The Heart Of Diabetes Part 6








Our look at Dr. Unger's Rolf Luft Award lecture has been going on for a while but we've only covered part of it, and this is too important to just glean over, so it will take a few more segments and I do like to break these articles down into digestible pieces for my readers, and we'll seed several more anyway to finish discussing this video, so we will now resume that.

So we left off talking about Dr. Unger's breakthrough discovery back in the 1970's that the body's glucagon secreting alpha cells are not just confined to the pancreas, and that the stomach also has been found to secrete glucagon, and in significant enough amounts to cause diabetes with dogs whose pancreas has been removed.

We already know that from Dr. Unger's research that if we control glucagon, we control blood sugar, even in the presence of no insulin.  When we remove the pancreas though this does not solve the problem of excess glucagon, and with no pancreas, this means no insulin is secreted to control glucagon, and we know that controlling glucagon is the main function of insulin as far as glucose homeostasis is concerned.

So Dr. Unger then set out to find the cells in the stomach that secrete glucagon, after he found glucagon emanating from the stomach, and he did find alpha cells present in stomach tissue.  These gastric alpha cells were also found to be true alpha cells, secreting glucagon just like the ones in the pancreas do.

Before we move on, I want to add that our view of insulin being required for sufficient glucose uptake in the periphery, in other words for the body itself to use glucose, has been completely trashed by the research of Dr. Unger.

The dogma, as Dr. Unger describes prevailing beliefs about diabetes, assumes that we need insulin in amounts many times higher than normal for proper glucose uptake. Not only is this untrue, but a sufficient amount of insulin will do for that, a low amount will do as well, and even no insulin at all will do, as far as a sufficient amount of glucose making it into our cells is concerned anyway, although insulin is indeed required in sufficient amounts to control glucagon, provided sufficient insulin sensitivity is maintained.

The dogma here actually arises out of some pretty stupid conclusions, that the fact that we have hyperglycemia in itself means that we aren't taking in as much glucose as we should, which is clearly false, and only arises when we completely neglect the counter regulatory mechanisms that the body uses to elevate blood sugar, that are clearly shown to be imbalanced toward raising blood sugar.

So when they see two subjects who eat the same meal, and one has normal blood sugar, and the other has high blood sugar, they assume that the person with the high blood sugar isn't taking in as much glucose, leaving the amount not taken in in the blood.

We know though, with no uncertainty, that the real reason behind this is that the diabetic not only has to deal with the glucose from the meal, they also have to deal with varying amounts of extra glucose, driven essentially by their high glucagon levels, and this extra glucose is over and above the normal requirements of the body.

So what happens when we try to force this extra glucose into cells is that we not only worsen the underlying problem of alpha cell insulin resistance, which is caused both directly and indirectly by too much insulin, we also force toxic amounts of both glucose and fat into our cells in general, including our alpha cells, and this is why this approach not only fails but it so harmful.

Dr. Unger attacks another view which he correctly describes as dogma, and this is one that is very prevalent, which is the notion that insulin replacement is a sufficient treatment for type 1 diabetes.  Very few people indeed would doubt this claim in fact.

Although injected insulin is a life saving therapy for type 1 diabetics, it is just a workaround for the body's lack of insulin production, and does not take the place of our own insulin, and I also want to throw in that it does not take the place of our own insulin with type 2 diabetics either, although in this case it's generally used to add to the toxic levels of insulin that we already have, and even in cases of insulin deficiency in late stage type 2, we overdose it because it simply does not work anywhere near as well as our own.

So Dr. Unger, in a graph, first looks at a normal distribution of blood glucose patterns in a non diabetic, and then compares this with what we see with type 1 diabetics on insulin replacement.  So in non diabetics this is kept in a tight range, about 12 mg/dl on average, and when we look at the graph of the patterns of type 1 diabetics we see some very wild fluctuations, from dangerously low to very high and everything in between.

So Dr. Unger then wonders why this is the case, why we see such poor results from injected insulin, and he then explains for us why this is the case, and the difference has to do with the way injected insulin works versus the way natural insulin works, and this ties in to the role of the alpha cells and glucagon as well.

I've mentioned this elsewhere on the site and this is one of the big problems with injected insulin but it was through the work of Dr. Unger that we know this, although it's not something that's talked about much.

The level of insulin secreted by the pancreas that reaches the proximate alpha cells is at a concentration of 2000 units per ml.  It then gets diluted to 1/40 of this concentration by the time it reaches the liver, another organ where insulin sensitivity is critical, and then gets diluted to 1/400 of the concentration in the pancreas once it reaches the periphery.

He then compares this with a dose of injected insulin at 20 units.  So instead of the 5 units that are normal for the periphery, this dose increases that fourfold, not something we want.  The liver, on the other hand, is accustomed to a concentration of 50 units, but only gets 20.  The alpha cells require a concentration of 2000 units per ml, but only get 20 as well.  So this won't control glucagon very well at all, nor will it control the liver, but it does a good job at promoting peripheral insulin resistance because the concentrations here are several times higher than normal.

If you are just thinking that the only thing that matters is peripheral insulin levels, in other words if you are very ignorant of the physiology involved here, then it might seem that this is a good way to go, and should be effective, but this is far from the way the body works.

There's more to talk about here which we will resume in Part 7.

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