976829
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Mapa Mental por kezzie.mutd, atualizado more than 1 year ago
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Criado por kezzie.mutd
quase 10 anos atrás
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2 or more biological explanations
of schizophrenia (AO2)
- Evaluation of family studies
- however studies are usually retrospective
- they look at the families of people already
diagnosed and therefore are inconclusive
- it could be that the greater risk is due to shared
environment rather than shared genes
- however studies are usually retrospective
- Evaluation twin studies
- 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
- to rule this out some researchers have looked at MZ twins reared apart
- Gottesman found concordance rates of 58% in MZ twins reared apart
- 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)
- as the twins share the same pre-natal environment,
environmental factors can still not be ruled out
- 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
- Evaluation of adoption studies
- adoption studies provide evidence of a strong
genetic link for schizophrenia
- however it still seems genes are only part of the story
- Tienari's data was re-examined
- 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
- adoption studies provide evidence of a strong
genetic link for schizophrenia
- Diathesis stress model
- seems that genes alone do not cause schizophrenia as the
concordance rates would be 100% in MZ twins
- a better explanation would be the diathesis stress model which suggests
we may inherit a genetic vulnerability for schizophrenia
- however would take an environmental trigger for the disorder to develop
- however would take an environmental trigger for the disorder to develop
- example of a trigger could be living in a family with poor
communication or experiencing stressful life events
- both have been found to influence relapses in schizophrenia
- both have been found to influence relapses in schizophrenia
- seems that genes alone do not cause schizophrenia as the
concordance rates would be 100% in MZ twins
- Molecular biology
- strong evidence for genetic factors has been
identified from molecular biology research
- Miyakawa et al (2003) - studied mutant mice
who lacked calcineurin in the forebrain
- reported that these mice developed schizophrenic type
behaviour - decreased social interaction, impaired attention,
impaired nesting behaviour, increased hyperactivity
- however we have to be careful extrapolating
findings from animals to humans particularly if we
are going to assign animals with human symptoms
- 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
- strong evidence for genetic factors has been
identified from molecular biology research
- Drugs do not always work
- in addition the drugs used to treat
schizophrenia that block dopamine
receptors do not work for all patients
- 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
- suggests that dopamine cannot be sole cause of schizophrenia
- suggests that dopamine cannot be sole cause of schizophrenia
- Healy (2000) - believes that the dopamine hypothesis has
been over promoted by the pharmaceutical industry
- they gain to make huge profits from developing
drugs that inhibit dopamine production
- they gain to make huge profits from developing
drugs that inhibit dopamine production
- in addition the drugs used to treat
schizophrenia that block dopamine
receptors do not work for all patients
- Evidence against - post mortem studies
- critics of the dopamine hypothesis suggest that there is very
little direct evidence for the involvement of the neurotransmitter
- one source of evidence for the hypothesis is that post-mortem studies
show that an increased level of dopamine in the limbic system
- however these have failed to account for whether the
patient has received treatment for the illness
- however these have failed to account for whether the
patient has received treatment for the illness
- it is possible that the drugs used to treat schizophrenia by blocking the
dopamine receptors are actually increasing dopamine levels
- been supported by other post mortem studies of schizophrenics which found
increased dopamine levels in patients who have been medicated
- those not medicated had normal levels
- those not medicated had normal levels
- leads to question of whether high dopamine levels cause schizophrenia
or whether high levels are a result of schizophrenia
- critics of the dopamine hypothesis suggest that there is very
little direct evidence for the involvement of the neurotransmitter
- Proximate and ultimate causes
- 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
- 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)
- for example high dopamine levels may be the proximate cause of symptoms such as hallucinations
- however the dopamine levels may have been ultimately caused by,
for example, genetic defects, stress or drug misuse
- 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
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