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Results: Longecity sponsored AML study

c60oo longevity cancer leukemia aml

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#31 Raza

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Posted 20 May 2015 - 07:18 AM

Sweet, new data!

 

So if I get this right, you injected immunocompromised mice with what were already cancerous human cells? I'm kind of surprised to see a result at all that way; wasn't the idea of C60 that it'd reduce mortality from cancer by reducing oncogenic mutations? (I'm a bit out of date on my C60 theory, mind). What was the hypothesis for an effect on the growth of or mortality from preexisting cancers?

 

At least this shows that Niner's theoretical worries about regular C60 dosing protecting existing cancers from the oxidation penalty of their high metabolism were unfounded, and apparently then some.

 

Also, question. What was the idea behind injecting the doses, rather than delivering them orally? Considering that we take them orally, and the Baati rats did, too? It seems like effects from oral would be both more educative and more strongly expected. And I worry that injecting volumes of undigested lipids would have detrimental effects of its own, which might exlain why the saline control did unexpectedly well compared to everything else, unless intraperitonal lipid injections are something standard, in which case nevermind.



#32 Raza

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Posted 20 May 2015 - 08:23 AM

Oh also, what were the presumed dosage equivalencies?



#33 kmoody

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Posted 20 May 2015 - 03:45 PM

How Much $$$?

Dozen rats or Mice divided each in two groups X 12 = 24 Rats or Mice

Group One C60 dosed 2 mg/per Kilogram for one month and control group dosed on ordinary Saline

Then we introduce same exact human cancer line to all the rats / mouse with a known longevity for controls 

Wait for them to pass away and record the times of death and Chart it

Nothing fancy  

Just a simple experiment.

I personally think a member of SENS could have performed this test with the millions they have in donations.

The amount of funding required depends on how much needs to be done. You are correct in that just running a basic experiment using death curves is simple and probably inexpensive. This is a good reference for an idea of basic housing costs:

https://www.research...rdiemrates.html

 

Keep in mind that 2mg/kg or 4mg/kg could be protective against cancer in a normal healthy individual, but introducing a massive bolus of cancer cells all at once is not consistent with how cancer naturally emerges in the body. Would you be better off to administer fewer cells? Or perhaps a better model might be to take a mouse line that is known to acquire a specific type of cancer very early in life and test c60oo as a preventative measure in that line?

 

Also note that not all human cancers engraft at 100% in these immunocompromised models. In fact, many have rather low rates of engraftment. So how do we know c60oo protects against cancer with this model? If there is a difference in cancer-free survival it could be chance (i.e. with a low n one group is bound to have lower engraftment success than the other) or perhaps c60oo inhibits engraftment... that would tell us nothing about a potential role for c60oo in cancer prevention. Alternatively, c60oo could actually PROMOTE engraftment... so we could see treated mice fair worse... but that could just be an artifact of messing with engraftment efficiencies and have nothing to do with cancer progression.

 

When I think about these sorts of issues, I like to try to think about what are the most worthwhile questions to answer, rather than how to answer them. Your question seems to be, "Can c60oo prevent someone from getting cancer?" I think this is a good question. We should brainstorm some other good questions, get a ballpark price for answering each, then rank order them by priority adjusted by price. At least, that would be my recommendation.

 

I'll volunteer a few questions...

1. Are the pharmacokinetic and biodistribution properties of c60oo similar in people and rodents?

2. How does c60oo compare to standard of care in our AML model (i.e. is it better than the recommended chemo regimens)?

3. Do basic growth curve studies in culture suggest c60oo selectively targets cancer, rather than healthy cells?

4. What is the mechanism of action for #3 (cytotoxicity, growth inhibition, other)?

5. Do we believe the results of our pilot study (low n, could be noise, worth repeating)?

6. Do we see similar results in primary cancer cells rather than just cancer cell lines?

 

Dear community... what questions do you want to see answered? :)

 

 

I personally think a member of SENS could have performed this test with the millions they have in donations.

SENS Foundation does not have a mouse facility at their laboratory.



#34 kmoody

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Posted 20 May 2015 - 03:54 PM

So if I get this right, you injected immunocompromised mice with what were already cancerous human cells? I'm kind of surprised to see a result at all that way; wasn't the idea of C60 that it'd reduce mortality from cancer by reducing oncogenic mutations? (I'm a bit out of date on my C60 theory, mind). What was the hypothesis for an effect on the growth of or mortality from preexisting cancers?

Correct, we injected with already cancerous human cells... and I promise I was more surprised than you were. :) Reducing mutations is one proposed mechanism, and this is not mutually exclusive with the data we're seeing. We wanted to track growth and mortality from AML in this study. Growth tracking by flow was not good... we need to use bone marrow aspirates next time to better answer this question because few of the AML cells make it into circulation, and they are not an accurate measure of tumor burden.

 

At least this shows that Niner's theoretical worries about regular C60 dosing protecting existing cancers from the oxidation penalty of their high metabolism were unfounded, and apparently then some.

In one cancer line that shares few properties with metastatic solid tumors, maybe? :)
 

Also, question. What was the idea behind injecting the doses, rather than delivering them orally? Considering that we take them orally, and the Baati rats did, too? It seems like effects from oral would be both more educative and more strongly expected. And I worry that injecting volumes of undigested lipids would have detrimental effects of its own, which might exlain why the saline control did unexpectedly well compared to everything else, unless intraperitonal lipid injections are something standard, in which case nevermind.

We wanted total control over dosing and IP is easier than gavage. Since absorption is similar we figured it didn't matter and we could go either way. To account for the potential liver toxicity associated with olive oil injections we did track liver enzyme levels (AST and ALT). We did not see a spike nor any other sign of liver toxicity. This is consistent with what was reported by Baati.

 

Oh also, what were the presumed dosage equivalencies?

I do not understand the question... we administered 2mg/kg, 4mg/kg, and 8mg/kg c60oo. Control mice were administered the highest volume of either saline or olive oil that the experimental mice received. The dosing used by Baati et al was 4mg/kg c60oo.


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#35 bixbyte

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Posted 22 May 2015 - 07:20 PM

 

So if I get this right, you injected immunocompromised mice with what were already cancerous human cells? I'm kind of surprised to see a result at all that way; wasn't the idea of C60 that it'd reduce mortality from cancer by reducing oncogenic mutations? (I'm a bit out of date on my C60 theory, mind). What was the hypothesis for an effect on the growth of or mortality from preexisting cancers?

Correct, we injected with already cancerous human cells... and I promise I was more surprised than you were. :) Reducing mutations is one proposed mechanism, and this is not mutually exclusive with the data we're seeing. We wanted to track growth and mortality from AML in this study. Growth tracking by flow was not good... we need to use bone marrow aspirates next time to better answer this question because few of the AML cells make it into circulation, and they are not an accurate measure of tumor burden.

 

At least this shows that Niner's theoretical worries about regular C60 dosing protecting existing cancers from the oxidation penalty of their high metabolism were unfounded, and apparently then some.

In one cancer line that shares few properties with metastatic solid tumors, maybe? :)
 

Also, question. What was the idea behind injecting the doses, rather than delivering them orally? Considering that we take them orally, and the Baati rats did, too? It seems like effects from oral would be both more educative and more strongly expected. And I worry that injecting volumes of undigested lipids would have detrimental effects of its own, which might exlain why the saline control did unexpectedly well compared to everything else, unless intraperitonal lipid injections are something standard, in which case nevermind.

We wanted total control over dosing and IP is easier than gavage. Since absorption is similar we figured it didn't matter and we could go either way. To account for the potential liver toxicity associated with olive oil injections we did track liver enzyme levels (AST and ALT). We did not see a spike nor any other sign of liver toxicity. This is consistent with what was reported by Baati.

 

Oh also, what were the presumed dosage equivalencies?

I do not understand the question... we administered 2mg/kg, 4mg/kg, and 8mg/kg c60oo. Control mice were administered the highest volume of either saline or olive oil that the experimental mice received. The dosing used by Baati et al was 4mg/kg c60oo.

 

 
Concept of study to prove if C60 can PREVENT cancer better than salt water.
And
Here is a study that you could use to help design a better mouse study and see if dosing with C60 for a period of time
and then inoculating the mice with the same cancer cell line: 
 
 
Results
Dox (total dose 2.5 mg/kg) combined with C60 fullerene (total dose 25 mg/kg) in tumor-bearing animals resulted in tumor growth inhibition, prolongation of life, metastasis inhibition, and increased number of apoptotic tumor cells and was more effective than the corresponding course of Dox treatment alone. C60fullerene demonstrated a protective effect against superoxide dismutase and glutathione peroxidase inhibition induced by Dox-dependent oxidative insult in the liver and heart.

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#36 Raza

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Posted 30 May 2015 - 01:22 PM

 

So if I get this right, you injected immunocompromised mice with what were already cancerous human cells? I'm kind of surprised to see a result at all that way; wasn't the idea of C60 that it'd reduce mortality from cancer by reducing oncogenic mutations? (I'm a bit out of date on my C60 theory, mind). What was the hypothesis for an effect on the growth of or mortality from preexisting cancers?

Correct, we injected with already cancerous human cells... and I promise I was more surprised than you were. :) Reducing mutations is one proposed mechanism, and this is not mutually exclusive with the data we're seeing. We wanted to track growth and mortality from AML in this study. Growth tracking by flow was not good... we need to use bone marrow aspirates next time to better answer this question because few of the AML cells make it into circulation, and they are not an accurate measure of tumor burden.

 

At least this shows that Niner's theoretical worries about regular C60 dosing protecting existing cancers from the oxidation penalty of their high metabolism were unfounded, and apparently then some.

In one cancer line that shares few properties with metastatic solid tumors, maybe? :)
 

Also, question. What was the idea behind injecting the doses, rather than delivering them orally? Considering that we take them orally, and the Baati rats did, too? It seems like effects from oral would be both more educative and more strongly expected. And I worry that injecting volumes of undigested lipids would have detrimental effects of its own, which might exlain why the saline control did unexpectedly well compared to everything else, unless intraperitonal lipid injections are something standard, in which case nevermind.

We wanted total control over dosing and IP is easier than gavage. Since absorption is similar we figured it didn't matter and we could go either way. To account for the potential liver toxicity associated with olive oil injections we did track liver enzyme levels (AST and ALT). We did not see a spike nor any other sign of liver toxicity. This is consistent with what was reported by Baati.

 

Oh also, what were the presumed dosage equivalencies?

I do not understand the question... we administered 2mg/kg, 4mg/kg, and 8mg/kg c60oo. Control mice were administered the highest volume of either saline or olive oil that the experimental mice received. The dosing used by Baati et al was 4mg/kg c60oo.

 

Thank you for your answers, kmoody. Good points, too. You've answered my last question by mentioning how the two ROAs compare for bioavailability. I'm still curious about what the hypothesis was, though. If you were surprised to find this, how did you come to be looking for it?

 

 

Results
Dox (total dose 2.5 mg/kg) combined with C60 fullerene (total dose 25 mg/kg) in tumor-bearing animals resulted in tumor growth inhibition, prolongation of life, metastasis inhibition, and increased number of apoptotic tumor cells and was more effective than the corresponding course of Dox treatment alone. C60fullerene demonstrated a protective effect against superoxide dismutase and glutathione peroxidase inhibition induced by Dox-dependent oxidative insult in the liver and heart.

Interesting. If you look at the full text, you see that the C60-only control also did significantly better than the no treatment control. The effect seems additive with, but not dependent on this Dox stuff.

But that's C60 without olive oil.
 


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#37 sensei

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Posted 21 June 2015 - 07:42 PM

   It's true that SCID mice can't fight a cancer quite as well as a normal mouse, but we're looking for the effect of the treatment.  The controls and the treatment group all had the same immunologic background.

 

 

 

 

As long as we add a caveat that states the results show the effect of C60 directly on the cancer cells.  

 

 

And that the results are not representative of the anti-cancer effect of C60 when one takes into account potential anti-tumor and anti-cancer mechanisms that are caused by:

 

direct action of the immune system on infected cells -- mediated by C60

indirect action due to downstream effects caused by the innate or active immune system -- mediated by C60


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#38 Kalliste

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Posted 06 July 2015 - 10:33 AM

What would the cost be of a repeat of the original study but with twice or thrice the n of animals used? (I'm sure there would be donations both here and from others as Mind noted)

 

Would it be possible to acquire already aged animals from a trusted source and then randomize them into groups and treat them with saline and C60 X number of times and look at biomarker differences (should be cheap?) Ideally with some different groups of dosages (2, 4, 12, 24 mg's)

 

 

 



#39 Mind

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Posted 06 July 2015 - 06:16 PM

There will likely be a more statistically relevant study coming soon. Can't say more than that right because I am unsure on the timing, n, what-not.



#40 Mind

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Posted 07 July 2015 - 11:04 PM

Here is a press release for C60oo aficionados: http://www.prweb.com...web12835073.htm


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#41 Kalliste

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Posted 08 July 2015 - 04:39 AM

Here is a press release for C60oo aficionados: http://www.prweb.com...web12835073.htm

 

That is great news! Godspeed Kmoody.



#42 bixbyte

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Posted 25 December 2015 - 03:35 PM

 

 

 

For each dosing, the olive oil control group received a volume equal to the largest dose by volume received by any of the c60oo mice. So the actual amount varied, but the general range was approximately 30-45uL depending on the day.

 

 

Doesn't that add a confounding variable, considering that phenol components of EVOO have known anti-cancer properties?

If the olive oil control performed well then yes, it could. However, these results are not consistent with a contribution from olive oil.

 

 

Who choose this mouse model (immuno compromised leukemia) and why?

I chose this model because, 1) low learning curve for my team (i.e. we could do this study for the community inexpensively), and 2) I prefer to use human cells whenever possible.

 

These results are so baffling:

 

Saline controls fared much better than 4mg C60oo group, close to EVOO group. EVOO group is almost on par with 1mg C60 group.

 

If the 8mg group did best (signifying C60oo had protective effect) and the 1mg one finished second how the 4mg one fared the worst of all (if there is a supposed dose-response relationship)??

This doesn't correspond to the clearly delineated mortality curves in Baati between saline , EVOO and C60oo groups as posted above.

 

 

It looks like megadosing C60oo was a good idea and anything else is statistical noise (due to the small sample size) not to be relied upon for any conclusions.

A few things to keep in mind, 1) Baati provided lifespan data in rats whereas we did an aggressive cancer model in immunocompromised mice, so these are not comparable studies in any way, 2) the sample size is VERY low (n=5 per group), so modest effects are not going to be seen in this study, 3) we were looking to see if there was a dose dependent relationship (we never use words like "supposed to be" in science) and based on median survival (which is probably the best place to compare the groups in such a small study) we DO see a dose-dependent effect, and 4) for the sake of redundancy I will reiterate that the sample size is VERY low.

 

This data may tentatively suggest there could be value in taking slightly elevated doses of c60oo if you have AML. These results cannot be ubiquitously applied to all cancers, and the chronic effects of high level c60oo supplementation have not been studied in any model that I am aware of. You may speculate all you want, but be careful what definitive statements are drawn from this study.

 

The EVOO control group looks so much worse that I wonder if the control oil wasn't filtered and thus contained pathogens that killed some of these immunocompromised mice. In fact, even filtered oil might become recontaminated unless care is taken.

Control oil was filtered (prepared identically to c60oo except that c60oo was not present). Syringes for injection were drawn up in a certified laminar flow hood (aka aseptic environment). So I am doubtful that this is the case, though we did not explicitly test for it.

 

 

 

I am starting to believe it, that if test subjects have cancer C60 has little or no benefit.

C60 in Olive Oil has been shown to possess prophylactic properties.

Whatever is the efficacy, it appears to be working in the spleen.

 

 

SO, I am ill informed and everyone disagrees with Me?

The second experiment proves I might be correct.

You should dose the test animal with C60 Olive Oil First.

And the inoculate them with the Cancer cell line.   



#43 kmoody

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Posted 25 December 2015 - 09:07 PM

SO, I am ill informed and everyone disagrees with Me?

The second experiment proves I might be correct.

You should dose the test animal with C60 Olive Oil First.

And the inoculate them with the Cancer cell line.   

What would this show? This xenograft model does not replicate de novo cancer formation. At best, prophylactic treatment would show efficacy for reducing tumor engraftment. This is analogous to showing that C60oo inhibits engraftment during a bone marrow transplant. Effects on engraftment from a donor and effects on de novo cancer formation are two very different things. I'm not quite following your logic on this.



#44 bixbyte

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Posted 26 December 2015 - 01:57 AM

 

SO, I am ill informed and everyone disagrees with Me?

The second experiment proves I might be correct.

You should dose the test animal with C60 Olive Oil First.

And the inoculate them with the Cancer cell line.   

What would this show? This xenograft model does not replicate de novo cancer formation. At best, prophylactic treatment would show efficacy for reducing tumor engraftment. This is analogous to showing that C60oo inhibits engraftment during a bone marrow transplant. Effects on engraftment from a donor and effects on de novo cancer formation are two very different things. I'm not quite following your logic on this.

 

 

 

Are you looking at C60 olive oil that can be marketed similar to Chemo?

How did you figure out this experiment?

That interestingly shows good results for the mice with a high dose of C60.

I am not trying to make a buck in the marketing of C60

and I believe that is  why you have difficulty in understanding why I think c60 might be best prophylactic

and you are doing grafting them with a human cell leukemia line.   ;)



#45 youngandold

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Posted 20 January 2016 - 01:43 AM

IMO oil injections, even worse INTRAPERITONEAL oil injections makes them sick.

Subcutaneous and intraperitoneal lipogranulomas following
subcutaneous injection of olive oil in Sprague-Dawley rats.
Macroscopically, multifocal white spots were found over the liver
and mesentery.
www.ncbi.nlm.nih.gov/m/pubmed/19770348/

as compared to 'Oral' oo
Incidence of pancreatic tumors and tumor precursors in
Sprague-Dawley rats after administration of olive oil
www.ncbi.nlm.nih.gov/m/pubmed/3291718/?i=6&from=/19770348/related
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#46 youngandold

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Posted 20 January 2016 - 01:59 AM

Keep in mind that C60 requires massive amounts of oil.
Massive amounts even for oral administration, let alone injections.

And yes injections increase the infection risk even if 'sterilized'.
Or some oo substances that are normally degraded by digestion are now passing freely to the bloodstream.

Bottom line
Repeat the study with oral (or gavage = force feeding) administration.
Who cares if intraperitoneal injections are easier than gavages?
Those LAZY lab workers should be sent to face Donald Trump
so they can hear YOU ARE FIRED! really loud
and possibly also banned from entering America LOL
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