Biological explanations of schizophrenia

AO1

• Researchers look to identify whether biological relatives are more likely to be affected by sz than non-biological relatives
• Relatives share a high proportion of similar genes, which means that if sz is genetic then it would be more apparent in closely related family members.
• Gottesman (1991)- Risk of developing sz is greater for those more closely related
  • When 2 parents have sz- 46%
  • When 1 parent has sz- 16%
  • When a sibling has sz- 8%   [Shows the influence of genes over nurture]

AO2

• Support- Kendler et al- Found that first degree relatives were 18x more likely to develop sz than general population(1%) [Supports the theory that genetics may be involved in sz onset]
• Against- Sz running in families may be more to do with common rearing patterns
  • E.g. Expressed emotion has shown that the negative emotional climate in some families may lead to stress beyond an individuals coping mechanisms-triggers a sz episode

AO1

• Allows researchers to investigate the relative contributions of genetic & environmental influences- MZ 100% same genes [more concordantin traits like sz], DZ 50% same genes [greater similarity is due to genetic factors]- Allows nuture to hopefully be discounted
• Joseph et al (2004)- When comparing twin studies:
  • Identical-40%
  • Non-identical-7.4% [High concordance rate presents a strong argument for genetic factors

AO2

• Support-Gottesman (1991)- Analysis of twin studies:
  • MZ-48%           DZ-17%
  • Also found concordance rates for MZ twins reared apart were very similar to MZ brought up together- Suggest high concordance rates is not due to being treated in a similar way in the family

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• Against- Torrey(1992)
  • Argued that many twin studies were inadequate- small sample size and biased allocation of twins
  • Reviewed 8 studies- MZ-28%               DZ-6%
  • His findings are lower than Gottesman but there is still a higher chance of developing sz
• Eval:
• Twin studies provide strong genetic evidence
  • As MZ are genetically identical & DZ are more like siblings- supports involvement of genetic factors
  • If genetic wern't important, and nurture was the key factor- then there should be no difference in the concordance rates between MZ and DZ twins
• Not 100% concordance- No studies show that there is a 100% concordance for MZ- suggest that sz cannot be entirely a genetic disorder

AO1

• Adopted children with biological parents suffering from sz are compared to a control group of adoptees with non-sz parents
• Aim- Help seperate the role of nature & nurture 
• Tienai et al. (2000)- Finland
  • Out of 164 adopted children whose mothers have been diagnosed with sz, 6.7% of children also shared a diagnosis compared to only 2% of 197 children with non-sz mothers
  • Supports the role of genetics influencing the onset of sz

AO2

• Wahlberg et al. (1997)- Reported additional findings that showed that environmental factors are important
  • Found that the genetic risk of developing sz was increasingly significant if the adopted family was high in communication deviance (communicating unclearly/confusingly)
  • Families with low communication deviance- children have good psychological health despite their genetic link to sz

• Sample size- All 3 studies casts doubt on the generalisability of the finding so population validity may be low [sample bias]
• Reductionist- Only focuses on biological factors and ignores psychological factors
  • Research on MZ twins had far from 100% concordance and so sz cannot be explained by genetics
  • Therefore, we should consider more that 1 level of explanation
  • Biological explanation alone is reductionist [simplistic]

• Dopaminne is 1 of many neurotransmitters that operate in the brain
• Dopamine hypothesis- Messages from neurones that transmit dopamine fire too easily or too often- leads to characteristic symptoms of sz
• sz patients usually have an abnormal amount of D2 receptors on recieving neurons -results in more dopamine joining togetherand therefore more neurones firing
• Key role played by dopamine in sz is highlighted by: Amphetamines, Antipsychotic drugs and Parkinson's disease

• Amphetamines
  • A drug with special relevance for our understanding of sz
  • Its a Dopamine agonist (a substance which initiates a physiological response when combined with a receptor)
  • Stimulates nerve cells containing dopamine causing the synapse to be flooded with this neurotransmitter
  • Large doses of the drug can cause hallucinations and delusions of a sz episode 

Antipsychotic drugs

• Various types of antipsychotic drugs- they all block the activity of dopamine in the brain
• By reducing stimulation of the dopamine system- drugs eliminate symptoms- e.g. hallucinations
• They make sz symptoms less severe- strengthened the case for being a significant contributory factor for sz

Parkinson's disease

• Low levels of dopamine activity are found in people who suffer from Parkinson's disease
• Grilly (2002)- Found that some people who were taking the drug L-Dopa to raise their levels of dopamine were developing sz-type symptoms

AO2

• Post-mortem studies: Haracz (1982)-Review of post mortem studies of sz patients
  • Found most of those studied who had high dopamine levels had received antipsychotics shortly before death. Post-mortems of sz patients who didn't recieve medication showed normal levels of dopamine