A discussion on what makes someone T2

[HSSS]

I’m not so sure that malfunction is the right word for the majority of type 2 (though it could be). Imuslin resistrance would be the place I lay the cause of type 2 label. Problem is that leads to “what causes insulin resistance?”

T 2 has two elements - Insulin Resistance and a pancreas that cannot produce and secrete enough insulin to overcome this resistance to insulin.

As shown by the chart above the pancreas will do an amazing job increasing insulin levels to overcome resistance and maintaining normal glucose level, sometimes for decades, or even forever in some people. But, every organ has it‘s limits. Once it’s reached flat out production if that’s not enough to overcome ever increasing resistance then it become “not enough” despite being at maximum and having high numerical levels. That’s not a faulty pancreas. It’s a job that’s unmanageable. So the insuffciency is relative to the situation, rather than like a type 1 who actually has less than normal or even no insulin production in absolute terms. As such I really dislike the references to type 2 starting out with insufficient insulin (even though after many years of high production it can begin to fail) as that tends to cause the underlying problem of increasing IR to be ignored unless the context of absolute and relative are included

There is another issue about first and second stage insulin responses and type 2 but I’ll be honest and say I still haven’t got my head around that issue even now.

I’m also 100% in agreement type 2 seems to have some definite sub sets in terms of what initiates the onset and what management works best. It seems to be diabetes that doesn’t fit into any other category of diabetes.

With regards to your diagnosis it seems you’d been inching closer for some time. It does seem a little odd that the second confirmation hba1c was done simultaneously with oral steroids those with their known effect though. I suspect that may be because drs/nurses assume the second test will only ever support the first regardless. That’s not always the case. My own mum just proved this when they tried to diagnose her on one test alone that was just above the cut off, and I insisted on a second test as per NICE and got her to go lower carb in between. I also reinforced she was dangerously close to the official diagnosis and action was the only thing that avoided it, rather than being an error. It does mean she avoided the triple medication they’d have put her on immediately despite that also not being the NICE guidance but a local area one. That hasn’t happened for you luckily and the eye tests for diabetes arent the same as the normal optician ones.

edited to remove superfluous quote.

 

[Lamont D]

Hi everyone. I'm a newbie to posting although I have followed the site for nearly a year. I've found everything I've read so interesting and helpful, particularly this thread, and learnt so much. I'm a woman in my 70s and have never been overweight. I had an HbA1c in May 2022 of 50 - my first one ever despite my family history being on my medical records. I thought I was only getting a cholesterol check. Two weeks later it was retested at 45. Since then I have gone low carb and finger prick tested, but my levels have remained firmly pre-diabetic at 46, 47 and 45 (July 2024). At least I now know the score.

I have a long family history of diabetes - my mother, my grandmother, my great-grandmother (who had a leg amputated), and my daugnter who is also now pre-diabetic and had gestational diabetes in 2015 with her second pregnancy. Has anyone here come across MIDD or Maternally Induced Diabetes and Deafness? I have worn hearing aids for some years. Is this it? My GP has never heard of it. My sister in Australia has a HbA1c of 41 and has already been prescribed metformin as a 'preventative measure' because of our family history - not a route I'm keen to follow.

I had a private Kraft Test (not cheap but worth it to me) in April 2023 which tests for glucose tolerance and insulin response side by side, and which showed I have a very poor insulin response, as though my pancreas is slowly wearing out, so maybe that is the weak link in my family history. I don't understand why more insulin testing doesn't take place as a general rule as surely it is a key piece of information in the jigsaw that is diabetes.

I identify completely with the phrase 'high blood sugar is a sympton, pancreas malfunction is the cause'! I shall keep on with my low carb diet and finger prick testing and just hope I can stay below that 48 figure. My GP has given me a prescription for the testing strips, sort of in return for my agreement to go back on statins. I stopped taking them for six months but it had made no difference to my BG levels.

Good luck on your journeys, everyone, and thank you for all your posts. I shall keep reading and learning.

When I had my second extended oral glucose tolerance test, the cannula fitted took blood samples which were sent off to a special laboratory for some tests, the one you refer to, was one of them whereas my glucose and insulin were tested as the eOGTT went on.
This has to be done by a specialist endocrinologist in hospital and as you can imagine, quite expensive.
Insulin testing is also more expensive than glucose testing and the reason why hba1c levels are used as a diagnostic basis.
Also my first phase insulin response was found to be weak, background insulin was low for the amount of glucose. This was the reason why, I had a abnormal high spike with the glucose.
There maybe other reasons for the weak insulin in the first phase. This is why, the pancreas responds with more insulin, sometimes, like me, too much.
As has been suggested a referral might get you the tests you need for a true diagnosis.

There are certain meds that are designed to help with weak first phase insulin.
However, depending on you or other factors or usual side effects issues found in pharmaceuticals.

Unless you have had heart issues previously, I would certainly consider not taking statins.
Over twenty years ago, I was advised because of my family history, to take statins. The side effects were worse.
My endocrinologist advised against them, a heart specialist asked why I wasn't taking them when he noticed my medical necklace. Then he told me not to bow down to GP's pressure.
I don't need them, at seventy, thanks to my diet, my heart health is very good.

Hope this helps.

 

[Melgar]

I understand what you are saying @HSSS I have a different angle on this. I agree with you on in fact every organ has its limits, but one can say that about any number of medical issues. It is just semantics on whether it’s faulty or overwhelmed or not producing enough, its failing because it cannot produce enough insulin to do the job it’s meant to do. If your pancreas cannot maintain a healthy blood sugar level, given a relatively normal diet then your pancreas is not operating as it should. The fact remains that Type Diabetes is an issue with the pancreas. Insulin resistance is definitely a component in classic T2 without question , but it is the inability of your pancreas to produce enough insulin to maintain ’normal’ blood sugars. please correct me if I’m missing your point. I’m jet lagged by 8 hours.
Edited to change the wording to “ different angle”.

 

[HSSS]

I understand what you are saying @HSSS but I disagree with you. I agree with you on in fact every organ has its limits, but one can say that about any number of medical issues. It is just semantics on whether it’s faulty or overwhelmed or not producing enough, its failing because it cannot produce enough insulin to do the job it’s meant to do. If your pancreas cannot maintain a healthy blood sugar level, given a relatively normal diet then your pancreas is not operating as it should. The fact remains that Type Diabetes is an issue with the pancreas. Insulin resistance is definitely a component in classic T2 without question , but it is the inability of your pancreas to produce enough insulin to maintain ’normal’ blood sugars. please correct me if I’m missing your point. I’m jet lagged by 8 hours.

It’s not semantics at all imo. If someone is producing 3 times the average amount of insulin for instance I’d say their pancreas was working pretty well. If other things have gone wrong in the body, in this case the IR, how can you blame the pancreas for not compensating enough if that would take such an enormous amount of extra work? That’s not to say a faulty pancreas cannot be part of the problem (and may even mean a type 3c diagnosis is more appropriate if the cause was externally induced) but it’s certainly not a requirement of type 2 according to everything I’ve read. I’d be interested if you have any articles etc supporting your view though (once you’re time adjusted etc)

 

[Melgar]

It’s not semantics at all imo. If someone is producing 3 times the average amount of insulin for instance I’d say their pancreas was working pretty well. If other things have gone wrong in the body, in this case the IR, how can you blame the pancreas for not compensating enough if that would take such an enormous amount of extra work? That’s not to say a faulty pancreas cannot be part of the problem (and may even mean a type 3c diagnosis is more appropriate if the cause was externally induced) but it’s certainly not a requirement of type 2 according to everything I’ve read. I’d be interested if you have any articles etc supporting your view though (once you’re time adjusted etc)

I understand what you are saying @HSSS , but there are none-diabetics with IR producing well over 1700pmol/ls of c-peptides and have normal blood sugars. There pancreas is capable of producing masses amounts of insulin because they have a tight, probably a large beta mass and very healthy islets of the Langerhans. Then you have diabetics producing 1000 - 1200 pmol/s with very high blood sugars. They have a pancreas that is incapable of producing enough insulin to compensate for their IR.

 

[Chris24Main]

The science around this is not 100% certain, and clearly as patients (I know this was true for me, there is a sense of "it could be insulin resistance, it could be the pancreas") we can be told conflicting things.

In the end, the only thing that "makes someone T2" is a certain level of blood glucose - but that's not really much help, because it also describes T1 - it is the insulin that differentiates the two, and my opinion is that we don't give that enough credence, for reasons outside the scope of the post.

There are massive differences in individual people and their pancreas capacity, and for that matter, the effect of the elevated insulin and resultant insulin resistance that follows, - there are plenty of people who remain relatively insulin sensitive and just put more and more weight on, but their blood glucose remains fine.

There are plenty of people who just tip into Colon Cancer (my father in law being one) and there are plenty of people that tip into Alzheimer's - but it's may not be on account of the relative capacity of the Pancreas, it follows from the insulin resistance due to elevated insulin over decades. I recently re-read the section in Prof Ben Bikman's "why we get sick" - and he is very clear that insulin resistance is the same as pre-diabetes. But he is a cellular biologist, just because he can surround pancreatic cells with glucose and see insulin resistance increase (and decrease on removing it) - doesn't mean that this is a 100% done deal - this is complex and we are all unique.

At the big-picture society level though, compensating for insulin resistance doesn't seem to me to be a strategy that's working (after all, that's really what most of the medical profession does with metformin until it also cannot compensate enough, then insulin and so on)


... edited to make it clear that I do not consider my opinion to be anything other than that.

 

[Melgar]

I agree that IR is very significant in many chronic conditions. So that isn’t an issue for me, I’m in agreement with that so cancer , dementia, chronic inflammation etc is related to IR. I still say that IR alone cannot cause T2 diabetes.
Edited to remove the statement I disagree plus a sentence that did not add to the discussion.

 

[Lamont D]

This all boils down to whether you think that it's the Pancreas's job to compensate for a diet that we're not evolved to cope with.
There are massive differences in individual people and their pancreas capacity, and for that matter, the effect of the elevated insulin and resultant insulin resistance that follows, - there are plenty of people who remain relatively insulin sensitive and just put more and more weight on, but their blood glucose remains fine.

There are plenty of people who just tip into Colon Cancer (my father in law being one) and there are plenty of people that tip into Alzheimer's - but it's not all on account of the relative capacity of the Pancreas, it follows from the insulin resistance due to elevated insulin over decades.

Compensating for insulin resistance doesn't seem to me to be a strategy that's working (after all, that's really what most of the medical profession does with metformin until it also cannot compensate enough, then insulin and so on)


... slight edit as it seemed too aggressive.
I guess I'm just thinking about the majority of cases. @Melgar - you are unique in many ways, but for the vast majority of T2DM cases, in all the literature I can find, there doesn't need to be anything wrong with the Pancreas. If there is, then for sure, it will have an effect - but even an edge case capacity Pancreas may hold your blood sugar down (for a while, or maybe even forever) - you still have a dangerously high level of insulin and insulin resistance which drives so many other chronic conditions.

Just to muddy waters a tad here.
Again, the relationship of all our organs, hormones, the gut, the brain, the system of how we cope with food.
The enteric system. And so on.
There may be more with the cell structure and other conditions that may impact on blood glucose, insulin response, and with Insulin resistance etc.

There is such a thing called the gut brain axis. That relays messages from brain to organs and so on, with the control of how much hormonal (insulin) response is required as well as the hormones etc.

The whole system is complicated and at about a million plus points could have an abnormal response.
So it cannot and will not be a single linear cause.
Over time, with many different factors attributing to a general decrease in healthy response to how we digest certain foods.
I know with my number of intolerances, how the different symptoms to the reactions of how different my spike is to different foods. Same portion size will produce a variance from single figures to high teens.
I do believe, having read research papers that inflammation of the cells in our organs is a precursor to an imbalance in the first phase response. As well as the precursor to insulin resistance, but the question is at the early stages, how much and how quickly will it develop. And the older we are, it does seem to cause more issues as old age does.
The boffins and researchers are only still just discovering different things that impact our thinking about how diabetes and related metabolic conditions like T2 develop. And are still in the last century with some of the way the doctors treat patients, mainly because the teaching of our doctors does rarely include T2.

 

[HSSS]

I understand what you are saying @HSSS , but there are none-diabetics with IR producing well over 1700pmol/ls of c-peptides and have normal blood sugars. There pancreas is capable of producing masses amounts of insulin because they have a tight, probably a large beta mass and very healthy islets of the Langerhans. Then you have diabetics producing 1000 - 1200 pmol/s with very high blood sugars. They have a pancreas that is incapable of producing enough insulin to compensate for their IR.

Maybe because the latter have higher IR? Maybe those that maintain normal blood glucose despite high IR or that can produce mega amounts of insulin are the outliers? Are all tests done the same way eg fasted or in response to glucose? Maybe some do in fact have pancreatic limitations. That’s not the same as it being a requirement of type 2 though. If your theory is right why have so many pancreas’ been damaged in the last generation compared to previous ones?

I’m not sure why you think all pancreas’ are supposed to be able to go on endlessly compensating for other deficiencies? Do you expect that of all body organs and systems or just this one?

I get you disagree, as is your right, but I’d love to read any literature that support your position when you are able to get some reasonable internet as it’s a position you’ve returned to several times and I’d like to see more on it if it’s avaliable as it isn’t consistent with the things I’ve found over the years.

 

[Melgar]

The above Posts have been moved by @Melgar from the discussion titled - What makes some diabetic? Click on link to see previous discussion
https://www.diabetes.co.uk/forum/threads/what-makes-someone-t2.206350/