How damaging is it?

[jasholden]

If you eat a meal that does this:

Before: 5.6 mmol
1h - 7.3 mmol
2h - 8.0mmol
2h 20 - 6.7mmol
3h - 5.7 mmol


And it happens once in a blue moon - as in when you eat at a party or at Christmas time or some other celebration.

Would you think anything of it even though the 2h is not exactly where you want it, but it didn't stay there too long.

My husband made a traditional dish, which he makes about once a year: Sarma - picked cabbage rolls (plenty of preserved meats) and polenta on the side (the carb that got me here).

I'm glad he only makes it once a year because I find it hard to stop at one helping. This was the first time I have eaten polenta (corn meal) since I've been testing my blood glucose.

I took a chance (couldn't help myself) and had a second helping... Kind of regret it now, and not just because I saw an 8.0 at the 2 hour mark.

Even my husband complained about the "food coma" it gave him.

If this only happens a few times per year, it would be a while before serious issues would set in, wouldn't it? Or will I regret it sooner?

This morning before breakfast I was 2.7, I decided to have my porridge with no injection, 2 hours later it was 14.2, so I injected - 1 hour later it was 3.3,

 

[Cocosilk]

This morning before breakfast I was 2.7, I decided to have my porridge with no injection, 2 hours later it was 14.2, so I injected - 1 hour later it was 3.3,

I have no experience of T3c but is it any better if you have, say, a bite of a banana (or teaspoon of honey if it helps with hypos quicker) and then have eggs instead of porridge?
I have only ever seen 13.8 mmol on my metre at the one hour mark during a GTT but I recently tried to reintroduce porridge and it put me up in the 8s, which for me is high considering I don't apparently have diabetes according to my doctor. I had gestational diabetes which puts me at risk.. and 13.8 mmol seems to be glucose intolerance.

 

[Walking Girl]

Yes but it's more complex than that. The etiology of resistant diabetes is decades of glucose buildup in the tissues long before diagnosis. With T2 the cells themselves are stuffed full of glucose for several years. This is the cause of the insulin 'resistance'. In T1 these same cells are largely unable to accept any glucose.

I’m curious if you have any links to articles or other references on this I can access? Always looking to learn more.

What tissues/cells are being referenced? From my understanding, BG is high in insulin resistance because insulin is unable to do its job of moving glucose into the muscle and skeletal cells, primarily where glycogen is stored other than the immediate reserves in the liver. It’s why they can tell T2 with a pretty high degree of accuracy on muscle ultrasounds, the muscle is brighter due to less glycogen in the cells. Also why insulin resistant people can have a harder time building muscles - less energy getting in. Also, less available glucose down regulates cell mitochondria activity and replication, which in turn causes the cells to seek less glucose so it’s a spiral leading to insulin resistant T2s having *less* glycogen in the cells, not more.

Not trying to drag the thread off topic, but I’m unclear why a T1s BG levels would no be comparable for purposes of complications, which is the OPs question.. (Although, I have read that some even minor insulin production may be protective in ways not yet understood.)

 

[Walking Girl]

4
Is there a test to measure how many beta cells you have left or is does the fasting insulin test tell you that?

A C-Peptide test is best for telling you how much insulin you are producing, which is what matters.

The only way to know how many beta cells you have is an autopsy, an electron microscope and a patient person to count

 

[Cocosilk]

A C-Peptide test is best for telling you how much insulin you are producing, which is what matters.

The only way to know how many beta cells you have is an autopsy, an electron microscope and a patient person to count

I think I'll skip the autopsy

 

[Member496333]

What tissues/cells are being referenced?

Every cell in the body.

In T2 resistant diabetes, the aetiology of the resistance is that each cell is already stuffed with glucose that has nowhere to go. The liver cannot accept more because it has run out places to store it as fat. A process that takes many many years. This is why the glucose then backs ups in the blood. In T1 the glucose remains in the blood because there is insufficient insulin to allow its transport into other cells. So, those same cells that are engorged with sugar in T2, are "empty" in the T1. Hence my original statement that glucose toxicity across the two types is not necessarily an apples for apples comparison.

Obviously there are nuances and some crossover, but that's the nuts and bolts of it as I understand it. You really need to intimately understand the fundamental differences between hyperinsulinemic "resistance" and insulin deficient autoimmune for it to make sense. It's also a new paradigm that is only recently becoming accepted over the old faulty lock & key idea. It's called the 'overflow hypothesis' of insulin resistance.

In summary, a T2 is more likely to have had every cell in their entire body engorged with super toxic glucose for many many years or even decades prior to diagnosis, whereas a poorly controlled T1, whilst still in danger, is less likely to have suffered the same all-body toxicity unless they have also become extremely resistant due to overuse of exogenous insulin. Which does of course happen.

This is all probably very off topic now, so I'll stop rambling. See the works of Jason Fung for better explanations. Specifically The Diabetes Code. A book that everyone should read at least once. Ive read it three times

 

[urbanracer]

Every cell in the body.

In T2 resistant diabetes, the aetiology of the resistance is that each cell is already stuffed with glucose that has nowhere to go. The liver cannot accept more because it has run out places to store it as fat. A process that takes many many years. This is why the glucose then backs ups in the blood. In T1 the glucose remains in the blood because there is insufficient insulin to allow its transport into other cells. So, those same cells that are engorged with sugar in T2, are "empty" in the T1. Hence my original statement that glucose toxicity across the two types is not necessarily an apples for apples comparison.

Obviously there are nuances and some crossover, but that's the nuts and bolts of it as I understand it. You really need to intimately understand the fundamental differences between hyperinsulinemic "resistance" and insulin deficient autoimmune for it to make sense. It's also a new paradigm that is only recently becoming accepted over the old faulty lock & key idea. It's called the 'overflow hypothesis' of insulin resistance.

This is all probably very off topic now, so I'll stop rambling. See the works of Jason Fung for better explanations. Specifically The Diabetes Code. A book that everyone should read at least once. Ive read it three times

I don't have the book and I am not about to buy it, so I cannot dispute what you have read.

I cannot help noticing though, that you refer to this as a 'hypothesis' and in that context I feel it has less credibility than the multiple sources of freely available information which puts forward a different route to insulin resistance.

The bottom line for me is that this is just one doctor's view / opinion (call it what you will) amongst a multitude of opinions from other medical professionals. Doesn't make it wrong but it doesn't have to be right just because it came from Dr Jason Fung.

 

[Brunneria]

Anyone who wants to ready Fung's 'New Paradigm' can do so for free here
https://thefastingmethod.com/new-paradigm-insulin-resistance-t2d/

It is simply a new discussion on the age old speculation of what goes wrong with the action of insulin when insulin resistance develops.

I have absolutely no problem with Fung presenting it as a theory, while discussing the short comings of the 'lock and key' analogy.
But it really shouldn't be presented as a fact, or anything more than a discussion point. No proof has been offered, as far as I am aware. If there is proof, I would be very interested to see it.

Additionally, while I don't have a problem with Fung presenting his theory on his blog and in his books, I am afraid that I do have a couple of problems with the way Jim has presented it in his posts.

My first concern is that @Jim Lahey claims that T2s swim in glucotoxicity for decades before diagnosis with diabetes.
While I am happy to agree that this can happen, the reality is different for many, many T2s. There is plenty of evidence, and some of it can be found on www.bloodsugar.101 , to suggest that different people develop insulin resistance and eventually T2 at different rates, and that their body copes with the rising IR in different ways. Jason Fung himself discusses this elsewhere on his blog in some of his many posts on IR. Some T2s develop raised blood glucose in a matter of weeks or months, and sometimes going in steps of rising blood glucose levels, sometimes post prandial, and sometimes fasting blood glucose. https://www.bloodsugar101.com/how-blood-sugar-control-works

My second concern is a development of my first. Jason Fung's paradigm is pretty clear that where possible the body copes with insulin resistance and rising blood glucose levels (glucotoxity) in T2s by tucking the glucose into the cells as fat. Until the cells are full. Yes. Absolutely. But then, in the majority of T2s, the next step is to increase the fat holding capacity by either creating new fat cells, or by enlarging the fat cells that already exist. For those developing T2s, the blood glucose levels do not simply escalate to toxic levels.

This is why for most T2s, they get fatter before their blood glucose gets out of control, because the body uses its fat storage mechanism to prevent the blood glucose levels from rising too high - right up until it can't cope any more - and that is when the blood glucose levels start to spiral up into diabetes levels.

Yes, of course, there are a minority of T2s who don't/can't gain weight, and yes, they are in a very difficult situation in that they are less likely to be tested for T2 because they don't look like T2s, and because they do indeed have higher levels of glucose in their blood and lack the fat cells to get rid of it into storage. They deserve a voice, and just as good quality treatment as any other person with diabetes. But they are still a minority, and their experience should not be used to make sweeping statements about how it works for all T2s.

Very important not to make general statements, especially when Fung's own paradigm discusses this aspect in detail.

 

[Member496333]

I don't have the book and I am not about to buy it, so I cannot dispute what you have read.

I cannot help noticing though, that you refer to this as a 'hypothesis' and in that context I feel it has less credibility than the multiple sources of freely available information which puts forward a different route to insulin resistance.

The bottom line for me is that this is just one doctor's view / opinion (call it what you will) amongst a multitude of opinions from other medical professionals. Doesn't make it wrong but it doesn't have to be right just because it came from Dr Jason Fung.

Yup. True enough. We're all free to believe as we wish.

 

[Member496333]

Another factor I suppose is that of insulin toxicity. Generally speaking, hyperglycaemia in a T1 will be as a result of insulin deficiency, whereas T2 is developed over a period (minutes, hours, days, years...) of too much insulin. Too much circulating insulin is also damaging to the body. Again..."as I understand it".

 

[Member496333]

But it really shouldn't be presented as a fact, or anything more than a discussion point. No proof has been offered, as far as I am aware. If there is proof, I would be very interested to see it.

Obviously there are nuances and some crossover, but that's the nuts and bolts of it as I understand it.

 

[Tophat1900]

I don't have the book and I am not about to buy it, so I cannot dispute what you have read.

I cannot help noticing though, that you refer to this as a 'hypothesis' and in that context I feel it has less credibility than the multiple sources of freely available information which puts forward a different route to insulin resistance.

The bottom line for me is that this is just one doctor's view / opinion (call it what you will) amongst a multitude of opinions from other medical professionals. Doesn't make it wrong but it doesn't have to be right just because it came from Dr Jason Fung.

I believe this is what @Jim Lahey was talking about, you don't have to buy the book now... lol

https://healthcareinamerica.us/what-exactly-is-insulin-resistance-2b0c62f343b0

Quick edit.... because I forgot to add the link, duh.

 

[Brunneria]

Nope. Sorry Jim winking and claiming that there are 'nuances and crossovers' does not justify the fact that you made the following clear, sweeping statement, which I disagree applies to the vast majority (90%?) of T2s. And is not supported by Fung's New Paradigm.

The etiology of resistant diabetes is decades of glucose buildup in the tissues long before diagnosis. With T2 the cells themselves are stuffed full of glucose for several years. This is the cause of the insulin 'resistance'.

 

[Member496333]

I will also add that I am not simply parroting Jason Fung's ideas. I have read (literally) two dozen books, hundreds of papers, listened to thousands of podcasts and tested everything on my own body before deciding that I believe the overflow hypothesis to be true. For one thing it perfectly explains the paradox of why the liver furiously responds to insulin by making fat, while the rest of the body has 'broken locks". A paraodox is simply a data point that disproves an existing theory. That alone is reason enough to bring the lock & key hypothesis into question.

But yeah sure enough we are all entitled to our views. But if someone asks me a question about my ideas I will answer it in detail to the best of my knowledge.

 

[Member496333]

Nope. Sorry Jim winking and claiming that there are 'nuances and crossovers' does not justify the fact that you made the following clear, sweeping statement, which I disagree applies to the vast majority (90%?) of T2s. And is not supported by Fung's New Paradigm.

The wink was to bring your attention to "as I understand it" in response to comments implying assertion of fact. But I'm sure we don't want to begin a tit-for-tat dissection of every individual statement. I've made my view as clear as I can make it, and others are free to disagree

 

[Brunneria]

But yeah sure enough we all entitled to our views. But if someone asks me a question about my ideas I will answer it in detail to the best of my knowledge.

Excellent!
I look forward to you producing some references that support your theories.

 

[Member496333]

https://healthcareinamerica.us/what-exactly-is-insulin-resistance-2b0c62f343b0

I'd forgotten that the central paradox is actually that the exact same cells in the exact same organ are - according to the lock & key theory - simultaneously insulin resistant and insulin sensitive. Thanks for the link. In typical Fung fashion, it's all very clearly put across.

 

[Tophat1900]

I'd forgotten that the central paradox is actually that the exact same cells in the exact same organ are - according to the lock & key theory - simultaneously insulin resistant and insulin sensitive. Thanks for the link. In typical Fung fashion, it's all very clearly put across.

I'm on board with Fung... he explains it so well, something I have trouble doing after reading stuff like that, but it makes sense to me, and in how T2dm is and has been treated for decades with worsening outcomes as he explains it.