Describe and evaluate the genetic explanation of sch., including supporting studies.
Schizophrenia has been observed to run in families, as show by a study by Gottesman and Shields (1991), who found the following sch. concordance rates:
- MZ twins - 48%
- DZ twins - 17%
- Siblings - 9%
- General population - 1%
(+) Significant difference between MZ twins and other family relations, suggesting an at least partial genetic influence.
(-) MZ rate is not even close to 100% so can’t be wholly genetic, i.e. must be some environmental influence.
(-) MZ twins share a more similar environment than DZ twins, so the difference between MZ and DZ may not be genetic at all, but instead environmental influences.
Candidate genes for sch. have been identified by Ripke (2014), who analysed the genetics of 37000 schizophrenic patients and 113000 non-sch. patients. Ripke identified 108 candidate genes, i.e. sch. is polygenic.
(-) The fact that sch. is polygenic makes it very difficult to treat in real life.
Describe and evaluate the neurochemical explanation of schizophrenia.
The dopamine hypothesis has two parts; hyperdopaminergia and hypodopaminergia.
Hyperdopaminergia says that sch ppl have too many dopamine receptor sites in the subcortex, specifically in Broca’s area. This explains positive symptoms e.g. auditory hallucinations (i.e. speech production in one’s head) and speech poverty (which DSM considers positive) i.e. poor speech production.
Hypodopaminergia says that sch. ppl have low levels of dopamine in the prefrontal cortex, which is responsibe for planning and decision making, which can explain the negative symptom of avolition.
(+) Drug treatments that target dopamine seem to be very successful at treating sch.
(-) Treatment-causation fallacy
(-) Some of the 108 genes involved in sch code for another NT called glutamate; dopamine hypothesis may not be fully comprehensive.
(-) It’s been suggested that high levels of dopamine could actually be a symptom of schizophrenia, and not a cause => correlation not causation.
Describe and evaluate the neural correlates explanation of sch.
Positive symptoms may be caused by low levels of activity in the superior temporal gyrus, which is responsible for auditory processing, so under-functioning can lead to auditory hallucinations. Sch. patients also struggle to comprehend pre-recorded speech, suggesting under-functioning in the STG.
Negative symptoms may be caused by low activity in the ventral striatum which is responsible for the anticipation of rewards and motivation. Sch. patients have underfunctioning here so cant anticipate rewards and lack motivation i.e. avolition.
(+) Juckel et al (2006) did fMRI scans on 10 male unmediated sch patients and found sig under functioning in the left ventral striatum compared to a control of 10 healthy males
(+) Matsumoto et al (2001) did brain scanning on 40 sch patients and found sig under functioning in the right superior temporal gyrus compared to a control group
(-) both small sample sizes (especially Juckel)
(-) too reductionist
(-) too determinist
(-) Correlation, not causation; we don’t know whether the abnormal brain structures and functioning caused the sch. or if it is a symptom of the sch.