Diabetes: Have We Got It All Wrong? (T2D)

[Member496333]

And no doubt genetics is behind many of the differences

Definitely, but it’s how we express our genes that matters. I’d never have become diabetic if I hadn’t eaten the Diewell plate, irrespective of whether or not I had the ability to gain any meaningful weight (which I don’t). Oh well, at least I found out eventually

 

[kokhongw]

I learn these in school. In T2 earlier phase, body is insulin resistance and hence it overcompensate to produce more insulin. In later phase, it burns out and insulin production reduces to very low. These do not seem to contradict with the paper presented. So what did we got it wrong in the first place?

That the chronic overcompensation with insulin is clinically harmless?

 

[AloeSvea]

I think the primary reason why very lean people become super resistant is because they aren’t able to easily become obese, and so the liver very quickly exhausts its capacity for lipogenesis.

Alas, I easily become obese, as do many Polynesians/Maori. I never dieted - I was a rare bird indeed in this sense. But my weight fluctuated a lot over the decades as an adult post 'diewell plate' (nice one) and franken-food and I had no idea why. (The carbs! Amongst other things.) I just need to look at a slice of bread and I put on fat, and bloat. But your point is very interesting regarding thin-on-the-outside (fat on the inside? is that the case?) folks with insulin resistance type two. It make sense for sure.

 

[AloeSvea]

So now... they have reworded it ever so slightly... but would anyone come away with the understanding that we are producing too much insulin to overcome our insulin resistance and hence struggle with weight/fat loss?

https://www.diabetes.org/diabetes/type-2
View attachment 36002

Yes. "Doesn't use insulin properly" has always irked me. What does that mean? It should of course be - 'produces a large and dangerous amount of insulin to deal with the excessive amount of glucose in the blood - introduced by eating and drinking excessive carbs' - that would really put it clearly. And make the first line of treatment extremely obvious. (Like stopping smoking for folks who are get diagnosed with obstructive lung disease.)

 

[millenium]

That the chronic overcompensation with insulin is clinically harmless?

In the last twenty years, there are a lot of research that pointed out hyperinsulinemia is a serious health concern. For example, it may cause wall of major blood vessels to thicken and lose elasticity. It definitely has many other negative consequences like depleting the insulin reserve in pancreatic cells and burning them out. Some theories linked it to autoimmune reaction in the late stage.

 

[kokhongw]

In the last twenty years, there are a lot of research that pointed out hyperinsulinemia is a serious health concern. For example, it may cause wall of major blood vessels to thicken and lose elasticity. It definitely has many other negative consequences like depleting the insulin reserve in pancreatic cells and burning them out. Some theories linked it to autoimmune reaction in the late stage.

Yes there has been no lack of evidence on the harm of chronic excessive insulin. As far back as Reaven's 1988 Syndrome X lecture
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30906-1/fulltext

Unfortunately, we have yet to see any concrete support for intervention that directly addresses the chronic excessive insulin. Only recently ADA and friends grudgingly included an escape clause, and accepted that "personalized nutrition", including low carb may be effective for some...pretending that they have been supportive all the while...and dishing out dietary recommendations that practically guarantees disease progression.

Mainstream providers have continued to discourage and disparage carbs reduction or fasting, two of the most effective way to move towards a insulin sparing lifestyle.

 

[Tophat1900]

Yes there has been no lack of evidence on the harm of chronic excessive insulin. As far back as Reaven's 1988 Syndrome X lecture
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30906-1/fulltext

Unfortunately, we have yet to see any concrete support for intervention that directly addresses the chronic excessive insulin. Only recently ADA and friends grudgingly included an escape clause, and accepted that "personalized nutrition", including low carb may be effective for some...pretending that they have been supportive all the while...and dishing out dietary recommendations that practically guarantees disease progression.

Mainstream providers have continued to discourage and disparage carbs reduction or fasting, two of the most effective way to move towards a insulin sparing lifestyle.

I think that is a fair summary. Although, I wonder how many people with T2 have ever visited sites like the ADA, for the first 10 yrs of being diabetic I never did and hadn't even heard of them, even while living in Colorado for 13 yrs. Perhaps I was lucky to not be influenced by them?

 

[kokhongw]

I think that is a fair summary. Although, I wonder how many people with T2 have ever visited sites like the ADA, for the first 10 yrs of being diabetic I never did and hadn't even heard of them, even while living in Colorado for 13 yrs. Perhaps I was lucky to not be influenced by them?

The problem is that people don't have to visit ADA to be impacted by their guidelines and dietary recommendation... They set the standard globally...

 

[millenium]

Yes. "Doesn't use insulin properly" has always irked me. What does that mean? It should of course be - 'produces a large and dangerous amount of insulin to deal with the excessive amount of glucose in the blood - introduced by eating and drinking excessive carbs' - that would really put it clearly. And make the first line of treatment extremely obvious. (Like stopping smoking for folks who are get diagnosed with obstructive lung disease.)

When the body do not react well to a hormone, it is because the cell receptors is insufficient in numbers, the shape of the type of receptors is less efficient to fit the specific hormone.

Yes there has been no lack of evidence on the harm of chronic excessive insulin. As far back as Reaven's 1988 Syndrome X lecture
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)30906-1/fulltext

Unfortunately, we have yet to see any concrete support for intervention that directly addresses the chronic excessive insulin. Only recently ADA and friends grudgingly included an escape clause, and accepted that "personalized nutrition", including low carb may be effective for some...pretending that they have been supportive all the while...and dishing out dietary recommendations that practically guarantees disease progression.

Mainstream providers have continued to discourage and disparage carbs reduction or fasting, two of the most effective way to move towards a insulin sparing lifestyle.

Carb reduction confirm works. We dun need to care about what those that only talk theories.

Those that said excessive insulin in the body do not cause harm is again talking rubbish. Insulin is something that is very anabolic, and it will definitely cause imbalance growth to certain body cells. When imbalance is going on long enough, the body will collapse. This is physiology common sense.

 

[Member496333]

When the body do not react well to a hormone, it is because the cell receptors is insufficient in numbers, the shape of the type of receptors is less efficient to fit the specific hormone.

The problem with the lock & key mechanism of insulin resistance is that it creates the 'central paradox'. That is - the same cells that are becoming resistant to insulin and thus rejecting glucose, are the same cells that are responding to it and thus furiously making fat. These are the same cells in the same organ that are purportedly both insulin resistant, and simultaneously insulin sensitive (the paradox).

This paradox is explained by replacing the lock & key model with the glucose overflow model, which proposes that there is no insulin 'resistance' at all in the truest sense - only hyperinsulinemia fed by hyperglycaemia. It's now widely accepted in many circles that the lock & key paradigm of resistance has been roundly disproven. In fact it's my understanding that it has been mechanistically shown that there is nothing at all wrong with the cell insulin receptors. The problem is that the cells are already overburdened with glucose and the liver is running out of places to store the requisite fat.

 

[kokhongw]

Carb reduction confirm works. We dun need to care about what those that only talk theories.

In reality, very few dare to disregard dietary advice by mainstream healthcare providers especially after a CVD event. My family went low fat for over 20 years after my father's first triple bypass, and stenting(angioplasty) every couple of years. and the tragic irony is that healthcare providers continue to think that non-compliance is the key reason why their dietary advice fails to stop T2D progression...

So we remain the unusual vocal miniority...

 

[millenium]

The problem with the lock & key mechanism of insulin resistance is that it creates the 'central paradox'. That is - the same cells that are becoming resistant to insulin and thus rejecting glucose, are the same cells that are responding to it and thus furiously making fat. These are the same cells in the same organ that are purportedly both insulin resistant, and simultaneously insulin sensitive (the paradox).

This paradox is explained by replacing the lock & key model with the glucose overflow model, which proposes that there is no insulin 'resistance' at all in the truest sense - only hyperinsulinemia fed by hyperglycaemia. It's now widely accepted in many circles that the lock & key paradigm of resistance has been roundly disproven. In fact it's my understanding that it has been mechanistically shown that there is nothing at all wrong with the cell insulin receptors. The problem is that the cells are already overburdened with glucose and the liver is running out of places to store the requisite fat.

I only know theory on this from school. So it is basically just full blown?

 

[ianf0ster]

In reality, very few dare to disregard dietary advice by mainstream healthcare providers especially after a CVD event. My family went low fat for over 20 years after my father's first triple bypass, and stenting(angioplasty) every couple of years. and the tragic irony is that healthcare providers continue to think that non-compliance is the key reason why their dietary advice fails to stop T2D progression...

So we remain the unusual vocal miniority...

Fortunately I studied Maths and Physics, so I was taught how to think for myself.
But I too 'doubled down' on my decades long High Carb Low Fat lifestyle after my 3x Bypass. I also allowed them to feed me Statins then, having resisted for many years. My excuse is just fear (father died aged 45yrs from heart attack).

However as soon as I was told that I was just a confirmatory HbA1C test away from being diagnosed as T2 D, I went back to the internet, found these forums and started educating myself about the various theories and studies done on both Diabetes and CVD.
It was almost immediately obvious that 'they' were killing me with their terrible advice based upon severely flawed pseudo science. So it was easy to completely reverse my dietary intake and go LCHF - job done! Except that I must take the immortal words of Pete Townsend of the Who to heart - Won't Get Fooled Again !

 

[alienskin]

I only know theory on this from school. So it is basically just full blown?

No, not at all.

The problem with Dr. Fung's argument is that there are two pathways to how the cell responds to insulin. The FoxO1 pathway for glucose and the mTORC1 pathway for lipids. The FoxO1 becomes resistant causing the glucose rise, but the non-resistance mTORC1 responds to the additional insulin causing additional lipogenesis. So there is no inherent contradiction as Dr. Fung claims: the cell is responding to insulin via the 'fat-producing' pathway while ignoring the glucose pathway.

That doesn't mean that his methods don't work and clearly do work for a lot of people, but his scientific explanation is not correct. Selective hepatic resistance which he calls a 'house build on no foundation' is precisely what you'd expect from the FoxO1/mTORC1 pathway 'split'. There is clearly a lot more going on at the cellular level. Read that paper then decide whether these scientists haven't considered such issues.

However, clearly the insulin resistance is a key component and the resulting insulin overproduction and understanding why the FoxO1 pathway stops responding is key, and he is certainly correct that we need to find ways to improve/normalize insulin sensitivity. Clearly, losing weight is a key element which is probably why both his and Dr. Taylor's work have shown success.

 

[millenium]

No, not at all.

The problem with Dr. Fung's argument is that there are two pathways to how the cell responds to insulin. The FoxO1 pathway for glucose and the mTORC1 pathway for lipids. The FoxO1 becomes resistant causing the glucose rise, but the non-resistance mTORC1 responds to the additional insulin causing additional lipogenesis. So there is no inherent contradiction as Dr. Fung claims: the cell is responding to insulin via the 'fat-producing' pathway while ignoring the glucose pathway.

That doesn't mean that his methods don't work and clearly do work for a lot of people, but his scientific explanation is not correct. Selective hepatic resistance which he calls a 'house build on no foundation' is precisely what you'd expect from the FoxO1/mTORC1 pathway 'split'. There is clearly a lot more going on at the cellular level. Read that paper then decide whether these scientists haven't considered such issues.

However, clearly the insulin resistance is a key component and the resulting insulin overproduction and understanding why the FoxO1 pathway stops responding is key, and he is certainly correct that we need to find ways to improve/normalize insulin sensitivity. Clearly, losing weight is a key element which is probably why both his and Dr. Taylor's work have shown success.



View attachment 36100

The way to improve body response to insulin will be to exercise and increase lean body mass. Just that it is very hard for health professionals to enforce this if they bother at all.

 

[kokhongw]

Clearly, losing weight is a key element which is probably why both his and Dr. Taylor's work have shown success.

Losing weight may be a very crude measure... I lost just over 10 kg shortly before my T2D diagnosis with HbA1c at 11%...all the while thinking that it is great that I have been losing weight...

 

[millenium]

Losing weight may be a very crude measure... I lost just over 10 kg shortly before my T2D diagnosis with HbA1c at 11%...all the while thinking that it is great that I have been losing weight...

I think losing weight is also a T1 symptom.

 

[Mr_Pot]

No, not at all.

The problem with Dr. Fung's argument is that there are two pathways to how the cell responds to insulin. The FoxO1 pathway for glucose and the mTORC1 pathway for lipids. The FoxO1 becomes resistant causing the glucose rise, but the non-resistance mTORC1 responds to the additional insulin causing additional lipogenesis. So there is no inherent contradiction as Dr. Fung claims: the cell is responding to insulin via the 'fat-producing' pathway while ignoring the glucose pathway.

That doesn't mean that his methods don't work and clearly do work for a lot of people, but his scientific explanation is not correct. Selective hepatic resistance which he calls a 'house build on no foundation' is precisely what you'd expect from the FoxO1/mTORC1 pathway 'split'. There is clearly a lot more going on at the cellular level. Read that paper then decide whether these scientists haven't considered such issues.

However, clearly the insulin resistance is a key component and the resulting insulin overproduction and understanding why the FoxO1 pathway stops responding is key, and he is certainly correct that we need to find ways to improve/normalize insulin sensitivity. Clearly, losing weight is a key element which is probably why both his and Dr. Taylor's work have shown success.



View attachment 36100

Here is a more recent article on the same subject....
https://www.sciencedirect.com/science/article/pii/S2352345X18301620
No mention of full suitcases or forcing passengers onto a train

 

[Member496333]

Here is a more recent article on the same subject....
https://www.sciencedirect.com/science/article/pii/S2352345X18301620
No mention of full suitcases or forcing passengers onto a train

Gee, that's some heavy reading that'll need multiple passes in order to tease anything out of it. I think it's worth noting that it doesn't actually draw any conclusions on the paradox and, so far as I can see, doesn't really discount the overflow hypothesis. Of course there is also systemic insulin 'resistance' to consider.

All very fascinating stuff. It's never been in doubt that Fung presents his theory in simplified form, but reading through all of that, it's easy to see why

 

[ickihun]

Diabetes: Have We Got It All Wrong?
Hyperinsulinism as the culprit: surgery provides the evidence

1. Walter J. Pories, MD, FACS⇓ and
2. G. Lynis Dohm, PHD

https://care.diabetesjournals.org/content/35/12/2438

View attachment 35955

OK.
The liver has a place to play.

I'd like to see results from ROUX-EN-Y patients who didn't need to do a liver shrinking diet.

From myself I didn't lose my IR immediately after my op. I reduced my insulin hugely before admittance to the ward. Eating to starvation before the op just so it wasn't cancelled changes your bodies need. I wonder how much insulin anyone needs on boiled chicken and boiled grey potato which I mixed with mushed carrot and nothing added. Fat nor gravy. I did see diet wasn't seen as the difference but hospital food and post similiar kiddies portion sized meals with fear (adrenaline and cortisol).
Conditions are alot different leading up to a major operation. Painkillers and rest immediately after "ALL THE DRAMA".
Are we surprised our liver and other organs expelled less hormones. They had just been in survival mode.
Shock to the heart restarts it.
This is the same, unfortunately.