Friday, July 3, 2009

Part two: insulin resistance

This is part two of a series of non-consecutive posts which attempt to explain in the simplest of terms the nature of a disease called diabetes mellitus.

Defined in the simplest terms I can think of, the disease we call diabetes occurs when the glucose in our bloodstream is unable to get inside the cells to provide the energy the cells need to carry on their essential life processes. The cells "starve" and die.

As the disease progresses, every system in the body begins to suffer. When small blood vessels block, terrible things happen to body tissues from lack of blood supply, and secondary diseases flourish. Some of these things will be covered in other posts.

The two reasons that glucose doesn't get into the cells are either that the pancreas is no longer making sufficient insulin to accompany the glucose, or a phenomenon called "insulin resistance" is occuring. Insulin resistance means the cells no longer properly "recognize" the insulin's "password", and will not allow the glucose to enter. More on this later as well.

Although the end result can be the same, there are two variations of the disease. You have probably heard of "Type I" and "Type II" diabetes. Again, trying to be as simple as possible, "Type II" is often self-inflicted, caused by poor diet and a sedentary lifestyle. "Type I" you can't prevent: you are born with a pancreas that doesn't produce insulin.

Type I was simply fatal in childhood in the old days. The increasing prevalence of "Type II" has prompted many advances in the treatment of the disease, although it is also still fatal pretty quickly if left untreated. Since the fairly recent ability of laboratories to synthesize human insulin, the days of early death for people born with "Type I" diabetes are over. This series of posts, however, is intended to talk more about the "self-inflicted" kind of diabetes. More to come.

This is a very important subject to the author of these posts. Because diabetes is important in today's world, your comments are encouraged even more than usual. However, I plan little actual interaction, comment-wise, until the entire series has been presented. This is because I realize how easy it will be to take "side trips" or, horrors!, to turn this into a medical text. The author intends to be ruthlessly simplistic in order to make the principles of the subject as clear as possible to those readers who don't already have a working knowledge of the disease, and, most of all, to explain to many of my readers who (whether they even know it or not yet) are now in the early stages of diabetes themselves, and what they need to do NOW to fight back.

Since, at the end of the series, I want very much to have step-by-step discussions, won't you please continue to comment anyway, so that we will have "notes" to go back to when it is discussion time? I am counting on you!


  1. I remember quite vividly a human biology lecturer explaining how diseases like type 1 diabetes are becoming more prevalent because they are no longer fatal. The patient is unlikely to die and will probably go on to have children who may inherit a susceptibility. Survival does of course depend on the patient doing as he's told.

    I remember it vividly not because of any particular interest in diabetes at the time, but because of the student who got to his feet to question the mental state of anyone who would marry a diabetic. The initial laughter gave way to startled silence when we realised he was serious.

  2. Since my mother has Type II, I have had gestational diabetes, have PCOS and am overweight, I am high risk.

    But I'm taking steps now to address it.

  3. @A. - Yes we've come a long way, medically-speaking. And in the way we look at things, too. For sure a genetic disposition (if your parents had it) but I think we are also pushing up the statistics because of our new lifestyles.

    @Stephanie B - I'm glad you realize you are at risk and because of that you are using the knowledge to fight back. So many other people don't have a clue, it seems. But the info seems to slowly be getting out there.



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