Bgs below traditional diabetes cut offs can cause damage

[EllieM]

It's an alternative way of testing to see what your hba1c is when there is reason to suspect regular hba1c's might be skewed due to, for instance, anemia.

It's also skewed to only cover the last 2 to 3 weeks, so gets used for pregnant women quite a bit. Though I don't know whether they've assigned specific diabetic/pre-diabetic/non-diabetic labels the way they do to hba1cs.

Going back to the diabetic damage/complications on pre-diabetic bgs issue, I think that a lot of people forget that many so called diabetic complications can be had by non diabetics, it's just that diabetes make them much more likely. eg I've got some cataracts (slowly) developing. Is that happening because I'm T1 or because I'm 59 and some people get cataracts in their 50s? So the condition may be diabetic related or it may just be the luck of the draw/genetics/environment.

 

[HSSS]

I don’t think it matters which BG test you use to determine where you are on the range of normal through prediabetic to diabetic. Though I have read – also in Jenny Ruhl's book, that the 1st/2nd phase insulin responses are the first to go when you get diabetes – these are shown broadly, though not perfectly accurately, by the OGTT, and further, that the FBGs are the last to go.

Each test shows a different thing that’s why it matters. As you then go on to partly explain. A longer term picture of how you are generally managing with hba1c (or fructosamine), a background level with fbg albeit influenced by dawn phenomenon or previous days food, a response to a meal showing if you have a normal response with pre and post prandial.

In fact if your beta cells are operating well then I’d suggest this pre and post meal would be highly informative and show a normal reaction (1st/2nd stage), as it would if they are still sub normal responses.

You’ve discussed (without numbers) testing fgb, hba1c and OGTT. Why avoid pre and post prandial? Are you concerned results might contradict your beliefs ?

And as for fbg being the last to go why is it that impaired fasting glucose and impaired glucose tolerance are two separate arms of pre diabetes, as opposed to full blown type 2?

 

[Tannith]

It's also skewed to only cover the last 2 to 3 weeks, so gets used for pregnant women quite a bit. Though I don't know whether they've assigned specific diabetic/pre-diabetic/non-diabetic labels the way they do to hba1cs.

Going back to the diabetic damage/complications on pre-diabetic bgs issue, I think that a lot of people forget that many so called diabetic complications can be had by non diabetics, it's just that diabetes make them much more likely. eg I've got some cataracts (slowly) developing. Is that happening because I'm T1 or because I'm 59 and some people get cataracts in their 50s? So the condition may be diabetic related or it may just be the luck of the draw/genetics/environment.

I ask myself the same question over my cataracts! Are they caused by T2 or just by age?

 

[Tannith]

Each test shows a different thing that’s why it matters. As you then go on to partly explain. A longer term picture of how you are generally managing with hba1c (or fructosamine), a background level with fbg albeit influenced by dawn phenomenon or previous days food, a response to a meal showing if you have a normal response with pre and post prandial.

In fact if your beta cells are operating well then I’d suggest this pre and post meal would be highly informative and show a normal reaction (1st/2nd stage), as it would if they are still sub normal responses.

You’ve discussed (without numbers) testing fgb, hba1c and OGTT. Why avoid pre and post prandial? Are you concerned results might contradict your beliefs ?

And as for fbg being the last to go why is it that impaired fasting glucose and impaired glucose tolerance are two separate arms of pre diabetes, as opposed to full blown type 2?

"In fact if your beta cells are operating well then I’d suggest this pre and post meal would be highly informative and show a normal reaction (1st/2nd stage), as it would if they are still sub normal responses."
Can you suggest a recognised standard scale, (perhaps from the ADA or similar organisation) which would tell me what was a "normal" reaction to Tuesday's dinner? And where it would put me on a scale of normal to prediabetic to diabetic? What, for example, is the bottom and top reading on the prediabetic section of the scale for Tuesday's dinner?

 

[lucylocket61]

"In fact if your beta cells are operating well then I’d suggest this pre and post meal would be highly informative and show a normal reaction (1st/2nd stage), as it would if they are still sub normal responses."
Can you suggest a recognised standard scale, (perhaps from the ADA or similar organisation) which would tell me what was a "normal" reaction to Tuesday's dinner? And where it would put me on a scale of normal to prediabetic to diabetic? What, for example, is the bottom and top reading on the prediabetic section of the scale for Tuesday's dinner?

Its not a scale like that. It's the size of the difference between the pre and post meal numbers. A non diabetic gets little change between the two at the 2 hours mark.

 

[HSSS]

"In fact if your beta cells are operating well then I’d suggest this pre and post meal would be highly informative and show a normal reaction (1st/2nd stage), as it would if they are still sub normal responses."
Can you suggest a recognised standard scale, (perhaps from the ADA or similar organisation) which would tell me what was a "normal" reaction to Tuesday's dinner? And where it would put me on a scale of normal to prediabetic to diabetic? What, for example, is the bottom and top reading on the prediabetic section of the scale for Tuesday's dinner?

As Lucy said above. It’s not a scale of prediabetic to full blown. It’s about assessing your ability to respond as normal, or not, to any given meal. The further from returning to the pre meal reading you are the more unsuitable the match between the meal and your ability to cope with the meal. This might well change over time. Hopefully improved.

If you can respond as normal to pretty much any meal then your beta cells must be coping ok mustn’t they?. If some or all meals are highly challenging then there’s a problem of some sort. You’d no doubt describe it as beta cells struggling, I’d call it insulin resistance in type 2.

I’ll try and dig out some data re this tomorrow

 

[Tannith]

Each test shows a different thing that’s why it matters. As you then go on to partly explain. A longer term picture of how you are generally managing with hba1c (or fructosamine), a background level with fbg albeit influenced by dawn phenomenon or previous days food, a response to a meal showing if you have a normal response with pre and post prandial.

In fact if your beta cells are operating well then I’d suggest this pre and post meal would be highly informative and show a normal reaction (1st/2nd stage), as it would if they are still sub normal responses.

You’ve discussed (without numbers) testing fgb, hba1c and OGTT. Why avoid pre and post prandial? Are you concerned results might contradict your beliefs ?

And as for fbg being the last to go why is it that impaired fasting glucose and impaired glucose tolerance are two separate arms of pre diabetes, as opposed to full blown type 2?

You said "And as for fbg being the last to go why is it that impaired fasting glucose and impaired glucose tolerance are two separate arms of pre diabetes, as opposed to full blown type 2?[/QUOTE]" I think you may be regarding IFG as an early stage in the course of diabetes development. It is my understanding that the T2 has been developing for some time before IFG, and that insulin resistance has preceded IFG by several years and actually levelled off by the time you get to diabetes and even before.
"The first stage in the development of T2D is insulin resistance. During this time beta cells are stimulated to increase insulin secretion in order to maintain normal glucose levels [10]. By the time T2D is diagnosed, around 40–50% of beta-cell function is already lost, with a further loss of 4–5% expected each year thereafter [11–13"

Figure 1. Natural history of type 2 diabetes. IFG, impaired fasting glycemia; IGT, impaired glucose tolerance. Mazze R, et al., Staged diabetes management: a systematic approach. 2nd Ed. John Wiley & Sons. Copyright © 2006 Matrex

https://www.tandfonline.com/doi/full/10.1080/00325481.2020.1771047

Beta-cell failure in type 2 diabetes: mechanisms, markers, and clinical implications

 

[Oldvatr]

You said "And as for fbg being the last to go why is it that impaired fasting glucose and impaired glucose tolerance are two separate arms of pre diabetes, as opposed to full blown type 2?

I do not agree with this review paper and its diagnosis. Other studies I have seen point to there being two seperate mechanisms of Insulin Resistance in play. The first mechanism is related to the Krebs cycle and concerns the role of insulin in the mitochondria only, This over time causes the hyperinsulinemia associated with T2D that leads ro the noted IFG and IGT symptoms of the disease. This in turn then leads to Metabolic Syndrome in many but not all T2D. The last stage affects the adipose tissues and develops the second form of IR, namely fat invading the pancreas,

This progression is demonstrated by the Newcastle Diet which seems to be able to remove the fat affecting the pancreas, thus reducing the second stage of IR, but leaving the first stage IR active and primed to start the cycle over again. This is why I think claims to reverse T2D with that treatment are premature, since ther is evidence that the success is not permanent long term.

I offer myself as a confounder to the study as well. I was DX;ed 30 years ago, so their 4-5% loss annually of beta cell function would have put me 6 feet under several years ago. The fact that I am now controlling my symptoms by diet control only proves that I still have beta cell function, I say control, because it is clear that I am not cured. But I can live with that.

 

[HSSS]

You said "And as for fbg being the last to go why is it that impaired fasting glucose and impaired glucose tolerance are two separate arms of pre diabetes, as opposed to full blown type 2?

" I think you may be regarding IFG as an early stage in the course of diabetes development. It is my understanding that the T2 has been developing for some time before IFG, and that insulin resistance has preceded IFG by several years and actually levelled off by the time you get to diabetes and even before.
"The first stage in the development of T2D is insulin resistance. During this time beta cells are stimulated to increase insulin secretion in order to maintain normal glucose levels [10]. By the time T2D is diagnosed, around 40–50% of beta-cell function is already lost, with a further loss of 4–5% expected each year thereafter [11–13"

Figure 1. Natural history of type 2 diabetes. IFG, impaired fasting glycemia; IGT, impaired glucose tolerance. Mazze R, et al., Staged diabetes management: a systematic approach. 2nd Ed. John Wiley & Sons. Copyright © 2006 Matrex

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https://www.tandfonline.com/doi/full/10.1080/00325481.2020.1771047

Beta-cell failure in type 2 diabetes: mechanisms, markers, and clinical implications[/QUOTE]


Just looking very quickly but the diagram you link to shows ifg and igt preceding type 2 diagnosis- which is what I said. I agree insulin resistance comes first and never said otherwise.