A guy i know wants to use Alpha lipoic acid (for long periods of time) which isn’t technically a diabetic drug but it can increase insulin sensitivity. Type 2 diabetes runs in his family and he is worried about a negative feedback loop. i.e., if ALA makes his body respond effectively to less insulin, his pancreas will respond by producing less insulin and over time his pancreas and Islet of Langerhans cells will atrophy as less insulin is needed to do the job. He fears this could cause an onset of Type 2 diabetes.
There is a class of Type 2 diabetic drugs called thiazolidinediones that also increase insulin sensitivity and i have never heard of a negative feedback loop occuring with them but does anyone know if there is a risk that drugs that increase insulin sensitivity will cause the pancreas to respond by producing less insulin?
Paging KarlGauss! If anyone here will really know, (as opposed to just searching the literature), It’ll be he.
(I’ve never thought about that question myself. I just beats 'em with metformin, sulfonylureas, glitazones, insulins, and ACE inhibitors till they gets better)
Hypoglycemia is described in this context as insulin resistance (insensitivity) leading to insulin oversufficiency leading to a large drop in blood sugar. This is amplified over time in a feedback loop that results in insulin overproduction, high ambient blood sugar, and the exhaustion of the pancreas.
A low-refined carbohydrate diet is recommended for people at risk of developing Type II. This is both to (a) decrease weight gain, and (b) decrease the demand for insulin.
JAMA describes low-carbohydrate alcohol (e.g., vodka) as increasing insulin sensitivity and thus providing a flatter insulin profile. They clarify that alcohol increases insulin sensitivity rather than causing hypoglycemia (though people taking Metformin, etc. should not drink without talking to their doctors).
Exercise does not just use up available blood sugar, but increases the body’s sensitivity to insulin.
It’s generally thought that the post-industrial diet we enjoy grossly overfeeds us with refined carbohydrates, accommodating which puts stress on the pancreas, which is doing more work than it is suited to do.
This suggests to me (and IANAMD) that activities/substances that increase insulin sensitivity DECREASE rather than INCREASE the risk of developing Type II diabetes. Type II diabetes is related to insulin OVERproduction and that the goal of Rx, diet and exercise interventions is in fact to decrease insulin production by increasing insulin sensitivity. Since we need insulin to stay alive, I will be so bold as to suggest that if your friend eats anything, his body will not cease to produce sufficient insulin, but that he may lower the threshold of insulin demand in a way that is salutary. NB: Insulin levels can be checked by a doctor.
Well, shucks, Qad, you make me blush :o (especially because I know you know the answer as much as anyone).
In a nutshell, yes, anything that improves insulin senstivity will lead to less insulin being produced by the pancreas. This would be expected to be a good thing, though. Trust your intuition here: if the pancreas is producing less insulin, it will have more reserve, and for longer.
Conversely, things that increase insulin secretion (or almost equivalently, things that increase insulin resistance) may, eventually, lead to exhaustion of the insulin-producing beta cells of the pancreas.
Things can get confusing, though. So, for example, if insulin secretion increases sufficiently that the glucose level is lowered, that may set in motion a set of effects that, ultimately, lead to improved insulin sensitivity to insulin and thus less insulin needing to be secreted. In other words, correction of hyperglycemia, by any means, leads to both improved sensitivity to insulin and less “toxicity” to the beta cells. This is a bit of a contentious issue, eg. drugs like glyburide increase insulin secretion. On the one hand, this may lead to a lower sugar level and thereby lead to decreased insulin resistance and less demand on the beta cells. On the other hand, the ongoing stimulation of the beta cells by the drug, may lead to beta cell exhaution. I think it’s still an open question.
Can i get your professional and/or educational credentials Guass? if Q.t.M. recommends you on a medical question then you probably have some pretty good ones. The guy im asking for, i think hes studying medicine in the UK so he will most likely want to know who is giving him this advice rather than me just saying ‘someone on the internet’.
I used to be an endocrinologist but then de-differentiated to become a mere general internist (although at a higher rank, mind you ):). So, in addition to medical school, I have four years post-grad training in Internal Medicine and three more in Endocrinology (plus more years of real-world experience than I care to admit!).
Let me use this opportunity to say that I am absolutely amazed by Qad’s consistently outstanding comments, insights, and advice. I guarantee you: few docs are as a eclectically gifted. Does everyone here know how unique he is, and how fortunate they are to have him? The man is amazing! (and I hear he’s a good kisser, too)
I don’t have time for a detailed answer right now. Bottom line, everything I know suggests the opposite will be true, i.e. a drug that makes you more sensitive to insulin will decrease the chance of you getting type II diabetes.
Thanks for the kudos, Karl, but don’t be ridikerous! I’m a basic generalist who just has an opinion on everything.
I am a good kisser, too. But only Mrs. Mercotan’s opinion counts, as she’s the only one with firsthand knowledge.
I also agree with your last statement. There’s no real way for the islet cells to atrophy just because they’re producing less insulin because they’ll always need to provide a constant amount of baseline insulin to take care of essential bodily glucose metabolism. So the pancreas is always on idle, and gets revved when carbs are ingested. That’s gotta be much better than gunning it all the time to produce more insulin.
