Research by Mikaywa et al has found that there must be a genetic explanation of schizophrenia due to the fact that concordance rates for environmental causes are not 100%. Also Mikaywa noticed that schizophrenia runs in the family, meaning there must be something other than environmental causes, causing the disorder. What Mikaywa studied was DNA from human families who were affected by schizophrenia and found that those with the disorder are more likely to have the defective gene: PPP3CC. The PPP3CC gene regulates the immune system, and therefore is an important gene in terms of genetic vulnerabilities which may be to the environment. The other biological explanation is The Dopamine Hypothesis.
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. In schizophrenics, dopamine activity is infrequent. This leads to the characteristic symptom of schizophrenia, such as anhedonia, flat affect and asociality. However research has also found that schizophrenics have abnormally high D2 receptors. Overall, the dopamine hypothesis suggests that schizophrenia is a result of high activity or high D2 receptors.
Research into dopamine hypothesis comes from medication given to schizophrenics and healthy individuals. Amphetamines are drugs which produce a state closely linked to paranoid schizophrenia. They can also exacerbate the symptoms of those who currently have schizophrenia. They release three neurotransmitters, the bulk of which is dopamine. Researchers are sure of the fact that the psychosis induced effect of amphetamines is due to increase in dopamine as antipsychotics are an effective treatment for amphetamine psychosis. However research has also found that, as well as excess of dopamine, increase numbers of dopamine receptors can be the cause of schizophrenia. Some post-mortem studies and PET scan looked at by Hietala et al and Tune et al show that dopamine receptor numbers are higher or hypersensitive in people with schizophrenia. Supporting this explanation is the success of clozapine (up-to-date antipsychotic) in treating the schizophrenia. Clozapine blocks dopamine receptors making less dopamine available, this effect has been proven by PET scans, thus providing greater biological evidence that dopamine receptors are responsible for some of the symptoms. However a greater number of dopamine receptors are not responsible for all the symptoms; they only account for the positive symptoms.
Although the dopamine hypothesis has good scientific support based on PET scans and post mortems, it has ignored the complexity of the biochemistry of the brain. Evidence from neuro imaging research has allowed researchers to study neurotransmitters and other chemicals associated with dopamine activity, such as metabolites. An example is the major metabolite of dopamine, homovanillic acid, was not found in greater amounts in patients with schizophrenia (Bowers). Wise and Stein also found that brain fluid in patients with schizophrenia who died in accidents had abnormally low levels of DBH, an enzyme that breaks down dopamine. similarly a US study found high levels of choline which is a chemical needed to make dopamine receptors work. What these studies show is that, high concentrations of dopamine not broken down and too much choline making D2 receptors over sensitive are important factors in explaining the complexity of brain biochemistry. It is also difficult to establish cause and effect; is increase dopamine activity caused by schizophrenia or does it cause schizophrenia.
In genetic explanations of schizophrenia, adoption, family and twin studies are used. In terms of family studies the main finding is that relatives of schizophrenics are at a risk of developing the disorder. This risk increases with the increase genetic relationship (50% first degree and 25% second degree). In support of this Kendler et al found that first degree relatives of those with schizophrenia are at 18 times more risk than the general population. Research has also found that schizophrenia symptoms may have a genetic component. This was suggested by Malaspina, who found that patients who have schizophrenia in their family histories are more likely to develop negative symptoms than those families who are schizophrenia free. In evaluation of family studies it may be concluded that they are not very reliable as they are retrospective. The studies for family studies where taken place when diagnosis was under a more liberal use of the term schizophrenia. Twin studies have also shown a genetic pre-disposition.
Gottesman found 48% risk of schizophrenia in MZ twins compared to only 17% in DZ twins. Similar to the Gottesman study two other studies showed higher concordance rates for MZ twins and lower in DZ twins however each had slightly different results. McGuffin et al argues this is because of the use of different diagnostic criteria, which may affect the validity of the results. On the other hand the researchers used blind techniques to obtain the results eliminating any researcher bias. Both family and twin studies face the problem of ignoring environmental impacts. In family studies, genetically similar members of the same family tend to spend more time together, therefore the environment would be similar. In twins, there has never been 100% concordance, suggesting genetic explanations cannot offer the full explanation. Adoption studies however allow for the consideration of both genetic factors and environmental factors, because they look at individuals whose biological mother has schizophrenia and brought up in an environment where schizophrenia is not present. Heston (1966), studied 47 people born between 1915 and 1945 to women with schizophrenia in a state mental hospital.
These infants were separated from birth and raised by adoptive parents. As well as the main group there was a control group of 50 participants chosen from the same foundling homes that had placed the children of the women with schizophrenia. The results revealed that 31 of the 47 children of mothers with schizophrenia were given a DSM diagnosis, compared to only 9 out of the 50 in the controlled group. None of the controlled group was diagnosed with schizophrenia versus 5 of the 47 whose biological mother had schizophrenia. Another finding of the study was that those whose biological mother was schizophrenic were more likely to be diagnosed as mentally defective, psychopathic and neurotic. They had also been found to be involved in criminal activity and spend more time in prison. Therefore this study provides strong support for the importance of genetic factors in the development of schizophrenia, as well as other psychiatric disorders. Another study in support is the prospective study by Kety et al. kety et al took a national sample from across Denmark and found high rates for diagnosis for chronic schizophrenia in adoptees whose biological parents had the same diagnosis, even though they had been adopted by healthy parents.
In evaluation of genetic explanations overall, it can be said that it is biological reductionism in that schizophrenia is a multi-factorial trait, spreading across a broad spectrum and a result of many genes (much more than we currently know of). Also we cannot assume that schizophrenia is a disorder completely determined by genetic transmission, as there is a key distinction between phenotype and genotype. Schizophrenia by behaviour is a phenotype, and is thus affected by the influence of genes and the environment. Therefore in terms of the diathesis stress model genetic factors can only provide a predisposition to the disorder, requiring an environmental trigger. A problem with this line of argument is that it is difficult to find out what the genetic predisposition or vulnerability is. A possible way could be to study relatives of schizophrenics, because although they may not have the disorder they are at increased risk and may carry the predisposition.
Something which links to the biological explanations is the evolutionary explanation. This is an important explanation because there is a debate as to the reason why the gene causing schizophrenia (if one exists) has not evolved out. Evolutionary theorists argue that although schizophrenia is maladaptive it is closely related to leadership qualities such as artistic ability, and creativity. These traits may be adaptive in the time our evolutionary ancestors were in the process of evolution and therefore persisted into our genes.
However the biological explanation is not the only one. Psychological (psychodynamic and behavioural) explanations have also been developed to account for Schizophrenia. One such explanation is the psychological explanation, an example of which is: high density (urban) living. Basically it is assumed that the urban environment (high pollution, noise and population) has a higher prevalence rate- (Tiennari et al).