I certainly don’t want people thinking that managing type 2 diabetes is merely a matter of controlling one’s diet, and we often need additional help to best manage this condition, and at times quite a bit of it. There are several therapeutic goals here, but the most fundamental one is looking to better balance our hormones, and in particular look to more normalize the hormones insulin and glucagon, although there’s more hormones that need balancing and more things that need fixing.
Diet needs to be the starting point though, the cornerstone of the treatment, because if we don’t fix this, we aren’t really going to address the underlying cause here which is high insulin. If our diets continue to produce too much insulin then we’re just going to be stuck in the mud and in fact sink deeper into it.
I’m going to wrap up this current FAQ of Dr. Hite’s that we’ve been looking at, but before I do I wanted to talk a bit more about this, and in particular, his view that high blood sugar means that insulin is not high enough.
The view he takes here could be called demand side glucose metabolism, just looking to increase the demand for it by using insulin to break down the barriers that our cells have erected to oppose it. I’m not even sure where people ever got the idea that this was the problem, but it likely just came from knowing that insulin does facilitate nutrient uptake, glucose uptake in particular, we have too much glucose in our blood, so we need to increase the uptake of it.
This is why we actually want to look at what really happens and not just assume, and not just assume for instance that this much glucose in our blood is normal, or that it’s even a good idea to accelerate the uptake of glucose by way of excessive amounts of insulin.
I’m going to talk more about this confusion later in the series, as Dr. Hite looks at this more specifically, but we know already that the real problem is one of oversupply, but this oversupply is actually worse than you may think.
One of the characteristics of alpha cell insulin resistance in type 2 diabetics is that insulin, instead of limiting glucagon secretion, actually tends to accelerate it. We can see this when we measure insulin and glucagon levels after a meal. Normally, insulin goes up, this puts glucagon down, our livers turn off their extra glucose production, because it’s not needed now, we’re getting glucose from the meal.
Much of the after meal spikes that we see from food isn’t from the food, it’s from the liver, and the liver not only doesn’t stop adding extra glucose now, but in the presence of the higher levels of insulin that we get after meals, especially after high carb meals, the liver increases its glucose production.
This is because it’s instructed by glucagon to do so and glucagon is the boss here, as it needs to be because this is the process that keeps us from dying just from going without food for a few hours.
So the more carbs you eat in a meal, particularly fast acting ones, the more glucagon rises. Now some of this is due to our lack of phase 1 insulin secretion, there’s none available because due to our higher blood sugar the beta cells release whatever insulin they make immediately, and therefore there’s none to save up to get a head start on meals.
This is not from lack of beta cell function by the way, it’s from their secreting too much insulin around the clock, they are too busy in other words and don’t ever get a rest, and don’t get to save up insulin so a bunch gets released initially following meals.
So during the early stages of the meal, insulin should be higher, glucagon isn’t suppressed like it should be, and this does factor into things, and this is one of the things that Dr. Unger discovered during his experiments.
That’s not enough to explain things though, and while glucagon doesn’t get turned down initially, this doesn’t explain why it goes up instead, or why it stays high as our delayed insulin response kicks in to typically several times healthy levels of insulin in our blood.
We’re not even exactly sure why this happens, but when you go up a lot from a high carb meal, it’s the meal secreting all that insulin that has caused glucagon to rise so much that is to blame, not the meal itself. Interestingly, we’ve isolated this by keeping glucagon in check like it is supposed to be, and give type 2 diabetics high carb meals, and they maintain normal blood sugar. So glucagon is to blame here as well.
For whatever reason, our alpha cells have evolved by way of their becoming toxic such that insulin itself is toxic to them as well, and while we are left to speculate as to the exact pathway here, it really doesn’t matter because we do know high levels of insulin cause these cells to go even more haywire, but what we need to do is limit their exposure to high insulin and then we can be affected by this less.
So the condition of type 2 diabetes is actually one called hyperglucagonemia, excessive high levels of glucagon, caused by hyperinsulinemia, excessively high levels of insulin. That’s type 2 diabetes right there in a nutshell, which is actually just a symptom of hyperglucagonemia.
Type 1 is also a condition of hyperglucagonenia, but this time the cause is a deficiency of insulin, not an excess. Hyperglucagonemia persists even with treatment with injected insulin, as the amounts needed to control glucagon excess properly would require blood levels of insulin to be needed to be kept so high that this would result in dying of low blood sugar, as this would bring our blood sugar down to dangerous levels or worse,.
So that’s what diabetes is, too much glucagon, although it is caused in each type by a different mechanism. It actually helps to know what is wrong with us by the way, because only then can we treat it properly.