biological explanations of schizophrenia

Question 1

genetic: inheritance

Answer 1

there is evidence that sz runs in families and is somewhat genetic

Question 2

family studies

Answer 2

• suggest the closer the genetic relationships to someone with sz, the greater the chance of developing it
• gottesman (1978) - the rate in the general population is 1%, the chance of 1st-degree relatives developing it is 12%, if both parents have it there’s a 40% a child of theirs will develop it
• tsuang et al (1990) - 1st degree relatives of someone with sz have a 5-20 x higher risk of developing it

Question 3

twin studies

Answer 3

• if mz twins have a higher concordance rate than dz twins, it suggests a degree of heritability
• gottesman and shields (1972) - concordance rate of 42% for mz and 5.3% for dz twins

Question 4

adoption studies

Answer 4

• an issue with comparing concordance rates of people in the same family is that they share the same environment
• adoption studies allow us to isolate the effects of environmental and genetic factors
• heston (1966) - compared 47 adopted children with sz mothers and 50 children who lived in the same homes as them. 17% of the experimental group and none of the control developed sz. the 47 were also more likely to have other disorders and be involved in crime

Question 5

genetic: specific genes

Answer 5

• many genes are implicated in sz, suggesting it is polygenic. and since different studies have identified different candidate genes, it appears to be aetiologically heterogeneous
• miyakawa et al (2003) - found those with sz were more likely to have a defective version of a gene PPP3CC
• sherrington et al (1988) - found a gene located on chromosome 5 linked in some extended families with sz
• research implicates different genes - is it one gene of several together?

Question 6

give a limitation of genetic explanations
1/3

Answer 6

genetic factors can’t be the sole factor as the concordance for mz is only 40-60%, so genes cannot wholly explain sz. a person may be predisposed to it making them more at risk. by focusing only on one factor (genes) it takes a biologically reductionist approach. using this approach leads to an explanation that doesn’t explain this 40-60% concordance rate

Question 7

give a limitation of genetic explanations
2/3

Answer 7

it is hard to separate nature and nurture in family and twin studies, the shared environment could increase the concordance rate irrespective of genes. high concordance rates between mz twins may be due to them being treated more similarly than dz twins or regular siblings. and mz twins raised apart still share the womb environment before birth. this shared environment could be a confounding variable as we can’t separate genetic and environmental factors

Question 8

give a limitation of genetic explanations
3/3

Answer 8

family studies collect retrospective data by comparing a cross-section of people who are already diagnosed, this can be unreliable as issues in memory and records are likely. prospective studies may be more accurate as they follow people over time and can allow for comparisons before and after the condition occurs

Question 9

give a strength of genetic explanations
1/1

Answer 9

lots of research support (see above)

Question 10

the dopamine hypothesis

Answer 10

• dopamine is a neurotransmitter that causes neurons to fire, its responsible for transmitting signals between neurons in the brain
• the theory was updated by davis et al (1991) as high dopamine levels aren’t found in everyone with sz. they found the anti-sz drug clozapine (with little dopamine blocking activity) worked against sz

Question 11

the original dopamine hypothesis

Answer 11

hyperdopaminergia in the sub cortex
- focused on the possible role of high levels or activity of dopamine in the subcortex
- this excessive activity causes the neurons that respond to dopamine to fire too often and transmit too many messages
- this overload may produce many symptoms of sz

Question 12

the recent dopamine hypothesis

Answer 12

hypodopaminergia in the cortex
- focused on abnormal dopamine systems in the brains cortex which could explain negative symptoms
- abnormally low levels of dopamine activity

Question 13

give a limitation of the dopamine hypothesis
1/3

Answer 13

newer drugs like clozapine are more effective than traditional ones. these affect other neurotransmitters like serotonin alongside dopamine, suggesting several neurotransmitters are involved in the development of sz. therefore this explanation may be too simplistic.

Question 14

give a limitation of the dopamine hypothesis
2/3

Answer 14

there is an issue with cause and effect: are the raised dopamine levels the cause or result of sz? lloyd et al state if dopamine is a causing factor, it is an indirect one mediated by environmental factors (e.g. abnormal family circumstances can cause high dopamine). therefore cause and effect cannot be established

Question 15

give a limitation of the dopamine hypothesis
3/3

Answer 15

dopamine abnormalities aren’t present in everyone with sz, especially those with neg symptoms. dopamine issues are associated more with pos symptoms so may only explain certain aspects of sz. davis et al (1991) suggests the variation of symptoms and types of sz implies several neurotransmitters are involved

Question 16

give a strength of the dopamine hypothesis
1/2

Answer 16

it has real-world practical applications such as the development of effective treatments. due to research drugs like clozapine have been developed, which is more effective in treating sz behaviour than neuroleptics. therefore psychiatrists can understand the role of neurotransmitters when treating sz

Question 17

give a strength of the dopamine hypothesis
2/2

Answer 17

research suggests people with sz have more dopamine receptors, which may lead to more neural firing and so an over-production of messages. autopsies show a larger number of dopamine receptors, and an increased amount of dopamine in the left amygdala, caudate nucleus and putamen in those with sz. this suggests there is evidence of dopamine abnormalities in the brains of people with sz

Question 18

neural correlates

Answer 18

• sz is due to structural and functional brain abnormalities, specific brain areas are linked to the disorders development
• research used to be limited to post mortems, but now uses non invasive scans like fMRIs. therefore the functioning of sz brains can be compared to those without it to identify brain areas linked to sz
• it proposes that sz is caused by enlarged ventricles (the fluid-filled gaps between brain areas), which are associated with damage to central brain areas and the prefrontal cortex which is linked to neg symptoms

Question 19

give a limitation of neural correlates
1/3

Answer 19

research suggests enlarged ventricles only explain certain symptoms. weyandt (2006) stated they are only associated with neg symptoms. therefore this explanation can’t explain all aspects of sz

Question 20

give a limitation of neural correlates
2/3

Answer 20

research into the role of enlarged ventricles is inconclusive. some people without sz have them and some with sz don’t have them. this contradicts the idea that sz is linked to a loss of brain. if this were the sole cause of sz, everyone with enlarged ventricles would have the disorder

Question 21

give a limitation of neural correlates
3/3

Answer 21

evidence suggests those with sz that don’t respond to medication are those with enlarged ventricles. it may in fact be that the sz causes long term brain damage (enlarged ventricles) rather than it causing sz