The State of T1D Outcomes published


@Mary67 It was wonderful before I moved, my Endo was a type 1 and her NP was a type 1 too.

They only took your pod to download and would just comment if they thought changes should be made, mostly they went over your blood work and asked if you needed help. You could ask them questions and they had experience themselves besides the benefit of seeing a lot of type 1’s so experience with that too. She actually ran meetings for type 1’s. You could also e-mail any questions you had and they would be answered,

That was one thing I knew I would miss when I moved and I have! I was glad I first got my pump and CGM under their tutelage! True gems !


Ted - I don’t believe what you’re suggesting takes into account the fact that in non-diabetics, glucagon is produced and released by the alpha cells as frequently as insulin from the beta cells. This occurs at near normal blood glucose levels - the bodies insulin is far superior to what we T1D’s & T2’s inject, and as often as not the amount of insulin produced to counter rises in sugars needs to be attenuated immediately (by glucagon).


Jim, I think what you’re saying is in line with Cryer’s theory that insulin secretion regulates glucagon secretion. This is probably the mainstream theory today of glucagon regulation, and it logically leads to the conclusion that the counterregulatory dysfunction is a result of exogenous insulin infusions not correctly mimicking endogenous beta-cell secretion.

However, the data about direct beta- to alpha-cell, paracrine control is mixed. For example, this study concluded the following: Thus, it is unlikely that suppression of insulin release during hypoglycemia modulates plasma glucagon responses in normal man and that lack of a decrease in intraislet insulin concentration is responsible for the lack of a plasma glucagon response to hypoglycemia in subjects with type I diabetes mellitus.

Another study concluded the following: (I)n the absence of diabetes, the majority of the glucagon response to insulin-induced hypoglycemia is mediated by redundant autonomic stimulation of the islet -cell.

As an aside, Jim, given the complexity of human physiology – which is an extremely complex, dynamic system of feedback and feedforward signals, experiments which artificially vary one or two components are often flat out wrong about how the system actually works. Which is why it is dangerous to lock in to any hypothesis without the results of carefully design clinical studies.

Anyway, I personally favor the concept of autonomic control of the glucose counterregulatory response for two reasons:

  1. It makes sense that the brain would be the tissue to raise the hypoglycemia alarm first.

  2. Pursuing this hypothesis in conjunction with certain other data could lead to a novel, testable hypothesis.

To fully develop that hypothesis, another aspect of glucagon secretion needs to be considered: normal glucagon secretion is suppressed following food intake. And, the alpha-cells in T1D patients do NOT reduce glucagon secretion in response to postprandial rises in blood glucose and exogenous insulin.

How can that be explained via the autonomous nervous system? What signal would it receive to suppress glucagon secretion?


Ted - Before replying to you, I’m consulting with the most qualified medical professional I know (a PhD in metabolic disorders).

I’ll report back when I’ve heard from him.


Good! The more the merrier. Ask him if he is aware of anybody working on a pharmaceutical approach to restoring the glucose/glucagon counterregulatory (CGR) response in T1D…


We are missing functioning beta cells