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STM Biological Rhythms and Sleep (basic outline of everything)
Transcript of STM Biological Rhythms and Sleep (basic outline of everything)
and Sleep Circadian
Rhythm Ultradian Rhythm Research - Dement
& Kleitman Stages of sleep
1-4 - NREM
5 - REM Outline Cycle length <24hrs Cycle length 24hrs Evaluation Biological approach Objective evidence Sleep Lab
*Lacks mundane realism Self report
method Cycle length >24hrs Evaluation Outline Miles Ex Shirffre Endo Morgan Endo Schochat Endo Biological Reductionism Biological approach Edongenous/Exogenous Schochat
+ Large sample
- Use of animals Contradictory Evidence
Folkard - Sleep/Wake cycle
and Temperature Rhythm Outline Evaluation Reinberg - Cave McClintock x2 -
- Armpit! Barlow - SAD Synchronisation is adaptive Objective Measuring pheramones? Practical applications Case studies Generalisability Biological Rhythms Jet Lag Jet lag occurs when the individual crosses time zones because it disrupts the natural rhythm of the biological clock. Klein - Westbound Flights Schwartz - Baseball Studies *Direction
* Time zones crossed
* Individual differences Factors Affecting * adjust to local zeitgebers immediately
* go out in morning daylight as soon as possible (melatonin)
* melatonin medication Beaumont et al (2004) Reducing Jet Lag Evaluation * anxiety night before * travel itself is tiring
* effects of alcohol and coffee
* low-oxygen cabin air * travelling is stressful * link between melatonin and sleepiness, melatonin tablets cure for jet lag.
* adopt the social rhythms of their destination Shift
Work Working patterns which enable factories and organisations to work around the clock. Monk and Folkard (1983) - Types of Shift
Work rapid rotation/slow rotation RESEARCH STUDIES Czeisler et.al. (1982) – chemical plant in Utah
Czeisler introduced a forward shift rotation = happier, healthier and more productive Coren (1996) – Rapid shift rotation
changing shifts every two or three days avoids trying to adjust RESEARCH STUDIES RESEARCH STUDIES RESEARCH STUDIES EVALUATION *light acts as a zeitgeber in maintaining the rhythm of the SCN > Workers exposed to a 4 hour pulse of bright light showed improvements in work performance.
*The negative effects of shift work are indisputable,
the accident record and workers’ self-reports
*Slow and fast rotation have negative consequences.
Fast rotation = constant state of disruption.
Slow rotation = permanently altering circadian rhythms, may cause lasting harm.
*Practical application - use of light to improve workers performance. CONCLUSION * many other factors affect shift work and jet lag
*Both jet lag and shift work have real consequences, many of them negative.
*Fortunately, research can be applied to finding ways to relieve the problems. * goes against the mainly endogenous,
* results in fatigue, headaches, and lack of concentration.
ACCIDENTS >all occurred between 1am and 4am,
* Chernobyl (nuclear explosion)
* Bhopal (explosion at a chemical plant),
* Three-Mile Island (near melt down of nuclear reactor)
*Exxon Valdez oil spill CONSEQUENCES OF
SHIFT WORK Seasonal Affective
Disorder "a form of clinical depression in which the sufferer experiences low levels of mood with the onset of Autumn and falling light levels" *studied Pat Moore
*suffered unipolar depression at start of winter
* tested the idea that light could affect Pat's mood
*used artificial lights in the morning to replicate sunlight
*Pat reported feeling less down within days Case Study *the brain very sensitive to light and day length, but the response to this can be negative, causing SAD.
*extra light = negative effects reduced, however, it is not a cure.
* single case study
* placebo effect
* Booker and Hellekson - incidence of SAD of about 9% in Alaska, Tondo et.al. (1993) found similar rates in Italy – a country known for its sunshine
*Treatment with selective serotonin reuptake inhibitors (SSRI’s) has also shown an improvement in mood Evaluation Disrupting Biological Rhythms Functions of Sleep Outline Evolutionary Theory Evaluation Sleep may serve an adaptive rather than a restorative function. This means that sleep has been naturally selected because it promotes survival. Webb 'Hibernation Theory' - One way in which sleep might help us survive is because it forces us to conserve energy at times when it would be inefficient for us to be awake. In this sense, sleep is like hibernation. Meddis (1979) the time that mammals spend asleep is related to whether it is a predator or a prey species. This is called the ‘safety needs hypothesis’. Therefore sleep is adaptive, it helps us stay safe and helps ensure the survival of our species. * Low adaptive value – in some species if sleep were simply adaptive then it should have been selected out.
* Lacks scientific validity – evolutionary theories are post hoc, i.e. they have been proposed retrospectively and consequently lacks empirical support
* Deterministic and reductionist – they ignore free will, therefore they are reductionist. Sleep is far too complex a process to have evolved solely as protection
* Evolutionary theories ignore the physiological and psychological functions of sleep and so are unlikely to provide a full explanation for sleep.
+ve Studies of sleep deprivation – the fatal effects shown in some of the sleep deprivation research confirm that sleep is necessary for survival.
-ve – Ratio of predator/prey sleep duration – the ratio of predator/ prey sleep duration seems to contradict Meddis’ theory that sleep provides protection from predators, prey should sleep longer than predators when in fact the opposite usually occurs. Restoration Theory Evaluation Outline OSWALD
The most well known restoration theory of sleep function is that proposed by Oswald (1966, 1980). According to Oswald, stage 3 & 4 sleep has 3 main functions:
• To restore depleted energy resources
• To eliminate waste products from muscles
• To recover physical abilities HORNE
Distinguished between core sleep and optional sleep. He proposed that core sleep was critical for restoration of the brain and normal functioning. SHAPIRO
Shapiro et al (1981) found that people who had competed in an ultra-marathon, a running race of 57 miles, slept an hour and a half longer than they normally did for two nights following the race. Stage 4 sleep occupied a much greater proportion of their total sleep time (about 45%) than normal (about 25%). Researcher Effects Reliability - Research is inconsistent and lacks reliability Face Validity - theory is highly plausible Objective measurements Growth Hormone - release of growth hormone at stage 4 supports Oswald Brain activity in REM - provides evidence for brain recovery Babies sleep patterns - babies spend 2/3s of the day asleep supporting the idea that REM is a source of restoration Duration of protein synthesis - can only occur for a limited time during sleep Not all sleep lost is recovered - if the function of sleep is restoration then lost sleep would need to be recovered, this is not always the case e.g. Gardner Sleep Disorders Insomnia “A condition whereby there are problems falling asleep and/or staying asleep. Sleep tends not to be deep and is easily disturbed.” Diagnostic criteria for insomnia requires one or more of the following:
* Sleep onset latency (time taken to fall asleep) of more than 30 minutes
* Sleep efficiency (time in bed actually asleep) of less than 85%
* Increased number of night-time awakenings Primary Insomnia The most common form of insomnia that has no underlying cause.
There is a clear problem with sleep, but there is no physiological or psychiatric cause.
It is likely that the sleep problem is the result of maladaptive behaviours or learning.
For at least one month the individual would have suffered insomnia.
This would not be linked with any other sleep disorder.
It would not be linked with another psychopathology such as depression, medication or substance abuse.
The most severe form of primary insomnia
It is a rare condition that begins in childhood and is effectively lifelong
In its most severe form, it does not vary with life circumstances or psychological well being
It may be associated with high levels of depression
It may be genetic; there is evidence that it can run in families
People learn to cope with idiopathic insomnia and function reasonably well Specific causes may include:
Sleep apnoea – the cessation of airflow during sleep preventing air from entering the lungs caused by an obstruction (stopping breathing)
Restless legs syndrome
Circadian rhythm disorders
Various medical, substance-use and emotional problems Secondary Insomnia Psychological disorders such as depression, schizophrenia and anxiety states; around 40% of patients seeking treatment for insomnia have an associated psychological disorder.
Medical conditions such as heart failure, Parkinson’s disease and asthma can also be linked.
It is often the medical treatments for the above illnesses that cause secondary insomnia. Causes Drug use can lead to insomnia:
Stimulants such as amphetamines
Misuse of sleeping pills
All of the above may lead to disruptive sleep patterns and increased insomnia. Drugs Factors Affecting As the brain is still active, alert and in day time mode, the natural changes that lead to sleep are unlikely to occur. Bedtime Behaviour The following factors can all contribute to insomnia:
Hot or cold rooms
An uncomfortable bed
A snoring companion Environmental
Factors Stress Acute stress, possible brought on by a major life event, can lead to insomnia.
Vahtera (2007) found that traumatic life events are highly correlated with sleep disorders in vulnerable personalities.
Vgontaz (2001) found that there is an association between insomnia and an increase in the stress hormone ACTH. Sleep Hygine Certain habits promote the calming and slowing down of the brain in preparation for sleep.
However, certain habits, for example smoking or drinking alcohol, may interfere with brain activity. Illness Medication may cause or contribute to insomnia. Personality An average nights sleep is approximately 7.5 hours long (although this varies).
However, Van Dongen et al. (2005)found there is no clear psychological or personality differences between long and short sleepers.
Research has found that people who suffer from an anxious personality are more likely to suffer from insomnia.
Monk et al. (2007) found a link between higher neuroticism as a personality trait and the timing and poorer quality of sleep
Sleep patterns can be linked to your chronotype:
Larks are ‘morning types’
Owls are ‘evening types’
Your chronotype is genetically determined; therefore, pretending you are an owl (if you are really a lark) and vice versa, may cause sleep disorders Evaluation Insomnia is a complex disorder and probably results from an interaction of many factors.
Spielman and Glovinsky (1991) suggest the predisposing, precipitating, perpetuating model to explain the onset and maintenance. This is similar to the diathesis-stress model we saw in abnormality at AS but takes it a stage further.
Predisposing: refers to the genetic component which makes the onset of the disorder more likely. As we’ve seen this predisposition seems to be mediated by greater cortical arousal making increasing the ‘tipping point’ for sleep. (This is the diathesis)
Precipitating: an environmental factor such as stress or anxiety that trigger the inability to sleep.
Perpetuating: During the insomnia patients have suffered anxiety due to inability to sleep and have learned to associate various nighttime habits and even the bedroom and the bed itself with sleeplessness..
Patients become dependent on the drugs and suffer even worse insomnia when they stop taking them.
Evaluation of research into insomnia
Dement (1999) believes there are so many variations of insomnia with so many causes that its barely worth trying to make general comments about the disorder. In fact he goes a step further and suggests that insomnia is not a disorder at all, merely the symptom of a whole host of other disorders. He suggests that doctors should not attempt treatments for insomnia but treat the underlying causes instead.
Very often diagnosis of insomnia is based on self-report. However, a lot of research suggests that patients claiming to be insomniac are in fact getting far more sleep than they believe, making this method very unreliable. Smith et al (2002) found evidence for physiological differences in the brains of insomniacs,
Nine women, five insomniacs and four controls slept in a sleep lab for three nights. They recorded brain activity, breathing, muscle tone etc) and on the third night they also underwent a brain scan.
It was found that the insomniacs had a significantly reduced flow of blood to various areas of the cerebral cortex suggesting abnormal activity during NREM sleep.
Morin et al (2003) investigated the link between stress and insomnia
67 participants comprising 40 insomniacs and 27 controls completed a series of questionnaires assessing:
•Their daily stressors (major life events and trivial daily hassles)
•Their pre-sleep levels of arousal
•The quality of their sleep
Although the insomniacs were experiencing similar numbers of stressful events to the control group they were reporting significantly higher levels of anxiety. Research