2523 replies to this topic

[Turnbuckle]

 

Even TB doesn't know what the most important elements are!

 

 

 

Nonsense.

 

Fusion and stem cell stimulation are equally important, as one does not work without the other. Fusion should occur before stem cell stimulation, and that doesn't have to be by much. GMS or DHM, adequately blended, appear to be more readily absorbed than C60/EVOO, and thus can be taken at the same time. A demethylase promoter almost doubles the results. AKG, again taken with the others, seems adequate for this purpose. Subsequently you can allow these new stem cells to be used as needed, or force things by using senolytics with fission to get rid of old cells faster.

 

There aren't "too many moving parts," as you claim.

Edited by Turnbuckle, 05 September 2022 - 03:03 PM.

[Turnbuckle]

"For C60, 50% of the animals live longer than the controls, and the other 50% die sooner than the controls. The overall increase in longevity seems to be zero."

 

I disagree with this reduction not least because it ignores the other 200 plus implicit controls of the other 20 groups. As stated, the top 6 or 7 longest lived are c60oo, out of 240 - this isn't massaging data to make c60oo look good. 

 

 

 

There are no "implicit controls," there is only one group of controls, and it is so labeled. As for these "6 or 7 longest lived," the site does not state that. That is your statement. But it doesn't matter. What we are interested in is the increase of longevity, and for the C60 group, was nonexistent over the controls. You need to compare these disappointing results with the results they are trying to replicate. Have you seen them? If not, I've attached it below. This is from the Baati 2012 paper, where I've erased the olive oil curve to keep things focused on C60/EVOO. Here the last control rat died at around 38 weeks, while the first treated rat didn't die for another 20 weeks. The difference is dramatic.

Attached Files

•  c60 vs water.png   492.77KB   0 downloads

Edited by Turnbuckle, 05 September 2022 - 03:16 PM.

[QuestforLife]

Nonsense.

 

Fusion and stem cell stimulation are equally important, as one does not work without the other. Fusion should occur before stem cell stimulation, and that doesn't have to be by much. GMS or DHM, adequately blended, appear to be more readily absorbed than C60/EVOO, and thus can be taken at the same time. A demethylase promoter almost doubles the results. AKG, again taken with the others, seems adequate for this purpose. Subsequently you can allow these new stem cells to be used as needed, or force things by using senolytics with fission to get rid of old cells faster.

 

There aren't "too many moving parts," as you claim.

 

The 'too many moving parts' phrase isn't a criticism of your protocol, more a statement of the complication of carrying this out in a lifespan study. Imagine explaining the above to Richard Miller at the ITP as a proposal for inclusion as a lifespan study. It would probably be rejected just because it requires multiple supplements with a timing element. 

 

Are you now suggesting that this protocol would work without senolytics or fission parts?

 

If so that is interesting and just what I was suggesting in terms of breaking down the protocol to increase our understanding.

 

I suggest some of your followers just do the fusion/C60 part and see how this impacts their methylation age.  

[Turnbuckle]

 

Are you now suggesting that this protocol would work without senolytics or fission parts?

  

 

Yes.

 

The body replaces some 300 billion cells a day, much of that via TACs (transit amplifying cells that are intermediate between SCs and somatic cells). TACs appear to be the locus of epigenetic aging in many tissues, so replacing TACs via SCs more frequently will lower the average epigenetic age of those tissues. A good number of those 300 billion replaced cells are physically lost (epidermal and epithelial cells, for example), but the others require apoptosis. Fission is required for apoptosis, but the fusion state is sticky, so you can speed things up with a fission supplement to banish fusion once it's not needed. Senolytics can take care of those senescent cells that that have become resistant to apoptosis.

 

Bottom line, an occasional C60/EVOO + mito fusion treatment will decrease epigenetic age (and can be expected to increase longevity as was seen in the Baati experiment). Adding a demethylase promoter will improve the results. Adding fission + apoptosis promoters (senolytics) with further improve the results.

 

The Baati experiment likely had C60/EVOO + mito fusion, but didn't appreciate what they had. They fasted rats overnight in their toxicity study, but failed to say anything about feeding with the subsequent longevity study. Overnight fasting would have been sufficient to produce a fasting-induced state of fusion, as rodents have a metabolic rate 6 times that of humans. But they made such a good case for C60 operating via an anti-oxidant mechanism that no one considered the mechanism might be completely different. And thus one attempt at replication has failed after another.

Edited by Turnbuckle, 05 September 2022 - 04:03 PM.

[ambivalent]

There is no other way to interpret the chart, that when all the other mice are dead around 40% of the c60oo group are alive. It is unambiguous. It is not my statement, it is a statement of the chart representing the study data. If it is BS, then of course all of this is for nothing - I am assuming it isn't. 

 

Thought experiment: suppose there was a secret group of 1000 controls in the study. Now you have to bet everything you own on either the control group of 10 or 12 mice or the 224 sample, excluding the c60 group being closest to the 1000 control figure. Would you dive in the on the small control group? I wouldn't especially looking at the chart, you're trading variance against experimental similarity. So yes, that's why I say it is a meaningful control, and in this case a better measurement, where a control group is there to illuminate the effect on the treatment group. 

 

If you have a 2 SD bad control group then all the groups could look good, the other way and they all look bad.

 

In a study like this I would say the meaningful outcomes are where there are big measurements of small groups, that's really what we're on the lookout for, because there are no big samples, except the total population. It's curious that 6 of the c60oo group were still alive when the controls were all dead, there might be a case for exceptional variance. But not the other 200, no there is something going on here. And you don't just take the average figure and throw it away, you open it up and explore. We wouldn't do that in humans, if a subgroup were doing something truly remarkable but taken together the group appeared normal.

 

As I said in a previous post, the average of c60oo compared to the control, is made up of one underperforming percentile and one overperforming percentile, I don't believe at all they are remotely equal in likelihood, even if they sum to zero, because we're measuring lifespan, not height: we don't expect symmetry unless the distribution is narrow. It might have been overlooked if just looking at the c60oo/control chart. But the comparison with the entire population lays this imbalance bare: they are not two sides of the same distribution coin. 

 

 

Edited by ambivalent, 05 September 2022 - 05:59 PM.

[ambivalent]

As an aside, to be on the thread - all I do is occasionally stearic acid + c60: does this still represent, say, 80% of the benefit as it seemed it used to be thought?

Edited by ambivalent, 05 September 2022 - 05:27 PM.

[Turnbuckle]

There is no other way to interpret the chart, that when all the other mice are dead around 40% of the c60oo group are alive. It is unambiguous. It is not my statement, it is a statement of the chart representing the study data. If it is BS, then of course all of this is for nothing - I am assuming it isn't. 

 

The chart makes no such statement. The way to compare them is by area under the curve, and by that method, the control seems slightly better. There is no point in continuing to beat this dead horse. It is just cluttering up the thread. 

 

As an aside, to be on the thread - all I do is occasionally stearic acid + c60: does this still represent, say, 80% of the benefit as it seemed it used to be thought?

 

If all you do is just use stearic acid with C60, you will get about 60% of the benefit in the body, and none in the brain, as stearic acid does not penetrate the BBB.

Edited by Turnbuckle, 05 September 2022 - 06:16 PM.

[ambivalent]

OK, thanks. Alright, so if only adding just one or only two to the protocol, which would you choose?

[Repack Racing]

All curves should show 100% until the first animal dies, and thereafter each curve should look like a staircase, with 90 degree angles. I did this freehand, making guesses where the break points are, and I see something quite different. For C60, 50% of the animals live longer than the controls, and the other 50% die sooner than the controls. The overall increase in longevity seems to be zero.

 

Agree - close to zero.

Agree - plot and study are a mess.

 

I do commend Bucky for their efforts - this was not an easy undertaking, but there are so many flaws as to make it useless.  Combining a dozen supplements into a test group makes no sense.  How can we possibility derive anything from that???

 

They said as much in their caveats - for example, doses were basically a "best guess."  I suppose that's all we have for a lot of the supplements.

 

At least C60, Mots-c, GDF and a couple others we tested independently, which is more meaningful.

 

The careful task of add/subtract as you have done simply isn't feasible for large-scale studies, unfortunately.

 

Thanks for the ongoing efforts!

[ambivalent]

ildr, I think you should add remarks to the other thread, if you want to follow this discussion up on interpretting the chart/data.

Edited by ambivalent, 05 September 2022 - 09:12 PM.

[Turnbuckle]

 

The careful task of add/subtract as you have done simply isn't feasible for large-scale studies, unfortunately.

 

The biggest problem with longevity studies is the time they take. Short lived species are used, but still it takes years. With epigenetic age as a proxy for longevity, and with tests now available for both humans and rodents, the process could be sped up considerably. 

[QuestforLife]

With epigenetic age as a proxy for longevity, and with tests now available for both humans and rodents, the process could be sped up considerably.

If and only if reversal of epigenetic age is proven to correlate strongly with lifespan extension. That has yet to be proven (and yes, that will require long lifespan studies in animals)

Edit: if samples have been kept from successful llfepsan studies (rapamycin, C60 Baati study, etc), this could shortcut the process.

Edited by QuestforLife, 05 September 2022 - 09:58 PM.

[Repack Racing]

Stem cell self-renewal

This is an update to post 1700.

  

Time 0 —

One brownie

 

 

 

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. 

 

Turnbuckle,.

 

I am in the midst of another all-day thread read - with a focus on getting all of the protocol spacing correct and eliminating any supplements that may interfere.

 

The latest Stem Cell protocol above is slightly confusing to me, and possibly to others.  I have a few clarifying questions when you have a moment.

 

1.  Presuming we follow the latest brownie recipe and take it at hour zero, which already includes dihydromyricetin, we take an additional 2-6 grams of dihydromyricetin at hour 3? Seems like a lot, so just checking.

2.  In several posts you mention that in lieu of the brownie, we can take 1-2g GMS + 2-3g dihydromyricetin, is that correct?

3.  In Q#2, is sunflower lecithin still needed?

4.  In Q#2, can the GMS/DHM be in pill form or is it important to blend them?

5.  Is it correct that if we are doing both the stem cell and mito protocols at the same time, the stem cell protocol would effectively "replace" the mito fusion day?

 

Thanks as always for the continued efforts!

 

[Kelvin]

The 'too many moving parts' phrase isn't a criticism of your protocol, more a statement of the complication of carrying this out in a lifespan study.

All they need to test is whether putting mice or rats into a fusion state (either by some supplement or by fasting) before giving them C60 extends lifespan.

[Kelvin]

If and only if reversal of epigenetic age is proven to correlate strongly with lifespan extension. That has yet to be proven (and yes, that will require long lifespan studies in animals)

Edit: if samples have been kept from successful llfepsan studies (rapamycin, C60 Baati study, etc), this could shortcut the process.

Epigenetic age is not the only measurement that could be used.

I and others have experienced multiple benefits with the protocol. In my case I had a reduction in gray hairs by at least 2/3rds, increased ability to keep muscle mass from lifting weights (which I as a natural ectomorph couldn’t maintain even when lifting weights years ago as a college student) and significant reductions in the amount of sleep I need each night.

Why not take the protocol yourself and see if you notice any benefits (with frequency of usage depending on your age)?

[QuestforLife]

All they need to test is whether putting mice or rats into a fusion state (either by some supplement or by fasting) before giving them C60 extends lifespan.

 

And how would they verify fusion, daily, in a mouse or rat lifespan study?

 

The only easy way I can think of would be to use fasting, but then you will fall foul of claims any resulting lifespan extension is a result of calorie restriction. 

 

Therefore, you'd need four animal groups: a control group CG (not fasted, no C60), a C60oo group (not fasted), an intermittently (over night) fasted group IFG and finally a IFG + C60oo group. To demonstrate lifespan extension independent of calorie restriction you'd have to prove statistical significance of IFG+C60oo vs. IFG.

 

It is going to take some persuasion to convince the ITP to do that. Anyone own a lot of mice or rats?

 

Interestingly, there is some evidence of an interaction between a mitochondrial antioxidant (ALA) and calorie restriction, as reported here.

Why not take the protocol yourself and see if you notice any benefits (with frequency of usage depending on your age)?

 

I tried it many years ago, when this thread was young!

 

I may try it again, but I'd really like to understand what is going on. 

[Turnbuckle]

Turnbuckle,.

 

I am in the midst of another all-day thread read - with a focus on getting all of the protocol spacing correct and eliminating any supplements that may interfere.

 

The latest Stem Cell protocol above is slightly confusing to me, and possibly to others.  I have a few clarifying questions when you have a moment.

 

1.  Presuming we follow the latest brownie recipe and take it at hour zero, which already includes dihydromyricetin, we take an additional 2-6 grams of dihydromyricetin at hour 3? Seems like a lot, so just checking.

2.  In several posts you mention that in lieu of the brownie, we can take 1-2g GMS + 2-3g dihydromyricetin, is that correct?

3.  In Q#2, is sunflower lecithin still needed?

4.  In Q#2, can the GMS/DHM be in pill form or is it important to blend them?

5.  Is it correct that if we are doing both the stem cell and mito protocols at the same time, the stem cell protocol would effectively "replace" the mito fusion day?

 

Thanks as always for the continued efforts!

 

I will be posting another protocol update soon. Normally I post what I have been doing lately, but his time I will try to be more complete with options, and give more of the rationales with it.

 

All they need to test is whether putting mice or rats into a fusion state (either by some supplement or by fasting) before giving them C60 extends lifespan.

 

I agree. And the control group would get exactly the same feeding regime, except water instead of C60 in oil.

 

...you'd need four animal groups: a control group CG (not fasted, no C60), a C60oo group (not fasted), an intermittently (over night) fasted group IFG and finally a IFG + C60oo group. To demonstrate lifespan extension independent of calorie restriction you'd have to prove statistical significance of IFG+C60oo vs. IFG.

 

 

Adding a C60oo/fasting/demethylase group would be good.

[stephen_b]

Turnbuckle, 

 

These are arguments against a positon I have clearly not taken: let me be clear:

 

You have suggested the study is not meaningul unless fusion is added. This doesn't make sense

 

If fusion is a critical variable that is not controlled for, then yes it makes sense as a possible explanation. Of course, it still needs to be verified, but it is a valid hypothesis.

[ambivalent]

If fusion is a critical variable that is not controlled for, then yes it makes sense as a possible explanation. Of course, it still needs to be verified, but it is a valid hypothesis.

 

That wasn't TB's position, though, which was to claim a c60oo longevity study was not meaningful without adding fusion, not without controlling for it, which is where I disagreed. 

[kurt9]

A question about the protocol. I did the three day cycle last week. Fusion was on Tuesday and fission was Wednesday and Thursday. I did not notice much. However, last night I began to experience flu-like symptoms that continue into today. The timing does not seem right (too long since fission - 4 days). But I have to ask. Could this be a delayed fission effect?

[Kelvin]

I agree. And the control group would get exactly the same feeding regime, except water instead of C60 in oil.

At least SOME of the C60 mouse studies that came after the Baati study SHOULD have tried fasting the test rodents.

Are the universities still teaching science research students how to do proper controls anymore?

This is a really easy control to setup (1 group of mice fast and get C60 while another group only fasts without C60) yet the studies keep screwing up whining about “But we can’t replicate Baati!”

You can’t because you didn’t setup test conditions identical to Baati, you damned fools.

Edited by Kelvin, 07 September 2022 - 12:06 AM.

[Kelvin]

A question about the protocol. I did the three day cycle last week. Fusion was on Tuesday and fission was Wednesday and Thursday. I did not notice much. However, last night I began to experience flu-like symptoms that continue into today. The timing does not seem right (too long since fission - 4 days). But I have to ask. Could this be a delayed fission effect?

When I tried the protocol 6 times earlier this year I got sneezing fits and mild fever on 2 of the cycles on my second fission day and for 2-3 days after.

both times.

I suspect that was the senolytics killing senescent cells but the immune system took a day or two to react and clear out the debris of the destroyed cells.

When was the last time you used senolytics?

Edited by Kelvin, 07 September 2022 - 12:12 AM.

[kurt9]

I did the senolytics part on Wednesday and Thursday of last week. I find it difficult to believe that I would have a reaction starting last night, four days after last day doing the senolytics portion. 

[Kelvin]

Maybe you have a mild cold?

Edited by Kelvin, 07 September 2022 - 01:48 AM.

[kurt9]

It must be. although it feels much more flu-like than a cold.

[Turnbuckle]

This is an extended update to post 1711. The updated protocol can be found near the end.

 

 

 

THE DE-AGING HYPOTHESIS

 

The human body is a work in progress. Some 300 billion cells are lost every day and must be replaced by stem cells (SCs). Given that viable SC numbers decline dramatically throughout life even while cellular replacement needs increase, the endogenous proliferation of stem cells should provide the most direct and comprehensive approach to restoring cellular maintenance and extending lifespan.

 

Each of the 200 different cell types in the human body has the same genetic code, but are distinguished by another code that resides above the genetic code and determines which genes are turned on or off for each cell type. This is the epigenetic code. Most of the epigenetic code is in the form of methylation of the DNA or the histones that carry them. With time, cells undergo epigenetic mutations (epimutations) that degrade cellular performance. These occur far more frequently than with the underlying genetic code, and there is no repair mechanism except replacement.  Thus replacing old epimutated cells with new cells derived from SCs having de novo methylation will improve the performance of organs and the body as a whole. It will also reduce the epigenetic age, which can be easily measured in a lab. Tests are available to the public, with one offered by Trumelabs.com presently the cheapest.

 

Cells are unaware of their epigenetic damage, but have a clock to determine when they are old and thus sufficiently damaged to require replacement. This is the telomeric clock. When it runs out (the Hayflick limit) cells commit suicide (apoptosis). Hopefully there are sufficient SCs to supply replacements. But with age, there aren’t, as SC niches become depleted.

 

So how to refill SC niches?

 

It’s known that SCs are quiescent due to high expression of uncoupling protein 2 (UCP2), which allow protons to dissipate through the inner mitochondrial membrane without producing ATP. It is also known that mitochondrial fusion will bias SC division to proliferation. Thus by simultaneously supplying a fusion supplement and a blocker for UCP2, quiescent SCs should awaken and begin proliferating, subsequently replacing senescent cells as needed.

 

A proposed method for reversing age can be divided into three parts:

1. Filling SC niches: Blocking proton leakage through UCP2 pores with C60* activates SCs while promoting mito fusion directs them to proliferation.
2. Replacement of senescent cells: Mitochondrial fission/apoptosis using senolytics removes senescent cells, which are replaced by cells derived from proliferated SCs of part A, at the direction of natural paracrine signaling.
3. Maximizing epigenetic age reversal: Supplying a demethylase promoter during parts A and/or B further reduces aberrant methylation and epigenetic age.

*The fullerene C60 dissolved in oil is proposed herein as a UCP2 blocker. The use of C60 to extend rodent lifespans was the subject of three papers. The first (in 2012, PMID 22498298) showed that feeding rats C60 in oil increased rat lifespans by 90% over controls, and attributed the increase to the antioxidant properties of C60. The next two (in 2021, PMID 33123847 and PMID 33849306) attempted to replicate this result in mice, but found no increase in lifespan. The discrepancy can be resolved by postulating a different MOA for C60 — UCP2 blocking rather than ROS quenching — and a different feeding regime for the three experiments. Although none of the papers precisely described how their test animals were fed, it is likely the research group of the first paper fasted their rats overnight (as they did in a previous C60 toxicology study), while research groups of the next two papers likely did not, as there was no suggestion to do so in the first paper. Rodents have a metabolic rate about six times that of humans, so a state of fasting-induced mitochondrial fusion would have been easily achieved in the first study, but no fusion would have occurred in next two.

 

 

SUPPLEMENTS FOR REDUCING EPIGENETIC AGE

 

 

For fusion, use one or more of the following:

 

Preferred: Dihydromyricetin (DHM): This can penetrate the BBB, but has terrible taste. It should be stirred into water or juice with a high speed blender. It can also be baked into brownies, but ruins the taste.

 

Stearic acid triglyceride (food grade stearic acid): This has low availability unless prepared properly (baked into a brownie, for instance) and taken 3 hours before other supplements due to its slow digestion.

 

Mito fusion brownies

 

Betty Crocker Fudge brownie mix* (519 g)

2 eggs

4-5 tbsp water

120 g food grade stearic acid

 

*Or any mix that requires ½ cup oil, but don’t use the oil. Diet versions don’t work well. 

Mix with power mixer and bake as directed on the box. Cut into 16 pieces, dust with flour to avoid sticking, and freeze. Dosage: 1 piece three hours before SC treatment.

 

Stearic acid monoglyceride (aka glycerol monostearate, GMS): This is a much more soluble and bioavailable form of stearic acid, if stirred into water of juice with a high speed blender. Both types of stearic acid have poor penetration of the blood brain barrier (BBB).

 

For fission: Nicotinamide (NAM). This may optionally be used with a like amount of ribose. Niacin may be used, but most will find the flush objectional. NR might be used, but it is essentially NAM + ribose that requires a time delay to be broken down. Apigenin is yet another possibility, but I prefer nicotinamide.

 

For UCP2 blocking: C60 dissolved in a biocompatible oil.

 

For SC nutrition: Lysine and methionine.

 

For promoting demethylase: AKG or source thereof.

 

 

 

UPDATED AGE REVERSAL PROTOCOL

(with DHM and GMS)

  

 

Day 1: Mito fusion/C60 —

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. GMS — 1-2 grams

5. Glutathione (reduced or liposomal) — .5-1 grams

6. AKG (alpha ketoglutarate) — 1 gram

7. AAKG (arginine alpha ketoglutarate)  — 2-3 grams

8. SAM-e — 200 mg

9. Lysine — 2-6 grams

10. Methionine — 1-3 grams

 

Astragalus root powder, every 10th treatment — 500 mg

 

Day 2: Mito fission, may be repeated for 2 days —

1. Nicotinamide — 1 gram

2. Ribose — 1-2 grams

3. AAKG  — 2-3 grams (AKG can also be used)

4. Lysine — 2-6 grams

5. Methionine — 1-2 grams

6. Fisetin — 100-200 mg

 

You may skip this fission step for the first month. 

 

Notes:

1. I generally add the C60 stack to water spiked with an orange/tangerine “water enhancer.” I take the fission stack as pills.

2. More lysine and methionine may be taken a few hours later.

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

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

5. I've dispensed with sulforaphane as a fusion agent, but it might be helpful for some people. 

6. Present schedule varies, but generally 4-5 times a month.

7. Sunflower lecithin helps the bioavailability of DHM and GMS and supplies a source of choline that find useful. Sunflower lecithin powder seems considerably superior to soy lecithin for this purpose.

8. Lysine and methionine provide SC nutrition.

9. Astragalus root powder provides a telomerase promoter, but using too much will ruin the epigenetic benefits, as it will lengthen the telomeres of TACs and somatic cells, and block their replacement.

10. I use both AKG (already dissolved by the manufacturer) and AAKG. The first is very fast acting (more important during fusion) and the other somewhat slower (more important during fission). Calcium AKG is expected to be even slower and may be used instead of AAKG. Other AKG salts or AKG conjugates may be used.

 

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. Do not add other random supplements. Telomerase promoters like resveratrol should definitely be avoided.

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:

Best epigenetic age result to date was 28 years below chronological. Baseline result in 2018 was half a year above chronological. Substantial improvements in appearance and general health, consistent with the drop in epigenetic age.

 

 

Edited by Turnbuckle, 07 September 2022 - 12:06 PM.

[Termophilus]

Thanks Turnbuckle,

 

I would like to ask how this protocol could be blended (if needed or if it useful at all) with your mitochondrial protocol, and if you think there is a rationale for Resveratrol + NMN in any space in beetween.

Thanks again for your effort and thoughtful experimentation, I've tried the mitochondrial protocol for almost two months circa (used NMN for Nicotinamide), and it helped a lot with stamina, and appetite suppression was evident, even if I used in fact every day resveratrol, like 500mg, which I undestood only later that is not suggested.

I've used NMN and Resveratrol (the Sinclair protocol) for quite some times, but I didn't notice too much, maybe estetic preservation, but I'm also 39 so its not so evident. 

[Turnbuckle]

Thanks Turnbuckle,

 

I would like to ask how this protocol could be blended (if needed or if it useful at all) with your mitochondrial protocol, and if you think there is a rationale for Resveratrol + NMN in any space in beetween.

Thanks again for your effort and thoughtful experimentation, I've tried the mitochondrial protocol for almost two months circa (used NMN for Nicotinamide), and it helped a lot with stamina, and appetite suppression was evident, even if I used in fact every day resveratrol, like 500mg, which I undestood only later that is not suggested.

I've used NMN and Resveratrol (the Sinclair protocol) for quite some times, but I didn't notice too much, maybe estetic preservation, but I'm also 39 so its not so evident. 

 

It's too late to add it now, but I meant to suggest the the mito protocol be used first. Resveratrol should never be used.

[Empiricus]

 

 

Day 2: Mito fission, may be repeated for 2 days —

1. Nicotinamide — 1 gram

2. Ribose — 1-2 grams

3. AAKG  — 2-3 grams (AKG can also be used)

4. Lysine — 2-6 grams

5. Methionine — 1-2 grams

6. Fisetin — 100-200 mg

 

 

 

Turnbuckle, would you care to share your reasoning behind adding fisetin?  

 

Suppose someone were to skip the fisetin altogether, what difference would that make?

Edited by Empiricus, 07 September 2022 - 06:19 PM.

[Turnbuckle]

Turnbuckle, would you care to share your reasoning behind adding fisetin?  

 

Suppose someone were to skip the fisetin altogether, what difference would that make?

 

If you're going to use a senolytic, this appears to be a good one, short of going to beyond supplements to drugs--

 

 

Findings

Of the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. Fisetin reduced senescence in a subset of cells in murine and human adipose tissue, demonstrating cell-type specificity. Administration of fisetin to wild-type mice late in life restored tissue homeostasis, reduced age-related pathology, and extended median and maximum lifespan.

https://www.ncbi.nlm...les/PMC6197652/

 

 

 

 

See the attached chart. Of course, once you've gotten rid of the recalcitrant senescent cells, fission alone might be enough.

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