I recently cited a good article on the progression of diabetes in a recent post on blood sugar and beta cell dysfunction. There's way more things of interest to talk about in this paper so I wanted to dedicate a separate article to discuss it.
What stands out the most is the fact that the discussion of beta cell function centers around using the HOMA model, which is actually a measure of insulin resistance, not insulin secretion. We can't really measure beta cells directly in live people, although in an autopsy they will look to measure beta cell mass and they do see that it is reduced significantly in diabetics, and there may be several reasons for this actually and some may actually be protective.
So the first thing I want you thinking about is that loss of beta cell function, while not in itself a good thing, is probably a good thing in the short and medium terms, although ultimately it may not be so good in the very long run if we allow our beta cell function to decline to the point where we get beta cell failure to the point that we no longer can secrete healthy amounts of insulin overall.
So this is indeed an area of concern, although not near as much as is thought generally. If we are already secreting toxic amounts of insulin, as type 2 diabetics generally do, then it is incredibly stupid actually to surmise that we have a loss of insulin secretory power overall, at least as far as being able to secrete normal amounts are concerned, although it is true that the timing of it tends to be off and that's something that could stand improvement.
If it's just the timing though, in other words reduced or absent phase 1 insulin release, the insulin that non diabetics store, then this in itself isn't going to present problems all that significant, although this will tend to elevate after meal (PP) readings somewhat. If you get rid of the insulin resistance that is present, in other words factor that out and only look at the impact of first phase, then the modest and short term increases in PP blood sugar is probably not going to affect overall blood sugar averages or A1Cs all that much.
So this probably would only be enough to qualify us as being glucose intolerant or prediabetic. So this is not what is behind type 2 diabetes at all, insulin resistance is, although diminished phase 1 does contribute to it.
There are some real differences as far as the delay of the insulin response in diabetics though, although we do peak later than non diabetics do, who peak around 30 minutes after a meal, party due to a proper phase 1 response. The work of Dr. Kraft is pretty instructive here as far as measuring the insulin response of diabetics, and most of what we know about this is thanks to the work of Dr. Kraft.
Some diabetics even have massive insulin levels even at the 30 minutes though, insulin levels of 200 for instance compared to the 60-80 we see in normal people. In spite of their going even higher later and seeing insulin peak at 2 hours, there's not only enough insulin at 30 minutes, insulin can be elevated at 3 times the normal level in certain diabetic subjects.
Part of the reason why it's assumed so much that we have a delayed insulin response is actually due to the higher need for insulin, it tends to take longer when you are producing many times the normal levels. Now there are a variety of presentations here, those who have beta cell failure won't ever produce normal levels, which defines the conditions, but that's the far end of the spectrum and only comprises a small percentage of type 2's, others may produce normal levels but it will take longer, and many produce too much but in a delayed fashion, where the initial response is diminished, and all of these patients may have similarly poor control.
This is one of the reasons why it's so important to measure insulin levels, to get an idea of what the heck is going on, although we of course don't bother with that much, and to this day, very few medical practitioners care a whit about insulin levels beyond distinguishing us with type 1's.
Our article takes the view that the primary mechanism of diabetes progression is beta cell failure, where failure here is not so much beta cell death as beta cell dysfunction, and it does properly recognize this, but the evidence of this loss of function is measured by measures of insulin resistance, and that's clearly a mistake.
So with the HOMA model that is used here we look at the levels of insulin relative to levels of blood sugar and when both are high, this is called a relative insulin deficiency and we blame the beta cells for not producing even more, so if both your blood sugar and insulin levels are 250 for instance, we surmise that the insulin levels should be much higher, even if this exceeds the physical limits of even the healthiest of pancreases, which is all preposterous.
So we can substitute beta cell failure with insulin resistance as we read this because this is what they are actually referencing, even though we know that there is a loss of beta cell function over time, where high glucose will reduce phase 1, high free fatty acids will reduce insulin secretion overall over enough time, and both in very high amounts will also cause beta cell death.
If we're wondering whether we are making enough insulin though, we have to look at the insulin levels themselves, and if we see that they are too high relative to normal, we can't say that there is any sort of deficiency, and if these abnormal levels aren't reducing blood sugar as they are supposed to, the problem surely isn't that the beta cells aren't secreting enough insulin if they are already secreting too much.
So beta cell health is certainly an important component of diabetes, you see things tried which claim to preserve it like medications do generally, and all medications do this in the short term as well, but diabetes progression rages on and the disease becomes more and more difficult to treat, so at the very least neither normalizing blood sugar or protecting against the loss of beta cell function works very well. In fact making these things our primary focus leads to failure, which is true beyond any question, and evidenced in this article as well, where each individual medication fails on average in just 2 years.
This is because the actual problem, insulin resistance, remains inadequately addressed, and while we are focusing on this more these days, where for years medication was limited to either insulin secretagogues or insulin itself, we still haven't made much progress in stopping the decline here, but that's because we still don't care about the primary driver of diabetes progression, which is excessively high and persistent insulin levels over time.