How can we "stimulate" mTOR?
- Thread starter Sushi
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i guess you don t mean anaerobic when saying non aerobic..walking is aerobic ,and every activity except the intense ones are aerobic..non aerobic aka anaerobic means you pass the threshold where your body can efectivelly use oxigen for energy,also is the time where lactate builds much faster in the blood than the ability to eliminate it..wich will force you to stop..so stick it to aerobic and be carefull to not push towards non aerobic/anaerobic
Hey you guys have started some good lists. But could you tell me where you read that Uridine is an mTor promoter? I read a lot on this one and it seems to behave like a FoxO promoter (the opposite). The pyrimidines are more likely to be inhibitory substances in general (in ray peat's generalizations, seems to be true) and it's the purines - intracellular adenosine and ATP (but even also extracellular, apparently) - that would help mTor the most.
There could a dose-dependent and cell type-specific response I suppose.
Like other poster wrote I think rhodiola is bad here (see examine.com). Maybe there are exceptions but herbs are a bad bet.
There could a dose-dependent and cell type-specific response I suppose.
Like other poster wrote I think rhodiola is bad here (see examine.com). Maybe there are exceptions but herbs are a bad bet.
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yes sorry I got my aerobic and heart rate zones confused (been a long weekend) ...what I was trying to say in a poor way was that low impact aerobic (under 60% of max total heart rate) is beneficial as long as it is managed to avoid PEM.
Was it this one maybe? https://www.ncbi.nlm.nih.gov/pubmed/26565787
I can see how a rectified uridine deficiency will help mTor (it rescues cells in therapies that lower pyrimidines), but beyond that it gets muddy.
I can see how a rectified uridine deficiency will help mTor (it rescues cells in therapies that lower pyrimidines), but beyond that it gets muddy.
I don't have time to read but there's no doubt they interact (both ways IIRC).
RE: Uridine, long story short it's safer to just supplement the precursors for de novo synthesis, which is Glutamine + ATP + B2 + B3 (overlaps conveniently) [+ aspartate + something else]
RE: Uridine, long story short it's safer to just supplement the precursors for de novo synthesis, which is Glutamine + ATP + B2 + B3 (overlaps conveniently) [+ aspartate + something else]
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Seriously?? How many of our doctors would have a clue about Tregg cells? or mTOR? The sad reality is that for most of us, we are on our own when it comes to taking supplements and OTC meds to help with CFS/ME.
My experiment with this was a pilates class, lying down with resistance machines. With a hefty dose of BCAAs before and after, no PEM. I've been doing pilates quite a while and have to do reduced reps, but normally it does give me PEM. I have been doing it anyway hoping that the trade--off (PEM for a day versus becoming a blob) was worth it.
Yoga can give me more PEM than weightlifting. I'm currently trialing Ketamine, one of if not the strongest mTOR activator. It's not conducive to Pilates though lol more like laying in bed or on the couch with music. Ketamine gets broken down into HNK and this is a potent antidepressant, mTOR activator and BDNF releaser, which further stimulates mTOR.
My doctor has suggested trying an IV of Ketamine at a low dose and with a long infusion. How are you taking it?
A downregulated mTOR could also be the consequence of the illness. Rather than running n=1 unblinded self rated experiments with no solid scientific basis, it would be better to donate to the OMF.
If you really can't resist the urge, rather than spending money on supplements, you can try the good old small frequent meals approach and having some amino acids with meals, like ricotta. Eating activates mTOR.
If you really can't resist the urge, rather than spending money on supplements, you can try the good old small frequent meals approach and having some amino acids with meals, like ricotta. Eating activates mTOR.
I dig skepticism but I think there are a few reasons why this is a false dichotomy:
1. Science is slow and plenty of forum members will be dead before official science finds a cure that works for them. Suggesting they simply sit and suffer without trying things (except "maybe consider eating"!!) is cruel.
2. Not everyone needs a cure that works on a large, placebo-controlled, double-blinded sample. They need something that works for them. Given the complex and multiple etiologies involved here, if you find something works for you that science says doesn't work, you may just be in an unidentified subgroup. Let's not deny patients' own lived experiences.
3. Hope keeps people alive. I'm not completely sure there is such a thing as 'false hope' in CFS. Falsifying the hope would require knowing that there is a proven better alternative. We have no idea what will cure CFS so if anything - be it crystals or mTor or whatever comes along next - can generate hope, I think its valid to try it. I'm on year 15 of being hopeful. Without hope I'm not sure where I'd be...
4. Before science can test hypotheses with large sample sizes, it needs suggestions. There is no doubt that a single patient's experiences, that make an observant doctor say "hmmm, that's interesting," can help shape the direction of science. In short, patients doing self experimentation in what looks like an ad hoc fashion can be the (blurry) leading edge of science.
TL;DR: try shit, but donate to the OMF too!
1. Science is slow and plenty of forum members will be dead before official science finds a cure that works for them. Suggesting they simply sit and suffer without trying things (except "maybe consider eating"!!) is cruel.
2. Not everyone needs a cure that works on a large, placebo-controlled, double-blinded sample. They need something that works for them. Given the complex and multiple etiologies involved here, if you find something works for you that science says doesn't work, you may just be in an unidentified subgroup. Let's not deny patients' own lived experiences.
3. Hope keeps people alive. I'm not completely sure there is such a thing as 'false hope' in CFS. Falsifying the hope would require knowing that there is a proven better alternative. We have no idea what will cure CFS so if anything - be it crystals or mTor or whatever comes along next - can generate hope, I think its valid to try it. I'm on year 15 of being hopeful. Without hope I'm not sure where I'd be...
4. Before science can test hypotheses with large sample sizes, it needs suggestions. There is no doubt that a single patient's experiences, that make an observant doctor say "hmmm, that's interesting," can help shape the direction of science. In short, patients doing self experimentation in what looks like an ad hoc fashion can be the (blurry) leading edge of science.
TL;DR: try shit, but donate to the OMF too!
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How about both--that is what I am doing. And n = 1 is working for me--so far so good.
I already had it in my supplement supplies--so no extra expense in my case. BCAAs are cheap though.
I already had it in my supplement supplies--so no extra expense in my case. BCAAs are cheap though.
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I followed some of the reference links from the Self-Hacked article. It seems Green Tea [EGCG] & Rhodiola are mTOR inhibitors. Ashwagandha also seems to be an inhibitor.
Can someone who's more technically proficient confirm this?
Also, I would urge everyone mentioning supplements as mTOR inhibitors or activators, to post them only after they have themselves actually read the research abstracts/articles [& not from just reading it somewhere else on the Internet], to avoid any confusion or worse, harm.
Wish better health to all.
Can someone who's more technically proficient confirm this?
Also, I would urge everyone mentioning supplements as mTOR inhibitors or activators, to post them only after they have themselves actually read the research abstracts/articles [& not from just reading it somewhere else on the Internet], to avoid any confusion or worse, harm.
Wish better health to all.
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Someone with a science background might be able to put that in language that is easier to understand. To me it looks like theanine is a "promoter"--but I may well be wrong.
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@Sushi I had based that on this report but it's about EGCG & not Theanine -
Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor.
https://www.ncbi.nlm.nih.gov/pubmed/21300025.
I googled & seems like Theanine is indeed mTOR activator. Hopefully, someone else will chip in, too. I will edit my other post [Done].
Epigallocatechin gallate (EGCG), a major component of green tea, is a dual phosphoinositide-3-kinase/mTOR inhibitor.
https://www.ncbi.nlm.nih.gov/pubmed/21300025.
I googled & seems like Theanine is indeed mTOR activator. Hopefully, someone else will chip in, too. I will edit my other post [Done].