Perhaps we could ask Telome to send emails or letters out to their customers at one year and two years for another test and then an advertisement for C60 with next. It's a three year plan, but it could turn up some good data. Especially if we find some good info from the C60 human trials and can use that to motivate the Telome customer base. Telome would get more revenue from tests this way, so Imagine they would be on board.
I must have missed something. Is there any evidence that C60 gets into the nucleus, much less lengthens telomeres? All the evidence I've seen to date points to an enhancement of mitochondrial function, and mitochondrial DNA has no telomeres. So not to say it's impossible, but it seems unlikely.
Telomeres seem to shorten by two processes. One is on division and the second from ROS or free radicals, and since C60 may block much of the ROS or free radical damage it may result in longer than normal telomeres, at least over time. This might be the explanation of longer lived mice getting C60-oo. Of course what all C60-00 does or doesn't do and how we don't know.
Longer telomeres are an unlikely explanation for the longer lifespans of the treated rats, as rats have far more telomere length than they need. Enough for several lifetimes. The lengths vary quite a bit, but the length doesn't translate into longer lifespans.
The strong telomere hypothesis states that absolute telomere length is irrelevant; relative loss of length since conception is what counts, at least so far as aging due to the telomere position effect is concerned. I would think that a short absolute length would still cause a mouse cell to experience replicative senescence. There are causes other than very short telomeres for cellular senescence in mice, obviously.
Mice have had their telomerase system shut down by genetic manipulation and still had enough telomere length to reproduce for several generations before running into a wall. So it can't be telomeres in the C60 study. There is also something called the mitochondrial theory of aging, which explains the Baati results better. First of all, the mitochondria are awash with ROS, so a good antioxidant would make the biggest difference there, and second, it's possible that C60 is acting epigenetically on the mtDNA, rejuvenating mitochondria that have picked up erroneous methyl groups, shutting down essential genes. There is some anecdotal evidence for that with the self-experimenters who see effects that could best be explained by activation of stem cells. Stem cells, like cancer cells, have quiescent mitochondria. Once you get them burning oxygen by removing those epigenetic markers--the methyl groups--they are differentiated into somatic cells.
The knockout mice are a puzzle, like why do they go so many generations with telomerase turned off and then by the 4th or 5th generation suddenly not make it much past 6 months and show signs of aging fast. Now do the mitochondria play out on them or is it the telomeres. I might also point to two other studies done with the knockout mice one at Harvard and the other at Mayo. The one at mayo stopped aging in the mice twice by taking out the senescent cells in them. Senescent cells are little nuclear radical causing agents trying to kill them cells. The one at Harvard showed a 30 days telomerase boost at old age near death caused the mice to reverse age, and the organs to grow back including their brains. They also had offsprings and lived a full lifespan of around 3 years. This is all from memory.
I would say the cells affect the mitochondria and not the other way around. Then you can get off into the species that never show age and are essentially immortals that produce gobs of telomerase. Gobs in this case is a scientific term
