2 or more biological explanations of schizophrenia (AO2)

kezzie.mutd
Mind Map by kezzie.mutd, updated more than 1 year ago
kezzie.mutd
Created by kezzie.mutd almost 6 years ago
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Mind Map on 2 or more biological explanations of schizophrenia (AO2), created by kezzie.mutd on 06/05/2014.

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2 or more biological explanations of schizophrenia (AO2)
1 Evaluation of family studies
1.1 however studies are usually retrospective
1.2 they look at the families of people already diagnosed and therefore are inconclusive
1.3 it could be that the greater risk is due to shared environment rather than shared genes
2 Evaluation twin studies
2.1 however it could be argued that there are still environmental influences as MZ twins would experience more similar environments than DZ twins as they look like each other
2.2 to rule this out some researchers have looked at MZ twins reared apart
2.3 Gottesman found concordance rates of 58% in MZ twins reared apart
2.4 however this represented a small sample (12 twins) and in many cases the twins were still brought up within the same family (e.g. by an aunt)
2.5 as the twins share the same pre-natal environment, environmental factors can still not be ruled out
3 Evaluation of adoption studies
3.1 adoption studies provide evidence of a strong genetic link for schizophrenia
3.2 however it still seems genes are only part of the story
3.3 Tienari's data was re-examined
3.4 found that it was only those children of a schizophrenic mother who were adopted into families with poor communication who were at increased risk of developing schizophrenia
4 Diathesis stress model
4.1 seems that genes alone do not cause schizophrenia as the concordance rates would be 100% in MZ twins
4.2 a better explanation would be the diathesis stress model which suggests we may inherit a genetic vulnerability for schizophrenia
4.2.1 however would take an environmental trigger for the disorder to develop
4.3 example of a trigger could be living in a family with poor communication or experiencing stressful life events
4.3.1 both have been found to influence relapses in schizophrenia
5 Molecular biology
5.1 strong evidence for genetic factors has been identified from molecular biology research
5.2 Miyakawa et al (2003) - studied mutant mice who lacked calcineurin in the forebrain
5.3 reported that these mice developed schizophrenic type behaviour - decreased social interaction, impaired attention, impaired nesting behaviour, increased hyperactivity
5.4 however we have to be careful extrapolating findings from animals to humans particularly if we are going to assign animals with human symptoms
5.5 however the research is backed up by studies in humans (e.g. Gerber) that suggest that people lacking the gene that produces calcineurin are more vulnerable to the disorder
6 Drugs do not always work
6.1 in addition the drugs used to treat schizophrenia that block dopamine receptors do not work for all patients
6.2 research suggests that approximately 25% of patients do not respond to medication and the medication only seems to be effective for the positive symptoms in others
6.2.1 suggests that dopamine cannot be sole cause of schizophrenia
6.3 Healy (2000) - believes that the dopamine hypothesis has been over promoted by the pharmaceutical industry
6.3.1 they gain to make huge profits from developing drugs that inhibit dopamine production
7 Evidence against - post mortem studies
7.1 critics of the dopamine hypothesis suggest that there is very little direct evidence for the involvement of the neurotransmitter
7.2 one source of evidence for the hypothesis is that post-mortem studies show that an increased level of dopamine in the limbic system
7.2.1 however these have failed to account for whether the patient has received treatment for the illness
7.3 it is possible that the drugs used to treat schizophrenia by blocking the dopamine receptors are actually increasing dopamine levels
7.4 been supported by other post mortem studies of schizophrenics which found increased dopamine levels in patients who have been medicated
7.4.1 those not medicated had normal levels
7.5 leads to question of whether high dopamine levels cause schizophrenia or whether high levels are a result of schizophrenia
8 Proximate and ultimate causes
8.1 one problem that the biological explanations have is that there are different types of schizophrenia and not one explanation seem to be able to explain all types
8.2 also it is not clear whether the explanations explain the immediate cause of certain symptoms (proximate cause) or the main cause of the illness (ultimate cause)
8.3 for example high dopamine levels may be the proximate cause of symptoms such as hallucinations
8.4 however the dopamine levels may have been ultimately caused by, for example, genetic defects, stress or drug misuse
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