Biological explanations

• Gottesman (1991)

  • Gottesman (1991) found that the closer a person's genetic relationship is to someone with schizophrenia, the greater their own risk of developing it
• concordance rate

  • The concordance rate for schizophrenia among identical twins was 48%, whereas for non-identical twins it was 17%. And this is supported by Cardano et al (1999), who found similar concordance rates for schizophrenia. Such studies support the idea that genetics play a role in schizophrenia
• AO3-A more holistic view

  • It's not like there's a single gene responsible for schizophrenia. Instead, multiple genes likely combine to increase a person's risk of developing schizophrenia e.g. 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 genetic explanation. Further, many of these genetic variations were related to dopamine transmission, so genetic explanations can be combined with the dopamine hypothesis for a holistic explanation of schizophrenia
• Enlarged ventricles

  e.g. Johnstone et al (1976) and Suddath et al (1990) found people with schizophrenia had enlarged ventricles compared to controls. This is particularly linked with the negative symptoms of schizophrenia, as shown in studies such as Andreasen et al (1982)
• AO3-Reduced grey matter and cortical thinking

  - MRI scans by Boos et al (2012) found schizophrenic patients had reduced grey matter and cortical thinking compared to their non-schizophrenic family members and the non-schizophrenic controls
• AO3-Facial emotion processing

  a common symptom of schizophrenia is difficulty perceiving emotions. A meta-analysis by Li et al (2010) compared fMRI scans of schizophrenic patients with non-schizophrenic controls during facial expression processing and found reduced activity in the bilateral amygdala and right fusiform gyri among the schizophrenic patients
• AO3-a problem with causation

  • As always, correlations do not prove causation e.g. reduced activity in the bilateral amygdala of schizophrenic patients may cause difficulties in emotional processing, but it could also be that reduced blood flow and activity in the bilateral amygdala is an effect of reduced emotional processing
• Dopamine hypothesis

  • The dopamine hypothesis of schizophrenia explains schizophrenia as a result of abnormal activity of the neurotransmitter dopamine
• Synder (1976)

  • Synder (1976) reported that several drugs that reduce schizophrenia symptoms are dopamine receptor antagonists: they reduce dopamine activity. The implication is that schizophrenia is caused by increased dopamine activity and that these drugs work by reducing dopamine activity
• Dopamine agonists

  these increase dopamine and have shown to worsened schizophrenia symptoms
• Brain scans and dopamine

  some studies using brain-scanning techniques have found increased dopamine activity in schizophrenic patients e.g. Lindstrom et el (1999) compared PET scans of 12 schizophrenic patients with 10 controls and found the schizophrenic patients had increased dopamine activity in the striatum and parts of medial prefrontal cortex (AO3)
• AO3-Conflicting evidence

  the dopamine hypothesis is controversial. Farde et al (1990) compared brain scans of 18 schizophrenic patients with 20 non-schizophrenic controls. They found no difference in dopamine activity between the two groups. Similarly, a review of post-mortem studies by Haracz (1982) found little evidence to support the dopamine hypothesis
• AO3-other neurotransmitters

  evidence suggests that other neurotransmitters besides dopamine are involved in the development of schizophrenia, such as glutamate e.g. a meta-analysis of brain scans by Marsman et al (2013) found decreased glutamate activity can successfully treat schizophrenia. But the glutamate hypothesis doesn't necessarily contradict the dopamine hypothesis- both neurotransmitters may be involved in schizophrenia
• AO3-Allegations of bias

  Psychiatrist David Healy (2004) 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.