Different carbs have different GIs so you are going to get meaningfully different responses from eating 50g of carbs from oatmeal compared to 50g of carbs from bananas or soda. Hell, you would probably get a different responses between regular oats and quick cook oats. But more to the point, how are you even going to interpret the result? Presumably where ever you have got this information from has also provided some standards to compare your results against, and if they did they almost certainly use the clinical standards we use for Oral Glucose Tolerance Testing. The problem with that (other than typically we use 75g of glucose – 50 is almost exclusively used for gestational diabetes) is that if you do not use the Glucola (the industry standard glucose drink) as the carb source then the results will not applicable against those standards.
What you have said there is wrong, as I have already pointed out. I will come back to that, but my point was that glucose measures and insulin resistance are not the same thing, even if obviously very closely related. If all you do is manage blood sugar by avoiding carbs then you are just managing the symptom. In many cases that can be beneficial, especially when it comes to blood glucose as chronic hyperglycemia can do some pretty awful things over the course of years. However, unless you couple it with weight loss, regular exercise and increased oxidative fitness then you aren’t going to improve the root cause of the problem by just avoiding carbs and reducing your post-prandial glucose spikes.
To come back to what actually is Insulin Resistance, is it the result of too much insulin? No. No, it isn’t. You are a physician, right? It is my recollection that you are, which is why I am engaging you on this possibly pedantic level, because you have made numerous statements in this thread that reveal a tremendous misunderstanding about what insulin resistance is, and I think a physician should know better, especially when they speaking from a position of authority.
Insulin resistance, other than for <1% of the population, is not related to the density or function of the insulin receptor, but the metabolic and hormonal milieu of the cell that impairs the signal transduction. In the skeletal muscle, which is the tissue most relevant in terms of management of blood glucose levels, at its most basic level it can be described as a dysregulation of the cellular metabolic interplay between fat and glucose oxidation. Essentially, a fat overload is experienced and interpreted by the cell as being in a state of starvation, and so compensatory mechanisms are employed to preserve blood glucose for the systemic circulation, thus the signal that should cause Glut-4 to translocate to the cell membrane is blocked. I suggest you read the 2001 Banting Lecture from John McGarry (published in Diabetes) for a primer. It is now quite old and so much of the field has moved on, but I think it’s still the best introduction for a professional to understand how wrong the simplistic the overexposure leads to downregulation paradigm is that so many people just assume to be the case.
http://diabetes.diabetesjournals.org...1/1/7.full.pdf
An aside about the compensatory hyperinsulinemia that occurs in insulin resistance, but it is largely achieved without any increase in production. The pancreas delivers insulin directly in to the portal vein, which means it has to go through the liver before it reaches the systemic circulation. The liver then regulates how much of that to allow to get through according to metabolic signals it is receiving. In a healthy person it may eliminate as much as 50% of the insulin, but as insulin resistance increases over time the liver allows more and more to pass though, producing a systemic hyperinsulinemia, but one that is reactive to the degree of insulin resistance registered by the liver. I dont think that is covered in the Banting Lecture posted above, but if you are interested in that, Richard Bergman did some great work in what he referred to as the Single Gateway Hypothesis in the late 90s that covered this.
I dont get what point you think it is I missed I acknowledged that weight training is an effective way to combat this. However, while we agree on this, we reached our respective conclusions for different reasons. That is important because it will likely have a bearing on how you may apply that knowledge. If you incorrectly believe the benefit is because of some effect of increased muscle mass providing more receptors for the insulin to work on, as you said a few times, then you might be inclined to believe that it would not be very effective outside of a novice lifter phase when muscle growth is going to be slow (or non-existent). However, with a correct understanding of insulin resistance you will realise that this is one those cases where even if all you are doing is exercising (vs training) you will get the benefits. What matters is that you have stressed the cells' oxidative functions, and that, for a short period of time, will somewhat normalize the signal transduction pathway that leads to glucose uptake and an associated reduction in the circulating concentration of insulin required to achieve normoglycemia.
I am not sure what relevance a home made version of this test has either, as I already said. What I was pointing out was that the information he thought he could get from it was not available from GI reference tables.
I am not sure what you mean by that. It seems like you denying the underlying physiology behind an OGTT, and I am sure that is not what you mean. It is the very fact that there are differences in carbohydrate metabolism that cause us to identify someone with impaired glucose tolerance after an OGTT or frank diabetes. While I do not think it would be worth it, as long as he totally standardized his procedure (exercise the day before, length of fast and made sure there was absolutely no change in the source of carbohydrate) Ben could use the test to judge how his carbohydrate metabolism was changing over time. Again, I dont see that it is worth if, but if 6 months from now his 30 minutes, 2 hour or total 2 hour Area under the curve measures for glucose were lower than the first time he did the test it would indicate an improvement in carbohydrate metabolism and (likely) insulin sensitivity.