Biological Rhythms and Sleep

Circadian Rhythms Sleep-Wake Cycle (AO1): A free running sleep-wake cycle is just over 24 hours. This has been found by studies e.g. that of Michael Siffre, who spent time living underground in the absence of exogenous zeitgebers, and whose sleep-wake cycle settled to 24 hours, and that of an experimental study that places participants in a WW2 bunker with no time cues, and found that their sleep-wake cycles settled to be 24-25 hours. There is evidence that the endogenous sleep-wake cycle is difficult to override. American submariners on an 18-hour day maintained circadian rhythms of 24 hours. Sleep-Wake Cycle (AO2): Case studies such as Michael Siffre are ungeneralisable, as we cannot conclude all people will respond in this way; it may be that his cycle is abnormal or that there is no such thing as a 'normal' cycle and his was coincidentally 24 hours (IDA - generalisability). Much of the experimental research is flawed because participants were not isolated from artificial light, as there is now evidence suggesting that circadian rhythms can be entrained even by dim, artificial light (IDA - methodology). There are large individual differences in the sleep-wake cycle, making blanket conclusions impossible. Sleep wake cycles have been found to vary from 13 to 65 hours and have different onsets and peaks (IDA - individual differences). There are cultural differences in sleep-wake cycles, as many cultures take a siesta in the afternoon. Most research does not consider this, whether it is entrained into their biological rhythms and if so, whether it also follows a 24 hour rhythm (IDA - culture). Core Body Temperature (AO1): Core Body temperature has been found to be lowest at 4:30 AM and highest at about 6 PM, indicating that it follows a circadian rhythm. There is also a slight trough in the early afternoon, that has been found to be endogenous and unrelated to the eating of lunch. Core Body Temperature (AO2): Bollani et al. studied babies in their first two days of life, monitoring their core body temperature every 10 minutes. After two days, all six babies were showing a clear 24-hour rhythm. It is unlikely that babies of this age would be responding to exogenous zeitgebers, so it was concluded that the cycle was innate (however - IDA - unrepresentative sample). The circadian variation in core body temperature has been found to link to cognitive abilities. Children who had stories read to them in the afternoon showed superior recall and comprehension than children who had stories read to them in the morning (however - IDA - cannot infer causality from correlation. Field experiment - extraneous variables (such as lack of sleep making children tired in the morning). Inconsistent findings - other research has found no link between core body temperature and cognitive ability). Hormones (AO1): Hormone production follows a circadian rhythm. Cortisol levels are lowest around midnight and highest around 6 AM (it is associated with alertness). Other hormones such as melatonin and growth hormone also follow a circadian rhythm, peaking at around midnight. Hormones (AO2):There is evidence from chronotherapeutics that hormones follow a circadian rhythm. Medications that act on certain hormones have no effect if taken when the target hormone's levels are at a dip in their cycle, however are fully effective if taken when target hormone levels are high. Ultradian Rhythms Basic Rest Activity Cycle (AO1): This is a 90 minute cycle characterised by different levels of excitement, movement, physiological arousal, rest and eating/drinking behaviour. In an observation of psychiatric patients, it was found that their eating and drinking fell into a 90 minute cycle. The cycles of timings in our everyday lives also seem to innately correspond to an underlying rhythm, e.g. length of lessons and lectures, coffee breaks. Basic Rest Activity Cycle (AO2): The BRAC suggests that sleep stages are part of a continuum and highlights the importance of the 90 minute cycle. This has lead to suggestions that the 90 minute cycle is a form of timing to ensure biological processes work in unison (supports idea of BRAC by explaining it). It is reductionist to suggest that all human behaviour falls into a biologically determined pattern. This one-size-fits-all approach may not be appropriate given that humans are complex moral characters with high intellectual abilities and large individual differences within the species (IDA - Reductionism). Sleep Stages (AO1): Stages 1 and 2 are light sleep. The brain produced beta waves that gradually slow to alpha, then theta waves. During theta waves there are bursts of brain activity call sleep spindles. At these stages, the sleeper is easily woken. Stages 3 and 4 are slow wave sleep. It is characterised by slow, delta waves. During these stages, most of the body's physiological repair work is done. The fifth stage is REM sleep, and is characterised by fast, desynchronised EEG activity that resembles the waking brain. It is when dreams are thought to take place. Cycles are around 90 minutes in length and continue throughout the night with REM periods getting longer and SW periods getting shorter. Sleep Stages (AO2):The link between REM sleep and dreaming has been demonstrated in a study that woke participants up either when their brainwaves suggested REM sleep or SWS. They were more likely to report dreaming during REM sleep (152 dreams were reported during REM compared to 39 during SWS). (However - suggests there is also dreaming outside of REM sleep, although this is difficult to know for certain as a person could be accidentally recalling a dream from earlier in the night or their brainwaves could be unusual for the sleep stage they were in. IDA - methodology). Infradian Rhythms Menstrual Cycle (AO1): The menstrual cycle is an infradian rhythm that takes place over a period of around 4 weeks. Its function is to regulate ovulation. The pituitary gland releases FSH and LH which stimulate a follicle to ripen an egg and release oestrogen. Once the egg has ripened, progesterone is produced, causing the lining of the womb to thicken. After two weeks, if there is no pregnancy, progesterone levels drop and the lining of the womb is shed. Menstrual Cycle (AO2): The menstrual cycle is thought to be mostly endogenous, however, it has been found that the timings can be controlled by exogenous cues. Research has shown that when women live together, they tend to menstruate at the same time each month. It has also been found that when daily samples of sweat were collected from one group of women and rubbed onto the upper lips of another group of women, the receiver's menstrual cycle synchronised with the donor's due to the pheremones in the sweat. PMS suggests that the menstrual cycle is endogenous. PMS is a syndrome affecting many women the week before menstruation, with symptoms including, depression, mood swings and fatigue. It has been found to be an physiological problem with psychological symptoms. Research into the causes and treatments of PMS is useful, as it can cause disruption to people's lives, and has even been used in a court case to explain murder. (IDA - Application to real life. However, IDA - determinism. Humans have higher order thinking skills and are not slaves to hormonal changes). Seasonal Affective Disorder (AO1):SAD is an infradian rhythm occurring over the winter months. It involves depression during winter and recovery in summer, and is thought to be caused by an increase in melatonin production (as melatonin is stimulated by darkness) and a decrease in serotonin production (as serotonin is stimulated by light).Seasonal Affective Disorder (AO2): Understand of SAD has allowed effective therapies such as phototherapy (exposure to light with the same wavelengths as natural light in the morning and evening to inhibit melatonin production) to be developed (IDA - application to real life). The explanation of SAD does not explain individual differences. It might be expected that everyone in the same climate experiences the same hormonal changes in winter, yet fewer than 5% of people experience SAD, and it is unclear why they should be more strongly affected. Endogenous Pacemakers and Exogenous Zeitgebers Suprachiasmatic Nucleus (AO1): The SCN is the main endogenous pacemaker in mammals. It is a cluster of nerve cells in the hypothalamus located above the place where the optic nerves cross over, and obtains light information via the optic nerve. If the endogenous clock is running slow, the SCN is able to shift it ahead, for example, at night, the SCN sends signals to the pineal gland to stimulate the production of melatonin. The SCN is made up of a pair of structures, the dorsal and ventral SCN. The ventral SCN is relatively quick to reset but the dorsal SCN takes much longer and is involved in causing jet lag. The SCN also coordinates the protein clock. This is made up of a number of proteins that interact in a negative feedback loop in order to keep bodily processes to time. Suprachiasmatic Nucleus (AO2): Normally the SCN coordinates bodily rhythms but in the absence of light, separate oscillators in the body will desynchronise, suggesting that although the SCN is endogenous, it is heavily dependent on exogenous cues. This has been displayed by a case study: Kate Aldcroft lived in a cave for 3 months and while her temperature rhythm settled to a 24 hour cycle, her sleep-wake cycle was 30 hours (However, IDA - case study, non generalisable). The role and importance of the SCN has been demonstrated in animal studies. Hamsters have been bred to have mutant 20 hour sleep-wake cycles, then their SCN was transplanted into other, normal, hamsters, which then adopted the 20 hour rhythm (IDA - extrapolation to humans). An evolutionary explanation for the role of the SCN is supported by a study of chipmunks, who has their SCNs leisoned and were then released into the wild. Within 80 days, all of the leisoned chipmunks had been killed by weasels, whereas the majority of a control group were still alive. The assumption was that as they had not gone to sleep at night, the weasels had heard them moving in their burrows and preyed on them (IDA - approaches). (This can also be used in support of the waste of time hypothesis.) Exogenous Zeitgebers (AO1): Light: Light is the dominant zeitgeber in humans. It can reset the SCN, and does so on a daily basis, so we can adapt to a 24 hour cycle despite our natural rhythms being very slightly over 24 hours. Light can also reset other bodily oscillators because one of the proteins in the protein clock is light-sensitive. Temperature: Some biological rhythms are entrained by temperature, for example, abscission and hibernation. Temperature is thought to be the dominant zeitgeber in the absence of light. Social cues: Although many behaviours appear to be entrained by social cues, it is more likely that they arose due to other rhythms, however, there are some rhythms that are entrained by social convention, for example, cells in the liver "learn" when mealtimes are. Exogenous Zeitgebers (AO2): Recent research has shown how sensitive humans are to light as a zeitgeber, as circadian rhythms can be entrained just by shining a dim light on the back of the knee. This suggests that our biological rhythms are primarily entrained by light. Genetic disorders affecting the protein clock suggest that rhythms are endogenous. Familial Advanced Sleep Phase Syndrome has been linked to a mutation in one of the genes that codes for a protein involved in the protein clock, and leads to sleep onset at around 7PM and spontaneous awakening at around 2AM (IDA - could be linked to application to real life). It is suggested that such neat divisions between an endogenous and exogenous system do not exist, and that the running of the biological clock is a blended system that involves both endogenous pacemakers and exogenous zeitgebers. Disrupted Biological Rhythms Shift Work (AO1): Night workers are required to be alert at night and to sleep during the day, which is the reverse to both our endogenous rhythms and exogenous cues, leading to decreased alertness. There is a circadian trough between midnight and 4AM when cortisol levels and body temperature are at their lowest. It also leads to sleep deprivation as noise and light reduces sleep quality and length. Daytime sleep is typically 1-2 hours shorter than nighttime sleep and REM is particularly affected. Shift lag can also affect health. There is a significant relationship between shift work and organ disease - individuals working shifts for more than 15 years were 3 times as likely to develop heart disease as non-shift workers. This could be directly caused by desynchronisation or more indirectly caused, e.g. by sleep deprivation. Shift Work (AO2): Research into shift work is valuable because the disruption of biological rhythms can have devastating consequences, for example, the Chernobyl nuclear disaster began at 1:25 AM, and most lorry accidents take place between 4 and 7 AM. It is estimated that accidents due to shift worker fatigue cost the US $77 billion annually. However, research into shift work can help reduce these harmful effects. It has been found that the most problems occur when people are on rotating shifts, and within these, shifts that follow a phase advance are harder to adjust to than those that follow a phase delay. (IDA - application to real life). Shift work effects could be due to other factors other than the disruption of biological rhythms. Individuals also experience social disruption, as it is difficult to spend time with family and friends. Divorce rates among shift workers are as high as 60%. Jet Lag (AO1): Jet Lag refers to the physiological effects of disrupted circadian rhythms. Our biological rhythms are not equipped to deal with sudden an large changes. It takes the dorsal SCN several cycles to resynchronise - estimated at one day per hour time change. Symptoms of jet lag include loss of appetite, fatigue and insomnia. We experience a phase delay when travelling west (when our behavioural rhythms are shifted later), and a phase advance when travelling east (our behavioural rhythms are shifted earlier). Phase advance tends to be more difficult to adjust to. Jet Lag (AO2): Jet lag may be affected by a number of other factors, such as travel being tiring, noise, caffeine or worry. The link between physiological effects is correlational, so causality cannot be established (IDA - methodology). Artificially-administered melatonin has been found to be effective at inducing sleep in people suffering from jet lag, allowing them to acclimatise to the new time zone. This has implications for real life as it could be commercially viable as a "cure" for jet lag (IDA - application to real life). There are significant individual differences in jet lag, as level of disruption caused by time zone change varies considerably from person to person, and this cannot be explained by our current understand of biological rhythms (IDA - generalisability). Lifespan Changes in Sleep Infancy (AO1): Babies sleep for around 16 hours a day, but their sleep is not continuous and they wake up every hour or so because their sleep cycles are shorter. Infants have sleep stages called quiet and active sleep that are immature versions of adult SWS and REM. At birth, sleep is predominated by active sleep. By 6 months, a circadian sleep-wake cycle is established, and by 1 year, infants are mostly sleeping through the night. The periods of quiet sleep lengthen and active sleep decreases. Infancy (AO2): An evolutionary perspective can explain why babies' sleep patterns are different from adults'. Night waking would have been evolutionarily adaptive as babies have small stomachs and need to be fed regularly, which night waking ensures (IDA - approaches) Infants' greater amount of active sleep can be explained by the immaturity of the infant brain, and the amount of learning that takes place. Active sleep has been linked to the consolidation of memories and neurotransmitter production. Childhood (AO1):By the age of 5, children have EEG patterns resembling those of an adult, but still sleep more (around 12 hours a day) and have more REM sleep (it is around 30% of the total sleep time). It is not uncommon to experience parasomnias such as somnambulism.Adolescence (AO1): Whilst during childhood need for sleep gradually decreases, during adolescence it increases slightly to 9-10 hours per night. Circadian rhythms change so that teenagers feel more alert at night and have difficulty getting up early. REM sleep in adolescent males is sometimes accompanied by orgasm and ejaculation, which is significantly less likely at other ages. Adolescence (AO2):Hormone production during adolescence can account for the changes in sleep patterns, as they are primarily released at night, and disturb sleep patterns.Adulthood (AO1):Normal adult sleep is around 8 hours a night, with 25% in REM sleep. Childhood parasomnias such as sleepwalking are less common, but parasomnias such as sleep apnoea and insomnia are more frequent.Old Age (AO1):Older people have more difficulty in going to sleep and wake up more frequently. REM sleep decreases to 20% of total sleep time, and SWS reduces to 0 to 5%. A phase advance is often also experienced.Old Age (AO2):The reduction in SWS leads to reduced growth hormone, resulting in decreased energy and lower bone density. This suggests that changes in sleep patterns in old age are linked to a reduction in function and the body's commencement of shutting down.Lifespan Changes in Sleep (AO2):The view presented in the description is one size fits all. However, there are significant individual differences in sleep at any age. This links to cultural differences in sleep - sleep habits are influenced by cultural values and lifestyle habits, and different cultures have different sleep behaviours, e.g. siestas (IDA - generalisabilty and culture). Functions of Sleep Restoration Theory (AO1): This theory suggests that the purpose of sleep is to restore the body's ability to function. Growth hormone is secreted during slow wave sleep. It is secreted in pulses throughout the day but mostly at night, as it is controlled by neural mechanisms that relate to slow wave sleep. It has been found that when sleep-wake cycles were reversed by 12 hours, the release of GH is also reversed, and that amount of SWS correlated with amount of GH released. In adults, GH enables protein synthesis and cell growth to take place. The immune system's antibodies must be regenerated during protein synthesis in SWS. Lack of SWS has been associated with reduced functioning of the immune system. REM sleep is needed for brain growth and consolidation of memory: active sleep is much higher in babies than in adults due to their rapid cognitive growth. It is suggested that the amount of REM sleep at birth in a species is directly proportional to the immaturity of the offspring at birth, for example, dolphins' offspring are mature from birth, and have no REM sleep. REM sleep also seems to allow a break in neurotransmitter activity, allowing neurones to regain their sensitivity and regenerate neurotransmitters. The antidepressant drug MAOI, which increases levels of the neurotransmitter serotonin, has the side effect of abolishing REM sleep. The suggestion is that REM sleep is no longer needed to revitalise neurotransmitter function as the drug does this. Restoration Theory (AO2): If restoration were the sole purpose of sleep, then we would expect to sleep more after an active day, however, research suggests that there is no relationship. In some animals no evidence of REM sleep has been found. Since sleep is universal, but REM sleep is not, it suggests that REM sleep does not play an important restorative function, as otherwise animals without it would not be able to survive (IDA - extrapolation to humans). Sleep deprivation studies further refute the theory, for example, the case studies of American DJ Peter Tripp, who stayed awake for 9 days, and student Randy Gardener, who stayed awake for 11 days, and experiences no long-term ill effects. This suggests that normal functioning can occur without sleep. However, the fact that they were unable to stay awake indefinitely suggests that sleep was required (IDA - case studies: generalisability). One study forced rats to remain physically active by rotating a disc they were standing on every time they began to go to sleep. By 33 days, all rats had died. This suggests that sleep is necessary for bodily function. However, this study is only correlational and their deaths could have been caused, for example, by the stress of the experience (IDA - correlation, IDA - extrapolation to humans). One study deprived participants of a certain type of sleep, ie, either SWS or REM. The next night, there was a 'rebound' of the type of sleep they had been deprived of the night before, where they entered into the type of sleep faster and stayed in it for longer. This suggests that these different stages of sleep are necessary to restoring bodily function, otherwise there would be no reason for the body to have to compensate for a lack of a certain type. Evolutionary Theory (AO1): This theory suggests that sleep has developed because it serves an adaptive purpose that enhances survival. Energy Conservation: This explanation suggests that sleep serves the purpose of enforcing a period of inactivity, thus using less energy. The implication of this is that small animals with high metabolic rates, for whom movement and maintaining body temperature use more energy, would sleep more. Enforced inactivity can be seen in hibernation. Foraging Requirements: This suggests that as the principle drive of animals is to eat, sleep has adapted according to the animal's eating habits. Herbivores that eat plants poor in nutrients need to eat more to get the nutrients they need, so sleep less. Carnivores whose diets are high in nutrients can afford to rest for much of the time. The theory also fits with the idea that carnivores are able to rest as they are not at risk of attack whereas herbivores, as prey, need to remain alert. Waste of Time Hypothesis: This explanation suggests that sleep is a way of ensuring that animals stay still when they have nothing else to do with their time, and helps prey stay out of the way of predators during the parts of the day when they are most vulnerable. Evolutionary Theory (AO2): Energy Conservation: It has been found that in general, small animals with high metabolic rates do sleep for longer. However, there are exceptions, such as the sloth, which sleeps for 20 hours a day, and the theory cannot explain these. Waste of Time Hypothesis: Although lying still and quiet to avoid predators makes sense, it does not follow that sleep serves this adaptive purpose, as it is illogical that during sleep an organism is unaware of their surroundings and could not protect themself if attacked. Waste of Time Hypothesis: This explanation is simplistic. It has been found that the relationship between predation and sleep is more complex, for example, animals that sleep in social groups tend to sleep for longer than solitary animals, and animals that sleep in exposed locations sleep for less long than animals that burrow or nest. Findings universally suggest that sleeping patterns differ between species, and are more similar in species that are more closely related. This suggests that sleep has evolved in response to the different selection pressures faced by different species and their ancestors (IDA - extrapolation of animals to humans: in modern day society, evolutionary factors do not apply in the same way they do for wild animals and for our ancestors). Research into animal sleep patterns may be flawed and incomplete. Of 5000 mammalian species, we only have data for 150. Within these, sample sizes are often fewer than 5 animals, and tests are completed in lab conditions, where animals may not be behaving in a natural way. Therefore, it is difficult to draw conclusions from this methodologically-flawed research (IDA - methodology). The Phylogeny of Sleep project has attempted to collect data on animal sleep. It has found that records are often conflicting with regards to certain species and therefore unreliable. For example, studies on giraffes differ in their recordings of NREM sleep from 1.5 to 3.6 hours and of REM sleep from 0.4 to 1.0 hours. Sleep Disorders Insomnia (AO1): There are two types of insomnia, primary and secondary. Primary insomnia occurs as a stand alone disorder, with no obvious cause, and secondary insomnia is sleeplessness caused by another underlying factor e.g. depression or stress. Women are more prone to insomnia than men due to the effects of menstruation and menopause on hormones and mood. Other risk factors include age (older people are more likely to have underlying health issues), personality traits (such as neuroticism and anxiety), sleep apnoea (as it disturbs sleep patterns) and stressful life events. Treatments for insomnia include good sleep hygiene (using the bedroom only for sleep and sex), benzodiazepines (to reduce anxiety) and sleeping pills. Insomnia (AO2): It is important to distinguish between primary and secondary insomnia because of the implications for treatment. However, recent research casts doubt on whether insomnia is an effect as often as it seems to be, rather than a cause of a mood disorder. A study found that insomnia more often preceded a mood disorder than followed it. Therefore, the distinction between primary and secondary insomnia is not as clear as suggested. Current practise does not distinguish between predisposing, precipitating and perpetuating factors. Predisposing factors such as genetics and personality are estimated to be about half of the cause of insomnia in people who develop it, but do not fully explain the disorder. Precipitating factors are triggers of the disorder, e.g. a stressful life event, and perpetuating factors are maintaining factors that continue to cause insomnia after the original cause has disappeared. Identifying these factors may help distinguish between acute and chronic insomnia in a patient, and have implications for treatment. Explanations of insomnia have enabled effective treatments to be developed (see AO1 for treatments. IDA - application to real life). Somnambulism (AO1): Sleepwalking is characterised by any form of movement whilst asleep. Risk factors include age, alcohol consumption, sleep deprivation, stress, fever and hormone fluctuation. There are two explanations as to why being of a young age is a risk factor in somnambulism. One is that SWS is linked to sleepwalking (brainwaves during sleepwalking have been found to be a mixture of beta and delta waves), and as children experience a lot of SWS due to the production of growth hormone, one would expect them to have a higher rate of sleepwalking accordingly. The other explanation is that the system that inhibits motor activity during sleep is underdeveloped in children (and some adults), a theory which is supported by neuroimaging research, which shows abnormally low levels of GABA in sleepwalkers. Somnambulism (AO2): There is evidence for a genetic predisposition to somnambulism. Concordance rates between dizygotic twins are 10-15% compared to 50% in monozygotic twins. This may explain why environmental risk factors only trigger sleepwalking in some people. There is evidence to support the claim that sleep deprivation is a risk factor for sleepwalking. One study observed people with sleepwalking problems on two occasions. The first night, 50% of participants sleepwalked. Then participants were prevented from sleeping for a night in order to deprive them of sleep. The night afterwards, 90% of participants sleepwalked. The theory that somnambulism in children is caused by an underdeveloped motor activity inhibitory system is reductionist. If this were the sole cause of sleepwalking, then all children would sleepwalk as it takes many years for this system to fully develop (IDA - reductionism). Narcolepsy (AO1): The clinical characteristics of narcolepsy are falling asleep at inappropriate times, fatigue, and cataplexy. Three explanations have been put forward to explain narcolepsy. One is to do with deregulated REM sleep, suggesting that narcolepsy is the result of a malfunction of the system regulating REM sleep. This is thought because narcoleptics tend to drop into REM sleep within 5 minutes of falling asleep, unlike most people. The second explanation is the Human Leukocyte Antigen (HLA) hypothesis, which suggests that narcolepsy is due to a mutation of the gene coding for this type of antigen. The third explanation is the Hypocretin hypothesis, which suggests that a mutation in the gene coding for hypocretin, a neurotransmitter involved in maintaining wakefulness, causes narcolepsy. Narcolepsy (AO2): Recording of neuronal activity in the brain stems of narcoleptic dogs suggests that cataplexy is linked to the activation of cells that are normally only active in REM sleep. However, research in general has failed to establish a causal link between deregulated REM sleep and narcolepsy. There may also be issues with extrapolating the research in dogs to humans, as the causes of the disorders could be different according to different sleeping habits (IDA - extrapolation from animals to humans). The HLA variant accused of causing narcolepsy is more common in narcoleptics, but is not found in all narcoleptics, meaning it cannot be the sole cause. Furthermore, if the disorder were caused by a mutation in a gene, that mutation should be inherited by both individuals in a monozygotic twin pair. However, concordance rates for monozygotic twins are only 32%. This suggests that this explanation is reductionist in its approach, as there must be more factors interacting than the biological factors it claims (IDA - reductionism). Research has found that narcoleptics have abnormally low levels of hypocretin in their cerebrospinal fluid. However, due to the lack of genetic link, it has been suggested that the reduction could be due to injury, infection or an auto-immune response, rather than a genetic mutation. Due to the HLA link, it is most commonly suggested that the HLA variant can cause an auto-immune response attacking hypocretin, but why this happens is unclear. WELL DONE YOU HAVE MADE IT TO THE END. NOW YOU KNOW BIOLOGICAL RHYTHMS AND SLEEP. HOPEFULLY.