AQA A-level Psychology Schizophrenia

The A-level psychology specification states you need to know the following for the classification of schizophrenia:

• Classification of schizophrenia. Positive symptoms of schizophrenia, including hallucinations and delusions. Negative symptoms of schizophrenia, including speech poverty and avolition. Reliability and validity in diagnosis and classification of schizophrenia, including reference to co-morbidity, culture and gender bias and symptom overlap.

Schizophrenia is a mental disorder which affects thoughts and emotions to a point where people lose contact with reality. About 1% of the population is affected by it at some point in their lifetime making it the most common psychotic disorder although many people can continue to lead normal lives after diagnosis and treatment. Schizophrenia is most commonly diagnosed between the ages of 15-35 with both genders affected equally.

To diagnose schizophrenia, a clinician would use a diagnostic manual such as The Diagnostic and Statistical Manual of Psychiatric Disorders which is also known as DSM-V (5).

DSM classifies and describes over 200 mental disorders grouping them in terms of their most common features. In the United States this DSM manual is most commonly used however in Europe another manual is more commonly used which is known as ICD (International Classification Of Diseases). The most recent version of ICD is ICD-10 with ICD-11 due to be published in 2017.

Under DSM-5 Criterion A, schizophrenia requires two or more of the following symptoms to be apparent for a one month period:

• Hallucinations
• Delusions
• Disorganised Speech
• Grossly disorganised or catatonic behaviour
• Negative symptoms
• Important to know: If delusions are bizarre or hallucinations consist of voices conversing with one another or keeping a running commentary on the persons thoughts and behaviours, then only one criterion A symptom is required from the list above.

Under Criterion B:

• Social/Occupational dysfunction: For a significant portion of time one or more major areas of functioning such as work, relationships or self-care or markedly lower than the level prior to onset.
• Criterion C) Duration: Continuous signs of the disturbance persist for at least a 6 month period.
• Criterion D) Exclusion of mood disorders with no major episodes of depression or elation have occurred concurrently with the
  psychotic symptoms.
• Criterion E) Exclusion of known organic causes: the disturbance is not due to the direct effects of drugs or a brain disorder

Positive symptoms are symptoms that reflect an excess or distortion of normal functioning. This involves the display of behaviours which demonstrate a loss of touch with reality involving hallucinations and delusions which generally occur in acute short episodes with normal periods of functioning in between.

Positive symptoms include:

• Hallucinations are bizarre unreal perceptions of the environment which may involve hearing voices, seeing things or even
  smelling things all of which do not exist. The person may even report that something is touching their skin or crawling underneath it such as bugs. Schizophrenics may even report auditory hallucinations such as hearing voices which may be insulting or obscene inside their heads which appear to form a running commentary or discuss the sufferers own behaviour.
• Delusions may involve the schizophrenic experiencing delusions of grandeur with inflated beliefs seeing themselves as more important in some form. The individual may also experience delusions of reference where they believe personal messages are being directed towards them e.g. through the television or radio. They may also believe they are famous or have special powers or abilities or the delusions may also be paranoid in nature believing themselves to be persecuted, followed or spied on.
• Disorganised Speech which is the result of abnormal thought processes and see’s the sufferer struggle to organise and filter their thoughts which show up in their speech. They may even display derailment where they are seen to switch from one topic to another mid-sentence with extreme cases displaying signs of incoherency that it is perceived as gibberish.
• Grossly disorganised or catatonic behaviour is characterised by the inability or motivation to initiate a task or complete it once started. This then causes problems in day to day life such as caring for ones own personal hygiene and looking after themselves. They may also dress or act in ways which appear bizarre to others such as wearing inappropriate clothing not suitable or the weather e.g. wearing thick clothing during summer time. Catatonic behaviour is characterised by reduced reaction to the environment, rigid postures and aimless motor activity by the sufferer.

Negative symptoms of schizophrenia are those that appear to reflect a diminution or loss of normal functions and may persist even during the absence of positive symptoms. Negative symptoms occur in chronic, long-lasting episodes and are mostly resistant to medication contributing the most towards a sufferers inability to function effectively within society, in relationships or at work.

Negative symptoms include:

Speech poverty is characterised by lessened speech fluency and productivity which is believed to reflect slowed or blocked
thoughts. Other characteristic signs of speech poverty may see them struggling with verbal tasks such as spontaneously naming as many animals as they can. Replies may also be brief with minimal elaboration.

Avolition is characterised by the inability to make decisions, lack of energy, enthusiasm and loss of interest in personal hygiene, sociability and affection. Sufferers may struggle to initiate and persist in goal-directed behaviour and sit in the house doing nothing for hours. The difference between this and poor social function or disinterest is avolition is the reduction of self-initiated involvement in activities that are available for them.

Affective flattening is characterised by a reduction in the range and intensity of emotional expression. This includes facial expressions, tone of voice, eye contact and body language. Sufferers show fewer body and facial movements, smiles and body movements associated with speech through the hands, head and face.

Anhedonia is the loss of interest or pleasure in activities or the lack of reactivity to normally pleasurable stimuli. The sufferer may display physical anhedonia which is the loss of physical pleasures such as eating or social anhedonia which is the inability to experience pleasure from interpersonal situations and social interaction. Physical anhedonia is seen as a more reliable negative symptom of Schizophrenia as it does not overlap with disorders such as depression (which social anhedonia does).

The specification specifically names co-morbidity, culture and gender bias as well as symptom overlap when we talk about reliability and validity - but what is reliability and validity?

• Reliability: Measures consistency. It is about the extent to which psychiatrists can agree on the same diagnoses when independently assessing patients.
• Validity: Is all about measuring what you want to measure, in our case how accurate diagnosis for schizophrenia is. If you create a test that does not measure schizophrenia then it is not valid.

These two go hand in hand, if a test is unreliable and keeps coming up with different conclusions when repeated then it cannot be valid (and vice versa).

In parts of the world the DSM diagnostic tool is used while other parts may use the ICD tool to diagnose Schizophrenia.

Issues with reliability first arise as both these tools have different diagnostic criteria’s; for example the DSM tool previously recognised 5 sub-types of schizophrenia while the ICD tool recognised 7 subtypes. Although now updated, this means diagnosis was not consistent between different parts of the world dependent on the tool being used. This means one country may have diagnosed someone as normal while another place with the same symptoms may see them as Schizophrenic. Therefore there is a clear cultural bias dependent on which identification tool is being used and where the individual is in the world highlighting how inconsistent and unreliable diagnosis actually is. This raises ethical concerns particularly when you consider the stigmatisation that follows a diagnosis of a mental disorder.

Cultural issues have contributed to significant variation between countries when it comes to the diagnosis of schizophrenia even when using the same criteria. Copeland (1971) gave 134 US and 194 British psychiatrists a description of a patient. 69% of US psychiatrists gave a diagnosis of schizophrenia while only 2% of British psychiatrists concluded the same highlighting issues with consistency and reliability.

In Britain people of Afro-Caribbean descent are more likely to be diagnosed as schizophrenic when compared to people who are white again highlighting diagnosis may not be valid. It could be argued the stress ethnic minority groups face contributes to this increased risk or that diagnosis itself is invalid. The fact that diagnosis is not consistent raises the issue of validity as we clearly cannot define schizophrenia correctly for a reliable diagnosis.

Gender bias in diagnosis is another issue although the accepted belief is that males and females are equally vulnerable to developing schizophrenia. Some argue that clinicians, most of which are men, misapply the diagnostic criteria to women and research findings show 50% more male sufferers due to this gender bias when diagnosing patients. Clinicians also fail to consider that males tend to suffer more negative symptoms than women and have higher levels of substance abuse while females have better recovery and relapse rates. Males and females also tend to have different predisposing factors giving them different vulnerability levels at different points in life and this is another factor clinicians tend to ignore contributing to this gender bias.

Gender differences in classification of the disorder occurs too, with first onset occurring earlier in males between the ages of 18 and 25. In females first onset is generally 4 and 10 years later between the ages of 25 and 35 years and this under-diagnosis and difference between genders highlights the lack of validity in diagnosis.

Symptom overlap is another issue affecting reliability and validity. Many of the positive and negative symptoms of schizophrenia are found in many other disorders such as depression and bipolar disorder. Ellason and Ross (1995) highlight how people with dissociative identity disorder (DID) actually have more schizophrenic symptoms than those diagnosed with schizophrenia themselves. Read (2004) also argued that most people with schizophrenia actually have enough symptoms that overlap with other disorders that they could receive one other diagnosis. This again calls into question the validity of both the classification and diagnosis of schizophrenia suggesting it may not be different to bipolar disorder or DID.

Co-morbidity is another issue undermining reliable diagnosis. This is when one or more additional disorders or diseases occur simultaneously with schizophrenia and this can affect reliable diagnosis as confusion arises over which disorder is being diagnosed. Schizophrenics often suffer from various forms of depression and this raises the issue of descriptive validity as having simultaneous disorders suggests schizophrenia may not be a separate disorder itself.

• One way of measuring how consistent and reliable diagnosis is through testing inter-rate reliability. This involves two assessors independently arriving to the same conclusion. Powell (1988) randomly selected 290 male and female psychiatrists to read two case vignettes of patients behaviour and give their diagnosis using the standard diagnostic criteria. When the patients were described either as “males” or their gender was not specified, 56% of psychiatrists gave a diagnosis of schizophrenia. When patients were described as “female” only 20% were diagnosed as having schizophrenia highlighting support for how much of a factor gender bias is in unreliable diagnosis. Also the interpretation of symptoms is subjective and down to the person doing the diagnosis so a great deal of importance is placed on the individual’s ability in diagnosis which may vary between health professionals. Therefore skill, experience and knowledge further affect reliability and diagnosis.

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• The fact that females tend to develop schizophrenia on average between 4 and 10 years later than males and develop a much later form of post-menopausal schizophrenia suggests different types schizophrenia exists. This in itself calls into question the validity of schizophrenia as we understand it currently and research findings suggest there is a case for different diagnostic considerations between genders. However this would then cast doubt on the validity of schizophrenia as a separate disorder.

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• Sim et al (2006) reported that of 142 hospitalised schizophrenics, 32% had an additional mental disorder highlighting the problem co-morbidity can create in achieving a reliable and valid diagnosis. Jeste er al (2009) stated that schizophrenics with co-morbid conditions are excluded from research yet form the majority of patients. This suggests research findings into the causes of schizophrenia cannot be generalised to most sufferers. This also has a knock-on effect in terms of the treatments sufferers should receive.

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• Peter Buckley (2009) found up to 50% of patients diagnosed with schizophrenia also fit into the diagnosis for depression and 29% suffered from post-traumatic stress disorder and OCD (23%). This poses a challenge for the validity of schizophrenia as a disorder itself because if we are unable to distinguish it from other disorders, the reliability of diagnosis by clinicians will also be inconsistent.
  Research suggests that the outcomes for patients diagnosed with schizophrenia varies with only 20% recovering their previous level of functioning, 10% achieving significant and lasting improvement and 30% showing some improvement with intermittent relapses. A diagnosis of Schizophrenia therefore has little predictive validity as some people never appear to recover from the disorder while others do. We cannot fully understand why this is and this highlights how our understanding of the disorder is limited.

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• Fernando (1988) argued that people from ethnic minorities experience greater levels of racism, prejudice, poverty and racism than the white population and these stressors trigger schizophrenia and explained cultural biases so should be expected in diagnosis. However Cochrane (1983) highlighted how it was only the afro-caribbean people who were more likely to be diagnosed and one possible explanation proposes the diagnosis of the disorder is valid but people of this background have little immunity to the flu (an illness common in Britain but not their country of origin). Children born to mothers who had the flu while pregnant have an 88% increased chance of developing schizophrenia which would explain higher levels of diagnosis in afro-caribbean people.

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• Hewitt et al (2001) compared 14 autistic patients with 14 schizophrenia sufferers finding none of the schizophrenics had symptoms of autism however 7 of the autistic patients had symptoms of schizophrenia. This shows support for the idea that there is symptom overlap and calls into question the classification of schizophrenia itself as a distinguishable disorder.

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• This is supported by Ophoff et al (2011) who assessed genetic material from 50k participants finding that seven gene locations associated with schizophrenia, three of them were also associated with bipolar disorder which suggests a genetic overlap between the two disorders. This genetic overlap presents real world applications as gene therapies might be developed which could simultaneously treat both disorders.

One biological explanation for schizophrenia proposes it is genetically inherited. Schizophrenia tends to run in families of people genetically related and the risk of developing the disorder is also much higher for related family members. It is believed numerous genes are responsible and although not automatically predisposing the individual to develop the disorder, it is believed they make an individual more vulnerable if other psychological stressors from the environment are present. The effects of genetics on schizophrenia has been measured using family studies, twin studies and adoption studies. Gottesmans (1991) family study established that schizophrenia was more common among biological relatives and the closer the relation, the higher the risk. Children with two schizophrenic parents had a concordance rate of 46% however this dropped to 13% when this was one parent and again down to 9% when compared to siblings had schizophrenia.

Twin studies compare genetically identical twins (who share 100% of the same DNA) and non-identical twins (who share 50%) to measure concordance rates between them. If identical twins have a higher rate then it is believed to be due to genetics however if non-identical share a higher concordance rate then it is due to the environment. As both sets of twins would share similar environments, this allows for the role of “nurture” to hopefully be discounted. Joseph (2004) found that when comparing identical twin studies, they had a concordance rate of 40% while non-identical twins had 7.4%. This higher concordance rate would present a strong argument for genetic factors.

In adoption studies, adopted children with biological parents suffering from schizophrenia are compared to a control group of adoptees with non-schizophrenic parents. The aim here is to help separate the role of nature (genes) and nurture (the environment) in schizophrenia’s development when those related are reared apart. Tienari et al found that out of 164 adopted children whose mothers had been diagnosed with schizophrenia, 6.7% of children also shared this diagnosis compared to only 2% out of 197 children with non-schizophrenic mothers. This supported the role of genes influencing the onset of schizophrenia.

Dopamine is one of the many different neurotransmitters that operate in the brain. The dopamine hypothesis states that messages from neurons that transmit dopamine fire too easily or too often leading to the characteristic symptoms of schizophrenia. Schizophrenics are thought to have abnormally high levels of D2 receptors on receiving neurons resulting in more dopamine binding and thus more neurons firing. One version of the dopamine hypothesis focused on high levels of activity of dopamine in the sub-cortex; excess dopamine in Broca’s area, which is responsible for speech, may be linked with poverty of speech or auditory hallucinations. Other explanations have focused on abnormal dopamine systems in the brains cortex with low levels in the prefrontal cortex (which is responsible for thinking and decision making) related to negative symptoms of schizophrenia. Therefore high and low levels of dopamine in different brain regions are thought to be linked to schizophrenia this way.

Neural correlates are measurements of the structure or function of the brain that correlate with an experience. Relating this to schizophrenia both positive and negative symptoms have neural correlates. Using fMRI techniques, researchers can observe the functioning of the brain in schizophrenics and compare them with non-schizophrenics to identify areas linked to the disorder. One negative symptom is avolition which involves the loss of motivation. Motivation itself involves the anticipation of a reward and regions of the brain such as the ventral striatum are believed to be involved in this anticipation and abnormalities in this area may be linked to avolition. Juckel (2006) measured activity in the ventral striatum in schizophrenics and found they had lower levels when compared to controls. A negative correlation between activity levels and the severity of overall negative symptoms was found and thus activity in the ventral striatum is a neural correlate of negative symptoms of schizophrenia. Positive symptoms also have neural correlates and Allen et al (2007) scanned the brains of patients reporting to suffer from auditory hallucinations and compared them to a control group whilst they identified pre-recorded speech as either theirs or others. Lower levels of activation in the superior temporal gyrus and anterior cingulate gyrus were found in the hallucination group who also made more errors than the control group. This reduced activity within these brain areas is therefore a neural correlate of auditory hallucinations.

• One major flaw for twin studies is the assumption that the environment shared between identical and non-identical twins are the same. Joseph et al highlighted how identical twins are more inclined to be treated similarly and be seen as one person therefore sharing the exact same environment. This could also be used to explain the higher concordance rates as being due to environmental factors (nurture) rather than necessarily genes alone (nature). Also the fact that even though identical twins share 100% of the genes, concordance rates remain at 40% and not 100% which suggests the environment (and nurture) still plays a huge mitigating role in schizophrenias onset. Also non-identical twins are more likely to be treated as individuals and two separate people due to different appearances and therefore the lower concordance rates between them may be explained due to differences in the environmental influence (nurture) rather than necessarily genes and nature. This may also be used as an explanation for why non-identical twins who share 50% of their genes have much lower concordance rates highlighting a strong case for the environment.

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• With adoption studies it may well be that adopting parents are influenced by selection bias. Such studies assume the selection of children is equal between parents who choose to adopt children with schizophrenic parents and those without. This may not be the case as in countries such as the US and Denmark, potential adopting parents are told of any disorders suffered by the biological parents such as schizophrenia. This may in turn influence their decision to adopt children skewing the results.

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• Irrespective of this there is strong evidence for a genetic basis for schizophrenia supporting biological explanations. Gottesman’s (1991) study does demonstrate how genetic similarity increases the risk of the disorder and Tienari (2004) demonstrated how children who were adopted but had schizophrenic parents still had a higher risk of developing the disorder too. There is also evidence from research conducted at the molecular level (Ripke 2014) showing particular genetic variations significantly increase the risk of developing schizophrenia. This provides strong evidence for genes playing an influential role in making people more vulnerable to develop schizophrenia.

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• A more holistic explanation may be that a diathesis-stress model explanation applies here with both nature (genes) and nurture (the environment) interacting and with the right amount of environmental triggers and stressors, causing a genetic vulnerability for schizophrenia to be activated. This would better explain the results of twin, family and adoption studies.

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• Support for the dopamine hypothesis comes from the success of drug treatments that work to reduce the effects of dopamine on the brain. Antipsychotic drugs reduce the effects of dopamine and also the symptoms of schizophrenia. Leucht et al (2013) carried out a meta-analysis of 212 studies that compared antipsychotic medication to placebo’s. The results found that antipsychotics were significantly more effective than the placebos in treating positive and negative symptoms of schizophrenia supporting the dopamine hypothesis.

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• Alternatively as antipsychotic drugs look to reduce dopamine and thus the symptoms of the disorder, drugs that increase dopamine should also increase symptoms if the dopamine hypothesis has validity. This is exactly what has been found with drugs such as amphetamines which increase dopamine in the brain (Curran et al 2004) and thus symptoms of the disorder supporting the dopamine hypothesis.

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• A weakness of the dopamine hypothesis is there is also evidence to suggest this is not a complete explanation. A major problem for the dopamine hypothesis is that drugs used to actually reduce dopamine levels can actually increase them as the body attempts to compensate for the sudden deficiency. Research in to postmortems of schizophrenics have shown that those with elevated levels had taken antipsychotics just prior to death. Those with normal dopamine levels had not taken any medication and this weakens the dopamine explanation. Also drugs designed to reduce dopamine levels work effectively after a few hours yet it takes many weeks for patients to have fewer schizophrenic symptoms and it is unclear why this is if excess dopamine is the sole cause. This suggests although dopamine may be involved; it may only be one of the many links in the chain that causes the disorder, possibly even an effect of schizophrenia rather than the cause.

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• One criticism with neural correlates is they actually tell us very little. Although a number of neural correlates for positive and negative symptoms exist and are useful for highlighting brain systems which may not be functioning correctly, this does not tell us whether this abnormality causes the symptoms. It may be that there is something wrong in parts of the brain such as the ventral striatum which is causing negative symptoms or it is just as possible that negative symptoms themselves cause less information to pass through the ventral striatum causing reduced activity.

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• Additionally with correlational data we cannot be sure of cause and effect. It may well be that schizophrenia causes these abnormalities in the brain and this is actually an effect of the disorder rather than a cause. Consideration must also be given to environmental factors in causing brain abnormalities such as substance abuse and stress levels which may damage brain tissue.

For psychological explanations of schizophrenia the specification states you need to know about family dysfunction and cognitive explanations, including dysfunctional thought processing.

One psychological explanation for schizophrenia is family dysfunction.

This explanation proposes it is maladaptive relationships and patterns of communications within families that are the sources of stress that influence the development of schizophrenia. Three dysfunctional characteristics found in parents of schizophrenics include high levels of interpersonal conflict, difficulty communicating with one another and being excessively critical and controlling of the children. Gregory Batesons (1972) double blind theory describes family dysfunction occurring when children receive mixed and contradictory messages from their parents and this influences the onset of schizophrenia. A developing child may find themselves trapped in situations where they fear doing the wrong thing but mixed messages about what this is leaves them unable to talk about this. When they do make mistakes this leads to the withdrawal of love from the parents leaving them seeing the world as confusing and dangerous. This is then reflected in symptoms such as disorganised thinking and paranoid delusions.

Another variable related to family dysfunction is a negative emotional climate or high degree of expressed emotions. This is a communication style where family members of the sufferer talk about the patient in a critical or hostile manner as well be overly involved or concerned with them. Schizophrenics may have a lower tolerance for emotionally charged intensive family environments and this may lead to stress levels that are beyond their ability to cope triggering schizophrenia.

Cognitive explanations of schizophrenia focus on dysfunctional thought processing and how schizophrenics process information differently. Frith et al (1992) identified two kinds of dysfunctional thought processing, metacognition (also known as metarepresentation) and central control. The monitoring of one’s own thought processes is known as metacognition and this includes a persons ability to detect errors in cognitive processing such as cognitive distortions. Metacognition also includes thinking about the feelings and behavioural reactions triggered by thoughts and feelings allowing them to view their own mental states and the intentions of others thus allowing them to make sense of their world. People suffering from schizophrenia are believed to experience a dysfunction in metacognition which results in them having dysfunctional thought processes which affect executive functioning and higher-level cognitive processes that manage cognitive and behaviroual processes. This impairs goal-directed behaviour, attention, memory, cognitive flexibility, self-monitoring, inhibition of inappropriate responses and physical motor-control of oneself.

Central control is the cognitive ability to suppress automatic responses while we perform deliberate actions instead. Schizophrenic symptoms such as disorganised speech and thought disorder are believed to be caused by this inability to suppress automatic thoughts and speech which are triggered by other thoughts. Schizophrenia sufferers tend to experience a derailment of thoughts and speech and this explanation proposes it is because each word during speech triggers associations the patient is unable to suppress.

• There is research supporting family dysfunction as a risk factor in developing schizophrenia. Tienari (1994) measured the prevalence of schizophrenia in adopted children finding children with biological parents with the Schizophrenia were most likely to develop the disorder but this only emerged when the adopting family were rated as disturbed. This supports the case for how psychological factors such as family dysfunction (nurture) can trigger a genetic vulnerability (nature) in people leading to the development of schizophrenia.

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  Although evidence links family dysfunction to schizophrenia, one criticism is the information about childhood experiences has generally been gathered after the development of symptoms. Schizophrenia itself may have distorted the patients recall of childhood experiences which raises the problem of validity undermining this explanation. Another problem with the dysfunctional family explanation is this has historically led to “parent-blaming” raising ethical and moral issues. Parents have gone through the trauma of watching their children develop schizophrenia and bear the lifelong responsibility for their care and then blame is added for the condition adding further insult to injury.

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• In addition, having a schizophrenic within the family can be stressful and problematic on family relationships itself and rather than dysfunctions within the families causing schizophrenia, it may well be that having someone with the disorder leads to family dysfunction as they struggle to cope. This is the major issue with such correlational data as you cannot be certain of cause and effect.
  The theory is however supported by the fact that therapies which successfully focus on reducing expressed emotions within the family have low relapse rates when compared with other therapies suggesting the explanation does have validity. However it could be argued that this merely masks the symptoms or teaches family members to tolerate them more rather than provide an effective solution for the disorder.

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• Research support for double blind theory comes from Berger (1965). This research found that schizophrenics reported a higher recall of double bind statements by their mothers when compared to non-schizophrenics supporting this explanation. This however may not be reliable as the patients recall may be affected by the schizophrenia itself undermining these findings. Other research has struggled to support double bind theory finding evidence to suggest it lacks validity. Liem (1974) measured patterns of parental communication within families and found no difference between families of a schizophrenic child and normal families. This was further supported by Hall and Levin (1980) who analysed data from previous studies finding no difference in families with a schizophrenia sufferer and those without when it came to verbal and non-communication.

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• There is strong evidence to support the idea that information is processed differently in the mind of a schizophrenics supporting dysfunctional thought processes. Stirling (2006) compared 30 patients with schizophrenia with 18 controls on a range of cognitive tasks one of which included the Stroop test. This tests their ability to suppress words as patients name the colors of words rather than reading the words which are named colors. In line with Frith’s explanation of central control dysfunction, patients with the disorder took over twice as long as the control group to name the ink colours supporting cognitive explanations of the disorder.
• One major issue with cognitive explanations such as dysfunctional thought processing is, although a link is clear, this does not tell us anything about the origins of abnormal cognitions or the condition itself. It could also be easily argued that dysfunctional thought processes are merely a symptom of a biological cause such as genetics rather than the cause itself which further undermines this explanation. It could be that both biological and psychological factors separately produce the same symptoms raising questions of validity and whether both outcomes are schizophrenia. We could also view this in terms of the diathesis- stress model where people may have a genetic vulnerability for the disorder but then it takes psychological factors such as family dysfunction or irrational cognitive thoughts to trigger the disorder.

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• If dysfunctional cognition can better characterise schizophrenia as Frith proposes, this presents to us real world applications as we can look to construct a specific cognitive deficit profile to help with the diagnosis of the disorder.Kane et al argued that including cognitive impairment within the diagnosis criteria for schizophrenia would help improve the currently poor reliability in diagnosis of the disorder. This could then help in creating more targeted treatment with cognitive enhancement being the primary goal.

The specification states that for schizophrenia and drug therapies, you need to know about typical and atypical antipsychotics.

The prime treatment for Schizophrenia is the use of anti-psychotic drugs and these fall into two types of antipsychotics which are Typical and Atypical antipsychotics.

The prime treatment for Schizophrenia is the use of anti-psychotic drugs and these fall into two types of antipsychotics which are Typical and Atypical antipsychotics.

The first typical antipsychotic created was Chlorpromazine and this primarily looked to treat positive symptoms such as hallucinations and thought disturbances which are caused by an overactive dopamine system. Typical antipsychotics are dopamine antagonists and work by arresting dopamine production by binding with and blocking D2 receptors in the synapses in the mesolimbic dopamine pathway. Typical antipsychotics therefore aim to reduce the effects of dopamine and thus positive symptoms. By reducing stimulation of the dopamine system in the mesolimbic pathway, this helps eliminate hallucinations and delusions. After starting treatment, hallucinations and delusions disappear within a few days although other symptoms may take several weeks to improve. Typical antipsychotics do not cure the patient of schizophrenia but instead dampens the effects of the disorder to a level where they may be able to function. They come in syrup form as well as tablet and also act as a sedative helping calm patients.

The side effects of typical antipsychotics includes effects on other neurotransmitter systems such as cholinergic, alpha- adrenergic, histaminergic and serotonergic mechanisms. Anti-cholinergic side effects include a dry mouth, urinary problems constipation and visual disturbance while effects on noradrenergic leads to low blood pressure, problems in sexual functioning and nasal congestion. Long-term use of typical antipsychotics also leads to tardive dyskinesia in 15% of sufferers which involves uncontrollable muscle movements usually around the mouth. In some patients this condition can become permanent.

Atypical anti-psychotics introduced in the 1990s such as Clozapine work by acting upon serotonin receptors as well as dopamine production systems and affect negative symptoms of the disorder such as reduced emotional expression and cognitive impairment.

Although atypical drugs are perceived as having fewer side-effects, it is not always known specifically how they affect the brain to alleviate symptoms. Similar to typical antipsychotics, these act on the dopamine system blocking D2 receptors however they only occupy them temporarily before rapidly dissociating to allow normal dopamine transmission. It is believed that this “rapid disassociation” may be responsible for the lower levels of side effects such as tardive dyskinesia however atypical antipsychotics have other side effects too. This can include weight gain, neuroleptic malignant syndrome, increased risk of stroke, cardiac arrest, blood clots and diabetes. They too can be taken in syrup or tablet form making consumption easy.

Davis et al (1989) performed a meta-analysis of more than 100 studies that compared antipsychotics with placebos. The results found antipsychotics were more effective with over 70% of sufferers seeing improvements after 6 weeks of use while less than 25% reported improvements with placebos. This shows that antipsychotics are effective in treating schizophrenia.

However one of the studies in Davis’s review was by Vaughn and Leff, who found that antipsychotic medication did make a significant difference but only for those living with hostility and criticism in their home environment. In such conditions, the relapse rate for those on medication was 53% but for those in the placebo condition the relapse rate was 92%. For individuals living in more supportive environments however there was no significant difference between those on medication and placebos (12% relapse and 15% relapse).

This shows that the environment people are surrounded by is very important and high amounts of hostility and criticism appears to be linked with higher relapse rates and environmental factors need to also be considered when deciding on the appropriateness of drug therapies. Supportive home environments yielded the best results regardless of being on medication or placebos which suggests drug therapies are most effective when certain environmental conditions are not always ideally suited.

Marder (1996) reported that atypical antipsychotics such as clozapine are as effective as typical antipsychotics with 30-61% of patients who were resistant to typical antipsychotics responding to them. This shows atypical antipsychotics may be more appropriate and effective when they do not respond to typical antipsychotics. Patients taking atypical antipsychotics also reported to have fewer side effects meaning patients are more likely to continue taking their treatment resulting in improved symptoms.

There is also recent evidence however that atypical drugs incur serious other side-effects such as the reduction in white blood cells which can lead to infection and even death making them inappropriate as the first port of call. Due to this blood tests are required regularly for white blood cell count and this is another reason why atypical drugs tend to be prescribed after conventional drugs are tried first due to the high risks of infection or illness.

The fact that typical antipsychotics carry a risk of developing permanent tardive dyskinesia could be argued to make them inappropriate as the effects of this may be seen as worse than that of schizophrenia by patients. Atypical antipsychotics also carry the risk of serious health problems ranging from weight loss to stroke, cardiac arrest and diabetes. The fact that both groups of antipsychotics carry such serious side effects may make them inappropriate and even unethical. For example critics argue that if the side effects, deaths and psychosocial consequences of the drugs were taken into account a cost-benefit would see it as having more costs than actual benefits for the drug. There is also a legal basis for this as one tardive dyskinesia sufferer in the US even won a large out-of-court settlement on the basis of this drug treatment breaching the human rights act 1988 (Chari et al 2002).

Antipsychotics are seen as effective as they are relatively cheap to produce and easy to administer providing positive effects on many sufferers allowing them to live a relatively normal life outside of mental institutions. Due to the high costs of providing specialistic care or psychological interventions this makes antipsychotics more appropriate even from an economic viewpoint. For patients not wanting the social confrontation of talking to specialists about their mental health problems, this makes them more appropriate as some people no doubt struggle to talk about their problems.

However a major criticism of antipsychotics is they are not effective in treating the underlying cause of schizophrenia instead only providing relief for the symptoms. Drug therapies do not cure the patient instead helping them to mask the symptoms and for this reason they need to be continuously used for many patients. Antipsychotics also have high relapse rates with up to 40% in the first year of treatment and then 15% in later years generally due to patients stopping their course because of the side effects and the impact this has on quality of life. This means for many sufferers they are not a effective long-term solution.

Ross & Read (2004) also argue that being prescribed medication reinforces the view that there is “something wrong with you” with patients. This, they argue prevents the individual from thinking about possible stressors that might be a trigger for their condition in turn reducing their motivation to look for possible other solutions beyond drug therapies. Reearch by Haslam (2004) actually found that when people were surveyed on the causes of schizophrenia many cited social factors such as poverty or traumatic childhood which patients may be less inclined to confront if they were simply given drugs to manage their symptoms. For this reason drug therapies may be inappropriate for many when social factors can be addressed instead first.

This next section focuses on 3 types of psychological therapies as per the A-level psychology specification.

These are cognitive behavioural therapy, family therapy and token economies.

CBT is the main psychological treatment used in treating schizophrenia and it works by modifying delusional beliefs and hallucinations within sufferers. CBT assumes it is these delusional beliefs which cause schizophrenia. These may occur due to incorrect interpretations the sufferer has of the world around them, themselves, other people, maladaptive thinking or distorted perceptions on how to approach problems and goals. The aim of CBT is to help the patient identify these “faulty” and distorted beliefs and address them. Sessions are conducted for between 5 and 20 sessions either in a group or one-to-one setting.

Patients may be encouraged to think back to when their schizophrenic symptoms first started to help them get a better idea of how they developed. Other methods may see them use self-talk to challenge any delusional beliefs or voices they may hear
 and how they could test their validity to help them see they are irrational. Drawings may be used to display links between the sufferers thoughts, actions and emotions using the ABC model helping them understand where symptoms may be originating from to alleviate any anxiety.

One form of CBT is Personal Therapy (PT) which looks at detailing the problems, experiences, triggers and consequences as well as potential strategies sufferers could use to cope. This may involve helping patients cope with intrusive thoughts and voices through distraction, learning to challenge the meaning of intrusive thoughts through self-talk, increasing/decreasing social activity to help distract the patient from troublesome moods as well as relaxation techniques. Patients can also be taught to recognize signs of potential relapses before they build up into schizophrenic symptoms again.

• McGorry et al found CBT was effective when comparing two samples of patients at high risk of having a schizophrenic episode receiving different treatments. After 6 months 36% of patients receiving psychotherapy developed schizophrenia while only 10% of those receiving CBT and drug therapy developed the disorder. This supports the use of CBT as an effective form of treatment when combined with drug therapies.

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• The NICE (2004) review of treatments for schizophrenia also found consistent evidence to show CBT was most effective when combined with antipsychotic medication. It was effective in reducing rehospitilisation rates up to 18 months following the end of treatment as well as reducing symptom severity compared to patients receiving only antipsychotics.

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• It is however questionable whether CBT is effective at all as lower relapse rates could have actually been mainly due to the drugs received rather than anything to do with CBT itself. Therefore the drug therapy administered may have been a confounding variable with results with CBT having little to no benefits making it potentially ineffective.

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• One major issue with CBT is the lack of availability. Despite it being recommended in the NICE study, it is estimated that as little as 1 in 10 actually get access to this form of therapy. Haddock et al (2013) found that of 187 randomly selected schizophrenics, only 13 had been offered the therapy and of those who were offered, many failed to attend or refused thus limiting the therapies effectiveness even more. The therapy also requires a trained professional to deliver the sessions over a number of months making it incredibly costly and time consuming. Patients may also struggle to open up or build rapport with a therapist and the effectiveness of the therapy is largely influenced by the skill of the practitioner also. Comparing this to drug therapies which are extremely cheap, easy to administer for patients and requires little time, it may make CBT inappropriate for most people.

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• CBT may in truth only be effective with people with milder forms of schizophrenia and enough level of insight and awareness into their own thinking to actually address this. Not all patients will be able to use CBT as they may lack the intelligence, insight or their symptoms are too severe and chaotic to control. Some studies have found that age may well be a factor with CBT being less effective for older patients compared to younger as they may not engage as well.

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• Other studies have brought into question the effectiveness of CBT as a treatment altogether. Meta-analyses into CBT have tended to reach unreliable conclusions on its effectiveness due to poor methodology and setup. For example participants were not always randomly allocated between a CBT group or control condition and interviewers were often aware of the treatment conditions further biasing results. Juni et al (2001) concluded there was clear evidence that problems associated with methodologically weak trials translated into biased findings about the effectiveness of CBT itself. Wykes (2008) actually found that the more rigorous a study was, the weaker the benefits of CBT suggesting the therapy was not really effective at all.

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• More recent methodologically sound meta-analyses tend to support this viewpoint. Jauhar et al (2014) conducted a meta-analysis finding only a “small” therapeutic effect on key symptoms of the disorder such as hallucinations and delusions suggesting it was not effective. Regardless when patients are not responding to drug treatments or their side effects are too severe, CBT may be more appropriate in cases such as these as it presents no side effects or risks to the patient.

The use of token economies is based on the principles of operant conditioning and was developed as a way to deal with negative symptoms and maladaptive behaviours and promote more functional behaviours from patients. The therapy does not cure schizophrenia however its aim is to improve the quality of life and make it easier for them to function outside the institutional setting.

Tokens are given to patients immediately when they display desirable behaviours that are targeted for reinforcement. Functional behaviours may vary dependent on the patients individual behavioural issues but could include getting dressed or making their bed. Giving a reward as soon as the desirable behaviour is displayed by the patient is important as this prevents “delay discounting” which reduces the effects if a reward is delayed. As a result of this process of classical conditioning, these neutral tokens become secondary reinforcers and so can be used to modify behaviours.

Tokens that patients gather can be swapped for tangible rewards which vary but can include sweets, cigarettes, magazines or privileges within the institution. The idea is that patients will then engage more often with desirable behaviours voluntarily because they become associated with these rewards. Additionally undesirable behaviours can also be removed by removing any reinforcers that maintain it and restructuring the environment so the undesirable behaviour is no longer reinforced allowing token economies to reinforce only desired behaviours. This treatment assumes the behaviour can then be carried on and maintained outside the hospital setting too.

The approach has its roots in a study reported by Ayllon et al. They were asked to visit a hospital where staff were finding it difficult to get withdrawn Schizophrenic patients to eat regularly and noticed staff had to coax patients into eating. They believed the special attention paid to such resistant patients was reinforcing their behaviour (the reward/reinforcement was the special attention) and decided to change hospital rules. For example if patients did not arrive on time for dinner they would be locked out and also to gain entry they would need to pay one penny. Staff were no longer allowed to interact with patients either thus removing any chance of them gaining “attention” and reinforcement for the behaviour. To earn the pennies for entry they would need to display desired behaviours. They found this to be a huge success resulting in patients displaying more desired and functional behaviours in the hospital. The desired behaviour was highest when reinforcements were imposed for behaviour and lowest when they were not. The token economy also had a positive effect on patient and staff morale with patients being less apathetic and irresponsible whist staff also became more enthusiastic in their jobs.

• Several other studies have confirmed the effectiveness of token economies and it is generally accepted that it is effective in producing a variety of positive behavioural changes at least in a setting where tokens are given. A major criticism Corrigan (1991) argues is applying this therapy in the community where patients are not under 24 hour care and tokens are not available. The concern here is like most behaviours reinforced using operant conditioning, when the rewards are removed so is the desirable behaviours making it an ineffective treatment to manage schizophrenic behaviour within the community.
  

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• Due to the setup of token economies, staff are required to give rewards immediately after the desirable behaviour is displayed. This in itself makes the therapy more effective in the hospital setting where staff can monitor patients around the clock. The therapy may be more appropriate only within the hospital setting where the behaviours of patients needs to be controlled for reasons such as risk to staff or suicide. The therapy also has the advantage of making the hospital environment more healthy and productive. Token economies therefore facilitate a safer more therapeutic environment and staff and patient injuries reduce with both having a more positive regard for one another which is motivational for patients and staff.
  

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• One issue however is token economies only remain effective if tokens can be exchanged for a variety of rewards as if they remain the same, satiation occurs and the behaviour decreases in frequency. For this reason it may only be effective in managing behaviour because the hospital setting can provide this variety unlike the community.
  

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• Another factor that affects token economies is the intelligence of patients and it is generally accepted it is best suited for patients of Schizophrenia with limited intellectual capacity. Therefore it may not be effective in patients with greater intelligence and some might even argue it is degrading in essence as it treats people in a patronising way. This raises ethical issues as some clinicians argue that participants are humiliated into obeying for necessities which makes it an inappropriate treatment.

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• Sultana et al (2000) conducted a meta-analysis review of token economy regimes over s 15 year period finding that they did reduce negative symptoms in schizophrenic patients showing their effectiveness in the management of schizophrenic symptoms. It was however unclear if these behavioural changed were maintained beyond the treatment programme themselves.

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• Ost et al treated 12 Schizophrenics with token economy regimes for 8 months finding positive changes in behaviour. Of the 5 patients discharged, none had been readmitted in the 1-year follow-up suggesting that behavioural changes can be maintained after treatment ends in the short-term at least. Whether this treatment was effective in the management of schizophrenic behaviour in the long-term however is still questionable.

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• Upper et al found that weight gain associated with the use of antipsychotics could be addressed with token economy regimes and schizophrenics were able to achieve a target of 3 pounds of weight loss a week. However the sample size was very small making it difficult to generalise the results to a wider population. This does suggest a combination of drugs and token economy treatment may be effective and appropriate in managing the side-effects of antipsychotics and promoting more positive behaviours such as exercise. This would help make the management of schizophrenia more effective as drug treatments help reduce the symptoms while token economies can then be used to promote more desired behaviours.

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• Although helpful in aiding staff manage patient behaviour, token economies alone merely mask the symptoms of schizophrenia with desirable behaviours making it ineffective as the underlying cause is not tackled in anyway.

Family therapy, also known as family-focused therapy, developed as a result of studies into the family environment and the effect this had on schizophrenia sufferers. Research has shown that the long-term outcome for an individual with schizophrenia is greatly affected by those that care for them. Positive relationships with those around them such as family members result in improved outcomes while poor relationships result in poorer outcomes and greater chance of relapse. Family therapy aims to provide support for carers to make the family life less stressful and reduce re-hospitalisation rates.

Family therapy is a form of psychotherapy and is based on the idea that as family dysfunction can affect the development of schizophrenia, altering the relationship and communication patterns within dysfunctional families and lowering levels of expressed emotions should in theory help schizophrenics recover. The treatment involves the whole family playing the role of a support network for the schizophrenia sufferer. The aim of family therapy is to improve positive communication and decrease negative communication, increase tolerance levels and reduce criticism between family members and to decrease feelings of guilt and responsibility for causing the illness on the schizophrenia sufferer.

Family members, the patient and therapists meet regularly to talk openly about the patient’s symptoms, behavior and progress and how they are affected by the illness. The aim is to form an alliance with carers to reduce the emotional stress experienced within the family and to support one another with each given a specific role in the rehabilitation of the sufferer. They are also taught to better anticipate and solve problems they may face and set reasonable expectations among one another for the patient’s progress.
Family therapy is given to schizophrenics for a set amount of time usually between 3 months to 1 year. The focus is to reduce symptoms, levels of expressed emotion and allow family members to develop skills they can continue to use to manage the patient after the therapy has finished.

• Research by Pharoah and Xiong appears to suggest family therapy is effective and does go some way in improving mental state and social functioning. One criticism however is this type of research is based on correlational data and we cannot be certain of cause and effect as confounding variables may lay in between affecting these results. For example the effectiveness of family therapy may be explained due to it increasing compliance among sufferers to take their medication regularly rather than anything to do with the therapy itself. Surrounded by encouragement and reminders, the benefits observed may actually be due to the antipsychotic medication and these studies into family interventions may therefore lack internal validity. This is because they are not measuring the effectiveness of family therapy itself but a confounding variable which is their medication being taken regularly rather than sporadically.

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• Family therapy presents to us real world applications particularly when we consider the economic benefits of it. The NICE review of family therapy studies (NCCMH, 2009) demonstrated that family therapy provides significant cost savings when combined with standard care. The extra cost of the therapy is offset by the savings from lower re-hospitilisation rates due to lower relapse rates. This would make the therapy not only more effective but more appropriate too.

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• However one criticism here is that family therapy puts significant burden on the family members who may be ill equipped to cope with the needs of schizophrenic sufferers. Specialist care and intervention may be better suited by staff that better understand the symptoms and problems and the use of family members may not be appropriate as this could then impact on their lives causing great stress as they cope to manage another person’s problems as well as their own. Another view is that the family environment, while offering lower relapse rates may simply be masking the symptoms of the sufferer as they have come to see them as a normal part of their personality.

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• Lobban et al (2013) offered an alternative view suggesting family therapy could have a positive impact on surrounding family members making it appropriate. Analyzing 50 family therapy studies which included an intervention to support relatives, 60% of these studies reported at least one positive outcome from the intervention. However this research suffered from poor methodological quality which makes it difficult to assess how effective it truly was.

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• The focus on being “open” could cause problems for family members who may be reluctant to share personal information as this may increase family tensions within the home environment. This reluctance to talk or even acknowledge problems may hamper the effectiveness of the therapy. If this could be overcome family therapy may be useful for patients who lack insight into their own illnesses or are unable to talk about it. Family members may have a greater awareness of the patient’s moods and behavior and raise these on their behalf although it could be argued this may be more indicative of the family’s problems than the patients themselves.

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• Garety et al (2008) conducted a study into the effectiveness of family therapy and this failed to show any improved outcome for patients receiving the intervention when compared to patients who had carers but no family therapy. Both groups had significantly lower relapse rates when compared to patients with no carers at all. This study also found most of the carers displayed low rates of expressed emotion which may reflect the knowledge and attitude change towards schizophrenia as a disorder. Garety et al believed for most people however family therapy did not improve outcomes beyond receiving a good standard of treatment as usual. Family therapy is a psychological treatment and assumes “nurture” can override a potential biological problem caused by “nature” and this may make the therapy inappropriate. For example people with schizophrenia likely have a biological cause and treating them through family therapy, which is a psychological treatment, may simply be papering over the cracks to manage their symptoms. Therefore the problem with this therapy is it does nothing to address the underlying problem that is causing schizophrenia (nature) making it ultimately ineffective for the patient.

This section focuses on one explanation which is the diathesis-stress model which offers an explanation for schizophrenia by proposing it is a combination of both biological factors and psychological factors that contribute towards the disorders onset.

The diathesis-stress model of schizophrenia is part of the interactionist approach to explaining schizophrenia. This explanation see’s schizophrenia developing due to an interaction between the biological (diathesis) and the environmental (stress) influences. Research using family studies have suggested a genetic vulnerability is inherited and this varies from those with a high vulnerability to a low vulnerability. The diathesis-stress model of schizophrenia assumes that the development of schizophrenia is determined by this vulnerability but also the environmental stresses they experience within their lives that triggers this vulnerability to cause schizophrenia. Relatively minor stresses may cause schizophrenia for individuals who are highly vulnerable while major stressful life events may cause the disorder in those with low vulnerability. This approach pre-supposes additivity, i.e. that diathesis and stress combine together to produce schizophrenia.

Twin studies into schizophrenia have provided a strong case for a genetic component being involved in schizophrenia and people having a genetic vulnerability for the disorder. The identical twin of a schizophrenia sufferer has been found to be at a much greater risk of developing schizophrenia themselves when compared to siblings or fraternal twins. Adoptive relatives have also been found to be at much lower risk than biological relatives (Tienari et al 2004). In 50% of cases where an identical twin has been diagnosed with schizophrenia, the other twin never meets the diagnostic criteria to be diagnosed with schizophrenia themselves. The fact that identical twins who share the same genetic DNA do not share the disorder presents a strong case for environmental factors also playing a role in triggering biological vulnerabilities as the diathesis-stress model proposes.

The diathesis-stress model also proposes psychological triggers such as family dysfunction, substance abuse and critical life events are all environmental triggers that can cause schizophrenia in those most genetically vulnerable. Critical life events cause stresses and psychological trauma and research by Varese (2012) found that children who experienced severe trauma before the age of 16 were three times more likely to develop schizophrenia when they are older compared to the general population.

As the interactionist approach acknowledges both biological and psychological factors play a role, treatment is therefore based on both. This model may combine antipsychotic medication with psychological therapies such as CBT to relieve psychological symptoms. The effectiveness of treatments is dependent on factors such as cost, relapse rates, degree of side effects as well as symptom reduction. The combination of treatments will vary dependent on the patients individual circumstances; for example family therapy may only be appropriate when patients have problems with dysfunctional family relationships. Antipsychotics are usually initially given to reduce symptoms to a manageable level so psychological treatments can then have a greater effect.

• Our understanding of how evolution works supports the diathesis-stress explanation of schizophrenia. Genes (nature) alone cannot determine outcomes as they need particular environmental pressures (nurture) to trigger them. Therefore genes that predispose someone to have an increased vulnerability to develop schizophrenia cannot alone cause the disorder requiring stressors to bring about the disorder supporting the diathesis-stress model.

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• Support for the interactionist approach comes from Walkers (1997) study. This reported how schizophrenics were found to have higher levels of cortisol than non-sufferers and higher levels were related to more severe symptoms. Stress-related increases in cortisol heightens genetically-influenced abnormalities in dopamine transmission triggering the onset of schizophrenia. This demonstrates the interaction of biological and environmental factors in the development of schizophrenia supporting the diathesis-stress model.

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• Murray (1996) reported how children born after flu epidemics and when their mothers had contracted the disease while pregnant during the second trimester, had an 88% increased chance of developing schizophrenia than those born at the time whose mothers did not contract the flu. Exposure to the flu during this trimester is suspected of causing defects in neural development which leads to increased vulnerability to develop schizophrenia due to brain damage. This illustrates how the onset of schizophrenia can result from an interaction of factors as the interactionist explanation of schizophrenia proposes.

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• Other research suggests diathesis may not be exclusively genetic undermining this explanation. Research by Verdoux et al (1998) found evidence to suggest brain damage caused by environmental factors alone can also increase the likelihood of developing schizophrenia. Individuals who experienced an obstetric complication at birth (prolonged labour which can cause oxygen deprivation) were four times more likely to develop schizophrenia than those who did not.

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• There are problems in determining the causal diathesis in this explanation. Hammen (1992) argued it was stressors earlier in life that set up maladaptive coping methods so the individual is then less able to cope with stress in later life. This highlights how it may not be genetics that determine a vulnerability that triggers schizophrenia but a lack of resilience to stress.

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• Stressors that contribute to the risk of developing schizophrenia include biological, environmental, psychological and social factors. However a problem is determining precisely how these risk factors contribute to the diathesis- stress interaction for any single person because specific causes will vary from one sufferer to another. This makes it difficult to validate this explanation fully as studies will often lack internal validity and struggle to measure what the dependent variable (and cause) is.

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• The differential susceptibility hypothesis extends the diathesis-stress model to include positive as well as negative environments. A biological vulnerability for the disorder combined with a stressor can cause schizophrenia however the same individual exposed to a positive environment such as a caring family may see positive outcomes and reduce the chances of developing the disorder. This raises implications for possible treatment as genetic vulnerabilities may not be controlled however environmental factors that trigger this may be addressed instead. This forms the basis for family intervention therapies which provide evidence of reduced relapse rates supporting this interactionist explanation as having validity.

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• Research has consistently shown that a combination of psychological and biological treatments has tended to provide the best results supporting the interactionist approach. Biological treatments help treat the biological elements reducing symptoms while psychological treatments can help address problems such as disordered thinking and teaching patients more functional behaviours. One issue however is the increased costs in treatment to provide both. In the long-term however the greater effectiveness should make combined treatments based on the interactionist approach more cost-effective.