One of the current theories about the cause of Type I (Insulin-Dependent, or Juvenile) Diabetes is that sufferers are predisposed to catching a virus which attaches itself to the outlet ports on the surface of the pancreas; these ports generate insulin. The body’s immune system generates antibodies which fight off this virus and, just to make sure, also kills off the ports (d’oh!). The antibodies remain in the bloodstream so that even if the ports heal, they just get killed off again. Some type II (non-insulin dependent) patients may have this happen, but enough ports stay functioning to generate some insulin.
There is a treatment being studied which involves transplanting insulin-creating ports from a healthy person to the surface of the pancreas, along with some bone marrow from the healthy person, so that the transplanted bone marrow sends the message to the immune system that these ports are okay and don’t need to be killed off. The patient needs to take immune-suppressing drugs for the operation to take hold, it only lasts for a couple years, and there is the possibility of an immune-system turf war taking place within the patient’s body.
Not for me, thanks.
The general roadmap for diabetes is that people acquire Type I diabetes before they’re 20 or type II (non-insulin dependent, or adult-onset) after they’re 50. In both cases, the patient will usually have been fairly overweight for most of his or her life (with the understanding that for the Type I patient, that’s 10 years, and for the type II patient, that’s 25-30 years).
I acquired Type II diabetes when I was 33, and I had been maybe 10 pounds overweight for about five years. This really annoyed my doctor. I then shifted to Type I about two years later when the diet/exercise thing stopped working for me.