You could be right. So maybe the thing is to lose the weight keep it off and avoid carbs. maintaining reversal or remission requires a life long change in habits. Or you end up with a relapse possibly.
In other words, if a T2 who achieved great results low-carbing, say (approach unimportant for this really), then wants to go back to eating as before diagnosis, they are risking a reversion to a less healthy state, versus a wider/more relaxed way of living.
The loss of fat from the pancreas is known to take a helluva lot longer
One effect that may be at play here is Liver Dump.
I don't know what changes I have made - so I can only advise - eat to your meter.
After all the work you did it seems such a pity to have ignored those high readings for a whole week.
It rather reminds me of someone I knew quite a while ago now. He spent weeks carefully rebuilding an old car, and as soon as it was running he took it on the motorway to see if it would 'do the ton' - he blew up the engine.
IMO the weight loss is only an indication that fat reserves are being used up, and not the cause of 'remission'. So, at present, and until I am proven otherwise, I will say that it is the reduction of bgl by either carb or calorie reduction that is key, and that the low food intake is similar to fasting in that the body is probably becoming 'fat burning' i.e. keto in a small way, and this is driving the weight loss and possible pancreas repairs(?).That's how I'm feeling about it at the moment, to be honest. It did *start* as eating and exercising to my meter, because I could eat a fair amount of carbs and get great readings straight afterwards through exercise. But a) it got addictive, b) the 'background level' of glucose crept up, and c) it wasn't possible to exercise one day.
Anyway I'm over it in terms of giving myself a good talking to. I'm still fascinated by the question of whether a strict approach to weight loss is key, however!
IMO the weight loss is only an indication that fat reserves are being used up, and not the cause of 'remission'. So, at present, and until I am proven otherwise, I will say that it is the reduction of bgl by either carb or calorie reduction that is key, and that the low food intake is similar to fasting in that the body is probably becoming 'fat burning' i.e. keto in a small way, and this is driving the weight loss and possible pancreas repairs(?).
Some of us using Low Carb diets find that fasting is a useful adjunct to the diet that seems to show some success in enabling a better beta cell response (or reduction of Insulin Resistance). But I find personally that while I am now able to eat the occasional higher carb meal without weeping, nonetheless I would suffer high bgl if I revert back to my old eating ways.
What I am wondering about is the idea that there is beta cell dysfunction at all. Most T2's start out with extremely high insulin levels and it is not until later in the course of the disease that the pancreas can no longer produce normal amounts of insulin.
How can someone be trying to heal the pancreas or know if it is healed if there is no way of knowing whether or not it is broken?
For me the compelling evidence comes from the ND report which showed they used a new method of interpretation of MRI scans taken before and after the diet plan that showed reduction in fatty tissue of both the liver and the pancreas. This is a clincher in my eyes.They also measured insulin levels using the insulin clamp technique to show that the diet reduced residual insulin levels. The ND study did its best to.use modern in vivo techniques to demonstrate their hypotheses to have merit, which is why for me ND is worthy study. I do not believe it is the only way of skinning the cat, but it does seem to have significant importance in the fight against T2D.Good points. So far RE the fat-in-beta-cells idea, I think what we have are two things: a correlation (fat in pancreas reduces and insulin response improves), and observations of beta cells in the lab which show that if there is fat in a beta cell it does not behave like a beta cell; remove that fat and it does. I find the combination of these two findings to be very compelling, but that, really, is it.
I think the basic observations far more compelling than the theory. We can see that the remission rate in gastric bypass patients is surprisingly high, and the remission rate (meaning here, the restoration of insulin response) in the first Newcastle experiment was shockingly high. What have both got in common? A sustained, continuous weight loss journey, largely involving liquid foods, and with no let-ups and carb binges along the way. In some ways attempting to work out why that works is like trying to explain gravity - interesting, but the important thing is it works.
That's a very very good question.
Edit: And it's just made me change the term "pancreatic function" to "insulin response" in my previous statement!
I would tend to suggest that the evidence of T2D on insulin actually using diet to be able to stop taking insulin and get good bgl is a demonstration of the beta cell recovery, although it could just be due to extreme high IR being reversed. I think that the C-peptide test shows if T2D have high or low insulin levels, and this is often the test used to initiate insulin replacement therapy. I am not a doctor, but I believe that insulin is given if c-peptide shows low insulin, as in the case of beta cell failure, but not when insulin is high. I know this is anecdotal evidence, and not proof per se.What I am wondering about is the idea that there is beta cell dysfunction at all. Most T2's start out with extremely high insulin levels and it is not until later in the course of the disease that the pancreas can no longer produce normal amounts of insulin. How can someone be trying to heal the pancreas or know if it is healed if there is no way of knowing whether or not it is broken?
We use cookies and similar technologies for the following purposes:
Do you accept cookies and these technologies?
We use cookies and similar technologies for the following purposes:
Do you accept cookies and these technologies?