Dave - I never meant ti imply metformin makes the pancreas work better. Quit the opposite. The pancreas is damaged and needs rest. Metformin has proven it can not and does not provide this needed rest period to allow the beta cells time to regenerate. We know with early insulin intervention we see this beta cell regeneration.
The issue for T2s is meal time sugar spikes. Metformin does not address the primary issue PWDs have. A PWD on meds in the perfect would reflect a non-diabetic; meal time sugar spike < 130 and back to ~83 in about 2 hours. Instead what we see are metformin PWDS not even hitting a 7.0 A1c which is an average BG of 154. IMO, with CGMs and better insulin the real target should be 5.5 which is an average BG of 97. How many metformin users are hitting that, < 90%+ ???
For newbies, if they really want to control and potential stop and in some cases reverse beta cell damage telling them metformin is a great first step is not good. In fact, all metformin is going to do is allow progressive beta cell damage to happen.
What fasting does is very much different. It directly affects the carb intake because if you are fasting you have none. This allows time for the pancreas to potentially get back to a FB state and rest. Going on a low carb diet also directly affects the pancreas as it will not need to address a high meal time spike. Exercise affects muscle structure and if you believe Mike Geger the muscles are affected by intramyocellular lipid caused by high fat meals - What Causes Insulin Resistance? - YouTube
Pretty much agree, except for two things:
This is a gross (and dangerous) oversimplification. T2 is not a single dysfunction and set of symptoms. It’s not a true diagnosis, but rather one of exclusion. When diagnostic tests don’t point to a clear and unambiguous diagnosis, patients are lumped together into the T2 category regardless of what the actual pattern is. Any statement you can make about T2s (such as the one above) will be true of some and not true of a significant number of others.
For example: the “classic” stereotype of T2 is plenty of insulin but lots of insulin resistance, making the pancreas work overtime but to little effect. That’s not me. I have next to no IR and next to no insulin.
Broad generalities about T2, how it behaves and how to treat it are just plain . . . false. And consequently dangerous.
And complicating the picture still further is the fact that substantial numbers of T1s are erroneously diagnosed as T2. One of our members, @Melitta, has written extensively about this. It’s a genuine problem.
The other part I have to take exception to is this.
My point, which I apologize for not being clear about, was that metformin and fasting each, in different ways, allow the pancreas to rest by giving it less work to do. Fasting does that by reducing exogenous carbs; metformin does it by reducing endogenously produced ones. Less carb is less carb, however it happens. And less carb means lower insulin requirements. Metformin also aids by reducing IR so that less insulin is needed to handle whatever carbs there are.
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