Psychology

The article in question appeared in the American journal of psychiatry and has been written and presented by a number of authors. It deals with the correlation between evidence of prenatal exposure and an infection of the upper urinary tract and its familial susceptibility. The authors purport that previous studies of this type have demonstrated a two, five even tenfold indication for the increased risk of schizophrenia caused by various other ailments and use these results in an attempt to bring legitimacy to this study. This essay will attempt to critique said article by presenting the research methodology employed and discussing the fallibility of said procedures (Clarke, Tanskanen, Huttunen, Whittaker,  Cannon, 2009).

The primary methodology by which this research study attempts to make its case is by creating correlation between the data contained within three registries. They are known as the Finnish Hospital Discharge Register, the Medical Birth Register, and the Finnish Population Register. The collection of this data was done at the National Research and Development Center for Health and Welfare and was used to identify all individuals born between 1947 and 1990 who were exposed to pyelonephritis prenatally. The study uses siblings of the individuals in question who were not exposed to the disease pre natal as a comparison group (Clarke, Tanskanen, Huttunen, Whittaker,  Cannon, 2009).

Using the Finnish Hospital Discharge Register psychiatric diagnosis was ascertained for all the exposed cases, the comparison group, as well as the parents of the subjects in question. The diagnosis were recorded according to the classification provided by the International Classification of diseases (ICD) provided by the world health organization. According to the timeline different versions of the ICD were employed with criteria for psychosis defined as having family or siblings with broadly defined history of psychosis (Clarke, Tanskanen, Huttunen, Whittaker,  Cannon, 2009).

The logistic regression model was employed in order to calculate the probability ratios for the occurrence of schizophrenia. In order to correlate the effects of the infection prenatally with the development of psychosis, the trimester in which the infection took place was taken into account. Other methods were also employed in order to assess the risk factors for pre supposed infectivity (Clarke, Tanskanen, Huttunen, Whittaker,  Cannon, 2009).

Of the recorded 9,596 individuals who were the subjects of this study and the comparison group of siblings composed of 13,808 individuals. The study found that the familial liability for developing schizophrenia was 6.4. The study also found that there was no correlation between the timing of the infection and the occurrence of the psychotic episode. However, the risk factors for those who had a family history of broadly defined psychotic disorder was much greater than for those who did not. The data also provides evidence to suggest that infection in the first trimester leaves the individual more susceptible to schizophrenia, however with the chosen sample only consisting of two people such a conclusion is hypothetical at best. Additionally, the scientific mechanism for the incidence of the psychiatric disease has also been provided, however such findings are inconclusive (Clarke, Tanskanen, Huttunen, Whittaker,  Cannon, 2009).

Unfortunately it must be said that the true fallibility of the writers research lies in the methodology which has been employed in order to ascertain the correlation between schizophrenia and pre natal exposure to pyelonephritis. While in theory the methodology is sound and cost effective, the primary analysis of the data requires the consideration of all patient data provided to be factual. While it is true that the chosen sample was quite large and the comparison subjects were also suitably large. Other variables such as age of incidence, sex, marriage, occupation, personal relationships, and previous mental health status were not taken into account. Additionally, the study admits it limitations concerning the absence of data regarding the number of therapies and medications prescribed to the individuals, as well as the antibiotics prescribed to the mothers during their pregnancies.

Not only does the primary diagnosis of schizophrenia employ the use of outdated diagnostic criteria, but also does not allow for the supposition of a misdiagnosis on the part of the attending psychiatrist. Additionally, while the logistic regression model which has been employed to assess the data is competent enough to assess the risk factors for the incidence of the disease. The employment of Discriminant analysis estimators also seems warranted.

The resulting risk factor calculated at 6.4 does not corroborate the theory for familial liability of upper urinary tract infections. In fact if a margin of error for the calculation is taken into account the number would be lower as well. The risk factor would further decrease if taken into account that a certain number of the parents had been diagnosed as having a broadly defined form of psychosis. Such a familial history of psychosis has been proven to be an important etiological factor for the incidence of schizophrenia and further show the fallibility of the authors contentions.

While the study is purported to use environmental factors as a reason for the incidence of schizophrenia in patients it does not take into account that there may be other factors in play here which may have induce such psychotic episodes.  Other studies which have attempted to compare the effects of first and second generation antipsychotics on schizophrenics have found that there are a variety of environmental factors which can increase the incidence of the disease and the outcome of the studies including but not limited to acute symptoms, substance abuse and other co-morbidities, lack of quality of life. These studies have admitted that the incidences of these factors are key in the measurement of the outcome of not only the incidence of the disease but also the effectiveness of the medication prescribed. They admit however, that such measures and real world clinical practice cannot always be taken into account (Altamura  Glick, 2010). In the case of this research study this point of contention particularly holds true as the data on the clinical practices employed, as well as antibiotic therapy are simply not available in order to exclude a viable cause.

While it may be true that schizophrenia may have ties to the incidence to disease pre-natally, especially in the first trimester. The data provided is insufficient to ascertain if upper urinary tract infections were truly the root cause of schizophrenia in these cases. It may be more prudent to conduct a long term study into the effects of urinary tract infections which takes the variables suggested into account. Although, the results of such a study would be subject to limitations as well, the inherent lack of appropriate data in this study does not make it a viable resource to make such a diagnosis. Additionally the conclusions which have been reached by the authors regarding the mechanism of action of this disease would also not be required to be based on supposition if they simply had the opportunity to conduct pathological and biochemical examinations.  The positive and negative syndrome scale can also be employed to ensure viability of the study and allow for differentiation of chronic and acute symptoms.