Family studies have found that schizophrenia is more common in the biological relatives of a schizophrenic, and the closer the degree of genetic relatedness, the greater the risk (Gottesman, 1991). Twin studies have shown that identical twins have a 48% risk of developing schizophrenia if their twin has the disorder compared to 17% for non-identical twins (Janicak et al, 2001). Adoption studies have shown that 14% of the biological relatives of adoptees with schizophrenia were classified as schizophrenic, compared to only 2.7% of their adoptive relatives (Kety el al 1988). Research in molecular biology has found that schizophrenics are more likely to have defective version of the gene PPP3CC, associated with the production of calcineurin an enzyme that regulates the immune system (Myakawa et al, 2003).
Evidence from genetic studies indicates that even when two individuals share the same genes (i.e. identical twins), there is less than 50% risk of both developing schizophrenia if one is schizophrenic, thus showing a significant environmental contribution to the disorder. The diathesis-stress model proposes that individuals may be genetically predisposed to become schizophrenics but the actual disorder depends on exposure to significant life stressors. A further problem for genetic explanations is that they cannot account for patients who have no family history of the disorder, which is the case for about two-thirds of schizophrenic patients (Stirling and Hellewell, 1999).However, if schizophrenia is caused by large numbers of genes, individuals who possesses only a few of these genes would not develop schizophrenia. Schizophrenia would only develop when a large number of these genes are present.
The dopamine hypothesis emphasises the role of excess dopamine activity in schizophrenia. In schizophrenics dopamine neurons fire too easily or too often, leading to the characteristic symptoms of the disorder. Dopamine neurons play a key role in guiding attention, so disturbances in this process may lead to the problems of attention and thought that are common in people with schizophrenia (Cromer, 2003). The importance of dopamine in schizophrenia was demonstrated by the effect of antipsychotic drugs, which bind to the D2 dopamine receptors, blocking the transmission of nerve impulses and consequently reducing schizophrenic symptoms. Low levels of dopamine activity are found in sufferers of Parkinson’s disease, and the drug L-dopa, which raises levels of dopamine, causes schizophrenic-type symptoms in some people (Grilly, 2002).
A problem with the dopamine hypothesis is that because antipsychotic drugs are effective only for the positive symptoms, this means that excess dopamine can only explain some types of schizophrenia. Newer atypical antipsychotics also affect levels of other neurotransmitters (eg serotonin) which suggest that dopamine is not the only biochemical factor involved in schizophrenia (Kasper et al 1999).Also; this hypothesis cannot explain why some schizophrenics have lengthy periods of remission, where they are relatively free from the symptoms of the disorder. This could be explained by a variation in dopamine levels over time, but there is no suggestion why this might occur.
Attempts to explain schizophrenia simply in terms of one biological cause are challenged by the fact that there are different types of schizophrenia. Type 1 schizophrenia (characterised by positive symptoms) and type 2 schizophrenia (characterised by negative symptoms) are believed to different causes rather than one single biological cause. Explaining schizophrenia from a purely biological perspective is further challenged by research which shows an important role for environmental influences in the development and maintenance of the disorder. Research by Linszen et al (1987), for example, found that patients returning to a family with high levels of expressed emotion (EE) were four times more likely to relapse than those in families with low levels of EE.