My latest protocol, my latest results, and a note of caution:
First the caution.
The hypothesis here is that
- Pools of endogenous stem cells can be refilled with this protocol, and
- Being to some degree unprogrammed (age zero), these stem cells can be used to replace old somatic cells and thereby lower epigenetic age.
The problem with part 2 is that adult stem cells do have some epigenetic programing, and thus the age of those programed genes cannot be brought down this way. In fact, by overdoing this protocol, one might actually age them to a degree much greater than somatic cells. The results from epigenetic testing are still too noisy to tell if this is happening or not. (See the results for 3 epigenetic tests at end of this post.)
Thus I suggest this protocol should be considered only for people 60+ years, and even then should be used judiciously. By that I mean using it only once a week or two, and not after effects have plateaued. (Of course I was too impatient to do stretch it out like that, but I’ve stopped now that the effects seem to have plateaued.) I advise getting an epigenetic test before and halfway through.
Attached is a chart showing the changes in the epigenetic/chronological age ratio between the test 1 (baseline), test 2 (after 34 endogenous SC treatments over 3 months), and test 3 (after another 21 treatments over 2 months), grouped by gene. The first gene (on the left) has the best correlation with chrono age according to Osiris Green, and shows a decline which is consistent with what I expected if old somatic cells were replaced with new ones having de novo methylation. The next two, however, are showing some wild behavior, which could be no more than testing noise and the possibility that the buccal stem cell source is already methylated for those genes. More testing will be needed.
Baseline chronological age is 67.4 years. I am waiting on test results from another company (mydnage.com) taken at the same time as the third test. They look at hundreds of genes but don’t report on them. They just give you an estimated age, which isn’t that informative if you have a bimodal age distribution.
Given that things have plateaued subjectively, I’ve stopped the treatments for now and will get more epigenetic age tests over the next months. Below is my last protocol, with a couple of speculative items in red that I don’t have enough experience with to say if they really add (though they seem to)—
Stem cell self-renewal, with C60
Time 0 —
Stearic acid — 10 g (in hot chocolate or brownie)
Cycloastragenol – 10 mg
Astragalus extract — 5 g
TUDCA — 500 mg
Liposomal glutathione — 1 g
SAM-e — 200 mg
Astaxanthin — 8 mg
Time 3:00 —
Threonine — 10 g
Methionine — 1 g
Liposomal glutathione — 1 g
Butyrate — 600 mg (from sodium butyrate)
C60 — 3 mg (in EVOO or MCT oil)
Time 5:00+ —
More threonine if necessary
Rationale for additions:
1. Given that this is not a protocol for the long term, I’ve restored the cycloastragenol and astragalus extract.
2. Methionine and SAM-e are methyl donors and new stem cells will need methyl groups. Hypomethylation is the major source of epigenetic aging.
3. Astaxanthin Improves Stem Cell Potency via an Increase in the Proliferation of Neural Progenitor Cells
The present study was designed to investigate the question of whether or not astaxanthin improves These results clearly showed that astaxanthin induces proliferation of NPCs via activation of the PI3K and MEK signaling pathways and improves stem cell potency via stemness acting signals.
https://www.ncbi.nlm...les/PMC3100832/
4. There are several papers on the use of sodium butyrate to jazz up the process of turning somatic cells into stem cells, and it also is useful with neuronal stem cells and in promoting the self-renewal of pluripotent SCs—
the administration of sodium butyrate significantly ameliorated the SIRT2-induced reduction in cell proliferation and neuroblast differentiation.
https://www.ncbi.nlm...pubmed/24963697
and
In the present study, we found that NaB [sodium butyrate] effectively promotes MSC [mesenchymal stem cells] differentiation into SMCs [smooth muscle cells]. NaB markedly inhibited the expression and enrichment of HDAC2 at SMC specific genes in MSCs, which further induced high levels of H3K9 and H4 acetylation and the subsequent expression of the SMC specific genes α-SMA, calponin and SM-MHC. These results provide a strategy and mechanism for promoting MSC differentiation that could potentially be applied in clinical tissue engineering and cell transplantation.
https://www.ncbi.nlm...les/PMC4280132/
and
We show that a narrow concentration of the naturally occurring short chain fatty acid, sodium butyrate, supports the extensive self-renewal of mouse and human ES cells, while promoting their convergence toward an intermediate stem cell state.
https://www.ncbi.nlm...les/PMC2719860/
Edited by Turnbuckle, 20 September 2018 - 07:53 PM.
