To what extent is it possible to explain Schizophrenia from a biological perspective?

Schizophrenia is a serious brain disorder. It is a disease that makes it extremely difficult for a person to tell the difference between real and unreal experiences, to think logically, to have normal emotional responses to others, and to behave normally in social situations. People with schizophrenia may also have difficulty in talking, remembering and behaving appropriately. Schizophrenia is one of the most common mental illnesses. Schizophrenia is a neurological disorder that affects the cognitive functions of an individual. The cause of this illness to this day is still unknown, but there are several theories of how an individual may get schizophrenia. Because there are so many symptoms of the disease and because the symptoms can vary quite significantly among several individuals and even within the same individual over time, the diagnosis of schizophrenia can be quite difficult.

Schizophrenia is sometimes seen as a functional disorder with professionals often referring to it as a sociological phenomenon, meaning patients with schizophrenia are normal people driven insane by the insane world (Gelder, et al., 1989). However, with many years and numerous advances in genetics/brain imaging, molecular biology and neuroscience over the years, evidence has been found for the biological bases underlying schizophrenia.

There have been quite a few theories of possible causes. Firstly, a lot of family studies indicate that a proneness to the disorder schizophrenia might be inherited. Although scientists carrying out these studies and advances still do not know how many genes are involved or how the genetic proneness is transmitted, and how the environment may interact with it. A further line of research has identified specific, refined abnormalities in the structure and function of the brains of schizophrenic patients and provided the evidence for significant, early biochemical changes. Although neurobiologist development on the other hand indicates that schizophrenia may be a result of the neurons forming inappropriate connections during fetal development. Having so many possibilities of explaining the causes of schizophrenia it is no surprise that it still remains one of the most challenging areas for scientific and medical researchers.

A well-known observation is that schizophrenia is hereditary, which is caused by genetic factors. Studies have been carried which support this statement to include family studies, twin studies and adoption studies.

With regards to family studies it is suggested that relatives of patients with schizophrenia have a greater risk of being diagnosed themselves as the genetic relationships become closer. The actual likelihood of a person developing schizophrenia is about 1 in 100, and if one biological parent has this illness the likelihood increases to 1in 5 and if both biological parents possess it, it increases to 1in3. The twin studies have assessed and looked at the concordance rates for schizophrenia for identical MZ and non-identical DZ twins, and the results of these studies suggested that likelihood is that both twins would develop the disease schizophrenia. Gottesman & Shields study 1966, concluded that for MZ twins its results was 64% and for DZ twins was 27%. A further study was also carried out in the whole of Europe and its results varied just slightly, with results for MZ being 48% and DZ being 17%. Although, it must be highlighted that, because MZ twins were not completely concordant, genes therefore cannot be the sole cause of the disorder. Researchers have stated that for the disorder schizophrenia to develop, physical or psychological trauma must occur to kick off the effect of the gene.

Further studies were also carried out in adopted children to explain if there was a genetic contribution to schizophrenia. The first being Heston’s (1996) study. Here he carried out a study of 47 children of schizophrenic mothers who were adopted at infancy by parents with who they had no biological relationship. This group was compared at maturity with a control group of 50 adoptees who were separated from non-schizophrenic mothers. The results obtained suggested a genetic aetiology of schizophrenia: whereas five children of schizophrenic mothers developed schizophrenia, none of the children of non-afflicted mothers developed the disorder. Kety’s (1975) study had two groups of adoptees, in one group of 33 adoptees had the illness schizophrenia and the other group which also consisted of 33 did not have the disease. This study looked at the rate of the disorder in the biological and adoptive families. The results found were that it was much higher among the biological relatives of schizophrenia adoptees. More or less stating that adoptees that were separated from a biological parent which had the disorder would develop it. Further results also showed that children born to non- schizophrenic parents but raised by a schizophrenic parent did not show any indication of the illness.

The studies explained above suggest that genetic factors appear to play a role in the development of schizophrenia. However, even if these factors are involved, they cannot be responsible fully.

A lot of studies have also stressed the possible role of brain neurotransmitters in the development of schizophrenia. The main focus of research has been aimed on the neurotransmitter called dopamine. Dopamine is a brain chemical that increases the sensitivity of the brain cells that promote an individual’s awareness of events around them, when they are in danger or under stress. If however the individual’s level of brain activity is already at a high level, then the effects of the additional dopamine activity may trigger the onset of a psychotic state, such as schizophrenia. This theory grew out of the finding that all effective anti-psychotic medications stop dopamine brain receptors, and that their power is linked to the strength of binding to dopamine type 2 (also referred to as D2) receptors in the brain. The support for the theory came from studies carried out by (Jones, & Pillows, 2002). That the administration of drugs which increase dopamine activity aggravates psychotic symptoms in some persons with schizophrenia

Neurotransmitter studies carried out on deceased persons have shown increased numbers of dopamine type 2 (D2) receptors in serious amounts of the brain, areas such as the basal ganglia and the limbic system. Although we know that not all studies have been consistent with these findings .The main argument being the fact that anti-psychotic medications are effective in treating psychosis of any origin, which suggests that elevated dopamine activity may not be specific to schizophrenia. And finally, studying the brains of deceased persons is maybe full with problems, simply because of the person’s medical history.

There are further biochemical explanations such as serotonin involvement and faulty metabolic brain processes. The evidence for serotonin participation comes from patients who have not been helped by dopamine alone but by a combination of drugs designed to treat symptoms of the disorder schizophrenia, these drugs block both dopamine and serotonin transmission. The faulty metabolic processes have been suggested to be the main blame for the production of the substances known as psychotogenes in the brain. Therefore they in turn might resemble the actions of some hallucinogenic substances in other words resemble the chemical structures of some neurotransmitters. Metabolic breakdown might cause the brain to convert some of the harmless molecules into such substances and produce schizophrenia like behaviours.

When we speak about neurological explanations, we are talking about the possible causes of the negative symptoms of schizophrenia and them being the structural abnormalities in the brain. MRI studies give images of a live brain. (Chua & McKenna) compared MRI images of the brains of schizophrenic and non-schizophrenics and found structural abnormalities in the person’s brain with the disorder. They found high densities of white matter in the frontal lobe and also unusually large ventricles. These MRI scans also showed that schizophrenics have a smaller hippocampus. CT scans reveal that schizophrenics’ show an increase in the size of the lateral cerebral ventricles – which is the fluid filled spaces in the centre of the brain. There were also findings of reduced blood flow in the frontal regions in schizophrenic patients. This therefore points out impaired functioning of that area and also lack of blood flow causes reduction in the size of the brain itself. Freedman et al., (1995) found that skull volume is reduced in persons with schizophrenia by 3.5%. Since brain growth drives skull growth, these findings indicate that the process causing schizophrenia takes place prior to the completion of brain growth (approximately age 18) (Elkins, et al. 1995). This therefore could suggest that the process leading to schizophrenia is a developmental error occurring prior to birth, rather than a degenerative or destructive process. Neurobiologists suggest that schizophrenia may be a developmental disorder resulting from neurons being miswired during fetal growth. These faults may lie dormant until puberty, when changes in the brain that occur normally during this critical stage of maturation start interacting badly with the faulty connections.

However, after these finding we are still at a lost, because we do not actually know if these structural abnormalities are actually a cause or a consequence of having the disorder schizophrenia, and whether they can explain all the symptoms. After all the above evidence discussed, to explain schizophrenia from a biological perspective it appears to be disorganised and more or less one sided in my opinion. It is necessary to take into account environmental and social factors which contribute to the psychological wellbeing of an individual. Factors such as family stress, poor social interactions, infections or viruses or trauma at an early age all might be contributors to the development of schizophrenia later in life.

The diathesis-stress model provides strong evidence of support that in fact schizophrenia could be caused by a number of combination factors whether it being environmental or social, such as major life-events, traumatic experiences or adverse family circumstances such as death, illness, loss of home

Taking all the reviewed possibilities into account, and the discussion of theories it is impossible to put the psychological and biological findings into a singular model of schizophrenia. It could be said that schizophrenia is most probably biologically predisposed condition but may not develop into a full blown disorder without environmental influences and stressors.

An overview of the evidence strongly indicates that there are several biological bases for schizophrenia. The studies carried out with genetic have also provided what is perhaps the most important contribution to the understanding of this disorder. However current and continuous research has still yet to discover the specific genes that underlie the disorder. It is definitely a result of interactions of complex systems, therefore a systems approach is needed for understanding its development.

Understanding these causes will be critical for the medical care of patients suffering from schizophrenia, so the doctors can if not cure, then at the least alleviate the suffering this disease brings on the patient and their family and friends.

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