Diabetes is a chronic disease that affects the way glucose is utilized in the body. The necessary mediator for glucose uptake and utilization is via a substance produced in the pancreas called insulin. Although factors associated with insulin are the primary causes of diabetes, the two types have very different pathologies in relation to insulin. Type one, known as insulin dependant, results from an insufficient insulin production, where the cells need glucose from the blood, but there is no insulin production to facilitate glucose transport into the cell. Type two is non-insulin dependant, and is associated with normal insulin production, with cellular resistance (Kumar, 2010).
Although there have been many hypotheses developed to describe the etiology of diabetes mellitus, one study by Barbeau, Bassaganya-Riera, and Hontecillas (2007) suggests that hygiene may be a significant factor in the development of type 1 diabetes, in what they refer to as a “hygiene hypothesis.” In this hypothesis, it is thought that individuals with a predisposition to diabetes that are more frequently exposed to infections have a lesser incidence of developing the disease. Epidemiological statistics supporting this theory show that there are significantly lower prevalence rates of diabetes type one in areas that are prone to infections, such as the tropics, as well as in highly populated areas, where infections can be spread easily and children are exposed at an early age (Barbeau et al., 2007). Furthermore, Barbeau et al. (2007) explains that, in an experiment involving mice with a genetic predisposition for diabetes, mice that were raised in a pathogen free environment had higher rates of diabetes development than other genetically predisposed mice raised in normal conditions with exposure to various pathogens such as viruses and parasites. The rational for then phenomenon is linked to the idea that diabetes is a disease of autoimmunity. Barbeau et al. (2007) advocates that “the protective role of infections observed in human autoimmune diseases may be due in part to “antigen competition (Bach, 2001),” in which, theoretically, if the immune system is preoccupied with infectious agents and inflammation, there would be a “down-regulation” in the development of diabetes (Barbeau et al., 2007). In addition, identical twin studies showed that the numbers of CD45RO+ CD4+ lymphocytes (immune cells involved in the inflammatory response) are higher in the twin without diabetes, than in the twin that does have diabetes, with a concordance rate of at least 50% (Wu, 2005).
These finding present many aspects of controversy to health care providers. When assessing a client with a family history of diabetes, it is important to consider these findings in educating our patients. Generally, when managing diabetes, it is beneficial to advise clients to avoid potential situations that promote exposure to pathogens, due to the increased susceptibility for infections that diabetics typically acquire (Kumar, 2010). When discussing with patients with a genetic predisposition, it might be beneficial to suggest the idea of early exposure to benign pathogens that might be a possible strategy for prevention. Furthermore, this provides a foundation for health care providers to seek more information through conducting more research on the subject in order to better accommodate or decline this theory.
Bach, J. (2001) Protective role of infections and vaccinations on autoimmune diseases,
Journal of Autoimmunity, 16: p. 347–353.
Barbeau, W., Bassaganya-Riera, J., & Hontecillas, R. (2007). Putting the pieces of the puzzle
together – a series of hypotheses on the etiology and pathogenesis of type 1diabetes.
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Kumar, V., (2010) Endocrine disease: Diabetes mellitus. Robbins and Cotran:
Pathologic basis of disease, 8th Ed. Online Case Studies. Philadelphia: Elsevier
Wu, D. (2005). Bacterial glycolipids and analogs as antigens for CD1d-restricted NKT cells,
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