207 replies to this topic

[niner]

 C60 may be binding into mitochondrial membranes with very long half-lives, and when you take C60 you may end up absorbing higher and higher densities into membranes for more than a year after you start taking it.

 

I do think that c60oo localizes to mitochondrial membranes and stays there for a long time, but once you stop taking it, I don't think that the concentration in the mitochondrial membrane will increase.  It just won't decrease very quickly.

[HighDesertWizard]

 

niner... Is there Evidence that C60 brown spots in splenic macrophages are a bad thing or is it just your Feeling that it's a bad thing?

 
Is there evidence that C60 brown spots in splenic macrophages are a good thing?

 

 

Yes.

• The evidence we have from the Baati study is that there is an association between the condition of brown spots in Splenic Macrophages because of C60 accumulation and longer lives.

• And there is an Explanation for the brown spots in Splenic Macrophages having a Longevity effect. I'll begin to sketch it below.

Table 2 in that study clearly shows C60 accumulation in the Spleen. In fact, the authors says themselves that C60 concentrations reached the limit of solubility in spleens.” And yet, the Baati study is confused about C60 accumulation in because it also says that the weakness of organ concentrations notably at D8 after 7 daily successive administrations of C60 dissolved in olive oil clearly shows that C60 molecules are eliminated from the organs in a few hours after both oral and i.p. administrations." I’ve posted about that confusion here.

 

The Spleen is not just a filter for the blood. It’s also plays a key role in the Vagus-HRV-CAIP nexus. As shown in the graphic figure below, Splenic Macrophages play a key role in inhibiting NF-kB Cytokine Transcription and that inhibition impacts Cytokine levels throughout the blood circulatory system.

 

 

 

More than that, in both Human and Animal studies, the Spleen has been shown to have Longevity effects as shown in the graphic figures below. You can find an 8 slide presentation that contains the three pics below and a sketch of the Explanation underlying them here.

 

 

 

 

I now believe that C60 accumulation in the Spleen was a Key Driver of the Baati study Longevity effect. And I’ve provided Evidence, an Argument, and an Explanation about a Positive Role for C60 brown spots in Splenic Macrophages and for saturation in the Spleen. And, by the way, the Explanation I'm just beginning to sketch Hard to Vary and is Falsifiable.

 

Evidence, Arguments, and Explanations, my friends, not just Arguments.

 

I asked if there is any evidence that the c60 brown spots in the Spleen played a negative role vis-a-vis the health of those C60 rats.

 

And now, with all due respect, can anyone provide Any Relevant Evidence that answers my question?

Edited by HighDesertWizard, 23 April 2015 - 01:56 PM.

[sagafemina]

So this (these) are what I mean by guessing.  I don't detect a pathologist in this group. 

 

 

Does anyone know what the violet colour means? It seems to be much more prevalent on the last figure.

 

 

 

 

niner... Is there Evidence that C60 brown spots in splenic macrophages are a bad thing or is it just your Feeling that it's a bad thing?

 

 

Is there evidence that C60 brown spots in splenic macrophages are a good thing?

 

And I am not one.  But no, the violacious colors in the slides are not the violet color some are seeing in formulations of c60.  It is a stain routinely used to detect different cell types.  It becomes more obvious when there are more of a particular type of cells present in the tissue after a certain intervention (such as c60 administration or a chemical or cellular reaction to same), or the stain color can change when there is a change in the chemistry of the cell, for example, something new is being eluted in response to a stimulus or there is sequestration of a substance. 

 

And who could know whether the brown spots (probably sequestration) are a good thing?  All that is known is that in the Bhati experiment, treated rats lived longer. 

 

I think the most curious thing about all of this is that there has only been the one study.  Yes, studies cost money and take time.  But someone paid for the first one.  Someone thought it worth while to know whether c60 was toxic or protective from liver injury (the French dry cleaning industry?) (CCl4) 

 

Obviously money is being made now on this product by some entrepreneurs.  Why isn't someone (or is anyone?) trying to duplicate (or refute) the results?  (Luna maybe?)

 

Except of course, people who are using themselves as guinea pigs. 

 

Who MIGHT, I hasten to add, have the last laugh!  (Or whose sacrifice may teach us something...)

 

 

[pone11]

 

 

I think the reason this thread was started was because Caliban gave up on moderating the purely scientific discussion since it was very hard to define or keep supposedly "pure science" separated from the experiences/questions of curious users/potential users.  So no need to apologize, IMO. 

tions.

 

Right, and already this thread is degenerating into personal protocols and experiences, nothing to do with science behind C60 at all.

 

There are other threads on Longecity that talk about personal experiences with C60 and protocols for how to take it.   A science thread should be about mechanisms of action, publishing other studies, and discussion of the original research.

 

Yeah, I didn't think it would be this bad.  Maybe we do need a strictly moderated thread, but there's always a subjective point over when a post is "sciency enough".  It's really rude to delete posts, but moving them into a different thread is a hassle with our software.

 

 

Perhaps the moderator could edit the wrongly focused posts with a warning at the top of the post.   That then teaches others about topic constraints by example, while preserving original content as a courtesy.

 

 C60 may be binding into mitochondrial membranes with very long half-lives, and when you take C60 you may end up absorbing higher and higher densities into membranes for more than a year after you start taking it.

 

I do think that c60oo localizes to mitochondrial membranes and stays there for a long time, but once you stop taking it, I don't think that the concentration in the mitochondrial membrane will increase.  It just won't decrease very quickly.

 

 

This is what I was trying to say.

[sagafemina]

 

Optical microscopy of spleen sections: (a) oral and (b) i.p. treatment with olive oil only; (c.) oral and (d) i.p. treatment with C60-olive oil. The arrows indicate C60 crystals-containing macrophages (brown). (Credit: T. Baati et al./Biomaterials)

Look at the Spleen Cells of the Test Animals treated with C6O and tell me if I am on the right track?

The Fullerenes changed the way the Spleen filters? 

 

No, bixbyte, I would say that in a and b slides the spleen had nothing (of substance) to filter.  There are probably macrophages in a and b, but they are empty of anything that has much color or that changes the staining.  Again, not a pathologist.   Going back to the study, it seems they should have offered an interpretation? 

[sagafemina]

 

 

niner... Is there Evidence that C60 brown spots in splenic macrophages are a bad thing or is it just your Feeling that it's a bad thing?

 
Is there evidence that C60 brown spots in splenic macrophages are a good thing?

 

 

Yes.

• The evidence we have from the Baati study is that there is an association between the condition of brown spots in Splenic Macrophages because of C60 accumulation and longer lives.

• And there is an Explanation for the brown spots in Splenic Macrophages having a Longevity effect. I'll begin to sketch it below.

Table 2 in that study clearly shows C60 accumulation in the Spleen. In fact, the authors says themselves that C60 concentrations reached the limit of solubility in spleens.” And yet, the Baati study is confused about C60 accumulation in because it also says that the weakness of organ concentrations notably at D8 after 7 daily successive administrations of C60 dissolved in olive oil clearly shows that C60 molecules are eliminated from the organs in a few hours after both oral and i.p. administrations." I’ve posted about that confusion here.

 

The Spleen is not just a filter for the blood. It’s also plays a key role in the Vagus-HRV-CAIP nexus. As shown in the graphic figure below, Splenic Macrophages play a key role in inhibiting NF-kB Cytokine Transcription and that inhibition impacts Cytokine levels throughout the blood circulatory system.

 

 

 

More than that, in both Human and Animal studies, the Spleen has been shown to have Longevity effects as shown in the graphic figures below. You can find an 8 slide presentation that contains the three pics below and a sketch of the Explanation underlying them here.

 

 

 

 

I now believe that C60 accumulation in the Spleen was a Key Driver of the Baati study Longevity effect. And I’ve provided Evidence, an Argument, and an Explanation about a Positive Role for C60 brown spots in Splenic Macrophages and for saturation in the Spleen. And, by the way, the Explanation I'm just beginning to sketch Hard to Vary and is Falsifiable.

 

Evidence, Arguments, and Explanations, my friends, not just Arguments.

 

I asked if there is any evidence that the c60 brown spots in the Spleen played a negative role vis-a-vis the health of those C60 rats.

 

And now, with all due respect, can anyone provide Any Relevant Evidence that answers my question?

 

Well, you are just beginning to sketch something but it seems hardly conclusive to me.  There seems to be a disconnect between assuming that seeing full macrophages in a spleen has demonstrated anything to do with longevity.  Or even inhibition of antiinflammatory pathways, alterations of vagal tone or increased heart rate variability, of all of which I am in favor! 

 

Some of your figures are interesting, but they are hard to read, for example the label on the red bar graphs at the right of the page with the mice. 

 

And frankly, if you restrict your requests to someone who can refute or even offer to answer in what you believe to be the only valid and unassailable form, you are not too likely to get any takers.  That does not make your assertions correct.  Or your questions any less valid.   Just less likely to get what you seem to want. 

[pone11]

Table 2 in that study clearly shows C60 accumulation in the Spleen. In fact, the authors says themselves that C60 concentrations reached the limit of solubility in spleens.” And yet, the Baati study is confused about C60 accumulation in because it also says that the weakness of organ concentrations notably at D8 after 7 daily successive administrations of C60 dissolved in olive oil clearly shows that C60 molecules are eliminated from the organs in a few hours after both oral and i.p. administrations." I’ve posted about that confusion here.

 

The Spleen is not just a filter for the blood. It’s also plays a key role in the Vagus-HRV-CAIP nexus. As shown in the graphic figure below, Splenic Macrophages play a key role in inhibiting NF-kB Cytokine Transcription and that inhibition impacts Cytokine levels throughout the blood circulatory system.

Evidence, Arguments, and Explanations, my friends, not just Arguments.

 

 

Macrophages increase cytokines and increase inflammatory response.     How are those pro-longevity effects?  

http://en.wikipedia....wiki/Macrophage

 

If you look at work Shoemaker has done on biotoxins (primarily mold) on genetically susceptible individuals, the entire mechanism of action is based on cytokines creating inflammatory responses, overall hypoxia in peripheral capillaries, and chronic fatigue from that hypoxia.   There are studies with C60 showing all kinds of elevated immune responses consistent with increased macrophage, IL-6, etc:

http://www.docdroid....cology.pdf.html

 

It's an extremely twisted conversation to try to hypothesize that increased levels of macrophages in the spleen would somehow lower immune responses - including cytokines - throughout the body.   It would be contradicted by many other studies showing macrophages increasing immune and inflammatory responses.

[ambivalent]

 The oral dose is a lot safer.  Because crystallization is a threshold effect, i.e., it doesn't happen until you hit a sufficiently high concentration, there shouldn't be any problem with lower doses taken for a longer time.  That's assuming, of course, that what we're seeing really is crystallization.  

 

This is probably a rather basic question: given there were a presence of c60 crystals would subsequent low-dosing of c60 be likely to cause the crystals to accrete?    

Edited by ambivalent, 23 April 2015 - 10:15 PM.

[niner]

The evidence we have from the Baati study is that there is an association between the condition of brown spots in Splenic Macrophages because of C60 accumulation and longer lives.

 

Actually, we don't have that.  The splenic macrophages were from the short term tox part of the paper where the animals were given higher doses, then sacrificed.  The long-lived animals were from the long-term tox arm of the study.  They didn't do a necropsy on any of the longer term animals, so we don't know what their spleens looked like.  We do know that there is a dose-response with the brown spots, in that the i.p. dosed animals had a lot more spots than the orally dosed animals.

[sensei]

I take the full dose about every 6 months or so. It is disgusting, but adding about a cup of oil to a tuna salad, somewhat helps. I wouldn't use DR caps as I agree with niner regarding the digestion and also because the caps don't do well with oils. The nitrogen protected Licaps we use for some capsules could be great to use, but you need a specialized machine that runs about $40,000 to $60,000. All in all, its not practical, specially for folks that take the full dose.

 

What conditions might benefit from C60oo?

From my personal experience ...

<Deleted>

 

​Sorry niner, I just read Calibans thread and took out my anecdotal observations.

 

Anthony -

 

Exactly how many mg constitutes your "full dose"?

[sensei]

Is there any known issue with interacting with pharmaceuticals?  For instance and particularly, would c60 blunt the effects or increase the rate at which the body excretes a pharmaceutical?  Say, such as an Angiotensin II receptor antagonist? 

 

Based on the number of consistent reports -- it is fair to say that C60 at a sufficient dose significantly blocks the effect of ethanol intoxication -- almost completely depending on dose -- and no hangover.

 

I can personally attest that a 45mg dose of C60 caused a significant drop in the efficacy of diazepam (valium) needing 14 mg to get the same effect as the normal 4 mg dose.

[aribadabar]

 They didn't do a necropsy on any of the longer term animals

 

How has it been determined, without necropsy, that they don't have any tumors at the time they died?

[Kalliste]

So this (these) are what I mean by guessing.  I don't detect a pathologist in this group. 

 

 

Does anyone know what the violet colour means? It seems to be much more prevalent on the last figure.

 

 

 

 

niner... Is there Evidence that C60 brown spots in splenic macrophages are a bad thing or is it just your Feeling that it's a bad thing?

 

 

Is there evidence that C60 brown spots in splenic macrophages are a good thing?

 

And I am not one.  But no, the violacious colors in the slides are not the violet color some are seeing in formulations of c60.  It is a stain routinely used to detect different cell types.  It becomes more obvious when there are more of a particular type of cells present in the tissue after a certain intervention (such as c60 administration or a chemical or cellular reaction to same), or the stain color can change when there is a change in the chemistry of the cell, for example, something new is being eluted in response to a stimulus or there is sequestration of a substance. 

 

And who could know whether the brown spots (probably sequestration) are a good thing?  All that is known is that in the Bhati experiment, treated rats lived longer. 

 

I think the most curious thing about all of this is that there has only been the one study.  Yes, studies cost money and take time.  But someone paid for the first one.  Someone thought it worth while to know whether c60 was toxic or protective from liver injury (the French dry cleaning industry?) (CCl4) 

 

Obviously money is being made now on this product by some entrepreneurs.  Why isn't someone (or is anyone?) trying to duplicate (or refute) the results?  (Luna maybe?)

 

Except of course, people who are using themselves as guinea pigs. 

 

Who MIGHT, I hasten to add, have the last laugh!  (Or whose sacrifice may teach us something...)

 

Fullerenes is an item that generated a Nobel prize for it's discovery. In the decades following it's discovery a very large number of papers have been written on the topic of exploring it's health effects. Many of these papers, by many different teams, have found the molecule to be interesting and worth investigation. It sounds like you have not really read much about fullerene science at all.

0. Very promising ADME, unlike most substances we discuss on this site.

1. Antioxidant. (Antioxidants are routinely screened against CCl4, do a pubmed search)

2. Possible use for drug administration (make money by pateting your new drug)

3. Some antiviral functions, for instance it binds to HIV in some forms.

4. Lubricant that could be used in applications that would contaminate the environment with their added C60, and lubricant in the sense that it could be used for direct injections into human tissue.

5. Photoactive, could be used for imaging and cancer therapy.
6. My favorite: C60 might have served as a catalyst for the start of life on Earth

 

Antioxidant:

 

We investigated the protective effects of three fullerene nanomaterials
as the inhibitors of reactive oxygen species (antioxidants
and free radical scavengers). The ESR spin trap technique provided
direct in vitro evidence that the three fullerene derivatives, gadolinium
endohedral metallofullerenol (Gd@C82(OH)22), fullerenol
(C60(OH)22), and carboxyfullerene (C60(C(COOH)2)2), can efficiently
scavenge different types of free radicals and inhibit lipid peroxidation.
Both of the reactive oxygen species and the nitrogencentered
free radical were intercepted by these fullerene materials.
We demonstrated in vitro by using human lung adenocarcinoma
cell line A549 or rat brain capillary endothelial cell line (rBCECs)
that they could reduce H2O2-induced cytotoxicity, free radical
formation and mitochondrial damage. These nanomaterials have
great potential in biomedical applications, for examples,
gadolinium endohedral metallofullerenols can be used for both of
MRI imaging and chemotherapy. The present findings provide
a molecular basis of the diseases for which oxidative stress may
play a key role.

The scavenging of reactive oxygen species and the potential for cell protection
by functionalized fullerene materials (2008)

 

Promising, but nobody know the full story yet:

 

Despite that, no categorical statement can
be made about the safety of these carbon-based agents; differences in
the purity of the samples, in the incorporation of bioactive molecules
through several chemical procedures and in the doses used during the
experiments do not allowany definite conclusion about the documented
higher efficacy or their toxicological profile.Many questions regarding
the safety of nanoparticles are still unanswered, the main concern
being their ability to trigger intense chemical reactions and anomalies
as nanospecies, while escaping from the normal phagocytic defenses
and depositing into organs and tissues. At the moment, available information
concerning the health risks to the environment and humans is
poor. The encouraging results that have been achieved so far suggest
that they are worth further investigation, although it is imperative to
fully address the biocompatibility of these formulations before concluding
that nano-carriers are safe delivery systems.

Gruber J, et al, Mitochondria-targeted antioxidants and metabolic modulators as pharmacological interventions to
slow ageing, Biotechnol Adv (2012), http://dx.doi.org/10...adv.2012.09.005

Edited by Cosmicalstorm, 24 April 2015 - 03:56 AM.

[Kalliste]

Here is a study on the substance IAC, which is not C60OO.  But I found it interesting and related. These rodents faired pretty well through different ordeals with IAC in their body at 30mg/kg. The full text is paywalled but I printed it from work. It's very interesting to read this study in parallel with reading the Baathi study. There is something peculiar about low molecular antioxidants. Unless something really nasty turns up soon I wonder if this new class of antioxidants will make a real commercial breakthrough. That could be the first time the supplement industry really sell something that lives up to their claims

 

 

Pancreas. 2007 Nov;35(4):e10-7.

Reduction of oxidative stress by a new low-molecular-weight antioxidant improves metabolic alterations in a nonobese mouse diabetes model.

Novelli M¹, D'Aleo V, Lupi R, Paolini M, Soleti A, Marchetti P, Masiello P.

Author information

Abstract

OBJECTIVES:

We have previously established a nonobese diabetes mouse model characterized by moderate hyperglycemic levels, like those usually occurring in human type 2 diabetes. As oxidative stress is considered a major mechanism of progressive beta-cell damage in diabetes, we tested in this model the protective effects of a new low-molecular-weight antioxidant, namely, bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)decandioate dihydrochloride (IAC).

METHODS:

Diabetes was induced in C57Bl/6J mice by streptozotocin (STZ) and nicotinamide (NA) administration. Two weeks later, STZ-NA mice were treated for 5 weeks with different doses of IAC (15 or 30 mg/kg per day intraperitoneally) and monitored for glycemia, insulinemia, glucose tolerance, and pancreatic insulin content.

RESULTS:

Streptozotocin-NA mice showed moderate hyperglycemia, hypoinsulinemia, glucose intolerance, growth impairment, and markedly reduced pancreatic insulin content (22% of controls). IAC-treated STZ-NA mice showed clear-cut reduction of hyperglycemia and attenuation of glucose intolerance, associated to higher residual pancreatic insulin content with respect to untreated diabetic animals. Plasma nitrotyrosine levels (an index of oxidative stress), enhanced 3-fold in diabetic mice, were significantly reduced by IAC treatment. Significant correlations were found between plasma nitrotyrosine values and either blood glucose levels or pancreatic insulin content.

CONCLUSIONS:

In the STZ-NA diabetic mouse model, the new antioxidant, IAC, improves diabetic metabolic alterations, likely by counteracting beta-cell dysfunction and loss associated with oxidative stress.

 

 

 

World J Gastroenterol. 2010 Aug 7;16(29):3642-50.

Non-peptidyl low molecular weight radical scavenger IAC attenuates DSS-induced colitis in rats.

Vasina V¹, Broccoli M, Ursino MG, Canistro D, Valgimigli L, Soleti A, Paolini M, De Ponti F.

Author information

Abstract

AIM:

To investigate the effects of the free radical scavenger bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)decandioate (IAC) in the dextran sodium sulphate (DSS) experimental model of ulcerative colitis.

METHODS:

Colitis was induced in Sprague Dawley male rats by administration of 5% DSS in drinking water. IAC (30 mg/kg, lipophilic or hydrophilic form) was administered daily (orally or ip) for 6 d until sacrifice. Colonic damage was assessed by means of indirect (Disease Activity Index score) and direct measures (macroscopic and microscopic scores) and myeloperoxidase (MPO) activity. Neutrophil infiltration within the tissue and glutathione S-transferase activity were also investigated.

RESULTS:

DSS-induced colitis impaired body weight gain and markedly increased all inflammatory parameters. Six-day treatment with lipophilic IAC significantly reduced intestinal damage caused by inflammation, induced a down-regulation in MPO activity (0.72 +/- 0.12 and 0.45 +/- 0.12 with lipophilic IAC po and ip, respectively, vs 1.10 +/- 0.27 in untreated DSS colitis animals) and minimized DSS-induced neutrophil infiltration, while hydrophilic IAC administered orally did not ameliorate DSS-induced damage.

CONCLUSION:

These results support the hypothesis that reactive oxygen metabolites contribute to inflammation and that the radical scavenger IAC has therapeutic potential in inflammatory bowel disease.

 

[sagafemina]

So, actually, cosmicalstorm ,I'm not sure how you can take from my comment,

 

 

 

I think the most curious thing about all of this is that there has only been the one study.  Yes, studies cost money and take time.  But someone paid for the first one.  Someone thought it worth while to know whether c60 was toxic or protective from liver injury (the French dry cleaning industry?) (CCl4) 

 

that

 

 

 

It sounds like you have not really read much about fullerene science at all.

 

*********************************************************************************************

 

Because actually, I have read almost every scientific article posted on this forum, as well as others I have found; and am not at all unimpressed with the potential for c60. 

 

I only explored with the group my curiosity as to why the ONE study which got the topic included in this forum devoted to longevity science has not yet been replicated. 

Perhaps I wasn't specific enough. 

 

We are all hopeful or we wouldn't be here.  Some are more knowledgeable than others, there seems to be a degree of expertise in varying areas; and certainly some are  motivated by circumstance or intellectual curiosity to delve more deeply than others.  Some have access to more resources and have generously shared that access. Some seem at times to be making rather loose connections, but the "Emperor's New Clothes" phenomenon can be quite stimulating to discovery! 

 

This synergy helps us all to learn and grow from participation here.   Especially when respect and civility are maintained. 

 

Not to mention tolerance when we inevitably go off topic from time to time!  As in this aside. 

 

 

 

 

[Anthony_Loera]

 

I take the full dose about every 6 months or so. It is disgusting, but adding about a cup of oil to a tuna salad, somewhat helps. I wouldn't use DR caps as I agree with niner regarding the digestion and also because the caps don't do well with oils. The nitrogen protected Licaps we use for some capsules could be great to use, but you need a specialized machine that runs about $40,000 to $60,000. All in all, its not practical, specially for folks that take the full dose.

 

What conditions might benefit from C60oo?

From my personal experience ...

<Deleted>

 

​Sorry niner, I just read Calibans thread and took out my anecdotal observations.

 

Anthony -

 

Exactly how many mg constitutes your "full dose"?

 

 

 

Hi Sensei,

 

I have been busy working too much lately so sorry about not answering earlier...

but here is my dose since 2012... (and I only take it 7 days straight every 6 months or so)

 

150mg of C60 in olive oil per day, every day for 7 days...

which uses 187.5 ml of oil a day... which turns out to be about 0.8 of a cup of oil.

From post: http://www.longecity...ndpost&p=511916

 

and the "tuna salad" does kind of look like this when I add the C60 Olive Oil....

 post-4527-133571970795.jpg   106.95KB   10 downloads

 

from post:

http://www.longecity...ndpost&p=513247

 

And niner... I understand your warning... it reminds me of something a wise Monty Python used to say...

 

I'm Not Dead Yet!

 

(Actually, if I find issues with my doc, I will obviously stop.. but none so far)

 

For everyone else...

here's my simple disclaimer on C60 Olive Oil:

Don't do what I do!

 

A

Edited by Anthony_Loera, 24 April 2015 - 09:22 PM.

[niner]

 

 They didn't do a necropsy on any of the longer term animals

 

How has it been determined, without necropsy, that they don't have any tumors at the time they died?

 

It was done by visual inspection.  The control rats had visible tumors, but the treatment rats had none.  A necropsy would have been nice, but that's the data.

[sensei]

Hi Sensei,

 

 

I have been busy working too much lately so sorry about not answering earlier...

but here is my dose since 2012... (and I only take it 7 days straight every 6 months or so)

 

150mg of C60 in olive oil per day, every day for 7 days...

which uses 187.5 ml of oil a day... which turns out to be about 0.8 of a cup of oil.

 

 

I've taken as much as 135 mg in one day (150 ml oil)

 

And I have also done 45 mg every other day until 24 doses are done. give or take a day here or there.

 

My yearly consumption is more than 2 grams -- like yours, although mine is spread out a bit more -- but done with large down times (a month to a few months) between

 

So, you could say our intake is comparable.

[pone11]

Table 1 in this study shows how much C60 is absorbed into different types of rodent tissues over time:

http://www.docdroid....cology.pdf.html

 

They inject a single dose of radiologically tagged C60 into rats and then measure at different intervals.   What is really strange here is that Table 1 shows gradually increasing saturation in muscle over time up to 14 days.   At the 30 day point the saturation begins to come down.    This alone seems strange because the blood levels are near zero at day 7.   How can the tissue saturation continue to grow so dramatically between days 7 and 14?   Does someone have a hypothesis about why that happens?

 

The final column in Table 1 shows an alternative experiment where they dose the rats five consecutive days and then wait 14 days.   The measurement they have in muscle for this alternative experiment is much lower than the 14 day measurement in muscle for a single dose of C60.   How is that possible?    Does someone have a theory to explain that?   I did not read most of the study and there may be an explanation there.

 

It's worth noting that the measurement in muscle is less at 30 days than 14 days, but at 30 days is still higher than seven days.    It really looks like the saturation from one dose takes a long time to work its way through mitochondrial membranes, and it is a shame in this study that they did not do measurements at two months, three months, etc, to establish how rapidly the C60 comes out of tissues.

 

 

Edited by pone11, 26 April 2015 - 07:14 PM.

[HighDesertWizard]

 

The evidence we have from the Baati study is that there is an association between the condition of brown spots in Splenic Macrophages because of C60 accumulation and longer lives.

 

Actually, we don't have that.  The splenic macrophages were from the short term tox part of the paper where the animals were given higher doses, then sacrificed.  The long-lived animals were from the long-term tox arm of the study.  They didn't do a necropsy on any of the longer term animals, so we don't know what their spleens looked like.  We do know that there is a dose-response with the brown spots, in that the i.p. dosed animals had a lot more spots than the orally dosed animals.

 

 

A great point niner... Thanks... But, strictly speaking, accumulation in the Spleen did take place in the rats that were sacrificed after 8 days... And it would be Unreasonable to assume that it Did Not take place in the Long Lived C60-OO consuming rats.

[tunt01]

What is the theory on how C60 is protective, yet simultaneously increasing 8OHdG?  Or is the hypothesis that C60oo is not the same as c60 and therefore there shouldn't be a rise in 8OHdG?

 

Also, what is the rationale that this collects in the lungs at such a large rate as compared to muscles?

 

[Mind]

Not exactly replicating Baati, of course, but Ichor's LongeCity-Sponsored C60oo study shows a somewhat "familiar" result: http://www.longecity...ored-aml-study/

 

N=5. Would be nice to see a bit larger study, eventually.

[niner]

What is the theory on how C60 is protective, yet simultaneously increasing 8OHdG?  Or is the hypothesis that C60oo is not the same as c60 and therefore there shouldn't be a rise in 8OHdG?

 

Also, what is the rationale that this collects in the lungs at such a large rate as compared to muscles?

 

This is an aggregated form of C60, and they often result in oxidative damage.  I don't think that we can compare this result to c60oo, which is a molecular species.  Foley et al. looked at the sub-cellular localization of a water-soluble c60 malonate derivative that was radiolabeled.  Here is what they found:

 

Sub-cellular particle: Counts per minute 14C/mg protein
Cytosolic fraction: 544
Membranous fraction: 5180
Mitochondria: 6727
Microsomes: 3013

 

You can see that (molecular) c60 localizes to membranes, particularly the mitochondrial membrane.  This was a study in cells rather than a whole animal study,  so it differs in more than one way.

Edited by niner, 27 April 2015 - 01:36 AM.

[tunt01]

This is an aggregated form of C60, and they often result in oxidative damage.  I don't think that we can compare this result to c60oo, which is a molecular species.

 

 

Thx Niner.  I was looking through the old science thread and I could not find the data that supported this viewpoint.  Is this an educated guess based on the outcome of Baati's rats combined with a theory of mechanism of action or is there some paper that demonstrates C60oo doesn't elevate this dna/rna damage biomarker (8ohdg) ?

[niner]

 

This is an aggregated form of C60, and they often result in oxidative damage.  I don't think that we can compare this result to c60oo, which is a molecular species.

 

Thx Niner.  I was looking through the old science thread and I could not find the data that supported this viewpoint.  Is this an educated guess based on the outcome of Baati's rats combined with a theory of mechanism of action or is there some paper that demonstrates C60oo doesn't elevate this dna/rna damage biomarker (8ohdg) ?

 

There's a lot of evidence that molecular fullerene compounds are potent antioxidants (e.g. Baati or Laura Dugan), whereas the aggregated particles are often associated with oxidative damage.    It's known that c60 reacts with alkenes and dienes by a variety of mechanisms, and the fact that it appears to "dissolve" in olive oil is consistent with reaction, since its physical solubility in the constituents of olive oil is vanishingly small.

[HighDesertWizard]

 

 

 

niner... Is there Evidence that C60 brown spots in splenic macrophages are a bad thing or is it just your Feeling that it's a bad thing?

 
Is there evidence that C60 brown spots in splenic macrophages are a good thing?

 

 

<< SNIP >>

 

More than that, in both Human and Animal studies, the Spleen has been shown to have Longevity effects as shown in the graphic figures below. You can find an 8 slide presentation that contains the three pics below and a sketch of the Explanation underlying them here.

 

 

 

<< SNIP >>

 

 

Some of your figures are interesting, but they are hard to read, for example the label on the red bar graphs at the right of the page with the mice. 

 

Actually... I provided a link to the graphic figures at that link highlighted in Red above... That's here. Take a look slides 1-3 and 8... The Explanation of those 3 figures about Longevity In Humans is the same as the Explanation for Slide 8. The Explanation itself is highlighted in the graphic figures in Slides 4-7. A study reference for each graphic figure is on each slide.

 

But you're right that I'm just beginning to sketch something. I'll have more about this, in more detail, soon.

[sagafemina]

Well, it does look interesting and is food for thought.  However, still can't read the axis on the far right graphs in slide 8 so don't know what it is trying to show.  Link to the original perhaps?

 

And still missing is a nexus between the appearance of clogged macrophages in Baati rat spleens and this phenomenon, IMO.  Next study should perhaps monitor HRV!

And more carefully examine what is coming out of those spleens...

[Kalliste]

Here is a tox study involving nC60 and two functionalized c60 groups not posted before.

 

Interactive overview of results can be found here:

http://www.quantworm.org/nano/

 

http://www.scienceda...50202144836.htm

 

The lowly roundworm is the star of an ambitious Rice University project to measure the toxicity of nanoparticles.

The low-cost, high-output study by Rice scientists Weiwei Zhong and Qilin Li measures the effects of many types of nanoparticles not only on individual organisms but also on entire populations.

The Rice researchers tested 20 types of nanoparticles and determined that five, including the carbon-60 molecules ("buckyballs") discovered at Rice in 1985, showed little to no toxicity.

Rice University postdoctoral researcher Sang-Kyu Jung checks an assay of roundworms like those used to test nanoparticles for toxicity. Rice scientists have developed a low-cost, high-throughput system that could cut the cost of determining which nanoparticles should be studied further for applications and for their effects on the environment. Click the image for a larger version. Photo by Jeff Fitlow

Others were moderately or highly toxic to Caenorhabditis elegans, several generations of which the researchers observed to see the particles' effects on their health.

The results were published by the American Chemical Society journal Environmental Sciences and Technology.

"Nanoparticles are basically new materials, and we don't know much about what they will do to human health and the health of the ecosystem," said Li, an associate professor of civil and environmental engineering and of materials science and nanoengineering. "There have been a lot of publications showing certain nanomaterials are more toxic than others. So before we make more products that incorporate these nanomaterials, it's important that we understand we're not putting anything toxic into the environment or into consumer products.

"The question is, How much cost can we bear?" she said. "It's a long and expensive process to do a thorough toxicological study of any chemical, not just nanomaterials." She said that due to the large variety of nanomaterials being produced at high speed and at such a large scale, there is "an urgent need for high-throughput screening techniques to prioritize which to study more extensively."

Rice's pilot study proves it is possible to gather a lot of toxicity data at low cost, said Zhong, an assistant professor of biosciences, who has performed extensive studies on C. elegans, particularly on their gene networks. Materials alone for each assay, including the worms and the bacteria they consumed and the culture media, cost about 50 cents, she said.

The researchers used four assays to see how worms react to nanoparticles: fitness, movement, growth and lifespan. The most sensitive assay of toxicity was fitness. In this test, the researchers mixed the nanoparticles in solutions with the bacteria that worms consume. Measuring how much bacteria they ate over time served as a measure of the worms' "fitness."

"If the worms' health is affected by the nanoparticles, they reproduce less and eat less," Zhong said. "In the fitness assay, we monitor the worms for a week. That is long enough for us to monitor toxicity effects accumulated through three generations of worms." C. elegans has a life cycle of about three days, and since each can produce many offspring, a population that started at 50 would number more than 10,000 after a week. Such a large number of tested animals also enabled the fitness assay to be highly sensitive.

The researchers' "QuantWorm" system allowed fast monitoring of worm fitness, movement, growth and lifespan. In fact, monitoring the worms was probably the least time-intensive part of the project. Each nanomaterial required specific preparation to make sure it was soluble and could be delivered to the worms along with the bacteria. The chemical properties of each nanomaterial also needed to be characterized in detail.

The researchers studied a representative sampling of three classes of nanoparticles: metal, metal oxides and carbon-based. "We did not do polymeric nanoparticles because the type of polymers you can possibly have is endless," Li explained.

They examined the toxicity of each nanoparticle at four concentrations. Their results showed C-60 fullerenes, fullerol (a fullerene derivative), titanium dioxide, titanium dioxide-decorated nanotubes and cerium dioxide were the least damaging to worm populations.

Their "fitness" assay confirmed dose-dependent toxicity for carbon black, single- and multiwalled carbon nanotubes, graphene, graphene oxide, gold nanoparticles and fumed silicon dioxide.

They also determined the degree to which surface chemistry affected the toxicity of some particles. While amine-functionalized multiwalled nanotubes proved highly toxic, hydroxylated nanotubes had the least toxicity, with significant differences in fitness, body length and lifespan.

A complete and interactive toxicity chart for all of the tested materials is available online.

Zhong said the method could prove its worth as a rapid way for drug or other companies to narrow the range of nanoparticles they wish to put through more expensive, dedicated toxicology testing.

"Next, we hope to add environmental variables to the assays, for example, to mimic ultraviolet exposure or river water conditions in the solution to see how they affect toxicity," she said. "We also want to study the biological mechanism by which some particles are toxic to worms."

Rice postdoctoral researcher Sang-Kyu Jung and alumna Xiaolei Qu, now an associate professor at Nanjing University, are lead authors of the paper. Co-authors are Rice research scientist Boanerges Aleman-Meza, graduate students Tianxiao Wang and Zheng Liu and alumna Celeste Riepe, now a graduate student at the University of California, Berkeley.

 

Edited by Cosmicalstorm, 27 April 2015 - 02:48 PM.

[katzenjammer]

 

Is there any known issue with interacting with pharmaceuticals?  For instance and particularly, would c60 blunt the effects or increase the rate at which the body excretes a pharmaceutical?  Say, such as an Angiotensin II receptor antagonist? 

 

Based on the number of consistent reports -- it is fair to say that C60 at a sufficient dose significantly blocks the effect of ethanol intoxication -- almost completely depending on dose -- and no hangover.

 

I can personally attest that a 45mg dose of C60 caused a significant drop in the efficacy of diazepam (valium) needing 14 mg to get the same effect as the normal 4 mg dose.

 

 

Yes, the alcohol effects I've experienced; and while I have rarely gotten a cold since trying c60, when I did get one I needed to sleep before an important day and took some nyquil - it had ZERO effect on my sleeping/symptoms, except maybe it got me wired a bit.  Maybe that's just a fluke.  

 

Anyway, so on that I started wondering if it might have an effect (either blunting or causing it to be excreted rapidly, etc.) on other pharmaceuticals, such as ACE inhibitors or Angio receptor antagonists, or anything else like that.   

 

Thought it was important because for some people it could be of some concern.  Was wondering if anyone here had noticed such effects on any prescription medicine they are taking.  

 

Thanks.    

[HighDesertWizard]

Well, it does look interesting and is food for thought. However, still can't read the axis on the far right graphs in slide 8 so don't know what it is trying to show. Link to the original perhaps?

And still missing is a nexus between the appearance of clogged macrophages in Baati rat spleens and this phenomenon, IMO. Next study should perhaps monitor HRV!
And more carefully examine what is coming out of those spleens...

The name of the study summary PDF that the mouse study pic is from is on Slide 8.

Understand a more specific linkage is important. I'm working on a post about it.

One other thing to remember... The Baati study said that "C60 concentrations reached the limit of solubility in spleen." The point is not just about Splenic Macrophages...

If you digest the key Tracey studies, it's no great leap to understand that Spleen functionality played some role. Problem is... It takes time and effort to digest the science of VAGUS-HRV-CAIP Physiology... .

Edited by HighDesertWizard, 27 April 2015 - 04:34 PM.