Biological explanations Flashcards
(20 cards)
What is the genetic explanation of psychology?
inherited disorder runs in families
faulty genes are passed on from generation to generation
How do Twin studies demonstrate Generic bias
Grottesman summarised findings of 40 twin studies and found concordance rate of 48% for MZ compaired to 17% for DZ
This shows that If MZ twins are more concordant than DZ twins then this suggests that the greater similarity is due to
genetics.
How do family studies demonstrate genetic bias?
Grottesman found that if both parents had schiz then there was a 46% chance of developing the disorder, 16% if one parent had schiz, 1% if there are no relatives with it
This shows that a higher concordance rate with children of two schizophrenic parents than just 1 suggests its due to genetics
How do adoption studies demonstrate genetic bias?
Tiernari studied 112 adopted children who were separated from their schiz mothers compared to 135 adopted kids without schiz mothers
By the time they reached adulthood 10.3% of those w/ schiz mothers developed schiz compared to 1.1% without
- shows that schiz genes still impacted children’s behaviour despite being in a different environment
What are candidate genes?
genes associated with risk of inheritance
How do candidate genes effect schizophrenia?
schizophrenia is polygenic - requires a no. of factors to work in combination
- schiz is aetiologically heterogeneous different combinations of factors lead to the condition
- shows there is no one single gene that causes schiz and multiple genes may have an influence
May explain why there are so many types of schiz
What are strengths of genetic bias as an explanation of Schizophrenia
Supported by evidence
Role of mutations
Evaluate supported by evidence as a strength of the genetic bias as an explanation of Schizophrenia
P: Evidence to support genetic vulnerability and the link to Schizo.
E: The Gottesman study clearly shows how genetic similarity and shared risk of schizophrenia are closely related. Adoption studies such as that Tienari et al. show that children of schizophrenia sufferers are still at heightened risk of schizophrenia even if adopted into families with no history of schizophrenia.
E: There is therefore overwhelming evidence for the idea that genetic factors make some people much more
vulnerable to developing schizophrenia than others.
L: This does not of course mean that schizophrenia is entirely genetic. There are a number of factors in the
environment associated with risk of schizophrenia, but the available evidence suggests that genetic susceptibility is
very important
Evaluate the role of mutations as a a strength of the genetic bias as an explanation of Schizophrenia
P: Role of mutation supports the genetic explanation
E: Schizophrenia can take place in the absence of a family history of the disorder. You would think this would critique
the genetic link. However, one explanation for this is mutation in parental DNA, for example, in paternal sperm
cells. This can be caused by radiation, poison or viral infection.
E: Evidence for the role of mutation comes from a study showing positive correlation between paternal age (associated with increased risk of sperm mutation) and risk of schizophrenia, increasing from around 0.7% with fathers under 25 to over 2% in fathers over 50
What is the dopamine hypothesis?
High and low levels if dopamine in different brian regions are involved in schizophrenia
What is hyperdopaminergia in the subcortex
Original version of the dopamine hypothesis
high levels of dopamine in the subcortex
- e.g an excess of dopamine receptors in the brocas area may be associated with poverty of speech and the experience of auditory hallucinations
What is hypodopaminergia in the prefrontal cortex?
Recent version of the dopamine hypothesis
low levels of dopamine in the prefrontal cortex (responsible for decision making) in the negative symptoms of schiz
What is a limitation of dopamine hypothesis?
Mixed evidence in support
Evaluate mixed evidence in support as a limitation of dopamine hypothesis?
P: We have mixed evidence in support.
E: Studies that support the hypothesis have found dopamine agonists like amphetamines that increase the levels of
dopamine make schizophrenia worse and can produce schizophrenia-like symptoms in non-sufferers
Antipsychotic drugs on the other hand, work by reducing dopamine Both kinds of drug study suggest an important role for dopamine in schizophrenia.
Studies that CRITIQUE the hypothesis show evidence to suggest that dopamine does not provide a complete
explanation for schizophrenia. Some of the genes identified in the Ripke et al study code for the production of other neurotransmitters, so it appears that although dopamine is likely to be one important factor in
schizophrenia, so are other neurotransmitters.
E: Evidence for the dopamine hypothesis can perhaps be best described as mixed and thus can it be considered a wholly accurate explanation of Schizophrenia considering it is the basis of the biological treatment.
Describe neural correlates of negative symptoms?
The negative symptom avolition involves the loss of motivation.
Motivation involves the
anticipation of a reward, and certain regions of the brain.
Abnormality of areas like the ventral striatum may be involved in avolition.
The ventral striatum are believed to be particularly involved in anticipation for reward.
Luckel et al measured activity levels in the ventral striatum in schizophrenia and found lower levels of activity than those observed in controls. They observed a negative correlation
between activity levels in the ventral striatum and the severity of overall negative symptoms.
Describe neural correlates of positive symptoms?
Allen et al scanned the brains of patients experiencing auditory hallucinations and
compared them to a control group.
They identified pre-recorded speech as theirs or others. Lower
activation levels in the Superior temporal gyrus and Anterior cingulate gyrus were
found in the hallucination group, who also made more errors than the control group.
We can thus say that reduced activity in these two areas of the brain is a neural correlate of auditory hallucination.
What is a limitation of Neural correlates as a genetic explanation of schizophrenia
Evidence is correlational
Evaluate correlational evidence as a limitation of Neural correlates as a genetic explanation of schizophrenia
P: There is a correlation-causation problem.
E: Although studies are useful in flagging up particular brain systems that may not be working
normally, this kind of evidence leaves some important questions unanswered. Most importantly, does the unusual activity in a region of the brain cause the symptom? Logically there are other possible explanations for the correlation.
E: For example, the correlation between levels of activity in the ventral striatum and negative symptoms of
schizophrenia. It may be that something wrong in the striatum is causing negative symptoms. However, it is just as possible that the negative symptoms themselves mean that less information passes through the striatum, resulting in the reduced activity.
L: We can never infer a cause and effect relationship and therefore this explanation is limited when attempting to
explain schizophrenia.
What is a limitation of the biological explanation of Schizophrenia
Reductionist
Evaluate reductionism as a limitation of the biological explanation of Schizophrenia
P: A limitation of the biological explanation is its failure to consider other explanations.
E: There are a number of other factors that could influence the probability of developing schiz such as the influence of the environment
E: Even in MZ twin studies we don’t have a 100% concordance rate suggesting other factors may be in play. There is
evidence that family functioning can play a role in the development of schizophrenia. This suggests that schiz may be the result of a both biological and psychological causes. This invokes the diathesis stress model which suggest you vulnerability and trigger for the development of the condition can be both biological and
psychological
