A good point that goes back to the title of the thread. How do you know that you are/were insulin resistant? Maybe you just don't produce enough insulin. You had a fasting insulin test that showed low insulin but that is to be expected when fasting and would mask low insulin production. If you produce low insulin you would expect high blood sugar, but you eat almost no carbs so limited insulin would be enough.They appear to have forgotten about those who are extremely insulin resistant and yet built like a bean pole.
How do you know that you are/were insulin resistant?
A good point that goes back to the title of the thread. How do you know that you are/were insulin resistant? Maybe you just don't produce enough insulin. You had a fasting insulin test that showed low insulin but that is to be expected when fasting and would mask low insulin production. If you produce low insulin you would expect high blood sugar, but you eat almost no carbs so limited insulin would be enough.
I suspect I am in the MARD category mentioned above, I was diagnosed at 67 and my moderately low carb diet keeps me in the range of my limited insulin capacity.
Yes.
When I first saw Jason Fung announcing in a lecture that ‘T2 is a disease of insulin resistance’ I remember doing a double take. That is simply incorrect.
In many (most?) parts of the world, T2 is the default diagnosis given to any adult in the absence of further testing to establish more detail. So T2s are not tested for insulin resistance, because they are given the diagnosis based on high blood glucose levels, with no further investigation.
Fung’s statement may apply to the majority of those who receive a T2 diagnosis, but not all. There are others (a large number worldwide) Who may not have insulin resistance (or the new trendy term hyperinsulinemia). Those individuals may have low or inadequate insulin production. For example, I can think of slim T2 members on the forum, requiring injected insulin, who find small doses are sufficient. Assuming that they have high levels of their own insulin seems illogical.
It is a great pity we don’t get tested for insulin production at diagnosis, isn’t it? Then we wouldn’t be making unfounded assumptions.
What would be even better would be a series of tests to check for changes in insulin production over the following years.
I’d take that a bit further and say that if ‘routine’ blood screening focused on insulin/insulin resistance rather than HbA1c, many cases of type 2 could be prevented or picked up a lot earlier. In turn that’d save the NHS a lot of money.
I think the problem is that it is very difficult to test for insulin. There is a fasting insulin test but that doesn't say anything about how well the pancreas can cope with the demands of meals. There is a clamp test but that is only suitable in a research environment. The C-peptide test shows if you are producing none or very little insulin to identify Type 1 but it can't measure the dynamic response in a Type 2.Yes.
When I first saw Jason Fung announcing in a lecture that ‘T2 is a disease of insulin resistance’ I remember doing a double take. That is simply incorrect.
In many (most?) parts of the world, T2 is the default diagnosis given to any adult in the absence of further testing to establish more detail. So T2s are not tested for insulin resistance, because they are given the diagnosis based on high blood glucose levels, with no further investigation.
Fung’s statement may apply to the majority of those who receive a T2 diagnosis, but not all. There are others (a large number worldwide) Who may not have insulin resistance (or the new trendy term hyperinsulinemia). Those individuals may have low or inadequate insulin production. For example, I can think of slim T2 members on the forum, requiring injected insulin, who find small doses are sufficient. Assuming that they have high levels of their own insulin (and insulin resistance) seems illogical.
It is a great pity we don’t get tested for insulin production at diagnosis, isn’t it? Then we wouldn’t be making unfounded assumptions.
What would be even better would be a series of tests to check for changes in insulin production over the following years.
I think the problem is that it is very difficult to test for insulin. There is a fasting insulin test but that doesn't say anything about how well the pancreas can cope with the demands of meals. There is a clamp test but that is only suitable in a research environment. The C-peptide test shows if you are producing none or very little insulin to identify Type 1 but it can't measure the dynamic response in a Type 2.
I think the problem is that it is very difficult to test for insulin. There is a fasting insulin test but that doesn't say anything about how well the pancreas can cope with the demands of meals. There is a clamp test but that is only suitable in a research environment. The C-peptide test shows if you are producing none or very little insulin to identify Type 1 but it can't measure the dynamic response in a Type 2.
Secondly, IMHO people should have a c-peptide test on diagnosis to confirm the level of insulin production.A decade or so back this might not have seemed significant as the treatment pathway was the same whatever, but if we had some reasonable baseline data we might not have to be having this discussion.
You think no type 2 is hyperinsulemia or that not all of them are? If it’s the latter I think that’s the gist of this thread really.Seeing as this thread is still going I will restate the above.
IMHO anyone stating that T2 is the same as hypreinsulemia needs to show the body of evidence from HOMAR/IR testing for all newly diagnosed T2s.
Which as far as I am aware is not being and has not been collected.
https://www.diabetes.co.uk/c-peptide-test.html
Describes a standard (and reasonably priced) test which is often used to differentiate between T1 and T2.
Forum post suggest that this is not routine even when there is doubt over T1/T2 diagnosis.
A move to gather more data would be a very good thing, if only to decide on the course of treatment to try and mitigate the problem.
You think no type 2 is hyperinsulemia or that not all of them are? If it’s the latter I think that’s the gist of this thread really.
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