Sleep_Deprivation

Outline one example of a circadian rhythm A circadian rhythm is a biological rhythm that’s happens every 24 hours. An example of a circadian rhythm is the sleep-wake cycle. Every day we will sleep and we have adapted to this over time as generally speaking we are awake in the morning and asleep at night. Exogenous zeitgebers and endogenous pacemakers work together to control this biological clock, to keep the cycle in-sync adjusting the inherited genetic clock with the environment by sensing when it is light through communication between the pineal gland and SCN, producing hormones such as melatonin to make us sleep. It is also shown that we will still go through the 24hr sleep wake cycle when our environment changes and there are no external factors, showing that our bodily functions are controlled inside in 24 cycles. Supporting this, the SCN, when in petri dish still works in a 24.5 hour cycle! Outline and evaluate one or more explanations for sleep disorders. Explanations of sleep disorders tend to have a behavioural and biological theory to explain them. Insomnia is one of them that has many genetic factors as well as environmental. Insomnia is a sleep disorder where you basically are unable to sleep. There are two types of insomnia, primary and secondary. Primary insomnia is the illness itself. The sleeplessness is not caused by a medical, psychiatric or environmental cause. This sleeplessness would have to last at least one month, does not occur purely during other sleep disorders such as narcolepsy and is not because of possible physiological effects from using drugs and medication. If there are other underlying causes to the disorder, it would then be secondary insomnia where a psychiatric (depression) or medical disorder (chronic pain) causes the sleeplessness. They range from causes such as hormone changes, asthma, stimulants and temperature etc. As I said earlier, primary insomnia is the illness itself and is not affected by medical and environmental causes. This leads us to believe if it is a disorder, if there is any biological research to show that insomnia is genetic. Dauvilliers did a study on chronic insomniacs to see if there was a link between them and their close family. After asking 256 repeated primary insomniacs to complete psychometric questionnaires, questionnaire about their family history, a clinical interview (and even a polysomnography in order to collect physiological recordings of the participant’s sleep) and using a control group to find an estimated base-rate incidence of insomnia in their families to understand what all the various data meant, he found a higher percentage in participants with primary insomnia reported familial insomnia compared with the non-insomnia control group. This research suggests a familial link to primary insomnia. This study collected a lot of data from numerous measures as well as using a large sample of chronic insomnias (who are sufferers of insomnia for a long period of time) and a control group, suggesting that the data collected is reliable. But do we really understand what it means, what does it actually show about insomnia' There is little scientific proof that this link exists, it all lies on the fact that the participants believe it’s in their family history. In order to prove that sleep disorders and insomnia are biological we must look at other research to show there is some evidence of this. Insomnia is inability to sleep; this suggests a problem with our sleep-wake cycle. It is a circadian rhythm affected by endogenous pacemakers as well as exogenous zeitgebers. We are able to adjust to our environment relatively well but if something happened to our endogenous pacemakers, this could result in a sleep disorder. Idiopathic insomnia supports this hypothesis. It occurs due to brain abnormalities in mechanisms that control the sleep-wake cycle. Normally this tends to occur in children but if the sleeplessness becomes trouble for the rest of their lives, it is attributed to an abnormality in the neurologic control of the sleep-wake cycle as it creates problems promoting wakefulness/sleep because it affects the brain reticular system and media forebrain. There is physiological research that supports the idea that there is an abnormality with biological components that are involved in sleeping. Smith conducted a study using 9 female participants, of which 4 were control, to look into neuro-imaging of NREM sleep in insomnia. The patients with insomnia showed consistent and significant decreases in blood flow compared to non-insomniacs, providing possible evidence for physiological abnormalities with central nervous system activity in insomniacs during NREM. However there are various problems with this supporting study. Firstly it was carried out in laboratory conditions; this will affect results as it is not a natural place for someone to sleep. Therefore this can affect the validity of the results as the sleeping pattern could be affected in a new artificial environment. On the other hand, even though this is the case there has been research into how effective studies are in a laboratory. Garcia found a positive correlation with rating scales against laboratory measures for the sleep disorder restless lag. This shows that the lab measures could give good indications of some sleep disorders. But we must bear in mind that a correlation shows just a relationship between two things and not the cause and effect of each other and the study can have differences as it was concentrating on a different sleep disorder. However I believe the biggest problem is the gender and extremely small sample size of participants. There will be individual differences as the findings are estrocentric and could not possibly be generalised for all insomniacs on a study with only 5 sufferers even with some evidence that laboratory measures may not affect results as much as we thought. Questioning the ability to use biological research to generalise the explanation of insomnia leads me on to see if the behavioural approach is a more valid explanation of it. Another type of primary insomnia is Psychophysiological insomnia. It is the form of insomnia that is learned and is primarily anxiety-induced. It is where we become worried about sleeping through the process of classical conditioning. For example some activities such as turning the lights out, drawing the curtains and getting changed into our pyjamas can become linked with sleeping. Once these activities are repeated, they can trigger over-arousal and then consequently insomnia. Unbelievably, only a few interrupted nights a month is enough to produce a vicious cycle. You could be worrying that you are tired during the day and not had enough sleep, so try hard to sleep during the night, the anxiety keeps you awake and increases your worrying the next day about not being able to sleep. Compared to the other explanations of primary insomnia, the treatment for Psychophysiological insomnia targets the stressors and not the insomnia itself. So is this then arguably secondary insomnia not primary, as secondary focuses on other underlying factors' The explanations of secondary insomnia are based on physical underlying conditions and lifestyle factors. One of the highly reported conditions is the psychiatric factor, depression. People who suffer from depression tend to sleep badly and are wake up much earlier than wanted. Secondary insomnia is therefore a symptom of depression and supported by treatment of depression suffering insomniacs, as they experience improved sleep after taking anti-depressants and have no effect on the sleeping patterns of non-depressed insomnia suffers. Decreased melatonin production is another factor. It is the hormone that helps control sleep and with age the body produces much less, suggesting that older people are more likely to suffer from insomnia. However, I think that melatonin production in itself could be a biological explanation because it is a hormone that is affecting our sleep-wake cycle. Just as children may have brain abnormalities which affect their sleep patterns, some people could be born/develop lack of this hormone or unable to produce sufficient amounts. This could be treated by sleeping pills which contain the previously deprived hormone. Taking medication seems to be the way to treat secondary insomnia and although it is affected by environmental, physical conditions etc, they all seem to have an effect on our sleep wake cycle just as much as something biological would. The fact that they all inhibit our sleeping patterns, may suggest that insomnia is affected biologically. It appears that nearly all of the factors do affect our sleep wake cycle or even just interrupts a night’s sleep. As there are so many factors, we are starting to wonder if insomnia is a sleep disorder at all or purely a misconception. As is said earlier, secondary insomnia is much more common than primary. I think this is because there are so many other factors, anyone with the slightest difficulty sleeping may think they are suffering from insomnia. This is supported by sleep state misconception. Many people sleep fine at night but feel they have not slept adequately. In one of Dement’s studies, a patient who complained he suffered from serve insomnia spent 10 days in the sleep lab. He completed a questionnaire every morning to say how long he thought it took for him to get to sleep. He overestimated every time as he reported times of 1-4 hours yet he never took longer than 30 mins to fall asleep. This gives us another view entirely. If many of us underestimate the time we think we’ve slept , we may psychologically believe that is all the sleep we’ve had as there is difficulty distinguishing from sleep and awake and feel the true symptoms of insomnia. We’ve looked at so many types of insomnia not just secondary and even found that some people sleep more than believed. This makes it difficult to generalise all of the findings. Dement said “ there are so many different types of insomnia caused by different causes, its nearly impossible to make generalisations that describe all of the causes of insomnia in a meaningful way” for example, to find a way of treating all insomnia by looking purely at melatonin pills, it may help the elderly and teenagers but not effective in curing it for everyone else. This suggests that insomnia is not a disorder at all; that we must find the main cause and treatment of this will help. Dement believes that it is purely a symptom created by a number of causes and the fact that most the secondary insomnia treatments target the condition, usually with medication, this may not be because it is a biological approach, as i previous thought, but just purely to treat the specific cause and not the reoccurring symptom that happens to be sleeplessness.