Biological explanations

• genetic basis evaluation: strength: research support= Gottesman shows risk increases with genetic similarity to a family member with schizophrenia. Tienari (2004) adoption study showed biological children of those with schizophrenia are at a heightened risk even growing up separately. Hilker (2018) found concordance rate of 33% for identical twins and 7% for non-identical twins. 
• Genetic basis evaluation Limitation: environmental factors= include biological and psychological influences. biological risk factors include birth complications and smoking cannabis in teenage years. psychological risk factors include childhood trauma leaving people more vulnerable to adult mental health issues. Morkved (2017) found 67% with schizophrenia reported at least one childhood trauma.
• genetic basis- family studies:

  • family studies shown risk of schizophrenia increases in line with genetic similarity
  • findings from Gottesman's 1991 family study= someone with an aunt with schizophrenia has a 2% chance of developing it,9% for sibling and 48% identical twin.
• genetic basis- candidate genes:

  • schizophrenia is polygenic (number of genes involved) most likely genes would be those coding for neurotransmitters including dopamine.
  • Ripke (2014) compared genetic make up of 37,000 people with SZ to 113,000 controls and found 108 separate genetic variations,increasing risk of SZ
• Genetic basis- role of mutation:

  • SZ can have genetic origin in absence of family history
  • one explanation is mutation in parental DNA, caused by radiation, poison or viral infection
  • evidence for mutation found in positive correlations between parental age and risk of SZ (increasing from 0.7% with fathers under 25 to 2% in over 50)
• Neural correlates-

  • This was once referred to as a brain structure explanation. The idea here is that it is the actual mechanical working of the brain that is the issue. 
  • A major problem is that we are not sure whether schizophrenia causes brain abnormalities or if the case is vice versa. 
• Neural correlates- the original dopamine hypothesis:

  • based on discovery that drugs used to treat SZ caused symptoms similar to those with Parkinson's disease (associated with low DA levels)
  • meaning SZ may result from high levels of DA in subcortical areas (speech production) of the brain, may explain symptoms like speech poverty
• Neural correlates- updated version of dopamine hypothesis:

  • Davis (1991) proposed abnormally low DA in brains cortex can also explain some symptoms.
  • Low DA in prefrontal cortex (thinking) could explain cognitive issues
• Neural correlates- Evaluation Strength: Evidence for dopamine

  • amphetamines increase DA and worsen symptoms in people with SZ and induce symptoms in those without
  • antipsyhotic drugs reduce DA activity and reduce intensity of symptoms
  • some candidate genes act on production of DA or DA receptors
  • all strongly suggest influence of dopamine
• Neural correlates- Evaluation Limitation: glutamate

  • Post mortem and live scanning studies have consistently found raised levels of neurotransmitter glutamate in people with SZ.
  • Several candidate genes for SZ believed to be involved in glutamate production
  • equally strong case for other neurotransmitters