L4: Biological Explanations - Genetics Flashcards
What did Ripke suggest (AO1)
- Schiz is polygenic & candidate genes might be responsible for causing the illness
- Meta analysis conducted
- 37000 Schiz sufferers & 11000 controls
- Found that 108 separate genetic variations associated with increased risk of Schiz
- Genes code for functioning of dopamine
- High dopamine = Schiz
Ripke (AO3)
(-) Cautious at looking at genetics alone, other approaches need to be considered e,g behavioural model suggests children learn abnormal behaviour via the env.
(-) Genetics doesn’t offer a full explanation. Just because someone has the gene, doesn’t mean they will get it. Diathesis Stress Model says genetics increases the chances but a factor in the env will trigger the illness.
(-) Schiz can occur in the absence of genetics. A mutation in parental DNA could cause Schiz in future offspring. A positive correlation was found between paternal age and risks of having Schiz. 9.7% if father is under 25 and 2% if father is over 50
(+)Research can be supported by the Dopamine hypothesis: high levels of dopamine cause Schiz. Ripke’s work is praised for linking biological mechanisms.
Gottesman & Shields on Twins and Schiz (AO1)
- Investigated 224 sets of twins
- 120 males and 104 females
- Average age of ppt were 46
- Conducted in a London hospital and was a longitudinal study for 25 years
- Study relied on one twin has Schiz and concordance rates were investigated, examining the likelihood of the healthy twin becoming a Schiz.
What methods did Gottesman and Shields use to diagnose Schiz?
- Interviews
- Doctors case notes
- DSM
What were the results of Gottesman and Shields study?
- 48% of MZ twins were concordant for Schiz
- 17% of DZ twins were concordant for Schiz
- Indicates Schiz has a genetic basis esp for MZ
- DZ is less prominent
AO3 of Gottesman and Shields
(-) Ignores behavioural approach. Identical twins copy and model each other’s behaviour so maybe the healthy twin copied that behaviour
(-) Study relies on interviews and Schiz patients have difficulty with speech and might have found it difficult to communicate their symptoms. This can have negative effects on the diagnosis and classification of Schiz.
(+) Longitudinal study = tracked over long periods of time = monitor development
(+) 48% MZ concordance and 17% DZ concordance, supporting the biological argument.
(+) Reliable and Valid: used 3 diff methods to diagnose Schiz. More chance of inter-rated reliability so higher validity.
The Copenhagen High Risk Study - Adoption AO1
- Prospective longitudinal study in Denmark
- 207 adopted children studied. Their mothers had been diagnosed with Schiz (high risk)
- Matched control group of 104 adopted children with healthy bio mums. (Low risk)
- Children ages 10-18 at the start and we’re matched in terms of age, gender, socioeconomic status
- 16.2 % of high risk diagnosed with Schiz, only 1.9% of low risk
- Schizotypal was diagnosed in 18.8% of high risk, but only 5% of low risk
- 35% of high risk has mental disorders and 6.9% of low risk group
The Copenhagen High Risk Study - Adoption AO3
(-) Hard to separate genes from env. Children born to Schiz mothers shared the same env as mums before being adopted. Needs to be considered
(-) Reliability is questioned. Mothers diagnosed with Schiz before introduction of diagnostic systems. Maybe mums didn’t have Schiz at all but something similar - Schizotypal personality disorder. Similar but milder.
(+) Advantage - all kids were carefully matched on variables. Study is fair and very controlled, helps eliminate CVs
(+) Other psychologist made New York High Risk Project. A longitudinal piece lasting 25 years and found similar results to Kety.
(+) A prospective longitudinal study is good because it looks at children before they have the illness and doesn’t rely on retrospective data because Schiz patients can have trouble with memory
