144 replies to this topic

[Logic]

Logic, What about Alpha Lipoic Acid, isn't it noted for energizing mitochondria as well?

First I have heard of it. Thx; I'll look into that.

Based on these hypotheses it seems like a good idea to take mitochondrial 'kickstarters' prior to and/or during taking C60oo.
Apart from DCA; Mebendazole, a de-worming Medication, and most other microtubule destabilizers, has also been shown to boost OXPHOS expression while suppressing ROS levels.

Let me see if I understand what you're getting at. Are you attempting to up-regulate ATP by boosting OXPHOS expression to keep healthy cells alive while suppressing ROS to choke out cancer cells? Being that Green Tea, PQQ and Resveratrol are all on my list, it might hold that a good time to take c60 is while I'm taking my phytochemical supplements. Sounds logical. Also, anything else that might fall into the MitoSENS category should booster this effect.

No; I think that 'kickstarting' mitochondria that have been switched off in pre/cancerous cells and then protecting them with C60oo will allow them to get their apoptosis signal out; killing the defective cell.
This just seems like a good idea as a means of getting to Baati's 'no cancer' result.

Green Tea, PQQ and Resveratrol are simply supps that I hypothise will have a similar effect to DCA.
There are studies saying that they, and Mebendazole, are anti-cancer and studies showing that they... 'boost' mitochondria, so perhaps part of the reason that they are effective is in their mitochondria 'boosting' properties.

How do you plan to take C60oo and cycle telomerase activators/de-activators given that many of the de-activators in cancer cells are activators in healthy cells?
Resveratrol is a case in point.

[Logic]

I was thinking about a hypothesis that could explain well basically everything. Let’s call it an unified theory of free radicals and disposable soma with an answer why those rats lived 15% longer on olive oil and 90% longer on C60-oo.

Ok, ROS are bad guys. They leak from complex I, III and IV in mitochondria and either damage mitochondria itself or the cell itself. Some of them are very reactive (HO) some of them are quite stabile (H2O2), unless they hit Fe/Cu and become 2 very reactive ones (HO). The rate of production of ROS is somewhere between 0,1 and 10% of consumed 02, but it is generally in the 2-4% range. That generally means 60K "liters of oxygen per kilogram consumed" = death from all those random ROS hits. The exception to that rule are birds which have better mitochondria because of flight and naked mole rats, humans and few deep diving animals that have evolved better defenses against ROS. The reason is hidden in the evolutionary race between high reproducing (low ROS) and long living (high ROS) but handicapped with all those resources that are needed for better ROS defenses. We live only as long as we can improve chanses that "our" genes will live longer then competing ones.

That 60K liters/kg is not a hard limit even in the specific organisms. We can extend that limit by either calorie restriction or with specific chemicals that target some genes. mTOR, FOXO and sirtuins come to my mind. But if you look closer one gene pops up almost always and it’s a nrf-2. Nrf-2 is a strange gene. Type almost any “antioxidant” and it is somehow related to Keap1-Nrf2-ARE pathway. http://onlinelibrary.../med.21257/full lists following substances as activatos: propolis (CAPE), garlic, bardoxolone methyl, diethyl maleate, quercetin, onion, coffe, resveratrol, green tea, rosmarin, broccoli, cabbage, brussel sprouts, arsen, ALA, selen, carrots, tomatos,.. The list goes on if you search pubmed the list goes on.. olive oil, metformin, chocolade, curumin, ashwaganda, boswellia, ginger,.. and let’s not forget exercise, toxins, radiation,..

So what is Nrf2?

It’s a peptide/gene that gets activated when things get oxidized or come under some kind of stress. For example, Bardoxolane methyl oxidizes glutathione. In response the Nrf2 upregulates about 200 cytoprotective genes. Keap1 is it's antagonist making it a homeostatis system. The interesting thing about Nrf2 is that it is inhibited by NAC, E vitamin and C vitamin. It makes sense. Lower ROS = lower Nrf2 activation. What all that means? Well.. if you eat your greens and eat “antioxidants” (toxins!) then you will have higher ROS protection, high free iron neutralization and upregulated gene and system repair. You will live longer, but since those things are everywhere nobody notices that, except if you have rats that eat boring food that just happens to have none of if. In that case small amounts of olive oil will make your rats live 15% longer. And if you test E vitamins (on humans) you will notice that it increases mortality and you will stop test and declare “E vitamin will kill you”. Nope. Lower Nrf2 activation will kill you.

Ok, now, what happens if you discover super-vitamin-E that is catalytic, does not wear out and happens to embed itself into mitochondrial lipid wall and into any other lipid wall (nucleoid wall?), but other than stopping ROS chain reactions and not wanting to leave lipid wall doesn’t do anything. Well, Nrf2 downregulates. It is upregulated only by all those chemical activators, but from ROS; NOTHING. If this would be your E vitamin test, your mice would die from ROS made from H2O2 catalised by Fe/Cu and by low running DNK and system repair. But, our super-vitamin reduces ROS damage to such a low level that it doesn’t matter. Rats live longer. And remember olive oil that is used to “dissolve C60” still has Nrf2 activators. That should help a little on that subject.

Our super-vitamin-E has changed “regular” mitochondrion into “super efficient, more bird like” mitochondrion. In our rats lifespan went from 60K liters/kg oxygen to 114K liters/kg oxygen before death.

Prediction: C60-oo with potent Nrf-2 activators that cause genetic removal of free iron and upregulate repair as much as possible should increase “liters/kg oxyen before death” even higher. And this could be testable even in short lived animals (yeast, flies, worms) since they all have mitochondria that produce ROS, regulate apoptosis (when x of them die, cell kills itself) and have nrf-2 pathway.

An interesting and logical hypothesis Taho. Thx.

[solarfingers]

Logic, What about Alpha Lipoic Acid, isn't it noted for energizing mitochondria as well?

First I have heard of it. Thx; I'll look into that.

Based on these hypotheses it seems like a good idea to take mitochondrial 'kickstarters' prior to and/or during taking C60oo.
Apart from DCA; Mebendazole, a de-worming Medication, and most other microtubule destabilizers, has also been shown to boost OXPHOS expression while suppressing ROS levels.

Let me see if I understand what you're getting at. Are you attempting to up-regulate ATP by boosting OXPHOS expression to keep healthy cells alive while suppressing ROS to choke out cancer cells? Being that Green Tea, PQQ and Resveratrol are all on my list, it might hold that a good time to take c60 is while I'm taking my phytochemical supplements. Sounds logical. Also, anything else that might fall into the MitoSENS category should booster this effect.

No; I think that 'kickstarting' mitochondria that have been switched off in pre/cancerous cells and then protecting them with C60oo will allow them to get their apoptosis signal out; killing the defective cell.
This just seems like a good idea as a means of getting to Baati's 'no cancer' result.

Green Tea, PQQ and Resveratrol are simply supps that I hypothise will have a similar effect to DCA.
There are studies saying that they, and Mebendazole, are anti-cancer and studies showing that they... 'boost' mitochondria, so perhaps part of the reason that they are effective is in their mitochondria 'boosting' properties.

How do you plan to take C60oo and cycle telomerase activators/de-activators given that many of the de-activators in cancer cells are activators in healthy cells?
Resveratrol is a case in point.

Logic,

I find your idea very compelling and it would work well with my idea of cycling telomeres and c60. Turnbuckle has on his profile that he currently takes 4 mg C60-EVOO once a week. Niner takes 15mg of c60-oo once a month. My current telomere cycle is two weeks of activation and two weeks of inhibition. I like the way Niner looks at this picture and have been thinking that taking c60-oo once a month would be a prudent thing since we do not know exactly what effect c60-oo will have on cancer. I also like Turnbuckles idea of giving healthy stem-cells time to proliferate. Basically, with these concerns in mind a daily dosage would not sound like the best idea. So if I decide to take c60-oo once a month when would be the optimal time during my telomere cycle? Yours, Taho's ideas and my current thinking on gene signal silencing would make me believe that the best time to take c60-oo would be once a month at the beginning of my telomere inhibiting cycle. Turnbuckle is taking 16mg a month and Niner is taking 15mg. I will likely follow suite on dosing.

Edited by solarfingers, 22 June 2013 - 04:42 PM.

[Kevnzworld]

I think it's too early to say with any type of accuracy what the best dosing regimen is. I've been doing the one week on, one week off schedule at 12 mg per month, recently raised to approximately 18 since 10/12..
I haven't changed anything else I supplement with because of C60 other than limiting or eliminating anything I took purely for its action as an antioxidant. The exception possibly being gamma E and a buffered ascorbate C.

[solarfingers]

I think it's too early to say with any type of accuracy what the best dosing regimen is. I've been doing the one week on, one week off schedule at 12 mg per month, recently raised to approximately 18 since 10/12..
I haven't changed anything else I supplement with because of C60 other than limiting or eliminating anything I took purely for its action as an antioxidant. The exception possibly being gamma E and a buffered ascorbate C.

Kevnzworld,

I don't disagree with you but I still would like to make an educated decision.

[Hebbeh]

There isn't enough data to warrant even an educated guess.

I've been using C60-EVOO for more than a year. Longer than most with the exception of Turnbuckle....whose subjective experiences differ from mine. Of course Turnbuckle also has a vastly different physiology with differing health conditions than me.

I've experimented over the past year with differing dosing schemes as recommended by others but have settled on daily dosing as I've found that the effects that I can subjectively "feel" as in increased daily energy and in considerably increased exercise endurance and tolerance quickly fade after 2 days of not dosing. I don't know if it is a rebound effect or just that my baseline without C60 is hard to compare to a year on C60 but I seem to struggle through workouts after 2 days without C60 compared to workouts I breeze through on C60. I will stick to daily dosing where I can "feel" positive effects on a daily basis. That's what it is all about to me.

[solarfingers]

I'm only saying in the light of the concerns posted by Turnbuckle and Niner do I make the choice to not take c60 daily. The choice of my timing is based upon other factors which may or may not be happening. If they are not happening... No foul. It they are then I believe my choices are prudent. Go the way of peace. I don't mean to disrespect anyone else or their choices. I am merely speaking for myself and trying to explain them.

[Kevnzworld]

I'm only saying in the light of the concerns posted by Turnbuckle and Niner do I make the choice to not take c60 daily. The choice of my timing is based upon other factors which may or may not be happening. If they are not happening... No foul. It they are then I believe my choices are prudent. Go the way of peace. I don't mean to disrespect anyone else or their choices. I am merely speaking for myself and trying to explain them.

I believe that one of the reasons that some here ( including me )don't dose daily is to allow for homesis.
http://www.anti-agin...-and-longevity/

[solarfingers]

I'm only saying in the light of the concerns posted by Turnbuckle and Niner do I make the choice to not take c60 daily. The choice of my timing is based upon other factors which may or may not be happening. If they are not happening... No foul. It they are then I believe my choices are prudent. Go the way of peace. I don't mean to disrespect anyone else or their choices. I am merely speaking for myself and trying to explain them.

I believe that one of the reasons that some here ( including me )don't dose daily is to allow for homesis.
http://www.anti-agin...-and-longevity/

Do you believe that c60-oo is creating or relieving stress in this process?

[Hebbeh]

There is no evidence that C60 is performing it's magic via hormesis and even if that was a factor, there is no reason that daily dosing wouldn't allow that to occur. Many things that we are exposed to on a daily basis very likely do have a hormesis component (such as exercise or many phytochemicals) but that doesn't mean intermittent dosing is better than daily dosing...quite to the contrary. We all can probably agree that C60 performs it's magic via multiple pathways but the one thing I believe all can agree on is the potent antioxidant capability of C60...especially at the mitochondrial level. And current wisdom indicates that the power of antioxidants is achieved through regular daily dosing so that the antioxidant is able to to quench ROS on a daily basis preventing as much cellular damage as possible. Intermittent dosing very likely doesn't take full advantage of the antioxidant power of C60. Anything else is purely hypothetical speculation. And the only reason Baati's rats weren't dosed daily to the end was not because intermittent dosing was more beneficial but because the dosing by gavage was by definition unduly stressful for the rats and therefor unnecessary to achieve the ends of the intended research. Even Vince suggests that the rats may have lived longer with daily dosing.

http://www.anti-agin...012/11/12/1424/

[solarfingers]

Hebbeh... allot of maybes and what ifs here to go around... You'll likely live past 200 and the rest of us intermittent dosers will all die at 150. If only we had listened.

[Kevnzworld]

There is no evidence that C60 is performing it's magic via hormesis and even if that was a factor, there is no reason that daily dosing wouldn't allow that to occur. Many things that we are exposed to on a daily basis very likely do have a hormesis component (such as exercise or many phytochemicals) but that doesn't mean intermittent dosing is better than daily dosing...quite to the contrary. We all can probably agree that C60 performs it's magic via multiple pathways but the one thing I believe all can agree on is the potent antioxidant capability of C60...especially at the mitochondrial level. And current wisdom indicates that the power of antioxidants is achieved through regular daily dosing so that the antioxidant is able to to quench ROS on a daily basis preventing as much cellular damage as possible. Intermittent dosing very likely doesn't take full advantage of the antioxidant power of C60. Anything else is purely hypothetical speculation. And the only reason Baati's rats weren't dosed daily to the end was not because intermittent dosing was more beneficial but because the dosing by gavage was by definition unduly stressful for the rats and therefor unnecessary to achieve the ends of the intended research. Even Vince suggests that the rats may have lived longer with daily dosing.

http://www.anti-agin...012/11/12/1424/

I didn't mean to imply that C60 was " performing its magic " via homesis, but that daily dosing of an antioxidant as powerful as C60 may prevent homesis.
I agree that all of this is speculative at best. Everyone should read as much as possible and design a protocol based on their own physiology and opinion.

[Hebbeh]

Hebbeh... allot of maybes and what ifs here to go around... You'll likely live past 200 and the rest of us intermittent dosers will all die at 150. If only we had listened.

Actually, you've misjudged my intentions. I have no desire to be immortal in this world or even live past 100 (although my chances are good as most of my relatives on both sides of the family lived well into their 90's and none of them lived a particularly healthy lifestyle IMO). My intentions are driven not by lifespan but rather by health span. I'd much rather die a dignified death at 95 and be active and enjoying life right up to the end rather than live to 150 and having to depend on others for my needs and spend the last 30 years with no quality and unable to either contribute or enjoy my time here. For the ones that plan on living to 150 or 200 and being productive and enjoyable right up to the end....well I wish you the best. For what it's worth, I live in Colorado and enjoy climbing what they call fourteeners here, with 54 14,000 ft peaks in the state to pick from and I would love to go out like Inestine Roberts who died at age 88 while making her 14th and final ascent of 14,110 ft Pikes Peak via the 26 mile round trip Barr Trail. There is a memorial plaque attached to a boulder at 12,000 ft just above treeline and I always enjoy taking a few moments to pay respect to her amazing life and accomplishments...which I would love to enjoy also.

No, I have no desire to live to even 120 but it would be cool to still be mountain climbing at 95 or 100 and pass on the summit....hopefully completing the journey a little quicker.

[free10]

Hebbeh... allot of maybes and what ifs here to go around... You'll likely live past 200 and the rest of us intermittent dosers will all die at 150. If only we had listened.

Actually, you've misjudged my intentions. I have no desire to be immortal in this world or even live past 100 (although my chances are good as most of my relatives on both sides of the family lived well into their 90's and none of them lived a particularly healthy lifestyle IMO). My intentions are driven not by lifespan but rather by health span. I'd much rather die a dignified death at 95 and be active and enjoying life right up to the end rather than live to 150 and having to depend on others for my needs and spend the last 30 years with no quality and unable to either contribute or enjoy my time here. For the ones that plan on living to 150 or 200 and being productive and enjoyable right up to the end....well I wish you the best. For what it's worth, I live in Colorado and enjoy climbing what they call fourteeners here, with 54 14,000 ft peaks in the state to pick from and I would love to go out like Inestine Roberts who died at age 88 while making her 14th and final ascent of 14,110 ft Pikes Peak via the 26 mile round trip Barr Trail. There is a memorial plaque attached to a boulder at 12,000 ft just above treeline and I always enjoy taking a few moments to pay respect to her amazing life and accomplishments...which I would love to enjoy also.

No, I have no desire to live to even 120 but it would be cool to still be mountain climbing at 95 or 100 and pass on the summit....hopefully completing the journey a little quicker.

I think you might be stuck in old world thinking, that long life means long suffering and very long life looks to be on its way barring any catastrophic events.To get to 200 for existence you must be pretty young and in great shape at 150-175 and having lots of fun, for example. It is the declining state of the body and mind that makes most long for death and welcome it IMHO.

Now 100 or so is quite a goal in the sense, as very very few men make it that far currently, but we know from mice age, or damage if you will, can be reversed several different ways, and both studies were done at Harvard just in the last few years. So we are no longer looking at just slowing the ageing and its damage but in the very near future reversing it possibly quite easily.

There is also a type of jellyfish that can revert all the way back to the embryonic state, for the ultimate in aging reversal. This shows this ability exist in more than one species and you can bet your bottom dollar reversal will be the next huge trend. Don't worry though you still won't be "immortal", as the lose your head you will lose your life rule will still apply (Highlander).

[solarfingers]

Actually, you've misjudged my intentions.

Honestly, I'm not judging at all. Just a friendly discussion here. What we are all missing is the premise of this thread. Namely, that c60 could POTENTIALLY allow cancerous cells to divide as long as it is present. The purpose of intermittent dosing would allow natural apoptosis of cancer cells to occur. Logic seems to see a mechanism here to prevent this:

I think that 'kickstarting' mitochondria that have been switched off in pre/cancerous cells and then protecting them with C60oo will allow them to get their apoptosis signal out; killing the defective cell.
This just seems like a good idea as a means of getting to Baati's 'no cancer' result.

The problem with this is if it were so, we run into the problem Turnbuckle is concerned with. Namely that artificially stimulating mitochondria in stem cells COULD cause them to differentiate. There is evidence that suggests it is POSSIBLE that c60 is causing stimulation the mitochondria of cells. If there is no end to this stimulation then the stem cells could potentially differentiate themselves out of existence. We need a break to allow healthy stem cells to differentiate.

I agree with Niner in that the real reason the Baati rats escaped cancer is simply because they started taking c60 at a young age before cancerous cells would have started to appear. c60 was able to prevent cancer from starting in young rats but it would likely not have stopped already progressing cancer in older rats. Niner actually stated a citation that would uphold this premise of cancer in older rats with c60. Albeit, if one has pristine cellular activity and there is no cancer cells present then it is very likely not to be a problem when c60 is started, no matter your age. But, being that an average of 1/4 of the population WILL get cancer in their lifetime we each have a 1 in 4 chance of having cancer cells in our bodies when we start c60. Sounds a little risky not to consider this problem.

So, IF and that is a BIG IF, either of the two scenarios presented by Niner and Turnbuckle are true then intermittent dosing would be prudent. Since it is POSSIBLE that intermittent dosing is less risky in this respect than more frequent dosing, IMHO, intermittent dosing is the most prudent methodology. We might miss the full benefit of taking c60-oo daily but we MAY skirt the possibility of destroying our stem cell population or contracting terminal cancer. I will hold this point of view until it can be demonstrated that neither of the two scenarios are not true.

Edited by solarfingers, 22 June 2013 - 10:38 PM.

[taho]

If C60-oo works its magic by stopping free radicals in mitochondria and in lipid walls, then the fact that it is hydrophobic and lipophilic means that the regime doesn’t matter. This isn’t your typical “antioxidant” that the liver is working hard to remove from the body in the matter of hours. My guess is that it’s not even recognized as anything other then two lipid acids weirdly conjugated together. It gets into lipid wall and stays there for a very long time. If that is the case, then cycling doesn’t matter and the daily dosage would probably be optimal. If you took everything at once, once a month, all you would do is load mitochondria until it is either removed or replaced by fresh ones (that have half of the contents of C60). It’s there, always on, always working, always cleaning up ROS and doing it’s magic.

And this is how it should probably be. Everything packed full of C60 with no daily ROS jumps up or down. ROS: Gone. Good riddance if you ask me.

What we would have to deal with is an unbalanced Keap1-Nrf2-ARE pathway. It is ROS or toxin/activators modulated. We need to bring it back into normal by upregulating Nrf2 and downregulating Keap1 by toxins (“antioxidants”) or via gene expressions, daily, more than few times a day probably. If we bring it into overdrive and keep it there all the better. That way we get to have mitochondria that look like it was extracted from the birds (1/3 normal ROS production compared to mammals) with superior damage control that humans already have but don’t use fully (disposable soma). Since there is no shortage of things that influence that pathway we can choose things that are preferably not too toxic to the rest of the organism. Since we use most of them already and are quite tolerable we would only have to find a good mix, increase the dosage and the frequency. Add a good mix of minerals and vitamins, things that help with lipofuscin, AGEs, and other stuff and that would be it.

Have I missed any big problem with this theory?

[solarfingers]

If C60-oo works its magic by stopping free radicals in mitochondria and in lipid walls, then the fact that it is hydrophobic and lipophilic means that the regime doesn’t matter. This isn’t your typical “antioxidant” that the liver is working hard to remove from the body in the matter of hours. My guess is that it’s not even recognized as anything other then two lipid acids weirdly conjugated together. It gets into lipid wall and stays there for a very long time. If that is the case, then cycling doesn’t matter and the daily dosage would probably be optimal. If you took everything at once, once a month, all you would do is load mitochondria until it is either removed or replaced by fresh ones (that have half of the contents of C60). It’s there, always on, always working, always cleaning up ROS and doing it’s magic.

And this is how it should probably be. Everything packed full of C60 with no daily ROS jumps up or down. ROS: Gone. Good riddance if you ask me.

What we would have to deal with is an unbalanced Keap1-Nrf2-ARE pathway. It is ROS or toxin/activators modulated. We need to bring it back into normal by upregulating Nrf2 and downregulating Keap1 by toxins (“antioxidants”) or via gene expressions, daily, more than few times a day probably. If we bring it into overdrive and keep it there all the better. That way we get to have mitochondria that look like it was extracted from the birds (1/3 normal ROS production compared to mammals) with superior damage control that humans already have but don’t use fully (disposable soma). Since there is no shortage of things that influence that pathway we can choose things that are preferably not too toxic to the rest of the organism. Since we use most of them already and are quite tolerable we would only have to find a good mix, increase the dosage and the frequency. Add a good mix of minerals and vitamins, things that help with lipofuscin, AGEs, and other stuff and that would be it.

Have I missed any big problem with this theory?

taho, I like your theory as it seems very logical. How does it deal with the problem of c60 turning on mitochondria in cancer that would otherwise go into apoptosis? If it is allowing cancerous cells to send their signals for apoptosis then how does it prevent stem cells from prematurely differentiating themselves out of existence with no proliferation? I'm sure you understand it but I can't see it. You have a wonderful theory of how c60 is doing it's magic yet where does our HYPOTHETICAL concerns about daily dosing get solved. Or, can we explain the problems away?

Thanks...

[Hebbeh]

I think you might be stuck in old world thinking, that long life means long suffering and very long life looks to be on its way barring any catastrophic events.To get to 200 for existence you must be pretty young and in great shape at 150-175 and having lots of fun, for example. It is the declining state of the body and mind that makes most long for death and welcome it IMHO.

Now 100 or so is quite a goal in the sense, as very very few men make it that far currently, but we know from mice age, or damage if you will, can be reversed several different ways, and both studies were done at Harvard just in the last few years. So we are no longer looking at just slowing the ageing and its damage but in the very near future reversing it possibly quite easily.

There is also a type of jellyfish that can revert all the way back to the embryonic state, for the ultimate in aging reversal. This shows this ability exist in more than one species and you can bet your bottom dollar reversal will be the next huge trend. Don't worry though you still won't be "immortal", as the lose your head you will lose your life rule will still apply (Highlander).

This type of research in mice and jellyfish has little to no carryover in humans. To suggest that in the very near future we will quite easily be reversing aging such that you'd be pretty young at 150-175....is wishful thinking at best. And although average lifespan has been creeping up since the 1950's, very few enjoy a quality health span if making it into advanced age in their 80's and 90's. Almost all end up spending their final years in a convalescent home waiting out there days with others like them. The very few that maintain a quality life into those years is so rare that it usually makes the news. Few if any are able to work beyond 70 (if they are lucky...although my Dad did work until 82, I know of few others) and have difficulty financing a retirement into advanced years....especially a retirement that involves convalescent care not alone the medical costs associated with attempting to afford the possible technology to keep your mind and body functioning. There is no technology on the horizon that will afford lifespans or health spans much beyond 100 years. And if the technology does develop some day, better buy all their stock you can so as to finance not only the cost of such technology but the cost of living that long...but I would suggest not holding your breath.

[Kevnzworld]

This study showed an 11% lifespan increase for mice just fed a fairly basic 30 ingredient nutrient cocktail.
http://biomedgeronto.../60/3/275.short
I figure that if you add AGE inhibitors, PQQ, and Metformin to that mix, maybe some conservative HRT , a lttle resveratrol and 15% wouldn't be out of the question. Practice some moderate CRON lifestyle for good measure..
Now add C60 OO , began in one's mid life, and a 20-25% healthy lifespan increase isn't all that unreasonable. ...
Probably wishful thinking, but it's all I got...

[Hebbeh]

This study showed an 11% lifespan increase for mice just fed a fairly basic 30 ingredient nutrient cocktail.
http://biomedgeronto.../60/3/275.short
I figure that if you add AGE inhibitors, PQQ, and Metformin to that mix, maybe some conservative HRT , a lttle resveratrol and 15% wouldn't be out of the question. Practice some moderate CRON lifestyle for good measure..
Now add C60 OO , began in one's mid life, and a 20-25% healthy lifespan increase isn't all that unreasonable. ...
Probably wishful thinking, but it's all I got...

Given the current average life expectancy in the USA is about 79 years (http://en.wikipedia....life_expectancy) then a increased life expectancy of 95-98 years isn't unreasonable...especially considering the accompanying increased health span.

[taho]

taho, I like your theory as it seems very logical. How does it deal with the problem of c60 turning on mitochondria in cancer that would otherwise go into apoptosis?

There are over 200 different kinds of cancer, so there can't be one answer. But, an easy answer is that many cancers don't have mitochondria in them or they are non-working.

If it is allowing cancerous cells to send their signals for apoptosis then how does it prevent stem cells from prematurely differentiating themselves out of existence with no proliferation? I'm sure you understand it but I can't see it. You have a wonderful theory of how c60 is doing it's magic yet where does our HYPOTHETICAL concerns about daily dosing get solved. Or, can we explain the problems away?

No mithochondrial enzimes = no apoptosis.

My thinking is, that if you get cancer that is not something that you deal with C60-oo. You prevent cancer by preventing DNK damage with C60-oo. If you get cancer you are in big trouble and you go to the doctor and he will try to kill it depending on what kind of cancer it is. You have a 43% chance of getting a cancer in your lifetime. C60-oo is not a "cure all" medicine it is more like super-vitamin-E. Vitamins don't cure cancer and C60-oo probably won't either.

[Logic]

Logic,

I find your idea very compelling and it would work well with my idea of cycling telomeres and c60. Turnbuckle has on his profile that he currently takes 4 mg C60-EVOO once a week. Niner takes 15mg of c60-oo once a month. My current telomere cycle is two weeks of activation and two weeks of inhibition. I like the way Niner looks at this picture and have been thinking that taking c60-oo once a month would be a prudent thing since we do not know exactly what effect c60-oo will have on cancer. I also like Turnbuckles idea of giving healthy stem-cells time to proliferate. Basically, with these concerns in mind a daily dosage would not sound like the best idea. So if I decide to take c60-oo once a month when would be the optimal time during my telomere cycle? Yours, Taho's ideas and my current thinking on gene signal silencing would make me believe that the best time to take c60-oo would be once a month at the beginning of my telomere inhibiting cycle. Turnbuckle is taking 16mg a month and Niner is taking 15mg. I will likely follow suite on dosing.

Thx Solarfingers. Do remember that I am no expert and it is simply a hypothesis at this time.

I think you need to reconsider your telomerase activation inhibition cycle:
The supps known to inhibit telomerase have been shown to do so in cancerous cells not healthy cells.
The question that needs to be asked, but often isn't, before deciding on a telomerase activation inhibition cycle is 'What do these supps do to telomerase in healthy cells?'
Quite often they are actually telomerase activators in healthy cells or at worst do nothing to telomerase in healthy cells.
This fact seems to have been largely ignored by most and has lead to the misconception that telomerase inhibitors in cancerous cells need to be avoided during a telomerase activation cycle.
http://www.anti-agin...-of-telomerase/
(There are some interesting replies below the blog post)

If I remember correctly one should be more worried about the correct fixing of DNA breaks that may occur during telomerase activation for some reason I don't recall.
Cat's Claw and Rooibos tea plus other supps are said to help here.
http://www.longecity...post__p__218220
(James Green is probably the most knowledgeable person I know of when it comes to telomerase activation)

When it comes to dosage and schedule for C60oo I, like everyone else, just don't know.
I did note that Agevivo's two mice that have been receiving C60oo every 7 days religiously seemed more energetic, healthy and less itchy when a dose was skipped due to Agevivo being on holiday...
A mouse's physiology is way different to a human's, so I don't know how to translate this info for human scheduling?
I think that going on how you feel and taking note of how long it takes for the positive effects of C60oo to wear off, with occasional breaks, is probably best.

[solarfingers]

No mithochondrial enzimes = no apoptosis.

My thinking is, that if you get cancer that is not something that you deal with C60-oo. You prevent cancer by preventing DNK damage with C60-oo. If you get cancer you are in big trouble and you go to the doctor and he will try to kill it depending on what kind of cancer it is. You have a 43% chance of getting a cancer in your lifetime. C60-oo is not a "cure all" medicine it is more like super-vitamin-E. Vitamins don't cure cancer and C60-oo probably won't either.

I agree... The question is cancer prevention. However, not all cancer cells will metastasize. This is something we want to prevent from happening. Mostly our bodies can deal with cells gone awry and send a signal for apoptosis. The problem presented is that c60 can potentially prevent the natural death of cancer cells and encourage them to differentiate. How many steps till they metastasize I do not know but it sounds like the kind of thing you don't want to happen. If you read my comments earlier about signalling cells to turn off chromosomal precursors to cancer you will see that we are somewhat similar in our thinking. So it sounds like we need to encourage the signalling necessary to send cancerous cells toward apoptosis and signals to prevent those things that cause cells to become cancerous in the first place. Like your concept natural supplements can be used to send signals to turn off chromosomal precursors to cancer. The only thing that I can see that will stop the natural process of apoptosis in cancer cells is c60 and that's the problem. The only natural response is give time from the advantageous action of c60 to allow cancer cells to signal cell death. During that same period of time stem cells will have the opportunity to proliferate and if we take supplements to encourage this we are on our way to a prescription for real success.

As far as there being a cure for cancer, one is right around the corner. A new discovery called CD47 has successfully destroyed all human cancer types in lab studies. "But when the anti-CD47 was present, the macrophages engulfed and destroyed cancer cells from all tumor types."

While it is prudent to see your doctor if you contract cancer, medicines ability to cure cancer is no more successful as the Gerson therapy. They have the same success rates and the Gerson therapy has been known to have cured 3rd stage esophageal cancer. This has not been done with clinical medical technology. Surprisingly, the Gerson therapy uses a combination of detoxification through juicing and coffee enemas to help your body cure cancer on its own. I would much rather go this route than chemotherapy any day.

[solarfingers]

Logic,

I find your idea very compelling and it would work well with my idea of cycling telomeres and c60. Turnbuckle has on his profile that he currently takes 4 mg C60-EVOO once a week. Niner takes 15mg of c60-oo once a month. My current telomere cycle is two weeks of activation and two weeks of inhibition. I like the way Niner looks at this picture and have been thinking that taking c60-oo once a month would be a prudent thing since we do not know exactly what effect c60-oo will have on cancer. I also like Turnbuckles idea of giving healthy stem-cells time to proliferate. Basically, with these concerns in mind a daily dosage would not sound like the best idea. So if I decide to take c60-oo once a month when would be the optimal time during my telomere cycle? Yours, Taho's ideas and my current thinking on gene signal silencing would make me believe that the best time to take c60-oo would be once a month at the beginning of my telomere inhibiting cycle. Turnbuckle is taking 16mg a month and Niner is taking 15mg. I will likely follow suite on dosing.

Thx Solarfingers. Do remember that I am no expert and it is simply a hypothesis at this time.

I think you need to reconsider your telomerase activation inhibition cycle:
The supps known to inhibit telomerase have been shown to do so in cancerous cells not healthy cells.
The question that needs to be asked, but often isn't, before deciding on a telomerase activation inhibition cycle is 'What do these supps do to telomerase in healthy cells?'
Quite often they are actually telomerase activators in healthy cells or at worst do nothing to telomerase in healthy cells.
This fact seems to have been largely ignored by most and has lead to the misconception that telomerase inhibitors in cancerous cells need to be avoided during a telomerase activation cycle.
http://www.anti-agin...-of-telomerase/
(There are some interesting replies below the blog post)

If I remember correctly one should be more worried about the correct fixing of DNA breaks that may occur during telomerase activation for some reason I don't recall.
Cat's Claw and Rooibos tea plus other supps are said to help here.
http://www.longecity...post__p__218220
(James Green is probably the most knowledgeable person I know of when it comes to telomerase activation)

When it comes to dosage and schedule for C60oo I, like everyone else, just don't know.
I did note that Agevivo's two mice that have been receiving C60oo every 7 days religiously seemed more energetic, healthy and less itchy when a dose was skipped due to Agevivo being on holiday...
A mouse's physiology is way different to a human's, so I don't know how to translate this info for human scheduling?
I think that going on how you feel and taking note of how long it takes for the positive effects of C60oo to wear off, with occasional breaks, is probably best.

Granted, few of us here are Biochemical experts but I do appreciate thoughtful discussions. If we only had someone who actually had the answers we could be off playing tennis instead of scouring the forums in search of reason. Reading what you have said in previous posts has made me pause and consider my telomere lengthening choices. I do believe that James Green splits his regimen into two distinct activation and inhibitor cycles. I found his site before becoming acquainted with Longecity and read a great deal of what he has posted about his choices. Here are excerpts from his blog:

I'll show you Jim's two week cycle. From what I can tell he prefers the astragalus extract.

"(1) Two weeks using telomerase activation with astragalus root powder ( < 33 grams/day) (emphasis mine), OR astragalus root extract (< 11 grams/day), astragalosides, other telomerase activators, with TRF1 t-loop closure protein stripping via tankyrase 1 phosphorylation with insulin expressed via Fenugreek and/or Gymnema Sylvestre to open telomere t-loops for access by the telomerase holoenzyme.

Simultaneously we downregulate P16INK4a (which can make recovery from senescence irrecoverable) with Id-1 helix-loop-helix transcription factor obtainable by stimultion with nerve growth factor obtained from acetyl-L-carnitine, PQQ, huperzine A, carnosic acid, rosemary extract, or other nerve growth factor boosters.
.... Black cohosh, perhaps the most inexpensive telomerase activator, may also be used. Black cohosh causes no estrogenic side effects in exercising males at 4 caps/day in standard formulations.

Exercise promotes 12 different endogenous telomerase activators such as HGH that may be further boosted by supplements such as alpha-GPC and arginine.

(2) Then we go two weeks using telomerase inhibitors [81s/TI] not used during the first two weeks.

This procedure is expected to produce telomere elongations of less than 38 base pairs per month, that is, less than 456 base pairs/year. I note that RevGenetics now recommends a two-week cycle for telomerase activation, alternating a telomerase activator like Astral Fruit C (cycloastragenol) or Astral Fruit (astragaloside IV) one week with life-extending telomerease inhibitors including resveratrol, quercetin and other supplements the next week.

About 50-200 telomere base pairs are typically lost per cell division, although antioxidants may reduce the loss rate. Humans have about 50 cell divisions available from the embryonic stage of development, so this procedure may outdistance the aging process, although treatment should continue for years. TA Sciences did as well as the maximum here in blood granulocytes, 230 base pairs during each 3-month telomerase-on pulse in the Patton protocol using TA-41, which was an astragalus extract. This corresponds to a rejuvenation rate of about 9 years backwards in time per year, or 0.75 years/month."

You can see that he doesn't really suggest an inhibitor here. I have to dig further into his writings to determine what he suggests.

"Telomerase inhibitors garlic, turmeric (curcumin), resveratrol, quercetin, vitamin E, green tea, melatonin, silymarin, fish oil EPA, cocoa, cacao bean products, chocolate, and dietary polyphenols may be taken during the 2nd two weeks, but must not be taken during the first two weeks. Retinoic acid, a telomerase inhibitor that also inhibits the expression of P16INK4A (which makes replicative senescence irreversible) can also be used during the telomerase inhibition phase. Retinoic acid inhibits P16INK4A expression in oral keratinocytes."

So you can see that I am following his regimen only a little less slightly. I do add ALCAR to my diet but not many other ngf with the exception of Lion's Mane which isn't on his list at all. During the inhibition phase I take Milk Thistle Seed powder which is on his list of inhibitors. I also take Resveratrol and Ashwagandha as inhibitors.

The question for me is where to place c60 in this picture. Since c60 will be at it's weakest during the inhibition phase it holds that as cancer cells are naturally going into apoptosis that it would be a good time to send out cancer preventing signals. Also, almost all of the cancer inhibiting herbs contain polyphenols of which most have some telomerase inhibitory features but also fight against telomerase activation. It makes you wonder why nature designed herbs with polyphenols to behave this way and perhaps we are following a natural pattern here... That's my thinking on it anyhow.

Edited by solarfingers, 23 June 2013 - 12:31 AM.

[taho]

The only thing that I can see that will stop the natural process of apoptosis in cancer cells is c60 and that's the problem.

The problem is, that this increase in ROS production (the original proposal on how to kill cancer) by decreasing ROS defenses depends on cancer killing itself with its own ROS production. Many cancers already have upregulated Nrf-2 so that strategy will not work to kill them. Those are some tough cells that will survive with or without C60. Some cancerous cells will of course die, but not all of them. Many will live and the increased mutation rate will probably result in mutations that turn back defenses (and those cells will proliferate). Remember, cancer is cells that divide uncontrollably because they already have many mutations that enable them to escape system of checks against that. It’s survival of the fittest and it’s every cell for itself. The cells that have mutations that upregulates local ROS defense will win the fight (and kill the organism and itself).
That Anti-CD47 would of course work with no regard what is inside of cell (unless it has a mutation against CD47). Macrophages would clean everything C60 or not. If it works it would be THE cure.

Rats didn’t get cancer. Many people that take C60-oo are still alive without cancer. Some of them will almost certainly get cancer, but will it be more then 43%? I think it will be lower. What will be the number? Who knows.. lower.. maybe much, much lower..

If you get cancer, then you deal with cancer. How? The answer probably isn’t C60-oo

[Hebbeh]

In regards to telomerase, actually more current research point to silymarin (milk thistle), ashwagandha, curcumin (turmeric), and resveratrol as being telomerase activators and as such, why they are supposedly the main ingredients of Product B (although I am not a proponent of Product B). From the Product B thread: http://www.longecity...n/page__st__450

[solarfingers]

Taho,

The problem is, that this increase in ROS production (the original proposal on how to kill cancer) by decreasing ROS defenses depends on cancer killing itself with its own ROS production. Many cancers already have upregulated Nrf-2 so that strategy will not work to kill them. Those are some tough cells that will survive with or without C60. Some cancerous cells will of course die, but not all of them.

Yes but those that will do... Is that not significant if they are being kept alive by c60? I think you underestimate the number of these kinds of mutations where the mitochondria send signals toward apoptosis.

Remember, cancer is cells that divide uncontrollably because they already have many mutations that enable them to escape system of checks against that. It’s survival of the fittest and it’s every cell for itself. The cells that have mutations that upregulates local ROS defense will win the fight (and kill the organism and itself).

What is it that you are saying here? Is it fruitless to fight cancer or is this a comment which contradicts the validity of the Gerson therapy? It really doesn't matter. Cancer prevention is the least expensive prescription. I don't believe anyone is suggesting c60 is the answer for curing cancer and Niner's stated concern actually agrees with this. I don't think evidence is on your side if you are suggest it doesn't prevent cancer.

[solarfingers]

In regards to telomerase, actually more current research point to silymarin (milk thistle), ashwagandha, curcumin (turmeric), and resveratrol as being telomerase activators and as such, why they are supposedly the main ingredients of Product B (although I am not a proponent of Product B). From the Product B thread: http://www.longecity...n/page__st__450

Yes, that is something that I find interesting and I believe this has something to do with Logic's question. Jim Green has Resveratrol on both lists as an inhibitor and an activator. As Logic and Niner both pointed out the nature of an inhibitor isn't what many think and you can actually take both at the same time. Activators cause growth and inhibitors prevent shortening. Why not both at the same time?. Well, because James Green and Vince Giuliano both cycle. James Green prescribes to a two week cycle and Vince Giuliano prescribes to a bi-daily cycle. Who's right? I don't want to hijack this thread with telomere discussions unless it includes c60. Where my c60 fits into my cycle and how it relates to hypothetical concerns about dosing is what I want to talk about.

Edited by solarfingers, 23 June 2013 - 01:30 AM.

[Hebbeh]

Not wanting to hijack the thread but since telomerase was brought into the scope of the discussion and seeing a need to keep factual, all the ingredients of Product B are telomerase activators (not inhibitors) as specified by hits in Sierra Sciences RT-PCR screen as described in the patent. Just to be clear.

[taho]

What is it that you are saying here? Is it fruitless to fight cancer or is this a comment which contradicts the validity of the Gerson therapy? It really doesn't matter. Cancer prevention is the least expensive prescription. I don't believe anyone is suggesting c60 is the answer for curing cancer and Niner's stated concern actually agrees with this. I don't think evidence is on your side if you are suggest it doesn't prevent cancer.

If you are cancer free or don’t know that you do have cancer, you take C60. The goal is reduction of ROS production and with it rate of mutations that could lead to cancer. If this keeps you in the 57% group that don’t get cancer – you won.

If you have cancer or suspect that you have gotten cancer, you go to the doctor. You are part of a 43% that got cancer – you lost. Instead of C60 you should be taking some nasty chemicals that will hopefully kill the cancer and not you. Or do whatever else will hopefully work to get you healthy again.

If the question is.. Will C60 help protect the small, undetected cancer to grow faster, then the answer is probably “yes”.

If the question is.. Should I NOT take C60 to slow down small, undetected cancer that could be growing inside of me, then the answer is probably “statistically your bets are better that you do take C60 to prevent cancer and deal with cancer when you know that it actually exists”