Biological Explanations for SZ AO3

• what is support for the genetic basis of SZ?

  • evidence that SZ is biological (and therefore partly genetic), particularly suggesting it runs in families
  • Gottesman and Shields 1966 graph showed strong empirical evidence that the more genes two individuals share (highest is MZ twins 48% and lowest in general population 1%), the higher the risk of developing SZ - support genetic basis
  • Gottesman and Shields 1991 also showed high concordance rates of SZ in MZ - 48% and DZ - 17% - twin studies show a genetic link
• what is a limitation of genetic basis of SZ?

  • however, MZ twins share 100% of genes so it would be assumed that is one had SZ the other would too, but G&S showed only a 48% risk so maybe genes aren't the only factor
  • perhaps a more holistic explanation like the diathesis-stress model would be better as it argues genes play a role in creating a predisposition to SZ, but symptoms won't develop unless triggered by a stressor (interactionist, both nature and nurture) - better as nature and nurture don't work in isolation in real life
• what is a further point about Gottesman and Shields findings?

  • high risk of SZ in MZ twins may be due to nurture not genetics - due to MZ twins being identical, there is an increased similarity in upbringing compared to DZ twins which would explain the high concordance rates, rather than shared genetics
• what is support/limitation for the dopamine hypothesis?

  • Curran et al 2004 - amphetamines induce SZ-like states in non-SZ individuals and exacerbate symptoms in SZs, drugs activate dopamine systems in brain and can induce similar symptoms in non-sufferers - suggests underlying cause of SZ is an excess of dopamine
  • However, if this is correct, drugs that reduce levels of dopamine should stop SZ - its been found that antipsychotic drugs (antagonist of dopamine) only reduce all of symptoms in 20% of patients
  • suggests the cause of SZ isn't completely biological and other factors may be involved
• how is RWA a strength of neural correlates?

  • development of anti-psychotic drugs like chlorpromazine which reduces symptoms of SZ by inhibiting dopamine transmission
  • Thornley - antipsychotic drugs associated with better functioning and reduced symptom severity compared with a placebo
  • further evidence which validates the dopamine hypothesis, if drugs that control levels of dopamine then cause a reduction in SZ symptoms, it can be suggested that dopamine is linked to development of SZ
• what is a limitation of neural correlates?

  • can't establish an accurate cause and effect relationship
  • is the raised dopamine levels the cause of SZ, or is the raised dopamine a result of SZ?
  • In research it is not clear which comes first, as research focuses on patients who have already been diagnosed with SZ
  • therefore, as we have no information about the patients pre-diagnosis, we need to be careful when establishing cause and effect relationships in SZ patients in relation to dopamine