Acarbose has very low bioavailability, less than 2% gets absorbed as the active drug, and 35% as metabolites, it’s believed that Acarbose extends lifespan by slowing glucose absorption.
But many diabetic drugs can also slow glucose absorption, but they can’t extend lifespan much like Acarbose.
I wonder beside the reduction of postprandial glucose blood concentrations, does Acarbose extend lifespan by other pathways? such as altering the microbiome on GI tract?
I am curious if we treat Acarbose on the fasting mice, can it also has anti-aging effect?
If taking Acarbose on the fasting can also extend lifespan, then it’s a good news that we can take mega dose of Acarbose on the fasting, while avoiding those annoying adverse effects.
Acarbose acts locally in the gastrointestinal (GI) tract with low systemic bioavailability (less than 2% gets absorbed as the active drug, and 35% as metabolites).
Good question… what is the overlap with caloric restriction? It hasn’t been tested, but it would be interesting to find out.
But ultimately maybe the better question is how well it works with other longevity medications because real Caloric Restriction with Optimal Nutrition (reducing caloric intake by 30% to 50% over many years while still getting all the important nutrients that your body needs) is so hard, and so unpleasant (I’ve tried it for a year) that I think the percent of people who could do it and would continue to do it for years, is likely under 1% of people, so its kind of irrelevant.
The more simple explanation sounds more plausible in my opinion. Glucose and insulin are both inflammatory. It seems to me that much about mammalian health links to glucose. The leading causes of death are strongly linked to glucose and the mechanism of so many known ways to improve health do so as well: caloric restriction, time restricted feeding, metformin, exercise, ketogenic diet, etc. What would be different about acarbose mechanism of action? I’m personally doubtful about the benefits of acarbose without food.
The multiple morbidities are actually secondary to diabetes rather than glucose per se . If it were strictly glucose then very strict glycemic control of diabetics would greatly lower end organ damage and mortality rates. Very major studies have shown that that is actually not the case.