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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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#1 Turnbuckle

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Posted 29 March 2018 - 03:01 PM


Summary: C60 is used with stearic acid to increase the pool of stem cells.

 

Background:  Stem cells predominately divide asymmetrically into 2 daughter cells, one a somatic cell the other a stem cell. Theoretically this would keep the population stable, but over a lifetime it does not, and the falling population becomes a major source of aging.

 

From The Stem Cell Theory of Aging (Wikipedia) 

 

The number of stem cells in young people is very much higher than older people and this cause a better and more efficient replacement mechanism in the young contrary to the old. In other words, aging is not a matter of the increase of damage, but a matter of failure to replace it due to decreased number of stem cells. Stem cells decrease in number and tend to lose the ability to differentiate into progenies or lymphoid lineages and myeloid lineages.

 

https://en.wikipedia...theory_of_aging

 

 

C60 stimulates mitochondria, and mitochondrial activity drives the activity of stem cells. Anecdotal reports (including my own) suggest that C60 is a powerful stimulant of stem cells, but the effect appears to fade, as if the stem cell pool is being depleted. In my opinion depletion of stem cells is second only to mitochondrial dysfunction in importance for aging. (Mito dysfunction can be reversed—see the thread, Manipulating Mitochondrial Dynamics.)

 

Increasing the SC pool: While stem cells generally divide asymmetrically, symmetric division is also possible, wherein one stem cell divides into two stem cells, called self-renewal. It appears that mitochondria direct the process. When mitochondria are in a state of fusion, symmetric proliferation is more common, thus increasing the population.

 

… we present a model whereby changes in mitochondrial structure direct the fate of stem cells. In this model, elongated [fused] mitochondria in NSCs [neural stem cells] maintain low ROS levels and promote self-renewal, while a transition of mitochondria to a more fragmented state [fissioned] results in a modest increase in ROS levels, thereby inducing the expression of genes that inhibit self-renewal and promote commitment and differentiation.

 

https://www.scienced...934590916300820

 

 

Supplement for fusion: C18:0 — stearic acid.

 

Regulation of mitochondrial morphology and function by Stearoylation of TfR1 

 

“We find that animal cells are poised to respond to both increases and decreases in C18:0 levels, with increased C18:0 dietary intake boosting mitochondrial fusion in vivo.”

 

 

My experiment: I’m presently using 10 g of stearic acid (120 mg/kg) and 1 teaspoon of C60 in olive oil half an hour later, doing this once a week or so. The oil is my own mix from 2016, which I’d stored in the freezer. It contained 0.6 mg/kg of C60 in Frantoio Pruneti EVOO which tested at 608 mg/polyphenols (mostly oleuropein), to which I added 1400 mg/kg hydroxytyrosol (HT). This oil with extra HT proved to be one of the better of my olive oil experiments for exercise.

 

Results: When I first tried C60 in 2012 I noted hair regrowth that filled in a bald spot to about 50% of the density of the rest of my hair. This faded slowly over a period of a year, and while there was some variability over the succeeding years, it seemed that something had changed, as if some easily stimulated stem cells had been used up. I noted physical changes as well, with my shoe size increasing from 9.5 to 10.5 over those years and my height increasing by one inch. The rate of these changes was slowing (with my use of C60 amounting to around 50-100mg/year), but are now increasing again, and the bald spot is filling in. It’s not to the point it was in 2012, but it’s better than at any point since then. I have also used a fusion mix topically, and this may have added to the hair regrowth. I can’t say for certain which is more responsible, as I did both oral and topical.

 

Oral dosing: Stearic acid is available as white waxy flakes. It can be consumed in a cup of hot chocolate if sufficient amount of lecithin is added (I use roughly equal amounts). It can also be stirred into hot foods such as oatmeal, or used in fudge or cookies.

 

Topical application: An oil with high levels of stearic acid is needed. As none are available, you can make your own using either olive oil or MCT oil with 30-40% added stearic acid (warmed to over 157F to melt it), then stirring in a little C60/EVOO before use. The high stearic acid oil should resemble coconut oil in that it is solid when cool but melts at skin temp. This should only be used at night due to the photosensitivity of C60. I’ve only used stearic acid in MCT oil to date, however MCT oil may cause inflammation for those with sensitive skin.


Edited by Turnbuckle, 29 March 2018 - 03:10 PM.

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#2 thedarkbobo

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Posted 29 March 2018 - 04:13 PM

Interesting find, how does it taste? Does it dissolve in hot water or not really? Is it okay to eat it raw?

Toxicity?

C17H35CO2H or C17H35COOH ?

From what I can see on internet it does not really dissolve in water.

 

https://www.ncbi.nlm.../pubmed/3689663

 

Let me add to this:

 

Decreased membrane rigidity is one of the characteristics of malignant cells, resulting in part from the desaturation of stearic acid into oleic acid. In this study we investigated the influence of stearic acid on tumour cell inhibition in vitro and tumour development in vivo. Stearic acid inhibited the colony-forming ability of 4 out of 5 rat and two human tumour continuous cell lines in vitro. In contrast, the colony-forming ability of rat fibroblasts was not inhibited and that of human foetal lung fibroblasts was inhibited at a higher dose than that required to inhibit human tumour cell lines. Using a model of rat mammary carcinoma induced by nitroso-methyl urea (NMU) the subcutaneous injection of stearic acid at weekly intervals prevented tumour development in 5 to 10 rats. Using iodostearic acid twice weekly, 11 of 19 rats were alive and tumour free at week 22 whilst all of 14 animals injected with NMU alone had died of tumour by the 16th week. The ratio of stearic to oleic acids in erythrocyte membranes was significantly reduced in the tumour-bearing rats, but was normal in tumour-free animals treated with stearic or iodostearic acid. These preliminary data indicate that stearic acid inhibits tumour development in rats.

 


Edited by thedarkbobo, 29 March 2018 - 05:10 PM.


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#3 thedarkbobo

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Posted 29 March 2018 - 05:26 PM

Since can't edit previous...toxicity:

https://toxnet.nlm.n...erm @DOCNO 2000

/HUMAN EXPOSURE STUDIES/ LD100 Human oral 14286 mg/kg; practically nontoxic: probable oral lethal dose (human) more than 1 qt (2.2 lb) for 70 kg person (150 lb).

 

/SIGNS AND SYMPTOMS/ The greatest danger from ingestion of large quantities...is intestinal obstruction. Skin sensitization is unusual. Aspiration or inhalation...could cause chem pneumonitis. Implantation...will cause foreign body reaction.

 

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/Rats fed 50 g/kg/day stearic acid for 24 weeks developed reversible lipogranulomas in adipose tissue. No significant pathological lesions were observed in rats fed 3000 ppm stearic acid orally for about 30 weeks, but anorexia, increased mortality, and a greater incidence of pulmonary infection were observed. Stearic acid is one of the least effective fatty acids in producing hyperlipemia, but the most potent in diminishing blood clotting time.

 

Looks good to me :)



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#4 Nate-2004

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Posted 29 March 2018 - 08:10 PM

I have a bit of C60 left from that company in Texas. It's been in a closet for a year now, hopefully it's stable outside of any olive oil solution. I haven't made the stuff in some time.

 

I have fresh EVOO I'll just mix it in that. Is the hydroxytyrosol all that necessary? 

 

What about the stearic acid, can it be taken just by itself?


Edited by Nate-2004, 29 March 2018 - 08:10 PM.


#5 Female Scientist

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Posted 31 March 2018 - 03:59 PM

I mix the stearic acid directly into crunchy peanut butter. Can’t even tell it’s there! Often I eat it with an apple for breakfast. Eliminates having to heat it.
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#6 Nate-2004

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Posted 03 April 2018 - 09:18 PM

I tried mixing the food grade stearic with lecithin in a cup of hot chocolate, it does not dissolve very well if at all. I expected it to all melt into the drink but it doesn't. Why lecithin anyway?


Edited by Nate-2004, 03 April 2018 - 09:18 PM.


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#7 Turnbuckle

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Posted 03 April 2018 - 09:44 PM

I tried mixing the food grade stearic with lecithin in a cup of hot chocolate, it does not dissolve very well if at all. I expected it to all melt into the drink but it doesn't. Why lecithin anyway?

 

Lecithin helps it dissolve. I use 10 g stearic acid, a like amount of lecithin, Hershey's unsweetened cocoa, low cal brown sugar, then stir up the dry powders before adding milk and microwaving. If you still have a problem, stir it into peanut butter as mentioned above.

 

Note: I've used C60 (in EVOO with added HT)/stearic acid six or seven times in the past six weeks, and already I've had to go up a half shoe size. For four decades I was stable at 9.5 and I'm now at 11. This growth began in 2012 when I first began experimenting with C60, but using it with stearic acid has accelerated it. This has been a good thing despite having to throw away shoes, as my feet never hurt anymore.


Edited by Turnbuckle, 03 April 2018 - 09:51 PM.

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#8 Nate-2004

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Posted 04 April 2018 - 12:55 PM

Weird effect there. I am not sure if I want bigger feet haha. I'm already a size 12. 

 

I will try that tonight, that's pretty much the exact ingredients and measurements I used, substituting splenda for sugar though. I used boiling water and a couple tbsps of "better-half" creamer, which is coconut and almond cream, not dairy.  That shouldn't have made much of a difference though. It was pretty gritty when I drank it. The lecithin is yellow granules and the stearic is the white flakes. We probably even got the same brand. Maybe I should put it in a shaker and shake it up?

 

I haven't started making the C60 EVOO yet, I just defrosted the relatively fresh EVOO I got in January (November harvest), I am also not sure what the stability is on C60 alone, but it's been sitting in a dark closet for a year and a half in the original capsule it came in.



#9 stephen_b

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Posted 05 April 2018 - 03:06 AM

Any thoughts about other purported stem cell enhancers? Here's a study on Stem-Kine. Astragalus + angelica have had good results too, if you are a rat with artificially induced diabetes. Or here in human in vivo.


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#10 lost69

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Posted 05 April 2018 - 06:40 AM

what about epimedium?

 

https://www.ncbi.nlm...les/PMC5355742/

 

https://www.ncbi.nlm...pubmed/29355456

 

http://www.anti-agin...um-and-icariin/

 



#11 Turnbuckle

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Posted 05 April 2018 - 08:20 AM

Any thoughts about other purported stem cell enhancers? Here's a study on Stem-Kine. Astragalus + angelica have had good results too, if you are a rat with artificially induced diabetes. Or here in human in vivo.

 

 

I've tried stearic acid with one gram of icariin (a constituent of Epimedium, aka horny goat weed) and separately with a combo of lesser amounts of icariin, DHEA and TUDCA. All are said to encourage stem cell proliferation in the brain, and likely elsewhere as well. It's hard to say how well they worked compared to C60/stearic acid without further experimentation, but to answer your question, any substance that augments stem cell proliferation ought to benefit from a mito fusion state to push proliferation into self-renewal.

 

 

Widely available supplements that increase neural stem cell proliferation—
 
DHEA 
TUDCA 
Icariin 
Piracetam 
Apigenin (also promotes fission, and thus not used here)
 
 

 

References:

 

 

Dehydroepiandrosterone Stimulates Nerve Growth Factor and Brain Derived Neurotrophic Factor in Cortical Neurons

 

In this study, we provided evidences that DHEA increased NGF and BDNF production, neuronal cell proliferation, neuronal cell survival, and neurite outgrowth. The microenvironment of the CNS plays a major role in controlling neurogenesis. Levels of neurosteroids in the blood and/or CNS are a significant determinant in the formation of new neuronal cells. Our results add a new point to this map: the neurosteroid DHEA promotes overexpression of NGF and BDNF.

 

https://www.ncbi.nlm...les/PMC3867952/

——————

 

Tauroursodeoxycholic acid increases neural stem cell pool and neuronal conversion by regulating mitochondria-cell cycle retrograde signaling.

 

In this study, we identified a novel role for TUDCA in enhancing both proliferation and neuronal conversion potential of NSCs. TUDCA prevented differentiation-induced mitochondrial alterations, without influencing cell death, while increasing self-renewal and proliferation levels of NSCs. Importantly, the mechanisms by which TUDCA modulates cell fate were shown to be dependent on mtROS and ATP regulation, ultimately favoring NSC commitment to a neuronal fate (Fig. 7).

 

https://www.ncbi.nlm...les/PMC4613652/

——————

 

Stimulatory effect of icariin on the proliferation of neural stem cells from rat hippocampus

 

The present study showed that icariin promotes the growth and proliferation of neural stem cells from rat hippocampus in a dose-dependent manner

 

https://www.ncbi.nlm...les/PMC5789743/

——————

 

Role of Mitochondrial Metabolism in the Control of Early Lineage Progression and Aging Phenotypes in Adult Hippocampal Neurogenesis

 

We found short-term piracetam treatment of aged animals to be sufficient to promote neurogenesis, suggesting mitochondrial metabolism as a potential pharmacological target to ameliorate age-associated hippocampal neurogenesis deficits.

 

https://www.ncbi.nlm...les/PMC5300896/

——————

 

Apigenin and related compounds stimulate adult neurogenesis

 

Apigenin and related compounds stimulate adult neurogenesis in vivo and in vitro, by promoting neuronal differentiation. Apigenin promotes learning and memory performance in the Morris water task. The application claims the use of apigenin and related compounds for stimulating adult neurogenesis and for the treatment of neurological diseases, disorders and injuries, by stimulating the generation of neuronal cells in the adult brain.

 

https://www.ncbi.nlm...pubmed/19441930


Edited by Turnbuckle, 05 April 2018 - 08:36 AM.

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#12 Kentavr

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Posted 05 April 2018 - 10:28 AM

and the division of bone marrow cells increases starvation (due to increased expression FOXO1). The number of bone marrow stem cells increases 6 times:



Controlled fasting should be 5-6 days, then a break of 25 days (within 25 days there is a recovery of the body, during this period one should eat well). The procedure must be repeated 8 times.
And not a penny of money.

Edited by Kentavr, 05 April 2018 - 10:33 AM.

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#13 Turnbuckle

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Posted 05 April 2018 - 12:23 PM

Here is research behind Kentavr's info, in English--

 

We tested whether the cycles of PF [Prolonged Fasting lasting 48–120 hr] alone could also stimulate HSC self-renewal. Results using bromodeoxyuridine (BrdU) incorporation assays indicated an approximately 6-fold increase of newly generated (BrdU+) HSPCs (i.e., LT-HSC, ST-HSC, and MPP) in PF mice, which represents 93.7% of the total increase in HSPCs after PF cycles (Figure 2A)...

 

Because during PF mammalian organisms minimize energy expenditure in part by rapidly reducing the size of a wide range of tissues, organs, and cellular populations including blood cells, the reversal of this effect during refeeding represents one of the most potent strategies to regenerate the hematopoietic and possibly other systems and organs in a coordinated manner. Here, we show that PF causes a major reduction in WBC number, followed, during refeeding, by a coordinated process able to regenerate this immune system deficiency by changes beginning during the fasting period, which include a major increase in LT-HSC and ST-HSC and redirection of the frequency of Ly-HSC/Bala-HSC/My-HSC leading to a lineage-balanced mode. In fact, we show that PF alone causes a 28% decrease WBC number, which is fully reversed after refeeding (Figures 7B and S2F). Even after WBCs are severely suppressed or damaged as a consequence of chemotherapy or aging, cycles of PF are able to restore the normal WBC number and lineage balance, suggesting that the organism may be able to exploit its ability to regenerate the hematopoietic system after periods of starvation, independently of the cause of the deficiency

 

Whereas PKA is implicated in stem cell differentiation, our study suggests that cycles of PF downregulate IGF-1 and PKA to promote stem cell self-renewal.

 

http://www.cell.com/...5909(14)00151-9

 

 


Edited by Turnbuckle, 05 April 2018 - 12:34 PM.


#14 QuestforLife

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Posted 10 April 2018 - 09:29 AM

 

Note: I've used C60 (in EVOO with added HT)/stearic acid six or seven times in the past six weeks, and already I've had to go up a half shoe size.

 

Wow, just wow. If this can be repeated by other users then this may well turn out to be your most impressive contribution to this forum Turnbuckle, and you've made many.

 

One word of caution from a self-declared telomere expert - more work probably needs to be done on stem cell symmetrical and asymmetrical division but I suspect both cause telomere shortening . If this is true then although you will be renewing your somatic tissues when they do differentiate, your stem cell pool will be losing its telomere reserve, even though the number of cells is maintained.

 

Women tend to live longer then men, and short people tend to live longer than tall ones (yes there are lots of confounding factors). This to my mind is evidence that greater proliferation causes a loss of telomere reserve and this is significant for aging.

 

You could try adding a telomerase activator to your stack - when cells divide HTERT becomes accessible, so you might get some synergy here. I did a successful experiment in prompting adipocytes to differentiate, and I used liposomal astralogosides IV (and incidentally also C60 on occasion) to protect telomeres.


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#15 QuestforLife

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Posted 10 April 2018 - 09:37 AM

A question Turnbuckle - I understand you are using Fusion to encourage Stem Cells to undergo symmetric division, but do you have any insight into what mechanism C60 is using to cause proliferation?

 

I wonder if there is a limit to how much C60 mitochondria can absorb (based on their membrane potential) and any remainder then does something else in the cell that is encouraging stem cell proliferation. This could explain why prolific users report different and more profound effects.  


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#16 Turnbuckle

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Posted 10 April 2018 - 11:22 AM

Wow, just wow. If this can be repeated by other users then this may well turn out to be your most impressive contribution to this forum Turnbuckle, and you've made many.

 

One word of caution from a self-declared telomere expert - more work probably needs to be done on stem cell symmetrical and asymmetrical division but I suspect both cause telomere shortening . If this is true then although you will be renewing your somatic tissues when they do differentiate, your stem cell pool will be losing its telomere reserve, even though the number of cells is maintained.

 

Women tend to live longer then men, and short people tend to live longer than tall ones (yes there are lots of confounding factors). This to my mind is evidence that greater proliferation causes a loss of telomere reserve and this is significant for aging.

 

You could try adding a telomerase activator to your stack - when cells divide HTERT becomes accessible, so you might get some synergy here. I did a successful experiment in prompting adipocytes to differentiate, and I used liposomal astralogosides IV (and incidentally also C60 on occasion) to protect telomeres.

 

 

You make some excellent points. Certainly stem cell aging via shortening of telomeres could explain the fading of C60 effects, assuming that C60 promotes stem cell proliferation as I think it does. And that could bring about a situation of getting anti-aging effects now and paying for it later by more rapid aging--something that would not be evident in short lived rats. Another point is timing. When stem cells proliferate, that provides a window of opportunity to lengthen their telomeres. And one possibility is controlling the nuclear redox state--keeping it in a relatively reduced state to raise the activity of telomerase.

 

Fusion itself lowers ROS and thus should tend to produce a more reduced cellular environment--

 

Conversely, genetic pro-fusion interventions (inducing mitochondrial elongation) were associated with reduced mitochondrial ROS production, whereas pro-fission interventions (leading to mitochondrial fragmentation) stimulated mitochondrial ROS production.

https://www.scienced...550413115002739

 

 

--and so will higher GSH levels, as GSH is the cells major reducing agent and is known to raise the activity of telomerase. --

 

Telomerase activity is maximal under reduced conditions i.e. when the reduced/oxidized glutathione ratio is high. Consequently glutathione concentration parallels telomerase activity. 

http://www.jbc.org/c...9/33/34332.full

 

 

Also, a reduced nuclear environment is associated with proliferating cells--

 

it was only relatively recently when the group of Dean Jones defining the cellular redox environment by estimation of the ratio of glutathione/glutathione disulfide couple concluded that each phase in the life of the cell is characterized by a particular redox state and that proliferating cells are in a most reduced state

https://www.ncbi.nlm...les/PMC2712766/

 

 

--thus supplements to aid this nuclear environment during stem cell self-renewal should help keep stem cells young. Fusion and supplements that increase GSH, in particular. 


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#17 Turnbuckle

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Posted 10 April 2018 - 12:53 PM

A question Turnbuckle - I understand you are using Fusion to encourage Stem Cells to undergo symmetric division, but do you have any insight into what mechanism C60 is using to cause proliferation?

 

I wonder if there is a limit to how much C60 mitochondria can absorb (based on their membrane potential) and any remainder then does something else in the cell that is encouraging stem cell proliferation. This could explain why prolific users report different and more profound effects.  

 

 

The mechanism is unknown, but it certainly exists--

 

Zero-dimensional fullerenes can modulate the biological behavior of a variety of cell lines. However, the effects and molecular mechanisms of proliferation and cardiomyogenic differentiation in brown adipose-derived stem cells (BADSCs) are still unclear. In this study, we report the initial biological effects of fullerene-C60 on BADSCs at different concentrations. Results suggest that fullerene-C60 has no cytotoxic effects on BADSCs even at a concentration of 100 μg/mL. Fullerene-C60 improves the MAPK expression level and stem cell survival, proliferation, and cardiomyogenesis. Further, we found that the fullerene-C60 modulates cardiomyogenic differentiation.

https://www.ncbi.nlm...pubmed/26848263

 

 

It is obvious that C60 increases mito function and ATP production, and it's known that stem cell mitochondria are more or less quiescent, and the proliferation process begins there. It's possible that C60 blocks uncoupling pores (UCP) and thus kickstarts stem cell mitochondria, as C60 is roughly the same size as those pores.

 

We have shown that only UCP2 is present in undifferentiated stem cells and it disappears simultaneously with the initiation of neuronal differentiation.

http://journals.plos...al.pone.0088474

 


Edited by Turnbuckle, 10 April 2018 - 12:57 PM.

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#18 Nate-2004

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Posted 10 April 2018 - 05:15 PM

Here is research behind Kentavr's info, in English--

 

Mice do not equal humans in even the remotest sense. It's *highly* unlikely that for a human, 8 cycles of 5 days out of 33 will result in what happened with the mice.  That's not to say it couldn't happen during a 28 day fast every 120 days, but that's insane and I don't think I or anyone else I know could ever go that long without food. 



#19 Nate-2004

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Posted 10 April 2018 - 05:21 PM

Turnbuckle what do you mean by "reduced"?

 

Also I don't know if astragalus root extract is a worthwhile addition since it's questionably effective as far as telomerase activation goes, but what about SkQ1?

 

 

I've been taking SkQ1 from Mitolab during fusion the last couple cycles.


Edited by Nate-2004, 10 April 2018 - 05:39 PM.


#20 lost69

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Posted 10 April 2018 - 11:26 PM

did you use actinovo.com liposomal astragalosides IV?i see their liposomals are very cheap, i hope quality is good as well

 

Wow, just wow. If this can be repeated by other users then this may well turn out to be your most impressive contribution to this forum Turnbuckle, and you've made many.

 

One word of caution from a self-declared telomere expert - more work probably needs to be done on stem cell symmetrical and asymmetrical division but I suspect both cause telomere shortening . If this is true then although you will be renewing your somatic tissues when they do differentiate, your stem cell pool will be losing its telomere reserve, even though the number of cells is maintained.

 

Women tend to live longer then men, and short people tend to live longer than tall ones (yes there are lots of confounding factors). This to my mind is evidence that greater proliferation causes a loss of telomere reserve and this is significant for aging.

 

You could try adding a telomerase activator to your stack - when cells divide HTERT becomes accessible, so you might get some synergy here. I did a successful experiment in prompting adipocytes to differentiate, and I used liposomal astralogosides IV (and incidentally also C60 on occasion) to protect telomeres.

 



#21 QuestforLife

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Posted 11 April 2018 - 11:14 AM

did you use actinovo.com liposomal astragalosides IV?i see their liposomals are very cheap, i hope quality is good as well

 

Yes I did. They told me that they'd achieved 90% liposome encapsulation on the last batch they tested in late 2017 and sent me some documentation to prove it. I'm sure they'd do the same for you if you asked.

 

Nate - telomerase activation is a complex subject with lots of things that can stop it working. I'd imagine a mitochondrial antioxidant would help as it will lower ROS and consequently inflammation - which is what you need to do to acheive a reduced (opposite of oxidised) state. It is well known that inflammation shortens telomeres dramaticlly,and it has also been well established that telomerase leaves the nucleus to protect mitochondria in times of high ROS, therefore it is not able to do its normal job. I expect C60oo and SkQ1 would be superfluous however, one would do this job (lowering ROS).

 

I've read all the old Geron and TA-Sciences patents on astralogosides and it seems they are the best bet at the moment for actually extending telomeres, atleast in vitro. (I don't know anything about Bill Andrew's telomerase activator, maybe someone else can inform us?) The problem seems to be that astralagosides are very poorly absorbed into the bloodstream. Cycloastranegol was an attempt to improve this biovailability rather than increase the potency of telomerase activation. It didn't work.  Hence TA Sciences now use a variant of Cycloastranegol called C3-(L)-Valyl-cycloastragenol.

 

Check out patent number US9403866B2; tables 4 (rats) and 5 (dogs) are particularly interesting, at least if you're a Beagle dog!

 

Anyway the practical implication of all this is that liposomes should solve the bioavailability problem. Certainly lots more work needs to be done here to solve the telomere problem, however.


Edited by QuestforLife, 11 April 2018 - 11:17 AM.


#22 lost69

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Posted 11 April 2018 - 02:20 PM

thanks for your feedback

 

i use terraternal Cycloastranegol, aswaganda and milk thystle as weak telomerase activators but i ll try activo astragalosides IV and liposoaml gsh instead terraternal combined with c60 and stearic acid

Yes I did. They told me that they'd achieved 90% liposome encapsulation on the last batch they tested in late 2017 and sent me some documentation to prove it. I'm sure they'd do the same for you if you asked.

 

Nate - telomerase activation is a complex subject with lots of things that can stop it working. I'd imagine a mitochondrial antioxidant would help as it will lower ROS and consequently inflammation - which is what you need to do to acheive a reduced (opposite of oxidised) state. It is well known that inflammation shortens telomeres dramaticlly,and it has also been well established that telomerase leaves the nucleus to protect mitochondria in times of high ROS, therefore it is not able to do its normal job. I expect C60oo and SkQ1 would be superfluous however, one would do this job (lowering ROS).

 

I've read all the old Geron and TA-Sciences patents on astralogosides and it seems they are the best bet at the moment for actually extending telomeres, atleast in vitro. (I don't know anything about Bill Andrew's telomerase activator, maybe someone else can inform us?) The problem seems to be that astralagosides are very poorly absorbed into the bloodstream. Cycloastranegol was an attempt to improve this biovailability rather than increase the potency of telomerase activation. It didn't work.  Hence TA Sciences now use a variant of Cycloastranegol called C3-(L)-Valyl-cycloastragenol.

 

Check out patent number US9403866B2; tables 4 (rats) and 5 (dogs) are particularly interesting, at least if you're a Beagle dog!

 

Anyway the practical implication of all this is that liposomes should solve the bioavailability problem. Certainly lots more work needs to be done here to solve the telomere problem, however.

 



#23 aribadabar

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Posted 11 April 2018 - 02:33 PM

Fascinating thread - thanks Turnbuckle!

 

I've read all the old Geron and TA-Sciences patents on astralogosides and it seems they are the best bet at the moment for actually extending telomeres, atleast in vitro. (I don't know anything about Bill Andrew's telomerase activator, maybe someone else can inform us?) The problem seems to be that astralagosides are very poorly absorbed into the bloodstream. Cycloastranegol was an attempt to improve this biovailability rather than increase the potency of telomerase activation. It didn't work.  Hence TA Sciences now use a variant of Cycloastranegol called C3-(L)-Valyl-cycloastragenol.

 

Check out patent number US9403866B2; tables 4 (rats) and 5 (dogs) are particularly interesting, at least if you're a Beagle dog!

 

Anyway the practical implication of all this is that liposomes should solve the bioavailability problem. Certainly lots more work needs to be done here to solve the telomere problem, however.

 

FWIW a technical brochure suggests that cycloastragenol is a smaller and more bioavailable molecule than astragaloside IV.

 

Does liposomal astragaloside IV better than cycloastragenol or they are roughly the same in terms of telomerase activation?

Or it's better to combine both?
 
Thanks for the C3-(L)-Valyl-cycloastragenol pointer - I have not heard of it before.

 

did you use actinovo.com liposomal astragalosides IV?i see their liposomals are very cheap, i hope quality is good as well

 

I see that you reported ingesting of cycloastragenol to good effect. Do you still experience any continued benefit?

 

 

The mechanism is unknown, but it certainly exists--

 

 

It is obvious that C60 increases mito function and ATP production, and it's known that stem cell mitochondria are more or less quiescent, and the proliferation process begins there. It's possible that C60 blocks uncoupling pores (UCP) and thus kickstarts stem cell mitochondria, as C60 is roughly the same size as those pores.

 

 

Doesn't the C60oo long-half life and its ability to stay within the cell supposedly for weeks, and even months, after repeated administration negatively interfere with the fission/fusion QA cycle as it saves marginally functioning mitochondria to be marked for mitophagy?

Or it is the "price to pay" for its stem cells renewal effect?

 



#24 QuestforLife

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Posted 11 April 2018 - 02:43 PM

The mechanism is unknown, but it certainly exists--

 

 

It is obvious that C60 increases mito function and ATP production, and it's known that stem cell mitochondria are more or less quiescent, and the proliferation process begins there. It's possible that C60 blocks uncoupling pores (UCP) and thus kickstarts stem cell mitochondria, as C60 is roughly the same size as those pores.

 

I'm slightly concerned by the concentrations required to elicit an effect in the paper you posted Turnbuckle.

 

The Baati study achieved blood levels of the order of 0.1-1ug/mL, tending to be towards the lower end with oral administration, but 'Fullerene mediates proliferation and cardiomyogenic differentiation of adipose-derived stem cells via modulation of MaPK pathway and cardiac protein expression' used 5-100ug/mL concentrations, with the best results at around 50ug/mL.

 

So either you have discovered we don't really need those levels to get the effects you are reporting, or the effects you're reporting are due to something other than C60, or maybe you have built up the fullerene in your system over a longer period, and the dose you are taking with stearic acid is not the only fullerene in your system.

 

What do you think?



#25 QuestforLife

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Posted 11 April 2018 - 02:52 PM

Fascinating thread - thanks Turnbuckle!

 

 

FWIW a technical brochure suggests that cycloastragenol is a smaller and more bioavailable molecule than astragaloside IV.

 

Does liposomal astragaloside IV better than cycloastragenol or they are roughly the same in terms of telomerase activation?

Or it's better to combine both?
 
Thanks for the C3-(L)-Valyl-cycloastragenol pointer - I have not heard of it before.

 

 

I see that you reported ingesting of cycloastragenol to good effect. Do you still experience any continued benefit?

 

 

 

 

Yes, cycloastranegol has the same backbone, with the same telomerase activation as astralogosides IV, but supposedly better bioavailability - but that study was done in rats and later found not to hold true for Beagles (and presumably humans). That's why they started trying other similar molecules. It's all in the patent, see the Tables that I suggested.

 

Liposomes should egress the digestive system intact, and even get into cells so removing the need to mess around with different variations on the molecule. I said SHOULD. I'm still not convinced this is doing all that much - bear in mind half life is probably only ~4 hours for the free molecule, and most cells guard their HTERT gene jealously. Knowing you're causing cell division is a good way to know that this is the right time to try and grow telomeres however, and this is why I think this might work well with Turnbuckle's procedure. We badly need a better telomere test to know for sure (leukocyte ones are mainly a waste of time and money IMO).


Edited by QuestforLife, 11 April 2018 - 02:54 PM.

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#26 Nate-2004

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Posted 11 April 2018 - 05:21 PM

So then what is the half-life of C60 supposedly? I took my first dose about 3 hours after stearic acid and broccomax.  I still have it running on the magnetic stirrer and it's been spinning about 5 days now. This is the last of my C60 unfortunately. It's around 6mg per ML.

 

I assume I should wait the usual week before trying again.  Wondering how long I should stay in fusion this time around.


Edited by Nate-2004, 11 April 2018 - 05:37 PM.


#27 aribadabar

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Posted 11 April 2018 - 06:34 PM

It's around 6mg per ML.

 

FYI - the maximum solubility of C60 in olive oil is about 0.9mg/ml. Putting more than that is a waste of C60.



#28 Turnbuckle

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Posted 11 April 2018 - 06:44 PM

I'm slightly concerned by the concentrations required to elicit an effect in the paper you posted Turnbuckle.

 

The Baati study achieved blood levels of the order of 0.1-1ug/mL, tending to be towards the lower end with oral administration, but 'Fullerene mediates proliferation and cardiomyogenic differentiation of adipose-derived stem cells via modulation of MaPK pathway and cardiac protein expression' used 5-100ug/mL concentrations, with the best results at around 50ug/mL.

 

So either you have discovered we don't really need those levels to get the effects you are reporting, or the effects you're reporting are due to something other than C60, or maybe you have built up the fullerene in your system over a longer period, and the dose you are taking with stearic acid is not the only fullerene in your system.

 

What do you think?

 

 

I use one teaspoon of .6 mg/ml, or 3 mg C60. I don't see any reason to use more. In fact, more may be less. I use it about an hour after stearic acid + NAC (1.8 g), and I expect the C60 to be gone from the mitochondria (if not the body) in a day or so. Am I sure about all these time frames? No.



#29 Kentavr

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Posted 11 April 2018 - 07:24 PM

I think the use of Ubiquinol will enhance the telomere lengthening effect.

Reason: an increase in the production of adenosine triphosphate. Consequently, all processes in the cells will occur more actively.

In addition, it is a mitochondrial antioxidant.

Edited by Kentavr, 11 April 2018 - 07:28 PM.


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#30 Nate-2004

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Posted 11 April 2018 - 07:30 PM

FYI - the maximum solubility of C60 in olive oil is about 0.9mg/ml. Putting more than that is a waste of C60.

 

I think I meant 0.6mg/ml, I put 60mg in 100ml. I'm bad at math.


Edited by Nate-2004, 11 April 2018 - 07:32 PM.






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