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
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
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
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
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
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
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
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
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
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
leads to question of whether high dopamine levels cause schizophrenia
or whether high levels are a result of schizophrenia
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