Best ignore whatever site that came from..I read it online
So it's not true?Best ignore whatever site that came from..
I would say not providing you can control your diabetes with diet then you won't be over stressing your pancreas so why would it fail? With Type 2 this shouldn't happen.So it's not true?
I read that the pancreas stops making insulin eventually i thought this was only the case with type 1's.How long before this happens? i was told i'm making insulin but not using it properly i was never told that my pancreas would stop making it eventually!!!
Nudge, nudge, wink, wink.Treat it gently and it will last a lot longer.
I would just argue that diabetes II is complex function of 5 variables: liver, pancreas, muscle mass, visceral fat and insulin resistance.T2 diabetes is either your body having so much insulin resistance that your pancreas can't keep up, or your pancreas throwing in the towel because it is knackered. Or a combination of the two.
For 30 years, I had thot as you did, that T2D leads to premature exhaustion of our pancreas and that is will eventually lead us to lifelong dependancy on insulin, just like T1D.
But one of the most surprising and life changing realization about T2D is that the above is often mis-represented and is actually misleading.
This is a well understood T2D progression chart
Looking at the lower graph, you can see that following standard dietary advice and treatment insulin levels will decline and beta-cells function approach zero after 30 years.
But note that for up to 10 years BEFORE and AFTER diagnosis, we typically continue to produce MORE insulin than normal. That means there is at least 10 years of excessive beta-cells demand that we can control.
The reason for this is exactly what the others have pointed out. The build up of insulin resistance means we need MORE insulin to process/handle the same amount of carbs.
Dr Joseph Kraft's graph illustrates this with great clarity
The obvious solution then is to reduce the amount of carbs so that we place minimal demand on our remaining functional beta-cells and achieve normal glucose/insulin levels. This will also give our pancreas a chance to regenerate more beta-cells than it is losing....many of us do this using a carbs lite fats friendly approach. Others choose a combination of very low calorie diet (Newcastle diet), Vegan diet, exercise, and intermittent fasting.
Welcome to the forum and your journey to beta-cells recovery...
All good informative stuff - however you say "This will also give our pancreas a chance to regenerate more beta-cells than it is losing". I think it should be made clear that it increases the possibility that the pancreas can recover, but there is no guarantee that it will.
I am diagnosed 10 years and I recently had an insulin resistance test. This showed that I had a higher fasting BG level (not sure how that happened) and a low level of insulin production. So I certainly wasn't over producing insulin.
However as I eat LCHF and am mainly in ketosis then I would expect a naturally low level of insulin production because there is a low daily requirement.
The one thing the test ruled out was that I was highly insulin resistant and still over producing insulin.
I would love to see the evidence of regeneration of human beta cells.
A few years ago when I first encountered the idea that beta cells could regenerate and insulin production could go back up, I got all excited and ransacked the internet for studies on the subject.
All I found were several over-excited articles by journalists promising a 'cure' 'within 10 years'
and a few rodent studies, where young lab mice and rats could grow new beta cells.
Hopefully the research has moved on since then, but I think it is a bit of a stretch to suggest that a middle aged human pancreas (with/without being a fatty pancreas) can regenerate beta cells like a young, non-fatty, rat or mouse pancreas.
Anyone know if there is evidence out there for studies on adult humans with prior diagnoses of T2?
Very interested to read them, if there are.
CONCLUSIONS
β-Cell mass in human obesity increases by ∼50% by an increase in β-cell number, the source of which is unknown. β-Cell mass is well preserved in humans with advanced aging.
Conclusions:
Therefore, although we concur that in type 2 diabetes there are endocrine cells with altered cell identity, this process does not account for the deficit in β-cells in type 2 diabetes but may reflect, in part, attempted β-cell regeneration.
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