144 replies to this topic

[Hebbeh]

http://www.scienceda...30621141806.htm

[Logic]

Think about cancer not as a disease but as big wall of cells that are chained by their genes to their place. All of them want to be free, but are blocked by many ways to stay in that wall to serve a “higher purpose”. Mutations happen. Great majority will do nothing since we are descendants of cells that had multiple redundant systems just because those cells survived compared to those that didn’t. The “higher purpose” demands that cells stay in that wall under threat of enforced suicide (enforced by mitochondria) or murder (macrophage).

But time goes on. Mutations in all those cells accumulate but the wall stands. Once, by chance, one of those billions of cells gets mutations that it enables to: ignore suicide, trick immune system not to kill it, enables telomerase and things like that it becomes “free”. It can finally start to do what it did before it became multicellular organism. It’s all about natural selection and evolution from then on. Those cells that don’t have mutations that will enable it to survive are killed and those that aren’t – those multiply further and further in mindless quest to pass on their genes into the next generation until it kills its “higher purpose”

Yes that means that are infinite number of types of cancer, but they are shaped by natural selection to share some similar traits. Those traits allow them to survive and multiply. It’s just that those specific cells are supposed to be “disposable soma” and are not supposed to do that. Your body is a “disposable soma” also, made to last about 80 years, have children and then die. There is no rule that you must die. If you take care of your body you will live as long as you live.

This is pretty much how I think of cancer too, but add to that silenced viral DNA that we inherit from our parents and DNA modified by virii.
I think that sometimes when DNA is modified by a virus the silenced, inherited viral DNA is somehow "turned on' again too and that this can lead to complicated health issues and sometimes cancer.
(Other things like toxins, short telomeres and heavy metals may also cause the activation of this silenced DNA)

As over 50% of virii are lipid coated and a bigger percentage of cancer causing virii seem to be lipid coated, it just makes sense to me to take supps that strip off this lipid layer.
This exposes the virus to the immune system for what it is rather than a nutrient and disables the virus's ability to dock with and infect cells.

Both Coconut Oil and BHT have this ability.
Niner is going to ask me how much Coconut Oil it takes to get this effect again and I am going to have to say I don't know, but that people seem to have success fighting Hep C, HSV and Flu at around 3 tablespoons per day.

I digress; my question remains:
Is the 'turning off' of mitochondria common to all cancers???

[Logic]

One thing to bear in mind is that Baati's rats got huge doses, relative to what most of us take. Anthony Loera was trying to match the rats on a mg/kg basis, and he was taking 140mg at a shot. If you use the "human equivalent dose" calculations, you would divide that by 6, giving 23mg per dose. However, those rules may or may not apply to membrane lipid turnover, which I think is the key factor here. Essentially, the rats got really saturated with c60-oo during the 7 month dosing phase, and it took a long time to drop down to a level that was no longer protective. With all this discussion of cycling c60, it would be good to know what the long term pharmacokinetics are.

Logic, how much were you taking, and how long after you stopped did you notice those effects falling off? A few months back, I had a pause in my c60 use while I was sorting out some GI issues. (antibiotic-induced...) I thought I had enough on board to carry me through, but I noticed a change in my response to alcohol, and, annoyingly, my eczema that c60 had finally cleared up suddenly came back. (that sucked...) Also annoyingly, I had gotten complacent about recording my doses, so I don't know exactly when I stopped. What I do know is that at the level I'd been dosing at, the protective effects go away in some number of weeks. I've since raised my dose, and the eczema is back under control. I'd been taking a fairly minimal dose before- 15mg/month. I've doubled that to 30/month.

I wish I had decent answers for you Niner.
The fact is that the Xmass season devolved into a haze of parties and my memory leaves a lot to be desired even without that confounding factor.
I was taking both C60oo and Epitalon and this had a perhaps too positive effect on my mood and outlook, (Can Do!!!) which is why I am loth to update my log.

I pretty much followed the Baati schedule with a week long loading phase around November, then weekly dosing, more or less, over the Xmass period.

I ran out of both some time in January.

Dosing is equally vague:
I took around a teaspoon-full at a time, but used a tablespoon to avoid messing, so probably 5 to 8 ml of carbon's product per dose.

I stopped partying soon after new years, but also went to gym very seldom due to having caught the attention of a young lady...

At a guess I would say that I was back to baseline within 2 months.

[niner]

It sounds like you must have had a 100ml bottle. Does that sound right to you?

[Logic]

It sounds like you must have had a 100ml bottle. Does that sound right to you?

About 150 ml: 3 bottles shared.

[mikeinnaples]

Tests for C60 were conducted on the blood, urine, liver, spleen, lungs and brain. When dissected the rats showed c60 in the spleen, brain and in the liver. There was no evidence of the c60 in the lungs. Presence of c60 in the brain demonstrates its ability to traverse the blood brain barrier. The time it takes the c60 to reach one half of the amount of the peak concentration in the blood shows that c60 is completely eliminated after 97 hours from the blood stream. The lack of c60 in the organs after 7 daily administrations of c60-oo shows that all of the c60 clears the organs a few hours after oral consumption. The presence of c60 had little effect if any in the spleen and the liver. In fact it was proven that the presence of c60 was a powerful agent in protecting the liver. The c60-oo is digested, later excreted through the bile duct and is eliminated through the feces. This would indicate to me the c60 that is eliminated is still clinging to a lipid form (olive oil) since that is how lipids are excreted from the body. No c60-oo is excreted through the urinary tract. Basically c60-oo was demonstrated to be extremely non-toxic and demonstrated super anti-oxidant effects.

I know this is in another discussion topic and it is bad form to do what I am doing, but it is relevant and wasn't really commented on there. The link to Solar's post is here.

[solarfingers]

I know this is in another discussion topic and it is bad form to do what I am doing, but it is relevant and wasn't really commented on there. The link to Solar's post is here.

Not sure if the citation belongs or not... It is from the actual paper. Is there a point or a question that you are using it to reference?

[taho]

Is the 'turning off' of mitochondria common to all cancers???

Almost all cancers have changed mitochondria metabolism. Why, how, can be best described as natural selection of “feral” cells that didn’t get eliminated. This is the evolutionary pressure and “reason” in a development of cancer. It is driven by change. Change caused by.. something.

Perhaps you should read Vincent's work "PART 1: Slaying Two Dragons with One Stone – How to Prevent Cancer and Aging with the Same Strategy"

Well, I like this article. It has good point that cancer and aging share many same things. And they do. It has a list of usual suspects: resveratrol, curcumin, ECGC, metformin and so on. What this combination won’t do is stop aging. Why? Because people have been consuming those things for thousands of years and all of them are no longer alive. If some good combination would work, odds are somebody would have found it by now. What those things do show is moderate extension in lifespan and better health. And if you look deep enough, you get to Nrf-2 and this is how I think they work. Many cancers have Nrf-2 turned on. It makes good evolutionary sense for them to upregulate production of ROS defenses. It makes those cells that much harder to kill, so they survive and multiply. ROS = (almost always) bad. Nrf-2 = (probably always) good.

What I am suggesting is that C60oo is special compared to all those usual suspects. It stops the change. Change caused by.. ROS. Change to mitochondria. Change to cell environment. Change to DNK. Change to cells from extracellular ROS (from lipofuscin, infections, radiation,..). By inbeding itself into lipid membranes it stops ROS chain reactions there. C60 is a special molecule unlike anything that we usually consume in its property to be catalisatic ROS scavenger. C60oo is special that it looks like food and is transported around the cells without much fuss and then it sticks around. It’s good. It’s very good.

But, is too much of a good thing, good?
What if there are no more ROS in the cytosol?
What happens to Nrf-2, NF-kB and other things that turn on/off depending on amount of ROS?

Ok, change is greatly reduced. That would explain no-cancer and long life of rats. But, rats could live 30 years or more if there would be evolutionary pressure for them to do so. Naked mole rats are not much different then them and they do live that long.

According to “disposable soma” theory:
- rats have low ROS defenses because they don’t need much better one.
- birds have better mitochondria because they need them.
- humans have high ROS defenses because we need them
- cancer cells have even higher ROS defenses because they need them

According to “disposable soma” theory, the one thing that is predicted is that cells only serve the whole body to serve genes. Cells only use as much resources to repair themselves as is needed to serve the interests of survival and replication of genes. If that “mission” means that the cell will die – it will and it must. If that means that its defenses are not 100% because genes would rather invest resources into making new body, then this is and must happen.

So, does our body work like that and downregulates ROS defenses because “it is not needed”?

Can we have bird like mitochondria (with c60oo) and cancer like ROS defenses (upregulated Nrf-2) without killing ourselves by some side affects?

Edited by taho, 24 June 2013 - 05:03 PM.

[solarfingers]

Perhaps you should read Vincent's work "PART 1: Slaying Two Dragons with One Stone – How to Prevent Cancer and Aging with the Same Strategy"

Well, I like this article. It has good point that cancer and aging share many same things. And they do. It has a list of usual suspects: resveratrol, curcumin, ECGC, metformin and so on. What this combination won’t do is stop aging. Why? Because people have been consuming those things for thousands of years and all of them are no longer alive. If some good combination would work, odds are somebody would have found it by now. What those things do show is moderate extension in lifespan and better health. And if you look deep enough, you get to Nrf-2 and this is how I think they work. Many cancers have Nrf-2 turned on. It makes good evolutionary sense for them to upregulate production of ROS defenses. It makes those cells that much harder to kill, so they survive and multiply. ROS = (almost always) bad. Nrf-2 = (probably always) good.

What I am suggesting is that C60oo is special compared to all those usual suspects. It stops the change. Change caused by.. ROS. Change to mitochondria. Change to cell environment. Change to DNK. Change to cells from extracellular ROS (from lipofuscin, infections, radiation,..). By inbeding itself into lipid membranes it stops ROS chain reactions there. C60 is a special molecule unlike anything that we usually consume in its property to be catalisatic ROS scavenger. C60oo is special that it looks like food and is transported around the cells without much fuss and then it sticks around. It’s good. It’s very good.

You ask some very good questions and your grasp of biochemistry is a magnitude greater than mine. I can only gleam answers from others and don't even pretend to know what I am talking about. When we look at aging there is obviously more than one thing going on as Niner had suggested to me in another thread. Cancer is just one of those things that must be dealt with to either achieve some longevity or immortality. So, I am very much in agreement with you. I certainly hope c60 is doing much good and having super bird-like mitochondria sounds advantageous. Let's you and I get together over a beer in 2050 and discuss it...

[taho]

I don't know everything. Far from it. That's why I ask those questions. Maybe we will get some new answers that we can use. I do try to look at the big picture. Far too often we can't see the forest because we are looking at all those trees. Simplify, find a big picture then go looking what doesn’t fit into that big picture.

So.. about that Nrf-2 v ROS? Yes/No? Anyone want to take some wild guesses?

[niner]

So.. about that Nrf-2 v ROS? Yes/No? Anyone want to take some wild guesses?

Nrf2 is a transcription factor that increases the expression of some antioxidant genes. Keap1 is a protein that acts as a sensor of oxidative stress- under low stress conditions, it degrades Nrf2. Under high stress conditions, it allows Nrf2 to build up in the cytosol, which leads to it getting into the nucleus and acting as a transcription factor. So basically Nrf2 is a major part of the system that responds to oxidative stress. I'm not sure I understand the question...

[taho]

Nrf2 is a transcription factor that increases the expression of some antioxidant genes. Keap1 is a protein that acts as a sensor of oxidative stress- under low stress conditions, it degrades Nrf2. Under high stress conditions, it allows Nrf2 to build up in the cytosol, which leads to it getting into the nucleus and acting as a transcription factor. So basically Nrf2 is a major part of the system that responds to oxidative stress. I'm not sure I understand the question...

There is a constant trickle of free radicals from mitochondria. My thinking is, that C60oo could reduce ROS production to such a low level, that the body would reduce systems that neutralize H2O2, reduce amount of enzymes like SOD, reduce DNK repair, reduce protein chaperones and those 200 genes that are regulated by Nrf2.

What would happen if that trickle of free radicals would come to a complete stop?

Wouldn’t it be better to have more defenses that would be mostly idle, then too little defenses because free radicals as a signal molecule isn’t working as it normally would?

If you blocked Keap1 and upregulated Nrf2 as high as possible, what effect would this have on a lifespan and health?

Edited by taho, 25 June 2013 - 03:35 AM.

[taho]

Ok, let’s play the “hypothetically it would work” game with unknown substance by looking at it from the “form follows function” maxim. Yes, most of the biochemists, philosophers and English majors will disapprove my way of using things, but, let’s try anyway. If anyone has any comments I would sure like to know them..

So, we have this new thing called C60-oo that looks like something that would not be used even in the 19^th century by quacks to describe “snake oil”. It sounds so good that even then the people would go “C’mon, this can’t be true. You are a crook out to get our money. Hang him!”. It will extend life, it will prevent cancer, it will make you smarter, it will make you stronger, it will make your lungs better, your blood run better, your hair grow better, prevent CVD, diabetes, Alzheimer’s, Parkinson’s and will make you survive nuclear war if it ever happens.

Could it be so? Well, there is no technical reason why it could not be true and we could live more then 122 years. If the trees could talk, they would tell us that we are amateurs when it comes to that survival stuff. They would of course complain, but their complaints would go something along the lines of “well, that firecracker at Nagasaki burnt my leaves. How rude was that. I had to grow new ones and it was not even spring. And those roman legions: let me tell you story about them..” (ginkgo’s have survived few km from the nuclear blast, and they can live hundreds even thousands of years).

So, “form follows function”. If the function of the body is to survive xx years, then this is what the form of that body will be. That is a nice way of getting past our incomplete knowledge of our own body. Maybe in 100 years we will know everything how it works, but we are not there yet. But, let’s try anyway.

Let’s simplify and say that C60-oo works and that it works by stopping ROS. What would that mean? Well, if our body would be system called “Country” how would things work there?

Immune system/damage control would be this semi-independent really paranoid industrial military complex. But as a saying goes if you are paranoid, that doesn’t mean that they are not out to get you, because they most certainly are. It’s a non-stop war against microbes, toxins, viruses, fungi, ROS, radiation, miss folded proteins, lipofuscin and anything else you can think of. It’s all there and it’s war 24/7. Now, you suddenly sprinkle some magical pixie dust and it’s a lot quieter all of a sudden. It’s a celebration, peace dividend, mass demobilization, retooling of factories to make ploughshares instead of swords and so on. The pixie dust protects and protects really good. But, what happens if there would exist a military threat that pixie dust just wouldn’t protect? What if you can afford to keep a large standing army because well you can have it and use it in full extend in case of emergencies. Yes, but, this army is special. It has a mind of its own. It can start shooting civilians because they all wear some weird hats. It can start to kill it’s own citizens because it’s a imaginary unlogical system that happens to do that sometimes (autoimmune disease). How do you keep your army ready and keep it from getting nuts. Well.. you put them on maneuvers. That will keep them occupied and ready to fight when the real war breaks out. But since it is a fake war, there is no damage being done.

Nrf2 activation / Keap1 inhibition would be that kind of fake war. Some combination of substances would keep your immune system/damage control in fighting condition. Which kind? Well, it could go from benign like lots of vegetables and physical activity, through more potent stuff (resveratrol, curcuma, metformin) to some quite dangerous stuff (dimethyl fumarate). This could theoretically possibly put things in the balance thus help in everything.

As for the cancer: It will possibly prevent it, but if you have it already you are in big trouble as it is. If the strains of cancer that have Nrf2 activated is any indication, then C60-oo will help it survive. But then, it could possibly help every cell in the body survive better and that means that you can increase radiation dosages/poisons to levels that would otherwise kill you and you will fry the cancer while the rest of the cells will get minimal damage. It depends on what kind of cancer you have and how you treat it.

The rest of my concerns are related to vitamin D synthesis (you need UV light to make it). C60-oo could reduce vitamin D levels and it is probably prudent to check how it is. It could act as a amplifier of light by making free radicals in the skin. That would increase photo damage to the skin, increase the chances of melanoma and could possibly even make you blind. It’s unlikely but it is a hypothetical concern. Then there is the unknown effects on the NF-kB and infection. If could possibly delay immune system’s response through reduced inflammation. And there could be more things since we are not quite rats and have better defenses..

What else could go wrong?

Edited by taho, 28 June 2013 - 01:12 PM.

[Turnbuckle]

C60 is a special molecule unlike anything that we usually consume in its property to be catalisatic ROS scavenger.

Actually, C60 in oil acts as a sacrificial antioxidant. It oxidizes and its antioxidant capacity is used up over time.

Unsaturated lipids when exposed to air at room temperature undergo a slow autoxidation. When fullerene C60 was dissolved in selected lipids (ethyl oleate, ethyl linoleate, linseed oil and castor oil) the spectrophotometric analysis shows that the oxidation is concentrated to C60 which is converted to an epoxide C60O.

http://www.sciencedi...009308410000496

C60 derivatives are known that do have catalytic properties--

Development of small molecules capable of eliminating reactive oxygen species, such as superoxide and H2O2, has been an important recent focus of biomedical research. We previously reported that malonic acid derivatives of buckminsterfullerene (C60) exhibit superoxide scavenging properties, as determined by electron paramagnetic resonance (EPR) spectroscopy. We have subsequently determined that one such C60 derivatives, the e,e,e tris malonic acid isomer (C3) is a catalytic scavenger of both superoxide and hydrogen peroxide, with a ki for superoxide of 3 x 106.

http://www.electroch...3/pdfs/1639.pdf

Edited by Turnbuckle, 28 June 2013 - 02:00 PM.

[taho]

C60 is a special molecule unlike anything that we usually consume in its property to be catalisatic ROS scavenger.

Actually, C60 in oil acts as a sacrificial antioxidant. It oxidizes and its antioxidant capacity is used up over time.

It's my understanding that C60 can capture and give electrons, thus can serve as a catalyst in the neutralization of free radicals, like it was discussed here. Is that not the case?

[Turnbuckle]

C60 is a special molecule unlike anything that we usually consume in its property to be catalisatic ROS scavenger.

Actually, C60 in oil acts as a sacrificial antioxidant. It oxidizes and its antioxidant capacity is used up over time.

It's my understanding that C60 can capture and give electrons, thus can serve as a catalyst in the neutralization of free radicals, like it was discussed here. Is that not the case?

I see people writing equations, but where is the experimental evidence?

[taho]

C60 is a special molecule unlike anything that we usually consume in its property to be catalisatic ROS scavenger.

Actually, C60 in oil acts as a sacrificial antioxidant. It oxidizes and its antioxidant capacity is used up over time.

It's my understanding that C60 can capture and give electrons, thus can serve as a catalyst in the neutralization of free radicals, like it was discussed here. Is that not the case?

I see people writing equations, but where is the experimental evidence?

Here is the mode of action on a similar molecule. It is described as catalytic dismutation of superoxide. But as for the specifics in C60-oo, this is little beyond my knowledge and will need someone else to answer that question.

http://www.ncbi.nlm....pubmed/15451059

Superoxide, a potentially toxic by-product of cellular metabolism, may contribute to tissue injury in many types of human disease. Here we show that a tris-malonic acid derivative of the fullerene C60 molecule (C3) is capable of removing the biologically important superoxide radical with a rate constant (k(C3)) of 2 x 10(6) mol(-1) s(-1), approximately 100-fold slower than the superoxide dismutases (SOD), a family of enzymes responsible for endogenous dismutation of superoxide. This rate constant is within the range of values reported for several manganese-containing SOD mimetic compounds. The reaction between C3 and superoxide was not via stoichiometric "scavenging," as expected, but through catalytic dismutation of superoxide, indicated by lack of structural modifications to C3, regeneration of oxygen, production of hydrogen peroxide, and absence of EPR-active (paramagnetic) products, all consistent with a catalytic mechanism. A model is proposed in which electron-deficient regions on the C60 sphere work in concert with malonyl groups attached to C3 to electrostatically guide and stabilize superoxide, promoting dismutation. We also found that C3 treatment of Sod2(-/-) mice, which lack expression of mitochondrial manganese superoxide dismutase (MnSOD), increased their life span by 300%. These data, coupled with evidence that C3 localizes to mitochondria, suggest that C3 functionally replaces MnSOD, acting as a biologically effective SOD mimetic.

another link that goes into specifics of catalytic Antioxidants:
http://www.ncbi.nlm....les/PMC2933572/

[Turnbuckle]

Here is the mode of action on a similar molecule. It is described as catalytic dismutation of superoxide. But as for the specifics in C60-oo, this is little beyond my knowledge and will need someone else to answer that question.

http://www.ncbi.nlm....pubmed/15451059

That's the same derivative I linked to above in post 134, but it's not C60 in oil.

[taho]

There is some quite similar molecule that is in fact being shown to work as a catalytic antioxidant. The precise structure is not known because nobody has went though all the trouble to find out what kind of structures are found in C60-oo and published that data in a peer reviewed journal. Effects on rats are more consistent with C60-oo being catalytic antioxidant then a sacrificial antioxidant based on time delay till death. What a true nature of C60-oo is not known, but that still doesn’t change the fact that it apparently works very well.

So, the question is still valid. What would happen if the amount of free radicals that influence Keap1 / Nrf2 pathway falls to very low level and that leads to down-regulated ROS defenses?

Do you have any comments on that matter?

Edited by taho, 28 June 2013 - 09:19 PM.

[niner]

The following isn't experimental- it's a fairly sophisticated quantum mechanical study of the reaction mechanism for fullerene-catalyzed dismutation of superoxide. The mechanism they propose should work with a c60-fatty acid adduct. Being in a less-solvated hydrophobic membrane environment should make it work even better, since the superoxide anion wouldn't be as stable in a less-aqueous environment.

Chemistry. 2010 Mar 8;16(10):3207-14. doi: 10.1002/chem.200902728.
On the mechanism of action of fullerene derivatives in superoxide dismutation.
Osuna S, Swart M, Solà M.

Institut de Química Computacional and Departament de Química, Universitat de Girona, Campus Montilivi, 17071 Girona, Spain.

We have studied the mechanism of the antioxidant activity of C(60) derivatives at the BP86/TZP level with inclusion of solvent effects (DMSO) by using the COSMO approach. The reaction studied here involves degradation of the biologically relevant superoxide radical (O(2)(*-)), which is linked to tissue damage in several human disorders. Several fullerene derivatives have experimentally been shown to be protective in cell culture and animal models of injury, but precisely how these compounds protect biological systems is still unknown. We have investigated the activity of tris-malonyl C(60) (also called C(3)), which efficiently removes the superoxide anion with an activity in the range of several biologically effective, metal-containing superoxide dismutase mimetics. The antioxidant properties of C(3) are attributed to the high affinity of C(60) to accept electrons. Our results show that once the superoxide radical is in contact with the surface of C(3), its unpaired electron is transferred to the fullerene. This process, which converts the damaging O(2)(*-) to neutral oxygen O(2), is the rate-determining step of the reaction. Afterwards, another superoxide radical reacts with C(3)(*-) to form hydrogen peroxide and in the process takes up the additional electron that was transferred in the first step. The overall process is clearly exothermic and, in general, involves reaction steps with relatively low activation barriers. The capability of C(3) to degrade a highly reactive oxygen species that is linked to several human diseases is of immediate interest for future applications in the field of biology and medicine.

PMID: 20119990

[niner]

C60 is a special molecule unlike anything that we usually consume in its property to be catalisatic ROS scavenger.

Actually, C60 in oil acts as a sacrificial antioxidant. It oxidizes and its antioxidant capacity is used up over time.

Unsaturated lipids when exposed to air at room temperature undergo a slow autoxidation. When fullerene C60 was dissolved in selected lipids (ethyl oleate, ethyl linoleate, linseed oil and castor oil) the spectrophotometric analysis shows that the oxidation is concentrated to C60 which is converted to an epoxide C60O.

http://www.sciencedi...009308410000496

But that oxidation happens in a high-oxygen tension environment, possibly with some UV around. In the body, there isn't all that much free O2 around. Such a reaction could still occur at a low rate, and maybe that has something to do with the need to take more c60-oo every couple weeks or months, depending on dose. It's conceivable that the c60 gradually degrades, but that doesn't mean that it isn't acting as a catalytic antioxidant with respect to superoxide. The c60 is probably still an effective antioxidant even if it's somewhat epoxidized. I would imagine there would be some point at which it was so highly epoxidized that it would cease to function well, but it probably takes a long time to get there, if it ever does.

[mikeinnaples]

So much back and forth on dosing and I feel no more confident on how/how much to dose than I was when I began taking C60.


1. Loading dose, followed by small dose daily for a month. Followed by a month off. (30 days on then 30 days off, would be somewhat quick to return to baseline)

2. Large, all at once dose per month. The would result in a large spike of C60 with a return to baseline over (x amount of days / weeks).

3. The same as #1 & 2 above but every 2 weeks instead.

4. The always-on approach with no period off so C60 is always in your system.


From reading and following everything, I almost think a legitimate case can be made for each of the 4 methods I listed. Personally, I have tried 2 of them already with no (known) ill effects, but who can say what kind of long term effects that would have.

[niner]

So much back and forth on dosing and I feel no more confident on how/how much to dose than I was when I began taking C60.


1. Loading dose, followed by small dose daily for a month. Followed by a month off. (30 days on then 30 days off, would be somewhat quick to return to baseline)

2. Large, all at once dose per month. The would result in a large spike of C60 with a return to baseline over (x amount of days / weeks).

3. The same as #1 & 2 above but every 2 weeks instead.

4. The always-on approach with no period off so C60 is always in your system.


From reading and following everything, I almost think a legitimate case can be made for each of the 4 methods I listed. Personally, I have tried 2 of them already with no (known) ill effects, but who can say what kind of long term effects that would have.

I would argue that these represent two fundamentally different methods. The first three get your membranes sufficiently loaded that you can pass through the next two to four weeks without taking any c60, yet you never fall below the effective concentration. The always-on approach is different on two counts- First, it keeps the membrane concentration constant, while 1-3 should result in a membrane concentration that rises and falls, though presumably staying above the effective concentration. Second, it constantly replenishes the plasma concentration, so there is always (or often) some c60 around that isn't in the membranes. Because there's free c60-oo floating around, it's available for other biological interactions, such as inhibiting an enzyme or otherwise binding to a biological macromolecule. This would be a good way to generate subtle side effects that might have long term consequences.

The first three dosing methods are the closest to Baati, which is the only long term evidence of no harm that we have at this point. Daily dosing is the most experimental, in that regard. I think that a lot of the allure of the daily dosing method comes from peoples familiarity with typical drugs and supplements that have fast pharmacokinetics, requiring dosing anywhere from daily to multiple times a day. There are, however, some drugs that have very slow pharmacokinetics, so you can get away with very infrequent dosing. For example, Actonel, a bisphosphonate, comes in two dosage forms- A pill that you take weekly, or a higher dose pill that you take once a month.

My preference is for intermittent dosing, but there is one dosing regimen that I would argue against- Don't stretch cycles out so far that you fall below the effective concentration. My concern with that is that c60 should be down-regulating our endogenous antioxidant defenses. If you drop below an effective concentration, you'll be left defenseless for some amount of time while your system is upregulating, and this may result in some oxidative damage. Doing this on a regular basis might eliminate the long term benefits of c60. I can't think of any reason why you would lose the ability to upregulate over time, so I don't see a need to regularly exercise that system.

Some people argue that they feel better using daily dosing. Maybe they aren't taking a large enough dose when they try intermittent dosing, maybe they are seeing some sort of non-membrane macromolecule interaction that's producing an effect they like, or maybe it's just a deep seated discomfort with long dosing regimens. Hard to say.

[mikeinnaples]

I pretty much agree with everything you are saying Niner. The source of my struggles wrapping my head around this, which I am sure can be echoed by many of us, is that we don't know what dosage it takes to get C60 to effective concentration or how long it remains at that effective concentration. I do understand the fundamental difference between #'s 1-3 and #4 to some degree, as I separated them that way with intent, but you explained it far more eloquently and expertly than I could have hoped to.

From my purely anecdotal experience, the single large dose followed by a month off didn't produce the same impact that my initial dosing did in my log. Placebo or not, I did at least have measurable and observable results with my initial dosing strategy which was large loading dose over 3 days. I followed that with nothing for 2 weeks and didn't notice any fall off (pure anecdote going forward as I switched up exercise routines and could no longer produce something comparable to baseline). I then began a smaller dose daily for 2 weeks and still didn't notice any decline. I followed that by a month off and I did 'feel' that there was a decline by the end of this period. The next month I hit up the huge initial dose, followed by the rest of the month off. I 'felt' something initially, but it gradually receded over the month completely.

With that said, I will give you my personal conclusion beginning with a base of pure personal anecdote, mixed with a touch of measurable results, and a dash of logic. It seems to me that with Baati's results and reasoning so eloquently detailed by Niner, that a 2 week dosing schedule is optimal for me in regards to risk/reward. Of course this doesn't really answer the question of 'how much' is optimal for a human, but it is a good start. Taking it a step further, in regards to dosage I did have directly measurable results from 45mg. Though I did take more than 45mgs total that initial month (between 55-60mg guestimation), I think it would be a good starting point.

15mg load -> remaining 30mg evenly split over 2 weeks -> 2 weeks off

[ambivalent]

Hi all,

Currently in possession of some c60oo and contemplating stepping into the void at some not too distant point: though I am still somewhat cautious. I have little domain knowledge and as such struggle to establish (personal) entry level criteria for using c60 or indeed for recommending it to other people (i.e. when it appears to be sufficiently low risk). One would imagine it no sooner than a decade away before it is deemed officially safe for humans, benefits established: perhaps that is optimistic. As such, in the meantime, I must take my cues from the good and knowledgeable people inhabiting these forums and the like.

My current intention, for what it is worth, is to take 1.5mg, twice a month. In addition, I plan to initiate a course of resveratrol (advice on levels would be useful: I am a 42 year old healthy male). Since, upon sampling this forum, it appeared that doses of c60 above allometric levels indicated no improvement in short-term efficacy I’d thought it probable that doses below this level would also show to be just as effective and perhaps reduce risk. In any case there seemed little low level dosing being recorded, so I thought it would have value. However, I was concerned, probably through ignorant interpretation, by niner’s remarks, that perhaps a low level dose regime, as I planned, would cause fluctuating regulation of the immune system (since c60 might not be able to establish an effective foothold at low levels), which he indicated would be damaging and offset some of the gains of c60. I am hoping though that my interpretation is false and that it would just be that my immune system would be consistently partially down-regulated: though I really don’t know what I’m talking about!

My intention is to record some simple before and after metrics (vision, hearing, scars etc). I’d also considered, a little reluctantly, to take one for the team as it were, to instigate some repeatable small injury and compare healing rates with and without c60. It seems, from what I’ve read here, there is, in healing rates, potentially a consistently measurable and largely objective metric to be explored. It struck me that this could be one way (especially if a placebo controlled study be put in place) of measuring the efficacy of dosing levels (at least on the axis of healing, I don’t know how optimal healing-levels would inform on other key axis) . So one could, say, establish healing rates when dose-doubling, dose-halving; healing rates when injured within 24 hours of dose, two weeks etc. So perhaps it would be interesting to establish some standardised form of self-injury (and healing criteria) that people would be willing to sign up to and repeat several times.

Thoughts and advice would be greatly appreciated. Thanks in advance.