Biological Explanations

• Ripke (2014) argues there are 108 gene variations identified in heightened risk of SZ. A person would have to inherit this gene mutation from a parent hence Schizophrenia is a genetic disorder. Many candidate genes appear to be involved in dopamine breakdown.
• COMT gene = breaks down dopamine.

  Normal dopamine levels are involved in processes such as thought, perception and emotion. In those with schizophrenia it is thought this breakdown process is disrupted. Disruption is associated with excess dopamine and the disorganised thinking, hallucinations and delusions
• Tienari et al (2004). Adoption study. 6.7% adoptees whose biological mother had SZ developed SZ compared to 2% without schizophrenic mothers. Suggests biological influence.

  If solely genetic would expect 6.7% to be higher because we share 50% DNA. 2% with no genetic predisposition got the disorder
• Gottesman (1991) - twin study. Concordance in MZ 48%, whereas DZ 17%. Supports genetic explanations as higher for those with 100% genetic similarity however not 100% concordance. Diathesis stress model may be a better explanation which considers environmental triggers to genetic vulnerabilities
• Hypodopaminergia

  Lower levels of dopamine in the prefrontal cortex may contribute to negative symptoms such as avolition.

  The frontal cortex is responsible for thinking and decision making so may explain loss of goal directed behaviour
• Hyperdopaminergia

  Increased levels of Dopamine in the subcortical areas may contribute to positive symptoms such as hallucinations and delusions. E.g broca's area is here and is responsible for language which may explain auditory hallucinations.
• Dopamine antagonists e.g. amphetamines increase levels of dopamine. This can produce-schizophrenia like symptoms in non sufferers and worsen symptoms in sufferers. Supports ideas that dopamine is implicated.
• Typical antipsychotics bind to D2 receptors, blocking dopamine action and are effective in reducing positive symptoms of schizophrenia.
• Limitation of dopamine hypothesis

  Other neurotransmitters such as serotonin and glutamate have been implicated in schizophrenia. Newer types of antipsychotics that appear to be more effective sz treatments do not block dopamine action as effectively as the older drugs. They seem to have more influence on neurotransmitters such as serotonin and glutamate. Limits efficacy of dopamine hypothesis as it is too simplistic
• Juckel (2006)

  Ventral striatum = area linked to reward anticipation. Found a negative correlation between ventral striatum activity and negative symptoms. Avolition is a reduction in motivation so this therefore makes sense and therefore activity in the ventral striatum is a neural correlate of schizophrenia.
• Brain imaging appears to show enlarged ventricles in the brain in those with schizophrenia compared to those without it. Gaps mean less grey matter/brain tissue.

  Believed to be present in 80% of sufferers

  Associated with brain damage and negative symptom
• Issue with neural correlates

  Correlation =/= causation. Cannot establish direction of causality. Enlarged ventricles could be a consequence of schizophrenia etc etc.
• Ho (2003) performed MRI scans on recent onset Schizophrenia patients

  Re scanned 3 years later

  Evidence of damage is present at diagnosis and worsens over time

  Brain damage can worsen as a consequence of schizophrenia. Argument is inconclusive however because some non schizophrenia patients have enlarged ventricles and not all schizophrenia patients do.

  Structural changes cannot be a sole cause
• • Biological evidence is inconclusive. Diathesis stress model may be more effective (interaction). Adoption studies seem to support this approach when considering genetic influence = triggers differ = we are only ever predisposed​
  • Stressful family life/abnormal familial circumstances can lead to higher than normal levels of dopamine = must consider environment= dopamine may be an indirect factor triggered by external experience​
• • Structural differences could easily be effect of SZ not cause =issues with correlational conclusions​
  • Dopamine hypothesis too simplistic = role of serotonin and glutamate. Biological reductionism. Nature/Nurture.