Biological explanations of SZ Flashcards

1
Q

Biological explanations of SZ

A

based on 2 factors:
- genetic basis
- neural correlates including the dopamine hypothesis

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2
Q

genetic basis

A

normally tested through:
- family
- twin
- adoption studies

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3
Q

family studies - genetic basis

A
  • find individuals who have SZ + determine whether their biological relatives are similarly affected more often than non-biological relatives
  • Gottesman (1991) found that if both parents were SZ, the likelihood of the offspring also having SZ was 46%
  • if only one parent, likelihood dropped to 13%
  • if a sibling, likelihood was 9%

= the closer you are genetically related, more likely to get SZ

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4
Q

twin studies - genetic basis

A

As MZ twins share 100% of their genes, whereas DZ share 50% (me and tanz)
= if SZ is genetic, then concordance rates should be higher for MZ than DZ twins
- Gottesman found 48% concordance rate for MZ and 17% for DZ
= more genetically similar you are then the more likely you are to get SZ

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5
Q

adoption studies - genetic basis

A

adoption studies carried out to understand the influence of nature + nurture

= a study carried out in Finland, found that 164 adoptees who biological mothers had SZ, 11(6.7%) were also diagnosed w/ SZ - compared to control group of 197 adoptees where only 4 (2%) were diagnosed w/ SZ

= shows that overall %age of children (who’ve been adopted by non-SZ parents) having SZ was very low

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6
Q

candidate genes

A

SZ is polygenic = there is a combination of different genes that have been implicated in SZ

  • study compared the genetic makeup of 37000 SZ patients worldwide + found that 108 separate genetic variations were associated with an increased risk of SZ

= the genes that were particularly vulnerable were the ones associated to the functioning of certain neurotransmitters e.g. dopamine

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7
Q

ads of genetic basis of SZ

A

there is a wealth of research evidence to support the genetic basis for SZ, shown through Gottessman, Joseph’s + Tienari’s study:
- there is a link between genes + SZ
- this is a strength cus if a child grows up in a family where both their bio parents has SZ, then the chances of them getting SZ is heightened compared to only one/ none of the parents having it
= genetics is an important factor

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8
Q

disads of genetic basis of SZ

A
  • separating nature + nurture
  • DNA mutation
  • diathesis stress model
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9
Q

separating nature + nurture - disads of genetic basis of SZ

A

difficult to separate nature (genes) from nurture (environment)
= look at adoption studies that attempt separate genes from the environment, children are raised by relatives in a similar way to biological parents
= adoption studies may not always be a good comparison for the effects of nature + nurture

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10
Q

DNA mutation - disads of genetic basis of SZ

A

SZ can take place in the absence of a family history
- may be a mutation in parental DNA
= supported by study where a positive correlation was found between paternal age + increased risk of SZ
- from around 0.7% w/ fathers under 25 to over 2% w/ fathers over 50
- no direct genes are involved, but a person can still get SZ if their father was older at the time of fertilisation

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11
Q

diathesis stress model - disads of genetic basis of SZ

A

the diathesis stress model suggests that there is a genetic vulnerability in SZ
= this vulnerability is only triggered if there is a stress-trigger - if your life is stress-free then you may not end up having the disorder
= thus we need to be cautious when looking at genetic factors since they alone may not trigger SZ

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12
Q

the dopamine hypothesis - neural correlates

A
  • neurotransmitters are the brains chemical messengers
  • claims that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with +ve symptoms fo SZ
  • the messages from neurons that transmit dopamine fire too easily + too often (more dopamine binding + neurons firing)
    = leading to hallucinations/ delusions
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13
Q

two consequences of the dopamine hypothesis

A
  • hyperdopaminergia
  • hypodopaminergia
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14
Q

hyperdopaminergia

A
  • consequence of the dopamine hypothesis
  • when there are high levels of dopamine which link to positive symptoms of SZ
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15
Q

hypodopaminergia

A
  • consequence of the dopamine hypothesis
  • when there are low levels of dopamine which link to negative symptoms
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16
Q

ads of the dopamine hypothesis

A
  • supporting research
  • antispychotic antagonist drugs
17
Q

disads of the dopamine hypothesis

A
  • other factors involved
  • correlation-causation problem
18
Q

supporting research - ads of the dopamine hypothesis

A

there is drug research to support the dopamine hypothesis
= dopamine agonists tend to increase dopamine levels + make the SZ symptoms worse, supporting the idea of hyperdopaminergia

19
Q

antipsychotic antagonist drugs - ads of the dopamine hypothesis

A

antipsychotic drugs act as antagonists to reduce the levels of dopamine (help control symptoms)
= supports the idea that dopamine levels are high in SZ + can be reduced through drugs

20
Q

other factors involved - disads of the dopamine hypothesis

A

the dopamine hypothesis cannot be seen as the sole cause of the SZ as there are other biological + psychological factors that contribute e.g. upbringing of family dysfunction or cognitive explanations
- also more research has found that dopamine may not be the only neurotransmitter responsible for SZ, research conducted on glutamate + seretonin

21
Q

correlation-causation problem - disads of the dopamine hypothesis

A

we don’t know whether the individual started having excess levels of dopamine + started experiencing symptoms of SZ OR did the individual first experience symptoms of SZ and consequently have high levels of dopamine?
= doesn’t explain cause + effect