109 replies to this topic

[Daniel Cooper]

As an example  - Think of all the patents granted for extended release versions of previously patented drugs.

 

The mechanics of making extended release compounds has been well established for decades now.  Yet, drug companies seem to be routinely granted patents for extended release versions of drugs that are (not coincidentally) about to come off their original patent.  Unless they have come up with a novel extended release mechanism, all of these patent applications should be rejected out of hand as being "obvious to one skilled in the art".  Yet, they seem to be routinely granted.  

 

This btw, has the perverse outcome of keeping extended release versions of drugs (which are often times useful) off the market for years until the original patent on a drug approaches the end of it's life.

 

 

 

[Iporuru]

Long-awaited results on C60 from Ichor:

 

C₆₀ in olive oil causes light-dependent toxicity and does not extend lifespan in mice

C₆₀ is a potent antioxidant that has been reported to substantially extend the lifespan of rodents when formulated in olive oil (C₆₀-OO) or extra virgin olive oil (C60-EVOO). Despite there being no regulated form of C₆₀-OO, people have begun obtaining it from online sources and dosing it to themselves or their pets, presumably with the assumption of safety and efficacy. In this study, we obtain C₆₀-OO from a sample of online vendors, and find marked discrepancies in appearance, impurity profile, concentration, and activity relative to pristine C₆₀-OO formulated in-house. We additionally find that pristine C₆₀-OO causes no acute toxicity in a rodent model but does form toxic species that can cause significant morbidity and mortality in mice in under 2 weeks when exposed to light levels consistent with ambient light. Intraperitoneal injections of C₆₀-OO did not affect the lifespan of CB6F1 female mice. Finally, we conduct a lifespan and health span study in males and females C57BL/6 J mice comparing oral treatment with pristine C₆₀-EVOO and EVOO alone versus untreated controls. We failed to observe significant lifespan and health span benefits of C₆₀-EVOO or EVOO supplementation compared to untreated controls, both starting the treatment in adult or old age. Our results call into question the biological benefit of C₆₀-OO in aging.

Edited by Iporuru, 31 October 2020 - 06:18 AM.

[Guest]

Given that many started to take C60-EVOO (commercially procured or home-made) based on that one french study by Baati et. al. ....

 

 

....and given that the replication study used larger cohorts (albeit mice instead of rats) and can be considered to be more neutral in terms incentives for over-/understating potential results - it even got funding from Longecity....

 

 

.... is anyone going to adjust their C60 consumption according to emerging evidence?

[Mind]

One can view a small screen capture of the figures contained in the paper (without purchasing the PDF). At least one of the graphs is relatively readable, C60-OO mice start out living longer but quickly "fall back" to end up matching OO controls at the end of life.

[Turnbuckle]

My impression has been from the beginning that less was more, and I typically use an oral dose of 3 mg (0.035 mg/kg), far less than in the rodent experiments. The Baati rat paper used an oral dose of 1.7 mg/kg, while the new paper used an oral dose of 4 mg/kg. There was mention of fasting in the Baati paper -- at least for the pharmacokinetics study -- and no mention at all in new paper. Fasting would tend to put mitochondria into a fusion state and push stem cells into proliferation rather than differentiation. 

 

Nutrient scarcity in organisms is linked to an increase in circulating glucagon and other stress hormones, such as norepinephrine, which generally increase intracellular cAMP levels and PKA signaling (Fig 2A). Under these circumstances, mitochondrial fusion is typically observed

https://www.ncbi.nlm...les/PMC4023882/

 

 

And

 

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

https://www.scienced...934590916300820

 

 

Is it possible that this made all the difference? Yes, if the longevity results came from SCs, because differentiation will deplete SCs while proliferation will increase them. The problem here is we don't know exactly how either paper fed their rodents during the long term studies. For my own use, I drive SCs to fusion with stearic acid.

 

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

https://www.ncbi.nlm...les/PMC4561519/

 

 

 

Edited by Turnbuckle, 31 October 2020 - 08:49 PM.

[Guest]

My impression has been from the beginning that less was more, and I typically use an oral dose of 3 mg (0.035 mg/kg), far less than in the rodent experiments. The Baati rat paper used an oral dose of 1.7 mg/kg, while the new paper used an oral dose of 4 mg/kg. There was mention of fasting in the Baati paper -- at least for the pharmacokinetics study -- and no mention at all in new paper. Fasting would tend to put mitochondria into a fusion state and push stem cells into proliferation rather than differentiation. 

 

 

And

 

 

Is it possible that this made all the difference? Yes, if the longevity results came from SCs, because differentiation will deplete SCs while proliferation will increase them. The problem here is we don't know exactly how either paper fed their rodents during the long term studies. For my own use, I drive SCs to fusion with stearic acid.

 

So you are saying:

 

the 4 mg/kg was such a profound overdosing compared to 1,7 mg/kg that the effects of 90% life-extension vanished?

 

The French team published the most profound life-extension in a mammal ever achieved in 200 years of biological research. But it is so fragile, that it vanishes at double the dose? In male and female mice. The survival curves in the replication study look as if there is no (positive or negative) effect of C60 at all.

 

 

 

Also what are you basing your low dose on? If your assessment is true, C60 has a very, very narrow therapeutic range - an Baati et al just were extremely lucky that they just hit the sweet spot in their experiment. So if you deviate from that (and it seems just doubling the dose is sufficent) you will have no effect.

 

 

 

The fasting was done in the pharmacokinetics test to ensure un-interfered measurements. It was not done before administration during the course of the lifespan of the rats. If that happened it was not published in their protocol.

[Turnbuckle]

So you are saying:

 

the 4 mg/kg was such a profound overdosing compared to 1,7 mg/kg that the effects of 90% life-extension vanished?

 

The French team published the most profound life-extension in a mammal ever achieved in 200 years of biological research. But it is so fragile, that it vanishes at double the dose? In male and female mice. The survival curves in the replication study look as if there is no (positive or negative) effect of C60 at all.

 

 

 

Also what are you basing your low dose on? If your assessment is true, C60 has a very, very narrow therapeutic range - an Baati et al just were extremely lucky that they just hit the sweet spot in their experiment. So if you deviate from that (and it seems just doubling the dose is sufficent) you will have no effect.

 

 

 

The fasting was done in the pharmacokinetics test to ensure un-interfered measurements. It was not done before administration during the course of the lifespan of the rats. If that happened it was not published in their protocol.

 

I'm pointing out the difference in oral dosage, and also that less seems to be more. But the more likely cause of the failure to see life extension in the most recent paper vs the first is a difference in mitochondrial morphology. The difference between SC differentiation and proliferation should be dramatic. I have seen this in my personal experiments.

Edited by Turnbuckle, 01 November 2020 - 07:23 PM.

[APBT]

FULL TEXT:

Attached Files

•  C60 in olive oil causes light-dependent toxicity and does not extend lifespan in mice.pdf   565.78KB   16 downloads

[Guest]

I'm pointing out the difference in oral dosage, and also that less seems to be more. But the more likely cause of the failure to see life extension in the most recent paper vs the first is a difference in mitochondrial morphology. The difference between SC differentiation and proliferation should be dramatic. I have seen this in my personal experiments.

 

 

That is not how supplements or medicine work.

 

There is a dose response-relationship, where there is an optimum and you see less health-effect by increasing or decreasing the dose (the first by secondary toxicity and the latter by under-dosing).

 

 

So what are you saying:

 

That using 1,7 mg/kg in the Baati et al study was already overdosing and less would result in even more than 90% life-extension? Like 150% oder 200% life-extension?

 

C60 is truly a miracle substance that stops all damages and causes of aging. (being ironic here)

 

 

 

And where do you get from, that there were:

 

a) differences in mitochondrial morphology (and supposedly stem cells) between the 2 studies?

 

b) that this differences can account between the greatest result ever reported in all of medicine and longevity science - and a complete Null-result?

Edited by Guest, 01 November 2020 - 07:36 PM.

[Turnbuckle]

 

 

And where do you get from, that there were:

 

a) differences in mitochondrial morphology (and supposedly stem cells) between the 2 studies?

 

b) that this differences can account between the greatest result ever reported in all of medicine and longevity science - and a complete Null-result?

 

As I said, the manner of feeding in the two papers is unknown. In the first paper, it is indicated for one study (fasting and thus likely fusion), but not in the longevity study, while in the second paper it is not indicated at all. And yes, the difference in morphology will make a huge difference, as that is the determinant of stem cell fate.

Edited by Turnbuckle, 01 November 2020 - 07:51 PM.

[yz69]

the 2020 result is not a complete NULL result.  If you check the  graphs, you will see the health span improves a lot with c60 treatment.

 

What's great about Turnbuckle's idea is he abandoned the mindset of "one pill save us all" and connected the dots between stem sell self-renewal , mitochondria dynamics and senescent cell removal.

 

Yes, the difference of tiny details between the 2012 C60 paper and the   2020 C60 paper could make a huge difference: in the 2012 paper, mice were fasted overnight before taking C60, the 2020 paper mice were allowed to eat ad libitum, this difference will have impact on mitochondria dynamics and stem cell fate.

Edited by yz69, 01 November 2020 - 07:52 PM.

[Guest]

the 2020 result is not a complete NULL result.  If you check the  graphs, you will see the health span improves a lot with c60 treatment.

 

What's great about Turnbuckle's idea is he abandoned the mindset of "one pill save us all" and connected the dots between stem sell self-renewal , mitochondria dynamics and senescent cell removal.

 

Yes, the difference of tiny details between the 2012 C60 paper and the   2020 C60 paper could make a huge difference: in the 2012 paper, mice were fasted overnight before taking C60, the 2020 paper mice were allowed to eat ad libitum, this difference will have impact on mitochondria dynamics and stem cell fate.

 

 

It is. Read the paper.

 

There is no statistical difference in lifespan. They're using different statistics and check for gender specific difference. If you want to go entirely by optics instead you see a slight survival advantage for early mortality and a slight disadvantage by late mortality (figure 4). Anyway, the fact remains: the curves are so close, that there is no statistical difference reported.

 

It is a Null result.

 

 

 

And again:

 

the Baati-paper does not report any specific feeding procedure (i.e. regular fasting) for the longevity part of their study. Read the paper.

 

There was an overnight fast for the purpose of the pharmacokinetics analysis. No such schedule is reported for the longevity part. And it would be highly unusual, as Caloric Restriction is an established life-extension procedure. So not to blur the CR effects with their own subject of study (C60) it is highly unlikely that their mice got constant intermittent fasts. And again: it is not reported in the study anyway. So you can't just assume that it happened without publishing it (that would be a huge part of the protocol if they did it - and against any scientific-ethics not to mention it in their paper).

 

 

 

@TB:

 

could you please provide a link, that the morphology is:

 

- relevant for C60 or alternatively it's supposed intra-cellular mechanism (presumably the anti-oxidant effects)?

- so important for lifespan effects

 

 

 

 

And I would still be interested in the plausibility of using much smaller dosing than used in the Baati et al paper. Do you mean, that Baati was already over-dosing?

[Hebbeh]

There was an overnight fast for the purpose of the pharmacokinetics analysis. No such schedule is reported for the longevity part. And it would be highly unusual, as Caloric Restriction is an established life-extension procedure. So not to blur the CR effects with their own subject of study (C60) it is highly unlikely that their mice got constant intermittent fasts. And again: it is not reported in the study anyway. So you can't just assume that it happened without publishing it (that would be a huge part of the protocol if they did it - and against any scientific-ethics not to mention it in their paper).

 

First, you're failing to realize the Baati study was NOT a longevity study or life extension study.  It was a toxicology study.

 

The study was not designed nor intended to explore C60 as a life extension or health extension substance.  The study was designed to measure adverse effects of exposure to C60 to determine safety of C60 as used in potential industrial applications.

 

The life extension aspect was an unexpected and surprising artifact.  Many people seem to forget the design and intent of the original Baati study and focus on the longevity artifact as if it was the designed intent when nothing could be further from the truth.

[Guest]

First, you're failing to realize the Baati study was NOT a longevity study or life extension study.  It was a toxicology study.

 

The study was not designed nor intended to explore C60 as a life extension or health extension substance.  The study was designed to measure adverse effects of exposure to C60 to determine safety of C60 as used in potential industrial applications.

 

The life extension aspect was an unexpected and surprising artifact.  Many people seem to forget the design and intent of the original Baati study and focus on the longevity artifact as if it was the designed intent when nothing could be further from the truth.

 

 

It sure as heck wasn't sold to the public as this, titled as "The prolongation of the lifespan of rats by repeated oral administration of [60]fullerene"

 

 

And what are you implying with that comment?

 

 

That the longevity results in the Baati et al study can't be taken serious?

[Hebbeh]

No where in the study do the authors show intent or discuss investigating longevity as an effect of C60.  The title of the paper was chosen not in relation to original study design but in bringing attention to the unusual and unexpected result artifact.

 

They do discuss in detail the intent of investigating the toxicity of chronic C60 ingestion which had never been studied before. In fact, once the life extension artifact became apparent, they ended the experiment treatment as the lack of toxicity had been apparent and therefore the study was complete at which time they sacrificed the last rat or 2.

 

Had it been a longevity study, they would not of ceased the C60 treatment and killed off the last rat or 2 but would have determined maximum lifespan which they did not do and had no interest in doing.  The study was complete after the first C60 rat to die had outlived controls which proved lack of toxicity and remaining rats were sacrificed as the study intent was concluded.

 

I can only suggest to read and study the full paper and accompanying discussions.

 

 

Edited by Hebbeh, 02 November 2020 - 12:28 AM.

[Guest]

I'm still not certain what bearing this has on the discrepancy between that original study and the recent replication study (which in fact was designed and statistically powered to investigate longevity). It sure doesn't mean that we can just assume a fasting regimen that was employed in the chronic intake part, but not reported in the paper.

[Hebbeh]

Baati's study was intended as a toxicity study and concluded no toxicity was detected (in fact, not only was no toxicity detected but unexpectedly the C60 dosed cohort outlived controls artifact).  In contrast, Moody's study determined a degree of toxicity.  That is the common thread between the 2 studies.  More questions than answers perhaps.  Are you feeling lucky?

[Turnbuckle]

Baati's study was intended as a toxicity study and concluded no toxicity was detected (in fact, not only was no toxicity detected but unexpectedly the C60 dosed cohort outlived controls artifact).  In contrast, Moody's study determined a degree of toxicity.  That is the common thread between the 2 studies.  More questions than answers perhaps.  Are you feeling lucky?

 

On the contrary, the researchers of the Baati study knew there was toxicity. Not of the C60 molecule itself, but of C60 derivatives. By exposing dissolved C60 to light, including red light that can penetrate amber bottles, you can create free radicals that produce all sorts of reactions. As Fathi Moussa (the lead researcher on the Baati paper) said five years before in 2007 -- 

 

Available data clearly shows that pristine C60 has no acute or sub-acute toxicity in a large variety of living organisms, from bacteria and fungal to human leukocytes, and also in drosophila, mice, rats and guinea pigs. In contrast to chemically--either covalently or noncovalently--modified fullerenes, some C60 derivatives can be highly toxic. Furthermore, under light exposure, C60 is an efficient singlet oxygen sensitizer. Therefore, if pristine C60 is absolutely nontoxic under dark conditions, this is not the case under UV-Visible irradiation and in the presence of O2 where fullerene solutions can be highly toxic through 1O2 formation. 

 

To sum up, this review shows that if pristine C60 is not toxic, the toxicity of each C60 preparation or each C60-derivative must be determined before use. For the promising medicinal applications of fullerenes, sufficient data regarding in vivo behaviour of fullerenes should be accumulated. 

https://pubmed.ncbi....h.gov/18217343/

 

 

Toxicity studies dating back to 1993 (referenced by Moussa et al in 2007) showed the C60 molecule itself to be non toxic. There was a good deal of evidence by the time of the Baati paper in 2012, so the statement by some here that this was purely a toxicity study is unwarranted.

[Hebbeh]

From Baati's paper:

 

However, although several independent research groups confirmed the innocuousness of pristine C60 [15e17] the toxicity of this fullerene is still a matter of debate [18,19]. As recently demonstrated, this is mainly due to the lack of characterisation of the tested materials [15e19]. Nevertheless, the metabolic fate and the in vivo chronic effects of C60 itself still remain unknown. In order to fulfil the potential of C60 and derivatives in the biomedical field these issues must be addressed.

 

Aqueous suspensions were previously used to investigate the acute and sub-acute toxicities as well as the in vivo antioxidant properties of pristine C60 [20,21]. But, such suspensions are not appropriate for determining toxicity at reiterated doses, because fullerene is active only in soluble form [21] and because the extremely slow dissolution of C60 in biological media prevents controlling accurately the active fraction [21]. This may be the reason for which the chronic toxicity of C60 has never been investigated to our knowledge.

 

 

 

5. Conclusion

The effect of pristine C60 on lifespan emphasizes the absence of chronic toxicity. These results obtained with a small sample of animals with an exploratory protocol ask for a more extensive studies to optimize the intestinal absorption of C60 as well as the different parameters of the administration protocol: dose, posology, and treatment duration. In the present case, the treatment was stopped when a control rat died at M17, which proves that the effects of the C60 treatment are long-lasting as the estimated median lifespan for C60-treated rats is 42 months. It can be thought that a longer treatment could have generated even longer lifespans. Anyway, this work should open the road towards the development of the considerable potential of C60 in the biomedical field, including cancer therapy, neurodegenerative disorders and ageing. Furthermore, in the field of ageing, as C60 can be administered orally and as it is now produced in tons, it is no longer necessary to resort to its water-soluble derivatives, which are difficult to purify and in contrast to pristine C60 may be toxic.

 

 

 

I'm short on time but it is clear they were studying toxicity and stopped C60 treatment and concluded the study with C60 cohorts still alive which would not have been done on a longevity study.

[Turnbuckle]

 

 

I'm short on time but it is clear they were studying toxicity and stopped C60 treatment and concluded the study with C60 cohorts still alive which would not have been done on a longevity study.

 

I don't see the logic. A better argument would be to note that the last C60 rats were euthanized (not mentioned in the paper), but this could have been the result of time constraints, and also patent considerations.

[Hebbeh]

I previously noted in a earlier post that they ended the study with C60 rats still alive at which time they sacrificed the rats to conclude the toxicity study as it was obvious that toxicity had not negatively affected life span and the intent of the study was therefore answered and the study was ended with no attempt to measure how much longer the final rats may have lived and which we will never know.

I already posted some excerpts from the study introduction which only discuss toxicity. The entire introduction only discusses aspects of toxicity and there is no mention of lifespan or longevity anywhere in the study introduction of study intent.

I'm puzzled in what you believe the intent of their study design is and what in the paper supports your opinion?

Edit: I also previously posted the concluding statement which I believe is the only mention of lifespan and is noted as an unintended artifact. I should also remind from a previous post that the toxicity that they were particularly interested in was chronic toxicity which had never been previously studied.

Edited by Hebbeh, 02 November 2020 - 02:13 PM.

[Turnbuckle]

I previously noted in a earlier post that they ended the study with C60 rats still alive at which time they sacrificed the rats to conclude the toxicity study as it was obvious that toxicity had not negatively affected life span and the intent of the study was therefore answered and the study was ended with no attempt to measure how much longer the final rats may have lived and which we will never know.

I already posted some excerpts from the study introduction which only discuss toxicity. The entire introduction only discusses aspects of toxicity and there is no mention of lifespan or longevity anywhere in the study introduction of study intent.

I'm puzzled in what you believe the intent of their study design is and what in the paper supports your opinion?

Edit: I also previously posted the concluding statement which I believe is the only mention of lifespan and is noted as an unintended artifact. I should also remind from a previous post that the toxicity that they were particularly interested in was chronic toxicity which had never been previously studied.

 

You don't understand the patent world. Moussa filed his first patent application in Tunisia in June 2011, nearly a year before the paper. It's typical of patent applications to say that a result is "surprising," as novelty is an essential element to patentability. So regardless of what they might have expected, they weren't going to say that in the paper published afterward, as that would have undercut patent applications in other countries.

 

The inventors of the instant invention have now discovered a surprising use of [60]fullerene as agent that promotes an increases in the overall length of the expected lifespan of mammals.

https://patents.just...ent/20140140985

 

[Hebbeh]

That's interesting but begs more questions than answers.

After securing patent rights, why didn't Moussa pursue additional studies and attempt to profit from his novel discovery?

Or did he perform additional studies and discover additional unexpected negative results affectively killing the project?

[Turnbuckle]

That's interesting but begs more questions than answers.

After securing patent rights, why didn't Moussa pursue additional studies and attempt to profit from his novel discovery?

Or did he perform additional studies and discover additional unexpected negative results affectively killing the project?

 

 

They did attempt to profit from it. At the time I saw pictures of Moussa at a Japanese company where he was discussing licensing. However, the failure of patents to issue would have made that difficult. The Tunisian patent was worthless, just a rubber stamp patent in a small country. Moussa hasn't given up, however, and his latest US filing (from 2018) is here.

 

The broadest remaining claims --

 

15. A stable biocompatible composition for use with the method of claim 22, the composition comprising: (a) a carrier selected from the group consisting of fats and oils; and (b) one compound selected from the group consisting of water-insoluble fullerenes, wherein said fullerenes are mostly dissolved in said carrier.

 

22. A method to prolong the expected lifespan of a mammal, which comprises a step of: administering to said mammal a stable biocompatible composition a water-insoluble C60 fullerene, wherein said composition is administered intravenously, intramuscularly, subcutaneously, intradermally, intrathecally, intraperitoneally, rectally by suppositories, sub lingually, orally, or by inhalation.

 

 

 

Edited by Turnbuckle, 03 November 2020 - 11:07 AM.

[Iporuru]

A short, pop-science overview of the C60 story and the recent study:

 

 

[OlderThanThou2]

Should there be an adjustment of the dosage caused by the fact that rats are heavier than mice? Not sure but I think that the heavier an animal is the lower the dosage. Say a rat weighs 5 times as much as a mouse, if the equivalent dosage is half, that means the difference between the 2 studies is not 4/1.7=2.35 but around 1. MAybe they adjusted the dosages to be equivalent. 

Edited by OlderThanThou2, 06 November 2020 - 01:37 PM.

[Hebbeh]

https://www.longecit...ga/#entry900113

[genX]

As far as I'm concerned the conclusion that C60/olive oil is of no value and should be avoided due to potential toxicity seems somewhat hasty due to the following:

 

1)  The effects of all supplements/medications are dose dependent (U-shaped curve as pointed out by Turnbuckle)

2) A large number of people have reported positive effects both in terms of symptoms and blood-work from taking C60/olive oil

3) The Ichor study itself found that in the absence of light exposure C60/olive oil is not toxic

4) The Ichor study also pointed out that it is a potent anti-oxidant (and again is not toxic if not exposed to light)

5) There's a big difference between taking it everyday, or perhaps once a week, or intermittently

6) Turnbuckle has a protocol in which he takes it once a week, followed by other supplements which he finds leads to age reversal

7) I tried C60/olive oil from different suppliers intermittently (e.g. at most I would take a teaspoon 2-3 days in a row) over a couple of years and while

it initially bothered me (brought back ringing in my right ear which is a long-standing problem) the last few times I took it (and I never took 

it more than 1-2 days in a row) I personally observed the following positive effects:

 

A) A month-long hip-injury/strained hip-ligament healed overnight

 

B) A long-standing (and untreated) tooth abscess (supposedly needing a root canal) was significantly reduced (at least temporarily)

 

Also, I periodically take 1 g of liposomal vitamin C (which is also an anti-oxidant) but never noticed such a powerful effect.

 

My tentative conclusion is that if one avoids exposure to ambient light (e.g. keeps it wrapped in a box and in a dark place etc.) then it can be

a powerful anti-oxidant and -based on the testimony of many others - can provide positive health benefits.

 

As far as being a "longevity" supplement, I know nothing of this and I wouldn't venture to say anything except again that

dose and frequency could play an important role in regulating its effects.  But certainly, if it can lead to short-term positive effects

as so many have reported, due it's very powerful anti-oxidant properties, then this can contribute to 'longevity" in humans in a number

of indirect ways.  

 

Getting back to the dose frequency issue, it is well known that taking anything regularly can reduce its effectiveness due to homeostasis (or something like that).

Also, there are issue of hermesis (occasional oxidative stress can be good).

 

Perhaps Turnbuckle has something to say about this.

 

I welcome any comments/corrections regarding my remarks.

 

Thank you.

 

 

[pherz]

Link:https://youtu.be/ve4q-1D_Ajo

Turnbuckle and Longecitizens, anyone familiar with Bret Weinstein and Carol Greider's interesting work on 'antagonistic pleiotropy theory of senescence' and telomere differences, in regards to lab bred mice vs wild mice, potentially corrupting and/or misleading drug/cancer research assumptions?

Think it may have significant implications for Moody vs Baati? On cursory review of Moody paper he appears mire unfaithful & cavalier than not to key science tenet of identical physical, biological, and methodical thesis replication to develop & help accurately test/evolve theory or as he apparently tries to falsify as conjecture.

[genX]

My impression has been from the beginning that less was more, and I typically use an oral dose of 3 mg (0.035 mg/kg), far less than in the rodent experiments. The Baati rat paper used an oral dose of 1.7 mg/kg, while the new paper used an oral dose of 4 mg/kg. There was mention of fasting in the Baati paper -- at least for the pharmacokinetics study -- and no mention at all in new paper. Fasting would tend to put mitochondria into a fusion state and push stem cells into proliferation rather than differentiation. 

 

 

I completely agree with this comment.  The typical human dose is one teaspoon a day (although Turnbuckle's protocol is more like 1 teaspoon once a week) which is around 4.5 g or around 0.045 - 0.06 mg/kg (for adult weight ranging  from 100 kg to 75 kg).    This is a dose per weight which is 70-90 times smaller than the Ichor dose per weight.   I'm sure that dose makes all the difference and I keep seeing anecdotal reports in many groups of significant positive results from taking C60 olive oil at this dosage.   I would suggest that a study be carried out on mice and/or rats with much lower dosage.