And no doubt genetics is behind many of the differences
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?
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.
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?
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.
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?
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.)
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.
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.
Carb reduction confirm works. We dun need to care about what those that only talk theories.
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.
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...
No, not at all.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.
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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...
Here is a more recent article on the same subject....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
OK.Diabetes: Have We Got It All Wrong?
Hyperinsulinism as the culprit: surgery provides the evidence
https://care.diabetesjournals.org/content/35/12/2438
- Walter J. Pories, MD, FACS⇓ and
- G. Lynis Dohm, PHD
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