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Comment by abtinf | Hacker News Reader

Note that glucose is only a proxy for the actual thing we want to control, which is insulin.

Um...no. Excess glucose kills you slowly with tissue damage and ketoacidosis. Too little glucose kills you quickly by starving your brain of something it needs. So glucose is very much the stuff we want to control. The mechanism for regulating glucose is insulin.

Excess glucose doesn't cause diabetic ketoacidosis, but rather too little insulin. You can run high blood sugar for literally years without going into DKA (although it does damage your body). It's even possible in certain, rare circumstances to enter DKA with normal blood sugar.

You're right. DKA is the result of the body burning fat for fuel when insufficient insulin prevents it from burning glucose. I should have remembered that. My patients with DKA always had a BGL of 500 or more (5x normal), so that's why I mistakenly associated DKA with high sugar.

Insulin controls blood glucose. So how do you figure blood glucose is merely a proxy for insulin and not the actual thing an artificial pancreas is intended to control?

My guess - where does the target blood glucose level come from in a non-diabetic? The thing the body can't produce is insulin. Higher than target blood glucose is a sign that not enough insulin is being produced. I can roughly see the logic there.

As I understand it, target blood glucose levels for diabetics are based on normal blood glucose levels in healthy (non-diabetic) individuals. So presumably a healthy body has some internal mechanism for determining when and how much insulin to produce/release into the blood stream.

As far as I know, we haven't figured out what that mechanism is. But I'm not diabetic and I'm much less prone to being hypoglycemic than I once was, so my reading on the subject is fairly casual compared to when I did things like wrote a research paper on Functional Hypoglycemia in part for my own edification.

That's wrong.

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