I discussed a video with you by Dr. Bryan Walsh on glucose a little while back, and I promised I’d be bringing you more from him, and I definitely will be doing several because his videos are top notch. While his videos are directed at practitioners, they are presented in a way that lay people can readily understand, which is the best part about them, although Dr. Walsh is plenty knowledgeable as well.
So this time we’ll be looking at a presentation of his on metabolic hormones, and obviously this pertains to diabetes a lot since it’s a metabolic disease. There are a lot of conditions that pertain to diabetes actually, either influenced by diabetes, or influencing diabetes, or both, and the body really is a holistic unit, in spite of how often we pretend that it is not.
So here he’s talking about a metabolic panel that looks at 3 markers, which are insulin, cortisol, and insulin like growth factor 1 (IGF-1). He starts out talking about insulin, and this is a fasting insulin test that is used, and what we’re looking for here is it not being too high, which is by the way not what doctors generally look for, but this stuff is designed for advanced practitioners who actually are aware of the negative consequences of high insulin levels.
So you’ll notice that the normal results by this test are expressed as low risk being less than 9, moderate risk being between 9 and 13, and high risk being over 13. With a lot of us, our fasting insulin levels can be a lot higher than 13 by the way, and the degree of risk goes up from there.
So we know already about the importance of insulin in glucose metabolism, and he discusses the GLUT4 transporter which is the major glucose transporter in the body, and how they need to be expressed properly. So insulin binds to the cell’s insulin receptors, and this promotes the expression of the GLUT4 transporters.
As previously discussed, he mentions that muscles during contraction do not require insulin for glucose uptake, and this is the main benefit of exercise on diabetics, although I do want to point out that this is just one factor in the process, and one’s blood sugar can actually go up from exercise in some patients.
Bryan mentions that insulin by itself is more meaningful in the context of other markers, and one of them is certainly glucose levels. This is how we measure insulin resistance actually, by comparing glucose levels and insulin levels, and can then figure out how well insulin is working to lower blood sugar and how much is needed to do that, and the more that is needed to get you to a certain level, the more insulin resistance you have.
So early on in the progression of diabetes, before diabetes results, we will see normal glucose levels but higher insulin levels, and this is indicative of a metabolic disorder and the one that both precedes diabetes and plays a central role in its development.
It’s not hard to see how this happens actually, as high levels of insulin cause insulin resistance, and when that increases, it’s just a matter of time before all the insulin the pancreas can produce, in spite of this resulting in some very toxic levels, eventually are not enough to regulate blood sugar properly. It’s not so much that the levels decline, it’s that our sensitivity to it keeps declining.
This happens because abnormally high levels of insulin causes downregulation of the cellular insulin receptors, which causes the pancreas to secrete even more insulin, which causes a further downregulation of insulin receptors, and we have a vicious circle here leading to diabetes.
So the next step on the road is where blood sugar starts to rise, and this is the point where the body is unable to regulate it, and Bryan gives an example of an A1C of 5.5, which is above normal but still below what is required for a diagnosis of prediabetes.
This process happens gradually and at this point the medical issues have generally already gone on for many years, and the sooner we get on top of this the better, preferably at the point where insulin starts to rise to unhealthy levels, way before blood sugar even rises a bit.
So then we get to the stage where both insulin and glucose levels are high, and this is due to insulin resistance getting worse, and now our bodies’ best efforts are not enough to prevent high blood sugar of various degrees, even extremely high ones.
I do want to point out as an aside that given that this is all the case, and it certainly is, if our strategy in managing blood sugar is to raise insulin levels to the point where glucose control is achieved, it’s not hard to see how such a strategy worsens the disease over time, by increasing insulin resistance even further.
So what we’re doing here is taking what has caused our diabetes in the first place and using medical intervention to perpetuate it, our insulin levels are too high, even the most our pancreases can produce isn’t enough, and those levels are toxic already, so we jack them up further, which eventually will cause us to be even more insulin resistant, and even massive amounts injected may eventually be not even enough to prevent dangerously high blood sugar.
So this is where doctors just throw up their hands, we did all we could, diabetes is progressive, yours has progressed, sorry, we’ll be there for you to amputate or put you on dialysis or whatever as needed. All the king’s horses and all the king’s men can’t help you much anymore, but they miss the part that this army has fought against you and not for you.
I’ll pick this up in part 2 of this discussion.