Biological and Environmental Models in Etiology of Schizophrenia - Essay Example

?Running Head: Developmental Psychopathology Strengths and Weaknesses of the Biological Model and Environmental Model in Determining the Etiology of Schizophrenia An Essay Name Course Title Name of Professor Date of SubmissionIntroduction 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, when analysing possible genetic roots of consequent psychopathology. An individual who inherited a particular gene or cluster of genes is predicted to show psychopathology at a later period. The biological model distinguishes several of the studies in the genetics of psychological disorder (Joseph, 2006). At this point, environmental factors, or the interface between them and the genes, serve hardly any function in the possible result. For instance, Kallman’s (1946 as cited in Joseph, 2006, 237) study on the genetic aspect of schizophrenia reinforces the application of the biological model, just like the presence or absence of specific substances on depression (ibid, p. 237). In all of these instances, the presence of specific attributes is presumed likely to influence a specific form of pathology. Even though the biological model is remarkable in its straightforwardness, it still has several limitations; for instance, not every individual who has a genetic indicator at a specific point in time is expected to display consequent psychopathology or a similar form of psychopathology (Miller & Mason, 2002). For example the case that every child of schizophrenic parents does not develop schizophrenia, or that not every monozygotic twin exhibits similarity in relation to schizophrenia indicates that other factors have to be taken into account. It is vital to emphasise that the failure to come across a significant prevalence of schizophrenic children of schizophrenic parents suggest that factors such as immunity, coping approaches, and invulnerability to stress, are protective factors in those with genetic vulnerability to schizophrenia (Weinberger & Harrison, 2011). For many years, the dominant belief about central nervous system pathologies was that they were either inherently psychological or neurological (Maj & Sartorius, 2002). Neurological pathologies were regarded to be those that changed the brain’s chemicals; psychological pathologies were those that encompassed emotional aspects. With the introduction of pharmacological substances, useful in the treatment of anxiety, depression, and psychosis, it became apparent that a psychological disorder could involve modifications of brain wiring and suggest a presence of a neurological pathology (Maj & Sartorius, 2002). Over the past three decades, this point of view has given momentum to development of studies, which focus on the effects of medication and pathophysiology of psychological disorders. Moreover, this period has been characterised by considerable development in the model of neuroscientists and psychologists of psychopathology research and how etiology of physiological disorders during adulthood, adolescence, and childhood is approached (Joseph, 2006). In particular, according to Frith and Johnstone (2003), various levels of analysis are required to gain accurate knowledge of how maladaptation versus adaptation influences pathological and normal development. A widespread assumption for schizophrenia’s etiology has been that individuals with this pathology could have disproportionate levels of dopaminergic functioning. With earlier family research reporting a more significant prevalence of schizophrenia among the next of kin of individuals with schizophrenia, it was proposed that genes might be the cause of the suggested boost of dopaminergic functioning (Ciccheti & Cohen, 2006). Nevertheless, seeing schizophrenia as a genetically transmitted pathology made some clinical findings ambiguous. For instance, the rate of similarity for the disorder among monozygotic twins was reported to be roughly 50%, making it practically unlikely to clarify the incidence of schizophrenia merely based on a hereditary attribute (Ciccheti & Cohen, 2006, 569). Furthermore, according to Csernansky (2001), because numerous schizophrenic individuals show a characteristic deterioration in functioning during the disorder’s initial period, it becomes apparent that a neurodegenerative mechanism could be present in the disorder’s etiology. It has traditionally been assumed that schizophrenia may characterise a diverse cluster of pathologies, with several patients having a neurodegenerative disorder and others a hereditary disorder (Frith & Johnstone, 2003). This assumption has had certain credibility because both etiologies might possibly clarify a number of the disparities in the medical appearance of individuals with schizophrenia (Frith& Johnstone, 2003). For instance, a number of patients display a prevalence of unfavourable syndromes— these symptoms are psychological capabilities which a schizophrenic cannot use anymore. Schizophrenics with observable unfavourable syndromes were discovered to be more prone to manifest ‘volume loss in computerised axial tomography scans of their brains’ (Ciccheti & Cohen, 2006, 217). Nevertheless, according to Joseph (2006), this classification has been unsuccessful in explaining the finding that majority of patients with schizophrenia manifest the prevalence of both unfavourable and favourable-- these favourable symptoms are psychological confusions in the schizophrenic’s subjective view of reality, such as delusions, hallucinations, etc.) attributes and cannot be simply divided into these two separate groups. However, a number of scholars contradict the biological model. They argue that schizophrenia is a composite neuro-developmental pathology that has considerable genetic roots and is affected as well by environmental factors in the first years of development (Torrey, 1994). However, a social perspective has a major influence at every stage in the pathogenesis and growth of schizophrenia. At the moment of gestation the social and cultural contexts are involved. For example, one of the determined risk factors for schizophrenia, which is influenced partly by socio-cultural aspects, is paternal maturity at gestation (Read, Mosher, & Bentall, 2004). The placenta, the developing infant, and the mother, during conception, work together as a network. The child develops into an individual after birth, and the family develops into one of the most important social groups. It introduces values nearest to the individual where development takes place. Furthermore, the family gives an important perspective for children regarding experiences acquired in wider social contexts (Read et al., 2004). It is likely that families maintain experiences acquired in a particular social context and bring them into a different social context, which influences children. For example, current studies examining the rural-urban disparity in schizophrenia showed that children raised in rural districts were at heightened vulnerability if their families had resided in an urban district before their birth (Carr, 2006). This emphasises the essence of the family as a social group for offspring during conception and early stages of development with regards to schizophrenia’s etiology. Nevertheless, according to Heinrichs (2001), the social environment affects not just the etiology but psychopathology’s development as well. As stated by Heinrichs (2001), studies comparing schizophrenia’s development in less developed nations with that of highly industrialised nations show that affected people in less developed societies encounter a more tolerable development of schizophrenia in spite of the comparative absence of pharmacological and other medications in these environments. It appeared that a two-factor perspective for schizophrenia could clarify more accurately these different findings. As stated in the two-factor model, if a slight brain problem takes place in the context of genetic vulnerability for schizophrenia, possibly both could cause the pathology (Ciccheti & Cohen, 2006). Therefore, a perspective of schizophrenia where both a premature brain problem and an influencing biological feature are indispensable for its development appears more likely. This two-factor theory of schizophrenia is in agreement with the assumption of Hebb (1949 as cited in Ciccheti & Cohen, 2006, 217) that both genetic makeup and environmental forces serve major functions in the development of psychological disorder. A major concern for a two-factor framework of schizophrenia is to recognise the genetic vulnerability for the pathology (Jang, 2005). Even though evidence for a main deficiency in dopamine activity has not been informative, a number of researchers have searched for other, more workable phenotypic symbols. For instance, adjustment of ‘smooth-pursuit eye movements’, which gives the eyes the ability to clearly see a moving object (Weinberger & Harrison, 2011, 75), that have been discovered in individuals with schizophrenia and their immediate kin could be associated with a basic disparity in the makeup of a person who bears a genetic material for the disorder. The biological model’s pursuit for ‘schizophrenia genes’ has been in progress for decades. Recent years have witnessed the reports from a number of studies declaring to have discovered an indicator for a schizophrenia gene (Frith & Johnstone, 2003). Consistently, these investigations were unsuccessful at replication. The report of Sherrington and associates (1988 as cited in Frith & Johnstone, 2003), for instance, to have recognised an indicator was followed up with a report by Kennedy and colleagues, who were unsuccessful replicating the results (Frith & Johnstone, 2003). However, despite the evidence to the contrary, Jang (2005) claims, there is a general knowledge that genetic indicators or genes for schizophrenia and other psychopathologies have been discovered. According to Frith and Johnstone (2003), the failure of the biological model to discover genes for schizophrenia does not indicate that these genes are nonexistent; however, the assumption that adoption and twin research has already verified the genetic source of the disorder is incorrect. It is quite surprising that, rather than verifying the findings of schizophrenia adoption and twin research, the unsuccessful search for schizophrenia genes possibly will encourage scholars to re-evaluate these seriously unsound and environmentally confused adoption and twin research. That schizophrenia’s genetic source is a basic verified finding in psychiatry reveals a lot about the failure of the biological model to decisively study the theories and techniques of its own studies. In numerous manuals in psychology, psychiatry and associated disciplines, professionals have discovered the same naive recognition of the findings of adoption and twin studies (Miller & Mason, 2002). Thus, the biological model necessitates a second look. In view of the above discussion about the biological model, it is concluded that the developmental psychopathology framework has developed and deepened current knowledge of schizophrenia by putting emphasis on the developmental roots and early signs of the pathology. As a result, research on schizophrenia’s developmental roots has supported developmental psychopathology by suggesting that it is applicable to both childhood and adult pathologies. Hence, it appears suitable to consider the importance of social perspective when looking at etiology of schizophrenia. Environmental Model and Schizophrenia The classic environmental model states that external forces affect development. However, there are two major difficulties in applying this model, namely, (1) the failure to take into account the effect of environmental factors throughout the life course, and (2) complexity in identifying what the environmental factors are (Shapiro, 2000). Indeed, the best type of the environmental model supports the suggestion that adjustment to existing environment, throughout the life span, is a primary influence in an individual’s socio-emotional being. The individual adapts as the environment changes (Torrey, 1994). According to Schumaker and Ward (2001), this forceful and shifting theory of adaptation and environments is in heavy opposition to the previous environmental theories, which suggest that factors influencing an individual occur just in the initial stages of life. Even though the environmental model has some inherent limitations, this model strongly and persuasively argues that the coexisting health condition of a child is established by environmental forces. As explained by Kerig and Wenar (2006), the environmental model is distinguished by the assumption that the stabilities, changes, and restrictions in the psychopathology of children depend not quite much on internal systems found in the child as in the child’s environment, system, and nature. As discussed earlier in the trait model, genetic aspects have a major influence in the root of schizophrenia. However, genetic aspects do not provide a complete explanation and other factors need to be taken into account. Other forces should contribute. An environmental model explaining the risk of psychosis relies upon the success of identifying or understanding the development of the personality of that individual (Joseph, 2006). One of the primary claims of the environmental model is that distressing emotional episodes produce psychological trauma that forces an individual to relapse to a previous phase of emotional development. Such relapse can be related to the development of psychotic syndromes (Joseph, 2006). In certain instances the individual takes up coping techniques for managing emotional tension, but as such tensions build up, the coping techniques are ultimately defeated and psychotic syndromes appear. The precise processes fundamental to the progression of these episodes are not detailed, but the apparent argument of the environmental model is that stressful episodes are a trigger for the development of psychoses (Read et al., 2004). This argument results in a quite verifiable proposition suggested by Read and colleagues (2004), that persons who have schizophrenia have experienced more emotional tension in the past than persons who do not develop this mental illness. Furthermore, family perspectives of schizophrenia emerged from within the environmental model. Bateson proposed that some parents continually communicate vague and contradicting messages to their children (Frith & Johnstone, 2003). This communication pattern would have a permanent impact upon children, so that in later stages of development these individuals may communicate in similarly abnormal ways resulting in a behaviour identified with schizophrenia. Later scholars have supported this assumption (Frith & Johnstone, 2003). According to Joseph (2006), Lidz and associates claimed that irregularities of parental bonds might force the child to be incapable of interacting with other people in a ‘usual’ way. However, the environmental model of schizophrenia has not, in general, given adequate attention to the variety of different indicators related to schizophrenia. Stresses, tensions, unsettled conflicts, and particularly responses to anomalous communication patterns within the family unit are brought into play to describe unfavourable symptoms like problems in building and maintaining rapport with others and social withdrawal, and favourable symptoms like mirage and fantasies (Sameroff et al., 2000). Nevertheless, outside the environmental mode, there is an extensive literature suggesting that social forces could have a particular function in the growth of unfavourable indicators in schizophrenia. This literature is mainly interested in the impacts of institutional care. The notion is that in an institution the unavoidable life impoverishment i will heighten and could produce the absence of encouragement and social withdrawal observed in schizophrenics (Read et al., 2004). It is generally agreed that a poor environment is harmful for individuals with schizophrenia. Moreover, most scholars would support the assumption that these environments possibly will worsen the problems cause by schizophrenia (Read et al., 2004). According to Maj and Sartorius (2002), the misfortune is that for numerous schizophrenics nowadays the physical, material, and social impoverishment related to institutional care will be possibly worse than what they would have encountered in the earlier, healthier institutions. In addition to this, arguments in the environmental model have also been put forth about several biological aspects in the early environment of the individual that could heighten the vulnerability to schizophrenia. These arguments are widely rooted in epidemiological research, which examines disease patterns in big populations (Frith & Johnstone, 2003). If it is discovered that an illness takes place more often in one location than in another, this can provide evidence about the cause/s of the illness. Furthermore, the environmental model states that some attributes of schizophrenia are influenced by gender (Frith & Johnstone, 2003): Many studies have shown that the average age of onset in men is about five years earlier than that in women. The two sexes have also been shown to differ in the course of the illness in more general terms. Women seem to have functioned better before the onset of the illness and are less disabled afterwards... One suggestion is that illness takes a more benign form in women through effects of estrogens (female sex hormones) on dopamine D2 receptors (ibid, p. 120). These assumptions of the environmental models, and its accompanied empirical methodologies evidently contributed to the understanding of the etiology of schizophrenia. However, just like the trait model, the environmental model cannot completely account for the cause/s of schizophrenia. Conclusions Hypothesis-oriented research in the field of developmental psychopathology, particularly in the arenas of biological model and environmental model, has generated few valid and reliable findings about the actual etiology of schizophrenia, even though due to the methodological problems the effect of life episodes cannot be taken for granted. But despite of these failures or limitations, these findings thus far are enlightening us about schizophrenia’s attributes and nature. Therefore, how the significant environment forces work together with genetic aspects could be fundamental, but currently assumptions in this field are more exploratory than evidence-based. References Carr, A. (2006). Handbook of Child and Adolescent Clinical Psychology: A Contextual Approach. London: Routledge. Ciccheti, D. (1989). The Emergence of a Discipline: Rochester Symposium on Developmental Psychopathology. Hillsdale, NJ: Lawrence Erlbaum Associates. Ciccheti, D. & Cohen, D.J. (2006). 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