biological explanations

Question 1

what are biological explanations for sz?

Answer 1

• genetics
• dopamine hypothesis
• neural correlates

Question 2

why is it difficult to untangle the genetic contribution to sz?

Answer 2

there is evidence that sz runs in families, but share the same environment. is it nurture or nature.

Question 3

is sz an inherited disorder?

Answer 3

there is a strong relationship between the genetic similarity of family members and likelihood of both developing SZ.

people don’t inherit schizophrenia but they inherit a genetic predisposition to the disorder.

Question 4

what were Gottesman’s 1991 findings?

Answer 4

• carried out a family study and found concordance rates for sz.
  MZ Twins - 48%
  DZ Twins - 17%
  Siblings - 9%

Question 5

why does Gottesman’s study also suggest that there is an environmental component to sz?

Answer 5

even though schizophrenia runs in families, so single gene is thought to be responsible.

schizophrenia is polygenic (many genes are involved)

Question 6

what is the role of genetics in the aetiology of sz?

Answer 6

different combinations of these genes can lead to sz.

it is therefore aetiologically heterogenous.

Question 7

what were the findings by ripke et al (2014)?

Answer 7

• studied 37,000 patients.
• found 108 separate genetic variations associated with increased symptoms.

Question 8

why are adoption studies helpful in determining the etiological role of genetics?

Answer 8

adoption studies are useful for disintangling shared genes from the same environment.

Question 9

why are twin studies of limited use?

Answer 9

even though MZ twins share 100% of same DNA - they have a shared environment.

Question 10

what are the findings of Tienari (2000)?

Answer 10

• carried out an adoption study in Finland.
• of 164 adoptees whose bio mothers had sz, 6.7% were also diagnosed.
• this is compared to 2% of 197 control group.

Question 11

what is Tienari’s study support for?

Answer 11

this is support fir a genetic explanation for sz, but only that it increased the likelihood of developing sz.

Question 12

difficult to separate the impact of nature and nurture - AO3.

Answer 12

difficult to seperate the impact of nature and nurture.

e.g. both family and twin studies investigate individuals who are sharing the same env could be increasing the concordance rates, irrespective of genes.

possibly - high concordance rates between MZ twins is really due to them being treated more similarly than DZ twins and not due to genetics. even MZ twins that are reared apart shared the same env before birth.

shared env could be a confounding variable in the role of genetics in sz - we can’t differentiate between genetic and environmental influences.

Question 13

strong evidence from multiple sources.

Answer 13

strong evidence from multiple sources.

e.g. gotessman (closer degree of relatedness, greater risk od developing sz). adoption studies e.g. tienari showed that children of sufferers are at heightened risk than adopted families with sz.

this is overwhelming evidence to support genetics making people more susceptible to developing sz.

may be that genetics aren’t the only factor but does suggest genetic vulnerability.

Question 14

what its the dopamine hypothesis of sz?

Answer 14

dopamine = neurotransmitter.

original hypothesis = sz caused by excessive activity of dopamine in sub cortex.

this causes the neurone to respond to dopamine to fire too often + transmit too many messages. message overload = produces symptoms of sz.

Question 15

what is hyperdopaminergia? where is it taught to occur in the brain in patients with sz?

Answer 15

high levels of dopamine in subcortical areas projecting to Broca’s area may be associated with auditory hallucinations and/ or speech poverty.

it is now thought that people with sz have high numbers of D2 receptors.

Question 16

what did the original dopamine hypothesis state about hyperdopaminergia?

Answer 16

• subcortex in patients is excessively hyperdopaminergia.
• original hypothesis focuses on hyperdopaminergia.

Question 17

what is an alternative explanation that would cause excessive dopaminergic activity?

Answer 17

hypodopaminergia in the cortex.

the more recent version of the dopamine hypothesis focuses on abnormal dopamine systems in the cortex.

Question 18

how does Goldman-Rakic’s (2004) work revise the dopamine hypothesis?

Answer 18

• identified how low levels of dopamine in prefrontal Corte in negative symptoms of sz such as abolition.

prefrontal cortex is responsible for thinking and decision making.

Question 19

how is hypo and hyper dopaminergia thought to relate to different symptoms of sz?

Answer 19

may be that both are correct explanations - but low and high levels of dopamine in different brain regions are involved in sz.

Question 20

limitation: dopamine hypothesis.

mixed evidence AO3

Answer 20

mixed evidence.

one hand - amphetamines increase levels of dopamine and can make sz worse and antipsychotics reduce levels of dopamine and can reduce symptoms. however - ripe suggests there are other significant neurotransmitters other than dopamine that play a role.

current research has shifted and investigating role of glutamate e.g. glutamate blocker (ketamine).

may be that dopamine plays some role in development of sz but isn’t a complete explanation.

Question 21

what did Moncrieff (2009) suggest about evidence for the dopamine hypothesis?

Answer 21

claimed that evidence is far from inclusive as dopamine levels can be affected by stress and smoking.

Question 21

what does the neural correlates of something mean?

Answer 21

refers to the measurements of the structure of function of the brain that correlate with an experience, positive and negative symptoms have neural correlates.

this explanation = proposes that sz is caused by enlarged ventricles. enlarged ventricles are associated with damage to central brain areas and the prefrontal cortex. such damage is often associated with negative symptoms.

Question 22

what are enlarged ventricles?

Answer 22

fluid filled gaps between brain areas.

Question 23

what is an example of the neural correlates of sz?

Answer 23

Johnstone et al (1976) found that sz’s had enlarged ventricles while non-sufferers didn’t. suggests sz is related to a loss of brain tissue.

Question 24

what did the study by Juckel et al on the neural correlates of negative symptoms find?

Answer 24

he found a negative correlation between ventral striatum activity and overall negative symptoms of SZ.

Question 25

what is the ventral striatum?

Answer 25

a part of the brain that is involved in the reward pathway.

loss of motivation may be explained by low activity levels in this part of the brain.

Question 26

limitation of neural correlates: AO3
results are only correlational

Answer 26

results are only correlational.

e.g. it may be that lower ventral striatum activity may cause negative symptoms of SZ such as abolition but this abnormal activity may be caused by some other factor such as trauma.

it is therefore difficult to use this correlational evidence to imply causation as there may be other intervening factors like the environment which causes this affect.

it may be that the neural correlates argument in the development of sz but further research to determine the cause of the abnormal brain activities is needed.

Question 27

in what regard is research into the bio basis of sz socially sensitive? AO3

Answer 27

biological explanations have been thought to make patients appear less accountable for their disorders, which could increase clinician’s empathy.

to the contrary, bio explanations evoked less sympathy.

the results are consistent with other research and the theory has suggested that biological accounts of psychopathology can exacerbate perceptions of patients as abnormal and even less than fully human.

although the ongoing shift toward biomedical conceptualisations has many benefits, Lebowitz (2014) results reveal unintended negative consequences.