Sleep walking is a parasomnia in which an individual engages in activities normally characterised by the awake brain. This is most common in childhood, affecting 20% of children and less than 3% of adults. It most commonly occurs during NREM and slow wave sleep (SWS). It is believed to be a disorder related to arousal with EEG recording during sleep walking showing a mixture of delta waves, typical of SWS, but also beta waves, characteristic of the awake brain. Theories propose it occurs when a person in SWS is woken but arousal in the brain is incomplete therefore causing the disorder.
Another explanation suggests sleep walking is a developmental disorder. It is suggesting that the system that normally reduces motor activity in SWS is not sufficiently developed in some children and it also may be underdeveloped in some adults causing the disorder.
Sleep walking can be explained using the diathesis-stress model which proposes that a genetic vulnerability may be the underlying cause. But, sufficient environmental triggers are needed to trigger the disorder. Other medical disorders such as fever, asthma, seizures, sleep apnoea and psychiatric disorders have been linked to sleep walking suggesting it may be the cause of a symptom of another underlying problem.
Broughton et al found it is ten times more likely for sleep walking to occur if a first degree relative has a history of sleep walking, compared to the general population, supported in twin studies and close family members both showing sleep walking, providing evidence of a genetic link for the disorder. However, sleep walking will not always despite a genetic vulnerability. Therefore environmental factors likely influence sleep walking e.g. stress, alcohol and sleep deprivation have been linked to sleep walking. This provides support for the diathesis-stress model and highlights how nature and nurture may interact causing an individual with a genetic vulnerability yo show the disorder.
Lecendreux et al reported a 50% concordance rate in MZ twins showing sleep walking compared to 10-15% in DZ twins suggesting a genetic link. This also highlights the importance of environmental influences as MZ twins did not have 100% concordance, suggesting the environment plays a mitigating role. MZ twins likely experience similar environmental influences due to them looking similar. This may have an influence on psychological development causing them to develop similar disorders due to being treated similarly by those around them. However, twin studies may lack external validity as twins will experience different environmental factors than the rest of the population therefore results may not be generalisable to the population therefore results may not be generalisable and findings may not explain how others develop sleep walking.
Understanding sleep walking has real world application. In some cases it has been used as legal defence for murder. Therefore it is important to establish the level of control an individual has while sleep walking. In one case Jules Low attacked and killed his elderly father, citing sleep walking as a defence. He was ultimately acquitted after tests showed he had a tendency to sleep walk. But, it is unclear whether this was the case during the attack. Some may voluntarily expose themselves to risk factors while others may not. Therefore improving our understanding of sleep walking is essential to establish whether individuals can be held responsible for behaviour.
Both Broughton and Lecendreux research focused on the assumption that sleep walking has a biological cause and both can be argued to have found evidence for such an assumption. However, through such research it is suggested environment plays a role too. Explaining sleep walking through purely biological means is reductionis and fails to explain the complex nature of sleep walking that occurs through the interaction of genes and the environment. Also such explanations do not consider the role of free will,therefore argued to be deterministic. However, if certain environmental stressors increase sleep walking occurrence, by controlling environmental factors we can reduce incidents of sleep walking, even with genetic vulnerabilities helping us to gain further understanding of sleep walking as a disorder.
Showing posts with label Sleep and biological rhythms. Show all posts
Showing posts with label Sleep and biological rhythms. Show all posts
Sunday, 31 May 2015
Outline and evaluate narcolepsy as a sleep disorder (8+16)
Narcolepsy means 'seized by sleepiness', symptoms include; bouts of extreme sleepiness during the day, cataplexy, a loss of muscle tone causing the individual to collapse. These are often brought on by extremes of emotion e.g. excitement or rage. Sleep paralyse may occur which is an inability to move just before falling asleep or waking up. Hypnagogic hallucination may occur when awake making it hard to distinguish between reality and hallucinations. Normally beginning in adolescents or early childhood and may continue throughout life.
One explanation is it is a malfunction in the system that regulates REM sleep. This may explain symptoms such as cataplexy and REM type hallucinations. Cataplexy may be explained through neurons in the medulla, that are normally active during REM sleep, become active while the individual is awake and sends signals to the spinal cord to suppress skeletal muscle movement during waking hours. Another explanation links to lower levels of hypocretin, and narcolepsy, as this is a hormone which promotes wakefulness. Mutations on genes that control hypocretin release have been linked to narcolepsy.
Nishino et al found those with narcolepsy had lower levels of hypocretin within their cerebrospinal fluid. However, correlational data cannot conclude whether low levels of hypocretin caused narcolepsy or whether it was only a symptom. Low levels of hypocretin have been suggested to have a genetic link however narcolepsy does not always run in families weakening a purely biological explanation to the disorder. Lower hypocretin levels maybe due to environmental factors such as brain injury, infection or a result of an auto-immune attack. To assume that hypocretin is solely responsible for narcolepsy is reductionist as we do not fully understand the complex process, and we may be over simplifying it to out own understanding.
Honda et al suggested another explanation of a link to a mutation in the immune system, linking to Nishino's suggestion of an auto immune attack being a possible cause. Studying narcoleptic patients they found an increased type of HLA. This link was observed in all Japanese patients studies with a similar association of 85% in Caucasians supporting the link. However, in African-Americans this was only present in 65-67% of narcoleptics. Therefore it is likely cultural and biological factors work together to predispose someone to narcolepsy. As this HLA variant was not found in all narcoleptics across cultures it suggests a lack of external validity and limits what generalisations can be made. A criticism for the HLA link is that higher amounts of HLA are present in both narcoleptics and the general population who do not suffer the disorder. Therefore suggesting HLA is the only cause is reductionist as it may be only indirectly involved.
A psychological explanation may be used in a small number of cases where narcolepsy has been found to run in families. Some form of the disorder may show and cause others to feel sleepy around them e.g. through yawning. Although, when considering the sever nature of symptoms, e.g. cataplexy, a psychological explanation in unlikely to be the cause, and most evidence points towards a biological cause.
Both Nishino and Honda's studies link narcolepsy to a biological cause, but ignores the role of environmental factors, making it reductionist, as these may trigger the disorder. Through such research it is suggested that nature and nurture work together in order to predispose someone to a narcoleptic attack. For example someone with a vulnerability to narcolepsy may need the right environmental trigger e.g. strong emotions for symptoms to show highlighting how the two work together. Therefore both biological and environmental factors will need to be considered in order to help those manage symptoms of the disorder. However, such studies often ignore the role of free will, making it deterministic. If emotional arousal causes its onset then, as we have some level of control over our emotions, we can control it to some extent. Therefore research has positive real world applications as mood controlling therapies such as CBT and self-talk may allow us to better control out emotions therefore we can have a better control of narcolepsy onset.
One explanation is it is a malfunction in the system that regulates REM sleep. This may explain symptoms such as cataplexy and REM type hallucinations. Cataplexy may be explained through neurons in the medulla, that are normally active during REM sleep, become active while the individual is awake and sends signals to the spinal cord to suppress skeletal muscle movement during waking hours. Another explanation links to lower levels of hypocretin, and narcolepsy, as this is a hormone which promotes wakefulness. Mutations on genes that control hypocretin release have been linked to narcolepsy.
Nishino et al found those with narcolepsy had lower levels of hypocretin within their cerebrospinal fluid. However, correlational data cannot conclude whether low levels of hypocretin caused narcolepsy or whether it was only a symptom. Low levels of hypocretin have been suggested to have a genetic link however narcolepsy does not always run in families weakening a purely biological explanation to the disorder. Lower hypocretin levels maybe due to environmental factors such as brain injury, infection or a result of an auto-immune attack. To assume that hypocretin is solely responsible for narcolepsy is reductionist as we do not fully understand the complex process, and we may be over simplifying it to out own understanding.
Honda et al suggested another explanation of a link to a mutation in the immune system, linking to Nishino's suggestion of an auto immune attack being a possible cause. Studying narcoleptic patients they found an increased type of HLA. This link was observed in all Japanese patients studies with a similar association of 85% in Caucasians supporting the link. However, in African-Americans this was only present in 65-67% of narcoleptics. Therefore it is likely cultural and biological factors work together to predispose someone to narcolepsy. As this HLA variant was not found in all narcoleptics across cultures it suggests a lack of external validity and limits what generalisations can be made. A criticism for the HLA link is that higher amounts of HLA are present in both narcoleptics and the general population who do not suffer the disorder. Therefore suggesting HLA is the only cause is reductionist as it may be only indirectly involved.
A psychological explanation may be used in a small number of cases where narcolepsy has been found to run in families. Some form of the disorder may show and cause others to feel sleepy around them e.g. through yawning. Although, when considering the sever nature of symptoms, e.g. cataplexy, a psychological explanation in unlikely to be the cause, and most evidence points towards a biological cause.
Both Nishino and Honda's studies link narcolepsy to a biological cause, but ignores the role of environmental factors, making it reductionist, as these may trigger the disorder. Through such research it is suggested that nature and nurture work together in order to predispose someone to a narcoleptic attack. For example someone with a vulnerability to narcolepsy may need the right environmental trigger e.g. strong emotions for symptoms to show highlighting how the two work together. Therefore both biological and environmental factors will need to be considered in order to help those manage symptoms of the disorder. However, such studies often ignore the role of free will, making it deterministic. If emotional arousal causes its onset then, as we have some level of control over our emotions, we can control it to some extent. Therefore research has positive real world applications as mood controlling therapies such as CBT and self-talk may allow us to better control out emotions therefore we can have a better control of narcolepsy onset.
Saturday, 30 May 2015
Outline and evaulate explanations for insomnia (8+16)
Insomnia is the 'inability to sleep', including struggling to fall asleep (initial insomnia), difficultly remaining asleep (middle insomnia) or waking up too early (terminal insomnia). Risk factors that influence insomnia can include age or gender with women being more likely to suffer. Older age groups may suffer health problems, which in turn affects sleep quality.
There are two types of insomnia; primary which is a disorder on its own and secondary which is a symptom of another underlying problem. Primary insomnia is sleeplessness not attributed to any medical, psychiatric or environmental cause, lasting over a month, according to the DSM. Primary insomnia consists of two sub types; pyschophysiological insomnia, a form of anxiety induce insomnia, referred to as learnt or behavioural insomnia. As the individual worries about falling asleep, and becomes tense making it harder to sleep. Idiopathic insomnia has no visible cause. It is a lifelong syndrome, apparent from birth, and is theorised to be caused by an under active sleep system or over active awakening system.
Horne suggested that there is only secondary insomnia and with 'primary insomnia' the cause is yet to be identified. Secondary insomnia is a symptom of another underlying cause e.g. depression or heart disease. It could also be due to due caffeine or alcohol intake or medication. Therefore treating the underlying cause should help treat the insomnia e.g. those suffering from depression may sleep better after taking anti-depressants.
Spielman et al proposed a distinction of component of insomnia. Predisposing factors may include a genetic vulnerability or physiological factors such as hyperarousal. In order for insomnia to be triggered the Diathesis-stress model proposes environmental factors are needed to expose the predisposed vulnerability, therefore triggering insomnia. Perpetuating factors such as stress and tension contribute to maintaining insomnia and may explain how chronic insomnia develops. This suggests that insomnia is a complex disorder and therefore it may be appropriate to consider these different component in deciding on appropriate treatment.
Morin et al examined the relationship between stress, coping skills and pre-sleep arousal between good sleepers and insomniacs. Both groups reported similar stressful events but insomniacs rated minor daily hassles with greater intensity compared to good sleepers suggesting personality may be a risk factor. Those with internalising problems will have higher levels of emotional arousal which can contribute to the onset of insomnia. However, with the correctional data we cannot establish cause and effect, it may be those who suffer insomnia also suffered more stress life events, and not reported all of them, than the control group. Therefore results may lack internal validity, and such confounding variables affect the generalisation of results therefore we cannot determine the extent to which personality and the ability to cope with stress links to insomnia. However, positive real world applications come from research such as developing therapies such as CBT in order to reduce symptoms. If stress can be managed it may reduce tendencies for insomnia.
Roth et al found insomnia often proceeded rather than followed cases of mood disorders suggesting it may be beneficial to treat the insomnia regardless of it being primary or secondary. This study used a large sample of 15,000 Europeans which is beneficial as it increases the reliability of findings allowing for wider generalisations. This gives us a greater understanding of the disorder and that in some cases the insomnia may cause other disorders.
Such research by Spielman, Morin and Roth highlights the complex nature of the disorder and suggests insomnia can have different attributable causes therefore it is deterministic to assume that all cases can be identified or attributed to a cause. Chronic insomnia is highly complex and for it to be broken down and explained in any simple way is reductionist. Reliability and validity of measures of insomnia have been criticised as they are based on reports of patients and interviews. Interviewers may interpret the information differently than what the patient intended, highlighting the subjective nature of diagnosing insomnia itself.
There are two types of insomnia; primary which is a disorder on its own and secondary which is a symptom of another underlying problem. Primary insomnia is sleeplessness not attributed to any medical, psychiatric or environmental cause, lasting over a month, according to the DSM. Primary insomnia consists of two sub types; pyschophysiological insomnia, a form of anxiety induce insomnia, referred to as learnt or behavioural insomnia. As the individual worries about falling asleep, and becomes tense making it harder to sleep. Idiopathic insomnia has no visible cause. It is a lifelong syndrome, apparent from birth, and is theorised to be caused by an under active sleep system or over active awakening system.
Horne suggested that there is only secondary insomnia and with 'primary insomnia' the cause is yet to be identified. Secondary insomnia is a symptom of another underlying cause e.g. depression or heart disease. It could also be due to due caffeine or alcohol intake or medication. Therefore treating the underlying cause should help treat the insomnia e.g. those suffering from depression may sleep better after taking anti-depressants.
Spielman et al proposed a distinction of component of insomnia. Predisposing factors may include a genetic vulnerability or physiological factors such as hyperarousal. In order for insomnia to be triggered the Diathesis-stress model proposes environmental factors are needed to expose the predisposed vulnerability, therefore triggering insomnia. Perpetuating factors such as stress and tension contribute to maintaining insomnia and may explain how chronic insomnia develops. This suggests that insomnia is a complex disorder and therefore it may be appropriate to consider these different component in deciding on appropriate treatment.
Morin et al examined the relationship between stress, coping skills and pre-sleep arousal between good sleepers and insomniacs. Both groups reported similar stressful events but insomniacs rated minor daily hassles with greater intensity compared to good sleepers suggesting personality may be a risk factor. Those with internalising problems will have higher levels of emotional arousal which can contribute to the onset of insomnia. However, with the correctional data we cannot establish cause and effect, it may be those who suffer insomnia also suffered more stress life events, and not reported all of them, than the control group. Therefore results may lack internal validity, and such confounding variables affect the generalisation of results therefore we cannot determine the extent to which personality and the ability to cope with stress links to insomnia. However, positive real world applications come from research such as developing therapies such as CBT in order to reduce symptoms. If stress can be managed it may reduce tendencies for insomnia.
Roth et al found insomnia often proceeded rather than followed cases of mood disorders suggesting it may be beneficial to treat the insomnia regardless of it being primary or secondary. This study used a large sample of 15,000 Europeans which is beneficial as it increases the reliability of findings allowing for wider generalisations. This gives us a greater understanding of the disorder and that in some cases the insomnia may cause other disorders.
Such research by Spielman, Morin and Roth highlights the complex nature of the disorder and suggests insomnia can have different attributable causes therefore it is deterministic to assume that all cases can be identified or attributed to a cause. Chronic insomnia is highly complex and for it to be broken down and explained in any simple way is reductionist. Reliability and validity of measures of insomnia have been criticised as they are based on reports of patients and interviews. Interviewers may interpret the information differently than what the patient intended, highlighting the subjective nature of diagnosing insomnia itself.
Outline the nature of sleep (8)
Sleep is a state of consciousness where responsiveness to external environment is diminished. It occurs daily as a circadian rhythm with the average adult sleeping for 8 hours out of 24. Within sleep itself, an ultradian rhythm exists with 5 distinguishable stages. EEG machines have helped us to identify these stages objectively.
Lifespan changes occur within sleep. Infants sleep up to 16 hours a day with 15% spent in REM. After 1 year REM decreases and total sleep time is about 13 hours a day, with an entire sleep cycle taking 45-60 minutes to complete. In childhood 30% of sleep is spent in REM with about 12 hours a day spent sleeping. In adulthood to complete on sleep cycle takes about 90 minutes and consists of both slow wave sleep (SWS) or NREM and rapid eye movement (REM) sleep. Throughout the night the length of time in REM increases with each cycle and NREM decreases.
The sleep stages consist of stages 1 and 2 which are periods of light sleep and people are easily woken. Alpha waves, characteristic of the awake brain begin to disappear. Slower theta waves, sleep spindles and k-complexes high in amplitude are recorded. Heart rates slows, metabolic rate and temperature drop and brain waves begin to slow down.
Stages 3 and 4 are states of deeper sleep and it is harder to wake someone in these stages. Delta waves become evident in brain activity. These stages are also known as slow wave sleep (SWS). During SWS growth hormones are released to repair proteins and cell synthesis occurs. Metabolic rate, heart rate and temperature are at their lowest points.
Stage 5 is also known as REM or rapid eye movement sleep. In this stage the body is paralysed but the eyes are moving. This state is often linked to dreaming and brain waves resemble that of someone who is awake.
Lifespan changes occur within sleep. Infants sleep up to 16 hours a day with 15% spent in REM. After 1 year REM decreases and total sleep time is about 13 hours a day, with an entire sleep cycle taking 45-60 minutes to complete. In childhood 30% of sleep is spent in REM with about 12 hours a day spent sleeping. In adulthood to complete on sleep cycle takes about 90 minutes and consists of both slow wave sleep (SWS) or NREM and rapid eye movement (REM) sleep. Throughout the night the length of time in REM increases with each cycle and NREM decreases.
The sleep stages consist of stages 1 and 2 which are periods of light sleep and people are easily woken. Alpha waves, characteristic of the awake brain begin to disappear. Slower theta waves, sleep spindles and k-complexes high in amplitude are recorded. Heart rates slows, metabolic rate and temperature drop and brain waves begin to slow down.
Stages 3 and 4 are states of deeper sleep and it is harder to wake someone in these stages. Delta waves become evident in brain activity. These stages are also known as slow wave sleep (SWS). During SWS growth hormones are released to repair proteins and cell synthesis occurs. Metabolic rate, heart rate and temperature are at their lowest points.
Stage 5 is also known as REM or rapid eye movement sleep. In this stage the body is paralysed but the eyes are moving. This state is often linked to dreaming and brain waves resemble that of someone who is awake.
Outline and evaluate lifespan changes in sleep (8+16)
Sleep changes occur throughout life with infants sleeping the longest, up to 16 hours a day. 15% of this is spent in REM sleep. However, sleep is not continuous and they tend to wake up every hour due to their sleep cycles being shorter than adults and their need to feed regularly. Sleep stages are similar to adult SWS and REM but are immature versions known as quiet and active sleep. After 1 year REM decreases and brain activity begins to resemble that of an adult with total sleep time being around 13 hours a day with the entire sleep cycle taking 45-60 minutes. In childhood 30% of sleep in REM with about 12 hours per day spent sleeping.
There are several explanations as to why babies have this longer sleep period. One explanation is based on an evolutionary approach. This suggests babies sleep longer to allow parents to carry out daily duties therefore this sleep pattern is adaptive. However, as with any evolutionary explanation that are purely speculative and cannot be proven conclusively as they are post hoc.
The biological approach provides a different explanation explaining that babies sleeping patterns are due to their immaturity. Longer sleep patterns may be due to the vast amount of learning that is taking place. REM has been linked to production of neurotransmitters and consolidation of memory. As babies are born immature, they are expected to sleep more therefore this approach suggests sleep is important for mental health and development. Evidence for this comes from non-human animal studies such as dolphins. They are born mature and are able to swim and have almost no REM sleep. This supports that a biological approach can explain lifespan changes in sleep and why babies spend a vast amount of time sleeping. However, results from non-human animal studies lack external validity due to differences of anatomy between them and humans. The study can only suggest why such sleep behaviours occur, it cannot provide conclusive evidence to explain babies sleep patterns. However, such studies can help towards drawing conclusions. Without any studies this approach would be purely speculative.
Stickgold et al suggest may link to human development as we age. Evidence suggests REM may be linked to consolidation of procedural memory whereas SWS may be important for semantic and episodic. This may explain why REM is high in babies as they rapidly develop and also whit it decreases with age. This supports the assumption of lifespan changes occurring within sleep. Therefore provides validity to the theory of lifespan changes occurring. However, them memory consolidation process is difficult to measure. Therefore we are making the assumption that REM is linked to this based on correctional data which may decrease its reliability. However, it can be concluded changes in REM and SWS occur as we age with evidence of this coming from EEG recordings.
Another significant lifespan change in sleep occurs during old age. Adults typically sleep for 8 hours going through the sleep/wake cycle stages, with 25% of sleep spent in REM sleep and in old age sleep time remains roughly the same. Although REM sleep decreases to 20% of total sleep time and SWS is as low as 5% or non-existent in some, meaning less growth hormone is released for bodily repair. Age may bring a phase advance in circadian rhythm, feeling sleepier earlier and waking up earlier.
The reduction of sleep in old age may be due to health problems which affect sleep, not purely due to lifespan changes. Sleep disorders such as sleep apnoea interrupts sleep and may be used to explain why SWS is lower as sleep is more easily disturbed resulting in less growth hormone being produced, from less time spent asleep. Therefore research has ed to practical application of treatments being created e.g. melatonin supplements to aid sleep. Highlighting how research can be used in the real world to produce treatments to aid in better sleep.
There are several explanations as to why babies have this longer sleep period. One explanation is based on an evolutionary approach. This suggests babies sleep longer to allow parents to carry out daily duties therefore this sleep pattern is adaptive. However, as with any evolutionary explanation that are purely speculative and cannot be proven conclusively as they are post hoc.
The biological approach provides a different explanation explaining that babies sleeping patterns are due to their immaturity. Longer sleep patterns may be due to the vast amount of learning that is taking place. REM has been linked to production of neurotransmitters and consolidation of memory. As babies are born immature, they are expected to sleep more therefore this approach suggests sleep is important for mental health and development. Evidence for this comes from non-human animal studies such as dolphins. They are born mature and are able to swim and have almost no REM sleep. This supports that a biological approach can explain lifespan changes in sleep and why babies spend a vast amount of time sleeping. However, results from non-human animal studies lack external validity due to differences of anatomy between them and humans. The study can only suggest why such sleep behaviours occur, it cannot provide conclusive evidence to explain babies sleep patterns. However, such studies can help towards drawing conclusions. Without any studies this approach would be purely speculative.
Stickgold et al suggest may link to human development as we age. Evidence suggests REM may be linked to consolidation of procedural memory whereas SWS may be important for semantic and episodic. This may explain why REM is high in babies as they rapidly develop and also whit it decreases with age. This supports the assumption of lifespan changes occurring within sleep. Therefore provides validity to the theory of lifespan changes occurring. However, them memory consolidation process is difficult to measure. Therefore we are making the assumption that REM is linked to this based on correctional data which may decrease its reliability. However, it can be concluded changes in REM and SWS occur as we age with evidence of this coming from EEG recordings.
Another significant lifespan change in sleep occurs during old age. Adults typically sleep for 8 hours going through the sleep/wake cycle stages, with 25% of sleep spent in REM sleep and in old age sleep time remains roughly the same. Although REM sleep decreases to 20% of total sleep time and SWS is as low as 5% or non-existent in some, meaning less growth hormone is released for bodily repair. Age may bring a phase advance in circadian rhythm, feeling sleepier earlier and waking up earlier.
The reduction of sleep in old age may be due to health problems which affect sleep, not purely due to lifespan changes. Sleep disorders such as sleep apnoea interrupts sleep and may be used to explain why SWS is lower as sleep is more easily disturbed resulting in less growth hormone being produced, from less time spent asleep. Therefore research has ed to practical application of treatments being created e.g. melatonin supplements to aid sleep. Highlighting how research can be used in the real world to produce treatments to aid in better sleep.
Outline and evaluate evolutionary explanations as a function of sleep (8+16)
The four main evolutionary theories all explain sleep as an adaptive response to aid survival.
Energy conservation theory suggests warm blooded mammals must conserve energy in order to maintain a constant body temperature. This is problematic for smaller mammals as they have higher metabolic rates therefore use more energy. Evolutionary theorists argue sleep enforces periods of inactivity to conserve energy, as metabolism is lower when asleep.
Food requirements have been suggested to determine sleep. All animals need to eat to survive therefore sleep may have evolved around this. Herbivores such as cows eat food low in nutrients therefore spend a vast amount of time grazing, and little time sleeping. Carnivores such as lions eat food high in nutrients therefore can afford to spend less time eating. they also have no predation risk therefore can spend more time sleeping.
Meddis proposed the 'waste of time hypothesis' suggesting sleep serves the purpose of helping animals to avoid predators when they are most vulnerable, as sleeping ensures they remain still when they have nothing better to do.
Predator avoidance links to this and Siegel et al argued it would be riskier for the animal to stay awake due to predator risk and risk on injury. He suggested sleep could enable both energy conservation and predator avoidance, as long as the animal sleeps in hidden safe places.
Cappellini et al found a negative correlation between metabolic rate and sleep in smaller mammals, having a higher metabolic rate but sleeping less supporting that food requirements may influence sleep. Smaller mammal, with a high metabolic rate, will have to eat more frequently in order to sustain their high metabolic rate, creating a restrain on sleep, as they must spend more time foraging. Suggesting a trade off between sleep and foraging. Within the study a standardised procedure was used therefore provides more reliable results with higher internal validity. However, this study only focuses on land mammals therefore may not be generalisable to all species, therefore lacks external validity. It also does not explain how evolutionary pressures affect sleep patterns for all species.
Horne et al proposed a combined approach to try and explain areas which a purely evolutionary theory failed to explain such as why we have a strong drive for sleep when deprived. This approach proposed some elements of sleep are for restoration and some are for occupying unproductive hours e.g. conserving energy, for small animals. This suggests that evolutionary approaches do have validity however individually they cannot fully explain function of sleep. Horne also proposed a distinction between core and optional sleep. Core sleep is equivalent to SWS and optional is equivalent to REM. Optional sleep is argued to be dispensable and used to occupy unproductive hours and used to conserve energy supporting the energy conservation theory. However, restoration theorists would argue REM plays an important role in brain functioning and is not simply used to waste time.
Both Capellini and Horne's research can provide support towards some explanations with the evolutionary approach of sleep. However, research cannot provide conclusive evidence towards one sole evolutionary theory highlighting the subject is inconclusive and debatable. However, they suggest how sleep has evolved to aid survival for example the Indus dolphin sleeps for short periods of time, of a few seconds, in order to avoid debris. Such pressures could be argues to play an overriding factor in sleep behaviour as they determine the animal's survival chances, providing support for an evolutionary function of sleep.
Many studies are based on animals therefore findings cannot be generalised to humans as our environmental pressures are different e.g. we have no predator risk and food is generally available. Therefore according to the evolutionary approach we should not need to sleep, but we sleep for 8 hours a day. This highlights a possible biological and restorative need rather than being controlled by evolutionary pressures. Humans generally dictate their sleep patterns, yet evolutionary explanations ignore this therefore are deterministic, ignoring our own conscious decisions in sleep patterns.
Energy conservation theory suggests warm blooded mammals must conserve energy in order to maintain a constant body temperature. This is problematic for smaller mammals as they have higher metabolic rates therefore use more energy. Evolutionary theorists argue sleep enforces periods of inactivity to conserve energy, as metabolism is lower when asleep.
Food requirements have been suggested to determine sleep. All animals need to eat to survive therefore sleep may have evolved around this. Herbivores such as cows eat food low in nutrients therefore spend a vast amount of time grazing, and little time sleeping. Carnivores such as lions eat food high in nutrients therefore can afford to spend less time eating. they also have no predation risk therefore can spend more time sleeping.
Meddis proposed the 'waste of time hypothesis' suggesting sleep serves the purpose of helping animals to avoid predators when they are most vulnerable, as sleeping ensures they remain still when they have nothing better to do.
Predator avoidance links to this and Siegel et al argued it would be riskier for the animal to stay awake due to predator risk and risk on injury. He suggested sleep could enable both energy conservation and predator avoidance, as long as the animal sleeps in hidden safe places.
Cappellini et al found a negative correlation between metabolic rate and sleep in smaller mammals, having a higher metabolic rate but sleeping less supporting that food requirements may influence sleep. Smaller mammal, with a high metabolic rate, will have to eat more frequently in order to sustain their high metabolic rate, creating a restrain on sleep, as they must spend more time foraging. Suggesting a trade off between sleep and foraging. Within the study a standardised procedure was used therefore provides more reliable results with higher internal validity. However, this study only focuses on land mammals therefore may not be generalisable to all species, therefore lacks external validity. It also does not explain how evolutionary pressures affect sleep patterns for all species.
Horne et al proposed a combined approach to try and explain areas which a purely evolutionary theory failed to explain such as why we have a strong drive for sleep when deprived. This approach proposed some elements of sleep are for restoration and some are for occupying unproductive hours e.g. conserving energy, for small animals. This suggests that evolutionary approaches do have validity however individually they cannot fully explain function of sleep. Horne also proposed a distinction between core and optional sleep. Core sleep is equivalent to SWS and optional is equivalent to REM. Optional sleep is argued to be dispensable and used to occupy unproductive hours and used to conserve energy supporting the energy conservation theory. However, restoration theorists would argue REM plays an important role in brain functioning and is not simply used to waste time.
Both Capellini and Horne's research can provide support towards some explanations with the evolutionary approach of sleep. However, research cannot provide conclusive evidence towards one sole evolutionary theory highlighting the subject is inconclusive and debatable. However, they suggest how sleep has evolved to aid survival for example the Indus dolphin sleeps for short periods of time, of a few seconds, in order to avoid debris. Such pressures could be argues to play an overriding factor in sleep behaviour as they determine the animal's survival chances, providing support for an evolutionary function of sleep.
Many studies are based on animals therefore findings cannot be generalised to humans as our environmental pressures are different e.g. we have no predator risk and food is generally available. Therefore according to the evolutionary approach we should not need to sleep, but we sleep for 8 hours a day. This highlights a possible biological and restorative need rather than being controlled by evolutionary pressures. Humans generally dictate their sleep patterns, yet evolutionary explanations ignore this therefore are deterministic, ignoring our own conscious decisions in sleep patterns.
Outline and evaluate restoration theory as a function of sleep (8+16)
Sleep is devided into slow wave sleep (SWS) and REM. Oswald proposed SWSaided in body repair and REM aided brain recovery. During SWS, growth hormone is released aigining in development during childhood and during adulthood it enables protei synthesis and cell growth aiding in bodily recovery. It has also been suggested that lack of SWS can result in redcued functionis of the immune system.
REM sleep is highest in babies and higher in premature babies. This may be due to humans being born immatues and requiring rapid brain growth and development. Animals born mature have little REM sleep suggesting a link between REM and neural development, another restorative function.
Siegel et al proposed REM sleep allowed for a break in neurotransmitter activity therefore allowing the neurons to regain sensitivity. Neurons are vital for bodily functioning. Anti-depressantcs have been seen to increase levels of neurtransmitter and abolist REM as a side effect, assumed to be due to receptors not needig to be regenerated. This highlights a possible link between neurtransmitter restoration and REM sleep.
Dement et al woke cats each time they entered REM sleep and found all the cats died highlighting lack of sleep can have serious consequences. However, other confouding variables such as stress of the environment may have contributed to the cats death therefore the study lacks internal validity as it was not purely a measure of sleep deprivation. Ethical issues are a concern as this could be have seen as a form of animal torture and it is questionable whether it can be justified as in the name of science. Results from cats cannot be generalised to humans therefore the study may not be justifiable and lacks external validity. However, it is clear that sever sleep deprivation has negative effects, even if indirectly linked to stress.
Horne proposed a distinction between core and optional sleep. Core sleep is equivalent to SWS and optional is equivalent to REM. Optional sleep is argued to be dispensible and used to occupy unproductive hours and used to conserve energy. However, restoration theorists would argue REM plays an important role in brain functionins and is not simply used to waste time. Evidence of the importance of sleep is seen in human case studies of deprivation.
Peter Tripp, stayed awake for 201 hours and suffered severe negative effects such as abusive, unpleasant behaviour and suffered hallucination and paranoia. Contrasting this, Randy Garner beat Tripp's record but suffered non eof the negative effects Tripp had shown. Restoration theories are reductionist as individual differences are not considered. From researchwe see individuals cope with deprivation differently and therefore will likely have different levels of restorative function from sleep. However, single case studies have low external validity making it difficult to draw firm conclusions regarding the restorative function of sleep. However, both experienced REM rebound helping conclude sleep likely provides a restorative function.
Restoration theories are limited as they cannot explain all sleep patterns. For example the EEG recordings of dolphins have found no evidence of REM sleep. Yet resoration theory suggests REM sleep is needed for brain restoration. Sleep differences cannot be explained and to suggest sleep only holds resorative function may be resductionist and over simplified. Some may argue an evolutionary approach would lead to better understanding of sleep as different environmental pressures would have shaped sleep patterns. However, during sleep animals become essentially paralysed leaving them vulnerable, suggesting sleep must have an important restorative function as they repeated put themsleves at risk during sleep.
Research findings from Dement and the two cases studies highlight that sleep deprivation has sever consequences. These uch consequences can vary between individuals, but most research can help us draw the conclusion that sleep aids in some restorative function, although we cannot determine the extent of restoration that sleep has. Positive application of research could aid towards better sleep hygiene helping to reduce the negetaive effects of sleep deprivation and/or help to prevent it.
REM sleep is highest in babies and higher in premature babies. This may be due to humans being born immatues and requiring rapid brain growth and development. Animals born mature have little REM sleep suggesting a link between REM and neural development, another restorative function.
Siegel et al proposed REM sleep allowed for a break in neurotransmitter activity therefore allowing the neurons to regain sensitivity. Neurons are vital for bodily functioning. Anti-depressantcs have been seen to increase levels of neurtransmitter and abolist REM as a side effect, assumed to be due to receptors not needig to be regenerated. This highlights a possible link between neurtransmitter restoration and REM sleep.
Dement et al woke cats each time they entered REM sleep and found all the cats died highlighting lack of sleep can have serious consequences. However, other confouding variables such as stress of the environment may have contributed to the cats death therefore the study lacks internal validity as it was not purely a measure of sleep deprivation. Ethical issues are a concern as this could be have seen as a form of animal torture and it is questionable whether it can be justified as in the name of science. Results from cats cannot be generalised to humans therefore the study may not be justifiable and lacks external validity. However, it is clear that sever sleep deprivation has negative effects, even if indirectly linked to stress.
Horne proposed a distinction between core and optional sleep. Core sleep is equivalent to SWS and optional is equivalent to REM. Optional sleep is argued to be dispensible and used to occupy unproductive hours and used to conserve energy. However, restoration theorists would argue REM plays an important role in brain functionins and is not simply used to waste time. Evidence of the importance of sleep is seen in human case studies of deprivation.
Peter Tripp, stayed awake for 201 hours and suffered severe negative effects such as abusive, unpleasant behaviour and suffered hallucination and paranoia. Contrasting this, Randy Garner beat Tripp's record but suffered non eof the negative effects Tripp had shown. Restoration theories are reductionist as individual differences are not considered. From researchwe see individuals cope with deprivation differently and therefore will likely have different levels of restorative function from sleep. However, single case studies have low external validity making it difficult to draw firm conclusions regarding the restorative function of sleep. However, both experienced REM rebound helping conclude sleep likely provides a restorative function.
Restoration theories are limited as they cannot explain all sleep patterns. For example the EEG recordings of dolphins have found no evidence of REM sleep. Yet resoration theory suggests REM sleep is needed for brain restoration. Sleep differences cannot be explained and to suggest sleep only holds resorative function may be resductionist and over simplified. Some may argue an evolutionary approach would lead to better understanding of sleep as different environmental pressures would have shaped sleep patterns. However, during sleep animals become essentially paralysed leaving them vulnerable, suggesting sleep must have an important restorative function as they repeated put themsleves at risk during sleep.
Research findings from Dement and the two cases studies highlight that sleep deprivation has sever consequences. These uch consequences can vary between individuals, but most research can help us draw the conclusion that sleep aids in some restorative function, although we cannot determine the extent of restoration that sleep has. Positive application of research could aid towards better sleep hygiene helping to reduce the negetaive effects of sleep deprivation and/or help to prevent it.
Outline and evaluate the consequences of disruption of biological rhythms (8+16)
Consequences of disruption of biological rhythms are seen in jet lag and shift work. Normally exogenous zeitgebers allow our bodies to adjust gradually. But, rapid changes can cause them to become desynchronised. Symptoms of desynchronisation include decreased alertness and performance, fatigue and nausea.
Shift work may involve working during the night when our internal body clocks are normally set to induce sleep, causing a breakdown between exogenous zeitgebers and endogenous pacemakers. In low light conditions melatonin is released to induce sleep. Therefore if awake during darkness hours this can cause decreased alertness. This also contributes to lower quality daytime sleep as melatonin levels are low. This can lead to sleep deprivation and a permanent state of dysychronisation. This can also increase stress levels which long term can have detrimental effects on health.
Jet lag is a physiological effect of a disrupted circadian rhythm which occurs through travelling through time zones quickly meaning our internal body clock does not match external zeitgebers. Biological clocks cannot cope with large shifts with the SCN taking several cycles to resynchronise. It is suggested to aid resynchronisation, and is most beneficial to, follow exogenous zeitgebers e.g. meals and sleep times and following the biological clock can cause synchronisation to take longer.
Recht et al studies US baseball teams who travelled coast to coast to play games. Results found teams travelling east to west, experiencing a phase delay, won 44% of games opposed to west to east teams, experiencing a phase advance, won only 37%. This difference may be explained through a disrupted rhythm therefore may provide support that disruption can lead to decreased performance. However, results were drawn based on correlation evidence therefore other confounding variables such as east coast teams being better at baseball and referee bias may have affected results. Therefore the study lacks internal validity. Also the difference in results between east and west coast teams was only 7% which may not be a high enough statistical difference to drawn conclusive results as to the affects that a disrupted biological rhythm has on performance.
As shift work and jet lag are unavoidable most research has focuses on how to reduce its harmful effects.
Boivin et al found artificial bright lights was effective in resetting biological rhythms. Four groups were exposed to varying light levels with the group exposed to the brightest light being the most responsive to having circadian rhythms rest. This suggests even artificial light can aid in helping reset disrupted rhythms. This has positive real world application as, if bright lights can be used in the workplace to aid in readjusting biological rhythms . This could help increase alertness during the night which may help to reduce the risk of work place disasters such as the Chernobyl disaster occurring.
However, this was a laboratory experiment therefore may lack external validity and findings may not be indicative of real life. Also participants were volunteers therefore may have been motivated to find a solution to their possible sleep problems therefore showed demand characteristics subconsciously. Therefore findings may apply to a real workforce and they may be less motivated and less likely to notice their rhythms change. Further issues arise within this study as it only focuses on the role light plays influencing biological rhythms despite temperature and social cues being found to have a strong influence. Therefore this study is reductionist and only focuses on a simplified understanding of exogenous zeitgebers.
Recht and Boivin's studies suggest that disruption occurs within everyone therefore needs to be treatable. However, such studies may be euro-centric as there is evidence of people coping in daylight year round e.g. Inuits. Therefore studies may be targeted at one specific culture and not generalisable to all. Therefore from research it is evident disrupted rhythms can cause problems, but the same factors do not cause disruption for all. Therefore the best method of treatment will also likely be subjective to the individual.
Shift work may involve working during the night when our internal body clocks are normally set to induce sleep, causing a breakdown between exogenous zeitgebers and endogenous pacemakers. In low light conditions melatonin is released to induce sleep. Therefore if awake during darkness hours this can cause decreased alertness. This also contributes to lower quality daytime sleep as melatonin levels are low. This can lead to sleep deprivation and a permanent state of dysychronisation. This can also increase stress levels which long term can have detrimental effects on health.
Jet lag is a physiological effect of a disrupted circadian rhythm which occurs through travelling through time zones quickly meaning our internal body clock does not match external zeitgebers. Biological clocks cannot cope with large shifts with the SCN taking several cycles to resynchronise. It is suggested to aid resynchronisation, and is most beneficial to, follow exogenous zeitgebers e.g. meals and sleep times and following the biological clock can cause synchronisation to take longer.
Recht et al studies US baseball teams who travelled coast to coast to play games. Results found teams travelling east to west, experiencing a phase delay, won 44% of games opposed to west to east teams, experiencing a phase advance, won only 37%. This difference may be explained through a disrupted rhythm therefore may provide support that disruption can lead to decreased performance. However, results were drawn based on correlation evidence therefore other confounding variables such as east coast teams being better at baseball and referee bias may have affected results. Therefore the study lacks internal validity. Also the difference in results between east and west coast teams was only 7% which may not be a high enough statistical difference to drawn conclusive results as to the affects that a disrupted biological rhythm has on performance.
As shift work and jet lag are unavoidable most research has focuses on how to reduce its harmful effects.
Boivin et al found artificial bright lights was effective in resetting biological rhythms. Four groups were exposed to varying light levels with the group exposed to the brightest light being the most responsive to having circadian rhythms rest. This suggests even artificial light can aid in helping reset disrupted rhythms. This has positive real world application as, if bright lights can be used in the workplace to aid in readjusting biological rhythms . This could help increase alertness during the night which may help to reduce the risk of work place disasters such as the Chernobyl disaster occurring.
However, this was a laboratory experiment therefore may lack external validity and findings may not be indicative of real life. Also participants were volunteers therefore may have been motivated to find a solution to their possible sleep problems therefore showed demand characteristics subconsciously. Therefore findings may apply to a real workforce and they may be less motivated and less likely to notice their rhythms change. Further issues arise within this study as it only focuses on the role light plays influencing biological rhythms despite temperature and social cues being found to have a strong influence. Therefore this study is reductionist and only focuses on a simplified understanding of exogenous zeitgebers.
Recht and Boivin's studies suggest that disruption occurs within everyone therefore needs to be treatable. However, such studies may be euro-centric as there is evidence of people coping in daylight year round e.g. Inuits. Therefore studies may be targeted at one specific culture and not generalisable to all. Therefore from research it is evident disrupted rhythms can cause problems, but the same factors do not cause disruption for all. Therefore the best method of treatment will also likely be subjective to the individual.
Outline and evaluate research into the role of endogenous pacemakes and exogenous zeitgerbers (8+16)
Endogenous pacemakers are biological clocks within organisms. In mammals the main pacemaker is the suprachiasmatic nucleus (SCN), located in the hypothalamus. The SCN receives information on light via the optic nerve, occurring even when our eyes are closed as light penetrates through our eyelids. This helps to keep circadian rhythms synchronised with the outside world. When the SCN receives information about light is sends a signal to the pineal gland which regulates the production of melatonin. In low light it increases production, as melatonin is the hormone which induces sleep through inhibiting brain mechanisms which provoke wakefulness.
Exogenous zeitgebers are external cues that help to regulate biological rhythms, known as entrainment. The opposite of this is free running where the biological clock operates without external cues. Light is the dominate zeitgeber in humans. The light sensitive protein CRY responds to light, shifting biological rhythms and has been found to reset the SCN and other bodily oscillators. Social cues such as meal times play a role as the liver and the heart are seen to be reset as the cells respond to eating. This suggests environmental factors play a role in biological cycles. Temperature is also important for the onset of hibernation in some animals. In the absence of light, temperature may become the dominant zeitgeber that resets biological rhythms.
Morgan et al bred 'mutant' hamsters with a circadian rhythm of 20 hours instead of 24. The mutant SCN was transplanted into normal hamsters,which then displayed the 20 hours rhythm. This highlights the importance of the SCN and the possible dominant role it plays in controlling our biological rhythms. However, this study does not explain how exogenous zeitgebers may have interacted with the SCN to maintain a 22 hour rhythm. It is reductionist to assume only the SCN plays a role as we know exogenous zeitgebers interact with endogenous pacemakers to keep rhythms synchronised. Ethical issues also arise as the animals were left permanently damaged. Research may be justified if it has an important application to human behaviour research. However, generalisation problems occur between non-human animals studies to humans, therefore limits the conclusions which can be drawn.
Campbell et al altered participants circadian rhythms through shining lights on the backs of participants' knees demonstrating the existence of other endogenous pacemakers. Their circadian rhythms shifted demonstrating other oscillators must exist to help keep the biological clocks synchronised. This supports the assumption that light acts as an exogenous zeitgeber through its interaction with the protein CRY to reset the biological clock. Highlighting that a relationship exists between exogenous zeitgebers and endogenous pacemakers. This also suggests humans do not solely need light to penetrate the eyes. Blood may also be a messenger carrying light signals from the sun to the brain. However, such explanations may be reductionist to assume light is the main exogenous zeitgeber as other external influences such as temperature and social cues work with endogenous pacemakers to maintain rhythms.
Both Morgan's and Campbell's studies demonstrate the importance of interaction of endogenous pacemakers and exogenous zeitgebers. They also highlight that most mammals have similar endogenous pacemakers to influence rhythms. Both studies took a biological approach ignoring the role of free will we have in overriding internal clocks, therefore is deterministic. We are not governed completely by biological programming and we can override them if we wish.
Also from such research we can identify that nurture has a strong influence. As, our environments interact with internal biological clocks suggesting both appear to be equally important. Our endogenous pacemakers can keep a rough measure biological rhythms but the environment and stimuli appear to be important in keeping it completely synchronised. However, we cannot determine the exact amount of influence endogenous pacemakers and exogenous zeitgebers have on our rhythms, we can only conclude they interact.
Exogenous zeitgebers are external cues that help to regulate biological rhythms, known as entrainment. The opposite of this is free running where the biological clock operates without external cues. Light is the dominate zeitgeber in humans. The light sensitive protein CRY responds to light, shifting biological rhythms and has been found to reset the SCN and other bodily oscillators. Social cues such as meal times play a role as the liver and the heart are seen to be reset as the cells respond to eating. This suggests environmental factors play a role in biological cycles. Temperature is also important for the onset of hibernation in some animals. In the absence of light, temperature may become the dominant zeitgeber that resets biological rhythms.
Morgan et al bred 'mutant' hamsters with a circadian rhythm of 20 hours instead of 24. The mutant SCN was transplanted into normal hamsters,which then displayed the 20 hours rhythm. This highlights the importance of the SCN and the possible dominant role it plays in controlling our biological rhythms. However, this study does not explain how exogenous zeitgebers may have interacted with the SCN to maintain a 22 hour rhythm. It is reductionist to assume only the SCN plays a role as we know exogenous zeitgebers interact with endogenous pacemakers to keep rhythms synchronised. Ethical issues also arise as the animals were left permanently damaged. Research may be justified if it has an important application to human behaviour research. However, generalisation problems occur between non-human animals studies to humans, therefore limits the conclusions which can be drawn.
Campbell et al altered participants circadian rhythms through shining lights on the backs of participants' knees demonstrating the existence of other endogenous pacemakers. Their circadian rhythms shifted demonstrating other oscillators must exist to help keep the biological clocks synchronised. This supports the assumption that light acts as an exogenous zeitgeber through its interaction with the protein CRY to reset the biological clock. Highlighting that a relationship exists between exogenous zeitgebers and endogenous pacemakers. This also suggests humans do not solely need light to penetrate the eyes. Blood may also be a messenger carrying light signals from the sun to the brain. However, such explanations may be reductionist to assume light is the main exogenous zeitgeber as other external influences such as temperature and social cues work with endogenous pacemakers to maintain rhythms.
Both Morgan's and Campbell's studies demonstrate the importance of interaction of endogenous pacemakers and exogenous zeitgebers. They also highlight that most mammals have similar endogenous pacemakers to influence rhythms. Both studies took a biological approach ignoring the role of free will we have in overriding internal clocks, therefore is deterministic. We are not governed completely by biological programming and we can override them if we wish.
Also from such research we can identify that nurture has a strong influence. As, our environments interact with internal biological clocks suggesting both appear to be equally important. Our endogenous pacemakers can keep a rough measure biological rhythms but the environment and stimuli appear to be important in keeping it completely synchronised. However, we cannot determine the exact amount of influence endogenous pacemakers and exogenous zeitgebers have on our rhythms, we can only conclude they interact.
Outline and evaluate research into infradian and ultradian rhythms (8+16)
Infradian rhythms are biological rhythms lasting more than 24 hours e.g. the menstrual cycle which is regulated by the secretion of oestrogen and progesterone over a month. It was originally thought to be controlled by the hypothalamus acting as an endogenous pacemaker. But, evidence shows external zeitgebers play a role. Another example is PMS which occurs a few days before menstruation and is characterised by loss of appetite, stress and poor concentration.
Russel et al used sweat of donor women causing other female participants menstrual cycles to become synchronised with that of the donor suggesting exogenous zeigebers influence a women's infradian rhythms and that endogenous pacemakers and exogenous zeitgebers interact to control infradian rhythms. However, a small sample was used and results may have occurred due to random occurrence raising issues of validity of findings. But, other research has found similar findings suggesting it is reliable and valid. The women used in the study has similar length menstrual cycles which may have acted as a confounding variable in whether their infradian rhythms synchronised or not, evidence of women with different length cycles synchronising would be needed to increase the external validity of findings. This study is reductionist and only focuses on the role of hormones and other factors such as the environment are ignored. Such factors may have acted as confounding variables influencing the menstrual cycle and thus the women's infradian rhythms.
Issues occur into research especially regarding PMS, as this has cited as a mental disorder and used as legal defence e.g. Ms English drove her car into her partner after an argument, killing him, using PMS as legal defence resulting in her being put on probation. Such anecdotes are deterministic and suggest women have no control over their behaviour when influenced by such infradian rhythms. This could result in responsibility being taken away from women who behave aggressively, and violent women being acquitted for violent acts.
Ultradian rhythms are biological cycles that last less than 24 hours. An example of this is the stages of sleep. Stages one and two are light sleep, heart rate reduces and muscles relax. Stage two also has noticeable sleep spindles and K-complexes. In stage 3 sleep spindles decline being replaced by delta waves. Stages 3 and 4 are slow wave sleep (SWS). Stage 4 is deep sleep, delta waves increase and metabolic rate is low. It takes about an hour to pass through stages 1-4 and after 90 minutes after falling asleep REM is entered. As the night progresses more time is spent in REM. This is fairly universal but there are developmental differences.
Dement and Klietman found participants when woken during REM sleep dreaming was reported 90% of the time and was recalled in detail. Only 7% reported dreaming in NREM. EEG recordings were used in order to wake participants up during different stages of sleep providing results with higher reliability and validity as researcher could determine which stage of sleep participants were in. From findings it could be assumed that REM sleep is dreaming sleep. However, this assumption is reductionist assuming all individuals will experience that same ultradian rhythms. Dreaming was not always reported in REM, additionally dreaming was reported in NREM although not as frequently. Results were inconclusive meaning the REM dream link is still unclear and that further research is needed in order to gain a better understanding of why dreams occur within this ultradian rhythm.
Russell, and Dement and Kleitman's research provides us with evidence of internal infradian and ultradian rhythms which help control cycles within the body. Such research is mostly conducted in a laboratory setting which lacks external validity as results may not generalise to real life settings. However, research has a piratical application to help us gain a better understanding of how our biological rhythms work. This may aid in providing better treatment for those who cannot synchronise rhythms or have difficultly controlling behaviour because of them.
Russel et al used sweat of donor women causing other female participants menstrual cycles to become synchronised with that of the donor suggesting exogenous zeigebers influence a women's infradian rhythms and that endogenous pacemakers and exogenous zeitgebers interact to control infradian rhythms. However, a small sample was used and results may have occurred due to random occurrence raising issues of validity of findings. But, other research has found similar findings suggesting it is reliable and valid. The women used in the study has similar length menstrual cycles which may have acted as a confounding variable in whether their infradian rhythms synchronised or not, evidence of women with different length cycles synchronising would be needed to increase the external validity of findings. This study is reductionist and only focuses on the role of hormones and other factors such as the environment are ignored. Such factors may have acted as confounding variables influencing the menstrual cycle and thus the women's infradian rhythms.
Issues occur into research especially regarding PMS, as this has cited as a mental disorder and used as legal defence e.g. Ms English drove her car into her partner after an argument, killing him, using PMS as legal defence resulting in her being put on probation. Such anecdotes are deterministic and suggest women have no control over their behaviour when influenced by such infradian rhythms. This could result in responsibility being taken away from women who behave aggressively, and violent women being acquitted for violent acts.
Ultradian rhythms are biological cycles that last less than 24 hours. An example of this is the stages of sleep. Stages one and two are light sleep, heart rate reduces and muscles relax. Stage two also has noticeable sleep spindles and K-complexes. In stage 3 sleep spindles decline being replaced by delta waves. Stages 3 and 4 are slow wave sleep (SWS). Stage 4 is deep sleep, delta waves increase and metabolic rate is low. It takes about an hour to pass through stages 1-4 and after 90 minutes after falling asleep REM is entered. As the night progresses more time is spent in REM. This is fairly universal but there are developmental differences.
Dement and Klietman found participants when woken during REM sleep dreaming was reported 90% of the time and was recalled in detail. Only 7% reported dreaming in NREM. EEG recordings were used in order to wake participants up during different stages of sleep providing results with higher reliability and validity as researcher could determine which stage of sleep participants were in. From findings it could be assumed that REM sleep is dreaming sleep. However, this assumption is reductionist assuming all individuals will experience that same ultradian rhythms. Dreaming was not always reported in REM, additionally dreaming was reported in NREM although not as frequently. Results were inconclusive meaning the REM dream link is still unclear and that further research is needed in order to gain a better understanding of why dreams occur within this ultradian rhythm.
Russell, and Dement and Kleitman's research provides us with evidence of internal infradian and ultradian rhythms which help control cycles within the body. Such research is mostly conducted in a laboratory setting which lacks external validity as results may not generalise to real life settings. However, research has a piratical application to help us gain a better understanding of how our biological rhythms work. This may aid in providing better treatment for those who cannot synchronise rhythms or have difficultly controlling behaviour because of them.
Outline and evaluate research into circadian rhythms (8+16 marks)
Biological rhythms are cycles with the body which are controlled by endogenous pacemakers and exogenous zeitgerbers e.g. light and social cues. Circadian rhythms are biological cycles that last 24 hours e.g. the sleep/wake cycle. The main biological clock in mammals is the suprachiasmatic neucleus (SCN) which aids in keeping biological rhythms synchronised with the outside world through regular events such as meal times.
The sleep wake cycle is governed by external cues e.g. light and social cues but there is also an endogenous clock which is free running, working without external cue. It sets a rhythm at about 24-25 hours. The external cues help the endogenous clock to remain synchronised with the outside world. Studies have shown circadian rhythms persist despite isolation from natural light, but are not accurate highlighting the importance of exogenous zeitgerbers.
Core body temperature is another circadian rhythms. It is it lowest around 4:30am at 36 degrees c and highest at 6pm at 38 degrees c with a slight dip occurring at midday, even without eating.
Hormone production also follows a circadian rhythm with cortisol levels being lowest around midnight and highest around 6am. Cortisol plays a role in making us alert therefore explains why awoken in the middle of the night we struggle to function. Melatonin and growth hormone also follow a circadian rhythm both peaking at around midnight.
Aschoff and Wever found participants to have circadian rhythms between 24 and 25 hours, when placed in an underground, with some as long as 29 hours. Rhythms persisted in the absence of external cues supporting the assumption of circadian rhythms being internal. Limitations of this study include low external validity as it was conducted in a laboratory setting therefore findings cannot be generalised to real life. However, it could be argued in a real life setting absence of external cues would never be an issue. But, such studies can be used to help gain further understanding of how our circadian rhythms work. However, participants may have shown demand characteristics as they were aware they were being monitored affecting the reliability and validity of results.
Michel Siffre spend 6 months in a cave without external cues and found his circadian rhythms varied from a 25-30 hours. This highlights the presence of an internal circadian clock but also highlights the importance of exogenous zeitgebers to regulate rhythms as his circadian rhythms were not maintained at 24 hours. However, results from a single case study may not provide accurate generalisations on how others would respond to a lack of external cues. Confounding variables such as temperature, air pressure and being connected to monitoring equipment may have affected sleep quality and length, therefore reliability and validity of results may be questioned. Also results suffer gender bias and it cannot be assumed women's circadian rhythms would have similar responses due to hormonal differences.
Research findings have positive real world application particularly in the area of chronotherapeutics, which recent research in Germany has found, to influence the effectiveness of drugs therapies. For example aspirin is effective in reducing the chance of a heart attack if taken in the evening as most attacks occur in the early hours of the morning. Therefore research into circadian rhythms may help to increase effectiveness of treatments for disorders and illnesses.
Both Aschoff and Wevers's and Siffre's studies suffer the issue of the use of abnormal environments. This may have affected length and quality of sleep, acting as a confound variable therefore affecting the validity of findings. Additionally, participants in both studies were able to us bright artificial lights which other research has found to cause rhythms to shift, further affecting the studies internal validity. Such research can be used to highlight the existence of free running circadian clocks. However, they are not accurate therefore suggesting the importance of interaction with external zeitgebers to maintain circadian rhythms.
The sleep wake cycle is governed by external cues e.g. light and social cues but there is also an endogenous clock which is free running, working without external cue. It sets a rhythm at about 24-25 hours. The external cues help the endogenous clock to remain synchronised with the outside world. Studies have shown circadian rhythms persist despite isolation from natural light, but are not accurate highlighting the importance of exogenous zeitgerbers.
Core body temperature is another circadian rhythms. It is it lowest around 4:30am at 36 degrees c and highest at 6pm at 38 degrees c with a slight dip occurring at midday, even without eating.
Hormone production also follows a circadian rhythm with cortisol levels being lowest around midnight and highest around 6am. Cortisol plays a role in making us alert therefore explains why awoken in the middle of the night we struggle to function. Melatonin and growth hormone also follow a circadian rhythm both peaking at around midnight.
Aschoff and Wever found participants to have circadian rhythms between 24 and 25 hours, when placed in an underground, with some as long as 29 hours. Rhythms persisted in the absence of external cues supporting the assumption of circadian rhythms being internal. Limitations of this study include low external validity as it was conducted in a laboratory setting therefore findings cannot be generalised to real life. However, it could be argued in a real life setting absence of external cues would never be an issue. But, such studies can be used to help gain further understanding of how our circadian rhythms work. However, participants may have shown demand characteristics as they were aware they were being monitored affecting the reliability and validity of results.
Michel Siffre spend 6 months in a cave without external cues and found his circadian rhythms varied from a 25-30 hours. This highlights the presence of an internal circadian clock but also highlights the importance of exogenous zeitgebers to regulate rhythms as his circadian rhythms were not maintained at 24 hours. However, results from a single case study may not provide accurate generalisations on how others would respond to a lack of external cues. Confounding variables such as temperature, air pressure and being connected to monitoring equipment may have affected sleep quality and length, therefore reliability and validity of results may be questioned. Also results suffer gender bias and it cannot be assumed women's circadian rhythms would have similar responses due to hormonal differences.
Research findings have positive real world application particularly in the area of chronotherapeutics, which recent research in Germany has found, to influence the effectiveness of drugs therapies. For example aspirin is effective in reducing the chance of a heart attack if taken in the evening as most attacks occur in the early hours of the morning. Therefore research into circadian rhythms may help to increase effectiveness of treatments for disorders and illnesses.
Both Aschoff and Wevers's and Siffre's studies suffer the issue of the use of abnormal environments. This may have affected length and quality of sleep, acting as a confound variable therefore affecting the validity of findings. Additionally, participants in both studies were able to us bright artificial lights which other research has found to cause rhythms to shift, further affecting the studies internal validity. Such research can be used to highlight the existence of free running circadian clocks. However, they are not accurate therefore suggesting the importance of interaction with external zeitgebers to maintain circadian rhythms.
Subscribe to:
Posts (Atom)