Sulforaphane has a lot of potential. I wish there were more human studies.

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I agree acarbose is well supported for male mice. Can you sketch the argument that this would translate to humans? My view has mostly been that whatever benefits acarbose has can be achieved by lifestyle modifications, but the overall point that aggressive glucose control might extend maximum lifespan is a good one.

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It’s supposed to boost MTORc2. That might do it alone. Also it might not be reducing the glycemic load that improves health as much as that the sugars go to the bacteria in the colon that make SCFA. This is fundamentally good.

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  1. Weight loss
  2. Statin
  3. BP Drugs
  4. Vaccines
  5. Vid D3
  6. Fish Oil
  7. Green tea / black tea / hibiscus tea / coffee…
  8. Rapamycin
  9. GlyNAC
  10. Some form of antidiabetic (Metformin, Acarbose, Pioglitazone, SGLT2, GLP1-RA…)
  11. AKG [Healthspan]

Studies:

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I didn’t know we could add more:

Pectasol every morning on an empty stomach and don’t eat for an hour.
Melatonin every night before bed. I use 24mg.
Yellow oyster mushroom powder for the ergothioneine, but there are more good things in there. You can’t overdo mushrooms.

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I think the two key arguments are fewer glucose spikes, and higher mTORC2. It would (from my experience) be really hard to keep your blood glucose between 80 and 110 or 120 mg/DL over the typical week and eating schedules and diets… but I find it very easy with acarbose (but I also use empagliflozin).

And I know of no other easy way to boost mTORC2 (other than fasting)… Acarbose, An mTORC2 Promoter We Should All Take?

While not definitive, the ITP studies do make a reasonable case that acarbose won’t be a net negative, and its cheap, with minimal side effects (with a non-wheat diet).

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With a higher dementia risk though in association studies (might not be causal, but just saying…): Predicting Alzheimers (and minimizing risk) - #189 by adssx

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Out of curiosity, in the acarbose ITP trial, after the mice die, do they perform any kind of autopsy to determine cause of death and a general assessment of tissue status, f.ex. signs of brain neurodegeneration? I guess I mean in any ITP trial, but if yes, then the acarbose one might be interesting for results. Also while the mice are alive do they perform any behavioral observations for signs of subpar functioning. I find it hard to believe, though of course not impossible, that the mice lived longer, but were more demented. Of course, these are mice, and mice don’t get AD, so this may all be moot.

The other thing to keep in mind, is what was the profile of the human subjects on acarbose, to what degree were they metabolically deranged, because we do know that drugs may not work the same in healthy vs morbid patients (f.ex. metformin). Someone who is not diabetic, exercises etc. may not have a given side effect with acarbose.

Finally, for those who take many meds at once, there may be unpredictable interactions, so acarbose in the individual who is also on a SGLT2i, ARB for BP modulation, lipid modulating agents etc. may behave very differently than in acarbose monotherapy. We have no way of knowing without some studies, but I guess it’s good to be aware of possible dangers.

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1 Life style (Exercise no 1/CR 20:4 /sleep/meditation/social connections)
2 Photobiomodulation/near infrared for brain + QEEG / neurofeedback training
3 Glycation control Mulberry leaf extract (alternative to Acarbose, may combine)
4 Peptides Thymalin and Epithalamin/Epithalon
5 Mitochondrial control still researching

Plan to resume Rapa when lymphocytes have recovered fully.

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  1. Use your organism consciously/wisely to be balanced in everyday activities so that it is working optimally all the time.

  2. Keep your spine young and flexible (by staying thin, strong especially in the middle, and of course exercising intelligently to gain and maintain that flexibility - I choose rigourous Pilates https://www.youtube.com/watch?v=r2UUl04-lvw)

  3. Rapamaycin.

4 Other drugs like metformin and tadalafil.

  1. Have a passion, preferably one that develops you.
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That’s a sick setup! what is that called and are there compact variations of that? I’ve always loved using a back hyperextension to do similar movements, reverse hypers, glute-ham raises, etc. but never found a simple solution to let me do all kinds of variation like yours. On occasion wanted to delve more into Pilates but never got around to it.

Edit: ah a Pilates ladder barrel…

My understanding is that the mechanism of acarbose, as far as known, is to slow the digestion of certain carbohydrates. Roughly it turns simpler carbs into more complex ones, and complex ones to fiber. Naively there’s not much reason to assume that you can’t do this with just eating complex carbs and fiber to begin with. Of course inulin supplementation did fail in the ITP. The situation is more complicated. But my concerns are:

  1. Digestion and nutrition are highly variable among species. So there’s a built-in translation problem for a drug that exclusively targets digestion.
  2. The ITP mice are purposely fed a sub-optimal diet, so one might suspect some of the observed effect is compensation for that.
  3. In the unlikely event that, say, the mTORC2 effect you cite is due to something other than the known target of acarbose, we don’t know what causes it so can’t say if it might translate.

Not to claim that acarbose won’t work for humans. Just that IMO the evidence is not at as high a level.

The broader point is that few people seem to understand the sheer depth of negative results in this field. Folks on the forum are throwing out huge lists of things, based on limited evidence. I have no special insight, but if history is any guide essentially all of them will have null effect on max lifespan.

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Thanks for posting! I’d like to look more into the details of this data…

See also this one: Predicting Alzheimers (and minimizing risk) - #190 by adssx

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Correct, the ladder barrel. :wink: and you have the spine corrector and also small barrel - but of course ladder is where its happening. Of course, the Reformer offers some nice challenges, too.

Can Recommend that you fall in love with Pilates!!

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Some further reading (of abstracts…) seems to indicate low or no effect on reducing dementia, but no increase in risk. Not concerned if that’s the case.

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Could you please provide the sources? Those I remember find with no effects had large CI so impossible to conclude. The two large studies of good quality found a detrimental effect. That was enough for me to eliminate acarbose. Even more so when SGLT2i exist.

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just need to find a way to fit that machine in my dwelling!

Will have to follow up when more time, but reading the paper you linked it was comparing Acarbose to SGLT2i, not non-use.

This paper for example found reduced dementia* risk comparing non-use with ever-use of Acarbose. And lowest risk with combination of drugs they studied.

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It was comparing to non use I think.

Single author paper from Taiwan analyzing 15k people. Non statistically significant risk reduction. Only in women. It’s also non sensical from a statistical point of view that acarbose prevents dementia in non metformin users AND in metformin users who also use pioglitazone but not in metformin users only. A garbage paper to me.

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