Some More Thoughts for Type I Diabetes

A really long prayerful dog walk around the NIH, as I contemplated the signs.  At 100 graves per sign, there would be a sign every 1/2 foot around the perimeter of the NIH.

Thinking about what is really needed right now in type I diabetes research, I think that one of the most significant advances that could be made in the near future would be a reliable method for detecting islet damage.  Islet autoantibodies are not good indicators of disease.  Although, apparently present 95% of the time over the course of islet destruction, not everyone possessing these autoantibodies progresses to type I diabetes.  Clearly, it is possible to modulate the immune system, so that tolerance develops, and patients do not lose all of their functioning islets.  One only needs 5-10% of islets to maintain correct blood sugar levels.  The key here is detection of the problem.  Is it possible to develop tests that will detect islet damage more directly?  For example, let’s say someone was infected with any of a variety of vectors containing an insulin gene – flu, pneumonia, TB, whatever.  Most people will start to make antibodies to insulin because damage is occuring at the site of infection (the lung, or the sinuses, etc).  How do we stop these antibodies from attacking the pancreas and destroying all the islets? 

It’s been done, the question is how.  What about the 5% who don’t have autoantibodies?  Could a PCR test be developed with a more direct marker of islet damage?  Would it be a macrophage?  How to detect damage?

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