25 replies to this topic

[reason]

The years of work that went into investigating the effects of fullerenes (spherical assemblies of carbon molecules, specifically C60 in this case) on life span in rodents are an example of the waste that can occur following the publication of a badly designed study that produces misleading data. The original 2012 study that led to the claim that supplementation with fullerenes dissolved in olive oil increases rat life span was carried out using only a small number of animals and was published in a journal that did not specialize in aging research. This is perhaps because the size of the life span extension claimed was large enough that it would be have been rejected by reviewers familiar with past results. It is too large to be taken at face value without resulting from a much larger and more rigorous study.

Later work showed that fullerenes in oil are in fact quite toxic unless very carefully manufactured, a hurdle requiring some years to pass, and not accounted for at all in the original paper. When tested robustly, using non-toxic formulations, fullerenes in olive oil were found to fail to extend rodent life span. The original study did not control for calorie intake, and so may have been reporting a disguised calorie restriction effect, or simply the result of an artifact of poor study design and execution.

We might then look at today's paper by a different group, in which the authors suggest that the problem is that olive oil on its own is quite harmful to rodent life span, while putting fullerenes into the olive oil counteracts some of these effects. The mechanisms of interest here revolve around oxidation of the lipid molecules in oils, as oxidized and otherwise altered lipids are harmful to cells, versus the sizable antioxidant capacities of fullerenes. At this point there is still at least one next step to conduct, which is to run life span studies based on delivery of water-soluble fullerenes without involving olive oil. This sort of approach has been tested in a preliminary way by a few groups for their ability to assist in control of localized inflammation, but not extensively.

Given the poor performance of systemic antioxidants to date in extending life in animal models, versus benefits for some types of antioxidant shown in inflammatory conditions, I wouldn't expect much to result from this work. The only antioxidant compounds that have produced increased life span are those that specifically target the mitochondria (such as MitoQ, SkQ1, and so forth), and even there the gains in life span in short-lived species are modest at best. These compounds have so far found their greatest success in localized treatment of inflammatory conditions, such as those of the eye.

Effect of long-term treatment with C60 fullerenes on the lifespan and health status of CBA/Ca mice

Several studies claimed C60 fullerenes as a prospective geroprotector drug due to their ability to capture free radicals effectively and caused a profound interest in C60 in life extension communities. Multiple additives are already sold for human consumption despite a small body of evidence supporting the beneficial effects of fullerenes on the lifespan. In order to test the effect of C60 fullerenes on lifespan and healthspan, we administered C60 fullerenes dissolved in virgin olive oil orally to 10-12 months old CBA/Ca mice of both genders for seven months and assessed their survival.

To uncover C60 and virgin olive effects, we established two control groups: mice treated with virgin olive oil and mice treated with drinking water. To measure healthspan, we conducted daily monitoring of health condition and lethality and monthly bodyweight measurements. We also assessed physical activity, glucose metabolism, and hematological parameters every three months.

We did not observe health deterioration in the animals treated with C60 compared with the control groups. Treatment of mice with C60 fullerenes resulted in an increased lifespan of males and females compared with the olive oil-treated animals. The lifespan of C60-treated mice was similar to the mice treated with water. These results suggest that the lifespan-extending effect in C60-treated mice appears due to the protective effect of fullerenes in opposition to the negative effect of olive oil in CBA/Ca mice.

View the full article at FightAging

[ambivalent]

Thank you so much for performing this additional research on c60oo, with so many using c60oo it is a deeply responsible pursuit.  

A great major scientific breakthroughs have been accidental in nature; the Baati study appeared to be one of those dramatic instances. The disinterest from the scientific community seemed to result from a vain allegiance to the scientific method. As scientific snobbery and elitism has escalated,  so its spirit and tradition of adventure and inquiry has waned. The complaint over sample size, is a seems to be a non-thinking trained response born out of the reputational risk averseness which seems endemic within the scientific community.

Sample size can't explain away huge effects: something was unquestioningly going on - accuracy is the only casuality of the meagre rodent enrollment, not certainty. And when the effect is close to doubling the lifespan, with the life-extended group achieving well beyond life expectation of the studied species, neither can poor experimental design: if so we need to capture that design error.

The response of the scientific community should have been to view the study like a prospector finding a nugget in a stream: if its not iron pyrite then shovel-up.  Money should have been immediately thrown into numerous parallel studies, one of which should be a large scale replication of Baati.  Science still can't trust in luck, even a 10% chance the study wasn't a fluke, would merit tens of millions of dollars of investment for mankind, but, of course, it wasn't a patented drug.  The heart and traditions of science inquiry is found on amateur communites, not in journals.

Nine years on we have to my knowedge yet to carry out a study upon the species in which the effects were observed while the work has been rather discredited through inter-species studies.

Around seven or eight years, I found a study and posted on longecity which showed at least when it comes to fasting at least rats aren't mice.

https://www.ncbi.nlm...les/PMC3119327/

https://pubmed.ncbi....h.gov/21410319/

There is too, other critical data, which has never been accumulated. When the longecity forum was alive with c60 users  there were some weirdly remarkable and seemingly independently observed effects, which experienced hackers and novices had never previously observed - such as burn healing, extreme alcohol intolerance.  That longecity data is an important validation of the study, but because it couldn't be accurately counted, then it is assumed not to count. However, after all, in life we take anecdotal evidence as evidence, especially when its harmful.

 

(Unable to post on FightAging) 

 

 

 

 

 

 

.

        

[Kentavr]

I wrote a comment on the FightAging website:

 

"For the correct preparation of C60EVOO, the following must be observed:

1. Stirring should be done WITHOUT ACCESS OF OXYGEN AND LIGHT (even red). Otherwise, TOXIC EPOXIES will form in the oil. It turns out OIL with EPOXY GROUPS. The container for cooking must be completely opaque, there must be nitrogen inside the flask. On the surface of fullerenes, heterogeneous catalysis of C = C bonds occurs with the participation of oxygen dissolved in oil.

2. The degree of crystallinity of C60 should be 99.5% (99.0% has more impurities, 99.9% dissolves worse due to the high degree of crystallinity). An ordered molecular lattice makes it impossible to effectively dissolve fullerenes.

3. You need to know how much antioxidants (oleorupein and hydroxytyrosol) were in the olive oil that the researchers used. If they take oil that is low in these antioxidants, the results will be different. C60 is thought to facilitate the delivery of antioxidants to mitochondria.

4. It is necessary to stir the C60 in EVOO for 2 weeks until the correct color (dissolution) is achieved.

And, MOST IMPORTANT: you must use NOT MICE, BUT RATS! Rats are closer to humans in terms of their functions, and MICE ABOVE POLYPHENOLS!

This research is FAKE!"

 

Do not believe those who want to mislead you.

[resveratrol_guy]

I haven't posted on Longecity in a long time, but I seem to have found myself in a unique position with respect to the C60 oil saga, so I thought I should point out few things.

I've read the Ichor study, and as you can see in some of my earlier posts, I've been taking C60 for the last 7 years, initially as c60oo, but almost exclusively c60mct for the back half of that. (I was compelled by Turnbuckle's argument that, independent of the question of toxicity or effectiveness, MCT must be more stable than EVOO.)

By chance, I was recently speaking to a friend of mine who happens to have extensively researched olive oil. While we weren't discussing C60, he advised me in particular to avoid any oils labelled as Italian -- even the name brands. He explained to me that they've suffered from a history of adulteration, from mislabeled vegetable oils with flavoring, to bastardized oils made from substandard olives more recently. I just took his advice because he's been a trusted friend for decades, but after reading the Ichor study that involved "high-quality EVOO from Central Italy", I had to investigate further. Here's an article from 2016 that summarizes the state of the problem at the time, which shows it to be far from contained and not long before Ichor started its experiments:

https://www.forbes.c...-keep-buying-it

Given that the study makes no mention of any attempt to authenticate the components of the oil, I'd have to label it as suspicious, given the gratuitous fraud outlined in the article. I don't blame Ichor for this. I blame the FDA for not doing their single most important job, namely, ensuring that food and drugs are what they say they are. It sounds like the cozy relationship between supermarket chains and Italian suppliers, in the absence of any acute toxicity experienced by consumers enthralled with low prices, is sustaining the abuse.

Moreover, it's time to admit that "olive oil" is a concept, not a substance. Even in the absence of fraud, there is a wide variation of chemical species dissolved within it, to say nothing of the age and composition of the oil itself. On the one hand, we have Jean Calment who reportedly lived to 122 and ingested copious amounts of olive oil; and on the other, these reports of pervasive fraud. Perhaps Calment happened to be faithful to a reliable brand untainted by the agro mafia. In any event, we need an oil that can be well defined and properly characterized. MCT is definitely a better candidate in this regard, in addition to its comparatively superior thermal stability. (I realize that coconut oil, and presumably MCT, increases morbidity in certain dietary contexts but the amount required for C60 dosing is rather minimal. For the record, I don't believe that this toxicity extends to ketogenic diets; it might rather be a calorie budget buster for CR folks.)

Looking at Figure 4 in the study linked above, it seems obvious that c60oo ("C60-EVOO") is superior to EVOO alone in older mice. The graph is at least consistent with the hypothesis that C60 somehow converted the older cohort of mice subject to adulterated EVOO into their control counterparts by shielding them from the toxicity. But we don't know because even if we knew the brand of EVOO employed, it's all but certain that no refrigerated sample still exists for testing purposes. The olive oil fraud has evolved over time in a cat-and-mouse game with consumers and enforcers, so the actual quality at the time of the experiment is unknowable.

In my view, the Ichor study definitively proves that a product labelled as high end EVOO can sometimes shorten average lifespan. That's quite valuable to know, even if it hasn't yet been proven in humans. But it has no bearing on the question of whether or not C60 in a thermally robust oil can extend lifespan or healthspan (not that Ichor attempted to test that).

The other damning finding of the Ichor study was photoinstability of c60oo and probably EVOO in general.

Baati may have been a careless experimenter but I lack the evidence to brand him a liar. It may be that the gross "error" in his study was due to the use of a trustworthy brand of EVOO.

I would implore anyone with the resources to more thoroughly investigate c60mct. Ichor did an outstanding job within the limitations of its knowledge at the time, and they would be as good a candidate as any for such experimentation. A much simpler experiment of high value would be to repeat the c60oo photodegradation study using MCT.

Finally, while I've read other studies on the matter, I'm still uncertain as to the severity of C60 degradation in the presence of ambient visible lighting, as one would encounter with typical cool white LED lab lights. It's clear that we should endeavor to keep the lights low during preparation, but how low, and how much time can we spend preparing the ingredients for stirring? And how much does oxygen actually matter? For instance, does it matter if we save a previously opened bottle of C60 powder in the fridge, given the column of atmospheric air inside the brown bottle? And what about the air column above the oil during stirring?

 

Let's not throw out the baby with the bathwater. Baati likely isn't a fraud. We just don't know exactly what he did "wrong".

 

Edited by resveratrol_guy, 24 July 2021 - 03:31 AM.

[resveratrol_guy]

Paging lead researcher Kelsey Moody... please invite him here if you can manage to get his attention. It would be good to get his input, or that of any other researcher with an interest in this.

 

A lot of consumers including me would pay a premium to have the confidence that we're consuming a c60mct product manufactured under tight controls derived from known rates of degradation under the influence of various environmental parameters, assuming of course that it actually shows a therapeutic benefit this time around. On the other hand, if it's all just poison, then it would be valuable to know that as well.

 

[Kentavr]

If we want to have an experiment with C60MCT, then he needs to add additional ingredients: oleuropein and hydroxytyrosol.

Without these molecules, C60 MCT will not work, since it is assumed that C60 is an agent for the delivery of these antioxidants to mitochondria.

Edited by Kentavr, 26 July 2021 - 07:27 AM.

[Turnbuckle]

If we want to have an experiment with C60MCT, then he needs to add additional ingredients: oleuropein and hydroxytyrosol.

Without these molecules, C60 MCT will not work, since it is assumed that C60 is an agent for the delivery of these antioxidants to mitochondria.

 

 

The antioxidant hypothesis is wrong. Oleuropein and hydroxytyrosol are not needed, nor is olive oil. Other solvents like MCT oil work perfectly fine. While C60 is a good antioxidant, this is not its mechanism of life extension. The Baati researchers were so impressed by the result of the toxicity trial that they made a wrong assumption. C60 actually appears to operate as a UCP2 blocker, and in conjunction with mito fusion is proliferating stem cells. Leave off the fusion, and you won't get proliferation. Nor will you get age regression or an increase in longevity. I saw no age regression without fusion, and more than twenty years with it. So I suspect Baati achieved fusion accidentally by fasting the rats. Fasting produces fusion, and rats, having a metabolic rate 6 times that of humans, will achieve that state overnight. The original study failed to mention fasting with the longevity trial (though they did with the toxicity trial), so likely Moody didn't do it. Thus the replication failed not because Moody did anything wrong, but because of a hidden variable that neither group appreciated.

Edited by Turnbuckle, 26 July 2021 - 11:16 AM.

[Kentavr]

The antioxidant hypothesis is wrong. Oleuropein and hydroxytyrosol are not needed, nor is olive oil. Other solvents like MCT oil work perfectly fine. While C60 is a good antioxidant, this is not its mechanism of life extension. The Baati researchers were so impressed by the result of the toxicity trial that they made a wrong assumption. C60 actually appears to operate as a UCP2 blocker, and in conjunction with mito fusion is proliferating stem cells. Leave off the fusion, and you won't get proliferation. Nor will you get age regression or an increase in longevity. I saw no age regression without fusion, and more than twenty years with it. So I suspect Baati achieved fusion accidentally by fasting the rats. Fasting produces fusion, and rats, having a metabolic rate 6 times that of humans, will achieve that state overnight. The original study failed to mention fasting with the longevity trial (though they did with the toxicity trial), so likely Moody didn't do it. Thus the replication failed not because Moody did anything wrong, but because of a hidden variable that neither group appreciated.

 

Turnbuckle,

 

Is olea25 required to be dissolved in MCT?

 

https://www.certifie...ucts_olea25.php

[ambivalent]

Turnbuckle, 

 

It isn't true you experienced no age regression without fusion, just that it was retraced, with no gains apparently held judged by lab tests at the beginning of these protocols. I assume you're not dismissing the antioxidant benefits of c60, but rather just c60's exclusive effect on age reversal. Plenty have had expereinced age reversing effects without fusion protocols, which you have posited is explained through depleted stem cell pools. There were few that seemed to display as dramatics effects from c60 as youurself - I remember for example dramatic improvement of miochondrial function, manifesting through physical endurace from just a 2ml of c60 - reversing statin damage; hair regrowth too. Niner recorded sustained improvements in breathing, from just c60. 

 

I have not kept tabs on on your threads recently, or longecity, but will experiment again most likely next year*  so I am inclined to wonder have you tried fasting as a fusion subsitute? 

 

 

 

 

* I recently dipped a toe into IV NAD (too early, but felt good) and tried out Alive by Science's sublingual liposmal fisetin gel  - I took above the recommended dose but experinced quite strong effects (eg pain in arthritic knee, a (personal) standard fisetin reaction) - so I would cautiously suggest it is a more penetrating senolytic, so perhaps worth adding to the protocol)    

Edited by ambivalent, 27 July 2021 - 11:54 AM.

[ambivalent]

The other damning finding of the Ichor study was photoinstability of c60oo and probably EVOO in general.

Baati may have been a careless experimenter but I lack the evidence to brand him a liar. It may be that the gross "error" in his study was due to the use of a trustworthy brand of EVOO.
.....

 

Let's not throw out the baby with the bathwater. Baati likely isn't a fraud. We just don't know exactly what he did "wrong".

 

The Baati study isn't fres in the memory, but iirc Wistlar Rats were known to be predisposed to cancer, and those on c60 didn't get it, moreover the rats lived long for Wistar. Admittedly, the fasting confounded things, however, there was an endorsement from Ichor's first study which led to further research. The AML study with mice did appear to demonstrate a reduction in disease progression with (inhouse) c60 treated mice. The subsequent study, with of the shelf c60, saw treated mice die quicker than controls.

 

No one has attempted to replicate Baatis study with Wistler rats - as far as I know - yet it is assumed the study isn't reproducible. It was a remarkable result, yet here we are years later and still it remains an enigma, not knowing the cause of a lifespan-doubling intervention. 

Edited by ambivalent, 27 July 2021 - 11:54 AM.

[Kentavr]

It seems to me that many influential people are not interested in the results of Baati's work being validated. Because it is very simple, radical, and it is not patented.

 

Moreover, if it is possible to greatly extend the life of one combination of drugs, and also along the way it will solve many related problems, it will be unprofitable.

 

Perhaps subsequent "explorers" are trying to undo Baati's research.

Edited by Kentavr, 27 July 2021 - 11:52 AM.

[Turnbuckle]

C60 has pleiotropic effects. It’s a good antioxidant, and it appears to block UCP2 pores in mitochondria. This second effect will have very different results in stem cells vs somatic cells. In somatic cells, UCP2 blocking will result in an increase in exercise performance — perhaps 20 percent or more — but this will be temporary. Stem cells have ten times as many UCP2 pores, and thus have quiescent mitochondria. Blocking them will banish quiescence and SCs will begin to divide. Whether they differentiate or proliferate is dependent on mitochondrial morphology. If they are in a fusion state, proliferation will be favored and stem cell pools will be increased. Fasting will get you there, but supplements will be easier and more reliable for most people.

 

The Baati group (actually Moussa et al.) tried to get a patent on C60 in food grade solvents. They got one in Tunisia, but Tunisia is just a registration system. That application was on Jun 30, 2011, before the first paper appeared. Their first US application was shot down as obvious in view of the prior art. It was already known that C60 could be dissolved in solvents, for instance, and was already known as an antioxidant (the prior art was a Moussa application from 2005).

 

Their first Moussa application for longevity in the US was in 2014, and the second in 2018. The first was abandoned. The second appears to be live.

 

 

Edited by Turnbuckle, 27 July 2021 - 03:53 PM.

[ambivalent]

It’s a good antioxidant

 

It does seem that it could be a little better than good, I remember this posted here years ago:

 

http://news.rice.edu...-flow-in-brain/

 

There were so quite rapid responses to burn injuries I and others found, it certainly appeared to quite rapidly reduce pain - I believe this was suggested to because of the suggested SOD mimicking property. Anyhow, without running off-track, there do appear to be a number of extreme, immediate and reliably powerful effects of c60oo which appeared independent of a prior fusion states (such as crazy alcohol tolerance).  

[resveratrol_guy]

Does anyone here have anything to add about the oxygen tolerance of C60 powder? For instance, do you reuse the same bottle over the months or years that it takes to consume it all, leaving it to mix with air locked inside the bottle in between times? Do you freeze the powder or refrigerate it? Or just leave it on the shelf (at what temperature)?

 

When I stir (for 3 or 4 weeks in the case of MCT at 800 mg/L), I leave about 30% of the beaker as room air at 26C, sealed under cling wrap. That's not intentional. It's just due to the limits of the stirring apparatus and the size of the beaker. I haven't ever noticed anything but the usual C60 benefits.

 

Still, perhaps I shouldn't be reusing C60 powder from previously opened SES bottles (small vials with a screw top, more accurately).

 

I'd also intrigued by the unappreciated fasting aspect of Baati's trial. So he fasted the EVOO and c60oo Wistar rats, but not the controls? Or what?

 

ambivalent, yes, that's what I recall as well: the rats were genetically predisposed to die of cancer, and then later in the initial Ichor investigations, Moody said something about getting dose-dependent life extensions until they outsourced the c60oo. Then it all fell apart in the study in question, and no one involved seems to have asked why.

 

Absent a rerun of the life extension study with MCT, I wonder if we can at least crowd fund an oxidation and photosensitivity assay to characterize degradation, both of the powder and the finished product. The Ichor study mentioned black products, so in principle one could just leave c60mct under a bright LED for a few days and take photos. That would be better than nothing, at least.

[Turnbuckle]

 

Absent a rerun of the life extension study with MCT, I wonder if we can at least crowd fund an oxidation and photosensitivity assay to characterize degradation, both of the powder and the finished product. The Ichor study mentioned black products, so in principle one could just leave c60mct under a bright LED for a few days and take photos. That would be better than nothing, at least.

 

 

See this thread. C60 and red light

 

Note that the prompt results I reported in that thread likely resulted from increased mitochondrial activity, but that was before I appreciated that C60 could be used to lower epigenetic age, which is an entirely different effect. Lowering epigenetic age appears to result from SC stimulation due to UCP2 blocking, and there's no reason to believe that red light would improve it.

Edited by Turnbuckle, 30 July 2021 - 08:59 AM.

[resveratrol_guy]

Thanks, Turnbuckle. I was thinking more in the context of photodegradation than photosensitivity in general. I did, long ago, read your comments about red light enhancing physiological effects (when delivered to the oil itself, quite apart from the vast literature on LLLT as a human therapy). My main concern here is just avoiding toxicity. For instance, we know that UV exposure must be avoided at all times (so keep the windows closed during prep, for starters).

I do have some data to share, though, in answer to my own question. It occurred to me that because a friend of mine had actually made some of my early c60mct batches, I should ask him how he kept the C60 powder for the 3 to 6 months in between deliveries. While I always kept the c60mct in the fridge inside a brown Boston bottle, which was only exposed to light for a matter of hours(?) over its months of use (due to opening the door to fetch food), he told me that he kept the C60 powder itself in a cabinet at around 24C. (I've asked for more specific data on the thermal band.) This means that the remaining portion of powder was kept in the presence of atmospheric air trapped inside the vial for months until it was consumed in the next batch. I must have consumed hundreds of mL of c60mct made with that "old" powder. It's been over a year since I finished the last of it and started making my own. I never noticed anything but the usual transient stomach upset I get with plain MCT. I even had c60mct (not necessarily made from old powder) in the trunk of a car for at least 45 minutes during a move, during which time the temperature would have been over 30C.

I've also asked him about light exposure during prep. But I know for sure that he stirred it in the same cabinet in the dark, so apart from the aforementioned fridge issue, there was no light exposure otherwise.

This makes me think that C60 isn't particularly oxygen-sensitive insofar as safe storage (even at room temperature!) is concerned. It's likely more that oxygen in the presence of intense light (maybe even visible) can cause cage damage over minutes to hours. So it doesn't surprise that doing the same to c60oo (let alone with adulterated oil) produced the extraordinarily toxic effects in the study. Never once did I observe discoloration of the c60mct of the sort described in therein. (Undissolved C60, which is not a manifestation of oil discoloration, forms a blackish sheen on the surface of an otherwise purple teaspoon dose. While I would recommend discarding the oil when you get that far down in the bottle, I've consumed at least tens of such tainted doses, which may account for my adrenal cysts, as I mentioned elsewhere. I no longer consume it, but it certainly wasn't acutely toxic.) Anyway, I don't use olive oil and I keep my c60mct in the fridge, which probably explains why I've never observed discoloration. I'm even careful to keep the bottle in my shadow when I pour out a dose so that no light can shine directly in through the open top. If I spill some oil or make a mess, I close the bottle and put it away before I clean up, all the while keeping it in my shadow with the windows closed.
 

[resveratrol_guy]

BTW I don't filter my oil (because I became convinced long ago, and perhaps in some part erroneously, that C60 powder is nontoxic). That's why I get undissolved C60 in the last several doses. In an effort to mitigate this problem, I moved to 23 days in the previously consumed batch and now 28 days of stirring in the current batch. My friend had been doing around 21 days.

Edited by resveratrol_guy, 31 July 2021 - 01:26 PM.

[resveratrol_guy]

I've started a stability experiment thread here. My first experiment failed to prove that c60mct is photounstable. At least, that's encouraging.

[orion22]

The antioxidant hypothesis is wrong. Oleuropein and hydroxytyrosol are not needed, nor is olive oil. Other solvents like MCT oil work perfectly fine. While C60 is a good antioxidant, this is not its mechanism of life extension. The Baati researchers were so impressed by the result of the toxicity trial that they made a wrong assumption. C60 actually appears to operate as a UCP2 blocker, and in conjunction with mito fusion is proliferating stem cells. Leave off the fusion, and you won't get proliferation. Nor will you get age regression or an increase in longevity. I saw no age regression without fusion, and more than twenty years with it. So I suspect Baati achieved fusion accidentally by fasting the rats. Fasting produces fusion, and rats, having a metabolic rate 6 times that of humans, will achieve that state overnight. The original study failed to mention fasting with the longevity trial (though they did with the toxicity trial), so likely Moody didn't do it. Thus the replication failed not because Moody did anything wrong, but because of a hidden variable that neither group appreciated.

what if the important factor is the autophagy you got from 3 g of nicotinamide the rats didn t get any nad+ boosters 

[Turnbuckle]

what if the important factor is the autophagy you got from 3 g of nicotinamide the rats didn t get any nad+ boosters 

 

Clearly that cannot explain the difference between the original rat study and the failed attempt to duplicate it, as no rats got any nad boosters.

[sensei]

What we can say from your evidence is the following:

C60 administered at the dose and frequency studied, in an Olive Oil vehicle, showed no statistically significant effect on the lifespan of xyz breed of mice.

What we can't state scientifically are the following:

Fullerenes don't extend life in all rodents. (there are many fullerenes, and many species of rodents)

C60 regardless of dose, has no effect on longevity. (the dose makes the poison or the cure, low dose naltrexone has clinical effects at 4mg not seen at normal doses)

Edited by sensei, 02 February 2022 - 04:13 PM.

[sensei]

Clearly that cannot explain the difference between the original rat study and the failed attempt to duplicate it, as no rats got any nad boosters.

However, in the original Baati Study, the oleocanthal in the EVOO would have induced significant autophagy due to MTORC1/P3IK inhibition.

[sensei]

MTORC1inhibition also affects stem cell maturation.

https://www.ahajourn...NAHA.119.044205

[Turnbuckle]

What we can say from your evidence is the following:

C60 administered at the dose and frequency studied, in an Olive Oil vehicle, showed no statistically significant effect on the lifespan of xyz breed of mice.

What we can't state scientifically are the following:

Fullerenes don't extend life in all rodents. (there are many fullerenes, and many species of rodents)

C60 regardless of dose, has no effect on longevity. (the dose makes the poison or the cure, low dose naltrexone has clinical effects at 4mg not seen at normal doses)

 

 

As I've pointed out several times now, the original study apparently used overnight fasting (as they did with the toxicity trial) while the attempted replication apparently did not. Rat metabolism is 6 times faster than humans, so overnight fasting would have inadvertently created a state of mito fusion. Mito fusion is key. Without it, you can expect SC niches to become depleted. I used C60 for some years and saw no epigenetic age reversal, while I saw substantial reversal after I began using fusion.

 

The original authors were so convinced that C60's activity was entirely due to its antioxidant properties that they neglected to give all relevant details about the longevity trial.

Edited by Turnbuckle, 02 February 2022 - 05:27 PM.

[sensei]

Rat metabolism is 6 times faster than humans, so overnight fasting would have inadvertently created a state of mito fusion. Mito fusion is key.

That even more solidly supports OLEOCANTHAL inhibition of MTORC1 as the driver of longevity, due to induction of mitochondrial hyperfusion.

The dose of olive oil and the oleocanthal and possibly ligsostride are paramount. Small doses of olive oil (EVOO) likely do not inhibit MTORC1 enough.

People like me, that gulp 240ml of C60EVOO to replicate the molar concentration of C60EVOO instead of allometrically reducing the rat dose, likely benefit. Little daily 5ml+ doses likely help less than the signal seen in the Mediterranean diet from oleocanthal at a daily EVOO consumption of 30ml on average.

Oleocanthal (and possibly ligstroside) as the driver of longevity through MTORC1 inhibition is supported by Jean Calment and the link below.

C60 action at the mitochondria is seemingly additive to the oleocanthal signal.

"Potent active-site mTOR inhibitors engender mitochondrial hyperfusion"

https://pubmed.ncbi....h.gov/28918902/

Edited by sensei, 02 February 2022 - 06:03 PM.

[Rocket]

I don't put any stock in these studies because I've seen other studies that were all lies in order to suppress knowledge and keep people sick.

If c60 did lengthen life you had better believe the world elite would to anything to keep it quiet and discredit it. The world elite are trying to reduce the population and not improve or lengthen life.