One theory of romantic relationships is the Reward/need satisfaction theory, this states that relationships are rewarding, and on the contrary being alone is unrewarding. Relationships can be formed through direct rewards (operant conditioning) by meeting psychological needs e.g. love, sex, or indirect rewards (classical conditioning) through associating the person with a positive circumstance for example if you’re in a happy mood the day you meet the person, you may associate that pleasant mood with the person, making you more likely to be attracted to the person. Another way in which relationships are formed is through reinforcement, positive reinforcement is simply through giving non-verbal signs such as smiling, reinforcing positive attitude. However, negative reinforcement can be through the person helping escape a negative mood for example if you’re feeling down about an aspect of your life and you meet someone and they cheer you up.
Support for this comes from May and Hamilton who asked female students how attractive they rated a picture of a male, they were split into three conditions; pleasant music, unpleasant music and a control group of no music, whilst they answered the scale. As predicted, those listening to pleasant music (classical conditioning) rated the male highest on attractiveness compared to the other two conditions. This suggests that the females associated the pleasant circumstance (music) with the stranger in the photograph. However, this study is gender biased as it only had female participants, and therefore we cannot generalise these results to males, as they may react differently. This study was also self-report data, meaning the internal validity is reduced as the participants may have lied to be more socially desirable, maybe they would feel guilty if they gave the male a low attractiveness score. Finally, the study lacks ecological validity seeing as the females rated attractiveness via a scale, this isn’t likely to happen in real life and therefore we cannot generalise these results outside of this condition.
This theory of relationship formation has been criticized for being reductionist as it simplifies relationship formation to only regarding receiving rewards, however Hays found that when examining student friendships as much value was given to rewarding other people, as to receiving rewards themselves. Furthermore, there is a cultural bias in the theory as Hill found that social relationships in non-western collectivist cultures show little concern for receiving reinforcement, therefore using this theory to explain relationships of a collectivist culture wouldn’t be applicable. Again in Lott’s study, he found that in many cultures women are socialised into being more attentive to the needs of other’s such as the husband or children, rather than focusing on their own personal needs, this theory therefore has a gender bias as it cannot be used to explain why in some cultures such as collectivists why females do not focus on their own needs, yet relationships are still formed.
This theory of reward/need satisfaction ignores the biological needs of reproduction in relationship formation, and only focuses on behavioural explanations. The next theory is an Evolutionary explanation which states that humans form relationships simply to pass on our genes via reproduction. There are differences in the challenges both males and females face when forming a relationship, for example males face the risk of cuckoldry which is the risk of investing resources into an offspring that is not your own, as males cannot be certain of paternity like females can. However females risk losing resources such as time and money for themselves and the offspring. This then extends to differences in what males and females look for in a partner; males tend to look for high reproductive value in terms of physical attractiveness as this means good quality genes, which is adaptive as offspring is more likely to survive. Females look for economic advantages such as wealth, parenting skills etc. which can assist in providing for the offspring and is adaptive in enhancing their survival.
Buss has supported this as a universal view of relationships; he studied 37 cultures with over 10,000 participants and found that males indeed wanted attractiveness in their female partner, and females wanted males with high economic resources and security. This shows that this theory is universal and there is no culture bias.
Waynforth and Dunbar also supported the evolutionary theory with the lonely hearts ad in American newspapers. He did a content analysis on what the females and males looked for in a partner and the results were that 44% male’s wanted attractiveness compared to only 22% of females. This suggests that physical attractiveness is more important to males than females, due to wanting good reproductive value. However, a criticism of this study is that it was based entirely on American participants, so these results cannot be generalised to other cultures.
This theory however is criticised for it being purely evolutionary and based on ancestors, this theory ignores proximate factors, such as the fact that in today’s society we no longer need the male to go out and hunt for food and resources in order to help our offspring survive, in today’s society the female can go shopping for food and resources herself. This theory also cannot be used to explain homosexual relationships, and has a heterosexual bias seeing as it is heavily based on reproduction. Due to the fact homosexual relationships do exist, there must be further reason for relationship’s forming other than reproduction.
“Discuss neural and hormonal explanations for aggression”
Neurotransmitters are chemicals that allow impulses within the brain to be transmitted from one area of the brain to another, the main neurotransmitter believed to play a part in aggression is serotonin, as low levels of serotonin can make a person impulsive and overly responsive, which often leads to aggressive behaviour.
Support for the serotonin link comes from Mann, who administered a serotonin depleting drug into 35 adults and then gave them a questionnaire to measure their hostility. The levels of hostility increased in males but not females. This suggests that when serotonin levels are low, aggressiveness does increase, however there is a clear gender bias as the aggression increased for males and not females, this could be explained by the use of self-report to measure aggression, as males may rate themselves as more aggressive due to demand characteristics and the stereotypical view that males are more aggressive than females. This study can also be criticised for having low ecological validity, due to the fact the aggression is measured on a hostility scale, which isn’t a real representation of aggression, therefore in a real life situation where serotonin is low, aggression could be displayed differently.
High levels of dopamine has also been linked with aggressive behaviour, although this is inconclusive as there is evidence to suggest that high dopamine levels are rewarding for a person and acts as a positive reinforcement. This suggests that individuals may seek out aggressive acts solely to increase dopamine levels and receive this rewarding feeling, therefore there is not conclusive evidence as to what the causal factor actually is.
Evidence to support the dopamine link comes from Buitelaar who administered a drug to reduce levels of dopamine in violent delinquents, which was found to reduce aggression levels, suggesting that when dopamine levels decrease, so does aggression. However, there is an issue with the sampling of this study, as the violent delinquents aren’t going to express the same level or type of aggressive behaviour as the wider population would on a day to day basis.
Further support for dopamine and serotonin link comes from Ferrari, who made rats fight at the same time every day for 10 days, then on the 11th day the rats were prevented from fighting, however they experienced high levels of dopamine and low levels of serotonin at the time the fights usually occur, suggesting the neurotransmitter levels were in anticipation of the fight. This suggests that neurotransmitters do play a role, however it is unclear whether the low or high levels of dopamine and serotonin cause the aggressive behaviour, or whether the aggressive behaviour causes the levels to increase or decrease. However, there are issues with this study relating to the use of non-human animals, as the results from this rat study must be generalised with caution as when applying to humans, the biological makeup and anatomy of rats and humans are significantly different, so these results may not be valid for humans.
The other explanation of aggressive behaviour comes from hormonal mechanisms, which have an important role in influencing aggression. There is a suggestion that high levels of testosterone can increase aggression, as Book did a meta-analysis of 45 studies and established a 0.14 correlation between testosterone and aggression. This is a positive correlation, however it is weak and correlational data isn’t valid as we cannot establish cause and effect, for example testosterone could cause aggression, or aggressive behaviour could lead to higher levels of testosterone.
More superior evidence comes from Pope, who tested the testosterone and aggression link scientifically using objective and empirical methods, a few key features of a science. Psychologists provided participants with testosterone drug, and some were given a placebo drug. This study was experimented using a double-blind technique, so neither the participants or psychologists knew who was given what drug. The participants were given these drugs for 6 weeks, and then were asked how much money they would take from a fictional character. Those given the testosterone drug took the most amount of money. This suggests that when testosterone levels increased from the drug, this led the participants to become more aggressive, however the measurement of aggression being asked to take money of a character, is not valid as It is unrepresentative of aggressive behaviour in the real world, for example shouting or violence would be a more appropriate measure, although because of the ethical issues involved in protecting participants from psychological and physical harm, this would not be able to be tested experimentally.
Further research suggests that the stress hormone cortisol is linked to aggression, it is suggested that there is an inverse correlation and that low cortisol leads to high aggression. Another suggestion is that cortisol levels being low creates an unpleasant feeling, which could mean that people then seek out aggressive acts to increase their cortisol levels and prevent this unpleasant feeling.
McBurnett provides support for the role of cortisol, as he evaluated 38 boys once a year for four years and found that the boys with the low levels of cortisol exhibited 3x more aggressive acts than those who had fluctuating or average levels of cortisol, suggesting there must be some relationship between the two. However, this is a longitudinal study and only provides a small insight into their aggressive behaviour, it could be on that specific day something happened which caused the boys to be aggressive, and the rest of the year there was little or no aggression shown. Popma however enhanced this theory by suggesting that cortisol is the mediator and that there is a positive correlation between testosterone and aggression, but only when the cortisol levels are also low.
Overall, the evidence is inconsistent as there is no clear evidence to show that hormones such as testosterone and cortisol solely cause aggressive behaviour, it could be the fact that aggression subsequently increases the hormones affected. The biological explanation of just hormonal and neural explanations is a reductionist view, as this ignores other biological areas of aggression such as genetics, both would be seen as a nature approach to aggression, which also doesn’t consider psychological explanations such as the social learning theory, which is more the nurture side, and may be a more valid explanation, as there is strong evidence for the idea that we observe and learn aggressive behaviour.
Genetic influence in aggression
In order to disentangle the nature (genetic influence) and nurture (environmental or social factors), researchers use a variety of studies including family, twin and adoption studies. In twin studies, MZ twins share 100% genes, compared to DZ who only share 50%. The traits of aggression are compared between the sets of MZ and DZ twins, and if the aggressive behaviour is solely down to genetics then the MZ twins should be alike – in terms of a concordance rate, this would be 100%.
Research support for the genetic influence in twins comes from McGuffin and Gottesman, who found a concordance rate of 87% for MZ twins and 72% for DZ. Although this does suggest some genetic influence as the MZ twins are more alike than DZ in terms of aggression, the behaviour can’t be said to be solely due to genetics, as the concordance rate for MZ is not 100%. Therefore, there must be other factors influencing the behaviour, such as environmental factors as sets of twins will share the same environment, therefore it is difficult to disentangle the influence of genes and environment, it is possible that they may work together with a gene-environment interaction.
To help disentangle the genetic or environmental influence, adoption studies are more effective. As if there is a positive correlation between a biological parent and an adopted child, it is likely to be due to genetics, however if a positive correlation occurs through the adopted child and adopted parents, it is likely to be environmental or social influence, such as the social learning theory.
Further support for genetics comes from Hutchings and Mednick, who studies 1400 adoptions in Denmark. There was a positive correlation between violent criminal convictions among the biological parents and the adopted sons, therefore this is a strong suggestion that genetic influence is a contributory factor, however as this is purely correlational we cannot say that genes cause aggressive behaviour, it could be a combination of genetic and social. Another criticism of this study is the use of adopted sons only, which creates a gender bias, as these results cannot be applied to females, which weakens the study as females may have different biological makeup or social influences that influences different levels of aggression than in males.
There is a major sampling issue with research into aggression, as the samples usually consist of violent criminals, which is not representative of aggressive behaviour amongst society as there are a great majority of the population that is aggressive but not convicted, also the issue that one criminal may be convicted of one murder offence, but hasn’t shown any other levels of aggressive behaviour. This means that the results of most studies cannot be generalised as it may not be the same aggression for general population.
There has also been a specific gene called MAOA that has been linked to aggressive behaviour. The MAOA gene regulates serotonin in the brain, and low levels of serotonin has been associated with aggressive behaviour. There is support for this gene from the Brunner Case Study, where one family in Netherlands, used urine samples to find MAOA levels and found a mutation on the X chromosome which affects production of MAOA. All 28 males had this mutation which led to mental retardation, however only 5/28 of the males were aggressive. This suggests that the aggression was not purely down to genetics as not all 28 were aggressive, the aggression may be caused by a predisposition to aggression and then becomes triggered by environmental factors such as stress. Further criticism of this study is that it was a case study, which means these results cannot be generalised to the whole population, as there may be individual differences or a certain role model in the family that has influenced the behaviour, rather than a genetic influence.
Overall, the genetic link as a theory is a reductionist theory alone, as it is solely one biological explanation and social and psychological factors play a huge role in aggressive behaviour, such as the social learning theory, which could be combined with this aggressive predisposition or influence. There is also evidence of free will regarding our aggressive behaviour, as just because our parents are aggressive it doesn’t mean we are all aggressive ourselves, this is ignored by this deterministic view.
There are also practical implications from this research toward the legal system, as if people are genetically predisposed to aggressive behaviour, treatments and sentencing of criminals may need to be reconsidered, and there are ethical concerns when labelling an individual as a violent criminal if it is beyond their control.
“Outline and Evaluate Psychological explanations for institutional aggression”
A prison is a type of institution which exhibits aggression within groups. One of the main model’s for institutional aggression in prisons is the importation model, which suggests that inmates import their own social histories and violent characteristics into the prison, which influences the behaviour within the prison. In addition to this, pre-prison gang membership is suggested to be a determiner of violence. This would be alongside the nature side of the nature/nurture debate, suggesting it is the individual’s makeup and characteristics that are the causal factor of the prison violence.
One strength of this model is that it can be supported by Harer and Stefensmiere, who studied 58 US prisons and found that black inmates had higher rates of violent behaviour than white inmates, and on the other hand white inmates had higher drug and alcohol usage in prison. This reflects the statistical differences found in the US society generally, therefore this is high in mundane realism to explain institutional aggression.
On the other hand, Delisi has criticised the idea that gang membership determines violence in prison, findings were that inmates with prior gang membership were no more likely than other inmates to engage in prison violence. However, this may be explained by sampling issues, as violent gang members are usually isolated from general inmate population, and this could reduce the aggression by 50%. Meaning this has a lack of internal validity and is therefore less of a criticism to the importation model.
The deprivation model, however suggests the opposite side to the importation model, this model focuses on the nurture side of the debate, suggesting that prison violence occurs due to the stressful conditions and environmental factors inside the prison itself; for example overcrowding and lack of social constraints. Sykes suggested that there are certain pains that an inmate has to deal with, such as loss of liberty and security, and that these environmental factors create a stressful situation for the inmates, and some inmates will cope with this through violent and aggressive behaviour.
Zimbardo has supported the deprivation model, as when conducting his Stanford prison experiment there were 24 males, which were psychometrically tested and were all healthy and non aggressive individuals, they played the role of the fake guards and prisoners, the institutional factors such as no social constraints and peer pressure from other participants, led to the guards brutal behaviour towards the prisoners due to there being no social norms throughout the experiment. The aggressive behaviour was so bad that the experiment had to be stopped earlier than planned. As the males were previously not aggressive, this is strong support for the deprivation model as there were no characteristics that could have been imported to cause this aggression. This study however can be heavily criticised, for it’s low ecological validity, because the experiment was not in an actual prison, meaning the behaviour in a real prison may differ, the amount of aggression shown could be due to demand characteristics, as we cannot say this is representitive of a real prison environment. However, there is a real life example as in the Abu Ghraib prison in Iraq, the brutal violence towards inmates was also demonstrated to be due to situational factors. Further critcism comes from the amount of ethical issues involved, for example the prisoners were not given fully informed consent and there was elements of deception involved that they were not aware of, for example the participants were arrested at their own homes, which they were not previously told about. There was also a great deal of psychological harm / distress involved, some participants stopped the experiment due to the amount of distress they recieved. This means that experiments such as this will not be able to be repeated in the furture.
McCorkle on the other hand studied a total of 371 US prisons and found very little evidence for the correlation between living conditions such as overcrowding, and violence. This suggests that there isn’t a strong link between the two variables, criticising the deprivation model for it’s lack of evidence. However, this could be explained by the cultural bias, as this study was only looking at US prisons, this lack of evidence may be due to the american culture, and this cannot be generalised to all cultures. For example prisons in a non westernised culture may have different conditions and violence correlation’s, therefore this weakens the criticism as it cannot be applied to other cultures outside of the US.
The deprivation model however has led to some real world practical applications, for instance Wilson found that when reducing the noise levels and providing more space for the inmates in Wood hull prison, the levels of aggression reduced, suggesting that conditions do have an impact on the inmates aggression. This research could therefore lead to reduced amounts of violence in many prisons.
Overall, these theories are deterministic, suggesting that the environment or characteristics of a person will lead to aggressive or violent behaviour, however this ignores those inmates that do not become aggressive or violent, regardless of their environment or prior characteristics, showing that there must be some free will involved, and providing evidence for individual differences amongst inmates, for instance the biology of each individual.
“Discuss explanations of sleep walking”
Sleep walking is a disorder that occurs in NREM sleep, and is mostly common among children rather than adults. The explanations for sleep walking are mainly biological, although there has been attempts at psychological explantations.
The first explanation is genetics, the idea that the disorder is inherited. Evidence for genetic inheritance comes from twin and family studies. In twin studies, we look at the concordance rate for MZ twins who share 100% of their genes, compared to DZ twins who only share 50%. If the disorder is purely down to genetics, then the MZ twins should have a 100% concordance rate. On the other hand with family studies, we compared the first degree relatives of a sleepwalker with a healthy control and if it is due to genetics then a first degree relative will have a high chance of developing the disorder also.
Evidence for genetic inheritance was found by Broughton who did a family study and found that first degree relatives of a sleepwalker are 10x more likely to suffer from sleepwalking themselves, suggesting some genetic link. However, Lecendrequx, compared the concordance rate of MZ and DZ twins for sleepwalking. The concordance rate for MZ was 50% compared to 10% for DZ twins. Therefore this suggests that there must be other factors involved, as it cannot be purely genetics otherwise the concordance rate would be 100% for MZ twins. Therefore, a genetic explanation for sleepwalking alone would be reductionist and would only consider the nature side of the debate, we must look at environmental factors or the nurture side of the debate. Therefore it has been suggested that there may be a genetic predisposition to the sleep walking disorder, which is then triggered by an environmental factor, such as stress. This is known as the diathesis stress model. Evidence for this comes from Zadra, who found that when sleep deprived, those genetically vulnerable showed signs of sleepwalking, compared to those who were not. Therefore sleep deprivation could be a stressor or trigger that in turn results in those with a genetic vulnerability to develop sleep walking.
The second explanation for sleep walking is brain development, as sleep walking is more prevalent in children, this suggests that it could be linked to the development of the brain, as children’s brain’s are developing more than adults. Oliverio supported this theory by comparing motor excitability levels in adult sleep walkers to normal controls, he found that sleep walkers had signs of immaturity in relevant neural circuits. Enhancing the idea that the brain may be under developed. This research would have been more superior if conducted with children participants, however this would be difficult to do due to the ethical issues involved in experimenting children.
Overall, these explanations alone would be seen as reductionist, although psychological explanations have been suggested, such as the idea that sleep walking occurs because the individuals are acting out their dreams. However, through further research into sleep and dreaming by Dement and Kleitman, it was found that dreams tend to occur in REM sleep, and sleep walking tends to occur in NREM sleep.
There are many practical implications from research into sleep disorders especially that of sleep walking, as there have been cases where criminals have claimed their sleepwalking caused them to murder and that they had no idea what they were doing due to being unconscious. Therefore it is important to research into finding out whether sleep walking is deterministic, and occurs as a result of an uncontrollable biological factor, or if there is evidence of free will which causes the individuals to murder. Therefore sleep walking research has practical implications to the legal system.
“Discuss research into disrupting biological rhythms”
Rhythms such as circadian sleep wake cycle can be disrupted when people work shift patterns or experience jet lag. The impact of desynchronisation can be negative in terms of decreased alertness, sleep deprivation and health problems. Shift workers who sleep in the day and work through the night are going against their natural circadian cycle and have difficulties entraining their rhythms.
Decreased alertness is one impact of shift work, as the circadian trough of decreased alertness occurs between midnight and 4am when cortisol levels are at their lowest and temperature is at it’s highest. Decreased alertness can increase the amount of accidents and reduction in focus occurring at work, therefore leaving you stressed.
Sleep deprivation is another impact which can occur, as Tilley and Wilkinson found that shift workers sleep 1-2 hours less than non shift workers. This is likely down to the noise, light or social demands that occur in the day, when the shift workers are trying to sleep, this disrupts their sleep and leaves them sleep deprived, which can have further impacts on their health, such as cognitive impairments.
Further health issues have been related to a disruption in biological rhythms from shift work, Knuttson found that individuals that have been doing shift work for 15 years are 3x more likely to develop heart disease. However, as this data is correlational, it is difficult to establish whether these problems are a result of disrupted rhythms (biological) or disrupted social routines for example (psychological). There are also extraneous variables not considered with shift work, for example the health related problems aren’t necessarily due to disruption of biological rhythms, there are a number of reasons why a person may develop heart disease, for example diet, stress, social factors such as life events, or a genetic predisposition.
Research into shift work has discovered practical implications, for example Czeizler studied chemical plant workers on night shifts, and changed their shift patterns to forward rotating shifts in a cycle of 3 weeks. Researchers then gave the participants a survey to fill out, Results were that the workers alertness increased and the amount of mistakes made decreased. This suggests that by adapting workers shifts correctly, these negative impacts can be reduced.
With regards to jet lag, travelling across time zones can also disrupt the natural circadian rhythm. There are two types of jet lag, travelling east to west causes a phase delay, and travelling west to east causes phase advance, this is harder to adapt to as individuals need to force themselves to go to sleep earlier. Evidence of phase advance having more negative impacts was found by Schwartz, who studied US baseball teams over a 3 year period. The teams that travelled East to West won 44% of the games, compared to teams that travelled West to East who only won 37%. This however ignores any extraneous variables such as the teams ability to play could simply be worse than the other.
The effects of jet lag being solely down to biological rhythms is reductionist, as it ignores social or psychological factors such as stress or anxiety from flying, noise or over crowded uncomfortable seats, all could prevent sleeping properly and then disrupt sleep for the next night, rather than the disruption in rhythms. Practical implications have occurred through this research into jet lag, as it has been found that melatonin injections, when given at the right point in the circadian cycle, can reduce the symptoms of jet lag. This further enhances the suggestion that jet lag symptoms are due to a disruption in biological rhythms, as melatonin is a chemical involved in the SCN process to maintain the sleep wake cycle.
“outline and evaluate explanations for insomnia”
Insomnia can be defined within DSM as experiencing sleep difficulties for 1 month, there are two known types of insomnia; primary which is when the insomnia itself is the disorder and there is no obvious other cause, secondary is when the insomnia is a result of another disorder such as sleep apnoea, or other trigger such as stress or anxiety.
Insomnia explanations are in majority biological, such as hyperarousal and genetics. Firstly, hyperarousal which is a state of long lasting arousal, has been suggested to be the cause of primary insomnia, symptoms are increased heart rate, stress hormones and anxiety levels. However, research has been done by Reimann who found that when comparing insomniacs levels of arousal to controls, the results were inconclusive, therefore there must be another explanation for insomnia, such as genetics.
Research has been conducted into genetics via twin studies. Twin studies use concordance rates of MZ twins who share 100% genes, compared to DZ twins who only share 50%, therefore if insomnia is genetically inherited, then the concordance rate for MZ twins should be 100%. However, in Watson’s study it was only 50%, which although still is a high indicator that genetics are involved, it can’t be solely a genetic inheritance as it is not 100%. Therefore, it has been suggested that genetics predispose individuals to the disorder, making those related to an insomniac vulnerable to developing insomnia themselves. This is then only further developed if those vulnerable come into contact with a precipitating factor, for example an environmental trigger such as stress or shift work related problems. This suggests that both environmental and biological factors combined may be the cause of insomnia, which is supporting both sides of the nature/nurture debate, which has been proven now that both sides do work together in some ways, such as gene environment interaction displayed here. Although, it has further been suggested there is also evidence of a perpetuating factor, in other words something that maintains the insomnia even when the original trigger has been removed. One example of this could be a self fulfilling prophesy, linked with the attribution theory. This suggests that the perpetuating factor, is the cognitive beliefs of the individual that they will have difficulty sleeping because they have insomnia, therefore attributing the sleep difficulties to insomnia. If convinced that the sleep difficulties are as a result of something else, the difficulties may stop.
To test this theory, insomniacs were given placebo drugs and were told that the drugs would either sedate or arouse them. Those insomniacs that were given the arousal drug went to sleep easier than those given the sedation drug. This can be explained by the attribution theory, as the insomniacs attributed their sleep difficulty to high arousal, and therefore were more relaxed knowing it was a result of something other than their insomnia.
Research such as this has major practical applications for treatments of insomnia, as cognitive treatments can now be used to help change the patients beliefs so they no longer attribute their sleep problems to insomnia.
However, this area of research is reductionist, as the biological predisposition along with cognitive beliefs fail to take into account why the insomnia occurred in the first place, it has been suggested by Dement that insomnia isn’t a disorder at all, but that it is a symptom of a range of other disorders, meaning there are major practical implications for treatments of insomnia, and it is hard to disentangle the casual factor, and it is difficult to generalise a cause.
“Outline and evaluate explanations of narcolepsy”
Explanations of narcolepsy are in majority biological. One explanation may be the lack of hypocretin, a chemical in the brain which regulates sleep and wakefulness. Therefore, a lack of cells producing hypocretin may explain sudden attacks of sleep, as sleep and wakefulness aren’t being regulated properly. Evidence for low levels of hypocretin has been found in narcoleptic dogs. The cause of low hypocretin in dogs has been found to be a mutation on a gene which affects the production of hypocretin. Superior research has been found in humans by Nishino, who also confirmed that narcoleptic patients had lower levels of hypocretin. However, This research is all correlational and we cannot establish cause and effect, for example low levels of hypocretin could actually be a consequence of narcolepsy, not the other way around. There is also questions surrounding the causes of low hypocretin levels, as genes have been found to be the cause in non-human animals such as narcoleptic dogs, although there isn’t a strong generic link for low levels in humans. Meaning there must be other causes such as; diet, stress, brain injury or an autoimmune attack.
This brings us into the second explanation for narcolepsy, a mutation in the immune system. There is an increased frequency of HLA, which coordinates the immune response, in narcoleptics, it has been found that 90% of narcoleptics have this HLA variant, although this has also been found in non-narcoleptics and is common in the population. Therefore, it cannot be purely down to the HLA variant.
Furthermore, an autoimmune attack, one of the possible causes of low hypocretin levels, is more likely to occur when suffering from this HLA variant. Therefore it is possible that the increased frequency in HLA, increases the chances of an autoimmune attack, and the autoimmune attack is responsible for creating low levels of hypocretin, which then goes onto develop narcolepsy.
There is one final explanation of narcolepsy, which is a believed malfunction in REM sleep of narcoleptics. This would explain the cataplexy (loss of muscle tone) symptom of narcolepsy and explain intrusions of REM via hallucinations when awake. Research by Vogel has supported this theory, as when observing REM sleep in narcoleptics he found that REM sleep occurred at the beginning of the patients sleep, whereas it usually occurs later on in the sleep cycle. This further supports the idea that narcolepsy occurs from a malfunction in the REM system. However, this research can be criticised for it’s small sample size, meaning it not generalisable to the wider population, as individual differences could be the extraneous variable of the results.
Overall, there is a strong link between narcolepsy and HLA/Hypocretin, and it is apparent that both may influence the disorder, however there is a lack of consistent evidence for the REM malfunction being a cause. These explanations, being solely biological, are a reductionist view towards the disorder, as they ignore other causes of narcolepsy such as any psychological explanations, or a combination of biological with other explanations.
Furthermore, there are practical applications that have occurred through this research into narcolepsy in the form of treatments, such as hypocretin based drugs which have been found to be effective, suggesting hypocretin is a likely contributory cause of narcolepsy.
“Discuss research into the nature of sleep including life span changes”
The sleep wake/cycle is a circadian rhythm occurring once every 24 hours, within this cycle there is the ultradian rhythm of the sleep stages, which lasts for about 90 minutes and occur more than once every 24 hours. Dement and Kleitman discovered the stages of sleep using EEG scans to measure brain activity objectively. The results were that stages 1 and 2 were considered ‘light sleep’ which is characterised by alpha and theta waves, this reflects relaxation and slows down bodily functions. Next are stages 3 and 4, which are deep sleep characterised by slow delta waves which slow down the rate of the heart and decreases body temperature. In stage 4, also known as slow wave sleep, the growth hormone is released which shows most of the bodily repairs occur in this stage. Finally there is stage 5, which is REM sleep (rapid eye movement). This is characterised by fast brain activity and is also commonly known as paradoxical sleep, this is because the brain and eyes are active but the rest of the body is paralysed. Further research by dement and kleitman has discovered that dreaming is most commonly occurring in REM sleep, this was also a result of EEG scans in a sleeping lab, and the participants were awoken during NREM and REM and asked to report any dreams, dreams were most commonly reported in REM sleep and were less vividly reported in NREM sleep.
The research by dement and Kleitman is praised for using EEG scans which are highly controlled and is an empirical method of measurement, this in turn makes the results more objective and can increase validity and reliability. However, criticisms of this study is that it lacks ecological validity due to the use of a sleeping lab, which may disturb the participants sleep and therefore won’t be a realistic representation of the natural sleep.
Practical applications have occurred from this research, as the use of EEG scans have provided a better method of identifying sleep, and in turn have helped in discovering explanations and treatments for sleep disorders such as narcolepsy.
Life span changes in sleep begin with infancy, babies sleep for 16 hours a day and there sleep cycles tend to be shorter, waking hourly. Babies have active and quiet sleep, similar to REM and NREM sleep. 50% of babies sleep is REM sleep, and a circadian rhythm is established at 6 months, when the amount of REM sleep reduces. Further support for babies sleep is that premature babies experience 90% REM sleep, suggesting that the more mature the human is, the less REM sleep is needed. It is suggested that babies sleep has an adaptive function, as the long amounts of sleep allows parents to complete survival enhancing chores such as finding food, cleaning etc. Although this is ignoring proximate causes such as that humans no longer need to go foraging for food, and can quickly get food from a shop and stock up in their home.
When moving from childhood into adolescence, there is an increased need for sleep, approximately 9-10 hours. Circadian rhythms change so that individuals will feel more awake at night and find it difficult to wake up, this is called delayed sleep phase syndrome. Practical implications have occurred from these research findings, as Wolfson and Carckdon have recommended that schools should start later in the day to accommodate for the poor attention and focus of adolescents in the morning, as this could improve their education.
Next we look at adult and old age, adults sleep approximately 8 hours and only 25% of that is REM. Elderly people have more difficulty going to sleep and wake up more frequently, therefore will nap during the day and this could results in negative effects as it interferes with their circadian rhythm. REM sleep further decreases to only 20% and SWS is as little as 5%. The lack of SWS results in a reduced production of growth hormones may explain some symptoms of old age such as the lack of energy and muscle and joint problems, which can help with practical applications such as treatments.
Overall, the life span changes appear to be deterministic, such as age predicting sleep length, however there is evidence of free will involved in this area as individuals do need more sleep than others, some need less sleep than others. Finally, the research on life span is culturally bias as most of the research is based on British and American samples, there are some differences within cultures that aren’t accounted for. 11 cultures were researched in Korea and the results found that there were less sleep in adolescents due to the amount of time spent outside the house, meaning they went to bed later, and the average sleep time was 6.5 hours, which highlight differences in the research we have found, therefore we hold a bias view towards life span changes.
Discuss endogenous pacemaker as a control of biological rhythms”
Endogenous Pacemakers (EP) are internal biological clocks that manage our rhythms. The Suprachiasmatic Nucleus (SCN) is the main EP, which maintains our circadian rhythm of the sleep/wake cycle. The SCN obtains light from the optic nerve, and sends signals to the pineal gland, this then regulates the production of melatonin and serotonin, regulating our sleep wake cycle.
Evidence for the SCN controlling our sleep wake cycle comes from Morgan, who bred mutant hamsters so they had a circadian rhythm of 20 hours, and transplanted the SCN of the mutant hamsters into unaffected healthy hamsters which had a regular rhythm of 24 hours. When transplanted, the healthy hamsters too developed a circadian rhythm of 20 hours. Which shows that EP’s do control our sleep wake cycle. This study can be criticised for it’s use of non-human animals, meaning the results need to be generalised with caution. This is because humans and hamsters have different autonomy and biological make-up, so we cannot be sure the same results would occur on human participants.
It has been suggested that endogenous pacemakers have an adaptive value in controlling our biological rhythms such as the sleep-wake cycle, suggesting it aids survival. This is shown through research by DeCoursey who found that removing the SCN in 30 chipmunks and returning them to their natural habitat proved costly for their survival. Therefore suggesting that the SCN aids survival by maintaining circadian rhythms alongside environmental cues- for instance going to sleep when predators such as foxes are out.
Isolating participants on 24 hour cycles from Exogenous Zietgebers (EZ) has found that our EP creates a free running cycle of 25 hours. This was found in a few studies, firstly Michel Siffre spent 6 months in a Texas cave with no EZ’s, this brain was monitored by EEG and at first his sleep wake cycle was very erratic, reaching over 40 hours, but eventually his sleep wake cycle did settle down to approximately 24-25 hours. Showing that EP do run on around 24 hours even when EZ’s aren’t present to guide them. This can be criticised for being a case study, as there are individual differences such as his bodily history and sleep patterns that mean these results cannot be generalised to the wider population.
Further, more superior research has been done by Aschoff and Wever, where participants were kept in an underground bunker in absence of social cues. Most sleep wake cycles were around 24 hours, however one was 29 hours. This shows that circadian rhythms persist to exist despite isolation from natural light and social cues. However, this study may lack internal validity as extraneous variables such as artificial light weren’t taken into account, and it has been found that artificial dim lighting can still have an impact in resetting the sleep wake cycle.
Overall, this suggests that EP’s predict our sleep wake cycle, making this a very deterministic view, however there is clear evidence of free will in our sleep wake cycle, for instance in Aschoff and Wever’s study there was one individual that had a 29 hour rhythm, showing that there are some individual differences involved and that our rhythms aren’t entirely determined by our internal clock. Furthermore, there is too much emphasis on the nature side of the nature/nurture debate, as it is evident that both interact with our rhythms, as EP’s and EZ’s do work alongside one another, and do not entirely work alone. Finally, this theory can be criticised for being reductionist as biological rhythms such as the sleep wake cycle could be a behavioural or social theory, as it is widely socially accepted that you fall asleep when it is dark, and wake up when it is light, therefore basing our rhythms entirely on biological factors is reductionist.
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