• Improvements in inter-observer reliability: Although research is conflicting (see studies above), more recent studies of schizophrenia diagnosis generally find higher concordance rates among psychiatrists compared to older studies. This suggests that diagnosis of schizophrenia has become more reliable over time.
• Low reliability between DSM and ICD: Cheniaux et al (2009) demonstrates different incidence of schizophrenia diagnosis by the same observer depending on which manual they use. In general, the DSM classification is considered more reliable as the descriptions of symptoms are more specific.
• Co-morbidity: People with schizophrenia often suffer from psychological disorders in addition to schizophrenia, which confuses diagnosis. For example, people with schizophrenia often suffer from depression as well. This can reduce the reliability of diagnosis as one evaluator may pick up on the depressive symptoms and diagnose the patient with depression, whereas another evaluator may pick up on the schizophrenic symptoms and diagnose the patient with schizophrenia.

• Improvements in validity: Although Rosenhan (1973) casts doubt on the validity of schizophrenia diagnosis, more recent studies suggest schizophrenia diagnosis has become more accurate. For example, Mason et al (1997) found that improvements to diagnostic manuals (DSM and ICD) over time led to more accurate diagnosis of schizophrenia.
• Symptom overlap: Schizophrenia shares symptoms with other psychological disorders, such as depression and autism. For example, both people with schizophrenia and people with autism often suffer with speech poverty. This overlap of symptoms may reduce the validity of schizophrenia diagnosis because an evaluator may incorrectly attribute these symptoms to a different disorder.
• Gender differences: Several studies suggest differences between men and women in the rates of schizophrenia, average age of onset, and severity of symptoms. For example, a meta-analysis from Aleman et al (2003) found men were 42% more likely to suffer from schizophrenia than women. This is supported by Castle et al (1993), who found that when diagnostic criteria were strictly defined, the rate of schizophrenia in men was more than twice that of women. Is this disparity a result of gender bias in diagnosis, or do these findings reflect a valid difference in the incidence of schizophrenia between men and women? Cotton et al (2009) suggest that the better interpersonal functioning of women may cause doctors to miss schizophrenia diagnosis in women, supporting the existence of gender bias. However, Kulkarni et al (2001) found that administration of estrogen (the female hormone) reduces schizophrenia symptoms, which suggests biological differences may partly explain gender differences in schizophrenia.
• Cultural differences: Several studies (e.g. Cochrane (1977), McGovern and Cope (1987), and Ineichen et al (1984)) have found ethnic minorities living in Britain (particularly those of Afro-Caribbean descent) are diagnosed with schizophrenia at higher rates than white people. However, rates of schizophrenia diagnosis among Afro-Caribbean people living in the Caribbean are roughly the same as white people in Britain. This suggests either:
  • Invalid diagnosis: Afro-Caribbean people in Britain are being overdiagnosed with schizophrenia due to cultural bias (or Afro-Caribbean people in the Caribbean are being underdiagnosed).
  • Valid diagnosis: The diagnosis reflects a valid difference in schizophrenia rates and so environmental stressors in Britain (e.g. racism, increased risk of flu) are causing increased rates of schizophrenia among people of Afro-Caribbean descent.

Strengths of genetic explanations of schizophrenia:

• Supporting evidence: The familial and twin studies of schizophrenia above support the genetic explanation of schizophrenia because they show that being closely related (and thus having similar genes) to someone with schizophrenia increases the likelihood of suffering from schizophrenia.
• Multiple genes: It is unlikely that there is a single gene responsible for schizophrenia. Instead, multiple genes likely combine to increase a person’s risk of developing schizophrenia. In a study of more than 36,000 schizophrenic patients, Ripke et al (2014) found 108 different genetic variations that were correlated with schizophrenia, supporting the existence of a genetic component to the disorder. Further, many of these genetic variations were related to dopamine transmission, so genetic explanations can be combined with the dopamine hypothesis to provide a holistic explanation of schizophrenia.

Weaknesses of genetic explanations of schizophrenia:

• Other factors: Although most studies suggest genetics play a part in the development of schizophrenia, it is clear that other factors are important too. If schizophrenia was 100% genetic, you would expect concordance rates between identical twins to be 100%. However, most studies find concordance rates among identical twins to be less than 50%, which suggests there is more to schizophrenia than just genetics. This suggests an interactionist approach is best for explaining schizophrenia.
• Methodological issues surrounding twin studies: Twin studies typically assume that twins have identical upbringings and so any differences in concordance rates between identical and non-identical twins must be explained by genetics. However, environmental factors likely play a role too. For example, looking identical probably makes parents treat identical twins more similarly than they would non-identical twins. As such, greater similarities in environment could contribute to higher concordance rates for schizophrenia among identical twins, with the influence of genetics being exaggerated.

Strengths of genetic explanations of schizophrenia:

• Supporting evidence: The studies above support several neural explanations of schizophrenia because they demonstrate correlations between neural structures and schizophrenia.

Weaknesses of neural explanations of schizophrenia:

• Conflicting evidence: Although several studies have found correlations between enlarged ventricles and schizophrenia, there are many exceptions. There are many people with enlarged ventricles who do not have schizophrenia, and there are many people with schizophrenia who do not have enlarged ventricles.
• Correlation vs. causation: Although there are correlations between schizophrenia and certain neural patterns, it can be difficult to determine whether abnormal brain functioning causes schizophrenia symptoms or whether it is an effect of schizophrenia. For example, does reduced activity in the bilateral amygdala of schizophrenic patients cause difficulties in emotional processing, or do schizophrenics’ reduced emotional processing (caused by some other factor) result in reduced blood flow and activity in the bilateral amygdala?

Strengths of the dopamine hypothesis of schizophrenia:

• Supporting evidence: The studies above support the dopamine hypothesis of schizophrenia in several different ways. For example, drugs that lower dopamine have been shown to reduce schizophrenia symptoms, and brain scans have shown higher dopamine activity in schizophrenic patients.

Weaknesses of the dopamine hypothesis of schizophrenia:

• Conflicting evidence: Farde et al (1990) compared brain scans of 18 schizophrenia patients with 20 non-schizophrenic controls. They found no difference in dopamine activity between the two groups. Similarly, in a review of post-mortem studies, Haracz (1982) found little evidence to support the dopamine hypothesis.
• Other neurotransmitters: Evidence suggests that other neurotransmitters besides dopamine are involved in the development of schizophrenia, such as glutamate and serotonin. For example, a meta-analysis of brain scans by Marsman et al (2013) found decreased glutamate activity in schizophrenic patients compared to controls. Further, like with the dopamine hypothesis, there is some evidence that drugs that alter glutamate activity can successfully treat schizophrenia. It’s important to note that the glutamate hypothesis does not contradict the dopamine hypothesis: Both neurotransmitters may be involved in schizophrenia. Serotonin may also be implicated in schizophrenia, as suggested by the efficacy of atypical antipsychotic drugs.
• Allegations of bias: Psychiatrist David Healy (2002) argues that pharmaceutical companies exaggerated the dopamine hypothesis of schizophrenia to sell more drugs. The overly-simplified hypothesis that schizophrenia is caused by high dopamine makes it easy to market antipsychotic drugs as ‘cures’ for schizophrenia.

In general, there is no one-size-fits-all drug therapy for schizophrenia. The different mechanisms of action and side effect profiles of the various drugs (both typical and atypical) mean the best treatment option will vary from patient to patient. Further, drug therapy can be combined with psychological treatments such as CBT.

Strengths of drug therapy:

• Evidence supporting drug therapy: Several studies have found both typical and atypical antipsychotics to be more effective than placebo in reducing schizophrenia symptoms.
• Atypical antipsychotics more effective than typical antipsychotics: A systematic review by Bagnall et al (2003) looked at data from over 200 trials of antipsychotic drugs. In general, atypical antipsychotics were more effective than typical antipsychotics. However, data supporting the most recent atypical antipsychotics was of poor quality.

Weaknesses of drug therapy:

• Criticism of the distinction between typical and atypical: While atypical antipsychotics were designed to be more effective with less side effects than typical antipsychotics, some studies question whether this is actually the case. Further, while typical antipsychotic drugs were thought to target the dopamine neurotransmitter only, more recent evidence suggests both generations of antipsychotics target other neurotransmitters such as serotonin. For these reasons, some commentators (e.g. Leucht et al (2013) and Tyrer and Kendall (2008)) have questioned whether the distinction between typical and atypical antipsychotics is a meaningful one.
• Side effects: All antipsychotics carry a risk of side effects to varying degrees. These side effects can range from mild (e.g. weight gain, dizziness) to potentially fatal (e.g. heart attack, stroke, neuroleptic malignant syndrome). Lieberman et al (2005) found that 74% of 1,342 schizophrenic patients discontinued antipsychotic drug treatment within 18 months due to side effects.

Strengths of the family dysfunction explanation:

• Evidence supporting the family dysfunction explanation: Adoption studies suggest that dysfunctional family environments increase the risk of schizophrenia. For example, in a follow-up to their longitudinal study described above, Tienari et al (2004) rated familial dysfunctionality among the adoptive environments of adoptees whose biological mothers had schizophrenia. They found that adoptees raised in families rated as dysfunctional had much higher rates of schizophrenia (36.8%) compared to adoptees raised in families rated as healthy (5.8%).
• Evidence supporting the role of expressed emotion: A meta-analysis of 26 studies by Butzlaff and Hooley (1998) found relapse rates are higher among schizophrenic patients who return to live with families with a high degree of expressed emotion. The role of expressed emotion in schizophrenia is further supported by the success of family therapies that aim to reduce expressed emotion. However, this research doesn’t support expressed emotion as a cause of schizophrenia, but it does suggest it contributes to maintaining schizophrenia.

Weaknesses of the family dysfunction explanation:

• Exceptions: Not everyone raised in a dysfunctional family goes on to develop schizophrenia, and not everyone with schizophrenia was raised in a dysfunctional family. This suggests that other factors are important in explaining schizophrenia, such as biology.
• Correlation vs. causation: Even if schizophrenia is correlated with family dysfunction, this doesn’t prove that family dysfunction causes schizophrenia – it could be the other way round. For example, it seems possible that having a schizophrenic family member could itself cause stress and dysfunction within the family, rather than that family dysfunction causes schizophrenia. It’s a chicken or egg scenario: Which comes first?
• Methodological concerns: Bateson et al’s double bind explanation of schizophrenia is based on a handful of case studies and interviews. Some critics have suggested researchers focus on examples that support the explanation while ignoring examples that conflict with it (selection bias).

Strengths of cognitive explanations:

• Evidence supporting cognitive explanations: Several studies have found evidence of cognitive impairment in schizophrenic patients. Bowie and Harvey’s (2006) review above cites many examples. Cognitive impairments are often present before the patient’s first schizophrenic episode and persist throughout the disorder, but therapies that reduce cognitive impairment (e.g. CBT) often improve schizophrenia symptoms. This all supports a role for cognitive explanations of schizophrenia.
• Practical applications: Cognitive explanations have been used to develop effective therapies for treating schizophrenia, such as CBT.
• Complements other explanations: Cognitive explanations can be combined with other explanations (e.g. biological) to give a more holistic account of schizophrenia.

Weaknesses of cognitive explanations:

• Evidence against cognitive explanations: Many people have the cognitive biases and cognitive deficits associated with schizophrenia (for example, as a result of brain damage) and yet do not develop schizophrenia. This suggests that cognitive explanations alone are too reductionist: There is more to explaining schizophrenia than just cognitive explanations.
• Does not explain the cause of schizophrenia: Cognitive theories simply describe the thought processes of schizophrenia but do not explain why people with schizophrenia have these thought processes in the first place.

Strengths of CBT for schizophrenia:

• Evidence supporting efficacy of CBT: Several studies have shown that CBT effectively reduces schizophrenia symptoms. For example, a meta-analysis of 14 studies involving 1,484 schizophrenia patients by Zimmermann et al (2005) found CBT significantly reduced positive symptoms of the disorder.
• Complements other treatments: CBT can be used in conjunction with other treatments, such as antipsychotic drugs. Some evidence suggests this combined therapy is more effective than antipsychotic drugs or CBT alone.
• Less side effects than antipsychotic drugs: CBT has very few side effects. By comparison, antipsychotic drugs carry a risk of serious and potentially fatal side effects such as pyramidal symptoms, increased risk of heart attack, and weight gain.

Weaknesses of CBT for schizophrenia:

• Conflicting evidence: Contrary to Zimmerman et al (2005), a meta-analysis by Jauhar et al (2014) found CBT only had minor effects on schizophrenia symptoms. Further, when the researchers looked at blinded studies only (i.e. studies where the researchers were not aware which patients received CBT and which didn’t), even this small effect size disappeared. This calls into question the efficacy of CBT and suggests that research supporting the efficacy of CBT for schizophrenia may simply be the result of researcher bias.
• Not suitable for all patients: An important aspect of CBT is developing a trusting alliance between patient and therapist. However, some schizophrenic patients may be too paranoid or anxious to develop such a trusting alliance and so are not suitable candidates for CBT.

Strengths of family therapy for schizophrenia:

• Evidence supporting efficacy of family therapy: Several studies have demonstrated lower rates of schizophrenia relapse among patients receiving family therapy. For example, a meta-analysis by Pilling et al (2002) looked at 18 studies of family therapy for schizophrenia and found that it had a clear effect on reducing relapse rates.
• Complements other treatments: Evidence suggests that family therapy plus antipsychotic drug therapy is more effective at reducing relapse than antipsychotic drug therapy alone. For example, Xiong et al (1994) randomly allocated 63 subjects to either a drug therapy group or a drug therapy plus family therapy group. After one year, relapse rates were lower in the drug therapy plus family therapy group (33%) compared to the drug therapy only group (61%).
• Less side effects: Family therapy has very few (if any) side effects relative to antipsychotic drugs.
• Cost effective: The Schizophrenia Commission (2012) estimate that family therapy results in cost savings of around £1000 per patient over a 3 year period.

Weaknesses of family therapy for schizophrenia:

• Could be counterproductive: Family therapy for schizophrenia emphasises being open and honest. However, in some families, open communication may reveal difficult truths or reignite old arguments. This could increase, rather than decrease, negative communication and potentially make the problem worse.
• Not suitable for all patients: Some schizophrenic patients do not have dysfunctional families and so family therapy is unlikely to be an effective treatment for them.

Strengths of token economies:

• Evidence supporting efficacy of token economies: Several studies suggest token economies can improve symptoms of schizophrenia. For example, a review of studies by McMonagle and Sultana (2000) found token economies reduced the negative symptoms of schizophrenia. However, the researchers note that the evidence is not conclusive, with questions about the replicability of the findings and uncertainty about whether behavioural changes can be maintained after the treatment ends.
• Complements other treatments: Token economies can be used in conjunction with other treatments, such as antipsychotic drugs.

Weaknesses of token economies:

• Ethical concerns: Use of token economies could be seen as unethical for several reasons. Firstly, some argue that token economies are dehumanising as they take away the patient’s rights to make their own choices. Secondly, some argue that token economies are discriminatory: Severely ill patients will have greater difficulty complying with behavioural demands and thus get fewer privileges than patients who are less severely ill. Token economies may thus discriminate against the most severely ill patients.
• Relapse: If improvements in behaviour are dependent on receiving tokens, the schizophrenic patient may relapse once token economy therapy is withdrawn.

Strengths of diathesis-stress model:

• Evidence supporting diathesis-stress model: There is strong evidence for both the genetic and environmental components of schizophrenia. For example, Gottesman’s family studies described above support a role for genetics but schizophrenia concordance rates among identical twins are much less than 100%, demonstrating environmental plays a role too. With regards to the diathesis-stress model specifically, several studies suggest that stress is a key environmental component. For example, a review by Walker et al (2008) found schizophrenia is associated with elevated baseline stress hormones (e.g. cortisol) and that drugs that increase stress hormones worsen schizophrenia symptoms. Further, a meta-analysis by Varese et al (2012) found that stressful events in childhood increase the risk of schizophrenia, further supporting the hypothesis that stress is a key trigger of schizophrenia in those genetically prone.
• Holistic: Rather than reducing schizophrenia to one single cause, the diathesis-stress model accounts for the multitude of factors that contribute to the disorder. This can be seen as a more complete picture of schizophrenia.

Weaknesses of diathesis-stress model:

• Incomplete: Although there is strong evidence supporting the role of both biological diathesis and stress in the development of schizophrenia, the mechanisms through which they cause schizophrenia are not clear.

Although interactionist treatment approaches seem to be most effective, there is no one-size-fits-all solution. For example, family therapy will be more beneficial to a schizophrenic patient who was raised in a dysfunctional family environment, and the most suitable antipsychotic drug therapy for each patient will vary depending on efficacy and side effects. Costs are another factor to consider: It might not be economically viable to provide all schizophrenic patients with every possible treatment option.

Strengths of interactionist treatment approaches:

• Evidence supporting interactionist treatment approaches: Several studies suggest combination therapy is more effective than monotherapy. For example, Xiong et al (1994) randomly allocated 63 schizophrenic patients to either a drug therapy group or a drug therapy plus family therapy group. After one year, relapse rates were lower in the drug therapy plus family therapy group (33%) compared to the drug therapy only group (61%). These findings are supported by a study of 103 schizophrenic patients conducted by Hogarty et al (1986), who reported relapse rates of 19% among patients treated with drug therapy plus family therapy compared to 41% for patients treated with drug therapy alone. Further, Sudak (2011) describes how cognitive behavioural therapy makes patients more likely to adhere to drug therapy because it helps the patient rationally understand the benefits of doing so. This suggests antipsychotic drug therapy plus cognitive behavioural therapy will be more effective than drug therapy alone.
• Holistic: There are both biological and psychological components to schizophrenia, but interactionist approaches treat both. This is a more complete approach to treatment, which might explain why interactionist approaches are more effective. For example, antipsychotic drugs may address the chemical imbalances of schizophrenia while cognitive behavioural therapy addresses the irrational thought processes.

Weaknesses of interactionist treatment approaches:

• Increased costs: Interactionist treatment approaches will be more expensive than monotherapy because you have to pay for multiple treatments (e.g. CBT, family therapy, and antipsychotic drugs) rather than just one. However, if interactionist treatment approaches lead to lower relapse rates than monotherapy, this may save money in the long run because it prevents further costs to the health service down the line.
• Conflicting evidence: Some studies raise questions as to whether some interactionist approaches to therapy really are more effective than monotherapy. For example, Jauhur’s meta analysis described in the AO3 points for CBT above questions whether CBT really is an effective treatment for schizophrenia. If CBT is not an effective treatment for schizophrenia, then CBT+antipsychotic drug therapy is unlikely to be any more effective than antipsychotic drug therapy alone.