Type 2 and insulin resistance - what I don't understand is...

[Callista]

Hi, I wonder if someone can enlighten me.

From what I currently understand (not much!), T2 is strong associated (caused?) by insulin resistance - our bodies can still make insulin, that isn't the issue as it is for T1, but for 'some reason' it's not very effective any more, ie, our body can't use it as well as it used to. So our pancreas pumps out more for a while, and then, at some point, throws in the towel, and we stop producing insulin. At that point we need insulin injections, like T1 patients.

Is that the set up?

If so, then I don't really understand why, if our bodies can't use the insulin we are still producing, indeed, over-producing, how we then make use of any injected insulin? Aren't our cells still resistant to insulin (ie, we still can't make much/any use of it?)

I appreciate there are other mechanisms for getting glucose into our cells than using the insulin-mediated transfer system, but from what I understand (??) insulin-mediated pathways are what our muscles use (or like to use!), and our liver also uses (needs?) those insulin-mediated pathways to soak up excess blood glucose and turn it into liver-storable glycogen (and then, eventually, through loads of other metabolic pathways, if that glycogen isn't broken back down again into glucose by insulin's 'opposite number' glygogon, to replenish our blood glucose needed to feed our cells, then unused/excess glycogen ends up as fat)

So, if muscle cells and liver (glycogen storage) cells need insulin to take blood glucose out of our blood and into our muscle cells or to store in liver cells as glycogen, then if we have insulin resistance, how are they going to do that effectively, whether it's our own insulin or injected insulin?

I guess my question boils down to: If we have insulin resistance, then the problem is not that we can't produce insulin (or have it injected), but that we can't use it to 'feed' our muscles, or store in the liver or, worst of all from a 'toxic' point of view, get it out of our bloodstream.

(I appreciate the whole 'mission' of T2 patients is to minimise/reverse resistance but it still rather begs the above question of what happens if we don't or can't....)





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[Admiral Benbow]

From what I understand from guys who are much smarter than me like Dr. Jason Fung, Dr. Eckberg, Dr. Berg, the Beat Diabetes guy, Type 2 diabetes insulin resistance is caused when too much sugar is in the blood and stored as visceral fat around internal organs. Insulin trys to push it into the cells but if the cells already have too much glucose, they can't get into the cells so they store in places they are not supposed to be like the the pancreas or oversaturate the liver causing fatty liver.
The way to eliminate glucose from the system is to burn it off by not putting as much in (changing our diet), exercising it off, or fasting it off.
Dr. Fung say's its an overfill problem, and you have to drain it out over time.

 

[Lucyr]

It’s not a flat “T2 can’t use insulin at all” it’s insulin resistance, so more a “T2 can’t use insulin as effectively so it takes more to get the job done”

 

[Inka]

Insulin resistance was described to me like trying to squeeze something through a tiny hole. It will still eventually go through but it needs a lot of work (ie insulin). So with injected insulin, Type 2s are often on larger doses of insulin than Type 1s because their bodies resist the insulin so they need a bigger amount. It’s not that they can’t use it at all.

 

[EmmaL76]

I often think about this too, as I don’t really have a proper diagnosis the endo did say that if it ends up a type 2, because of my slim build and lack of metabolic issues etc I would always end up on insulin in the end. My question is, we know too much sugar in the blood is not good for you but what about too much insulin ? If we overproduce and inject the stuff is hyper insulin ok

 

[Admiral Benbow]

I often think about this too, as I don’t really have a proper diagnosis the endo did say that if it ends up a type 2, because of my slim build and lack of metabolic issues etc I would always end up on insulin in the end. My question is, we know too much sugar in the blood is not good for you but what about too much insulin ? If we overproduce and inject the stuff is hyper insulin ok

I would think too much insulin is bad because that means there is too much glucose in the blood and the insulin is trying to lower it. The way I look at it is like this, if the liver glycogen stores are constantly being emptied by good diet, fasting, and exercise (in that order), the blood sugars will stay low and so will the insulin. However, if one starts drinking lots of Coca Cola, eating french fries, and lots of sugar, spiking the blood sugars repeatedly and never giving the body a chance to get rid of the sugars, the insulin will rise trying to find a place to park the glucose. If it can't park it in the cells, because they are already saturated and now insulin resistant, it will park it (the glucose) as visceral and subcutaneous fat. The Doc's and Big Pharma treat the blood sugar, first with metformin, later with insulin, not the metabolic imbalance leading to the disease which is why I am absolutely terrified of being diagnosed with diabetes and hoping never to get into the vicious never ending cycle as I fear being reliant on Big Pharma. My strategy is shut down the source of insulin rising by lowering everything that could raise it, carbs sugar, and giving the body once a week complete rest from digestion for 48 hours by fasting. If my numbers are good on my next test I will go 24 hours a week only, but it looks like fasting is with me for life now, as I know during those hours insulin can only rise in response to glycogen being released by the liver.

 

[Windy]

This is my understanding - Insulin resistance is caused by too much fat around the liver and pancreas. This paper explains it. They say T2 is caused by "hepatic [liver] insulin sensitivity ..." and abnormal "beta cell insulin secretion" in the pancreas. They used weight loss to address both of these. There's a great graphic explaining the hypothesis:


Image from: Taylor, R., 2013. Banting Memorial Lecture 2012 Reversing the twin cycles of Type 2 diabetes. Diabetic medicine, 30(3), pp.267-275.

But the long and the short of it are that if you lose weight, it also goes from your liver and pancreas, and you have a chance to get diabetes remission if you lose 15% of your body weight, as you break the cycle causing insulin resistance.

PS "Big Pharma" is on a hiding to nothing with the medications that I have been prescribed, ramipril and atorvastatin. They're both out of patent, and for atorvastatin, it costs the NHS just over a pound per month to prescribe, compared to over £30 for the branded version, lipidor. I'm assuming ramipril was similar, but I haven't looked for the costs of that yet.

 

[rebrascora]

I see it similarly to how @Inka has described it. The cells store excess glucose as fat and once they reach a certain limit, they don't want to accept any more... this may be the "personal fat threshold" that Professor Taylor talks about. Up to that point, insulin works reasonably easily and efficiently although I believe there is an element of insulin resistance that we all experience, varying throughout the day and with BG levels, but once you hit that personal fat threshold the cells start to say enough is enough and don't want to take anymore, so more insulin is needed to force them to take it. Of course, if you do exercise and use up some of the stored glucose, the cells have capacity to take more for a short time and will do so more willingly, but if you keep putting the glucose into your blood stream without regularly burning off what is stored, gradually you approach a situation where your system is going to grind to a halt, because the pancreas eventually burns out and then you need to inject large doses of insulin to overcome that resistance. The difference generally comes down to the amount of insulin you need to inject between insulin dependent Type 1s and Type 2 and is one of the reasons why some Type 2s are eventually recognized as actually being Type 1 like @Eternal422, because they clearly only need "normal" amounts of insulin.

I believe there is another element to Type 2 where the liver and pancreas get enveloped and clogged with fat even if the patient isn't carrying a lot of weight in the rest of their body/fat in their other cells. The liver and pancreas then have problems communicating efficiently to balance BG levels and I do wonder if this situation can initially perhaps exhibit as Reactive Hypoglycaemia in some people whereas others experience a slow insulin response, so levels spike after a meal and take too long to come back down.

Some Type 2s may only experience one of those elements and some may experience both and I am sure there are also more variations of mechanisms at play... The body is very complex. 🙄

Anyway, that is my totally non medically trained take on the situation.

 

[Deleted member 21371]

From what I understand from guys who are much smarter than me like Dr. Jason Fung, Dr. Eckberg, Dr. Berg, the Beat Diabetes guy, Type 2 diabetes insulin resistance is caused when too much sugar is in the blood and stored as visceral fat around internal organs. Insulin trys to push it into the cells but if the cells already have too much glucose, they can't get into the cells so they store in places they are not supposed to be like the the pancreas or oversaturate the liver causing fatty liver.
The way to eliminate glucose from the system is to burn it off by not putting as much in (changing our diet), exercising it off, or fasting it off.
Dr. Fung say's its an overfill problem, and you have to drain it out over time.

Not with me.
Purely calories that produces visceral fat in my case.

 

[Deleted member 21371]

This is my understanding - Insulin resistance is caused by too much fat around the liver and pancreas. This paper explains it. They say T2 is caused by "hepatic [liver] insulin sensitivity ..." and abnormal "beta cell insulin secretion" in the pancreas. They used weight loss to address both of these. There's a great graphic explaining the hypothesis:

View attachment 24916
Image from: Taylor, R., 2013. Banting Memorial Lecture 2012 Reversing the twin cycles of Type 2 diabetes. Diabetic medicine, 30(3), pp.267-275.

But the long and the short of it are that if you lose weight, it also goes from your liver and pancreas, and you have a chance to get diabetes remission if you lose 15% of your body weight, as you break the cycle causing insulin resistance.

PS "Big Pharma" is on a hiding to nothing with the medications that I have been prescribed, ramipril and atorvastatin. They're both out of patent, and for atorvastatin, it costs the NHS just over a pound per month to prescribe, compared to over £30 for the branded version, lipidor. I'm assuming ramipril was similar, but I haven't looked for the costs of that yet.

This seems like the best explanation I've seen.
The trick is to get the body working properly again.
And yes , the normal drugs, that seem to work well, cost next to nothing now.

 

[EmmaL76]

I see it similarly to how @Inka has described it. The cells store excess glucose as fat and once they reach a certain limit, they don't want to accept any more... this may be the "personal fat threshold" that Professor Taylor talks about. Up to that point, insulin works reasonably easily and efficiently although I believe there is an element of insulin resistance that we all experience, varying throughout the day and with BG levels, but once you hit that personal fat threshold the cells start to say enough is enough and don't want to take anymore, so more insulin is needed to force them to take it. Of course, if you do exercise and use up some of the stored glucose, the cells have capacity to take more for a short time and will do so more willingly, but if you keep putting the glucose into your blood stream without regularly burning off what is stored, gradually you approach a situation where your system is going to grind to a halt, because the pancreas eventually burns out and then you need to inject large doses of insulin to overcome that resistance. The difference generally comes down to the amount of insulin you need to inject between insulin dependent Type 1s and Type 2 and is one of the reasons why some Type 2s are eventually recognized as actually being Type 1 like @Eternal422, because they clearly only need "normal" amounts of insulin.

I believe there is another element to Type 2 where the liver and pancreas get enveloped and clogged with fat even if the patient isn't carrying a lot of weight in the rest of their body/fat in their other cells. The liver and pancreas then have problems communicating efficiently to balance BG levels and I do wonder if this situation can initially perhaps exhibit as Reactive Hypoglycaemia in some people whereas others experience a slow insulin response, so levels spike after a meal and take too long to come back down.

Some Type 2s may only experience one of those elements and some may experience both and I am sure there are also more variations of mechanisms at play... The body is very complex. 🙄

Anyway, that is my totally non medically trained take on the situation.

See I can’t be type 2, I had all my organs scanned and all blood tests done. Found no evidence of fatty anything. Plus I was thin. I’ve heard of the term skinny fat but that really wasn’t me. I haven’t had any input for a while but I believe I will be having another c peptide done at some point up until the 5 year mark, then if I’m still producing adequate insulin then it’s type 2. I try not to get too stressed out by this but I’m in a constant state of confusion. I was quite young for type 2, I feel like I’ve got decades to struggle with this! I only just passed the gestational diabetes test, so that is the only thing I can connect it to, can women who have had GD get type 2 even if they don’t have fatty organs and stay slim and active ? My brain is a puddle

 

[harbottle]

I would think too much insulin is bad because that means there is too much glucose in the blood and the insulin is trying to lower it. The way I look at it is like this, if the liver glycogen stores are constantly being emptied by good diet, fasting, and exercise (in that order), the blood sugars will stay low and so will the insulin. However, if one starts drinking lots of Coca Cola, eating french fries, and lots of sugar, spiking the blood sugars repeatedly and never giving the body a chance to get rid of the sugars, the insulin will rise trying to find a place to park the glucose. If it can't park it in the cells, because they are already saturated and now insulin resistant, it will park it (the glucose) as visceral and subcutaneous fat. The Doc's and Big Pharma treat the blood sugar, first with metformin, later with insulin, not the metabolic imbalance leading to the disease which is why I am absolutely terrified of being diagnosed with diabetes and hoping never to get into the vicious never ending cycle as I fear being reliant on Big Pharma. My strategy is shut down the source of insulin rising by lowering everything that could raise it, carbs sugar, and giving the body once a week complete rest from digestion for 48 hours by fasting. If my numbers are good on my next test I will go 24 hours a week only, but it looks like fasting is with me for life now, as I know during those hours insulin can only rise in response to glycogen being released by the liver.

Insulin is released for meals high in protein as well, in fact, beta cells respond to amino acids as they have receptors for it and they still work even if the receptors for glucose don't. Insulin is also use to metabolise fats, and in T2s this is also broken as fat becomes insulin resistant as well (This is why GPs tend to put T2s onto statins) It doesn't get 'parked' anywhere, it all ends up in the bloodstream with nowhere to go.

Insulin resistance is all about cells being broken by having fewer insulin receptors or not being able to process insulin properly and/or the liver not responding properly to signals due to excess fat. Nothing to do with getting 'full'. Insulin is also used to metabolise fats, so when fat becomes insulin resistance it leads to raised fatty acids in the bloodstream (Which is why High Triglycerides and poor lipid profiles are a good indication of insulin resistance.) and this just makes it all worse as this interferes with how insulin works and leads to more insulin resistance.

 

[harbottle]

See I can’t be type 2, I had all my organs scanned and all blood tests done. Found no evidence of fatty anything. Plus I was thin. I’ve heard of the term skinny fat but that really wasn’t me. I haven’t had any input for a while but I believe I will be having another c peptide done at some point up until the 5 year mark, then if I’m still producing adequate insulin then it’s type 2. I try not to get too stressed out by this but I’m in a constant state of confusion. I was quite young for type 2, I feel like I’ve got decades to struggle with this! I only just passed the gestational diabetes test, so that is the only thing I can connect it to, can women who have had GD get type 2 even if they don’t have fatty organs and stay slim and active ? My brain is a puddle

There are a small number of 'T2s' that aren't fatty anything and it's a bit of a mystery as to why they develop it.
Are you on medication or anything for it?

 

[Deleted member 21371]

I would think too much insulin is bad because that means there is too much glucose in the blood and the insulin is trying to lower it. The way I look at it is like this, if the liver glycogen stores are constantly being emptied by good diet, fasting, and exercise (in that order), the blood sugars will stay low and so will the insulin. However, if one starts drinking lots of Coca Cola, eating french fries, and lots of sugar, spiking the blood sugars repeatedly and never giving the body a chance to get rid of the sugars, the insulin will rise trying to find a place to park the glucose. If it can't park it in the cells, because they are already saturated and now insulin resistant, it will park it (the glucose) as visceral and subcutaneous fat. The Doc's and Big Pharma treat the blood sugar, first with metformin, later with insulin, not the metabolic imbalance leading to the disease which is why I am absolutely terrified of being diagnosed with diabetes and hoping never to get into the vicious never ending cycle as I fear being reliant on Big Pharma. My strategy is shut down the source of insulin rising by lowering everything that could raise it, carbs sugar, and giving the body once a week complete rest from digestion for 48 hours by fasting. If my numbers are good on my next test I will go 24 hours a week only, but it looks like fasting is with me for life now, as I know during those hours insulin can only rise in response to glycogen being released by the liver.

If you do go low carb and 48 hour fasting, bear in mind you trigs could/will be raised, and your fasting glucose could/will be high, so make allowances for that before your next tests.

 

[harbottle]

This seems like the best explanation I've seen.
The trick is to get the body working properly again.
And yes , the normal drugs, that seem to work well, cost next to nothing now.

This is pretty much what I was told to do in a rushed phone call.
Stop overeating, lose weight, reverse the low-HDL and high-LDL.

"Some people can go into remission by doing this. Takes some tablets."

 

[Deleted member 21371]

This is pretty much what I was told to do in a rushed phone call.
Stop overeating, lose weight, reverse the low-HDL and high-LDL.

"Some people can go into remission by doing this. Takes some tablets."

"Stop overeating, lose weight, reverse the low-HDL and high-LDL"

They'd been telling me that for years.

I should have listened a lot sooner!

 

[EmmaL76]

There are a small number of 'T2s' that aren't fatty anything and it's a bit of a mystery as to why they develop it.
Are you on medication or anything for it?

I was on metformin for a few months on diagnosis. Had no impact on BGs but they were really high at that point. I was antigad positive but my current endo doesn’t see much significance in that, but the last one prescribed insulin and the story of how I get on with that is for another day

 

[EmmaL76]

I was on metformin for a few months on diagnosis. Had no impact on BGs but they were really high at that point. I was antigad positive but my current endo doesn’t see much significance in that, but the last one prescribed insulin and the story of how I get on with that is for another day

And just to add, I actually saw a professor of diabetes once in Liverpool. He recommended several drugs but went on to say that I pose a significant challenge to the NHS

 

[Admiral Benbow]

If you do go low carb and 48 hour fasting, bear in mind you trigs could/will be raised, and your fasting glucose could/will be high, so make allowances for that before your next tests.

Yeah, I am planning to fast only 3 days prior while the day or two before the test only eat nonglycemic foods like eggs, meats, and vegetables. I am hoping that the fast will get out any remaining sugars and the meats will stop any spikes on the morning of the fasting glucose test.

 

[Proud to be erratic]

Great original question @Callista.
Provoked lots of thought, you have a multitude of responses along with various interpretations and slightly different understandings about T2. Here are my non-medically trained thoughts to add to the mix!

I often think about this too, as I don’t really have a proper diagnosis the endo did say that if it ends up a type 2, because of my slim build and lack of metabolic issues etc I would always end up on insulin in the end. My question is, we know too much sugar in the blood is not good for you but what about too much insulin ? If we overproduce and inject the stuff is hyper insulin ok

@EmmaL76, there is a condition called hyperinsulemia. This is when one's blood has more insulin than normal AND high insulin resistance. So the normal consequence of going hypoglycaemic because of excessive insulin doesn't occur. Hyperinsulemia can be an indicator of pre-diabetes or T2 - so can exist even before someone with T2 ends up taking insulin injections.

Hyperinsulemia is a consequence of high insulin resistance and thus an accumulation of insulin in the blood. Hyperinsulemia exists in our blood, even before some (note some, but by no means all) people with hyperinsulemia end up with a T2 diagnosis. Hyperinsulemia would not in itself always be identified as existing, since there doesn't seem to be symptoms unique to hyperinsulemia - until other T2 symptoms occur and those symptoms leads HCPs to a diagnosis of DM. The HCPs may (or may not) formally test for or confirm the existence of hyperinsulemia - not least because it is a condition which doesn't seem to be easily recognised without DM symptoms. As far as I can tell hyperinsulemia as a 'state' isn't even a specific criterion for a T2 diagnosis, which as we generally understand has several origins (some of which are not actually understood!). But that's all for a different thread - methinks.

PS : Emma, my brain is frequently a puddle sometimes a swamp and no more so than reading this thread where responses are flooding in faster than I can absorb the individual replies!

But @Callista asked:

I guess my question boils down to: If we have insulin resistance, then the problem is not that we can't produce insulin (or have it injected), but that we can't use it to 'feed' our muscles, or store in the liver or, worst of all from a 'toxic' point of view, get it out of our bloodstream.

(I appreciate the whole 'mission' of T2 patients is to minimise/reverse resistance but it still rather begs the above question of what happens if we don't or can't....)

My italics. So, is there any evidence that an excess of insulin in our blood is actually a 'toxic' state for someone with high insulin resistance?

I can't find anything on the internet that says this is a toxic situation. Until DM symptoms occur, it would appear that you can have an excess of insulin and not necessarily be medically compromised. What I did find specifically for hyperinsulemia (when diagnosed rather than T2) was treatment included losing weight and regular exercise. No great surprise there really, since these are reasonable guidelines for healthy living anyway.

I suspect those people with hyperinsulemia and not pre-diabetic or T2, just flush the excess insulin out as we do for many other blood impurities.