since we know now that taurine (and same with glycine as discussed here in another topic) increases MTORC1 and still increase lifespan significantly, are we sure that MTORC1 is the real reason why rapamycin does increase lifespan ?
**Did they tested already a mice model where they knocked down genetically MTORC1 and actually showed it did improve lifespan ?
so far if yes, we have a conflicting role for MTORC1 and then have 2 hypothesis :
1/ it is tissue specific : so we have to understand if MTORC1 in insulin response is the same as in the muscle
2/ it is the over activation / long term wich is a problem, so take rapamycin in high dose and far away (like weeks to month) is especially beneficial and can even improve the benefits of glycine and taurine…
The main point is that the body is a dynamic system. It has cycles. There is the daily circadian cycle, there are the ultradian cycles, there is an annual vitamin D cycle.
The body needs to be fed at times, it then needs to sequester the nutrients, it then needs to stop feeding and move into autophagy (where Rapamycin helps).
Interesting. It’s worth knowing the many influences on mTOR, but we should recognize that there is more to health and longevity than mTOR. Deficiency in any of the many nutrients needed to run the machine will cause problems.
If taurine + glycine activate mTOR, are people offsetting those supplements relative to weekly rapa dosing? I looked through the taurine thread but do not see this mentioned anywhere. It seems like everyone in that thread mentions taking taurine daily.
I have been doing ~4 grams of taurine in the morning, 4 grams of glycine at night before bed, and 7 mg rapa weekly. Should we wait to take taurine + glycine a few days after rapa?
Rapamycin blocks MTOR completely. No other chemical that activates MTOR will activate any pathways blocked by Rapamycin. It takes precedent over any amino acids.
Also any activation by taurine or glycine will only happen during the 4 hour window you take it. The biggest downside here is that Rapamycin may be blocking some of the benefits of glycine and taurine near dosing time. The further away from dosing, the better. So, I wouldn’t bother taking Taurine or glycine in the first four hours after taking Rapamycin. Get it done before dosing Rapa.
Blocking MTOR is necessary for autophagy. Rapamycin does this very well.
Think of it in this way. Your body is like a jukebox. When you take Rapamycin, you are filling up the slot you put the quarters in with glue. It doesn’t matter how many quarters you have in your pocket (MTOR1 activators like taurine), you aren’t going to play any music until the glue is removed.
One can only guess. But taking both with Rapa seems counterproductive. Wish there were more info on that.
Do we know that mtor activation is the only mechanism by which Taurine works?
It is not a definitive answer that longevity is because of blocking of Mtor by Rapamycin, Glycine and Taurine technically activates Mtor and they have been shown to increase life span as well, albeit not as much as Rapamycin. Even experts that has studied this for decades does not have a 100% certainty.
There was a video by Michael Lustgarten that showed the connection of Candida growth in older people and dementia, as candida gets in the blood stream. Centenarians have notoriously low candida growth. Rapamycin is a solid treatment for Candida, so the more rapamycin the less candida you will have as you age.
Rapamycin’s effect on longevity is not only based on inhibition on Mtor, other things as well, gut microbiome, killing off candida as so on.
I thought that proteins in general activated mTOR. Especially Whey BCAA, milk and meat?
Are glycine better than other amino acids att activating mTOR? Or are we just looking all supplements thru rapamycin-glasses. I mean, maybe their mediating effects has nothing, or very little to do with mTOR.
Where could I learn more about the annual vitamin d cycle sir? Thank you
During the summer there is more sun, hence people whose skin encounters that have more vitamin D. My personal view is that from an evolutionary perspective this would advantage creatures which have optional genes which only function when there is plenty of food around.
Taurine has been discussed in other threads, but it does seem to indicate that it might be on the essential anti-aging list. It is interesting that there is a relationship between rapamycin and taurine.
I divide my supplements into two categories, health span, and life span.
“Supplementation with taurine slowed key markers of aging such as increased DNA damage, telomerase deficiency, impaired mitochondrial function, and cellular senescence. Loss of taurine in humans was associated with aging-related diseases, and concentrations of taurine and its metabolites increased in response to exercise. Taurine supplementation improved life span in mice and health span in monkeys”
Taurine deficiency as a driver of aging
Can we think about rapamycin and mTORC1 with some additional granularity? What I mean is, if one takes rapamycin, their mTORC1 activity will be lowered, but to what extent should depend on the dose. Just pulling some numbers out of my hat, let’s say I take 6 mg rapamycin once per week for a year and reduce my mTORC1 activity throughout my body (where it can get to, anyway) by 60%. Maybe if I went down to 3 mg per week my overall mTORC1 activity would just be reduced by 30%. I’m not sure how much I’d have to take to turn my mTORC1 activity to zero, but I bet it would be a very large dose. Someone let me know if this concept is just wrong.
So moving on to something that’s purported to increase mTORC1, like lifting heavy weights or eating lots of protein, I would guess those activities move the needle much less, relatively speaking. Let’s say I decide to put some muscle on, so I hit the weights hard and increase my protein intake 40%. Again pulling some numbers out of my hat, I’d guess doing that might increase mTORC1 by maybe 10% to 30%. I’ve never come across any quantitative guidance about this, so if anyone has any insight on this, I’m all ears!
One point I am making is that if we take rapamycin to crank our mTORC1 way down, and we simultaneously eat more protein, or whatever, we can still be in a state of reduced mTORC1 and get those benefits, while also getting benefits from something that purportedly raises mTORC1.
I am basing this on my understanding that our overall mTORC1 activity is not a switch that is either on or off, it’s a dial that we can tweak up or down as we see fit.