2523 replies to this topic

[Turnbuckle]

A question has arisen in me when reading the last posts:
Do you know if stem cells have a mechanism for repairing damaged mitochondria?
I remember reading that they suffer less ROS than somatic cells, but that they can also suffer DNA damage.

It would be great to know that stem cells can effectively repair their nuclear and mitochondrial DNA damage.
 

 

 

Yes they can get rid of damaged mitochondria, but only during differentiation. As I noted in post 56 -- And there's a second advantage to asymmetric division as defective mitochondria are partitioned to the somatic daughter where mito QC can get rid of them.

 

Here is the reference--

 

By dividing asymmetrically, stem cells can generate two daughter cells with distinct fates. However, evidence is limited in mammalian systems for the selective apportioning of subcellular contents between daughters. We followed the fates of old and young organelles during the division of human mammary stem-like cells and found that such cells apportion aged mitochondria asymmetrically between daughter cells. Daughter cells that received fewer old mitochondria maintained stem cell traits. Inhibition of mitochondrial fission disrupted both the age-dependent sub-cellular localization and segregation of mitochondria, and caused loss of stem cell properties in the progeny cells. Hence, mechanisms exist for mammalian stem-like cells to asymmetrically sort aged and young mitochondria, and these are important for maintaining stemness properties.

https://www.ncbi.nlm...les/PMC4405120/

 

[ryukenden]

Where do I buy Stearic acid to ingest?

[ceridwen]

The only thing that seems to have caused any improvement in my condition is MitoQ what does that imply?

[BieraK]

All of this could be applied to MitoQ?
MitoQ looks safer compared to c60, some users reports similar effects of MitoQ compared to the first weeks of c60. In my case C60 was excellent at the beginning, but over time began to produce negative effects, as if it lost its effects. Alcohol tolerance remained albeit at a lower level, however hangovers returned. I did not feel as oxygenated as at the beginning.
MitoQ on the other hand has studies that support its safety and effectiveness
For example this recent study:
 

 

Chronic Supplementation With a Mitochondrial Antioxidant (MitoQ) Improves Vascular Function in Healthy Older Adults

Matthew J. Rossman, Jessica R. Santos-Parker, Chelsea A.C. Steward, Nina Z. Bispham, Lauren M. Cuevas, Hannah L. Rosenberg, Kayla A. Woodward, Michel Chonchol, Rachel A. Gioscia-Ryan, Michael P. Murphy, Douglas R. Seals

 

Abstract

Excess reactive oxygen species production by mitochondria is a key mechanism of age-related vascular dysfunction. Our laboratory has shown that supplementation with the mitochondrial-targeted antioxidant MitoQ improves vascular endothelial function by reducing mitochondrial reactive oxygen species and ameliorates arterial stiffening in old mice, but the effects in humans are unknown. Here, we sought to translate our preclinical findings to humans and determine the safety and efficacy of MitoQ. Twenty healthy older adults (60–79 years) with impaired endothelial function (brachial artery flow–mediated dilation <6%) underwent 6 weeks of oral supplementation with MitoQ (20 mg/d) or placebo in a randomized, placebo-controlled, double-blind, crossover design study. MitoQ was well tolerated, and plasma MitoQ was higher after the treatment versus placebo period (P<0.05). Brachial artery flow–mediated dilation was 42% higher after MitoQ versus placebo (P<0.05); the improvement was associated with amelioration of mitochondrial reactive oxygen species–related suppression of endothelial function (assessed as the increase in flow-mediated dilation with acute, supratherapeutic MitoQ [160 mg] administration; n=9; P<0.05). Aortic stiffness (carotid–femoral pulse wave velocity) was lower after MitoQ versus placebo (P<0.05) in participants with elevated baseline levels (carotid–femoral pulse wave velocity >7.60 m/s; n=11). Plasma oxidized LDL (low-density lipoprotein), a marker of oxidative stress, also was lower after MitoQ versus placebo (P<0.05). Participant characteristics, endothelium-independent dilation (sublingual nitroglycerin), and circulating markers of inflammation were not different (all P>0.1). These findings in humans extend earlier preclinical observations and suggest that MitoQ and other therapeutic strategies targeting mitochondrial reactive oxygen species may hold promise for treating age-related vascular dysfunction.

 

Edited by BieraK, 06 May 2018 - 10:29 AM.

[Turnbuckle]

All of this could be applied to MitoQ?
MitoQ looks safer compared to c60, some users reports similar effects of MitoQ compared to the first weeks of c60. In my case C60 was excellent at the beginning, but over time began to produce negative effects, as if it lost its effects. Alcohol tolerance remained albeit at a lower level, however hangovers returned. I did not feel as oxygenated as at the beginning.
MitoQ on the other hand has studies that support its safety and effectiveness
For example this recent study:
 

 

 

That's interesting. Stem cells appear to be driven into proliferation by the awakening of their mitochondria. C60 appears to do that, and from what you describe, mitoq might do that as well. I have never tried the latter so I can't say from direct experience. But if so, using mitoq with a fusion protocol might get you back to the good results you were obtaining initially. I am certainly seeing that with C60, and will be posting an updated protocol soon. 

 

Note: Stem cells are kept in a quiescent state by the large number of UCP pores in their mitochondria. They thus get their energy from glycolysis instead of glucose oxidation, and when the UCP pores disappear, energy production shifts to oxidation and the cells wake up with the burst of ATP. I've previously speculated that C60 might be the right size to block those pores, and in fact there are other nanoparticles (such as gold and silver) that can stimulate stem cells, though the mechanism has not been recognized. Mitoq will certainly not block the pores, but might stimulate ATP production enough to kick start the process. 

 

Edited by Turnbuckle, 06 May 2018 - 11:37 AM.

[QuestforLife]

Arterial rejuvenation has also been achieved by using very low dose sartan and statin combination, supposedly through higher telomerase levels. (It does not say whether this is due to having more stem cells, or just more telomerase).

https://www.ncbi.nlm...ubmed/26214555/

Full text through sci-hub.

I wonder what the thread connecting these is.

[Andey]

There is also a recent paper that shows the effect of 24h fast on mice intestinal stem cells

Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging

http://sci-hub.tw/ht...5909(18)30163-2

Is it sensible to think that there is some synergy could be obtained with a protocol + fasting?

[QuestforLife]

My take on fasting is that it gives the (stem) cell time to clear out junk, including faulty mitochondria (mitophagy), and this means that when the time comes to divide, it is more likely to be able to do so.

I think with Turnbuckle's new protocol we are assuming good mitochondria (due to previous cycles of fission), so any fasting should probably fall in that portion of the cycle.

Here we are trying to use those good mitochondria to spur rejuvenation through tissue proliferation, and from what Turnbuckle is reporting (C60 back to its original effectiveness), it may be working

[Turnbuckle]

Arterial rejuvenation has also been achieved by using very low dose sartan and statin combination, supposedly through higher telomerase levels. (It does not say whether this is due to having more stem cells, or just more telomerase).

https://www.ncbi.nlm...ubmed/26214555/

Full text through sci-hub.

I wonder what the thread connecting these is.

 

 

I don't trust any research saying anything good about statins (though these guys don't have any obvious connection to the industry). And I'm not sure there is any connection to stem cell self-renewal. Stem cells don't typically have a problem with enough telomerase, so the major consideration is to make sure they aren't eroded during replication by ROS.

[QuestforLife]

Stem cells don't typically have a problem with telomerase?

It is my understanding that though stem cells have more telomerase and longer telomeres than the somatic tissues they supply, they still have a limit on their number of replications.

Mesenchymal stem cells, a kind of backup stem cell that can become many different types of tissues, show replicative senescence and also a tendency to become one the rather than another cell depending on how many times they've divided:

https://www.ncbi.nlm...les/PMC2374903/

[Turnbuckle]

Stem cells don't typically have a problem with telomerase?

It is my understanding that though stem cells have more telomerase and longer telomeres than the somatic tissues they supply, they still have a limit on their number of replications.

Mesenchymal stem cells, a kind of backup stem cell that can become many different types of tissues, show replicative senescence and also a tendency to become one the rather than another cell depending on how many times they've divided:

https://www.ncbi.nlm...les/PMC2374903/

 

 

They don't blame the decline on telomerase, but on a epigenetic degradation that they speculate might set a senescence program running--

 

Our results indicate that replicative senescence is associated with very reproducible changes in gene expression of MSC from different donors as well as under different culture conditions. Genes involved in DNA replication and repair are successively down-regulated. The final existence of a senescence associated program remains to be proven and specific factors that would activate or regulate such a program are yet unknown. However, the parallel nature of the molecular changes described in this study further indicates that senescence represents a somehow organized process. It is also striking, that these changes increase successively with every passage in a continuous fashion and that they are not restricted to the end of long-term in vitro culture.

 

 

Maybe, but speculative. Another paper says that while telomerase alone will not produce immortality, adding LT antigen will--

 

Neither hTERT nor U19tsA58 LT antigen alone was sufficient for immortalization of either mammary fibroblasts or endothelial cells. A combination of both genes, in whatever order and at both early and late passage, however, resulted in their high-frequency immortalization. Importantly, temperature-shift experiments showed that in such lines, functional telomerase alone was unable to maintain the immortal state, which remained dependent on functional LT antigen.

https://www.ncbi.nlm...icles/PMC14642/

 

 

Simian virus LT antigen is used to immortalize cells, but that is not very useful to us at present.

[QuestforLife]

They might not blame replicative senescence on telomere attrition (the hint is in the name!) but that is what is causing it alright - in every in vitro experiment with any non immortalised cell type ever. You're not suggesting stem cells are immortalised, are you?

Saying things like 'Our results indicate that replicative senescence is associated with very reproducible changes in gene expression of MSC from different donors as well as under different culture conditions' and 'the parallel nature of the molecular changes described in this study further indicates that senescence represents a somehow organized process' whilst making out this is somehow a new discovery and not completely explained before in a hundred papers is absolutely hilarious, and I must apologize for bringing this paper to your attention. It was simply the first paper I saw demonstrating replicative senescence in stem cells, but the researchers are obviously a bunch of clowns.

'It is also striking, that these changes increase successively with every passage in a continuous fashion and that they are not restricted to the end of long-term in vitro culture.'

This is referring to the fact some researchers think shortening telomeres only exert an effect when they get very short. But it's been shown by Shay and Wright amongst others

http://journals.plos...al.pbio.2000016

that the telomere affects gene expression both in the subtelomeric region, and over long distance, by the way the telomere folds back and associates with the chromosome and how this changes as it shortens long before it becomes short enough to cause arrest. So, it's not a mystery that changes 'are not restricted to the end of long-term in vitro culture.'

The second paper is well out of date. Researchers used to argue about exactly what was needed for immortalisation, whether you needed to inhibt p16 as well, etc., but no longer. Telomerase is all it takes.

Of course none of this changes the fact that we can't immortalise all our somatic cells (or even stem cells) without an absolutely rock solid anti cancer strategy. But lengthening them periodically (should that become feasible) seems like a non brainer and essential for living a really long time.

Edited by QuestforLife, 06 May 2018 - 07:55 PM.

[Kentavr]

I do not recommend using "MitoQ"

 

Reason: The molecule "MitoQ" when the dosage is exceeded is 2 times converted from an antioxidant to a pro-oxidant.

 

For the molecule "SkQ1" it is necessary to exceed the dosage by 1000 times.

 

https://link.springe...06297908120018 

 

The advantage of SkQ1 is that the difference in the concentrations between pro- and antioxidant activity is 1000. Experiments on mitochondria have shown that SkQ1 begins to exhibit antioxidant properties already at concentrations of 1 nM, and pro-oxidant at concentrations of about 1 μM. For comparison, the concentration of MitoQ should be increased to 0.5 μM - less than twice, so that the compound began to increase the production of AFK mitochondria. The appearance of antioxidant activity of MitoQ begins only at concentrations of 0.3 μM

Edited by Kentavr, 06 May 2018 - 08:08 PM.

[QuestforLife]

There is also a recent paper that shows the effect of 24h fast on mice intestinal stem cells
Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging
http://sci-hub.tw/ht...5909(18)30163-2
Is it sensible to think that there is some synergy could be obtained with a protocol + fasting?

Just had another look at this - fasting causes a switch to lipid metabolism and this is what is credited with stem cell self renewal. I wonder then whether this is a case of mitochondrial fusion state, similar to what we are trying with stearic acid? If this is the case then maybe a fast could be combined with C60 as an alternative.

Interesting also that they used a banned substance

https://en.m.wikiped...g/wiki/GW501516

To show fasting was using the PPAR delta pathway to burn fats, but worrying too, as this substance can cause cancer.

[Kentavr]

By the way, pay attention to this article:

 

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

 

Activation of telomerase leads to accelerated epigenetic aging.

I agree with the author.

Here's more news:

 

https://22century.ru...d-health/61352 

 

I ask you to read it.

 

 

[QuestforLife]

By the way, pay attention to this article:

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

Activation of telomerase leads to accelerated epigenetic aging.
I agree with the author.
Here's more news:

https://22century.ru...d-health/61352

I ask you to read it.

Don't get me started on how wrong this is. Plus it would completely derail the thread.

[Kentavr]

Don't get me started on how wrong this is. Plus it would completely derail the thread. 

 

I speak very little English.

I ask you to explain in more detail and simply your phrase.

Edited by Kentavr, 06 May 2018 - 08:56 PM.

[QuestforLife]

I speak very little English.
I ask you to explain in more detail and simply your phrase.

There must be another thread discussing the telomerase - epigenetic age link.

Very briefly - the Horvath clock is correlated to chronological age. The newer phenoAge clock is correlated with mortality. And the phenoAge clock is correlated the right way around with (leukocyte) telomere length, I.e. longer telomeres, younger PhenoAge. So it's a statistical thing with the Horvath Clock, probably based on people with longer telomeres either hanging onto cells for longer, or those cells being more metabolically active, so being more likely to acquire those semi random epigenetic changes. I'm sure this will all be cleared up in a few years.

That's just my take - but from a stem cell point of view I don't think we need to worry we'll have too much telomerase. I'm interested to see what else we can find out using Turnbuckle's protocol about restocking our stem cells and then putting them to work.

Edited by QuestforLife, 07 May 2018 - 06:56 AM.

[Andey]

 

I do not recommend using "MitoQ"

 

Reason: The molecule "MitoQ" when the dosage is exceeded is 2 times converted from an antioxidant to a pro-oxidant.

 

For the molecule "SkQ1" it is necessary to exceed the dosage by 1000 times.

 

https://link.springe...06297908120018 

 

The advantage of SkQ1 is that the difference in the concentrations between pro- and antioxidant activity is 1000. Experiments on mitochondria have shown that SkQ1 begins to exhibit antioxidant properties already at concentrations of 1 nM, and pro-oxidant at concentrations of about 1 μM. For comparison, the concentration of MitoQ should be increased to 0.5 μM - less than twice, so that the compound began to increase the production of AFK mitochondria. The appearance of antioxidant activity of MitoQ begins only at concentrations of 0.3 μM

 

 

  Its a study done by the SkQ1 inventor's group. SkQ1 and MitoQ are competing products, and I assume it's not that hard to `massage` study design to get the result you want.

[Kentavr]

Yes, it is possible, but the difference of 500 times is not the difference that can be distorted. Too much risk to spoil the reputation. Nobody will do this.

[Nate-2004]

SkQ1 is obnoxiously expensive and difficult to obtain in the amounts required to achieve the desired effect.

 

MitoLab sells SkQ1 in useless, miniscule doses that amount to nothing, 5mcg, where 3mg is optimal. Easier to just use a conservative, low dose (10mg) MitoQ in the mornings.

 

Back on topic:

 

I did another round of the fusion protocol with C60 this weekend but this time I had already run out of the liposomal astragalus. After doing some reading I figure that's probably not doing much to preserve telomere lengths anyway. Even TA-65 is horrible at significantly boosting telomerase in any way. 

 

I do notice some differences in my skin quality at this point after more than 3 rounds of this so far. I got a picture taken in good light and I look way better than usual. All subjective of course.

Edited by Nate-2004, 07 May 2018 - 02:32 PM.

[lost69]

i use both mito q oral and sqk1 drops in the eyes, although difficult to say what mitoq does among all other supps and interventions but i feel absolutely no difference when i stop it for 2-3weeks when shipments of new bottles are late, i just use it because it shouldn t hurt anyway

 

sqk1 drops have an effect on eyes and when i stop it for more than 4 days eye sight worsen a little but nothing so big

 

if i stop c60 i do feel the difference within days, c60 vs mito Q/sqk1.....the second ones are so wek effect i could not say where they stand

 

 

Edited by lost69, 07 May 2018 - 02:42 PM.

[Turnbuckle]

Experimental stem cell protocol, biased for self-renewal

 

 

Time 0 —

Stearic acid — 10 g, in hot chocolate or brownie (Fusion)

 

Time 1:00 —

TUDCA — 500 mg (Mitochondrial biogenesis & stem cell self-renewal)

PQQ — 40 mg (Mitochondrial biogenesis)

Jiaogulan — 800 mg (AMPK activator)

L-Threonine — 5 g (Stem cell nutrition)

Taurine — 5 g (Stem cell nutrition)

Core brand Liposomal Glutathione — .5 g (Master antioxidant, telomere protection/lengthening)

ALA — 300 mg (Antioxidant, stimulates stem cell proliferation)

 

Time 2:00 —

C60 — 1 teaspoon of .6 mg/ml in oil, 3 mg C60 (Mitochondria and stem cell stimulant)

Vitamin C — 1 g (Antioxidant to protect telomeres)

L-Threonine* — 5 g (Stem cell nutrition)

Taurine* — 5 g (Stem cell nutrition)

*Again later if feeling fatigue

 

 

 

Suggested schedule—Three days in a row, then a break of two or more days.

 

 

 

Notes:

 

It appears that fusion does not completely dictate self-renewal over differentiation, but only biases stem cells in that direction. So while fission may be necessary for rapid mito QC, it is likely unnecessary for this stem cell protocol. https://www.scienced...934590916300820

 

Creating new stem cells is relatively fast and can be considered completed after 24 hours. New somatic cells take longer — days to weeks for most cell types, and more than a year for neurons. https://www.ncbi.nlm...les/PMC5669577/

 

I used glutathione and other antioxidants to maintain and potentially lengthen telomeres during self-renewal. Liposomal glutathione is more available orally, and I used Core brand Liposomal Glutathione as it had the highest rating on Amazon. (I haven't tried any others.)

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

 

Stearic acid in brownies or hot chocolate on an empty stomach speeds up the digestion and absorption. Digestion of raw stearic acid powder or flakes will likely take a long and variable amount of time. These options were discussed previously in this thread. My source of stearic acid was Amazon (US) — 3 Lbs Stearic Acid White Flakes - Food Grade NF/USP

 

Stem cell nutrients L-Threonine and taurine were mixed into fruit juice—1.5 teaspoons each. The powders are almost tasteless. I’ve noticed fatigue an hour or more later if I don’t take them. This is especially true for L-Threonine.

https://www.scienced...873506112000232

https://www.ncbi.nlm...les/PMC4206991/

 

I deleted DHEA and NAC used in previous trials due their hypertensive effects. In any case, one should have a BP monitor available when using this protocol, esp. if one is hypertensive.

 

The C60 was either dissolved in EVOO or in MCT oil. In the latter case I grafted CoQ10 to it with red light under vacuum. The effect is subtly different, but it is too soon to make a recommendation. This I discussed on another thread a couple of years ago. See post #24.

 

[aribadabar]

Experimental stem cell protocol, biased for self-renewal

 

 

Time 0 —

Stearic acid — 10 g, in hot chocolate or brownie (Fusion)

 

Time 1:00 —

TUDCA — 500 mg (Mitochondrial biogenesis & stem cell self-renewal)

PQQ — 40 mg (Mitochondrial biogenesis)

Jiaogulan — 800 mg (AMPK activator)

L-Threonine — 5 g (Stem cell nutrition)

Taurine — 5 g (Stem cell nutrition)

Core brand Liposomal Glutathione — .5 g (Master antioxidant, telomere protection/lengthening)

ALA — 300 mg (Antioxidant, stimulates stem cell proliferation)

 

Time 2:00 —

C60 — 1 teaspoon of .6 mg/ml in oil, 3 mg C60 (Mitochondria and stem cell stimulant)

Vitamin C — 1 g (Antioxidant to protect telomeres)

L-Threonine* — 5 g (Stem cell nutrition)

Taurine* — 5 g (Stem cell nutrition)

*Again later if feeling fatigue

 

 

 

Suggested schedule—Three days in a row, then a break of two or more days.

 

 

 

Notes:

 

It appears that fusion does not completely dictate self-renewal over differentiation, but only biases stem cells in that direction. So while fission may be necessary for rapid mito QC, it is likely unnecessary for this stem cell protocol. 

 

Thank you for sharing your insights with the community.

 

So is it a good idea to blend in the mito fusion phase with this SC protocol i.e. maintain not only the the overlapping components (stearic acid, PQQ, vit C)  but also leucine, hydroxytyrosol, vit B complex?

 

Is cycloastragenol a good addition too, and if so, is it better to be ingested in the beginning or more towards the later stages of the SC regimen? 

 

In your opinion, what is the best way to sync this protocol with the AD detox one?

 

Thanks!

[Turnbuckle]

Thank you for sharing your insights with the community.

 

So is it a good idea to blend in the mito fusion phase with this SC protocol i.e. maintain not only the the overlapping components (stearic acid, PQQ, vit C)  but also leucine, hydroxytyrosol, vit B complex?

 

Is cycloastragenol a good addition too, and if so, is it better to be ingested in the beginning or more towards the later stages of the SC regimen? 

 

In your opinion, what is the best way to sync this protocol with the AD detox one?

 

Thanks!

 

If you have symptoms of AD, that is an emergency situation and you'd want to address that first. Then when the symptoms abate you can back off of a daily AD protocol and fit these other things in. Next I'd suggest you clean up your mitochondria (as mito dysfunction is tied in to AD but is not the root cause), and finally try this stem cell protocol. Ultimately, each is something you might do intermittently and as needed.  As for cycloastragenol, I've never tried it and have no opinion on it, other than it is probably not going to deliver much bang for the buck. My goal for all these things is to find the cheapest, readily available supplements that actually work.

[Female Scientist]

Looking forward to trying this. But since I am a LLLT/Red Light user, would it make sense to swap LLLT for the C60 in this protocol? Basing this on your comment about LLLT being good for SC.  You also mentioned that Fullerenes don't respond well to light. Thanks as always for your dedication to the subject...

 

Experimental stem cell protocol, biased for self-renewal

 

 

Time 0 —

Stearic acid — 10 g, in hot chocolate or brownie (Fusion)

 

Time 1:00 —

TUDCA — 500 mg (Mitochondrial biogenesis & stem cell self-renewal)

PQQ — 40 mg (Mitochondrial biogenesis)

Jiaogulan — 800 mg (AMPK activator)

L-Threonine — 5 g (Stem cell nutrition)

Taurine — 5 g (Stem cell nutrition)

Core brand Liposomal Glutathione — .5 g (Master antioxidant, telomere protection/lengthening)

ALA — 300 mg (Antioxidant, stimulates stem cell proliferation)

 

Time 2:00 —

C60 — 1 teaspoon of .6 mg/ml in oil, 3 mg C60 (Mitochondria and stem cell stimulant)

Vitamin C — 1 g (Antioxidant to protect telomeres)

L-Threonine* — 5 g (Stem cell nutrition)

Taurine* — 5 g (Stem cell nutrition)

*Again later if feeling fatigue

 

 

 

Suggested schedule—Three days in a row, then a break of two or more days.

 

 

 

Notes:

 

It appears that fusion does not completely dictate self-renewal over differentiation, but only biases stem cells in that direction. So while fission may be necessary for rapid mito QC, it is likely unnecessary for this stem cell protocol. https://www.scienced...934590916300820

 

Creating new stem cells is relatively fast and can be considered completed after 24 hours. New somatic cells take longer — days to weeks for most cell types, and more than a year for neurons. https://www.ncbi.nlm...les/PMC5669577/

 

I used glutathione and other antioxidants to maintain and potentially lengthen telomeres during self-renewal. Liposomal glutathione is more available orally, and I used Core brand Liposomal Glutathione as it had the highest rating on Amazon. (I haven't tried any others.)

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

 

Stearic acid in brownies or hot chocolate on an empty stomach speeds up the digestion and absorption. Digestion of raw stearic acid powder or flakes will likely take a long and variable amount of time. These options were discussed previously in this thread. My source of stearic acid was Amazon (US) — 3 Lbs Stearic Acid White Flakes - Food Grade NF/USP

 

Stem cell nutrients L-Threonine and taurine were mixed into fruit juice—1.5 teaspoons each. The powders are almost tasteless. I’ve noticed fatigue an hour or more later if I don’t take them. This is especially true for L-Threonine.

https://www.scienced...873506112000232

https://www.ncbi.nlm...les/PMC4206991/

 

I deleted DHEA and NAC used in previous trials due their hypertensive effects. In any case, one should have a BP monitor available when using this protocol, esp. if one is hypertensive.

 

The C60 was either dissolved in EVOO or in MCT oil. In the latter case I grafted CoQ10 to it with red light under vacuum. The effect is subtly different, but it is too soon to make a recommendation. This I discussed on another thread a couple of years ago. See post #24.

 

[Turnbuckle]

Looking forward to trying this. But since I am a LLLT/Red Light user, would it make sense to swap LLLT for the C60 in this protocol? Basing this on your comment about LLLT being good for SC.  You also mentioned that Fullerenes don't respond well to light. Thanks as always for your dedication to the subject...

 

 

Insofar as LLLT may work for superficial treatments, a topical treatment of stearic acid enriched oil might stimulate SC self-renewal in the target area. You could also try going the other way by adding apigenin to a topical oil, which might enhance SC differentiation. Apigenin has also been found to stimulate neural stem cells, as well as collagen synthesis. I've tried apigenin (dissolved in high oleic oil then added to coconut oil) on a knee without LLLT, and it seemed to make a difference. Applying a red LED flashlight half an hour later might be interesting, as I doubt coherent light is actually required.

Edited by Turnbuckle, 07 May 2018 - 10:22 PM.

[Female Scientist]

We often use LLLT for pain management as well. -- As to your new SC protocol -- might there be benefit in following the SC protocol, but swapping the C60 for the LLLT? Thanks again.

Insofar as LLLT may work for superficial treatments, a topical treatment of stearic acid enriched oil might stimulate SC self-renewal in the target area. You could also try going the other way by adding apigenin to a topical oil, which might enhance SC differentiation. Apigenin has also been found to stimulate neural stem cells, as well as collagen synthesis. I've tried apigenin (dissolved in high oleic oil then added to coconut oil) on a knee without LLLT, and it seemed to make a difference. Applying a red LED flashlight half an hour later might be interesting, as I doubt coherent light is actually required.

 

[Turnbuckle]

No. You can't make a straight swap.

[Kentavr]

The very high efficiency of SkQs allows the use of extremely low doses of these antioxidants for in vivo treatments, which decreases the probability of adverse side effects. Concerning possible overdose, such effects are not excluded, first of all, due to the fact that SkQs, like the great majority of antioxidants, become prooxidants when their concentration is increased. Fortunately, the window between anti- and prooxidant activities for plastoquinone and its derivatives is very large (from 30 to 1,000 times). For MitoQ, a CoQ derivative, the window is much smaller [11,54]. Nevertheless, even MitoQ was shown to have favorable in vivo effect in treating animals suffering from several oxidative stress-related pathologies, namely cardiac ischemia/reperfusion injury [55], negative consequences of nitroglycerin therapy [56], hypertension [57], sepsis [58,59], doxorubicin toxicity [60], diabetes [61], cocaine toxicity [62], insecticide toxicity in rats [63], and hepatic stenosis in ethanol-consuming rats [64]. For SkQs, this list is even longer (which is hardly surprising since their antioxidant activities are higher and the therapeutic windows are much larger than for MitoQ). It includes, as already mentioned, such pathologies as rhabdomyolysis, sepsis caused by pyelonephritis, stroke, myocardial infarction, arrhythmia, lymphomas in p53–/– rats, uveitis, dry eye syndrome, glaucoma, cataract, macular degeneration, etc.

 

---

 

Effects of SkQs and MitoQ cannot be explained by the assumption that they operate as scavengers

of non-mitochondrial ROS, stimulating antioxidant functions of mitochondria (“mitochondria as an

intracellular sink for ROS” [1]). Being a small hydrophilic cation, O2•– cannot penetrate a membrane. 

 

The ROS species OH• and HO2• are so aggressive and short-lived that their translocation from cytosol to the

mitochondrial interior is highly improbable. As to H2O2, a long-lived penetrant, it does not interact with

quinols.

 

https://www.scienced...1735X?via=ihub 

 

http://sci-hub.tw/ht...1735X?via=ihub