331 replies to this topic

[Turnbuckle]

I’m posting this because I’ve seen a number of reports of poor results from continuous use of C60, and continuous use is likely a bad idea.

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While C60/EVOO is certainly an anti-oxidant, there is also a spectrum of effects that appear to be persistent if not permanent. One possible explanation is that C60 is modifying the epigenetics of the mitochondrial DNA (mtDNA), as epigenetic changes produce very long lasting effects.

Some background:

The epigenetic content of mtDNA is due to methyl groups that attach to DNA and act as off switches. These are copied after DNA replication to the daughter strand by an enzyme known as methyltransferase, which must contact both strands to copy the switch positions. It is believed from a theoretical study that C60 is attracted to the DNA groove between strands. There it may act as a physical barrier--a methyltransferase inhibitor like procaine*, which is also attracted to the DNA groove and has been shown to extend the lifespan of rats.

The theory:

If the methylation of mtDNA is randomly reduced (and thus has fewer genes turned off) in some fraction of mitochondria this will prove to be advantageous and the population of a cell’s mitochondria (of which there are typically hundreds or thousands) will in time become dominated by the better functioning mitochondria as they are constantly dividing and the defective ones removed by mitophagy. Thus it would be important to take regular breaks from C60 treatment to allow the population of better functioning mitochondria** to increase without further modification--a dosing schedule the Baati rat study may have stumbled upon by accident.

The bottom line:

This process of replication and mitophagy is selection of the fittest at the intracellular level. Taking C60 continuously may result in degrading the better functioning mitochondria as it doesn't allow time for the replication and selection process to work.
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*Procaine is sold for longevity as "Gerovital". In 1965 researcher Anna Aslan reported that it increased the lifespan of Wistar rats (males only) by 20%. The dosing schedule was intermittent with injections of procaine 3 times a week for 4 weeks, followed by 4 weeks off. According to one paper: "Procaine can also demethylate densely hypermethylated CpG islands, such as those located in the promoter region of the RAR beta 2 gene, restoring gene expression of epigenetically silenced genes. This property may be explained by our finding that procaine binds to CpG-enriched DNA."

** There is also a process of mitochondrial sex involving fusion and fission whereby the double-stranded loops of mtDNA (of which there may be ten or so per mitochondrion) are randomly exchanged so that after fission one daughter mitochondrion might contain a preponderance of defective strands and thus is recycled by mitophagy.

[Kevnzworld]

If your theory is correct, and that is a big if, this shouldn't become evident as a result of very short term use. The lethargy, soreness etc reported by a few suggest at least to me something else. I have not experienced anything that I can identify as negative in my 1 week f use.
The effects on the immune system and TNF-a could be why some but not all experience somewhat negative effects. I posted a few studies in this post.


In Topic: C60 experiments @ home
Today, 02:52 PM
It does seem from the following that C60 does up regulate the immune system which could account for some of the flu like. " symptoms " being described here.   Maybe autoimmune like would be a better characterization .  

"Immunostimulatory properties and enhanced TNF- α mediated cellular immunity for tumor therapy by C60(OH)20 nanoparticles"
http://iopscience.io...84/20/41/415102

The results indicate that C60(OH)x enhances the phagocytosis of peritoneal macrophages and elevates the activity of arginase and acid phosphatase in vivo. The tumor necrosis factor alpha production of C60(OH)x-treated macrophages also increases in vitro
http://onlinelibrary...enticated=false

If C60 increases TNF-a, it would then also increase inflammation in some people.   Many of the symptoms described are inflammatory in nature (  Turnbuckle ).

As of now I think most of us agree, an intermittent dosage regimen at lower doses would be the most prudent. I will have new blood tests in 10 days.... I will add sed rate going forward.

[Turnbuckle]

If your theory is correct, and that is a big if, this shouldn't become evident as a result of very short term use.

Why not? Mitochondria are active beasties with half-lives of less than two days. And since there are about a thousand of them in the average cell, you could notice effects in an hour or two. Assuming you had some epigenetic deficiency to begin with.

Many of the symptoms described are inflammatory in nature ( Turnbuckle ).

Like what? I haven't seen any with C60, though I've seen such effects from resveratrol and astragalus extract.

As of now I think most of us agree, an intermittent dosage regimen at lower doses would be the most prudent.

I certainly agree, although judging by the poll, most are using continuous dosing. But the only thing we have to go by--the rat study--used weekly dosing after the first week.

Edited by Turnbuckle, 30 November 2012 - 01:25 AM.

[Kevnzworld]

Many of the symptoms described are inflammatory in nature ( Turnbuckle ).

Like what? I haven't seen any with C60, though I've seen such effects from resveratrol and astragalus extract.

There are so many posts on C60 I mis remember names, sorry. Most complain of lethargy and lack of mental clarity.
Here is one example of pains being reported


scorpe, on 22 November 2012 - 01:45 AM, said:
I am a healthy male rat 1.75 cm  75 kg and 66 years. Started yesterday at 2 pm with 1.5 mg and after abt 30 minutes my left elboo became painly and after a few m. later the right one. Abt 10 m.later it was gone. Never had this before.

Niner replied:
"We've had a number of reports of weird transient pains in people's arms.  It seems to only occur upon first starting c60, then never again.  I have no idea what's going on there, buy you certainly aren't the first to report it. "

I think that since C60 increases TNF-a and upregulates immune function, this could trigger an inflammatory response and flu like symptoms ( transient pain, lethargy ) in some people. Remember most people taking C60 haven't reported negative reactions, including me.

[Andey]

Any chance to check this theory in measurable way ? To exclude possibility of individual reactions on c60.

For me I dont think that Baati experiment in any kind proves intermittent regimen - they use huge doses and there is very little chance that rats was cleaned from c60 before new dosage.

[Turnbuckle]

Many of the symptoms described are inflammatory in nature ( Turnbuckle ).

Like what? I haven't seen any with C60, though I've seen such effects from resveratrol and astragalus extract.

There are so many posts on C60 I mis remember names, sorry. Most complain of lethargy and lack of mental clarity.
Here is one example of pains being reported


scorpe, on 22 November 2012 - 01:45 AM, said:
I am a healthy male rat 1.75 cm 75 kg and 66 years. Started yesterday at 2 pm with 1.5 mg and after abt 30 minutes my left elboo became painly and after a few m. later the right one. Abt 10 m.later it was gone. Never had this before.

Niner replied:
"We've had a number of reports of weird transient pains in people's arms. It seems to only occur upon first starting c60, then never again. I have no idea what's going on there, buy you certainly aren't the first to report it. "

I think that since C60 increases TNF-a and upregulates immune function, this could trigger an inflammatory response and flu like symptoms ( transient pain, lethargy ) in some people. Remember most people taking C60 haven't reported negative reactions, including me.

If there is an epigenetic effect in the mtDNA, then that will affect every cell in the body, and in some quite different ways. For instance, in cells like stem cells and cancer cells where mitochondria are turned off, turning them on again will stimulate differentiation in one and apoptosis in the other. By enhancing mitochondrial function in muscle cells, it might result in a sudden improvement in the gym. In immune cells, it might have the negative effect you're mentioning. So you get a spectrum of effects that is otherwise hard to explain.

Edited by Turnbuckle, 30 November 2012 - 11:18 AM.

[Turnbuckle]

Any chance to check this theory in measurable way ? To exclude possibility of individual reactions on c60.

It could be checked by measuring the methylation of the mtDNA before and after treatment. If correct, there would be less methylation afterward. This wouldn't be the only case of a drug acting this way. Procaine has been shown to increase the longevity of rats (with intermittent treatment) and bind to DNA where it acts as a methytransferase inhibitor.

For me I dont think that Baati experiment in any kind proves intermittent regimen - they use huge doses and there is very little chance that rats was cleaned from c60 before new dosage.

Clearance from the blood was quite rapid in Baati. From Fig. 1, the blood concentration reaches a peak in about 5 hours then drops by a factor of 10 in 24 hours and by a factor of a 100 in 48. In organs it isn't so clear, however Baati says--

Nevertheless, the weakness of organ concentrations notably at D8 after 7
daily successive administrations of C60 dissolved in olive oil clearly
shows that C60 molecules are eliminated from the organs in a few
hours after both oral and i.p. administrations.

Edited by Turnbuckle, 30 November 2012 - 11:23 AM.

[niner]

The continuous decline in the number of reps I could do before onset of muscle fatigue after cessation of c60 is inconsistent with the epigenetic hypothesis (this is not a theory, it has not been tested in any way). All the effects that have been observed with c60-oo are consistent with biphasic kinetics and a very low threshold concentration in mitochondrial membranes. The c60-oo is rapidly cleared from blood, but the very low concentration that remains in membranes is cleared very slowly. If Baati didn't see it in organs, the concentration was probably below the limit of detection for the chromatographic method he used. A 14C label experiment would be the way to test this.

[DeadMeat]

Clearance from the blood was quite rapid in Baati. From Fig. 1, the blood concentration reaches a peak in about 5 hours then drops by a factor of 10 in 24 hours and by a factor of a 100 in 48. In organs it isn't so clear, however Baati says--

Nevertheless, the weakness of organ concentrations notably at D8 after 7
daily successive administrations of C60 dissolved in olive oil clearly
shows that C60 molecules are eliminated from the organs in a few
hours after both oral and i.p. administrations.

How can they claim that without knowing the organ concentrations after for example 5 hours?

Also they measured the tissue concentrations at day 1 and 8 of oral daily dosing in table 2(from the blood concentration at day 1 I assume this is 24 hours after dosing). There the concentrations in the tissues(and blood) increases linear(ish)ly. As you would expect from something that stays in the body for a very long time. I mean if it was mostly gone in 24 hours, the concentrations would not change with repeated dosing.

Edited by DeadMeat, 30 November 2012 - 02:20 PM.

[Turnbuckle]

Clearance from the blood was quite rapid in Baati. From Fig. 1, the blood concentration reaches a peak in about 5 hours then drops by a factor of 10 in 24 hours and by a factor of a 100 in 48. In organs it isn't so clear, however Baati says--

Nevertheless, the weakness of organ concentrations notably at D8 after 7
daily successive administrations of C60 dissolved in olive oil clearly
shows that C60 molecules are eliminated from the organs in a few
hours after both oral and i.p. administrations.

How can they claim that without knowing the organ concentrations after for example 5 hours?

Also they measured the tissue concentrations at day 1 and 8 of oral daily dosing in table 2(from the blood concentration at day 1 I assume this is 24 hours after dosing). There the concentrations in the tissues(and blood) increases linear(ish)ly. As you would expect from something that stays in the body for a very long time. I mean if it was mostly gone in 24 hours, the concentrations would not change with repeated dosing.

I don't get it either. It's not the first inconsistency in this paper, unfortunately, but perhaps they will clear this up before long. They say, “A complete biodistribution study including intestine, skin, bone and fatty tissue is in progress in our laboratory.”

[Andey]

Any chance to check this theory in measurable way ? To exclude possibility of individual reactions on c60.

It could be checked by measuring the methylation of the mtDNA before and after treatment. If correct, there would be less methylation afterward. This wouldn't be the only case of a drug acting this way. Procaine has been shown to increase the longevity of rats (with intermittent treatment) and bind to DNA where it acts as a methytransferase inhibitor.

For me I dont think that Baati experiment in any kind proves intermittent regimen - they use huge doses and there is very little chance that rats was cleaned from c60 before new dosage.

Clearance from the blood was quite rapid in Baati. From Fig. 1, the blood concentration reaches a peak in about 5 hours then drops by a factor of 10 in 24 hours and by a factor of a 100 in 48. In organs it isn't so clear, however Baati says--

Nevertheless, the weakness of organ concentrations notably at D8 after 7
daily successive administrations of C60 dissolved in olive oil clearly
shows that C60 molecules are eliminated from the organs in a few
hours after both oral and i.p. administrations.

So if you (and Baati) are right than dosage volume must be irrelevant with such clearance speed. If you increase dosage in 10 times it mean only that it last for one or two hours longer.
Am I right ?

P.S. Sorry for overquoting but I dont want to loose context

Edited by Andey, 30 November 2012 - 03:11 PM.

[Turnbuckle]

Any chance to check this theory in measurable way ? To exclude possibility of individual reactions on c60.

It could be checked by measuring the methylation of the mtDNA before and after treatment. If correct, there would be less methylation afterward. This wouldn't be the only case of a drug acting this way. Procaine has been shown to increase the longevity of rats (with intermittent treatment) and bind to DNA where it acts as a methytransferase inhibitor.

For me I dont think that Baati experiment in any kind proves intermittent regimen - they use huge doses and there is very little chance that rats was cleaned from c60 before new dosage.

Clearance from the blood was quite rapid in Baati. From Fig. 1, the blood concentration reaches a peak in about 5 hours then drops by a factor of 10 in 24 hours and by a factor of a 100 in 48. In organs it isn't so clear, however Baati says--

Nevertheless, the weakness of organ concentrations notably at D8 after 7
daily successive administrations of C60 dissolved in olive oil clearly
shows that C60 molecules are eliminated from the organs in a few
hours after both oral and i.p. administrations.

So if you (and Baati) are right than dosage volume must be irrelevant with such clearance speed. If you increase dosage in 10 times it mean only that it last for one or two hours longer.
Am I right ?

P.S. Sorry for overquoting but I dont want to loose context

Generally speaking, if you increase the dose by a factor of ten without any change in the elimination rate constant, then it will take slightly more than three half lives to get back to the level of your original dose. So when you say it would last one or two hours longer, that would only be true if its half life were 20 to 40 minutes.

That said, I've tried single doses from .5 to 30 mg and I haven't seen any advantage from levels higher than 2 mg or so (.025 mg/kg), and I don't recall anyone here saying that higher levels are better from actual experience. Thus this may be a case of more is not better. And also a case of longer is not better as more people have reported that the effects fade with continuous use than not.

Edited by Turnbuckle, 30 November 2012 - 04:02 PM.

[Andey]

So if you (and Baati) are right than dosage volume must be irrelevant with such clearance speed. If you increase dosage in 10 times it mean only that it last for one or two hours longer.
Am I right ?

P.S. Sorry for overquoting but I dont want to loose context

Generally speaking, if you increase the dose by a factor of ten without any change in the elimination rate constant, then it will take slightly more than three half lives to get back to the level of your original dose. So when you say it would last one or two hours longer, that would only be true if its half life were 20 to 40 minutes.

That said, I've tried single doses from .5 to 30 mg and I haven't seen any advantage from levels higher than 2 mg or so (.025 mg/kg), and I don't recall anyone here saying that higher levels are better from actual experience. Thus this may be a case of more is not better. And also a case of longer is not better as more people have reported that the effects fade with continuous use than not.

I am also thinking in half times terms, this mean that curve of clearance is similar to expotential curve.
I just want to find one protocol that suits both theories - plain antiox and epigenetic. Personally I think that antiox theory is more probable, but I am also trust your knowledge and gut ) Also if wrong regimen could harm the cells it would be not clever at all to ignore such possibility.
If for epigenetic theory dosage does not really matter, and for pain antiox theory intermittent intervals are ok while your dosage is bug (with suggestion that C60 stores in membranes with very low clearance rate), then large intermittent dosage will be a compromise variant until we can prove one of the theories.
Would it work ? What do you think about large intermittent dosage ?

[Turnbuckle]

If for epigenetic theory dosage does not really matter...

I didn't mean to give that impression. What I was trying to say was I haven’t seen any immediate advantage from taking larger doses. Could their be a drawback? Certainly. Mitochondria don't have a lot of methylation but it's there so there must be a reason for it. Would a sufficiently big single dose be the equivalent of taking it continuously and eliminating any good effects by excessive demethylation? Possibly.

[nowayout]

If C60 increases TNF-a, it would then also increase inflammation in some people. Many of the symptoms described are inflammatory in nature ( Turnbuckle ).

Oops, then C60 could be BAD BAD BAD for people like me with autoimmune problems (AS, RA, Chrohn's etc.). The cornerstone of therapy for these conditions is currently TNF inhibition. For example, I am already on a TNF inhibitor for AS.

Good question why every promising anti-aging substance seem to be dangerous for autoimmune patients. First resveratrol, now this.

[Mind]

This is a great conversation. I love to see theories hashed out. Everyone can learn from this and provide a foundation for further insight.

However, let me rain on the parade (someone has to)....

Don't get your hopes up too high. Through the years it is very rare to find a life extension or rejuvenation-type supplement that works in mice AND humans. Even CR, which is spectacular for mice is not so spectacular (to put it mildly) in long-lived primates. Just remember that mice are not humans. We are talking herbivores vs. omnivores, short-lived species vs. long-lived species.

I sincerely hope that C60 is a "good" supplement for human health (thus I have been working with AgeVivo to first replicate the Baati study), but I would not be surprised if it has little to no effect in humans.

[mait]

I wonder if C60 causes demethylisation only in mitochondrial DNA or also in nuclear DNA. Here is one of the studies showing that demethylisation of nuclear DNA decreases with age (http://www.pnas.org/...nt/109/26/10522). An it has also been shown that inhibiting or knocking out gene responsible for methyltransferase synthesis in mice results in decreased memory performance: the memory performance is improved in old mice by increasing methyltransferase and decreased in young mice inhibiting it.

[Andey]

This is a great conversation. I love to see theories hashed out. Everyone can learn from this and provide a foundation for further insight.

However, let me rain on the parade (someone has to)....

Don't get your hopes up too high. Through the years it is very rare to find a life extension or rejuvenation-type supplement that works in mice AND humans. Even CR, which is spectacular for mice is not so spectacular (to put it mildly) in long-lived primates. Just remember that mice are not humans. We are talking herbivores vs. omnivores, short-lived species vs. long-lived species.

I sincerely hope that C60 is a "good" supplement for human health (thus I have been working with AgeVivo to first replicate the Baati study), but I would not be surprised if it has little to no effect in humans.

Its hydrated form C₆₀HyFn have some studies (even from different sources) that confirms their anticancer abilities - this is similar to efffect of C60oo on mice.
I think that any not specific anticancer supplement need to work on very ground level of human body and certainly can change whole pattern of aging.


On a bigger scale I am kind of skeptical on any supplement that already exists in our body and take part in body signalling and feedback loops (like Epitalon for example). But C60 is alien in human body and thats why I think its effect is not restricted by evolution.

[Andey]

If for epigenetic theory dosage does not really matter...

I didn't mean to give that impression. What I was trying to say was I haven’t seen any immediate advantage from taking larger doses. Could their be a drawback? Certainly. Mitochondria don't have a lot of methylation but it's there so there must be a reason for it. Would a sufficiently big single dose be the equivalent of taking it continuously and eliminating any good effects by excessive demethylation? Possibly.

I didnt mean that you give such expression.
I just trying to make a logical chain based on:
1. Baati used a very high dose on their rats - his results with rats tolds us that big dosages not doing harm at least.
2. Baatis rats intermittent regimen proves that it could work also.

I also think that plain antiox theory is somehow weak because the concentration of C60 found in organs is very low. Its just not enough to work as disposable chemical reagent.
So at the end I can recognise 2 theories -
1st you epigenetic theory with c60 comes, turns mito evolution on and result could last for very long. (the actual exposure time of c60 depends on dosage, but I think that any dosage mg/kg lesser then Baatis could overexposure us)
2nd that C60 is a kind of catalyst antioxidant (copiright to Grigoriy Andrievsky)

[niner]

I also think that plain antiox theory is somehow weak because the concentration of C60 found in organs is very low. Its just not enough to work as disposable chemical reagent.

It's not a disposable reagent; it's catalytic. Like you said, this was pointed out by Andrievsky, and also by the work of Laura Dugan.

How can we explain this data, in which muscle fatigue onset returned to baseline over the course of a little over two weeks, not to mention the very rapid onset of the effect, if the cause was epigenetic?

[Andey]

I also think that plain antiox theory is somehow weak because the concentration of C60 found in organs is very low. Its just not enough to work as disposable chemical reagent.

It's not a disposable reagent; it's catalytic. Like you said, this was pointed out by Andrievsky, and also by the work of Laura Dugan.

How can we explain this data, in which muscle fatigue onset returned to baseline over the course of a little over two weeks, not to mention the very rapid onset of the effect, if the cause was epigenetic?

Honestly, I dont see any explanation from epigenetic point of view.
Main problem is that we can operate mostly on our subjective experiences and than build theories based on it. Human experiences may vary greatly - good example is resveratrol. Supplements can also interfere with other supplements and it dont help either.

At the end I feel more an more confused with all this competative theories floating around )
We need more objective scientifical data.

P.S. I remember that I read your post where you mentioned Laura Dugan - its just passed away from me at that time (

[Kevnzworld]

If C60 increases TNF-a, it would then also increase inflammation in some people. Many of the symptoms described are inflammatory in nature ( Turnbuckle ).

Oops, then C60 could be BAD BAD BAD for people like me with autoimmune problems (AS, RA, Chrohn's etc.). The cornerstone of therapy for these conditions is currently TNF inhibition. For example, I am already on a TNF inhibitor for AS.

Good question why every promising anti-aging substance seem to be dangerous for
autoimmune patients. First resveratrol, now this.

I doubt that C60's upregulation of TNF-a is responsible for it's potential anti aging benefits, just some of it's negative side effects. I take many TNF-a inhibitors like curcumin and resveratrol. It might be more accurate to refer to them as anti TNF-a over expressers. I think they might help mitigate some of the reported C60 side effects. People like Mikey, Anthony and I who take these haven't noticed the side effects others have. Just an observation.

Edited by Kevnzworld, 01 December 2012 - 01:37 AM.

[Turnbuckle]

I also think that plain antiox theory is somehow weak because the concentration of C60 found in organs is very low. Its just not enough to work as disposable chemical reagent.

It's not a disposable reagent; it's catalytic. Like you said, this was pointed out by Andrievsky, and also by the work of Laura Dugan.

How can we explain this data, in which muscle fatigue onset returned to baseline over the course of a little over two weeks, not to mention the very rapid onset of the effect, if the cause was epigenetic?

Honestly, I dont see any explanation from epigenetic point of view.
Main problem is that we can operate mostly on our subjective experiences and than build theories based on it. Human experiences may vary greatly - good example is resveratrol. Supplements can also interfere with other supplements and it dont help either.

At the end I feel more an more confused with all this competative theories floating around )
We need more objective scientifical data.

P.S. I remember that I read your post where you mentioned Laura Dugan - its just passed away from me at that time (

What you're looking at is one anecdotal report. It's certainly possible that the effects of C60 are a combination of antioxidant and epigenetic effects, what I said in the OP. But no purely antioxidant theory can explain enhanced longevity, hair regrowth, the disappearance of scars, or the boosting of stem cell injections. It has simply never happened before with any antioxidant. But a drug that isn't an antioxidant but does have epigenetic effects has been shown to have longevity effects. This is procaine. And the theoretical studies suggest that C60 acts in a similar fashion.

Edited by Turnbuckle, 01 December 2012 - 01:37 AM.

[Andey]

What you're looking at is one anecdotal report. It's certainly possible that the effects of C60 are a combination of antioxidant and epigenetic effects, what I said in the OP. But no purely antioxidant theory can explain enhanced longevity, hair regrowth, the disappearance of scars, or the boosting of stem cell injections. It has simply never happened before with any antioxidant. But a drug that isn't an antioxidant but does have epigenetic effects has been shown to have longevity effects. This is procaine. And the theoretical studies suggest that C60 acts in a similar fashion.

Yep, I understand that ) But hair regrowth, the disappearance of scars are also anecdotal. May be it works different for different persons, may be endurance increase effect works separatly from others, may be some of effects are not from C60 actually.
You and niner both look right and niner have advantage because antioxidant idea is the way many other scientists think.
At the moment we just dont have enough information to judge with theory is right (if any). I hope future studies will reveal this soon.

I will wait until all this will settle, and until then I will take large dosage (7-15ml) with longer rest periods (1 to 2 weeks). Of course this regimen may also be wrong )

Edited by Andey, 01 December 2012 - 11:47 AM.

[niner]

no purely antioxidant theory can explain enhanced longevity, hair regrowth, the disappearance of scars, or the boosting of stem cell injections. It has simply never happened before with any antioxidant.

An antioxidant has been shown to enhance longevity- Skulachev's mitochodrially-directed plastoquinones. The reason that most common antioxidants don't seem to do much is that they have lousy pharmacokinetics, don't localize where they are most needed, and require regeneration. c60-oo is unlike all the other antioxidants to date, other than the various c60 analogs that have also shown profound biological effects.

[Turnbuckle]

What you're looking at is one anecdotal report. It's certainly possible that the effects of C60 are a combination of antioxidant and epigenetic effects, what I said in the OP. But no purely antioxidant theory can explain enhanced longevity, hair regrowth, the disappearance of scars, or the boosting of stem cell injections. It has simply never happened before with any antioxidant. But a drug that isn't an antioxidant but does have epigenetic effects has been shown to have longevity effects. This is procaine. And the theoretical studies suggest that C60 acts in a similar fashion.

Yep, I understand that ) But hair regrowth, the disappearance of scars are also anecdotal. May be it works different for different persons, may be endurance increase effect works separatly from others, may be some of effects are not from C60 actually.
You and niner both look right and niner have advantage because antioxidant idea is the way many other scientists think.
At the moment we just dont have enough information to judge with theory is right (if any). I hope future studies will reveal this soon.

I will wait until all this will settle, and until then I will take large dosage (7-15ml) with longer rest periods (1 to 2 weeks). Of course this regimen may also be wrong )

I said it was ONE anecdotal report, but there are many anecdotal reports that suggest something beyond an antioxidant effect. For instance, hair growth. Last time I looked, three people here are reporting hair regrowth in the C60 poll, and Luna has reported hair growth de novo using C60 and has filed a patent application on it. So how is this hair growth possible? One explanation is that C60 somehow encourages the differentiation of stem cells. And how would it do that? By turning on mitochondria that are turned off, which is the first thing that happens during stem cell differentation. The usual way of keeping mitochondria turned off is to methylate the promotor regions of the mtDNA, and so we're back to the demethylation theory of action I proposed in the OP.

Pluripotent blastomeres of mammalian pre-implantation embryos and embryonic stem cells (ESCs) are characterized by limited oxidative capacity and great reliance on anaerobic respiration. Early pre-implantation embryos and undifferentiated ESCs possess small and immature mitochondria located around the nucleus, have low oxygen consumption and express high levels of glycolytic enzymes. However, as embryonic cells and ESCs lose pluripotency and commit to a specific cell fate, the expression of mtDNA transcription and replication factors is upregulated and the number of mitochondria and mtDNA copies/cell increases. Moreover, upon cellular differentiation, mitochondria acquire an elongated morphology with swollen cristae and dense matrices, migrate into wider cytoplasmic areas and increase the levels of oxygen consumption and ATP production as a result of the activation of the more efficient, aerobic metabolism. Since pluripotency seems to be associated with anaerobic metabolism and a poorly developed mitochondrial network and differentiation leads to activation of mitochondrial biogenesis according to the metabolic requirements of the specific cell type, it is hypothesized that reprogramming of somatic cells towards a pluripotent state, by somatic cell nuclear transfer (SCNT), transcription-induced pluripotency or creation of pluripotent cell hybrids, requires acquisition of mitochondrial properties characteristic of pluripotent blastomeres and ESCs.

http://www.ncbi.nlm....pubmed/19521804

Turning on mitochondrial genes can theoretically produce a spectrum of effects that antioxidants cannot, from promoting the differentiation of stem cells, to killing cancer cells (which shut down their mitochondria to avoid autophagy), to enhancing oxygen utilization in muscle cells.

[Turnbuckle]

no purely antioxidant theory can explain enhanced longevity, hair regrowth, the disappearance of scars, or the boosting of stem cell injections. It has simply never happened before with any antioxidant.

An antioxidant has been shown to enhance longevity- Skulachev's mitochodrially-directed plastoquinones. The reason that most common antioxidants don't seem to do much is that they have lousy pharmacokinetics, don't localize where they are most needed, and require regeneration. c60-oo is unlike all the other antioxidants to date, other than the various c60 analogs that have also shown profound biological effects.

I'm not so sure he's shown that. He said in Dec. 2011--

It was found that substitution of a LP [Low Pathogen] vivarium for a conventional (non-LP) one doubled the lifespan of female outbred mice, just as SkQ1 did in a non-LP vivarium.

http://www.ncbi.nlm....les/PMC3249456/

So the effect was not due to an increase in the potential lifespan, but to a reduction of mortality due to disease.

Edited by Turnbuckle, 01 December 2012 - 01:11 PM.

[FunkOdyssey]

And also a case of longer is not better as more people have reported that the effects fade with continuous use than not.

You can add me to the list of people who observed initial benefits that faded away to roughly baseline after continuous use (couple months of 2.4mg daily).

[Junk Master]

Add me to the list too.

[Andey]

Add me to the list too.

You can add me to the list of people who observed initial benefits that faded away to roughly baseline after continuous use (couple months of 2.4mg daily).

Did you tried to withdraw C60 and measure athletic performance before and after ? (as I understand we are talking now only about endurance enchancments)

Edited by Andey, 03 December 2012 - 09:07 AM.