It is thought that genetic factors play a role in schizophrenia. However, research has failed to identify one or a small number of genes that are responsible for the disorder. Therefore the 'polygenic threshold model' has been suggested. This assumes that a genetic influence comes from an accumulation of small effects from a larger range of genes.
Current research from twin, adoption and family studies suggest that genetic influence is not enough to account for the rate of those who are genetically related to develop schizophrenia. This led to the conclusion that environmental factors also contribute to schizophrenia onset.
The Dopamine-Hypothesis states that the neurons transmitting dopamine fire too easily and too often leading to characteristic symptoms of schizophrenia. Schizophrenics are thought to have abnormally high levels of D2 receptors on receiving neurons resulting in more dopamine binding and thus more neurons firing. Dopamine plays a role in attention therefore disturbances in this process may lead to problems related to attention, perception and thoughts which are found in schizophrenics.
Joseph analysed data of schizophrenic twins finding a concordance rate of MZ twins of 40.4% and for DZ twins 7.4%. More recent methodologically sound studies e.g. 'blind' diagnosis, where the research does not know whether they are testing MZ or DZ twins, reported lower concordance rates for MZ twins. Despite this researchers still argue findings suggest a genetic link and MZ concordance is often higher than DZ concordance rates. Such research studies are inconclusive as to the exact degree of influence genetics has in determining likeliness of developing schizophrenia. It is likely other factors influence whether schizophrenia is developed when there is a biological predisposition.
An issue with twin studies is they assume that MZ ans DZ twins share the same environments. However, Joseph et al highlighted that identical twins are more likely to be treated similarly and may be seen as one person, therefore share similar environments. This could explain the higher concordance rates with MZ twins due to environmental factors rather than genes alone. Also MZ twins share 100% of genes, the concordance rate remains at 40% and not 100% suggesting the environment still plays a mitigating role in schizophrenia onset.
The diasthesis-stress model may apply here with both nature (genes) and nurture (environment) interacting. Schizophrenia onset may be caused by having a genetic vulnerability as well as being exposed to certain environmental triggers. This theory can be applied to help individuals with a genetic predisposition to avoid situations that may cause schizophrenic symptoms to show.
Cross et al found in post-mortem examinations comparing schizophrenics and a control group, found that a higher level of D2 receptors were found among schizophrenics, providing evidence to support the dopamine hypothesis. Other post mortem studies had concluded it was the drug treatments that the schizophrenics had been taking which caused this. However, Cross et al reported that these schizophrenics had not been taking drug treatment at the time of death, so contradicting other such studies that suggest anti-psychotics caused changed in the brain's response to dopamine.
Both Joseph and Cross' studies support a biological explanation, with study support for genetics remaining greater than that of the dopamine hypothesis, however neither are conclusive. Both genetic and neurochemical explanations have been criticised for being reductions as the ignore the role of free will and suggests all human being are driven by biological impulses that are beyond our control, which is untrue.
The nature/nurture debate suggests that out innate biological makeup gives us a predisposition to develop schizophrenic tendencies, but it is nature which is important in creating the circumstance for these behaviours to show. Therefore a consideration of both biological and psychological factors may be the most accurate explanation of how schizophrenia is developed.
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