biological explanation of schz Flashcards
outline the genetic explanation of schz.
there is a strong relationship between the degree of genetic similarity and shared risk of schizophrenia.
while the rate of schz in the general population is 1%, if a parent has the illness there is a 6% likelihood that their child will also develop it. if one identical twin has it, that likelihood increases to 48% - Gottesman (1991).
schz is said to be polygenic - requires a number of genes to work in combination.
because different studies have identified different candidate genes it also appears that schz is aetiologically heterogenous - different combinations of genes can lead to developing the disorder.
discuss research evidence to support as a strength of the genetic explanation.
a strength of the GE is evidence from research support.
Gottesman (1991) found that there was a concordance rate of 48% for MZ twins and 17% for DZ twins for schz.
MZ twins share 100% of their DNA whereas DZ twins share around 50% - so these concordance rates suggest that genes do have at least some influence on the development of schizophrenia, supporting the explanation.
HOWEVER -
MZ twins only have a concordance rate of 48% despite sharing 100% of their DNA, which suggests that other factors must also be involved, such as psychological explanations including family dysfunction - limiting the validity of the explanation.
ADDITIONALLY -
there is further evidence that schz is not purely genetic, and environmental factors may influence the development of the condition. Gottesman around that fraternal twins have a higher risk of developing schz than normal siblings despite sharing the same number of genes.
As twins are likely to have been raised in a more similar environment than siblings, this suggests environment is a factor of schz and challenges further the validity of the explanation.
discuss adoption studies and evidence of candidate genes as a strength of the genetic explanation.
however, adoption studies clearly show that there is a genetic influence on the development of schz.
Tienari et al (2004) looked at adopted children whose biological mothers had schz and they had a concordance rate of 7%, compared to a 2% rate in adopted children who had parents without schz.
this clearly shows that despite their environment, children with a genetic similarity to someone with schz are at heightened risk of developing the disorder - supporting the explanation.
ADDITIONALLY -
there is also evidence showing particular genetic variations significantly increase the risk of schz.
for example, Ripke et al (2014) found 108 genetic variations that were associated with an increased risk of schz.
there is therefore evidence for the idea that genetic vulnerability increases risk of schz, supporting the genetic explanation.
outline the dopamine hypothesis as an explanation of schz.
dopamine is a neurotransmitter that is important in the functioning of several brain systems that may be implicated in the symptoms of schz.
the original version of the hypothesis focused on the possible role of high levels of dopamine in the subcortical areas of the brain (hyperdopaminerga) . an excess of dopamine receptors in Broca’s area may be associated with speech poverty or experiences of auditory hallucinations, for example. e
more recent versions of the hypothesis have instead focused on abnormally low dopamine levels in the prefrontal cortex. For example low levels of dopamine have been identified as associated with negative symptoms.
Discuss research evidence to support the dopamine hypothesis.
A strength of the dopamine hypothesis is that there is research evidence to support.
Wise and Stein 1973 report abnormally low levels of DBH in post mortem studies of schizophrenia patients. This would suggest abnormally high dopamine activity as DBH is needed to break dopamine down, which provides support for the original dopamine hypothesis - hyperdopaminerga.
HOWEVER -
we can’t rule out cause of death or post-mortem changes as a source of error causing low levels of DBH, so the support this evidence can provide the hypothesis is limited.
HOWEVER -
further evidence has found that schizophrenic patients do produce more dopamine.
researchers found that chemicals needed to produce dopamine are taken up faster in the brains of schizophrenia sufferers than control groups, suggesting they produce more dopamine.
this supports hyperdopaminerga, and increases the validity of the original dopamine hypothesis.
discuss evidence that abnormal dopamine levels isn’t a full explanation as a limitation of the dopamine hypothesis.
A limitation of the dopamine hypothesis is that there is evidence to suggest abnormal dopamine levels do not provide a full explanation for schizophrenia.
Researchers found that an overdose of amphetamine bracket (DA antagonist) can produce schizophrenia like symptoms, and schizophrenic patients have an abnormally large response to low amphetamine doses.
While this does provide support for the role of dopamine and schizophrenia as proposed by the hypothesis, it does suggest that the role of dopamine might be more complicated than the original hypothesis suggests - suggesting that the hypothesis may be too simplistic.
ADDITONALLY -
there is also evidence for other neurotransmitters that may be responsible for schizophrenia.
researchers found evidence for the role of glutamate in which it appeared that schizophrenia sufferers have a deficiency in glutamate function.
this suggests that the dopamine hypothesis is reductionist, and schz is not purely down to dopamine levels as a hypothesis suggests limiting the validity of the hypothesis.
outline the neural correlates explanation of schz.
Neural correlates are measurements of the structure or function of the brain that correlate with an experience, in this case schizophrenia. Both positive and negative symptoms have neural correlates.
Neural correlates include but are not limited to dopamine levels. There are other neural correlates which link to the symptoms of schizophrenia - such as brain areas.
Negative symptoms -
the brain area ventral striatum is highly involved and reward anticipation - If there is no anticipation of a reward there is no reason to engage in behaviours to bring about the reward.
Therefore the VS is a neural correlate of negative symptoms such as avolition, which involves motivation.
positive symptoms -
The Superior Temporal Gyrus contains the primary auditory cortex which is responsible for processing sounds.
Less activity here may lead to difficulties in detecting the origins of a voice, which could explain why auditory hallucinations occur.
discuss empirical evidence as a strength of neural correlates.
One strength of the neural explanation of schizophrenia comes from empirical evidence.
fMRI scans are used to detect a lower activity that has been observed in both these superior temporal gyrus and ventral striatum of patients. These objective recordings of abnormalities have been correlated with the expression of clinical symptoms of schizophrenia.
This is a strength of the neural explanation as there is empirical evidence to support neural corollaries in schizophrenia.
HOWEVER -
Despite this scientific evidence clearly demonstrating abnormalities in patients there is a problem with cause and effect.
Whilst it is clear the abnormalities in these superior temporal Gyrus and eventual striatum exist, due to the research being correlational we cannot determine if this is a cause of symptoms, or a result of symptoms.
this is a problem of causation as although we can see a clear pattern between symptoms and areas of the brain, we are unsure which one came first.
therefore, limiting our understanding of whether neural correlates can be said to be a true cause of schizophrenia.
discuss biological determinism as a limitation of neural correlates.
A further weakness of the neural explanation is that it is biologically deterministic.
whilst abnormalities in specific brain areas may well have an impact, just because someone has the specific abnormality it does not necessarily mean they will develop schizophrenia.
Therefore, the proposition that singular brain areas may be responsible for symptoms is a biologically deterministic standpoint.
This is a weakness of the explanation as it demonstrates that it does not account for other explanations, such as the environment or protective factors.
