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Biological Explanations of Schizophrenia (24 Marks)

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Discuss biological explanations of schizophrenia
AO1- (4 marks)
Biological explanations of schizophrenia argue that the causes of schizophrenia and physiological rather than psychological. Evidence to support this comes from research into genetics, as well as biochemical factors. Firstly, genetic research has considered rates of schizophrenia found in biological relatives, monozygotic twins (MZ) and dizygotic twins (DZ). This research includes family studies. Schizophrenia is more common among biological relatives with schizophrenia and the closer then family member e.g. a sister the greater the risk of developing schizophrenia. They found children with 2 schizophrenic parents have a concordance rate of 46% compared with children who have one schizophrenic parent, concordance rate is 13%. In addition, MZ twins have a higher concordance rate at 40.4% than DZ twins at 7.4% in terms of developing schizophrenia. Researchers have also tried to find twins separated at birth and at least one twin was diagnosed with schizophrenia. Gottesman and Shields found 58% of twins were concordant for schizophrenia. In contrast, more recent studies, using blind studies, have reported lower concordance rates for MZ twins. However, it is still arguing findings support the genetic inheritance of schizophrenia. Similarly, adopted children are looked at to test whether schizophrenia is an environmental influence or genetically inherited. They have been looking at children who were adopted and later diagnosed with schizophrenia, then comparing them to their adopted and biological parents. Tienan found 164 adoptees whose biological mother had been diagnosed with schizophrenia was 6.7% and 194 control participants (non schizophrenic parents) was 2%.
AO2- (8 marks)
Evidence that supports schizophrenia having a genetic cause comes from Kety who looked at supporting evidence e for a genetic cause. They looked at twin studies to distinguish whether schizophrenia is caused by genetics than environment. They found twins separated at birth that develop schizophrenia were 21% more likely to have a relative with schizophrenia. Compared with their adoptive family, where it is 5% more likely to have schizophrenia. This tells us that genetic links produce a higher concordance rate than adoptive parents when looking at schizophrenia. As the percentage is higher, this provides sufficient proof it is partly caused by genetics.
However, there are problems with the genetic explanation. This is shown by a reductionist critique. This point argues, if schizophrenia were entirely genetic the results from the studies would be 100% for MZ twins and 50% for DZ twins. However findings from genetics studies are a lot lower than this. Therefore other factors must be involved such as stressful life events such as divorce that could set off schizophrenia. This suggests that schizophrenia is not only genetic but has to have external influences too. This means the genetic theory is unable to explain the onset of schizophrenia alone.
A further weakness is problems with environmental control. Joseph pointed out that MZ twins are more likely to have the same lifestyle and do similar activities than DZ twins. They are more likely to have identity confusion (being treated as 1 rather than 2). Therefore the concordance rate have little to do with genetics but the environment they’re in. This shows that the genetics argument is invalid due to the two sets of twins having different upbringings and the DZ twins having a more separate lives. This means the concordance rates are directly linked to this suggesting it is not nature but nurture.
A further weakness is family studies focussing on the past rather than the present. Family studies focus on the past events when they should look at longitudinal studies. It is more valid this way as it follows participants over a period of time, and make comparisons before and after diagnosis and treatment. This suggests that as the criteria is ever changing, the past studies cannot be compared to current studies.
AO1- (4 marks)
Secondly, biochemical factors such as dopamine levels in the brain have found to be linked to schizophrenic symptoms. Dopamine is a neurotransmitter (a chemical that acts as a messenger in the brain, transmitting impulses from one nerve cell to another across synapses). The dopamine hypothesis states that the presence of and excess dopamine receptors in the brain contributes to schizophrenia or the dopamine receptors fire too easily, leading to characteristics of schizophrenia. Evidence for the role of dopamine in schizophrenia has been found across 3 areas: Amphetamines, anti- psychotics and Parkinson’s disease. Amphetamines increase the effects of dopamine, this stimulates nerve cells containing dopamine. Large doses of this creates hallucinations and delusions. This means dopamine must be linked to schizophrenia as the symptoms are similar. Antipsychotics block to activity of dopamine. This leads to a reduced sense of hallucinations. This is a strength in the point that dopamine is involved in the symptoms of schizophrenia. Parkinson’s disease sufferers contain low levels of dopamine so have to take medication which increases the levels of dopamine. They can develop symptoms of schizophrenia, such as violence and hallucinations.
AO2- (8 marks)
Evidence that supports schizophrenia having a biochemical cause comes from post mortems, seen an increase in dopamine receiving parts of the brain. However, post mortems could be misleading. When examining a body, there is no indication that a person received treatment for the condition. The excess of dopamine could be a treatment for Parkinson’s rather than a natural occurrence. This suggests that dopamine levels do not directly relate to schizophrenia. The levels could suggest Parkinson’s rather than schizophrenia.
A limitation of the biological theory is, there is difficulty in establishing cause and effect. There is confusion among psychologists that we are unsure whether one causes the other. For example does the increase in dopamine cause schizophrenia or is an increase in dopamine the result of schizophrenia. This suggests, there is still controversy over cause and effect, this then lacks validity. As the dopamine levels could just be because the person has schizophrenia it is difficult to distinguish the cause and therefore it is not valid.
Another limitation is, there are problems with the effectiveness of drug treatment. There is reason to suggest that biochemistry is not the only factor to cause schizophrenia. This means, levels of dopamine may not at all cause schizophrenia. Some people do not react at all to drug therapy and some react differently depending on the type of schizophrenia. This suggests, biochemistry alone cannot be the sole cause of the schizophrenia and extraneous variables should be taken into account.
Lastly, the biochemical theory is reductionist. This means a complex disorder such as schizophrenia is reduced into simple levels of explanation. For example, an imbalance of chemicals in the brain. The argument is, it ignores any other cause such as stress levels or irrational thought processes. This suggests that schizophrenia is not simple enough to be explained by one element. It is a mixture of several complex aspects which the biochemical explanation ignores.

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