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Schizophrenia is an incapacitating disease affecting people with a first occurrence typically starting in the teen age up to adult (mid 30s approximately) (Day & Semrad, 1978). The indications of schizophrenia are varied but the results are the same, causing a breakdown of individuality and the consequent inability of the personage to purpose in reality. About one percent of the people undergo some form of schizophrenia in their lifetimes (Day & Semrad, 1978).
For investigators researching schizophrenia or experts curing schizophrenia, heterogeneity, or the differentiations within groups, is the universal attribute of the illness (Heinrichs, 2001). Indications will vary from individual to individual just as their environments and histories differ as well.
The origins of schizophrenia are varied as well. Throughout the past several decades, investigation on the sources of schizophrenia has budged between the powers of the hereditaries or “natural world” of the person versus the sways of the surrounding or “nature” of the person. The dispute of nature versus nurture and the communication between the two has been widely researched, developing with new study and approaches in medicine and technology.
Seymour Kety cites the complete twin study in Great Britain by Gottesman and Shields as an instance of heredity and schizophrenic origins. Through a meticulous assessment process, they were able to recognize twenty-four monozygotic twins and thirty-three dizygotic twins with at least one schizophrenic associate of every pair. The monozygotic twins, having equal genes, showed a concordance of 40 to 50 percent against a nine to ten percent concordance in the dizygotic twins (Kety, 1978). The vivid divergence in concordance rates points to a genetic factor, but given the lack of a 100% concordance, atmosphere has to be viewed contributing to fraction of the dissimilarity.
A group of personalities closely related to schizophrenics but who had lived separately from them, separating the influence of surroundings, was researched in Iceland in 1966. Kety explains the outcomes where this group displayed a high rate of schizophrenia in difference to the general populace and also in difference to a group of citizens who were cured with schizophrenics but were not hereditarily related (Kety, 1996). In a study of Oregon state psychiatric hospitals also in 1966, investigators located 47 people born to known schizophrenic mothers who were brought up apart from their mothers. Of this group five persons became schizophrenic.
Balanced to another control group of 50 born to non-schizophrenic mothers, but also raised by others, no schizophrenia was found (Kety, 1996). With environmental impacts inaccessible, these researches show the influence of heredity as a cause of schizophrenia, though, these researches also failed to support an exclusive hereditary origination.
There is more vagueness in research of the role of setting or nurture as a reason of schizophrenia. Seymour Kety offers that in hereditarily helpless children, the risk for schizophrenia is relatively thoughtless. Kety cites the above Oregon study to demonstrate the quality of parenting to be neutral as a cause of schizophrenia in genetically high-risk children.
Kety points out that the genetically high-risk children reared in foster care versus those raised in foundling institutions showed no significant difference in rates of schizophrenia. This is counter to Theordore Lidz’s assertion that dysfunctional parental communication and behavior has been shown to contribute to schizophrenia. Lidz considers the double bind communication of contradictory messages from parents’ causal in schizophrenic children (Lidz, 1973). Parental narcissism, which binds a schizophrenic child to a parent who can not establish proper frames, is also fundamental, according to Lidz (1973). In cases like these, the performance of a parent donates to surroundings that can originate schizophrenia in the kid.
The surroundings of the womb and other biological impacts have a basis as grounds of schizophrenia. The study of Finnish occupants depicted in a 1957 influenza plague revealed increased occurrence of schizophrenia in children gestating in the second trimester at the time of their mother’s decease. The timing of the sickness damaged brain expansion of the fetus, making a brain idiosyncrasy and the promising consequent incidence of schizophrenic in maturity (Mednick, et al., 1998).
Genetic and environmental aspects have been researched to show that both causes have a role in originating schizophrenia. Genetics play a brawny part as a reason, but as yet no exact concentration can be decided. Environmental impacts have been demonstrated to play a position in originating schizophrenia, but precise sources are not easily located as well. The interconnectedness of these reasons also makes it difficult to describe the derivations of the illness. Given these conditions, the study schizophrenia will necessitate more examination for some time to come.
References
Aldhous, P. (1993). Disease gene search goes big science. Science, 259, 591-592.
Bower, B. (1998). DNA links reported for schizophrenia. Science News, 154, 151.
Day, M. & Semrad, E.V. (1978). Schizophrenic reactions. In A.M. Nicholi, Jr. (Ed.). TheHarvard Guide to Modern Psychiatry (pp. 207-209). Cambridge, MA: The Belknap Press of Harvard University Press.
Gottesman, I.I., & Moldin, S.O. (1998). Genotypes, genes, genesis, and parthenogenesis in schizophrenia. In M.F. Lenzenweger & R.H. Dworkin (Eds.). Origins and development of schizophrenia (pp.5-11). Washington, DC: American Psychological Association.
Heinrichs, R.W. (2001). In search of madness: Schizophrenia and neuroscience. New York: Oxford University Press.
Keltner, N.L., James, C.A., Darling, R.J., Findley, L.S., & Oliver, K. (2001). Nature vs. nurture: Two brothers with schizophrenia. Perspectives In Psychiatric Care, 37, 88-94.
Kety, S.S. (1978). Genetic and biochemical aspects of schizophrenia. In A.M. Nicholi, Jr. Ed.). The Harvard Guide to Modern Psychiatry (pp.93-96). Cambridge, MA: The Belknap Press of Harvard University Press.
Kety, S.S. (1996). Genetic and environmental factors in the etiology of schizophrenia. In S.Matthysse, D.L. Levy, J. Kagan & F.M. Benes (Eds.). Psychopathology (pp.477-485). New York: Cambridge University Press.
Lidz, T. (1973). The Origin and Treatment of Schizophrenic Disorders. New York: Basic Books.
Mednick, S.A., Watson, J. B., Huttunen, M., Cannon, T.D., Katila, H., Machon, R., Mednick, B., Hollister, M., Parnas, J., Schulsinger, F., Sajaniemi, N., Voldsgaard, P., Pyhala, R., Gutkind, D., & Wang, X. (1998). A two-hit working model of the etiology of schizophrenia. In M.F. Lenzenweger & R.H. Dworkin (Eds.). Origins and Development of Schizophrenia: Advances in Experimental Psychopathology (pp. 34-60). Washington, DC: American Psychological Association.
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