Evaluation of the Biological Explanation for Schizophrenia

• genetic explanation strengths

  • multiple sources of evidence for genetic susceptibility
  • role of mutation
• multiple sources of evidence for genetic susceptibility

  family studies: Gottesman (1991):

  • children with 2 schizophrenic parents= concordance rate of 46%
  • children with 1 schizophrenic parent= 13%
  • siblings= 9%

  Twin studies: Joseph (2004)= calculated that the pooled data for all schizophrenia twin studies carried out prior to 2001 showed a concordance rate for MZ twins of 40.4% and 7.4% for DZ twins
• multiple sources of evidence for genetic susceptibility COUNTER

  MZ twins are treated more similarly and encounter more similar environments compared to DZ twins. the differences in concordance rates could be nothing more than environmental differences rather than genetic differences
• role of mutation

  it has been found that schizophrenia can take place in the absence of a family history of the disorder. a possible explanation for this is mutation in parental DNA. this can be caused by radiation, poison or viral infection

  evidence has shown a positive correlation between parental age (associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50. this evidence also highlights the genetic influence on schizophrenia
• neural correlates strengths

  • evidence from brain scanning research
  • evidence for dopamine hypothesis from drugs
• evidence from brain scanning research

  Juckel et al. (2006)- measured activity levels in the ventral striatum in schizophrenics and found lower levels of activity than observed in controls
• evidence from brain scanning research COUNTER

  correlation-causation problem= does not show a causal relationship, only correlational. can we confidently include that the unusual activity in the region of the brain causes the symptom?

  e.g. the correlation between activity in the ventral striatum and negative symptoms of schizophrenia- it is possible that the negative symptoms themselves mean that less information passes through the striatum, resulting in the reduced activity
• evidence for dopamine hypothesis from drugs

  
  

  there has been successful drug treatment for schizophrenics which attempt to change levels of dopamine activity in the brain:

  1. drugs that increase dopaminergic activity= amphetamines (not used as a medicine)= increase levels of dopamine. 'normal' individuals exposed to amphetamines can develop characteristic symptoms of a schizophrenic episode, which disappear when they stop taking drugs
  2. drugs that decrease dopaminergic activity= antipsychotic drugs- block activity of dopamine and so eliminate symptoms such as hallucinations and delusions. this strengthens the case for the important role of dopamine in schizophrenia
• evidence for dopamine hypothesis from drugs COUNTER

  it has been argued that psychotic drugs do not alleviate hallucinations and delusions in about one third of people. in addition, in some people, hallucinations and delusions are present despite levels of dopamine being normal