Why Our Phase 1 Insulin Is Diminished

phase 1 diminished









When we look at the glucose and insulin curves of type 2 diabetics, we do see a delayed response, leading to greater blood sugar excursions, as well as delayed insulin release patters compared to non diabetics.

One of the concerns that we do have is that we tend to go up too much from meals, our blood sugar that is, and if we were able to put out more insulin initially, right after the meal, we would do better with this, but not for the reasons that you might think.

What you need to realize is that with type 2 diabetics typically, our insulin does go up plenty, even though it is delayed.  However, it may go up several times normal, as evidenced in the seminal work of Dr. Joseph Kraft, who had this odd idea that perhaps insulin levels should be measured during a glucose challenge.

I was speaking to a gentleman the other day who is doing epidemiological research for the government on diabetes, and he had never heard of Dr. Kraft, nor did he seem to be aware of hyperinsulinemia playing any role in type 2 diabetes.  I did encourage him to look into the matter, whether he does or not is another thing, but it's so sad that Dr. Kraft still remains a relative unknown even among people considered to be somewhat experts.

You have to do a little more digging than looking at the standard, conventional literature we could call it to discover a lot of the truths behind this disease, and the companies who make countless billions aren't lining up to embrace this knowledge to say the least, anything that disturbs the status quo and their huge profits is not seen as favorable.

So even massive excursions of insulin levels aren't enough to normalize our blood sugar by the way, as evidenced in the sheer amount that we do put out typically, once again several times the amount a healthy person would.  We still can sit there with blood sugar several times normal as well.  This is what insulin resistance does though.

So our getting the timing wrong with phase 1 insulin response isn't a big deal at all on those terms, and would be fairly meaningless actually.  It does matter though, and you have to look to the main mechanism of insulin on blood sugar, which is regulation of glucagon.

The main reason, by the way, that we see both high insulin and high glucose isn't so much that insulin isn't effective, it's not as effective but this still isn't the main cause, a bigger reason is that our livers are pumping out very large amounts of glucose right along with what we've eaten, still thinking that we are starving.

Ironically, liver dumping, as it is often called, is highest after we've eaten a meal, not in between, as we might think, and this is because glucagon levels are highest then.  Glucagon is of course the primary hormone that raises our blood sugar, and while insulin is supposed to turn it down, with us if often gets turned up even more after meals and after insulin is increased.  This spells real trouble.

At least part of this broken and strange response is due to a lack of phase 1.   Our beta cells normally keep a reserve of insulin at the ready to be used at mealtime and this is what phase 1 is.

If our beta cells are putting out too much insulin all the time though, there's little or no reserve for meals, so it must make it on the fly.  Dr. Unger has shown clearly that when phase 1 is absent, glucagon goes significantly higher, and once that starts, then our blood becomes quickly overwhelmed with glucose from the liver, and this can be more than even a heightened insulin response later can handle, especially in the presence of the insulin resistance we all have to various degrees.

So there are two separate but related pathologies here, the lack of glucagon suppression in the alpha cells that is the hallmark of type 2 diabetes really, and the fact that our alpha cells are secreting too much insulin around the clock and have little or none in reserve to evoke a healthy phase 1 response post prandial.

In a real sense, we never really get to true fasting levels, because due to high glucagon all the time, our bodies are acting just like we're eating all of the time.  With type 2 diabetics typically, the majority of our blood glucose does not even come from the diet, even if we eat a high carb diet, even if we live across the street from McDonalds and use that as our dining room.  Even more glucose than that provides comes from the liver, so liver glucose is significant indeed.

Those with persistently high blood sugar get a particularly large percentage from the liver, and contrary to popular belief, this glucose just doesn't stay in the blood, it is constantly being taken out by insulin and more is constantly added by the liver.

One of the first steps in looking to understand type 2 is to realize that it's not that we can't handle sugar, we just make too much of it, and unless you get that, you are going to be on the wrong track essentially and probably will just make the disease worse and worse.  This confusion engulfs all of conventional medical thinking though in spite of the science telling a different tale, science is only paid attention to if it supports their views, the ones that don't, don't make the hit parade at all, like all of the work of Roger Unger for instance.

So if we're going to try to fix our phase 1, we don't need more insulin, we need less, and specifically, we need to be secreting less during what is supposed to be fasting times, even though they don't represent fasting very much physiologically.

Some think that adding exogenous insulin will help here, and it can take the load off the beta cells, but by increasing insulin levels, all you will do over time is to damage the alpha cells further, inevitably leading to more and more lipotoxicity of the alpha cells and more and more glucagon excursions.  This means higher and higher blood sugar in the end, period.

So things to reduce insulin, like dietary management, as well as certain supplements which take the load off here, as well as anything that reduces insulin resistance, especially things that reduce chronic cellular inflammation, will take us in the right direction to trying to improve our phase 1 response, and in doing so, this can really help our blood sugar management.

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