However this view has been challenged on several fronts. Primarily, those that support the environmental factors notion argue that if genetic factors were solely responsible, the concordance rate for identical twins would be 100%. In reality the concordance rate has been found to be somewhere between 22-44%. As Joseph (2003) notes, use of twin studies are based on the equal environment assumption – identical twins are treated no more alike than fraternal. However, Joseph reported several studies where concordance rates of fraternal twins were compared with those of non-twin siblings. Due to genetic similarity we might predict similar concordance rates. In fact, concordance rates were consistently higher for fraternal twins than for non-twin siblings. This suggests there might be something special about twins, making it difficult to draw conclusions from them.
Despite large differences in concordance rates reported across twin studies and disagreements of their validity, two findings have been obtained repeatedly: identical and fraternal twins who have a co-twin with schizophrenia are much more likely than random members of the population to suffer from the disorder, and; among twins having a co-twin with schizophrenia, identical twins are at significantly greater risk than fraternal twins. This undoubtedly suggests that genetic factors play a significant part in the explanation of schizophrenia. Although, it may be better to consider environmental factors also.
This can be seen in the study of adopted children. Tienari (1991) compared 155 adopted children who had a schizophrenic parent with 155 adopted children who did not have a schizophrenic parent. In all, 10.3% of those children with schizophrenic mothers developed the disorder, compared to only 1.1% of children without schizophrenic parent. Wahlberg et al. (1997) reported additional findings from this study, showing that environmental factors are also important. They found that children at genetic risk due to schizophrenic mothers had very good psychological health if raised by adopted families low in communication deviance (tendency to communicate in unclear and confusing ways). By contrast, children who were at genetic risk and were raised by adopted families that were high in communication deviance showed high levels of thought disorder. Therefore this suggests environmental factors have to be considered side by side with genetics, and that developing schizophrenia is the result of an interaction or combination of genetic and environmental factors.
Genetic factors can also lead to differences in brain chemistry; this would make the brain chemistry the immediate causal factor of schizophrenia. Biochemical abnormalities might be important in the development and maintenance of schizophrenia. For example, schizophrenia might result in part from abnormally high levels of the neurotransmitter dopamine (Seidman 1983). A slightly different view is that the neurons in the brains of patients with schizophrenia are oversensitive to dopamine. This is known as the dopamine hypothesis.
According to the original version of the dopamine hypothesis, patients with schizophrenia have excessive levels of dopamine. Dopamine is a neurotransmitter, and there are various reasons for arguing that it might play a role in schizophrenia. For example, there is strong evidence that the main antipsychotic drugs share the ability to block dopamine receptors. There is also more direct evidence based on post-mortem studies of schizophrenic patients. These showed that such patients had a greater density of dopamine receptors in certain parts of the brain than individuals not suffering from the disorder.
There are, however, several problems relating to the dopamine hypothesis. Firstly, it is hard to assess brain levels of dopamine in patients with schizophrenia, this can only be done in a direct way by post-mortem assessment. It is also possible to assess dopamine in an indirect way. However this involves inserting a needle into the spine, which can be dangerous. The findings have generally been negative – patients with schizophrenia do not seem to produce more dopamine than other people.
In conclusion, dopamine is probably of importance in understanding schizophrenia. However, it looks increasingly as if there are various complex differences in dopamine functioning between those with schizophrenia and healthy individuals. There is also the causality issue. If we find an association between having schizophrenia and having high levels of dopamine, the excessive dopamine levels might have played a part in causing the schizophrenia. However, it is also possible that elevated dopamine levels are in part a consequence of having schizophrenia.
