This has always been one of my favourite topics, both to study and to teach.  We begin with a look at biological rhythms in general, looking at research into the different types.  We then consider what happens when these rhythms get disrupted, most likely through jet lag or shift work.

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One of the rhythms we consider is the ultradian rhythm of sleep.  This leads us almost seamlessly into a discussion of the nature and possible explanations of sleep.  Sleep is still an enigma.  We spend longer practising this behaviour than any other.  An adult living to an average age of around 80 years will have spent over 25 of those asleep.  So what’s it all about this sleep thing?  Dreaming is no longer on the specification but it is a major psychological characteristic of REM sleep and is always worth a brief chat!

Finally we look at sleep disorders.  Some of these are common, insomnia being the one most widely suffered. Others are thankfully rare but nevertheless fascinating.  The best example of this second category being narcolepsy.  Until very recently narcolepsy was a mystery with no known obvious cause.  In recent years research has pointed the way to possible future treatments for what is a most debilitating disorder.  We shall also consider somnambulism (sleep walking) and sleep apnoea, as a possible secondary cause of insomnia. 

You will notice, as we progress, that inevitably there is some overlap between topics.  It would be difficult to consider biorhythms without looking at the stages of sleep for example. 

 
Biological Rhythms

Introduction

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).

What has become apparent in recent years is the ancient nature of the rhythms.  Clocks have been found to exist in the very simplest forms of life, algae.  It therefore seems reasonable to assume that they have been around since the beginning of life on Earth.  Biological rhythms allow organisms to adapt to the cycle of day and night and they appear to control nearly all behaviours and physiological processes. 

In this topic we consider the three main categories of biological rhythms and the extent to which they are controlled by internal and external factors.  We then consider what happens when our rhythms are disrupted. 

• Circadian Rhythms (about 24 hours)
• Infradian Rhythms (greater than 24 hours)
• Ultradian Rhythms (less than 24 hours at night)
  

There are others that we might mention en passant:

Circannual rhythms, as the name suggests rhythms that cycle over a period of one year.  These are therefore a subset of infradian.

Diurnal rhythms that are less than 24 hours but confined to daytime or waking hours, as opposed to ultradian at night or during sleep. 

Circadian

Variation is a cycle that repeats 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.


Is the circadian rhythm determined by internal mechanisms or external factors?
As second year psychologists you should be able to guess the answer to this one.  Whenever faced with an ‘is it nature or is it nurture’ question, it’s always BOTH!

First some terminology:

• Endogenous: refers to internal, physiological factors
• Exogenous: refers to external or environmental/social factors
  

Zeitgeber: we also have the added complication of this German word that roughly translated means ‘time giver’ and refers to exogenous factors that indicate times of day. 

We shall consider the role played by endogenous and exogenous (zeitgebers) in the control of the circadian rhythm. 

Endogenous
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 agreed to spend time cut off from the outside world in a disused WWII bunker in Munich.  After a month or so cut off from external cues they adopted a 25 hour daily cycle.  

Background info for interest only!
French geologist (and speleologist) 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!  He receives no unsolicited contact with the outside World, but does shout to co-workers at the cave entrance when he wakes, prior to sleep and before meals. 

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.  He spent new year’s eve eating foie gras and quaffing champagne.  He subsequently discovered that his celebrations were over three days late!  Each time his body clock extended form the usual 24 to around 24.5 hours.  Occasionally this extended to 48 hours, 36 hours awake and 12 to 14 hours asleep.  However, as he points out, these days appeared no longer at the time! 

Working with other volunteers he has also noticed a correlation between day length and REM duration.  For every 10 minutes that a day extends, REM seems to lengthen by one minute.  

This appears to suggest two things:

There is internal control of the circadian rhythm, since even in the absence of external cues we are able to maintain a regular daily cycle.

There must usually be some external cue that keeps this cycle to 24 hours.  When this is removed we adopt this very strange 24.5 or 25 hour cycle. 

 

Evaluation
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.

Folkard (1985) showed the limitation of purely exogenous factors in controlling the rhythm.  He got 12 volunteers to spend 3 weeks in isolation with no natural light.  They were instructed to go to bed when the clock suggested 23.45 and set alarms for 07.45.  After a few days the clock was speeded up so that the supposed 24 hours were passing in only 22.  Only one of the volunteers kept pace.  The other twelve all maintained a 24 hour rhythm, suggesting internal biological factors were over-riding exogenous factors (in this case quite literally ‘time-giver’ in the form of a clock!).

Body clocks are 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).  

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!).

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. 

Bringing this up to date (extension material or general interest)
Work is being carried out apace into biological rhythms.  Recent research (Albus et al 2005) has shed light (sorry) on the structure of the SCN. 

The hypothalamus crops up all the time in A-level psychology.  If there’s a brain area involved chances are it’s gonna be the hypothalamus!  To imagine its location, think of a line travelling back from the bridge of your nose.  Where this crosses another line from just forward of your ears is approximately where you should find yours!  However, it isn’t a unitary structure.  Instead this pea-sized bundle of miracles is in fact comprised of a number of distinct areas called nuclei (one of which is the SCN).  Like most brain structures it also appears in both hemispheres.  Albus added to the complexity of the SCN by splitting each of these into a ventral (forward) and dorsal (back).  According to Albus, the ventral portion is more sensitive to light so tends to keep pace with changing environments whereas the dorsal is not so easy to re-set.  It is more likely to ‘run free.’  This could provide part of the answer to the issue of desynchronisation (jet lag) that we shall consider later. 

 
External Factors (zeitgebers)
Light appears to be crucial in maintaining 24 hour cycles: 

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.  However, the question remains, how do the majority of blind people still manage to maintain a 24 hour cycle?

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. 

The above study suggests that light detection in the body may be more complex than we might believe.  The fact that most blind people seem to be detecting light to reset their body clock also suggests cells other than rods and cones may be responsible. 

The rods and cones both contain light sensitive opsin molecules.  However, a mutant strain of mice that have retinal degeneration lose their rods and cones but retain their biological rhythms.  Severing the optic nerve in mice however, does destroy the rhythm.  This appears contradictory, unless we assume that there are receptors in the eye other than rods and cones! 

There are a number of possible candidates.  Initially Sancar and others suggested that cryptochromes (which detect blue light) might be passing on the information to the body clock.  These are particularly interesting since they are also present in plants.  Later research has implicated another chemical melanopsin.  Eckler et al (2008) found that killing these cells in mice made entrainment impossible.  The mice could not adapt to changing light conditions suggesting these cells are the detecting mechanism.  This would explain Mile’s blind man study.  Although the blind man has lost the ability to detect light using rods and cones (so is unable to consciously perceive light) other cells like those containing melanopsin are still detecting light at an unconscious level and passing on this information to the body clock. 

Severing the optic nerve however, would prevent all information from the eyes, be it conscious perception or unconscious reaching the brain.  Presumably the case that Miles studied had damage to his optic nerve.  

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

Recent research
It seems that most people in the industrialised world are out of synchronisation with the natural world and this might be posing all sorts of risks for our physiological and psychological health.

A recent study looked at the extent to which our natural clock might be lagging behind sunrise and sunset and how this can quickly be adjusted.  A small group of volunteers were tested.  It was found that most were going to sleep after midnight and that as a result their melatonin levels were still high when they woke up in the morning and often were still high two hours after waking.  This meant that they were working against their natural cycles.

However, after one week’s camping in Colorado, no artificial light other than campfire allowed, their clocks were back in tune with sunrise and sunset.  On average they had shifted backwards by two hours so were sleeping and rising earlier, although total sleep time had not been affected.  Melatonin was being secreted earlier and levels were dropping long before waking.  Crucial to this shift appeared to be natural light.  It was estimated that total exposure to natural light had increased fourfold.  (Wright 2013)

Practical applications of research into the body clock
Think back to the Horizon documentary using the body clock to better treat cancers and improve the psychological health of patients with Alzheimer’s. 

Dr Reddy’s research at the University of Cambridge (2012):

The body’s immune system is more effective at certain times of the day.  For example, patients with blood poisoning are more likely to die between the hours of 2 and 6 am when the body’s defences are at their weakest.

Reddy and his co-workers have found that a protein TLR9 which detects the DNA of microbes such as bacteria and viruses is controlled by the body clock, at least in mice!  Immunising mice when their body clock is at its peak is most effective in fighting off a range of infections, much as treatment with chemotherapy we saw in the video. 

They have concluded that drugs need to be administered at certain times of the day perhaps longer term, drugs can be administered to alter the body clock to its optimum level.


Conclusion
This is how I’d conclude my essay on biological rhythms, especially one answering the old favourite on internal and external control of rhythms. 


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.  This could be fatal if winter came earlier than expected and animals had failed to prepare for winter in time or were still stuck in colder parts of the World. 

If control was entirely external our rhythms would be too erratic and change day to day depending on weather conditions etc.  We therefore have an internal mechanism that keeps us relatively stable but is sensitive to environmental factors that allow for adjustments based on weather conditions and available food. 



Ultradian

These occur more than once in a 24 hour cycle and at night time. We shall consider 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.  We shall cover it as an example of a rhythm but some of the information is also relevant to the section on sleep, particularly a question covering the physiology of sleep.

History
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.


Aserinsky and Kleitman (1957)
Nine participants were studies (seven male and two female)

Participants ate normally (excluding coffee and alcohol) then arrived at the laboratory just before their normal bedtime. They went to sleep with electrodes attached beside the eyes (EOG) and on the scalp (EEG). Participants were woken by a doorbell at various times during the night and asked to describe their dream if they were having one, then returned to sleep.

Participants were woken either in REM or NREM (but not told which). They confirmed whether they were having a dream and described the content into a recorder.

The direction of eye movements was detected using electrodes around the eyes. Participants were woken after the persistence of a single eye-movement pattern for more than one minute and asked to report their dream. The eye-movement patterns were either: mainly vertical, mainly horizontal, both vertical and horizontal, very little or no movement.

 
Findings:
Uninterrupted dream stages lasted 3-50 minutes (mean approx 20 minutes), were typically longer later in the night and showed intermittent bursts of around 2-100 REMs.

The cycle length varied between participants but was consistent within individuals, eg 70 for one, 104 for another.

When woken in NREM participants returned to NREM, but when woken in REM they typically didn’t dream again until the next REM phase (except sometimes in the final REM phase).

Participants frequently described dreams when woken in REM but rarely did so from NREM sleep (although there were some individual differences) and this differences was marked at the end of the NREM period (within 8 minutes of cessation of REM – only 6 dreams recalled in 132 awakenings). In NREM awakenings, participants tended to describe feelings but not specific dream content.

Accuracy of estimation of 5 or 15 minutes’ of REM was very high (88% and 78% respectively). REM duration and number of words in the narrative were significantly positively correlated.

Eye movement patterns were related to dream content, eg horizontal movements in a dream about throwing tomatoes, vertical ones in a dream about ladders and few movements in dreams about staring fixedly at something.

 
Conclusion:
Dreaming is reported from REM but not nREM sleep, participants can judge the length of their dream duration and REM patterns relate to dream content.

Evaluation
As with most sleep research, sample size is very smalln making generalisations difficult, particularly when there are such great individual differences between participants.

Sleep laboratories are very artificial settings.  The participants’ pre-sleep routine is very different to at home, they are in unfamiliar surroundings and covered with a plethora of electrodes and wires.  They also know that they’re being observed. 

However, sleep studies like this do allow for physiological measurements which are objective and replicable.  Unfortunately self-report techniques are just the opposite, subjective and non-verifiable.  Given the fragile nature of dreams self report of these must be seen as particularly unreliable. 

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. 



Infradian

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, and some in the evening.  Another 39 were exposed to negative ions (a placebo group). 

Findings
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 infradian.  Like other rhythms, the menstrual cycle appears to be under the influence of both internal (endogenous) mechanisms, and external zeitgebers. 

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.

For information
The menstrual cycle is divided into two phases--the follicular phase; and the luteal or ovulatory phase. The follicular phase includes the time when menstruation occurs and is followed by proliferation or the growth and thickening of the endometrium. This phase typically lasts from 10 to 14 days, starting with the first day of menstruation. Oestrogen and progesterone levels are at their lowest during menstruation. When bleeding stops, the follicular phase begins causing the endometrium to grow and thicken in preparation for pregnancy. During the next (approximately) two weeks, FSH levels rise causing maturation of several ovarian follicles and the size of the eggs triple. 

FSH also signals the ovaries to begin producing estrogen which stimulates LH levels to surge at around day 14 of your cycle triggering one of the follicles to burst, and the largest egg is released into one of the fallopian tubes.  This premenstrual period lasts approximately 14 days. After ovulation, LH causes the corpus leuteum to develop from the ruptured follicle. The corpus leuteum produces progesterone.  Together estrogen and progesterone stimulate the endometrium to prepare a thick blanket of blood vessels that will support a fertilized egg should pregnancy occur. When pregnancy occurs, this blanket of blood vessels becomes the placenta which surrounds the fetus until birth.

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. 


Armpit 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. 

Findings
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.

Evaluation
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. 

However
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).  Wilson (1992) believes her results are due to statistical errors and that when these are corrected the effect disappears. 

Wilson analyzed the research and data collection methods McClintock and others used in similar studies. He found significant errors in the researchers' mathematical calculations and data collection as well as an error in how the researchers defined synchrony. Wilson's own clinical research and his critical reviews of existing research demonstrated that menstrual synchrony in humans has yet to be proven. Wikipedia

 
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 that found that the onset of menstruation (menarche) is more likely in the winter months when light levels are low.  The menarche also 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?

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.

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. 


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.  

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 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 as 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.

• Phase advance: Getting up or going to bed earlier than usual (flying W to E)
• Phase delay: Getting up or going to bed later than usual (flying E to W)
  

In general it is easier to adjust to phase delay, possibly because of the reasons mentioned above but also because phase delay is effectively lengthening our day.  As we’ve seen our internal rhythm is greater than 24 hours.  Phase delay therefore brings external factors closer in line with internal whereas phase advance moves them further away.  

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 as 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; Per1 and Bmal1 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.

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 natural melatonin a licence in Europe since the potency and purity of the tablets cannot be sufficiently well regulated.  However, tasimelteon (a selective agonist for melatonin receptors) i.e. it mimics melatonin has proved effective in early trials.  450 volunteers were kept awake 5 hours past normal bedtime to mimic jet lag.  Taking tasimelteon increased eventual sleep duration by up to 2 hours compared with control groups (Klerman 2009).

 

Recent research (2013)

As we’ve seen, light acts as a sort of reset button for the body clock in the SCN, ensuring it sticks to a 24 hour cycle.  A large number of genes in the SCN appear to be light sensitive and adjust their activity depending on whether it is light or dark.  They do this quite quickly so should be able to adapt to new time zones.  However, recent research at Oxford has found that a protein SIK1 goes round switching all these proteins off again. 

The researchers, using mice, found that reducing the activity of this protein allowed the mice to switch their body clocks faster.  Using artificial lighting they advanced the mices’ day by six hours, similar to flying from the UK to India.  Instead of the usual 6 days it would normally take to adapt the mice were able to adapt in six hours! 

Practical applications:  A number of psychological disorders such as schizophrenia as well as neurological conditions such as Alzheimer’s, have been linked to disrupted biological clocks.  Dr Reddy of Cambridge University suggests that SIK1 is a ‘very drugable target’ and believes drugs may soon be available to allow faster switching to new time zones. 

 

 

 

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 et al  (2008) suggests that as well as the main ‘master’ clock in the SCN there is also a ‘feeding clock’ which depends on food intake.  In mice, this feeding clock seems to over-ride the master clock and keeps them awake until food has been found. 

So if we are flying from London to New York and need to adjust to the new time zone by staying awake longer than the master clock would expect we need to starve ourselves before and during the flight and then eat when we land.  This way we can postpone the master clocks drive to get us to sleep.  Saper and his team recommend fasting for 16 hours before eating!


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 is 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 shift workers 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

Cooper et al (2005) compared rotating shift patterns with fixed.  Oil rig workers on either twelve hour day shifts or twelve hour night shifts were compared to workers on a split-shift pattern (working seven days of night shifts followed by seven days of night shifts).  Urine tests measuring melatonin levels showed that those on split shifts never fully synchronised.  They also had significantly higher levels of circulating fatty acids putting them at greater risk of CHD and hypertension. 


Clockwise or anticlockwise
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).  
  

Conclusion
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. 

 
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

Introduction
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

Restoration: 

• Sleep helps us to repair damage done to our bodies during the day
  
• Sleep restores the brain’s levels of neurotransmitters
  

Evolutionary (ecological) theory


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 harm’s 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 and metabolic rate is used instead.  The lion has a large protein-rich intake every few days.  Because of its size it has a relatively low metabolic rate.  As a result it has time to sleep for over twenty hours a day.

Herbivores with their impoverished diet of grass need to be eating all the time so don’t have the time to sleep.

Summarizing Meddis

Animals sleep for short periods if: 

1.  They high metabolic rates so need to be constantly eating.

2.  They are likely to be eaten.

Animals sleep longer if:

1.  They have low metabolic rate, eat less and therefore have more time available to sleep.

2.  They have no natural predators


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?

Evaluation
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. 

Siegel (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 affect 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.   Repack 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 first 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 stopped there 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 night’s 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

Humans
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, and kittens; looking through drawers for money that wasn't there; insisting that a technician had dropped a hot electrode into his shoe. 


Secrets of Sleep: Peter Tripp (part 1 of 2)

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.

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.

Note:
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 dysfunction.  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!

Evaluation
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-Weidman who collated the data from a large number of sleep deprivation studies.  The findings are summarised in the table:

Nights without sleep

1

2

3

4


5

6

Symptoms


Discomfort

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. A feeling of tightness around the head.

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.

Evaluation
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 night’s 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.

Humans
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 night’s 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.


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.”



Lifespan changes

The amount that we sleep and also the pattern and quality of sleep vary as we get older.  These changing patterns of sleep may provide clues as to the purpose of sleep.

Age

Newborn




1 year



5 to 10 years




10 to 12 years



Adolescence


18 to 30 years

30 to 45 years



45 to 60 years



60 onwards

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.

Total sleep time drops to about 13 to 14 hours 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.

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

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.

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.

Apparently hormone levels start to decrease (all downhill from here on in).  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.

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)

Infancy
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 overtime to assimilate all this new information by making new and ever more complex interconnections.  According to Oswald this would be facilitated by plenty of REM sleep.

Evolutionary sleep theorists suggest all this infant sleep is designed to take the pressure off of parents who can get on with essential chores such as finding food. 

Adolescence
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. 

Adulthood
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)

Co-sleep
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 this 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 lines J

 

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
  

Insomnia

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.   Derivation: Latin; In (not) and somnus (sleep).

Insomnia often appears a trivial disorder, however, the Mental Health Foundation report (2011) entitled ‘Sleep Matters’ based on a self-selecting sample of 7000 volunteers found links between insomnia and poor relationships, low energy and inability to concentrate.  However, being self-selecting it is unlikely to be a representative sample. 

Insomnia can be classified in a number of ways including:

• Transient: inability to sleep lasts for less than one week (causes such as jet lag, noise etc)
  
• Acute: problem lasts for less than one month (perhaps an issue with stress)
  
• Chronic: inability to sleep persists for over one month and may be present for many years.

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 insomnia: does the insomnia appear to have no known physical or psychological cause
  
• Secondary insomnia: is there an obvious cause such as an underlying physical or psychological illness
  

Insomnia and ill-health
A few recent studies have claimed to have shown a link between hours spent asleep and long-term health issues or life expectancy.  A large scale study on over 1 million US citizens aged between 35 and 55 suggested that the optimum daily amount of sleep was between 6½ and 7½ hours per day in terms of mortality.  Sleeping either more than 8 ½ hours or less than 4 ½ hours per day increased mortality rates by 15%.  However, as the researchers themselves pointed out, most of this increase can actually be accounted for in terms of co-morbidity.  That is other disorders being suffered alongside the insomnia such as stress, cancers, CHD and depression.  Once these are factored in the risk to life expectancy caused by too much or too little sleep is very small.

Women are 40% more likely to suffer from insomnia than men.  Some of this has been attributed to hormonal factors.  However, Miller (2009) found that insomnia is more likely to increase the risk of CHD in women than it is in men.  Sleeping fewer than 7 hours per night increased levels of the hormone interleukin-6 which causes inflammation.  In a study of 4,000 civil servants (mostly men) she suggested that the increased susceptibility to CHD in women was due to hormone levels. 

Primary insomnia

This has no obvious cause so appears to be an illness in its own right. 

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. 

Brain chemistry
The neurotransmitter GABA (gamma amino butyric acid) is known to be involved in the process of inhibition of many brain areas.  Put simply it helps the brain to shut down!  Winkelman et al (2008) studied 16 long-term insomniacs (their average duration of insomnia was over ten years).  Data on sleep patterns was collected using a polysomnograph (measure of EEG, EMG, EOG etc) and a non-invasive technique for measuring levels of GABA was also used.

Patients suffering from long-term insomnia had a 30% lower level of GABA than non-insomniacs.  Furthermore, there was a significant correlation between levels of GABA and severity of insomnia as measured by both the physiological measures and more subjective sleep measures. 

It is worth mentioning also, that hypnotic benzodiazepines often used to treat severe insomnia appear to work by increasing the activity of GABA neurons. 

Measures such as this are scientific and carried out in sleep laboratories.  Be sure to mention all the usual good and bad points.  Scientific suggests tight control of variables (allowing cause and effect relationships to be established), objective techniques such as EEG that can be also be replicated.  However, they tend to lack validity.  In this case, the studies would have been carried out in sleep laboratories ensuring a less than natural night’s kip.  Small sample size (sixteen) also makes generalisation difficult.

However, that aside, you could point out that since benzodiazepines have had some success in treating insomnia and since these act by raising GABA activity it does suggest that the theory has some validity.

 
Brain structure
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.  


Research evidence for idiopathic 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.

However, although this is a lab experiment with tight control of variables allowing for cause and effect relationships to be established, consider the validity.  Trying to get a normal night’s sleep wired like this is far from natural!

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. 

Left: Measures taken during a polysomnograph

Evaluation of research into insomnia
The methods used to study insomnia lack validity:

Self-report techniques are never the best way of getting valid information but because of issues already discussed are particularly troublesome with insomniacs.

Sleep laboratory studies.  Clearly patients in unfamiliar surroundings with an altered sleep routine and wired up to a plethora of gadgets is not going to make for a typical night’s sleep.  However, rather than get a worse night’s sleep, insomniacs often sleep better due to the altered environment breaking the perpetuating factor of learned associations.  Either way, sleep labs are not an ideal measure of real-life insomnia. 


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.

In about 50% of all cases of diagnosed insomnia there is also a known existing psychiatric disorder.  Often the insomnia appears to pre-date the psychological issues so appears to be a significant risk factor in the development of psychopathologies such as depression.

There are issues with the validity of diagnosis due to the huge variations between individuals in the amount of sleep they actually need.  This also varies across a person’s lifetime as we’ve already seen. 

Stress
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. 

Vgontzas et al (2001) reported a link between insomnia and various stress hormones such as cortisol and ACTH.  More recently he has suggested that middle-aged men may be more susceptible to stress-related insomnia due to their increased sensitivity to such hormones. 

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

Findings
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.

Conclusion
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. 

Evaluation
A major weakness of studies like this is their reliance on self-report of sleep quality.  This is a notoriously inaccurate measure so dramatically reduces the internal validity of this study.  For a variety of reasons people, particularly insomniacs seem to underestimate their quality as well as quantity of sleep.  More on this when we look at sleep-state misperception.

 
Age
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 if any deep sleep and often complain of insomnia and tiredness.  However, the effects may be more indirect.  Older people are more likely to be on medication that may affect sleep.  They are also more susceptible to sleep apnoea and restless leg syndrome (RLS). Unfortunately relatively little research is carried out into the sleep of elderly people so it isn’t clear what constitutes a normal or healthy sleep pattern for this age group. 

Medical conditions
Allergies such as hay fever, asthma, heart disease, and conditions resulting in pain can all disrupt a night’s sleep.

Drugs
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, reducing stages three and four and suppressing REM.  As already mentioned some prescription drugs such as the analgesic codeine and opioids also disrupt sleep.

A word of warning here.  Remember the AO1/AO2 balance.  Most of what has just been mentioned is AO1.  Lots of description of possible causes of insomnia.  The text books, particularly the big red one focusses excessively on describing causes.  Ensure you focus on research evidence wherever possible.  Stress is a good secondary factor to discuss because of the Morin study.  There is little, if any AO2 to be had from a discussion of age, environment, medication etc.  The rest of this discussion of insomnia will be AO2 heavy.


Perceived insomnia (sleep-state misperception)
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! 

Dement (1999) reported the case of a supposed insomniac male. When studied in the labs he was typically taking 15 minutes to nod off each night.  However, when asked to report how long he was laying awake in the lab he was reporting anything up to four hours. 

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. 

Psychophysiological insomnia
The insomnia results from a learned or behavioural condition

Over a period of time the patient has learned to associate their bedroom routine with an inability to sleep.  This creates a vicious circle of anxiety prior to going to bed which makes nodding off even less likely.  Not only the bedroom but pre-bedtime and bedtime routine has become associated with stress which might start as soon as darkness falls or whilst brushing teeth etc.   Treatment for this type of insomnia would best involve some programme of ‘unlearning’ in which bedroom routine once again becomes associated with sleep. 

Unravelling cause and effect
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 underlying causes instead.

However, others disagree and turn Dement’s argument on its head.  Dement is arguing that disorders such as depression, anxiety and ill-health are the real culprits that lead to a symptom of insomnia.  Research by Ohayon and Roth (2003) suggests that insomnia often predates the onset of depression and other psychological disorders suggesting it is the cause rather than the symptom.  If this is correct then doctors need to be targeting the insomnia in an attempt to treat the resulting anxiety and depression. 

In a similar vein, insomnia can also result in a weakened immune system.  Here cause and effect becomes especially difficult to disentangle.  Is insomnia having physical effects on our immunity or is the resulting stress the culprit?  “Vein”… Kiecolt-Glaser?  Get it? J


Tying all of this together (wall to wall 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 or biological component or any other underlying issue such as personality which makes the onset of the disorder more likely. 

Precipitating: refers to factors that trigger a period of insomnia.  This could be environmental such as uncontrollable noise or a hot spell in the summer.  It could be a period of physical illness perhaps resulting in pain or in need of medication.  More likely it will be a period of stress or anxiety.

In addition insomnia requires a perpetuator, since the insomnia usually continues long after the precipitator 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. 

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. 


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 hypoapnoeas 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 polysomnograph.  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!

Causes
Anything that restricts airflow through the throat can cause OSA. 

• Blocked nose due to a build of mucus, as with a cold or hay fever, or more rarely due to nasal polyps that may develop as a result of hay fever. 
• 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. 

Symptoms
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. Gozal and Pope looked at the cases of 1500 primary school children.  Of those who reported heavy snoring 13% were in the bottom 25% in terms of attainment and behaviour compared to only 5% in the top 25%.  They believe that disordered breathing during this period of crucial brain development, caused by OSA, can result in ACHD, increased aggression, allergies and reduced academic performance. 

In a similar study Gozal also reported twice as many cases of ACHD in heavy snoring six year olds.  Treatment of the snoring reduced ACHD or in some cases seemed to have removed it altogether. 



Narcolepsy

Is a neurological 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. 

Symptoms

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. 


What causes narcolepsy?
This will form the bulk of an answer/essay on this sleep disorder.  In the past few years there has been a wealth of new information suggesting that narcolepsy is in fact an autoimmune disorder.  As yet little if any of this research has reached the A-level texts.  I shall break this section into two parts.  Firstly discussing earlier research which gave clues to the genetic and neurochemical cause of the disorder and secondly looking at very up to date research which builds on the simpler, earlier theory.

Early work
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

Hypocretin
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 of cataplexy, as had been observed in narcoleptics. 

We now know that hypocretin plays an important role in keeping us awake.  During the day it acts on the locus coerulus (shoo ru lus) to keep us awake, at night time production of the chemical by the hypothalamus stops so we can nod off

Dogs
Work by Mignot on his dogs isolated a fault on the hypocretin-2 gene that produces hypocretin.  This might result in lowered levels of hypocretin production and explain the resulting narcolepsy.

Mice
This was further supported by Dement’s work on mice that were unable to produce hypocretin.  Their symptoms were consistent with the symptoms seen in narcoleptics.  Clearly there are issues here with generalization.  Narcolepsy does not appear to be as genetically determined in humans as it does in dogs, suggesting that there could be different underlying causes.

Human People :)
However, 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 seems to suggest that the work of Mignot and Dement was relevant to humans too. More recently low levels of hypocretin have been found in the CSF of humans with the disorder.

Treatments based on this initial work
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. 

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. 


Tying the early research together
It seemed clear that the lack of hypocretin in dogs and cats was able to produce symptoms strikingly similar to narcolepsy.  Human narcoleptics seemed to have damage to their hypocretin-producing cells. It seems clear that there is a link between lowered levels of hypocretin and narcolepsy. 

However there were a number of issues that were unclear.


What was causing these lowered levels was unclear.  An obvious candidate was genes.  But if this were the case we’d expect
a.     Narcolepsy to run in families, which it doesn’t
b.     There to be concordance between MZ twins, which there isn’t!


In addition, if it was genetic, i.e. we were born with it, then why did it remain dormant for so long.  It is very rare for children to be diagnosed with the disorder.  Typically it doesn’t seem to develop until late teens/early 20s.  Clearly there must be an additional, perhaps environmental trigger.

In addition, some narcoleptics appeared to have no obvious damage to their hypocretin system. Some people with damage haven’t developed narcolepsy.  Clearly there is not a simple causal relationship between damaged hypocretin systems and narcolepsy.

Mahowald and Schenck (2005) report that ‘the absence of hypocretin is neither necessary nor sufficient to explain all the cases of narcolepsy [in humans].’

Put another way: there are patients with a damaged hypocretin system who show no signs of narcolepsy and narcoleptics with no obvious damage to the hypocretin system.  The former can be explained by predisposition and precipitators.  The latter is more difficult to explain.

The missing clue
In 1983, Honda suggested a link between narcolepsy and one type of HLA (human leukocyte antigen).  These HLA molecules are found on the surface of white blood cells and help control the body’s immune response when attacked.  They single out foreign invaders and mark them for attack by the body’s defence system. It seemed that many narcoleptics had a faulty variant of one of these HLAs (HLA DQB1*0602). Don’t even consider trying to remember this!

This is where it gets interesting
In 2009, Mignot suggested that the immune system of narcoleptics might be attacking their own bodies.  Rather than targeting alien invaders it was turning on its own cells.  This is what we call an autoimmune response and is the cause of diseases such as AIDS.

The immune system uses HLAs to distinguish between ‘self’ cells and ‘other’ cells.  If the HLA system is faulty then it might start to attack ‘self’ cells as well.  We have already seen that many narcoleptics have a faulty variant of an HLA.  Perhaps this is causing the body’s defences to attack the hypocretin cells of the hypothalamus.  If so what might be triggering such an auto-attack?

Tribble Trouble 
Tribbles are segments of RNA that build up in cells of the body.  The cells of the hypothalamus that produce hypocretin seem to produce a lot of a tribble called trib2.  This builds up in the cells of the hypocretin cells.  

The faulty HLA DQB1*0602 found in narcoleptics leads to an over-production of antibodies that attack trib2.  It seems that during this attack on trib2 the hypocretin cells are killed so levels of hypocretin fall dramatically in narcoleptics.  

Having dramatically reduced or even destroyed all the brain’s hypocretin cells would explain the EDS and the cataplexy found in narcoleptics.

Right: the impossible attractive Captain Kirk having Tribble trouble himself!

However there is more to the story
Mignot (2009) studied 1800 patients with the faulty variant of HLA.  Over 800 of these had been diagnosed with narcolepsy.  This suggested a link between the two but also suggests that not all people with the variant develop narcolepsy.   Clearly other, perhaps environmental factors, were also needed for narcolepsy to develop.

In 2009 antibodies for the streptococcus bacterium were found to be significantly higher than expected in many narcoleptics.  Usually, following an attack by the bacterium, levels of antibody fall back to normal within days.  In narcoleptics they remained raised for up to three years.  Perhaps this was the trigger that turned the immune system on itself.

Very recent research (March 2012) has also implicated the swine flu vaccination in possibly triggering the disorder.  The incidence of new cases of reported narcolepsy in Finland in 2010 were seventeen times higher than they had been in the previous eight years.  This followed a programme in 2009 to vaccinate against swine flu. 

Children aged 4 to 19 who had been given the vaccination had a thirteen-times greater chance of developing the disorder than those who hadn’t been jabbed. 

We seem to have a case of biological/genetic predisposition that is then triggered into action by environmental factors… infections.

Some of this increase may be due to an increased awareness of narcolepsy in Finland in recent years but it seems unlikely that could explain such a massive rise. 

It is also worth mentioning that despite such huge percentage increases the numbers involved were relatively small. Only 1 in 16,000 of children given the injection got the disorder.  However, it does raise the possibility that viruses or bacteria are the trigger for an underlying predisposition. 

Other evaluation points
The drug modafinil has been used as an effective treatment for some cases of human narcolepsy.  It is thought that it works by increasing levels of hypocretin which supports the basic theory.  However, as with all chemicals working in the brain its precise mechanism isn’t clear.

There is clearly a genetic component to narcolepsy as shown in dogs were colonies of narcoleptic dogs can be specifically bred.  However, in humans it appears to be more complex.  MZ twins show a high level of discordance.  When one twin has narcolepsy there is only a 30% chance that the other will have a similar diagnosis.  This might be partly attributable to an issue with diagnosis.  It does appear however, that other precipitating factors are needed.  It would also appear that these occur outside the womb otherwise both twins would be exposed to them.

One final point. The symptoms of narcolepsy in humans vary significantly from patient to patient.  Patients showing no signs of cataplexy still have the loss of hypocretin cells found in patients with cataplexy.  So we have a common underlying cause resulting in different symptoms.  Again this is not easy for the medical model to explain. 

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. 

Right: BBC News report on the dangers of sleepwalking:

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 one episode per night.  Usually sleep-walkers have no recollection of the event when they wake up the next morning.  


Causes

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.

Genetic
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-amino butyric 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. 


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.
  

Findings
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.  

The case of 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? :)