Insulin Resistance or Lack of Insulin

[Mr_Pot]

They appear to have forgotten about those who are extremely insulin resistant and yet built like a bean pole.

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.

 

[Member496333]

How do you know that you are/were insulin resistant?

Because I had type 2 diabetes. A symptom of hyperinsulinemia.

ETA: low fasting insulin is not to be expected at all if you have T2DM. The opposite is true.

 

[Brunneria]

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 (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.

 

[Goonergal]

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.

 

[Brunneria]

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.

yes indeed!

 

[Mr_Pot]

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.

 

[Goonergal]

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.

The HOMA-IR test is a pretty good guide to insulin resistance. It’s a calculation based on fasting insulin and fasting BG. Doesn’t seem to be available on the NHS, but Medichecks offer it.

 

[Brunneria]

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, and glucose dysregulation develops in a whole variety of ways (the www.bloodsugar101.com website goes through the various ways that often happen to people labelled T2). These include slow development over years, to fast over weeks or months, weight gain, or not, raised fasting readings and/or after meals, and so on. Lots of variation.

 

[AloeSvea]

Do remember the sick fat cell theory. It accounts for the slim insulin resistant type twos.

But great to see the Swedes' different types of type two diabetes being discussed in this thread - MODs and MARDS and SIRDs and so on. They also come with a percentage of how many, are in each particular sub-group, based on their own research (Lund University). I am the only one so far who states what type I am in my signature! Be marvellous to see more folks do so!

I am a SIRD (15% of all diabetics say Lund Uni) - I get my C-peptide, as in my insulin production, tested along with my regular HBA1c. I sent my GP who writes my blood test prescription the material from the Swedes, and she was the one who diagnosed my PCOS in my 20s, and my T2D in my 50s - it was easy to convince her in my case!

The severly insulin deficient diabetics - not autoimmune - is around 17% (say Lund uni)n - so a significant percentage group.

 

[MrsA2]

My husband says I've always been MARDy.
He's not a professional doctor- does his opinion still count?

 

[finsit]

I would say first thing you need to look is at your genes. If the D2 runs in the family then you have higher chances of beta cell issues than the insulin resistance. However, i am still unclear if we say D2 runs in a family, it maybe that insulin resistance runs in the family? You can only find this if you do the insulin/HOMA-IR test. Other way round is to work on your resistance by reducing carbs and lowering your visceral fats and see how much glycaemic load you can take to keep your spikes in the range.

I almost believe that once you have been declared D2, you can not go back to normal food and eating like in your 20s. However, i also believe that you can achieve perfectly normal BGs or close to normal at the cost of lifestyle changes.

 

[LittleGreyCat]

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.

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.

 

[HSSS]

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.

 

[LittleGreyCat]

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.

Minority not hyperinsulemia is what I am suspecting.
Like the 80/20 rule of overweight/obese vs normal weight on diagnosis.