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\title{Sleep and Sleep Deprivation}
\author{Roger Dingledine
        \\
        9.00: Introduction to Psychology
        }
\date{\today}

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	Since the beginning of recorded history, humans have been curious
about the
functions of sleep.  Though the specific needs that
sleep fulfills are still for the most part unknown, it is clear that
the act of sleep is necessary to maintain our awareness and ability to
interact with our environment.  The effects of sleep deprivation, or an
extended partial or total loss of sleep, are
interesting from a scientific viewpoint
for several reasons.  First, studying sleep deprivation
gives us a better understanding of the purpose of sleep itself.
By preventing the body from receiving its normal amount of sleep, we can
determine which processes are affected, and how much a given amount of
sleep loss affects them.  Second, the practical consequences of loss of sleep
can be determined -- the extent to which it interferes with physical or mental
activity, and which
activities are affected most and least.  Third, examination of people who
have endured extended loss of sleep allows us to understand more fully its
effects on mental and physical health.  Today, sleep deprivation plays
a role in the lives of many important people in our society.

	Sleep deprivation study can be approached in several different ways in order
to gain insight into the functions of sleep itself.  By selective
deprivation of only certain parts of the sleep cycle, we can determine the
functions of those stages of sleep, and their importance to the body and
mind.  By partial deprivation of all stages of sleep at once (the most frequent type of
sleep loss), we can examine the impact lack of sleep has in moderation.
This kind of study might also provide a basis for the development of drugs that
specifically promote the types of sleep (e.g., REM) that we need, for those
of us who can't afford to sleep much.
By total deprivation of sleep for an extended period of time, we can identify
what functions sleep performs for our bodies and minds over the long term.

	The function, or purpose, of sleep has been the subject of much
debate over the past millenia.  In a general sense, the purpose of sleeping
is believed to be ``to restore the organism's capacity to be awake.'' (Webb 1993) 
This was called the ``restorative model.''  In the last few centuries, several
variations to this model have been proposed, such as the idea that sleep
plays a preventive role in keeping us from becoming exhausted; it maintains
our level of performance and our capacity to match external demands.  Scientists
noticed a significant correlation for both animals and humans between body weight,
metabolism, and
amount of sleep.  Smaller animals tended to sleep more (up to 18 hours) than
larger animals (as low as 3 to 4 hours of sleep in a 24 hour period). (Webb 1991)
A greater amount of sleep helps to conserve energy, simply because the organism
is not active while asleep.  This new realization, gained from analyzing and
reviewing data pertaining to sleep patterns of animals, led to a new model
termed the ``adaptive model,'' which stated that sleep activities were based in large
part on the behavior of the organism.  Predators have more flexible sleep schedules,
grazing animals sleep for only a couple hours at a time due to herding and the
constant danger of predators, and small burrowing animals with high pressures from
predators sleep more than those with fewer predator pressures.  This model showed,
in short, that ``the purpose of
sleep was to aid the survival of the animal in relationship to environmental pressures.''
(Webb 1991)

	The restorative model of the purpose of sleep is excellent in explaining
sleep deprivation results, as well as the observation that not sleeping makes us
tired whereas sleeping lets us recover.  However, the restorative model
implies that the amount of recovery sleep, the sleep after an extended period of wakefulness,
should be linearly related to the amount of lost sleep.  In reality, studies have found that
recovery sleep is related to lost sleep, but not nearly the one to one relation that we
would expect.  In addition, the restorative
model does not sufficiently explain such conditions as jet lag (alterations
in timing and length of sleep play a key role in sleep's restorative abilities, whereas
the restorative model does not indicate that timing is relevant to quality of sleep).  On
the opposite
end of the spectrum, the adaptive model explains the varying range of sleep needs for
different species, as well as the timing of those needs, but it does not explain the
effects of sleep deprivation or recovery (it merely treats sleep as an adaptive behavior
designed to keep organisms out of danger at certain times of the day or night).  By combining
these two models of sleep and adding a behavioral component, we can get a much more versatile
model of the purpose of sleep.  Rather than exposing the organism 
to the environment at dangerous times of day, sleep for each species is timed to occur
at the best time and for the best duration to ensure its survival, based on foraging
needs, dangers of predation, and physiological limitations such as the inability to
see clearly in the dark.  The sleep process attempts to maintain itself: the arousal
threshold to external stimulation is dramatically increased during sleep, so that
the organism can sleep through soft noises.  Similarly, sleep can easily resume after
an awakening if there is no danger present.  Sleep provides the organism with the
flexibility necessary to stay awake longer, sleep at different times in the day,
or wake up if necessary to protect its safety; like breathing and circulation, the
act of sleep requires no learning or conscious effort.  However, despite this general
understanding of the function of sleep,
physiological and neurophysiological reasons for feeling tired and for the mechanics
of recovery sleep are still poorly understood.

	Now that we have an understanding of what scientists currently believe to be
the purpose of sleep, we can move on to the two principal types of sleep.
NREM (non rapid eye movement) sleep ``constitutes the majority of mammalian sleep
patterns,'' (Klerman 177) whereas REM sleep constitutes the remainder.  NREM sleep is
characterized by slow and regular breathing, reduced muscle tone levels, minimal
eye movements, lowered neuronal activity in most regions of the brain, and slow-wave
brain activity.  (Slow wave sleep, or SWS, is the slow and stable behavior of brainwaves
connected with NREM sleep.) On the other hand, REM sleep is characterized by very different
phenomena, including complete absence of muscle tone (this might be done to keep the body
still during the more realistic dreams), more rapid eye movement, irregular breathing
patterns, and a much higher level
of activity in the neurons of most brain regions (higher than NREM levels, and often
higher than waking levels!) (Bonnett 1993).  REM sleep is the state in which most vivid dreams
occur.  The arousal threshold to external stimulation is much higher during REM sleep.
REM and NREM sleep intervals alternate during sleep, and adult humans average roughly
1.5 to 2 hours of REM sleep per night.  

	REM sleep deprivation (RSD) is a state wherein only REM sleep is reduced;
NREM sleep is not reduced for the most part.  From selective deprivation of REM sleep,
researchers have learned that REM sleep appears to play an important role in mental
health and related behaviors, in learning and
consolidation of memories, and in thermal regulation of the body.  (Vogel 1993)  
Researchers produce actual RSD by awakening subjects as soon as the onset of REM sleep
is identified in their brainwaves.  ``Because NREM sleep necessarily follows wakefulness,
the awakened subject returns to NREM sleep.  After a period of NREM sleep, REM sleep
begins and another awakening is made.'' (Bonnett 1993)  When REM sleep is deprived in
this way, during recovery there is a selective increase in REM sleep. This
indicates that somehow REM sleep is vital to the organism, and a deficit can be built
up.  Curiously, REM sleep deprivation of this sort seems to be influential in ameliorating
endogenous
depression, a very severe variant of depression.  Some antidepressant drugs are believed to
work in part by reducing REM sleep.  While selective deprivation of REM sleep produces
significant results, selective deprivation of NREM sleep seems to be much less
noticeable.  Unfortunately, because NREM sleep precedes REM sleep, a study that
reduces NREM sleep must also necessarily reduce REM sleep.  After NREM sleep deprivation,
a selective increase in NREM sleep does occur during recovery sleep, though the amount
of recovery sleep time spent in SWS is not linearly related to the amount of sleep
lost.  Unlike selective REM sleep deprivation, no further psychological or
performance changes have been found from selective loss of NREM sleep.

	Partial sleep deprivation is a reduction in the total amount of
sleep obtained in a 24 hour period.  When severe, its effects are similar to those of total
sleep deprivation.  There have been many studies examining the effect of several
nights of reduced sleep on performance capacity.  Wilkinson (1968), for example,
performed experiments that allowed subjects 0, 1, 2, 3, 5, or 7.5 hours of sleep
per night.  At levels of sleep below three hours for one night or five hours for
two consecutive nights, decreases in vigilance performance (the ability to stay
awake and vigilant for a period of time) were noticeable.  When five
hours of sleep per night was maintained for four nights, increased sleepiness as
measured by sleep latency (the amount of time it takes the subject to fall asleep)
was observed.  With a reduction of the time allowed for sleep to six hours over a
period of 42 nights, performance differences were not significant; however, when
the sleep per night was reduced to 5.5 hours over a period of 60 days, the last two weeks
showed some general performance degradation.  Over the course of the study, time spent in
REM sleep was reduced by a quarter, and REM sleep latency, the amount of time spent
in NREM sleep before moving to REM sleep, was reduced by as much as half an hour.
Sleep latency itself did not show a significant change until the last week of the
study, where it slightly decreased.

	In a different study, subjects had the amount of time available for sleep
reduced in half hour steps, every two to four weeks, until the subjects were no longer
willing to continue reducing their sleep time.  For both groups of people who ordinarily slept
8 hours and groups of people who ordinarily slept 6.5 hours, the average amount of time spent
in bed that they were able to reduce to was 5 hours.  Although significant decline in
performance was not found in subjects who received 6 hours of sleep, they complained
of discomfort and fatigue.  Intriguingly, those subjects who had originally slept
only 6.5 hours a night soon returned to their baseline sleep schedules, but the
subjects who had originally slept for 8 hours a night reported that they were
sleeping between 6.1 and 6.4 hours per night over the next entire year. (Bonnet 1994)  Most of
the studies of partial sleep deprivation demonstrate that most normal young adults
can tolerate a chronic sleep reduction of up to three hours a night without building
up a loss of sleep or having to sleep more afterwards to compensate for the lost
sleep.  In fact, there is a growing school of thought that holds that human beings
have a core sleep requirement of roughly four to six hours per day. (Horne 1987, as
cited in Bonnet 1994)  Though I found no reported results to directly support this, it is
speculated that any sleep beyond that core requirement might serve to create a buffer against
unknown demands in the future that might require a more flexible sleep schedule.  

	Total sleep deprivation refers to denial of all sleep stages over a period
of time.  The first published studies about total sleep deprivation, first on puppies
and then on humans, are from the end of the nineteenth century.  The study of puppies
indicated that prolonged sleep loss can be fatal.  Later, ``Allan Rechtschaffen reported, in
1983, that sleep deprivation when well controlled and sustained, was uniformly
fatal to rats.'' (Hobson 1989)  The impact of total sleep loss in
humans varies greatly from person to person and situation to situation.  For instance,
performance during an extended period of wakefulness is very dependent on amount and
distribution of prior sleep, length of time awake, and what times the subject normally
sleeps. Similarly, situational characteristics such as the amount of noise nearby,
exercise prior to performance testing, temperature of the environment, and any
stimulants or other drugs, as well as subject characteristics such as motivation to
perform well, history of exposure to sleep loss, age, personality, and psychopathology
all play important roles in the ability of the subject to perform well during total
sleep deprivation.  Finally, the task itself is of critical relevance to performance
capacity.  Such attributes as the length of the test, immediate performance feedback,
test pacing, level of proficiency at performing the task, and the difficulty and
complexity of the task itself have all been shown to affect performance ability.

	One of the most famous examples of long term total sleep deprivation is the
case of Randy Gardner, a 17-year-old high school student who stayed
awake for 11 days (264 hours) starting in 1964.  His experiment gained national
press, and William C. Dement and other sleep researchers studied him
intently over the final six days, learning much about the physiological
and behavioral effects of sleep deprivation.  Near the end of the
eleven days, Gardner ``played a penny arcade baseball game with Dement
and won every one.  Before going to bed... Gardner held a news
conference at which he was `very coherent and conducted himself in
impeccable fashion.' '' (Dement, cited in Gray 1994)  Of course,
the excitement of the press conference was certainly a contributing factor in
his alertness, since sleep deprived people have the most trouble when performing
repetitive, boring, or passive
tasks. The effects on Gardner's physiology reinforce what was stated earlier
with regard to one of the likely functions of sleep, regulation of
energy and body temperature.  ``Late in deprivation he had a 1 C
decrease in body temperature and a 10 C decrease in skin temperature,
along with severe performance deficits.'' (Bergmann 1993)

	After being awake for those eleven days, Gardner
``slept for 14 hours and 40 minutes, and
appeared entirely refreshed upon awakening.  He subsequently remained
awake for 24 hours before having a second sleep episode of normal
duration of approximately eight hours.'' (Thorpy and Yager, 1991, 202)
Clearly, the amount of sleep required to recover from extended sleep
deprivation is not equal, or even linearly related, to the amount of
sleep lost. Bonnet reported similar findings in experiments he did
involving 205 or more hours of sleep deprivation. In these experiments,
``mild nystagmus [a rapid involuntary oscillation of the eyeballs], hand tremor,
intermittent slurring of speech, and ptosis [drooping of the upper eyelid] have
been noted. Sluggish corneal reflexes, hyper-active gag
reflex, hyper-active deep tendon reflexes, and increased sensitivity
to pain were reported after more extensive deprivation.  All of these
changes immediately reversed after recovery sleep.'' (1991) Amazingly,
Bonnet reported in his conclusions that after as many as 64 hours of
sleep loss, young adults appear to be able to fully recover to baseline
sleep levels after only a single 8 to 10 hour period of sleep. (1993)

	Many drugs have been studied in conjunction with lack of sleep.
Though usually used for weight reduction, amphetamines such as dextroamphetamine
sulfate ``have their most beneficial effect in counteracting or preventing
performance deteriorating that results from fatigue and/or sleep loss.'' (Higgins 1975)
It has been established that amphetamines are generally not only more effective than
caffeine, but also produce fewer and less severe side effects.  For instance,
the human body does not appear to build up a significant tolerance for amphetamines
and cocaine, whereas a tolerance is easily built up for opiates and caffeine. (Roehrs 1993)  
However, in extremely high doses, "complex movements are replaced by stereotyped,
simple movements and a sense of anxiety and danger is engendered." (Mitler 1993)  
Of course, amphetamines have larger long-term side effects, such as strong withdrawal
effects (such drugs require strict controls because of their potential for
abuse and addiction). Dextroamphetamines were used by the Apollo 11 crew, and
have been shown to maintain complex task performance capacity at a significantly
higher level after 24 hours with no sleep, when subjects are given 15mg in three
doses at four hour intervals. Even eight to sixteen hours after the last capsule
was ingested, performance increase was noticeable compared to the placebo effects.

	Though amphetamines are generally regarded as one of the most effective stimulants,
often a weaker form of stimulant such as caffeine can be used instead with much the same
results over a shorter period of time. Because caffeine is commonly available in various
beverages and foods, from carbonated drinks to coffee to chocolate, and because it is
freely available in tablet form without a prescription, it should be examined first as a
viable option to reversing the sleep deprivation effects on alertness and mood. A
group at the Walter Reed Army Institute of Research led by David Penetar conducted
a study on caffeine, concluding that their study ``quantifies the ability of caffeine
to reverse the alertness and mood changes produced by long periods of sleep deprivation
in humans.  Caffeine was not able to reverse fully the effects of 48 hours of sleep
deprivation in modest users of caffeine, but was effective in producing significant
alerting, and long-lasting improvements in mood.'' (Penetar 1993)  Furthermore,
``doses of 100-300 mg are associated with improved or positive aspects
of mood, especially in regular users of caffeine.'' (Griffiths et al.,
cited in Penetar 1993)  The group's report states that caffeine concentration in
the bloodstream was highest 90 minutes after ingestion, and remained significant for the
subsequent twelve hours.  However, much like amphetamines, it has been found that
``among the prominent symptoms reported by individuals discontinuing
excessive caffeine use... are lassitude, drowsiness, fatigue, and
decreased performance. These symptoms are reversed by the
administration of caffeine.'' (Sawyer, Julia, and Turin, 1982, cited in
Carskadon 1993)  Further, a caffeine tolerance can develop in humans
relatively quickly, yielding fewer significant advantages in taking more
caffeine and increasing the effects of withdrawal if excessive caffeine use
is stopped or greatly reduced.

	The need for humans to sleep is clear from both common sense and scientific
study.  ``Sleep loss affects `divergent' thinking, or the ability to think creatively,
flexibly, and spontaneously.'' (Kribbs 1993)  After about 36 hours of sleep deprivation,
there are major changes in mood and performance, with fatigue, irritability, impaired
perception and orientation, and inattentiveness due to sleep deprivation.  Despite these
important effects, though, all of these symptoms disappear very quickly once a sufficient
amount of recovery sleep is obtained.  Indeed, such geniuses as Edison are said to have
survived adequately on only four or five hours of sleep a night.  The capacity for
sleep in animals is ingeniously adapted to be able to perform adequately in many different
environments.

\newpage

\section{Works Cited or Consulted}

\begin{singlespace}
\noindent
Bonnet, Michael H. (1993). Deprivation, Partial. In {\it The
     Encylopedia of Sleep and Dreaming} (pp. 176-177). New York:
     Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Bonnet, Michael H. (1993). Deprivation, Total: Behavioral Effects. In
     {\it The Encylopedia of Sleep and Dreaming} (pp. 180-183). New
     York: Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Bonnet, Michael H. (1994) Sleep Deprivation. In {\it Principles and
Practice of Sleep Medicine} (pp. 50-64). London: W. B. Saunders.
\end{singlespace}

\begin{singlespace}
\noindent
Bergman, Bernard. (1993). Deprivation, Total: Physiological Effects. In
     {\it The Encylopedia of Sleep and Dreaming} (pp. 183-187). New
     York: Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Carskadon, Mary A. (Ed.). (1993). Caffeine. In {\it The Encylopedia
     of Sleep and Dreaming} (pp. 88-90). New York: Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Dinges, David F. (Ed.). (1993). Napping. In {\it The Encylopedia of
     Sleep and Dreaming} (pp. 392-395). New York: Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Gray, Peter. (1994) {\it Psychology}. New York: Worth.
\end{singlespace}

\begin{singlespace}
\noindent
Higgins, E. A. et al. (1975) {\it The Effects of Dextroamphetamine on
    Physiological Responses and Complex Performance During Sleep Loss}.
    Oklahoma City: FAA Civil Aeromedical Institude.
\end{singlespace}

\begin{singlespace}
\noindent
Hobson, J. Allan. (1989). {\it Sleep}. New York: Scientific
American Library.
\end{singlespace}

\begin{singlespace}
\noindent
Horne J. 1987. {\it Why we sleep}. New York: Oxford University Press.
\end{singlespace}

\begin{singlespace}
\noindent
Irwin, Michael, et al. (1996). Partial night sleep deprivation reduces
natural killer and cellular immune responses in humans. {\it FASEB
Journal}, 10, 5, pp. 643-653.
\end{singlespace}

\begin{singlespace}
\noindent
Klerman, Elizabeth B. (1993). Deprivation, Selective: NREM Sleep. In {\it The
     Encylopedia of Sleep and Dreaming} (pp. 177-178). New York:
     Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Kribbs, Nancy B. (1993). All-Nighters. In {\it The
     Encylopedia of Sleep and Dreaming} (p. 26). New York:
     Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Mitler, Merrill M. (1993). Amphetamines. In }\it The
     Encyclopedia of Sleep and Dreaming} (pp. 33-34). New York:
     Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Penetar, David, et al. (1993). Caffeine reversal of sleep deprivation
effects on alertness and mood. {\it Psychopharmacology}, 112,
pp. 359-365.
\end{singlespace}

\begin{singlespace}
\noindent
Roehrs, Timothy A. (1993). Drugs of Abuse. In {\it The Encyclopedia
     of Sleep and Dreaming} (pp. 195-196). New York: MacMillan.
\end{singlespace}

\begin{singlespace}
\noindent
Thorpy, Michael J. and Yager, Jan. (Eds.). (1991) {\it The
Encyclopedia of Sleep Disorders}. New York: Facts on File.
\end{singlespace}

\begin{singlespace}
\noindent
Vogel, Gerald. (1993). Deprivation, Selective: REM Sleep. In {\it The
     Encylopedia of Sleep and Dreaming} (pp. 178-180). New York:
     Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Webb, Wilse B. (1993). Functions of Sleep. In {\it The
     Encylopedia of Sleep and Dreaming} (pp. 257-258). New York:
     Macmillan.
\end{singlespace}

\begin{singlespace}
\noindent
Wilkinson RT. 1968. Sleep deprivation: Performance tests for partial and selective sleep
deprivation. {\it Prog Clin Psychol} 8:28-43.
\end{singlespace}

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