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Biological Explanations for Schizophrenia

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Outline and evaluate 2 biological explanations for schizophrenia.’ 24 Marks

One biological explanations for schizophrenia is genetic factors, which can be studied through twin studies. If the concordance rate is 100% in MZ twins it means that the characteristic is genetically determined because monozygotic twins share the same genes and environment. This was shown by Gottesman and Shields, who reviewed the results of 5 twin studies looking for concordance rates for schizophrenia. These studies looked at 210 MZ twins and 319 DZ twins. It was found that in MZ twins there was a concordance rate of 35-58% compared with dizygotic (DZ) twin rates that ranged from 9-26%. They also found a concordance rate in MZ twins of 75-91% when the sample was restricted to the most severe form of schizophrenia. This can show that there is a link with genetics and schizophrenia. However, the twin studies have all assumed that the shared environmental effects for MZ and DZ twins are equal which may be incorrect. In addition twins are not representative of the wider population. This is because it is a very small sample and there are very few MZ twins in the population and only 1% are Schizophrenic. This shows the sample may not be generalizable to the public.

In addition family studies support the idea that there is a genetic influence in schizophrenia. For example, if a parents is schizophrenic and a child becomes schizophrenic it would be likely that genetic factors responsible because children share 50% of their genes with each of their parents. Research has shown that the risk of schizophrenia risk rises with degree of genetic relatedness. For a child of someone who has schizophrenia, they have a 13% risk of getting schizophrenia. Whereas a spouse only has a 1% chance of getting schizophrenia which is the same as the general public. This shows that there could be a genetic factor towards getting schizophrenia as opposed to living with someone with schizophrenia without being biologically related.

In the same way, if adopted children have a higher concordance rate for Schizophrenia with their biological parents than with their adoptive parents, it would support the influence of genetic factors. Tienari (2000) study found that 6.7% of people were likely to get schizophrenia when their biological mother had schizophrenia in comparison to 2% of the control group. This research shows that there is a higher risk of developing schizophrenia when there is a biological influence, as opposed to an environmental influence.

The neuregulin gene supports the idea that there is genetic factors that influence schizophrenia. In 2006, an Edinburgh University team found people carrying a variant of a gene called Neuregulin had a higher chance of developing psychotic symptoms. However since then, research has shown that Schizophrenia involves a huge number of genes with each of them making only a small contribution to the development of the disorder (Robin Murray.)

The prevalence of schizophrenia is the same all over the world (about 1%) which supports a biological view as prevalence does not vary with environment.

However, there are variations within broad geographical areas. For example there were higher rates of Schizophrenia in Ireland (4%), Croatia and Scandinavian countries but low in Spain, Italy in some parts of Africa (Torrey 2002.) This shows that the environment may have a greater factor to explain schizophrenia.

Another biological explanation for schizophrenia is Biochemical Model. This suggests that there is a dysfunction of several neurotransmitter systems that are thought to play a part in schizophrenia. For example dopamine, 5-hydroxytryptamine and Glutamate.

The dopamine hypothesis supports the biochemical model as it suggests that Schizophrenia is caused by excessive DA activity. This causes abnormal functioning of DA-dependent brain systems, resulting in schizophrenic symptoms. DA can increase or decrease brain activity depending on the system. Furthermore the dopamine hypothesis states that the brain of schizophrenic patients produces more dopamine than normal brains. Evidence for this comes from studies with drugs, post mortems and pet scans.

From a post mortem Falkai (1988) found that people with schizophrenia have a larger than usual number of dopamine receptors. The increase of DA in brain structures and receptor density (left amygdala and caudate nucleus putamen.) He concluded that DA production is abnormal for schizophrenia.

Furthermore drugs, such as, Amphetamines (agonists) lead to increase in DA levels. Large quantities of these can lead to delusions and hallucinations. If drugs are given to schizophrenic patients their symptoms get worse. However, drugs may influence other systems that impact on schizophrenia so we can’t be 100% sure about their effects. In addition, there is a lack of correspondence between taking the drugs and signs of clinical effectiveness. It takes 4 weeks to see any sign that the drugs are working when they begin to block dopamine immediately. We cannot seem to explain this time difference.

PET scans have also shown how there can be a biochemical model for explaining schizophrenia. Lindstroem (1999) radioactively labelled a chemical L-Dopa and administered it to 10 patients with schizophrenia and 10 with no diagnosis. L-Dopa was taken up quicker with schizophrenic patients which suggests they were producing more DA than the control group. Although PET scans have also suggested that drugs did not reduce symptoms of patients diagnosed with disorder for 10 years or more.

Overall, this hypothesis shows that elevated level of dopamine in the brain are found in schizophrenic patients. Neurons that use the transmitter ‘dopamine’ fire too often and transmit too many messages or too often. Certain D2 receptors are known to play a key role in guiding attention. To help remove the symptoms of schizophrenia, DA activity could be lowered.

There can be many criticisms with the biochemical model such as it could be that the development of receptors in one part of the brain may inhibit the development in another. Therefore, it is questionable whether faulty chemicals cause schizophrenia or whether schizophrenia causes faulty chemicals. This can show that other things are involved for explaining schizophrenia such as other neurotransmitters, social and environmental factors. Therefore biological explanations can’t be used to explain schizophrenia alone.

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