A03: Biological Explanations for Schizophrenia

• Evaluation A03: Biological Explanations 


  GENETIC BASIS OF SZ:

  -Not just genes

  +Research Support

  
  

  NEURAL CORRELATES OF SZ

  -limitation is evidence for a central role for glutamate

  +Support for dopamine in the symptoms of SZ

  
  

  BIG PEEL
• -ve:Not just genes- A03: Part 1

  P: Although Gottesman's study provides support for heredity in the risk of developing Sz, some findings actually detract from role of genes.

  E: E.G, states that identical twins (monozygotic) share 100% genes, but only have 48% risk & half siblings expected to have half risk of siblings but HS have higher risk then expected - influence of env factors

  E: Biological risk factors includes birth complications (morgan et al 2017) and smoking THC-rich cannabis in teenage years (Di FOrti et al 2015).
• -ve:Not just genes - A03: Part 1

  E:Psy risk factors include childhood trauma e.g 67% with Sz (38% matched controls) reported at least one childhood trauma (Morkved et al 2017)

  E: This problem as genes shared in these relationships doesn't reflect the concordance rate. Perhaps the env of twins is more similar than the env of siblings. Similarly HS may had trauma like parental divorce/death.

  L: Indicating although there clear genetic pattern, there other influences & these should be considered alongside role of genes. So genes alone cant provide a complete explanation for Sz.
• A03: Research Support: Part 1

  P: But, research adds support for a genetic explanation

  E: Tienari et al 2004 found 155 adopted kids born to sz mum had 10% risk of developing sz as opposed to 1% in those who born to non-sz mothers

  E: Show that biological children of parents with sz are at a greater risk even if they grown up in an adoptive family. Study also shows that adoption is not a risk factor as the rates for control group remained at 1%.

  E: This show despite the schizophrenogenic env being removed, the risk was much greater where the mum had it.
• A03: Research Support: Part 2

  E: Family studies like Gottesman, shows risk increases with genetic similarity.

  E: And twin study found 33% concordance for MZ and 7% for DZ twins (Hilker et al 2018)

  L: This add support for genetic vulnerability of the illness & give suggestions on how to improve risk for those who are genetically vulnerable (which is to place them in homes where there no risk of sz). This shows that some people are more vulnerable to sz because of their genes.
• PEEL P1 A03 - Bio Explanations

  P: There is lots of evidence from therapeutics to show the dopamine hypothesis in action

  E: Research has shown that drugs that increase levels of dopamine (e.g amphetamines) produce psychotic symptoms meaning dopamine is somehow implicated in +ve symptoms of SZ, supporting the hyperdopaminergia hypothesis

  E: An excess number of dopamine receptors have been found in Broca's area, which is linked to speech production, this can help to explain disorganised speech auditory hallucinations as overstimulation of Broca's area by dopamine can cause overactivity.
• PEEL P2 A03 - Bio explanations

  E: Antipsychotic drugs that reduce Sz do so blocking the dopamine receptor (i.e reducing the amount of dopamine) meaning further support for the hyperdopaminergic explanation as these drugs dopamine transmission & reduce +ve symptoms.

  E: Low levels of dopamine have been linked to negative symptoms of Sz such as avolition meaning support for the hypodopaminergic explanation as education of dopamine activity in the prefrontal cortex is observed in Sz sufferers which typically suffer with negative symptoms like avolition.
• PEEL P3 A03 - Bio explanations

  E: However, there are some issues associated with evidencing the casual influence of dopamine

  E: It s difficult to assess brain levels of dopamine in Schizophrenics meaning there may be issues of causality when trying to understand the illness.

  E: High levels of dopamine could actually be a symptom of Sz rather than a cause, suggesting it may actually be another, unknown factor which caused sz to occur.
• PEEL P4 A03 - Bio Explanations

  E: Clozapine is the most effective drug at reducing schizophrenic symptoms. It acts on serotonin as well as dopamine meaning that serotonin must be involved in schizophrenia - not just dopamine. Therefore meaning the dopamine hypothesis is not a complete explanations.

  L: This inconsistency in evidence means our understanding of the role of dopamine in the development of Sz is inconclusive making it difficult to accept this as a sole explanation (Interactionism)
• Hyperdopaminergic explanation SUPPORT?

  ?

  A) ?

  
• Support for dopamine in the symptoms of Sz - Bio Exp A03

  • Amphetamines (Increase DA) mimic symptoms (Curran et al. 2004). Antipsychotic drugs (reduce DA) reduce intensity of symptoms (Tauscher et al 2014)
  • Candidate genes act on the production of DA or DA receptors.
  • This strongly suggests that dopamine is involved in the symptoms of sz.
• limitation is evidence for a central role for glutamate - Bio Exp A03

  • Post Mortem and scanning studies found raised glutamate in people with sz (McCutcheon et al 2020)
  • Also several candidate genes for sz are believed to be involved in glutamate production or processing.
  • This means that a strong case can be made for a role for other neurotransmitters in sz.
  • NOT JUST DOPAMINE - SO INCOMPLETE STUDY