Wednesday, February 14, 2007

Sea change coming in type I diabetes treatment

Two decades ago, it was learned that Type 1 diabetes is the result of an auto-immune disease where the patient's own immune system attacks and destroys the islet cells that make insulin. Since that time it has been learned that the body is quite resilient and has more islet cells than it needs. Therefore the disease is well underway before symptoms occur because the body is able to deal with the loss of islet cells for some time before enough islet cells are destroyed to cause a reduction in insulin production. At that point, the die is cast. The body can no longer compensate for the lost islet cells. In research published in this months' Scientific American magazine, it has been shown that there are three antibodies that appear in between 70% and 90% of those that are diagnosed with type 1 diabetes. It is thought that these antibodies, which includes an antibody against insulin itself, as well as antibodies against glutamic acid decarboxylase (GAD), and a protein called Islet Antigen-2 (IA-2), are responsible for the destruction of islet cells. But even if they are not the bad actors themselves, they serve as markers for those who's islet cells are under attack. That is the key, because if those individuals who's islet cells are under attack but have not started showing symptoms yet can be identified, the disease can be stopped before any further damage is done, sparing them (or at least delaying) a life of needles and blood sugar tests and disease complications. Immunosuppressive drugs like those used for Rheumatoid Arthritis and Lupus such as Enbrel and for eczema like Elidel hold promise that the autoimmune reaction can be damped down in order to spare the islet cells. This is obviously not a cure, but it can clearly prevent or delay onset of active diabetes.

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