The article under review is, “Applying Bradford Hill’s Criteria for Causation to Neuropsychiatry: Challenges and Opportunities,” which was published in “The Journal of Neuropsychiatry and Clinical Neurosciences.” This article makes use of Hill’s guidelines. This review has made extensive use of Hill’s guidelines in hypothesizing causality based on the assessment of the literature on Neuropsychiatry. The review reveals the benefits of using proven standards in coming up with assertions regarding causation in Neuropsychiatry. It also demonstrates the various challenges associated with the contentions of causation.
This article refers to various aspects of the Hill’s guidelines although some of them are problematic in their implementation during the assessment. This review strengthens and facilitates the use of the Hill’s guidelines and criteria in Neuropsychiatry. Hill’s criteria allow the researcher to be critical about the strengths and the barriers of causation arguments. This also facilitates the potential upgrading of research development and methodology in researches of causation within Neuropsychiatry (Van-Reekum, Streiner & Conn, 2001).
It is evident that some of the Bradford Hill’s guidelines are significantly relevant, or practicable to be utilized in Neuropsychiatry rather than others. Illustrations of a correlation between the causative instrument and the outcome, a biological rationale, the relevant temporal sequence, and the regularity of the findings are all prerequisite criteria that are reasonable to achieve (Aschengrau & Seage, 2008). Despite being relevant, they may experience potential difficulties in the execution. It is noted that biological gradient, specify criteria, analogous evidence, and coherence may not be appropriate for Neuropsychiatry. However, where they can be illustrated, they will increase the contention for causation. Experimental evidence is quite convincing. However, it is hampered by ethical issues. Despite some of these guidelines having their own limitations, their systematic application leads to an immense rigor as compared to non-systematic contentions of causation (Van-Reekum, Streiner & Conn, 2001).
This article has highlighted the purpose for rigorous criteria to determine causation in Neuropsychiatry. However, it fails to address the procedure for determining an argument of causation. What eventually convinces the researcher that factor “X” also causes outcome “Y”? Ultimately, the researcher has to make that decision based on the researcher’s reevaluation of the evidence. Nevertheless, individuals appreciate the perspectives taken by others, mostly from the experts. It is only when there is an agreement between the experts that humans accept an argument of causation. However, caution should be taken as experts are also human, and may be biased to some aspects. The aspect of bias is most evident in a court of law. Legal experts from the different sides argue with great enthusiasm, and usually from the same combination of evidence, as to whether a certain laceration in the brain can be attributed to a given characteristic of behavior. Knowledge of the criteria for developing arguments about causation, as well as research strategies with their strengths and limitations used to tackle these criteria, minimizes the risk of being disoriented by the knowledge of other experts (Van-Reekum, Streiner & Conn, 2001).
Despite this argument, many scholars practicing epidemiology argue that biological plausibility and determinism are significant considerations when determining the nature of a correlation. The central idea of causality is closely associated with the notion of determinism. Various scholars associate causality with strict causal determinism and the possibility of reason and logic. A good example is a study done on hospitalized cardiac patients in which one half was prayed by Christian volunteers participating in the study. In this study, the patients who were prayed had fewer heart attacks and rarely contracted pneumonia than those who did not receive prayers. Many epidemiologists do not subscribe to this due to the lack of a biological framework to justify it.
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