3585 replies to this topic

[stephen_b]

Tell me you're using an Omega 3 Oil... EPA/DHA... My response would be a positive one...

That would also be a long chain fatty acid, like olive oil. So it should mostly be processed through the lymph system, bathing a lot of tissues of the body along the way with C60. My understanding is that MCT oil would not.

Are there other purified long chain fatty acid choices out there (along the lines of MCT oil, a purified medium chain fatty acid)?

[HighDesertWizard]

The Buckyball study we're talking about documented an astounding result of life extension in rats. I truly don't understand why, at this stage of experimentation in humans, the conversation has shifted from "how can we replicate the study methods as closely as possible" to brainstorming and implementing methods we imagine might be more optimal...

And I really don't understand why this makes sense when Turnbuckle has made such a positive statement about his experience with the methods (C60s and Olive Oil) of the study.

Did I misread what you used Turnbuckle? You used Olive Oil? Or did your experience turn sour at some post later in this thread and I missed it?

If he did use Olive Oil and his experience was positive, HappyPhysicist, why would you want to try anything else? This is your LIFE, right?

Have I understood you correctly to say that "ease of filtering" would keep you from trying to replicate the methods of the study closely to achieve its profound result and the remarkable oxygen utilization result Turnbuckle reported?

A development as incredible as the study itself...

Edited by wccaguy, 16 May 2012 - 08:42 PM.

[Turnbuckle]

Did I misread what you used Turnbuckle? You used Olive Oil? Or did your experience turn sour at some post later in this thread and I missed it?

Yes, I used olive oil as the solvent and had positive results within a few hours. I took it for ten days (2-20 mg daily), stopped, and then tried it for another three days at 10 mg without seeing any additional benefit...at least, not anything as dramatic as that first day when I went running and found that I wasn't out of breath after 100 yards. Since then I've seen improvements at the gym, increasing the weights by 20-50%. My cholesterol has ticked back up, but is still running 20 points lower than when I started. No change to BP.

One of my dogs also benefited noticeably from a few days treatment. He's now able to jump into the back of my car without a problem and he's regained his ability to catch a tennis ball in the air, an ability he'd lost some time ago.

Unfortunately, I seem to be the only one who has posted results here. Either no one else has tried it, or no one is saying.

[nowayout]

I would be the first to wish that this direction of research is successful.

One thing that bothers me, though, is that the median life span of Wistar rats is known to be around 30 months. That the control rats lived for 22 months, so much less than the known median lifespan, rings alarm bells...

A Japanese paper gives the average lifespans for male Wistar Mishima and male Wistar/Lobund rats as 731 days and 707 days respectively. That’s 24 months and 23 months, which isn’t far off from this set of male “Wistar” rats.

Not sure about that. Could we get some clarification re. the lifespan of Wistar rats? This paper gives it as 29-30 months. And this paper gives it as about 930 days which is 30 months. This paper on Han:Wistar rats find a median life expectancy of between 30-33 months for females and 33-36 months for males.

If this is correct, my objection remains. If the size of the study is so small that 30% shorter than 30 months is noise, then 30% longer than 30 months is also just noise.

Edited by viveutvivas, 16 May 2012 - 09:57 PM.

[Turnbuckle]

There are many Wistar lines, some inbred, some outbred.
See http://www.harlan.co...earch_models.hl
So you'll have to know which one was used before you can say the controls didn't live long enough. There is one that is listed as just plain Wistar--General-purpose albino stock--but the spec sheet doesn't give a lifespan for it.

Edited by Turnbuckle, 16 May 2012 - 10:33 PM.

[HappyPhysicist]

wccaguy, I'm a habitual tinkerer, I'm always saying to myself "what if I try this...", anyway I plan on sticking with Olive Oil for the most part but I will take some swigs of the MCT combo. By the way after about 8 hours it is now a deep purple but not all of the C60 has dissolved. Usually by the second day it is all dissolved (at least visibly) in the olive oil.

I have been taking C60/OO for about 8 days now, approximately 10 mg per day = 10 mg/85 kg = 0.01 mg/kg. I have not noticed any improvement but I'm probably not a great test subject because of my disease which is busy taking away all my strength day by day. An excellent outcome for me would be if it slowed my rate of decline, but that is almost impossible to perceive. It will take a few months before I find out if this is the case.

Edited by HappyPhysicist, 17 May 2012 - 12:10 AM.

[Turnbuckle]

One thing I should add is that I've taken PQQ for over a year now and that was also very helpful. The effect of PQQ was fast, but not nearly as fast as C60. It's possible that PQQ and C60, both operating on the mitochondria as they do, are synergistic.

Edited by Turnbuckle, 17 May 2012 - 12:39 AM.

[testerer]

Another interesting article, dealing with atherosclerotic rats, C60 in saline solution and resulting in vasomotor balance shift towards vasorelaxation:

http://www.particlea...m/content/6/1/5

[testerer]

This article tests varios nanoparticles toxicity during pulmonary exposure to CarbonBlack, fullerene C60, single-wall nanotubes, gold particles and quantum dots. The result was that all except C60 and gold are toxic. Gold was used at a much lower dose than others, so the least toxic was C60.

http://www.springerl...77tp575r017911/

[nowayout]

There are many Wistar lines, some inbred, some outbred.

Hmm, it is indeed possible that they used a strain with a shorter lifespan, but if that is the case, that would problematic for a different set of reasons. Lab strains with shorter lifespans often have specific problems that make them less suitable for longevity studies per se; for example, they may be short-lived because they are more prone to cancer, in which case a result like this could be more about cancer prevention (for example) than about longevity.

[niner]

The experimental results show that the solubility of fullerenes appears to be dependent on the unsaturation level of the fatty acids composing the vegetable oils being lower in oils with higher unsaturation level. Franco Cataldo

Has anyone found a chart which orders the various oils in terms of "unsaturation" level?

It was already pointed out by someone in this forum that MCT is a pure saturated fat, and therefore has a low "unsaturation level" (If I understand that term correctly), and therefore should have a higher solubility of C60. The question is does the C60 still go along for the ride to the cells or mitochondria.

Here's a chart that gives the content of key unsaturates in various oils. Cataldo's statement that as the oil gets more unsaturated, the solubility of fullerene goes down doesn't totally make sense. If the solubility is driven by adduct formation, for which Diels Alder condensation is an example, it should behave the opposite way, which is what the cryptic Russian paper (Pogorelij et al.) found. Of course, they also found solubilities that were two orders of magnitude too large, so go figure.

[PWAIN]

There are many Wistar lines, some inbred, some outbred.

Hmm, it is indeed possible that they used a strain with a shorter lifespan, but if that is the case, that would problematic for a different set of reasons. Lab strains with shorter lifespans often have specific problems that make them less suitable for longevity studies per se; for example, they may be short-lived because they are more prone to cancer, in which case a result like this could be more about cancer prevention (for example) than about longevity.

According to the paper, of the untreated rats, the first died at 17 months old from a tumor, the next to die was about 26 months old (imprecise because taken from graph) and the longest lived was 38 months old. That makes the longest lived of the untreated mice 3 years and 2 months old. Only the non-parametric Kaplan-Meier EML lifespan was 22 months (the straight median is 29.7 months) and this was probably not helped by having a rat die at 17 months from a tumor. The straight median lifespan comes out to 32 for 5 rats and if you add the age of death of the 5 and divide by 5 you get 32 average. So looks like small sample size bites.

Now consider that the C60 treated rats to between 59 months and 66 months. SERIOUSLY if these rats were normally living to even 4 years, they have still totally outlived any fiddly quibbles about normal lifespan, poor treatment etc.

[HighDesertWizard]

Tell me you're using an Omega 3 Oil... EPA/DHA... My response would be a positive one...

That would also be a long chain fatty acid, like olive oil. So it should mostly be processed through the lymph system, bathing a lot of tissues of the body along the way with C60. My understanding is that MCT oil would not.

Are there other purified long chain fatty acid choices out there (along the lines of MCT oil, a purified medium chain fatty acid)?

Thanks for this comment stephen_b... You're right...

... the best way to ensure Buckyball delivery to the "systemic circulation" is to dissolve them in a PUFA oil. A great way to limit the tissues that get exposed to the Buckyballs is to use an MCT OIl.

--------------------------

Lipid-based delivery systems and intestinal lymphatic drug transport: A mechanistic update

After oral administration, the majority of drug molecules are absorbed across the small intestine and enter the systemic circulation via the portal vein and the liver. For some highly lipophilic drugs (typically log P > 5, lipid solubility > 50 mg/g), however, association with lymph lipoproteins in the enterocyte leads to transport to the systemic circulation via the intestinal lymph. The attendant delivery benefits associated with lymphaticdrug transport include a reduction in first-pass metabolism and lymphatic exposure to drug concentrations orders of magnitude higher than that attained in systemic blood. In the current review we briefly describe the mechanisms by which drug molecules access the lymph and the formulation strategies that may be utilised to enhance lymphatic drug transport. Specific focus is directed toward recent advances in understanding regarding the impact of lipid source (both endogenous and exogenous) and intracellular lipid trafficking pathways on lymphatic drug transport and enterocyte-based first-pass metabolism.

--------------------------
--------------------------
...MCT's energy sustaining powers can be explained as follows: when MCT oil is metabolized in the body, it behaves more like a carbohydrate than a fat. Remember that the fuel of preference for the body is carbohydrate. Unlike other fats, MCT oil does not go through the lymphatic system. Instead, it is transported directly to the liver where it is metabolized so it releases energy like a carbohydrate and creates lots of ketones (which can be used for fuel) in the process.
http://www.bodybuild.../fun/issa23.htm

--------------------------
--------------------------
Supporting study reference...

medium-chain triacylglyerols (MCT) are edible oils composed of triacylglycerols with saturated medium-chain fatty acids (MCFA) moieties of six to ten C atoms. These have been introduced into clinical nutrition programmes because of their rapid absorption and solubility (Seaton et al. 1986). MCT are metabolized differently from LCT. They are transported to the liver directly via hepatic portal circulation and are oxidized to ketones, whereas LCT are absorbed via the intestinal lymphatic ducts and transported in chylomicrons through the thoracic duct to reach the systemic circulation (Bach & Babyan, 1982; Senior 1990).
--------------------------

niner... After reviewing the above links, do you still maintain the position that deviating from the Buckyball study protocol by using an MCT Oil vs. the study choice of a PUFA is a choice of no consequence? If you do still maintain that position, please provide the rationale and supporting study link support for your view...

Edited by wccaguy, 17 May 2012 - 12:15 PM.

[Hebbeh]

Tell me you're using an Omega 3 Oil... EPA/DHA... My response would be a positive one...

That would also be a long chain fatty acid, like olive oil. So it should mostly be processed through the lymph system, bathing a lot of tissues of the body along the way with C60. My understanding is that MCT oil would not.

Are there other purified long chain fatty acid choices out there (along the lines of MCT oil, a purified medium chain fatty acid)?

Thanks for this comment stephen_b... You're right...

... the best way to ensure Buckyball delivery to the "systemic circulation" is to dissolve them in a PUFA oil. A great way to limit the tissues that get exposed to the Buckyballs is to use an MCT OIl.

--------------------------

Lipid-based delivery systems and intestinal lymphatic drug transport: A mechanistic update

After oral administration, the majority of drug molecules are absorbed across the small intestine and enter the systemic circulation via the portal vein and the liver. For some highly lipophilic drugs (typically log P > 5, lipid solubility > 50 mg/g), however, association with lymph lipoproteins in the enterocyte leads to transport to the systemic circulation via the intestinal lymph. The attendant delivery benefits associated with lymphaticdrug transport include a reduction in first-pass metabolism and lymphatic exposure to drug concentrations orders of magnitude higher than that attained in systemic blood. In the current review we briefly describe the mechanisms by which drug molecules access the lymph and the formulation strategies that may be utilised to enhance lymphatic drug transport. Specific focus is directed toward recent advances in understanding regarding the impact of lipid source (both endogenous and exogenous) and intracellular lipid trafficking pathways on lymphatic drug transport and enterocyte-based first-pass metabolism.

--------------------------
--------------------------
...MCT's energy sustaining powers can be explained as follows: when MCT oil is metabolized in the body, it behaves more like a carbohydrate than a fat. Remember that the fuel of preference for the body is carbohydrate. Unlike other fats, MCT oil does not go through the lymphatic system. Instead, it is transported directly to the liver where it is metabolized so it releases energy like a carbohydrate and creates lots of ketones (which can be used for fuel) in the process.
http://www.bodybuild.../fun/issa23.htm

--------------------------
--------------------------
Supporting study reference...

medium-chain triacylglyerols (MCT) are edible oils composed of triacylglycerols with saturated medium-chain fatty acids (MCFA) moieties of six to ten C atoms. These have been introduced into clinical nutrition programmes because of their rapid absorption and solubility (Seaton et al. 1986). MCT are metabolized differently from LCT. They are transported to the liver directly via hepatic portal circulation and are oxidized to ketones, whereas LCT are absorbed via the intestinal lymphatic ducts and transported in chylomicrons through the thoracic duct to reach the systemic circulation (Bach & Babyan, 1982; Senior 1990).
--------------------------

niner... After reviewing the above links, do you still maintain the position that deviating from the Buckyball study protocol by using an MCT Oil vs. the study choice of a PUFA is a choice of no consequence? If you do still maintain that position, please provide the rationale and supporting study link support for your view...

But how do we not know that the Buckyballs do their magic in the liver rather than the individual mitochondria throughout the body? There simply wasn't enough Buckyballs ingested in relation to the number of mitochondria in the body....not even close....it's got to be something separate from the gazillions of mitochondria.

[niner]

niner... Do you still maintain the position that deviating from the Buckyball study protocol by using an MCT Oil vs. the study choice of a PUFA is a choice of no consequence? Inquiring minds want to know... If you do still maintain that position, please provide the rationale and supporting study link support for your view...

I never maintained that position in the first place. My personal choice, were I to try this, would be a PUFA. I would most likely use olive oil. As I mentioned yesterday, my working assumption, and I'll note that it's a hypothesis at this point, is that a fullerene / fatty acid adduct is the active species. I think you would get easier adduct formation with an unsaturated oil. The Russian paper (Pogorelij et al.) says that adduct formation is easier with PUFA than with MUFA, which is consistent with a Diels Alder mechanism, subsequent to a rearrangement in the fatty acid to a conjugated diene.

[Turnbuckle]

But how do we not know that the Buckyballs do their magic in the liver rather than the individual mitochondria throughout the body? There simply wasn't enough Buckyballs ingested in relation to the number of mitochondria in the body....not even close....it's got to be something separate from the gazillions of mitochondria.

Have you ever heard of Avogadro's number? There's plenty enough C60 to do the job.

10E12 cells in the human body and 1000 mitochondria/cell = 1.0E16 mitochondria
20 mg C60 = .00003 mole = 1.7E19 molecules
Which is 1,700 C60 molecules/mitochondria

Edited by Turnbuckle, 17 May 2012 - 01:46 PM.

[Turnbuckle]

Assuming my hypothesis that C60 acts to strip methyl groups from the mitochondrial DNA is correct, then curcumin (which I've taken for some time) might act synergisticly--

Genomic DNA was extracted from a leukemia cell line exposed to curcuminoids at concentrations of 0, 1, 3, and 30 μM for 72 hours. Analyses of global DNA methylation levels showed stability at 1 μM curcumin, but decreased by approximately 15% to 20% at 3 μM and 30 μM curcumin compared with untreated basal methylation levels, which was equivalent to decitabine-induced decreases in global DNA methylation levels. These data show that curcumin is a potent DNA hypomethylating agent, which is consistent with its broad activity in inflammation, cancer, and many other diseases, while remaining relatively safe in normal healthy cells.

Development of curcumin as an epigenetic agent.

[HighDesertWizard]

Assuming my hypothesis that C60 acts to strip methyl groups from the mitochondrial DNA is correct, then curcumin (which I've taken for some time) might act synergisticly--

Genomic DNA was extracted from a leukemia cell line exposed to curcuminoids at concentrations of 0, 1, 3, and 30 μM for 72 hours. Analyses of global DNA methylation levels showed stability at 1 μM curcumin, but decreased by approximately 15% to 20% at 3 μM and 30 μM curcumin compared with untreated basal methylation levels, which was equivalent to decitabine-induced decreases in global DNA methylation levels. These data show that curcumin is a potent DNA hypomethylating agent, which is consistent with its broad activity in inflammation, cancer, and many other diseases, while remaining relatively safe in normal healthy cells.

Development of curcumin as an epigenetic agent.

Turnbuckle...

You may recall that I posted the figure below with a reference to the way that 5-Lipoxygenase (5-LO) inhibitors reduced ROS (and, btw, Olive Oil inhibits ROS and Curcumin also is a profound 5-LO inhibitor). The implication for longevity is clear given the Sirt1 refrence in the figure... I was thinking that your hypothesis must be consistent with mine. We can both find study backing for them. I've imagined that the difference in our hypotheses must have to do with some Unit of Analysis Level question or some internal process sequence issue. Hopefully, you and I and others can keep this kind of discussion going.

I absolutely believe that the *explanation* for the Buckyball study result already exists implicitly in the literature. If we discuss it, even argue about it, we can find that explanation. And in finding that explanation, can we come up with some *home remedy* sorts of approaches, clearly non-toxic, that might be beneficial? I think we might... Looking for more discussion...



Truth is, I don't understand what the heck methylation is and so, well, I thought I'd do a little google scholar about it... A few choice studies...

Epigenetic Changes Induced by ReactiveOxygenSpecies in Hepatocellular Carcinoma: Methylation of the E-cadherin Promoter

ReactiveOxygenSpecies (ROS)––Induced genetic and epigenetic alterations in human carcinogenesis

And there's this from...

http://www.hindawi.c...gi/2010/302051/

[HighDesertWizard]

Turnbuckle... re: Curcumin... I've got two bottles with me all the time. One Curcumin 95, the other Curcumin C3. I take both just to be sure that I've taken both. I just became aware recently that Revgenetics sells Sky Curcumin. What do you recommend?

[HappyPhysicist]

I have been taking C60/OO for about 8 days now, approximately 10 mg per day = 10 mg/85 kg = 0.01 mg/kg.

For some reason I can't edit my post. There was a typo. Should have been 0.1 mg/kg.

[Mind]

Assuming my hypothesis that C60 acts to strip methyl groups from the mitochondrial DNA is correct, then curcumin (which I've taken for some time) might act synergisticly--

Genomic DNA was extracted from a leukemia cell line exposed to curcuminoids at concentrations of 0, 1, 3, and 30 μM for 72 hours. Analyses of global DNA methylation levels showed stability at 1 μM curcumin, but decreased by approximately 15% to 20% at 3 μM and 30 μM curcumin compared with untreated basal methylation levels, which was equivalent to decitabine-induced decreases in global DNA methylation levels. These data show that curcumin is a potent DNA hypomethylating agent, which is consistent with its broad activity in inflammation, cancer, and many other diseases, while remaining relatively safe in normal healthy cells.

Development of curcumin as an epigenetic agent.

Turnbuckle...

You may recall that I posted the figure below with a reference to the way that 5-Lipoxygenase (5-LO) inhibitors reduced ROS (and, btw, Olive Oil inhibits ROS and Curcumin also is a profound 5-LO inhibitor). The implication for longevity is clear given the Sirt1 refrence in the figure... I was thinking that your hypothesis must be consistent with mine. We can both find study backing for them. I've imagined that the difference in our hypotheses must have to do with some Unit of Analysis Level question or some internal process sequence issue. Hopefully, you and I and others can keep this kind of discussion going.

I absolutely believe that the *explanation* for the Buckyball study result already exists implicitly in the literature. If we discuss it, even argue about it, we can find that explanation. And in finding that explanation, can we come up with some *home remedy* sorts of approaches, clearly non-toxic, that might be beneficial? I think we might... Looking for more discussion...



Truth is, I don't understand what the heck methylation is and so, well, I thought I'd do a little google scholar about it... A few choice studies...

Epigenetic Changes Induced by ReactiveOxygenSpecies in Hepatocellular Carcinoma: Methylation of the E-cadherin Promoter

ReactiveOxygenSpecies (ROS)––Induced genetic and epigenetic alterations in human carcinogenesis

And there's this from...

http://www.hindawi.c...gi/2010/302051/

There is also this older Longecity discussion about epigenetic methylation and aging.

[Turnbuckle]

Turnbuckle... re: Curcumin... I've got two bottles with me all the time. One Curcumin 95, the other Curcumin C3. I take both just to be sure that I've taken both. I just became aware recently that Revgenetics sells Sky Curcumin. What do you recommend?

I'll bet Anthony could recommend one.

[HighDesertWizard]

I've written upthread that I know a bit about 5-Lipoxygenase. A reminder about it's importance...

• The LEF said earlier this year that it was involved in 7 of the 10 most lethal diseases in the US.

• A study of more rapid aging in space--up to 10 times--found 5-LO to be the probable cause.

• Curcumin is a 5-LO inhibitor.

• And my own list of 5-LO diseases... one abstract per disease

That said, it occurred to me likely that other 5-LO inhibitors are also likely DNA hypomethylating agents. Here's a sample of the literature I pulled out pretty quickly.

Boswellia
http://www.landesbio.../article/19604/

Quercetin
http://pubs.rsc.org/...1/FO/c1fo10049a

Polyphenols
http://www.sciencedi...308814611013860

Silymarin, Green Tea and Several Other Polyphenols
http://www.dkfz.de/e...a-Gerhauser.pdf

Finally, a nuanced but relevant and important point from a Youtube TED Talk...

William Li says that "food anti-angiogenesis synergy" (aka 5-LO inhibitor synergy) has a more powerful effect than merely one anti-angiogenesis food.. (beginning at 12:55)
http://www.youtube.com/watch?v=B9bDZ5-zPtY

------------------------
I understand Turnbuckle to say that Curcumin is complementary to Buckyball activity. Does that mean the action of the Olive Oil was irrelevant?

just trying to put more data on the table here that's related to the discussion to get more insight...

Edited by wccaguy, 17 May 2012 - 07:54 PM.

[HappyPhysicist]

Some picts of C60/MCT before and after 1 day of mixing.

Attached Files

•  MCT after.jpg   100.57KB   17 downloads
•  MCT before.jpg   147.14KB   16 downloads

Edited by HappyPhysicist, 17 May 2012 - 08:52 PM.

[Junk Master]

I've been doing some preliminary reading/research on C60 and can't find any reason to not go the "low tech" Turnbuckle route. Are there any studies I should read that show toxicity?

I like the idea it might even be liver protective, at least in aqueous suspension--

"Other studies could not establish the toxicity of fullerenes: on the contrary, the work of Gharbi et al. (2005)^[46] suggested that aqueous C₆₀ suspensions failing to produce acute or subacute toxicity in rodents could also protect their livers in a dose-dependent manner against free-radical damage."

[Krell]

I am training for my annual 5k road race on June 2. Since I have about 10 years of race history and this race is electronically timed, I am thinking about using it to test C60/OI.

My 500ml of Bertolli Extra Light Olive Oil + 0.40 grams of SES C60 has been mixing for 8 days, so it should be ready in time for the race.

I am going the "low tech" Turnbuckle route with occasional hand shaking to encourage mixing.

Edited by Krell, 17 May 2012 - 09:30 PM.

[Junk Master]

Excellent! Reading some Russian studies using C60 in aqueous suspension that mentions they help red blood cell levels return post chemo.

Here's a study of toxicity of INHALED C60 on rats. Apparently, nothing to worry about.

http://toxsci.oxford.../101/1/122.full

[Anthony_Loera]

I work at RevGenetics, so I am a bit biased when it comes to the Sky Curcumin.

Dr V has sent me a Vaccum filtration system "rapid 500" by TPP for small samples, however for ongoing filtration of multiple liter samples I am looking at a larger system to see if it's feasible, and start making it available.

Cheers
A

[nowayout]

Curcumin is well known to be estrogenic. It may not be a suitable supplement for at least some men, if not all men.

[niner]

I am training for my annual 5k road race on June 2. Since I have about 10 years of race history and this race is electronically timed, I am thinking about using it to test C60/OI.

My 500ml of Bertolli Extra Light Olive Oil + 0.40 grams of SES C60 has been mixing for 8 days, so it should be ready in time for the race.

I am going the "low tech" Turnbuckle route with occasional hand shaking to encourage mixing.

Thanks for posting. I think the light olive oil is a good choice in this case because you can evaluate colors a lot easier. What does it look like? Are all the solids dissolved? You might want to start dosing soon in order to evaluate mitochondrial biogenesis. I don't think that would happen overnight. I don't really know what will happen to your athletic performance. You might get a boost, or it might be that if you're already in good shape, you won't notice that much. Maybe your recovery will be accelerated. Or not... Keep us posted on your dosage schedule and observations.