635 replies to this topic

[HappyPhysicist]

But these were comparisons between carboxyfullerenes. I'd like to see a carboxyfullerenes vs lipofullerene cage match.

[niner]

But these were comparisons between carboxyfullerenes. I'd like to see a carboxyfullerenes vs lipofullerene cage match.

Yes, ultimately this is what we need. It will take some time, I think. That the carboxy and hydroxy fullerenes have such potent radical protection and show the lifespan extension that they do makes me suspect that lipofullerenes will be more potent, given that they ought to be able to become a permanent part of the mitochondrial membrane. If anyone were to attempt replicating the rat tox study, I'd suggest the following twist: Prepare a selection of fullerene / oleic acid analogs with the double bond in different positions and/or with different chain lengths, and try a diverse selection of such adducts in different groups of animals. That way we could see which one worked the best.

For comparison, SkQ1, the prototypic Skulachev ion, a designed mitochondrial protectant, has a phosphonium polar head attached to a plastoquinone electron shuttle by a ten carbon linker. If C60 binds to oleic acid in the 9 position (at the double bond), then the dimensions would be similar. The C60 would be analogous to the plastoquinone of SkQ1, while the carboxylate would be the polar head group. (SkQ1 structure) See also this recent paper. and this recent open access (full text) paper. The charge at the carboxylate would be opposite that of the triphenylphosphonium of SkQ1, so this might affect mitochondrial targeting, if not actual membrane incorporation.

[Turnbuckle]

...That the carboxy and hydroxy fullerenes have such potent radical protection and show the lifespan extension that they do makes me suspect that lipofullerenes will be more potent, given that they ought to be able to become a permanent part of the mitochondrial membrane....

When it comes to mitochondria, there is no such thing as permanence. Far from it. The turnover rate can be as rapid as a day or two.

We estimated the actual [mouse] liver mitochondrial half life as only 1.83 days, and this decreased to 1.16 days following 3 months of dietary restriction, supporting the hypothesis that this intervention might promote mitochondrial turnover as a part of its beneficial effects.

Source: http://www.ncbi.nlm....les/PMC2659384/

So the only thing that remains after a few weeks or months is the memory of the mitochondria--the information on its DNA.

Edited by Turnbuckle, 13 May 2012 - 01:35 PM.

[niner]

...That the carboxy and hydroxy fullerenes have such potent radical protection and show the lifespan extension that they do makes me suspect that lipofullerenes will be more potent, given that they ought to be able to become a permanent part of the mitochondrial membrane....

When it comes to mitochondria, there is no such thing as permanence. Far from it. The turnover rate can be as rapid as a day or two.

But what would happen to the molecular components of the membranes? They probably get reused.

[Turnbuckle]

...That the carboxy and hydroxy fullerenes have such potent radical protection and show the lifespan extension that they do makes me suspect that lipofullerenes will be more potent, given that they ought to be able to become a permanent part of the mitochondrial membrane....

When it comes to mitochondria, there is no such thing as permanence. Far from it. The turnover rate can be as rapid as a day or two.

But what would happen to the molecular components of the membranes? They probably get reused.

Re-utilization is discussed in the paper I referenced, and is a problem for the techniques used because it gives an overly long value for the half-life. But nevertheless, there is no permanence. Even if there were 90% recycling, less than .01% of the original material would remain after six months.

[niner]

...That the carboxy and hydroxy fullerenes have such potent radical protection and show the lifespan extension that they do makes me suspect that lipofullerenes will be more potent, given that they ought to be able to become a permanent part of the mitochondrial membrane....

When it comes to mitochondria, there is no such thing as permanence. Far from it. The turnover rate can be as rapid as a day or two.

But what would happen to the molecular components of the membranes? They probably get reused.

Re-utilization is discussed in the paper I referenced, and is a problem for the techniques used because it gives an overly long value for the half-life. But nevertheless, there is no permanence. Even if there were 90% recycling, less than .01% of the original material would remain after six months.

Fullerenes might exist in a more longer-lived reservoir, like in the membrane of a long-lived somatic cell. I apologize for the use of the heinously misleading term "permanent". Can we move on from that? My point is that it is at least conceivable that they stay in the body for a very long time. This doesn't require any heretofore-unheard of chemistry or biophysics. It could be tested by administering a C14-labeled fullerene fatty acid adduct, then monitoring animals over time with a scintillation counter. This would allow you to derive a rate constant for disappearance from the body. Until something like that is done, it's a hypothesis. Your hypothesis that fullerenes are causing epigenetic modifications that result in a near doubling of lifespan is troubling for several reasons. For one thing, how would a chemical agent know how to remove the right epigenetic markers while leaving the ones that needed to stay? Where would the specificity come from? For another thing, what sort of chemistry are you proposing for these putative epigenetic modifications? How would a fullerene methylate or demethylate a CpG?

[Turnbuckle]

...That the carboxy and hydroxy fullerenes have such potent radical protection and show the lifespan extension that they do makes me suspect that lipofullerenes will be more potent, given that they ought to be able to become a permanent part of the mitochondrial membrane....

When it comes to mitochondria, there is no such thing as permanence. Far from it. The turnover rate can be as rapid as a day or two.

But what would happen to the molecular components of the membranes? They probably get reused.

Re-utilization is discussed in the paper I referenced, and is a problem for the techniques used because it gives an overly long value for the half-life. But nevertheless, there is no permanence. Even if there were 90% recycling, less than .01% of the original material would remain after six months.

Fullerenes might exist in a more longer-lived reservoir, like in the membrane of a long-lived somatic cell. I apologize for the use of the heinously misleading term "permanent". Can we move on from that? My point is that it is at least conceivable that they stay in the body for a very long time. This doesn't require any heretofore-unheard of chemistry or biophysics. It could be tested by administering a C14-labeled fullerene fatty acid adduct, then monitoring animals over time with a scintillation counter. This would allow you to derive a rate constant for disappearance from the body. Until something like that is done, it's a hypothesis. Your hypothesis that fullerenes are causing epigenetic modifications that result in a near doubling of lifespan is troubling for several reasons. For one thing, how would a chemical agent know how to remove the right epigenetic markers while leaving the ones that needed to stay? Where would the specificity come from? For another thing, what sort of chemistry are you proposing for these putative epigenetic modifications? How would a fullerene methylate or demethylate a CpG?

The papers I quoted before spoke of a epigenetic drift of aging DNA, which is presumably stochastic since it effects different cells differently. Apparently during replication, methylation is reproduced but not always exactly. There are gains and losses, and also movements in position. This noise thus changes the expression of genes randomly and make the mitochondria less vital and that makes the cell less vital. It's what passes for aging. As one paper said about calorie restriction (CR): "Reversal of aberrant DNA methylation during aging is believed to be the most effective mechanism for CR to maintain chromatin function and subsequently influence aging processes." And if it's the most effective mechanism for CR, why not also C60?

As I'm not a chemist, I won't speculate on how C60 might operate to remove methyl groups from mtDNA, but once these are removed, you might expect them to be replaced in a default pattern. Off hand I don't know of any experiment that shows this to happen, but the paper I quoted before suggested that "CR is likely to recover these aging-induced aberrant DNA methylation patterns, but by specific loci control rather than globally." So how does CR know what to do? What to add and what to take away? Wouldn't the simplest answer be that there is a default pattern that DNA reverts to--equivalent to reverting software to its factory presets?

From the chapter "Methylation Pattern and the Control of Transcription"-- http://www.ncbi.nlm....books/NBK10038/

"In the primordial germ cells that give rise to the sperm and egg, all methylation differences are wiped out. The DNA is almost entirely unmethylated. However, as the germ cells develop into sperm or eggs, their genes undergo extensive methylation."

So my hypothesis is that fullerenes wipes out the methylation, the DNA automatically recovers it, and the effective age is set to zero. The DNA will begin to age again, and a later treatment can reset it back to zero. Keep resetting every few years and the ultimate limit then passes to the telomeres and epigenetics of the nuclear DNA.

Edited by Turnbuckle, 14 May 2012 - 01:24 AM.

[niner]

So my hypothesis is that fullerenes wipes out the methylation, the DNA automatically recovers it, and the effective age is set to zero. The DNA will begin to age again, and a later treatment can reset it back to zero. Keep resetting every few years and the ultimate limit then passes to the telomeres and epigenetics of the nuclear DNA.

There are seven different forms of aging damage that SENS aims to deal with. One of them is in fact nuclear mutation and epimutation, but these aren't a noticeable cause of aging until we are very very old, if ever. The real problem with mutation is that it may cause cancer which can kill us. CR may induce some epigenetic changes, which aren't done by CR itself but by the body's enzymatic machinery, in response to the perceived starvation. CR changes the expression rate of a huge number of genes. If you think about it, starvation is something that all animals have faced throughout evolution, so it stands to reason that we would have developed sophisticated responses to it. We have never been exposed to C60-fatty acid adducts in our evolutionary history, so we aren't likely to have a major genetic response to it.

It's very clear that C60 has mitochondrial activities; for example, animals treated with C60 are more resistant to radiation effects, and are far more resistant to the oxidative damage from carbon tetrachloride ingestion. That isn't just a reset to a youthful state, because youthful animals would be injured by both radiation and CCl4.

[Turnbuckle]

We have never been exposed to C60-fatty acid adducts in our evolutionary history, so we aren't likely to have a major genetic response to it.

You could say similar things about most products of the pharmaceutical industry. But novelty doesn't equate to a lack of function.

It's very clear that C60 has mitochondrial activities; for example, animals treated with C60 are more resistant to radiation effects, and are far more resistant to the oxidative damage from carbon tetrachloride ingestion. That isn't just a reset to a youthful state, because youthful animals would be injured by both radiation and CCl4.

I agree that important aspects of C60 are its affinity for the mitochondria and its affinity for radicals. Add to that an affinity for methyl groups and we'll be on the same page. Other substances are known to have such an affinity, and not in a good way, such as arsenic, which can reduce methylation, increase DNA oxidation, and enhance cell survival. The last thing is rather strange, but could be explained if it is resetting the mitochondria even as it damages it.

Edited by Turnbuckle, 14 May 2012 - 01:09 PM.

[DeadMeat]

Then there was this one, which reports lifespan extension in wild-type mice from a carboxy-fullerene "SOD Mimetic". I haven't seen the full text of that one, and don't have any details.

The full text of that one is on dr Dugans website.
http://thebronxproje... Aging 2006.pdf
And supplement A:

Attached Files

•  supplementA.pdf   11.02KB   14 downloads

[DeadMeat]

I wonder to what extend the C60 in olive oil can escape the lipid phase by binding to proteins.
http://www.ncbi.nlm....pubmed/16933357

It seems to be able to bind to quite a lot of proteins.
http://www.ncbi.nlm....pubmed/20359241

Baiting proteins with C60.
Calvaresi M, Zerbetto F.
Dipartimento di Chimica "G. Ciamician", Universita' di Bologna, V. F. Selmi 2, 40126 Bologna, Italy. matteo.calvaresi@studio.unibo.it

About 20 proteins are known to modify their activity upon interaction with C60. Their structures are present in a database that includes more than 1200 protein structures selected as possible targets for drugs and to represent the entire Protein Data Bank. The set was examined with an algorithm that appraises quantitatively the interaction of C60 and the surface of each protein. The redundancy of the set allows to establish the predictive power of the approach that finds explicitly the most probable site where C60 docks on each protein. About 80% of the known fullerene binding proteins fall in the top 10% of scorers. The close match between the model and experiments vouches for the accuracy of the model and validates its predictions. The sites of docking are shown and discussed in view of the existing experimental data available for protein-C60 interaction. A closer exam of the 10 top scorers is discussed in detail. New proteins that can interact with C60 are identified and discussed for possible future applications as drug targets and fullerene derivatives bioconjugate materials.

The experiments detailing the binding of C60 to HIV protease, cysteine and serine proteinases, glutathione S-transferase and reductase, cytochrome P450, ATPase, tubulin, antibody Fab fragment, glutamate receptors, nitric oxide synthase, troponin, ion channels, serum albumin, HIV-reverse transcriptase, acethylcholineaterase, lysozyme, and a set of proteins that inhibit allergic response provide clear evidence that C60 and proteins are a good if not perfect match.

Attached Files

•  C60protein2010.pdf   1.07MB   25 downloads

[nowayout]

This whole subject reeks of the Pons and Fleischmann cold fusion scandal. It is simply too implausible. So I wouldn't get my panties all in a knot unless and until it gets replicated.

Edited by viveutvivas, 15 May 2012 - 04:23 PM.

[HappyPhysicist]

This whole subject reeks of the Pons and Fleischmann cold fusion scandal. It is simply too implausible. So I wouldn't get my panties all in a knot unless and until it gets replicated.

I think everyone here would generally agree that this is reminiscent of cold fusion. That is exactly why we are experimenting with it right now. For a few of us we will be dead long before anyone replicates this study. So waiting is simply not an option.

[Turnbuckle]

This whole subject reeks of the Pons and Fleischmann cold fusion scandal. It is simply too implausible. So I wouldn't get my panties all in a knot unless and until it gets replicated.

I think everyone here would generally agree that this is reminiscent of cold fusion. That is exactly why we are experimenting with it right now. For a few of us we will be dead long before anyone replicates this study. So waiting is simply not an option.

We'll all be dead before anyone replicates Pons and Fleischmann. The trouble was they used palladium rather than fullerenes.

Interesting fact: Palladium, like arsenic, can increase the lifespan of animals: "Mice given palladium(II) chloride in drinking-water (5 mg palladium/litre) from weaning until natural death showed suppression of body weight gain together with longer life span (in males, but not in females; mean age of palladium-fed males 555 days versus 444 days in controls)..." So you wonder, if they had been given just a short exposure during middle age, would they have done even better.

Edited by Turnbuckle, 15 May 2012 - 06:50 PM.

[HighDesertWizard]

...That the carboxy and hydroxy fullerenes have such potent radical protection and show the lifespan extension that they do makes me suspect that lipofullerenes will be more potent, given that they ought to be able to become a permanent part of the mitochondrial membrane....

When it comes to mitochondria, there is no such thing as permanence. Far from it. The turnover rate can be as rapid as a day or two.

But what would happen to the molecular components of the membranes? They probably get reused.

Re-utilization is discussed in the paper I referenced, and is a problem for the techniques used because it gives an overly long value for the half-life. But nevertheless, there is no permanence. Even if there were 90% recycling, less than .01% of the original material would remain after six months.

Fullerenes might exist in a more longer-lived reservoir, like in the membrane of a long-lived somatic cell. I apologize for the use of the heinously misleading term "permanent". Can we move on from that? My point is that it is at least conceivable that they stay in the body for a very long time. This doesn't require any heretofore-unheard of chemistry or biophysics. It could be tested by administering a C14-labeled fullerene fatty acid adduct, then monitoring animals over time with a scintillation counter. This would allow you to derive a rate constant for disappearance from the body. Until something like that is done, it's a hypothesis. Your hypothesis that fullerenes are causing epigenetic modifications that result in a near doubling of lifespan is troubling for several reasons. For one thing, how would a chemical agent know how to remove the right epigenetic markers while leaving the ones that needed to stay? Where would the specificity come from? For another thing, what sort of chemistry are you proposing for these putative epigenetic modifications? How would a fullerene methylate or demethylate a CpG?

Emphasis in quote added...

Thanks to Turnbuckle for referencing this earlier discussion... I'm getting a better handle on his proposed hypothesis about why the study result happened...

re: the question about how a fullerene would methylate or demethylate a CpG... EPA, of course, is an Omega 3 and Olive Oil is partly Omega 3 also...

Eicosapentaenoic Acid Demethylates a Single CpG That Mediates Expression of Tumor Suppressor CCAAT/Enhancer-binding Protein δ in U937 Leukemia Cells

I don't know much about genetics, but I can still pull this kind of study out pretty easily... In my last post I referenced a few 5-LO inhibitors that performed this kind of task (Boswellia, Polyphenols, including Green Tea, etc).. There are a lot more inhibitors and study links.

• The fact that quite a few 5-LO inflammatory cascade inhibitors clearly or likely play a cancer related (de)methylating role ought to give us pause as we brainstorm potential Fullerene Solvents that don't have studies suggesting they play such a role. (AFAIK, MCT does not have such studies.) On the other hand... Hot off the press...

Boswellia sacra essential oil induces tumor cell-specific apoptosis and suppresses tumor aggressiveness in cultured human breast cancer cells (published December 2011)

Boswellic acid induces epigenetic alterations by modulating DNA methylation in colorectal cancer cells (published May 2012)

• In my last post, the point of the William Li video was to raise the question of synergy across (de)methylating substances used as Fullerene solvents... How about mixing half the daily fullerene dose in Olive Oil and half in EPA/DHA and getting synergy from ingesting the fullerenes from both? Or dividing the fullerene dose into 3rds or 4qts, Olive Oil, EPA/DHA, Boswellia, and Curcumin? Check this study out and then watch the portion of the William Li video I pointed to again...

Dietary fish oil and curcumin combine to modulate colonic cytokinetics and gene expression in dextran sodium sulphate-treated mice

The abstract punch line...

"... Mucosal microarray analysis revealed that dietary FO, curcumin and FO plus curcumin combination differentially modulated the expression of genes induced by DSS treatment. These results suggest that dietary lipids and curcumin interact to regulate mucosal homeostasis and the resolution of chronic inflammation in the colon."

That's what we want, right? ... differential modulation? ... what William Li calls Synergy?

• Might the benefit of the Fullerenes be magnified using different solvents that play methylating roles? It's not that hard to come up with a short list of potential solvents. I suggest starting with known 5-LO inhibitors, um, like maybe Pomegranate Oil...

Pomegranate Extract Induces Cell Cycle Arrest and Alters Cellular Phenotype of Human Pancreatic Cancer Cells

• I keep noticing an assumption in some folk's posts that the Fullerenes were the only substance in the study having a positive impact. IMHO, if they're going to continue to make that assumption, I suggest that NOW would be a good time to point us to the place in the Buckyball study that says the Fullerenes were the only mechanism having a non-trivial (solvent only) impact. I think getting this assumption sorted out now, before MORE people take a fancy to trying this out with something less than what is likely to make a difference, is a good idea....

Edited by wccaguy, 19 May 2012 - 11:36 PM.

[HighDesertWizard]

This looks interesting and the PDF is downloadable for free...

From April 2012...

Virgin olive oil in preventive medicine: From legend to epigenetics

Edited by wccaguy, 20 May 2012 - 12:18 AM.

[revenant]

I have a hypothesis: Because of its hydrophobic propensity, C60 incorporates itself into cell membranes thereby presenting the adducted olive oil which disrupts the signaling pathways of arachidonic acid in the phospholipids therein while also sopping up supersoxide everywhere the C60 finds it, nice "one-two".

How/why does the C60 pass through the cytosol into the mitochondrial membranes? Wouldn't it want to stay in the cell membrane? Is it shunted through the cell membrane by a channel protein or an inner membrane channel protein? Is there a charge graident involved? Is it just possible that because it behaves like a wave also...it makes for the mitochondria and leaves the olive oil in the cell membrane?

Edited by revenant, 20 May 2012 - 05:50 AM.

[revenant]

After a bit of half educated half baked thought..I am guessing there is a saturation of the cell membrane first..then the molecules can enter the mitochondria via a charge graident maybe?

[revenant]

After a bit of half educated half baked thought..I am guessing there is a saturation of the cell membrane first..then the molecules can enter the mitochondria via a charge graident maybe?

mmm this is silly

[Metrodorus]

Harman,in this 2001 paper posits that fullerene may work in the mitochondria as a blocking agent.

Many antioxidants,at therapeutic doses,actually decrease the efficiency of the mitochodria, which is why possibly we do not see increases in the maximum lifespan.

If fullerene is indeed a blocking agent, then it acts by stopping oxygen from generating reactive oxygen species and superoxide formation, while having no negative impact on mitochondrial functionality.

Other studies posit it is a superoxide dismutase mimetic.

[HighDesertWizard]

Harman,in this 2001 paper posits that fullerene may work in the mitochondria as a blocking agent.

Many antioxidants,at therapeutic doses,actually decrease the efficiency of the mitochodria, which is why possibly we do not see increases in the maximum lifespan.

If fullerene is indeed a blocking agent, then it acts by stopping oxygen from generating reactive oxygen species and superoxide formation, while having no negative impact on mitochondrial functionality.

Other studies posit it is a superoxide dismutase mimetic.

Thanks for the Harman reference Metrodorus. Do you have a study link related to antioxidants decreasing mitochondrial efficiency?

I posted this figure earlier. It helped me to understand the mechanism of action that may be played by Reactive Oxygen Species reduction vis-a-vis the Sirt1 related mechanism of Resveratrol. It also illustrates the hypothesis that Metrodorus relates from Harman about a potential role for Fullerene.

The graphic figure is from this literature overview of the action of P53...

http://www.ncbi.nlm....38/?tool=pubmed

Edited by wccaguy, 20 May 2012 - 11:07 PM.

[niner]

For one thing, how would a chemical agent know how to remove the right epigenetic markers while leaving the ones that needed to stay? Where would the specificity come from? For another thing, what sort of chemistry are you proposing for these putative epigenetic modifications? How would a fullerene methylate or demethylate a CpG?

re: the question about how a fullerene would methylate or demethylate a CpG... EPA, of course, is an Omega 3 and Olive Oil is partly Omega 3 also...

Eicosapentaenoic Acid Demethylates a Single CpG That Mediates Expression of Tumor Suppressor CCAAT/Enhancer-binding Protein δ in U937 Leukemia Cells

Thanks for the example, wccaguy. Drugs, diet, or exercise are all capable of changing gene expression; for example, resveratrol alters the expression level of on the order of 1000 genes. It's very likely that fullerenes change the expression level of numerous genes as well. For the vast majority of these genes, the changes in expression are transient, and when the drug is withdrawn, expression returns to normal. In some cases, however, there are apparently long-lasting changes put in place by CpG (de)methylation, histone (de)acetylation, etc. These are epigenetic modifications. Turnbuckle's idea was entirely reasonable, though I was thrown off by the proposed chemical mechanism, which is highly implausible. However, epigenetic modifications made via the organism's enzymatic machinery is entirely possible. When a drug study is run in the pharmaceutical industry, sometimes they will take great pains to find subjects that are "drug-naive"; i.e., that have never in their lives had the drug in question nor any analogs of it. It's a known effect that the very first time you take a drug, it may behave differently than it will ever after. I've even had this experience myself- the first time I took diazepam, I had some weird side effects, like bleeding from my nose. Even with multi-year gaps in use, I never saw that again. An epigenetic change could explain an effect like that, though it's probably not the only way it could happen.

Thanks for stimulating my thought on this; I appreciate that.

[Allen Walters]

If THC would transport the c60 to different parts of the body, what would the different JWH-XXX compounds do? Some have an affinity for cb1 and cb2 receptors, and otheres are specific to only one. It's also oil soluble, and JWH-133 has anti cancer properties.

[Turnbuckle]

If THC would transport the c60 to different parts of the body, what would the different JWH-XXX compounds do? Some have an affinity for cb1 and cb2 receptors, and otheres are specific to only one. It's also oil soluble, and JWH-133 has anti cancer properties.

I was just speculating about THC, but are you saying replace the oil or the C60 with JWH?

[Allen Walters]

No, just saying it goes to the same place in the body as THC. Besides the JWH's come in powder form which could be dissolved along with the c60 in the olive oil. I didn't know if it would take the c60 along with it to the same places THC would. Take what I say with a grain of salt, I'm not as smart as the members on this board. I just was thinking out loud.

[Logic]

I'm probably going to make a complete ass of myself, (again! ) but ...:

Mammalian Mitochondria Possess Homologous DNA Recombination Activity
http://www.jbc.org/c...1/44/27536.full
It may be possible to improve mitochondrial function (and thereby enhance levels of mitochondrial homologous DNA recombination activity) by supplementing the culture media with high levels of the ketone body 3-hydroxybutyrate.

3-hydroxybutyrate derivatives can be used as nutritional supplements to increase physical performance and as therapeutics to ameliorate symptoms of medical conditions, particularly neurological conditions, such as Alzheimer's and similar conditions:
http://www.google.co...s/US20060280721

3-hydroxybutyrate production seems to be improved by Oleic Acid:
http://www.springerl...7g24232121n272/

Oleic Acid is most prevalent in Olive Oil:
http://www.wisegeek....-oleic-acid.htm

so... ???

[Logic]

I'm probably going to make a complete ass of myself, (again! ) but ...:

Mammalian Mitochondria Possess Homologous DNA Recombination Activity
http://www.jbc.org/c...1/44/27536.full
It may be possible to improve mitochondrial function (and thereby enhance levels of mitochondrial homologous DNA recombination activity) by supplementing the culture media with high levels of the ketone body 3-hydroxybutyrate.

3-hydroxybutyrate derivatives can be used as nutritional supplements to increase physical performance and as therapeutics to ameliorate symptoms of medical conditions, particularly neurological conditions, such as Alzheimer's and similar conditions:
http://www.google.co...s/US20060280721

3-hydroxybutyrate production seems to be improved by Oleic Acid:
http://www.springerl...7g24232121n272/

Oleic Acid is most prevalent in Olive Oil:
http://www.wisegeek....-oleic-acid.htm

so... ???

Ok so everyone knew that mitochondrial DNA could be repaired and that the process is probably helped by 3-hydroxybutyrate?
No one thinks its possible that the production of 3-hydroxybutyrate or similar could have something to do with C60 in Olive Oil?

Edited by Logic, 23 May 2012 - 09:34 PM.

[Metrodorus]

Interestingly, fullerenes have come under scrutiny at SENS
http://www.sens.org/node/1327

[Metrodorus]

Interesting phd thesis on fullerenes
http://www.tesisenre....pdf?sequence=1

[niner]

About your first thought... Based on a discussion between niner and Turnbuckle, I'd been thinking that the C60s afforded greater (and longer lasting?) affinity to mitochondria. I've also imagined that the study solvent provided "the potion" with an affinity for the cell types that Olive Oil had an affinity for. That's how I've imagined it. I have no idea if this is a "correct" way to imagine it.

There's nothing about naked C60 that would target it to mitochondria specifically; it's exceptionally hydrophobic, so it would be expected to partition into lipids wherever it encountered them. The (covalent) addition of a long chain fatty acid, on the other hand, would create a molecule that would have an affinity for lipid membranes in general, of which the mitochondrial membrane would be an example. I suspect that the C60 that finds its way into non-mitochondrial membranes isn't hurting anything, and may be helping some, but the fraction that gets into mitochondrial membranes is what's doing the magic, because it's close to the source of damaging superoxide ions.

But given this imagining... I've been thinking about a mix of oils. Not MCT... I've been saying in my posts that, if the solvent is important at all, then it makes sense to use a 5-Lipoxygenase Inflammatory Cascade Inhibitor. The most profound of these inhibitors have been shown to have (de)methylating effects. (And, in fact, I'm pretty sure I experienced such an effect using very high dose Boswellia a few years ago.)

So that means Omega 3 (EPA/DHA), Boswellia, etc. So how about 25% Olive Oil, 25% EPA/DHA, and fill in the rest. Alternate the potion taken on different dose days.

I'd really advise against using EPA/DHA. Highly unsaturated fatty acids like that are extremely oxidation prone, and have been shown to result in an increase in lipid peroxidation in the body. Other vegetable oils could be used if one is so inclined, though given the quantities of oil involved, I would want to stay away from omega 6 varieties. Personally, I'd stick with olive oil, which has very good epidemiology associated with it.

Here's a question for the more informed science types.... How might the "the potion" be effected if an additional substance was added to it. Say, Curcumin, Boswellia (AKBA), or Resveratrol Powder added to the Olive Oil in addition to the Fullerenes?

While some of those substances might be useful as co-supplements, I can't think of any way in which they would help if they were added directly to the mixture. With some of them, you might run into solubility problems, or possibly even a chemical interference of some sort.