Insulin resistance

[KK123]

Agreed. As far as I know, most/all T2s have developed insulin resistance (so tend to be over-weight) and most/all T1s produce no/not enough insulin (so tend to be under-weight). However, in T2s the pancreas can get exhausted by producing more and more insulin to try and overcome severe resistance, so the T2 develops T1 and needs artificial insulin. In T1s, injecting lots of insulin can lead to insulin resistance, so the T1 develops T2 (maybe gains weight) and needs even more injected insulin. Both conditions are known as "double diabetes". Apologies for unscientific résumé. If I have got this wrong, I hope someone will instruct me better.

Hi Alexandra, I get what you are trying to say but even a type 2 with an exhausted pancreas cannot become a type 1. Yes they may well have to use insulin in the same way but the causes between the two types are completely different.

 

[HICHAM_T2]

Because the root cause has not been fixed. There are people who regain some insulin sensitivity but even they must admit that to return to their former 'normal' diet would see their blood glucose levels compromised.
There is no cure but there can be excellent management.

So where is the problem? We know there are healthy people who eating what they want without problems accumulating

 

[Guzzler]

No Not I am just i download it

Thank you, I was wondering about the part of the diagram that shows 'Islet triglyceride' as this is a term I have not come across before.

 

[Guzzler]

So where is the problem? We know there are healthy people who eating what they want without problems accumulating

No one knows why some people become insulin resistant but others do not. There is a hypothesis that genetic predisposition could be the answer but, as I said, no one truly knows.

 

[HICHAM_T2]

No one knows why some people become insulin resistant but others do not. There is a hypothesis that genetic predisposition could be the answer but, as I said, no one truly knows.

For this reason we must all work in search of a solution why not We are concerned,?

 

[Seacrow]

Is there anyone here with what alexandra100 quotes as "double diabetes", i.e, having type 2 symptoms, when youre a type 1, and is there an actual diagnosis term for it? I was thinking about this earliar. If I become insulin resistant when im older to the point where insulin is ineffective, then what
? Or does this not happen as extreme as what im making out

I've got both. Started out with auto-immune reaction, lost all insulin production from the pancreas, then developed insulin resistance.

Doctors ignore the type one, and treat purely as a type two.

It’s just called having insulin resistance. I don’t like using the term ‘double diabetes’ or having ‘type 1 and type 2’. It doesn’t help with the educating about type 1 and type 2 being two different conditions. Also as a type 1 I can’t have type 2 ever. My pancreas cannot start producing insulin again.

Not true. A type one with no insulin production can still develop insulin resistance, becoming type two. I know because I did.

 

[NicoleC1971]

Hi @HICHAM_T2 my friend.

One could transplant a whole new heathy pancreas into a patient with insulin resistance. It would not solve the issue..
The "tactic" is using more insulin (with injecting for T2.) than is naturally produced, to "ramp up" the message to the receptors.?

As I understand it the gummed up lock with insulin as the key is not actually what happens though it is an easy to understand analogy. I believe this is the story:
The condition starts with excess insulin in response to excess carbs (that cannot be stored as energy in the muscles or fat cells (everyone has an individual tolerance for the expansion of their fat cells), then the person becomes increasingly insulin resistant in that their insulin fails to turn off the liver's production of glucose (gluconeogenesis). At the end of the process, the huge demands upon the beta cells cause a drop in insulin production such that the bg rises to 'diabetic' levels but in fact the person has been diabetic 'in situ' or insulin resistant for many years prior to that. It has recently been proved that those beta cells can recover production once the person fasts, has bariatric surgery, goes low carb or does a very low cal diet all 3 of which strip the liver of stored energy and allow it to respond normally to the body's insulin again.
Treating a type 2 with exogenous insulin is therefore analagous to giving alcohol to an alcohol dependent person; the root casue of the problem is insulin resistance and not insufficient insulin.
Some very large people can be metabolically healthy because their fat cells expand expedentially to protect their bodies from toxic blood sugar levels whereas the converse is true for the skinny type 2s who turn their excess carbs into fat around the liver and pancreas.

 

[ziggy_w]

No one knows why some people become insulin resistant but others do not. There is a hypothesis that genetic predisposition could be the answer but, as I said, no one truly knows.

I agree. I don't believe we know for sure what causes insulin resistance and that there must be some kind of genetic component to it. However, I also think that lots of people are potentially predisposed towards insulin resistance (as evidenced by rising worldwide rates of T2 diabetes and prediabetes) and that there is also some environmental trigger -- may it be excess carbs or vegetable oils in the diet, chronic stress and sleep deprivation, or something else or any combination of these factors.

There is also an interesting hypothesis centering on the role of fat cells in the development of insulin resistance. If I understand this theory correctly (and I may not) is that there are two types of people.

One set of people develop the maximum number of fat cells before birth or in childhood and these are all the fat cells, they will ever have. Once these fat cells reach their maximum size and are overfilled, they will become insulin resistant and will have problems absorbing any more glucose. Insulin levels rise, but because very little addtional glucose can be absorbed by fat cells, fat now starts depositing on the inner organs, including pancreas and liver (leading to improper functioning, such as lower insulin production and liver insulin resistance and increased release of glucagon from the liver) and eventually blood glucose levels will start to rise.

The other set of people, based on this theory, can grow new fat cells even later in life, so there is theoretically no limit to absorbing excess glucose and turning it into fat. These people would then never become insulin resistant, but would continue gaining weight in response to excess glucose.

What makes this theory attractive, in my mind, is that it can explain why there are some thin T2s and some not so thin T2s -- the difference might just be the number of fat cells we come pre-equipped with.

Interesting theory, anyway, I believe.

If you interested into looking more into this, I think Gabor Erdosi talks some about this and here is also a link to an article which provides some support for this: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018284

 

[Guzzler]

I agree. I don't believe we know for sure what causes insulin resistance and that there must be some kind of genetic component to it. However, I also think that lots of people are potentially predisposed towards insulin resistance (as evidenced by rising worldwide rates of T2 diabetes and prediabetes) and that there is also some environmental trigger -- may it be excess carbs or vegetable oils in the diet, chronic stress and sleep deprivation, or something else or any combination of these factors.

There is also an interesting hypothesis centering on the role of fat cells in the development of insulin resistance. If I understand this theory correctly (and I may not) is that there are two types of people.

One set of people develop the maximum number of fat cells before birth or in childhood and these are all the fat cells, they will ever have. Once these fat cells reach their maximum size and are overfilled, they will become insulin resistant and will have problems absorbing any more glucose. Insulin levels rise, but because very little addtional glucose can be absorbed by fat cells, fat now starts depositing on the inner organs, including pancreas and liver (leading to improper functioning, such as lower insulin production and liver insulin resistance and increased release of glucagon from the liver) and eventually blood glucose levels will start to rise.

The other set of people, based on this theory, can grow new fat cells even later in life, so there is theoretically no limit to absorbing excess glucose and turning it into fat. These people would then never become insulin resistant, but would continue gaining weight in response to excess glucose.

What makes this theory attractive, in my mind, is that it can explain why there are some thin T2s and some not so thin T2s -- the difference might just be the number of fat cells we come pre-equipped with.

Interesting theory, anyway, I believe.

If you interested into looking more into this, I think Gabor Erdosi talks some about this and here is also a link to an article which provides some support for this: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018284

Absolutely agree with all that you have said. There has to be a cohort of triggers.

 

[Seacrow]

The condition starts with excess insulin in response to excess carbs (that cannot be stored as energy in the muscles or fat cells (everyone has an individual tolerance for the expansion of their fat cells), then the person becomes increasingly insulin resistant in that their insulin fails to turn off the liver's production of glucose (gluconeogenesis). At the end of the process, the huge demands upon the beta cells cause a drop in insulin production such that the bg rises to 'diabetic' levels but in fact the person has been diabetic 'in situ' or insulin resistant for many years prior to that. It has recently been proved that those beta cells can recover production once the person fasts, has bariatric surgery, goes low carb or does a very low cal diet all 3 of which strip the liver of stored energy and allow it to respond normally to the body's insulin again.
Treating a type 2 with exogenous insulin is therefore analagous to giving alcohol to an alcohol dependent person; the root casue of the problem is insulin resistance and not insufficient insulin.
Some very large people can be metabolically healthy because their fat cells expand expedentially to protect their bodies from toxic blood sugar levels whereas the converse is true for the skinny type 2s who turn their excess carbs into fat around the liver and pancreas.

So, given I had type one, and my beta cells are all dead I should in theory be able to get down to a 'normal' insulin dose rather than the bucketloads I take right now? Sounds good, but for me it doesn't work. There have been multiple times I have fasted for three or four days. It does absolutely nothing to my insulin resistance.

While I can see your point that treating insulin resistance with insulin is not a perfect solution, there is one major point. It keeps people alive, and not in hospital with dka.

And for those going with the genetic susceptibility theory, I have types 1 and 2 and I am the first and only one from five generations. Always was an awkward s#d though.

 

[KK123]

I've got both. Started out with auto-immune reaction, lost all insulin production from the pancreas, then developed insulin resistance.

Doctors ignore the type one, and treat purely as a type two.



Not true. A type one with no insulin production can still develop insulin resistance, becoming type two. I know because I did.

Hi Seacrow. I get that a type 1 can develop symptoms that a type 2 might get but does that mean they are then a type 2 or a type 1 still but with extras (double whammy!!).? Insulin resistance does not just apply to type 2s in any case. I suspect plenty of type 1s have insulin resistance. I also don't get what's the difference being treated 'purely as a type 2', in what way? I'm guessing you are still on insulin so what else do you get, metformin for example? Fascinating.

 

[HICHAM_T2]

I think the solution would be to study insulin type 2 diabetic patients its very important
must be Comparisons between insulin for healthy people and The patients people may have a difference in genetic composition who is know ?

 

[Seacrow]

Hi Seacrow. I get that a type 1 can develop symptoms that a type 2 might get but does that mean they are then a type 2 or a type 1 still but with extras (double whammy!!).? Insulin resistance does not just apply to type 2s in any case. I suspect plenty of type 1s have insulin resistance. I also don't get what's the difference being treated 'purely as a type 2', in what way? I'm guessing you are still on insulin so what else do you get, metformin for example? Fascinating.

It's a definition thing. If you define type two as increased insulin production due to insulin resistance, possibly followed by pancreas burnout, then I'm not type two. If you define type two as insulin resistance, then I am. All the doctors I see classify me as type two.

I think of myself as type 1 + type 2, beta cells killed by immune system and severe insulin resistance. In the doctors notes I'm classified as ( type 2, pump ). My gp mentioned the libre at my last visit, then said I didn't qualify because I was type 2. He had to check all the way back to find my antibody tests and confirm I was type 1 as well.

My consultant has tried to prescribe every single drug used on type 2s, even gliclazide. (Glic is the drug that makes your pancreas produce more insulin. Didn't work for some reason .) I can't tolerate metformin or exenatide, the 'gliptin didn't work, pioglitazone didn't do anything to my bg but did horrible things to my cholesterol. He has sent me for testing for: hypothyroidism, no; hypoparathyroidism, yes; ovarian cysts, yes; kidney cysts, yes; fatty liver, yes; gastroparesis, yes; hyperhaemotosis, no; pheochromocytoma, ?; paraganglioma, ?. He is determined to find every single metabolism affecting condition I have.

I think the attitude I've caught from the doctors is that type 1 is an unfortunate but one-off event (the triggering of an immune reaction) and needn't affect your health, but type 2 is indicative of an entire metabolic system that isn't working and WILL come with added complications.