In science, there is often a predilection toward conceptualizing cognitive events in a discrete, measurable fashion. This tendency has been most prevalent in investigating intelligence through an intelligence quotient, yet this kind of approach has also been applied to mental disorders. Psychiatrists now speak of depression in terms of serotonin and dopamine, not necessarily in how one experiences the feelings and emotions behind certain behavior.
Although this is often taken as dehumanizing, it is a natural human tendency to believe that there is some sense of self-efficacy to be obtained in overcoming our own biology. This is of course a foolhardy idea in that one cannot overcome what one is at a physical level in any phenomenological sense. Yet, it provides us with a necessary illusion that we have control over our worldly actions. Simply stated, individuals often believe that people are depressed simply because they cannot tolerate the world or that anorexia is simply a manifestation of not attaining some sense of being able to control the world.
This brings us to a scientific article in the Proceedings of the National Academy of Sciences by Fetissov et al. expanding on previous work looking at molecular markers for the eating disorders anorexia and bulimia. Looking at a diagnosed population of 12 anorexic patients and 42 bulimic patients versus 41 healthy individuals, they found that in addition to their early work demonstrating the production of autoantibodies to two neuropeptides, alpha-melanocyte-stimulating hormone and adrenocorticotropic hormone, individuals with anorexia also contain autoantibodies against oxytocin and vasopressin. Further, alpha-melanocyte-stimulating hormone demonstrated a correlation with the intensity of disease symptoms of eating disorder. These antibodies against the body's own signaling devices are believed to interfere with the normal melanocortin functioning that include regulation of appetite.
More interestingly, the discussion of this paper details an odd and as of yet unproven hypothesis: These autoantibodies are the result of molecular mimicry by infectious agents. Certain pathological agents, such as Escherichia coli, Helicobacter Pylori, and influenza A virus have proteins with a stretch of five amino acids that are in common with both adrenocorticotropic hormone and alpha-melanocyte-stimulating hormone perhaps providing a mechanism for microintestinal flora causing eating disorder behavior.
What makes this article truly interesting is not the novelty of the concept, but rather the entire lack of support that exists for it. The only connection between infection and eating disorders is that autoantibodies, which themselves are not known to be pathogenic entities in eating disorders, have a five amino acid sequence similarity with two agents which autoantibodies are made against.
This hypothesis is actually a manifestation of current paradigm as opposed to the evidence that exists. Besides a small sequence similarity that one likely can find occurring naturally by chance, there is not a shred of evidence presented to support the influence of infection in eating disorders. It is much more plausible that the production of these autoantibodies is in response to stress, but this is not mentioned. It would seem that the desire to produce consistent hypotheses for a paradigm focused on simple, discrete phenomena has superceded a rational, methodical approach to the problem at hand. It would behoove scientists to take into account paradigmatic bias when approaching problems within science.
Michael can be reached at michaelmcduffie@virginia.edu
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