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One biological explanation for schizophrenia is the dopamine hypothesis. This explanation argues that the neurotransmitter dopamine is the main cause of schizophrenia. It suggest that schizophrenia is caused by an excess activity of dopamine in certain parts of the brain. It is not the amount of dopamine, but the sensitivity and density of dopamine receptors. Weinbereger (1987) argues that schizophrenia is due to dopamine overactivity in the pathways linking the midbrain to the limbic system, and under activity linking the midbrain to the cortex. This explanation was developed after it was found that antipsychotic drugs which lesson the symptoms of schizophrenia seem to decrease the dopamine activity. It could alternatively be that schizophrenic symptoms are caused by a high number of dopamine receptors on the receiving neurones, resulting in more dopamine binding to the neurones, thereby increasing the amount of dopamine in the system. Dopamine receptors control attention, this explains why disturbances in the dopamine receptors may well lead to problems in attention, perception which a symptom of schizophrenia.

Research by Davis updated the dopamine hypothesis as it showed that not all schizophrenics show high levels of dopamine. Davis suggested that high levels of dopamine in the prefrontal cortex system are associated with positive symptoms. Low levels of dopamine in the receptors of the prefrontal cortex are associated with negative and cognitive symptoms

A wealth of research such as supporting evidence for the dopamine hypothesis can be found by Wong et al (1986) 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. This supports the role of anti-psychotic drugs that work by either blocking dopamine receptor sites or depleting the levels of dopamine in the brain. This supports the dopamine hypothesis as if the symptoms of schizophrenia are reduced by the biological treatment (anti-psychotic drugs) then the biological cause must be plausible. This also suggest, the dopamine hypothesis does have practical applications because research by Wong has led to understanding of the brain’s functioning, Phenothiazines are used to treat schizophrenia by decreasing dopamine activity in the brain. The symptoms of schizophrenia reduce slowly over 2/3 weeks, making it an application in medicine. This is supported by Davis et al who carried out a meta-analysis asking the effectiveness of the dopamine treatment to a placebo and found that relapse occurred in 55% of placebo patients as opposed to 19% of those on the drugs, therefore suggesting the dopamine hypothesis does work and has practical applications.This therefore increases the validity of the dopamine hypothesis as an explanation for schizophrenia and the generalisability of the explanation.

However, the dopamine hypothesis is not entirely valid when looking at the causes of schizophrenia and is therefore reductionist. This is due to the explanation’s main proposal being excessive dopamine activity which cannot be the main cause of schizophrenia. By only focusing on the nature side of the nature and nurture debate and ignoring other behavioural and cognitive factors the explanation ignores individual differences and free will. This reduces the validity of the dopamine hypothesis as an explanation of schizophrenia.

Another biological explanation of schizophrenia is the genetic explanation. The genetic explanation argues that maladaptive genes or a combination of genes that can be inherited are the cause of schizophrenia. The genetic predisposition explanation argues that certain individuals inherit maladaptive genes which increase the likelihood of  the individual developing schizophrenia although, will only develop schizophrenia when interacting with other factors such as environmental and social factors. The absolute genetic explanation believes that genetics plays a major role in the cause of schizophrenia and indicates that the closer the genetic relationship to someone with schizophrenia the greater the chance of developing the disorder. Family and twin studies have consistently found the closer the genetic relationship between two people, if one of them has schizophrenia the greater the chance of them both having the disorder.

Gottesman carried out a meta-analysis and reported that whilst the rate of schizophrenia is 1% in the general population, if one MZ twin pair has schizophrenia there is a 48% chance of the other MZ twin developing schizophrenia. If both parents have schizophrenia there is a 46% chance of their child developing schizophrenia and the concordance levels for DZ twins were found to be 17% which is the same as one parent having schizophrenia. This research clearly supports the view that genetics are associated with schizophrenia as the concordance rates for MZ twins which are genetically identical are significantly higher than the DZ twins which are non-identical. However, critics are quick to point out that the finding of the study are not absolute. As if schizophrenia was purely based on genetics the concordance rates for MZ twins would be 100% and the concordance rates for DZ twins would be 50% however the studys findings showed MZ twins only had concordance rates of 48% and DZ twins 17%. This clearly shows environmental factors play a role in the cause of schizophrenia. Furthermore however, Gottesman reports that even when MZ twins are separated at birth the concordance rates for schizophrenia are much higher for MZ than DZ twins reared together which also shows a clear genetic role in the cause of schizophrenia. Even though the findings do not fully support the absolute genetic explanation, the genetic predisposition explanation can support the findings with their prediction that only some individuals with the inherited maladaptive gene will actually show symptoms of schizophrenia after interacting with other factors. Therefore weakening the validity of the absolute genetic explanation however strengthening the genetic predisposition explanation. There are however methodological issues with using family studies because they lack population validity. Only small samples can be used because twins are hard to find, meaning the results can’t be extrapolated to the general public. Furthermore, in family studies it’s hard to distinguish whether schizophrenia is caused by nature or nurture because families often share the same environment (nurture), thus making research into family studies low in internal validity because it’s not sure what’s being measured.

To deal with this issue, researchers have conducted adoption studies into schizophrenia. Tienari et al found that with 155 adopted children 10.3% of children with biological schizophrenic mothers had developed by adulthood compared to 1.1% of the control group. These finding support the genetic basis of schizophrenia.

Despite a large body of supporting research there is no conclusive evidence of a genetic marker that can be linked to all or even most types of schizophrenia. However, just because a gene has not been identified we cannot conclude the gene does not exist. Ridley argues that the Human Genome Project is making progress on identifying possible genes for schizophrenia and suggests that future research may one day identify a single gene or combination of genes that can account for all or most types of schizophrenia. Therefore giving valuable insight and reason for further research in the genetic explanation.