vervet monkey, hedgehog 10
Rhesus monkey, chimpanzee, baboon, red fox 9
Human, rabbit, guinea pig, pig 8
Gray seal, gray hyrax, Brazilian tapir 6
Tree hyrax, rock hyrax 5
Cow, goat, elephant, donkey, sheep 3
Roe deer, horse 2
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Fourth, many studies have tried to identify some char- acteristic that identifies various species as long sleepers or short sleepers. Why do cats tend to sleep about 14 hours a day and horses only about 2? Under the influence of re- cuperation theories, researchers have focused on energy- related factors in their efforts. However, there is no strong relationship between a species’ sleep time and its level of activity, its body size, or its body temperature (see Siegel, 2005). The fact that giant sloths sleep 20 hours per day is a strong argument against the theory that sleep is a com- pensatory reaction to energy expenditure—similarly, en- ergy expenditure has been shown to have little effect on subsequent sleep in humans (Driver & Taylor, 2000; Youngstedt & Kline, 2006). In contrast, adaptation theories correctly predict that the daily sleep time of each species is related to how vulnerable it is while it is asleep and how much time it must spend each day to feed itself and to take care of its other survival requirements. For example, zebras must graze almost continuously to get enough to eat and are extremely vulnerable to predatory attack when they are asleep—and they sleep only about 2 hours per day. In con- trast, African lions often sleep more or less continuously for 2 or 3 days after they have gorged themselves on a kill. Figure 14.4 says it all.
14.3 Effects of Sleep Deprivation
One way to identify the functions of sleep is to determine what happens when a person is deprived of sleep. This section begins with a cautionary note about the interpre- tation of the effects of sleep deprivation, a description of
the predictions that recuperation theories make about sleep deprivation, and two classic case studies of sleep deprivation. Then, it summarizes the results of sleep-dep- rivation research.
Interpretation of the Effects of Sleep Deprivation: The Stress Problem I am sure that you have experienced the negative effects of sleep loss. When you sleep substantially less than you are used to, the next day you feel out of sorts and unable to function as well as you usually do. Although such ex- periences of sleep deprivation are compelling, you need to be cautious in interpreting them. In Western cultures, most people who sleep little or irregularly do so because they are under extreme stress (e.g., from illness, exces- sive work, shift work, drugs, or examinations), which could have adverse effects independent of any sleep loss. Even when sleep deprivation studies are conducted on healthy volunteers in controlled laboratory environ- ments, stress can be a contributing factor because many of the volunteers will find the sleep-deprivation proce- dure itself stressful. Because it is difficult to separate the effects of sleep loss from the effects of stressful condi- tions that may have induced the loss, results of sleep- deprivation studies must be interpreted with particular caution.
Unfortunately, many studies of sleep deprivation, particularly those that are discussed in the popular media, do not control for stress. For example, almost weekly I read an article in my local newspaper decrying the effects of sleep loss in the general population. It will point out that many people who are pressured by the de- mands of their work schedule sleep little and experience a variety of health and accident problems. There is a place for this kind of research because it identifies a problem that requires public attention; however, be- cause the low levels of sleep are hopelessly confounded with high levels of stress, many sleep-deprivation stud- ies tell us little about the functions of sleep and how much we need.
Predictions of Recuperation Theories about Sleep Deprivation Because recuperation theories of sleep are based on the premise that sleep is a response to the accumulation of some debilitating effect of wakefulness, they make the fol- lowing three predictions about sleep deprivation:
● Long periods of wakefulness will produce physiologi- cal and behavioral disturbances.
● These disturbances will grow steadily worse as the sleep deprivation continues.
● After a period of deprivation has ended, much of the missed sleep will be regained.
Have these predictions been confirmed?
36114.3 ■ Effects of Sleep Deprivation
FIGURE 14.4 After gorging themselves on a kill, African lions often sleep almost continuously for 2 or 3 days. And where do they sleep? Anywhere they want!
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Two Classic Sleep-Deprivation Case Studies Let’s look at two widely cited sleep-deprivation case stud- ies. First is the study of a group of sleep-deprived stu- dents, described by Kleitman (1963); second is the case of Randy Gardner, described by Dement (1978).
The Case of the Sleep-Deprived Students While there were differences in the many subjective expe- riences of the sleep-evading persons, there were several features common to most. . . . [D]uring the first night the subject did not feel very tired or sleepy. He could read or study or do laboratory work, without much attention from the watcher, but usually felt an attack of drowsiness between 3 A.M. and 6 A.M. . . . Next morning the subject felt well, except for a slight malaise which always ap- peared on sitting down and resting for any length of time. However, if he occupied himself with his ordinary daily tasks, he was likely to forget having spent a sleepless night. During the second night . . . reading or study was next to impossible because sitting quietly was conducive to even greater sleepiness. As during the first night, there came a 2–3 hour period in the early hours of the morning when the desire for sleep was almost overpowering. . . . Later in the morning the sleepiness diminished once more, and the subject could perform routine laboratory work, as usual. It was not safe for him to sit down, how- ever, without danger of falling asleep, particularly if he at- tended lectures. . . .
The third night resembled the second, and the fourth day was like the third. . . . At the end of that time the in- dividual was as sleepy as he was likely to be. Those who continued to stay awake experienced the wavelike in- crease and decrease in sleepiness with the greatest drowsi- ness at about the same time every night. (Kleitman, 1963, pp. 220–221)
The Case of Randy Gardner As part of a 1965 science fair project, Randy Gardner and two classmates, who were entrusted with keeping him awake, planned to break the then world record of 260 hours of consecutive wakefulness. Dement read about the project in the newspaper and, seeing an opportunity to collect some important data, joined the team, much to the comfort of Randy’s worried parents. Randy proved to be a friendly and cooperative subject, although he did com- plain vigorously when his team would not permit him to close his eyes for more than a few seconds at a time. How- ever, in no sense could Randy’s behavior be considered abnormal or disturbed. Near the end of his vigil, Randy held a press conference attended by reporters and television crews from all over the United States, and he conducted
himself impeccably. When asked how he had managed to stay awake for 11 days, he replied politely, “It’s just mind over matter.” Randy went to sleep exactly 264 hours and 12 minutes after his alarm clock had awakened him 11 days before. And how long did he sleep? Only 14 hours the first night, and thereafter he returned to his usual 8-hour schedule. Although it may seem amazing that Randy did not have to sleep longer to “catch up” on his lost sleep, the lack of substantial recovery sleep is typical of such cases.
(From Some Must Watch While Some Must Sleep by William C. Dement, Portable Stanford Books, Stanford Alumni Association, Stanford University, 1978, pp. 38–39. Used by permission of William C. Dement.)
Experimental Studies of Sleep Deprivation in Humans Since the first studies of sleep deprivation by Dement and Kleitman in the mid-20th century, there have been hun- dreds of studies assessing the effects on humans of sleep- deprivation schedules ranging from a slightly reduced amount of sleep during one night to total sleep depriva- tion for several nights (see Durmer & Dinges, 2005). The studies have assessed the effects of these schedules on many different measures of sleepiness, mood, cognition, motor performance, physiological function, and even molecular function (see Cirelli, 2006).
Even moderate amounts of sleep deprivation—for exam- ple, sleeping 3 or 4 hours less than normal for one night— have been found to have three consistent effects. First, sleep-deprived individuals display an increase in sleepiness: They report being more sleepy, and they fall asleep more quickly if given the opportunity. Second, sleep-deprived individuals display negative affect on various written tests of mood. And third, they perform poorly on tests of vig- ilance, such as watching a computer screen and respond- ing when a moving light flickers.
The effects of sleep deprivation on complex cognitive functions have been less consistent (see Drummond et al., 2004). Consequently, researchers have preferred to assess performance on the simple, dull, monotonous tasks most sensitive to the effects of sleep deprivation (see Harrison & Horne, 2000). Nevertheless, a growing number of stud- ies have been able to demonstrate disruption of the per- formance of complex cognitive tasks by sleep deprivation (Blagrove, Alexander, & Horne, 2006; Durmer & Dinges, 2005; Killgore, Balkin, & Wesensten, 2006; Nilsson et al., 2005) although a substantial amount of sleep deprivation (e.g., 24 hours) has often been required to produce con- sistent disruption (e.g., Killgore, Balkin, & Wesensten, 2006; Strangman et al., 2005).
The disruptive impact of sleep deprivation on cognitive function has been clarified by the discovery that only some cognitive functions are susceptible. Many early studies of
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the effect of sleep deprivation on cognitive function used tests of logical deduction or critical thinking, and per- formance on these has proved to be largely immune to the disruptive effects of sleep loss. In contrast, performance on tests of executive function (cognitive abilities that ap- pear to depend on the prefrontal cortex) has proven much more susceptible (see Nilsson et al., 2005). Executive function includes innovative thinking, lateral thinking, insightful thinking, and assimilating new information to update plans and strategies.
The adverse effects of sleep deprivation on physical performance have been surprisingly inconsistent consid- ering the general belief that a good night’s sleep is essen- tial for optimal motor performance. Only a few measures tend to be affected, even after lengthy periods of depriva- tion (see Van Helder & Radomski, 1989).
Sleep deprivation has been found to have a variety of physiological consequences such as reduced body tem- perature, increases in blood pressure, decreases in some aspects of immune function, hormonal changes, and metabolic changes (e.g., Dinges et al., 1994; Kato et al., 2000; Knutson et al., 2007; Ogawa et al., 2003). The prob- lem is that there is little evidence that these changes have any consequences for health or performance. For exam- ple, the fact that a decline in immune function was dis- covered in sleep-deprived volunteers does not necessarily mean that they would be more susceptible to infection— the immune system is extremely complicated and a de- cline in one aspect can be compensated for by other changes. This is why I want to single out a study by Cohen and colleagues (2009) for commendation: Rather than studying immune function, these researchers focused di- rectly on susceptibility to infection and illness. They ex- posed 153 healthy volunteers to a cold virus. Those who reported sleeping less than 8 hours a night were not less likely to become infected, but they were more likely to de- velop cold symptoms. Although this is only a correla- tional study (see Chapter 1) and thus cannot directly implicate sleep duration as the causal factor, experimen- tal studies of sleep and infectious disease need to follow this example and directly measure susceptibility to infec- tion and illness.
After 2 or 3 days of continuous sleep deprivation, most study participants experience microsleeps, unless they are in a laboratory environment where the microsleeps can be interrupted as soon as they begin. Microsleeps are brief periods of sleep, typically about 2 or 3 seconds long, during which the eyelids droop and the subjects become less responsive to external stimuli, even though they re- main sitting or standing. Microsleeps disrupt perform- ance on tests of vigilance, but such performance deficits also occur in sleep-deprived individuals who are not ex- periencing microsleeps (Ferrara, De Gennaro, & Bertini, 1999).
It is useful to compare the effects of sleep deprivation with those of deprivation of the motivated behaviors
discussed in Chapters 12 and 13. If people were deprived of the opportu- nity to eat or engage in sexual activity, the effects would be severe and unavoidable: In the first case, starvation and death would ensue; in the second, there would be a total loss of reproductive capacity. Despite our powerful drive to sleep, the effects of sleep deprivation tend to be subtle, selective, and variable. This is puzzling. An- other puzzling thing is that performance deficits observed after extended periods of sleep deprivation disappear so readily—for example, in one study, 4 hours of sleep elimi- nated the performance deficits produced by 64 hours of sleep deprivation (Rosa, Bonnett, & Warm, 2007).
Sleep-Deprivation Studies with Laboratory Animals The carousel apparatus (see Figure 14.5) has been used to deprive rats of sleep. Two rats, an experimental rat and its yoked control, are placed in separate chambers of the apparatus. Each time the EEG activity of the experi- mental rat indicates that it is sleeping, the disk, which serves as the floor of half of both cham- bers, starts to slowly rotate. As a result, if the sleeping experimental rat does not awaken immediately, it gets shoved off the disk into a shallow pool of water. The yoked control is exposed to exactly the same pattern of disk rotations; but if it is not sleeping, it can easily avoid getting dunked by walking in the direction opposite to the direction of disk rotation. The experimental rats typically died after about 12 days,
36314.3 ■ Effects of Sleep Deprivation
FIGURE 14.5 The carousel apparatus used to deprive an ex- perimental rat of sleep while a yoked control rat is exposed to the same number and pattern of disk rotations. The disk on which both rats rest rotates every time the experimental rat has a sleep EEG. If the sleeping rat does not awaken immediately, it is deposited in the water. (Based on Rechtschaffen et al., 1983.)
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while the yoked controls stayed reasonably healthy (see Rechtschaffen & Bergmann, 1995).
The fact that humans and rats have been sleep-deprived by other means for similar periods of time without dire consequences argues for caution in interpreting the re- sults of the carousel sleep-deprivation experiments (see Rial et al., 2007; Siegel, 2009). It may be that repeatedly being awakened by this apparatus kills the experimental rats not because it keeps them from sleeping but because it is stressful. This interpretation is consistent with the pathological problems in the experimental rats that were revealed by postmortem examination: swollen adrenal glands, gastric ulcers, and internal bleeding.
You have already encountered many examples in this book of the value of the comparative approach. However, sleep deprivation may be one phenomenon that cannot
be productively studied in nonhu- mans because of the unavoidable confounding effects of extreme
stress (see Benington & Heller, 1999; D’Almeida et al., 1997; Horne, 2000).
REM-Sleep Deprivation Because of its association with dreaming, REM sleep has been the subject of intensive investigation. In an effort to reveal the particular functions of REM sleep, sleep researchers have specifically deprived sleeping volunteers of REM sleep by waking them up each time a bout of REM sleep begins.
REM-sleep deprivation has been shown to have two consistent effects (see Figure 14.6). First, following REM- sleep deprivation, participants display a REM rebound; that is, they have more than their usual amount of REM sleep for the first two or three nights (Brunner et al., 1990). Second, with each successive night of deprivation, there is a greater tendency for participants to initiate REM sequences. Thus, as REM-sleep deprivation pro- ceeds, participants have to be awakened more and more frequently to keep them from accumulating significant amounts of REM sleep. For example, during the first night of REM-sleep deprivation in one experiment (Webb & Agnew, 1967), the participants had to be awak- ened 17 times to keep them from having extended peri-
ods of REM sleep; but during the seventh night of deprivation, they had to be awak- ened 67 times.
The compensatory increase in REM sleep following a period of REM-sleep dep- rivation suggests that the amount of REM sleep is regulated separately from the amount of slow-wave sleep and that REM sleep serves a special function. This finding, coupled with the array of interesting physi- ological and psychological events that de- fine REM sleep, has led to much speculation about its function.
Considerable attention has focused on the potential role of REM sleep in strength- ening explicit memory (see Chapter 11). Many reviewers of the literature on this topic have treated the positive effect of REM sleep on the storage of existing memories as well established, and researchers have moved on to study the memory-promoting effects of other stages of sleep (e.g. Deak & Stickgold, 2010; Rasch & Born, 2008; Stickgold & Walker, 2007) and the physio- logical mechanisms of these memory- pro- moting effects (e.g., Rasch et al., 2007). However, two eminent sleep researchers,
364 Chapter 14 ■ Sleep, Dreaming, and Circadian Rhythms
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