describe and evaluate one or more natural
Outline and evaluate one or more biological explanations of schizophrenia. In your evaluation you should refer to research facts. 24 represents According to the hereditary hypothesis, the more closely related the loved one to the schizophrenic the greater their chance of developing the disorder. Evidence via twin, family and adoption studies has maintained to indicate schizophrenia to have a hereditary component though a major problem is separating away environmental influences.
Recently gene mapping studies have been performed that review genetic materials from households with a high and low incidence of the disorder with results indicating several family genes rather than a solitary one to become at work to create increased weeknesses to expanding schizophrenia.
Support for the genetic disagreement was provided by Gottesman and Shields 1976 who examined 5 twin studies to find a concordance level of up to 91% between MZ identical twin babies with serious forms of schizophrenia implying genes to have a greater influence on chronic schizophrenia.
This was further more supported by Kety et al 1992 who also identified schizophrenics who had been used and in contrast the rate of schizophrenia to get 10 times larger among natural relatives, implying genes to play a much much larger role than environmental elements.
Nevertheless Leo 06\ argues Kety et al’s evidence being suspect because sample sizes were tiny making generalisation difficult and many of the biological relatives were rather far away ones just like half siblings and therefore low biological likeness.
In addition double studies never have gone devoid of criticism possibly; they may suggest a genetic influence although often usually do not consider the influence of social category and socio-psychological factors between twins. Furthermore Hedgecoe 2001 argues that scientists possess tried to construct schizophrenia being a genetic disease by using facts from double and usage studies in a biased method to create a story about schizophrenia that discreetly prioritises hereditary explanations.
As well even in rare cases wherever MZ baby twins are reared apart they still share the same environment in the tummy before labor and birth so the contribution of environmental factors cannot be entirely cheaper. A second biological explanation is definitely the dopamine speculation which believes schizophrenia symptoms occur as a result of overproduction from the neurotransmitter dopamine or of the super-sensitivity of the dopamine receptors.
Supporting evidence for the dopamine hypothesis comes from research into medicines that influence dopamine amounts in the mind. In healthful patients these kinds of drugs cause effects comparable to Parkinson’s disease and research has indicated that Parkinson’s disease is the result of a lack of dopamine in an area of the brain referred to as the fondamental ganglia. Amphetamines seem to improve the level of dopamine in the mind and studies have shown that giving amphetamines to sufferers of schizophrenia often worsens their symptoms.
Further support comes from post-mortem examinations which have shown schizophrenia patients had a greater denseness of dopamine receptors in certain parts of the brain than people not suffering from schizophrenia (Owen et ing 1978). However a problem with studies accomplished into amounts of dopamine and schizophrenia is they carried out “post mortem. Just for this we cannot say in case the increase in dopamine is a trigger or a result of schizophrenia. Furthermore brain-imaging studies have developed rather varying results. Farde et al. 1990) located no difference in the number of dopamine receptors between a schizophrenia group and a control group. The dopamine hypothesis is also over simplistic (reductionist).
Not necessarily as simple to express schizophrenics have got too high dopamine levels, such as other factors such as cognitive dysfunction and abnormal brain expansion (enlarged ventricles) also impact the happening of schizophrenia. There is also a insufficient consistency in the evidence for instance a studies have got found bigger levels of dopamine function nevertheless others have not.
This lack of reliability could possibly be due to the reductionism of only focusing on dopamine. Additionally dopamine does not take into account the variety of schizophrenic symptoms and seems more relevant to the positive symptoms. Finally effectiveness of medication used to concentrate on levels of dopamine do not help all patients and whilst they obstruct the dopamine receptors instantly, symptom comfort takes days or weeks, which displays there is not a direct link between dopamine and schizophrenia.
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