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Biological Rhythms and Sleep
Transcript of Biological Rhythms and Sleep
Endogenous Pacemakers and Exogenous Zeitgebers
Endogenous pacemakers : Internally managed rhythms
Disruption of biological rhythms
Lifespan changes in sleep
Functions of Sleep
Rhythms that last about 24 hours.
Regulated by an internal biological ‘clock’ that is readjusted every day according to environment cues, our cycle is free-running without these cues.
Michel Siffre (1975) was a French cave explorer who was interested in the human internal clock.
1. 61 days in the Alps, resurfaced on 17th September thinking it was 20 August.
2. 6 months in a Texan cave. His natural rhythm was 24 hours, although fluctuated to 48 hours.
3. Aged 60 in 1999 he found his biological rhythms ticked much more slowly with age.
Aschoff and Wever (1976) placed participants in an underground WW11 bunker. It was found that the circadian rhythms of the volunteers were between 24/25 hours some were as long as 29 hours.
Folkard et al. (1985) had 12 adult volunteers living in cave for 3 weeks. They went to bed when the clock read 11:45 and woke at 7:45. Initially the clock ran normally (24 hours) then sped up to 22 hours. only 1 participant could adapt, showing the clock is normally 24 hours.
Duffy et al (2000) found that morning people prefer to rise early and go to bed early (about 6.00am and 10.00pm), whereas evening people prefer to wake and go to bed later (about 10.00am and 1.00am).
All researchers need to be aware of the power of artificial lighting.
Core body temperature
Core body temperature can indicate circadian rhythm.
It is highest at 6pm and it falls about 2 degrees Celsius over the next 12 hours to its lowest at 4.30am.
There is a slight dip in temperature just after lunch (which isn’t due to eating – as the dip remains even when no food is consumed).
In some countries an afternoon siesta is common, and coincides with this temperature decrease.
Cognitive behaviour has been found to vary with differences in temperature.
Folkard et al (1977) tested memory recall in children aged 12-13. They were read stories at either 9am or 3pm, after one week the afternoon group (higher core body temperature) showed both superior recall and comprehension, retaining 8% more information. So long-term recall is better when body temperature is highest.
Gupta (1991) found IQ test results were better at 7pm, than 9am or 2pm. Maybe this should be considered for exams!
Less than one day
There are five stages to sleep; the first four stages are called NREM sleep (non-rapid eye movements) and the fifth stage is called REM sleep (rapid eye movements).
One sleep cycle goes through all five stages and lasts 90 minutes.
There are 4 stages to NREM sleep.
Stage 1 and 2 are shallow stages of sleep (alpha and theta waves), you then progress into deep or slow wave sleep (SWS) which is stages 3 and 4 (delta waves).
The progression through the stages is marked by a decreasing frequency and increasing amplitude (size).
This change in frequency and amplitude is measured using a electroencephalograph (EEG) machine.
The final stage of sleep is REM sleep.
There is a fast and desynchronised EEG activity that resembles the awake brain.
These cycles continue through the night with the SWS getting shorter and the REM periods getting slightly longer as the night progresses.
Each cycle is about 60 minutes in early infancy this increases to 90 minutes during adolescence.
The assumption that REM = dreaming is incorrect according to Dement and Kleitman (1957).
They woke participants when their brain indicated REM sleep and they were highly likely report dreaming (but not always). However, when they were woken outside of REM they also reported dreams.
Hobson and McCarley (1977) suggest that dreams are simply an set of random electrical signals typical of REM.
More than one day, but less than a year
The pituitary gland releases hormones which stimulate a follicle in one ovary to ripen an egg and release the female hormone oestrogen.
Once the egg is ripened the ruptured follicle secretes progesterone which causes the lining of the womb to prepare for pregnancy.
Two weeks after ovulation if there has been no pregnancy the level of progesterone falls causing the line of the womb to be shed.
Evidence of a cycle was also found in males, Empson (1977) found some evidence for a periodic variation of both body temperature and subjective ratings of morning alertness, with a cycle length of 20 days.
Exogenous zeitgebers : external cues resetting the rhythms
The suprachiasmatic nucleus
This is the main pacemaker for humans. It is found in the hypothalamus, just above where the optic nerves of the eye cross.
It obtains information about light from the eye (even when our eyes are shut). If our endogenous clock is running slow the SCN will shift it forwards.
Each is divided into dorsal and ventral SCN.
- Ventral is reset quickly by external cues.
- Dorsal is less affected by light and more resistant to being reset.
The pineal gland and melatonin
Morgan (1995) bred mutant hamsters so they had a circadian rhythm of 20 hours instead of 24 hours. Their SCN was then implanted into normal hamsters. The normal hamsters then displayed the mutant rhythms.
DeCoursey et al (2000) disconnected the SCN in 30 chipmunks. The chipmunks were returned to their natural habitat and observed alongside two other groups of chipmunks – 24 surgical controls and 20 intact controls. After 80 days, significantly more of the SCN-lesioned chipmunks had been killed by weasels. This was presumably because these chipmunks remained awake in their burrows and the weasels could hear the noise and were able to locate the chipmunks.
The SCN sends signals to the pineal gland.
This increases the production of melatonin at night.
Melatonin induces sleepiness and inhibits brain mechanisms for wakefulness.
SAD is a consequence of a disrupted circadian rhythm.
People become depressed during the winter months and recover during the summer.
Research studies have shown that the hormones melatonin and serotonin are secreted when it is dark (by the pineal gland); the more darkness, the more melatonin and serotonin.
In the UK, as the seasons change from summer to winter, the circadian rhythms may be thrown out of phase.
People continue to get up at about the same time but often go to bed earlier because it is darker earlier.
This means that the biological system gets the impression that time is shifting and the result is similar to jet lag.
Light is a dominant zeitgeber in humans. Light resets the SCN.
It can also reset other oscillators within the body that are light-sensitive.
Campbell and Murphy (1998) found that if you shine light on the back of participants’ knees their circadian rhythms shifted!
In cave studies (Ashoff and Wever, and Siffre) participants were exposed to artificial light. It was assumed that this would not entrain rhythms.
Other research supports Campbell and Murphy – Boivin et al (1996) found circadian rhythms can be entrained by dim lighting, though bright lighting was more effective.
The fact that we live in an artificially lit world could have a negative effect. Stevens (2006) suggests that as melatonin disruption occurs in dim lighting it could explain the high rate of breast cancer in the industrialised world.
During childhood the need for sleep decreases, but in adolescence it increases slightly (9-10 hours per day)
Circadian rhythms also change, so teenagers feel more awake at night and have difficulty getting up (phase delay).
One factor that distinguishes adolescent REM is that males have accompanied orgasm and ejaculation (this is significantly less likely at other ages).
Normal adult sleep is 8 hours per night with 25% REM
Parasomnias (sleep walking) are more rare, but there is an increase in apnoea and insomnia.
Redline (2004) meta analysis found that as we age
Total sleep decreases
Time to get to sleep increases
Night time wakings increases
Feeling refreshed on waking increases
Feeling sleepy in the day increases
Daytime naps increase
As we age total sleep time remains the same, but you may have more difficulty going to sleep and may wake frequently (up to 6 times per night)
Need to nap in the day to satisfy sleep needs
Pattern of sleep changes
REM decreases to 20%
SWS is significantly reduced to 5% or none
Other kinds of NREM sleep increase
Phase advance can be experienced, feel sleepy earlier in the evening and wake earlier
Newborns spend about 16 hours a day sleeping, but their sleep is not continuous.
Sleep cycles are shorter than the adults 90 minute cycle.
Sleep stages are similar to adults, called quiet sleep and active sleep, these are immature versions of SWS and REM.
More active sleep than adult REM (about 50% is active sleep).
While adults normally go straight into deep sleep, babies initially have a light period of sleep, after 20 minutes they enter deep sleep.
By 6 months babies sleep longer due to an established circadian cycle (one sleep-wake cycle)
By age 1 infants sleep mainly at night (with one or two naps in the day).
At age 5 the EEG of a child’s sleep looks like an adult, but they still sleep more (12 hours per day).
There is also more REM (30% of total sleep time).
Boys sleep slightly more than girls.
It is normal for children to have sleep disorders (parasomnias) e.g. night terrors.
Between the ages of 5 and 12, total nocturnal sleep drops to about 9 -10 hours.
Pre-teens seem to experience sleep-wake utopia. During the day they are bursting with energy, at night they sleep soundly and they are wide awake and fully rested from the moment they open their eyes in the morning (Dement, 1999).
Babies sleep is an adaptive mechanism to make parents’ life easier. Parents can get on with chores while baby sleeps in the daytime.
Waking through the night is adaptive, as babies have small stomachs and need to be fed regularly.
REM sleep related to immaturity of the infant brain. REM sleep is linked to the production of neurotransmitters and consolidation of memories. Premature babies spend 90% of time in REM/active sleep. Psychologists suggest that REM activity may present images which further stimulates the brain.
Hormones are normally released at night and can disturb sleep.
‘Adolescent’ behaviours (e.g. irritability, moodiness) are also associated with lack of sleep.
Crowley (2007) showed that adolescent sleep patterns vary with the school year. Circadium rhythms reset on school Mondays result in jet-lag.
Wolfson and Carskadon (2005) suggest schools should begin later in the day to accommodate poor attention span in morning lessons.
Tynjälä et al. (1993) looked at sleep patterns across cultures. 400,000 11-16 year olds from 11 countries were studied. Found Swiss children slept the most and Israeli children slept the least. Factors that affected this are number of nights spent away from home. This shows that sleep is influenced by cultural practices.
Too much sleep is linked to increased mortality risk.
Kripke et al. (2002) surveyed 1 million adults and found those sleeping 6/7 hours had reduced mortality risk, those sleeping 8 hours had 15% higher mortality risk, and those sleeping 10 or more hours had a 30% higher mortality risk.
But this is correlational data and does not account for intervening variables (e.g. if you have a health problem you often sleep more).
Older adults often have problems staying asleep (due to sleep apnoea or medical illness).
SWS reduces and the elderly are more easily woken.
Reduced SWS also means lower growth hormone production which is associated with the lack of energy and lower bone density found in older adults.
To treat the problems with sleep the elderly can use relaxation techniques or take melatonin.
Growth hormone is secreted during SWS which then stimulates growth – this is very important during childhood.
In adults, growth hormone allows proteins to synthesise and cells to grow. Uninterrupted sleep is vital for GH release.
Sassin et al (1969) found that when sleep was reversed by 12 hours, GH also reversed. Suggesting that GH is associated with SWS.
GH correlates with the amount of SWS (van Cauter and Plat).
Lack of SWS also reduces the effectiveness of the immune system.
Brain growth is linked with REM sleep.
REM/active sleep is far higher in babies than adults and even higher in premature babies.
It has been suggested that the amount of REM sleep needed correlates with immaturity at birth.
Siegel (2003) found the platypus has 8 hours of REM per day as it is immature at birth, whereas the dolphon (born mature) has no REM.
Siegel and Rogawski (1988) suggest that REM sleep allows for a break in neurotransmitter release, which allows the neurons to regain their sensitivity and the body to function properly.
Support comes from MAOIs (drugs to increase dopamine and serotonin) a side effect is REM is abolished.
REM has been found to be important for consolidation of procedural memories.
Shapiro et al (1981) found that runners in a marathon slept for an hour more on the two nights following a race. SWS also increased supporting the view that NREM sleep is associated with physical recovery.
Research for the importance of sleep comes from case studies (e.g. Peter Tripp stayed awake for 201 hours, after 3 days he was unpleasant and abusive, after 5 days he began to hallucinate. At the end of the experiment he slept for 24 hours, and then woke feeling normal).
The problem with this is that it only tells us one person's need for sleep.
It has been suggested that during sleep deprivation microsleep occurs (this is where EEG recordings show patterns of sleep while awake).
Non-human animals have shown us the importance of sleep. Rechtschaffen et al. (1983) forced rats to stay awake for 33 days on a rotating disc - they all died. But could this be due to stress?
When a person is deprived of REM sleep (e.g. wake them when their eyes dart around), they have a tendency to go straight back into REM the following night. This shows the importance of REM.
And if you get really stuck...you can use the evolutionary approach to evaluate restoration.
Metabolic rate refers to the chemical processes that take place in the body.
All activities use energy.
Animals with a high metabolic rate use more energy when foraging or escaping from predators; so they sleep to conserve energy.
Webb (1982) described this as the hibernation theory of sleep.
Time spent sleeping is restricted by food intake.
Animals such as cows and horses have to spend a great deal of time foraging for food (e.g. grass) which is poor in nutrients.
Animals such as cats and dogs are carnivores and their food is higher in nutrients, they therefore eat less and can spend more time sleeping.
An animal that is a predator (e.g. fox) sleeps for longer.
Prey species need to be vigilant to avoid predators and so sleep time is therefore reduced.
As sleep is needed to function they sleep when they are less vulnerable.
Waste of Time
Meddis (1975) suggested that sleep helps prey animals to stay out of harm’s way when they are most vulnerable.
For most animals this means sleeping at night or where they are hidden. This is referred to as the ‘waste of time’ hypothesis.
Young (2008) added to this, there is greater likelihood of passing on your genes if you can sleep for as long as you can get away with.
Evolutionary theories aim to explain why we sleep by showing other benefits:
Criticisms of research into animals' sleeping patterns are...
out of 5000 mammalian animals we have data on only 150 animals
we do not know the REM and SWS of these animals
we do not know the amount of sleep of different aged animals
The phylogeny of sleep project aimed to correct these problems but the data is not always reliable (e.g. less than 5 of one species studied, in a lab, for less than 12 hours of observation.
Allison and Cicchetti (1976) found that animals with a high danger rating did sleep less (apart from the rabbit, who slept as much as moles who have a low danger rating).
Zepelin and Rechtschaffen (1974) found smaller animals with higher metabolic rate do sleep more than larger animals (apart from the sloth who is large but sleeps 20 hours a day).
According to Capellini et al (2008) the energy conservation hypothesis may be wrong and foraging and predator avoidance may be correct - they found a negative correlation between metabolic rate and sleep (not supporting energy conservation), but they did support the foraging hypothesis. They also found that animals who sleep in an exposed position sleep less, but time spent sleeping is also reduced in animals which sleep socially.
Types of Insomnia
Initial insomnia = trouble falling asleep
Middle insomnia = trouble remaining asleep
Terminal insomnia = waking up early
Insomnia is classified as...
transient = short term
intermittent = occasional
chronic = constant and long term (occurs for 1 month or more).
Where there is a single underlying medical, psychiatric or environmental cause.
Insomnia can be a symptom of a main disorder such as depression, it is therefore secondary.
It is typical of people who do shift work or who have circadian rhythm disorders.
It can also be the result of environmental factors, e.g. too much caffeine, tea, alcohol or even chocolate.
According to the DSM definition is when insomnia occurs on its own with no known cause for more than 1 month.
Insomnia is the individual’s primary problem.
The individual may be stressed, they may have developed bad sleeping for example staying up to late.
Sometimes insomnia may have a cause that has now disappeared but insomnia persists because of an expectation of sleep difficulty.
Causes of Insomnia
Ohayon and Roth (2003) carried out a study of almost 15000 Europeans and found that insomnia often preceded rather than followed cases of mood disorder. This means that insomnia should be treated regardless of whether it is primary or secondary in cause.
Consequences of insomnia:
Cognitive impairment - memory loss and poor concentration in the daytime.
Accidents - sleepiness and cognitive difficulties make it dangerous to drive. Arendt et al (2001) compared those deprived of sleep for one night to a group of adults drinking alcohol. They found that even staying awake by three hours was comparable to modest amounts of alcohol. Zammit et al (1999) estimate that 1500 deaths a year are linked to sleepiness.
Psychological disturbance - insomnia is often the cause of depression and anxiety.
Immunity - Savard et al (2003) found fewer immune cells in people with insomnia compared to good sleepers. Although we have a problem with cause and effect.
Spielman and Glovinsky (1991) explain insomnia with the 3Ps:
genetic vulnerability to insomnia. Watson et al (2006) found that 50% of the variance in insomnia could be due to genetic factors.
events trigger insomnia in a vulnerable individual. E.g. stress at work, exams, or shift work.
some factors maintain insomnia when original cause has disappeared, e.g. you are tense at bedtime as you fear you will not sleep.
Two main symptoms;
1. Feeling sleepy all the time
2. Episodes of cataplexy (loss of muscular control) during the day.
Episodes can be triggered by different emotional arousals e.g. stress.
Individuals can also experience hallucinations, sleep paralysis, these are experienced when feeling asleep or waking up, night time sleep can also be interrupted by frequent waking.
Narcolepsy often begins in adolescence/early adulthood it’s estimated that 1 in 2000 people are affected, this number may be larger as many may go undiagnosed since some people only experience minor symptoms.
What is narcolepsy?
Explanations of narcolepsy
There are three explanations for narcolepsy:
In the 1960s narcolepsy was thought to be linked to a malfunction in the system which regulates REM and explains some of the symptoms of narcolepsy, e.g. Cataplexy
During the day narcoleptics can also experience hallucinations, linked to REM-type sleep, and have abnormal REM at night.
In the 1980s narcolepsy was thought to be linked to a mutation in the immune system – Honda et al. (1983) found an increased level of HLA in narcoleptic patients. HLA is found on the surface of white blood cells and coordinates the immune system response. 90% of people with narcolepsy have this variant of HLA.
Recently research has found a link between the neurotransmitter hypocretin and narcolepsy. Hypocretin plays a role in wakefulness.
It has been found that narcoleptics have lower levels of hypocretin-producing cells, resulting in narcolepsy. Narcoleptic dogs have been found to have a mutation in chromosome 12 which disrupts processing of hypocretin
Lehrman and Weiss (1943) suggest that narcolepsy disguises sexual fantasies.
Vogel (1960) proposed the REM hypothesis for narcolepsy. Research was supported by recording the neuron activity in the brainstem of narcoleptic dogs, which showed that cataplexy activated the cells that are normally only active during REM.
Mignot et al (1997) criticised the HLA-narcolepsy link – the HLA variant is common in not only narcoleptic individuals, but is also high in the general population. Additionally, not all narcoleptics have the variant.
Hypocretin seems to be the most promising lead. Findings from narcoleptic dogs have been confirmed in humans e.g. chromosome 12 in dogs seemed to be mutated. Nishino et al (2000) found low levels of Hypocretin in human narcoleptic patients’ cerebrospinal fluid. But low levels of hypocretin are not likely to be inherited as narcolepsy is not genetic (does not run in families or concordant in twins). The reduction could be due to stress, diet, infection, or auto-immune attack (linking back to HLA explanation).
Explanations of Sleep Walking
EEG recordings made during sleep walking show a mixture of delta waves (typical in SWS), and higher frequency beta waves (which are characteristic of the awake state). It may be that sleep walking occurs when a person in SWS is awakened but arousal of the brain is incomplete. This abnormal arousal may be genetic.
Sleep deprivation, alcohol, fever, stress, or psychiatric conditions...
can also lead to sleep walking. Hormonal changes during puberty and menstruation can also trigger sleep walking.
Children have more SWS than adults. Oliviero (2008) suggests that the system which inhibits motor activity in SWS is not sufficiently developed in children, and possibly underdeveloped in some adults. In the study motor excitability was tested in adult sleep walkers and it was found that compared to controls the sleep walkers showed signs of immaturity in the relevant circuits.
Sleep walking fits the diathesis-stress model – the diathesis (vulnerability) comes from genetics.
Lecendreux et al (2003) found a 50% concordance in MZ twins and 10-15% in DZ twins. The stress part of the model can be explained by SWS; sleep deprivation, alcohol and fever all increase SWS and can trigger sleep walking.
A gene has been identified as critical to sleep walking.
Zadra et al (2008) studied 40 sleep walking patients. On the first night they slept normally. On the second night they were prevented from falling asleep for 25 hours. On the first night 50% of the patients sleepwalked. After sleep deprivation this rose to 90%. This shows that sleep deprivation could be a ‘stressor’.
The high levels of SWS that children have could also explain why they sleep walk more. The high levels of SWS are the diathesis.