Biological Rhythms and Sleep

Psychology A2 question 1


Biological rhythms AO1

Biologically driven behaviour that is periodically repeated

Controlled by endogenous pacemakers (internal mechanisms)


Exogenous zeitgebers (external factors) E.g. daylight

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Circadian rhythms AO1

24 hour period we sleep/wake once

Normally sleep/wake pattern is entrained (clocks, meal times, daylight changes)

Free running daily cycle governed by our endogenous body clock

Michel Siffre 1972 spent 6 months in an underground cave. Sleep/wake cycle settled down to 25-30 hours.

Endogenous rhythm controlled to a limited amount

Folkard 1985 used artificial light to reduce the circadian cycle. Participants coped at a 23-hour cycle. But when reduced to 22hours, their bodies reverted to a natural cycle.

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Circadian rhythms AO1

Core temp rises and falls during the day. Along with heart rate, urine secretion, others that indicate metabolic rate.

Trough at 4am and returns to normal level at 8pm

Colquhon 1970 concluded from research, cognitive performance is positively correlated with temp

Monk and Embrey 1981 suggest long term recall is best when body temp is lowest, in the early morning and early evening.

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Circadian Rhythm AO2

Individual differencesAschoff and Wever 1976 observed some people, when isolated from daylight, maintain a 24-25 hour cycle. Others developed idiosyncrasies such as 29 hours awake and 21 hours asleep.

Marks and Folfard 1985 ‘morning’ types may peak in their daily rhythms a few hours earlier than ‘evening’ types.

Applicationchronotherapeutics aims to match medical treatments to circadian rhythms to maximise benefits of certain treatments and minimise adverse effects.

Asthma symptoms worsen during the night, possibly due to increased levels of cortisol. Some doctors prescribe unequal doses of medication.

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Infradian rhythms AO1

Menstural cycle occurs once a month

Controlled endogenously by hormones produced by the pituitary gland

Reinburg 1967 documented the menstrual cycle of a woman who spent 3 months in a cave, with only dim lighting.

Sleep/wake cycle lengthened slightly and menstrual cycle became shorter.

However, menstrual cycle can be synchronised by extreme factors

Russell 1980 collected daily samples of women’s underarm sweat mixed with alcohol and applied it to the upper lip of their female participants.

Their menstrual cycles synchronised, due to pheromones that acted as exogenous zeitgebers.

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Infradian rhythms AO2

Purpose of menstrual cycle is to conserve energy. Better to restrict periods of fertility, therefore there is a need to have endogenous control of the rhythm

Side effects of the menstrual cycle – pre-menstrual tension has been associated with aggression. Been used as a defence in criminal trials. Lewis 1990

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Infradian rhythms AO1

Circa-annual rhythms

MigrationGwinner 1986 kept wild birds in cages for 3 years, exposing them to 12 hours of light and darkness. They still showed signs of migratory, suggesting endogenous control.

HibernationPengelly and Fisher 1957 artificially controlled squirrels exposure to light and temp. Squirrels hibernated between Oct to Apr

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Infradian rhythms AO2

Seasonal affective disorder (SAD) affect some people during winter, becoming depressed.

Darkness leads to increased production of melatonin, which affects mood.

Led to phototherapy as a treatment. Exposure to bright light for several hours a day reduces the effects.

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Ultradian rhythms AO1

During a night’s sleep you pass through different sleep cycles. Each cycle takes about 90mins.

Daytime biorhythms follow the same 90mins cycle.

Klein and Armitage 1979 tested participant’s performance on verbal and spatial tasks. Found a 96mins cycle.

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Ultradian rhythms AO2

90min cycle appears to be controlled by a different biological clock to the one governing the circadian rhythm.

If the circadian rhythm was destroyed, the 90min cycle would continue.

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Exogenous Zeitgebers AO1

External stimuli are rhythmic.

Day length is the dominant zeitgeber.

Important are the seasons, weather, temperature, phases of the moon, tides, availability of food, and social stimuli.

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Exogenous Zeitgebers AO1

Miles 1977 studied a blind man who had a 24.9 hour circadian rhythm despite being exposed to a variety of zeitgebers that should have set his ‘clock’ to 24hours, like the radio.

Had to use stimulants and sedatives to coordinate his sleep/wake cycle with the rest of the world.

Demonstrates that light really is the dominant time-giver.

Light cues can be overcome. Demonstrated by Luce and Segal with those who live in the Arctic Circle who sleep for 7 hours, despite the sun never setting during the summer months.

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Exogenous Zeitgebers AO2

Adaptive to have biological rhythms to govern biochemical processes

Also adaptive for these endogenous rhythms to be reset by external cues so that animals are in tune with seasonal variations.

Dangerous to be solely at the mercy of environmental cues, endogenous cues are important.

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Disrupting biological rhythms AO1

Phase delay – delaying the internal clock

Phase advance – skipping ahead

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Disrupting biological rhythms AO1

Shift work – on average it takes about 3 days to adjust to a 12-hour shift in time.

Artificial lighting is moderately effective in re-setting the circadian rhythm

Performance is affected as some body clocks take longer to re-adjust, therefore body rhythms are desynchronised.

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Disrupting biological rhythms AO2

Individual differences – people whose circadian rhythms change least may cope best overall Reinburg 1984

Harmful effectsshift workers suffer from sleep deprivation because it is more difficult to sleep during the day due to light and noise. It also disrupts family and social life, which can lead to depression

ApplicationsDawson and Campbell 1991 exposed participants to a 4-hour pulse of bright light on their first night. Helped their subsequent adjustment as measured by body temp

Czeisler 1982 tested the effects of rotating shifts with the clock, rather than against. People were doing early shifts and then later shifts.

Workers felt better and management reported an increase in productivity.

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Disrupting biological rhythms AO2

Jet lagKlein 1972 found that adjustment was faster for westbound flights.

Schwartz 1995 found East coast US Baseball teams did better when travelling west than West coast teams travelling east.

Shows phase delay has less effect.

However on short trips, when returning home may be easier that outward journeys. Other body clocks haven’t changed, meaning that on the return home it may take less time to readjust.

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Disrupting biological rhythms AO2

Coping with jet lagRedfern 1989 use of benzodiazepines to increase melatonin levels and resynchronise the body clock. -  One reason for jet lag may be the body temp may not have reset as easily. Meaning the body is experiencing desynchronised rhythms

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Sleep Stages AO1

Sleep is an altered sate of consciousness.

Decreased responsiveness to the external environment.

Occurs daily and has distinct stages

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Sleep Stages AO1

Stage 1relaxed state, waves change from beta (being awake) to alpha, which are slower, more regular and have a greater amplitude. Transaction from stage 1 is often accompanied by a hypnagogic state. May include hallucinations.

Stage 2Slower, larger brain waves, short bursts of high-frequent sleep spindles and K-complexes. Light sleep and the sleeper is easily woken.

Stage 3Slowing down of the brain waves and bodily activity. Long, slow delta waves, with some sleep spindles.

Stage 4Slow wave sleep with more delta waves than stage 3. Hard to be woken except by personally significant noises, like baby crying. Some physiological activities take place, production of growth hormones. Sleep walking and night terrors are experienced in the stage.

Stage 5 or REM SleepStage four sleep is followed by stage 3, 2 and then 5, rapid eye movement sleep. There are active brain waves. Jouvet called this paradoxical sleep because of the contradictions: eye movement, heart rate, breathing, etc. But the body is the state of near paralysis and is difficult to wake a person up.

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Sleep Stages AO1

Most people have 5 cycles of sleep a night that last approximately 90 minutes.

Electroencephalographs (EEGs) measure electrical activity or brain waves, electro-oculograms (EOGs) measure eye movement, and electromyograms (EMGs) measure muscle movement and have been used to distinguish the stages and cycles of sleep

1st cycle (90 min) - 1, 2, 3, 4, 3, 2, REM (10 min)

2nd cycle (90 min) 2, 3, 4, REM (10 min)

3rd cycle (90 min) - 2, REM (40 min)

4th cycle (90 min) -2, REM (60 min)

5th cycle (90 min) - 2, REM (60 min)

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Sleep Stages AO2/AO3

Objective evidence – EEG, EOG and EMG illustrate Psychology as a science 

Artificiality of sleep laboratory – extrapolation issues

Universality – stages & cycles of sleep have been found across cultures

Individual differencesreductionist – simplifies all sleep to a set range of stages & cycles of sleep – people will differ 

AO3 - Weakness of the self-report method – The self-report method yields data that may be subject to social desirability bias

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Functions of Sleep AO1

Sleep patterns have evolved because they are adapted to the needs of individual’s species.

Each species developed different sleep habits and patterns to deal with environmental pressures.

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Functions of Sleep AO1

Sleep may serve an adaptive rather than a restorative function - sleep has been naturally selected because it promotes survival.

Species that sleep have survived to reproduce & carry sleep into the next generation as an adaptive behaviour - If it was non-adaptive, i.e. does not have an evolutionary purpose, then it should have disappeared.

Meddis (1975) suggested that sleep is adaptive because the immobility of sleep keeps animals safe from predators and that it occurs when normal activities (such as feeding) are impossible.

Webb (1982) proposed the hibernation theory that suggested the adaptive function of sleep is energy conservation.

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Functions of Sleep AO2

Genome lag - may have been more relevant in our evolutionary past. However, such explanations may not be true of human sleep today as predators no longer pose such as threat. It may well be that sleep patterns will change in time as evolution is a gradual process and so the patterns we have at the moment may be due to genome lag, which occurs because the environment changes much more quickly  than the genes.

Low adaptive value - In some species if sleep were simply adaptive then it should have been selected out.

Lacks scientific validity - Evolutionary theories are post hoc, i.e. they have been proposed in retrospect and consequently lack empirical support, and so they lack scientific validity. Difficult to dismiss and so they are neither verifiable nor falsifiable.

Deterministic & Reductionist - Evolutionary theories are deterministic as they ignore free will. People can and do choose when they want to sleep. Sleep is far more complex a process to have evolved solely as protection as this does not explain why we have the different stages and cycles of sleep or why we need to catch up on some of our missed sleep. Evolutionary theories ignore the physiological and psychological functions of sleep and so are unlikely to provide a full explanation for sleep.

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Restoration Theory AO1

Purpose of sleep is to repair and recharge the brain and body

Oswald (1980) claimed that NREM sleep restored the body and REM sleep restored the brain 

Horne (1988) distinguished between core (stage 4 & REM) and optional (stages 1 to 3) sleep and claimed that only core sleep was critical for restoration of the brain as restoration of the body can occur during resting wakefulness.

Stern and Morgane (1974) REM sleep allows the brain to replenish neurotransmitters

Hartmann (1973) REM sleep is a time for synthesising noradrenaline and dopamine  

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Restoration Theory AO2

 Case Studies - The studies of sleep deprivation in humans are mainly case studies or small samples  - difficult to extrapolate from (Randy Gardner)

Objective measurement - The physiological measures of sleep, e.g. REM activity and levels of neurochemicals, are objective, which means that they are less subject to bias

Multi-perspective - The sleep deprivation research suggests that effects are more psychological than physiological (Huber-Weidman, 1976 and the Peter Tripp case study) and so the main function of sleep may be to recover psychological functioning.

Androcentricity – all of the sleep deprivation research is based on male participants

Animal research – can you apply findings from Rechstaffen’s rats or Jouvet’s cats to human behaviour?

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Lifespan AO1

Sleep needs vary by age, both qualitatively (different stages of sleep) and quantitatively (how much sleep).

New-born's sleep an average of 16 to 18 hours a day. In the early months, an infants sleep is divided equally between REM and non-REM sleep. A new-born baby will often enter REM sleep immediately and it is not until they are 3 months old that the sequence of NREM and REM sleep is established.

By the age of 5-10 years, the sleep stage cycle increases to approximately 70 minutes (Borbely, 1986) Between the ages of 5 and 12, total nocturnal sleep drops to about 9 -10 hours.

Young adults (18-30 years) tend to start sleeping less than during adolescence and do not experience such deep sleep.

In middle age (30-45 years), people may start to notice a shallowing and shortening of sleepIncreased signs of fatigue are a sign of middle age.

In late middle age (45-60) sleep duration drops to about 7 hours and stage 4 sleep virtually disappears. There is a corresponding increase in lighter stages of sleep such as stage 1.

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Lifespan AO2

Objective measurements  - Research into lifespan changes in sleep has been conducted in numerous sleep laboratories throughout the world - Dement (1999) himself carried out a detailed 7 year longitudinal study called the Stanford Summer Sleep Camp, which used twenty-four 10, 11 and 12 year olds.

External factors and co-sleep (Reductionism) - There are numerous factors that affect the quality and quantity of sleep experienced. Work patterns, children, aches and pains, and medication can all affect sleep patterns. Individual Differences - Borbely (1986) warns against the use of generalisations about sleep patterns for different age groups. Extrapolation could be difficult

Operationalisation of sleep - One difficulty with sleep research is to agree when sleep occurs. Sleep onset is gradual and entails a predictable sequence of events rather than a discrete event. If it cannot be operationalised, it should not be measured.

Cultural traditions - In Europe and North America, adults tend to adopt a so-called monophasic pattern of sleep (that is, they sleep for one long period during the night) and much of the research outlined would only be applicable to these countries.

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Insomnia AO1

Primary Insomniachronic insomnia occurring in the absence of any psychological or physical (medical) condition.

Secondary Insomnia = chronic insomnia that can be explained by a pre-existing psychological or physical (medical) conditions.

There are numerous primary insomnia subtypes including: Psychophysiological insomnia, Idiopathic insomnia and Sleep state misperception.

Psychophysiological insomnia - This is a form of anxiety-induced insomnia and is sometimes known as learned insomnia or behavioural insomnia. The primary components involved are intermittent periods of stress, which result in poor sleep and generate two maladaptive behaviours.

Idiopathic insomnia - This was originally called childhood-onset insomnia because it tends to occur at a very early age. It is thought to occur due to an abnormality in the brain mechanisms that controls the sleep-wake cycle.

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Insomnia AO2

Physiological support - Smith et al (2002) conducted a study into the neuro-imaging of NREM sleep in insomnia and found clear evidence for physiological abnormalities in insomniacs.

External validity of sleep studies - Studies have examined whether findings from sleep laboratories relate to reported sleep disorders from patients.

Difficulty in extrapolation - Melatonin does appear to be effective in small group of elderly patients with insomnia who have low melatonin levels. However, it is considered  ineffective in the general treatment of insomnia, and the precise role of melatonin in sleep still needs to be clarified.

Not a sleep disorder at all! –Dement (1999)

Reliability and validity of sleep insomnia measures: One major obstacle to explaining the cause of insomnia is that there is controversy over the identification of insomnia in the first place!

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Narcolespy AO1

Narcolepsy is a disorder of the system that regulates the sleep-wake cycle. It results in sudden and uncontrollable attacks of sleep at irregular and unexpected times, which may last minutes or hours

The most obvious symptom of narcolepsy is a sudden loss of muscular control (cataplexy) triggered by amusement, anger or excitement.

Narcolepsy usually begins in adolescence and may have a biological basis. It affects 0.02% - 0.06% of the population (so is very rare).

It may be the result of a genetic abnormality (related to the HLA complex on chromosome 6), the result of an auto-immune disease or caused by a shortage of the neurotransmitter hypocretin.

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Narcolepsy AO2

Animal research - Understanding of narcolepsy stems primarily from research involving narcoleptic dogs (for example, special laboratory-bred Dobermans and Labradors).

Effective treatments and animal research: treatments for narcolepsy often involve stimulant drugs. The drug (Provgil) has proved useful in the treatment of narcolepsy.

Reductionism – reduces the explanation of narcolepsy to hypocretin only.

Biological approach – explains narcolepsy in terms of a physical (biological) response

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Sleep Walking AO1

Sleepwalking affects about 20% of children and only about 1-3% of adults (Hublin, 1997). Adolescents and adults with SW tend to have an increased prevalence of anxiety and personality disorders.

The causes of sleep-walking are not fully known but it is thought to be triggered by: Sleep deprivation and/or an irregular sleep schedule.

SW occurs during NREM sleep.

Research has found that SW has a significant genetic component. Evidence comes from familial studies. For example, Broughton (1968).

They have also identified a gene that may be critical in SW – the DQB1*05 gene.

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Sleep Walking AO2

Nature/Nurture - It remains unclear what the exact nature of the relationship between the HLA gene and sleepwalking is.

An additional problem with the Bassetti study is that the sample of sleepwalkers studied may not be representative of the general population of sleepwalkers. Extrapolation issues.

Dement (1999) recognises that the possibility of sleep deprivation plays a part in sleepwalking – however is this reductionist?

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