Biological explanation

• What are the 2 biological explanations of SZ?

  • Genetic basis of schizophrenia
  • Neural correlates of schizophrenia
• How is the genetic basis of SZ further divided?

  • Schizophrenia runs in families
  • Candidate genes
  • Role of mutations
• Schizophrenia runs in families

  • Investigations have looked at the extent to which genetic similarity between family members is associated with the likelihood of developing SZ.
  • There have been some studies investigating genetic similarity and the risk of SZ.
  • Gottesman carried out a large-scale family study, which suggests that the more genetic similarity, the higher the chance for developing SZ. For example, identical twins share 100% of their genes and they have 48% chance of developing SZ. Whereas non-identification twins who share 50% of their genes only have 17% risk of developing SZ.
• Candidate genes

  • Individual genes are associated with the risk of inheritance.
  • Schizophrenia is polygenic.
  • Schizophrenia is aetiologically heterogenous (different combinations of factors can lead to the condition)
  • Research support: Ripke et al
• Research support for candidate genes

  • Ripke et al, genetic make-up of 37,000 patients was compared to that of 113,000 controls.
  • 108 separate genetic variations were associated with increased risk of schizophrenia.
  • Genes associated with increased risk included those coding for the functioning of a number of neurotransmitters including dopamine.
• Role of mutation

  • Schizophrenia can occur without any family history of the disorder.
  • One explanation of this is mutation in parental DNA.
  • Mutation of sperm cells can be caused by radiation, poison or viral infection.
• Research support for role of mutation

  • Positive correlation between paternal age (associated with increased risk of sperm mutation) and the risk of developing SZ.
  • Increasing from 0.7% with fathers under 25 to over 2% in fathers over 50.
  • Brown et al
• Research support for genetic vulnerability

  • Gottesman family study clearly shows how genetic similarity and shared risk of SZ are closely related.
  • Tienari et al, adoption studies show children of people with SZ are still at heightened risk of SZ if adopted into families without a history of SZ.
  • There is evidence which in favour of the role genetic factors play which makes people more vulnerable to developing schizophrenia than other.
  • However not entirely genetic as environmental factors are associated with SZ.
• Environmental factors not included in the genetic explanation

  • Morkved et al found that 67% of people with SZ and related psychotic disorders reported at least 1 childhood trauma.
  • This shows that psychological risk factors like childhood trauma leaves people more vulnerable to developing SZ.
  • Therefore this suggests that genetic factors alone cannot provide a complete explanation of SZ.
• Real life application of genetic explanation

  • For example, based on Gottesman’s study there will be a 2% probability of developing SZ if a child has an uncle or aunt with SZ, and 6% probability if they have a half-sibling with it.
  • This shows if one or more potential parents have a relative with SZ, they risk having a child who would go on to develop the condition.
  • Genetic counselling involves informing potential parents of these probabilities so they can make informed decisions of whether to have children as they may have a poor quality of life if they develop SZ.
• Neural correlates

  • Refers to when measurement of structures or functions of the brain correlate with SZ
• The dopamine hypothesis

  • The brains chemical messengers appear to work differently in the brain of a patient with SZ.
  • In particular dopamine is widely believed to be involved.
  • Dopamine is important in the functioning of several brain systems that may be implicated in the symptoms of SZ
• Original dopamine hypothesis: Hyperdopaminergia

  • Hyper= high
  • Excess amounts of dopamine receptions in the BROCA’S area may be associated with speech poverty or auditory hallucinations.
  • Schizophrenics are thought to have high numbers of dopamine receptions on receiving neurones, resulting in more dopamine binding therefore more dopamine firing.
• Updated dopamine hypothesis: Hypodopaminergia


  Hypo= Low

  • Davis et al, found low levels of dopamine in the brain’s cortex.
  • E.g low levels of dopamine in the prefrontal cortex could explain cognitive problems e.g negative symptoms of SZ
• How can we determine which dopamine hypothesis to use?

  • It may be that both hyperdopaminergia and hypodopaminergia are correct explanations.
  • Both high and low levels of dopamine in different brain regions are involved in SZ.
• Evidence for dopamine

  • Amphetamine increases levels of dopamine and can make SZ worse by producing schizophrenia-like symptoms in non-sufferers.
  • Antipsychotic drugs reduce levels of dopamine and can reduce the intensity of SZ symptoms.
  • Suggests that dopamine is involved in the symptoms of SZ.
• Contradictory evidence for glutamate

  • McCutcheon et al, Post-mortem and live scanning studies have consistently found raised levels of glutamate in several brain regions of people with SZ.
  • Other candidate genes for SZ are believed to be involved with glutamate production.
  • Therefore this means other neurotransmitters are involved in SZ other than dopamine.
• Use of correlational research in neural correlates. Why is this bad?

  • It is not clear whether abnormal dopamine level cause SZ or whether it is a result of SZ.
  • Shows that the causes of SZ may not be as a result of dopamine levels alone. The abnormal brain activity could be caused by another factor such as trauma.
  • It is difficult to use correlational evidence to imply causation because there may be other intervening factors such as the environment that causes this effect.