When considering twin or adoption researchers have to be cautious because they are retrospective and diagnoses may be biased by knowledge that other family members have been diagnosed. This suggests there could be problems of demand characteristics.
A final weakness of the genetic explanation is that it is biologically reductionist; the genome project has increased understanding of the complexity of the gene. Schizophrenia is a multi-factorial trait as it is the result of multiple genes and environmental factors. This suggestsresearch into gene mapping is too simplistic as schizophrenia is not due to a single gene and that any pattern of inheritance is likely to be very complex.Nurture needs to be considered and the evidence suggests environmental factors must play a part. Without knowing the specific genes involved we can’t explain how these contribute to the development of schizophrenia, however the current advances in research into the mapping of genes may bring more insight to the process.
Recent research has suggested that genetic factors affect the hard wiring of the brain. The research focused on the brain biochemistry (neurotransmitters). Although there have been many neurotransmitters associated with schizophrenia, Dopamine seems to be the most important. The dopamine hypothesis says that schizophrenia is caused by an increased reaction to dopamine in the brain. This could be because there is too much of the hormone dopamine in the brain, or conversely because there is an abnormally high number of dopamine receptors in the brain. This model says the excess sensitivity to dopamine results in the brain, causes the symptoms of schizophrenia.
Evidence comes from the fact that amphetamines increase the amounts of dopamine large doses of amphetamines given to people with no history of the disorder produced behaviour which is very similar to paranoid schizophrenia. Small doses given to people already suffering from the disorder tend to worsen their symptoms. L-dopa is a drug used to treat Parkinson's disease it acts by increasing dopamine levels; it can also produce symptoms of schizophrenia in previously unaffected individuals, although not all patients developed these side effects. Main antipsychotic drugs such as Phenothiazine’s block the dopamine receptor cells and reduce symptoms
However Phenothiazine’s do not work for everyone diagnosed with schizophrenia, this suggests something else must cause schizophrenia as well otherwise the drugs would help all the patients. They also tend to alleviate the positive symptoms rather than the negative symptoms this implies that the dopamine hypothesis can at best only explain some types of schizophrenia. Newer atypical antipsychotic drugs such as Clozapine have been more effective than traditional ones in successfully treating the symptoms of schizophrenia despite blocking fewer dopamine receptors. This suggests there is refuting evidence for the notion of dopamine being the main contributing factor associated with schizophrenia.
Further support for the dopamine hypothesis comes from the post-mortems of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale (Falkai et al. 1988). However these examinations have been carried out on people who have taken neuroleptic drugs for years. Therefore it's difficult tell whether increased dopamine levels are the result of drug therapy rather than the cause of schizophrenia. Owen et al 1978 found evidence of increased dopamine receptor density in the caudate nucleus putamen however this evidence was varied and inconclusive.
Wong et al. (1986) shows in live patients using pet scans that the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies; this implies this research is not reliable.
A criticism of the dopamine hypothesis is there is a problem with the chicken and egg. Is raised dopamine levels the cause of schizophrenia, or is it the raised dopamine level the result of schizophrenia? It is not clear which comes first. This implies that one needs to be careful when establishing cause and effect relationship.
A final weakness of the dopamine hypothesis is that it is biologically deterministic. The reason for this is that if a person does have excess amounts of dopamine, then does that really mean they will develop this chronic and disabling disease? The dopamine hypothesis does not account for individual free will and implies other forces beyond our control, causes us to develop this disorder.
Advances in brain scanning technology are allowing medical researchers to seek structural, organic abnormalities in the brains of people who exhibit behavioural disorders. Two such scanning technologies are Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI). Using these new technologies researchers have discovered that many schizophrenics have enlarged ventricles, cavities in the brain that supply nutrients and remove waste. The ventricles of a person with schizophrenia are on average about 15% bigger than normal (Torrey 2002).
Evidence for neuro-anatomical explanations has been shown by Brown et al (1986) who found decreased brain weight and enlarged ventricles. Flaum et al. (1995) also found enlarged ventricles along with smaller thalamic hippocampal and superior temporal volumes. Buchsbaum (1990) found abnormalities in the frontal hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified. Strength of these studies is that they have high reliability; the reason for this is that the research is carried out in highly controlled environments with specialist high tech equipment.
One weakness of the neuroanatomical explanation is the of problem cause and effect. Causation cannot be inferred as associations have only been identified. The brain dysfunction may be a symptom of the disorder rather than the cause as the flexibility of the brain means it may change as a result of abnormalities.
The critical time period for the onset of schizophrenia is not usually before adolescence. Therefore if the brain abnormalities precede the onset of clinical symptoms this would confirm the view that schizophrenia is a developmental disorder. Castner (1998) subjected monkeys to brain damaging x rays during foetal development and found that they showed no ill effects in childhood compared to the control group, but at puberty they developed symptoms of schizophrenia such as hallucinations. There are of course ethical issues associated with animal research of this kind. This study could have shed light on the direction of causality but as it’s carried out only on animals it is difficult to generalise the findings to humans.
Birth complications have recently been thought to cause schizophrenia and provided evidence for both structural and neurochemical abnormalities in the brain of schizophrenics but do they result from a genetic defect or birth complications? A longitudinal study by Dalman et al 1999 found links between birth complications and later development of schizophrenia, with pre-eclampsia being the most significant risk factor. However suggesting the birth complication are the main cause is reductionist there are other factors to consider. Secondly its very deterministic not everyone who's been through birth complications is destined to develop this disease, in fact it’s very unlikely that conditions like pre-eclampsia are the sole cause as this is a common problem yet not all infants become schizophrenic.
In contrast to the biological explanations the psychological explanations rejects the view that schizophrenia is caused by genetics and brain chemistry. Instead it favours the idea that the disorder is caused by life events, the environment and upbringing. For example, research shows that dysfunctional family interaction where there is a lot of expressed emotion can lead to schizophrenia. Also many schizophrenics come from a lower social class which implies that poverty and housing are involved. This suggests that the biological account does not provide a full explanation of schizophrenia.
In conclusion the Diathesis Stress Model, states that there is a genetic vulnerability to a disorder, but it is only triggered when an individual has been exposed to a stressful life event. Both of these factors are necessary for a disorder to develop. This is why not all the children with schizophrenia develop the disorder, and why the concordance rate for schizophrenia for MZ twins is nowhere near 100%.
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