Biological explanations for Sz Flashcards
what does the genetic explanation say about schizophrenia
- multiple gene alleles that increase the risk of developing schizophrenia
- if members of our family have schizophrenia we are more likely to develop schizophrenia
- the more genetic risk alleles a person has, the more likely they are to develop schizophrenia
what was tienari et al method for the adoption study on schizophrenia
- study supports the genetic explanation
- the experimental group was adopted children whose biological mothers had schizophrenia
- the control group was adopted children whose biological mothers did not have schizophrenia
what were the finding about the adoption study
- children with biological mothers with schizophrenia were more likely to develop schizophrenia themselves
- similarities between child and biological mother were due to genetics
- genetics had more of an influence on schizophrenia development than the environment
what are limitation of adoption studies
- they assume that any similarity between biological parent and adopted child is solely down to genetics
- they ignore similarities in environment shared by biological parent and adopted child
what are the limitations of Tienaris adoption study
- assume similarities between biological parent and adopted child is solely down to genetics - ignore similarities shared by biological parent and adopted child
what is Gottesman family studies
both parents suffer from Sz = 46% chance
1 Sz parent = 13%
sibling with Sz = 9%
the more genetically similar relatives are, the higher concordance rate is found
weakness of Gottesman family studies
problem of nature vs nurture. Very difficult to separate the differences. the fact that the concordance rate cannot wholly be explained by genes + could be that the individual has a predisposition to Sz which simply puts them more at risk. This suggests that the biological account cannot give a full explanation of the disorder
what did Gottesman find in the twin study
gottesman found that Mz twins have a 48% risk of getting Sz but Dz have a 17% risk rate. Evidence shows the higher the degree of genetic relatives ness higher risk of getting Sz
evaluation of Gottesman twin studies
- fail to look at the social class and social psychological difference, between twins
- tend to use small samples
Joseph (2004) pointed out that Mz twins are treated more similarly that Dz. so still could be a cause of environmental factors
Question $3.$ Explain what assumption about the phenotypes expressed by an individual is made in twin studies
Phenotype is the characteristic we express when our genes interact with the environment. Twin studies assume that the environmental impact on phenotype is equal for both monozygotic and dizygotic twins. This means that any difference in concordance between monozygotic and dizygotic twins must be due to their genetic similarity.
limitation of adoption in essay format
Adoption studies assume that the biological parent has no environmental influence on the child. However, children are often paired with adoptive parents who come from a similar background and live in a similar area. Therefore, while there is no direct influence, the adopted child may still grow up in an environment similar to how they would have grown up with their biological parent. This is a limitation because adoption studies may be over-exaggerating the genetic influence on the child, because they are ignoring the potentially shared environment between the adopted child and biological parent.
what does the neural correlates of schizophrenia say
say that schizophrenia is caused by abnormal brain structure
people with schizophrenia have larger ventricles and smaller frontal cortex
what did joseph (2004) point out about twin studies
pointed out that MZ twins are treated more similarly than DZ, so there still could be a cause from environmental factors
neural correlates: support study
Torrey conducted MRI scans on people with schizophrenia
Torrey compared scans with people with schizophrenia and people with healthy
what are the findings of Torreys brain imaging study
Torrey found that people with schizophrenia had 15% large ventricles than those in the control groups
Torrey study supports the neutral correlates of schizophrenia
what are the limitations of the neural correlates hypothesis
- we do not have sufficient evidence to conclude that brain abnormalities cause schizophrenia, because the evidence obtained from MRI studies are correlational (cant establish cause and effect)
- the drugs that patients take to treat schizophrenia may act as a confounding variable in studies of neural correlates
- there are individual differences in the brain abnormalities displayed in patients with schizophrenia- not all patients display enlarged ventricles, study support doesn’t always replicate
Sarah was always an eccentric child, who grew into an adult with symptoms consistent with schizophrenia. She was diagnosed in her early 20’s, and was given lots of medication to reduce her symptoms.
However she became skeptical of this diagnosis, and asked for another doctor to take a closer look. The doctor conducted an MRI scan, and was able to show Sarah that she had a brain structure that had similarities with someone typically experiencing schizophrenia (i.e. enlarged ventricles.)
Question $6$. Explain one limitation of studies investigating the neural correlates hypothesis, with reference to the scenario given.
One limitation is that the evidence from these studies is correlational - it does not prove that brain abnormalities are causing schizophrenia, only that there is a correlation between these two factors. For example, taking certain medications could cause a side effect where people develop larger ventricles, which could act as a confounding variable in the research. In Sarah’s case, she may have developed enlarged ventricles after consistently taking the medication she was given after her diagnosis. Therefore, studying people who are already on medication does not necessarily show that they have schizophrenia because of these enlarged ventricles.
what are neural correlates
variations in neural structure and biochemistry that are correlated with an increased risk of developing Sz
what does dopamine do
involved in processing reward and in controlling attention
what are dopamine levels like in people with schizophrenia
- people with schizophrenia have higher levels of dopamine than healthy people
- the neurones with people with schizophrenia generate more electrical activity than those without schizophrenia
what does the dopamine hypothesis say
people with schizophrenia have a higher level of dopamine than normal in their mesolimbic system which causes higher activity of neurones in mesolimbic system leading to hallucination’s and delusions
what is true according to the revised dopamine hypothesis
- people with schizophrenia have higher levels of dopamine in the mesolimbic pathways
- overactivity in the mesolimbic system causes the positive systems of schizophrenia
- people with dopamine have lower levels of schizophrenia in the frontal cortex
- underactivity causes negative symptoms
According to the dopamine hypothesis, which symptoms of schizophrenia are caused by overactivity of the mesolimbic system?
positive symptoms
- hallucinations
- delusions
Question $4$. What does the original dopamine hypothesis state about the frontal cortex?
The original dopamine hypothesis did not say anything about the frontal cortex. This came later in the revised dopamine hypothesis.