Some practical notes of advice:
The possible questions on this topic are limited and will most likely be
along the lines of:
Discuss two types of biorhythm or
Discuss what psychological research has told us about
Discuss the roles played by endogenous (internal factors)
and zeitgebers (environmental factors) in determining bodily rhythms.
Describe research into biological rhythms (eg circadian, infradian,
Consider the consequences of disrupting biological rhythms (eg shift
work, jet lag).
Criticisms of theories or research is limited so evaluation marks are
going to be obtained by comparing studies and highlighting how they show
different things or combine to produce a more complete picture of the
Most human and non-human animal functions are cyclic, alternating over a
period of time. Obvious examples include the sleep-wake cycle which
repeats over a 24 hour cycle, or the hibernation patterns of some
creatures that typically rest through the winter months and awaken in
spring. The major debate, similar to the nature/nurture in some
respects, but without the controversy, is to what extent biological
rhythms are determined by internal clocks (endogenous factors) and by
environmental factors (so called zeitgebers).
Types of biorhythm
Variation is over an approximate 24 hour period. The word stems from
the Latin; circa (meaning ‘about’) and diem (meaning
‘day’). There are some cycles that we are consciously aware of; the
sleep/wake cycle being an obvious one, but most cycles we are not
usually aware of. For example our core body temperature fluctuates over
a 24 hour period. Generally it peaks mid afternoon at about 37.1 C and
troughs in the wee small hours at about 36.7 C. This may not sound like
a lot but you may nevertheless have noticed the effect and found
yourself shivering unexpectedly as you’ve walked home after a late night
party, even in August!
Other examples of human circadian rhythm include heart rate, metabolism
and breathing. These follow a similar pattern to temperature, which may
not seem surprising, since they match our patterns of activity.
However, people on shifts, who are sleeping through the day and more
active at night still keep the same circadian rhythms with body
temperature, metabolism and resting heart rate still peaking mid
Blood clotting also shows a circadian rhythm, peaking in the morning and
coinciding with increased incidence of heart attack
It is worth mentioning that there are big differences between
individuals. The most noticeable being the larks/owls division; larks
being morning types and owls preferring the evenings. Typically when
studied larks seem to be clock advanced having rhythms about two hours
ahead of owls.
For a detailed
overview of research into these rhythms, seel the later notes on
endogenous and exogenous control of rhythms, for example the work of
Siffre and Morgan.
These occur more than once in a 24 hour cycle. Most are confined to
either day or night, for example the stages of sleep. As you should be
aware, a typical night’s sleep takes you from stage 1 to 4 then back to
2 and finally into REM. This whole cycle then repeats itself three or
four more times during the night, each cycle lasting about 90 minutes.
There are a number of similar cycles during the daytime too. Sometimes
these are referred to as diurnal. Examples include eating
(approximately every four hours), smoking and drinking caffeine (in
those addicted), and urination.
Stages of sleep
This section fits logically into both the ‘biorhythms’ and the ‘sleep’
sections of this particular topic area. As far as our set text is
concerned its rightful place is in ‘sleep’ but I see no reason why it
could not be used as an example of a biological rhythm.
Sleep is the perfect example of an ultradian rhythm, that is, one that
repeats itself over a period of less than 24 hours. The cycle of sleep
typically lasts about 90 minutes and during a typical nights sleep we
will repeat this cycle four or five times.
know that Henry Ford said that this was ‘bunk’ but the history of sleep
is useful from the point of view of research into the stages of sleep.
Until the 1930s there was no scientific or objective way of measuring
what was happening in the brain. Following the invention of the
electroencephalogram (EEG), it became possible to record the electrical
activity of the brain. This was crucial, since as you should be aware
by now, the activity of the brain is mainly electrical in nature.
1937: Loomis et al discover that during sleep the waves generated by the
brain slow and become larger. For the scientists amongst you, the
frequency falls as the wavelength increases.
1952: Aserinsky was checking to make sure that his newly acquired EEG
was working properly. He placed the electrodes of the machine near to
the eyes of his eight year old son, Armond whilst he was asleep. At
regular intervals he noticed that there were bursts of electrical
1953: Aserinsky & Kleitman coin the phrase ‘Rapid Eye Movement’ or REM.
1957: Dement & Kleitman realise that there appears to be a link between
REM sleep and dreaming. They tested 5 participants, waking them either
5 or 15 minutes into periods of REM sleep. Participants would normally
report dreams and the length of the dream would correspond to the time
that they had spent in REM.
1968: Rechtschaffen & Kales record four other distinct stages of sleep.
All this is important because prior to the 1930s it was assumed that
sleep was sleep. Nobody even considered the possibility of different
stages or patterns of activity.
recording brain activity
recording muscle activity
recording eye activity
noticeable features are how similar the eye and brain recordings
are between awake and REM sleep and the loss of muscle activity
in REM sleep.
brain is obviously active and shows what is called beta activity (see
EEG above). When we relax, for example close our eyes or meditate the
brain shows alpha activity. These are slower waves with higher
Stage 1 sleep (15
This occurs at the start of a nights sleep. It lasts a matter of
minutes and you will all be familiar with it since we often wake from
this stage. For example sat watching ‘Big Brother’ gradually losing the
will to live or certainly to stay awake, we may nod off. We may wake
from this stage and think that we’ve been dreaming. In fact these
hallucinations are referred to as hypnogogic phenomena and usually
comprise fleeting images rather than the bizarre stories more
characteristic of dreaming. The eyes may roll slowly. Sometimes we may
wake without realising that we’ve even nodded off. Brain waves are
slower and are called ‘theta.’ Other times we may wake with a jerk or
Stage 2 sleep (20
After about a minute or so we enter stage 2. This is characterised by
bursts of high frequency waves called ‘sleep spindles.’ We are still
aware of sounds and activity around us and the brain responds to this
with K-complexes. At this stage we are still very easily woken.
Stage 3 sleep (15
The brain waves start to slow and become higher in amplitude and
wavelength. These are called delta waves and are associated with deep
sleep. We are now more difficult to wake. First time round in the
night this stage is brief, only a few minutes, but we spend longer in it
later in the night.
Stage 4 sleep (30
In many respects this is a continuation of stage 4, however, delta waves
now constitute most of the brain activity and we are now at our most
relaxed. At this stage we are very difficult to wake up and even
vigorous shaking may not be sufficient to wake some people, me
included. However, a quiet but meaningful sound such as a baby crying
can be sufficient, again indicating that the brain still retains some
degree of awareness to external stimuli! Heart rate and blood pressure
fall, muscles are very relaxed and temperature is at its lowest.
We have now been asleep for about an hour. We start to ascend back
through these stages in reverse order, i.e. back to level 3 and then to
level 2. However, instead of going back to level 1, after just over an
hour we enter a very bizarre state of consciousness.
REM sleep (10 minutes
at start of night, up to an hour later in the night)
Sometimes referred to rather unimaginatively as stage 5, or more
descriptively ‘paradoxical sleep.’ REM is strange. The brain now
becomes very active, almost indistinguishable from a waking brain.
Remember the activation-synthesis theory of dreaming? The pons in the
midbrain throws out bursts of electrical activity into the cortex
lighting it up like a Christmas tree. Heart rate and blood pressure
increase, as does body temperature, and the eyes twitch rapidly giving
this stage its name. But, despite this frantic activity the body
remains motionless, cut off from the brain by the pons. We are
paralysed and unable to act out the brain’s bizarre thoughts.
REM is now thought by some to be the deepest stage of sleep since it is
now that we are most difficult to wake up. However, this could be as a
result of being so absorbed in our dreams.
Paralysis appears to be to prevent the body acting out our dreams and
endangering our lives. Cats that have had lesions to the pons do in
fact appear to act out their dreams. Remember, however, that we have no
certain way of knowing whether lower species do dream; it is merely
assumed that they do because all warm blooded creatures (birds and
mammals), with the exception of the very early egg-laying mammals, have
Our first visit to REM typically lasts about for about 10 minutes and we
start our journey back down to stage 2, stage 3 and stage 4 sleep. This
cycle repeats throughout the night, however, as the diagram below
illustrates, we spend most of the first half of the night in deep sleep
(slow wave or NREM), and most of the second half in REM sleep.
The last cycle is referred to as the ‘emergent cycle’ since it is during
this one that we wake up. This last cycle contains no stage 3 or stage
4 sleep so under normal conditions we will emerge from either REM or
stage 2 and the waking process may be accompanied by further hypnogogic
images as was mentioned in stage 1. (Strictly speaking on waking these
are referred to as hypnopompic).
The outline above describes a typical or average night’s sleep.
Obviously there are large individual differences between people. Some
may sleep much shorter periods, others who have been sleep deprived will
spend longer in stage 4 and REM, and the pattern changes with age.
These occur over a period of time greater than 24 hours. In humans the
best examples are menstrual cycle and PMS (Pre-Menstrual Syndrome) which
occurs a few days prior to the onset of bleeding and is characterised
(information for the boys), by loss of appetite, stress, irritability
and poor concentration. There are a number of rhythms that are cyclic
over about one year. A human example would be SAD (Seasonal Affective
Disorder), more on this later; and in the animal world migration, mating
patterns and hibernation of some species.
Seasonal Affective Disorder (SAD) (Infradian or circadian?)
Although it is
apparently normal for most people to feel more cheerful in the
summer months than in winter, a small number of people suffer an
extreme form of this that appears to be related to the lack of
bright light in the winter months.
you’ll remember from the stuff we did on the physiology of
sleep, light levels, as detected by receptors in the eye,
influence levels of melatonin and serotonin. Additionally as
you will hopefully recall from your work on depression,
serotonin is implicated in mood. See how eventually all these
strands knit together! At night low light levels stimulate the
production of melatonin, this is what triggers sleepiness.
Therefore you would expect the lower light levels of the winter
months to have a similar affect.
In areas where light levels are exceptionally low for prolonged periods,
such as the
Polar regions, you would expect the effects to
be particularly noticeable.
Terman (1988) found that SAD was five times more common in
New Hampshire, a northern state of the
USA, than in
Florida, obviously a sunnier clime.
The symptoms of SAD can be reduced in polar regions by sitting patients
in front of very bright artificial lights for at least one hour per
day. This lowers the levels of melatonin in the bloodstream which in
turn reduces the feelings of depression. The precise mechanism for this
is still unclear, it could be that melatonin (released from the pineal
gland) has a direct affect on mood or it could have its influence
indirectly through serotonin. Drugs used to treat depression such as
Prozac and other MAOIs (monoamine oxidase inhibitors), appear to work by
altering serotonin levels. Terman et al (1998) researched 124
participants with SAD. 85 were given 30 minute exposure to bright
light, some in the morning, some in the evening. Another 39 were
exposed to negative ions (a placebo group).
60% of the am bright light group showed significant improvement compared
to only 30% of those getting light in the evening. Only 5%of the
placebo group showed improvement.
The researchers conclude that bright light administered in this way may
be acting as a zeitgeber and resetting the body clock in the morning.
Research into SAD has led to effective treatments suggesting that the
theory has some validity. However, there does also appear to be a
Note: SAD varies
over a yearly cycle so can be viewed as an infradian (or circannual)
cycle. However, it appears to disrupt the sleep/wake cycle so can also
be viewed as circadian. SAD can be discussed in an essay on disruption
of biological rhythms.
Obviously a cycle that lasts about one month, so this cycle is infradain.
Like other rhythms, the menstrual cycle appears to be under the
influence of both internal (endogenous) mechanisms, and external
zeitgebers. It is worth reminding you that menstruation itself, usually
considered to be the start of the cycle, is in fact the termination of
The cycle is under the internal control of hormones, particularly
oestrogen and progesterone, secreted by the ovaries. These cause a
number of physiological changes within the body including the release of
at least one egg (ovum) from the ovaries and the thickening of the
lining of the womb (uterus), in preparation for the arrival of the egg.
If the egg is not fertilised then the lining of womb is shed and
menstruation occurs. The contraceptive pill mimics the effects of
pregnancy and cons the body into ceasing production of further eggs.
External control (zeitgebers)
It has long been known that the menstrual cycle can be influenced by
external factors, most notably by living with other women. The most
likely mechanism for this is by the action of pheromones, chemical
substances similar to hormones but which carry messages between
individuals of the same species.
pits, pheromones and
the McClintock effect
Martha McClintock (1971) was the first to notice possible
synchronisation of menstrual cycles amongst women living in close
proximity whilst still an undergraduate student at Wellesley women’
liberal arts college in Massachusetts.
In 1988 McClintock & Stern published their findings of a 10 year
longitudinal study into external control of the menstrual cycle. They
had followed 29 women (aged 20-35) who had had a history of irregular
menstrual cycles. Sweat samples from the armpits of 9 of the women had
been collected, sterilised and dabbed onto the upper lip of the other
On 68% of occasions the recipients of the sweat donation had responded
to the pheromones.
Armpit compounds collected from the nine donors in the follicular phase
of the menstrual cycle shortened the cycles of 20 recipients
by 1.7 ± 0.9 days. Conversely, when the nine donors were
in the ovulatory phase, the compounds lengthened the cycles
of the same 20 recipients by 1.4 ± 0.5 days.
McClintock’s earlier work as well as the above study are supported by
Russell et al (1980) who also placed dabs of sweat taken from the arm
pits of sexually inactive women and placed on the upper lips of other
women. Four out of five of the women had menstrual cycles that had
synchronised to within one day of the sweat-donor.
Due to the small sample size, the entire effect might have been due
to just one or two subjects who had a disproportionate effect.
Additional questions are raised by the following statement (Stern
McClintock, 1998): `Any condition
preventing exposure to the compounds, such as nasal
congestion anytime during the mid-cycle period from 3 days
before to 2 days after the preovulatory, could weaken the
effect. We analysed the data taking this into account'. It
would be useful to know what a priori criteria were employed
in making such adjustments, and whether the data analysis part
of the project was done blind
McClintock’s work has also been criticised for its lack of statistical
rigour. Wilson (1992) believes her results are due to statistical
errors and that when these are corrected the effect disappears.
advantages of external control of the menstrual cycle
Bentley (2000) believed that synchronisation between women living in
close proximity would ensure that the women would conceive and give
birth at similar times. This would be beneficial since they could share
breast feeding, a behaviour observed in other species. Similarly,
McClintock (1971) found that women who work in a mostly male environment
have shorter menstrual cycles. In the past this would be of
evolutionary advantage since it would provide more opportunities for
Reinberg (1967) reported the case of a young woman who lived in a cave
for three months with the only light being provided by a miner’s lamp.
The woman’s daily cycle lengthened to 24.6 hours, (compare to Michael
Siffre) and her menstrual cycle shortened to 25.7 days. It took a year
before her cycle returned to normal! Reinberg believed that light
levels could therefore influence the period of the cycle (no pun
intended!). This theory is backed by research on 600 German girls (no
armpit jokes), which found that the onset of menstruation (menarche) is
more likely in the winter months when light levels are low.
Timonen et al (1964) found that women were far more likely to conceive
in lighter months of the year than in darker months. This was
attributed to the effects of light on the pituitary gland, which exerts
its influence on the cycle via the ovaries.
This is a collection of symptoms that usually occurs four or five days
before menstruation. Typically symptoms include irritation, depression,
headaches and a decline in alertness. Other possible symptoms,
according to Luce (1971) include insomnia, cravings for certain foods
and even nymphomania!
However, it is the psychological affects that have been most widely
studied. Dalton (1964) alarmingly reported a sharp increase in crimes,
suicides, accidents and a decline in schoolwork associated with PMS.
More recent studies have played down these findings, for example Keye
(1983) concluded that although a small minority of women may suffer in
this way, such extreme symptoms are relatively rare.
to have an underlying physiological cause, as evidenced by the
fact that it is reported in all cultures. This is contrary to
earlier theories that attributed it to cultural factors and a
denial of femininity!
reported similar symptoms in other primates.
or external zeitgebers?
There is plenty of evidence to suggest that our biological rhythms are
inherited. For example although within a species there is variation of
rhythm, each individual tends to have a pattern of rhythm that shows
little variation over a lifetime. Even the most extreme of
environmental factors such as anaesthesia (not the late Russian
Princess), alcohol and drug abuse, brain damage and loss of
consciousness have little effect on our rhythms.
To study endogenous clocks it is necessary to isolate people from
external cues for many months. In 1962 Aschoff and Wever studied a
number of volunteers that agrred to spend time cut of from the outside
world in a disused WWII bunker in Munich. After a month or so cut off
from external ues they adopted a 25 hour daily cycle.
French geologist Michael Siffre is the daddy! Over the past 40
years or so he has regularly spent extended periods of time in
various caves around the World and agreed to be studied during
the process. His first stint was in 1962 when he spent 61 days
in a cave in the Alps. He emerged on September 17th
but thought it was August 20th! (Note: if you add
this up it simply doesn’t make sense. This means he had lost 28
days which is more than 1 hour a day!). In 1972 he was
monitored by NASA in the caves of Texas and in 1999 he missed
the millennium celebrations in a cave in some part of the
World. Each time his body clock extended form the usual 24 to
around 24.5 hours.
Left: we see
Siffre wired for various physiological readings during his 1972
isolation in Midnight Cave, Texas
This appears to suggest two things:
There is internal
control of the circadian rhythm, since even in the absence of
external cues we are able to maintain a regular daily cycle.
There must usually
be some external cue that keeps this cycle to 24 hours. When this
is removed we adopt this very strange 24.5 or 25 hour cycle.
Some have criticised this research since it is so artificial. In
particular they object to the use of strong artificial light by the
participants. On waking the volunteers such as Siffre switch on lights
which are likely to artificially re-set the body clock. Czeisler et al
(1999) has argued this is the equivalent of providing powerful drugs.
In their own version, Czeisler et al kept 24 participants in constant
artificial low-level light for one month and put them on a 28 hour
cycle. When readings of body temperature and blood chemicals were
analysed they were shown to have adopted a cycle of 24 hours and 11
minutes, much closer to the 24 hours we would expect.
Others however, disagree with Czeisler. In an attempt to find the
endogenous clocks’ period volunteers have been exposed to severe
variations in clock alteration, for example, exposing participants to
artificial lighting simulating a 28 hour day. (So if ‘sunrise’ was at
6am on day 1 it would be at 10am on day 2 and so on). The body cannot
adjust to such extremes and the body clocks ‘run free.’ In all cases
the cycle is greater than the usual 24 hours but estimates vary as to
the exact length. Some put the increase at as little as 11 minutes
whereas others claim one hour.
The biological rhythm often comes into conflict with external cues,
however, although disruption may occur the cycle remains intact. If you
have ever stayed up all night at a party and walked home in the early
hours you may have felt cold, perhaps getting the shivers, even though
it was August. This is your natural dip in body temperature still
occurring despite the night’s activities.
Biological basis of
In lower species the pineal gland appears to be the brain structure
responsible for regulating bodily rhythms, especially the sleep/wake
cycle. The pineal gland lies at the top of the brainstem and in lower
species this means it is close to the surface of the skull. As well as
having an inbuilt cycle it also has light sensitive cells that receive
information through the skull about external light levels and these seem
to keep it synchronised with fluctuating environmental conditions. The
pineal gland secretes melatonin which is known to have an influence on
In humans the pineal gland is still situated in the same place, at the
top of the brainstem, but we have an extensive cerebral cortex overlying
this. (When I say ‘we’ I refer to most of us!). This means the pineal
gland is situated deep inside the brain so has no direct contact with
conditions outside. (In fact the Greeks considered the pineal gland to
be a possible site for the ‘soul’ since it was situated in the centre of
In humans the suprachiasmatic nuclei (SCN) appears to take over the
role. This is situated in the hypothalamus and just behind the eyes and
receives sensory input about light levels through the optic nerve. The
SCN then appears to regulate melatonin production from the pineal
gland. Removal of the SCN in rats causes the usual sleep/wake cycle to
disappear. Studies of the electrical activity of the SCN show it to have
a cyclic activity varying over a 24.5 hour cycle. This cycle persisted
even after the SCN had been removed from the brain (so called
Humans certainly have a bunch of fibres (the retino-hypothalamic tract)
that connects, as the name suggests, the retina of the eye to the
hypothalamus. As early as 1929 Bailey found that patients with brain
tumours close to the hypothalamus suffered from odd sleep/wake cycles.
Evidence suggests that there is more than one internal clock. Damage to
the hypothalamus of squirrel monkeys alters their sleep/wake cycle but
leaves other cycles such as metabolism and temperature unaltered,
(Fuller et al 1981).
Body clocks everywhere
The SCN appears to be the location of the main clock but there are
certainly others. Yamazaki et al (2000) found that tissues from the
liver, lungs and other organs could maintain a constant 24 hour cycle
despite being kept in vitro (outside the body).
Additional biological content for extension
Krishnan et al
(1999) reported that the fruit fly has body clocks in its
antennae. In an ingenious experiment on fruit flies Kay et al
(1997) paired what they termed the ‘period gene’ (a gene they
believe responsible for body clocks) with a gene from jelly fish
that produces a green fluorescent dye. They then exposed the
flies to different patterns of light and found that all parts of
the body were developing green spots. They concluded that genes
responsible for the internal clocks of fruit flies are found in
all of their tissues.
evidence provided by Hall (1999) suggests these peripheral
clocks may also be present in humans. The adrenal glands
secrete a hormone cortisol each morning just before dawn, (‘the
darkest hour’ according to Mama Cass!). Cortisol therefore must
be controlled by a clock mechanism. Hall removed tissue from
the gland and grew it in culture and found that it continued to
secrete cortisol at the same time each day. Hall concludes that
the tissue in our adrenal glands must possess an endogenous
The SCN may regulate other cycles. Rusak & Morin (1976) found that
lesions to the SCN disrupted their breeding pattern (infradian rhythm).
Instead of just producing testosterone during the mating season, the
hamsters produced it all year round. Morgan (1995) removed the SCN from
some hamsters and found that their rhythms ceased. However, when they
received SCN transplants from other hamsters the cycles were
re-established. In a follow up they transplanted the SCN from mutant
hamsters (15 feet long!) who had shorter circadian rhythms. The
hamsters receiving these SCNs developed these mutant cycles. (However,
they did not grow to the same length!).
Mutant hamsters have
been used as a green source of electrical energy in London. Using the
London Eye as a giant wheel they can generate enough electricity to
power Westminster and half of Kensington!
Its role in the breeding cycle of humans is not so clear cut. We do
know however, that light levels can influence the menstrual cycle. The
menarche (onset of menstruation) is more likely to occur in the winter
months and generally occurs earlier in girls that are blind. In
Finland, during its very long summertime daylight hours, conception
rates increase significantly. Perhaps you can think of other
contributory factors! No football for example
However, much of
the research has been carried out on non-human animal species so we have
issues of generalisation. Breeding behaviour in humans is far more
complex. The females of many species, including rats, simply need to be
exposed to the right pheromone for them to adopt the lordotic stance
(legs akimbo, bottom raised mating position). Clearly, outside of Essex
at least, this is not the case with human females.
participants have been involved they have tended to be case studies of
individuals, and very often individuals with medical conditions, so
again, generalisation is an issue.
External Factors (zeitgebers)
Light appears to be crucial in maintaining 24 hour cycles:
Campbell & Murphy (1998), in a bizarre experiment, shone bright lights
onto the back of participants’ knees and were able to alter their
circadian rhythms in line with the light exposure. The exact mechanism
for this is unclear, but it seems possible that the blood chemistry was
altered and this was detected by the SCN.
Miles et al (1977) reported the case study of a blind man who had a
daily rhythm of 24.9 hours. Other zeitgebers such as clocks, radio etc.
failed to reset the endogenous clock and the man relied on stimulants
and sedatives to maintain a 24 hour sleep/wake cycle.
Luce & Segal
(1966), however, have shown that light levels can be over
ridden. In the Arctic Circle people still maintain a reasonably
constant sleep pattern, averaging 7 hours a night, despite 6
months of darkness in the winter months, followed by six months
of light in the summer. In these conditions it appears to be
social factors that act to reset endogenous rhythms rather than
Our biological rhythms therefore appear to be internally and externally
controlled. Left to their own devices our internal clocks seem to be
set to about a 25 hour cycle but external cues, especially light, resets
our clocks daily. So why do we need internal and external control? If
control was entirely internal we would not be sensitive to external
changes such as light levels. Species that hibernate or migrate would
not adjust their behaviour. If control was entirely external our
rhythms would be too erratic and change day to day depending on weather
Disruption of biorhythms
In some respects biorhythms are like stress in that they developed in
response to situations we found ourselves in hundreds of thousands of
years ago. Like stress, our body’s in built and inherited biorhythms
are outdated in a modern world that has a 24 hour culture.
In normal circumstances our in-built body clocks are not in conflict
with external zeitgebers. The daily pattern of life, waking in the
morning at or around sunrise, working through the day when our
metabolism, body temperature etc. are at their peak and going to sleep
at night when it gets dark, causes no disruption. However, given modern
life there are situations now when our internal clocks do come into
conflict with external cues, such as dark/light. The two most obvious
examples are shift work when we operate on a rotating schedule of hours
and jet lag when we travel across time zones either east to west or west
Jet lag or
desynchronosis is caused by the body’s internal body clock being out of
step with external cues. This results in a number of symptoms including
fatigue, insomnia, anxiety, constipation (or diarrhoea), dehydration and
increased susceptibility to illness.
Suppose you leave London Heathrow at 6pm (GMT). The flight to New York
JFK will take about six hours. However, because time on the east coast
of America is five hours behind you will arrive at 5pm local time.
However, your body clock assumes that its midnight since the flight has
taken six hours. As a result your internal clock is ready for bed, your
temperature is starting to fall and your metabolic rate is slowing.
External cues however, are telling you something quite different, its
still light, people are still shopping, the roads are still busy etc.
To overcome this conflict between internal and external effects is not
difficult. Provided you keep yourself well stimulated for the next five
or six hours you should be able to stay awake ‘til 11pm local time (4am
body clock time) and adapt to the new time zone.
But, suppose you leave JFK airport in New York at 12 noon (Eastern
standard Time) heading for London Heathrow. The flight is six hours.
You arrive in London at 6pm (New York Time) but this is 11pm GMT (London
time). Are you with me so far? Your endogenous clock has just lost
five hours! Your body clock still thinking it’s only 6pm, is not ready
for bed. Your body temperature, metabolism etc. is still at its peak.
To adapt to the new time setting you must now go to bed! This is not so
easy as going east to west. Going to sleep when you are wide awake is
not as easy as staying awake when you’re tired. As a result flying east
to west is more troublesome and takes longer to adapt.
evidence provided by Schwartz et al (1995) supports this theory.
They studied the results of baseball games involving
teams on the west and east coasts of
The time difference here is three hours.
They found that east coast teams travelling to play away
games on the west coast won significantly more games that west
coast teams travelling to the east.
A bit of biology:
we have two distinct time keeping centres in the brain, one sticks to
the body’s internal clock and the other is influenced more by external
cues such a levels of light. Normally these two centres are
synchronised but during jet lag desynchronisation occurs. Dr Horacio de
la Iglesia (2004) exposed rats to artificial days and nights lasting
eleven hours rather than the usual twelve. Gradually over a period of
days the rats started to exhibit daytime behaviour at night.
Dr de la Iglesia
discovered that their SCNs contained two proteins; Perl and Bmall and
also that the SCN could be seen as having a top half and a bottom half.
Now for the technical bit.
During a normal day
the rats would have the protein Perl in both halves of the SCN whereas
at night both halve would contain the protein Bmall:
However, when the
rats became desynchronised and started exhibiting daytime behaviour at
night Perl was found in the top half and Bmall in the bottom half.
The bottom half of the SCN appears to stick to the body’s internal 24
hour cycle whereas the top half responds to external cues or zeitgebers
such as light.
Using melatonin to
reset the body clock
melatonin is used by American military pilots to adapt to differing time
zones. Melatonin is the chemical secreted at night and enables us to
switch off the RAS (that keeps us awake during the day). Taken just
prior to bedtime in the new time zone, melatonin has been shown to be
effective in allowing sufferers of jet lag to get to sleep sooner than
their body clock would normally allow. At present the EU has not given
melatonin a licence in Europe.
Using fasting to reset
the body clock
Recent research has
also shown that social factor can play a role in resetting biological
rhythms and alleviate some of the symptoms of jet lag. For example a
period of fasting before travel followed by eating at times relevant to
the new time zone. Apparently food is very good at altering biological
rhythms (Fuller et al 2008)
suggests that as well as the main ‘master’ clock in the SCN there is
also a ‘feeding clock’ which depends on food intake. In mice, this
feeding clock seems to over-ride the master clock and keeps them awake
until food has been found.
So if we are flying
from London to New York and need to adjust to the new time zone by
staying awake longer than the master clock would expect we need to
starve ourselves before and during the flight and then eat when we
land. This way we can postpone the master clocks drive to get us to
sleep. Saper and his team recommend fasting for 16 hours before eating!
Other species abide by natural laws and are governed by their inbuilt
biological rhythms. It is only humans with their 24 hour lifestyle that
suffer desycnchronisation due to working against biorhythms. Twenty
percent of workers in the industrialised world work some form of
rotating or permanent unsocial shift pattern.
Shift work results in:
Fatigue, sleep disturbance, digestive problems, lack of concentration,
memory loss and mood swings.
Shift work is
usually more troublesome than jet lag since it involves
prolonged conflict between internal clocks and external
stimuli. As a result during the day when metabolism etc. is at
its peak the person is expected to sleep. At night when body
temperature etc. are low the person is expected to be working.
This situation is often compounded by 1. the person reverting to
‘normal’ sleep/wake cycles at the weekend and 2. shifts altering
from one week to the next. As a result the person never adapts
to a new rhythm, leaving their biorhythms in a permanent state
of desynchronisation! It is estimated that 20% of Western
employees work shifts.
In the very least this can result in reduced productivity and reduced
employee morale. In extreme cases it can have catastrophic
consequences. Major disasters such as Chernobyl and Three-mile Island,
Bhopal (explosion at a chemical plant in India), Exxon Valdez (oil
tanker spillage in Alaska and many other major incidents have occurred
in the early hours of the morning and been attributed to tiredness.
Additionally on the roads in Britain there are a disproportionately high
number of fatal accidents in the early hours of the morning
In addition to accidents and disasters there are also health risks
associated with regular shift work. These include increased risk of
heart disease and digestive disorders and regular tiredness. Twenty
percent of shiftworkers report falling asleep whilst at work. This
clearly has implications both for safety and for productivity and
Shifts can follow a number of patterns:
Rotating of fixed
rotating pattern involves working different hours each week or month. A
typical three shift system covering a 24 hour period would involve
6am to 2 pm
2pm to 10pm
10pm to 6am
In addition the rotation can be clockwise or anticlockwise. In the
example above, week 1 would be 6am to 2pm in the first week and moving
to the pm to 10pm in week to…and so on. This is clockwise. A backward
(or anticlockwise) rotation would involve starting at am to 2pm in week
one and then moving to the 10pm to 6am in week two…and so on.
With a rotating shift pattern there can be permanent desynchronisation
between internal and external factors with the person never fully
adjusting to the new shift.
Fast or slow rotation
Although most research suggests a clockwise rotation is to be preferred,
there is disagreement over the speed of rotation. Czeisler (main man in
this area) recommends a slow rotation, for example spending at least
three weeks on each shift. Bambra (2008) however, prefers a faster
rotation of just 3 to 4 days on each pattern so the body never has time
to adjust to the new cycle.
Fixed shifts tend to be rarer, mostly because of the unsociable hours
involved. For example working a permanent 10pm to 6am shift. Although
this allows time for resynchronisation with the worked adjusting to the
shift pattern it does create problems at weekends when people revert
back to a normal sleep-wake pattern.
Czeisler et al (1982) were called in to sort out shift related problems
at a chemical plant in Utah, USA. Having implemented the changes
suggested above a number of benefits were reported. These included
greater productivity, fewer accidents, increased morale and improvements
to the health of workers.
It is worth mentioning that work by Monk & Folkard (1983) reported that
rapidly rotating shifts (i.e. working 2 or 3 days on any one shift) were
preferable to slower rotation of shifts. This seemingly contradicts the
work of Czeisler.
Even with a constant shift pattern such as 10pm to 6am (night shift)
there are issues. Although the worker will adapt to this pattern by
experiencing a shift in biological rhythm there will be disruption at
the weekend when presumably, not being at work, they will adopt a more
sociable day pattern of recreation before restarting the night shift the
Using artificial light
to reset the body clock
Boivin et al (1996)
put 31 male participants on an inverted sleep pattern (so they were
awake at night and slept during the day). This lasted for three days.
Each day when they woke they were sat in front of dim lights for 5 hours
and then placed in one of four conditions:
temperature was recorded and used as a measure of how well they were
adapting to the new rhythm.
After three days:
Group 1 had
advanced by five hours (they were adapting to the new pattern best)
Group 2 had
advanced by three hours
Group 3 had
advanced by one hour
Group 4 had drifted
backwards by one hour (were failing to show any signs of adapting).
even ordinary room light can help us adapt our biological rhythms to
suit the environment, however, brighter light is even more effective.
Clearly this could
be useful in the workplace to help shift workers to adapt to changing
phase syndrome (DSPS)
desynchronisation (as experienced in jet lag) this results in a mis-match
between the body’s internal biological rhythm and the external world
(light, social activities etc). However, this failing seems to be due
to a delayed internal mechanism that results in the endogenous clock
being three or four hours behind what would be expected. As a result
patients with this ‘disorder’ find it difficult to get to sleep before
2am and typically wake about 10am. Amount of sleep is therefore not an
issue. Problems arise with social expectations, particularly schooling
and work. Often referred to as ‘owls’ (as opposed to the ‘larks’ that
are early risers), the condition is thought to affect about 7% of
teenagers and is a major contributory factor to cases of chronic
states that you need to know about disruption of biological rhythms…
clearly suggesting more than one. The two obvious ones suggested
above are the effects shift work and of jet lag. However, SAD is a
disrupted biorhythm that can be seen as either circadian or infradian so
can also be discussed in a question on disruption of rhythms.
However, a much
richer vein of material would be a discussion of the effects of sleep
deprivation studies, covered in the sleep section. Work by Dement,
Jouvet, Rechtschaffen, Huber-Weidman and the case studies of Randy
Gardner and Peter Tripp look at the effects of disrupting the stages of
sleep (ultradian) and the sleep-wake cycle (circadian).
If the question asks
for disruption of biorhythms you can discuss sleep deprivation, shift
work, jet lag and SAD and DSPS
What the board expects you to know:
The nature of
sleep, including evolutionary explanations and restoration
changes in sleep
All birds and
mammals sleep and other creatures have a dormant period during the 24
hour cycle, suggesting that sleep must perform some vital purpose.
such as horses and giraffes can sleep whilst standing but must lie down
for REM when muscle paralysis sets in, otherwise they’d fall over.
Birds tend to have a much shorter cycle of sleep, and according to
Wikipedia do not lose muscle tone to the same extent as mammals when
they enter REM.
However, in humans
the amount of sleep needed by individuals does show considerable
variation. Meddis (1979) reported the case of a woman who only slept
for one hour per night but showed no ill effects. This case however is
unusual and it is estimated that in the UK with an average of 7.5 hours
sleep per night, that most of us are in a state of mild sleep
deprivation. Sleep deprivation studies highlight the need for sleep to
maintain normal levels of awareness and cognitive ability as well as
psychological health. Three or four nights without sleep can result in
symptoms of mild paranoia and hallucinations. Yet, even in the most
extreme cases, such as Randy Gardner’s eleven nights without sleep, the
effects are not long lasting.
The nature of sleep
It is possible that you will be faced with a short question
on the nature of sleep. If so use the material on the stages of sleep
(see the biorhythms booklet) covering stages 1 to 4 and REM and the
characteristics of each. Later in this booklet we will also look at
lifespan changes and the way in which sleep patterns alter with age. If
this wasn’t enough it might also be possible to include material on
sleep disorders, again to be covered later in this booklet.
Theories of sleep
Why then do we
sleep, and why do we spend almost one third of our lives in this state
of reduced consciousness? There are two main theories
helps to protect us from harm at night
helps us to conserve energy
helps us to repair damage done to our bodies during the day
restores the brain’s levels of neurotransmitters
‘The lion and the lamb shall lie down together but the
lamb will not be very sleepy!’
Woody Allen (from Love and Death)
1. Protection (Meddis 1975)
In our evolutionary past night time would have been a time
of great danger. Since as a species we have poor night vision we would
have been unable to forage, likely to fall and hurt ourselves and wide
open to predation from species with better night sight. Sleep would
have been an evolutionary advantage since it would have kept us out of
harms way. As a result, those members of the species that slept would
have been more likely to have survived to maturity and passed on their
genes, ensuring that as an activity, sleep would have been retained in
our behavioural repertoire. The theory also considers the metabolic
rates of other species, predicting that animals with high metabolic
rates will need to spend more time eating so have less time to sleep.
Animals such as the shrew are safer since they have a burrow
to return to, but due to their high metabolic rate (heart rate of 800
beats per minute) and need to be eating constantly only have time to
sleep for two hours per day. Generally speaking smaller species have
higher metabolic rates because of their large surface area to volume
ratio. This results in loss of a lot of heat energy in comparison to
species that are larger.
Larger preyed-upon species, e.g. ground squirrel, have
burrows where they are safe, similar to the shrew, but since they are
larger and have a lower metabolic rate, they need to eat less often and
so can spend longer tucked away in their burrows asleep.
However, there are some glaring anomalies. On the face of
it you would expect species most at risk to sleep longer (in order to
get added protection) but often the opposite is the case. Species most
at risk such as herbivores sleep least (a few hours a day in brief
naps), whilst species that are at little risk such as big cats sleep for
most of the day! Since this can’t be explained by one aspect of the
theory (protection), food intake is used instead. The lion feeds once
every few days so spends the rest of its time asleep… because it can!
Herbivores with their impoverished diet of grass need to be eating all
the time so don’t have the time to sleep.
Other obvious evaluation comments
If the only purpose of sleep is to protect from harm, then
why do species that face the most risk when asleep bother to
sleep at all. Surely it would make more sense to stay awake and alert
to danger. Research in India for example has suggested that given a
choice, lions are happier tucking into a sleeping human than a more
active one! Evans (1984) sums it up nicely: ‘The behaviour patterns
involved in sleep are glaringly, almost insanely, at odds with common
Sleep can also be dangerous in other respects as these two
dolphin examples illustrate:
The Indus dolphin is at constant risk from being hit by logs
and other big river debris being swept down the River Indus. Clearly,
loss of consciousness is life threatening since it means loss of
vigilance. However, despite this it still grabs quick naps of a few
seconds at a time. In effect, this dolphin is risking its life to
sleep. How can this be protective?
The Bottlenose dolphin sleeps with one hemisphere of its
brain at a time (unihemispheric slow wave sleep) so it can remain partly
conscious and return to the surface to breathe. This takes place in two
hourly cycles with one half of the brain always remaining fully
conscious. The fact that it has evolved such a bizarre sleep pattern
suggests sleep is serving an essential purpose.
…in fact it
sleeps for most of the day too!
If sleep is there to protect us from
predation why would a creature at the top of the food chain with
no natural predators spend up to 22 hours a day asleep?
Meddis’ theory does try to explain the diverse sleep
patterns found across various species, unlike the restoration theory
that we’ll look at in a while.
Siegal (2005) in reviewing the data on different sleep
patterns, varying from a few hours per day in sheep and herbivores to 20
hours or more a day in lions, bats and opossums believes it’s difficult
to see how sleep can be serving the same purpose in all species. Killer
whales and dolphins barely sleep at all in the first few months of
life. Compare this to the human infant that sleeps 18 or more hours a
day during the same stage of development. How can sleep be serving the
same purpose in both? In humans it is assumed that we sleep more to aid
in development. If so, perhaps dolphins take care of these
developmental issues whilst the young are still in the womb so don’t
need the extended sleep pattern once born (Blumberg). Horne also
suggests that sleep may be serving a different purpose in different
If sleep is designed to make us inconspicuous at night, why
do we snore! (Bentley 2000).
of energy (Webb
A variation on Meddis is the Hibernation Theory which
is also sees sleep as an adaptive behaviour, but this time
designed to conserve energy. It compares sleep to hibernation. During
hibernation body temperature falls and the animal becomes inactive as a
way of conserving energy when food is scarce. The more at risk we are
from predators the longer we will sleep. Other factors will also effect
the time spent sleeping, for example the time we need to spend each day
searching for food. Again, in the case of early human species night
time would have been an unproductive period when we would have been
unable to forage. Sleep would have been one way of conserving our
resources by lowering our metabolic rate.
Evaluation of conservation theory
Research has shown that energy metabolism is significantly reduced
during sleep (by as much as 10 percent in humans and even more in other
species). For example, both body temperature and caloric demand decrease
during sleep, as compared to wakefulness. Such evidence supports the
proposition that one of the primary functions of sleep is to help
organisms conserve their energy resources.
Meddis criticises the theory on the grounds that it is
over-simplistic. According to Meddis (as seen above), the amount of
time spent sleeping is a compromise between protecting from danger and
Just being inactive at night would save almost as much
energy but without the added danger of loss of vigilance. It is
estimated that the calories we save by sleeping rather than simply
resting, is equal to the calories in a slice of bread, though it is
higher in other species.
Evaluation of evolutionary theories in general
On a positive note,
the evolutionary theories do attempt to explain the sleep patterns of
various species and generally they are able to predict the sleep times
of species. However, to do this they have adopted a catch-all
approach. For example with Meddis, if threat of predation doesn’t work
then metabolic rate will!
If sleep serves no other purpose other than safety, why do
we suffer psychological problems when deprived of sleep and why as
Rechtschaffen found in rats do animals die without sleep.
Empson (1993) describes sleep as ‘a complex function of the
brain involving far reaching changes in body and brain physiology’
adding that it must have some restorative function. He famously refers
to the evolutionary theories as ‘waste of time’ theories as they see
sleep merely as a way of passing time.
In an attempt to explain REM in evolutionary terms it has
been suggested that active sleep is most prominent in birds and mammals
- both warm-blooded. Perhaps REM keeps brain active and prevents it
dropping to dangerously low temperatures.
Evolutionary theories are unable to explain the complexities
of sleep. For example why do we have five stages of sleep (including
the very bizarre REM stage)?
Finally, some have argued that sleep would now be pointless
in most human societies because we are much more advanced and able to
protect ourselves against harm at night. However, as already pointed
out, our change in behaviour as come about very quickly (in evolutionary
terms), particularly with the discovery of electricity. Evolution of
biology and physiology on the other hand is much slower, so we wouldn’t
expect to see big changes in our sleep pattern for hundreds of years at
least: the genome lag
(1966) suggested that sleep restores depleted resources of
energy, removes waste from muscles and repairs cells. For example
during the day waste chemicals build up in the muscles following
physical exertion and neurotransmitters used for communication
throughout the nervous system are likely to be used up. Sleep therefore
might be an ideal time for the body to remove this waste and
restock/replenish its levels of neurotransmitters in preparation for
activity the next day. As some have put it…life disrupts homeostasis;
sleep restores it.
In addition the body could carry out repairs to damaged
cells and growth could occur the young
Non REM sleep
According to Oswald, NREM sleep is a time for replenishing
the body. Oswald points out that most NREM sleep, especially stages 3
and 4, occur at the start of the night when the body is most tired.
During stages 3 and 4 we secrete greater levels of growth hormone into
the blood which would help in the repair process, seeming to offer
support to his theory. (Good evaluation phrase!). We do know that
many restorative functions appear to occur during sleep, for example
digestion, removal of waste from muscles etc. and protein synthesis for
repair and growth. However, these processes also occur whilst we are
Evidence in support of restoration theory
Further support is
(1981) who studied ultra marathon runners who had completed a 57-mile
run. It was found that they slept for 90 minutes longer than usual for
the next two nights. REM sleep decreased whilst stage 4 of quiet or
NREM sleep increased dramatically from 25% of nights sleep to 45%.
However, lack of
exercise does not reduce amount of deep sleep as this model would predict.
Ryback and Lewis (1971) got healthy students to spend 6 weeks in bed and
observed no change in their sleep patterns. (Note: Carrying our sleep research
on student sleep patterns seems to be as valid as research on the sleep patterns
Other evaluation points
When we lose sleep
and are given the opportunity to make it up we only catch up on a small
proportion of it. This suggests that not all sleep is needed. Why
therefore would we need non-essential sleep?
Amino acids are not
stored in the body and only remain in the bloodstream for about eight
hours before being broken down or excreted. As a result we would expect
protein synthesis to stop half way through a night’s sleep. This would
explain why deep sleep occurs in the irst half of a night’s sleep. Of
course this also assumes that we eat just prior to going to sleep!
Oswald (1980) and Hartman (1984), built on the theory to
include restoration during REM sleep. They believe that REM is for
restoration of the brain. Stern & Morgane (1974), believed that
neurotransmitter levels within the brain may be restored during REM
sleep. The young brain is growing and developing at its fastest rate so
young children, especially babies sleep for much longer than adults. In
the newborn about 9 hours a day is spent in REM compared to about 2
hours in adults.
theories of sleep make cognitive sense since we suffer so many
unpleasant consequences when deprived of sleep
It is important to
remember that this seeks to explain the
state of REM sleep and makes no mention of the psychological state of
dreaming. Therefore it is
to be used in a
question that asks for theories of dreaming.
Research in support of
The most obvious
support comes from aspects of the sleep deprivation studies to be
discussed in the next section. First some other evidence:
Disruption of stage 4 sleep can cause fibrositis, a
condition of the lower back caused by muscle wasting.
Growth hormone, essential for production of amino acids
and proteins is secreted during deep sleep.
Babies sleep for much longer than adults and spend up to 9
hours in REM. This would allow time for growth and development
of the brain.
Following brain insults i.e. damage caused by ECT,
strokes, drug overdoses etc. Patients spend longer in REM for
an average of 6 weeks. This suggests time is being spent
carrying out repairs by laying down new proteins and building
It has been suggested that neurotransmitters are
replenished during REM. When patients are prescribed
antidepressants e.g. tricyclics or monoamine oxidase inhibitors
(MAOIs) they spend less time in REM.
However, when treatment is stoppedthere is no REM
rebound. Perhaps this is due to the drugs providing whatever
chemical REM sleep usually provides. Antidepressants increase
levels of serotonin and dopamine. Stern and Morgan (1974). So
perhaps REM is a time for the brain to replenish its supply of
neurotransmitters that it has used up during the day.
This is not
easy so I shall spend time explaining it in class
According to Oswald and Horne loss of these
neurotransmitters would explain problems in perception memory and
attention experienced following sleep deprivations e.g. Randy Gardner
and Huber-Weisman (1976)
synthesis occurs 24 hours a day, not just during stage 4 - although it
does seem to peak in stage 4.
of sleep does not appear to decrease when our level of daytime activity
decreases, (as shown by Ryback & Lewis, and others).
Following great physical exertion the amount of additional sleep we need
may only be negligible. Horne & Millard (1985) found that although we
usually fall asleep quicker we do not usually sleep for longer.
brain is very active during REM so runs counter to the idea that it is
an ideal time for repair.
model is over simplistic since in fact neuro-chemicals appear to be
produced throughout a night’s sleep and not just during REM.
miss out on sleep it doesn’t seem to affect our physical well-being. A
good night’s sleep and we’re back to normal.
Other research contradicting the theories
Returning briefly to animal studies; this theory predicts
that more active species will sleep longer. However, one of the least
active creatures, hence its name, the sloth, sleeps for about 20 hours a
day, whereas some very active humans get by on a few hours only. At the
other end of the scale, shrews are very active and presumably would need
plenty of restoration, nut only sleep a couple of hours a day.
Whilst looking at other species. Oswald assumes a single
and essential purpose for sleep. If this is the case why are there so
many different patterns of sleep across other species. Why do lions
need to sleep so long and herbivores sleep so little? It seems unlikely
that big cats suffer so much more damage on a daily basis.
The different patterns of sleep in other species do seem to
be related more to their differing lifestyle needs rather than a more
If sleep served only one purpose we would expect the results
of sleep deprivation studies to show similar results. This is not the
case; we only need to look at the very different outcomes of Peter Tripp
and Randy Gardener.
One final comment on this section that is always worth
making: Horne (1988) distinguishes between core and non-core sleep.
Core sleep (stages 4 and REM) appear to be essential and present in all
species, whereas non-core sleep (stages 2 and 3) appears not to be so
vital. Evidence for this is: following sleep deprivation we spend
longer in REM and stage 4 suggesting that we need to catch up on these.
Other theories of sleep function:
This is not
mentioned specifically on the syllabus but I thought I’d give it a
mention. Apart from being of general interest, you may be able to
incorporate some of the information into an essay on sleep function or
use it to evaluate one of the two main theories.
is provided by the way we feel so refreshed and renewed after a good
nights sleep. Other evidence is provided by
Kales et al
(1974) who found that insomniacs suffer from more psychological problems
and disorders. Hartman (1973) reported that we sleep more during times
of stress, e.g. changing job or moving house, and I told you about the
Greenberg et al (1972) study in which men showed footage of a
circumcision being carried out reported less anxiety each day when it
was shown again. However, if deprived of REM sleep they were just as
anxious on subsequent screenings.
Sleep deprivation studies
These are interesting in their own right, but from a
practical point of view can be used:
evidence for the restoration theory of sleep
essay on the methods used in the study of sleep
example of disruption of biological rhythms
Total sleep deprivation
These studies tend to be carried out on student participants
at various universities, for example Loughborough and Edinburgh in the
UK. There are also the two infamous cases of sleep deprivation for the
purposes of charity and notoriety in the Guinness book of records.
Peter Tripp spent 201 hours and 10 minutes awake, much of it sitting in
a glass booth in Times Square, spinning records and bantering into his
microphone three hours a day.
When Mr. Tripp
began to fall asleep, nurses shook him; doctors joked with him, played
games with him and gave him tests to take. After a few days, he began to
hallucinate, seeing cobwebs, mice, kittens; looking through drawers for
money that wasn't there; insisting that a technician had dropped a hot
electrode into his shoe.
His last 66 hours
awake were spent under the influence of drugs administered by the
doctors and scientists observing him. Asked at the end of his stunt what
he wanted the most, Mr. Tripp said, not surprisingly, that he wanted to
sleep, which he then did for 13 hours and 13 minutes.
Mr. Tripp's career
was indelibly tarnished by the 1960 payola scandal, in which he and
several other disc jockeys and radio station employees were indicted on
charges of accepting money from record companies in exchange for playing
their records. Tripp later blamed his involvement, at least in part, to
his sleep deprivation.
during his wakeathon attempt
completing his feat he is taken to bed with electrodes attached to monitor
Randy Gardner (1965) stayed awake for a record breaking 11 nights as part
of a school science project!!!. He reported blurred vision, slurred
speech, mild paranoia in which he began to believe that the researchers
watching him thought he was stupid. When Randy was allowed to sleep he
did so for 14 hours and 40 minutes on the first night and two hours longer
than usual on the next two nights. So, despite losing about 90 hours
sleep he only made up about 11. However, he did catch up on a
disproportionate amount of his lost stage 4 (68%) and REM sleep (53%)
suggesting that these are the vital stages. There were estimated to be 67
hours of sleep that he did not make up. Despite his exploits he suffered
no long term consequences.
In fact Randy
never made it into the Guinness Book of Records because,
according to Wiki, a month later Toimi Soini of Finland beat the
record by a few hours. (Why so little about this effort is
known I’m not sure). In 1989 the record was removed from the
book because of fears that it would encourage others to risk
their health by attempting to beat it.
year, Tony Wright of Penzance stayed awake longer than Gardner
but unaware of Toimi Soini’s record fell just short of the last
Guinness World Record
Accounts of the degree to which Gardner suffered during the
attempt vary. The official report by Dement paints a picture of little
or no cognitive disfunction. On the tenth day of his ordeal Dement
interviewed Gardner and then took him for a game of pinball, which
Gardner won. However,
J. Ross a commander of the U.S. Navy Medical Neuropsychiatric Research
Unit in San Diego, who was called in by Gardner’s parents, describes a
more serious loss of ability.
first few days these included problems focusing, inability to repeat
simple tongue twisters and moodiness. By day four there was memory loss
and the first hallucination, he imagined that a street light was a
person. Later in the same day he had a delusional episode, imagining
himself to be a famous black footballer!
end of the first week speech had slowed and become slurred and he was
having problems…. *
last two days his loss of cognitive ability was far more marked than
Dement suggests. When asked to count backwards from 100 in evens he
stopped at 65. When asked why he said he couldn’t remember what he was
supposed to be doing. He became paranoid and his speech was slow and
It is difficult to generalise to the general population with
case studies like this that by definition have a very small sample size,
particularly with such different findings between studies. Most
research since has backed this up. Greatest impairment appears to be in
boring tasks and those requiring close attention. Sleep deprived radar
operators in the war would miss enemy planes appearing on the screen.
Tired car and lorry drivers may have accidents following a few seconds
of micro sleep in which consciousness fades and the eyes de-focus.
In cases of fatal familial insomnia, people sleep normally
until middle age when they suddenly stop. Death is usually within two
years! Lugaressi et al (1986) reported the case of a man with brain
damage who as a result slept very little. He was unable to live a
normal life and eventually died as a result!
Larger studies on
The main study is the meta-analysis carried out by Huber-Wiedman
who collated the data from a large number of sleep deprivation studies.
The findings are summarised in the table:
Urge to sleep especially between 2 and 4 in the morning
Cognitive tasks requiring concentration are seriously
impaired, especially if they are repetitive or boring.
Periods of micro sleep are unavoidable and the volunteer
becomes irritable and confused. The ‘hat phenomenon’ occurs.
Still irritable and confused and may also become
Person becomes depersonalised with a loss of self
identity. This is referred to as ‘sleep deprivation psychosis.’
Webb & Bonnett (1978) used a different method of sleep
deprivation. They got their participants to gradually reduce their
sleep by 2 hours. Participants reported no ill effects. In a follow up
they got them to reduce sleep to only 4 hours per night, again without
Even with larger
sample sizes such as this study there are still serious issues with the
methodology. The participants are under tightly controlled conditions
and know that they’re being watch 24 hours a day. This will involve
massive demand characteristics and presumably with people that have
volunteered to remain awake for long periods they will probably view it
as a competition. This will not only create a level of stress but also
significantly increase motivation.
Dement himself admits that his own observations of participants are a
big source of bias due to his own expectations when observing
Overall evaluation of human deprivation studies
On the face of it they do appear to support the restoration
theory. However, with some of the studies it could be stress resulting
from deprivation rather than deprivation per se that caused the
effects observed. Hence we have problems with cause and effect
Dement’s work was carried out in sleep laboratories and this
in itself may have caused disruption to the night’s sleep. In the case
of Webb & Bonnet there is also the issue of social desirability bias
with participants just wanting to look psychologically tough.
The concept of total sleep deprivation is very artificial.
It is exceptionally rare for people in real life to go completely
without sleep for any length of time. As a result the studies lack
ecological validity, more so than studies of partial deprivation. Betty
Schwartz in the USA studies cases of supposed total insomnia, in which
patients claim that they never sleep. However, when tested under lab
conditions it is usually found that they have quite a good nights sleep,
but without realising it.
One finding that does appear common to animal studies and
human case studies is that total sleep deprivation is fatal and as yet
we don’t understand why!
human studies participants are aware that they are being observed and
this may well affect their behaviour. Bentley (2000) says that Dement
recognised this as being an issue in his 1960 study.
Animal studies (total sleep deprivation)
Rechtschaffen et al (1983) placed rats on a disc over
water. Each time that its EEG suggested it was falling asleep the disc
would rotate forcing the rat to walk to stay out of the water. A second
rat was used as a control. This had to do the same amount of walking
but was able to sleep when the other rat was awake. The experimental
rats started to lose weight after a week due to increased metabolic rate
started to eat more. Despite this, the weight loss continued and after
about three weeks the rats started to die. After 33 days all the sleep
deprived rats were dead.
Partial sleep deprivation
In these procedures volunteers are deprived of part of their
night’s sleep, i.e. deprived of REM or deprived of NREM sleep only.
Dement (1960) deprived volunteers of either REM or NREM
sleep and observed the consequences. He found that REM deprivation was
most dramatic with participants becoming more aggressive and having very
poor concentration. He also reported REM rebound effects, in which
participants would try and catch up on lost REM sleep. For example
going straight into REM when allowed to go back to sleep. By the
seventh night Dement reported that participants were averaging 26
attempts per night to enter REM. After the procedure when they were
allowed an uninterrupted nights sleep they spent much longer in REM.
This is similar to the results reported following the Randy Gardner
study and again reinforces the apparent importance of REM sleep.
In practice partial sleep deprivation is not possible over
any period of time since participants need to be woken so often it
quickly deteriorates into total sleep deprivation.
Jouvet (1967) used the flower pot technique to deprive cats
of REM sleep. They would be placed on an upturned flower pot in a tank
of water. This allowed them to sleep, but when they entered REM and lost
muscle tone they would fall into the water. They then climb back onto
the flowerpot renter the stages and fall back in once REM is reached.
In fact after a number of trials the cats become conditioned. On
reaching REM they wake up before falling into the water on many of the
trials. The study again is very unethical and cruel. On average the
cats survive for 35 days.
I couldn’t find a
picture of Jouvet’s cats on a flowerpot, however, this is a rat on a
flowerpot in a bowl of water.
of animal deprivation studies
animal studies there are clearly issues of generalising to humans.
animal studies are particularly cruel since unlike humans the animals
have no idea that the experiment will eventually end!
Conclusions on sleep function (courtesy of Dwyer and
The evolutionary theories of sleep are unable to explain why
sleep deprivation has such adverse effects whereas theory restoration
can. However, it is clear that sleep is essential for survival and this
is in agreement with the evolutionary theory’s adaptive value of sleep.
Modern ideas assume that restoration does in itself serve an adaptive
function so both evolutionary and restoration theories may be relevant.
Furthermore, sleep may serve other useful purposes as yet not
considered. One of these could be to allow us to dream. As
Shakespeare put it; “to sleep perchance to dream.”
The Physiology of sleep
On occasions the question on the paper has asked for you to outline or
discuss the physiology of sleep. Given this question you could of
course talk about the stages of sleep and what we know about the brain
activity etc. associated with each. Better still you could also mention
some of the stuff that follows here… but be warned there are some long
words and scientific terms!
Let’s consider the
procedure in three stages:
1. Staying awake:
The midbrain has a
large structure running down its centre called the RAS (reticular
activating system). We have long known that this increases arousal.
Bremner (1937) cut
the brainstem above the RAS in cats. Result permanent sleep. When he
cut below the RAS cats still had a normal sleep wake cycle. Reason:
cutting above it prevented electrical impulses from the RAS passing to
higher centres in the brain to keep the brain awake.
Moruzzi & Magoun
(1949) found that passing small electric currents through the RAS of
sleeping cats would wake them up whereas damaging the RAS would cause
2. Getting to sleep:
To nod off in the
first place the RAS needs to be switched off. We think this is achieved
by two chemicals serotonin and melatonin. This was covered in
detected by the eyes. This message is passed to the suprachiasmatic
nuclei (SCN) which acts as the main human body clock. This influences
another structure in the brain called the pineal gland* situated higher
in the brain. At night this gland starts to secrete melatonin.
Melatonin in turn causes serotonin to be produced by a structure in the
midbrain called the raphe nuclei. Serotonin from this group of cells
appears to shut down activity in the RAS.
Jouvet (1967) found
that damaging the raphe nuclei of cats caused severe insomnia (prevented
sleep). In humans natural damage to this area of the brain has similar
*the pineal gland
(sometimes called the third eye) was thought by the Greeks to be the
seat of the soul because of its central location within the brain.
3. Switching from NREM
to REM sleep
a night’s sleep we shift from the quiet of NREM sleep to the activity
that is REM. This appears to be triggered by a structure called the
locus coeruleus (pronounced ‘shu ru lus’). This produces the
neurotransmitter noradrenaline which passes to the brains higher centres
and appears to trigger REM.
Also crucial is the
brain chemical acetyl choline and the pons of the midbrain. Oswald
likened this process to a machine gun loading. The pons fills up with
acetyl choline. At a certain point it fires and triggers REM, lasting
about 15 minutes. When the acetyl choline runs out REM stops. It then
takes another 90 minutes to reload (NREM sleep) until it is ready to
Article found online
suggesting that we are in fact all sleep deprived:
the advent of the lightbulb, people sleep 500 hours less each year than
they used to. Unfortunately, our current "sleep diet" is significantly
less than evolution intended. Most other primates (e.g., apes and
monkeys) have a 24-hour sleep and activity cycle that is similar to that
of humans who live in cultures where the siesta is still practiced.
These animals have a long sleep at night, and a shorter sleep in the
midafternoon, with a daily sleep total of about 10 hours. Humans seem to
naturally need about the same amount of sleep. For instance, when the
pressure of work, alarm clocks, social schedules and advanced technology
is removed, people tend to sleep longer. Thus, in many less
industrialized societies, the total daily sleep time is still around
nine to 10 hours as it is for people when they are on unstructured
holidays (Coren, 1996a).
Useful study for
inclusion in an essay on biological rhythms:
Confirmation of these natural sleep durations comes from Palinkas,
Suedfeld and Steel (1995). These researchers spent a summer above the
arctic circle where there is continuous light 24 hours a day. All
watches, clocks and other timekeeping devices were removed, and only the
station's computers tracked the times that the team went to sleep and
awakened. Individual researchers did their work, and chose when to sleep
or wake according to their "body time." At the end of the experiment,
they found that their overall average sleep daily time was 10.3 hours.
Every member of the team showed an increase in sleep time, with the
shortest logging in at 8.8 hours a day, and the longest almost 12 hours
a day. This study, like many others, seems to suggest that our
biological need for sleep might be closer to the 10 hours per day that
is typical of monkeys and apes living in the wild, than the 7 to 7.5
hours typical of humans in today's high-tech, clock-driven lifestyle.
Other theories of sleep function:
‘Sleep that knits up the ravell’d
sleeve of care,
The death of each
day’s life, sore labours bath,
Balm of hurt minds,
great nature’s second course,
Chief nourisher in
Macbeth (Or the
‘Scottish Play’ for the thespians amongst you).
This is not
mentioned specifically on the syllabus but I thought I’d give it a
mention. Apart from being of general interest, you may be able to
incorporate some of the information into an essay on sleep function or
use it to evaluate one of the two main theories.
evidence is provided by the way we feel so refreshed and renewed after
a good nights sleep. Other evidence is provided by
Kales et al
(1974) who found that insomniacs suffer from more psychological
problems and disorders. Hartman (1973) reported that we sleep more
during times of stress, e.g. changing job or moving house, and I told
you about the Greenberg et al (1972) study in which men showed footage
of a circumcision being carried out reported less anxiety each day
when it was shown again. However, if deprived of REM sleep they were
just as anxious on subsequent screenings.
(similar to Oswald’s
theory is the idea that REM helps us to consolidate memories)
(1976), showed that rats that had spent the day learning a maze spent
longer in REM that night, suggesting that memories are being
constructed in REM.
spend longer in REM having spent the day learning how to avoid
electric shocks. (Smith 1997).
Students spend longer in REM when cramming for exams.
The amount that we
sleep and also the pattern and quality of sleep varies as we get older.
These changing patterns of sleep may provide clues as to the purpose of
Pattern of sleep
18 hours of
sleep (9 hours of which is REM)
first few months of life there is little in the way of a
pattern. This doesn’t emerge until about 20 weeks when the NREM/REM
cycle appears. In the first few months the infant often goes
straight into REM from the outset and this REM is often restless
with lots of facial movements and unlike in later life arms and
legs may move too
time drops to about 13 to 14 hors a day and the ultradian sleep
cycle takes about one hour (compared to the 90 minutes later in
life). The developing child remains awake most of the day (from
10am until 8pm) perhaps with one nap during that time.
5 to 10
time is now 9 to 10 hours with an adult pattern of 75% NREM and
25% REM sleep.
The bulk of
NREM occurs in the first half of the night.
ultradian cycle is now extended to 70 minutes.
10 to 12
(1999) describes the sleep pattern at this age as ‘ideal.’
child typicallyhas plenty of energy during the day and can nod
off quickly into deep, uninterrupted sleep waking the following
morning totally refreshed!
child should still be spending 9 to 10 hours asleep but for the
first time the pattern is frequently disrupted due o late
nights, schooling etc.
growth hormones are released for the first time and the
increasingly sexual nature of dreams can result in wet dreams.
18 to 30
body still requires as much sleep as early teens but this is
rare at this age.
this age are permanently sleep deprived.
Environmental factors such as babies, snoring, work patterns and
anxieties keep us awake.
30 to 45
continues to decrease and people in this age group experience
deep sleep, especially stage 4 sleep decreases.
factors such as less exercise, alcohol, caffeine interfere with
the sleep pattern.
45 to 60
hormone levels start to decrease (all down hill from here on in
tendency is to go to bed earlier but quality of sleep begins to
time drops to around 7 hours but with little or no stage 4
however, remains at about 2 hours per night.
retirement when we have more time to sleep, the overall
quality of sleep deteriorates significantly.
estimates that in a typical night’s sleep at this age there
could be up to 1000 brief awakenings per night each lasting just
a few seconds.
are unaware of these ‘micro-arousals’ they do leave us tired the
Changes over a
lifetime (more detail)
infant child sleeps much longer than an adult. In the first year of
life a child will typically spend about 16 hours asleep, half of this
being in REM. By the age of one this has dropped to about 12 hours of
total sleep with about four hours of REM. Lots of sleep in early life
does seem to tie in with restoration theory, since this is a time of
rapid growth both in the body and in the brain. Early life is a steep
learning curve so presumably the brain is working over time to
assimilate all this new information by making new and ever more complex
interconnections. According to Oswald this would be facilitated by
plenty of REM sleep.
Evolutionary sleep theorists suggest all this infant sleep is designed
to take the pressure off of parents who can get on with essential chores
such as finding food.
adolescence hormones seem to be playing an ever-increasing role in the
sleep pattern. Hormone production at night is disturbing sleep and
leading to sleep deprivation. Studies suggest that adolescents need
more sleep that pre-adolescents not less. However, schools usually
expect the older age group to start earlier than the younger age group.
Recent research is suggesting that many adolescents have DSPS (mentioned
in biorhythms) that results in later sleep onset and difficulty waking
in the morning. As a result some schools are now experimenting with a
later start to the school day and are reporting improved performance and
the time we have reached maturity we usually sleep for 8 hours with only
one quarter (2 hours) being spent in REM. Note, people who sleep longer
tend to spend much of the extra time in REM. As a species, in the West
we sleep less than we did a century ago. It is estimated that in the UK
we now spend only 7.5 hours asleep per night compared with 9 hours in
Kripke et al (2002) report that sleeping longer is correlated with
ill-health. In a huge survey of over one million adults they found that
those sleeping six or seven hours have a greater life expectancy than
those sleeping eight hours longer. However, you have probably noticed
the weak link in this argument… the word ‘correlated!’ It would seem
likely that people who are ill may need to sleep longer, so underlying
health problems are causing the increase in mortality and the increased
need for sleep.
The wrinkly years
we get older still there are further changes. REM continues to
decrease, and by the time we reach 60, stage 4 is non-existent. As a
result older people are more easily awoken and often complain of
insomnia. This loss of deep sleep may explain the deterioration seen in
later life. No deep sleep, no growth hormone for repairs. As a result
there is increased loss of muscle tone, lack of energy and increased
risk of osteoporosis as bone density declines.
Research into age lifespan changes
Cauter et al (2000) carried out a longitudinal sleep study on 149 male
participants (aged 16 to 83) over a 14 year period (though I’m not sure
how many of the 83 year olds would have seen the study through to the
particular interest was their finding that deep sleep and as a result
production of growth hormone, deteriorates in two stages:
Between 16 and 35 years and then again
Between 35 and 50 years
Meaning that between these years the amount of repair to body tissues is
reduced. In fact by the age of 45 there is so little growth and repair
that muscle tone begin to fade, exercise becomes more difficult and
obesity is more likely.
researchers considered this from an evolutionary perspective.
our ancient past when we were still hunter-gatherers, our life
expectancy would have been less than half of what it is in the Western
World today. Certainly 30 would have been getting on a bit and it’s
unlikely that many would have ever reached 45. As a result, with death
so imminent what would have been the point of producing growth hormone
and carrying out repairs to a decrepit body? No growth hormone needed…
no deep sleep needed.
These findings are supported by other studies that suggest as we get
older there are
- decreases in
total sleep time, deep sleep time and REM sleep time
- increases in
sleep latency (time taken to nod off) and stages 1 and 2 sleep time.
Dozing and depression in the elderly
older people there may also be a link between dozing and depression.
Foley et al (2000) carried out a telephone poll and questioned people on
their sleeping habits and mood. A significant correlation was found.
However, telephone polls are a notoriously poor way of obtaining a
sample since people are even less likely to be honest on the phone than
they are face to face.
Also being a correlation I’m sure you can also tell me we can’t prove a
cause and effect relationship. The assumption is that the depression
results from the dozing but it is just as likely that being depressed is
leading to dozing or even more likely that a third event such as
bereavement or lack of job is causing both.
However, in support of the theory it has been suggested that older women
who report sleeping well suffer fewer problems with mood, memory and
issues of attention and are less likely to suffer from physical
disorders such as diabetes and CHD. (Aneoli-Israel 2008)
Most older people sleep with a partner. Relatively little research has
been carried out into the affect this has on sleep patterns.
Kloesch et al (2006) found that the male sleep pattern seems to be most
disrupted, to the extent where cognitive functioning is impaired.
Eight unmarried, childless couples in their twenties were asked to spend
ten nights sleeping together and ten nights sleeping apart. They were
given questionnaires and asked to complete a variety of tasks the next
men reported sleeping better with a partner despite their sleep
appearing to be more disturbed. Co-sleeping also raised the levels of
men’s stress hormones. Women on the other hand were found to sleep more
Stanley believes that we are not designed to sleep together. Few other
species do, but modern human society sees it as the norm. He describes
it as ‘bizarre thing to do.’
Evaluation points to make on lifespan changes
measures used for testing age differences are scientifically rigorous,
use objective measures of sleep such as EEG, EMG and levels of
breathing. As such they are replicable and appear to be reliable.
However most information is gathered in sleep labs which are very
artificial and may affect sleep patterns. Participants are wired to
electrodes over large parts of their head, face and body. They have
straps to measure their breathing and sometimes even penile erections
(not so widely used in women). They are aware of being watched and
expected to sleep in unfamiliar beds. Research therefore lacks mundane
realism so it is difficult to generalise the findings to real life!
That is ecological validity is low.
Self report methods used in dream research is subjective and may be open
to researcher bias.
There is a big
question mark over whether or not older people really do sleep so much
less than younger adults. There certainly appears to be less nocturnal
sleep, however, some or all of tis could be made up by afternoon naps.
Borberley et al (1981) reported that 60% of 65 to 80 year olds regularly
take naps in the afternoon.
There is also a big
discrepancy in research into the different age groups. In the past
twenty years or so there has been a focus on infant sleep patterns and
habits, largely due to research into sudden infant death syndrome (what
the tabloids call ‘cot death). In contrast to this relatively little
research has been carried out on the middle aged. Dement attributes
this lack of information to practical reasons; namely the constraints on
this age group such as pressures of work and families etc. They simply
don’t have the time to spend in sleep labs for weeks on end as the other
age groups do.
Despite their being
obvious average differences in the amount we sleep at different ages,
research also points to there being huge individual age differences
within each grouping. So within my age group there will be those
managing perfectly well on four hours of sleep whilst others will be
suffering tiredness despite eight or nine hours. It seems that
individual differences are every bit as important as age differences
when studying sleep.
In Northern and
Central Europe, North America sleep is usually monophasic (one long
period of nocturnal sleep, typically lasting 7 or 8 hours). Text books
seem to consider this to be the norm; yet another example of
ethnocentricism, imposed etic and ‘West is Best’ attitude.
Those travelling to
southern Europe or South America may have noticed a different and more
practical sleep pattern in these sunnier climes. The afternoon siesta,
often lasting two or three hours followed by a much later nocturnal
sleep is considered the norm and appears to produce no additional
deficits to monophasic sleep.
Hope you found this interesting. I
quite enjoyed writing this section on age differences in sleep. As I
said you could incorporate this information into a question on sleep
research or a question on biorhythms. Even if you have no opportunity
to use it, I’m sure that you could bore friends with it endlessly at
parties or adapt it as a source of chat up line
Disorders of sleep
What the board expects you to know:
Explanations for insomnia, including primary and secondary
insomnia and factors influencing insomnia, for example, apnoea,
Explanations for other sleep disorders, including sleep walking
Is a condition that most of us experience to a greater or lesser extent
at sometime during our lifetime. Insomnia is either an inability to
fall asleep, an inability to stay asleep or both. Not surprisingly the
symptoms are similar to those of sleep deprivation: tiredness, fatigue,
inability to concentrate, irritability etc.
According to Dement insomnia should not be classed as a sleep disorder
in its own right, merely a symptom of other disorders, which at times
may be unknown. For doctors this also raises the question; whether to
treat the sleep loss or the underlying cause.
Primary and secondary insomnia
One way of categorizing insomnia is to consider whether or not there is
a known disorder causing the condition.
This has no obvious cause so appears to ne an illness in its own right.
It is by far the most common form of insomnia.
To be diagnosed with primary insomnia (according to DSM IV):
Patient must have had problems sleeping for at least one month
The lack of sleep has resulted in social or occupational impairment
The insomnia is not the result of any other sleep disorder such as
narcolepsy or sleep walking
The insomnia is not the result of any other psychological disorder
such as anxiety or depression
The insomnia is not due to a physiological disorder such as cancer
or heart disease.
The inability to sleep is the result of some other known disorder such
as apnoea, restless leg syndrome (RLS), depression, anxiety etc. Other
possible causes include: Jet lag or shift work resulting in
desynchronisation of biological rhythms. Attempting to sleep is in
opposition to the sleep-wake cycle. Physical injuries or conditions
resulting in pain
Certain drugs such as codeine (prescribed as an analgesic) and various
Explanations of primary insomnia
The insomnia results from a learned or behavioural condition
A cycle of anxiety resulting in an inability to sleep that becomes
Regular routines that pre-empt sleep and which have become
associated with an inability to sleep. For example brushing teeth,
hanging up clothes, putting on your Paddington Bear PJs or even the
bedroom itself, which over time have become associated with bedtime
and create stress since they are linked to the forthcoming,
This second one is clearly an example of classical conditioning and
almost creates a phobia-like situation. As a result sufferers often
find that they can sleep better if they break some of these habits, for
example when they sleep elsewhere on holiday.
This usually starts early in life and appears to be the result of the
body’s sleep-wake cycle. Brain mechanisms such as the raphe nuclei and
reticular activating system (RAS) seem to be at fault.
As discussed in biorhythms, the sleep/wake mechanism is a balancing
act. During daylight hours we are kept awake by the RAS which creates
arousal in the higher centres of the brain. In order to sleep these
must be inhibited (or switched off) by the sleep centres such as raphe
nuclei and locus coerulus. As night falls a build up of melatonin opens
the sleep gate and the balance tips from waking to sleeping. Patients
with idiopathic insomnia appear to be predisposed to greater arousal in
the higher centres and as a result struggle to switch off the waking
mechanisms. Bonnet and Arand (1995) suggest insomniacs have higher
levels of cortical activity both when awake and asleep.
There is a tendency for many of us, insomniacs or not, to underestimate
the amount of sleep we get. Often when patients claiming to be severe
insomniacs are tested in sleep laboratories they are found to be having
near-normal nights of sleep.
Typically patients are wired to EEGs and left in labs overnight. They
may also be asked to press switch every 20 minutes (perhaps in response
to a quiet tone). The following morning they report having little or no
sleep, but their EEG patterns suggest otherwise, as does the fact that
they haven’t responded to the tone!
This is not surprising. We all know that our perception of the passage
of time slows when we are bored. Fifteen minutes laid awake at night
seems like a lifetime and often we drift in and out of sleep without
Family links (nature or nurture)
Dauvilliers et al (2006) put insomniacs through a battery of tests,
questionnaires and clinical interviews. They found that 73% of
insomniacs reported a family history of insomnia compared to only 24% of
non-insomniacs. Clearly this doesn’t explain the family link. The
assumption here appears to be something genetic. However, as with
phobias and other anxieties in families, it could simply be a learned
Explanations of secondary insomnia
This tends to be more common and whenever possible it would seem to make
more sense to treat the underlying condition rather than the insomnia
If you cast your minds back to AS; stress results in increased activity
in the sympathetic branch of the ANS (autonomic nervous system). Likely
causes of modern day stress will be life events such as divorce and
examinations, as well as relationship and money issues and occupational
stressors. Acute (short-lived) stress will result in temporary insomnia
but sleep patterns should return to normal when the stressor is dealt
with. However, chronic stress can result in long term disruption and is
likely to become a vicious circle of anxiety causing sleeplessness and
inability to sleep increasing the anxiety experienced.
As we saw with lifespan changes in sleep patterns, as we get older we
tend to sleep less and by the age of sixty the body is producing very
little melatonin. As a result, pensioners get little is any deep sleep
and often complain of insomnia and tiredness.
Allergies such as hayfever, asthma, heart disease, and conditions
resulting in pain can all disrupt a night’s sleep.
Many drugs, prescription and recreational can interfere with the
ultradian rhythm. Caffeine and nicotine are both stimulants so create
increased activity in the nervous system. We often take caffeine to
keep ourselves awake or to help wake us up in a morning. Alcohol seems
to help us nod off but it disrupts the pattern of sleep, particularly in
the second half of the night. As already mentioned some prescription
drugs such as the analgesic codeine, also disrupt sleep.
We are all familiar with this one! Hot summer’s nights, (like the ones
we used to get before global warming), bright lights, uncontrollable
noise, uncomfortable bed etc. can all disrupt sleep. Less familiar may
be high altitudes which result in the blood becoming more alkaline as
oxygen levels drop.
all of this together (useful for AO2)
Insomnia is a complex disorder and probably results from an interaction
of many factors. Spielman and Glovinsky (1991) suggest the
predisposing, precipitating, perpetuating model to explain the onset and
maintenance. This is similar to the diathesis-stress model we saw in
abnormality at AS but takes it a crucial stage further…let me explain:
refers to the genetic component which makes the onset of the disorder
more likely. As we’ve seen this predisposition seems to be mediated by
greater cortical arousal making increasing the ‘tipping point’ for
sleep. (This is the diathesis)
an environmental factor such as stress or anxiety that trigger the
inability to sleep. (This is the stress).
In addition to diathesis stress, insomnia requires a perpetuator, since
the insomnia usually continues long after the stress has been sorted
Perpetuating: During the insomnia patients have suffered anxiety due to
inability to sleep and have learned to associate various nighttime
habits and even the bedroom and the bed itself with sleeplessness.
After the stress has been lifted this negative association still exists
and as a result so does the insomnia.
Note: the term ‘sleep hygiene’ refers to improving your sleeping health
by reducing alcohol, caffeine etc and by improving the sleep environment
such as quieter and darker environment. Increasing exercise and
avoiding afternoon naps also improve sleep hygiene.
Treatments for insomnia usually concentrate on the perpetuating factors
and attempt to improve sleep hygiene. Often insomnia leads to habits
that create poor sleep hygiene. Inability to sleep at night often
results in patients taking afternoon naps to compensate. Tiredness
results in less exercise and patients often resort to alcohol to help
trigger sleep. All of these need to be discouraged to improve hygiene
and help break the perpetuating cycle.
Sleeping pills (usually benzodiazepines) that were so popular in the
seventies are no longer prescribed in such massive numbers. Patients
become dependent on the drugs and suffer even worse insomnia when they
stop taking them.
Evaluation of research into insomnia
Dement (1999), the undeniable expert in the area, believes there are so
many variations of insomnia with so many causes that its barely worth
trying to make general comments about the disorder. In fact he goes a
step further and suggests that insomnia is not a disorder at all, merely
the symptom of a whole host of other disorders. He suggests that
doctors should not attempt treatments for insomnia but treat the
underling causes instead.
Very often diagnosis of insomnia is based on self-report. However, a
lot of research suggests that patients claiming to be insomniac are in
fact getting far more sleep than they believe, making this method very
Research into insomnia
Two useful studies:
Smith et al (2002)
found evidence for physiological differences in the brains of
Nine women, five insomniacs and four controls slept in a sleep lab for
three nights. They were studied using a polysomnograph (recording brain
activity, breathing, muscle tone etc) and on the third night they also
underwent a brain scan.
It was found that the insomniacs had a significantly reduced flow of
blood to various areas of the cerebral cortex suggesting abnormal CNS
activity during NREM sleep.
Morin et al (2003) investigated the link between stress and insomnia
67 participants comprising 40 insomniacs and 27 controls completed a
series of questionnaires assessing:
Their daily stressors (major life events and trivial daily hassles)
Their pre-sleep levels of arousal
The quality of their sleep
Although the insomniacs were experiencing similar numbers of stressful
events to the control group they were reporting significantly higher
levels of anxiety. They also reported their lives as being more
stressful and were more likely to using emotion-focused coping
The researchers concluded that actual stressors were not the cause of
the insomnia, rather the insomniacs’ perception of the stress that they
were under. Although they were not suffering significantly more stress
in their lives it was creating much higher levels of anxiety. The
researchers therefore recommended that the best course of treatment
would be better coping strategies, preferably problem-focused
Apnoea (properly obstructive sleep apnoea (OSA)) is brief pauses in
breathing resulting in a suspension of the movement of gases between the
lungs and the air. This is brought about by a blockage preventing
oxygen entering the lungs. NB: Gaseous exchange within the alveoli of
the lungs and cellular respiration continue as normal. This reduction
of air movement is called hypopnoea).
Clinically speaking, apnoea occurs when breathing ceases for ten seconds
or more at least ten times per hour and results in a drop in blood
oxygen saturation and/or a 3 second or greater alteration in the EEG
(electro-encephalogram). Apnoea is not an issue during waking hours
since there is sufficient muscle tone to keep the air passages open.
The brain, aware of the drop in oxygen levels wakes the person to
unblock the obstruction and this waking is often accompanied by a loud
Apnoea can be relatively mild or severe. The level is assessed using
the API (apnoea/hypopnoea index) which does exactly what it says on the
tin… it measures the number of apnoeas and hypopnoeas per hour. Fewer
than ten such events per hour is likely to cause few problems and will
probably go unnoticed by the patient.
Diagnosis and assessment of severity often requires an overnight stay in
hospital with the patient attached to a polysomnogram. This measures
EEG, EMG, chest movements, airflow through the nose and mouth, pulse
rate and blood oxygen levels…oh yes and often video footage of the
patient snoring and waking!
Anything that restricts airflow through the throat can cause OSA.
due to a build of mucus, as with a cold or hayfever, or more rarely
due to nasal polyps that may develop as a result of hayfever.
especially when it results in an increased diameter of the neck.
The additional fat tissue puts pressure on the throat causing
top of the list for these is alcohol, but others such as tobacco,
painkillers and sedatives can all result in OSA.
OSA becomes more common as we get older, probably due to a
combination of the above factors, especially being overweight and
drinking more alcohol.
Adenoids and tonsils:
enlarged adenoids and tonsils is the most common cause of OSA in
Pretty much as you’d expect: these include tiredness and deficits in
cognitive functions. Macey et al (2002) believes that repeated
starvation of oxygen causes damage to the neurons of the brain.
Childhood OSA can result in an inability to concentrate, poor memory and
attention span and lowered IQ as well as poor performance at school.
Is a disorder of the sleep-wake cycle which results in excessive
sleepiness and often a loss of muscle tone resulting in cataplexy.
About 1 in 2,000 people suffer from the disorder and worldwide it is
estimated that there are 3 million sufferers. Until very recently the
cause was unknown but major advances have been made in the past 10 years
that are now giving hope that a successful treatment can soon be found.
Excessive daytime sleepiness (EDS) is usually the first symptom to present itself.
Initially patients try very hard to stay awake but find that if they do
this then they are faced with involuntary attacks of sleep that can
strike at any time. Periods of micro-sleep resulting in brief naps
lasting less than 30 seconds are also common. Very often the patient
themselves are unaware of these though observers find them
EDS can cause knock on effects with memory loss, focusing of eyes and
tiredness. Often friends initially find these first symptoms signs of
rudeness, laziness or lack of interest.
(muscle paralysis) is the other major symptom, although 25% of
narcoleptics never seem to experience this. Until recently it had been
argued that cataplexy was an essential symptom of the disorder but
recently it was decided that the disorder could be diagnosed even in
those that never suffer from it.
The paralysis may only affect the muscles of the face but in more severe
cases can result in loss of all muscle tone causing the patient to
collapse on the floor. Although the paralysis usually lasts a matter of
minutes, repeated attacks can result in the patient being immobilized
for up to half an hour, particularly if the trigger, such as excitement
Very often cataplexy doesn’t develop or many years following the initial
first signs of narcolepsy (usually EDS) which makes an early diagnosis
of the disorder unlikely. It is usual for narcoleptics not to be
diagnosed until 12 to 15 years following the first symptoms!
Although the patient may sleep for many hours a day, night time sleep is
constantly interrupted by waking, increased heart rate, periods of
alertness and hot flushes.
The day time attacks of cataplexy are often accompanied by vivid
hallucinations which seem to be due to REM sleep encroaching on
wakefulness. The patient is still fully conscious and aware of what is
going on around them so such hallucinations can be frightening and
difficult to distinguish from reality. Similar to this are the very
vivid hypnogogic and hypnopompic hallucinations that we often experience
on falling asleep and just prior to waking up respectively.
are also experienced. The patient behaves as if on autopilot, carrying
out every day behaviours, often unaware, and often getting them wrong,
for example pouring milk into the teapot.
as we’ve already seen, our first bout of REM sleep usually occurs after
60 or 70 minutes of NREM or slow wave sleep, before reoccurring every 90
minutes or so (the ultradian rhythm). Narcoleptics often nod off
straight into REM sleep at the start of the night.
Age of onset
First signs of the disorder (EDS) usually occur between 15 and 30 years
of age, but can be as young as five. As already mentioned, it may take
many years for the full symptoms to appear and for a correct diagnosis
to be made.
Narcolepsy is NOT a psychological disorder but a neurological condition
resulting in a fault in the mechanisms controlling the normal,
circadian, sleep-wake cycle resulting in REM sleep occurring at
Research on dogs by Mignot and others has suggested a genetic
link with the disorder. Dr Emmanuel Mignot has bred a colony of
narcoleptic dogs (Labradors and Dobermans ) at his laboratory
Stanford University. However, the disorder doesn’t appear to be
so clearly defined in humans with what appears to be a lesser
In recent years the neurotransmitter hypocretin (sometimes referred to
as orexin) has been implicated in the disorder. In the late 1990s Dr
Yanagisawa was testing hypocretin’s use as an appetite suppressant on
rats. He bred mice that couldn’t produce hypocretin and found that they
ate far less than normal. However, he noticed that over time they
actually put on weight rather than lost it as would be expected. When
he taped their behaviour he found that instead of being very active at
night they were having frequent attacks o cataplexy, as had been
observed in narcoleptics.
Work by Mignot on his dogs isolated a fault on the hypocretin-2-gene
that produces hypocretin which seemed to support the earlier work.
Siegel et al (2000) managed to acquire the preserved brains of 4
narcoleptics and after a close examination they were found to have 93%
fewer hypocretin neurons than a non-narcoleptic’s brain. This was
subsequently supported by Mignot.
More recently low levels of hypocretin have been found in the CSF of
humans with the disorder.
Further research is still ongoing. It has been found that small
injections of hypocretin can reduce the cataplexy in dogs, however
larger injections make the cataplexy work. This seems to be due to
different areas of the midbrain responding in different ways to the
chemical. The locus coerulus (already mentioned in the physiology of
sleep) seems to be crucial in the whole process.
Hypocretin certainly plays an important role in keeping us awake.
During the day it acts on the locus coerulus o keep us awake, at night
time production of the chemical by the hypothalamus stops so we can nod
Evaluation of narcolepsy research
The drug modafinil has been used an effective treatment for some cases
of narcolepsy. It is thought that modafinil stimulates production of
hypocretin by the hypothalamus.
As we’ve already seen, injections of hypocretin can reduce the cataplexy
experienced by narcoleptic dogs.
There is clearly a genetic component to narcolepsy but as shown in dogs
and with a limited tendency for the disorder to run in human families.
However, the research by Mignot on dogs does suggest that there are
serious issues of generalisation between the two species. In dogs one
group of genes (the so called HLA complex on chromosome 11) appears to
be responsible for narcolepsy.
In humans, however there is a high level of discordance in MZ twins. If
one twin as narcolepsy there is only a 30% chance that the other will
develop the disorder.
Although levels of hypocretin is a major contributory factor, further
clarification of its precise role is needed. Mahowald and Schenck
(2005) report that ‘the absence of hypocretin is neither necessary nor
sufficient to explain all the cases of narcolepsy [in humans].
Sleep walking (somnambulism)
Sleep walking is a surprisingly common condition with an estimated 10%
of the population experiencing it in some form at one time or another in
their lifetime. (note: some texts put the estimate as high as 20%).
One thing is clear, it is far more common in children. Only about 3% of
adults experience sleep walking.
The Hollywood, cartoon depiction of sleep walkers with arms out in front
walking like a robot is far from the mark. Sleep-walkers move quite
naturally and other than the glazed expression in the eyes may appear to
be awake. There are annual reports of people driving cars and even
riding horses whilst asleep.
Somnambulism is associated with deep sleep (not REM obviously) and also
night terrors. Because of its link with stages 3 and 4 of sleep it is
more common in the first half of the night and in severe cases there can
be more than on episode per night. Usually sleep-walkers have no
recollection of the event when they wake up the next morning.
There appears to be an issue of arousal. EEG monitoring of sleepwalkers
shows that typically they have delta activity (a characteristic of deep
sleep) with beta activity (characteristic of being awake) mixed in.
Researchers believe that sleepwalking occurs when the patient wakes from
deep sleep but the arousal is incomplete so as a result they are not
fully woken. There appears to be a genetic component to this.
Sleepwalking certainly appears to run in families (Horne 1992) which in
itself may suggest a genetic component. Hublin et al (1997) in a study
of Finnish twins reported that there is a concordance of 66% for boys
and 57% for girls. Again these are high figures suggesting a genetic
Recent genetic evidence
Bassetti (2002) claims to have isolated a specific gene that may be a
risk factor in sleepwalking. HLA DQBI*05 (the gene, not a random string
of characters) was found to be present in about 50% of sleepwalkers he
tested. The same gene was only present in about 25% of
non-sleepwalkers. The gene is part of a group of genes involved in the
production of the protein HLA and has also been implicated in some cases
However, the sample size used was very small. Out of 74 patients
studies only 16 underwent genetic testing and 8 of these were found to
have the gene.
The researchers asked for volunteers. As you should know from AS
research methods, this sort of self-selecting sample is the worst
possible way of getting participants. Most sleepwalkers do not seek
medical attention or are not even aware of their condition. Those that
do are usually the more serious cases and often include those who have
sustained injuries or caused a nuisance. As a result, they are not a
typical cross-section of the sleepwalking fraternity.
A neuro-chemical explanation:
Antonio Oliviero (writing for Scientific American 2008)
“During normal sleep the chemical messenger gamma-aminobutyric acid (GABA)
acts as an inhibitor that stifles the activity of the brain’s motor
system. In children the neurons that release this neurotransmitter are
still developing and have not yet fully established a network of
connections to keep motor activity under control. As a result, many
[kids] have insufficient amounts of GABA, leaving their motor neurons
capable of commanding the body to move even during sleep.”
Olivero goes on to explain that in some this inability to produce
sufficient GABA may persist into adulthood.
Olivero also offers a simpler explanation for why sleepwalking is more
common in childhood. Sleepwalking is associated with stage 4 sleep and
as we’ve already seen children spend much longer in this stage, which
gradually decreases as we get older and completely disappears in the
Sleepwalking is more common when people are sleep deprived and
tired. Sleepwalking is closely related to restless leg syndrome
(RLS) which is a risk factor for insomnia and as a result
RLS is a genetic condition. This may help explain the genetic
component of sleepwalking.
Left: this style of sleepwalking portrayed in cartoons and films
is a myth!
Tiredness, sleep deprivation and sleepwalking
Although there are clearly biological predispositions for somnambulism
an important trigger appears to be tiredness.
Zadra et al (2008) tested 40 sleepwalking volunteers under laboratory
Night one: designed to measure baseline sleep habits. The participants
were observed sleeping in the laboratory
Night two: participants were kept awake. In fact they went without
sleep for 25 hours
Night three: recovery sleep was allowed, with participants being
observed again as they slept.
On the first night, the 40 participants had a total of 32 sleepwalking
episodes between them
On the third night (participants sleep deprived) this rose to 92
This seems to suggest that tiredness can trigger sleepwalking
However, the sample size is relatively small and the first night, used
as a control for comparison purposes would have been the first night in
the sleep lab. Perhaps participants were getting used to the new
The greatest danger to sleepwalkers is self-harm. It is very rare for
them to harm or attack others.
Jules Lowe (2003)
In Manchester, 2003, a 32 year old man, Jules Lowe attacked and
killed his 82 year old father. When questioned by police he
claimed to have no recollection of the event and to have been
sleepwalking at the time.
Dr Irshaad Ebrahim was called in as an expert witness to
investigate the case and run a variety of tests on Lowe. It was
found that despite a history of sleepwalking, Lowe had never
been violent before.
Lowe was found ‘not guilty’ of murder but was believed to be
suffering from ‘insane automatism’ and has subsequently been
compulsorily detained indefinitely in a secure psychiatric*
* does psychiatric mean guessing right three times in a row?