It’s the Insulin, Stupid, Part 3

I’m returning back to the series on looking at Amy Berger from Tuit Nutrition’s series It’s The Insulin, Stupid, which is excellent in itself and certainly worthy of going over in detail here.  Her series does cover a lot of ground so my version of it no doubt will as well, and it’s obvious that we both have been blessed with the ability to write long passages on topics.

Her series is 8 parts long, and I’m still working my way through part 1 and I’m on part 3 of mine, so who knows now many segments this will take us but we want to do all this stuff justice because it’s that important.

We left off talking about Dr. Joseph Kraft and his over 10,000 oral glucose tolerance tests in which he measured both insulin and glucose levels at regular intervals over 4 hours.  The information he compiled over the years is extraordinarily valuable, the only database of its kind really, sadly enough, as we don’t generally care about insulin levels very much.

Among the treasures that emerged here is the fact that over 80% of the people he tested had issues with glucose processing, what he calls diabetes in situ.  In situ means basically in its natural state, and if diabetes is to be understood as disturbances in glucose tolerance, then the in situ version certainly qualifies as diabetes.

The way I would describe this is to call all of this what it is, disturbances of insulin secretion, both in magnitude and timing, too much insulin and at the wrong time in other words.  This is a disease in itself, apart from type 2 diabetes, and it’s called hyperinsulinemia, where more insulin is secreted than normal, and his numbers do tell the story here as these days we know that about 8 people in 10 have this, which matches Dr. Kraft’s results.

So 8 people in 10 have this metabolic disease, and you would think that this would scare a lot of people, but no one really pays attention to this.  They do pay attention to the most popular symptom of this, which is becoming overweight, and that’s what too much insulin does, it stores too much fat.

Insulin’s other important function is to suppress excess glucagon from the pancreas to be secreted, and over time the alpha cells become poisoned by all the excess toxic fat in our blood that hyperinsulinemia causes, and it starts to lose its sensitivity to insulin, and this is when our blood sugar starts to get out of control.

So it’s not even a relative lack of insulin that does us in here, as crazy an idea as that is actually when you think of it, it is a loss of insulin sensitivity by the alpha cells, and this has been well proven, starting with the work of Dr. Roger Unger decades ago.  Diabetes really is the state of excess glucagon, caused by years or even decades of too high insulin.

So given that more and more people have high insulin levels these days, should we be surprised that more and more people are becoming overweight and obese, and more and more people are getting type 2 diabetes?  Both these common conditions have a common cause, hyperinsulinemia, and this condition causes a number of other things, virtually all of the modern chronic diseases as a matter of fact.

There’s nothing that predicts one’s likelihood of diabetes more accurately than insulin levels, not weight, lifestyle, genetics, nothing.  This was the main mission of Dr. Kraft actually, to get us to screen for this by testing people’s insulin levels, this all fell upon deaf ears in the medical community though and to this day we rarely test anyone for insulin levels, not even type 2 diabetics, not even type 2 diabetics that we are giving insulin therapy to!!!

Anyone who knows even a little about the role that hyperinsulinemia plays in the etiology of type 2 diabetes will not be surprised by this data, showing such a strong correlation and predictive value with insulin levels and diabetes, but the truth is, they just don’t care to screen for diabetes at all, so why would they care that this works best?

The most significant data that we got from Dr. Kraft’s work though, which would be a real eye opener to a lot of people if they paid attention to any of this, was the degree of hyperinsulinemia that was shown in type 2 diabetics.  So many still wrongly assume that our beta cells are three quarters dead by the time we get type 2 and our insulin secretion levels suffer, but those who have paid attention to Dr. Unger’s work and what has followed would know that this is not the case at all, that this is a disease of insulin excess, but no one bothered even looking at this on a big scale, testing type 2 diabetics, a bunch of them, and seeing where their insulin levels were at.

We couldn’t even scrape enough data for a good metastudy because once again, we’re not tested for this, especially during an oral glucose tolerance test.  It is good to know what our fasting levels are, virtually no one tests insulin after meals and this is very important information as well, we need to see just how high we go.

Now some type 2 diabetics have blunted insulin curves overall, but the majority secrete way too much, and way too much will just make us sicker and sicker.  In a great number of these patients with full blown hyperinsulinemia, we increase their high insulin levels even further with medication or insulin injections, which is utter madness unless the goal is to make them worse.  Perhaps that is the goal though.

Insulin is the only hormone that we administer without careful monitoring so that we don’t go over healthy amounts, but with insulin, we don’t have a care in the world about either how high someone is already or how much higher we may drive them, we only look at their blood sugar, which by the way is  beyond malpractice, it’s pure idiocy.

So the battle cry with this one, as opposed to let’s screen people for this, is let’s test the levels of people who already have diabetes, with at least a bit of an understanding of why this might even matter.  This is something that the medical community lacks though, completely, they have no idea why high insulin would ever matter, let alone be aware of its fundamental role in the etiology and progression of type 2 diabetes.

We’ll resume this in part 4.

Please follow and like us:

Leave a Reply

Your email address will not be published. Required fields are marked *