Biological explanations for schizophrenia

• AO3 - Multiple sources of evidence for genetic susceptibility:

  The Gottesman (1991) study clearly shows how genetic similarity and shared risk of schizophrenia are closely related. There is also evidence from studies conducted at a molecular level showing that particular genetic variations specifically increase the risk of schizophrenia (Ripke et al. 2014). There is thus overwhelming evidence for the idea that genetic factors make some people more vulnerable to developing schizophrenia than others.
• AO3 - Evidence for the dopamine hypothesis:

  Curran et al. (2014) found that dopamine agonists like amphetamines that increase the levels of dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in people not diagnosed with schizophrenia. This drug study suggests an important role for dopamine in schizophrenia.
• AO3 - The correlation-causation problem:

  For example, the correlation between levels of activity in the ventral striatum and negative symptoms of schizophrenia. It may be that something wrong in the ventral striatum is causing negative symptoms. However, it is just as possible that the negative symptoms themselves mean that less information passes through the striatum, resulting in the reduced activity. The existence of neural correlates in schizophrenia therefore tells us relatively little in itself.
• AO3 - The role of the psychological environment is important but unclear:


  There is also evidence to suggest an important role for environmental factors, including psychological ones such as family functioning during childhood.