“Biological Explanations of schizophrenia tell us all you need to know about the disorder.” Critically consider biological explanations of schizophrenia with a reference to the issue raised in the quotation above.
...disorder were entirely genetic. Also, the fact that family members who are more similar genetically tend to spend more time together means that environmental factors play an influential role. Clearly, looking at adoption studies is one way round the problem of controlling environmental factors. Heston (1966) compared 47 children of schizophrenic mothers adopted before the age of one month, with 50 children raised in the home of their biological and non-schizophrenic mothers. He found that the control children were significantly less disabled than the children born to schizophrenic mothers. 60% of those children born to schizophrenic mothers were given a psychiatric diagnosis, compared to only 18% of the control group. This study shows there is a strong genetic component in the explanation of schizophrenia. Kety et al (1974) found that the rate of schizophrenia did not differ for adoptive families that had adopted a child who became or did not became, schizophrenic. These studies indicate the significance of genetic factors and that environmental factors had little impact on the development of schizophrenia. For what has been said, genetic factors appear to play some role in schizophrenia. However, attempts to identify the gene or genes responsible have not been successful. As noted, even if the genes are involved, genetic factors alone cannot be responsible. One way in which genes may influence behaviour is through biochemical agents in the brain. Biochemical abnormalities may be important in the development and maintenance of schizophrenia. For example:- schizophrenia may result in part from excess levels of the neurotransmitter dopamine. Various kinds of evidence suggests that dopamine plays a role in schizophrenia. For example neuroleptic drugs that block dopamine seem to reduce the symptoms of schizophrenia. The phenothiazines are neuroleptic drugs that block dopamine at the synapse. The phenothiazines typically reduce many of the symptoms of schizophrenia (Davison and Neale, 1996). Other evidence supports the notion that dopamine is involved in schizophrenia. For example, the drug L-dopa, which increases dopamine levels, can produce many of the symptoms of schizophrenia (Davidson et al, 1987). In similar fashion, the symptoms of schizophrenic patients often become worse when they are given amphetamine, which activates dopamine. Patients suffering from Parkinson’s disease have been found to have low levels of dopamine including the uncontrolled movements of the limbs. Similar, uncontrolled movements are found in the schizophrenics given neuroleptic drugs, presumably because these drugs reduce dopamine levels. Although, the evidence linking dopamine to schizophrenia is impressive, its causal role has been questioned. For example, excess levels of dopamine could just be a factor in the development of schizophrenia rather than the only factor. Furthermore, drugs like phenothiazines have been found to have more affect on positive symptoms such as delusions and hallucinations than on negative symptoms such as apathy and immobility (Crow et al, 1982). This has lead to the proposal that the positive symptoms have one cause (possibly related to dopamine), whereas the negative symptoms have some other cause. Other problems identified with the dopamine hypothesis are that neuroleptic drugs block dopamine fairly rapidly, but generally fail to reduce the symptoms of schizophrenia for days or weeks after. This is puzzling considering that high levels of dopamine are responsible for maintaining the symptoms. The dopamine hypothesis is further confounded by the fact that clozapine (a new drug) is more effective than neuroleptic in reducing schizophrenic symptoms. As according to the dopamine hypothesis it should be less effective because it block dopamine activity less than neuroleptic. This can be explained in the view that clozapine blocks both neurotransmitters, dopamine and seratonin, that exaggerate the symptoms of schizophrenia, which is not the case with the neuroleptic. The evidence on the relationship between schizophrenia and dopamine levels is mostly correlational in nature. As a result, it is uncertain whether the altered dopamine activity in schizophrenics occurs before or after the onset of the disorder. If it occurs after, then clearly dopamine plays no part in causing schizophrenic symptoms. One possible cause of the negat...