Topic I: Bio-rhythms (separated into six essay topics) Biological rhythms:
There are three types of biological rhythm; circadian, ultradian and infradian. Circadian rhythms are those which complete a cycle in a 24 hour period such as the sleep-wake cycle, heart rate or metabolism. People have variations within the circadian rhythms, notably the owl/lark division describing people who have biological clocks which run ahead or behind the average. Ultradian rhythms are those which occur more than once in a 24 hour period, for example eating or the sleep cycle which repeats approximately four times per night.
Infradian rhythms are those which occur over a period greater than 24 hours, such as the menstrual cycle and PMS. These and SAD (seasonal affective disorder) are the infradian rhythms which have attracted the most psychological research. The stages of sleep are an example of an ultradian rhythm, repeating roughly every 90 minutes while asleep. Since the invention of the EEG in the 1930’s the research into stages of sleep has drastically increased. In 1968, Kales and Rechtschaffen discovered four distinct stages people entered during sleep.
Stage 1 usually lasts for roughly 15 minutes at the beginning of the cycle and is characterised by slower ‘theta’ brain waves. Stage 2, lasting about 20 minutes is characterised by sleep spindles (bursts of high cognitive activity) and K-complexes. Following this is stage 3, which lasts for 15 minutes. In this stage, brain waves slow and increase in amplitude and wavelength, developing into delta waves. Stage 4 is similar to stage 3 and is when a person is most relaxed and most difficult to wake. The fifth stage of sleep is called REM (as opposed to stage 1-4 which are NREM stages).
During REM sleep the brain is almost as active as it is during the day. Sleep paralysis also occurs, meaning that while brain activity is high, because the pons disconnects the brain from the muscles, the body effectively becomes paralysed. There are a few infradian rhythms which have attracted a fair amount of research. Seasonal affective disorder affects a small number of people. It is a disorder where low light levels stimulate melatonin production (a neuro-chemical which induces sleepiness) and decrease serotonin production (which can lead to depression).
Terman et al. (1998) researched 124 participants with SAD; 85 were exposed to a bright light in the morning or evening while others were exposed to negative ions and acted as a placebo group. 60% of the morning light group showed an improvement, as opposed to 30% of the evening light group and only 5% of the placebo group. Therefore, it has been concluded that bright light acts as an exogenous zeitgeber, resetting the biological clock in the morning. The menstrual cycle, lasting roughly a month uses both endogenous pacemakers and exogenous zeitgebers.
On an internal level, this is controlled by levels of oestrogen and progesterone, both secreted by the ovaries. These cause the release of eggs from the ovum and the thickening of the uterus lining. One notable external factor is living with other women, which alters the cycle likely due to the secretion of pheromones which carry messages between individuals of the same species. This was investigated by McClintock and Stern (1988) in a 10 year longitudinal study. In this study sweat samples from 9 women were collected and dabbed on the upper lip of a separate 20 with histories of irregular menstrual cycles.
68% of recipients responded to the pheromones. This is supported by Russell et al (1980) who conducted a similar study where four fifths of participants responded to the pheromones. However, McClintock’s study has been criticised for a low sample size and Wilson (1992) believes that the results were due to statistical errors and when these are corrected the effect disappears. Reinberg (1967) reported on a woman who lived in a cave for 3 months; her menstrual cycle shortened to 25. 7 days. Therefore it may be possible for light levels to affect the cycle.
This is supported by Timonen et al. (1964) who found women were less likely to conceive during darker months due to the effect of light on the pituitary gland, which may have an evolutionary advantage. Endogenous pacemakers are internal factors which are able to regulate biological rhythms. To study these, Siffre (1962) spent 61 days in a cave in low light conditions. During this period, his body clock extended to a 24. 5 hour day and when he emerged he believed it was 28 days earlier than it in fact was.
This suggests that there is internal control of circadian rhythms because a regular cycle was maintained but also there must be exogenous zeitgebers that shorten the cycle to a 24 hour cycle instead of a 24. 5 hour cycle. There is conflicting evidence from Czeisler who conducted a study where participants were kept in constant low light conditions. In this study, a roughly 24 hour cycle was maintained; this is known as ‘free running’. However, a major criticism of Siffre’s study is that it was a case study and therefore, because of individual differences, other people may react differently.
The basis for endogenous pacemakers is the pineal gland, which secretes melatonin (the neurotransmitter that induces sleepiness). In some animals, this itself has photoreceptors that monitor light levels. However in humans, the SCN (suprachiasmatic nucleus) receives sensory input via the optic nerve and regulates melatonin production. Morgan (1995) transplanted the SCNs from mutant hamsters (with abnormal circadian rhythms) into regular hamsters. It was discovered that this caused the hamsters to develop abnormal circadian rhythms, implicating the SCN in the regulation of circadian rhythms.
But there are issues with generalising these results across species and releasing the hamsters into the wild. ***** Disrupting rhythms: Under normal circumstances biological rhythms are not in conflict with the daily lives of people, however there are two main examples of when conflict can occur; jet lag and shift lag. Jet lag (desynchronosis) is caused by the body’s internal clock being out of sync with external cues and has symptoms including fatigue, insomnia, anxiety and dehydration. Schwartz et al.
(1995) studied the performance and reaction times of baseball teams flying from the East to West coast of America and vice versa (a 3 hour time difference). It was found that teams travelling West performed considerably better than those travelling East. However, this was performed on sports teams who are likely to be trained to have high reflexes/ reaction times so there are difficulties in generalising the results of this study. De la Iglesia (2004) exposed rats to artificial days lasting 11 hours rather than 12. It was found that gradually, the rats began to exhibit daytime behaviour at night.
De la Iglesia went on to discover that both the top and bottom of the SCN contained the protein Perl during the day and the protein Bmall at night. However, during desynchronosis the top half contained Perl and the bottom half contained Bmall suggesting that the bottom half of the SCN continues to rely on endogenous pacemakers whereas the top half is affected by exogenous zeitgebers. Saper (2008) suggested that there is a food clock which is capable of over-riding the master biological clock and therefore fasting during flights and eating at the correct times in new time zones may in fact reset the biological clock.
Shift lag is a serious problem as it can result in fatigue, sleep disturbance, lack of concentration, memory loss and usually occurs over extended periods of time. There are a number of shift patterns currently in use; fixed shifts and clockwise/ anti-clockwise rotating shifts. Czeisler et al (1982) recommended a slow rotation with a phase-delay system (moving a shift forward every time) to factory workers in a Utah chemical plant and a number of benefits including increased morale and health were reported. Boivin et al.
(1996) put 31 male participants on an inverted sleep pattern for three days. After waking on each day they were subjected to one of the following conditions: very bright light, bright light, ordinary room lighting or dim lighting. To measure the adjustment, core body temperature (a known circadian rhythm) was measured. Participants in the very bright light condition adjusted by five hours within three days. The other conditions did also advance but not by as much and the participants in condition four did not adjust at all.
It was concluded that bright light can help biological rhythms adjust to shift lag and this research could be implemented in various companies where employees work on shifts. Alternatively, Sharkey (2001) found that the hormone melatonin could be used to aid adjustment to shift patterns and increase sleep during periods of non-work. However this is currently only available in America as it has not been given an EU licence yet. ***** Sleep states: Sleep appears to be necessary for all animals to survive. It has been estimated that humans sleep on average for 7. 5 hours per night.
Of course, there are individual differences and Meddis (1979) even reported the case study of a woman who slept for 1 hour per night with none of the side effects associated with sleep deprivation. The stages of sleep (slow wave 1-4 and REM) are covered in biological rhythms. There are two theories concerning the development of sleep, these are the evolutionary theory and the restorative theory. The evolutionary theory (Meddis) states that due to poor vision in low light, sleep has an evolutionary advantage to humans because it keeps the species safe at night; and therefore more likely to survive to pass on genes.
This theory also takes into account that animals with higher metabolic rates spend more time eating and so sleep for smaller periods at a time. Evans (1984) criticises this theory, stating ‘ the behaviour patterns involved in sleep are glaringly at odds with common sense’ referring to the fact that while this theory proposes animals sleep for protection, they are in fact at their most vulnerable during this state. Siegal (2005) reviewed the sleep patterns of numerous species and concluded that it could not be performing the same function in every species because of the diversity of sleep patterns.
Webb proposes a variation on the evolutionary theory, known as the hibernation theory which sees sleep as an adaptive behaviour designed to conserve energy. This theory compares sleep to hibernation in the way that it occurs to conserve energy so that an animal does not need to constantly feed. In humans, sleep lowers the metabolic rate by up to 10% thus conserving energy/ resources during time when early humans were unable to forage or hunt (eg. night time, as described in the previous paragraph).
Meddis criticises this theory for being too simplistic and not taking into account the role of sleep in protection from danger. Empson(1993) described sleep as ‘a complex function involving far reaching changes in brain and body physiology’ suggesting that sleep must have a restorative function and cannot purely be evolutionary. Evolutionary theories are also unable to explain the complexities of sleep such as the REM stage (although it has been suggested that the brain activity observed in this stage is to prevent brain temperature from dropping too low).
Some psychologists argue that sleep would now be pointless in human societies, however the evolutionary response is that behaviour changes much more rapidly than biology or physiology through evolution – known as the genome lag. Oswald (1966) suggested that sleep restores energy, removes waste from muscles and repairs cells, as well as allow growth to occur. One example of this is the build up of neurotransmitters used in the nervous system throughout the day, the restoration theory states that these can be removed and levels restored during sleep.
Oswald noticed that greater amounts of the growth hormone is released into the bloodstream during stages 3 and 4 NREM sleep, supporting this theory. However, many of the other processes that occur during sleep, such as protein synthesis also happen while awake. Further support is provided by Shapiro (1981) who studied ultra- marathon runners. It was found that on the two nights after the marathon, participants slept for 90 minutes longer than usual, while REM sleep decreased and stage 4 slow wave sleep increased from 25% to 45%.
Further support for why deep sleep occurs in the first half of the night is provided by the fact that amino acids only remain in the bloodstream for eight hours; therefore protein synthesis could only occur during the first half of the night. Hartman (1984) extended this theory to include restoration during REM sleep, however restoration of the brain and not the body. Stern and Morgane (1974) found that levels of neurotransmitters within the brain may be restored during REM sleep.
Further support comes from the fact that more time is spent in REM sleep during childhood as opposed to adulthood (when the most brain development occurs). Most research into the purpose of REM sleep comes from sleep deprivation, and will be discussed in the next section. However, other supporting evidence comes from people with brain injuries. It has been found that people with brain damage caused by ECT, strokes etc. spend longer in REM sleep for roughly 6 weeks, suggesting that restoration and repair to the brain is being carried out in this time.
Also, patients on MAOI antidepressants spend less time in REM sleep, but when the treatment is stopped, there is no REM rebound. Naturally, it has been suggested that the antidepressants (which are known to increase serotonin and dopamine levels) are providing what REM sleep would otherwise provide. Evidence against this theory includes; Horne and Millard (1985) who found that even after physical exertion, although people fall asleep quicker, they do not sleep for longer. Also, Ryback and Lewis discovered that the amount of sleep required does not decrease when daytime activity decreases.
Finally, it is worth noting that Horne (1988) distinguishes between core sleep, comprised of stage 4 slow wave sleep and REM sleep, and non- core sleep, comprising of stages 2 and 3 slow wave sleep. Core sleep is present in all animals but non-core sleep is not, suggesting it is not essential. ***** Sleep deprivation: Peter Tripp is an example of a total sleep deprivation case study after spending 201 hours and 10 minutes awake. When he began to fall asleep he was wakened by doctors and nurses, however after a while, he began to hallucinate and suffer from delusions.
A second case study in this area is that of Randy Gardner (1965) who stayed awake for 11 consecutive days. During this time, he reported blurred vision and mild paranoia. When he did sleep, he slept for 14 hours and 40 minutes on the first two nights and longer on the following two. In total, he only reclaimed roughly 11 hours sleep, however he spent much more time in stage 4 NREM and REM sleep compared to usual, suggesting that they are important. Of course, being case studies, the results of these are difficult to generalise to the entire population, but other research has backed up these findings.
In severe cases of fatal familial insomnia, a person, upon reaching middle age, stops sleeping until the point of death. Huber- Weidman carried out a meta-analysis of sleep deprivation studies and found that symptoms ranged from 1 night without sleep causing discomfort, to 6 nights without sleep, where the participant experienced a loss of self identity. Another study, this one by Webb and Bonnett (1978) reduced participants sleep to four hours per night and found no negative consequences. However, in all sleep deprivation studies there will be demand characteristics and there will be experimenter bias due to expectations of participants.
Partial sleep deprivation studies deprive participants of only one part of a nights sleep; either NREM or REM. Dement (1960) deprived participants of either REM or NREM sleep and observed the consequences. He found that participants deprived of REM sleep found concentrating difficult, became more aggressive and displayed REM rebound. By the 7th night, these participants were attempting to enter REM sleep 26 times, thus deteriorating into total sleep deprivation. Another study is provided by Jouvet (1967) who placed cats on upturned flower pots in water.
This meant they could sleep, but once REM sleep was reached and sleep paralysis occurred, they would fall into the water. Many of the cats became classically conditioned and would wake before entering REM sleep. On average, the cats survived for 35 days. Dwyer and Charles concluded that evolutionary theories do not explain why sleep deprivation causes so many adverse effects, however restorative theories do. That said, there are important advantages to evolutionary explanations so an eclectic approach may be the most suitable. As well as this, there are three stages to the physiology of sleep highlighted by sleep deprivation studies.
The first is staying awake which is mainly controlled by the RAS (reticular activating system). Support for this is provided by Bremner (1937) who discovered lesioning the brain stem above the RAS in cats caused a permanent coma, however lesioning the brain stem below the RAS caused no disturbance. This is because lesioning above the RAS prevents electrical impulses passing from it to the higher brain centres. The second stage is getting to sleep, which requires the RAS to be switched off; a process completed by the neurochemicals melatonin and serotonin.
The mechanism here is when a lack of light is detected by the eyes, an electrical impulse is passed to the SCN which influences the pineal gland and stimulates the production of melatonin. Melatonin in turn causes serotonin to be produced in the raphe nuclei. The serotonin is then able to switch off the RAS. This is supported by Jouvet (1967) who discovered that damaging the raphe nuclei of cats caused severe insomnia. The third stage is switching from NREM to REM sleep, which is triggered by two processes; the first is the locus coeruleus producing noradrenaline which passes to the higher brain centres.
The second is the neurotransmitter acetyl choline entering the pons and activating REM sleep which lasts 15 minutes, and then taking 90 minutes for the process to repeat. ***** Lifespan changes: A brief overview of the pattern of sleep at different ages is as follows. Newborns sleep for 18 hours per night, 9 hours of which is REM sleep. In the first few months, babies can directly enter REM sleep; it is only after this period when the REM/NREM cycle is established. At 1 year the total time asleep drops to 14 hours per day and the ultradian sleep cycle increases to 60 minutes.
Between 5 and 10 years, the total sleeping time drops to 10 hours, with 75% NREM and 25% REM sleep. The ultradian cycle increases to 70 minutes. Between 10 and 12 years old is described by Dement (1999) as sleep/wake utopia. During adolescence, the same amount of sleep should be kept, but social and environmental factors often prevent this. Between the ages of 18 and 30 most people’s sleep decreases and many people become sleep deprived. Between 30 and 45 sleep continues to decrease and people tend to feel tired upon waking; the amount of deep sleep (particularly stage 4 sleep) decreases.
At the age of 45 and lasting to the age of 60, hormone production decreases and quality of sleep decreases. Total sleep time drops to 7 hours and there is little or no stage 4 sleep, however REM sleep remains constant at 2 hours per night. From the age of 60 onwards, the quality of sleep deteriorates rapidly and Dement estimates that there could be up to 1000 micro-arousals during every night’s sleep which have a profound effect on the restorative effect of sleep. Van Cauter et al. (2000) carried out a longitudinal sleep study on 149 male participants over a 14 year period.
They found that hormone production decreases between the ages of 16 and 35, then again between the ages of 35 and 50. This means that between these periods the amount of growth and physiological repair carried out during sleep decreases from a restorative perspective. From an evolutionary perspective, it is unlikely for early humans to have lived past 45 and therefore the gradual decrease of hormones was natural because after this point, restoration was no longer needed. This is supported by other studies which suggest that as age increases there is a
decrease in total sleep time and notably slow wave sleep, and there is an increase in sleep latency. Kloesh et al. (2006) found that the male sleep pattern is disrupted by sleeping with a partner. The study comprised of 8 unmarried childless couples sleeping together for 10 days and apart for 10 days. Each day they were asked to complete a series of tasks. The study found that co-sleeping raises the levels of stress hormones in men but women spend more time in deep sleep and it is therefore beneficial for them. The methods used for testing sleep pattern differences at different ages are rigorous and include EEG, EMG etc.
However, most information is gathered in sleep laboratories which is a highly artificial environment and may in itself affect sleep patterns (low ecological validity). Self reporting is also widely used in sleep studies which again is unreliable and can often result in socially desirable results. There is also dispute over whether older people do in fact sleep much less than younger people. Borberley et al (1981) reported that 60% of over 65 year olds take regular afternoon naps; although there is a wide consensus that older people do have less nocturnal sleep.
Of course, while there are many average differences such as this one, individual differences also play a large role in sleep differences at different ages. As well as individual differences, there are also cultural differences. Most research has been into monophasic sleep, however in some cultures afternoon naps or two shorter periods of sleep are more common. This is therefore an example of ethnocentric research. ***** Disorders of sleep: There are a number of sleep disorders and most people will suffer from at least one of these at some point during their life.
The most common are: primary and secondary insomnia, somnambulism and narcolepsy. Primary insomnia is said to be an inability to fall or remain asleep due to anything other than a disease process (ie. not psychiatric or environmental causes). Vgontzas et al. (2005) found that insomniacs have increased levels of ACTH and cortisol, which has been associated with higher levels of arousal. This suggests that some insomniacs may be in a state of hyper-arousal. Nofzinger et al. (2004) found that usually in the transition to sleep, brain activity in the thalamus and prefrontal cortex decreases; however this change is smaller in insomniacs.
This may help explain why insomniacs experience difficulty falling asleep. Winkelman et al (2008) proposes that insomnia is caused by changes in brain chemistry. This study found that people who had suffered from insomnia for more than 6 months had reduced levels of GABA, which inhibits brain function and thus shows an alternative explanation for insomniacs’ inability to fall/ remain asleep. A third explanation is genetic- Beaulieu-Bonneau et al. (2007) found that 34. 9% of insomniacs surveyed had a first degree relative with insomnia.
Further, Watson et al (2006) found a correlation of 0. 47 between MZ twins and 0. 15 between DZ twins, suggesting that while genetics is not predictive of insomnia, it is an influencing factor. Studies have also implicated personality factors in the onset of primary insomnia. One such study was by Kales et al. (1976) which used the MMPI to test 128 insomniacs and found that insomniacs tended to have an internal locus of control. This original study had a biased sample with no control, therefore the study was repeated with a sample of 300 insomniacs and a control group of 100.
This Kales et al. (1983) study found similar results and that insomniacs had the following traits in common: obsessiveness, inhibition of anger and negative self image. Kales concluded that this caused insomniacs to be in a constant state of emotional arousal, contributing to their trouble sleeping. Secondary insomnia is a form of insomnia caused by or made worse by either psychiatric or environmental factors. A range of medical conditions have been shown to produce insomnia as a side effect, including; chronic pains, respiratory diseases and endocrine conditions. Katz et al.
(2002) conducted a study on 3,445 patients with a range of these conditions and found that 50% reported (this was conducted using questionnaires) symptoms indicative of insomnia. Bardage and Isacson (2000) found that 20% of patients using drugs to treat hypertension had insomnia like symptoms. Even sleeping drugs can cause insomnia because they can cause dependence and therefore ‘rebound insomnia’ when they are removed leading to increased dependence. Other drugs that may amplify the effects of insomnia include alcohol and tobacco. Aside from biological causes, secondary insomnia is also associated with mental health problems. Weiss et al.
(1962) found that 72% of psychiatric patients reported sleep disturbance, as opposed to 18% of a sample. In fact, insomnia is so closely associated with depression that it is in fact a criterion for diagnosis. Benca and Peterson (2008) suggest that patients with depression may have similar abnormalities in the genes associated with circadian rhythms as insomniacs. The HPA, which produces cortisol, is linked to depression. However, cortisol reaches its lowest levels during the first few hours of sleep, but remains elevated in patients with depression; furthering the potential link. Brain injury is also a common cause of secondary insomnia.
Cohen et al. (1992) compared the sleep complaints of 22 hospitalised with 77 discharged patients finding rates of 72. 7% and 51. 9% respectively. Both of these are much higher than the general population. In a study by Ayalon et al. (2007) between 40% and 60% of patients with brain injury complained of insomnia. However, of this sample of 42, it was found 15 had CRSD (circadian rhythm sleep disorder) which is commonly misdiagnosed as insomnia. However, unlike insomnia, people suffering from CRSD are able to get enough sleep if allowed; it is simply a problem with the timing of circadian rhythms.
Narcolepsy is a sleep disorder characterised by excessive daytime sleepiness. In addition to this, patients may also suffer from cataplexy, disturbed sleep, hypnagogic hallucinations and sleep paralysis. Narcolepsy usually begins in the late teens or early 20s, but around 25% of sufferers do not experience the onset until the age of 40. There is little evidence that narcolepsy is caused by brain damage. Scammell et al. (2001) report the case of a 23 year old who acquired narcolepsy due to damage to the hypothalamus after a stroke. Further testing revealed reduced levels of Hcrt, which is a popular theory for explaining narcolepsy.
It is thought that it may be caused by a loss of cells that secrete Hcrt. However, Gerashchenko et al (2003) found a correlation between the number of cells lost and the decline in the level of Hcrt. Further support for Hcrt comes from Parkinson’s disease (a disease which destroys brain cells). Many people suffering from this complain of symptoms similar to those of narcolepsy. Thannickal et al (2007) conducted post mortems on brains of sufferers of Parkinson’s disease and found that up to 62% of Hcrt producing cells had been lost.
An alternative explanation for narcolepsy is the genetic one. Nishino and Mignot (1977) found that narcoleptic Dobermans have a genetic mutation affecting Hcrt, however research showed that the defect did not apply to humans. In fact it seems highly unlikely that genetics play a role in the onset of narcolepsy. One further explanation, provided by Overeem et al. (2008) is that because over 90% of narcoleptics carry particular subtypes of a human leukocyte antigen (HLA), then it may be being destroyed as part of an autoimmune response. However this is not yet any evidence for this hypothesis.
_______________________________________________________________________________________________ Topic II: Aggression (separated into three essay topics) Social psychological explanations: One explanation of aggression is what is known as individuation – the process by which a person loses self awareness. Le Bons (1895) suggested that when a crowd, when combined with anonymity, suggestibility and contagion, acts as one mind. Deindividuation is characterised by lowered self- evaluation and lowered concerns of others view of the self. This means that the person and group is un-inhibited by personal morales.
Zimbardo suggested that uniforms increase the effects of deindividuation because of the anonymity they provide. This is supported by his Stanford prison study; which was stopped after just 6 days because of the levels of abuse that the guards subjected the prisoners to. Another Zimbardo study (1969) studied 4 groups of female students as they were asked to administer electric shocks to other students in a ‘learning exercise’. There were two conditions, in the deindividuated conditions participants wore lab coats and hoods and were never referred to by name.
In the individuated condition, participants wore ordinary clothes and were introduced to each other beforehand. It was found that the deindividuated group shocked for twice as long. Further support is provided by Watson (1973) who studied warriors from 24 cultures and found that the most aggressive were those that painted their faces. However, not all large anonymous crowds perform aggressive acts, and Postmes and Spears (1998) concluded that there is insufficient evidence to support the deindividuation theory after a meta-analysis of 60 studies.
The theory is also highly deterministic, as it states that the presence of a group determines the aggressive behaviour. One of the more prominent social psychological explanations for aggression is social learning theory. This is a theory that was introduced by Bandura (1963). It states that behaviour is influenced by inherent socio- environmental and psychological factors. The 4 basic principles of social learning theory are: attention, retention, repetition and motivation. In essence these steps describe the process of observing the behaviour, remembering it, then copying and gaining the motivation to repeat the behaviour.
Bandura believed that role models played an important part in influencing children to either become aggressive or passive in their behaviour. He also stated that a role model of the same gender as the child will have more influence than a role model of the opposite sex. Bandura’s theory has led to three models of how aggressive behaviour is encouraged or discouraged. The first is vicarious reinforcement; where a child witnesses a role model being rewarded for performing an aggressive act. The second is direct reinforcement; where the child themselves is rewarded or punished for certain behaviours (this is also known as operant conditioning).
The third is self- efficacy; where a child reaches a level of self confidence through mastery experiences, social modelling, social persuasion and psychological responses which will allow them to perform a particular behaviour. The most notable study into this is the ‘Bobo doll study’ conducted by Bandura (1963) who studied 72 children between the ages of 3 and 6. The experimental group was made up of 24 children with an aggressive role model and 24 children with a non-aggressive role model. In each group 12 children had a role model of the opposite gender.
All children went through the same procedure; watching their role model and then being presented with the same toys to play with. The results showed that children exposed to an aggressive role model behaved more aggressively towards the Bobo doll. Children with same sex role models imitated behaviour more accurately and levels of aggression were higher in boys. This study has high face validity, as it does go some way to explaining why children from abusive families may develop aggressive personalities later in life. However, the ethics of this study are questionable. While the confidentiality of the participants na