Factors that contribute to the development of schizophrenia
A lot of emphasis is put on investigating biological, scientific causes of schizophrenia and there is an ongoing hunt for identification of specific genes that can be targeted as the root of the problem. as this mystery gene/group of genes is yet to be established it becomes necessary to explore the contributions of other approaches such as the social and environmental theories to determine potential causes or stressors of schizophrenia this view is evident when u looking at certain biological theories.
Numerous studies involving the use of twins and concordance rates have been carried out to try and determine whether or not schizophrenia is caused by hereditary genes. Research implies that the higher the concordance rates established for MZ twins as opposed to DZ twins signifies a genetic link. (Gottesman & Sheilds, 1990; Tsaung, Gilbertson & Farone, 1991). Results indicate the monozygotic twins are more than 4x more concordant than Dizygotic twins providing strong evidence that schizophrenia is genetically determined. Despite the sufficient evidence however the results of the study illustrate that there must be other factors that contribute to the progression of the illness.
As cited in Carlson (1998) If schizophrenia was caused solely by the existence of such genes the results would be very different. If the gene was dominant at least 50% of children possessing two schizophrenic parents should be diagnosed with the illness and similarly “if it were recessive, all children of two schizophrenic parents should become schizophrenic”. As this is not the case other influences must be considered.
After reviewing adoption studies, Gottesman et al (1982) concluded that they provide adequate support for the genetic theory allowing researches to focus their research on “environmental stressors which activate the genetic predisposition”. Furthermore Zubin and Spring (1977) concur that we in all probability actually inherit a “degree of vulnerability to exhibit schizophrenic symptoms; whether or not we do will depend on environmental stresses”.
As cited in Gross (1992). The relevance of this point is highly important when related to the distinction between reactive and process schizophrenia. Reactive schizophrenia usually appears later on in life any symptoms manifest themselves quite suddenly, often in response to high levels of stress ( E.g. a death in the family). Conversely process schizophrenia describes individuals whose symptoms at some level have been apparent for many years.
Read (2001) conducted many experiments in to the histories of psychiatric patients and sufferers of schizophrenia. His results indicated the vast majority of people (two-thirds) suffering from schizophrenia had suffered physical and or sexual abuse in their lifetime suggesting that this form of trauma may have an influence on the progression of the illness, if not, in terms of reactive schizophrenia the source. Boydell (2004) suggests “the experience of abuse may create a biological or psychological vulnerability for the development of psychotic symptoms.”
Despite this however it’s difficult to determine whether or not these events have in fact taken place due to the nature of the illness. People suffering from Schizophrenia can experience delusions that are immovable beliefs in something very unlikely or bizarre. Patients often experience paranoid delusions where they feel people may be stalking them, or poisoning them or simply trying to hurt them in some way. It is therefore difficult to establish the validity of such claims, especially regarding such a sensitive topic which may bring conclusions made from Read’s (2001) investigation in to question.
A lot of research into the environmental and social causes for schizophrenia has been focused on the relationship between the family and the development of schizophrenia. Studies have investigated both pre and post natal familiar problems and particularly maternal problems that may prove to be potential catalysts to the onset of schizophrenia.
Huttunen & Niskanen (1978) noted that there were significantly higher numbers of people suffering from schizophrenia who were born during World War II and had lost their fathers in combat consequently demonstrating a link between the levels of stress endured by the mother impacting on the child’s mental health.
Similarly research findings suggest that post-natal loss or separation from a parent may also be a major stimulus in the development of schizophrenia. Both Heads et al (1997) and Pert et al (2004) separately conducted research that indicated vast numbers of patients suffering from schizophrenia had experienced some form of parental separation during their childhood. The stress and anxiety experienced during this time seems to have had great consequences on the minds of the individuals stressing the importance of functional families helping provide stable environments for children to develop in emotionally.
In addition to Huttunen & Niskanen (1978) research, the mother-child relationship has been further demonstrated as a potential impetus for the development of schizophrenia in terms of the “Double Bind Theory”, introduced by Bateson et al (1956). The “Double Bind Theory” insinuates that the communication style a mother adopts can influence the potential development of schizophrenia. It is the confusing “contradictions” within the communication style that predisposes children to schizophrenia. The child finds it difficult to respond to the demand correctly as its actions will undoubtedly be construed as wrong; this creates an internal conflict within the child.
Nonetheless as cited in Gibney, 2006, Hoffman (1982) suggests that its actually the attempts to “communicate concern, control respect and some limits” with somebody who suffers from schizophrenia that creates the feelings of contradictions and conflicting messages rather than the communication problems being the cause for schizophrenia.
Furthermore Fromm-Reichman’s (1984) research findings infer that a mother can “induce psychosis” in her child by responding to the child with behaviours considered negative or rejecting ,he labelled these women “schizophrenogenic mothers” showing again the negative impact of unstable mother-child relationships on a child’s mental health. Dispute regarding the credibility of this theory however indicates that like “Double Bind theory” it cannot be established whether this is simply effect of schizophrenia rather than a cause (Liem, 1974).
It is argued that the use of cannabis can lead to “acute transient psychotic episodes” in some people (D’Souza et al, 2004) and it has also been reported to produce a relapse in pre-existing symptoms of people who seem to be recovering from schizophrenia or at least responding well to medicine (Thornicroft, 1990; Mathers & Ghodes, 1992; Hall & Degenhardt, 2004). There is little evidence and much debate as to whether the use of cannabis can cause schizophrenia. There is significant cross-cultural evidence confirming rates of long term cannabis abuse amongst people suffering from schizophrenia in comparison to control groups of non-sufferers (Grech et al, 1998; Mc Creadi, 2002). The problem however is determining whether the use of cannabis is a cause or an effect of schizophrenia.
Hambrecht & Hafner (1996) reported on an investigation of patients suffering from schizophrenia, the study involved 232 patients disclosing their previous drug habits. The results showed that one third of participants had used drugs at least a year before the beginning of their illness, one third had used drugs and developed their illness within a year and the final third used cannabis after the onset of their schizophrenic symptoms.
Furthermore, Cantwell et al (1999) investigated 168 sufferers of schizophrenia. It was found that 37% showed evidence of substance and alcohol abuse before being presented to mental health services.
Evidence for a causal relationship between cannabis and schizophrenia comes from and relies solely on contemplative self-report studies. In order for more substantial evidence with higher validity, more prospective studies need to be carried out where bias and other such factors cannot confound the results.
Epidemiological studies have been carried out to determine whether any patterns in the distribution and causes of schizophrenia exist. Factors such as the season in which people are born, their proximity to the equator and population density have all been identified as potential influences.
Mortenson et al, (1992) carried out an investigation with a sample size of over 1.75 million participants and found that the longer time spent in urban areas under the age of 15, the higher the risk of a later development of schizophrenia. It can be concluded that this correlation may be attributed to a number of factors such as over exposure to infectious diseases, (densely populated environments encourages the spread of such infections) higher levels of stress, adversity, depression, poverty and higher levels of unemployment; all of which can influence the development of schizophrenia. According to Susser (1999) "It's not clear if it is birth in cities, or upbringing in cities, but there is something about city living that increases risk," he believes that the environment in which we are born and raised can be more of a determinant for schizophrenia than having a genetic predisposition.
The seasonality effect shows that there are disproportionately higher instances of people diagnosed with schizophrenia who are born during late winter and early spring. Kendall and Adams (1991) investigated the birth months of over 13,000 patients suffering from schizophrenia between 1914 and 1960 and found that significantly more participants were born in February, March, April and May. These results have been cross culturally (Takei et al, 1995; Tam and Sewell, 1995; McGrath, Welham and Pemberton, 1995). Pallast et al (1994) points out those babies born during this period will be developing in their second trimester during flu season. A time in which significant brain developments are occurring for the baby coincide with high outbreaks of the flu infection which may explain why the proportions of schizophrenia suffers born in these months are so high. This viral explanation may also give further support to that of population density contributing to the development of schizophrenia as infections are readily transmitted in these environments. The seasonality effect theory is strengthened in that it is more of a holistic approach combining both an environmental and biological explanation.
Finally peoples geographical positioning in terms of their proximity to the equator has been found to be yet another unusual factor seemingly influencing the development of schizophrenia. Labelled the “latitude effect” Dalen et al (1968) found that people born further from the equator are at a higher risk of becoming schizophrenic. As cited in Carlson 1998 an explanation for this may involve the climate as temperatures are lower in higher altitudes and considering that temperatures further decrease in the winter months it may be that the latitude effect is in fact another example of the seasonality effect.
Assessing both social and environmental explanations allow for insight to be gained in to the development and progression of schizophrenia. The problem however is It remains impossible to completely disregard all other explanations firstly because many are inextricably linked and cannot be separated for analysis such as the research into twin studies and the empirical evidence showing that more than one factor needed to be considered. Secondly, by critically analysing many different approaches, a more in depth non-reductionist view can be created which allows for strengths of different theories to complement each other providing a better explanation.
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