True, but there is still a dose response. We just don’t know why…
But - it does seem like the benefit maxes out around the 1000ppm, so perhaps thats the ideal intestinal concentration for this drug. There is no added benefit at 2500ppm over the 1000ppm.
more benefit in males, whose median lifespans were increased by the three doses by 11%, 17%, and 16%,
Am I the only one that thinks this is a bit odd. SGLT2’s work in the kidneys which have decreased activity at night. An SGLT2 isn’t going to deplete body glucose, and I don’t know what it means to declutter a mitochondria?
For an average person, taking a SGLT2 inhibitor at night would have an addictive effect on natural circadian rhythm and functions- that’s the hypothesis anyway.
SGLT2 will not “deplete” glucose but yes, the drug will perform functions regulate glucose over night. I can’t think of why it wouldn’t, but regardless it’s proven to do so- day or night.
Results: T max increased by 35% in the evening phase compared to the morning phase, while C maxdecreased by -6.5% in the evening dose compared to the morning dose. Additionally, AUC 0 to ∞increased in the evening phase by 8.25% compared to the morning phase. The mean cumulative amount of glucose excreted (UGE ( 0-24)) increased by 43% in the evening dose compared to the morning dose
Conclusion: Despite the difference in pharmacokinetics parameters between evening and morning doses, C max, AUC 0-t, AUC 0-∞, didn’t differ on the bioequivalence level. In addition, as UGE ( 0-24) didn’t statistically differ, thus, we can conclude that there is no statistical significance between the morning and evening doses.
Biologically speaking, their cannot be a meaningful difference. I don’t mean this personally, but if you do not have a background in molecular biology this can all be difficult to understand, but this website has a group of people with these backgrounds- myself inc. that you can learn from. I have learned so much, we’re lucky to have such a strong forum.
Isn’t this what we really care about , the amount of glucose exerted? I mean you could argue that we don’t really care about the “Cmax”, or “Tmax” or AUC in this case - its the results that matter; glucose excreted?
Of course, if the benefits we seek are coming from something other than just blood glucose reduction (which increasingly seems likely given the plethora of beneficial effects of SLT2 inhibitors), you want all of these. But at least if you take it at night you can feel comfortable knowing that " C max, AUC 0-t, AUC 0-∞, didn’t differ on the bioequivalence level."
Before starting a Carnivore diet, I was taking acarbose, but it caused terrible gas. I’m curious about the effects of acarbose on my pure Keto diet. Are there any benefits beyond blocking carbohydrate absorption?
I experienced the same thing when I first started taking acarbose and even stopped taking it because of the gas etc.
Then I went on a low-carb diet and started retaking it because I had ordered a year’s supply from India on hand and believed it might have other beneficial effects.
Of course, there was a little gassiness even with low-carb meals, but I had less than I had before. I was only taking it if the meal wasn’t low-carb, so I didn’t take it for every meal.
After a while, I noticed when I took acarbose with a high-carb meal, even ones that had a wheat content that I had little or no gas from the acarbose. I am not taking probiotics.
My theory is that over time, acarbose changed my gut microbiome.
So, it would be interesting to know if anyone else had the same experience; that acarbose changes your gut microbiome, and your body adjusts to it.
Just to add on to DesertShores’ comment - I too had unbelievable gas when I first started Acarbose. Over time and with a shift in my diet away from wheat products, my gas has gone down to a minimal level (still more than normal, but not at a bothersome level). I take acarbose with every meal.
I think it depends on different variables. In the context of a healthy population, maybe, but not in the case of diabetes which half the population has a varying degree of processing and utilizing energy. The problem is it’s difficult to measure metabolic dysfunction in all its complexities at an end-tissue level.
Doesn’t that seem to make sense. Why would we be reducing blood glucose into our urine at night? If we did, we’d be up all night peeing and that doesn’t happen as far as I can tell.