Sunday, March 31, 2013

First Respondent— Integrating the Causes of Chronic Diseases

 Paul Ewald's informative piece on chronic diseases, in particular atherosclerosis highlights an essential but lacking facet of modern day medicine and how humans approach health complications. Modern day health professionals often seek to cure proximate causes, and are thus limited to proximate-level perceptions. I bring this common pattern up, as does Ewald. He demonstrates how this constricted thinking has caused many individuals to overlook ultimate-levels of causation in denoting chronic diseases. By eliminating and curing symptoms, it is inevitable that the root of the disease itself is not cured, and the ability for it to rise up again is very likely, in a fashion far more dangerous and less preventable.

Before this week's reading, I had never realized the spectrum of complexity the mere term "risk factor" holds: primary and secondary correlations instead of causation. Often it is thought, by myself in particular, that possible risk factors can be considered as adverse causes the stronger and detrimental they are to the individual. In other words, if a risk factor of a disease or medication is high blood pressure, the prior existence of high blood pressure greatly increases just how negative the risk factor is. This in turn, is what may appear to be the "cause" of a chronic disease as opposed to the mere correlation; especially because the risk factors accounted for are not present in all people. As mentioned before, Chapter 19 focused on the ultimate causation of one chronic disease through three possible hypotheses. It was warming to notice that these hypotheses were actually based off of concepts we have already discussed in class. For example, the rich diet hypothesis hints at how change (environmental, societal, and technological) has been developing far too quickly for biological evolution and natural selection to adapt to. This aligns with the thrifty genotype hypothesis which sheds light on the mismatch theory. The bad allele hypothesis looks at fitness trade-offs; for example the presence of an allele in all humans for the degree of its expression and purpose it serves. And lastly, the longevity hypothesis demonstrates how the persistent existence of alleles (even the bad ones) don’t have to be experienced in a species until environmental factors trigger them. Thus, many confounding factors are able to complicate our understanding in the exact cause of chronic diseases.

Overall, the significance of understanding all possible causes of infectious and chronic diseases is critical to diagnose, treat and even more importantly prevent stronger strains. But the causes stem beyond our typical perceived understanding into realm of risk factors. As a result, we retain integrated influences that work together to provide holistic measures and analyses of chronic diseases.
After reading this chapter, it brought to my attention once again the issue of the treatment of chronic diseases. It seems that drugs versus holistic care of infections approach risk factors and causation through different angles. In my opinion, holistic care uses a more integrated perspective of the above hypotheses whereas prescribing drugs is limited to more of the “bad allele” hypothesis. Perhaps the evolution of medicine will recognize the integration of both these viewpoints. 

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