As a solution to this problem adoption studies have been proposed; adoption studies won’t face this problem as the children will have been raised in a different environment but will still share the same genes. This means that the effect of nature can be observed without the confounding variable of the effect of nurture. Adoption studies also support the claim that genetic factors play a part in the development of schizophrenia; a large scale study of 5500 adults adopted early in childhood shows that 14% of their biological relatives were diagnosed as schizophrenic compared to 2.7% of their adopted relatives.
However, a key criticism to note is that genetic factors cannot provide a complete explanation; if the cause of schizophrenia was purely genetic then concordance rates between monozygotic twins would be 100% as they share the same genes. The genetic explanation does not explain why 52% of monozygotic twins do not develop schizophrenia if their other twin has it.
The dopamine hypothesis provides a second biological explanation of schizophrenia; the dopamine hypothesis states that schizophrenia is caused by an excess of dopamine which causes neurons to fire too often and transmit too many messages causing a ‘message overload’ and resulting in schizophrenia. Research into this shows that large doses of amphetamines given to people with no history of schizophrenia show behaviour similar to paranoid schizophrenics and small doses given to people already suffering from the disorder worsen their symptoms.
Further drug research shows that antipsychotic drugs used to treat schizophrenia work by blocking dopamine receptors. In addition to this, L-Dopa, a drug used to treat Parkinson’s disease (caused by a lack of dopamine) produces symptoms similar to schizophrenia on individuals with no history of the disorder.
A variation of the dopamine hypothesis is that people with schizophrenia had an excess of dopamine receptors (as opposed to just dopamine) leading to more firing and an overproduction of messages. This is supported by Owen et al (1986) who found an unusually large number of dopamine receptors in the autopsies of schizophrenics.
However, Farde et al (1997) failed to find a difference in the amount of dopamine receptors between schizophrenics and non sufferers. Kapur and Remington fount that recent drugs successful in controlling schizophrenia block fewer dopamine receptors but also block receptors for the neurotransmitter serotonin, therefore, it is likely that schizophrenia is a result of interaction of serotonin and dopamine rather than dopamine alone. These inconsistent findings show that research into the dopamine hypothesis isn’t reliable. Schizophrenia may be a result of excess dopamine receptors, but it is equally likely that there is no connection between dopamine receptors and schizophrenia.
The biological approach therefore provides an incomplete explanation of schizophrenia; this suggests that there is another factor affecting the development of schizophrenia.
The above explanations appear to provide an incomplete explanation of schizophrenia; there seems to be a genetic link but that link is not 100% so the genetic model cannot be regarded as full explanation for schizophrenia. As a solution to this, the diathesis-stress model has been proposed. The diathesis stress model claims that people have a biological predisposition to schizophrenia and environmental factors encourage or discourage the transition of the predisposition to schizophrenia itself. Tienari et al (1994) found that no adopted children raised in “healthy” families developed schizophrenia whereas 9% raised in “mildly disturbed” families and 11% in “severely disturbed” families developed schizophrenia. The adopted children were children were of schizophrenic mothers, this shows that although they were born with a predisposition those placed in “healthy” families were not affected by this predisposition.
