Biological Explanations

• Biological explanations


  The genetic basis of schizophrenia

  Schizophrenia runs in families - there is a strong relationship between the degree of genetic similarity and shared risk of SZ. Gottesman's (1991) large-scale family study showed that identical twins have a 48% chance of developing SZ if the other has it. However there is only a 17% risk between fraternal twins.
• Biological explanations


  The genetic basis of schizophrenia

  Candidate genes - because studies have identified different candidate genes that each appear to confer a small increased risk of SZ, it appears that SZ is polygenic (influenced by multiple genes) and aetiologically heterogeneous (influenced by different combinations of genes). Ripke et al. (2014) carried out a huge study combining all previous genome-wide studies of SZ and found that 108 genetic variations were associated w/ increased risk of SZ.
• Biological explanations

  The dopamine hypothesis

  The original version focused on the association between high levels of dopamine (hyperdopaminergia) in the subcortex and the experience of positive symptoms of SZ. However, more recent versions have focused on the association between low levels of dopamine (hypodopaminergia) in the prefrontal cortex (responsible for thinking and decision making) and the experience of negative symptoms of SZ. It may be that both explanations are correct - both high and low levels of dopamine in different brain regions are associated w/ SZ.
• Biological explanations


  Neural correlates of schizophrenia

  The ventral striatum is believed to be involved with motivation which the negative symptom avolition lacks. Therefore abnormality of the ventral striatum may be involved in the development of avolition. Juckel et al. (2006) found that activity levels in the ventral striatum are lower in schizophrenia than those observed in controls. Thus activity in the ventral striatum is a neural correlate of negative symptoms of SZ.
• Biological explanations - evaluation


  Multiple sources of evidence for genetic susceptibility. Gottesman's study clearly shows how genetic similarity and shared risk of SZ are closely related, and Ripke's study provides evidence that particular genetic variations significantly increase the risk of SZ. There is thus overwhelming evidence for the idea that genetic factors make some people much more vulnerable to developing SZ than others. However, this does not o mean that SZ is entirely genetic as there are a number of factors in the environment associated w/ risk of SZ.
• Biological explanations - evaluation 2


  Support from a number of sources for abnormal dopamine functioning in SZ. Dopamine agonists like amphetamines that increase the levels of dopamine make SZ worse and can produce SZ-like symptoms in people not diagnosed w/ SZ, suggesting an important role for dopamine in SZ. However, there is also evidence to suggest that dopamine does not provide a complete explanation for SZ. Much of the attention of current research has shifted to the role of glutamate, meaning that evidence for the dopamine hypothesis can perhaps be best described as mixed.
• Biological explanations - evaluation 3


  The existence of neural correlates in SZ tells us very little in itself. For example, it may be that something wrong in the ventral striatum is causing negative symptoms or that the negative symptoms themselves means less information passes through the striatum, resulting in reduced activity. Therefore, important questions are left unanswered in relation to this correlation-causation problem.