Salvador Dali: Sleep A2: bio-rhythms

Biological Rhythms

Disrupting rhythms

Sleep states

Sleep deprivation

Lifespan changes

Disorders of sleep


Salvador Dalí. Dream Caused by the Flight of a Bee around a Pomegranate. One Second before Awakening.

































































































































































































































































































































































































































































































































































































































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Biological Rhythms


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 biorhythms or

Discuss the roles played by endogenous (internal factors) and zeitgebers (environmental factors) in determining bodily rhythms.

(a) Describe research into biological rhythms (eg circadian, infradian, ultradian) (12)

(b) Consider the consequences of disrupting biological rhythms (eg shift work, jet lag).  (12 marks)

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 mechanisms involved.


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 afternoon!

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.

Research into circadian rhythms

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.


I 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 activity.

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.



EEG is recording brain activity

EMG is recording muscle activity

EOG is recording eye activity

The most 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.


AwakeThe 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 amplitude.

Stage 1 sleep (15 minutes)

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 knee twitch. 

Stage 2 sleep (20 minutes)

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 minutes)

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 minutes)

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 REM sleep. 

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. 

As hopefully 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. 

Research evidence

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 genetic component. 

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. 


The menstrual cycle

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!

Endogenous control

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. 

Sweaty 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 twenty. 


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 and 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 (Strassmann 1998).

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. 


Evolutionary 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 pregnancy.

Light levels

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.


Pre-menstrual Syndrome (PMS)

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. 



 PMS appears 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!  


Janiger reported similar symptoms in other primates. 






Endogenous clocks 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. 



However, 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:

  1. 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.
  2. 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 circadian rhythms

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 sleep patterns.

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 the brain).

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 ‘hypothalamic island’). 

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 purposes


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. 

Recent 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 clock.


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!


Evaluation of endogenous factors

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. 

When humans 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 light levels. 




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 conditions etc.


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 to east.

Jet lag

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.


Research 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 America.  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:

Research suggests 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:


Daytime   Night time

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

Apparently 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)

Saper (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!

Shift work

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 efficiency. 

Shifts can follow a number of patterns:

Rotating of fixed

A rotating pattern involves working different hours each week or month.  A typical three shift system covering a 24 hour period would involve people working

  • 6am to 2 pm
  • 2pm to 10pm
  • 10pm to 6am

Clockwise or anticlokwise

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 following week. 


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:

  1. Very bright light
  2. Bright light
  3. Ordinary room light
  4. Continued dim light

Core body 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). 


Artificial light, 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 sleep-wake cycles. 


Delayed sleep phase syndrome (DSPS)

Like 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 insomnia. 

Exam advice:

The specification 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



Sleep states

What the board expects you to know:


Sleep states


·         The nature of sleep

·         Functions of sleep, including evolutionary explanations and restoration theory

·         Lifespan 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.  Some herbivores 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

Evolutionary theories:

·                     Sleep helps to protect us from harm at night

·                     Sleep helps us to conserve energy


·                     Sleep helps us to repair damage done to our bodies during the day

·                     Sleep restores the brain’s levels of neurotransmitters


Evolutionary (ecological) theory


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 sense.’ 

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. 


According to the song

‘The lion sleeps tonight’

…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 species.

If sleep is designed to make us inconspicuous at night, why do we snore! (Bentley 2000).


2.  Conservation 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 dietary requirements. 

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


Restoration theory

Oswald (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 awake too!

Evidence in support of restoration theory

Further support is provided by Shapiro (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 of cats). 


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!

REM 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. 

Note: restoration 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 biological state of REM sleep and makes no mention of the psychological state of dreaming.  Therefore it is not to be used in a question that asks for theories of dreaming.


Research in support of restoration theories

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 new tissues

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)

Research against restoration theories

·         Protein synthesis occurs 24 hours a day, not just during stage 4 - although it does seem to peak in stage 4.

·         Amount 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.

·         The brain is very active during REM so runs counter to the idea that it is an ideal time for repair.

·         The model is over simplistic since in fact neuro-chemicals appear to be produced throughout a night’s sleep and not just during REM.

·         When we 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 endogenous purpose. 

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.

Anecdotal 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.


Sleep deprivation studies

These are interesting in their own right, but from a practical point of view can be used:

·         As evidence for the restoration theory of sleep

·         In an essay on the methods used in the study of sleep

·         As an 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.

Case studies

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.

Peter Tripp

Left: during his wakeathon attempt

Right: On completing his feat he is taken to bed with electrodes attached to monitor his sleep.




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. 

Earlier this 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, John 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. 

In the 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!

By the end of the first week speech had slowed and become slurred and he was having problems…. *

By the 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 without intonation.

*finishing sentences!



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 human participants

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:


Nights without





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 delusional.


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 problems.


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. 

Additionally, Dement himself admits that his own observations of participants are a big source of bias due to his own expectations when observing volunteers. 


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!

·         In the 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. 

Overall evaluation of animal deprivation studies

·         With animal studies there are clearly issues of generalising to humans. 

·         The 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 Charles).

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 permanent coma.

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 biorhythms:

Darkness is 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 results. 

*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

Periodically during 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 fire again. 



Article found online suggesting that we are in fact all sleep deprived:


Because of 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:


Psychological Restoration


                      ‘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 life’s feast.’


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.


Anecdotal 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.


Memory function (similar to Oswald’s theory is the idea that REM helps us to consolidate memories)


·         Bloch (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.

·         Rats 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.



Lifespan changes

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 sleep.




Pattern of sleep


18 hours of sleep (9 hours of which is REM)

In the first few months of life there is little in the way of a discernable

sleep 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


1 year

Total sleep 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 years

Total sleep 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. 

The ultradian cycle is now extended to 70 minutes. 

10 to 12 years

Dement (1999) describes the sleep pattern at this age as ‘ideal.’ 

The  child typicallyhas plenty of energy during the day and can nod off quickly into deep, uninterrupted sleep waking the following morning totally refreshed! 



Ideally the 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. 

Sex and growth hormones are released for the first time and the increasingly sexual nature of dreams can result in wet dreams.

18 to 30 years

Again the body still requires as much sleep as early teens but this is rare  at this age. 

Most people this age are permanently sleep deprived.

Environmental factors such as babies, snoring, work patterns and anxieties keep us awake.

30 to 45 years

Sleep time continues to decrease and people in this age group experience  more tiredness. 

Amount of deep sleep, especially stage 4 sleep decreases.

Social factors such as less exercise, alcohol, caffeine interfere with the  sleep pattern.

45 to 60 years

Apparently hormone levels start to decrease (all down hill from here on in L ). 

The tendency is to go to bed earlier but quality of sleep begins to deteriorate. 

Total sleep time drops to around 7 hours but with little or no stage 4 sleep. 

REM however, remains at about 2 hours per night.

60 onwards

Following retirement when we have more time to sleep, the overall  quality of sleep deteriorates significantly. 

Dement 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. 

Although we are unaware of these ‘micro-arousals’ they do leave us tired the following day. 



Changes over a lifetime (more detail)


The 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. 


By 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 results. 


By 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 Victorian times. 

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

As 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

Van 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 end!). 

Of 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. 

The researchers considered this from an evolutionary perspective. 

In 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

  1. decreases in total sleep time, deep sleep time and REM sleep time
  2. increases in sleep latency (time taken to nod off) and stages 1 and 2 sleep time.

Dozing and depression in the elderly

In 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 day.

The 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 deeply. 

Dr 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

The 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. 


Cultural differences

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, personality

Explanations for other sleep disorders, including sleep walking and narcolepsy



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.

Primary insomnia

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. 


Secondary insomnia

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 recreational drugs


Explanations of primary insomnia

Psychophysiological insomnia

The insomnia results from a learned or behavioural condition

  1. A cycle of anxiety resulting in an inability to sleep that becomes self-reinforcing
  2. 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, inevitable insomnia. 

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.


Idiopathic insomnia

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. 


Perceived insomnia

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 knowledge. 

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 response. 


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 that results.


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.

Medical conditions

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.

Tying 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:

Predisposing: 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)

Precipitating: 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 out.

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 unreliable.

Research into insomnia

Two useful studies:

Smith et al (2002) found evidence for physiological differences in the brains of insomniacs,

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 mechanisms.


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 techniques. 


Sleep Apnoea

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 snore!   

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. 

  • Blocked nose 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. 
  • Obesity: especially when it results in an increased diameter of the neck.  The additional fat tissue puts pressure on the throat causing closure.
  • Drugs: top of the list for these is alcohol, but others such as tobacco, painkillers and sedatives can all result in OSA.
  • Age: 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 kiddies. 


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 disconcerting. 

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. 

Cataplexy (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 persists. 

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!

Other 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. 

Automatic behaviours 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. 

Early REM: 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 inappropriate times. 


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 genetic component. 



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 off.


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. 


Incomplete arousal

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 component. 

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 of narcolepsy.

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 elderly. 



Other factors

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 excessive tiredness. 

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 conditions. 

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 sleepwalking episodes

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 environment. 

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* hospital.



* does psychiatric mean guessing right three times in a row? J