New Paradigm For Insulin Resistance

Could you supply a reference to this new theory, please?

Yes, I have seen this new paradigm recently too.

Was it Fung?
Will have a look and check.

Yup, here you go:
https://intensivedietarymanagement.com/new-paradigm-insulin-resistance-t2d/

Fung's article is annoyingly short of references. He is usually better than that. I remember thinking this the first time I read it, too. lol.

I have read similar but not for people not as clever when reading scientific papers, like myself.

In someone with T2, the amount of glucose and insulin is excessive and it makes sense that the glucose gives you hyperglycaemia and the excess insulin goes to visceral fat! But which came first, the excess insulin or glucose. I think it can be both, as one would lead to the other and therefore T2.
It has been proved that excessive insulin leads to obesity then T2. Bit I believe that too much glucose will lead to exactly the same scenario.
This is probably why, the meds work for some but not the others. Thus the ones the meds don't work lead to poor management and problems down the line.

Now for us RH ers, and I'm guessing here, the glucose is normal or below normal, the excess insulin would lower the glucose in the blood hence the hypos, the horrible hypo symptoms will increase because your body wants more glucose, so it's use to getting its glucose source from carbs and sugars. The hunger pangs, the thirst, the body wants more glucose. So we eat carbs the sugar (glucose) surge, hyperglycaemia, the pancreas creates too much insulin and the cycle continues. Fluctuating blood glucose levels. Hypos, hypers, dreadful symptoms that don't make it any easier.

I actually think that this new theory has a lot going for it.

But, then I could be talking rubbish, and I have been known for that!!

Brunneria said:

Fung's article is annoyingly short of references. He is usually better than that. I remember thinking this the first time I read it, too. lol.

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Thanks for the link. Yes, as you say there are no references that I can find. I've also been unable to find anything in peer-reviewed publications, as yet. If no-one has measured higher glucose concentrations within the cell then all we have here is a hypothesis, not a new paradigm.

I didn't know this was a new paradigm. Quite a time ago Malcolm Kendrick said something very similar and it made so much sense at the time that I took it on board as part of my understanding of the subject.

I feel diabetes type 2 is the creation of the wrong 'fat' cells and how those cells reject insulin.
Insulin resistance is due to those fat cells not being processed, everytime as only the right 'fat' cell can be accessed.
The more wrong cells, the more insulin resistant. Has dr fung or anyone explored the wrong fat cell theory?
I'm sorry if I'm dum but this theory feels right to me.
Carb intolerance causes the wrong fat cell but in reducing carbs it reduces the amount of wrong fat cells being made.
Total conversion only possible when more good fat cells more than bad fat cells which need killing off in the body asap.
Low bad fat cells will cure type 2 diabetes.
Empty bad fat cells still confuse insulin.

I feel fat cells are the problem. Not pancreas in type 2. Nor insulin.

Ok I will give it a go but I am not an expert in this. This is just the way I see it.

People come equipped with fat cells unless they have Beradinelli-Siep generalised lipodystrophy in which case they come without any fat cells and are the thinnest people you can get. They all have diabetes though. What a bummer.

Eating carbohydrates produces glucose and then insulin. The muscle and tissue cells need glucose for energy and the insulin helps them to receive it. If you keep on eating carbohydrates when your muscle and tissue cells are full then you produce more glucose and more insulin. The glucose is converted into triglycerides and this is stored away in your pre existing fat cells. This is a one way ticket since insulin can get things into cells but cannot get them out again.

If you keep on eating carbohydrates then you start to run out of places to put the glucose/triglycerides and you exhibit what looks like insulin resistance and when someone measures your blood glucose levels you are diagnosed as diabetic.

This process makes you fat if you are well equipped with fat cells and eventually gives you type 2 diabetes.

Apologies to Briffa and Kendrick

Squire Fulwood said:

Ok I will give it a go but I am not an expert in this. This is just the way I see it.

People come equipped with fat cells unless they have Beradinelli-Siep generalised lipodystrophy in which case they come without any fat cells and are the thinnest people you can get. They all have diabetes though. What a bummer.

Eating carbohydrates produces glucose and then insulin. The muscle and tissue cells need glucose for energy and the insulin helps them to receive it. If you keep on eating carbohydrates when your muscle and tissue cells are full then you produce more glucose and more insulin. The glucose is converted into triglycerides and this is stored away in your pre existing fat cells. This is a one way ticket since insulin can get things into cells but cannot get them out again.

If you keep on eating carbohydrates then you start to run out of places to put the glucose/triglycerides and you exhibit what looks like insulin resistance and when someone measures your blood glucose levels you are diagnosed as diabetic.

This process makes you fat if you are well equipped with fat cells and eventually gives you type 2 diabetes.

Apologies to Briffa and Kendrick

Click to expand...

Wow. They all have type 2 diabetes?
So fat and diabetes are very very related.

Thanks for clarification.

ickihun said:

Wow. They all have type 2 diabetes?
So fat and diabetes are very very related.

Thanks for clarification.

Click to expand...

I think it's because they run out of places to put the spare glucose before anyone else might and so miss out the stage of getting fat and go straight to diabetes. Fat cells exist in certain parts of the body and accept triglycerides at those places but if you have no fat cells you are stuffed.

I was watching a Gary Taubes lecture where he said that someone had a skin transplant on their hand and the skin used was from a fat area so now they get a fat hand.

Also I remember films about the Kalahari Bushmen who have fat cells mainly in their buttocks and look quite odd when they put on weight.

As for the relationship between diabetes and fat I have always viewed it as the same thing that makes you fat also gives you diabetes and so I regard the fat as a symptom.

If you are into professors Unger and Lustig then visceral fat plays a huge part. It seems that fructose (table sugar is 50% fructose) and alcohol are metabolised into fat directly in the liver and as this builds up you reach a point where the pancreas goes mammeries up. Any glucogon produced by the alpha cells does not see the highly concentrated insulin normally produced by the beta cells because they are glued up. Unger says that injecting insulin is a crude way of correcting this. It's better than dying I suppose.

I'm using insulin injections to keep my blood glucose lower. I havent added any weight. In fact im losing.
Have you heard of insulin takers losing weight?
I have great energy. I could run a half marathon in my mind. I feel tiredness is a thing of the past. I restricted my insulin alongside restricting my carbs to 30g. I ate too much protein otherwise I would have needed less insulin than my 44mixed units.
I increased my carbs to 100g on supervision but more than doubled my insulin need to conveet into energy.
Im a more involved, active diabetic on 100g carb and converting insulin.
Ive had diabetes for 4 decades. I havent been checked for antibodies. Obese so assumed still type2. (Assumed im making my own insulin still). Im making some insulin on my own as I level off in 20s in previous carb craves. Of which I dont have now. Or any urges gets veg'd on. Low carb has given me carb craving awareness and control.

ickihun said:

Have you heard of insulin takers losing weight?

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I have never asked any. My DN says that her type 1's are often skinny. The only thought that occurs is that insulin users are often advised to eat anything they like and to use the insulin to deal with it. You seem have taken a more intelligent route.

Interesting stuff; I haven't read it yet but the discussion here seems to suggest that the problem with T2s is that they run out of fat cells and so have nowhere to store the spare BG.

I am struggling with this concept because as I understand it you don't generally create new fat cells but the ones you have grow larger. I may be wrong on this, though.

If it was just around fat cells, then if you lose for example a kilo of fat from your existing cells then you should normalise your BG until they fill up again. Unless the fat cells are insulin resistant and refuse to fill up quickly enough.

Edit: O.K. now I have read it and I can't quite track the logic.

It seems to suggest that "tissues" (I assume the liver and muscles and other organs) are crammed full of glucose and not insulin resistant.
O.K. that doesn't sound earth shattering; most T2s seem to have normal energy levels and also exhibit the normal "quick 4 lbs drop" when crash dieting which is attributed to the glucose stores (held in water) being depleted.

The article also says that the liver is turning glucose into fat (so listening to insulin) but still producing glucose (so not listening to insulin); this is where I start to lose the train of logic.

As I understand it, blood glucose is stored preferentially in the liver and muscles to provide an immediate energy source.
Once these tissues are full, then any remaining BG is converted to fat and stored in fat cells against future need.
This is encouraged by insulin, and while BG is elevated insulin is provided to encourage the cells to take up the spare glucose/glycogen.
Once the BG levels fall then insulin production drops and all is well.

However if BG levels aren't falling then the storage mechanism seems to be failing; Jason seems to be saying that the muscles and internal organs aren't insulin resistant so the logical culprit is the fat cells.

The liver is (possibly) trying to do all the right things but something isn't working in the rest of the system. Or there are two different metabolic pathways in the liver; one for converting glucose to fat for storage, and one for generating more glucose. Both these activities seem to be happening so perhaps one of these pathways is defective and not the other?

The article says

How in seven hells can this insulin resistant liver selectively be resistant to one effect of insulin yet accelerate the effect of the other? In the very same cell, in response to the very same levels of insulin, with the very same insulin receptor? That seems crazy. The same cell is insulin resistance and insulin super-sensitive at the same time!

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That seems to be the big question; the liver seems to be still generating more glucose when insulin should prevent this. The fact that it is producing glucose when it shouldn't be could be a key part of the equation. Although later on it is suggested that the liver isn't producing more glucose but there is just nowhere for the glucose to go so the assumption that the liver is producing more glucose is possibly incorrect..

All this seems to point to the fat cells.
If the fat cells take up glucose as mediated by insulin then become full, this suggests that either there are not enough fat cells or there is a problem within the cells converting glycogen to fat and so the problem is not in the insulin receptors (insulin resistance) but in the fat conversion process being too slow to clear the glucose already in the fat cells to make room for more glucose to enter the queue for conversion to fat.

Think of a bank with the front doors wide open but only one ageing and partially deaf bank clerk trying to process the ever growing queue until the queue spills out onto the pavement.

However we go round the loop again because as far as I can tell from trawling the Internet the process of converting glucose to fats within the fat cells is stimulated by insulin.

So perhaps what Jason is saying that it may be that the insulin receptors on the boundary of the cells may not be the issue - the "key and lock" analogy - but instead there is something not responding to insulin (or perhaps some trigger further into the cycle) or perhaps just not working fast enough within the fat cells to convert glucose to fat so the pancreas just keeps pushing harder and eventually gets tired and gives up.

This would tie in with the issue I mentioned further up; if you empty a fat cell then why doesn't it fill up again quickly and take the BG levels down.

Bottom line; there seems to be resistance built into the insulin cycle however it may be inside the cell itself instead of at the cell boundary. If you could transplant fat cells from a non-diabetic into a diabetic and monitor their performance this might give interesting results.

LittleGreyCat said:

Interesting stuff; I haven't read it yet but the discussion here seems to suggest that the problem with T2s is that they run out of fat cells and so have nowhere to store the spare BG.

I am struggling with this concept because as I understand it you don't generally create new fat cells but the ones you have grow larger. I may be wrong on this, though.

If it was just around fat cells, then if you lose for example a kilo of fat from your existing cells then you should normalise your BG until they fill up again. Unless the fat cells are insulin resistant and refuse to fill up quickly enough.

Click to expand...

I think that you can lose subcutaneous fat and get thin but you won't affect your diabetes much unless you lose visceral fat. There are exceptions I am sure but this seems to gel with Prof. Unger's work.

We can definitely grow more fat cells. But it only happens when our original fat cells are full. So it takes a level of obesity before the body says 'yikes, my existing fat stores are full, I had better make more cells to cope.'

This is one of the reasons why it is so much more difficult for obese people to slim down and stay slim than for slightly overweight people to slim down and stay slim.

Once your body has created these extra fat cells, they are likely to be there for a very long time. They don't pop out of existence if we lose weight. And the body keeps them functioning, so expects to have fat stores in them... What effectively happens, is that once you have created extra fat cells, then your body re-sets its 'normal' fat storage levels higher, and will fight to maintain that level.

So losing weight below that level becomes more challenging, because our own body is trying to bounce us back up to the 'normal' it likes. This is one of the reasons why rebound weight gain is so common.

@Brunneria @Squire Fulwood please read massive edit above