Psychology

Biological Explanations Of Schizophrenia

Biological Explanations Of Schizophrenia

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Biochemical Explanation

One biological explanation of schizophrenia is the dopamine hypothesis. This biochemical explanation suggests that the characteristic symptoms of schizophrenia are the result of the overactive transmission of dopamine (a neurotransmitter in the brain). Schizophreniacs are thought to have abnormally high numbers of D2 receptors on reviving neurons, resulting in more dopamine binding and therefore more neurons firing. Dopamine neurons play a key role in guiding attention, so disturbances in this process may well lead to the problems relating to attention, perception and through found in people with schizophrenia (Comer).

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Evidence to support dopamine hypothesis comes from drug research; amphetamine drugs are dopamine agonists which means that they stimulate neurons containing dopamine causing the synapse to be flooded with this neurotransmitter. It has been found that large doses of these drugs cause hallucinations and delusions, similar to the symptoms seen in Paranoid Schizophrenia.

Similarly, research has shown that L-dopa, a drug used to treat Parkinson's disease  which also works by raising levels of dopamine, can result in symptoms similar to the positive symptoms of schizophrenia. This seems to show that an overactive transmission of dopamine could explain some of the positive symptoms of schizophrenia such as hallucinations.

A major strength of the dopamine hypothesis is that is had practical applications in developing treatments for schizophrenia. Typical antipsychotic drugs used to treat schizophrenia are all dopamine antagonists. This means that they work by reducing the stimulation of neurons containing dopamine by blocking D2 receptors and in doing so, reduce positive symptoms of schizophrenia. such as hallucinations and delusions. 

This is positive as not only does it show that the dopamine hypothesis has been useful in developing treatments that benefit the everyday lives of schizophrenia sufferers, it further strengthens the idea that dopamine is a key factor in explaining schizophrenia because reducing levels seems to reduce symptoms.

However it is wrong to assume that just because a treatment works by reducing a particular action in the body (dopamine reception) then this action must have caused the problem in the first place, this is known as the treatment-aetiology fallacy.

In fact, post-mortem studies have shown that schizophrenics who had high levels of dopamine had received antipsychotic drugs shortly before death whilst those that had not received medication, showed normal levels of dopamine. Therefore, this may indicate that high levels of dopamine in schizophreniacs may simply be a result of their medication. Indeed it has been suggested that by taking antipsychotic drugs that block dopamine reception, this makes neurons work even harder to try and compensate for this sudden reduction in levels leading to an increase in dopamine levels over time.

Furthermore newer antipsychotic drugs (called atypical antipsychotics) only temporarily block dopamine receptors (so in a sense they block dopamine less well), whilst also acting on serotonin receptors (another neurotransmitter) and these drugs have been shown to be more effective an the typical antipsychotics in reducing symptoms of schizophrenia. This seems to suggests that dopamine is not the sole cause of schizophrenia symptoms, the neurotransmitter, serotonin may also play a part in its onset.

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Genetic Explanation

The genetic explanation argues that schizophrenia is passed on from one generation to the next through genetic inheritance, therefore, in theory, the closer a family member is to the schizophreniac genetically, the more chance there is of them developing the disorder. Much of the evidence for this explanation comes from family, twin and adoption studies, these studies are used to establish a concordance rate (the degree to which the relatives share the same disorder). For example monozygotic (MZ) and dizygotic (DZ) twins, where one of each twin pair has schizophrenia, can be compared to see how often the other twin also shows signs of the illness. If schizophrenia is genetic then it is argued that MZ twins should have a higher concordance rate for the disorder than DZ twins.

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Evidence to support the genetic explanation comes from family studies, Verma found that 16% of first degree relatives of schizophreniacs developed the disorder compared to only 7% of the controls. This therefore supports the genetic explanation because there is an increased risk of schizophrenia if it runs in the family. 

Furthermore there is also support from Joseph who found a concordance rate of 40% for MZ twins compared to only just over 7% for DZ twins. This suggest the more genetically related you are with someone with schizophrenia, the more likely you to share the disorder.

- This essay is unfinished -

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