Biological Explanations of Sz Flashcards
How do genes influence schizophrenia?
the more genetically similar you are to another person with schizophrenia, the more likely you are to develop schizophrenia too.
Evaluate the genetic explanation.
Good scientific val. based on objective methods such as gene mapping. gurling - 7 families. genetic mutation on chromosome 5 in all schizophrenic relatives, suggesting a direct link to genes. however further research points out that mutations have also been found on chromosome 9, 10, 11, 18 and 19.
Reductionist - explain Sz solely through genes. does not account for other factors such as EE. multi-dimensional approach is needed to explain the complex interaction between nature and nurture.
Deterministic - suggests that genes inevitably cause Sz. ignores the role of free will to change irrational thoughts (e.g. hallucinations).
Outline Gottsman’s research (twin studies).
studied 40 twins.
concordance rate for MZ twins is 48%.
DZ = 17%.
Outline Cardino’s research (twin studies).
Concordance rate of 26.5% for MZ.
0% for DZ.
Evaluate twin studies.
Correlation - no C+E.
Lacks reliability - different studies use diagnostic criteria, calculate concordance rates differently. difficult to gain consistent results into the influence of genes on Sz.
Outline Tienari’s research (adoption).
155 adopted children whose biological mothers had schizophrenia.
Concordance rate of 10%, compared to 1% for someone whose parents do not have Sz.
Strong evidence for the link between genes and Sz.
Outline Gottesman’s Research (family studies).
both parents have Sz = 46% chance of developing Sz.
Compared to 1% for someone selected at random.
The more genetically similar you are to your relatives, the more concordance is found.
Evaluate family studies.
Contradict genetics - genetically similar family members spend more time together. therefore Sz could be explained through environmental factors such as SLT. supports the role of nurture in Sz.
Gottesman - meta-analysis, over 40 research studies. research used a larger sample than single studies. increases pop val. however - used a range of methods and different diagnostic criteria (changes over time) - difficult to make comparisons, reducing rel. Researcher bias - Gottesman may have interpreted the findings to suit his expectations. Reduces int val - partial support.
Outline the dopamine hypothesis.
Excessive dopamine/over-sensitivity to dopamine can lead to Sz.
High levels of dopamine can be due to several factors:
- excessive dopamine being produced.
- hypersensitivity of dopamine receptor sites.
- too many dopamine receptor sites.
What are the strengths of the dopamine hypothesis?
drugs which block dopamine receptors reduce symptoms of Sz. this shows a link between dopamine levels and Sz.
L-DOPA - drug used to treat parkinsons by increasing dopamine levels. found to increase Sz symptoms. this shows a clear link between dopamine and Sz.
Post mortems of Sz sufferers show high levels of dopamine in the brain.
What are the weaknesses of the Dopamine Hypothesis?
Phenothiazines do not work for everyone - difficult to establish C+E between dopamine and Sz - there may be other causes such as the environment (SLT).
Aetiology fallacy - because the treatment (reducing dopamine) works, doctors believe dopamine is the sole cause of Sz. Too simplistic - Sz is a complex disorder with more than one cause.
Excessive dopamine only linked to positive symptoms not negative - cause of Sz must be more complex.
Diathesis Stress Model.
Resolves the nature nurture debate.
some people born with biological predisposition to Sz.
triggered by environmental factors e.g. life changes.
