Diabetes Basics Part 12


In the last part we left off talking about a diabetic feeling hungry and Dr. Hite saying this was because he or she wasn’t getting enough glucose into their cells, when we know this is an excess of hormones.

I mentioned high insulin levels and this is well known to make us feel hungrier, and there’s a reason for this, it is because this is a signal that we need to eat to counter the higher levels of insulin in our blood, to help the body manage the tendency for low blood sugar.

Now it does this just fine on its own but eating of course augments this.  Our bodies will do anything to keep our blood sugar from going too low, as our survival depends on it, it will even cannibalize itself here, and we actually see this happen in type 2 diabetics as well, and even type 1’s, and this is actually the reason why untreated type 1’s wither away to skin and bones, and I’ll explain a bit more about this in a moment.

Both type 2 and even type 1 diabetes are widely misunderstood, and Dr. Hite brings this out well in his next FAQ, where he is asked to explain the various types of diabetes.  The answers given are the fairly uneducated ones though, which is not what we’re after.

I’m not just out to poke this guy by the way for the sake of having an academic discussion, all of this has practical consequences in our management of diabetes, and in order to treat it properly, we must first understand what is actually going wrong, lest we make it worse instead of better, and making it worse instead of better is certainly the hallmark of conventional type 2 diabetes treatment that’s for sure, as I will explain.

Dr. Hite once again asserts that type 2 diabetes is high blood sugar caused by our cells not taking in enough glucose.  If this were really true, type 2 diabetes would be wonderfully easy to manage, you just give us some insulin and insulin increases cellular uptake of nutrients so that would be a cure actually.

This is basically what we look to do when we treat diabetes conventionally, to increase glucose uptake, but this not only misses the real problem here, it makes things worse and worse.

Insulin has two main functions, to suppress glucagon and to store excess nutrients.  In terms of blood sugar regulation, it’s function is to suppress glucagon, and when this doesn’t happen, and glucagon levels get too high, our blood sugar gets overregulated, and too much glucose is put into the blood.

This causes both types of diabetes, or we could say all three if we count type 1.5, which has components of both.  In type 2, glucagon is not suppressed properly, it goes too high, this puts too much sugar in our blood, and there’s actually no good way to dispose of this.  Insulin tries to and this makes us fat and even more insulin resistant, and it’s not the cells in our body that matter here, it’s the cells in our pancreas that secretes glucagon that matter, and to a lesser extent our liver.

If we just assume that the only problem we have is that this glucose isn’t getting into cells, we’re going to need a higher disposal rate than normal, from a higher insulin level than normal, but this is going to make glucagon go up even more over time, as the alpha cells of the pancreas get poisoned from this excess insulin and all the lipotoxity this produces.

So type 2 diabetes isn’t our cells in the periphery, our fat and muscle cells, not taking in enough glucose, it’s too much glucose being put into the blood in the first place, from the liver mostly, and from being told to do this by a confused pancreas, who thinks we’re low on insulin when in fact it is too high.

So the way out of this isn’t to raise insulin further, and promote more peripheral uptake of glucose, it’s to do the opposite, to look to normalize insulin  such that the pancreas and liver become more sensitive to it and stop going so crazy by pumping so much excess glucose in our blood.

This is all very well known by the way in case you are wondering, this is not just a matter of competing theories, this one versus the one that Dr. Hite espouses, his is just a bad guess where the hormonal explanation is very well proven.

Type 1 diabetes is also a matter of insulin not suppressing glucagon, although in this case, without endogenous insulin secretion, glucagon runs unopposed and raises blood sugar to extremes.  The reason why type 1’s have to inject insulin to survive is not to cover the carbs they eat as most of them think, it is to control excess glucagon.

We’ve done experiments and brought both glucagon and insulin down to zero and we see normal blood sugar, insulin isn’t required for that, and our cells will take in the glucose they need, and the amount they get from the diet is fine.  When you pile on extra blood sugar from the liver from excess glucagon, this is where things get out of hand, proportional to the degree of glucagon excess.

If we could control glucagon more effectively in type 1 diabetics, we would need to use less insulin, and also would have more stable blood sugar.  We have to elevate their blood insulin levels several times higher than normal, producing hyperinsulinemia, the disease of high insulin levels, because injected insulin cannot suppress glucagon anywhere near as well as secreted insulin, because its concentration in the pancreas and the liver is much higher than levels in the blood, where it becomes much more diluted.

So glucagon levels remain too high, although less so, and then the insulin disposes of the extra glucose that results, in our fat and muscle cells, but if we could control the secretion of this extra glucose better, we’d do a whole lot better job of managing this condition.

Controlling glucagon better is also a target for type 2 management as well, as this is what is wrong with us too.  One of the ways to control it is to attack the problem at its source, which involves normalizing insulin levels as a starting point, whereby the glucagon secreting alpha cells of our pancreas can start to heal, as the toxic load of ceramide from fat from excess insulin is brought more under control.

Dr. Hite claims that diabetes develops when insulin is ineffective at driving glucose into cells, but we should add that this is the case when it is no longer effective in driving all this excess glucose that is produced by our livers into our cells, but whether we even want this excess glucose driven into cells is a whole other question.

Regardless though, this is not where the defect is, we have to look upstream, and if we don’t, look out.

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