Does Metformin inhibit recovery and muscle building?

[Pluripotent]

I would argue it addresses blood sugar (mostly post-prandial glucose excursions), but not insulin resistance per se, and they are not the same thing. It is a band aid, but sometimes a band-aid is better than going without. And while the insulin resistance is kinf of pernicious in the way it kills you, ultimately it is the hyperglycemia that does a lot of the nasty stuff like destroying your kidney, making you go blind and making you lose your limbs, so symptom management is still a good idea even if it doesnt address the root cause.

What is the root cause of insulin resistance? Perhaps too much insulin relative to insulin receptors? Why does a person go about producing so much insulin? Answer that, and you have your root cause.

Not really. Outside of rare genetic issues, neither receptor number nor affinity are the issue in insulin resistance. The issue is altered cell metabolism that impairs signal transduction. From a practical PoV, it is of little practical difference though. If you said that to encourage the sort of training that builds muscle, then the same action goes a long way to normalizing the hormonal/metabolic mileau that would allow for improved signalling. The advantage of this being the truth though is that it allows the acute effect of the training session to continue to provide benefit long after muscle growth has plateaued.

You've missed the point. I'll give you a hint.. What is the title of this web site?

He's not talking about GI, which refers to the food. He is talking about a homemade version of an OGTT, which tests his personal response to a type of carb. I'd still argue it's not particularly useful, but that's because his version has no standardization of the carb source (at least the way he tells it).

I'm not sure what you would do with the information gathered from this test. I'm not convinced carbohydrate metabolism is that different among different people, and this seems like an odd way to test it.

I think it's important to acknowledge the psychological aspect of hunger. The vast majority of people are brought up with carbs as the primary source of food, and eliminating that can lead to feelings of restriction, even if the other hormonal and physiological signals are telling you that you should be satisfied. The handful of times I have experimented with low carb/keto I routinely felt so dissatisfied after meals (how can you have eggs without potatoes, or bread?), feeling as if a part of the meal was missing. Psychologically I interpreted that as hunger, and that was regardless of how much of everything else I had eaten. I am sure it is something that one can acclimate to, and the speed of that is probably related to how much one believes in the merits of going low carb, but for me it was just an experiment and so had no skin in the game. Two days without being able to eat something like Oatmeal for breakfast and I didn't want to get out of bed in the morning.

Like I said a few pages back, people don't eat what they like as much as they like what they eat. You are not a slave to your childhood diet. Try the soda test, if you are a soda drinker. Stop drinking sweet drinks for a month, then when you drink it next, it will taste way too sweet. You have effectively reset your likes.

[LimieJosh]

How would you standardise it?
The process as I understand it is to wake up in the morning, eat a food containing 50g of carbohydrate - so that might be say 70g of oats, or 2 apples, or whatever. Eat nothing else - set a timer for 2 hours and test your blood sugar at that point.

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 is the root cause of insulin resistance? Perhaps too much insulin relative to insulin receptors? Why does a person go about producing so much insulin? Answer that, and you have your root cause.

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.

You've missed the point. I'll give you a hint.. What is the title of this web site?

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'm not sure what you would do with the information gathered from this test.

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'm not convinced carbohydrate metabolism is that different among different people

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.

[Pluripotent]

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.

This is a lot to write when what you want to say is to eat less sugar and lift. (when did I say that increased muscle mass was the only benefit of training? Of course it changes your metabolism. That's why it works. You are splitting a fair number of hairs here. I'll let those on the boards decide who has the better understanding of the topic. I don't currently have time to go through your objections point by point. And I'm only speaking from the authority derived from "some guy on the internet" status.

[BenM]

BenM, i understand you are aware of the main criticism of GI which this protocol seems similar to.

Briefly, that it's not a real world situation, since a normal meal contains protein and fats, which have their own insulin response, as well as alter the insulin response relative to that of constituent carbs alone.

Yes, you're correct - it's not a real world situation, but that doesn't mean it might not have some practical application.

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.

<snip>

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.

<snip>

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.

Thanks Josh / Pluripotent, you've both given me some interesting food for thought. Yes - there are standards in the book - basically that ideally 2 hours after eating the carbs, blood glucose should be between 90 and 115 mg/dl, any higher than this and this food is 'probably not a good fit for you' (direct quote).

One of the reasons I thought about doing it is the further I go down the fitness/strength rabbit hole, the more I want to experiment on myself and try new things to see how I can optimise performance, body composition and just general feelings of wellness. I want to try keto, I want to try IF, and many other things, purely for my own curiosity as much as anything. This particular one seemed like something that was fairly simple to do, low cost, and won't have the same difficulties that a complete diet change will (my wife has this strange idea that we as a family should eat the same meals together, and that I should eat breakfast as an example to my daughter... so keto and IF are off the table for the time being). But if as you say it doesn't have a lot of practical value other than possibly tracking change in carbohydrate metabolism over time, it might not be worth the effort. I _think_ my insulin sensitivity is generally OK.

[David Clark]

So to build on this thread, I cannot change what got me here I can only change what happens next. I have been a type 2 diabetic for 15+ years. I have controlled it with diet, exercise at times and a variety of medications. It was not under control for the last year and in response to an A1c of 9.8 I added 10 units of basal insulin to my regimen. I substantially changed my lifestyle. My blood sugar is under control and my August A1c was 6.0. I am 62, male, receiving biweekly injection for low testosterone. I am doing LP on a two day a week schedule as well as making sure I am much more active every day. I take 2000 mg of metformin and 10 units of basal insulin. I am not looking for medical advice. My question is this. Assuming I can cut back on medication, cutting which would have the greatest benefit as far as strength gains and muscle growth?

Thanks

[Pluripotent]

So to build on this thread, I cannot change what got me here I can only change what happens next. I have been a type 2 diabetic for 15+ years. I have controlled it with diet, exercise at times and a variety of medications. It was not under control for the last year and in response to an A1c of 9.8 I added 10 units of basal insulin to my regimen. I substantially changed my lifestyle. My blood sugar is under control and my August A1c was 6.0. I am 62, male, receiving biweekly injection for low testosterone. I am doing LP on a two day a week schedule as well as making sure I am much more active every day. I take 2000 mg of metformin and 10 units of basal insulin. I am not looking for medical advice. My question is this. Assuming I can cut back on medication, cutting which would have the greatest benefit as far as strength gains and muscle growth?

Thanks

Personally, I don't think this is an important question. You realize that insulin is sometimes used by body builders for its anabolic effect? I'm not saying that you should be on insulin for this reason, however. It would make it more difficult to lose weight, if that is an issue for you. It's probably best to come off meds in reverse order: stop insulin first, then metformin or other orals. Insulin actually makes diabetes worse because of its anabolic effects. Most docs try to keep people off it as long as possible, only starting it when there are no other options. You will probably notice that it's much easier to keep your waist under control if you are able to keep your sugars under control without insulin. Ultimately, the advantages of being able to reduce your meds far outweigh the specifics of which meds those are.

[David Clark]

Personally, I don't think this is an important question. You realize that insulin is sometimes used by body builders for its anabolic effect? I'm not saying that you should be on insulin for this reason, however. It would make it more difficult to lose weight, if that is an issue for you. It's probably best to come off meds in reverse order: stop insulin first, then metformin or other orals. Insulin actually makes diabetes worse because of its anabolic effects. Most docs try to keep people off it as long as possible, only starting it when there are no other options. You will probably notice that it's much easier to keep your waist under control if you are able to keep your sugars under control without insulin. Ultimately, the advantages of being able to reduce your meds far outweigh the specifics of which meds those are.

Thanks. My preference is to get off the insulin as quickly as possible.

[Pluripotent]

So, currently taking my mom to cataract surgery, so I have some time to kill. We can dig into this a little.

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.

How various carbs are broken down into sugar is a different mechanism than how that sugar is subsequently absorbed by the tissues. What I'm saying is that the initial metabolism of carbs isn't different enough among people to require individualized testing beyond what you can gather by knowing the glycemic index of the food. Isn't that good news?

How your body handles sugar is a different matter.

What you have said there is wrong as I have already pointed out.

No it isn't. I was speaking in a very broad, general manner, as the point was not to put forth a concise description of insulin resistance at the cellular level. Nothing I said was wrong, although I admit I left a lot out.

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.

You can restate this by saying that you are managing blood sugar by managing sugar intake. How is that managing a "symptom?" Insulin resistance develops from a breakdown is sugar management which starts from chronic sugar overload. How is that a "symptom?" It is a cause, if not the cause.

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.

When do I ever advice to tackle this problem with diet alone?

To come back to what actually is Insulin Resistance, is it the result of too much insulin? No. No, it isn’t.

You are misrepresenting what was said. Of course something is driving increased levels of insulin. That was my point. What might that be? There's your root cause.

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.

I never offered up a detailed description of insulin resistance at the cellular level. Is this completely necessary? Here's an overview of the topic:

Exercise, GLUT4, and Skeletal Muscle Glucose Uptake.

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.

So far, so good..

Essentially, a fat overload is experienced and interpreted by the cell as being in a state of starvation

Huh?

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.

Dysregulation of glut-4 is at the heart of insulin resistance, however I think your mechanism is flawed. Excess fat is at the root, but this is not an indication to preserve glucose in the blood. Rather, excess blood glucose remains there because of an overload of the glucose storage mechanism, which eventually gets stored as fat. But the obese person overloaded with sugar just can't deal with it that fast.

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

I'll take a look, but you are again misinterpreting what I said.

An aside about the compensatory hyperinsulinemia that occurs in insulin resistance, but it is largely achieved without any increase in production.

That's just not the case.

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.

This is a very novel understanding of insulin regulation. Insulin is released directly into the bloodstream by pancreatic beta cells and travels throughout the body, it is then removed from circulation by the liver and the kidney. However the liver does not store or subsequent release insulin.

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).

I didn't say it was the only reason resistance training works. It also improves the glucose receptor function. More muscle mass is unquestionably better for a lot of reasons, but even when you stop creating more, you are still improving what you have.

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.

This article gets into the details, if anyone is interested:

Update on the effects of physical activity on insulin sensitivity in humans

I'm not sure what other info you'd need.

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.

Like I said earlier, initial sugar metabolism is not the problem, and is likely not that different among people. It's the subsequent metabolism of the resulting sugar load that is at issue. Perhaps I wasn't that clear about that. Once the sugar is in the blood, it doesn't matter a whole lot which foods it came from, which is why I don't think you're going to get much useful info out of this test beyond what's available through standard diabetic screening and the existing glycemic index of carbs.

[Yonason Herschlag]

I just came across a relevant find; a teaspoon a day of MCT oil (medium chain triglyceride oil - usually from coconut oil) improves insulin resistance and helps speed up the catabolism of fat. It appears it is most effective (for losing weight) when on the keto diet. A person can be on a calorie restricted diet, but if his metabolism slows down, he won't lose weight. The MCT oil not only speeds up the metabolism, but it enables and "encourages" the body to burn body fat as a source of energy. Here's one study in humans, and here's another.

Another natural insulin sensitizer is ginseng; see this study.

And yet another natural insulin sensitizer is cloves; see this study.

[Pluripotent]

I just came across a relevant find; a teaspoon a day of MCT oil (medium chain triglyceride oil - usually from coconut oil) improves insulin resistance and helps speed up the catabolism of fat. It appears it is most effective (for losing weight) when on the keto diet. A person can be on a calorie restricted diet, but if his metabolism slows down, he won't lose weight.

And how does the metabolism "slow down?" Perhaps from modern life imitating the sea anemone?

The MCT oil not only speeds up the metabolism, but it enables and "encourages" the body to burn body fat as a source of energy. Here's one study in humans, and here's another.

Another natural insulin sensitizer is ginseng; see this study.

And yet another natural insulin sensitizer is cloves; see this study.

I suppose you could do all that. Or you could just lift.

From Exercise, GLUT4, and Skeletal Muscle Glucose Uptake:

"Exercise training remains the most potent stimulus to increase skeletal muscle GLUT4 expression, an effect that may partly contribute to improved insulin action and glucose disposal and enhanced muscle glycogen storage following exercise training in health and disease."