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  • Created by: alex
  • Created on: 27-12-13 14:21

Circadian Rhythm

  • Circadian rhythms (a type of biological rhythm) - rhythms that last about 24 hours
  • The most studied example is the human sleep-wake cycle in which we sleep around 8 hours every 24 hours.
  • One of the best indicators of the circadian rhythm is core body temperture which is at its lowest around 4:30am (about 36*) and highest at around 6:00pm (around 38*).
  • Hormone production also follows a circadian rhythm - cortisol is at its lowest around midnight and peaks at around 6:00am. Melatonin (which induces sleepiness) and growth hormone are two other hormones that have a clear circadian rhythm, both peaking at around midnight.
  • Internal circadian clock - free running (works without external cues) setting a cycle of about 24-25 hours
  • Under normal circumstances, the internal clock does not work alone, there are external cues (e.g. daylight) that help adjust the internal clock to the environment in which we live.
  • Studies show that circadian rhythms persist despite isolation from natural light which demonstrates the existance for endogenous clock.
  • However, research also shows that external cues are also important because clock was not perfectly accurate; it varied from day to day.
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Circadian Rhythm: studies

  • Siffre studied his own biological rhythms by staying underground in a cave with no external cues for 61 days in the Southern Alps, he resurfaced again believing it was about month earlier than it actually was. He also spent 6 months in a Texan cave and found that his circadian rhythm settled to just over 24 hours but sometimes would change to as much as 48 hours.
  • The only factor influencing his behaviour was his internal (endongenous) clock, therefore, this research shows that circadian rhythms persist despite isolation from natural light which demonstrates the existance of an internal (endogenous) clock.
  • Siffre's research is supported by other studies such as that of Aschoff and Wever who placed participants in an underground WWII bunker in the absence of any environmental and social time cues. They found that most participants displayed circadian rhythms between 24-25 hours in length and some being as long as 29 hours.
  • It shows that our Circadian Rhythms continue regardless of  external cues such as light, as the cycle remained around 24hours, which backs up Siffre's findings. However, the research also shows that external cues are important as the clock was not perfectly accurate: it varied from day to day - it sometimes was unusually long (29 hours), thus external factors must still be influential.
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Circadian Rhythm: studies

  • In fact, research supports the importance of external cues. Folkard conducted an experiment to see if external cues could override the internal clock. 12 participants lived in a cave for 3 weeks and agreed to go to bed and get up at a certain time on the clock. Initially the clock ran normally, but gradually it was quickened so it indicated the passing of 24 hours when in fact only 22 hours had passed. At first, the participants' circadian cycle matched the clock, but not as it quickened.
  • This suggests that the circadian rhythm can only be guided to a limited extent by external cues (such as a clock) and cannot override the internal clock.
  • However, from Siffe's 1962 study to Folkard's 1985 study, this early research meant that there was an important flaw when estimating the 'free-running' cycle of the human circadian rhythm.
  • In the studies, participants were isolated from natural light but not artificial light, because it was thought that dim light would not affect the circadian rhythm. However, more recent research such as that of Czeisler (1999) altered participants' circadian rhythms down to 22 hours and up to 28 hours just by using dim lighting, suggesting that even dim, artificial light affects the circadian rhythm.
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Circadian Rhythm: studies

  • Individual differences could also affect the sleep-wake cycle, such as the cycle length, which, from research suc as that of Czeisler et al, has been found to vary from 13 hours in some people to 65 hours in others.
  • Another individual difference is cycle onset; individuals appear to be innately different in terms of when their circadian rhythms reach their peak. For example, Duffy et al found that larks (morning people) prefer to rise early and go to bed early, and owls (evening people) prefer to go to bed late and get up late.
  • The circadian variation in core body temperature has been linked to cognitive abitlty. For example, Folkard looked at the learning ability of 12-13 year olds who had stories read to them at either 9:00am or 3:00pm. He found that the afternoon group (which would have a higher body temperature at that time) showed superior recall, retained 8% more information than the morning group. This suggests that long-term recall is best when body temperature is at its highest. This is a factor which might be an important consideration when taking examinations.
  • A fundamental flaw with Miche Siffre’s experiment is that it’s a case study, there may be individual differences as he may have different bodily behaviours in comparison to other people. However, because it was experiment and he controlled some extraneous variables (light), allowing for cause and effect to be established.
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Circadian Rhythm: studies

  • It’s a reductionist approach, as human behaviour is more complex than this as people can override biological determined behaviours by making choice of what they do. Thus, just using the biological approach is reductionist, as we have the freewill to stay up over 24hours and are able to override the biological approach. On the other hand we may not be able to override biological rhythms, an example of a young man who was blind from birth and had a circadian rhythm of 24.9 hours. H ewes exposed to various exogenous zeitgebers such as clocks and social cues, yet found great difficulty in reducing his internal place. But when given external queues (clocks/social cues) he found it very difficult to adapt to the rhythm. This suggests that his body clock was the main factor for his cycle to run smoothly, as a result of this it suggests that this is deterministic rather than reductionist.
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Ultradian Rhythms:

  • An ultradian rhythm exists within the sleep portion of the sleep-wake cycle of humans. The first four stages are called NREM sleep (Non-rapid eye movements) and the fifth stage is REM sleep (rapid eye movement). One sleep cycle goes through all five stages and lasts about 90 minutes.

  • Stages 1 and 2 are light sleep, characterised by a change in the electrical activity of the brain. The awake brain produces typical pattern called a beta wave. As you become more relaxed, you’re brain waves become slower, and more regular, and have a greater amplitude (Alpha wave). As you go to sleep the waves slow down even further and have a greater wave frequency (Theta wave).

  • Stage 3 and 4 are characterised by even slower delta waves. These waves are called slow wave sleep (SWS). In deep sleep, most of the bodies physiological repair work is undertaken (production of growth hormones) and important biochemical processes take place (e.g. production of growth hormone). In REM sleep, there is fast, desynchronised EEG activity resembling the awake brain.

  • These cycles continue throughout the night with the SWS period getting shorter and the REM periods getting slightly longer as the night progresses Each time the sleep cycle is about 60 minutes in early infancy, increasing to 90 minutes during adolescence.

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Infradian Rhythms:

  • The most obvious being the menstrual cycle driven by fluctuating hormone levels, with a periodicity of 28 days.
  • Hibernation in some animals such as bears and squirrels is another example, which takes place on an annual basis - they prepare for hibernation for example, by producing extra layers of fat.
  • Seasonal Affective Disorder (SAD) is another example. People who are affected by this become depressed during the winter months and recover during the summer. Reseasrch has shown that the hormones melatonin and serotonin are secreted (by the pineal gland) when it is dark; more darkness means more melatonin, and more melatonin means less serotonin and low levels of serotonin are associated with depression.
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Ultra&Infra Rhythms Evaluation:

  • One issue with studies on REM sleep is the assumption that it is a dreaming sleep. Dement and Kleitman were the first to demonstrate this link. They woke participants up at the times when their brain waves were characterised of REM sleep and found that participants were highly likely to report dreaming. However they also found that dreams were recorded outside REM sleep and that sleepers when awoken in the REM sleep were not always dreaming. The importance of the REM/Dream link is that it potentially provides a way to identify when someone is dreaming and therefore might provide theorists with a way to explain dreaming – for example Hobson and McCarley proposed that dreams are just a psychological read out of random electrical signals typical of REM sleep. Although, such theories of dreaming are based on the erroneous assumption that REM activity = dreaming. 
  • Exogenous cues, the menstrual cycle normally governed by an endogenous system, the release of hormones under the control of the pituitary gland. However, it can be controlled by exogenous queues. Research has shown that when several women live together and do not take oral contraceptives, they tend to menstruate around the same time every month. In one study daily samples of sweat were collected from one group of women and rubbed on the upper lip of women in a second group. The groups were kept separate yet their menstrual cycles became synchronised with their individual odour donor (Russell). This suggests that the synchronization of menstrual cycles can be affected by pheromone chemicals.
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Ultra&Infra Rhythms Evaluation:

  • SAD has been explained in terms of being a natural outcome of infradian rhythms, but alternatively it could be the consequence of a disrupted circadian rhythm. IN the UK, as the seasons change from summer to winter, the circadian rhythms may be through out of phase. People continue to get up at about the same time but often go to bed earlier because its darker earlier. This means the biological systems gets the impression that time is shifting, and the result is similar to jet lag. So external queues may be effecting this. The low levels of these hormones may be a result of these shifts.
  • The understanding of the role of darkness in SAD has led to effective therapies most notably the use of phototherapy as illustrated below. This uses strong lights in the evening / early morning to change the levels of melatonin and serotin. The lights are between 6000 and 10000 lux which is the equivalent to full daylight; a 60 watt light bulb produces about 1000 lux. Sad Suffers have reported tat daily use of such boxes is enough to relieve them of their feelings of lethargy, depression and other related symptoms. However, these are some question about whether this may be due to placebo effect. One study found that a placebo condition was less effective but 32% of participants did improve with the placebo alone (Eastman).
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Ultra&Infra Rhythms Evaluation:

  • Deterministic approach; PMS has been used as a legal defence for examples, in one case a Ms English drove her car into her married lover after an argument, killing him. She was charged with murder but ultimately placed on probation because it was argued in court that her actions were related to severe PMS (Johnson). This suggests that the biological rhythms may be beyond our control. On the other hand, there is evidence that we can will our biological rhythms to change, one study found that people who were told to wake up at earlier times of the night than usual had higher levels of the stress hormone ACTH (which contributes to the waking up process) than normal at the designated time they woke up earlier (Born).
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Endogenous Pacemakers:

  • The main endogenous pacemaker in mammals is the suprachiasmatic nucleus (SCN), which lies in the hypothalamus.
  • The SCN obtains information about light from the eye via the optic nerve. 
  • If endogenous clock is running slowly, morning light automatically shifts the clock ahead, making the rhythm correct with the world outside again.
  • Albus found that the ventral SCN is relatively quickly reset by external cues, but the dorsal SCN is much less affected by light and more resistant to being reset. SCN sends signals to the pineal gland making it produce melatonin at night, melatonin creates sleep because it inhibits the brain mechanisms that promote wakefulness.
  • The imporstant role of SCN has been demonstrated in animal studies. Morgan selectively bred hamsters that had 'mutant' circadian rhythms of 20 hours instead of 24. He then transplanted the SCNs to normal hamsters and found that they displayed the mutant rhythms. Therefore, this implies there is strong evidence to support the theory as it shows how vital the SCN is.
  • DeCoursey removed the SCN of Chipmunks who were then returned to the wild along with a control group with intact SCNs. After 80 days most of the chipmunks without SCNs had been killed by predators because without an SCN they stayed awake foraging and were easier to be located by nocturnal predators.
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Endogenous Evaluation:

  • However, there is a methodological flaw with using animal studies in this area. This is they have been performed on animals. As a result of this, it is difficult to generalise the results displayed by the animals to humans. This is because human beings are far more complex creatures and also systems differ from animal to animal. For example, the biological rhythms of reptiles have a direct input to the pineal gland, whereas for mammals along with humans, the process is mediated by the SCN. Also, there are serious ethical issues to consider when talking about animals, DeCoursey's chipmuks were made more vulnerable to predators. Although, if we acknowledge that this research does have important applications for human behaviour, then the harm to animals might be considered acceptable as long as the key ethics of non-human animal research remain.
  • For ethical reasons, it is difficult to carry out the same experiments on humans (i.e. removing the SCN to study the effect on circadian rhythms) as it would cause physical harm. However, other studies have supported the importance of the role played by the SCN.
  • Siffre spent spent 179 days in a cave in Texas, deprived from any natural light to reset his SCN each day. Siffre's sleep-wake cycle settled to between 25 and 37 hours. This shows that the SCN naturally runs a little slower than 24 hours and must be corrected each day by exposure to natural light.
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Exogenous Zeitgebers:

  • The process of resetting the biological clock with exogenous zeitgebers (entrainment). Opposite is free-running - the biological clock operates in the absence of exogenous cues.
  • Light is the main zeitgeber which resets the body's circadian rhythm each morning, also resets other oscillators located throughout the body because the protein CRY, part of the protein clock, is light sensitive. Light is received via the eyes by the SCN which causes the pineal gland to stop the release of melatonin, and the person awakes.
  • In conditions where people are deprived of light it is difficult to maintain a 24-hour circadian rhythm. People also find it difficult when they travel across time zones because they receive external light cues to wake up (or go to sleep) at times that feel strange to the body.
  • Social cues such as mealtimes and the taking of medications can also act as zeitgebers because they provide cues to the internal clock.
  • This theory has good evidence. Campbell and Murphy found that if you shine a light on the back of the knee, then their circadian rhythms will shift. Consequently, this proves the theory useful as it demonstrates proof that light is the main exogenous zeitgeber.
  • Stevens implies that the exposure to artificial lighting disrupts circadian rhythms and therefore disrupts melatonin production. This could essentially explain why women in industrialised (and well-lit) societies are more likely to develop breast cancer. This is a positive application because it means that we can warn people about the dangers of having lots of lights on all the time.
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Exogenous Evaluation:

  • In some societies , it is not possible to use light and dark as zeitgebers. The inuit in Greenland have periods in the year of 24 hours of light or 24 hours of darkness. Yet they maintain normal 24 hour sleep-wake cycles. For them, the social and work habits, rather than light, are used to synchronise the sleep-wake endogenous pacemaker with the outside world.
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Disruption of biological rhythms:

  • Long distance jet travel can disrupt our circadian rhythms because our internal body clock is no longer synchronized with external zeitgebers such as light and dark. The effects of jet lag can include feelings of tiredness and lack of concentration. These effects tend to worsen when travelling from West to East  (phase advance) than East to West (phase delay). This is because when travelling from West to East, the biological clock is behind local time and so has to catch up. As a result, our circadian rhythms are dramatically disrupted and the symptoms tend to worsen than when the biological clock is ahead of local time. The SCN gradually adjusts to the changed external zeitgebers but takes a few days to do so.
  • A study that supports the claim that West-East travel is more disruptive in terms of circadian rhythms is that of Recht who analysed the performance of American baseball teams over 3 seasons. He found that teams won 37% of away games when they had travelled West to East and 44% after travelling East to West. He claimed that jet lag had affected the players' performance and were worse after phase advance.
  • The problem with this study is that there are many uncontrolled variables that could influence the results, such as the ability of the other team or injuries etc. which makes it difficult to draw conclusions.
  • Other studies such as that of Cho investigated the disruption of bodily rhythms in people who are regularly exposed to jet travel.
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Disruption of biological rhythms:

  • Cho studied aircrew and found that many had raised levels of stress hormones and performed relatively badly on tests of memory compared to a control group. Research studies like these conform that jet travel can lead to problems with cognitive processes and stress-related illness.
  • However, because these studies are correlational, only a casual link can be found and it cannot be assumed that there is a cause and effect between jet travel and symptoms associated with jet lag.
  • However, studies like these have led to improved knowledge of what causes jet lag which in turn has led to an interest in treatments to ease its symptoms.
  • For example, it is claimed that exposure to bright light can shift circadian rhythms during long distance jet travel. Boulos used a head-mounted light visor on an East-West flight across 6 time zones. However, there was no improvement in jet lag symptoms.
  • Shift work also disrupts circadian rhythms because when working at night, a person must be active at a time when their biological clock is telling them to sleep - we are going against our circadian rhythms, trying to maintain alertness when our body is telling us to sleep. Additionally, workers on night shifts must therefore sleep during the day when external zeitgebers such as light and distractions such as noise make sleep difficult. This means that night-shift workers suffer from mild sleep deprivation which makes it difficult to draw conclusions about the effects of disrupting biological rhythms through shift work.
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Disruption of biological rhythms:

  • The negative effects of shift work was demonstrated in the study of Gold who found that nurses on a night-shift had significantly more road accidents than those working during the day.
  • There is also evidence such as that of Davis that the disruption of bodily rhythms through shift work is associated with an increase in the chances of developing breast cancer or heart disease. This is because exposure to light at night time suppresses the normal nocturnal production of melatoninby the pineal gland - and melatonin is thought to be important in preventing tumor growth. In fact, Davis found that women who frequently do not sleep when melatonin levels are usually at their highest have a 14% increase in breast cancer risk.
  • Knowledge of the relationship between biological rhythms and external zeitgebers particularly light has led to applications to cope with the negative effects.
  • E.g. Czeisler changed shift patterns at a chemical plant to make them rotate less frequently and to rotate forwards rather than backwards so that there would be enough time for the resynchronisation of the biological clock.
  • After 9 months on the new shift pattern, there as less absenteeism and workers reported feeling less stressed and with fewer sleep and health problems.
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Nature of sleep:

  • The first four stages are called NREM sleep (Non-rapid eye movements) and the fifth stage is REM sleep (rapid eye movement). One sleep cycle goes through all five stages and lasts about 90 minutes.

  • Stages 1 and 2 are light sleep, characterised by a change in the electrical activity of the brain. The awake brain produces typical pattern called a beta wave. As you become more relaxed, you’re brain waves become slower, and more regular, and have a greater amplitude (Alpha wave). As you go to sleep the waves slow down even further and have a greater wave frequency (Theta wave).

  • Stage 3 and 4 are characterised by even slower delta waves. These waves are called slow wave sleep (SWS). In deep sleep, most of the bodies physiological repair work is undertaken (production of growth hormones) and important biochemical processes take place (e.g. production of growth hormone). In REM sleep, there is fast, desynchronised EEG activity resembling the awake brain.

  • These cycles continue throughout the night with the SWS period getting shorter and the REM periods getting slightly longer as the night progresses Each time the sleep cycle is about 60 minutes in early infancy, increasing to 90 minutes during adolescence.

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Lifespan changes in sleep:

  • As humans grow from infancy to old age there are major changes in the amount and kind of sleep experienced. In newborn babies, REM sleep accounts for over half the total sleep time. They tend to sleep about 16 hours a day, but their sleep is not continuous. By the age of six months a circadian rhythm has become established (one main sleep wake cycle). By the age of five, children have EEG patterns like those of adults but they are still sleeping more and having more REM activity.

  • During childhood, the need for sleep decrease, but in adolescence increases, to about nine of ten hours a night. Circadian rhythms also change so that teenagers feel naturally awake later at night and have more difficulty getting up early (a phase delay).

  • Young adults have about 20% of total sleep time in REM and older adults (70+) having only 10% of their sleep in REM. There is also a reduction in total time sleeping as people age, mostly in the amount of time people spend in stage 3 and 4. People over 60 have half as much stage 3 and 4 sleep compared to someone of 20. Breedlove found that people over the age of 90 lose these stages of sleep completely. Older people also experience a phase advance of circadian rhythms – feeling sleepier early in the evening and waking up earlier.

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Lifespan changes in sleep:

  • One suggestion as to why babies’ sleep patterns are so different from those of adults is that their sleep is an adaptive mechanism to make their parents life easier – daytime sleep means that parents can get on with their chores which enhances survival. Infants’ greater amount of active/REM sleep may be explained in terms of the relative immaturity of the brain, and is related to the considerable amount of learning taking place. REM sleep has been linked to to the production of neurotransmitters and this explains why babies have a significantly greater amount of REM sleep as their brains are greatly developing. It if further supproted by the fact that premature babies (whose brains are even less mature) spend 90% of their time in REM sleep.
  • The change of sleep patterns in adolescence may be linked to changes in hormone production at this age. These hormones are primarily released at night and therefore sleep patterns are disturbed leading to sleep deprivation. Hormone changes can also explain the upset to the circadian clock, which has been described as a delayed sleep phase syndrome by Crowley et al. In fact, research such as that of Wolfson and Carskadon has led to some schools beginning later to accommodate the poor attention span of adolescents in the early morning.
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Lifespan changes in sleep:

  • In adults, the common perception is that a good night’s sleep is related to good health. To test this, Kripke et al surveyed over a million adults and found that there in an increased mortality risk associated with too much sleep. However, this was a correlational theory, and therefore does not account for extraneous variables. This means that a casual relationship cannot be established. It could be that underlying illness or the medication treatment for the illness may lead to increased sleep, and the illness itself led to mortality.

  • The research in this area shows that sleep patterns vary considerably with age, but these patterns are also influenced by cultural values as well as lifestyle habits (such as consumption of a alcohol, amount of exercise and so on). Tynjala et al found that sleep may also reflect cultural differences. Shin found that in Korea, the mean sleep time was about 6.5 hours, and Glanizadeh found that the mean sleep time in Iran was 7.5 hours, both supporting the view that sleep duration is shorter in Asia then Europe. Therefore, such research shows that sleep duration is influenced by cultural practices and reminds us that our view may be biased as it ignores such influences.

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Functions of sleep: Evolutionary

  • The evolutionary theory claims there are 2 major functions for sleep. Webb suggests that when animals sleep, they conserve energy, particularly at a time where it is not easy to forage because most animals are not adapted to be active at night. It is vital for mammals to conserve as much energy as possible to mainatin a constant body temperature, and sleep serves the purpose of providing a period of inactivity to conserve energy.
  • A second adaptive function for sleep is that sleep is constrained by predation risk. If an animal is a predator then it can sleep for longer to conserve energy, whereas for prey, their sleep time is reduced as they must remain alert as much as possible to avoid predators - but still must have some time to sleep as it is a vital function.
  • Meddis claimed that the amount of time that animals spend asleep depends on how safe thay are while sleeping, so animals that sleep in the open would sleep less than animals that slept in nests or burrows.
  • The energy conservation explanation is supported by Phillips; the observation that animals sleep more when food is scarce (many animals hibernate during the winter months), so they are conserving energy at times when it cannot be easily replaced.
  • In addition, Phillips noted that the temperature of mammalian species' bodies drops by 2* while they sleep, which conserves energy. This explanation is further supported by the fact that small animals that have a higher meatbolic rate sleep longer than larger animals with a lower metabolic rate.
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Functions of sleep: Evolutionary

  • This explanation fails to explain why the animal becomes unconscious during normal sleep. However, because the brain uses a large proportion of the body's calories, conservation of energy is best served by limiting its sensory inputs.
  • Research such as that of Allison and Cicchetti supports the predator avoidance explanation. They looked at sleep patterns of 50 species and confirmed the prediction that prey species sleep for less time than predator species. They also confirmed that animals with safe sleeping places sleep longer thatn animals that sleep in the open, where they would be more vulnerable to predators.
  • However, Capellini argued that this previous research was flawed because the methods used to collect the data on sleep from different animals were not standardised and therefore comparisons were meaningless. They carefully selected data from the studies using standardised procedures and found found a negative correlation between metabolic rate and sleep which does not support the energy conservation hypothesis. However, it does support the view that animals with a high metabolic rate need more time to forage for more food and therefore less time to sleep.
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Functions of sleep: Restoration

  • Restoration theorise of sleep argue that sleep is homeostatic, restoring the equilibrium of the body's physiological systems that have been active during the day.
  • Oswald suggests that the high level of brain activity during REM sleep meant that this type of sleep was to restore brain systems. He also noted that during the deeper stages of NREM sleep, there was a surge in growth hormone release, which indicated that NREM sleep was for the restoration of the body's physiological systems.
  • Horne proposed that REM and the deeper levels of NREM sleep  make up 'core sleep' which was essential for the maintenance of brain systems rather than bodily restoration.
  • Oswalds theory is challenged by the finding that strenuous exercise should make people sleep longer to restore the physiological processes that have been active, yet this is not the case. Breedlove found that although in such circumstances people do fall asleep quicker than usual, they do not tend to sleep for longer. He observed that there is a surge of growth hormone during NREM sleep and this has an importanat role in protein synthesis (for the restoration of body tissue).
  • However, Horne pointed out that amino acids, which are necessary to build proteins, are only available for a few hours after a meal so by the time we sleep, the level of available amino acids is low, which means that very little tissue restoration could take place during sleep.
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Functions of sleep: Restoration

  • Horne's claim that core sleep is essential for brain growth is supported by research such as that of Harrison who found that participants who underwent 36 hours of sleep deprivation performed significantly worse on tests of reasoning.
  • However, most sleep deprivation studies taske place in labs that do not reflect real life - people are usually sleep deprived because of stressors such as family, work etc.
  • Although the restoration theory explains the valid point that sleep is important for the maintenance of brain function, the evolutionary approach explains things that the restoration approach can't. Such as if sleep is important for the maintenance of brain function, then don't animals such as dolphins need it as well? EEGF studies have shown that they have no REM sleep. Such sleep patterns may be related to the process fo evolution.
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Insomnia:

  • Primary insomnia is linked to a state of 'hyperarousal'. Heart rate and stress hormones are raised in people with primary insomnia and they tend to shoe high levels of anxiety, which also increases arousal.
  • One explanation is that a period of extreme stress leads to insomni, which is then maintained by the high level of arousal and anxiety about not being able to sleep.
  • Insomnia can also be a secondary effect of a number of conditions such as depression and post-traumatic stress disorder, or the overuse of stimulants such as caffeine and alcohol.
  • Reseasrch such as that of Watson has shown that some people are genetically vulnerable to insomnia in response to these conditions.
  • A problem with the hyperarousal explanation is that reseasrch findings are not consistent. For example, Riemann's study has supported the claim that people with primary insomnia are more likely to have high arousal levels compared to a control group. However, other studies have failed to find any significant difference in levels of arousal between those with primary insomnia and a control group. Adding to this, Morin suggested that there may also be gender differences that need to be taken into account for the diagnosis of primary and secondary insomnia, as women have higher levels of neuroticism and anxiety than men.
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Insomnia:

  • Research has suggested that one of the main causes of primary insomnia is that people may develop the belief that they are unable to sleep, so this expectation then becomes self-fulfilling because the person is tense and anxious when trying to sleep; they have learned to attribute their sleeping difficulties to insomnia.
  • Nisbett used this idea to develop a treatment of insomnia - the reverse placebo effect. They found that insomniacs went to sleep faster than usual when they tooke the placebo pill thought to be arousal pills as they attributed their arousal to the pill and therefore actually relaxed.
  • It is also difficult to identify a casual relationship between psychological disorders and secondary insomnia. For insomnia to be a secondary consequence of depression, the depression must be shown to proceed the insomnia. In order to establish this, information needs to be collected from patients through the use of self-reports which can be unreliable as a way of establishing exactly how depression and insmnia are related for the individual.
  • For example, research such as that of Lichstein showed that although it may be assumed that depression has caused the insomina, insomnia may also lead to depression. Also, Stepanski found that therapeutic interventions for insomnia also simultaneously reduced symptoms of depression, suggesting that insomnia rather than depression was the primary problem.
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Insomnia:

  • A problem for the study of sleep disorders is that it often requires the use of techniques to measure EEG changes in a laboratory. A problem with this approach is that the highly controlled environment may leak to a lack of ecological validity as it cannot be generalised to other situations. For example, the person may regularly sleep with another person whose sleeping patterns contribute to the individual's sleeping difficulties.
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Narcolepsy:

  • Narcolepsy is thought to result from abnormal hypocretin functioning. Hypocretin levels have been found to be very low in patients with narcolepsy; as hypocretin regulates the activity of the hypothalamus (part of brain associated with sleep), it plays an important role in maintaining wakefulness, so a deficiency of hypocretin can trigger the sleep attacks experienced by those with narcolepsy.
  • Mignot found that most patients with narcolepsy do not have abnormal hypocretin gene mutations, which explains why it is not genetic in humans to the same extent as it is for dogs. It also suggests that therefore, it must be due to the damage of the cells that normally secrete hypocretin - and the reason why these cells die is thought to be due to an abnormality in the immune system.
  • Evidence for the role of hypocretin in narcolepsy was discovered by MIgnot who studied canine narcolepsy. He found that these dogs had a mutation in a hypocretin receptor gene, which caused the narcolepsy. He then attempted to breed a colony of narcoleptic zebra fish by obtaining a mutanat fish that lacked hypocretin receptors. However, they did not respond in the same way as narcoleptic humans and therefore did not provide insight into the role played by hypocretin to humans. This shows the limitation of using animals to try and understand the behaviour of humans as zebra fish have hypocretin cells organised in a different way to mammals so their validity to the understanding of humans is limited.
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Narcolepsy:

  • However, there is evidence for the importance of hypocretin in human narcolepsy from Thannickal who found that the brains of individuals with narcolepsy contain less than 10% of the usual number of hypocretin neurons. This reinforces the claim that low levels of hypocretin are associated with the development of narcolepsy.
  • The important role played by hypocretins has implications for the treatment of narcolepsy. As the cause of narcolepsy seens to by a hypocretin deficiency, hypocretin replacement therapy appears to be a suitable option for treatment. In fact, there is some evidence for the effectiveness of this treatment in animals. Hypocretin administration to dogs has shown to lead to increased activity and Sakurai found that injections of hypocretin in rats increased the time the animals spent awake.
  • However, Nishino claimed that the administration of hypocretin is not an effective treatment because it does not cross the blood brain barrier and are limited because they treat the symptoms and not the cause. He suggested therefore that modafinil would be more effective because it treated the cause - by activating the hypocretin-containing neurons.
  • Evidence for the effectiveness of modafinil comes from Broughton, and an additional advantage of modafinil is that it has less potential for abuse than stimulant drugs which are other present drug treatments for narcolepsy.
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Narcolepsy:

  • Despite evidence from dogs, it appears that hypocretin loss in humans is rarely due genes, and it generally doesn't seem to be inherited. This is indicated by Mignot's findings that in cases where one twin has the disorder, it has not been found in the other twin.
  • It is more likely therefore, that hypocretin deficiency is due to an autoimmune disorder.
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Sleep Walking:

  • Sleep walking is a disorder of arousal; a person who is sleep walking is partly awake in the sense that they are normally engaged in activities normally associated with the waking state, but they are also in slow wave sleep (SWS).
  • Recordings of the brain during an episode of sleep walking shows a mixture of delta waves typical of SWS as well as higher frequency beta waves typical of the awake state. Therefore, it looks as if sleep walking occurs when a person in deep sleep is awakened but the arousla of the brain is incomplete.
  • Plazzi found that certain factors seem to increase the likelihood of of sleep walking such as sleep deprivation, alcohol or stress. However, the fact that these factors trigger sleep walking in only some people (i.e. not everyone with sleep deprivation experiences sleep walking) suggests that some individuals may have an inherited vulnerability for sleep walking.
  • In fact, there is evidence that sleep walking may be inherited from research such as that of Broughton who found that the prevalence of sleep walking in first-degree relatives of the affected person is at least 10 times more than that of the general population. Further research from Lecendreux found a 50% concordance rate in identical (MZ) twins compared to 15% DZ twins. This suggests that sleep walking is due to inheritance - and to reinforce this idea, the gene critical for sleep walking (B1*05 gene) has been identified.
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Sleep Walking:

  • However, the diathesis-stress model proposes that genes merely provide a vulnerability for the disorder but it will only occur due to environmental factors. Research such as that of Zadra shows evidence of this. Zadra studied 40 patients who were referred to a sleep lab for suspected sleep walking and were prevented from falling asleep. He found that 50% showed signs of sleep walking on the first night and on the second night, rose to 90%. Therefore, this shows that the sleep deprivation does not lead to sleep walking for normal individuals but acted as a stressor for individuals with a vulnerablity for sleep walking.

  • The diathesis-stress model can also be used to explain the higher frequency of sleep walking in children. It shows that children are more likely than adults to sleep walk because the higher level SWS in childhood acts as a diathesis. The idea that children are more likely than adults because they have more SWS has been supported by other research such as that of Oliviero who found that the system which inhibits motor activity in SWS has not properly developed yet in children, and may be underdeveloped in some adults.

  • Research into sleep walking is important for not only treatment for the disorder but also in aspects such as court cases. There have been murder cases where the disorder has been claimed as a defence. One such example was that of Mr Lowe, accused of killing his father but claimed that he had not recollection of the attack because he was sleep walking - and indeed, tests confirmed that he frequently did sleep walk and so the defence case was proved.

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Clinical characteristics of depression:

  • The formal diagnosis of major depressive disorder requires the presence of five symptoms which must cause clinically significant distress or impairment in general functioning.
  • For a diagnosis of depression, these symptoms must be present all or most of the time and should persist for longer than 2 weeks.
  • There are four general groups of symptoms that apply to all forms of depression. These are affective symptoms (depressed mood or feelings of sadness), cognitive symptoms (inability to concentrate or lowered self-esteem), behavioural symptoms (social withdrawal and restlessness) and physical symptoms (change in sleep pattern or appetite).
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Issues of diagnosis/classification:

  • The reliability of diagnosis is determined by whether the same diagnostic criteria are likely to produce the same diagnosis on two separate occasions and whether or not two independent doctors give the same diagnosis when presented with the same symptoms.
  • One of the main issues around the diagnosis of depression is that reliability is not always as high as it should be . For example, in a study using DSM-IV, Keller found that the reliability of diagnosis over a 6 month period was poor for major depression. He suggested that one of the reasons for this is that a diagnosis of depression requires a minimum of 5/9 symptoms. If an individual is just at the threshold for depression, a disagreement about one iten could result in either a diagnosis or not.
  • In the UK, diagnosis is frequently left to the GP who might get it wrong. Mitchell claimed that depression is misdiagnosed more frequently than it is missed, and this is probably due to the ambiguous criteria of classification systems such as DSM.
  • For a valid diagnosis to be made, the doctor must distinguish between depression and other disorders showing similar symptoms as well as different forms of depression. However, McCullough compared nearly 700 patients and found an overlap of symptoms and responses to treatment, which made it difficult to diagnose accurately.
  • For a doctor to make a valid diagnosis of depression, they must first rule out other possibilities and make sure that physical symptoms are not due to injury or illness.
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Biological Explanations of Depression:

  • A number of studies have shown an increased risk for depression among first-degree relatives of individuals with major depression, with the chances of developing the disorder seemingly dependent on the closeness of the genetic relationship. Family studies have compared individuals of known genetic similarity to see if those who share more of their genes with an individual with depression also have greater risk of developing the disorder themselves, therefore supporting the claim.
  • One such study is that of Gershon who analysed the results of ten family studies and found that the rates of depression in first-degree relatives was 30% higher than rates in the general population. 
  • However, this increased risk of developing depression when a close family member already has been diagnosis of the disorder might not be entirely due to genetics. It may instead be the result of a shared environment, with children acquiring their depressed mood and associated behaviours as a result of observing their parents.
  • In fact, twin studies have also provided evidence for the link between genetics and depression. MZ twins have identical genetic material, whereas DZ twins share only 50% of their genetic material. If we assume that twins share roughly the same environment, then any greater similarity between MZ twins compared to DZ twins in term of depression can be explained in terms of their greater genetic similarity.
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Biological Explanations of Depression:

  • Studies support this such as that of McGuffin who found a concordance rate of 46% for MZ twins and 20% of DZ twins, suggesting that depression has a substantial genetic component. However, this also demonstrates that genetics cannot be the only explanation, as otherwise the concordance rate for MZ twins would be 100%. This might be explained by the diathesis-stress model, which suggests that individuals may inherit a vulnerability for depression, which only leads to depression when the individual is exposed to significant life stressors.
  • However, a problem with the use of twin studies is that twins share their environment and so tend to be subject to the same influences. This has meant that researchers are turning to adoption studies as a better test of the genetic explanation, because such studies can use individuals who are genetically related but exposed to different environments as a result of being adopted. This enables researchers to study the influence of genetics without the confounding influence of environment.
  • The largest adoption study in this area was carried out by Wender et al (1986). They interviewed people who had been adopted and found that they were eight times more likely to develop depression if their biological parents were depressed.
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Biological Explanations of Depression:

  • However, more recent studies have suggested that having an adoptive parent with depression was also a significant risk factor for developing depression. Tully et al (2008) found that adopted children who had an adoptive parent with depression were significantly more likely to develop depression themselves than were children in an adoptive family with no evidence of depression. These two studies suggest that both genetics and rearing environment are influential in the development of depression.
  • The influence of genetics is also demonstrated in a study by Kendler who studied over 15000 twins using the Swedish Twin Registry and estimated from the data that the heritability of major depressive disorder is 38%, with a higher risk for women than men. There are many explanations for why women should be more at risk of depression than are men. One explanation is that any gene for depression may be located in the X chromosome. Women have two X chromosomes, while men only have one, which might explain why women are generally twice as more likely to be diagnosed with depression than men. However, psychological explanations – for example male reluctance to report illness, are more generally accepted as an explanation for this gender difference.
  • Trying to establish which genes are involved in depression has been a challenge for researchers. Some studies have found a defect in the 5-HTT gene responsible for the transmission of serotonin in people suffering from depression. Low levels of serotonin has been associated with depression.  
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Biological Explanations of Depression:

  • However, some argue that genes such as 5-HTT do not directly cause depression but instead change the way the person responds to environmental stressors, which for some people makes depression more likely. This is further evidence for the diathesis-stress model, as it demonstrates that some people are more likely to develop depression because of an inherited vulnerability, in this case an abnormality in the 5-HTT gene.
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