As Emily Litella says " You learn somethin new every day. 
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Sure, but mice in the ITP are not eating a āwhole foodā diet. They claim to give them āmice chowā but that chow are basically industrialized food with lots of carbs in it. Just see how fat are the control mice compared with those on Acarbose.
And yes, metformin did nothing to the mice because the mechanism of action is different. Acarbose blocks the absorption of carbs in the gut. Very different approach. But once you block the absorption, then you get a healthier mice. At the end, all what ITP is doing is finding drugs to protect mice from their terrible food.
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Iād argue that the typical Western diet of ultra processed food does not differ much nutritionally from mice chow.
They are not specifically chewable tablets, and the prescribing instructions donāt say to chew them, but Iām glad theyāre essentially tasteless and easy to chew anyway, even if some of the tablet gets stuck in my teeth.
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Acarbose seems amazing but has anyone found an effective way to address the 3000-pound gorilla in the room?
The gas.
Or are we stuck with the gas since the gas is a side effect of feeding the bacteria in the gut?
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Iāve found the best way to eliminate the gas (mostly, not completely) is removal of wheat from my diet.
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Do we know that the mice ate that had a life extension using acarbose? Is it the wheat plus acarbose that gives all the benefit? Probably not but wouldnāt that be a kick in the butt.
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It is the gas which causes the life extension
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Unless I get murdered because of it.
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The gas gets better over time. Itās still there, just not as bad as in the beginning.
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I notice that some take Jardiance instead of Acarbose.
What are the comparative benefits of each?
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I donāt know that buy thatā¦as a non-diabetic who uses an SGLT2 inhibitor, when I use a glucose urinalysis stick I can see Iām excreting a lot of glucose (way more than I normally do).
So that glucose must be coming from the kidneys, via the blood that they are filtering. That surely must be impacting my blood glucose levels, and even it has no impact on postprandial levels, it must surely lower the baseline on which the postprandial glucose sits ?
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This would be unfortunate. One primary motive for considering acarbose is to mitigate the post-prandial effects of wheat. However, if I need to steer clear of wheat due to gas, this undermines the original reason for taking acarbose.
Iām not sure this is a great trade off. I guess I could still use it for riceā¦
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If you have normally glucose in urine your glucose concentration must exceed 180-200 mg/dl which is renal threshold. In metabolically healthy people this occurs really seldom. If you take SGLT2i in my understanding you lower renal threshold by about 30%. There is still some glucose reabsorption in place.
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Intriguing, youāre right in that my blood glucose never reaches those levels.
Yet I know that I get a 10-20 fold increase in urinary glucose output when I take an SGLT2 inhibitor.
Iāll have to investigate further.
Iām in the middle of a study at the moment but when that ends, Iāll stop my SGLT2 inhibitor, do a 24 hour glucose collection, restart the inhibitor and do another collection.
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Unless you have kidney disease, which also rules out metaformin.
My current thinking is that metformin is not a big deal. There is nothing in the literature that I have read that says metformin is a significant life extender in humans. Metformin is one of the drugs that has an extensive history of use in humans. It seems to have other benefits than glucose control but they are not well studied.
As far as glucose control is concerned, there is nothing I have read that says controlling glucose in non-diabetic people has any life-extension properties. I know glucose control is a popular subject in the forum threads.
On the off chance that it does, I take acarbose and linagliptin. I am currently off of metformin because it has side effects for me that I donāt like. Metformin seems to cause digestive tract issues in a significant percentage of people who take it.
Bottom line: If you are not diabetic I wouldnāt worry about the supposed life-extension benefits of metformin.
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I am trending toward this conclusion. I have blood sugar issues genetically (family history) but I am doing so many things that I think metformin is not necessary for me (to accept its drawbacks). I think acarbose and canagliflozen plus berberine and ALA will be enough. That will be my next test, using HbA1c as a guide. I will not tolerate going above 5.5.
I plan to drop Farxiga for Cana, and metformin for acarbose, to stay under my limit of 10 chemicals.
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Metformin use should not be abandoned in those with Chronic Kidney Disease. Most paranoia about Metformin is based on its predecessor, Phenformin, which was discontinued in the U.S. in 1978, due to excess deaths due to lactic acidosis. Although Metformin, like Phenformin, is a biguanide, it is much safer, and rarely causes lactic acidosis. If one has CKDāeven Stage IVāMetformin can be safely used if the dose is reduced (500-1,000 mg/day) and its effects and side effects are monitored.
[MetformināA Candidate Drug for Renal Diseases](https://Metformin--A Candidate Drug for Renal Diseases)
METFORMIN IN CHRONIC KIDNEY DISEASEāTIME FOR A RETHINK.pdf (647.1 KB)
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