The case of Genain quadruplets, which is described by Perese (2012), can be used to demonstrate the fact that genetic and nongenetic as well as prenatal and postnatal influences tend to form complex and unique combinations, which define human development.We will write a custom Adult Psychiatry: Schizophrenia in Quadruplets specifically for you
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Four Genain quadruplets developed schizophrenia, but the course of the disease was different for each of them. A history of psychological issues could be found in the genealogy of their father, which implies that their schizophrenia is likely to have been defined by the genetic predisposition. Genes can be regarded as a matrix or template for a person’s development; in particular, they exert varied influence during the prenatal stage on different brain areas, and they can be responsible for schizophrenia predisposition (Perese, 2012, p. 80). The predisposition was the same for the girls since they were monozygotic quadruplets. Moreover, other prenatal factors, for example, the diet of the mother of the girls, which could have an impact on their development (Saugstad, 2004), were also the same for all the quadruplets. However, the courses of schizophrenia and its manifestations were very different for the girls, which suggests that the genes are not the only influence of importance. For example, while all the girls had low birth weight, Nora was almost twice as big as Hester. Coincidentally, Nora was also the last to develop schizophrenia, while Hester was the first to exhibit issues. In fact, the girls with greater birth weight fell ill later than the girls with lower birth weight, which allows suggesting a connection between the two factors.
Apart from the low birth weight, it is noteworthy that the parental attitudes that the girls were subjected to were far from healthy: they had a domineering and abusive father who was reported to be addicted to alcohol, and their mother would not recognize them as individuals. It was also established that the girls were restricted from socializing by their parents. All these factors could contribute to the development of the girls’ diseases as postnatal external influences (Perese, 2012). From the case materials, it is not clear whether the girls were exposed to these factors to a similar extent.
To sum up, even though the girls were identical quadruplets, the specifics of their disease development was also influenced by a number of other factors. In fact, the events that are mentioned in the case might not be exhaustive, and other experiences of the girls that were not known to the observers might have had an impact as well.
As a psychiatrist, I am naturally interested in the topics discussed by Esch and Stefano (2010) and Saugstad (2004). Also, both articles are of importance from the point of view of the integrative, holistic approach: the former considers stress and its regulation, and the latter investigates the way human development is affected by diet. The articles are united by the neurobiological perspective, but they have different topics, which makes it difficult to establish which one of them is more useful. However, I suppose that the former article is of greater consequence since it is more recent. Moreover, it is also of greater interest to me as a professional due to its value for the practice of stress management. Esch and Stefano (2010) discuss the biology of stress management, analyzing stress coping techniques from the point of view of the biological effects that they have. The authors especially highlight the fact that the human body has a potential for stress regulation. The article is most informative and insightful, and it can be used to guide the stress management element of holistic and integrative nursing practice.
Esch, T., & Stefano, G. B. (2010). The neurobiology of stress management. Neuroendocrinology Letters, 31(1), 19-39.
Perese, E. (2012). Psychiatric advanced practice nursing. Philadelphia, PA: F.A. Davis Co.Get your
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Saugstad, L. F. (2004). From superior adaptation and function to brain dysfunction – The neglect of epigenetic factors. Nutritional Health, 18(1), 3-27.