Although twin studies show a strong genetic link with schizophrenia they do not use the same diagnostic criteria. McGuffin found that different definitions produce different concordance rates and therefore comparisons cannot be made within these studies.
Another limitation is that MZ twins are very rare. 1% of the world are schizophrenics and only a small portion of these are MZ twins. This sample is small and we cannot have lots of research to then successfully generalise these findings.
One of the main criticism is that both twins live in the same environment and therefore we cannot determine whether it is all down to genes or if there are environmental factors that contribute to developing schizophrenia.
However, research by Kety supports a strong genetic component showing a higher rates in those with those with biological parents who had the disorder but had been adopted by healthy parents. This highlights, a genetic role in schizophrenia even though the environment was different.
Genetic expression may be in the form of DA regulation rather than a gene for schizophrenia per say. Hence the biochemical approach for schizophrenia. This states that schizophrenia results from excess dopamine activity at certain synaptic sites. This could be caused by an excess of dopamine receptors, over sensitivity or release of receptors or release of excess dopamine by presynaptic neurons.
Phenothiazine, a drug treatment that blocks dopamine at the synapse is effective in alleviating major symptoms of schizophrenia. Therefore, this approach must be logical if this treatment which is based on is effective.
Seeman found increase dopamine in dopamine receptors between 60-110% in schizophrenics compared to a control group. This supports the dopamine hypothesis as it shows a positive correlation between increased dopamine levels and schizophrenics.
Similarly, post mortem examinations of schizophrenics showed an increase of levels of dopamine in parts of the brain compared to non-schizophrenics further supporting this.
However, it is not possible to accurately say whether this increased level is causal to schizophrenia or a result of the disorder. Therefore, this lack causality as post mortems are carried out retrospectively.
Overall, the biological approach favours the nature side of the nature/nurture debate because it only favours the biology that could affect the development of schizophrenia rather than environmental factors that could play a large role in the development. This then means that the approach is reductionistic because it is narrow minded because it only focusses on our biology only and doesn’t consider behavioural or cognitive contributions. Lastly, this approach suggests we are a product of our biology and ignores free will making this approach deterministic.
Given that no biological explanation accounts for all cases of schizophrenia or even for all aspects of the disorder within an individual, it seems likely that social and psychological factors play a part, and therefore a more holistic explanation is needed.
