Yes but acarbose doesn’t feed the good bacteria – it’s the undigested starches that do this. If you take acarbose but don’t eat starch, there’s still no extra fuel for the bacteria. No side effects (gas, etc) but no benefits either, unless I’m missing something.
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No, good point. I eat veg and berries and this time of year I eat whatever my wife brings to the field. I think they’re getting something.
I’m sure the mice fed acarbose and rapa are fed starch. Most people get some starch, and it’s probably ok to eat the amount you can burn. Though I think, having been low carb for awhile, it is also important to be a fat burner and consumer. So I do try to keep it way down.
Not sure if a true keto person would get benefit from acarbose or not. Also not sure how much it raises mtor2.
Blue Zones are cherry picked to support an agenda. They’re bogus.
Do you have evidence to support the contention that keto/carnivore diets promote increased health span and/or life span when compared to diets rich in whole fruits/vegetables/beans/whole grains? Note that both dietary approaches are low or absent in processed junk, refined sugars, white flour and sweetened beverages.
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Yes, ketogenic diet extends lifespan and healthspan in mice. Giving glucose to C. elegans shortens its lifespan.
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Guess I’ll have to cut back on the Glucola. Given that we have human data for non-ketogenic diets and health span/life span, I’m going to go with that, but to each his own.
Blagosklonny Tweet
Koschei anti-aging formula that included
Rapamycin,
Captopril or Lisinopril,
metformin, aspirin and
low carb diet (instead of acarbose)
I see no point in taking acarbose when eating keto or low carb meals. I only take it when indulging in a pizza or pasta on occasion.
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That’s how I’m going to use it as well, but also time it so I don’t have horrible gas at work. Looks like Friday night is PIZZA NIGHT! 
Neuroprotective Effect of SGLT2 Inhibitors - PMC => the brain has SGLT1/2 receptors. But most of the neuroprotective effects of empagliflozin shown in diabetic models.
It says canagliflozin > empagliflozin.
Damnit. Ugh this is really going to cut into my berry and even tomato juice consumption. There are fruits that ARE responsive to acarbose but those are {mangoes/peaches/nectarines/oranges/grapefruit/apricots}. Still quite a few though… WOW, to imagine that I might finally prefer bread over berries…
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I personally stuck to acarbose as mentioned quite a while ago and it’s a much more elegant solution to glucose/SCFAs/AMPK.
Yep SGLT2i has off-target effects which may or may not be significant and has some potential risks regarding urinary infections and high-dose rapamycin increasing bacterial infection risk as you alluded to if you’re taking it long term. I have considered Cana intermittently with acarbose. Gonna wait for more human data on this one.
Cana is not necessarily a “bad” drug but it is a “dirty” drug like metformin to some extent - the main issue with acarbose is “acarbose resistance” but I already detailed the solution before - multiple inhibitors via food.
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Why are you concerned about the fructose content if you’re just taking 1-2 servings of blackberries or raspberries?
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Dr. Rami,
You write: " SGLTI should never be seen as a substitute for Acarbose. If someone wants to take them together then that’s another story."
So what is the other story? Do you think its a good idea to take both SGLT Inhibitors and Acarbose? Any negatives to do this?
Still…rapamycin+acarbose had additive effects. I suspect acarbose might be better at some pathways and rapa at some.
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If you recall, Matt K got a 60% life extension in male mice by giving very large doses of rapamycin leading to more mTOR inhibition.
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Acarbose shares pathways with rapamycin, and is an mTOR inhibitor in several tissue types. So it’s possible that acarbose is merely giving greater TOR inhibition, like giving a higher dose of rapamycin . It’s unfortunately not clear.
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Miller had pubs for the effects of rapa vs acarbose on a few proposed pathways which showed some differences. Hard to say if it’s not just the TORi but acarbose isn’t quite the same as rapa on TOR pathways. I think he was somewhat upset Matt K didn’t want to go with acarbose and went with rapa first since he believes the glucose effects are very much different than rapa and rats don’t get diabetes.
This number is often misunderstood. This was 60% increase on the “remaining life” (given extremely high transient dosing of rapamycin) - not a 60% increase on the total lifespan. I’ve talked with the researchers (interviewed Allesandro Bitto ) … and the percent of the % total lifespan increase was about the same as what they saw in the ITP studies (mid teens) for middle range dosing (14ppm).
But you are right, if this protocol was started at a younger age (e.g. 9 months) and continued fully through the mouse lives, we may have seen very high lifespan increase. I’d like to see that study.
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Good point.
Thanks for the correction.
It’s possible that it’s the change in the microbiome that’s additive with acarbose. Of course, rapamycin also causes a change, more specifically an increase in the segmented filamentous bacteria. So, is there something special about acarbose in this regard? Maybe.
One could also argue that it’s the glycemic control, but the Accord study in diabetics showed no improvement in total mortality with strict glycemic control.
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Ouch! I fear you are right.
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