Neural and Hormonal causes of aggression. However, control females only given testosterone as adults did not react in this way Edwards ,
This essay will cover both genetic and neural explanations of schizophrenia. Most evidence comes from research using family studies which indicate that the closer the genetic relationship to someone with schizophrenia the greater the chance of developing the disorder Gottesman Overall, Tsuang et al estimate that if stringent criteria are used, a first degree relative of schizophrenia has times higher risk of it developing than those with no relatives.
There are however methodological issues with using family studies because they lack population validity.
Further evidence to support the genetic explanation comes from twin studies. In general, it is reasonable to assume that if identical twins MZ have a higher concordance rate than fraternal DZ twins, then this indicates a degree of inheritability. Although other studies have shown other rates, all twin studies have shown a significantly higher rate among MZ than DZ twins, therefore suggesting that research into this area is reliable, making the genetic explanation academically credible to explain schizophrenia.
However, there are issues with using twin studies. Joseph would argue that the differences in concordance rates between MZ and DZ twins reflect nothing more than the environmental differences that establish the two types of twins.
Taking this argument, twin studies like family studies also fail to distinguish between nature and nurture. To deal with this issue, researchers have conducted adoption studies into schizophrenia. Tienari et al used Finnish adoptees whose biological mothers had been diagnosed with schizophrenia.
Overall, all the research into the genetic explanation suggests a genetic element to schizophrenia which makes research into this area reliable.
The theory is also reductionist because it ignores the main role of nurture, however it does state that a predisposition is inherited allowing for the role of nature in the initiation of the illness. Alternatively, the dopamine hypothesis suggests that schizophrenia occurs from an excess activity of dopamine in certain parts of the brain.
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It is not the amount of dopamine, but the sensitivity and density of dopamine receptors. Weinbereger argues that schizophrenia is due to dopamine overactivity in the pathways linking the midbrain to the limbic system, and underactivity linking the midbrain to the cortex.
Supporting evidence for the dopamine hypothesis can be found by research by Wong et al who conducted PET scans on medication free schizophrenics, those taking phenothiazines and normal controls matched for age.
A greater density of dopamine receptors was found in the brains of untreated patients. Phenothiazines are used to treat schizophrenia by decreasing dopamine activity in the brain.
In conclusion, the dopamine hypothesis is not entirely valid when looking at the causes of schizophrenia and is therefore reductionist.According to the importation model, institutional aggression is caused by the people in the institution rather than a result of the institution itself.
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