635 replies to this topic

[Turnbuckle]

My deepest inside hope is that if C60 is not discontinued, taken regularly in small, normal doses, with some pauses; will lead to an order lifespan increase.

Why do you think that there are some need for pauses on C60 intake ?

Most everyone here seems to believe that it works as a super antioxidant, even though no antioxidant has ever been shown to extend the lifespan of rats. My theory is that it acts as a demethylating agent, in which case it is similar to procaine, which has also been shown to extend the lifespan of rats and is sold as a longevity supplement. C60 concentrates in the mitochondria, and if it demethylates the mitochondrial DNA, this would turn on genes that had been turned off and essentially act as a reset. If, however, some of those genes are better turned off for optimal functioning, then you could go too far with the treatment. If you take too much, for instance, or take it every day, you might wipe out all the epigenetic programming of the mtDNA and not be able to get it back.

I've posted a more complete explanation on my profile page--under "3. C60 theory."

But most people here beleive that C60 is accumulating in cells and this point look proven for some degree because C60 effects are not dissapear immediatly after canceling its intake.
Do you think that small rest periods are enough for C60 removal from mitochondria ?
And what pause duration do you think optimal ? Once a week intake ? Two times per week ? Every other day ?

How could it be proof when epigenetic changes are even more permanent?

As for the needed rest period, that will depend on how much you are taking, and for how long. The C60 has to stick around long enough to prevent methytranferase from doing its job, and then, if there is sufficient change to make a difference, any mitochondria that are improved will then have to be promoted over the others. That process will vary by cell, but even the fastest turnover is more than a day or two, and there are around a thousand in the average cell. So if taking a few mg for a few days, a week to a month rest period would be ideal, I'd guess.

I've experimented with many dose protocols, but the effects are so persistent it would take a designed study to say which is best. A conservative approach consistent with the epigenetic theory of action would be to take 2-3 mg (.03 mg/kg) for 2-3 days and then a week or two off.

Edited by Turnbuckle, 29 October 2012 - 11:51 AM.

[Andey]

My deepest inside hope is that if C60 is not discontinued, taken regularly in small, normal doses, with some pauses; will lead to an order lifespan increase.

Why do you think that there are some need for pauses on C60 intake ?

Most everyone here seems to believe that it works as a super antioxidant, even though no antioxidant has ever been shown to extend the lifespan of rats. My theory is that it acts as a demethylating agent, in which case it is similar to procaine, which has also been shown to extend the lifespan of rats and is sold as a longevity supplement. C60 concentrates in the mitochondria, and if it demethylates the mitochondrial DNA, this would turn on genes that had been turned off and essentially act as a reset. If, however, some of those genes are better turned off for optimal functioning, then you could go too far with the treatment. If you take too much, for instance, or take it every day, you might wipe out all the epigenetic programming of the mtDNA and not be able to get it back.

I've posted a more complete explanation on my profile page--under "3. C60 theory."

But most people here beleive that C60 is accumulating in cells and this point look proven for some degree because C60 effects are not dissapear immediatly after canceling its intake.
Do you think that small rest periods are enough for C60 removal from mitochondria ?
And what pause duration do you think optimal ? Once a week intake ? Two times per week ? Every other day ?

How could it be proof when epigenetic changes are even more permanent?

As for the needed rest period, that will depend on how much you are taking, and for how long. The C60 has to stick around long enough to prevent methytranferase from doing its job, and then, if there is sufficient change to make a difference, any mitochondria that are improved will then have to be promoted over the others. That process will vary by cell, but even the fastest turnover is more than a day or two, and there are around a thousand in the average cell. So if taking a few mg for a few days, a week to a month rest period would be ideal, I'd guess.

I've experimented with many dose protocols, but the effects are so persistent it would take a designed study to say which is best. A conservative approach consistent with the epigenetic theory of action would be to take 2-3 mg (.03 mg/kg) for 2-3 days and then a week or two off.

I am just trying to formulate comprimising protocol - that could work either if C60 primarly is antioxidant or if it is a demethylating agent.
For now for it looks as subject of probability because eithre theory didnt have absolute proofs on its side.
So may be could make compromising protocol that would not push not to the faith or not territory ? )
What if taking C60 every day for a month or two and than do a long rest period for 2 weeks ?

[niner]

Most everyone here seems to believe that it works as a super antioxidant, even though no antioxidant has ever been shown to extend the lifespan of rats. My theory is that it acts as a demethylating agent, in which case it is similar to procaine, which has also been shown to extend the lifespan of rats and is sold as a longevity supplement. C60 concentrates in the mitochondria, and if it demethylates the mitochondrial DNA, this would turn on genes that had been turned off and essentially act as a reset. If, however, some of those genes are better turned off for optimal functioning, then you could go too far with the treatment. If you take too much, for instance, or take it every day, you might wipe out all the epigenetic programming of the mtDNA and not be able to get it back.

Previous antioxidants were not getting into the mitochondria where they could really do some good, and/or they were one-shot antioxidants that required recycling. Many so-called antioxidants don't even have much antioxidant activity at all, outside of a test tube. I'm pretty sure that Skulachev's mitochondrially targeted plastoquinones did provide some life extension, though nothing to write home about. (It got to the right place, but was a lousy antioxidant)

C60-oo is special because it gets into the mitochondrial (and other) membranes, and it acts catalytically to reduce superoxide, the primary damaging ROS.

C60 Doesn't last forever, like you would expect from the epigenetic hypothesis. It simply has biphasic elimination kinetics:
When you dose C60-oo, there is an initial rapid clearance from blood. Most is being excreted, but the rest partitions into membranes and other lipid compartments. It then slowly diffuses out of those compartments, leading to a gradual decrease in C60-oo effects. Here is an example of a muscle fatigue metric that spikes after dosing, and drops back to near baseline in about 2 weeks. That was from a dose of 6mg spread over 4 days. Repeated huge doses (like Anthony's 3500mg would last for months or years, on the basis of this kinetic behavior.

[Turnbuckle]

C60 Doesn't last forever, like you would expect from the epigenetic hypothesis.

Epigenetics is much more malleable than genetics, especially in mitochondria that divide every couple of days. They are modified by the availability of food, for instance, and other environmental factors. So the epigenetic effects of C60 will last a long time, but can be expected to fluctuate and drift along with the population of a cell's mitochondria.

Thus, mtDNA mutations provide heritable and stable adaptation to regional differences while mitochondrially-mediated changes in the epigenome permit reversible modulation of gene expression in response to fluctuations in the energy environment.

http://www.ncbi.nlm....pubmed/20818725

Edited by Turnbuckle, 29 October 2012 - 01:59 PM.

[taho]

Rats where given CCl4, and those with c60-oo were much more resistant to it, then the controls that have not gotten c60.

Would an epigenetics hypothesis be able to explain resistance to CCl4?

[Turnbuckle]

Rats where given CCl4, and those with c60-oo were much more resistant to it, then the controls that have not gotten c60.

Would an epigenetics hypothesis be able to explain resistance to CCl4?

I'm not saying that C60 isn't a good antioxidant, just that the long term effects are epigenetic.

[clairvoyant]

• Why I think C60 should be paused? Because it is fat soluble, it stays long in the body and by doing some pauses it will be evenly distributed everywhere as well as without peaks in the body’s concentration.

• I could explain the long lasting effect of C60 by both:

8]First: long presence in the body’s fat tissue

8]Second: “repair” of the body’s peroxidated fats into normal ones. One will have more time to live, to smoke so as to get himself back to his initial condition.

I have one more thing about the dosage: the fatter you are the greater you dose will be. The fat tissue acts like a sponge. It slowly loads and unloads.

[clairvoyant]

This is my explanation on how C60 in olive oil works.
...
C60 acts like catalyst and is not spent. C60 repairs damaged lipid, included but not limited to cell and mitochondrial membranes.
That is how we can explain improvement of the Turnbuckle’s skin and hair. It is so called Turnbuckle effect.
To me C60 not only stops the time (aging) but reverses it, too. To turn back the hands of time is equal to rejuvenation.
My deepest inside hope is that if C60 is not discontinued, taken regularly in small, normal doses, with some pauses; will lead to an order lifespan increase.

Hi )
Thank you for such descriptive post - its time to mr to recall some chemistry from school)

Why do you think that there are some need for pauses on C60 intake ?

Most everyone here seems to believe that it works as a super antioxidant, even though no antioxidant has ever been shown to extend the lifespan of rats. My theory is that it acts as a demethylating agent, in which case it is similar to procaine, which has also been shown to extend the lifespan of rats and is sold as a longevity supplement. C60 concentrates in the mitochondria, and if it demethylates the mitochondrial DNA, this would turn on genes that had been turned off and essentially act as a reset. If, however, some of those genes are better turned off for optimal functioning, then you could go too far with the treatment. If you take too much, for instance, or take it every day, you might wipe out all the epigenetic programming of the mtDNA and not be able to get it back.

I've posted a more complete explanation on my profile page--under "3. C60 theory."

Turnbuckle, do you think that compound C60-(CH3) methyl radical exists? On the other hand C60(OH)24 exists, C60(O) also exists.

[Turnbuckle]

This is my explanation on how C60 in olive oil works.
...
C60 acts like catalyst and is not spent. C60 repairs damaged lipid, included but not limited to cell and mitochondrial membranes.
That is how we can explain improvement of the Turnbuckle’s skin and hair. It is so called Turnbuckle effect.
To me C60 not only stops the time (aging) but reverses it, too. To turn back the hands of time is equal to rejuvenation.
My deepest inside hope is that if C60 is not discontinued, taken regularly in small, normal doses, with some pauses; will lead to an order lifespan increase.

Hi )
Thank you for such descriptive post - its time to mr to recall some chemistry from school)

Why do you think that there are some need for pauses on C60 intake ?

Most everyone here seems to believe that it works as a super antioxidant, even though no antioxidant has ever been shown to extend the lifespan of rats. My theory is that it acts as a demethylating agent, in which case it is similar to procaine, which has also been shown to extend the lifespan of rats and is sold as a longevity supplement. C60 concentrates in the mitochondria, and if it demethylates the mitochondrial DNA, this would turn on genes that had been turned off and essentially act as a reset. If, however, some of those genes are better turned off for optimal functioning, then you could go too far with the treatment. If you take too much, for instance, or take it every day, you might wipe out all the epigenetic programming of the mtDNA and not be able to get it back.

I've posted a more complete explanation on my profile page--under "3. C60 theory."

Turnbuckle, do you think that compound C60-(CH3) methyl radical exists? On the other hand C60(OH)24 exists, C60(O) also exists.

That's of no importance since C60 would not act directly but as a methyltrasferase inhibitor by its presence in the DNA groove, as the enzyme has to act over the groove from one strand to the other. So if C60 stayed there long enough, the daughter strand would not pick up the matching methyl group.

Attached Files

•  C60-DNA.png   147.2KB   6 downloads

Edited by Turnbuckle, 29 October 2012 - 03:45 PM.

[maxwatt]

It seems to be that to to its effects on defective mitochondria (inducing apoptosis or cell death) if resveratrol would be a useful complement to C60, especialy if epigenetic changes account for the effects. I doubt that one could tell except perhaps by comparison of a long time period.

Is anyone else currently using both?

[Mind]

Good job keeping the discussion mostly science focused. This is the "hard science" thread on C60. Try to limit anecdotal reports or post them in different threads.

[niner]

Rats where given CCl4, and those with c60-oo were much more resistant to it, then the controls that have not gotten c60.

Would an epigenetics hypothesis be able to explain resistance to CCl4?

I'm not saying that C60 isn't a good antioxidant, just that the long term effects are epigenetic.

But the epigenetic hypothesis is just a hypothesis, right? Is there any evidence to support it?

[niner]

That's of no importance since C60 would not act directly but as a methyltrasferase inhibitor by its presence in the DNA groove, as the enzyme has to act over the groove from one strand to the other. So if C60 stayed there long enough, the daughter strand would not pick up the matching methyl group.

Turnbuckle, what's the source of the image you posted showing C60 in the major groove of a piece of DNA? It looks like it was built with a molecular modeling program. The contacts look kind of close; do you have any idea what the energy of this interaction is? The reason I ask is that C60 seems energetically unlikely to be a major groove binder. The major groove is full of hydrophilic groups to which real major groove binders will typically form hydrogen bonds. C60 wouldn't be capable of this, and stuffing a big hydrophobe like C60 into the major groove just doesn't look like something that would happen spontaneously.

Edited by niner, 29 October 2012 - 08:56 PM.

[Turnbuckle]

That's of no importance since C60 would not act directly but as a methyltrasferase inhibitor by its presence in the DNA groove, as the enzyme has to act over the groove from one strand to the other. So if C60 stayed there long enough, the daughter strand would not pick up the matching methyl group.

Turnbuckle, what's the source of the image you posted showing C60 in the major groove of a piece of DNA? It looks like it was built with a molecular modeling program. The contacts look kind of close; do you have any idea what the energy of this interaction is? The reason I ask is that C60 seems energetically unlikely to be a major groove binder. The major groove is full of hydrophilic groups to which real major groove binders will typically form hydrogen bonds. C60 wouldn't be capable of this, and stuffing a big hydrophobe like C60 into the major groove just doesn't look like something that would happen spontaneously.

That's from the theoretical paper showing that C60 was attracted to the minor groove.

[Turnbuckle]

Rats where given CCl4, and those with c60-oo were much more resistant to it, then the controls that have not gotten c60.

Would an epigenetics hypothesis be able to explain resistance to CCl4?

I'm not saying that C60 isn't a good antioxidant, just that the long term effects are epigenetic.

But the epigenetic hypothesis is just a hypothesis, right? Is there any evidence to support it?

Yeah, the hypothesis is a hypothesis. I put the argument for it on my profile page, third section.

[caliban]

MODERATION NOTE

The thread was split weeks ago to disentangle scientific discussions from anecdotal reports.

Whereas almost the whole of this sub-forum is flooded with the latter, this is the thread for the former.

You can discuss do-it-yourself science here (personal use), here (equipment), or in fact anywhere suitable in this forum.

As indicated in the first post for this topic, I will delete (not move, not split, not archive)

1- any further posts posts in this thread that contain, reference or incorporate personal observations (whether it is to how they are feeling, how their hair is growing back in measurable increments, what the mixture looks like in their home fridge or how your mice are faring).

2- any posts that mix proper scientific references and theory-making with the type of stuff under (1)

3- any posts commenting on this policy in any way

If this means that this thread receives no further posts, it might illustrate that scientific discussion which does not rely on home-brew experiences has been exhausted.

I have deleted 30+ posts in this thread since that notice was posted.


EDIT: Predictably. I just deleted another half a dozen posts in contravention of Rule No.3 above.

To clarify once more:

1) the above criteria are specific enough. You can engage in wild theory making as long as you don't base it on 'homebrew data'. As soon as that line is crossed the post is toast.

2) The rule only applies strictly in this thread since the warning was posted (although an attempt was made to split some of the non-compliant older discussions, which involved me reading every single post in this thread to date.)

3) LongeCity does not favour outright deletions for non-spam. This is a drastic step because previous pleas were simply ignored, including by Moderators.

4) The rule only applies in this thread which is supposed to be the guarantor that there is at least one such topic in this sub-forum. If you don't like it, post in any of the many, many other threads or open your own.

5) I'm affixing this explanation (and breaking rule No.3 in the process) because I deleted some explanatory text to the original warning which was felt to be 'to cynical'. Some information was lost in the process, for example that if you want to complain, you can contact someone like Shannon via PM, send me abusive emails or post in "forum issues" or something, but not in this thread.

[Turnbuckle]

My deepest inside hope is that if C60 is not discontinued, taken regularly in small, normal doses, with some pauses; will lead to an order lifespan increase.

Why do you think that there are some need for pauses on C60 intake ?

Most everyone here seems to believe that it works as a super antioxidant, even though no antioxidant has ever been shown to extend the lifespan of rats. My theory is that it acts as a demethylating agent, in which case it is similar to procaine, which has also been shown to extend the lifespan of rats and is sold as a longevity supplement. C60 concentrates in the mitochondria, and if it demethylates the mitochondrial DNA, this would turn on genes that had been turned off and essentially act as a reset. If, however, some of those genes are better turned off for optimal functioning, then you could go too far with the treatment. If you take too much, for instance, or take it every day, you might wipe out all the epigenetic programming of the mtDNA and not be able to get it back.

I've posted a more complete explanation on my profile page--under "3. C60 theory."

But most people here beleive that C60 is accumulating in cells and this point look proven for some degree because C60 effects are not dissapear immediatly after canceling its intake.
Do you think that small rest periods are enough for C60 removal from mitochondria ?
And what pause duration do you think optimal ? Once a week intake ? Two times per week ? Every other day ?

Do most people believe this? Really? In my opinion, from taking sub-milligram doses, it sticks around for less than a day.

[Guest]

To the people who complain about the rules for this particalur thread:

I personally appreciate an enforced focus on basic scientific arguments. This would have been needed in the Resveratrol forum a long time ago. As mentioned: if you like to fantasize, make up your own facts or try to draw vast conclusions from your personal anecdots you are free to open your own thread, but they can not be part of a rational debate. This is laymen scientists discussing science and not a presedential election.


To add to the topic: I would urge everyone invested in this discussion to have a read at this old slate article:

http://www.slate.com...n_disease_.html


to bring some of the more far reaching theories down to earth. The effect of chemical compounds on mice is a very delicate thing and C60 certainly is no exception. The next step would be to get short lived monkey, possibly already middle aged ones, and repeat the experiment. The observations in mice are so pronounced, that we would expect to see something in monkeys - if not, it would be a just another fluke in a rodent model, as usual.

[clairvoyant]

To the people who complain about the rules for this particalur thread:

I personally appreciate an enforced focus on basic scientific arguments. This would have been needed in the Resveratrol forum a long time ago. As mentioned: if you like to fantasize, make up your own facts or try to draw vast conclusions from your personal anecdots you are free to open your own thread, but they can not be part of a rational debate. This is laymen scientists discussing science and not a presedential election.


To add to the topic: I would urge everyone invested in this discussion to have a read at this old slate article:

http://www.slate.com...n_disease_.html


to bring some of the more far reaching theories down to earth. The effect of chemical compounds on mice is a very delicate thing and C60 certainly is no exception. The next step would be to get short lived monkey, possibly already middle aged ones, and repeat the experiment. The observations in mice are so pronounced, that we would expect to see something in monkeys - if not, it would be a just another fluke in a rodent model, as usual.

We already have human testimonials. Experience with rats proves that C60 is not toxic, after all.

[clairvoyant]

To Turnbuckle

Turnbuckle, I respect your theory of mitochondria DNA demethylation though I am scared of it because I already personally took C60.
Could you give us some idea how it can be proven? For example, if a substance interferes with nuclear DNA then it will be seen on the next generation. If a substance does it with nuclear DNA methylation then all the tissues will loose theirs functioning and death will occur. What is mitochondrial DNA methylation for, what is going to happen if removed? How it can be proven? For example with electron microscope or by the behavior of the laboratory animals.

[Turnbuckle]

To Turnbuckle

Turnbuckle, I respect your theory of mitochondria DNA demethylation though I am scared of it because I already personally took C60.
Could you give us some idea how it can be proven? For example, if a substance interferes with nuclear DNA then it will be seen on the next generation. If a substance does it with nuclear DNA methylation then all the tissues will loose theirs functioning and death will occur. What is mitochondrial DNA methylation for, what is going to happen if removed? How it can be proven? For example with electron microscope or by the behavior of the laboratory animals.

The bolded part is right. If you were to start demethylating nDNA randomly, you would suffer for it. Epigenetics is how the body distinguishes one cell type from another, and you wouldn't want your organs to revert to a jelly-like, undifferentiated state. Fortunately, this does not appear to happen. C60 in OO seems to be directed preferentially to the mitochondria as fuel. Besides, mtDNA has a life cycle about a hundred times faster than nDNA and thus is much more sensitive to a methyltransferase inhibitor, and is very lightly methylated to begin with. In fact, for a long time people thought there was no methylation, and even now the reason for it isn't well understood. Fortunately, there are now techniques for analyzing the methylation of mtDNA, so this theory is testable.

Here is a recent paper that not only measured the methylation, but correlated it with disease--http://www.ncbi.nlm....pubmed/22879518

[niner]

To add to the topic: I would urge everyone invested in this discussion to have a read at this old slate article:

http://www.slate.com...n_disease_.html

to bring some of the more far reaching theories down to earth. The effect of chemical compounds on mice is a very delicate thing and C60 certainly is no exception. The next step would be to get short lived monkey, possibly already middle aged ones, and repeat the experiment. The observations in mice are so pronounced, that we would expect to see something in monkeys - if not, it would be a just another fluke in a rodent model, as usual.

As usual? Are you saying that the majority of rodent results are flukes? I think you're being overly cynical. C60 has shown life extension in multiple species, and the observed effects in humans suggest that it is working as a powerful mitochondrial antioxidant, consistent with observations in animals. Most of us who are taking c60 now don't have 15 or 20 years to wait for primate experiments to be planned, funded, run and analyzed. In fact, even if it doesn't add one second to human lifespan, a number of us are very happy with the impact that c60 has already had on our health.

[Turnbuckle]

I think rodents are different from humans in one very important way--they have enough telomeres for four lifetimes so their lifespans are more likely limited by their mito machinery than ours. Thus for longevity, we need a two pronged approach that addresses the health of both nuclear and mitochondrial DNA.

[Guest]

@niner:

I was more generally speaking for medical science and testing for individual chemical compounds. And yes: it is no oversimplification to state, that the majority of chemicals (aka medicine) that work in mice (speaking for all kinds of diseases) do not work in humans as intended or have side effects not observed in mice which prevent their application in humans. If most of the headlines proclaiming to cure diseases in mice would have translated into humans, medical progress would have been much faster than we see today.

That said, I do not doubt, that you see real effects from C60 and I concurr with your reasoning, that if you do not have the time to wait, you can take the gamble (Ray Kurzweil has this approach, though somewhat more extreme). I'd just suggest, that we do not get overexcited over something, that possibly might be just another resveratrol-like case.

It would be useful to build a comprehensive theory of the action of C60. If it does significantly enter cells in vivo and if it indeed somehow manages to capture free radicals at mitochondria (which is not self explanatory - a lot of chemical compounds, including some vitamins, are actively directed within the cell - e.g. via the cytosceleton hig ways) it would be useful to first establish, how the mitochondria cause aging. Aubrey de Grey grants it some validity in SENS, though there is no phatology he directly attributes to mitochondrial free radicals. Also there is the notion, that long lived organisms inherently evolved better mechanisms to deal with free radicals and thus antioxidants might not be able to improve upon it as much as they presumely do in mice.


@Hebbeh:
I apologize if I insulted you. If it was your impression that I was specifically referring to you (which I was not), well...

Also I was not saying that you "are all fantasizing and making up facts"... But there is a tendency in some people, to enthusiastically jump on new dicoveries and in turn throw scientific logic and necessary scepticism over board. And I am not special - I am just like most people in this forums trying to use a scientific mindset in analysing life extension claims and merits.

Edited by TFC, 11 November 2012 - 06:53 PM.

[niner]

I was more generally speaking for medical science and testing for individual chemical compounds. And yes: it is no oversimplification to state, that the majority of chemicals (aka medicine) that work in mice (speaking for all kinds of diseases) do not work in humans as intended or have side effects not observed in mice which prevent their application in humans. If most of the headlines proclaiming to cure diseases in mice would have translated into humans, medical progress would have been much faster than we see today.

Are you sure you aren't getting mice mixed up with in vitro experiments? If a drug works in a mouse, it has passed a hell of a lot of hurdles that drugs doing interesting things in yeast have not passed. Resveratrol comes to mind here. The Resveratrol craze was based on yeast results, IIRC. A long placebo controlled experiment in rats is a far cry from that. Obviously, rodents aren't people, but the phenomena involved here appear to be physical rather than receptor-mediated, so I don't expect a big genetic component. OTOH, you are correct in noting that long lived species like humans have evolved better antioxidant defenses than rats and mice. Anyone who expects to live to 150 on the basis of c60-oo alone is going to be disappointed.

[Guest]

Are you sure you aren't getting mice mixed up with in vitro experiments? If a drug works in a mouse, it has passed a hell of a lot of hurdles that drugs doing interesting things in yeast have not passed. Resveratrol comes to mind here. The Resveratrol craze was based on yeast results, IIRC. A long placebo controlled experiment in rats is a far cry from that. Obviously, rodents aren't people, but the phenomena involved here appear to be physical rather than receptor-mediated, so I don't expect a big genetic component. OTOH, you are correct in noting that long lived species like humans have evolved better antioxidant defenses than rats and mice. Anyone who expects to live to 150 on the basis of c60-oo alone is going to be disappointed.

I might be doing a more comprehensive search later, for the moment we can refer to this article and its sources:
http://www.guardian....g-safer-methods

Considering the low success rate of drugs entering clinical trials, which presumaly have been tested in mice before, my estimate is roughly in line. You are certainly right, that certain kind of drugs who have receptor mediated actions are different than C60. But generally mice are just different enough from humans (short lived with different metabolisms, developing other kinds of phatologies than humans etc.) to warrant caution.

Monkeys are much more useful to estimate drug effects on humans, but their life spans can be measured in decades, which makes them kind of useless in practical terms to establish the long run effects of drug use. All we can say at the moment is, that C60 is non-toxic in the short run and possibly in the long run. We don't know about interaction with other kinds of drugs or supplements etc. (invocing the (in-)famous study relating betacarotenes to earlier death in smokers) or if it indeed has any real life extension effect in long lived primates.

If one has the kind of money to afford it and runs out of time to wait for results or results from other fields of research I can relate to taking it (though fortunately I am not yet in that situation).

[Logic]

TFC you must remember that the experiments, trials and FDA approval cost vast amounts of money.
80 Million USD is a figure I have seen mentioned quite a lot.
If the compound is not going to make even vaster sums of money that money will not be spent. (Yes it IS all about the money..!)
Natural substances are not patentable and therefore not profitable and therefore you will never see the tests you desire.
In fact the chances are very good that you will see the opposite with really effective natural treatments being suppressed.
You may even see bogus publications designed to scare people away from cheap, effective cures.

An ounce of prevention is better than a pound of cure...
Do you have the time to wait for something with a track record of never happening, to happen while you wither away? Or would you better serve yourself by doing your own research and deciding for yourself what is most likely to be effective at increasing your health/lifespan?

[niner]

Monkeys are much more useful to estimate drug effects on humans, but their life spans can be measured in decades, which makes them kind of useless in practical terms to establish the long run effects of drug use. All we can say at the moment is, that C60 is non-toxic in the short run and possibly in the long run. We don't know about interaction with other kinds of drugs or supplements etc. (invocing the (in-)famous study relating betacarotenes to earlier death in smokers) or if it indeed has any real life extension effect in long lived primates.

If one has the kind of money to afford it and runs out of time to wait for results or results from other fields of research I can relate to taking it (though fortunately I am not yet in that situation).

I agree that monkeys are essentially out of the question. An alternative approach is to look at compounds in multiple short-lived species, which can uncover more problems than a single species. At the moment, we're doing a large primate study, with ourselves as the subjects. There is no significant short term tox, though we know nothing about long term, reproductive, or developmental toxicities. There are profoundly beneficial effects in certain disease states, but we know nothing about life extension in long-lived primates.

If you make your own c60-oo like many of us do, it's very cheap. My total expenditure for a two year supply was $160, which included the cost of a mortar and pestle to grind the c60. (grinding eliminates the need for mechanical stirring; filtration isn't necessary, and centrifugation is useless)

[caliban]

Gents, while current discussions on patenting etc. don't break the 'no anecdotes' rule for this thread the topic here is supposed to be 'scientific discussions'.
The may be some overlap, but if you want to explore the patenting/commercialisation angle further, please do so in a separate topic.

[maxwatt]

Please Note:

I have moved the posts concerning patenting here: http://www.longecity...ic-discussions/ to keep the topic pure as to scientific discussion. I do hope any errant anecdotes and other off topic but possibly otherwise worthy posts in future are moved there rather than getting deleted.