Developmental theories embody perspectives about environmental forces and human essence that build a path of human development. Developmental psychopathology theories embody these perspectives as well, and the information from ‘normal’ and ‘pathological’ human life courses enlighten current models of development (Davies & Bhugra, 2004). Thus, for instance, the healthy child and the biological model both agree that certain predetermined behavioural pattern may be impervious to environmental forces. Similarly, knowledge about relapse to previous patterns of behaviour necessitates the re-evaluation of the idea that every process of development is a change and; that every previous pattern of behaviour is transformed into entirely new one (Haugaard, 2008). Undoubtedly, developmental models should be relevant to both normal and pathological development.
This essay discusses two models of developmental psychopathology, namely, the (1) biological model and the (2) environmental model to critically evaluate how they are able to account for the etiology of schizophrenia. These two models, which are antecedents of the different developmental perspectives, explain how these perspectives differ and how they can be applied to gain better knowledge of the etiology of psychopathology. It is crucial to regard them in this way so as to identify their weaknesses and strengths. Biological Model and Schizophrenia
Numerous scholars adopt several variants of the stress-vulnerability model of schizophrenia, and one of the most widely used is the biological model of psychopathology. The biological model uses the concept of ‘diathesis’ to explain vulnerability to pathologies. A ‘diathesis’, in particular, is usually viewed as a “biological predisposition to develop a disease or morbid condition” (Shean, 2004, 79). The biological model largely claims that risk for schizophrenia is a polygenetic imperfection that is outside the boundaries of healthy discrepancy. In addition, it is believed that harmful episode at some point in prenatal development that may lead to a brain defect which increases the risk for development of schizophrenia (Shean, 2004). According to Ciccheti and Cohen (2006), vulnerable people are believed to be inclined to react with pathological responses to the common pressures of life.
Stress-vulnerability models differ concerning their arguments about whether stress and diathesis are believed to be needed, adequate, or causal factors. Scholars also disagree on the question of whether the genetic risk for schizophrenia is inherently polygenetic or monogenetic (Shean, 2004). Advocates of the polygenetic theory take up some kind of a supplementary model of stress-vulnerability relationship, where diverse genetic stressors and variables add to a risk point (Heinrichs, 2001). According to Jang (2005), the influence of environmental forces is believed to be a component of the scale of genetic risk. Individuals biologically above the point need slight or no stress to have schizophrenia, individuals merely below the point will have the pathology under almost all situations, individuals slightly below the point need extreme stress to have the pathology, and individuals way below the point are not prone to have short psychotic responses even under situations of severe stress (Shean, 2004). Numerous theorists believe that the genetic risk for schizophrenia is somewhat confined in the general population. As a result, life stressors are seen as a comparatively minor component in schizophrenia’s etiology. Some scholars believe that the polygenetic effects that add to diathesis for schizophrenia are extensively dispersed in the normal population (Weinberger & Harrison, 2011). Because nobody has successfully discovered a genetic indicator for schizophrenia, the character and importance of a genetic risk for vulnerability to schizophrenia are still one of guesswork. The biological model has numerous valuable uses, for instance,...
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