2523 replies to this topic

[Turnbuckle]

Stem cell self-renewal

This is an update to post 1700.

  

Time 0 —

One brownie

 

Body and brain mito fusion brownies

For use with the Stem Cell protocol

 

Betty Crocker Fudge brownie mix* (519 g)

2 eggs

4-5 tbsp water

30 g (4 tbsp) Sunflower lecithin powder  

30 g (7 tbsp) Dihydromyricetin powder

120 g stearic acid

 

*Or any mix that requires ½ cup oil, but don’t use the oil. Diet versions don’t work well. More water may be used if necessary.

 

Mix with power mixer and bake as directed on the box. Cut into 12 brownies, dust with flour to avoid sticking, and freeze. The dihydromyricetin degrades the taste a bit, but freezing improves it. The lecithin is to make the dihydromyricetin more bioavailable and to supply phospholipids for new brain cell myelination.

Previously described in post 1648

 

 

 

Time 3:00 C60 stack (mito fusion) —

1. C60 — one teaspoon if in olive oil, 1.5-2 teaspoons if in MCT oil

2. Sunflower lecithin — 2-4 grams

3. Dihydromyricetin — 2-6 grams

4. Liposomal glutathione — .5-1 grams

5. AKG (alpha ketoglutarate) — 1 gram

6. AAKG  — 2-3 grams

7. SAM-e — 100-500 mg

8. Lysine — 2-6 grams

9. Methionine — 1-3 grams

 

Astragalus root powder, every 4th treatment — 500 mg

 

Next day (mito fission, may be repeated for 2 days) —

1. Nicotinamide — 1 gram

2. Ribose — 1-2 grams

3. AAKG  — 2-3 grams

4. Lysine — 2-6 grams

5. Methionine — 1-2 grams

 

Notes:

1. I generally add the stack to OJ along with a slug of olive oil, and blend it. I believe the olive oil will slow absorption of the C60 and remove any need to space it out from the other ingredients.

2. More lysine and methionine may be taken a couple of hours after the C60 stack.

3. Threonine (not listed) is optional. I have used 5-10g on occasion, so I can't say with certainty.

4. The second dose of dihydromyricetin may be unnecessary, as it is in the brownie. It degrades the taste of both the brownie and the stack, but is not that terrible.

5. The solubility of C60 in MCT oil is less than in olive oil, so I use more with MCT oil.

6. I use both AKG and AAKG to get short and long term action. The short action is more important with the C60 stack. AKG salts can also be used.

7. I've dispensed with sulforaphane, but it might be helpful for some people. 

8. Present schedule varies, but generally 1-2 times a week.

 

Caveats:

1. This is a work in progress.

2. It is intended as a geriatric treatment for age reversal.

3. One should avoid alcohol during this treatment.

4. A link to the latest protocol can always be found on my profile page.

5. All amounts are approximate and based on a 180 pound individual.

  

Results:

    Present epigenetic age (TruMe) is 28 years less than chronological. 

Edited by Turnbuckle, 21 March 2022 - 08:25 PM.

[yz69]

I do TruMe tests every month. I am 53, here are my last five TrueMe results: 38.7,  45.4,  43.3, 47.8, 41.2. I follow TB's protocol once a week, I can see lifestyle changes can affect the TruMe result a lot. After the 1st test, I did a lot of international travel, visited many cities on a tight schedule, when I was back home to do the second test, the trume result shoot up 6+ years. Then I managed to lower the Trume results with a no-so-busy normal schedule, then in January some shit happened in my life, had some sleepless nights, pretty stressful, and the test result shot up again. Then after February,  things settle down, stress level down, so is the Trume result.

 

I also do blood tests every 2 months. The biggest changes in my blood test are MCV and RDW, from 92/14.6 in 2019 to 90/13.2 now. Baseline TruMe test was 47.5 done in January 2020, before I tried TB's protocol.

 

BTW, according to Trume Labs' founder Yelena Budovskaya, if someone's test result is significantly lower then the chronological age, they will test again to double check.

 

Edited by yz69, 22 March 2022 - 12:04 AM.

[kurt9]

An update on my TruMe epigenetic age. It is now -28 years from my chronological age. I'm presently doing the protocol 1-2 times a week.

 

Congratulations! You made it past a full quarter century!

[DJSwarm]

Is there a special reason for the 5 gms of Lysine?  I find it difficult to take 2gms but will bear it, if needed.

 

Be careful taking too much Lysine to often. Had a friend with cold sores who found out the hard way too much long term high dose Lysine can damage your stomach and kidneys.

[DJSwarm]

You have to be judicious in using agents to lengthen telomeres, as you can easily end up blocking stem cell replacement of aging TACs, thus increasing epigenetic age rather than decreasing it. This has been discussed here several times. 

 

I think you may be looking at it reversed.

 

Just in general I don't continuously do any treatment. These are all experimental and the body handles acute insults way better than chronic ones and breaks give recovery time if I dip into body resources. I'm on a break right now after trying some of your recommendations.  

 

Senescent cells accumulate over time, constantly, and they are always a problem at our level. It seems extremely unlikely you could remove sufficient senescent cells that you end up with less than you had at say at age 20. Based on the rates of accumulation, my age, and a desire to not find side effects; I do an anti-senescent cell run about once a quarter. I tend to not do other things with the senolytics since they are working to trigger apoptosis. For example, NAC in particular seems to block them.

 

Lengthened telomers from Ep, so far, has resulted in longer lifespans and increased numbers of cell divisions without reported increases in cancer rates or other negative side effects. Since Astra/TA-65 works on short telomers but and increases health span but not lifespan (aka, cell division), it seems that lengthening of telomers in cancer may be a side effect instead of a cause. I.E., I'm not "blocking" replacing aging cells, I'm de-aging cells so they don't need to be replaced yet.

 

Improving Mito performance makes everything happier and then there is the whole mTOR effectors like rapamycin and berberine.

 

Of course it looks like if Yamanaka factors can be safely applied, that seems to result in full cell rejuvenation. Watching that closely.

 

BGE-175 (asapiprant) is pretty exciting if you didn't catch it:

 

New BioAge Drug Prevents Death From COVID-19 in Old Mice by Reversing Immune Aging

Oral drug that reverses immune aging effectively prevents death in COVID-19 mouse model

 

Nothing so far is a silver bullet. for example, we don't have a universal senolytic, each one misses certain cell lines.  So please, let me know if I'm missing a point of attack here.

 

Finally, you seem pretty knowledgeable on the testing aspects. I wouldn't mind your recommendations. You can send that directly if it is too off topic and in anticipation - Thanks!

[Turnbuckle]

I'm not "blocking" replacing aging cells, I'm de-aging cells so they don't need to be replaced yet.

 

 

 

When you reverse the telomeric clock, cells can get endlessly older epigenetically. So it's far better to replace them for maximum performance.

 

Most cells outside the brain are replaced 1 or more times during a lifetime. The turnover is enormous -- about a third of a trillion cells are replaced ever day. Some cells live only a couple of weeks, while most neurons and cells in the lens of the eye may last a lifetime. Here are a few examples --

 

Heart muscle cells: 40 years

Intestinal cells (excluding lining): 15.9 years

Skeletal muscle cells: 15.1 years

Fat cells: 8 years

Hematopoietic stem cells: 5 years

Liver cells: 10-16 months

Pancreas cells: 1 year

 

Skin cells and the cells of the intestinal lining live only a few weeks. The body has stem cell niches tucked away everywhere to replace them. But with time the niches become depleted (see the attached plot). Some niches may disappear forever, and the first to go are typically the very small ones that reside in individual hair roots. Aging is the failure of the body to keep this replacement process running at a youthful level. What you are promoting -- interfering with the telomeric clock -- allows epigenetically old and therefore dysfunctional cells to continue living and to continue to grow ever more dysfunctional. This may allow you to live longer, but only as an old person, not as a young one.

 

 

 

Improving Mito performance makes everything happier 

 

 

Take a look at my mitochondria protocol. 

Attached Files

•  Stem cell decline.png   423.94KB   1 downloads

[DJSwarm]

 

When you reverse the telomeric clock, cells can get endlessly older epigenetically. So it's far better to replace them for maximum performance.

 

[...]

 

Some niches may disappear forever, and the first to go are typically the very small ones that reside in individual hair roots. Aging is the failure of the body to keep this replacement process running at a youthful level. What you are promoting -- interfering with the telomeric clock -- allows epigenetically old and therefore dysfunctional cells to continue living and to continue to grow ever more dysfunctional. This may allow you to live longer, but only as an old person, not as a young one.

 

Take a look at my mitochondria protocol. 

 

 

"Age" at the cellular level is a misconception. They have, with the Yamanaka factors, shown that cells can completely rejuvenate back to pl. stem cells. This tracks with how cells in newborns are able to become fresh again as well and how bacteria and cancer cells behave as well. Our cells could clean up and preserve us until mechanical failure. Age seems to be imposed on eukaryotes at individual as an evolutionary tactic to speed up the process of replacement for the species and it seems that can be interrupted and reversed, to a degree at least. 

 

Consider, our cells have been continuously matralinearly alive for 3.5 billion years, just the same as all other life. The difference between us and bacteria is that we have generational breaks where our old colony is shead to form a new one again from a single cell. 

 

Also you are kinda playing both sides here. You can't call out senolytics burning out my stem cells replacing bad zombie cells; and then say, "it's far better to replace them for maximum performance" when I'm saving working, but older cells by telomere extension.

 

Seems like removing bad cells, which does burn some stem cells but alleviates all kinds of age related issues, and keeping working cells working, which preserves stem cells for those who need them more while also giving them a chance to de-age further; is a reasonable strategy. 

 

I've been enjoying watching your protocol evolve. I might eve try C60, though I'm still considering that one.

 

I was just reading an article on dihydromyricetin and how it can ameliorate alcoholism.  Dihydromyricetin As a Novel Anti-Alcohol Intoxication ... - NCBI

[Turnbuckle]

"Age" at the cellular level is a misconception. They have, with the Yamanaka factors, shown that cells can completely rejuvenate back to pl. stem cells. 

 

 

The 200 types of nucleated human cells are distinguished only by their epigenetic patterns, and epigenetic aging is the scrambling of the patterns so that a less than ideal mix of proteins is produced for a given cell type. An epigenetically old cell might be perfectly happy, but not the organ in which it resides. If you erase those old scrambled patterns with Yamanaka factors and allow cells to reprogram themselves with de novo methylation, then they will be young again, as will the organs in which they reside. The heavily funded Altos Labs is looking into this (along with many others) but as of today no protocol is available to the public. The protocol of this thread uses the body's own systems to do the job, tricking existing stem cells into proliferation to top up SC niches to a more youthful state, then allowing the body's own processes to take it from there (with a little mito fission help). All the ingredients are available to the public, so anyone can do this today.

Edited by Turnbuckle, 23 March 2022 - 10:18 AM.

[timedilation]

I wonder if photobiomodulation (low level light therapy) can be used to serve the same role as C60 in this protocol.  It is known to stimulate mitochondrial cytochrome c oxidase and ultimately increase ATP production.  It has also been shown to induce stem cell activity and produce wound healing.  Taken together, those facts seem to imply that LLLT could stimulate quiescent stem cells into activation, and then the other aspects of this protocol could push the activated stem cells into symmetric division. 

 

Here is a review article that suggests basically the same thing: https://www.ncbi.nlm...les/PMC5844808/

 

 

Due to the intense interest in possible therapeutic applications of stem cells, many investigators have asked how PBM and various light therapy interventions affect stem cell proliferation and differentiation. Although the exact mechanisms by which PBM can activate stem cells is not known, there are some theories. The first theory is that stimulation of the mitochondria leads to a switch from anaerobic glycolysis to oxidative phosphorylation. This switch acutely increases the demand for oxygen by the newly activated mitochondria. However in the hypoxic niche (that is characteristic of stem cells) the oxygen supply is strictly limited. When the cells suddenly require more oxygen they must leave their niche and go in search of a higher pO₂ level (107). Whether they then proliferate or differentiate is governed by the specific cues they encounter in their new environment.

 

This idea could provide a new route to stem proliferation that can be used in a much more targeted manner.  Those with chronic injuries could rebuild stem cell pools right around their most distressed areas without having to resort to systemic treatments.  Interested to hear more thoughts on this.

 

[Turnbuckle]

I wonder if photobiomodulation (low level light therapy) can be used to serve the same role as C60 in this protocol.  It is known to stimulate mitochondrial cytochrome c oxidase and ultimately increase ATP production.  It has also been shown to induce stem cell activity and produce wound healing.  Taken together, those facts seem to imply that LLLT could stimulate quiescent stem cells into activation, and then the other aspects of this protocol could push the activated stem cells into symmetric division. 

 

Here is a review article that suggests basically the same thing: https://www.ncbi.nlm...les/PMC5844808/

 

 

This idea could provide a new route to stem proliferation that can be used in a much more targeted manner.  Those with chronic injuries could rebuild stem cell pools right around their most distressed areas without having to resort to systemic treatments.  Interested to hear more thoughts on this.

 

 

Very unlikely, as the mitochondria of stem cells are rich with UCP2 pores that allow H⁺ ions to pass freely without doing work. Light of specific frequencies would thus increase the ATP production of normal cells, but not of stem cells.

[timedilation]

Hmm, then I guess the question would be, how do stem cells normally deactivate UCP2 in the course of natural replication and can PBM reproduce this phenomenon?  Cytochrome c oxidase itself pumps protons across the mitochondrial membrane, so it seems plausible that there could be mechanisms linking it to UCP function.  Given the many documented effects of LLLT on wound healing and recovery, it would be strange if it didn't affect stem cell activity.  But perhaps the effects on somatic cells are simply strong enough to compensate

Edited by timedilation, 24 March 2022 - 06:19 PM.

[Turnbuckle]

Hmm, then I guess the question would be, how do stem cells normally deactivate UCP2 in the course of natural replication and can PBM reproduce this phenomenon?  Cytochrome c oxidase itself pumps protons across the mitochondrial membrane, so it seems plausible that there could be mechanisms linking it to UCP function.  Given the many documented effects of LLLT on wound healing and recovery, it would be strange if it didn't affect stem cell activity.  But perhaps the effects on somatic cells are simply strong enough to compensate

 

UCP2s are heavily expressed in stem cells --

 

UCP2 is expressed in hPSCs and repressed during differentiation

 

To identify a mechanism(s) controlling the unique mitochondrial metabolism of hPSCs, we re‐analysed three expression profiling studies to search for metabolism‐regulating genes that were differentially expressed between hPSCs and differentiated cells. Two studies compared gene expression between hPSCs and fibroblasts (Lowry et al, 2008; Maherali et al, 2008) and a third study evaluated gene expression with hESC differentiation to embryoid bodies (EBs) and cardiomyocytes (Cao et al, 2008). Notably, UCP2 expression was 5‐ to 10‐fold higher in hPSCs than in human fibroblasts

 

https://www.ncbi.nlm...les/PMC3243621/

 

 

 

Clearly a variety of chemical signals can activate SCs, and they must funnel into a common signal to alter UCP2 production. But how, exactly, I don't know. I haven't seen it in the literature. C60 seems to work by a backdoor, going directly to the pores and blocking them.

 

Stem cells aren't  involved in wound healing to nearly the degree that TACs are, though TACs can stimulate SC activity by secreting the Sonic Hedgehog (SHH) protein, and SCs can secrete signals to attract other types of cells. TACs derive from SCs and do most of the work of replication.

 

Early on, it was observed that TACs were ephemeral; they divided faster and differentiated rapidly, while SCs were almost nonproliferative in steady-state conditions [11, 15]. Indeed, SCs from adult organisms replicate very slow, as in mice where hematopoietic SCs (HSCs) replicate once every 2.5 weeks [47] or in humans where HSCs replicate every 10 months [48]. During development, SCs proliferate faster while serving as the source of cells for new organs and tissues. However, as organisms mature, SCs divide less and less, moving towards a quiescent state, which may be related to avoiding premature exhaustion and minimizing mutational events [5]. This behavior is critical for therapeutic cell transplants since low proliferation rates may limit tissue repair. In contrast, TACs are highly proliferative making cell cycle dynamics one of the main differences between SCs and TACs.

 

 

And --

 

Essential knowledge about how TACs are regulated come from studies in mammals on the hair follicle (HF). The HF is a particularly useful system in which to study SCs and their progeny since hair growth is fueled by SCs during development, and in adults, the HFs continuously regenerate in alternate cycles of growth (anagen), destruction (catagen), and quiescence (telogen) [29]. Furthermore, mouse HFs are an ideal system to explore possible interactions and regulation between SC and TAC populations. The TACs associated with HFs are located surrounding the dermal papilla (DP) at the base of the HF; these TACs are embedded in matrix cells that enclose the DP. The DP is a specialized niche compartment, and their signals (such as TGFB2 and FGF7) have a strong influence in regulating TAC proliferation, migration, and differentiation. At the same time, TAC signals have a role in SC regulation. For example, the TAC-secreted ligand Sonic Hedgehog (SHH) induces quiescent SCs at the HF bulge, to proliferate [8], hence promoting the anagen hair growth phase.

https://www.thefreel......-a0555409880

 

Bottom line, PBM ought to stimulate TACs, and there might be some back-signaling to SCs, and thus some indirect effect. Whether that would be enough to significantly lower epigenetic age is another question. Certainly it would likely be more effective in superficial tissues.

Edited by Turnbuckle, 24 March 2022 - 10:14 PM.

[DJSwarm]

The 200 types of nucleated human cells are distinguished only by their epigenetic patterns, and epigenetic aging is the scrambling of the patterns so that a less than ideal mix of proteins is produced for a given cell type. An epigenetically old cell might be perfectly happy, but not the organ in which it resides. If you erase those old scrambled patterns with Yamanaka factors and allow cells to reprogram themselves with de novo methylation, then they will be young again, as will the organs in which they reside. The heavily funded Altos Labs is looking into this (along with many others) but as of today no protocol is available to the public. The protocol of this thread uses the body's own systems to do the job, tricking existing stem cells into proliferation to top up SC niches to a more youthful state, then allowing the body's own processes to take it from there (with a little mito fission help). All the ingredients are available to the public, so anyone can do this today.

 

None of which makes me think that I should hold on to senescent cells, or, that rescuing old but functional cells is a bad idea (every extra division is a SC not used). The telomere studies have had both improvement to health span (ast. / TA65) and increased health and life span (epitalon). I quite agree that refreshing mito and replenishing SCs is also good, but without removing senescent cells you're still subject to their inflammatory and procancer factors. No matter how nice your mito are, if you runout of telomeres, the cell dies or goes senescent. And of course there is whatever mTOR1 (rapamycin) inhibition is doing.

 

Nothing yet is catching everything. Even the "well tested" stuff is mainly still in mouse or early human trails. (Except for rapamycin and dasatinib.)  This is why I go with intermittent runs and rotate through various protocols based on what studies I find. On the other hand, a lot of this stuff is already known to be GRAS in its previous suppliment life and they have pretty nice safety profiles (like fisetin). 

 

So far my strategy seems to be producing reasonable results within my risk tolerance. I must admit I'm suspicious of "maximum" performance when I don't know what the real limits are.

[DJSwarm]

Very unlikely, as the mitochondria of stem cells are rich with UCP2 pores that allow H⁺ ions to pass freely without doing work. Light of specific frequencies would thus increase the ATP production of normal cells, but not of stem cells.

 

Specifically there seems to be some evidence that FIR - NIR light at 1000-600 ish nm is able to stimulate cells (670-580 nm normal red diode) in the retina, improving visual performance (but strangely this effect happens only if you do it first thing in the morning upon waking. Other times did not produce the effect.) These frequencies can penetrate bone and there is a Dr. in England who is using this to treat Alzheimer's, also mentioned in places are skin rejuv and reducing baldness. Near Infrared (NIR) Light Therapy of Eye Diseases: A Review Low-level light therapy of the eye and brain

[eigenber]

Has this article been evaluated yet. I may have missed it but didn't find mention of it on this thread. 

C60 in olive oil causes light-dependent toxicity and does not extend lifespan in mice

https://link.springe...357-020-00292-z

[Danniel]

SAM-e is included to make sure there are enough methyl groups available. Epigenetic age is not based on too many or too few methyl groups per se, but in those methyl groups being in the right place. Thus the protocol supplies a promoter of demethylase to clean up aberrant methylation, and a methyl source to provide the raw materials for establishing the epigenetic code. The cells do these things in the right order on their own, given the proper raw materials.

Would it be possible to replace SAMe with a different methyl donor? Would Methionine be a good candidate?

 

Does anyone know a good source for Dihydromyricetin in Europe (Germany)?

Also, what would be a decent replacement?

[Kentavr]

Would it be possible to replace SAMe with a different methyl donor? Would Methionine be a good candidate?

Does anyone know a good source for Dihydromyricetin in Europe (Germany)?
Also, what would be a decent replacement?

The amino acid methionine is negatively correlated with lifespan in animal models.

I suspect that all amino acids containing sulfur are somehow capable of shortening a person's lifespan. But, unfortunately, I do not have conclusive evidence on this issue.

[Turnbuckle]

The amino acid methionine is negatively correlated with lifespan in animal models.

I suspect that all amino acids containing sulfur are somehow capable of shortening a person's lifespan. But, unfortunately, I do not have conclusive evidence on this issue.

 

 

The mystery is why an anti-oxidant like methionine would shorten lifespan, and I think the answer is in its up-ticking stem cell activity. If you use up stem cells when you are younger, you will run out of them at an earlier age. This is thus the basis of the calorie and methionine restriction ideas for living longer. But it's not necessary (and actually counterproductive) when used with this protocol, where we are expanding SC pools.

 

That methionine can increase SC activity is shown below--

 

The intestinal epithelium is derived from intestinal stem cells (ISCs) and has direct contact with nutrients and toxins. However, whether methionine (Met) or a methionine hydroxyl analogue (2-hydroxy-4-(methylthio)butanoic acid (HMB)) can alleviate deoxynivalenol (DON)-induced intestinal injury remains unknown...our findings reveal that Met and HMB alleviated DON-induced intestinal injury by improving ISC expansion...

https://pubmed.ncbi....h.gov/31532211/

 

[stephen_b]

I just got my second TruMe report back.

 

First test date 2021-08-04

Biological age: 40.7 years

Chronological age: 57.5 years

Delta: 16.8 years

 

Second test date 2022-03-06

Biological age: 37.8 years

Chronological age: 58.1 years

Delta: 20.3 years

 

I started the stem cell protocol rounds on 2020-09-04. I did 11 rounds before my first test and 8 rounds between the 1st and 2nd tests. I kept up with the protocol updates along the way.

[FWP]

Does anyone know a good source for Dihydromyricetin in Europe (Germany)?

https://cerebra-noot...hydromyricetin/

[QuestforLife]

Does anyone know a good source for Dihydromyricetin in Europe (Germany)?

https://cerebra-noot...hydromyricetin/

 

Would someone remind me what the rationale is for inclusion of myricetin to the protocol (doesn't have to be Turnbuckle)

 

Cheers

[JamesPaul]

 

4. Liposomal glutathione — .5-1 grams

 

You're sure that's not too much?  Dr. Brad Stanfield posted a video containing a caution about liposomal glutathione.

 

“NAC (& Glutathione) Crucial New Research,” Dr. Brad Steinfeld, Nov 21, 2021 

https://www.youtube....h?v=rdOJa5J6eoM

“The last thing we want to do is boost the glutathione levels in the brain, because the brain simply doesn't need it”.  Paraphrasing, he said liposomal glutathione can build up to toxic levels. It bypasses the liver's detox mechanisms.

 

His caution applies only to the liposomal form.  His comment may apply only to regular ongoing consumption.  Because I don't know, I thought I'd post this question.

[JamesPaul]

Would someone remind me what the rationale is for inclusion of myricetin to the protocol (doesn't have to be Turnbuckle)

 

Cheers

 

Turnbuckle posted the following in post 1619:

 

“Three mito fusion promoters are used for maximum effect. Unlike stearic acid (from GMS), dihydromyricetin and sulforaphane can penetrate the blood brain barrier. Dihydromyricetin is much longer acting than sulforaphane.”

 

Post 1619 is here:

 

https://www.longecit...ndpost&p=909987

[QuestforLife]

I just got my second TruMe report back.

 

First test date 2021-08-04

Biological age: 40.7 years

Chronological age: 57.5 years

Delta: 16.8 years

 

Second test date 2022-03-06

Biological age: 37.8 years

Chronological age: 58.1 years

Delta: 20.3 years

 

I started the stem cell protocol rounds on 2020-09-04. I did 11 rounds before my first test and 8 rounds between the 1st and 2nd tests. I kept up with the protocol updates along the way.

 

It's good to see another person (other than Turnbuckle) with a very significant delta.

 

What we really need now is validation of the epigenetic/methylation age measure against 'real' physical biomarkers. Is this just a 'paper exercise' where the biomarker is reversed to a youthful level but the person is unchanged? Or is this a genuine age reversal?

 

Do you habitually monitor anything like heart rate variability, blood pressure, heart rate, etc...? If so we could start to build a correlation with epigenetic/methylation age.

Edited by QuestforLife, 01 April 2022 - 02:14 PM.

[Turnbuckle]

It's good to see another person (other than Turnbuckle) with a very significant delta.

 

What we really need now is validation of the epigenetic/methylation age measure against 'real' physical biomarkers. Is this just a 'paper exercise' where the biomarker is reversed to a youthful level but the person is unchanged? Or is this a genuine age reversal?

 

Do you habitually monitor anything like heart rate variability, blood pressure, heart rate, etc...? If so we could start to build a correlation with epigenetic/methylation age.

 

 

The positive health effects of C60 were quite evident in the first rat experiments by the Moussa group. The treated rats were healthier all along and lived 90% longer than the controls. Unfortunately, the researchers ascribed the remarkable benefits to the anti-oxidant properties of C60, and thus missed an uncontrolled variable. So when the Moody group (funded in part by Longecity) tried to reproduce it, they failed. The uncontrolled variable was mitochondrial morphology -- in particular, mito fusion, which is necessary for stem cell proliferation, and ultimately for epigenetic age reversal.

[Danniel]

Turnbuckle posted the following in post 1619:

 

“Three mito fusion promoters are used for maximum effect. Unlike stearic acid (from GMS), dihydromyricetin and sulforaphane can penetrate the blood brain barrier. Dihydromyricetin is much longer acting than sulforaphane.”

 

Post 1619 is here:

 

https://www.longecit...ndpost&p=909987

 

Then why drop the sulforaphane? Could Dyhidromyricetin be replaced with two pills of Sulforaphane taken a few hours apart?
 

[QuestforLife]

The positive health effects of C60 were quite evident in the first rat experiments by the Moussa group. The treated rats were healthier all along and lived 90% longer than the controls. Unfortunately, the researchers ascribed the remarkable benefits to the anti-oxidant properties of C60, and thus missed an uncontrolled variable. So when the Moody group (funded in part by Longecity) tried to reproduce it, they failed. The uncontrolled variable was mitochondrial morphology -- in particular, mito fusion, which is necessary for stem cell proliferation, and ultimately for epigenetic age reversal.

I'd agree it is a strange omission - feeding ad libitum rather than overnight fasted before dosing, but then the Baati study was ad hoc, dosing C60 daily, then weekly, then every other week, then not at all! It's a miracle they discovered the life span effect and it's not surprising replication failed.

The 'replication' study also used mice, not rats.

But I think you're right, for the full C60 benefits, fasting is required - and in humans anything but a prolonged fast would be ineffective (because of our slower metabolism relative to rats), hence the necessity of your mito-fusion additions.

All that being said, I'd still like some independent (of methylation test) verification of the protocol.

Edited by QuestforLife, 01 April 2022 - 05:25 PM.

[Turnbuckle]

The difference between rodent and human metabolism (about a factor of 6) many have ruined many other drug studies as well, in which mito morphology was an unrecognized factor.

Edited by Turnbuckle, 01 April 2022 - 05:35 PM.

[Kentavr]

The difference between rodent and human metabolism (about a factor of 6) many have ruined many other drug studies as well, in which mito morphology was an unrecognized factor.

Do you plan to do a detailed blood test?
It is very interesting to know what exactly has changed in your analyzes and by what amount.

[Paravani]

Does anyone know a good source for Dihydromyricetin in Europe (Germany)?

https://cerebra-noot...hydromyricetin/

 

If you can't find Dihydromyricetin, look for "Hovenia Dulcis Extract" or "Ampelopsis grossendentata extract".  

 

A rose by any other name...