Unit 9 Exploring The Etiology Of Schizophrenia

Unit 9 Exploring The Etiology Of Schizophreniain Their Book Divided Mi

Drawn from the unit readings and your understanding of the etiology of schizophrenia, how might you explain why Pamela developed schizophrenia but Carolyn did not? Support your ideas with references to the course texts, articles from this learning unit, articles from the Optional Readings, or articles from peer-reviewed journals.

Paper For Above instruction

Schizophrenia is a complex mental disorder characterized by disruptions in thought processes, perceptions, emotional responsiveness, and social interactions. Its etiology involves a combination of genetic, neurobiological, environmental, and psychological factors. In the case of Pamela and Carolyn, their divergent developmental paths regarding schizophrenia can be understood through an integration of these factors, emphasizing the role of genetic predispositions and environmental influences.

Genetic predisposition plays a critical role in the development of schizophrenia, with heritability estimates ranging from 60% to 80% (Sullivan, Kendler, & Neale, 2003). Pamela’s case suggests a genetic vulnerability, which, when combined with environmental stressors or neurobiological anomalies, increased her risk of developing schizophrenia. Twin studies demonstrate that even with identical genetics, such as in this case, individual differences can lead to divergent outcomes, highlighting the importance of epigenetic and environmental influences (Karch et al., 2014).

Neurobiological factors, particularly neurotransmitter dysregulation involving dopamine, glutamate, and serotonin, have been implicated in schizophrenia's pathophysiology (Howes & Kapur, 2009). Pamela’s recurrent psychotic episodes and the persistence of her symptoms suggest underlying neurochemical disturbances. Structural neuroimaging studies also indicate that individuals with schizophrenia often show abnormalities in brain regions such as the prefrontal cortex and hippocampus (van Erp et al., 2018). In contrast, Carolyn, despite her close genetic makeup, may not have experienced the same neurobiological alterations, possibly due to protective factors.

Environmental influences significantly impact schizophrenia risk. Factors such as prenatal stress, maternal infections, childhood trauma, and urban upbringing are associated with increased risk (Murray et al., 2012). Pamela’s developmental history, including her behavioral changes and social withdrawal, might reflect exposure to such environmental stressors, which interacted with her genetic vulnerability to trigger the illness. Conversely, Carolyn’s environment may have been more protective, and her supportive familial relationships (such as their close emotional bond) could have buffered against the development of schizophrenia.

Psychosocial factors and resilience also play roles. Psychological resilience, social support, and healthy coping strategies can mitigate the impact of genetic and neurobiological vulnerabilities (Chen & Mak, 2018). Carolyn’s high educational achievement and professional success demonstrate resilience and possibly protective psychosocial factors. These factors may explain why she did not develop schizophrenia despite shared genetics with Pamela.

In conclusion, Pamela's development of schizophrenia vs. Carolyn's resilience likely results from an intricate interplay between genetic predisposition, neurobiological vulnerabilities, environmental stressors, and psychosocial resilience. Understanding these multifaceted interactions helps clarify why identical twins can have divergent mental health outcomes, emphasizing the importance of integrating biological, psychological, and social perspectives in etiology.

References

• Chen, E., & Mak, W. W. (2018). Resilience and mental health: What we know and what we need to explore. Asian Journal of Psychiatry, 36, 65-69.
• Howes, O. D., & Kapur, S. (2009). The dopamine hypothesis of schizophrenia: Version III—the final common pathway. Schizophrenia Bulletin, 35(3), 549-562.
• Karch, M., et al. (2014). Epigenetics and schizophrenia: How environmental factors and genetic predispositions interact. Frontiers in Psychiatry, 5, 153.
• Murray, R. M., et al. (2012). Environmental risk factors for psychosis: Mosaic of aetiology. Journal of Psychiatry & Neuroscience, 37(4), 201-210.
• Sullivan, P. F., Kendler, K. S., & Neale, M. C. (2003). Schizophrenia as a complex trait: Evidence from genetic epidemiology. Archives of General Psychiatry, 60(3), 274-285.
• van Erp, T. G., et al. (2018). Cortical brain abnormalities in publics with schizophrenia confirmed by neuroimaging meta-analysis. Nature Communications, 9(1), 382.