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Insulin Resistance or Lack of Insulin

Mr_Pot

Mr_Pot

Well-Known Member
It used to be said that Type 2 diabetes occurs when not enough insulin is produced or insulin resistance prevents glucose being absorbed. I have noticed recently on the forum that the "not enough insulin" explanation seems to have been dropped. As an example in a thread today someone said of insulin resistance; "that is what Type 2 is". In view of the fact that many people develop Type 2 in later life, age 67 in my case, is it not plausible that the pancreas goes the way of eyesight and hearing and just doesn't work as well as you get older. Low carb diets offset this by ensuring that the amount of glucose is within the capacity of the limited amount of insulin. Hopefully further deterioration will be slow and not result in recourse to external insulin but it won't be the case for everyone.
 
Type 2 diabetes occurs through insulin resistance as the cells stop responding to insulin, and on diagnosis, the body produces higher than normal levels of insulin to compensate. Over a long time, twenty years or more, if not managed, high sugars can kill off the beta cells, and eventually not enough insulin is produced. Insulin resistance will still be present.
This is different from type 1 diabetes when on diagnosis, non enough insulin is produced because the immune system mistakenly attacks the beta cells, and kills them off.
 
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Type 2 is an umbrella term that people use to label anybody with higher blood glucose readings, who doesn’t fit into any of the other classifications.

so yes, many people who have been diagnosed with T2 have insulin resistance, others have failing beta cells with or without insulin resistance, others simply have not yet been diagnosed with something else, and so on.

The moment someone announces ‘this is what T2 is’ I shrug and know they don’t have a big enough overview, because if they actually had a better grasp, they wouldn’t be making such statements.

One size does not fit all. But we all know that really, don’t we?
 
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ert said:
Type 2 diabetes occurs through insulin resistance as the cells stop responding to insulin, and on diagnosis, the body produces higher than normal levels of insulin to compensate. Over a long time, twenty years or more, if not managed, high sugars can kill off the beta cells, and eventually not enough insulin is produced. Insulin resistance will still be present.
This is different from type 1 diabetes when on diagnosis, non enough insulin is produced because the immune system mistakenly attacks the beta cells, and kills them off.
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I agree with what you say but I am still puzzled by insulin resistance. I can understand that reduced insulin production either from damage due to long periods of high sugar or deterioration due to age would be permanent. However why does insulin resistance persist? Once someone has controlled their blood glucose by changing their diet and got rid of excess weight what causes insulin resistance?
 
Mr_Pot said:
Once someone has controlled their blood glucose by changing their diet and got rid of excess weight what causes insulin resistance?
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Well nothing as they should then be in remission surely?

But quite a few people (docs in the field of research for example) are now avoiding the "insulin resistance" term and instead using "hyperinsulinemia" as a definition of T2.

In my view this might make more sense as T2 are insulin over-producers whereas T1's and many of the varieties under that banner are under-producers.
 
Mr_Pot said:
It used to be said that Type 2 diabetes occurs when not enough insulin is produced or insulin resistance prevents glucose being absorbed. I have noticed recently on the forum that the "not enough insulin" explanation seems to have been dropped. As an example in a thread today someone said of insulin resistance; "that is what Type 2 is". In view of the fact that many people develop Type 2 in later life, age 67 in my case, is it not plausible that the pancreas goes the way of eyesight and hearing and just doesn't work as well as you get older. Low carb diets offset this by ensuring that the amount of glucose is within the capacity of the limited amount of insulin. Hopefully further deterioration will be slow and not result in recourse to external insulin but it won't be the case for everyone.
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Ah... Nuances. Context. The statement was mine, though I put it a little differently: "That is kind of what T2 is", so no absolutes there. And then I proceeded to explain what went on in a newly diagnosed body, with an overproduction of, and insensitivity to, insulin. Far as I understood it, the pancreas does get knackered after a while, and production can certainly diminish, yeah... But to start off with, it seemed to kind of make sense. But I guess not. I'm not a doctor, though they seem more clueless than I feel, half the time.

You know what, I give up. I keep making stupid mistakes anyway, it seems. And I can't seem to pour everything that is relevant into posts without absolutely overwhelming the person asking for help. But next time someone says something, feel free to call them out on it in the relevant thread: it could very possibly help the OP get more of the answers they seek, after all.
 
If we routinely tested insulin rather than obsessing over glucose until it's too late then we would have our answer. Unfortunately most doctors seem to think that insulin testing is some kind of mumbo jumbo black magic, but there we have it.
 
bulkbiker said:
Well nothing as they should then be in remission surely?

But quite a few people (docs in the field of research for example) are now avoiding the "insulin resistance" term and instead using "hyperinsulinemia" as a definition of T2.

In my view this might make more sense as T2 are insulin over-producers whereas T1's and many of the varieties under that banner are under-producers.
Click to expand...

Agreed. T2DM is basically synonymous with hyperinsulinemia. Anything else is a misdiagnosis or misunderstanding. Yes those with T2 can also develop an eventual deficiency, but they will still be resistant to anything they produce or inject.
 
Hi. Many GPs haven't a clue with regard to diabetes so thank goodness for this forum and the other one. I think until the C-Peptide test has come into more frequent use it was assumed (guessed) that T2 could in some cases be the result of too little insulin production. It was also thought (guessed) that T1 was only a childhood condition caused by antibodies. It has now become clearer that true T2 is more commonly the result of insulin resistance and T1 can occur later in life through more than antibodies. So typing is becoming clearer and there will always be genetic exceptions. I agree that it seems feasible that age could cause beta cell loss and then there is the debate as to whether that is T2 or T1. The C-Peptide test can help decide but what if you are mid-range? What type is that....
 
JoKalsbeek said:
Ah... Nuances. Context. The statement was mine, though I put it a little differently: "That is kind of what T2 is", so no absolutes there. And then I proceeded to explain what went on in a newly diagnosed body, with an overproduction of, and insensitivity to, insulin. Far as I understood it, the pancreas does get knackered after a while, and production can certainly diminish, yeah... But to start off with, it seemed to kind of make sense. But I guess not. I'm not a doctor, though they seem more clueless than I feel, half the time.

You know what, I give up. I keep making stupid mistakes anyway, it seems. And I can't seem to pour everything that is relevant into posts without absolutely overwhelming the person asking for help. But next time someone says something, feel free to call them out on it in the relevant thread: it could very possibly help the OP get more of the answers they seek, after all.
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No, no no! I simply won't have it :). None of us can hope to get every word we utter 100% accurate and it is very easy for someone to pick up on something contained within many, many paragraphs and posts and view it out of context or just take those few words to comment on. I don't find anything wrong with that as such (unless someone is seriously misquoted or it's implied they said something that clearly wasn't meant). Anyway Jokalsbeek, PLEASE keep on posting, I rarely (if at all) see a mistake on your part and would hate for you to feel underappreciated. Your posts are spot on along with your nutritionally thingy which makes me smile every time I see it. x
 
JoKalsbeek said:
Ah... Nuances. Context. The statement was mine, though I put it a little differently: "That is kind of what T2 is", so no absolutes there. And then I proceeded to explain what went on in a newly diagnosed body, with an overproduction of, and insensitivity to, insulin. Far as I understood it, the pancreas does get knackered after a while, and production can certainly diminish, yeah... But to start off with, it seemed to kind of make sense. But I guess not. I'm not a doctor, though they seem more clueless than I feel, half the time.

You know what, I give up. I keep making stupid mistakes anyway, it seems. And I can't seem to pour everything that is relevant into posts without absolutely overwhelming the person asking for help. But next time someone says something, feel free to call them out on it in the relevant thread: it could very possibly help the OP get more of the answers they seek, after all.
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I purposely started a new thread as my question wasn't relevant to the OP. I didn't quote you directly as your remarks were only one example of a trend I had noticed, that insulin resistance was now the only the problem with Type 2 and not diminished insulin production. I didn't suggest that you had made a mistake and I agree with @KK123 that none of us are accurate all the time, how can we be when there a no hard facts and experts have differences of opinion.
 
JoKalsbeek said:
Ah... Nuances. Context. The statement was mine, though I put it a little differently: "That is kind of what T2 is", so no absolutes there. And then I proceeded to explain what went on in a newly diagnosed body, with an overproduction of, and insensitivity to, insulin. Far as I understood it, the pancreas does get knackered after a while, and production can certainly diminish, yeah... But to start off with, it seemed to kind of make sense. But I guess not. I'm not a doctor, though they seem more clueless than I feel, half the time.

You know what, I give up. I keep making stupid mistakes anyway, it seems. And I can't seem to pour everything that is relevant into posts without absolutely overwhelming the person asking for help. But next time someone says something, feel free to call them out on it in the relevant thread: it could very possibly help the OP get more of the answers they seek, after all.
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Thank goodness you're not a doctor! At diagnosis mine told me my pancreas was failing. I said I knew I was insulin resistant and he said what's that? At first I wasn't sure if he was serious or not but as the conversation continued it was clear that he was.

Of course an aging pancreas will probably work less well but if a person is an obese T2 chances are there is some level of insulin resistance there. I am with you on this. Please keep posting.
 
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Jim Lahey said:
Yes those with T2 can also develop an eventual deficiency, but they will still be resistant to anything they produce or inject.
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That's the bit I don't understand, what has permanently changed in the body so that it remains insulin resistant. I am not saying it doesn't happen, I just don't know what the mechanism is.
 
Mr_Pot said:
I agree with what you say but I am still puzzled by insulin resistance. I can understand that reduced insulin production either from damage due to long periods of high sugar or deterioration due to age would be permanent. However why does insulin resistance persist? Once someone has controlled their blood glucose by changing their diet and got rid of excess weight what causes insulin resistance?
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I agree with you entirely. If you could answer this question, then you could cure diabetes rather than put it into remission.
 
Mr_Pot said:
That's the bit I don't understand, what has permanently changed in the body so that it remains insulin resistant. I am not saying it doesn't happen, I just don't know what the mechanism is.
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Well I have my views on that but since you have disagreed with them in the past more than thrice, there’s not much point in elaborating.
 
I tend towards the view that T2 isn't really about 'Insulin Resistance'. But that it is all about the carbs eaten and the body's ability to deal with them.

Though not perfect the best analogies are with Japanese trains or adding more to an already overstuffed holiday suitcase:

We all (should) know that Carbs turn to Blood Glucose and Insulin stuffs the Blood Glucose into muscle and fat cells.
When a Japanese train is half empty, no external pressure is required in order for more passengers to get on it. But when all seats and much standing space has been taken up, they use physical pressure from 'pushers' in order to pack more people into the train.
What is called 'Insulin resistance' is just fat cell overload caused by excess carbs. The body responds to the higher Blood Glucose by (trying) to produce more and more Insulin (more Japanese train passenger pushers) in order to get that dangerous Glucose safely out of the blood stream.
It is thought that this process has been going on for as much as decades before the takes becomes impossible and Blood Glucose finally gets high enough for T2D to be diagnosed and that by that stage the pancreas is no longer able to produce the peak Insulin that it was previously capable of (either by 'wearing out' or because of 'old age').

I have seen that some forum members post claims that their T2D is 'cured' i.e. they are able to eat 'normal' (though not excessive) amounts of carbs without spiking their BG. That would seem to support this view of Insulin Resistance. However it seems that for probably the majority either the Insulin production will never be high enough for them to achieve this, or at least they don't have the confidence to risk trying to see if they are 'cured'.
 
Hello all,

Really interesting question.

Generally, I agree with @Brunneria -- we shouldn't overly generalize as T2 seems to be a bit of a catch-all category unless there is testing to specifically determine type. As we all know this really doesn't happe often enough. Instead type is usually guessed at based on age (and often weight). But even assuming that diagnosis is correct and we are truly T2, there still seems to be a lot of interindividual variation.

This having been said, for many of us T2s (maybe even most), producing too much insulin in response to a carb-heavy life style (probably due to a genetic predisosition) seems to be common at least initially.

There are a couple of interesting sources that may support this assumption:

This is an figure from a presentation (red line for average c-peptide levels for low HbA1cs included by me) by Ken Sikaris, a clinical biochemist from the University of Melbourne:

upload_2020-9-30_19-9-45.jpeg

As seen in this graph, average c-peptide levels for elevated HbA1cs seem to be higher than for normal HbA1cs (though more pronounced in the prediabetic range). Average c-peptide levels are still higher for very high HbA1cs in the range of 12% or 108 mmol. Furthermore, it appears that for elevated HbA1cs at least 2/3 of the results are higher than the average for a low HbA1c. I believe this also should be seen in the light of who is likely to be tested for c-peptide -- in my mind this is probably in many cases to be a person suspected of having T1 or LADA. So, in fact this graph would probably be a conservative estimate of the c-peptide production for a T2s (meaning after taking out T1 or LADAs , the average c-peptide production will very likely be higher).

In another article, also found tables comparing characteristics for T1, LADA and T2. Here, insulin production seems to be one of the distinguishing characteristics (https://www.e-enm.org/journal/view.php?doi=10.3803/enm.2018.33.2.147)

upload_2020-9-30_19-49-8.jpeg


Here is also an article, which looks at what happens to insulin production in T2s over time (https://pubmed.ncbi.nlm.nih.gov/16939949/). The authors conclude that insulin production often declines for T2s with time, but that this is not inevitable.
 
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