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Stem cell self-renewal with C60

c60 stem cells mitochondria fusion stearic acid aging hydroxytyrosol olive oil mct oil proliferation

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#1171 kurt9

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Posted 03 March 2020 - 07:48 PM

My latest epigenetic age test result, ten weeks after the last one, is 14.2 years below chronological age. Over that period I used the modified SC treatment on this post, with one treatment per week. The test was TruAge from Trumelabs.

 

To recap. 

 

Test date...Epigenetic age - chronological age

2/2018 ... +.5 years (This was baseline, before treatments)

6/2018 ... -11

 

I began to use telomerase stimulants at this point, and my epigenetic age began to increase. When I stopped telomerase stimulants, epigenetic age stabilized and slowly began to fall with continued SC treatments. Cycloastragenol and astragalus extract screwed up my age regression for a year.

 

12/2019 ... -13

2/2020 ... -14.2

 

This is kick ass! Its not something I would do at my current stage in life. But it is nice and reassuring that something like this is available for when I need to do it some time down the road.

 

BTW, I finished week 6 of the mitochondrial fission/fusion thing. I then had to stop because I was travelling last week and am getting over a bug I picked up on the flight (No, It not COVID-19). So, I resume next week and will continue for another 3 weeks and possibly 6 weeks.


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#1172 ryukenden

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Posted 04 March 2020 - 06:45 AM

Have you reversed your grey hair with the epigenetic age reduction?

Is there alternative to stearic acid? I am worried about whether it can cause atherosclerosis.

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#1173 thenewwildone

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Posted 04 March 2020 - 07:16 AM

My latest epigenetic age test result, ten weeks after the last one, is 14.2 years below chronological age. Over that period I used the modified SC treatment on this post, with one treatment per week. The test was TruAge from Trumelabs.

To recap.

Test date...Epigenetic age - chronological age
2/2018 ... +.5 years (This was baseline, before treatments)
6/2018 ... -11

I began to use telomerase stimulants at this point, and my epigenetic age began to increase. When I stopped telomerase stimulants, epigenetic age stabilized and slowly began to fall with continued SC treatments. Cycloastragenol and astragalus extract screwed up my age regression for a year.

12/2019 ... -13
2/2020 ... -14.2


I’ve been following this topic from the beginning and I really want to believe that you’re really getting younger. The problems are that it’s possible that you’re actually depleting your stem cell pool. People who have diseases that mimic aging have epigenetic ages that correlate to their age, but their telomeres are depleting almost twice as much as normal. This tells me that telomeres maybe more important than epigenetic age.

Ultimately there are only 2 ways to prove if any method is working.

1. Actually look younger after doing a protocol/protocols.

2. Live significantly longer than the average lifespan and be able to do things that people your age can’t. This one maybe objective.

All these test results mean preciously little unless they lead to one or both of the above and for #2 we won’t know for a while. I don’t know your age, but if you’re not capable of easily doing things that people 13 years younger can do physically (can be objective) and don’t look 13 years younger, you’re not younger.
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#1174 Turnbuckle

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Posted 04 March 2020 - 09:22 AM

Have you reversed your grey hair with the epigenetic age reduction?

 

 

 

So far graying may have been arrested, but not dramatically reversed. My feeling is that, if a stem cell niche is completely depleted, it's much harder to recover.

 

 

I’ve been following this topic from the beginning and I really want to believe that you’re really getting younger. The problems are that it’s possible that you’re actually depleting your stem cell pool. People who have diseases that mimic aging have epigenetic ages that correlate to their age, but their telomeres are depleting almost twice as much as normal. This tells me that telomeres maybe more important than epigenetic age.

Ultimately there are only 2 ways to prove if any method is working.

1. Actually look younger after doing a protocol/protocols.

2. Live significantly longer than the average lifespan and be able to do things that people your age can’t. This one maybe objective.

All these test results mean preciously little unless they lead to one or both of the above and for #2 we won’t know for a while. I don’t know your age, but if you’re not capable of easily doing things that people 13 years younger can do physically (can be objective) and don’t look 13 years younger, you’re not younger.

 

The epigenetic results closely parallel physical results. See post #201. In addition to those things noted in that post, I experienced an elimination of a distortion in the Amsler grid that I'd seen for some years. The increase in shoe size I noted there finally stopped. 



#1175 Turnbuckle

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Posted 04 March 2020 - 10:09 AM

This is an update from post #1149. The only change is with resveratrol. After I added that, I felt there was an acceleration in age reduction, but the drop I saw in the epigenetic test results wasn't significant enough to say it actually improved anything. So best to take it out for now.

 

 

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.

  

 

Part 1: Stem cell self-renewal

 

 

Time 0 —

1Stearic acid — 5-10 g (food grade, in brownie)

 

  

Time 3:00 —

2Sulforaphane — 100 mg

3Liposomal glutathione — 1 g

4SAM-e — 500 mg

 

 

Time 3:30 —

6C60 — 3 mg (in oil)

7Amino acids: Threonine  2-3 g, Lysine — 2 g, Methionine — 1 g, Leucine — 1 g

 

These amino acids should be repeated as necessary every couple of hours, and perhaps days.

 

 

Part 2: Senescent cell replacement (24 hours later)

 

8Nicotinamide — 2g, Ribose — 2g

9Curcumin (liposomal or phytosomal) — 2g

7Lysine — 2 g, Methionine — 1 g, Leucine — 1 g

 

These amino acids should be repeated as necessary every couple of hours, and the entirety of Part 2 may be repeated the next day as well.

 

 

 

Notes:

 

(1) This is for mito fusion, which directs SCs to self-renewal. 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. Use ½ to 1 brownie for this protocol. With the addition of sulforaphane, I've been using ½. Stearic acid has much longer half life than sulforaphane (11 vs 4 hours), and thus may interfere with subsequent senescent cell replacement, which requires mito fission. It may be possible to use sulforaphane alone, but I've been content with just cutting it back.

 

(2) 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)

 

(3) Primary antioxidant.

 

(4) Methyl group donor.

 

(5) --

 

(6) UCP2 blocker. A teaspoon of commercially available C60 oil.

 

(7) These can be used in caps or tablets, though I use a commercial blend of essential amino acids here, adding extra lysine, methionine and leucine. Pluripotent cells have a special need for these three. I would spread out the doses as indicated, to avoid nausea. Note that I deleted threonine in the last update, but I got negative results by leaving it off. This became increasingly apparent after a few weeks, thus I restored it.

 

(8) Used together, nicotinamide and ribose rapidly increase NAD+, which drives mitochondrial fission, required for senescent cell apoptosis and replacement.

 

(9) Senolytic


Edited by Turnbuckle, 04 March 2020 - 10:10 AM.


#1176 QuestforLife

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Posted 04 March 2020 - 11:42 AM

So far graying may have been arrested, but not dramatically reversed. My feeling is that, if a stem cell niche is completely depleted, it's much harder to recover.

 

 

 

The epigenetic results closely parallel physical results. See post #201. In addition to those things noted in that post, I experienced an elimination of a distortion in the Amsler grid that I'd seen for some years. The increase in shoe size I noted there finally stopped. 

 

Even with younger looks and performance, there is at this point, no way outside of giving a bone marrow telomere sample to determine if the bone marrow is being used up at an increased rate (as the price for greater health), or whether genuine rejuvenation has taken place.

 

On the bright side, mouse studies such as this one [https://onlinelibrar...1111/acel.13110 , see Figure 1], where there was a control group who had increased bone marrow mobilisation (but no exogenous replacement), experienced a normal lifespan (you could argue it was slightly reduced but it wasn't statistically significant). 

 

So Turnbuckle's advice that this is a geriatric treatment only, is probably wise. 


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#1177 Turnbuckle

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Posted 04 March 2020 - 12:48 PM

Even with younger looks and performance, there is at this point, no way outside of giving a bone marrow telomere sample to determine if the bone marrow is being used up at an increased rate (as the price for greater health), or whether genuine rejuvenation has taken place.

 

 

 

 

I very much doubt that telomere length of bone marrow is predictive of anything, particularly aging or longevity.

 

 

Background and aim of the work: Bone marrow failure syndromes (BMFS) includes inherited and acquired conditions.... We have found that there is a significant difference in relative telomere length between congenital group and controls (p=0.001), also a significant difference between acquired group and controls (p= 0.029). However, there is no significant difference between congenital and acquired groups (p= 0.479). There is no significant correlation between the telomere length and the overall survival or prognosis of the patients of BMFS.

 


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#1178 QuestforLife

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Posted 04 March 2020 - 02:42 PM

I very much doubt that telomere length of bone marrow is predictive of anything, particularly aging or longevity.

 

 

 

There are diverse conditions that lead to BM failure; some of which result in shorter telomeres in circulating cells and some of which do not. See: https://www.ncbi.nlm...les/PMC4281312/

 

Most dyskeratosis congenita telomere lengths were below the 1st percentile, while only 2 Fanconi anemia and one each Diamond-Blackfan anemia and Shwachman-Diamond syndrome were that low. However, Fanconi anemia, Diamond-Blackfan anemia and Shwachman-Diamond syndrome clustered in the bottom half of the normal range

 

Moreover in the study you reference you are cherry picking the telomere lengths of an acquired vs. inherited condition, which were not significantly different from one another as you might expect, rather than the differences between either condition and unaffected controls, which was significant.

 

Finally, the abstract of your referenced study does not specify what tissue was used to measure telomere lengths. The whole crux of my argument is that you need to measure BM stem cell telomere lengths NOT a one off measurement of a dynamic population like leukocytes (as is common), the latter are influenced by a multiplicity of contradictory factors.   


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#1179 Turnbuckle

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Posted 04 March 2020 - 03:13 PM

An experiment with cultivated stromal cells found that, with multipotential stromal cells, methylation changes but not telomeric length correlate with survival--

 

Results. Regardless of donor age, cultures’ osteoprogenitor content correlated better with remaining lifespan (population doublings before senescence, PD-BS) than proliferative history (accrued PDs). Individual gene’s expression or telomere length did not predict PD-BS but methylation of individual CpG islands did...

 

In spite of literature supporting the loss of telomere length being a feature of MSC replicative ageing [9, 10, 16] no correlation was found in either culture expanded MSCs or osteodifferentiated MSCs, although the differentiated MSCs did have significantly shorter telomeres. Modelling calculations in conjunction with SPARC were attempted but were not predictive.

 

The methylation of CpG islands [12] collectively had very strong associations with PD, which remained for PD-BS albeit reduced...

https://www.hindawi....i/2017/6129596/

 

 

 

Telomere length is simply not predictive. It's only a sell-by for individual cells.



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#1180 QuestforLife

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Posted 04 March 2020 - 08:11 PM

Telomere length is simply not predictive. It's only a sell-by for individual cells.


Yes it's the rate of shortening that matters but that is besides the point. Adult stem cells are notoriously sensitive to culture conditions and in general behave quite differently in vitro to how they do in the body. You can't draw any firm conclusions from a Petri dish study.

It is well known stromal stem cells produce less osteocytes and more adipocytes with age, so that would be a good predictor of their function. The fact that this correlates with their potential population doublings in vitro indicates to me that it is related to telomere shortening. It is easy to see how this relationship might be obscured by the variation in telomere length between a small number of donors. There is also a great heterogeneity in stromal cells even within a single individual. Senescence independent of telomere length is also a factor, but this is much more common in high O2 (high ROS) culture conditions than in the body, again highlighting the caution required when interpreting in vitro studies.
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#1181 Turnbuckle

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Posted 04 March 2020 - 09:12 PM

You can't draw any firm conclusions from a Petri dish study.

 

 

And all you get from in vivo are scatter charts with only a vague trend.

Attached Files


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#1182 kurt9

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Posted 16 March 2020 - 01:50 AM

Can this C60 protocol be used to repair the lung fibrosis damage that some COVID-19 survivers are reporting?



#1183 yz69

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Posted 17 March 2020 - 03:07 AM

interesting paper "Hyperactivation of sympathetic nerves drives depletion of melanocyte stem cells"

 

https://sci-hub.se/1...1586-020-1935-3

 

 

Under conditions of stress, the activation of these sympathetic nerves leads to burst release of the neurotransmitter noradrenaline (also known as norepinephrine). This causes quiescent melanocyte stem cells to proliferate rapidly, and is followed by their differentiation, migration and permanent depletion from the niche. Transient suppression of the proliferation of melanocyte stem cells prevents stress-induced hair greying.

 

Does this mean one has to have sex under mito fusion mode so the stem cells go to self renewal instead of  differentiation?

 

 


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#1184 Graviton

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Posted 18 March 2020 - 12:01 AM

interesting paper "Hyperactivation of sympathetic nerves drives depletion of melanocyte stem cells"

 

https://sci-hub.se/1...1586-020-1935-3

 

 

Does this mean one has to have sex under mito fusion mode so the stem cells go to self renewal instead of  differentiation?

In addition, exercise is known to induce mitochondrial fission and it seems to temporarily secretes NE.


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#1185 ryukenden

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Posted 18 March 2020 - 02:47 AM

Would you consider taking the following stem cell supplement from LE with your regime? It may be helpful for you?

http://www.lifeexten...aspx?item=02401

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#1186 yz69

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Posted 18 March 2020 - 06:37 AM

Interestingly, this article suggest NE is also pro mito fission:

https://www.nature.c...es/ncb2950.pdf 

 

Norepinephrine promoted protein kinase A (PKA)-mediated phosphorylation of the pro-fission protein Drp1, and its localization with the mitochondria.

 

Any idea about how to reverse the hair greying?

 







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