A study by Tienari compared 112 adopted children of schizophrenic birth mothers with a control group of 135 children of non-schizophrenia birth mothers. Only 1.5% of the control group was diagnosed with schizophrenia later in life compared to 7% in the experimental group. This again suggests a genetic component to schizophrenia.
All these studies support each other and this therefore shows there is a predisposition to schizophrenia. However, concordance rates are not 100%, so it cannot be said that genetics is the only cause.
The dopamine hypothesis applies only to type 1 - positive, paranoid schizophrenia. There is some evidence for the dopamine hypothesis. Phenothiazines (Anti-Psychotic drugs since schizophrenia is called as a Psychotic illness) block dopamine levels in the brain and they reduce the positive symptoms of delusions and hallucinations, but have little effect on negative symptoms such as apathy and immobility.
Taking amphetamines in large doses causes an individual to show symptoms similar to schizophrenia for example, hallucinations and delusions. Amphetamines are known to increase levels of dopamine in the brain.
There is also evidence against the dopamine hypothesis. Phenothizines block dopamine in the brain rapidly but fail to reduce the symptoms of schizophrenia for days or weeks thereafter.
It has been noted that Clozapine (a new drug for schizophrenia) blocks dopamine activity less then Phenothiazies and therefore should be less effective in treating schizophrenia. However, there is growing support for the view that Serotonin as well as dopamine plays a part in producing the symptoms of schizophrenia and Clozapine blocks both of these neurotransmitters.
A study by Kammen shows that on certain occasions taking amphetamines can lead to a reduction in the symptoms of schizophrenia.
The evidence for the dopamine hypothesis is correlational, therefore it cannot be concluded that schizophrenia is caused by an excess of dopamine.
Another explanation is Neuroanatomy, there seems to be evidence that there are structural differences in the brains of schizophrenia and non-schizophrenics. Brown for example has noted that many schizophrenics have lighter brains with enlarged ventricles. However, a study by Pearlson has failed to replicate these findings. It is also possible that the ventricular enlargement could be the result rather than the cause of schizophrenia. Coger and Seraftinides suggest that enlargement of the corpus callosum is associated with the negative symptoms of schizophrenia and there is some support for this. However, we need to consider how these differences in brain structure have occurred. Seidman states only around 25% of schizophrenica have any form of brain abnormality and this may be the result of anti psychotic drugs. Mednick disagrees and states that differences in brain structure are the result of an infection by a virus during foetal development. There is evidence that mothers exposed to flu during their third to sixth month of pregnancy are more likely to have schizophrenic children than those exposed to the flu in other periods of pregnancy.
The biological explanation is a reductionism explanation because it explains complex behaviour by the simplest terms, genetics, inheritance, neurotransmitters, neuroanatomy and the flu virus.
The biological approach emphasizes nature and ignores nurture; this approach therefore ignores the stress part of the diathesis stress model and so ignores psychological and environmental triggers.
High expressed emotion in families has been linked with schizophrenia. Brown found that schizophrenic patients returning to high expressed emotion homes were more likely to relapse then those returning to low expressed emotion homes. This is supported by Vaughn and Leff who found a 51% relapse rate in high expressed emotion homes compared to 13% in low expressed emotion homes. It is important to remember however that high expressed emotion does not cause schizophrenia but explains how it is maintained and why the symptoms may reappear.
The social causation hypothesis states that schizophrenia is caused by factors to do with social class. Hollingshead and Redlich found that schizophrenia was twice as likely to be found in the lower social classes especially those living in densely populated and inner city areas. A study by Farris supports this. Farris found a higher rate of schizophrenia in working class areas with poor housing, overcrowding and high crime rates, than in the more middle class areas. They also found that the schizophrenics had always lived in these areas and had not drifted into them because of their disorder.
From this we can conclude that the biological approach does not explain everything. The biological approach is deterministic in that it believes all behaviour is caused by factors other then one’s on will.
The biological approach does not tell us all we need to know about schizophrenia. The biological approach is reductionistic, deterministic, emphasizes nature and ignores nurture. Therefore it ignores psychology and environmental triggers such as high expressed emotion and social causation. However, the biological approach explains a genetic predisposition to schizophrenia but for a full understanding the diathesis stress model needs to be used.
