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The Etiology of Schizophrenia

The Etiology of Schizophrenia

The etiology of schizophrenia, along with the biological basis of conscience, the physiological function of dreams, and countless other organic phenomena is still a vexing subject to psychiatric researchers. While correlational data indicates that schizophrenia is largely due to neurological dysfunction at a cellular and molecular level, the complexity of the disorder revolves around the issue of genetic versus environmental influence.

Schizophrenia Etiology Influences

What causes schizophrenia at the biological level so that we can treat it? What causes schizophrenia at the environmental level so that we can prevent it?

Schizophrenia and Genetics

It is widely known that schizophrenia is highly heritable, as the risk of developing the disease increases significantly with the amount of genes shared between blood related individuals. Among the general population, the incidence of schizophrenia is as low as 1 to 3 percent compared to the 17 percent risk between dizygotic twins and the 48 percent risk between monozygotic twins. This hereditary trend, while tremendously significant, does not account for the prevalance of the disorder within the general population. Although almost insignificant, researchers cannot look away without theorizing that some other environmental variable is at play alongside nature. From a biological perspective, the ‘inheritance’ of schizophrenia is possible only if we understand the mode of transmission. This means that there is a certain gene coding for the disorder itself, or a series of genes that combine to create biochemical reactions that lead to the development of the disorder. For example, a genetic pre-determination of dopamine or serotonin levels (both substances are tied to the development of schizophrenia). Because of extensive studies on twins and adoption cases, many researchers believe that schizophrenia is indeed due to one gene whose location must be discovered. However, as has been the case in countless mental disorders before, one gene hardly ever accounts for the complexity of such a dynamically destructive disorder- much less one primarily affecting the brain.

Schizophrenia and Dopamine

The use of drugs in the treatment of psychological disorders is highly controversial, yet in using them, researchers have been able to learn valuable information about the body’s reaction to neurotransmitter manipulation. In the case of schizophrenia, important observations concerning dopamine and schizophrenia’s relationship were noticed. Positive symptoms of schizophrenia can be successfully treated with drugs that inhibit dopamine release, thus supporting the theory that schizophrenia is to some extent caused by an excess of dopamine production. Another supporting observation is that patients suffering with Parkinson’s disease can experience schizophrenic symptoms as a result of using drugs that contain L-dopa, a neurological substance preceding dopamine. Parkinson’s disease is caused by a deficiency of dopamine in the basal ganglion cells. It is also important to note that patients treated for schizophrenia with antipsychotic drugs can develop symptoms similar to those of Parkinson’s disease as a result of the lack of dopamine. The dopamine theory of schizophrenia basically gets most of its validation from the fact that drugs that block dopamine receptors reduce schizophrenic symptoms and drugs that increase dopamine levels either produce schizophrenia like symptoms or worsens symptoms in diagnosed patients. Despite evidence supporting this theory, the most modern drugs also influence serotonin and glutamate levels and seem to have the same effect in treating the positive symptoms of schizophrenia. This may indicate a more complex relationship, one involving dopamine, serotonin, and glutamate. Given that we already produce a variety of dopamine blocking drugs, if the cause of schizophrenia were due to the function of that one neurotransmitter, a cure would have already been found. Thus, the dopamine theory is far too simplistic.

Neurological Structure and Schizophrenia

Patients diagnosed with schizophrenia show significant differences in brain structure compared to their non-schizophrenic peers. Differences in the volume, shape, and size of the brain, especially the frontal lobe, hippocampus, and temporal lobes are noticeably abnormal. The difference in brain structure among schizophrenics takes the form of enlarged ventricles (fluid-filled cavities at the center of the brain) and decreased amounts of gray matter. During early development, the central nervous system undergoes an interesting phenomenon whereby it destroys newly formed synapses on a continuous basis. Scientists have postulated that this occurs in order to fine-tune the connections between neurons. However, researchers have also made a connection between faulty neuronal connections in early development, and later development of schizophrenia due to large changes in the brain that occur after puberty. It is also interesting to note that the prodromal symptoms of schizophrenia can be seen during young adulthood when these brain changes are occurring.

Schizophrenia and The Environment

Adoption studies indicate that environmental exposure to stressful or abusive situations can trigger an early onset of schizophrenia in twins with a high hereditary-based risk for the disorder. In these studies, while the heritability of schizophrenia almost always predicted future development of the disorder, environmental variables significantly affected when the first symptoms appeared and how severely symptoms manifested in the individual. Environmental factors are also significant in the development of neurological structure, especially in young adulthood when the brain undergoes major changes.The most recent studies suggest that disruption in brain development is predisposed and certain environmental factors are the decisive cause of later development of the disease.  In cases where the individual has a high risk for developing schizophrenia, negative environments can cause neurological changes that worsen brain structure and promote earlier onset of the disease.

A new approach to understanding the etiology of schizophrenia is called the bio-psycho-social model and it states that biological predisposition and psychosocial conditioning as a result of environmental exposure are a combined system for understanding mental disorders. Although schizophrenia is highly heritable and related to some extent to dopamine, glutamate, and serotonin levels, to really understand the cause of the disorder, we must view it as a dynamic and complex process and try to integrate theories of the schizophrenia etiology rather than seek one dominant theory.

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