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October 23, 2016
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Going Viral — The Damage in its Wake

While researchers have isolated in the vicinity of two dozen genes associated with autoimmune (type 1) diabetes, we still haven't figured out how one of a pair of identical twins might develop type 1 diabetes, while the other remains diabetes-free. (Such a case exists.) This suggests that while genes may be part of the equation, they're not the sum total of "why someone gets type 1 diabetes".


One theory I've read is the "trigger event" theory. There is a significant percentage of the type 1 community whose diagnosis stories include having had some sort of virus or flu shortly before developing the typical diabetes syndrome (incessant hunger and thirst, frequent urination, lethargy, unusual and rapid weight loss, etc.). At least one published theory suggests that a specific enterovirus may be the triggering factor in these cases. The question remains, though, why a once-through virus might cause lifelong damage...


Then I am reminded of the aftermaths of viral diseases such as polio (which confined US president Franklin Roosevelt to a wheelchair), mumps (which can make an adult man sterile), and smallpox, as well as bacterial diseases such as the rheumatic fever which left my great-aunt with lifelong heart problems. The acute stages of these diseases have killed many thousands. While "garden varieties" of flu kill more people than we'd like to believe, most people survive without any permanent damage as do most people who get a stomach virus.


In Advanced Placement Biology which I must admit to have taken nearly 35 years ago (when our knowledge of genetics and immunology was based on empirical, rather than molecular and microbiological, evidence) we were taught that viruses replicate (reproduce) by injecting their RNA into cells in a way that turns those cells into virus factories. Some scientists believed that cancer worked in a similar fashion, though they did not know what turned a particular cell, or locus of cells, into "cancer cells" (or, conversely, what would cause a person's body to not recognize the cancer as "foreign" and destroy it before fatal damage occurred). While we've located genes (BRCA1 and BRCA2) that have high association rates with particular types of cancer (early-onset, rapidly-developing breast cancer), and we know that toxins in the environment can cause mutations in human tissue that are also associated with cancer (as well as other chronic or fatal medical conditions), we still can't pinpoint exactly what happens, and why the body's immune system doesn't "come to the rescue".


If flu shot recommendations are to be taken at face value, the message is that "people with weakened immune systems are those most likely to die from an influenza virus". It is also said that diabetes weakens our immune systems. This is somewhat confusing, since the common belief is that people with autoimmune conditions (like type 1 diabetes) have immune systems that "work overtime"... How do we reconcile that seeming contradiction? What if the real underlying issue is that the genes associated with autoimmune disorders like the genes associated with breast cancer are those of an impaired immune system in the first place, allowing the enterovirus (or other triggering factor) to attack the immune system? And what if what that enterovirus does is change the RNA of target immune cells to attack the body's beta cells (or the tissues associated with any other particular autoimmune disease)?


I'll admit it's a pretty long-shot, through-my-hat sort of speculation. But it puts diabetes (and other autoimmune conditions) in a class of diseases that includes cancer, explains the implied immunodeficiency/autoimmunity connection, and potentially relates them all with known virally-transmitted immune system diseases (including HIV), as well as historical "scourge" diseases.


Which probably makes the theory too simple, and too simplistic, to be anything near correct.

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