OxfordAQA International A-level Psychology (9685): 3.3.1 Psychology of sleep – Study Guide

This guide covers section 3.3.1 Psychology of sleep in the OxfordAQA International AS and A-level Psychology (9685) specification, Version 3.1 (International A-level exams May/June 2020 onwards). The section sits in Unit 3: Advanced topics and research methods 2. The specification says Unit 3 is a 1 hour 30 minute written exam worth 90 marks and 30% of the International A-level, and that Section A, Psychology of sleep, carries 30 marks of compulsory questions.

Use it with the sleep revision notes and the sleep practice questions. The 9685 course hub and 9685 checklist show the rest of the course. The nervous system and hormones you need here are taught in the Unit 2 biopsychology guide.

Coverage table

Syllabus reference	What you must know or be able to do (from the document)	Where assessed
3.3.1 bullet 1	Biological rhythms: circadian, infradian and ultradian. The effect of endogenous pacemakers and exogenous zeitgebers on the sleep/wake cycle	Unit 3, Section A
3.3.1 bullet 2	Disruption of biological rhythms: the effects of shift work and jet lag	Unit 3, Section A
3.3.1 bullet 3	The nature of sleep: types of sleep, non-REM and REM	Unit 3, Section A
3.3.1 bullet 4	Functions of sleep: evolutionary explanations; restoration theory; memory consolidation	Unit 3, Section A
3.3.1 bullet 5	Sleep disorders: insomnia, including the role of personality factors and genetics; narcolepsy	Unit 3, Section A
3.3 (all Unit 3)	Demonstrate knowledge (AO1), apply it in a range of contexts (AO2), analyse, interpret and evaluate theories and studies (AO3); evaluate therapies and treatments	Unit 3

The specification also says research methods, practical skills and mathematical skills are assessed in Unit 3. Expect sleep questions built around data or a study design. Your teacher will confirm the question styles and mark tariffs.

Biological rhythms, pacemakers and zeitgebers

Key terms

• Circadian rhythm: a cycle of about 24 hours, such as the sleep/wake cycle or core body temperature.
• Infradian rhythm: a cycle longer than a day, such as the menstrual cycle (about a month) or seasonal affective disorder (yearly).
• Ultradian rhythm: more than one cycle in 24 hours, such as the roughly 90-minute cycle of sleep stages.
• Endogenous pacemaker: an internal biological clock. The main one is the suprachiasmatic nucleus (SCN) in the hypothalamus.
• Exogenous zeitgeber: an external cue that resets the clock. Light is the main one; meal times and social routines also act as zeitgebers.
• Entrainment: resetting the internal clock to match the outside world.

How it works. Light reaches the retina. A pathway from the retina carries the signal to the SCN. The SCN sends signals to the pineal gland, which releases melatonin when it is dark. Melatonin promotes sleepiness. In bright light, melatonin output falls. So the SCN keeps time on its own, and light keeps it in step with the day.

Evidence

• Siffre (1962) spent about two months in a cave with no daylight or clocks. His sleep/wake cycle kept going but ran slightly longer than 24 hours. This shows an endogenous clock that needs light to stay on a 24-hour day.
• Aschoff and Wever placed volunteers in an underground bunker with no natural light. Most settled into cycles a little longer than 24 hours.
• Ralph et al. (1990) transplanted SCN tissue between normal hamsters and mutant hamsters with short (20-hour) rhythms. The recipients’ own SCN had been destroyed. The recipients took on the donor’s rhythm, whichever direction the transplant went. This points to the SCN as the main pacemaker.
• DeCoursey et al. (2000) damaged the SCN in chipmunks and returned them to their natural forest habitat. More of them were killed by weasels than control chipmunks, possibly because their restlessness at night helped predators find them.
• Stern and McClintock (1998) found that odourless compounds from other women’s armpits changed the length of women’s menstrual cycles. This suggests pheromones can act as a zeitgeber for an infradian rhythm.

Evaluation

• Strength: converging evidence from human isolation studies and animal lesion and transplant studies.
• Limitation: Siffre was a single case. Isolation studies often allowed artificial light, which may itself reset the clock.
• Limitation: animal studies raise ethical problems and may not generalise to humans.
• Counter-evidence: Campbell and Murphy (1998) reported that light shone on the back of the knee shifted the rhythm, but later work failed to replicate this.
• Many totally blind people have sleep/wake cycles that drift out of step with the day. This supports light as the key zeitgeber.
• Interaction: the clock and the cues work together, so studying either alone is reductionist.

Worked paragraph. “The sleep/wake cycle is controlled by an endogenous pacemaker, the SCN, which is reset each day by light (AO1). For example, a student who studies in a windowless room under constant lighting may find their bedtime drifting later each day, because the SCN’s own cycle runs slightly over 24 hours (AO2). Siffre’s cave study supports this, since his cycle continued without daylight but lengthened (AO3). However, Siffre was one person, so the finding needs the bunker and hamster studies to support it (AO3).”

Disruption: shift work and jet lag

Both disrupt rhythms by making the internal clock out of step with external cues. This is desynchronisation.

Shift work. Night workers must sleep in daylight, when melatonin is low and body temperature is rising. Their sleep is shorter and lighter. Alertness is lowest in the early hours of the morning, so errors are more likely then. Rotating shifts mean the clock never fully adjusts. Long-term shift work has been linked with health problems, including heart disease, but most of this evidence is correlational.

Czeisler et al. (1982) studied workers on rotating shifts. When rotas were redesigned to fit circadian principles, rotating forwards (days to evenings to nights) and changing less often, workers were more satisfied with their schedules and rated their health better, staff turnover fell and productivity rose. Rotating forwards asks the body to phase delay (stay up later), which is easier than a phase advance.

Jet lag. Crossing time zones moves the light/dark cycle. Flying east shortens the day, so the body must phase advance. Flying west lengthens the day, a phase delay. Because the SCN runs slightly over 24 hours, phase delay is easier. Recht et al. (1995) analysed American baseball results and found that teams who had just flown east performed worse than teams who had flown west.

Evaluation

• Strength: findings have practical value, for example forward-rotating rotas.
• Limitation: jet lag studies are natural or correlational. Travel stress, alcohol and cabin conditions are confounding variables.
• Limitation: shift workers also face family disruption and poorer diet, so not all effects are rhythm effects.
• Individual differences: some people adjust faster than others.

Worked paragraph. “Jet lag happens because the SCN cannot reset instantly to a new light/dark cycle (AO1). A traveller flying east must fall asleep earlier than their clock allows, so they lie awake and then feel tired the next day (AO2). Recht et al.’s baseball data support the east/west difference (AO3). However, the data were not experimental, so other features of travel may explain some of the effect (AO3).”

The nature of sleep: non-REM and REM

Sleep has two broad types. Researchers record them with EEG (brain waves), EOG (eye movements) and EMG (muscle tone).

Stage	Main features
NREM stage 1	Light sleep; theta waves; easy to wake
NREM stage 2	Sleep spindles and K-complexes on the EEG
NREM stages 3 and 4	Slow-wave sleep (SWS); delta waves; hard to wake; growth hormone released
REM	Fast, desynchronised EEG like waking; rapid eye movements; near-paralysis of body muscles; vivid dreams

Many textbooks use four NREM stages. Newer clinical scoring merges stages 3 and 4 into one stage, N3.

A full cycle lasts about 90 minutes, an ultradian rhythm. A typical night has four to five cycles. Early cycles contain more SWS. Later cycles contain more REM. REM is called paradoxical sleep because the brain looks awake while the body is still. Dement and Kleitman (1957) found that people woken from REM usually reported dreams.

Evaluation

• Strength: EEG gives objective, reliable measurements.
• Limitation: sleep labs are artificial, so the first night is often unusual.
• Limitation: links between REM and dreaming rely on self-report on waking.

Worked paragraph. “Sleep follows an ultradian cycle of about 90 minutes, moving from light NREM sleep into slow-wave sleep and then REM (AO1). If a sleep lab record shows mostly delta waves in the first two hours and long REM periods near morning, this is the typical pattern (AO2). EEG makes this objective (AO3), but a single lab night may not reflect normal sleep (AO3).”

Functions of sleep

Evolutionary explanations say sleep exists because it helped survival.

• Energy conservation: sleep lowers metabolism. Zepelin and Rechtschaffen (1974) found smaller animals with faster metabolic rates tend to sleep more.
• Predator-prey (safety): Meddis (1975) argued sleep keeps an animal still and hidden when it cannot forage. Allison and Cicchetti (1976) compared 39 mammal species and found that species in more danger from predators tended to have less REM (paradoxical) sleep.
• Evaluation: there are many exceptions to these patterns. Sleep also makes an animal unresponsive, which is dangerous. Bottlenose dolphins sleep with one brain half at a time, which suggests sleep is needed and not just a way to stay safe. The explanations are hard to falsify.

Restoration theory (Oswald) says SWS restores the body (growth hormone, tissue repair) and REM restores the brain. Horne split sleep into core sleep (SWS and some REM, needed) and optional sleep.

• Support: Shapiro et al. (1981) found increased SWS and total sleep time in runners after a 92 km ultramarathon. Randy Gardner stayed awake for 264 hours in 1964. He made up only a fraction of the lost sleep, but a larger share of SWS and REM, which fits core sleep.
• Limitation: tissue repair also happens while awake. Exercise does not always increase sleep. Gardner was a single case.

Memory consolidation. Sleep strengthens and reorganises new memories. A common view is that SWS supports declarative memory (facts) and REM supports procedural memory (skills), with the hippocampus replaying new learning to the cortex.

• Support: Jenkins and Dallenbach (1924) found better recall after sleep than after the same time awake. Plihal and Born (1997) found early-night (SWS-rich) sleep helped word recall, while late-night (REM-rich) sleep helped a mirror-tracing skill. Stickgold et al. (2000) found improvement on a visual task depended on sleep in the first night after training. Rasch et al. (2007) found that an odour present during learning, re-presented during SWS, improved later recall.
• Limitation: Siegel (2001) pointed out that some antidepressants greatly reduce REM, yet users show no obvious memory problems. Also, sleeping after learning reduces interference, which is not the same as active consolidation.

Worked paragraph. “Restoration theory proposes that slow-wave sleep repairs the body (AO1). A long-distance cyclist who sleeps longer and deeper after a race fits this account (AO2). Shapiro et al.’s ultramarathon findings support it (AO3). However, the theory struggles to explain why repair also happens while awake, so restoration may be one function among several, alongside memory consolidation (AO3).”

Sleep disorders: insomnia and narcolepsy

Insomnia is persistent difficulty getting to sleep or staying asleep, or sleep that does not feel refreshing, with problems during the day. It can be short-term or long-term. Secondary insomnia results from another condition, such as pain. Primary insomnia has no clear separate cause.

Personality factors. People high in neuroticism, anxiety-proneness, worry or perfectionism seem more likely to have insomnia. They may be more physically and mentally aroused at bedtime (hyperarousal) and ruminate in bed. Spielman’s 3P model describes predisposing factors (such as personality and genes), precipitating factors (such as a stressful event) and perpetuating factors (such as long periods awake in bed).

• Evaluation: most personality evidence is correlational and uses self-report. Poor sleep may increase anxiety, so the direction of cause is unclear.

Genetics. Insomnia runs in families. Twin studies suggest a moderate genetic contribution. Large genome-wide studies have found many genetic variants, each with a small effect. Fatal familial insomnia is a rare inherited prion disease caused by a single gene mutation, but it is not typical of everyday insomnia.

• Evaluation: families share environments as well as genes. A diathesis-stress view, where genes and personality create vulnerability and stress triggers it, fits the evidence best.

Narcolepsy involves excessive daytime sleepiness and sudden sleep episodes. Many people with narcolepsy also have cataplexy (sudden loss of muscle tone, often triggered by strong emotion), sleep paralysis and vivid hallucinations as they fall asleep. It is often explained as REM sleep intruding into waking.

• Lin et al. (1999) found that inherited narcolepsy in dogs was caused by a mutation in a gene for a hypocretin (orexin) receptor. In humans with narcolepsy with cataplexy, most hypocretin-producing neurons in the hypothalamus are lost.
• A link with an immune system gene (HLA-DQB1*06:02) suggests an autoimmune cause. Cases rose in some European countries after a 2009 H1N1 flu vaccine, which fits this idea.
• Evaluation: the dog findings are single-gene, but in humans the cause is more complex. The hypocretin account fits narcolepsy with cataplexy better than narcolepsy without it.

Worked paragraph. “Personality factors such as high neuroticism may predispose people to insomnia through hyperarousal at bedtime (AO1). A student who worries about exams and lies awake replaying the day fits this pattern (AO2). However, the evidence is correlational, so insomnia could increase anxiety rather than the reverse (AO3). Family history suggests genes also matter, which supports an interactionist, diathesis-stress view (AO3).”

Common errors

• Calling the sleep/wake cycle ultradian. It is circadian. The sleep stage cycle is ultradian.
• Saying jet lag is worse flying west. East is usually worse because it needs a phase advance.
• Calling melatonin a zeitgeber. It is a hormone. Light is the zeitgeber.
• Describing REM as “deep sleep”. Deep sleep is SWS. REM is paradoxical sleep.
• Writing about insomnia without naming personality factors and genetics, which the specification lists.
• Treating fatal familial insomnia as typical evidence for a gene for ordinary insomnia.
• Evaluating every study with “it was a lab study”. Name the specific problem, such as a single case or an animal sample.

Where to go next

Test yourself with the sleep practice questions and plan your revision with the 9685 exam preparation guide.

Official syllabus

OxfordAQA International AS and A-level Psychology (9685) specification, Version 3.1 (International A-level exams May/June 2020 onwards), section 3.3.1 Psychology of sleep, with the Unit 3 assessment details in section 2.3 and the assessment objectives in section 4.3.