Psychology March mocks
Schizophrenia:
Classification of schizophrenia. Positive symptoms of schizophrenia, including hallucinations and delusions. Negative symptoms of schizophrenia including speech poverty and abolition. Reliability and validity in diagnosis and classification of schizophrenia, including reference to co-morbidity, culture and gender bias and symptom overlap
Definition- a serious mental disorder that is characterised by severe disruptions in psychological functioning such as delusions, hallucinations, disorganised speech and behaviour, and other symptoms that may disrupt social and/or occupational functioning
Classification:
Schizophrenia is classified by two systems:
The DSM-5- diagnostic and statistical manual of mental disorders, published by the American psychiatric association
Criteria A:
Two or more of the following symptoms must be present for a significant portion of time during a two month period.
At least one of these should include an active symptom
Delusions
Hallucinations
Disorganised speech
Alongside other symptoms including
Grossly disorganised or catatonic behaviour
Negative symptoms (i.e. diminished emotional expression or avoltion)
Criteria B:
There should be a reduction in one or more major areas of functioning such as work, interpersonal relations, or self-care
Criteria C
Continuous signs of the disturbance must persist for at least six months, during which the patient must experience at least one month of active symptoms
ICD-10- international classification of diseases, published by the world health organisation
The two systems differ, in that the DSM requires at least one positive symptom to be present for a diagnosis is schizophrenia but this is not present in the ICD. The ICD also recognises a range of subtypes of schizophrenia but these were removed from the DSM-5
There are two main types of schizophrenia:
Type 1 schizophrenia, characterised by positive symptoms
Positive symptoms of schizophrenia
Hallucinations- these are unusual sensory experiences (visual, auditory, smell, touch or taste). About 70% of people with schizophrenia suffer from auditory hallucinations
Delusions- these are irrational beliefs that have no basis in reality. Delusions can make a sufferer or schizophrenia behave in ways that make sense to them but seem bizarre to others.
Delusions of grandeur- this is when a person believes they are an important historical or religious figure, such as the queen or the pope
Delusions of persecution- this is the belief that they are being spied spied on or plotted against by others such as the government
Type 2 schizophrenia, characterised by negative symptoms
Negative symptoms:
Any behavioural deficit (the loss of usual abilities and experience)
Speech poverty- this is a decrease in speech fluency and productivity. They produce fewer words in a given time on a task of verbal fluency. This is not due to less verbal ability than people without schizophrenia, but more a difficulty spontaneously producing them. Patients will often slur their responses, not pronouncing consonants clearly, and their words may trail off into a whisper
Abolition- a reduction of interests and desires as well as an inability to initiate and persist in goal directed behaviour. Abolition is distinct from poor social functioning, which can be the result of other circumstances such as having no friends and family available to have social contact with. To be classed as avolition, there must be a reduction in self-initiated involvement in activities that are available to the patient
Reliability and validity in diagnosis and classification of schizophrenia:
Reliability:
Reliability refers to the consistency in the diagnosis. In this case, whether there is agreement in the diagnosis of schizophrenia by different psychiatrists across time and cultures. This is known as inter-rather reliability. Reliability can also be seen in whether diagnostic tests are consistent on different occasions. This is known as test-retest reliability
Co-morbidity- comorbidity is an issue for the reliability of the diagnosis of schizophrenia. it refers to the presence of one or more additional disorders or diseases simultaneously occurring with schizophrenia. For example people with schizophrenia also more commonly suffer with the following conditions substance abuse (47%) anxiety/panic disorder (15%) symptoms of depression (50%). If I suffer I can experience simultaneous disorders. This suggests that schizophrenia may not actually be a separate disorder. This could lead a different medical professional professionals giving different diagnosis at the same patient.
Culture bias – the extent of which the diagnostic system reflects belief about what is viewed as normal and acceptable in western predominantly white cultures. Culture buyers reduces the validity of the diagnostic system. Both the ICD and DSM were developed by western clinicians and a criticise for lacking cultural relativism. Therefore, people who show behaviours such as hearing voices, which may be normal in their own culture, are classified as having schizophrenia. Culture bias can also affects the reliability of the diagnostic system. Research suggests there is a significant variation between cultures when it comes to diagnosing schizophrenia. Copeland (1971) they’ve 134 US and 194 British psychiatrists a description of a patient. 60% of the US psychiatrist diagnose schizophrenia, only 2% of the British Homsted showing diagnosis was unreliable across different cultures.
Evaluation:
There is criticism that the DSM and ICD tools are routinely used for the high level of reliability by mental health clinicians. Cheniaux (2009) as two psychiatrist to independently diagnosed 100 patients using both of DSM and ICD. In rate a reliability was poor, for example, using the DSM, once psychiatrist diagnosed 26 patients with schizophrenia whilst the other only diagnosed 13 this is a weakness of the diagnostic system as they failed to produce consistent results and therefore shows that the reliability of diagnosing schizophrenia is poor. However, recent research has found that the reliability for diagnosed schizophrenia has improved. Osorio at al (2019), reported excellent reliability for the diagnosis of schizophrenia using the DSM five. Pair of interview is achieved into rate to reliability of around 0.97 and test retest ability of around 0.92. This suggests that the diagnostic system is consistently applied and therefore has a good reliability. Furthermore, even if the reliability of the classification systems are not perfect, they do provide clinicians with a common language, permitting communication of research ideas and findings, which may ultimately lead to a better understanding of a disorder and more effective treatments.
There is a lot of body of evidence so suggest that many sufferers do also have issues of substance abuse. Buckley (2009) found that 50% of patients with schizophrenia also have depression or substance abuse. Alcohol, cannabis and cocaine or substances that can be abused by people with schizophrenia (possibly as a way of self-medicating) and not only does such morbid substance abuse make a reliable diagnosis of schizophrenia difficult to achieve, it’s also Leesa lower levels of functioning, increased hospitalisation and lower compliance of medication, which makes effective treatment more difficult to achieve. This is the strength because it demonstrates the complexity is involved in giving a reliable diagnosis if the person schizophrenia is also using recreational drugs. Suffer to use recreational drugs may find it difficult to achieve a reliable diagnosis as it’s difficult to know what symptoms are a direct offensive having schizophrenia and what are the symptoms of substance abuse. Additionally, Jeste at all, (1996) states that those sufferers of schizophrenia with comorbid conditions are excluded for research and yet for the majority of patients, which suggests that research findings into the cause of schizophrenia may not be based on reliable research as the sample samples used are not consistent.
Research suggested that the diagnosis of schizophrenia is affected by culture bias. Pinto and Jones (2008) reported this in Haiti Iszy some people believe that voices are communications from ancestors. British people of African – Caribbean origin, and sometimes more likely to receive a diagnosis and white British people, although people living in African Caribbean countries are not, ruling out a genetic vulnerability. This is a weakness of the diagnostic system because it highlight the difference in diagnostics statistics of some cultural groups is due to the biased over interpretations of symptoms by some psychiatrist. However, the higher statistics could represent the effects of poor housing, higher rates of unemployment and social isolation that are more commonly experienced by minority group such as African Caribbean groups
Validity:
This is the extent of which the methods used to measure schizophrenia are accurately measuring schizophrenia. For example, the patient may have hallucinations but it’s not suffering with schizophrenia (symptom of comorbidity) or maybe the psychiatrist. I’m misinterpreting the behaviour of the patient (agenda/culture bias). Additionally, different assessment systems may arrive at completely different diagnosis we can assess validity by using predictive validity – if a diagnosis needs a successful treatment, then diagnosis as soon as valid.
The research findings on whether the diagnosis of schizophrenia is valid are very mixed. Some researchers report that when you match patients diagnosed with schizophrenia to the DSM criteria there is a good correlation, suggesting that diagnosis is valid.
However, to diagnose patients can differ greatly on the precise symptoms each displays (for example, one showing delusions, but the other not – but they both have a diagnosis of schizophrenia). This suggests that a single label of schizophrenia is not valid. Perhaps it is more valid to use the presence or absence of positive and negative symptoms to distinguish different form of schizophrenia, as the DSM five does.
Gender bias in the diagnosis of schizophrenia occurs when the accuracy of diagnosis is dependent on the gender of an individual. The diagnostic criteria may be gender biased or clinicians made judgement on stereotypical beliefs about gender. Gender bias refers to the differential treatment of males and females on the diagnosis of schizophrenia. Statistically, since the 1980s, men are diagnosed schizophrenia more often than women. It may be that due to genetic factors, women on genetically less vulnerable than man. However, it seems more likely that women are underdiagnosed because they are more likely to have support around them and therefore function better than men. Cotton (2009) found inpatient with schizophrenia that female patient function better than male patients. For example, they are more likely to work and have good family relationships. This may explain why women are not diagnosed schizophrenia as frequently as men. It appears that they’re better interpersonal functioning may buy a clinicians to under diagnose schizophrenia in women. This also explains why the age of onset tends to be much younger in males than female females.
Symptom overlap occurs when symptoms of schizophrenia are also found in other disorders. For example, positive symptoms, such as delusions and negative symptoms such as avolition occur in both schizophrenia and bipolar disorder. This makes it difficult for clinicians to accurately decide which particular disorder someone is suffering from when diagnosing
Evaluation:
A threat to the validity of diagnosing schizophrenia is highlighted by the fact that in the same way that people diagnosed with schizophrenia rarely share the same symptoms, likewise there is no evidence that they share the same outcomes. The prognosis for patients diagnosed with schizophrenia varies with about 20% recovering their previous level of functioning, 10% achieving significant and lasting improvement and about 30% showing some improvement with intermittent relapses. This is a problem because a diagnosis has little predictive validity because some people never appear to recover from the disorder, while many do. Additionally what does appear to influence outcome is more to do with gender and psycho-social factors such as social skills, academic achievement, and family tolerance of schizophrenic behaviour.
Research suggests that gender bias is often a problem in the diagnosis of schizophrenia and the subsequent treatment offered. Evidence shows that males could be more likely to be committed to psychiatric institutions (referred to as being hospitalised) when they show mild signs of schizophrenia due to the risk of socially deviant patients. Females, on the other hand, are likely to be voluntary patients because they are more likely to seek help earlier. This is a strength as it supports the idea that gender differences in diagnosis exist. Their better interpersonal functioning may bias clinicians to under diagnose schizophrenia in women. This therefore threatens the validity of the diagnostic system because people may get an incorrect or no diagnosis based not heir gender, rather than their symptoms
Research suggests symptom overlap can cause issues when accurately and reliably diagnosing schizophrenia. Ophoff (2011) found a genetic overlap between bipolar disorder and schizophrenia. Three of the seven gene locations on the genome associated with schizophrenia were also associated with bipolar disorder. Both schizophrenia and bipolar disorder involve positive symptoms and negative symptoms. This highlights the problem when trying to distinguish schizophrenia from other illnesses and in terms of classification this suggests that schizophrenia and bipolar disorder may not be two different conditions but variations of the single condition. Furthermore Ellison and Ross (1995) point out that, not only is there a great deal of overlap between SZ and bipolar disorder, but people with another disorder-DID- actually have more symptoms of schizophrenia than people being diagnosed as being schizophrenic. This is a problem as it brings into question whether SZ, bipolar disorder and DID are separate disorders or all part of the same spectrum. Due to symptom overlap, this can lead to years of delay in receiving relevant treatment, leading to further degeneration in mental health and an increase in suicidal risk. This again calls into question the validity of the methods used to assess schizophrenia. Despite these issues, the fact that the classification and diagnostic symptoms are updated and revised is one way to try and improve the accuracy and reliability by creating more clear and distinct labels for illnesses
A major consequence of invalid or unreliable diagnosis of SZ relates to the social stigma of being incorrectly labled- such inaccurate diagnosis can have a long term lasting negative impact on the lives of those diagnosed. Despite these problems, the classification systems do at least allow professionals to share a common language which helps in communicating ideas and allows greater opportunities for research which can lead to a better understanding of schizophrenia
Biological explanations for schizophrenia: genetics and neural correlates, including the dopamine hypothesis
Neural correlates:
Neural correlates are measurements of the structure or function of the brain that correlate with an experience (in this case schizophrenia). These correlates have allowed abnormalities within specific brain areas to be associated with the development of schizophrenia
Dopamine hypothesis:
One biological explanation of schizophrenia is the dopamine hypothesis. This biochemical explanation suggests that the positive symptoms of schizophrenia are the result of the overactive transmission of dopamine. Sufferers of SZ are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more dopamine binding and therefore more neurons firing. Dopamine plays a key role in guiding attention, so disturbances in this process may well lead tot he problems relating to attention and thought found in people with schizophrenia.
For example, an excess of dopamine has been found in the Broca’s area. As Broca’s area is responsible for speech production, an excess of dopamine in this area may be responsible for auditory hallucinations.
Recent versions of the dopamine hypothesis have focussed on abnormal dopamine levels in the prefrontal cortex (outer layer of the brain). For example low levels in the prefrontal cortex (responsible for thinking and decision making) are linked to the negative symptoms of schizophrenia. Therefore, it appears that both high and low levels of dopamine, in different brain regions are involved in schizophrenia
Evaluation:
There is support with the use of PET scans for the dopamine hypothesis as an explanation for schizophrenia. Wong found an increase in the number of dopamine receptors in several brain regions in patients with schizophrenia. This is a strength because it supports the view that schizophrenia is caused by unusually high levels of these receptors, increasing the validity of the dopamine hypothesis
Further support for the dopamine hypothesis as an explanation of the cause of schizophrenia has come from studies into drug use. Drugs such as cocaine and amphetamines increase dopamine levels in the brain, causing schizophrenic-like symptoms in normal people. Additionally, Parkinson’s disease is caused by a lack of dopamine in the brain and a drug called L-dopa is used to increase these levels. However, if the dosage is too high, patients suffer from schizophrenic-like side effects. These examples are a strength because they lend further support to the view that dopamine is the primary cause of many schizophrenic symptoms
The dopamine hypothesis revolutionalised the treatment of schizophrenia in psychology. It led to the creation of antipsychotic drugs, which reduce the amount fo dopamine in the brain and therefore reduce positive symptoms of schizophrenia. This is a strength because the success of these drugs strengthens the validity of the dopamine hypothesis as an explanation for schizophrenia- if the drugs help reduce the symptoms of schizophrenia by reducing the levels of dopamine this suggests the symptoms are caused by high levels of dopamine. However, this may not be the case. The drugs affect dopamine levels quickly but for many sufferers the effect on the symptoms of schizophrenia can take several weeks. This suggests that the cause of schizophrenia is more complex than simply high levels of the neurotransmitter dopamine. Additionally, atypical antipsychotic drugs such as clozapine which affect serotonin as well as dopamine are more successful than typical antipsychotics that only alter dopamine levels. This highlights that the dopamine hypothesis may be oversimplifying the cause of schizophrenia and that many other neurotransmitters are involved.
Enlarged ventricles
Originally evidence was limited to post-mortems conducted upon the brains of dead people who had suffered with schizophrenia, but research now uses non-invasive scanning techniques such as fMRI which gives a picture of the brain in action using magnetic fields
Early research was focussed on people with schizophrenia having enlarged ventricles (the fluid-filled gaps between brain areas). Enlarged ventricles are especially associated with damage to central brain areas and the prefrontal cortex, which recent scanning studies have also linked to the disorder. Early research focuses on the sufferers of schizophrenia having enlarged ventricles and these were associated with the negative symptoms of schizophrenia such as avolition and speech poverty.
Neural correlates of negative symptoms- one negative symptom is avolition, the loss of motivation. Motivation is the anticipation of receiving a reward, one area of the brain ventral striatum is involved in anticipation. It is therefore logical that abnormality of this area may be involved in the development of avolition. Juckel (2006) measured the activity levels in the venal striatum in schizophrenics and found lower levels of activity than those in the control group. They observed a negative correlation between activity levels in the venal striatum and the severity of overall negative symptoms. Therefore, activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia
Neural correlates of positive symptoms- positive symptoms also have neural correlates. Allen (2007) scanned the brains of patients experiencing auditory hallucinations and compared them to the control group brains whilst they identified pre-recorded speech as theirs or others. Lower activation levels in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucinations group, who also made more errors than the control group. Therefore, reduced adaptivity in these two areas of the brain is a neural correlate of auditory hallucinations
Evaluation:
There is a wealth of supporting biological evidence for neural correlates theory. Yo net al (2013) used fMRI scans to examine the brains of 18 patients with schizophrenia and 19 people without schizophrenia performing a memory task. Schizophrenic participants had decreased activity in the prefrontal cortex and diminished connectivity between other parts of the brain (the striatum), the stronger the symptoms of schizophrenia were. This suggests that abnormal functioning of the prefrontal cortex-basal ganglia brain circuit may be related to the cognitive deficits experienced by schizophrenics. The use of objective, replicable brain scans as evidence for this explanation has increased the scientific credibility of this explanation for schizophrenia as it allowed for a direct objective comparison of the neurological differences between brains of patients with the disorder and those without schizophrenia.
As much of the evidence to support neural correlates is correlational, it is impossible to establish causation. For example it is possible that the schizophrenic symptoms cause changes in the brain, rather than the other way round. Furthermore, not all patients with schizophrenia have evidence of enlarged brain ventricles and some people have enlarged but do not suffer with schizophrenia. This is a weakness because it makes it difficult to draw firm conclusions about the role of neural correlates in the causes of schizophrenia, thus reducing validity of this theory and clearly demonstrating how using the enlarged ventricles theory alone to explain the cause of all types of schizophrenia is not possible
The neural correlates explanation is no longer accepted as a complete explanation of schizophrenia. According to the diathesis-stress model, faulty levels of dopamine alone are unlikely to cause the disorder. Instead, it would suggest that while faulty dopamine levels may make a person vulnerable to developing schizophrenia, the onset of the condition must be triggered by a stressful life events such as family problems or drug abuse
The genetic explanation:
Another explanation of schizophrenia is the genetic explanation. Here, it is argued that schizophrenia is passed on from one generation to the next through genetic inheritance. Therefore, in theory, the more closely related the family member is to the person with schizophrenia, the greater their chance of developing the disorder. No single gene is thought to be responsible for the development of schizophrenia and it is more likely that different combinations of genes make individuals more vulnerable to the disorder and so schizophrenia is believed to be polygenic.
Much of the evidence for this explanation comes from family studies, twin studies and adoption studies. These studies are used to establish a concordance rate (or the degree to which relatives share the same disorder). For example, identical (monozygotic) and non-identical (dizygotic) twins where one of each twin pair has schizophrenia can be compared to see how often the other twin also shows the illness. If schizophrenia is genetic then it is argued that monozygotic twins should have higher concordance rates for the disorder than dizygotic twins
Gottesman found that children with two schizophrenic patients had a concordance rates of 46%, children with one schizophrenic parent a rate of 13%, and sibling a concordance rate of 9%
Specific genes identified- genes associated with increased risk included those coding for the functioning of the neurotransmitter dopamine. It has been found that the NRG3 gene variants interact with both NRG1 and ERBB4 variants
Evaluation
Supporting evidence from twin studies- there is strong support for genes associated a cause of schizophrenia. Twin studies have found a concordance rate of 40% for MZ twins compared to only just over 7% for DZ twins (Joseph, 2004). This suggests a genetic cause of scizophrenia since the MZ twins share 100% of their genes and had the higher concordance rates for the disorder compared to the DZ twins who share only 50% of their genes. However, if schizophrenia is caused by genetic factors alone then the concordance rates would be expected to be 100% for identical twins since they have the exact same genetic makeup. Furthermore, some critics have claimed that the higher concordance rates for MZ twins compared to DZ twins is because they are more likely to be treated similarly and have the same environmental experiences. This suggests that the genetic explanation of schizophrenia may not provide a complete explanation
Supporting evidence from family studies- evidence to support the genetic explanation for schizophrenia has been provided from family studies. Varma found that 16% of the first degree relatives of someone with schizophrenia developed schizophrenia compared to only 7% of the controls. This is a strength of the genetic explanation because it demonstrates that the closer genetic relatedness to someone with schizophrenia, the greater the chance of developing the disorder. However, it is possible that the increased rate of schizophrenia amongst those with parents with schizophrenia was due to environmental rather than genetic influences. This means that it is not possible to firmly conclude that schizophrenia is caused by maladaptive genes
Supporting evidence from adoption studies- adoption studies allow for the separation of nature and nurture factors so we are able to investigate if genetic factors are more of an influence on the development of schizophrenia. Tienari et al compared adopted children whose biological mothers has SZ amongst those whose biological mothers had SZ. This is a strength because even when the environmental influence of the biological mothers was removed, the genetic risk was still evident therefore supporting the theory that genetic factors cause schizophrenia. However, it was found that a healthy adoptive family could protect against those with a high genetic risk developing schizophrenia onset as well. A reasonable conclusion is that schizophrenia is caused by a complex interaction of both genetic and environmental factors and it is not possible to say with certainty which contributes the most. Most psychologists believe that genes predispose certain individuals toward schizophrenia but this will only become apparent under particular environmental conditions
Supporting evidence from gene mapping studies- through the use of gene mapping, gene variants have been discovered. Benzel et al (2007) used gene mapping to find studies suggesting that NRG3 gene variants interact with both NRG1 and ERBB4 gene variants to create a susceptibility to developing schizophrenia. This is a strength as it provides scientific and objective evidence for the influence of genetic factors. However, although gene mapping offers the possibility of developing tests to identify high-risk individuals, it does raise socially sensitive and ethical concerns about how this information is shared and used.
Overall, all biological explanations of schizophrenia could be said to be deterministic. This means that the disorder is inevitable in those with the wrong genes (genes influence neurotransmitters and how the brain develops). Nobody would try to argue that a person with schizophrenia has free willl and choice in their experience of suffering with the illness but taking a deterministic view when explaining the illness can be controversial
This deterministic view of the cause of SZ could be viewed both positively and negatively. On the one hand, biological explanations could be said to be more humane because the sufferer is not blamed for their illness as it is not something they can control
On the other hand, a biologically deterministic explanation could have a negative impact because a sufferer may feel that they are ‘sick’ and that there is little they can do to recover from this disorder
However, the diathesis-stress model doesn’t claim a deterministic view. It suggests people with genetic abnormalities may have a predisposition (an increased risk). If a person reduces their risk factors they can influence whether they develop schizophrenia or not
Furthermore, biological explanations could also be said to be reductionist because they focus wholly on one level of explanation ie internal factors such as genes and neurochemistry and ignore environmental factors. Indeed, there are psychological explanations of schizophrenia such as family explanations which argue that the way parents treat their child is the main influence on schizophrenia onset or that poor people are more at risk of schizophrenia. As a result, biology alone may not explain all aspects of schizophrenia
Psychological explanations for schizophrenia: family dysfunction and cognitive explanations, including dysfunctional thought processing
Family dysfunction:
Many of the psychologically explanations of schizophrenia have focussed on the role of the family. Family dysfunction explanations claim that the risk of schizophrenia is increased when there are abnormal patterns of communication within the family. Parents of sufferers often display three types of dysfunctional characteristics:
1. High levels of interpersonal conflict
2. Difficulty communicating with each other
3. Being excessively critical and controlling of their children
The double bind hypothesis- Bateson (1956) suggested children can find themselves trapped in situations where they fear doing the wrong thing but are not given clear guidance on what the wrong thing is. When they do ‘get it wrong’ the parent withdraws affection/love as a punishment. The child frequently receives contradictory messages from parents where a verbal message is given but opposite behaviour is exhibited. For example, if a mother tells her son she loves him, yet at the same time turns her head away in disgust, the child receives two conflicting messages about their relationship. Bateson argued this was reflected in symptoms such as disorganised thinking and paranoid delusions. The double-bind behaviour from parents where/;caregiver can lead to a negative reaction from the child of social withdrawal and flat affect (a lack of emotional expression) to escape double bind situations. Bateson was also clear he viewed these double-binds as a risk factor rather than the sole cause of schizophrenia
High expressed emotion
High expressed emotion refers to the level of negative emotion expressed towards a patient by their carers. Expressed emotion contains several elements:
Verbal criticism of the patient
Hostility towards the patient
Emotional over-involvement in the life of the patient
These high levels of expressed emotion towards the patient are a serious source of stress for the patient. It is argued that this stress can trigger the onset of schizophrenia in a person who is already genetically vulnerable to the disorder. Expressed emotion has been primarily linked to the course of the disorder rather than being seen as the cause. High levels of expressed emotion in carers have been found to lead to poorer outcomes and an increased likelihood of relapse and a return to psychotic experiences for the patient
Schizophrenogenic mother- according to Fromm-Reichmann (1948) a schizophrenogenic mother (schizophrenia causing) is cold, rejecting, controlling and tends to cause a family environment characterised by tension and secrecy. This leads to distrust which may manifest itself into paranoid delusions in the child. There is often a family schism or skew with a dominant mother and passive father
Evaluation:
There is evidence to support the double bind theory of family dysfunction as a risk factor for schizophrenia. Berger (1965) found that sufferers of schizophrenia reported higher recall of double-bind statements from their mothers than non-sufferers. This seems to suggest contradictory messages during upbringing may increase the risk of SZ later in life. However, most professionals now agree that while there is evidence that poor childhood experiences within the family are associated with adult schizophrenia there is very little support for the double bind and schizophrenogenic mother explanations. These theories have been based on clinical observations and personality assessments of the mother of someone with SZ and are not viewed as valid in comparison to other objectively supported theories
There is support for the role of expressed emotion in the course of schizophrenia. Tienari et al (2004) assessed adopted children whose biological mother had SZ compared to a control group of adoptees without any genetic risk. He found that when the parenting style of the adoptive family was characterised as highly critical with low levels of empathy, this greatly increased the risk of SZ but that being reared in a ‘healthy’ adoptive family had a protective effect on those at a high genetic risk. This suggests that expressed emotion in families can increase the risk of SZ but also that being in a low expressed emotion family can help prevent SZ. However, there is difficulty in establishing cause and effect with this theory. For example, having a child suffering with schizophrenia within a family can be problematic and stressful on family relationships. Therefore, rather than dysfunctional families causing schizophrenia, it could be that having an ill child within a family leads to dysfunction.
One advantage of family dysfunction is that they have led to practical applications. This means that the focus on the role of the family in SZ has led researchers to develop family therapy to increase the patients chance of recovery and decrease chances of relapse. Evidence for this comes from NICE (2009) who found that the relapse rate in a family therapy condition was 26% compared to 50% relapse in a control group recieving ‘standard’ care. This is positive as it suggests family dysfunction theories have led to psychological therapies that have benefitted peoples real lives. By supporting the family it allows the sufferer of schizophrenia a reduced chance of relapse.
Cognitive explanations
The cognitive approach is based on mental processes and explains symptoms of schizophrenia as being a result of a disruption of normal thought processing. Compared to controls, research has found evidence of dysfunctional thought processing in people with schizophrenia- they process information differently to those without the disorder
Metarepresentation- is the cognitive ability to reflect on our own thoughts and behaviour. It is believed that a dysfunction in metarepresentation contributes to the onset of hallucinations. For example, a person may start to believe that their actions and thoughts are being carried out by others. A dysfunction in metarepresentation may also cause the patient to believe that their own inner voices are actually the thoughts of others being projected into their heads
Central control- is the cognitive ability to suppress automatic responses while we perform deliberate actions instead. Disorganised speech and thoughts disorder could result form the inability to suppress automatic thoughts and speech triggered by other thoughts. For example, sufferers with schizophrenia tend to experience derailment of thoughts and spoken sentences because each word triggers association and the patient has difficulty suppressing an automatic response to these
Evaluation:
There is research evidence for dysfunctional thought processing. O’Carrol (2000) reviewed available evidence and found that cognitive impairments existed in 75% of people with schizophrenia comes from Stirling (2006) who compared performance on a range of cognitive tasks in 30 people without schizophrenia. Tasks included the Stroop test where participants have to name the font-colours of colour words, so have to suppress the tendency to read the words aloud. As predicted by Frith’s central control theory, people with schizophrenia took over twice as long on average than the control group to name the font colours. Both studies show clear support for the cognitive explanation of schizophrenia because it demonstrated the impairment in cognitive processes in sufferers compared to those without SZ
A major strength is that the cognitive explanation of schizophrenia has led to practical applications. This is because cognitive explanations have helped in the development of cognitive behavioural therapy for psychosis (CBTp) which has been extremely effective in treating SZ. Evidence for this comes from NICE (2014) who reviewed a range of treatments for SZ and found that, compared with antipsychotic drug therapy, CBTp was far more effective in reducing symptom severity and improving social functioning. This is positive as the theory leading to treatment has benefitted real peoples lives in helping them to develop strategies to cope with and improve their dysfunctional thought processes
It has been suggested that the cognitive impairments found in schizophrenia may be due to antipsychotic medication. This medication has serious side effects that may account for some of the deficits found in patients with schizophrenia. It has also been suggested that the cognitive differences are a result of neural correlates and abnormal neurotransmitter levels rather than the cause for SZ. Therefore casting doubt on the belief that the cognitions are to blame for schizophrenia.
Cognitive theories have been criticised for only identifying the reason for current symptoms. The theories identify faulty cognition as the cause of some of the symptoms such as disordered thinking and deficits in processing but does not explain what led to the cognitive impairments int he first place. Therefore faulty cognition explains symptoms, but not causes. This is a weakness because it suggests that we cannot fully explain the cause of schizophrenia using a cognitive theory alone.
Drug therapy: typical and atypical antipsychotics
Drug therapy is the most common treatment for schizophrenia. Antipsychotics are used to treat even the most debilitating types of schizophrenia. Drug therapy works on the basis that SZ is caused by an excess of dopamine and so drug therapy aims to reduce the effect of dopamine in the brain
There are two main groups of antipsychotic drug therapies- typical and atypical antipsychotics
Typical antipsychotics:
Chlorpomazine is a dopamine antagonist that works to reduce the effects of dopamine. They achieve this by binding to dopamine receptors (particularly the D2 receptors) but not stimulating them, thus blocking their action. By reducing the effects of dopamine, the positive symptoms of schizophrenia, such as hallucinations and delusions are reduced. These symptoms are liked to the excesses of dopamine and are reduced
Atypical antipsychotics:
Atypical antipsychotics such as Clozapine and Risperidone are the ‘newer’ types of drug treatments. Clozapine acts on the dopamine system by blocking D2 receptors. Unlike the typical antipsychotics, these drugs only temporarily block dopamine receptors before dissociating to allow normal dopamine transmission. The effect being that it reduces the positive symptoms of schizophrenia and the temporary effect on the D2 receptors leads to less extra-pyramidal side effects (movement disorders). Atypical antipsychotics also affect serotonin (5-HT) receptors in the brain, particularly the 5-HT2A receptors which are considered to be vital in the role of the negative symptoms of schizophrenia. The atypical drugs help improve patients mood and improve cognitive sunctioning
Evaluation
Supporting evidence for typical drugs- there is a wealth of research support for the effectiveness of typical antipsychotic drugs in the treatment of schizophrenia. Thornley (2003) reviewed studies comparing the effects of Chlorpromazine to reduce symptoms. Some sufferers were given the drug and others were given a placebo. The data included over 1,000 participants and found that chlorpromazine was associated with overall better functioning and reduced symptoms and also that the relapse rate was lower when the drug was taken, compared to the placebo group. This quantitative data shows clear support for the effectiveness use of typical antipsychotics, and also has used a scientific way of conducting the research with control group comparisons. Additionally, antipsychotics are effective, relatively cheap to produce, easy to administer and have positive effects on many sufferers, allowing them to live normal lives outside of mental institutions. Less than 3% of people with schizophrenia in the uk live permanently in hospital. This further supports the use of antipsychotics as they have practical applications and benefits to the economy
Supporting evidence for atypical drugs- there is also a wealth of supporting research for the effectiveness of atypical antipsychotic drugs when treating schizophrenia. In a review, Meltzer (2012) concluded that clozapine (an atypical antipsychotic)was more successful in treatment resistant cases of schizophrenia than typical antipsychotic (30-50% more effective). This is clear support for the use of atypical antipsychotic medication to treat schizophrenia and supports the idea that schizophrenia is caused by a chemical imbalance as the drugs correct the imbalance of neurotransmitters. However, critics have argues that there are serious flaws with the evidence showing drug therapy is an effective treatment for schizophrenia. Healy (2012) claims most studies only focus on short term effects and the positive effects have been exaggerated because the data has been published numerous times. This means that caution should be observed when evaluating the success of drug therapy as an effective treatment for schizophrenia
Side effects- one major issue with using drugs to treat schizophrenia is that serious side effects can occur. Serious side effects of typical antipsychotics can lead to movement disorders (extrapyramidal side effects) such as tardive dyskinesia. This is characterised by involuntary chewing and sucking, jerky movements and twisting of the mouth and face, all of which can be permanent. About 30% of people taking antipsychotic medication go on to develop tardive dyskinesia. This side effects is irreversible in 75% of cases (Hill, 1986). This is a weakness because it often leads to sufferers stopping the medication and suggests that drug therapy is not the most effective treatment for some sufferers of schizophrenia. However, one strength of atypical antipsychotic drugs is that rates of tardive dyskinesia have been found to be much lower for typical antipsychotics at just 5%. This suggests that atypical antipsychotics may ultimately be more appropriate than conventional antipsychotics as they have fewer side effects, which in turn means patients are more likely to continue their medication and therefore see more benefits
Dropout rates- a problem with all drug treatments for SZ is that the side effects can lead to problems with patient compliance. It has been argued that, on average, 50% of schizophrenia patients stop taking their medication after a year, and 75% after two years. This causes what is known as revolving door syndrome- where the patient is reluctant to take their medication and regularly relapses before being admitted for care, treated successfully with drugs again, only to then avoid taking them when released. This is a problem as it raises doubt over how appropriate antipsychotic treatments are if they rarely lead to a long-term and stable recovery. This also suggests that at least for some patients. They may benefit from psychological treatments in addition to drug therapy to prevent relapse.
Cognitive behaviour therapy and family therapy as used in the treatment of schizophrenia. Token economies as used in the management of schizophrenia
Cognitive behaviour therapy:
Cognitive behavioural therapy for psychosis (or CBTp) is the name given for CBT for patients with schizophrenia (SZ). It usually takes place for between five and twenty sessions, either in groups or individually. A CBT therapist begins by developing a trusting relationship with the schizophrenic patient, helping them to see that many of their symptoms, such as having paranoid thoughts, are more common than they think (normalisation), thus helping to reduce anxiety levels.
The basic assumption of CBTp is that it is not events themselves that cause the person problems but the beliefs they have about events. If a person has distorted beliefs this will, in turn, have a negative effect on their feelings and behaviours. For example, someone with SZ may believe their behaviour is being controlled by something else. CBTp is used to help the patient identify and correct these faulty interpretations or beliefs.
The therapist will discuss with the patient how likely these irrational beliefs are to be true (reality testing) and consider other more rational beliefs instead. By doing this, CBTp allows the patient to make sense of how their delusions and hallucinations impact on their feelings and behaviours. For example, if a patient hears voices and believes the voices are demons, they will naturally be very afraid. By thinking about these more rational, disputing beliefs, the client should feel the effect of challenging irrational thoughts and become less anxious which will have a positive effect on their behaviour. This process is sometimes called the ‘ABCDE’ model
Patients are also encouraged to develop coping strategies. A common coping strategy employed to deal with auditory hallucinations is to limit the time they actively listen to voices, eg 30 minutes per day. The rest of the time the patient is encouraged to ignore the voices
Evaluation:
There is some support showing the benefits of CBTp when treating SZ. Terrier (2005)- reviewed 20 studies using CBTp and found persistent evidence of reduced positive symptoms, lower relapse rates and a faster recovery rate in ill patients in the short term. Jauhar (2014) reviewed 34 studies and concluded that CBTp has a significant by fairly small effect on both positive and negative symptoms. These findings suggest that CBTp is an effective therapy for helping people with schizophrenia control their symptoms
Unlike drug therapy, CBTp produces no side effects and therefore, could be considered a more suitable treatment for many people with schizophrenia, making the condition more manageable and improve patient’s quality of life. For example, CBTp helps to raise the patient’s self esteem by helping them realise that healthy people also sometimes experience delusions and hallucinations (normalisation).
Many patients with severe symptoms of schizophrenia drop out of CBTp. Tarrier (1993) found 45% of the sample refused to cooperate or dropped out during the trial. Patients need to be highly motivated and have the ability to put in the time and effort for the therapy to be a success. Some patients with Sz suffer with avolition so engaging in a lengthy therapeutic process will be problematic for those patients in particular. Therefore, this suggests CBT may not be a suitable treatment for all patients suffering with SZ and alternative treatments such as drug therapy may be more appropriate
The effectiveness of CBT is increased when mixed with combinations of treatments and may depend on the stage of the disorder
Addington and Addington (2005) claim that in the initial phase of SZ, self-reflection on symptoms is not particularly appropriate. However, following stabilisation of the symptoms with antipsychotic medication, individuals can benefit from group based CBT which can help normalise their experience by meeting other individuals with similar issues. This suggests that CBT may only be useful for specific stages of treatment and may need to be constantly adapted. However, despite its success for many patients, CBT is not suitable for all patients, especially those too disorientated, agitated or paranoid to form trusting alliances with practitioners. Therefore CBT may not be effective for all patients with schizophrenia and alternative treatments may be necessary
Family therapy
Family therapy is a form of psychotherapy which is based on the idea that communications and interactions amongst the family of patients with schizophrenia are dysfunctional. The therapy involves the patients whole family and aims to improve the quality of communication and interactions between family members and to reduce the levels of expressed emotion and stress. Family therapy is usually offered for a period of between 3 and 12 months and at least 10 sessions
Family therapists aim to improve the functioning of a family with a member suffering schizophrenia by employing a number of strategies:
Forming a therapeutic alliance with all family members
Reducing the stress of caring for a relative with schizophrenia
Problem solving
Reduction of anger and guilt
Helping family members achieve a balance between caring for the individual with schizophrenia and maintaining their own lives
Improving beliefs and behaviour towards schizophrenia
NICE recommends that family therapy should be offered to all individuals diagnosed with schizophrenia who are in contact with or live with family members. They also stress that such interventions should be seen as a priority where there are persistent symptoms or high risk of relapse
Evaluation:
Family therapy has been found to be effective. Pharaoh et al (2010) conducted a meta-analysis of 53 studies to compare the effectiveness of family therapy for the treatment of schizophrenia with antipsychotic medication. They found a reduction in the risk of relapse and a reduction in hospital admission during treatment and in 24 months after. The use of family therapy also increased patient’s compliance with medication. This suggests that family therapy is an effective treatment, which could hint that better family relationships are the key element in helping a patient to recover
There are economic benefits of family therapy. The NICE review of family therapy studies show that family therapy is associated with significant cost savings when offered to patients with schizophrenia. The extra cost of family therapy is offset by a reduction in costs of hospitalisation because of lower relapse rates
A further strength of family therapy as a treatment for schizophrenia is that it is useful for patients who lack insight into their schizophrenia. This is because family members are able to assist with providing lots of useful information about the patients schizophrenia in a coherent way, whereas the patient may be unable to do so. They have insight into the patients moods and are able to speak for them when the patient cannot speak for themselves. This can help them start to receive therapy immediately and is a clear strength of family therapy in helping to treat schieffectively.
Studies have suggested that family therapy is also highly beneficial for family members and not just the sufferer of schizophrenia. Lobban et al (2013) analysed the results of 50 family therapy studies that had included an intervention to support relatives. 60% of these studies showed a positive impact of the intervention on at least one outcome for relatives eg coping and problem solving skills. This therefore shows that investment in family therapy can have positive consequences for many family members which in the long term should be cost effective in reducing the relapse and re-hospitalisation of the person with schizophrenia and the mental health of carers
However not all evidence suggests that family therapy is effective in treating schizophrenia. Garety et al (2008), found little difference in the improvement of symptoms of schizophrenia in patients that received family therapy compared to patients that received no family therapy but had carers. Patients in both groups had low incidences of relapse. Researchers found that the carers has low levels of expressed emotion and this could explain why there was little difference between the two groups. This clearly shows that low levels of expressed emotion are important for improving symptoms of schizophrenia, but it also shows that family therapy may not necessarily be any more effective than a high-quality standard of care provided by emotional responsive carers
Token economy
Token economy is a form of behavioural therapy used primarily in hospitals. This is passed on the principles of operant conditioning. The aim of token economy is to change maladaptive behaviours (negative symptoms such as social withdrawal and poor motivation) shown by individuals with schizophrenia into more desirable behaviours through the use of tokens. The tokens reinforce desirable behaviour. This helps in the management of schizophrenia. The idea is that the token (a coloured disk) is given immediately on completion of a desired behaviour such as getting dressed in the morning. The tokens can be later swapped for material treats such as sweets, magazines or for services such as having a room cleaned, breakfast in bed or privileges such as walks outside the hospital
These modified behaviours do not cure schizophrenia but rather improve the patients quality of life and increase the likelihood of living outside a hospital/care setting
During the early stages of the token economy, frequent exchange periods mean that patients can be quickly reinforced, and target behaviours can then increase in frequency. Over time, to encourage further improvements, more may be expected of patients to achieve token rewards. For example, they may only be rewarded for helping others or completing chores. In this way, their behaviour can be developed and shaped over time, working towards being more and more able to function and look after themselves and become less reliant on staff, carers and medication.
Evaluation:
One strength is that there is evidence for token economies being effective in managing the symptoms of schizophrenia. Glowacki (2016) identified 7 studies published between 1999 and 2013 and reported that all studies had shown a reduction in negative symptoms and a decline in the frequency of unwanted behaviours. The findings demonstrate support for the view that token economies are effective in managing schizophrenia in hospitalised patients. This is because it is possible to control the environment and ensure that patients are rewarded consistently for desirable behaviours. The tokens can be tailored to the individual patients’ requirements and used to target different behaviours.
However, critics argue that using only 7 studies to support the effectiveness is limited and may not accurately represent the effectiveness of token economies to manage symptoms of schizophrenia.
One problem with token economies is that they are not effective in managing all symptoms of schizophrenia. Token economy is only really effective in treating the negative symptoms which involve social withdrawal yet not effective in treating the positive symptoms such as hallucinations and delusions. It has also been argued that token economies produce only token learning. For example, it is possible that what patients learn in token economies is merely to imitate normal behaviour without any deeper changes in their thoughts and beliefs. This suggests the therapy may be limited in terms of its effectiveness in that it may be superficial and temporary. Additionally, it may only be useful within an institution and may not provide the patient with skills for living in the outside world
There are ethical issues surrounding the use of token economies. Most significantly, the privileges and services become more accessible for patients with milder symptoms, and less avaliable for patients with severe symptoms. In addition, it has the potential for abuse. Corrigan (1995) claimed that token economy can be abusive and humiliating. It has the potential for taking away the power from the patient and allowing others to have power over the patient. This suggests token economy therapies may not always be appropriate when they are used for reasons other than the treatment of patients
The importance of an interactionist approach in explaining and treating schizophrenia; the diathesis stress model
Explaining
The interactionist approach (sometimes called a biosocial approach) is an approach that acknowledges that there are biological and psychological/societal factors that contribute to the development of schizophrenia. Biological factors include genetic vulnerability, neurochemical abnormality and neurological abnormality. Psychological/societal factors include stress and poor-quality family interactions
Diathesis- underlying vulnerability
Stress- the generic name which refers to the trigger for the development of schizophrenia. In the context of schizophrenia, stress means a negative psychological experience. The diathesis-stress model suggests that an individual must have the genetic vulnerability and an stress-trigger present in order to develop the condition. An individual may have more than one underlying biological factor which would make them vulnerable to developing schizophrenia, but the onset of schizophrenia is triggered by stress. Psychological triggers for schizophrenia can be things such as family dysfunction, substance abuse and stressful life events
In Meehls (1962) original model, diathesis was also biological, and stress was always psychological/societal.
However, research has led to a modern understanding of diathesis-stress in which explains:
Diathesis can be biological or psychological. We know that many genes have been linked to causing schizophrenia ‘polygenic’. We also know that early and severe stauma can affect the developing brain. For example, the HPA system becomes more over-active, this makes the person more vulnerable to later stress and so can also be a diathesis as well as genes
Stress can be caused psychological, societal or biological factors. For example, much recent research has looked at cannabis as a triggering ‘stress’ factor, due mainly to the fact that cannabis appears to increase schizophrenia rates by 7 times. This is probably because cannabis interferes with the dopamine system
Evaluation
There is evidence to support the dual role of vulnerability and stress in the development of schizophrenia. Tienari et al (2004): they assessed adopted children whose biological mother was a sufferer of schizophrenia compared to a control group of adoptees without any genetic risk. He found that parenting style characterised as high levels of criticism and conflict with low levels of empathy was implicated in the development of the disorder but only for the children with high genetic risk and not in the control group. This suggests that both genetic vulnerability and family-related stress are importantly in the development of schizophrenia and that poor parenting could be a possible source of stress
Furthermore Varese (2012) found that children whose biological mother experience severe trauma before the age of 16 were three times as likely to develop schizophrenia in later life compared to the general population. There was a relationship between the level of trauma and the likelihood of developing schizophrenia, with those severely traumatised as children being at greater risk. This suggests that the early trauma is a diathesis meaning the person was vulnerable to developing SZ later due to the presence of a stress trigger later in life. This evidence supports the modern understanding of a diathesis in the diathesis stress explanation of SZ
Although there is much evidence to suggest SZ is caused by genetic inheritance. MZ twin concordance rates for schizophrenia seldom rise above 50% supporting the view that environmental factors must also play a role in determining whether a biological vulnerability actually develops the disorder. This supports an interactionist view when explaining the development of SZ because it clearly demonstrated that a genetic vulnerability alone does not automatically lead to the disorder developing. If genes alone were the cause, we would be expecting 100% concordance for MZ twins when one of the twins has schizophrenia
Treating
As the interactionist model of SZ acknowledges both biological and psychological factors in schizophrenia it is therefore compatible with both biological and psychological treatments. The model would recommend to combine antipsychotic medication and psychological therapies (most commonly CBT). Turkington (2006) believes it is possible to believe in biological causes for schizophrenia and still practice CBT to relieve psychological symptoms. For many patients, they will be treated with a number of treatments such as CBT and family therapy alongside antipsychotic medication
There is lots of evidence that combining treatment for schizophrenia is highly effective. Terrier (2004) studied 315 patients who were randomly allocated to either 1. Medication and CBT, 2. Medication and counselling or 3. Control group (medication only). Terrier found symptom levels were lower in both combination groups compared to the control group although there were o differences in the rates of hospital readmissions. This clearly demonstrates the benefits of adopting an interactionist approach when treating schizophrenia
However, a problem with using a combination of treatments is that it is difficult to assess which treatment is the most successful. As for the evidence above suggests, a combination of antipsychotic and CNT is the most effective treatment for schizophrenia, but it is uncertain which of these therapies is having the greatest effect. In addition, just because a treatment is effective does not mean that the cause was biological or psychological (depending on the treatment)
Aggression:
Neural and hormonal mechanisms in aggression, including the roles of the limbic system, serotonin and testosterone. Genetic factors in aggression, including the MAOA gene
Neural mechanisms
The limbic system
The limbic system is a set of structures deep within the brain, including the cingulate gyrus, hypothalamus and amygdala. The amygdala has been linked to how humans and animals assess threats in the environment and how they respond emotionally to these threats.
Evidence from fMRI scans have shown that damage or underactivity in the pre-frontal cortex leads to a lack of ‘control’ over the limbic system, meaning people and animals may show sudden and unexpected aggressive responses to perceived threats in the environment. Over-reactivity in the amygdala has the same effect; if this part of the limbic system is activated, both humans and animals show high levels of aggression.
Serotonin
Serotonin is a neurotransmitter which is associated with communication of impulses between neurons; it has an inhibitory or calming effect on the brain. Low levels of serotonin in the orbits-frontal cortex have been linked to poor self-control and impulsive behaviours including aggression
Aggressive behaviours may be split into impulsive or non impulsive. Low serotonin levels seem to explain why some people may ‘flip’ and loose control over their aggression, for example, evidence comparing the cerebrospinal fluid of violent-impulsive and violent non-impulsive offenders showed significantly lower levels of serotonin metabolite in the violent-impulsive offenders. The violent-impulsive offenders also reported more difficulties sleeping compared to the non-impulsive group, suggesting that their nervous system was in an excited state (fight or flight)
Evaluation:
There is supporting evidence showing the role of the amygdala in playing a key role in how we assess and respond to environmental threats. Hospice et al (2011) carried out brain scans on participants in a lab-based game that provoked aggression. Scans showed aggressive reactions were associated with a fast and heightened response by the amygdala. Benzodiazepine (reduces arousal of the autonomic nervous system) taken before the game halved the number of aggressive reactions and decreased amygdala activity. This is a strength because it demonstrates the influence of higher activity in the amygdala on impulsive behaviour and therefore could explain impulsive behaviour and therefore could explain impulsive behaviour
There is supporting evidence showing that drugs that increase serotonin activity also reduce levels of aggressive behaviour. Bremen et al (2009) split participants into two conditions where participants were given either a placebo or a dose of paroxetine (a drug which enhances serotonin activity). Participants then took part in a lab-based game where they gave and recieved electric shocks in response to provocation. The placebo group gave more intense shocks than the group given paroxetine because the paroxetine group has experienced an increase in ther serotonin levels. This was only true of participants who had a prior history of aggressive behaviour. This study therefore demonstrates the link between serotonin levels and aggression. (Low serotonin can lead to aggression and increasing serotonin can lower aggression)
There is also supporting evidence from case studies for the neural explanation for aggression from case studies such as Phineas Gage
Hormonal mechanisms
It is a reliable observation that males are more aggressive than females, which has led psychologist to look into the role of the male sex hormone, testosterone. Testosterone is responsible for the development od masculine features during puberty such as height, build, deep voice and body hair, and is thought to be linked to displays of aggression.
Evidence suggests that the prevalence of aggressive behaviours tend to correlate with fluctuating testosterone and males show more aggressive behaviours than females in the majority of animal studies as well as humans. Experiments on animals have shown that when testosterone levels are reduces, then the number of aggressive behaviours are also lower
Evaluation:
There is supporting evidence showing the role of testosterone in aggression from animal studies. Gramma do et al (2005) showed experimental increases in testosterone are related to aggression. Conversely, castration studies leading to a decrease in testosterone and therefore a reduction in aggressive behaviour. This is a strength because it shows a direct link between the hormone testosterone and aggression in animals
Evidence to support the role of testosterone in human aggression comes from Dabbs et al (1987). They measured testosterone in the saliva of criminals and found those with the highest levels had a history of primarily violent crimes, wheras those with the lowest levels had committed only non-violent crimes. This suggests that testosterone levels may have caused this difference in aggression.
Genetic factors
Twin studies
Twin studies have compared the aggression levels of MZ and DZ twins, for example by looking at people with a history of violent and criminal behaviour, and comparing them with their twin. The higher the concordance rate for aggressive behaviour between the twins, the higher the likelihood that their behaviour was biologically determined, for example through genes. Because MZ twins share 100% if the same genes, and DZ twins share 50% of the same genes, we would expect that if aggression is genetic, then there would be a higher concordance rate for aggression between MZ twins. Coccaro et al found in male participants with a history of physical assault, there was a 50% concordance for MZ twins and 19% for DZ, corresponding with their shared genetic profile
Adoption studies
Adoption studies such as Ritter et al, compare the aggressive behaviour of adoptees to that of their biological parents (nature) and their adoptive parents (nurture). Research has suggested that criminality and aggression does have some inherited factors, as the participants’ aggressive history was more similar to their estranged biological parents (inherited factors could explain around 41% variance) compared to the adoptive parents who brought them up
MAOA gene
MAOA is an enzyme which breaks down neurotransmitters such as serotonin, dopamine and noradrenaline. Some people develop an underactive MAOA gene which only produces low levels of MAOA enzyme which in turns means there are higher levels of the neurotransmitters in these peoples brains. Low activity of MAOA has been associated with high levels of aggressive behaviour, hence showing the inherited behaviour of a ‘warrior’
Evaluation
There is supporting evidence showing genetic factors in non-human aggression. Godar et al (2014) used genetic depletion techniques to knock out the MAOA gene in mice. When the mice has the MAOA gene knockout, they showed increased serotonin levels in the brain and hyper aggression. When the mice were given an SSRI (selective serotonin reuptake inhibitor) they reverted back to their non-aggressive behaviours again. This is a positive because this scientific research highlights the link between MAOA gene and serotonin activity however the findings may only be applicable to explaining aggression in animals rather than humans
There is supporting evidence showing genetic factors in human aggression. Brunner et al (1993) studies 28 members of a Dutch family who all has a history of impulsively violent and aggressive behaviour, including physical assaults, rape and attempted murder. Findings showed that all these men has the ‘warrior gene’ MAOA-L which has led to low levels of the MAOA variant in their brains and thus high levels of serotonin and noradrenaline. This is a strength because this research could potentially help identify individuals at risk of becoming violent if it is possible to detect this genetic variation early on
Some research has identifies MAOA is linked to aggression but only in individuals who have experienced early trauma. Frazzetto et al (2007) found an association between antisocial aggression and low MAOA gene variant in adult males but only in those who experiences significant trauma during the first 15 years of life. Those who has not experience trauma were not especially aggressive as adults even if they possessed the low-activity gene variant. These findings suggests that a genetic explanation alone cannot fully account for aggression and therefore a diathesis stress explanation may be more appropriate. Furthermore, twin studies such as Coccaro et al (1997) found concordance rates for direct physical aggression in MZ twins is 50% and DZ 19%. This shows that genes alone cannot fully explain aggressive behaviour
An issue of the genetic explanation is that twin studies may lack validity. Twins will share the same environment as each other however MZ twins tend to be treated more similarly than DZ twins, especially by parents. This means that the concordance rates may be inflated and the genetic influences on aggression may not be as high as the twin studies suggest
The ethnological explanation of aggression, including reference to innate releasing mechanisms and fixed action patterns, evolutionary explanations of human aggression
The ethological approach studies natural animal behaviour. Konrad Lorenz (1966) defined aggression as innate, “the fighting instinct in beast and man which is directed against members of the same species”
Adaptive functions of aggression
The theological explanation looks at aggression as an adaptive response which is beneficial for survival. When two members of the same species fight, they rarely kill their opponent but instead defeat them, and the victor gains territory, resources and mates
Aggression also serves a purpose of establishing social hierarchies within a group of animals. The most dominant male will exert power over the others in the social group, gaining special status such as being given the first opportunity to feed after a hunt, or having mating rights over the females. This can be seen in many animal species, including chimpanzees and lions
Ritualistic aggression
A ritual involves carrying out certain behaviours in a specific set order. This can be seen in animal aggression, for example, through certain ritualistic displays of aggression which occur before a physical fight. These techniques are used to scare off the opponent before it reaches the point of physical aggression such as bearing teeth or claws, growling or roaring.
Lorenz also identified ritualistic behaviours of a defeated animal, for example, cowering or whimpering. Chimps who loose a fight offer a subordinate hand display and lower their head to the victor. Wolves who are defeated expose their neck to show that the victor could rip out their throat with one bite and kill them if they wished. It is very rare that the victor would actually kill their opponent as this would affect their own genetic blood line, therefore these rituals work to clearly display the winner of the fight
Innate releasing mechanisms and fixed action patterns
innate releasing mechanisms are built in psychological processes or structures, for example particular circuits in the brain, which are triggered by environmental stimuli. Once triggered, IRMs activate a certain sequence of behaviours which an animal is compelled to carry out, fixed action patterns
Lea (1984) identified the main features of FAPs:
Ballistic- an inevitable course which must be completed
Response to so specific stimulus which is viewed as a physical threat
Universal to the species
Stereotypical, unchanging sequences of behaviour
Hasn’t been learnt
Evaluation
There is supporting evidence showing the roles of IRMs and FAPs in non human aggression. Tinbergen (1951) found that, when male sticklebacks were presented with a series of models, the sticklebacks would attack in the same way, regardless of the shape of the model, if it had a red spot, but would not attack if no red spot was present, even if the model looked like a realistic stickleback. This supports the idea that members of the same species do have an IRM that is triggered by a sign stimulus . It also supports Lea’s features of FAPs because, for example, the FAPs we’re unchanging from one encounter to another and the attack always ran its course to completion
The idea that behaviour patterns of a species are ‘fixed’ has also been criticised. Hunt (1973) argued that Lorenz underestimated the role of the environment in developing these behaviour patterns and that learning and experience interacts with innate factors to produce subtle variations in behaviour. For example, members of the same species have been shown to differ in the duration of each behaviour, and even in the same animal from one encounter to another. This is a problem that led ethnologists to move away from the term ‘fixed action patterns’ and replace it with the term ‘behaviour patterns’ to reflect the fact that these behaviours can be modified by experience
There is some evidence against the idea of ritualistic aggression. Goodall (2010) observed chimpanzees in a national park in Tanzania. The aggression of the two rival communities of male chimpanzees was not impulsive but coordinated and planned like a military operation to the point that she dubbed it the ‘four-year-war’. One group of males systematically slaughtered the other community in a gang fashion, holding down individual chimps and carrying out prolonged attacks. They ignored the victim’s signals of defencelessness and defeat, hitting and biting them until they were dead. This is a weakness because it questions the idea that animal aggression is often ritualistic rather than real
Findings cannot be generalised to explain human aggression. Animals are qualitatively different to humans in their aggression; Tinbergen studied fish, Lorenz studied birds and mammals. However, both researchers extrapolated their findings to try to explain human aggression. Humans are more complex than animals and show a range of different aggressive behaviours; active or passive, impulsive or calculated. It would be invalid to compare human aggression directly to animal aggression. Therefore these findings may not be able to explain the complex and less predictable ways humans show aggression.
Evolutionary explanations of human aggression
Evolutionary psychologists argue that aggression is adaptive (good for survival) as it would have been effective for solving a number of survival and reproductive issues among early humans. For example, acquiring and defending resources, intimidating or eliminating male rivals for females, and deterring mates from sexual infidelity. Solving these problems enhanced the survival and reproductive success of the individual and therefore these behaviours would have spread through the gene pool, becoming common amongst all humans (particularly males)
Sexual competition- ancestral males seeking females would have had to compete with other males (intra-sexual selection). One way of eliminating this competition would have been through aggression. The successful individual would have increased their social status and been more successful in acquiring and protecting their mates from competing males and so would be more successful in passing on their genes to the offspring. This would then have led to the development of a genetically transmitted tendency for males to be more aggressive to other males
Sexual jealousy- male aggression may also occur as a result of sexual jealousy, this arises as a result of paternal uncertainty. Unlike women, men can never be entirely certain that they are the fathers of their children. Therefore men are always at risk of ‘cuckoldry’- when a man is deceived into raising and investing in offspring that are not his, thus aiding the survival of genes that are not his. Wilson and Daly (1996) identified several mate retention strategies used by males including:
Direct guarding- vigilance over their partner, keeping tabs on them to ensure they are not seeing other men
Negative inducements- threatening their partners if they act in a way which he doesn’t want them to
Evaluation:
There is supporting evidence that aggression may be motivated by a response to the threat of sexual jealousy and/or sexual competition. Shackelford et al (2005) aimed to investigate intimate partner violence in heterosexual couples. 107 married couples who had been married for less than one year completed questionnaires about their relationship. Men completed the ‘mate retention inventory’ where they rated how likely they were to use different mate retention techniques. Women completed the ‘spouse influence report’ where they rated the extent of their partner’s violence in the relationship. They found a strong positive correlation between the men’s reports of their mate retention strategies and the women’s reports of their partner’s aggressive behaviours. This is a strength because it supports predictions from the explanation about aggression being caused by the threat of infidelity, cuckoldry and that aggression can have an adaptive value
In addition further support for evolutionary explanations of aggression comes from crime data. For example, male sexual jealousy is claimed to be the single most common motivation for killings in domestic disputes in the US and sexual jealousy is reported to account for 17% of cases of murder in the UK. This seems to show that there is a large body of evidence from controlled research and criminal statistics that support the link between sexual infidelity in males, jealousy and increased aggression
Evolutionary explanations account for gender differences in aggression. Males are physically bigger and stronger than women, and use aggressive behaviours to gain resources and assert their dominance. Women feel like they have ‘more to lose’ in a fight, and don’t want to risk their own survival or that of their children so avoid situations involving physical aggression and resort to verbal aggression to resolve disputes. This is a strength of evolutionary explanations of aggression because they can explain why men are more likely to be aggressive than women, particularly physically violent.
There are cultural differences in aggression. If aggression is due to evolutionary principles, we would expect all humans to universally show the same levels of aggressive behaviours regardless of upbringing, however there are clear differences. The ¡Kung San look down on those who use aggression and will extradite those who use violence against another member of the tribe. However the Yanomamo use aggression as a status- a female will only marry another member of the tribe if he had proven himself to be a strong warrior. These examples demonstrate a weakness of evolutionary explanations of aggression because it seems likely that these aggressive/non-aggressive behaviours have been influenced by socialisation and cultural norms rather than a result of an evolved instinctive way of dealing with rivals
Social psychological explanations of human aggression, including the frustration-aggression hypothesis, social learning theory, as applied to human aggression, and
Frustration aggression hypothesis- Dollard (1939) originated the frustration aggression hypothesis based on psychodynamic beliefs about the role of catharsis in aggression. According to the hypothesis, aggression usually occurs in an outburst after a person feels that their actions or goals are being blocked by some obstacle. Catharsis is about relieving feelings of frustration; aggression makes a person feel better when they have an opportunity to vent or ‘let off steam’
Indirect expression- often the person cannot express their true feelings of anger directly at the obstacle causing the frustration. For instance, it may be a person in higher power or it could be anger at a situational factor. People therefore use the defence mechanism displacement to direct their anger at someone or something else. Aggression can be expressed physically, verbally or through a fantasy
Environmental cues- Berkowitz (1989) suggested that frustration does not make us instantly aggressive, but may create a ‘readiness’ for aggression. When people feel frustrated this heightens their emotional state meaning they are more likely to act on impulse if prompted by an environmental cue. For example, someone is more likely to snap at an annoying friend if they are having a ‘bad day’ but they might not have shown aggression if they hadn’t seen the friend. This shows that aggressive behaviour from internal anger can be triggered by external factors
Evaluation:
There is supporting evidence showing the role of frustration in aggression. Green (1968) investigated the effects of frustration on aggression in a lab setting. In the first part of the experiment, male university students were asked to complete a jigsaw puzzle while frustration was altered in different conditions:
Group one- the puzzle was impossible to solve
Group two- another student (confederate) kept interfering causing them to run out of time
Group three- the confederate kept insulting the participant for not being able to solve the puzzle
In the second part of the experiment, participants were given the opportunity to give electric shocks to the confederate when they made a mistake on another task. On average, group three gave the most electric shocks and group one gave the least electric shocks. Green also repeated the study using a non-frustrated control group who were the least likely of all conditions to give any electric shocks. This supports the idea that people are more aggressive the more they are feeling frustrated
There is supporting evidence showing the role of environmental cues in aggression. Berkowitz and LePage (1967)- students were given electric shocks by confederates to induce feelings of frustration. Participants were later given the chance to shock the confederate in return. Half of the participants were randomly allocated to a condition where two guns were present on a table next to the shock machine. Participants in the ‘weapon’ condition gave an average of 6.07 shocks which was significantly higher than the control group (no weapons) who gave an average of 4.67 shocks. This research suggests frustration causes a readiness to aggress
This explanation could be seen as overly simplistic/reductionist, as it does not account for biological factors in aggression
Some evidence shows that aggression does not have a cathartic effect. Bushman (2002) found participants who vented anger by repeatedly hitting a punch bag became more aggressive rather than less aggressive. He concluded that venting to reduce anger is like using petrol to put out a fire. This is a weakness of the frustration-aggression hypothesis as it criticises validity. It could be that exposing someone to aggression increases their likelihood of future aggressive behaviours
There are individual differences in people’s reactions to frightening situations. Some people are more pessimistic in nature and are more likely to experience emotions of self-defeating, depression or guilt rather than feeling guilty rather than angry or aggressive. Equally, some people act aggressively for reasons that don’t seem to be associated to frustration. This is a weakness of the frustration- aggression hypothesis as it cannot help us to predict when aggression will occur as aggression does not always follow feelings of frustration.
Social learning theory
Direct and indirect learning:
Bandura originated the Social Learning Theory (SLT) building on the behavioural approach to acknowledge that aggression may be learnt directly or indirectly. SLT suggests that direct learning of aggression happens through operant conditioning, for example a child who angrily snatches a toy from their sibling and receives no reprimand to punishment for their behaviour Will learn that aggression leads to rewards
Additionally, we can learn aggression indirectly (vicariously); if the child’s friend watched this aggressive behaviour, they might be motivated to imitate, believing that they too will not be punished. Children observe the behaviours of their role models are motivated to imitate these behaviours, particularly if it seems to lead to positive consequences. Therefore, SLT would suggest that if a child witnesses aggressive behaviours from role models they are more likely to act aggressively than a child who has not observed aggression, or one who has seen people being punished for aggression
Cognitive control
Bandura also acknowledged that people do not passively imitate aggression and have some cognitive control over their actions, so he focussed on the following mediational processes involved in social learning
The four mediational processes involved are attention, retention, reproduction and motivation
Self-efficacy
Sefl-efficacy means whether a person is confident that their behaviour will lead to a particular goal. If a child regularly uses aggression to reach their goal then they learn how much force or aggression is necessary and become confident in using their own physical strength as a means of getting what they want. Each time they successfully achieve their goal, their self-efficacy grows, meaning they believe that as aggression has worked for them in the past, it will solve similar problems in the future
Evaluation:
There is supporting evidence showing the role of social learning in aggression. Bandura et al (1961) found children who had observed the aggressive behaviours of an adult model in a video, imitated almost identically what they had seen and acted aggressively towards the Bobo doll. A control group who has not watched the aggressive role models, did not act aggressively. A replication of Bandura’s research showed that the adult being rewarded or punished for their aggressive behaviours. Children who observed an adult being rewarded were four times more likely to be aggressive than those who saw the model being punished. These findings demonstrate support for several key aspects of SLT including the role of vicarious reinforcement in the learning of aggressive behaviours
Social learning theory has real-life application to everyday aggression. There have been cases such as the Columbine high school massacre and the Jamie Bulger murder which the media have dubbed ‘copycat killings’ , where children have observed violence in films and then imitated them on victims on real life. OFCOM have brought out age restrictions on certain media, as well as the watershed to censor some aggression being witnessed by children, implying that they do believe the children may imitate the aggressive behaviours that they observe. This is a strength because this application of SLT as an explanation of aggression has been used to help improve society by limiting young peoples exposure to aggressive models and using prosocial role models whose behaviour is being reinforced
A strength of SLT as applied to aggression is that it is scientific. This means the theory focuses on observable and measurable behaviour which can be tested in controlled conditions. For example, Bandura’s bobo doll research is highly controlled and the learning demonstrated by the children was clear to observe and measure. This is a strength as it means the SLT explanation of aggression is supported by empirical evidence.
However, the mediational processes cannot be observed which means factors like attention and motivation have to be inferred. This is a problem as this inference could be mistaken meaning we cannot empirically measure all aspects of the SLT explanation of aggression
Deindividuation
Factors leading to deindividuation
Deindividuation is a term coined by LeBron (1895) to explain why some people lose their sense of personal responsibility, for example when in a crowd, in a uniform or disguise. If the individual feels anonymous, they feel less responsible for their actions and are more likely to go along with the group behaviour, which often includes acting aggressively towards rival groups. This is commonly known as ‘mob mentality’ where people stop thinking like they normally would as an individually and instead act aggressively as part of the faceless crowd
Self awareness
Prentice-Dunn and Rogers (1982) explained the link between agression and deindividuation in terms of two types of self-awareness:
Private self awareness- this regards paying attention to our own thoughts, feelings and behaviour, something we monitor when we are acting on out own. This is restricted when in a crowd as our attention is focussed outwardly rather than inwardly, meaning we are more perceptive of environmental factors such as the mood of the crowd, and absorb that energy, including aggression.
Public self awareness- this concerns how much we care about other people’s judgement and opinion of our behaviour, and this is also reduced in crowds. We believe that others would be less likely to identify us for out actions, and do the consequences seem less likely, meaning we are more likely to behave aggressively and not feel accountable for it.
Evaluation
There is supporting evidence showing the deindividuation in aggression. Zimbardo’s (1969) Stanford prison experiment demonstrated that when some people lose their sense of identity, they become disinhibited, stop monitoring their behaviour, forget about potential consequences for their actions and act impulsively and emotionally. This can ultimately lead people to carry out violent and aggressive acts that they never would have thought themselves capable of.
Further support from deindividuation leading to aggressive behaviour comes from Dodd (1985) who asked 229 of his undergraduate psychology students to anonymously answer the following question ‘if you could do anything humanly possible with complete assurance that you would not be detected or held responsible, what would you do?’. Three independent raters who were not aware of the hypothesis then read the answers and categorised them. He found 36% of the responses were classed as antisocial, 26% were actual criminal acts, the most common was to ‘rob a bank’. Some responses were very violent such as murder, rape or assassination of a political figure. Only 9% of the responses were prosocial and helpful. This research suggests anonymity leads to a higher chance of aggression.
Deindividuation has real-life application to everyday modern aggression. Douglas and McGarty (2001) looked at aggression online, in chat rooms and instant messaging. They found a strong correlation between anonymity and sending threatening messages to other users. This shows that people are more likely to act aggressively online when they feel anonymous. This is exactly what the theory predicts- people do not self-monitor when part of a group in chat rooms and therefore can be more aggressive because they take on the mood of the group and do not feel personally identifiable
Research has demonstrated that deindividuation can lead to pro-social rather than anti-social behaviour like aggression. Johnson and Downing (1979) found, in a replication of Zimbardos electric shock study, that participants shocked more than a control group when dressed like the Ku Klux Klan, but actually shocked less than controls when dressed in nurses uniforms. This suggests that aggressive behaviour is dependent upon the norms associated with the uniform as opposed to the uniforms themselves.
Institutional aggression in the context of prisons: dispositional and situational explanations
Dispositional explanations- the importation model
Dispositional explanations for aggression focus on the personality factors that the people have before they enter prison and how they might prime them for aggression inside the institution. The importation model was decided by Irwin and Cressey (1962) who believed there are certain factors that criminals ‘import’ into prison that lead to aggression such as beliefs, values norms and attitudes, as well as personal characteristics such as gender, race and class.
Statistically, most aggressive inmates tend to be young ethnic minority males from lower class backgrounds; this could be due to a variety of reasons. There is also higher aggression levels shown by prisoners who had issues such as addictions, or were members of gangs before being arrested. These groups’ aggression levels within the prison environment mirror their behaviour before they entered the prison, and often a history of impulsive aggression and violence is the reason they were sent to prison in the first place.
Evaluation:
There is evidence to support the dispositional explanation comes from Poole and Regoli (1983). They fond that the best indicator of violence amongst juvenile offenders was their level of pre-institutional violence, regardless of any situational factors in the institutions. This suggests the importation model may be a stronger explanation of institutional aggression than the deprivation model
There is supporting evidence showing aggressive characteristics can be imported into prison. DeLisi et al (2011) studied 813 juvenile delinquents in Californian institutions who imported with them, a range of negative dispositional features, including experience of childhood trauma or abuse, addictions and anger. A positive correlation was observed; inmates with the most negative dispositional features were the most likely to be brought in front of the parole board for being aggressive in the institution. Compared to a control group, they were also more likely to engage in self-harm and suicide. This is a positive because it can provide an insight for which individuals are more likely to be aggressive based on their characteristics before entering prison. This can be an important practical application because these individuals could receive targeted support as soon as they enter the institution. Fischer (2001) found that isolating known gang members in a special management unit reduced the rates of serious assault by 50%. This suggests research into the importation model can help to reduce prison violence
Situational explanation for institutional aggression- the deprivation model
Situational explanations for aggression focus on the prison environment itself and how the harsh conditions cause stress and strain for the prisoners, leading them to retaliate by acting aggressively. The Deprivation Model was devised by Clemmer 1958) who identified a number of deprivations experienced by prisoners which correlated with aggression; Freedom, Independence, Material Goods, Safety and Intimacy
When a person has their regular routine and luxuries taken away, this leads to a loss of social norms (anomie) so they adopt behaviours of others rather than acting like they normally would, leading to some deindividuation and in turn aggression. Prisons that are overcrowded and regularly use punishments such as lock-ups or taking away luxuries such as TV time' are more likely to experience prisoners acting aggressively. Deprivation of material goods and services can also lead to frustration and competition, so aggression becomes a means of solving this problem.
Evaluation:
There is supporting evidence showing characteristics of the prison itself is linked to aggression. Iberia (2011) took a stratifies sample from all 117 US federal bureau and gave them a questionnaire on conditions at their prison. This was matched to prison records of violence. The Explain / Expand: Bierie (2011) took a stratified sample of prison staff from all 117 US federal bureau of prisons results showed extreme inmate violence was significantly higher in prisons with poor physical conditions such as noise level, poor hygiene and a lack of privacy for inmates as well as in prisons with more white staff and few female staff. These findings are a strength of the situational explanation of aggression because they suggest that the actual prison environment itself can influence the level of violence in prison.
One strength of this research is that it has clear practical applications. In the early 1990s, Wilson set up two units at HMP Woodhill that were less 'claustrophobic' and gave a view of the outside world, masked prison noise with music from a local radio station and lowered the temperature so it was no longer so extremely hot. It was found that these changes virtually eradicated assaults on prison staff and other inmates. This suggests that the deprivation model can be used to help improve safety and security for staff and inmates alike by improving the prison environment.
There is contradictory research that criticises the situational explanation for aggression. Hensley et al (2002) studied two prisons in Mississippi where inmates were allowed 'conjugal visits', meaning they were not deprived of sexual intimacy with their romantic partner. These prisons had the same levels of aggression as those who did not allow conjugal visits. This is a problem as it suggests the deprivation of heterosexual relationships does not affect prison violence.
Media influences on aggression, including the effects of computer games.
Experimental Studies:
Conducted in a lab, short term effects of media on aggression
Bartholow and Anderson (2002)
Procedures: Student volunteers were randomly allocated to one of two conditions; they either played a violent game 'Mortal Kombat' or a non-violent game PGA Tournament Golf' for ten minutes then carries out a standard task that measures aggression (delivering blasts of white noise at chosen volumes to an opponent).
Findings and conclusions: Those who played the violent game gave significantly louder blasts of noise to their opponent (mean of 6.0 compared to 4.6 decibels). It was concluded that violent computer games can cause an immediate increase in aggressive behaviour.
Correlational Studies:
Relationships between real life variables in media and aggression
DeLisi et al (2013)
Procedures: Used structured interviews to study 227 juvenile offenders with histories of serious aggression such as hitting a teacher, parent, or gang fighting.
Findings and conclusions: The offenders' aggressive behaviour was significantly correlated with how often they played violent computer games, and how much they enjoyed them. It was concluded that computer game violence is a serious risk factor for aggression.
Meta-Analysis
Greitemeyer and Mugge (2014) performed a meta-analysis of 98 studies and found that violent video game use was linked to an increase in aggression whilst exposure to prosocial games was linked to an increase in prosocial behaviour.
It was concluded that a range of evidence supports the link between violent computer games and aggression.
Evaluation
One strength of the laboratory experiment research is that it had a high degree of control over variables. variables to be controlled. For example, the type of violent game plaved and for how long. This means the research is conducted in the controlled setting of a laboratory which allows extraneous variables to be controlled. This is a strength as the research has high internal validity. It is therefore it is more likely we can make a cause and effect conclusion i.e, to say that it is the playing of an aggressive computer game that has led to the aggressive behaviour.
However, a major weakness of these laboratory experiments is that researchers have not measured 'real-life' aggression. This means that ethical issues have restricted researchers to alternative measures of aggression. For example, administering 'noise blasts' has been used in place of real aggression which is very different, not least because it does not involve any fear of retaliation. This is a problem as the research may not represent real-life aggression.
Additionally, it is argued research has overstated the effects of the media. This means, although many results have been significant, they typically report only small-medium effect sizes. Furthermore, when focusing on the small of number of studies that measure aggression towards another person (as opposed to alternative measures), the influence of the media on aggression is actually close to zero. This suggests the influence of the media on aggression many be much smaller than is often thought.
One weakness of correlational studies is that they do not establish cause and effect. This means that correlations only establish a relationship between two co-variables but cannot say that one co-variable 'caused' the change in the other. For example, although they might seem to show that violent computer games cause people to become more aggressive, they might also only show that people who are already aggressive select aggressive media.This is problematic as it limits the extent to which the researcher can draw firm conclusions from the research.
A strength of research into media influence on aggression is that it has practical applications.This means it shows the negative effects violent media can have, but also the positive influence prosocial media can have on people which can be used to ensure the media has a positive influence on society. For example, greater censorship of aggressive media and promotion of prosocial media (e.g. computer games where the aim is to help others) may well have positive effects on people. This is positive as ongoing research can help ensure the media is a force for good in society as much as possible.
The role of desensitisation, disinhibition and cognitive priming
Desensitisation
Physiological responses to aggression are based on the fight or flight response; when someone witnesses violent actions, their sympathetic nervous system is activated, raising heart rate and blood pressure ready to respond to the threat. However, the more often people are exposed to aggression, the less sensitively their nervous system reacts to it, meaning the more they play violent computer games, or watch violent media, the less of a physiological arousal they show. This in turn suggests that people, particularly children, who have large exposure to violent media show less emotion in response to aggression in real life.
Evaluation:
Support for the role of desensitisation comes from Krahé et al (2007). They found that participants who reported regularly viewed violent media (including violent films and computer games) showed lower levels of arousal (e.g. sweating) when shown violent film clips than non-regular viewers. Lower arousal was correlated with unprovoked aggression in a 'noise blast' task. This supports the view that regular exposure to media aggression does serve to 'desensitise' the viewer, but also that this desensitisation is linked to higher levels of unprovoked aggression. However, this research has been criticised for not measuring real-life aggression. This is because, delivering blasts of white noise at chosen volumes to punish a (non-existent) opponent is very different to real aggression, not least because it does not involve any fear of retaliation. Furthermore, as aggression is only correlated with 'desensitisation", we cannot say desensitisation causes aggression, merely that they are linked.
However, desensitisation is thought to have both positive and negative real-life consequences. On the positive side, for army troops, they can become desensitised to the horrors of combat and therefore become a more effective soldier. One practical application may therefore be to use violent media such as computer games to desensitise soldiers as part of their conflict training. On the negative side though, Bushman et al (2009) suggest that exposure to violent media and the resulting desensitisation can reduce helping behaviour which might otherwise be offered. They become 'comfortably numb' to the pain and suffering of others and are consequently less helpful. This suggests awareness of the role desensitisation in peoples behaviour is important in a range of situations
Disinhibition
The normal belief is that aggression is harmful and unacceptable in a society; children are taught that aggressive behaviour will receive punishments (i.e. formal or informal sanctions) directly through operant conditioning or indirectly through social learning theory. If children continue to interact with violent media, especially if they perceive that the aggression was rewarded or not punished, then their usual moral restraints become looser; they minimise the effects of violence and justify its use meaning they may act aggressively themselves in future.
Evaluation:
Support for the role of disinhibition in aggression comes from Berkowitz et al (1973). They found that, participants that watched a film depicting aggression as vengeance gave more (fake) electric shocks of longer duration to a confederate. This suggests that media violence may disinhibit aggressive behaviour when it is presented as vengeance, possibly because vengeance is seen as a strong justification for violence and therefore more socially acceptable. However, the chances of disinhibition occurring may depend on other factors. Heath et al (1989) found that children growing up in households with strong norms against violence are unlikely to experience sufficient disinhibition for them to exhibit aggressive behaviour, whereas the disinhibition effect is stronger in families where children experience physical punishment from their parents and where they identify with violent heroes. This suggests there may be practical applications of this research in encouraging parents to prevent their children from feeling the effects of disinhibition by establishing clear household norms and expectations around violence.
Cognitive priming
According to Huesmann 1998), our life experiences help to write our schema or 'script about violent situations which is stored in our memory ready to play out' when we encounter such situations in the future. For people who have had large amounts of exposure to violent media, including violent computer games, music and other media, they show more of a readiness to act aggressively. They are primed for aggression which means their schema may be 'triggered' by cues that they perceived to be more aggressive than others.
Evaluation
Support for the role of cognitive priming in aggression comes from Bushman (1998). They found that, when undergraduates watched a 15 minute segment of a violent film, they had faster reaction times to aggressive words than those who had watched a non-violent film. This suggests that exposure to violent media does increase the 'accessibility of violent thoughts and ideas, as predicted by the theory. Furthermore, Anderson and Dill (2000) found that participants who played violent computer games had more cognitively accessible aggressive thoughts than did those who played non-violent computer games. They concluded that a single incident of violent game play was enough to prime aggressive thoughts.
However, blaming aggression on the influence of the media may ignore the role played by biological factors. For example, it is possible that aggressive behaviour may be, at least in part, genetic. Brunner 1993) discovered a defective 'MAOA gene' in a Dutch family with a history of male violence. Furthermore, testosterone has been shown play an important role in determining some aggressive behaviour. This suggests media influence explanations of aggression may be limited in the amount of aggressive
Gender:
Sex and gender. Sex-role stereotypes, androgyny including the Bem Sex Role Inventory
Sex and gender
The difference between sex and gender is that sex is innate in nature whereas gender is at least partly environmental. This would suggest that a person’s sex cannot be changed. A person’s gender however is seen to be a person’s psychosocial status. It is assumed that a person may be more masculine or feminine depending on the social context they are in
Imperato-McGinley et al conducted a study on a unique family known as the Batista family who lived in the Dominican Republic. Four of the children were identified as being female at birth and raised as such, however they were actually genetically male. This very rare genetic condition meant that when hormonal changes occurred in puberty, their vaginas closed over and they developed penises. All of the boys abandoned their female gender and identified as male from that point forward. This would suggest gender is flexible
Sex-role stereotypes
Societies expectations of what is seen to be appropriate for males or females re often communicated and reinforced by parents, teachers and the media. For example, Furnam and Farrager (2000) analysed tv adverts and found that when men are more likely to be shown in autonomous roles in professional contexts, whereas women were depicted in familial roles within domestic settings
Although some sex role stereotypes have an element of truth behind them, many do not, which leads to sexist views being formed. For example, recent research has found that women do seem to cope better with multi-tasking than males but there is no strong evidence to suggest that women struggle to control their emotions in the workplace
Androgyny
Androgyny means to show an even balance of qualities or characteristics that are typically associated with the genders.
Both males and females can be describes as being androgynous. For example, an individual who is aggressive and competitive in work but a kind and sensitive parent is displaying typically male and female characteristics
Androgynous individuals tend to have more positive mental health outcomes than typically masculine or typically feminine individuals
Measuring androgyny- Bem Sex role inventory
Bem (1974)- designed the Bem sex role inventory to measure androgyny. It is a self report with 60 items all rated on a seven point likert scale. 20 items are related to stereotypically masculine characteristics, 20 are related to stereotypically feminine characteristics and 20 are gender-neutral filler items. The scores are calculated to identify the individuals overall type. The BSRI is an indication of psychological well-being and mental health rather than just having masculine or feminine characteristics
Scoring of the BSRI- scores are classified on two dimensions- masculinity/femininity and androgynous/undifferentiated
Evaluation:
Burchardt and Serbin (1982) provided supporting research for a positive correlation between androgyny and good mental health, particularly in relation to lower levels of depression in androgynous females. Androgynous collagen males also scored lower on social introversion than feminine females. The findings therefore support the importance of androgyny as an indicator of positive mental health
Peters of Cantrell (1993) used the BSRI to provide supporting evidence that androgynous females had the best quality of relationships, supporting the idea of a positive correlation and it being associated with higher interpersonal functioning than individuals who are predominantly masculine or feminine. Therefore this decreases the validity of the BSRI as a measure of psychological wellbeing
Whilst there is supporting research evidence for a correlation between positive mental health and androgyny critics argue that androgyny is not always associated with positive mental health. For example, androgynous individuals may demonstrate negative masculine characteristics such as aggressiveness and negative feminine characteristics such as being too timid. This therefore criticises Bems idea of positive psychological wellbeing
A strength of the BSRI is that it has good test-retest reliability. Research has demonstrated high correlation co-efficients of .76 and .94 over a 4 week period. Furthermore, the shorter version of the test which has 30 items has improved test-retest reliability with a correlation of 0.90. This therefore suggests that the inventory is a reliable way to measure androgyny
However a limitation of the BSRI is that its temporal validity has been questioned. This is because it was created by data generated from American students in the 1970s and typical gender behaviour may have changed since then. For example more contemporary research was conducted on a group of 400 undergraduates who were asked to rate the items on the BSRI as masculine or feminine, only two of the items were still considered to be masculine or feminine. This therefore suggests that the BSRI is outdated as a measure of androgyny,
The role of chromosomes and hormones (testosterone, oestrogen and oxytocin) in sex and gender.
From the biological perspective, sex and gender are the same. Behavioural, psychological and social differences between the sexes are seen to be the result of anatomical, chromosomal and hormonal differences in the body. From this perspective our biological sex determines out gender development
The role of chromosomes:
There are 46 chromosomes in the human body which are arranged into pairs. Each person has 23 pairs of chromosomes. Each of these chromosomes carries hundreds of genes containing instructions about physical and behavioural characteristics such as eye colour and predisposition to certain mental illnesses
One pair of chromosomes are called the sex chromosomes because they determine an individual’s biological sex. A females chromosomal structure is XX and a male is XY
A mother’s egg always contains an X chromosome, the sperm fertilising the egg will carry either an X or a Y chromosome. If it carries an X, the baby will then have XX chromosomes and be female, if it carries a Y then the baby will have XY chromosomes and be male
Up to about 6 weeks into pregnancy, male and female foetuses look the same i.e. their gonads (sexual organs) are no different. However around the 6th week the sex chromosomes will begin to have an effect. If the fertilising sperm contained an X chromosome then the gonads will develop into ovaries. lf, however, the sperm had contained a Y chromosome then the gonads would develop into
testes.
The Y chromosome carries a gene called the SRY gene which causes testes to develop in an XY embryo. The testes produce androgens (male sex hormones) which cause the embryo to become a male, without them the embryo would develop into a female
The role of hormones
Chromosomes initially determine a person's sex but most gender development occurs through the influence of hormones. Prenatally in the womb, hormones act upon brain development and cause the development of reproductive organs. At puberty, a burst of hormonal activity triggers the development of secondary sexual characteristics such as pubic hair. Males and females produce many of the same hormones but in different concentrations.
Testosterone
Testosterone is a male hormone which is produced prenatally and controls the development of male sex organs. Testosterone also affects brain development both prenatally and later in childhood. Much research has focussed on the behavioural effects of testosterone and its link to aggression. Human and animal studies have demonstrated the influence of increased testosterone on aggressive behaviour.
Oestrogen
Ostrogen is a female hormone that determines female sexual characteristics and menstruation. The default gender is female and so females do not need hormones to direct prenatal gender development. Ostrogen plays a major role from puberty onwards promoting secondary sexual characteristics such as breast development and directing the menstrual cycle. Ostrogen also causes some women to experience heightened emotions and irritability during their menstrual cycle.
Oxytocin
Women typically produce oxytocin in much larger amounts than men and is sometimes referred to as the love hormone. Oxytocin is released in massive quantities during labour and after childbirth and makes the new mother feel 'in love' with the baby. The hormone stimulates lactation making it possible for women to breast feed and reduces the stress hormone cortisol facilitating bonding. The fact that men produce less Oxytocin has fuelled the stereotype that men are less interested in intimacy and closeness in a relationship.
Evaluation
Supporting evidence by Dabbs et al (1995) has found, that in a prison population, offenders with the highest levels of testosterone were more likely to have committed violent or sexually motivated crimes. Furthermore, Van Goozen et al (1995) studied transgender individuals who were undergoing hormone treatment and being injected with hormones of the opposite sex. Transgender women (male-to-female) showed a decrease in aggression and visuo-spatial skills whilst transgender men (female-to-male) showed the opposite. These studies therefore support the role of sex hormones in gender-related behaviour such as aggression
Tricker et al (1996) gave males either 10 weekly injections of testosterone or a placebo and found no significant differences in aggression. This is consistent with further research, which has found that sex hormones had no consistent effect on gender development. This therefore questions the view that sex hormones determine behaviour.
Research into cross cultural gender differences has been used to criticise the role of chromosomes and hormones in sex and gender. Mead (1935) conducted research into three tribes in Papua New Guinea. In the Arapesh, both males and females displayed non-aggressive gentle, typically feminine behaviour.
In the Mundugumor tribe both males and females behaved in an masculine way-aggressive and assertive and in the chambuli tribe sex role behaviour was completely reversed. This therefore suggests that the environment has a larger influence on gender development as if the main cause was biological (e.g. Hormones) then the same gender differences would be seen across all tribes.
The biological accounts of gender oversimplify a complex concept. Gender is reduced to the level of chromosomes and hormones and underplays the importance of alternative explanations for gender development. For example, the psychodynamic approach would suggest that childhood experiences such as interactions within family are important for gender identity. Therefore, just focusing on biological factors is too simplistic.
A limitation of research into the role of sex hormones such as oestrogen is that it can lead to negative stereotypes. Some people object to the medical category premenstrual syndrome on the grounds that it a social construction rather than a medical fact. Therefore, some feminists would argue that this encourages damaging stereotypes of 'irrational women' and this can affect how women are treated in society.
Atypical sex chromosome patterns: Klinefelter’s syndrome and Turner’s syndrome
Klinefelter's Syndrome:
Individuals who have this condition are biologically male, with the anatomical appearance of males and have an additional X chromosome. Their sex chromosome structure is XXY. Approximately 1 in 1000 males have this condition.
Physical characteristics
• Reduced body hair
• Underdeveloped genitals
• Some breast development at puberty and a 'softening' or 'rounding' of body contours
• More susceptible to health problems found in females such as breast cancer
Psychological characteristics
• Poorly developed language skills and reading ability
• Passive and shy
• Lack of interest in sexual activity
• Tend not to respond well in stressful situations
Turner’s syndrome
This is caused by an absence of one of the two allocated X chromosomes and is referred to as XO. This means the individual has 45 chromosomes rather than the usual 46. This occurs in about 1 in 2000 females at birth.
Physical characteristics
• Underdeveloped ovaries, leading to a lack of monthly periods
• Do not develop breasts at puberty and instead have a broad chest
• Low set ears and a webbed neck
• Physically immature and retain appearance of pre-pubescent girls
Psychological characteristics
• Higher than average reading ability
• Lower performance on spatial, visual memory and mathematical skills
• Socially immature
• Have trouble relating to their peers and 'fitting in'
Evaluation:
A strength of research into atypical sex chromosomes is that the research has practical applications. Herlihy (2012) showed that individuals identified and treated from a very young age has significant benefits compared to those who had been diagnosed in adulthood. Further research is likely to lead to earlier diagnosis and an increased understanding of those issues faced by those syndromes. Such research will therefore have a direct benefit to people who have these atypical chromosomal patterns as well as increasing our understanding of atypical development.
Studies into atypical sex chromosome patterns are beneficial as they contribute towards our understanding of the nature-nurture debate in gender development as a whole. By comparing individuals with these conditions with individuals who have typical chromosomal patterns it allows researchers to identify differences in gender behaviour. For example, individuals with Turner's syndrome tend to talk more than 'typical girls. This therefore leads researchers to conclude that this is due to chromosomal differences providing evidence for the role of nature in gender development.
A limitation of research into atypical sex chromosome patterns is that is there is a lack of causal relationships. It is possible that the impact of environmental and/or social influences are more important than the research suggests. For example, social maturity in females with Turner's syndrome maybe due to the way others respond to their physical immaturity rather than a biological cause related to their chromosomes. Therefore, it is difficult to establish the cause of social maturity as being due to the atypical chromosome patterns
A further criticism of research into this area is that there is no such thing as typical and atypical gender behaviour. One of the symptoms of Turner's syndrome is that females are socially immature compared to the vast majority of females. Research by Maccoby and Jacklin has actually found that there are significantly more gender differences within the sexes than between them. This therefore suggests that assumptions about typical gender behaviour are often based more around stereotypes than fact.
Cognitive explanations of gender development, Kohlberg’s theory, gender identity, gender stability and gender constancy, gender schema theory
Kohlberg’s theory
Kohlberg believes that gender development including gender identity and gender roles is determined by a child's level of thinking and understanding
When children have the cognitive ability to understand that gender is fixed and constant, at about 7 years, they develop schemas of appropriate and inappropriate same sex behaviour and characteristics, such as clothing, hairstyles, occupations and personality
Gender schemas and gender roles develop through environmental interactions in which children actively seek out and imitate same sex models and focus on other gender information of how to behave like a boy or girl, Kohlberg called this self-socialisation
Kohlberg argues that children go through three distinct stages in the development of full gender identity:
Stage one is gender identity and occurs between about 2-3 years. This is when a child understands that they are a boy or a girl, but believe that gender can change
Stage two is gender stability and occurs between 3-5 years. The child understands that their gender is fixed over time and that boys become men and girls become women but they are unable to apply this to other people and other situations. They are also confused by changes in appearance so if a man has long hair, they will think he is a woman
Stage three is gender constancy and occurs between 6-7 years. At this stage the child understands gender remains fixed over time and different situations. Children are cognitively ready to develop appropriate gender roles and behaviour
Evaluation:
McConaghy (1,979) found that when a doll was dressed in transparent clothes so there was a discrepancy between its clothing and its genitals. 3 to 4 year old children decided on the dolls gender on the basis of clothing. This study therefore supports Kohlberg's theory of gender development because it suggests that gender constancy has not yet been achieved by this age in line with what Kohlberg predicts. Furthermore Munroe et al 1984) found that Kohlberg's three stages of gender identity development was similar and occurred in the same order in six cultures (USA, Kenya, Nepal, Belize and Samoa). This study provides evidence that the three stages may be universal and based on biological maturation of cognitive structures as Kohlberg claims which strengthens the explanation.
However there is contradictory evidence to Kohlbergs theory. Martin and Little (1990) found that children under the age of four, who showed no signs of gender stability or constancy still demonstrated strong sex typed behaviour and attitudes. Furthermore Bussey and Bandura found that children as young as 4 said they felt good about playing with gender-appropriate toys and bad about playing with gender-inappropriate toys. These findings dispute Kohlberg's claim that children only begin to demonstrate gender-appropriate behaviour once they reach the gender constancy stage and are more in line with gender-schema theory which suggests that children absorb gender-appropriate information as soon as they identify themselves as either male or female at around 2 years of age
Another issue is that there are methodological problems with Kohlberg's theory. Kohlberg's theory was developed using interviews with children who were as young as 2 years. Despite the questions being tailored towards that particular age group, the children may have lacked the vocabulary needed to express their understanding of gender. This may have lowered the validity of the interviews as the children may not have been able to express what they truly felt and therefore the findings are not representative of the children's understanding of gender and could ower the validity of Kohlberg's stages
Furthermore, there is evidence to suggest that boys tend to show stronger sex-typing than girls With males being less flexible than females. These differences are difficult to explain by Kohlberg's theory because if gender development was purely due to maturation there would be no difference in male and female gender identity. This suggests the less flexibility is due to socialisation, and psychologists have found that fathers react more negatively towards their sons' feminine play than mothers did, suggesting environmental influences such as this could be responsible for boys being less flexible and showing greater resistance to opposite-sex activities Therefore, social explanations maybe a better explanation of gender development than cognitive.
However Kohlberg's explanation of gender development unlike most other explanations can be given credit for taking into account both nature and nurture, because the three stages of gender development are universal and not limited by cultural relativism so are based on nature, and self-socialisation focuses on experiences so is based on nurture. By considering both nature and nurture, it could be argued that this makes Kohlberg's explanation of gender development more reasonable and therefore acceptable.
Gender schema theory
A gender schema is an organized set of attitudes, beliefs and values stored in memory about gender behaviour. A child's thinking and understanding about experiences determine the development of gender schemas and therefore gender development
Gender schema theory proposes that we learn gender schemas about what is appropriate and inappropriate gender behaviour through our observations and interactions with others. These gender schemas develop from about 2 years of age, after basic gender identity is established and children are most interested in and therefore focus on schemas which match their own in-group gender identity and avoid out-group gender schemas
In-group schemas develop concerning expectations and attitudes about one's own gender and out-group schemas about the other gender. Gender schemas provide the basis for what is perceived to be appropriate and inappropriate gender role behaviour. Gender schemas determine what information children pay attention to; how children interpret behaviour and social situations and what children remember from their experiences
Gender schemas change and become more complex as a child's cognitive abilities develop. By adolescence gender schemas become more flexible as children understand that gender roles are socially constructed, and many teenagers become less sex-typed and more androgynous
Evaluation:
There is supporting evidence by Martin and Halverson who found that children under the age of inconsistent behaviours when tested a week later. Children tended to change the sex of the six were more likely to remember photograns of ander consistent behaviours than gender person carrying out the gender - inconsistent activities in the photographs when asked to recall them which supports that memory is distorted to fit in with existing gender schemas
Further research to support comes from Martin and Little 1990). They found that children under the age of four, who showed no signs of gender stability or constancy still demonstrated strong sex typed behaviour and attitudes. This therefore supports the gender schema theory whilst contradicting Kohlberg's theory
However, a criticism of the gender schema theory is that the key assumptions are unsupported The theory suggests that it should be possible to change a child's schemas and that by adolescence gender schemas become more flexible; however, this has shown to be very difficult. For example, many people have strong views regarding sex equality and division of labour in the home, but this often fails to show in their day-to-day behaviour. Therefore, this demonstrates that attitudes do not necessarily lead to behaviour, yet the gender schema theory assumes that child's attitudes (schemas) do affect their behaviour, this therefore questions the validity of gender schema theory
The gender schema theory has been criticised further for exaggerating the importance of schemas. The theory does not pay sufficient attention to social factors such as the roles of parental influence and the role of reward and punishment. For example, a girl may be punished for being assertive and dominant whereas a boy may be praised for showing these qualities
Therefore it would be inappropriate to conclude that schemas alone are responsible for gender role development and that other factors should be taken into consideration when trying to explain such a complex behaviour as gender
It has been suggested that the gender schema theory and Kohlberg's theory can actually be seen to complement one another as oppose to being in direct conflict. Researchers have argued that gender schemas and gender constancy may be two different processes. Gender schemas explain how information is organised and stored in memory whereas gender constancy related to motivation. Once a child has established their concept of what it means to be a boy or girl they are then motivated to find out more. It would therefore perhaps be more appropriate to look to combine these gender theories to provide a wider understanding of gender development
Psychodynamic explanation of gender development, Freud’s psychoanalytic theory, Oedipus complex, Electra complex, identification and internalisation
Pre-phallic children
According to Freud, children have no concept of gender identity prior to the phallic stage. Freud described these pre-phallic children have no sense that they are neither masculine nor feminine. Gender identity begins to form in the phallic stage (3-5 years) when the focus of pleasure switches to the genitals, and the child experiences the Oedipus complex (boys) or the Electra complex (girls). Resolving these conflicts effectively is vital for healthy gender development.
Oedipus complex
Freud proposed that boys
experience the Oedipus complex whereby they desire their mother. They then see their father as a rival and as a result, develop murderous hatred for their father who stands in the way of the boy possessing his mother. However, the boy recognises that the father is more powerful than he is and fears he may be castrated by the father for his feelings towards the mother. This is known as castration anxiety. To resolve the conflict, the boy gives up his love for his mother and begins to identify with his father. It is through this identification with that the boy internalises his father's gender identity.
Electra complex
Girls experience the Electra complex; upon discovering she doesn't have a penis, the girl develops penis envy blaming the mother for a lack of a penis, believing that she was castrated by her. The girl also sees the mother as a love rival standing in the way of the father. Over time, the girl comes to accept that she will never have a penis and substitutes penis envy for the desire to have children. This reduces the anger towards her mother, causing her to identify with her mother and internalise her feminine gender behaviours.
Identification and internalisation
For both sexes, identification with the same-sex parent is the means of resolving their respective complexes. A boy will give up his desire for his mother and identify instead with his father, likewise the girl passively identifies with her mother. Identification leads to internalisation. This is the processing of adopting the attitudes, values, and the gender identity of the same-sex parent. A boy will internalise the views and behaviour of his father and likewise the girl does the same with her mother, assuming their values as the child's own
Evaluation
Reckers and Morey (1990) rated the gender identity of 49 boys aged 3-11 based on interviews with the boys and their families. Of those who had been judged as having issues with their gender identity, 75% had neither their biological father nor a substitute father living with them. This suggests that being raised without a father was having a negative impact on their gender identity which is inline with Freud
Freud supported his theory with the use of case studies (e.g., Little Hans). This research lacks validity. Based on one case, we cannot be certain that all young boys suffer from castration anxiety.
Additionally, Freud's theory implies that the sons of very strict and harsh fathers should go on to develop stronger gender identity than other boys. This is because the high levels of castration anxiety experienced by these boys should produce stronger identification with the aggressor However, this is not supported by evidence and in fact, the reverse would seem to be true - boys with more liberal (easy-going) fathers, tend to be more secure in their masculine identity (Blakemore and Hill, 2008) which would go against the key ideas of Freud's theory
Freud's theory relies on a child having two parents of different genders. This implies that raising a child in a non-nuclear family, would have a negative effect on the child's gender development.
However, evidence does not support this assumption. For example, Susan Golombok (1983) demonstrated how children from single-parent families went on to develop normal gender identities
Similarly, Richard Green 1978) studied 37 children who were raised by gay or transgender parents and discovered that only one had a 'non-typical gender identity.
Freud wrote extensively about the Oedipus complex and focussed much more on male gender identity, admitting that that women were a mystery to him. As such, Freud's theory of female gender identity, especially the notion of penis envy, has been heavily criticised for reflecting the patriarchal Victorian era in which Freud lived. Indeed, the feminist psychoanalyst Karen Horney argues that a more powerful emotion than penis envy is the male experience of 'womb envy' - a reaction to women's ability to give life.
Furthermore, Horney argues that Freud's theory of female gender development is flawed as it is founded on the idea that women desire to be like men illustrating Alpha Bias
Freud argued that gender identity is formed at the end of the phallic stage (age 6), when the child identifies with the same sex parent. Prior to this, the child is described as bisexual, neither male nor female. This contrasts with other explanations of gender development, such as Kohlberg's theory, which suggests that the child's concept of gender develops gradually across a number of stages, which coincide with increased cognitive abilities. Freud failed to consider the growing cognitive abilities of the child; therefore, his theory is too simplistic
Social learning theory as applied to gender development. The influence of culture and media on gender roles
Social Learning Theory (SLT) explains the influence of the environment (nurture) in shaping our gender identity. This includes the influence of parents, peers, as well as culture and the media
Direct reinforcement: Children are more likely to be reinforced (praised) for demonstrating behaviour that is gender appropriate. The way in which boys and girls are encouraged to show gender-appropriate behaviour is called differential reinforcement. It is through this differential reinforcement that a child learns their gender identity (I am a boy). Behaviours that are reinforced are then imitated. A child is more likely to imitate behaviour that has been reinforced (rewarded). This reinforcement may be direct or indirect
Indirect (vicarious) reinforcement: If the consequences of another person's behaviour are pleasant, that behaviour is more likely to be imitated by a child.
If the consequence of the behaviour leads to punishment, behaviour is less likely to be imitated
Identification: This is the process whereby a child attaches themselves to a role model. Role models tend to be attractive, high status and usually, the same sex as the child. Give some examples of same sexed role model you had whilst growing up.
Include people that were within your immediate environment as well as those from the media
When a child imitates the behaviour of a role model, this is called modelling. E.g., when a little girl copies her mother setting the table, or feeds her doll using a toy bottle, she is modelling the behaviour she has witnessed.
Evaluation:
Smith and Lloyd (1978) dressed 4-6-month-old babies in either girl's clothes or boy's clothes. They found that adults interacted with the babies differently. For example, when it was assumed the baby was a boy the adults selected a hammer shaped rattle and were more adventurous and active with the baby. When the adults believed the baby was a girl, they reinforced passive behaviour and selected a cuddly doll to play with the child. This study suggests that gender behaviour is reinforced at an early age, supporting the SLT.
Changing views regarding stereotypically masculine and feminine behaviours in our society can be explain by a shift in cultural norms and the way that these new forms of acceptable gender behaviour have been reinforced. As there has been no corresponding change in people's basic biology within the same period (e.g. males still have XY chromosomes) such a shift is much better explained by SLT than the biological approach.
Critics have argued that SLT does not provide an adequate explanation of how learning processes change with age. For example, a toddler is incapable of imitating a parent vacuuming the living room because they are not strong enough to push a vacuum cleaner. However, the general implication is that modelling of gender-appropriate behaviour can occur at any age. The influence of age and development on learning behaviour is not a factor considered by SLT and this may be a limitation of the explanation.
SLT is contradicted by the case of David Reimer. David was born biological male but due to an accident during surgery he was raised as a female. David never felt like he was female and when told as a teenager that he was biologically male, he then changed his gender identity to male. He reported that he always felt that he was in the wrong gender identity. This case study suggest that biology has a stronger influence on gender identity than socialisation.
Social learning theory in relation to the media
Indirect (vicarious) reinforcement: If a child observes in the media that the consequences of another person's gender behaviour are pleasant, that behaviour is more likely to be imitated by a child. If the consequence of the behaviour seen in the media leads to punishment, the gender specific behaviour is less likely to be imitated
Identification: This is the process whereby a child attaches themselves to a role model. Role models tend to be attractive, high status and usually, the same sex as the child. Individuals in the media tend to be seen as having high status and more likely to be influenced by their gender behaviour
When a child imitates the behaviour of a role model, this is called modelling. E.g., when a little girl copies a TV character setting the table, or feeding her doll using a toy bottle, she is modelling the behaviour she has witnessed.
Evaluation
Research into the effects of the media on gender roles provides support for the social learning theory explanation of gender. This is because it clearly illustrates the effects of learning through imitation and observation on gender role behaviour.
The media provide role models with whom children may identify and want to imitate. A study of TV adverts by Furnham and Farragher (2000) found that men were more likely to be shown in autonomous roles within professional context e.g., the company boss, whereas women were often seen in domestic setting, e.g child rearing. This suggests that the media may play a role in reinforcing widespread social stereotypes concerning male and female behaviour.
Furthermore McGhee and Frueh (1980) conducted research on the amount of TV children watch and their knowledge of sex-role stereotypes. They found that children aged 6-12 who watched more than 25 hours of TV a week held more sex-stereotyped perceptions than those who watched 10 hours or less.
This study suggests that the media is a source of information for sex-role stereotypes and was especially seen for male teenagers.
However, correlational research, cannot establish whether the TV viewing causes sex-role stereotypes. Additionally, is cannot be ascertained how this increase in knowledge affects the behaviour of the children.
However in recent years there have been many examples of counter-stereotypes in the media, such as the Disney movie Brave, which challenges traditional gender roles and Marvel's top selling movie, Captain Marvel, using strong female role models in the media. It is hoped that these counter-stereotypes may help in
reducing gender stereotyping and gender discrimination in society.
Also, the Advertising Standards Authority (ASA) has toughened rules on ads that ar deemed to present activities as only appropriate for one gender or another, or that mo those who do not conform to stereotypical gender roles. Ads that perpetuate sex stereotypes, from men bungling housework to girls being less academic than boys, will banned under rules being proposed by the industry watchdog.
Social learning theory in relation to culture
Cross-cultural research is noted for its valuable contribution to the nature-nurture debate
Cultural differences: One of the earliest cross-cultural studies of gender roles was carried out by Margaret Mead 1935) of tribal groups on the island of New Guinea
• Arapesh were gentle and cooperative (similar to Western stereotype of femininity)
• Mundugumor were aggressive / hostile (similar to Western stereotype of masculinity)
• Tchambuli women were dominant and organised village life. The men were passive and considered to be 'decorative', (the reverse of the Western stereotypes)
Mead concluded that gender is culturally determined and that gender roles are acquired through socialisation and adherence to cultural norms
However, Mead's research has been criticised for not separating her own opinions from her description of Samoan life (observer bias) and making sweeping generalisations based on a relatively short period of study. In a follow up study by Freeman (1983) he said that Mead had been mislead by some of her participants and that her own preconceptions of what she would find had influenced her judgements. We can therefore question the validity her findings into the role of culture on gender as her findings may not be objective
Evaluation:
Cultural similarities: There is evidence to support that gender is more biological than cultural.
There are many cross-cultural similarities in gender roles. For example, Buss (1955) found similar patterns in mate preferences in 37 countries across all continents. In all cultures, women sought men who could offer wealth and resources, whilst men looked for youth and physical attractiveness in a potential partner. These findings would therefore suggest that if some gender roles are universal then they must have a biologically origin rather than a cultural one
Imposed ethics: There is a danger that researchers, armed with theories and methods that have been developed in the West, impose their own cultural interests and understandings pon the people they are studying. Berry (2002) refers to this as an imposed etic. To counteract this, Berry suggested that at least one member of the local population should be ncluded within the research team. This is what Buss did in this research, increasing its ultural validity.
Nature or nurture? Although cross-cultural research can provide an insight into the effect of different cultural practices on gender-role behaviour, such research does not solve the nature-nurture debate. In reality, it is impossible to separate the two influences on the development of gender roles. As soon as children are born, their socialisation into society begins (see Smith and Lloyd study). Therefore, it becomes very difficult to determine where nature (biology) stops, and nurture (social influence) begins.
Atypical gender development: gender dysphoria, biological and social explanations for gender dysphoria
Some men and women experience a mismatch between their biological sex and the gender they feel that they are (their gender identity).
Individuals who have gender dysphoria do not identify as their sex given at birth. For many people who experience this, gender dysphoria is a sourced of stress and discomfort and is thus recognised as a psychological disorder in the DSM-5.
Biological explanations
Brain sex theory:
This suggests that gender dysphoria is caused by specific brain structures that are different in males and females. Zhou (1995) found that a particular area within the thalamus (the bed nucleus of the stria terminalis or BSTc), is around 40% larger in males than females
In a post-mortem study of six transgender female, the BSTc was found to be a similar size to that of a cis female brain. This was confirmed by Kruijver (2000) who studied the same brain tissue and found that the number of neurons in the BSTc of these transgender individuals was similar to that of a cisgender female brain. This leads to the suggestion that people with gender dysphoria have a BST which is the size of the gender they identify with, not the size of their biological sex
Genetic factors:
Evidence suggests that gender dysphoria may have a genetic basis
Coolidge, 2002, assessed 157 twin pairs for evidence of gender dysphoria and found that 62% of gender dysphoria cases were accounted for by genetic variance. Similarly, Heylens (2012) compared 23MZ and 21DZ twins, where one of each pair was diagnosed with gender dysphoria, They found that 39% of the MZ twins were concordant for gender dysphoria compared to none of the DZ's. Both of these studies suggests that there is a strong heritable component to gender dysphoria.
Evaluation:
Contradictory evidence for BSTc: Although most transgender people report gender confusion in early childhood, Chung et al (2002) found that hormonal influences that affect the size of the BSTc volume are not triggered until adulthood. This evidence casts doubt on the idea that brain differences are present in early childhood and therefore, that gender dysphoria is directly caused by the BSTc volume.
Twin studies are inconclusive: The concordance rates for gender dysphoria are not very high (39%). This makes it very difficult to separate the influence of nature and nurture within these investigations. Twins, especially MZ twins, may influence each other, and the environmental conditions they are exposed to are likely to be very similar. E.g., one twin may simply be imitating the behaviour of the other by dressing and acting as the opposite sex. Also due to the fact that gender dysphoria occurs so rarely, sample sizes in twin studies tend to be extremely small, limiting the extent to which effective generalisations can be made.
Social-Psychological explanations
Psychoanalytic theory: It has been argued that gender dysphoria in biological males is caused by the child experiencing extreme separation anxiety before gender identity has been established. The child fantasises of a symbiotic fusion with his mother to relieve the anxiety, and the danger of separation is removed. The consequence is that the child becomes overly close to the mother and adopts a female gender identity.
Stoller (1973) interviewed gender dysphoric biological males and found that they had overly close mother-son relationships, which could lead to greater female identification and confused gender identity in the long term. It is suggested that severe paternal rejection is the cause of gender dysphoria in biological females. Unconsciously, the child identifies as a male to gain acceptance from the father (Zucker 2004)
Evaluation:
Supporting evidence: Zucker et al (1996) studied 115 boys with concerns about their gender identity. Of the boys who were diagnosed with gender dysphoria, 64% were diagnosed with separation anxiety disorder. Zucker also found high levels of emotional involvement in the mothers of boys with gender dysphoria. This suggests that gender dysphoria in males is linked to their relationship with their mothers, supporting the psychanalytical explanation. However, it should be noted that separation anxiety is very difficult to test as it relies on retrospective data, e.g., recalling events that happened in childhood which means that the research might be subject to retrospective bias and the emotional involvement of the mother in gender dysphoria may not be as a valid as Zucker suggests.
Social constructionism
This theory suggests that gender identity is not due to underlying biological differences, it is 'invented' by society. Individuals who have gender dysphoria experience the gender confusion because society forces us to be either a man or a women and act accordingly.
This theory suggests that gender dysphoria is not a pathological disorder, rather it is a social phenomenon arising when individuals are forced to pick one of two paths.
Evaluation:
A strength of social construction theory is that there is supporting evidence. In some cultures, for example the Fa'afafine in Samoa, they recognise more than two genders and the fact that more people are identifying as non-binary in modern society suggests that gender identity and therefore gender dysphoria is more a social construction rather than a biological fact.
Furthermore, Drummond (2008) followed a sample of 25 biological females who had been diagnosed with gender dysphoria in childhood. Only 3 out of 25 still were still classified as having gender dysphoria when followed up at the age of 24. These findings suggest that gender dysphoria is more a social/psychological issue rather than a biological issue because if the issue was biological then they should still have gender dysphoria as an adult.