Critically Consider Biological Explanations of Schizophrenia

The term 'schizophrenia' covers a group of serious psychotic disorders characterised by a loss of contact with reality. It comes from two Greek words: schiz meaning 'split' and phren meaning 'mind'. DSM IV (1994) estimate that the occurrence rate of schizophrenia ranges from 0.2%-2.0% worldwide. There are two main explanations of schizophrenia: the biological explanations and the psychological explanations. In this essay I will critically consider the biological explanations. These include genetics, neurochemistry, brain structure and evolution.

Genetic factors of schizophrenia can be explained using studies on twins and studies on family history. With twin studies researchers want to establish the degree of concordance. This is the probability that if one twin has the disorder, the other twin will also have it. Monozygotic (MZ) twins share 100% of their genes and dizygotic (DZ) twins share about 50%. Gottesman (1991) summarised 40 twin studies and found that the concordance rate for MZ twins was 48% and the concordance rate for DZ twins was about 17%. Concordance rates were also studied by Cardano et al. (1999) using the Maudsley twin register. They found concordance rates to be 40% for MZ twins and 17% for DZ twins.

Although this is strong evidence for genetic factors in schizophrenia, concordance rates are not 100% and therefore there must be some environmental input. Loehlin and Nichols (1976) argued that the reason for the higher concordance rates in MZ rather than DZ twins was due to MZ twins being treated more similarly so producing a greater environmental similarity.

However, there are two arguments against this view. MZ twins may produce more similar treatment from their parents than do DZ twins (Lytton, 1977). This therefore suggests that the higher genetic similarity of MZ twins may be the cause, rather than the effect, of their more similar parental treatment. Also the schizophrenia concordance rates for MZ twins who are brought up apart are similar to those of MZ twins who are brought up together (Sheilds, 1962). So presumably the high concordance rates of MZ's brought up apart is not due to environmental similarity. However it has been suggested that some of the twins who had been brought up separately in Sheilds study had not always spent their whole childhood apart and some were raised by relatives and even went to the same school (e.g. Kamin, 1977).

Family studies also aid to explain how genetic factors influence schizophrenia. Gottesman (1991) found that if you have a sibling with the disorder you have an 8% chance of being schizophrenic, if you have one parent with the disorder you have a 16% chance of being schizophrenic and if you have two parents with the disorder you have a 46% chance of being schizophrenic. These concordance rates should all be compared to the 1% chance that a person randomly selected from the population would be schizophrenic.

Gottesman and Bertelsen (1989) also reported some convincing findings on the importance of genetics. The found that participants had a 17% chance of being schizophrenic if they had a parent who was an identical twin and who had schizophrenia. This could be due to heredity or environment. They also found that participants had a 17% chance of being schizophrenic if they had a parent who was an identical twin and did not have schizophrenia, but whose identical twin did. This therefore shows that the most important factor is genetics.

The evidence reported by Gottesman is criticised because although it indicates that schizophrenia runs in families and that concordance rates are much higher between relatives who have higher genetic similarity, it does not account for the fact that family members who are more genetically similar are likely to spend more time together. This means that environmental factors are also indicated in this evidence.

The importance of the genetic component is supported by adoption studies. Tienari (1991) looked at adopted children in Finland with schizophrenic biological mothers. He compared 155 adoptive children of schizophrenic mothers with 155 adoptive children of non-schizophrenic mothers. There was a large difference in the incidence of schizophrenia when they were adults between the two groups. The group with schizophrenic mothers were found to have a 10.3% chance of being schizophrenic and the group with non-schizophrenic mothers were found to have only a 1.1% chance of being schizophrenic.

Kety et al. (1978) examined early-age Danish adoptees matched on gender and age. 50% of these adoptees were diagnosed as schizophrenic and 50% were not. They found that the incidence of schizophrenia was greater among the biological relatives of those with schizophrenia than those without. This is expected if genetic factors are important. They also found that the rate of schizophrenia was no different for adoptive families who had adopted a child who became schizophrenic compared to those who had adopted a child that did not become schizophrenic. This therefore suggests that environment is of little importance.

However Kety et al.'s (1978) study is criticised due to the fact that they drew their adoptees from 1924-1947 and gathered their statistics from a time-span of over 70 years. This means that the uniformity of the diagnostic criteria must be queried due to the change in interpretations of symptoms.

Genetics can cause differences in brain chemistry and biochemistry may be important in the development and maintenance of schizophrenia. The dopamine hypothesis suggests that excess levels of dopamine are associated with schizophrenia. It has been found that neuroleptic drugs that block dopamine seem to reduce the symptoms of schizophrenia. Phenothiazines are neuroleptics drugs that block dopamine at the synapse. These typically reduce many of the symptoms of schizophrenia (Davison and Neale, 1996). However they have more effect on positive symptoms such as hallucinations and delusions than on negative symptoms such as apathy and withdrawal.

More support for dopamine's role in schizophrenia comes from the drug L-dopa, which increases dopamine levels. When given this, schizophrenic symptoms may occur (Davison et al., 1987). Van Kammen, Docherty and Bunney, 1982 have also found that symptoms of schizophrenic patients may become worse when given amphetamines, which activates dopamine. Also the symptoms of amphetamine psychosis are similar to paranoid schizophrenia (Prentice, 2000).

Patients suffering from Parkinson's disease provide more support for the dopamine theory. Parkinson's disease is associated with low levels of dopamine and patients suffer uncontrollable limb shaking. Similar uncontrolled movement is found in schizophrenic patients given neuroleptics drugs, most likely due