2503 replies to this topic

[Turnbuckle]

Could you tell us how long had you taken the telomerase stimulants after the second test, and how much older your epigenetic age result you got from the previous test?

Just curious of how much impact of telomerase stimulants on epigenetic age, because, if the rise after taking telomerase stimulant is small enough, the rise in the epigenetic age may be due to something else or it might be a random error.

 

 

There's no mistake. That telomere length and higher rates of epigenetic ageing are correlated is known, so I was only surprised by how sensitive it is. A study published in 2018 showed that gene variants associated with longer telomere length are associated with higher intrinsic epigenetic age acceleration (IEAA). The P level is so close to zero that there is no chance of it being accidental. And while the paper calls the relationship paradoxical, it isn't. Imagine if telomeres never got shorter and cells never became senescent, then old cells would never be removed and they would just get epigenetically older and older and older. There is no paradox because telomere length is not a root cause of aging. It is only a sell-by date. Only removal of epigenetically old cells that have reached their sell-by dates and replacement with epigenetically young cells can stop the epigenetic aging process.

 

 

[Gene] Variants associated with longer leukocyte telomere length (LTL) in the telomerase reverse transcriptase gene (TERT) paradoxically confer higher IEAA (P < 2.7 × 10−11).

https://www.nature.c...467-017-02697-5

 

Edited by Turnbuckle, 19 August 2019 - 03:03 PM.

[sholay75]

Epigenetic aging is mostly the result of errors by methyltransferase. It has nothing directly to do with growth factors. As for your link, it proves my point--

 

 

Likewise, if you replace the oldest ten percent of your cells with somatic cells derived from endogenous stem cells, those new cells will begin aging normally from a starting point that is near zero. Cells age at a rate that is specific to the cell, not to the organism. This goes on all the time, thus the body is a melange of cellular ages. If the body's repair machinery were to work perfectly, you would reach a certain average epigenetic age and plateau there. That you do not is due to depletion of stem cell pools and failure to eliminate senescent cells. Address those issues and you can stop and even reverse aging.

I agree with you Epigenetic aging has nothing directly to do with growth factors. During the growth phase after birth , there is abundance of stem cell population which is rapidly growing to support growth, but in the presence of these stem cells, the population of these Epigenetically aged cells is also growing. In this growth environment there is no depletion of stem cells, instead there is accretion, and these Epigenetically aged cells are allowed to increase their numbers. 

 

Another possible way that the protocol designed by you is reversing Epigenetic age could be that the cocktail is accelerating the push of these Epigenetically aged cells towards senescence, which would show up as younger epigenetic age.

[Turnbuckle]

I agree with you Epigenetic aging has nothing directly to do with growth factors. During the growth phase after birth , there is abundance of stem cell population which is rapidly growing to support growth, but in the presence of these stem cells, the population of these Epigenetically aged cells is also growing. In this growth environment there is no depletion of stem cells, instead there is accretion, and these Epigenetically aged cells are allowed to increase their numbers. 

 

Another possible way that the protocol designed by you is reversing Epigenetic age could be that the cocktail is accelerating the push of these Epigenetically aged cells towards senescence, which would show up as younger epigenetic age.

 

No, you are completely wrong about the depletion of stem cell pools. The numbers of functional stem cells decline with age, even as the numbers of cells reaching senescence accelerates. You are making one statement after another about what you believe that is just flat out wrong. You should research these things before posting here.

[Werper]

Testosterone would be the most interesting hormone, and if the right supplement were added to the protocol, it's possible that testerone levels could be restored to a more youthful profile, and to even go beyond that. 

 

The main source of testosterone in men is Leydig cells. And while Leydig stem cells (LSCs) exist, they don't seem to be too anxious to proliferate. 

 

 

The reason is that LSCs require certain signals. This appears to be the hedgehog signaling pathway, which also impacts other SC types, like those in hair follicles. Stimulating the sonic hedgehog gene in mice grows new hair.

 

So stimulating that gene would increase the value of this protocol, if there were a supplement that was commonly available. And there's at least one. Resveratrol, for instance--Resveratrol Activated Sonic Hedgehog Signaling...

 

So can simply adding resveratrol to the protocol grow hair like Stalin and muscles like Stallone? We'll see.

 

cialis -     "For example, there is scientific research that was conducted in 2010. Doctors and scientists found that Tadalafil (the active ingredient of Cialis) can increase the production of testosterone by Leydig cells. These cells are located in male testicles. The experiment was conducted on laboratory rats. This became possible due to increasing of cAMP levels. Then cAMP works like a messenger between cells and hormones. That is why elevated levels of cAMP in the blood allows a body to increase the level of testosterone."
 

Edited by Werper, 19 August 2019 - 08:29 PM.

[sholay75]

No, you are completely wrong about the depletion of stem cell pools. The numbers of functional stem cells decline with age, even as the numbers of cells reaching senescence accelerates. You are making one statement after another about what you believe that is just flat out wrong. You should research these things before posting here.

You are right that the numbers of functional stem cells decline with age, but the numbers of functional stem cells increase during the growth phase till maturity, my point is during the growth phase, when the stem cell pool is increasing the Dnam clock shows that numbers of epigenetically aged cells is also increasing. There is no co-relation that increasing the stem cell pool will result in decline of epigenetically aged cells.

[NeilR]

I believe that stem cells are an important aspect of aging, and that‘s what makes me interested in this protocol. I do however wonder if this is working as good as it is supposed to. Is it really feasible for people to wait until their 50’s to start anti-aging? If a person doesn’t “age enough” according to this theory before then, is it possible it’s not even accurate? I mean we start aging well before 50, so a good method should theoretically work once the body passes its peak in the late 20’s/early 30’s. If you don’t lose enough stem cells by your 50’s for you to be old enough to reverse aging, then it sounds as if it’s just a minor effect of aging and certainly not it’s cause.

I also read this article:

https://joshmitteldo...-and-downgrade/

The above article’s comments seem pretty convincing in disproving the idea that a lower epigenetic age is a sign of successful anti-aging methods.

“What if epigenetic age is just a measure of time since a somatic cell line was spawned from it’s stem cell progenitor (which by definition will be younger epigenetically)? That means older people would naturally have an older epigenetic age because their stem cells are less active and somatic cells are replaced less often. It also means an individual with sightly more telomerase (and longer telomeres) would naturally have longer lasting somatic cells, so at any given time their tissues would be older epigenetically because they are also replaced less often. If this is true it means there are two separate but easily confused correlations: older people having less often replaced somatic cells due to tired stem cells, and people who have longer telomeres needing replacement less often (but probably with better preserved stem cells as a result).”

Turnbuckle received a lower epigenetic age on his test results, but is it possible that he actually biologically got older?

I think that the only real way to prove if any protocol is working is by serving before and after pictures from a user, showing that their aging has been either reversed or halted. You can feel 25 after a particular protocol, but if one looked 70 last year and doesn‘t look any younger this year, then I suspect that the protocol isn’t working as well as the think. I know that it’s possible that anti-aging may work on the “inside” but not the “outside”, but then we need to wait years and see if the person reaches 120 years (the supposed limit of how long a human can ultimately live) and even passes it, besides I suspect that most of us care just as much about our external appearance when it comes to aging interventions.

Edited by NeilR, 20 August 2019 - 06:22 AM.

[QuestforLife]

I had my epigenetic age tested shortly before I began (I was slightly older epigenetically than people my age, but within the error bars), and it dropped over 11 years after just 3 months of treatment. I then began using telomerase stimulants, and saw it begin to rise again. I thought I could use them with the protocol as stem cells would be mostly impacted, but I neglected to consider transit amplifying cells, which replicate far faster than stem cells and produce most of the new cells in many organs. So I cut the telomerase stimulants and saw my epigenetic age stabilize and begin to fall (more slowly this time), and according to the latest test I'm epigenetically younger than 96% of the population my age. So epigenetic age is far more malleable than people realize.

What epigenetic aging test did you use to get these results? Was it a blood test?

White blood cells turn over in 5 days or less, so I find it hard to imagine that a telomerase activator could extend that, although plausibly progenitor cells could be affected. More likely they can simply reproduce in larger numbers.

There is quite a lot of evidence that telomeres ARE critical to aging. For example the fact that the rate of telomere shortening predicts lifespan in multiple species (https://www.pnas.org...nt/116/30/15122).

You could argue telomere shortening and loss of stem cells are different sides of the same coin, and the problem might be stem cell loss rather than telomere loss. There is evidence that though telomere lengths are different in different tissues, they all shorten at the same rate. A possible explanation is that stem cells produce more progenitor cells in blood that, say, muscle, because of the requirements on replacement for that tissue during life. Hence blood has more progenitor cells with shorter telomeres that muscle. But over a course of a lifetime muscle loses a similar amount of telomeres to blood because it has less cells to do the replicating (https://www.nature.c...cles/ncomms2602).


I believe that no stem cell apart from pluripotent/embryonic stem cells have sufficient telomerase to offset continuous replication. So long term your protocol could erode stem cell telomeres.

Nevertheless, even with sufficient telomerase, it is likely other factors are required to assure continuous ability to replicate. For example this paper that has inspired my own research in ROCK inhibitors (https://stemcellres....10.1186/scrt449).

Thus, ultimately I think we'll have to use telomerase, epigenetic reprogramming factors and senolytics judiciously to achieve the end we all want, namely rejuvenation.

[Turnbuckle]

What epigenetic aging test did you use to get these results? Was it a blood test?

White blood cells turn over in 5 days or less, so I find it hard to imagine that a telomerase activator could extend that, although plausibly progenitor cells could be affected. More likely they can simply reproduce in larger numbers.
 

There is quite a lot of evidence that telomeres ARE critical to aging. For example the fact that the rate of telomere shortening predicts lifespan in multiple species (https://www.pnas.org...nt/116/30/15122).

 

 

 

I've had tests done with urine, blood, buccal swabs, and mixtures of those. I had tests done from two different companies on the same day, one using only buccal swabs and one using all three, and the results came out virtually the same, within the error bars. As for the aging of blood, don't think that it goes from stem cells to white blood cells in one step. There's an intermediate step of transit amplifying cells, and epigenetic aging occurs there. Those cells carry the replicative burden in many organs, with notable exceptions being the brain and liver. Multipotent stem cells are held in reserve, and there appears to be a population of pluripotent stem cells that are an even deeper reserve.

 

As for telomeres, when you look at long lived species such as humans, there appears to be little correlation between individual chronological age and telomere length, though you can statistically find a trend line that's headed down for large populations. And that's to be expected, as the numbers of cells aging out steadily increases with chronological age, even as stem cell pools dry up and fail to replace them. So aging is a failure of the maintenance process that consists of apoptosis/replacement. Nevertheless, I expect that someone doing this protocol with no telomerase stimulants would find that his telomeres had indeed gotten longer. That would be an effect, not a cause, the natural result of having a larger population of young cells.

[QuestforLife]

As for the aging of blood, don't think that it goes from stem cells to white blood cells in one step. There's an intermediate step of transit amplifying cells, and epigenetic aging occurs there. Those cells carry the replicative burden in many organs, with notable exceptions being the brain and liver. Multipotent stem cells are held in reserve, and there appears to be a population of pluripotent stem cells that are an even deeper reserve.

https://www.nature.c...s2602/figures/4

Yes you can see support for that in the Figure 4 from my second reference. More progenitors/amplifying cell replication from the same size stem cell pool means shorter telomeres, so having longer telomeres would allow them to divide for longer before having to go back to the pool (See attachement; apologies can't paste it in the text as I'm away from my computer).

Our positions on what causes aging don't seem to be far apart. Unfortunately they are sufficiently far apart to recommend different interventions.

Let's look at your results. You initially lowered you epigenetic age - presumably it's highly malleable if your cells are turning over rapidly, which you'd expect with short telomeres. Then you took a telomerase activator and your epigenetic age rose because those cells were being replaced from the stem cell pool less often. But have you actually shortened your life? Doubtful, as your stem cells will have been used less and hence you'll have more in reserve.

You then went back to your protocol without telomerase activators and saw the epigenetic age fall. So you were back to using up more stem cells.

How do you know you won't run out?

Attached Files

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[Turnbuckle]

https://www.nature.c...s2602/figures/4

Yes you can see support for that in the Figure 4 from my second reference. More progenitors/amplifying cell replication from the same size stem cell pool means shorter telomeres, so having longer telomeres would allow them to divide for longer before having to go back to the pool (See attachement; apologies can't paste it in the text as I'm away from my computer).

Our positions on what causes aging don't seem to be far apart. Unfortunately they are sufficiently far apart to recommend different interventions.

Let's look at your results. You initially lowered you epigenetic age - presumably it's highly malleable if your cells are turning over rapidly, which you'd expect with short telomeres. Then you took a telomerase activator and your epigenetic age rose because those cells were being replaced from the stem cell pool less often. But have you actually shortened your life? Doubtful, as your stem cells will have been used less and hence you'll have more in reserve.

You then went back to your protocol without telomerase activators and saw the epigenetic age fall. So you were back to using up more stem cells.

How do you know you won't run out?

 

 

I used the telomerase activators with the protocol, and not just once, but many times, having no idea that the combination of astragalus extract plus cycloastragenol would be that effective. Unfortunately it takes 2 weeks for buccal cells to make their way to the surface to be collected, and epigenetic tests were taking 6-8 weeks (and still are), so there was a 2-3 month delay in which I was flying blind. If I had seen this immediately I would have stopped earlier. Still, telomerase activators with the protocol might be OK if done very infrequently. Just keep in mind of the potential downside. As for running out of stem cells, that is the purpose of this protocol, to shift stem cell dynamics to proliferation over differentiation, with a special emphasis on pluripotent cells.

[sholay75]

I believe that stem cells are an important aspect of aging, and that‘s what makes me interested in this protocol. I do however wonder if this is working as good as it is supposed to. Is it really feasible for people to wait until their 50’s to start anti-aging? If a person doesn’t “age enough” according to this theory before then, is it possible it’s not even accurate? I mean we start aging well before 50, so a good method should theoretically work once the body passes its peak in the late 20’s/early 30’s. If you don’t lose enough stem cells by your 50’s for you to be old enough to reverse aging, then it sounds as if it’s just a minor effect of aging and certainly not it’s cause.

I also read this article:

https://joshmitteldo...-and-downgrade/

The above article’s comments seem pretty convincing in disproving the idea that a lower epigenetic age is a sign of successful anti-aging methods.

“What if epigenetic age is just a measure of time since a somatic cell line was spawned from it’s stem cell progenitor (which by definition will be younger epigenetically)? That means older people would naturally have an older epigenetic age because their stem cells are less active and somatic cells are replaced less often. It also means an individual with sightly more telomerase (and longer telomeres) would naturally have longer lasting somatic cells, so at any given time their tissues would be older epigenetically because they are also replaced less often. If this is true it means there are two separate but easily confused correlations: older people having less often replaced somatic cells due to tired stem cells, and people who have longer telomeres needing replacement less often (but probably with better preserved stem cells as a result).”

Turnbuckle received a lower epigenetic age on his test results, but is it possible that he actually biologically got older?

I think that the only real way to prove if any protocol is working is by serving before and after pictures from a user, showing that their aging has been either reversed or halted. You can feel 25 after a particular protocol, but if one looked 70 last year and doesn‘t look any younger this year, then I suspect that the protocol isn’t working as well as the think. I know that it’s possible that anti-aging may work on the “inside” but not the “outside”, but then we need to wait years and see if the person reaches 120 years (the supposed limit of how long a human can ultimately live) and even passes it, besides I suspect that most of us care just as much about our external appearance when it comes to aging interventions.

you are connecting the epigenetic age to the presence/ absence of stem cells. The Dnam clock shows epigenetic age increases right from birth, when the population of stem cells also increases.

epigenetic age increases regardless of the stem cell population, and this is demonstrated by the Dnam clock. epigenetic aging is not affected by growth or maturity. these epigenetically aged cells have been shown to be dysfunctional by partial reprogramming researchers and these cells are shown to be rejuvenated by partial reprogramming. These epigenetically aged are dysfunctional, but they are not harmful at least during the growth phase,because the body does not eliminate them and allows them to increase their population. These cells progress to senescence, but in a young and growing environment the immune system eliminates them, but in the aged body it becomes increasing difficult for the immune system to eliminate.

[sholay75]

https://www.nature.c...s2602/figures/4

Yes you can see support for that in the Figure 4 from my second reference. More progenitors/amplifying cell replication from the same size stem cell pool means shorter telomeres, so having longer telomeres would allow them to divide for longer before having to go back to the pool (See attachement; apologies can't paste it in the text as I'm away from my computer).

Our positions on what causes aging don't seem to be far apart. Unfortunately they are sufficiently far apart to recommend different interventions.

Let's look at your results. You initially lowered you epigenetic age - presumably it's highly malleable if your cells are turning over rapidly, which you'd expect with short telomeres. Then you took a telomerase activator and your epigenetic age rose because those cells were being replaced from the stem cell pool less often. But have you actually shortened your life? Doubtful, as your stem cells will have been used less and hence you'll have more in reserve.

You then went back to your protocol without telomerase activators and saw the epigenetic age fall. So you were back to using up more stem cells.

How do you know you won't run out?

Is there any study which shows less used stem cells will increase their reserve

[sholay75]

Is there any study which shows increasing the stem cell pool reverses epigenetic aging, because according to this study epigenetic ageing is not affected by replicative senescence, telomere length, somatic cell differentiation, cellular proliferation rate or frequency.

[Kentavr]

I read it all, and no one wrote about MicroRNA!
Why do not you take their expression as a true measure of age?
I really have little time now to give arguments. However, I read that 60% of all gene expression is controlled precisely by MicroRNA

[Turnbuckle]

I believe that stem cells are an important aspect of aging, and that‘s what makes me interested in this protocol. I do however wonder if this is working as good as it is supposed to. Is it really feasible for people to wait until their 50’s to start anti-aging? If a person doesn’t “age enough” according to this theory before then, is it possible it’s not even accurate? I mean we start aging well before 50, so a good method should theoretically work once the body passes its peak in the late 20’s/early 30’s. If you don’t lose enough stem cells by your 50’s for you to be old enough to reverse aging, then it sounds as if it’s just a minor effect of aging and certainly not it’s cause.

I also read this article:

https://joshmitteldo...-and-downgrade/

The above article’s comments seem pretty convincing in disproving the idea that a lower epigenetic age is a sign of successful anti-aging methods.

“What if epigenetic age is just a measure of time since a somatic cell line was spawned from it’s stem cell progenitor (which by definition will be younger epigenetically)? That means older people would naturally have an older epigenetic age because their stem cells are less active and somatic cells are replaced less often. It also means an individual with sightly more telomerase (and longer telomeres) would naturally have longer lasting somatic cells, so at any given time their tissues would be older epigenetically because they are also replaced less often. If this is true it means there are two separate but easily confused correlations: older people having less often replaced somatic cells due to tired stem cells, and people who have longer telomeres needing replacement less often (but probably with better preserved stem cells as a result).”

Turnbuckle received a lower epigenetic age on his test results, but is it possible that he actually biologically got older?

I think that the only real way to prove if any protocol is working is by serving before and after pictures from a user, showing that their aging has been either reversed or halted. You can feel 25 after a particular protocol, but if one looked 70 last year and doesn‘t look any younger this year, then I suspect that the protocol isn’t working as well as the think. I know that it’s possible that anti-aging may work on the “inside” but not the “outside”, but then we need to wait years and see if the person reaches 120 years (the supposed limit of how long a human can ultimately live) and even passes it, besides I suspect that most of us care just as much about our external appearance when it comes to aging interventions.

 

In your link, Mitteldorf says: Telomerase promotes epigenetic aging, while lack of telomerase promotes cellular senescence.  “If the ’gaitors don’t getcha then the ’skeeters will.”

 

Rather flip on his part, and the last bit is wrong. As I've been pointing out for some time, telomere shortening is not a cause of aging. It's an expiration date. You want telomerically old cells to become senescent so you can get rid of them, as those cells are generally epigenetically old as well. When you replace them with young cells, you get a net age reversal. As for other evidence that this protocol is working, I've posted my observations before. For instance, pain in both knees and joint instability in one knee that had troubled me for years faded and disappeared in a couple of months, as did a needle-like pain in one patella when kneeling. Tighter and smoother skin and disappearance of all age wrinkles most broken capillaries on face. A skin pinch test (time to recovery after pulling up neck skin with two fingers) went from 3 seconds to 1. Greater muscle mass and less fat, greater stamina. My formerly flat feet developed a noticeable arch. Tenosynovitis in one palm disappeared. A distortion I'd seen in the Amsler grid that had remained stable for approximately 15 years also disappeared. People who haven't seen me in a while are shocked.

[kurt9]

Turnbuckle,

 

You have two protocols. One is the senolytic protocol with stem-cell replacement. The other is stem-cell self-renewal with mitochondrial biogenesis. Correct me if I'm wrong. But it is my impression that both of these should be done in conjunction with each other. The first protocol is going to require the second protocol in order to restore the reproductive fitness of the stem-cells in question. Is this correct? Both of these appear to be daily protocols. Do you do them everyday for, say, a week or two weeks? Or do you do them, say, 2-3 days per week for a number of weeks?

 

I am currently not in a situation where I need them. I might try them maybe 5 years down the road, assuming you have not superseded them with something new. I do plan on trying your mito fission/fusion one early next year.

 

It would seem to me that anyone wanting to do the previous afforemented protocols ought to do the mito fission/fusion protocol first. Then do the other two as needed. I think this as I have a bias towards mitochondrial theories of aging over others.

[dlewis1453]

Turnbuckle,

 

You have two protocols. One is the senolytic protocol with stem-cell replacement. The other is stem-cell self-renewal with mitochondrial biogenesis. Correct me if I'm wrong. But it is my impression that both of these should be done in conjunction with each other. The first protocol is going to require the second protocol in order to restore the reproductive fitness of the stem-cells in question. Is this correct? Both of these appear to be daily protocols. Do you do them everyday for, say, a week or two weeks? Or do you do them, say, 2-3 days per week for a number of weeks?

 

I am currently not in a situation where I need them. I might try them maybe 5 years down the road, assuming you have not superseded them with something new. I do plan on trying your mito fission/fusion one early next year.

 

It would seem to me that anyone wanting to do the previous afforemented protocols ought to do the mito fission/fusion protocol first. Then do the other two as needed. I think this as I have a bias towards mitochondrial theories of aging over others.

 

 

Hi Kurt, 

 

You are confusing the protocols.

 

There is:

(1) the mitochondria protocol and,

(2) the stem cell protocol, of which there are two sub-protocols that accompany the main stem cell protocol, these are

          (a) the senolytic protocol, and

          (b) the muscle satellite cell protocol

 

Both (a) senolytic protocol and (b) muscle satellite cell protocol can be found within this thread. The senolytic protocol is an integral part of the overall stem cell protocol if you want to get maximum age reversal. The muscle satellite cell protocol is  separate from the main stem cell protocol and is meant for people who want to increase their fitness or muscle mass. 

 

The mitochondria protocol and the stem cell protocol should not be done simultaneously, as they may interfere with each other. You should do the mitochondria protocol first until you no longer feel much effect from it. Once you don't feel much during the fission phase, that is a sign that your mitochondria have been repaired and are now healthy and they will only need occasional small repairs going forward. 

 

Once you have finished the mitochondria protocol, you can move on to the stem cell protocol. You can find a link to the latest version of the stem cell protocol on Turnbuckle's profile page. Turnbuckle explains all the dosing details on that post if you follow the link. In general, assuming you are aged, and based on what I have read here, I believe the best practice is to do the stem cell protocol at most once a week at the beginning while you get the initial quick results , but you should not do it at that rate forever. After you have gotten some good results, you can slow down and do it intermittently going forward. I recommend you go back and reread the past 8 pages or so of this thread to get a good grasp of the latest information. 

[Nate-2004]

Turnbuckle which stearic acid are you using these days?

[Andey]

Tighter and smoother skin and disappearance of all age wrinkles most broken capillaries on face.

 

  Is it fair to say that your skin became thicker and that moved broken capillaries from being visible near the surface to deeper layers?

I think general consensus in dermatology is that broken capillaries dont go away by their own (and strictly speaking they are working just fine, only widened, body doesnt care)

Same thing with wrinkles, once they are etched its the new structure of a cellular matrix  and there is no mechanism to 'fix' it as its now a new normal for the body. 

 

I ve noticed my facial skin thickness increased, hided some broken capillaries, tightened up the skin and wrinkles are less visible but they are still there. My wrinkles are mimic ones so when I wake up they are barely there but at the end of a day if I laugh or talk too much, they became very visible.

[Vivian]

Hi Vivian, 

 

Go here to see Turnbuckle's senescent cell clearance protocol: https://www.longecit...ndpost&p=866728

 

The C60 effects you listed are very interesting. Were you suffering from hashimoto's thyroiditis by any chance? 

 

Since you have become mildly hyperthyroid while on your new reduced dose of thyroid medication, I'm cautiously optimistic that the protocol may have repaired damage to your thyroid. That would be incredible. 

 

Keep in mind that C60's mechanism of action is still speculative but can be boiled down to three main parts: (1) stem cell stimulation, (2) anti-oxidant/ anti-inflammatory, and (3) immunomodulatory.

 

Each effect appears to have a different duration in the human body.   The rejuvenation that results from the stimulation of stem cells is long lasting, while the anti-oxidant, anti-inflammatory, and immunomodulating effects are short term and eventually fade away after you stop consuming C60. For anti-aging purposes, the stem cell effect is the  most important, and this is paired with the senescent cell protocol to maximize age reversal. In your case, since it sounds like you suffer from inflammatory issues, effects 2 and 3 listed above may be most important for your current quality of life. This means that the senescent cell protocol may not be as important for you, and you may benefit from more frequent consumption of C60 than Turnbuckle. Turnbuckle appears to be using C60 exclusively for age reversal, which means he doesn't need to take C60 all that often once he has refilled his stem cell pools. By contrast, your inflammatory symptoms clearly return once you stop taking C60, so you may want to establish a regular intermittent dosing protocol of C60, while occasionally refilling your stem cell pools with Turnbuckle's protocol. Current best practice is to take C60 intermittently, rather than everyday. If at some point you want to pursue age reversal more aggressively, then you could add in the senescent cell protocol. 

 

Also, please bear in mind that none of the above is "medical advice." 

 

I hope this helps!

 

Thanks for this!

Yes, I have Hashimoto's.  I'm due for another TSH test in mid-September.  Previously I was on 150mcg Synthroid.  After C60, I'm taking less than 100mcg per day....

Inflammation has always been a big issue for me.  The glands in my neck have been swollen my whole life.  Doctors always commented on it, but never had any remedy or advice.

 

On Aug 5th I completed 3 cycles of Turnbuckle's SC renewal protocol. 

 

I'm on a break now, still a little uncertain about how I'm going to proceed RE the C60.....

In the meantime, I'm sitting here with a lot of supplements left over from the SC renewal protocol.  I feel like some of these supplements (maybe all?) were helping me to feel stronger and healthier, but hard to know which ones, because I introduced them all at the same time.  My strength seems to be slowly waning.

 

My new question is:  Which of these supplements are advisable to continue to take outside the renewal protocol?  I won't be taking c60 nor Stearic acid.

But what about the glutathione, threonine, Taurine, Methionine, lysine, sulforaphane, PQQ, SAM-e, Reveratrol, curcumin. apigenin, butyrate, quercetin, leucine. 

 

Are any or all of these healthy to take daily?

 

Do I need to separate any of these supplements from each other? Like are there supplements here that should not be taken together in the same day? 

 

Are the dosages in the SC protocol the same as what I should take outside of the protocol? 

 

Thanks for any thoughts on this!

Vivian

 

 

 

 

 

 

 

[Turnbuckle]

Vivian, this SC protocol is good for epigenetic age regression, but not for treatment of autoimmune disorders. Stem cells treatments have been considered for autoimmune situations, but they are complicated and dangerous, involving destruction of endogenous stem cells responsible for the immune response and replacement with fresh stem cells via autologous transplant. Thus I wouldn't expect stimulating endogenous SCs to be helpful, and since you discontinued it, it must not have been. However, since inflammation plays a part in the disease, liposomal glutathione ought to be helpful.

Edited by Turnbuckle, 26 August 2019 - 09:01 PM.

[Vivian]

Vivian, this SC protocol is good for epigenetic age regression, but not for treatment of autoimmune disorders. Stem cells treatments have been considered for autoimmune situations, but they are complicated and dangerous, involving destruction of endogenous stem cells responsible for the immune response and replacement with fresh stem cells via autologous transplant. Thus I wouldn't expect stimulating endogenous SCs to be helpful, and since you discontinued it, it must not have been. However, since inflammation plays a part in the disease, liposomal glutathione ought to be helpful.

 

Thank you!  I appreciate all your contributions on this site. 

V

[lost69]

hi vivian

 

i have subclinical hypothyroidm not autoimmune or supposed not because all antibodies always negative, due to peginterferon treatment.no symptoms and i felt bad on t4 and t3 medications so i don t take them

 

it is not exactly like yours but i have response from something normalizing tsh from 9 to 5 when i did stemcell protocol (i also did infrared light at that time so still not 100% sure it was stemcellprotocol to repair), when i stopped stemcells protocol tsh went back to 9.i only had ft4 low normal range but this time despite tsh 9 ft4 stayed well within normal range

 

c60 never had any effect on my thyroid, are you sure it is c60 to have effects on your thyroid?

Thanks for this!

Yes, I have Hashimoto's.  I'm due for another TSH test in mid-September.  Previously I was on 150mcg Synthroid.  After C60, I'm taking less than 100mcg per day....

Inflammation has always been a big issue for me.  The glands in my neck have been swollen my whole life.  Doctors always commented on it, but never had any remedy or advice.

 

On Aug 5th I completed 3 cycles of Turnbuckle's SC renewal protocol. 

 

I'm on a break now, still a little uncertain about how I'm going to proceed RE the C60.....

In the meantime, I'm sitting here with a lot of supplements left over from the SC renewal protocol.  I feel like some of these supplements (maybe all?) were helping me to feel stronger and healthier, but hard to know which ones, because I introduced them all at the same time.  My strength seems to be slowly waning.

 

My new question is:  Which of these supplements are advisable to continue to take outside the renewal protocol?  I won't be taking c60 nor Stearic acid.

But what about the glutathione, threonine, Taurine, Methionine, lysine, sulforaphane, PQQ, SAM-e, Reveratrol, curcumin. apigenin, butyrate, quercetin, leucine. 

 

Are any or all of these healthy to take daily?

 

Do I need to separate any of these supplements from each other? Like are there supplements here that should not be taken together in the same day? 

 

Are the dosages in the SC protocol the same as what I should take outside of the protocol? 

 

Thanks for any thoughts on this!

Vivian

 

[lost69]

Turnbuckle

i ve had a new development after the new round of stemcells renewal, i also take gdf11 and this substance works on very very low dose and if the dose is more than you need you get opposite results on hrv, rmssd, pulse, BP, reactive times and so on......after this second round of stemcell renewal all paramenters except BP have worsen to lower than baseline years ago especially rmssd reached values of 13-16 and hrv as low as 30 and so on.

muscles are also decreasing, excess gdf11 acts as myostatin (very similar and can share receptors when gdf11 is overdosed) and can worsen cardiac function and muscles, now i stopped gdf11 15days and parameters are slowly rising, this would be incredible if your portocol can rise gdf11 inside platelets again and make them work similar to stemcells on repairs

 

shall i also use your protocol for stemcells in muscles to balance excess myostatin?

 

i am also having a very hard time to gain weight (176cm 67kg) even eating a lot of carbs, cookies, sweets the weight does not move and if i swimm too much i risk going to 65-66kg my weight when a teen, the face does not look sagging but it would be ideal to gain some brown fat there, have you checked anyway to increase brownfat?did you also experience these problems with lowering weight?

Edited by lost69, 29 August 2019 - 12:06 PM.

[Turnbuckle]

Turnbuckle

i ve had a new development after the new round of stemcells renewal, i also take gdf11 and this substance works on very very low dose and if the dose is more than you need you get opposite results on hrv, rmssd, pulse, BP, reactive times and so on......after this second round of stemcell renewal all paramenters except BP have worsen to lower than baseline years ago especially rmssd reached values of 13-16 and hrv as low as 30 and so on.

muscles are also decreasing, excess gdf11 acts as myostatin (very similar and can share receptors when gdf11 is overdosed) and can worsen cardiac function and muscles, now i stopped gdf11 15days and parameters are slowly rising, this would be incredible if your portocol can rise gdf11 inside platelets again and make them work similar to stemcells on repairs

 

shall i also use your protocol for stemcells in muscles to balance excess myostatin?

 

i am also having a very hard time to gain weight (176cm 67kg) even eating a lot of carbs, cookies, sweets the weight does not move and if i swimm too much i risk going to 65-66kg my weight when a teen, the face does not look sagging but it would be ideal to gain some brown fat there, have you checked anyway to increase brownfat?did you also experience these problems with lowering weight?

 

 

One thing is obvious: gdf11 is a bad idea. As for being unable to gain weight, that may also be due to gdf11--

 

Exogenous GDF11 Induces Cardiac and Skeletal Muscle Dysfunction and Wasting

By day 9, body weights of GDF11 mice were significantly reduced compared to the control mice; this difference was even greater at day 13 

https://www.ncbi.nlm...les/PMC5833306/

 

 

The following paper suggests that gdf11 increases differentiation and apoptosis of stem cells (neither of which you want), and that blocking gdf11 might be a better idea.

 

Taken together, our current findings implied that GDF11 might be a potential target for pharmacologic blockade instead of a rejuvenated factor for neural stem cells.

https://www.ncbi.nlm...les/PMC6128255/

 

[lost69]

One thing is obvious: gdf11 is a bad idea. As for being unable to gain weight, that may also be due to gdf11--

 

 

The following paper suggests that gdf11 increases differentiation and apoptosis of stem cells (neither of which you want), and that blocking gdf11 might be a better idea.

 

i'll definitely stop gdf11, its rejuvenating effects are only on the 0.05ng per week dosing but even this is too much for me now.

i ve also tried some nmn for 2.5 months but i don t think this is the reason of what happened, it did increase reactive C protein from 0.1 to 0.6 (inflammation from senescence cells probably).what would it best now keep stemcells renewal and senescence protocol combined with your protocol for muscles stemcells or using some nmn to repair damage on muscles due to myostatin?

 

appart from the readings i feel great, full of energy and eye sight keeps improving to the point i can avoid reading glasses complitely, i just keep them using PC because they filter blue light

 

thank you very much for your help
 

[dlewis1453]

i'll definitely stop gdf11, its rejuvenating effects are only on the 0.05ng per week dosing but even this is too much for me now.

i ve also tried some nmn for 2.5 months but i don t think this is the reason of what happened, it did increase reactive C protein from 0.1 to 0.6 (inflammation from senescence cells probably).what would it best now keep stemcells renewal and senescence protocol combined with your protocol for muscles stemcells or using some nmn to repair damage on muscles due to myostatin?

 

appart from the readings i feel great, full of energy and eye sight keeps improving to the point i can avoid reading glasses complitely, i just keep them using PC because they filter blue light

 

thank you very much for your help
 

 

Hi Lost,

 

You might consider discontinuing most supplementation for a couple weeks or so and see where you stabilize. You may be having several interactions. For example, interactions between c60 and nmn, interactions between c60 and gdf11,  and interactions between gdf11 and nmn. Based on anecdotal reports from multiple people, boosting NAD+ levels with supplementation while on gdf11 can cause blood pressure to increase. Boosting NAD+ levels while on C60 can cause side effects as documented here on Longecity. Supplementing C60 and GDF11 at the same time may have side effects since both compounds have a strong effect on stem cells.

[lost69]

Hi Lost,

 

You might consider discontinuing most supplementation for a couple weeks or so and see where you stabilize. You may be having several interactions. For example, interactions between c60 and nmn, interactions between c60 and gdf11,  and interactions between gdf11 and nmn. Based on anecdotal reports from multiple people, boosting NAD+ levels with supplementation while on gdf11 can cause blood pressure to increase. Boosting NAD+ levels while on C60 can cause side effects as documented here on Longecity. Supplementing C60 and GDF11 at the same time may have side effects since both compounds have a strong effect on stem cells.

 

thanks, yes i stopped nmn also for more than 15 days.now im keeping only 9ml c60 once/twice a week or in the stemcell renwal protocol.i notice a decrease in vision sharpness stopping c60 complitely for long time and i also notice improvement at every stemcells cycle

 

i know i dint have interactions between gdf11, c60 and oral NR because i used them altogether in the past years and observed all changes knowing interactions between gdf11 and NR.i just had a huge boost in swimming performance when adding all of them and no BP, HRV interactions

 

but you are right now after stemcells renewal something might be different and also sublingual nmn might be different to nr and no  need to mix all this stuff
 

[granmasutensil]

 

An experimental protocol for stem cell proliferation and mito biogenesis (updated) —

 

 

 

1. This is a work in progress.

 

2. It is intended as a geriatric treatment, not for young people.

 

3. While this should be less sensitive to alcohol use than previously, one should still avoid alcohol the same day.

 

4. A prior protocol is at post #694. A link to the latest protocol can always be found on my profile page.

 

 

 

  

 

 

 

Stem cell self-renewal with mito biogenesis

 

This is where stem cell pools and mito numbers are expanded

 

 

 

Time 0 —

 

¹Stearic acid — 10 g (food grade, in brownie)

 

Liposomal glutathione — 1 g

 

 

 

  

 

Time 3:00 —

 

Threonine — 5 g

 

²Taurine — 5 g

 

³Methionine — 3 g

 

³Lysine — 2 g

 

⁴Leucine — 5 g

 

⁵Sulforaphane — 50 mg

 

PQQ — 20mg

 

Liposomal glutathione — 1 g

 

C60 — 3 mg (in oil)

 

SAM-e — 500 mg

 

 

 

 

 

 

 

Notes:

 

 

 

(1) Food grade stearic acid is a waxy triglyceride with about 50% stearic acid moieties. It has a high melting point and will have very poor availability unless properly prepared. Baking it into brownies is one option: Using a box mix that calls for 1/2 to 2/3 cups of oil, eliminate the oil and add 120 grams of stearic acid flakes or granules, leaving the rest of the recipe unchanged. Mix at room temp using a power mixer, bake according to directions on the box, then divide 3x4 and freeze most of it for later use.

 

 

 

(2) Taurine stimulates neurogenesis.

 

 

 

(3) Methionine is the primary nutrition for pluripotent cells, though threonine also seems necessary. So is lysine.

 

 

 

(4) Leucine stimulates both mito biogenesis and stem cell proliferation.

 

 

 

(5) Sulforaphane penetrates the BBB to produce mito fusion there, while stearic acid is blocked. 50 mg caps can be obtained from Amazon — Thorne Research - Crucera-SGS - Broccoli Seed Extract for Antioxidant Support - Sulforaphane Glucosinolate (SGS)

 

 

 

 

Turnbuckle are we going back to stearic acid instead of glyceryl stearate or was that a mistake?

 

Also as a side note about Leydig cells/testosterone brought up and Shh. Polygonum multiflorum/Fo-Ti also seems to up regulate Shh.

https://www.ncbi.nlm...pubmed/21419834

 

Werper also brought up Tadalafil increase the production of testosterone by Leydig cells by increasing cAMP. Forskolin increases cAMP.

https://www.ncbi.nlm...pubmed/22393824

 

 

[Turnbuckle]

Turnbuckle are we going back to stearic acid instead of glyceryl stearate or was that a mistake?

 

Also as a side note about Leydig cells/testosterone brought up and Shh. Polygonum multiflorum/Fo-Ti also seems to up regulate Shh.

https://www.ncbi.nlm...pubmed/21419834

 

Werper also brought up Tadalafil increase the production of testosterone by Leydig cells by increasing cAMP. Forskolin increases cAMP.

https://www.ncbi.nlm...pubmed/22393824

 

 

I never went away from stearic acid. As a source of stearic acid, food grade stearic acid triglyceride works very well, though it has to be done in two steps due to slow digestion. Glyceryl monostearate or distearate will be fine with many, probably, but the rise in fusion is so fast that it can spike blood pressure in some, especially with the monostearate. It's possible that adding oleic acid may control that-- https://www.ncbi.nlm...pubmed/18772370