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.
In keeping with this I should mention that James Green prescribes a two week activator, two week inhibitor cycle as cancer preventing protocol... Also, I think you missed the point that a supplement can be both an activator and an inhibitor at the same time. Why a activator/inhibitor is used for a inhibitor phase is beyond my understanding but they are used that way. For example... Resveratrol.
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.
In keeping with this I should mention that James Green prescribes a two week activator, two week inhibitor cycle as cancer preventing protocol...
No disrespect to James Green but all prescribed recommendations are simply guesses at best. There is no research or even anecdotal evidence to suggest how telomerase activators and inhibitors will interact with the possibility of decreasing the probability of developing cancer.
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.
In keeping with this I should mention that James Green prescribes a two week activator, two week inhibitor cycle as cancer preventing protocol...
No disrespect to James Green but all prescribed recommendations are simply guesses at best. There is no research or even anecdotal evidence to suggest how telomerase activators and inhibitors will interact with the possibility of decreasing the probability of developing cancer.
Very true... It depends on your comfort with risk when it comes down to it. When reputable researchers suggest it does which contradicts reputable researchers who suggest it doesn't what do you do? I'll go the path of least risk... especially when cancer is the prize... Which is the same path when dealing with c60.
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.
In keeping with this I should mention that James Green prescribes a two week activator, two week inhibitor cycle as cancer preventing protocol...
No disrespect to James Green but all prescribed recommendations are simply guesses at best. There is no research or even anecdotal evidence to suggest how telomerase activators and inhibitors will interact with the possibility of decreasing the probability of developing cancer.
Very true... It depends on your comfort with risk when it comes down to it. When reputable researchers suggest it does which contradicts reputable researchers who suggest it doesn't what do you do? I'll go the path of least risk... especially when cancer is the prize.
I don't understand your comment. What reputable researchers are you referring to? And what contradictory research are you referring to? And please elaborate on what path of least risk you are referring to.
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.
In keeping with this I should mention that James Green prescribes a two week activator, two week inhibitor cycle as cancer preventing protocol...
No disrespect to James Green but all prescribed recommendations are simply guesses at best. There is no research or even anecdotal evidence to suggest how telomerase activators and inhibitors will interact with the possibility of decreasing the probability of developing cancer.
Very true... It depends on your comfort with risk when it comes down to it. When reputable researchers suggest it does which contradicts reputable researchers who suggest it doesn't what do you do? I'll go the path of least risk... especially when cancer is the prize.
I don't understand your comment. What reputable researchers are you referring to? And what contradictory research are you referring to? And please elaborate on what path of least risk you are referring to.
Boy, you are beginning to wear me down. I regress, researcher's suggested that telomerase could caused cancer and there was research in the lab that showed it didn't. Just like the Baati study it should be replicated in the lab to prove the results are repeatable. I would go look for some citations but this is getting boring and I'm no longer enjoying this for the moment, so either take it or not. The path of least risk I am referring to is the path that has the least likelihood of cancer. If given two choices of something that MAY cause cancer and there is an alternative that May prevent it, I will choose the alternative that MAY prevent it. That's all I mean. Sorry for sounding curt but I am getting tired. I should step away from the computer for a time and give it a rest. Perhaps I will be in a better mood to respond later.
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.
People are usually forced to retire, even actors and actresses because of their age and the world does have its prejudices on age and many other things and once you break the routine it is usually down hill.
The economics of aging and lifespan can shift fairly fast though not in some worlds. Those in medical are pretty much stuck in a system that greatly lags behind the science, and the science is like a snowball going downhill faster and faster and getting bigger and bigger, as the knowledge keeps doubling and doubling in ever shorter time periods. At the same time, the availability of this knowledge to the person on the street keeps expanding through more devices and at faster and faster speed. Also the restriction are not there on what people can say or tell others, so that peer reviewed publishing, and human trials, and the FDA can no longer be the gate keepers of the old ways.
Look at C60 as an example. An amazing result is published in an obscure publication, and the internet news flashed the story and that got people to talking and figuring out how to make it at home, or buy/sell it to try it for themselves and all this took how long. Years down the road did not happen and there is no telling how it might extend our lifespans or in dogs and once that news spreads then the demand for it goes up and up. You may think mice or jellyfish are not connected to us, but I sure wouldn't bet on it. Or why do you think the longevity and reverse aging is being done in mice?? Or fruit flies or worms.
Regeneration study in mice..one day humans
“This is encouraging because the similarities give us hope that we will be able to induce human regeneration in the not-too-distant future,” Tulane University molecular biologist Ken Muneoka told Nature’s Ed Yong.
Then we have this one from so many months back and it is not just the heart but other organs and even the spine, and they think all from one protein which is available now. For research of course. Does it work in humans, well my guess there are people in the world already quietly finding out.
Five years ago a guy grew part of his finger back, including the finger nail with Pixie Dust. No human trials, or FDA approval but he had a connection who sent him the Pixie dust and told him to just sprinkle it on the stump left of his finger, and in 4 weeks it grew back in 2008. Hey it had worked in mice.
Do you see what I am saying?? Anything might be announced tomorrow, and if it can be made by labs somewhere in the world, and sold it will be available for those who want to go first, and for some there is not a lot of choice, if they want to stay out of those hospitals and homes and keep making the big money. The cost may be less than what they spend in a month, for their FDA approved meds.
Don't hold your breath waiting for me to hold mine My lungs don't work to well.
People are usually forced to retire, even actors and actresses because of their age and the world does have its prejudices on age and many other things and once you break the routine it is usually down hill.
The economics of aging and lifespan can shift fairly fast though not in some worlds. Those in medical are pretty much stuck in a system that greatly lags behind the science, and the science is like a snowball going downhill faster and faster and getting bigger and bigger, as the knowledge keeps doubling and doubling in ever shorter time periods. At the same time, the availability of this knowledge to the person on the street keeps expanding through more devices and at faster and faster speed. Also the restriction are not there on what people can say or tell others, so that peer reviewed publishing, and human trials, and the FDA can no longer be the gate keepers of the old ways.
Look at C60 as an example. An amazing result is published in an obscure publication, and the internet news flashed the story and that got people to talking and figuring out how to make it at home, or buy/sell it to try it for themselves and all this took how long. Years down the road did not happen and there is no telling how it might extend our lifespans or in dogs and once that news spreads then the demand for it goes up and up. You may think mice or jellyfish are not connected to us, but I sure wouldn't bet on it. Or why do you think the longevity and reverse aging is being done in mice?? Or fruit flies or worms.
Regeneration study in mice..one day humans
“This is encouraging because the similarities give us hope that we will be able to induce human regeneration in the not-too-distant future,” Tulane University molecular biologist Ken Muneoka told Nature’s Ed Yong.
Then we have this one from so many months back and it is not just the heart but other organs and even the spine, and they think all from one protein which is available now. For research of course. Does it work in humans, well my guess there are people in the world already quietly finding out.
Five years ago a guy grew part of his finger back, including the finger nail with Pixie Dust. No human trials, or FDA approval but he had a connection who sent him the Pixie dust and told him to just sprinkle it on the stump left of his finger, and in 4 weeks it grew back in 2008. Hey it had worked in mice.
Do you see what I am saying?? Anything might be announced tomorrow, and if it can be made by labs somewhere in the world, and sold it will be available for those who want to go first, and for some there is not a lot of choice, if they want to stay out of those hospitals and homes and keep making the big money. The cost may be less than what they spend in a month, for their FDA approved meds.
Don't hold your breath waiting for me to hold mine My lungs don't work to well.
It's a huge leap from growing back a finger tip (which has been happening from the beginning of time...pixie dust or not) to regrowing organs or more.
And if this wonderful pixie dust really did anything...and with the doubling of technology like you mentioned...can you explain why nothing more has become of this pixie dust in the past 5 years? Perhaps because there is no magic in this pixie dust? Much so called technology never pans out.
And mice, flies, and worms are often used in experiments not because the science transfers over to humans (it often doesn't) but due to the short life span of these type of organisms where they can often see results in days, weeks, months instead of the years it would take in higher life forms....not to mention that it would be unethical and illegal to directly perform experiments on humans. These lower life forms give science a place to start but seldom do the results transfer well to humans. I doubt that even the C60 experiment in Baati's rats will transfer very well as humans already have a very well developed endogenous antioxidant system as compared to rodents and part of the reason humans already live 20 times longer.
And I've never known of anybody forced to retire against their will. If anything, people are working longer and longer out of financial necessity. People retire either when they can afford to or more often when they are no longer capable of performing their job due to the effects of aging. They are not forced to retire....they are simply unable to continue of their own free will...their mind and body no longer cooperate...and they make their own decisions when the time comes. I see it happening all around me. But never see anybody forced out over age who could still do their job....quite the opposite really. In fact, at 56, I was recently recruited away from an excellent job to an even better job. Experience comes with age and savvy employers know this. In fact, if anybody is fired due to age discrimination, there are some very tough federal penalties that cover those situations and they would not only be facing costly fines but also lose a costly discrimination law suit.
And the jury is certainly still out on the long term effects of C60 in regards to humans...I doubt we're really going to see 150 or 200 with C60.
And you'll need something more potent than pixie dust to prolong human life beyond anything else currently available.
...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?...
Now I'm confused Solarfingers!?
From the first sentence above I thought you had misunderstood me and thought that C60oo's protecting mitochondria from being 'turned off' in pre/cancerous cells prevented cancerous cells from going into apoptosis.
Your second sentence is correct according to my hypothesis.
...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?...
Now I'm confused Solarfingers!?
From the first sentence above I thought you had misunderstood me and thought that C60oo's protecting mitochondria from being 'turned off' in pre/cancerous cells prevented cancerous cells from going into apoptosis.
Your second sentence is correct according to my hypothesis.
???
Sorry, it was obvious that I was wearing out later in the day. Let me gather myself here and see just what it was I was getting at.
We want c60 to stimulate mitochondria so that it would allow cancer cells the opportunity to send the signal for them to go into apoptosis. If c60 is stimulating cancer cell mitochondria we end up stimulating stem cell mitochondria (which serve a different function than normal cell mitochondria) and we may be causing uncontrolled stem cell differentiation without any proliferation. So, I guess the question is how can we have the advantageous effect of c60 turning on mitochondria in cancer cells causing apoptosis and not send stem cells into out of control differentiation? The answer to me still seems that we have to have some cycling going on in order to prevent our stem cells from being depleted.
The Batti rats would not have run into this problem because they were intermittently given c60. They were also given c60 at a very young age before any kind of negative cell mutations would have likely been happening in the first place.
So it seems that Turnbuckle's and Niner's hypothetical concerns about daily dosing are on opposite sides of the coin. It still may be possible that c60 does not turn on mitochondria in cancer cells and no signal for apoptosis is happening. It is also possible if it does that we may be depleting our stem cells if not controlled. If either is true you still will need intermittent dosing in order to prevent their downsides.
However, neither may be true and it doesn't matter. So, in summary, intermittent dosing can only be a form of insurance that we won't be causing some harm. Nobody is saying daily dosing of c60 WILL cause harm but only that HYPOTHETICALLY it may. I like Niner's choice of monthly intermittent dosing but I see no reason why intermittent dosing could not be more frequent, say bi-weekly. Bi-weekly may allow more of the advantages of c60 without the downsides. Weekly seems to be too short to allow c60 to pass out of the body in order for the body's natural processes to work. I'm a week away from starting my first intermittent dose of c60. I will likely take a small sample to ensure I don't have some sort of reaction in advance.
I would like to see a study conducted to examine these issues. It would be good to see exactly what effect c60-oo has on normal cells, per-cancerous cells and stem cells. I guess we will have to see the results of the second Baati rat study. I would hope they would raise these questions.
We want c60 to stimulate mitochondria so that it would allow cancer cells the opportunity to send the signal for them to go into apoptosis. If c60 is stimulating cancer cell mitochondria we end up stimulating stem cell mitochondria (which serve a different function than normal cell mitochondria) and we may be causing uncontrolled stem cell differentiation without any proliferation. So, I guess the question is how can we have the advantageous effect of c60 turning on mitochondria in cancer cells causing apoptosis and not send stem cells into out of control differentiation? The answer to me still seems that we have to have some cycling going on in order to prevent our stem cells from being depleted.
I don’t think “stimulate mitochondria” is the right phrase that we should use to describe effects of C60-oo. It would be better to describe it more along the line of “return mitochondria to normal”.
Cancer killing hypothesis hinges on improvements of mitochondria from non-working to working. Those suddenly working mitochondria would then be able to apoptosis their cells and kill the cancer that way. Since I very much doubt that mitochondria are turned “off” instead of “damaged beyond repair” C60-oo can’t help in that case.
Cancer promoting hypothesis hinges on improvement of ROS environment in and around cancer cell. C60-oo will probably improve this thus helping the cancer grow faster. Or it will help other parts of the body reduce inflammation markers and thus help the immune system focus on the part of the body that does have cancer. We don’t know what exactly will happen in that case, but we must weigh possible good (possibility of a much longer, healthier life) v bad (higher growth of cancer that would grow anyway). Cycling in long breaks will reduce C60oo in new cells, thus make ROS environment worse for those cells, but since we don’t know the optimal dosage or removal halftime we would be shooting in the dark. My guess is that this strategy would not give full benefit of C60oo but it could theoretically help with cancer. We don’t know enough to make any good predictions either way.
Stimulating stem cell mitochondria is not something that I have any good hypotesis why it should happen, neither any facts to point that this is actually happening. If anything it should just help more stem cells keep mitochondria in a good health, thus keep everything “normal”. Stem cells shouldn’t be effected one way or another with C60oo and will probably protect them.
So.. cycling could or could not help. What we know is that rats got weekly cycle that in my opinion is not long enough to hinder the cancer in the “worse ROS environment” way. What we do know is they lived long and cancer free lives. Based on the gap between the end of the supplementation and rats deaths and properties of C60oo (lipophilic) I think it takes months or even years for concentrations to fall to such a low level that they are not working any more. That (IMHO) makes the whole cycling C60-oo idea unfeasible and unworkable.
Your hypothetical assumptions are pretty much as valid as Niner's and Turnbuckle's and no more. Secondly, we need to disassociate the Baati rat study from the discussion for the reason we have stated previously. Namely, the Baati rats were given c60-oo prior to an age where they would have started seeing pre-cancerous mutations. Secondly, your assertion that they were only given weekly dosages is categorically incorrect. They were administered daily for the first week. Thereafter, till the end of the second month they were given a weekly dosage. After the second month they were given bi-weekly administration until the 15th month. They were given bi-weekly dosages for 12 months! So the cycling idea is both feasible and workable.
You are right. It was bi-weekly dosages. But it went only from when rats were 10 months old to when they were 17 months old. when the first control rat died, so 7 months. First C60-oo rat died when it was 60 months old. That’s one long gap since the last control died 38 months old (all based on data/graph from the article).
I think that the most important way C60-oo works is probably by reducing ROS from mitochondria and lipid walls thus even bi-weekly cycle isn’t really a cycle. New mitochondria get made with splitting of existing mitochondria, thus still have C60-oo in them. It’s has half of it, but since you don’t really need much of it and since it’s catalytic thus has no time limit on its functionality it should work in new mitochondria even if you rats haven’t consumed C60-oo in the past 14 days. It should take a much longer cycle for C60-oo to fall to low enough level to not work any more.
The only way cycle would work is if we knew exactly the dosage that is needed and the half life and its effects. Since C60-oo doesn’t look like its toxic, has fantastic potential (life extension counted in years or even decades) the whole low dosage/cycle because somebody didn’t want to torture rats too much isn’t something that I care about. I am inclined to go with “Forget small dosage/bi-weekly cycle. Let’s flood the system with C60-oo and deal with homeostasis in some other way” idea.
But, everybody should be aware that this substance is completely untested, unknown, possibly dangerous, could possiblly not work and could make you die in some horrible disease or infliction. If you aren’t prepared to take that risk, then don’t take it. If you wish, you can give it to your rat, cat or whatever and help everybody get more data so we could make better hypothesis about this new strange substance.
You are right. It was bi-weekly dosages. But it went only from when rats were 10 months old to when they were 17 months old. when the first control rat died, so 7 months. First C60-oo rat died when it was 60 months old. That’s one long gap since the last control died 38 months old (all based on data/graph from the article).
I re-read the study. I stand corrected they stopped treating the rats after 7 months as they were only 17months old. The "at [M17]" terminology threw me off but if you examine the graph it is clear that they are talking about the age of the rats and not the month of the test. This means that they continued bi-weekly administration for 7 months and not the 12 that I asserted.
Cancer killing hypothesis hinges on improvements of mitochondria from non-working to working. Those suddenly working mitochondria would then be able to apoptosis their cells and kill the cancer that way. Since I very much doubt that mitochondria are turned “off” instead of “damaged beyond repair” C60-oo can’t help in that case.
I am somewhat disappointed that you seem to have written off my hypothesis without following a single link Taho. If DCA is able to 'turn on' mitochondria in cancerous cells the mitochondria have to be present and functional. Perhaps you are asserting that the DCA studies are flawed and that DCA, like PQQ is capable of Mito-genesis?
Note that nowhere in the hypothesis is C60oo considered a Mitochondrial 'booster/on switch' like DCA, and possibly Green Tea, Mebendazole, resveratrol or PQQ (Mito-genesis). C60oo is considered an excellent mitochondrial 'protector' however.
So.. cycling could or could not help. What we know is that rats got weekly cycle that in my opinion is not long enough to hinder the cancer in the “worse ROS environment” way. What we do know is they lived long and cancer free lives. Based on the gap between the end of the supplementation and rats deaths and properties of C60oo (lipophilic) I think it takes months or even years for concentrations to fall to such a low level that they are not working any more. That (IMHO) makes the whole cycling C60-oo idea unfeasible and unworkable.
A good point. However we have a tiny hint in that Agevivo's mice seemed healthier after skipping one of their weekly doses. Slim pickings for sure but then all these hypotheses are based on conjecture at this point.
Due to the fact that no-one knows for sure and the very slim evidence on which all this conjecture is based; I like Solarfinger's hypothesis of dosing bi-weekly with known mitochondrial... 'boosters'
On the other hand one can imagine a synergy between C60oo and telomerase activators.
At the end of the day everyone is following their own minds and posting here. That's a very good thing as we will all learn from it eventually.
As someone who has not taken C60oo (and Epitalon) since January, I can tell you that I am back to baseline IMHO and I miss the combo like a 20 something year old honey smiling at me. (That actually happened 4 times)
As someone who has not taken C60oo (and Epitalon) since January, I can tell you that I am back to baseline IMHO and I miss the combo like a 20 something year old honey smiling at me. (That actually happened 4 times)
Man, I really have to read up more on Epitalon. Why the hell is it so expensive!
As someone who has not taken C60oo (and Epitalon) since January, I can tell you that I am back to baseline IMHO and I miss the combo like a 20 something year old honey smiling at me. (That actually happened 4 times)
Man, I really have to read up more on Epitalon. Why the hell is it so expensive!
Yep; people who hadn't seen me in 2 years would actually take a step back in surprise and say: 'Damn! You're looking good!" or similar. I enjoyed the reactions of the young ladies you didn't yet know me a lot more though!
A gram lasts quite a while @ 3mg per day especially if you take breaks. Also it seems that you can scale back to a maintenance dose of 1 mg/day after a year. The 2nd best price was 750USD/gram!
As someone who has not taken C60oo (and Epitalon) since January, I can tell you that I am back to baseline IMHO and I miss the combo like a 20 something year old honey smiling at me. (That actually happened 4 times)
Man, I really have to read up more on Epitalon. Why the hell is it so expensive!
Yep; people who hadn't seen me in 2 years would actually take a step back in surprise and say: 'Damn! You're looking good!" or similar. I enjoyed the reactions of the young ladies you didn't yet know me a lot more though!
A gram lasts quite a while @ 3mg per day especially if you take breaks. Also it seems that you can scale back to a maintenance dose of 1 mg/day after a year. The 2nd best price was 750USD/gram!
I sure hope to win the California lottery before the genetic lottery wins...
I am somewhat disappointed that you seem to have written off my hypothesis without following a single link Taho. If DCA is able to 'turn on' mitochondria in cancerous cells the mitochondria have to be present and functional. Perhaps you are asserting that the DCA studies are flawed and that DCA, like PQQ is capable of Mito-genesis?
I have not written your hypothesis off. I think it has some merit and could be a good tool to fight some cancers. DCA is able to “turn on” mitochondria, because it blocks anaerobic pathway through which cancer produces ATP. (cancer) cells then either die or find a way of turning to other sources of energy – mitochondria. If cancerous cells manage to do that, mitochondria will multiply and then the apoptosis via mitochondria once again becomes functional. That with a good combination of toxins, drugs, radiation and anything else that is thrown at it would hopefully kill the blob of uncontrollably expanding cells that is called cancer. DCA is just one of many tools and that’s why I said that if you get cancer, forget about C60oo, don’t take it lightly and go to the doctor that hopefully will be able to kill your blob of cells.
What I don’t think is that C60oo will prevent or reverse cell’s metabolism. I don’t think mitochondria get shut down because of ROS. I think the cell shuts down mitochondria because it is a trigger that controls apoptosis. That way the cancer can ignore all those “kill yourself” signals and grow, grow, grow. I think there are lots of unknowns here and I could be wrong on that subject, but once again: those rats did live long and cancer free lives.
Cycling works by boosting something then stopping. In that way the homeostatic systems will not get totally out of whack, boosting again on, off, on, off in a cycle. You can’t do that if the “stopping” doesn’t stop anything. C60oo gets into mitochondria and stays there for probably a long time. I think that delay before death in our rats is a symptom of how long does it stay there. Until we get a better theory, I will take it over “those mice look a little bit better”. If you can’t stop your boosting, then you must plan around it. And frankly “low, low ROS” with “extra boosted cell defenses” doesn’t really sound as such a bad plan. If anyone sees any big wholes in that plan I will be more then interested in knowing them.
I have not written your hypothesis off. I think it has some merit and could be a good tool to fight some cancers. DCA is able to “turn on” mitochondria, because it blocks anaerobic pathway through which cancer produces ATP. (cancer) cells then either die or find a way of turning to other sources of energy – mitochondria. If cancerous cells manage to do that, mitochondria will multiply and then the apoptosis via mitochondria once again becomes functional. That with a good combination of toxins, drugs, radiation and anything else that is thrown at it would hopefully kill the blob of uncontrollably expanding cells that is called cancer. DCA is just one of many tools and that’s why I said that if you get cancer, forget about C60oo, don’t take it lightly and go to the doctor that hopefully will be able to kill your blob of cells.
The last thing I feel like doing is re-reading the DCA studies right now, but I'll get to it. Be that as it may; the Mitochondria have to be present and functional to be turned back on, not “damaged beyond repair”?
What I don’t think is that C60oo will prevent or reverse cell’s metabolism. I don’t think mitochondria get shut down because of ROS. I think the cell shuts down mitochondria because it is a trigger that controls apoptosis. That way the cancer can ignore all those “kill yourself” signals and grow, grow, grow. I think there are lots of unknowns here and I could be wrong on that subject, but once again: those rats did live long and cancer free lives.
Here I agree with you completely. C60 seems to protect mitochondria in healthy cells and possibly prevent their being 'turned off' DCA and possibly the other supps mentioned are able of 'turning on' mitochondria again and THEN C60oo will be helpful once again.
Cycling works by boosting something then stopping. In that way the homeostatic systems will not get totally out of whack, boosting again on, off, on, off in a cycle. You can’t do that if the “stopping” doesn’t stop anything. C60oo gets into mitochondria and stays there for probably a long time. I think that delay before death in our rats is a symptom of how long does it stay there. Until we get a better theory, I will take it over “those mice look a little bit better”. If you can’t stop your boosting, then you must plan around it. And frankly “low, low ROS” with “extra boosted cell defenses” doesn’t really sound as such a bad plan. If anyone sees any big wholes in that plan I will be more then interested in knowing them.
Here I cannot really argue as, Agevivo's observation excepted, the limited evidence supports this view. Maybe the C60oo is still in my mitochondria. All I can say is that subjectively it does not feel like it as hangovers after partying are back as is the euphoric feeling after gym.
As I said before I am glad we all have different dosage schedules as we wouldn't learn what is best otherwise. I do hope studies are done soon to test all these theories.
Be that as it may; the Mitochondria have to be present and functional to be turned back on, not "damaged beyond repair"?
That depends on what kind of mutations cells in your specific kind of cancer has. Maybe your cancer has a DNK mutation that makes mitochondria non-functional. Or maybe you have mitochondria present in few cells but there is mutation that stops them proliferating in sufficient quantities. Or maybe you have mutation that controls metabolism. Or any other mutation that will allow the cells to avoid lever for an apoptotic guillotine that is in the mitochondria’s enzymes.
If you turn off alternative sources of ATP then your cancer cells will die all over the place. But, remember cancer cells live in a high mutation environment so few of the millions could have some mutation that will work around that. Those will survive and then you will have cancer that has mitochondria “turned on” even if your cancer had them “damaged beyond repair”
If this thread would be about cars, then this is where we would talk about how to change oil, filter, tires, how to paint or do things that will make sure your car serves you well and long time. The question “Do I change oil even if my car is total wreck from the accident?” would be kind of weird. Yes, well maintained car will be safer, but if you crash it there is no point in changing oil. Go talk to someone that will fix that car then come back and talk about filters and stuff..
I think you mistake our zeal for prevention as a cure.... Of course this isn't about how c60-oo effects existing cancer. Our discussion is and has always been about prevention... When we talk about cancer, in a generic way we mean pre-cancerous cells which have mutations that can lead to cancer. Mostly these kinds of cells die on their own and we don't usually have to worry about them. I prefer VGs theory of turning off as many signals to the chromosomes that create cancer to begin with. All you need is the proper mix of polyphenols. Stop cancer at the source.
There is an idea from a paper that says c60 could find a home in a groove in the DNA that causes methyl esters (If I have that straight) to stimulate the mitochondria. That paper also found that this process caused the DNA to unravel. The paper is generally flawed because it is poorly executed and is merely a computer model. Niner generally discredits this paper. So, this is where the idea of "stimulating mitochondria" comes from. Who's to say it's true or not? Obviously our DNA is not unwinding on c60-oo but could methyl esters be stimulating mitochondria? Some speculate that this is why they are experiencing so much more energy while on c60-oo. I'm merely trying to hedge the bets.
Be that as it may; the Mitochondria have to be present and functional to be turned back on, not "damaged beyond repair"?
That depends on what kind of mutations cells in your specific kind of cancer has. Maybe your cancer has a DNK mutation that makes mitochondria non-functional. Or maybe you have mitochondria present in few cells but there is mutation that stops them proliferating in sufficient quantities. Or maybe you have mutation that controls metabolism. Or any other mutation that will allow the cells to avoid lever for an apoptotic guillotine that is in the mitochondria’s enzymes.
So what you are saying is that there are an almost infinite number of types of cancer and that not all 'switch off' their mitochondria to avoid apoptosis? I was under the impression that disabled mitochondria were common to all cancers, much like the CD47 protein that sends out a 'Don't eat me' signal to macrophages. Do you have any further info I can learn from?
If you turn off alternative sources of ATP then your cancer cells will die all over the place. But, remember cancer cells live in a high mutation environment so few of the millions could have some mutation that will work around that. Those will survive and then you will have cancer that has mitochondria “turned on” even if your cancer had them “damaged beyond repair”
I have often used this point to advocate attacking a cancer from every epigenetic angle so as to get all the cancerous cells no matter their mutation. This argument flies out the window when you can use a trait common to all cancers to kill it though. I also note that this is a trait cancer has in common with Virii and that one in six cancers are caused by virii according to a recent study. http://www.longecity...ble-infections/
I think you mistake our zeal for prevention as a cure.... Of course this isn't about how c60-oo effects existing cancer. Our discussion is and has always been about prevention... When we talk about cancer, in a generic way we mean pre-cancerous cells which have mutations that can lead to cancer. Mostly these kinds of cells die on their own and we don't usually have to worry about them. I prefer VGs theory of turning off as many signals to the chromosomes that create cancer to begin with. All you need is the proper mix of polyphenols. Stop cancer at the source.
I wish to prevent cancer also, but to do that we must first have a good understanding of what is going on. To do that we must have solid theories that matches facts as they are. All this “cycling” business does not fit the facts. You can’t cycle something that you can’t cycle. To focus on things that are not important or not relevant to specific condition does not lead to better understanding.
What is cancer? ROS = DNK damage = mutations = 15.000.000.000.000 cells with random mutations = most of them die/are killed = some survive = 43% chance that you will get cancer in your lifetime
How do you prevent cancer? a) stop ROS b) fix the damage c) kill cells that are in danger of becoming “feral” (cancer) d) cancer – kill it before it kills you!
If you focus on the last point at the expense of previous points you are setting yourself for fail. Find ways to improve a) b) and c) and hopefully you will not have to deal with d).
C60oo deals with a) but it can possibly negatively impact b) and c) via Nrf-2 inhibition or some possible other ways. I would very much like to discuss a) b) and c). What and how to do that and yes, if we would have to cycle something to do that and why and how that would be very good information to have.
When you have d) -> this discussion is not relevant anymore.
There is an idea from a paper that says c60 could find a home in a groove in the DNA that causes methyl esters (If I have that straight) to stimulate the mitochondria. That paper also found that this process caused the DNA to unravel. The paper is generally flawed because it is poorly executed and is merely a computer model. Niner generally discredits this paper. So, this is where the idea of "stimulating mitochondria" comes from. Who's to say it's true or not? Obviously our DNA is not unwinding on c60-oo but could methyl esters be stimulating mitochondria? Some speculate that this is why they are experiencing so much more energy while on c60-oo. I'm merely trying to hedge the bets.
I don’t like “stimulating mitochondria” idea. Somehow C60 wedges itself into DNK and this somehow makes one organelle better without any other effects on a cell? How about we go with simple less damage = better working mitochondria until we get an idea that has some possible (preferably testable) concrete mechanism behind it.
The more logical thing why some have more energy is that either mitochondrion is working better somehow or feedback mechanism is impacted by lower ROS environment somehow. How? Yes. Let’s discus that one..
So what you are saying is that there are an almost infinite number of types of cancer and that not all 'switch off' their mitochondria to avoid apoptosis?
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.
I also note that this is a trait cancer has in common with Virii and that one in six cancers are caused by virii according to a recent study. http://www.longecity...ble-infections/
That probably gets you cancer since your immune system uses free radicals to kill infections. Those free radicals damage DNK. That gets you cancer.
Cycling works by boosting something then stopping. In that way the homeostatic systems will not get totally out of whack, boosting again on, off, on, off in a cycle. You can't do that if the "stopping" doesn't stop anything. C60oo gets into mitochondria and stays there for probably a long time. I think that delay before death in our rats is a symptom of how long does it stay there. Until we get a better theory, I will take it over "those mice look a little bit better". If you can't stop your boosting, then you must plan around it. And frankly "low, low ROS" with "extra boosted cell defenses" doesn't really sound as such a bad plan. If anyone sees any big wholes in that plan I will be more then interested in knowing them.
Here I cannot really argue as, Agevivo's observation excepted, the limited evidence supports this view. Maybe the C60oo is still in my mitochondria. All I can say is that subjectively it does not feel like it as hangovers after partying are back as is the euphoric feeling after gym.
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 am not trying to cycle to the point that I've dropped out of the protective range. I suppose it could be argued that if you did that, you might be more likely to keep your endogenous antioxidants upregulated, but taking my cue from Baati, I'm planning on staying in the protective range full time. My "hypothetical concern about daily dosing" was pretty hypothetical, and lately I've been doing some reading, trying to put it on a firmer footing. The cancer/redox rabbit hole is pretty deep and murky, and I think there may be a lot of red herrings along the way.
My "hypothetical concern about daily dosing" was pretty hypothetical, and lately I've been doing some reading, trying to put it on a firmer footing. The cancer/redox rabbit hole is pretty deep and murky, and I think there may be a lot of red herrings along the way.
Have you found anything particulary interesting?
What are your thoughts on Nrf-2 up/downregulation?
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