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Evaluation of biological explanations to Schizophrenia. - Coggle Diagram
Evaluation of biological explanations to Schizophrenia.
Genetic Explanations.
2/3 sufferers don't have relatives with Sz.
Could potentially be a gene mutation?
As paternal age increases, higher risk of sperm mutation.
Risk of Sz also increases from 0.7% to 2% of over 50 year olds.
Difficult to separate nature/nurture
Both family and twin studies look at people sharing the same environment.
This increases concordance rates regardless of genetics.
Even MZ share the womb, even if separated on birth.
Makes it hard to distinguish between genetic and environmental influences.
Concordance rates of 40% for MZ twins.
If it's genetic, why not 100%?
Genes therefore can't wholly be blamed for Sz.
Therefore biologically reductionist
Family studies
Conducted retrospectively
This can be unreliable as fact recall may be poor so data inaccurate.
Prospective studies more reliable.
These follow people over time so make comparisons before and after condition occurs.
Dopamine hypothesis.
Evidence: sufferers have more dopamine receptors.
More receptors = more neural firing.
Post mortem: Sz have more dopamine receptors.
More dopamine in amygdala.
Evidence of dopamine abnormalities in Sz.
Dopamine abnormalities not in all Sz patients.
Especially those with negative symptoms.
Dopamine more likely to impact those with positive symptoms.
May only impact certain aspects of the illness.
Implies several NT involved, not just dopamine
Practical application
Developed effective treatment.
Psychiatrists can understand role of NT.
This improves quality of life.
Issue with cause and effect.
Is too much dopamine causing it, or a result of it?
Not clear which comes first.
Dopamine increases could be result of environmental factors, such as abnormal family circumstances.
Newer drugs more effective than older ones.
New drugs affect dopamine and other NT
Several NT may be involved in Sz.
Hypothesis therefore reductionist.
Neural correlates.
Sz not responding to medication are those with enlarged ventricles.
Suggests enlarged ventricles result from prolonged Sz.
Enlarged ventricles caused by Sz, not creating Sz.
Research into enlarged ventricles is inconclusive.
Non Sz can also have enlarged ventricles.
Not all Sz have enlarged ventricles.
Goes against Sz being directly linked to loss of brain tissue.
If the sole reason, everyone with enlarged ventricles would have Sz.
Enlarged ventricles only explain some symptoms.
Weyandt (2006).
Only associated with negative symptoms.
Explanation cannot explain ALL symptoms.