Dr. Amy Nett: So, I think, okay. Interpreting this I think how I would piece this together is that I would agree with you that the pathogenesis of type 2 diabetes absolutely involves inflammation, insulin resistance, and it may or may not be somewhat autoimmune mediated, but I’m going to put the autoimmune component somewhat aside and say that 1.5 or LADA is unique. So we’re talking strictly about type 2 diabetics, where we don’t have autoimmune-mediated antibodies that have been identified. I think that inflammation is probably a driving factor, and if you on Facebook, I think last week, I posted up a paper in response to one of Laura’s questions about how to assess the degree of beta cell destruction. And I think that paper might have talked about some of the mechanisms that lead to type 2 diabetes.
I think the issue with type 2 diabetes is that it begins with inflammation and there’s a development of insulin resistance. And I think that that inflammation progresses to destruction of the beta cells. And so what Chris is saying is in this “full-blown type 2 diabetes” you end up with beta cell destruction. So and that’s as opposed to, and this is kind of again what Laura’s question was, was like, well, wait a minute, we have patients and they’re pre-diabetic or maybe they’re actually in that diabetes range. But if we can, I don’t want to say “save them,” but if we can improve their blood sugars they don’t necessarily become insulin-dependent. So there’s that group of patients that’s showing insulin resistance, they’re showing inflammation, they have blood sugar dysregulation, but we can get them back on track. And they might be defined as type 2 diabetes for a period until we bring them back into more normal blood sugar control and they do not have complete beta cell destruction. And that’s why they’re able to recover.
So what Chris is saying is full-blown type 2 diabetes is often when that blood sugar dysregulation has gone on for such a long time that you get destruction of the beta cells and the type 2 diabetes becomes essentially irreversible at that point. And again, I think I mentioned last time, I had a patient and her fasting blood sugar was something like 187, her hemoglobin A1C was eight or nine, I don’t even remember, and she really, she really didn’t want to go on medication and wanted to do this through a functional approach. But she isn’t able to do that anymore. I applaud her for trying, but we probably just started too late in the process. Because at that point, yes, when there is that degree of beta cell destruction and you can’t get a fasting blood sugar to be less than 180 even with intermittent fasting, the potato hack diet, protein-sparing modified fast, we tried everything.
So she’s probably gonna be insulin dependent because you’re going to need insulin at some point to get the glucose into the cells. And once you’ve progressed to the stage, and again, you’re absolutely spot on from inflammation. Once you’ve progressed to this stage of blood sugar dysregulation, where there’s been just so much inflammation and the body is overproducing insulin for so long that the beta cells give up, they die, and that’s when it’s essentially at that irreversible place where they become insulin dependent and actually do require medication. So that’s where we want to try to avoid getting people, but hopefully that clarifies because I think you’re absolutely right. It’s initially it’s insulin, insulin all the time, inflammation all the time, but then it leads into the destruction of the beta cells, loss of having any insulin, and that’s what we call full-blown type 2 diabetes. So send some other questions if that doesn’t make any sense and I’ll go back into the previously submitted questions. But yep, let us know. Because it’s a great question and diabetes is pretty tricky. A lot going on with that.