Biological explanations

• Three biological explanations:

  Genetic basis, dopamine hypothesis and neural correlates
• Schizophrenia runs in families- strong relationship between genetic similarity of family members and likelihood of both developing schizophrenia
• Grottesman's family study found MZ twins have a 48% shared risk of schizophrenia. DZ twins have a 17% shared risk and siblings (about 50% genes shared) have a 9% shared risk.
• Schizophrenia is polygenetic and aetiologically heterogeneous
• Existence of different candidate genes indicates the following:

  • Each individual gene confers a small increased risk of schizophrenia (i.e. schizophrenia is polygenetic)
  • Different combinations can lead to schizophrenia (i.e. schizophrenia is aetiologically heterogeneous)
• Ripke et al. studied 37,000 patients and found 108 separate genetic variations associated with increased risk; many coded for the dopamine neurotransmitter
• Dopamine (DA) is widely believed to be involved in schizophrenia because it is featured in the functioning of brain systems related to the symptoms of schizophrenia
• High dopamine activity (hyperdopaminergia) in subcortex (central areas of the brain) associated with hallucinations and poverty of speech (e.g. excess of dopamine receptors in Broca's area)
• More recent versions of the hypothesis have focused on low levels of dopamine (hypodopaminergia) in the prefrontal cortex (responsible for thinking and decision-making)
• Neural correlates are measurements of the structure or function of the brain that correlate with the positive or negative symptoms of schizophrenia
• Neural correlates: brain activity linked with symptoms
• Ventral striatum is involved in anticipation of reward (linked to motivation). Loss of motivation (avolition) in schizophrenia may be explained by low activity levels here. Supported by Juckel et al.
• Juckel et al. found a negative correlation between ventral striatum activity and overall negative symptoms
• Allen et al. found that patients experiencing auditory hallucinations recorded lower activation levels in the superior temporal gyrus and anterior cingulate gyrus
• Strength: strong evidence for genetic vulnerability

  The Grottesman family study shows how genetic similarity and shared risk of schizophrenia are closely related. Adoption studies (Tienari et al.) show children of people with schizophrenia are still at heightened risk of schizophrenia if adopted into families without a history of schizophrenia. So schizophrenia may not be entirely genetic, but there is overwhelming evidence that genetic factors make some people more vulnerable
• Limitation: correlation-causation problem

  The question that remained is whether unusual activity in the brain causes the symptoms or whether there are other possible explanations for the correlation. A negative correlation may suggest that low activity in the ventral striatum causes avolition. But it could be that avolition means that less information passes through the striatum resulting in the low activity. Therefore, although neural correlates exist, they tell us relatively little about the causes of schizophrenia
• Strength: role of mutation supports genetic explanation

  Schizophrenia can take place in the absence of family history of the disorder (e.g. through mutation of paternal DNA in sperm cells caused by radiation, poison or viral infection). Brown et al. found a link between paternal age (associated with increased risks of mutation) and risk of schizophrenia, increasing from 0.7% in fathers under 25 to 2% in fathers over 50. This evidence supports the importance of genetic factors in the development of schizophrenia
• Limitation: it is clear the environment is also involved

  After all, the probability of developing schizophrenia even if your identical twin has it is less than 50%. There is evidence that environmental factors (e.g. family functioning during childhood) can also play a role in the development of schizophrenia. This suggests that schizophrenia may be the result of a combination of biological and psychological approaches (as acknowledged by the interactionist approach)