Sleep - Whole Topic

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  • Created on: 26-05-16 09:41

Biological Rhythms - AO1

Rhythms - Circadian rhythms are cycles which last 24 hours, Infradian rhythms take longer than 24 hours to complete, and Ultradian rhythms take less than 24 hours. Sleep-wake is circadian, the menstrual cycle is infradian, and the stages of sleep are ultradian.

Endogenous Pacemakers - Biological clock located in the suprachiasmatic nucleus, which is part of the hypothalamus. This nucleus is linked to the retina, where light impulses are recieved. These impulses are passed to the pineal gland. Here, serotonin is convertde into melatonin, which acts of the raphe nuclei, which uses this hormone to send information to the reticular activating system, where sleep is induced.

External zeitgebers - These are external time givin cues. The co-ordination of these rhythms is what controls our sleep-wake cycle, such as the co-ordination between light cues and hormone production which work to induce sleep. This is a process known as entrainment. Without zietgebers like light, our biological clock would run free and settle into a 25-27 hour cycle, rather than a 24 hour cycle.

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Endogenous Pacemakers - AO2

Support (SCN) - Stephan and Zucker (1972) damaged rats' SCN to see how circadian rhythms were disrupted. They were exposed to equal time periods of light and dark. Those with damaged SCN lost their circadian drinking and activity pattern. This suggests that the SCN is the key pacemaker in circadian rhythms.

Further support - Morgan (1995) found that the removal of the SCN from hamsters caused their circadian rhythms to cease, however when they recived a transplant of an SCN from other hamsters, their rhythms were re-established. This is biologically sound proof that the SCN controls circadian rhythms.

IDA - Both of these studies relied on animals for the research, which are anatomically dissimilar to humans. However, the fact that ther research is focused in the limbic system suggests that it would be possible to apply the findings to human populations due to this area of the brain being the place which all animal brains are said to have evolved from.

Science - These studies support psychology as a science as they are objectively measured using control groups, and have falsifiable biological support due to the research being neurologically based.

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External Zeitgebers - AO2

Support - Siffre (1972) spent 6 months in an underground cave away from external zeitgebers. He had control of unnatural light, meaning he could sleep/wake whenever he wanted. His sleep cycle settled to between 25 to 30 hours, suggesting that his circadian rhythm ran free without the control of natural zeitgebers.

But - This study was a case study, meaning that the sample size is extremely small, thus hard to generalise to a wider population as the results lack population validity. This study, therefore, does not account for individual differences.

Criticism - Czeisler et al (1999) kept 24 participants in a constant level of low light, and established a 28 hour cycle. When readings of temperature and blood chemicals were taken, participants were shown to have adpoted a cycle of 24 hours and 11 minutes. This suggests that external zeitgebers are less important in maintaining circadian rhythms.

IDA - Entrainment provides a more whollistic approach to sleep cycles than the biologically reductionist approach of only considering endongenous pacemakers. Studying the co-operation between the two means that both biological and behavioural factors are considered.

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Disruption of Rhythms - AO1

Jet Lag - This happens when our bodily rhythms become desychronised by flying quickly from one time zone to another. Symptoms include extreme tiredness and slower physical/mental reactions. Phase advance (travelling from west to east) produces more severe jet lag than phase delay (east to west). Some people are more tolerant to jet lag, and experience fewer to no effects, which is known as phase tolerance.

Shift Work - Means that employees are often required to work when they should be sleeping, and is comparable to phase advance in terms of the body's adjustment. There are non-fluctuating shifts and fluctuating shifts, where employees works continually changing shifts week to week. Changing shifts every week does not allow the body time to sychronise with the new circadian rhytm, meaning that sleep is disrputed, causing impaired job performance and health problems.

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Disruption of Rhythms - AO2

Support (JL) - Recht, Lew and Schwartz (1995) studied a US baseball team as they travelled across 4 time zones for games, and analysed their game performance over a 3 year period. It was found that those travelling east to west won 44% of the matched, but those travelling west to east only won 37%, thus suggesting that phase advance negatively effected their game performance.

Study Eval - High ecological validity, as the study was naturalistic, meaning it is possible to generalise the findings. However, the study does not account for individual differences, for example the teams may have had lower talent levels than teams they played, which accounts for the loss rather than the phase advance.

Support (SW) - Czeisler et al (1982) carried out field research in a chemical plant where employees worked backwards shift rotation which changed weekly. They reported high rates of stress, sleep difficulties and health problems. This study provided good applications as Czeisler recommended moving to a forwards rotation every 3 weeks, which gave workers more time to adjust. Nine months later, both worker satisfaction and chemical output had increased.

IDA - These studies have led to useful applications of melatonin to help with phase advance, for example Sharkey (2001) found that it helped to increase body clock adjustment in shift workers.

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Nature of Sleep - AO1

Stages - The stages of sleep is an ultradian rhythm. There are five stages of sleep, four being slow wave sleep (SWS) and the other being rapid eye movement (REM). These cycles occur approximately every 90 minutes.

Characteristics - Stage 1 is the lightest sleep, where alpha waves are replaced by slower, small activity. Stage 2 is still light sleep, but contained K-complex activity, which indicate sleep is becomin deeper. Stage 3 is deep sleep, where there are large amplitude delta waves. Stage 4 is very deep sleep, and is comprised of only delta waves. REM sleep is associated with dreams, and EEG activity shows high frequency, small amplitude patterns similar to wakefulness.

Lifespan - Babies sleep more than adults (16-20 hours), and 50% of this is REM. Children sleep for 7 to hours, with 30% in REM. Teens sleep around 9 to 10 hours, but hormone changes alter their circadian rhythms meaning they are often awake later in the night and have difficulty getting up. Adults sleep for 6 to 8 hours and spend 20% in REM. Elderly sleep around 6 hours with 10% in REM. Stages 3 and 4 also decline in old age. It is difficult to identify how much elderly people sleep as they often nap during the day without realising.

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Nature of Sleep - AO2

IDA - The use of EEG monitors to measure the brain's activity means that research like this supports psychology as a science as it is biologically sound, and used subjective, falsifiable methods of measurement.

Criticism - One argument is that using an EEG could disturb people's sleep due to their awareness of the experiment, thus creating a pattern of sleep which is not their usual pattern, for example spending more time in stage 1 and 2 due to the machine's disturbance. Using an EEG also doesn't show specifically where the brain activity is coming from, such as the limbic system.

Support (Lifespan) - Plat et al found that time spent in SWS between the ages of 25 and 35 drops 15% from 20% in stages 3 and 4, to only 5% in stages 3 and 4. This shows how the body's dependency on restorative sleep decreases with age, compared to children and teens who spend large amounts of time in SWS due to their development.

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Restoration Explanations - AO1

Restoration Theory - Oswald (1980) argued that increased brain activity during REM indicated that the brain was recovering, whilst increased hormonal activity during SWS was the body's restoration and recovery. During SWS, a growth hormone is released which is important for protein synthesis. Thus, the theory suggests that SWS is necessary for bodily growth and repair.

Core Sleep/Optional Sleep - Horne (1988) argues that REM and stage 4 sleep are core sleep which are vital for restoring normal brain functioning, but the other three stages of sleep are optional sleep. This is based on findings that people with sleep deprivation tend to catch up on significant amounts of stage 4 and REM sleep, but not the other three stages. Horne believes that sleep deprivation causes few adverse physical effects, so sleep itself is not necessary for physical restoration.

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Restoration Explanations - AO2

Support - Rechtschaffen and Bergman (1995) deprived rats of sleep for 4 weeks, while observing their appetite, body weight, metabolism and brain activity. The rats started to eat more, but actually lost weight. After two weeks, temperature had become unstable, and weight loss very marked despite increased food intake. Within 3 weeks, they showed signs of immune failure, and most had died within the 4 week study. Sleep appears to be necessary for bodily function to continue, significantly the immune system. This supports the resortation theory.

But - Rats and humans are biologically dissimilar, so the findings may not be applicable to humans. They are also very different in how they use their wakefulness, as they are considerably more active than humans. The results of this study could actualy be due to stress, rather than sleep deprivation, as the methods used to keep the rats awake may have been too stressful and actually led to the immune failures.

Case study support - Randy Gardener stayed awake for 264 hours, and the following week, he experienced a rapid increase in the amount of time spent in stage 4 and REM sleep, suggesting his body needed to recover.

Further support - Coren found that older dogs tend to die after 13 days of sleep deprivation, while puppies die after only 6 days. This suggests puppies need more sleep for growth.

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Evolutionary Explanations - AO1

Protection Theory - Meddis (1975) argues that sleep is an adaptive behaviour to keep us safe from danger. For our early ancestors, night time was a time of danger due to predators and a lack of light, so they were unable to forage. Sleep provided an adaptive way of keeping us out of danger as animals are largely motionless and qiet during sleep, thus they do not draw a predators attention to them.

Hibernation Theory - Webb (1982) argues that sleep is an adaptive behaviour to conserve energy. Sleep, similar to hibernation, is a time when body temperaure falls, and an animal is still, thus uses far less energy than during waking times. Therefore, it makes sense for us to sleep when food is scarce or it is too dangerous to go looking for more e.g. at night. Webb suggests that humans still sleep due to an evolutionary hangover. Sleep is linked into basal metabolic rate, as smaller animals sleep more, and have higher basal metabolic rate, so require more sleep to conserve energy.

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Evolutionary Explanations - AO2

Support (PT) - Lesku et al did a meta-analysis of 54 species sleep patterns. They found that animals with exposed sleeping sites slept for less time than those with hidden sleeping sites e.g burrows. This supports protection theory as it shows that animals who were protected in their sleeping sites were able to sleep for longer.

Criticism - Allison and Ciicchetti (1976) studied sleep in 39 species and found that prey slept for less time than predators, whereas evolutionary theorists would argue that prey would sleep for longer in order to keep out of danger. They suggested that difference in sleep patterns may be due to herbivore/carnivore status or predator/prey status. This means that evolutionary explanations can be contradictory.

IDA - These studies are focused on non-human animals, meaning that the results may not be applicable due to both biological differences and differences in lifestyle e.g. humans do not have predators in every day life. Thus, the use of animal studies means that the results cannot be generalised to modern humans as the findings do not reflect modern lifestyles, due to low time validity.

IDA - In terms of animals, evolutionary theory avoids reductionism as they consider both biological reasons for sleep patterns as well as the factor of the animal's lifestyle.

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Insomnia - AO1

Overview - Primary insomnia is usually chronic, and has no overt medical reason. Secondary insomnia is usually short-term, and can be influenced by other conditions such as Parkinson's or drug addictions. Idiopathic insomnia is a lifelong problem which begins in childhood.

Brain - It is suggested that low levels of GABA can be attributed to sleeplessness. In terms of idopathic insomnia, the reticular activating system (RAS) seems to be at fault. During daylight hours, the RAS keeps us awake, as it stimulates arousal in the brain. This is usually inhibited by areas such as the raphe nuclei. However, patients wih idiopathic insomnia appear to be predisposed to greater arousal, thus suggesting they have an overactive RAS, or underactive raphe nuclei.

Anxiety/stress - Stress causes increased activity in the sympathetic ANS. Modern stress can be things such as divorce, examinations, and money problems. Acute stress can cause insomnia, however the insomnia will usually stop after the stress is solved. Chronic stress can lead to longer term insomnia which can become a vicious cycle of anxiety causing sleeplessness, and sleeplessness causing anxiety. For example, Heath et al (1998) found that the neurotic personality trait links into high levels of reported insomnia.

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Insomnia - AO2

Support (B) - Winkelman et al (2008) studied 16 long-term insomniacs using a polysomnograph, and a non-invasive method of measuring of GABA. They had, on average, 30% lower levels of GABA than non-insomnias. There was also a correlation between levels of GABA and the severity of insomnia. This suggests that low levels of GABA may be linked into sleeplessness.

Aetiological Fallacy - Benzodiazepines used to treat severe insomniacs work by increasing activity of GABA neurons, which has led doctors to believe GABA influences sleeplessness. However this is an aetiological fallacy, as a conclusion is being drawn due to the actions of drugs, while another factor may actually be influencing sleep, such as the psychological actions of actually taking a drug which is supposed to help their insomnia.

Support (S/A) - Morin et al (2003) investigated the role of stress and arousal levels in insomniacs/non-insomniacs. Participants complete self-reports over a 3 week period to record number of stressful events. Insomniacs reported the same number of stressful events as non-insomniacs, but rated them more severely, thus suggesting that a key factor in insomnia is how well people cope with stress.

IDA - Application of theory. Led to stimulus control therapy where patients learn to reassociate bed with sleep, and CBT is often prescribed to help with anxiety relating to sleeplessness.

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Somnambulism - AO1

Overview - More common in childhood, and usually occurs in stages 3 and 4 during the first stage of the night. There are two kinds: sleepwaking, where a person leaves their bed and walks around as if awake, and REM behaviour disorder, which involves the individual acting out a dream.

Bio - Oliviero (2008) suggests that GABA acts an inhibitor during sleep to prevent activity. In children, the neurons involved are still developing, therefore they have insufficient GABA to fully control motor neurons, meaning they move in their sleep. This helps to explain why sleepwalking is more common in childhood.

Genetics - Sleepwalking is ten times more likely if a first degree relative has had a history of sleepwalking, suggesting a genetic link with the disorder. It has been suggested that a specific gene in the family which produces HLA proteins could be linked into the disorder.

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Somnambulism - AO2

Support (B) - Hubin et al (1997) found that while 20% of children are affected by sleepwalking, only 2% of adults are, suggesting that there is a link between development and sleepwalking.

But - However, it could be argued that children are observed more in sleep, thus are more likely to be noticed when sleepwalking. Adults could live alone, which means they may not know they suffer from sleepwalking, which explains the lower percentage of cases.

Support (G) - Lecendreux et al found a 50% concordance rate in MZ twins in comparison to DZ twins where the rate is only 10-15%. This suggests a genetic factor in sleepwalking as MZ twins share 100% of their DNA.

But - As the concordance rate is not 100% for MZ twins, it cannot be concluded that genetics is the only factor which influences sleepwalking. A further factor, such as social or emotional factors may influence a person's likelihood of sleepwalking.

IDA - Research into sleepwalking is biologically deterministic as it suggests that sleepwalking is determined by factors beyond the control of the individual, thus they cannot be held accountable for their actions during an episode of sleepwalking. For example, a crime in which a person drove 14 miles and stabbed his mother-in-law to death was aquitted due to claims of sleepwalking.

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Narcolepsy - AO1

Overview - Narcolepsy is a sleep disorder where the individual experiences frequent sleepiness during the day, and includes symptoms such as cataplexy (loss of muscle tone after emotional stimulation) and hypnogogic hallucinations.

Hypocretin - This is a neurotransmitter thought to be involved in keeping us awake by controlling arousal functions. Narcolepsy is linked to low levels of hypocretin, and even low levels of hypocretin receptors. According to Nishino et al (2000), human narcopletics have lower levels of hypocretin in their brain due to a deteriorative process.

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Narcolepsy - AO2

Support - Lin et al (1999) studied narcolepsy in dogs, and found that a genetic mutation on chromosome 12, which disrupts the way hypocretic is processed, is linked to the causes of narcolepsy in dogs. These findings support the role of low hypocretin in narcoplepsy, as it is a fault with hypocretin which is linked with narcolepsy.

Support - Thannicakel et al (2000) found that human narcopletics have lost around 90% of their hypocretin neurons, thus suggesting that this is linked into the disorder.

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