Boo1979
Well-Known Member
- Messages
- 1,849
- Type of diabetes
- Other
- Treatment type
- Tablets (oral)
I wasnt saying its worked for me, quite the opposite! - My view is that it is very simplistic
The quote is from Jason Fung
I wasnt saying its worked for me, quite the opposite! - My view is that it is very simplisticProbably because it is.
I've never put sugar in anything, I have very rarely drunk any fizzy drink, I have rarely eaten biscuits, never been a chocolate lover, very rarely ate cake . . . . . . . . .
Have avoided processed foods since warned off frozen WW meals by dietician in 1989.
I'm no stranger to exercise, maybe not continuously but I have recently noticed with the aid of my FS Libre that my BG can actually go up when I exercise.
It's actually exactly like trying to lose weight, if that was a simple as eat less and exercise more, there would be more successful dieters in the world.
Glad it has worked for you, hope it works for many others, I think there's a little more to it especially when there are metabolic problems. ATP is the thing, I believe, that muscles use and we'd have to have a look at how glucose is metabolised in the individual. It's not straight forward.
No no other tests. One medic raised the question of monogenic diabetes but no tests have ever been done. I generally manage to keep my overnight fasting BM in the 6-7 range. Ive been under the hospital diabetes team for years
That's a shame. My opinion is that it's more complicated, only an opinion.I wasnt saying its worked for me, quite the opposite!
So if you have gone past the 20+ years it may be helpful to determine your insulin levels
Home > Blog > David Spero > Can Beta Cells Be Healed?
[paste:font size="6"]Can Beta Cells Be Healed?
Beta cells in Type 2
People with Type 2, however, recover beta cell function all the time. A study done in Seattle found that beta cells subjected to high glucose levels (about 288 mg/dl in a test tube) lost function rapidly. But when switched to a low-glucose environment (about 15 mg/dl), most of them recovered normal insulin production.
The longer the cells had stayed in the sugary solution, the longer it took them to recover. The researchers said that the damage might be irreversible after too much time in the glucose bath. They couldn’t say how long that time would be.
In 2011, a widely-reported British study found that beta cells recovered in a couple of weeks in most (not all) people eating 600 calories a day. Most of these people had been diagnosed with Type 2 fairly recently.
Insulin resistance in muscle and liver and β-cell failure represent the core pathophysiologic defects in type 2 diabetes. It now is recognized that the β-cell failure occurs much earlier and is more severe than previously thought. Subjects in the upper tertile of impaired glucose tolerance (IGT) are maximally/near-maximally insulin resistant and have lost over 80% of their β-cell function.
In addition to the muscle, liver, and β-cell (triumvirate), the fat cell (accelerated lipolysis), gastrointestinal tract (incretin deficiency/resistance), α-cell (hyperglucagonemia), kidney (increased glucose reabsorption), and brain (insulin resistance) all play important roles in the development of glucose intolerance in type 2 diabetic individuals.
Collectively, these eight players comprise the ominous octet and dictate that:
1) multiple drugs used in combination will be required to correct the multiple pathophysiological defects,
2) treatment should be based upon reversal of known pathogenic abnormalities and not simply on reducing the A1C, and
3) therapy must be started early to prevent/slow the progressive β-cell failure that already is well established in IGT subjects.
A treatment paradigm shift is recommended in which combination therapy is initiated with diet/exercise, metformin (which improves insulin sensitivity and has antiatherogenic effects), a thiazolidinedione (TZD) (which improves insulin sensitivity, preserves β-cell function, and exerts antiatherogenic effects), and exenatide (which preserves β-cell function and promotes weight loss).
Sulfonylureas are not recommended because, after an initial improvement in glycemic control, they are associated with a progressive rise in A1C and progressive loss of β-cell function.
It's pretty close to my 20th anniversary of being prescribed something. My insulin production last January was in the normal range and my insulin resistance index has dropped from 2.4 to 1.8 (should be < 1).
I also dont quite fit the theory re sulfonylureas either - Ive been on Gliclizide for over 20 years at a stable dose, although I have had closely monitor my diet to maintain hba1c in the 40-46 range its been happily sitting at - that stability is what led one medic to think about monogenic diabetes which apparently responds well to sulfonylureas ( or rather a couple of the different monogenic gene mutations do)Howver I believe for T2D, beta-cells regeneration and restoration is a possibility. But glucose levels have to be sufficiently low...
http://www.diabetes.co.uk/forum/blog-entry/t2d-beta-cells-regeneration.1910/
And Dr RA Defronzo 2009 paper explains why he would proposed a different treatment paradigm that is more protective of the beta cells...
http://www.diabetes.co.uk/forum/blo...e-treatment-of-type-2-diabetes-mellitus.1897/
I also dont quite fit the theory re sulfonylureas either - Ive been on Gliclizide for over 20 years at a stable dose, although I have had closely monitor my diet to maintain hba1c in the 40-46 range its been happily sitting at - that stability is what led one medic to think about monogenic diabetes which apparently responds well to sulfonylureas ( or rather a couple of the different monogenic gene mutations do)
Its on my list for next annual review to ask about further tests, I think the outcome may depend on whether I end up seeing the consultant this time or not
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