2523 replies to this topic

[eigenber]

Looking for advice, probably from Turnbuckle, on possible interactions.

I am trying to destroy a prostatic bacterial biofilm using an enzymatic cocktail of several fibrinolytics (including nattokinase-serrapeptase), EDTA, NAC, chitosan, followed by artemisinin, lactoferrin, silver nanoparticles, and sulfamethoxazole. 

Do you see any possible interference of these with the compounds in your protocol? 

[ambivalent]

Not been around too much lately, apologies if this has been posted - if it hasn't I'll put on the senolytics forum.

 

So thoughts on this? Likely that stem cell renewal addresses this potential problem of other senolytics - was it Navitoclax which caused clotting failures? 

 

It has been previously reported that selective removal of senescent cells was sufficient to maintain trabecular bone mass in aged mice (Farr et al., 2017). Surprisingly, 2 weeks of in vivo administration of navitoclax did not improve, and instead significantly decreased trabecular bone volume fraction in aged female and male mice (−60.1% females, −45.6% males)

 

https://www.frontier...2020.00354/full

[Turnbuckle]

Not been around too much lately, apologies if this has been posted - if it hasn't I'll put on the senolytics forum.

 

So thoughts on this? Likely that stem cell renewal addresses this potential problem of other senolytics - was it Navitoclax which caused clotting failures? 

 

It has been previously reported that selective removal of senescent cells was sufficient to maintain trabecular bone mass in aged mice (Farr et al., 2017). Surprisingly, 2 weeks of in vivo administration of navitoclax did not improve, and instead significantly decreased trabecular bone volume fraction in aged female and male mice (−60.1% females, −45.6% males)

 

https://www.frontier...2020.00354/full

 

 

There are paracrine factors that tell stem cells to replace dying cells. If you try to replace too many cells at once, or interfere with paracrine communication or stem cell differentiation, the process could fail. So it would have been interesting to see this trial done one dose at a time, with an interval between treatments. 

Edited by Turnbuckle, 02 August 2020 - 09:35 PM.

[QuestforLife]

I got back the results of my June TruMe test.

 

Chronological Age: 41.6

Biological Age 41.9

 

Intervention: 3 1/2 months of AKG. I also did a few rounds of TB's Stem Cell protocol (with no senolytics).

 

This is disappointing as it means there has been no change since my March 2020 methylation age test result from Zymo (42 yo).

 

Possible explanations:

TruMe uses a saliva test, which is less reliable than the blood or urine results from Zymo, and might have been affected by my bad hayfever during May and June.

I also took a Vit D and K2 supplment as a precaution against all the calcium in the AKG supplement. Vit D is a telomerase activator.

In my case having reversed my telomere age by 3 years recently through epitalon (and increased my methylation age by the same amount), I might need significantly longer to reverse my methylation age. 

 

Future plans: i have another TruMe test ready to go. My hayfever has relented and i've now replaced the VitD/K2 with just K2. I'll continue the AKG with occasional TB Stem Cell cycles (note I'm omitting any senolytics at this point) and report back when I done the next test (Sept or Oct).

Edited by QuestforLife, 03 August 2020 - 01:15 PM.

[Turnbuckle]

I got back the results of my June TruMe test.

 

Chronological Age: 41.6

Biological Age 41.9

 

Intervention: 3 1/2 months of AKG. I also did a few rounds of TB's Stem Cell protocol (with no senolytics).

 

This is disappointing as it means there has been no change since my March 2020 methylation age test result from Zymo (42 yo).

 

Possible explanations:

TruMe uses a saliva test, which is less reliable than the blood or urine results from Zymo, and might have been affected by my bad hayfever during May and June.

I also took a Vit D and K2 supplment as a precaution against all the calcium in the AKG supplement. Vit D is a telomerase activator.

In my case having reversed my telomere age by 3 years recently through epitalon (and increased my methylation age by the same amount), I might need significantly longer to reverse my methylation age. 

 

Future plans: i have another TruMe test ready to go. My hayfever has relented and i've now replaced the VitD/K2 with just K2. I'll continue the AKG with occasional TB Stem Cell cycles (note I'm omitting any senolytics at this point) and report back when I done the next test (Sept or Oct).

 

 

If you've taken a lot of telomerase activators, it could take quite a while to recover. My expectation is that lengthened telomeres will block senescence/replacement of TACs. The TruMe test is likely measuring the aging of epidermal cells that derive from and reflect the aging of TACs. See the following paper--

 

Aging Epidermis Is Maintained by Changes in Transit-Amplifying Cell Kinetics, Not Stem Cell Kinetics

[yz69]

Trume measures white blood cells in saliva:

https://secureserver...logical-age.pdf

 

I asked Trueme founder Yelena what happened to my test results, she told me this:

 

Quickly, I will say that your biological age went down because of only improvement of several markers in one loci out of 4. This loci is responsible for upregulation of genes involved in inflammation.

 

 

 

 

 

[Turnbuckle]

Trume measures white blood cells in saliva:

https://secureserver...logical-age.pdf

 

I asked Trueme founder Yelena what happened to my test results, she told me this:

 

 

It's a combination. From your link--

 

Saliva is not just a watery substance containing some digestive enzymes and some epithelial cells (buccal cells) that is produced by glands in your mouth area. Studies show that up to 74% of the DNA in saliva comes from white blood cells.

 

 

 

That appears to be a maximum, and it's not clear to me what the average is. I don't see in the references where they are getting this.

[yz69]

According to this paper https://www.scienced...030422058902196

 

The white blood cells in saliva are in the orders of 100-1000 per uL

 

 

In the toothless, healthy mouth the leukocyte count is considerably lower (1 to 143 cells per 1 c.mm.) than in the healthy mouth with teeth (110 to 1,364 cells per 1 c.mm.); in mouths with inflammation, the count increased quite remarkably (770 to 11,896 cells per 1 c.mm.). 

 

Edited by yz69, 03 August 2020 - 05:42 PM.

[QuestforLife]

If you've taken a lot of telomerase activators, it could take quite a while to recover. My expectation is that lengthened telomeres will block senescence/replacement of TACs. The TruMe test is likely measuring the aging of epidermal cells that derive from and reflect the aging of TACs. See the following paper--

Aging Epidermis Is Maintained by Changes in Transit-Amplifying Cell Kinetics, Not Stem Cell Kinetics

A very interesting article. And it makes sense when we consider that various 'destructive' skin treatments like retin-A, derma rolling, acids, etc. all seem to make skin look younger, whereas when I tried a telomerase activator on my face it actually seemed to make me look older.

Would you care to comment on whether this result in the epidermis can be extended to other aging tissues?

[Turnbuckle]

According to this paper https://www.scienced...030422058902196

 

The white blood cells in saliva are in the orders of 100-1000 per uL

 

 

That is meaningless unless you know what the buccal cell count is. And where does the 74% breakdown come from? The first reference mentions a 74%, but not in the same context.

[Turnbuckle]

A very interesting article. And it makes sense when we consider that various 'destructive' skin treatments like retin-A, derma rolling, acids, etc. all seem to make skin look younger, whereas when I tried a telomerase activator on my face it actually seemed to make me look older.

Would you care to comment on whether this result in the epidermis can be extended to other aging tissues?

 

 

I think it can, even in cases where there are no TACs. If the progression is directly from adult SCs to somatic cells, then epigenetic aging can only take place in the SCs, or by the decline in the SC niche populations. So where do replacement SCs come from? One obvious source is the blood supply, which contains VSELs that originate in the bone marrow. As they are pluripotent, they should have very low epigenetic age. The following article is pay only until Feb. of next year--

 

Very Small Embryonic-Like (VSEL) stem cells are a proposed pluripotent population, residing in adult tissues. VSELs have been described in multiple tissues including bone marrow, cord blood, and gonads. They exhibit multiple characteristics of embryonic stem cells including the ability to differentiate into cellular lineages of all three germ layers, including cardiomyocytes and vascular endothelial cells. However, their presence in adult solid organs such as heart in humans has not been established. VSELs are valuable source of stem cells for tissue regeneration and replacement of cells for turnover and usual wear-and-tear. The purpose of our study was to explore the existence of human VSELs (huVSELs) in human heart tissue and examine the changes in their prevalence with aging and cardiac disease. Human heart tissue, collected from healthy and ischemic heart disease subjects was examined for the prevalence of VSELS, defined as CD45-/CD133+/SSEA4+. Both epicardial and endocardial tissues were examined comparing VSEL numbers across different age groups. Our data confirm the existence of huVSELs in adult hearts with decreasing prevalence during aging. This is the first evidence of huVSELs in adult cardiac tissue. Cardiac huVSELs could be further explored in future studies to characterize their primitive potential and therapeutic potential in regenerative studies.

https://pubmed.ncbi....h.gov/31758373/

 

 

My hypothesis is that, insofar as SCs are somatic cell backups and VSELs are SC backups, the decline of VSELs is the root cause of aging, and that this C60/fusion protocol proliferates VSELs in vivo.

[yz69]

The first reference is very interesting is that they measure donor's DNA (which only exist in white blood cells) from bone marrow transplant patients. If 74% of DNA in mouthwash was donor's, they conclude that 74% DNA comes from white blood cells.

[Turnbuckle]

The first reference is very interesting is that they measure donor's DNA (which only exist in white blood cells) from bone marrow transplant patients. If 74% of DNA in mouthwash was donor's, they conclude that 74% DNA comes from white blood cells.

 

 

All right then, I'll buy that. But the result is highly variable. Out of 13 samples, the amount coming from the donor (presumably white blood cells as compared to buccal cells) ranged from 16-95%.

[QuestforLife]

I think it can, even in cases where there are no TACs. If the progression is directly from adult SCs to somatic cells, then epigenetic aging can only take place in the SCs, or by the decline in the SC niche populations. So where do replacement SCs come from? One obvious source is the blood supply, which contains VSELs that originate in the bone marrow. As they are pluripotent, they should have very low epigenetic age. The following article is pay only until Feb. of next year--

Thanks, I'll check that paper out. I've read quite a few papers on VSELs already, and find your argument persuasive. I still worry that VSELs are too rare and that if we amplify adult SCs we'll exhaust them via telomere attrition. But the evidence does seem to be leaning in your direction.

Edited by QuestforLife, 03 August 2020 - 08:49 PM.

[lost69]

I got back the results of my June TruMe test.

 

Chronological Age: 41.6

Biological Age 41.9

 

Intervention: 3 1/2 months of AKG. I also did a few rounds of TB's Stem Cell protocol (with no senolytics).

 

This is disappointing as it means there has been no change since my March 2020 methylation age test result from Zymo (42 yo).

 

Possible explanations:

TruMe uses a saliva test, which is less reliable than the blood or urine results from Zymo, and might have been affected by my bad hayfever during May and June.

I also took a Vit D and K2 supplment as a precaution against all the calcium in the AKG supplement. Vit D is a telomerase activator.

In my case having reversed my telomere age by 3 years recently through epitalon (and increased my methylation age by the same amount), I might need significantly longer to reverse my methylation age. 

 

Future plans: i have another TruMe test ready to go. My hayfever has relented and i've now replaced the VitD/K2 with just K2. I'll continue the AKG with occasional TB Stem Cell cycles (note I'm omitting any senolytics at this point) and report back when I done the next test (Sept or Oct).

 

i just started AKG after submitting my second mydnage test.shall i stop AKG until we get more results from you?could it be possible it interferes with stemcell protocol instead of boosting its results?

 

after my shoulder bone edema and small area of necrosis on humeral head in december 2019 i m using stemcells protocol 3-4days a week without senolytics (using pure stearic acid from sigma) nor any nicotinamide for fission.when i have some pain this protocol always fixes that

Edited by lost69, 04 August 2020 - 12:11 PM.

[QuestforLife]

i just started AKG after submitting my second mydnage test.shall i stop AKG until we get more results from you?could it be possible it interferes with stemcell protocol instead of boosting its results?

 

 

That is a decision you have to make for yourself.

 

I feel fine and intend to continue AKG until my next test in Sept or Oct. 

[Turnbuckle]

i just started AKG after submitting my second mydnage test.shall i stop AKG until we get more results from you?could it be possible it interferes with stemcell protocol instead of boosting its results?

 

 

 

How could anyone know if it interferes without even an hypothesis about its mode of action? It might act, for instance, as one of the following --

 

 

1. A senolytic.

2. A stem cell stimulant.

3. A somatic cell reprogramming agent.

4. A methyltransferase agonist, either maintenance or de novo.

 

From last year --

 

Here we show that alpha-ketoglutarate (delivered in the form of a Calcium salt, CaAKG), a key metabolite in tricarboxylic (TCA) cycle that is reported to extend lifespan in worms, can significantly extend lifespan and healthspan in mice. AKG is involved in various fundamental processes including collagen synthesis and epigenetic changes. Due to its broad roles in multiple biological processes, AKG has been a subject of interest for researchers in various fields. AKG also influences several age-related processes, including stem cell proliferation and osteoporosis. To determine its role in mammalian aging, we administered CaAKG in 18 months old mice and determined its effect on the onset of frailty and survival, discovering that the metabolite promotes longer, healthier life associated with a decrease in levels of inflammatory factors. Interestingly the reduction in frailty was more dramatic than the increase in lifespan, leading us to propose that CaAKG compresses morbidity.

https://www.biorxiv....0.1101/779157v1

 

 

 

And it seems there is a link between AKG and methyltransferase --

 

Embryonic stem cell renewal and differentiation is regulated by metabolites that serve as cofactors for epigenetic enzymes. Increase of α-ketoglutarate (α-KG), a cofactor for histone and DNA demethylases, triggers multilineage differentiation in human embryonic stem cells (hESCs). To gain further insight how the metabolic fluxes in pluripotent stem cells can be influenced by inactivating mutations in epigenetic enzymes, we generated hESCs deficient for de novo DNA methyltransferases (DNMTs) 3A and 3B. Our data reveal a bidirectional dependence between DNMT3B and α-KG levels: a-KG is significantly upregulated in cells deficient for DNMT3B, while DNMT3B expression is downregulated in hESCs treated with α-KG. In addition, DNMT3B null hESCs exhibit a disturbed mitochondrial fission and fusion balance and a switch from glycolysis to oxidative phosphorylation. Taken together, our data reveal a novel link between DNMT3B and the metabolic flux of hESCs.

https://pubmed.ncbi....h.gov/32652733/

 

 

So will AKG work with or against the C60/fusion protocol? My guess is that it will help, and will help the most when used with the senolytic/fission step.

[QuestforLife]

On the other hand, this paper suggests AKG helps iPSCs maintain pluripotency.

Intracellular α-ketoglutarate maintains the pluripotency of embryonic stem cells

https://pubmed.ncbi....h.gov/25487152/

Consequently, naive ES cells exhibit an elevated αKG to succinate ratio that promotes histone/DNA demethylation and maintains pluripotency. Direct manipulation of the intracellular αKG/succinate ratio is sufficient to regulate multiple chromatin modifications, including H3K27me3 and ten-eleven translocation (Tet)-dependent DNA demethylation, which contribute to the regulation of pluripotency-associated gene expression. In vitro, supplementation with cell-permeable αKG directly supports ES-cell self-renewal while cell-permeable succinate promotes differentiation.

This seems like the perfect supplement to expand VSEL numbers whilst avoiding differentiation, so it would go with the fusion part of the protocol.

[Turnbuckle]

On the other hand, this paper suggests AKG helps iPSCs maintain pluripotency.

Intracellular α-ketoglutarate maintains the pluripotency of embryonic stem cells

https://pubmed.ncbi....h.gov/25487152/


This seems like the perfect supplement to expand VSEL numbers whilst avoiding differentiation, so it would go with the fusion part of the protocol.

 

 

It might be preferable to use Vitamin C for that purpose.

 

...Global DNA demethylation occurs in the early embryo and the germ line, and may be mediated by Tet ... enzymes,* which convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Tet enzymes have been studied extensively in mouse embryonic stem (ES) cells, which are generally cultured in the absence of vitamin C, a potential cofactor... Here we report that addition of vitamin C to mouse ES cells promotes Tet activity, leading to a rapid and global increase in 5hmC. This is followed by DNA demethylation of many gene promoters and upregulation of demethylated germline genes. ... Collectively, the results of this study establish vitamin C as a direct regulator of Tet activity and DNA methylation fidelity in ES cells.

https://www.ncbi.nlm...les/PMC3893718/

 

*TET enzymes are instrumental in DNA demethylation.

Edited by Turnbuckle, 05 August 2020 - 04:58 PM.

[mister_blue]

Apologies in advance for the ignorant question among that thread of great knowledge. I studied math and phycics but I stopped biology after high school. I hope you will pardon me, but I've been asking so many people and I want so much to find the answer to those questions.

 

Does the body naturally renew the pool of stem cells after we stop C60 ? If not, could it be dangerous to take C60, reverse aging short term, and then maybe age a lot quicker later in life because we lack stem cells ?

 

Another question, if applied topically (on the head for hair loss), will the stem cells from another part of the body "migrate" there ? (Probably a laughable question but I wanted to check). In other terms, do I use up my stem cell pools for my hair instead of using them for something more useful ?

 

Thanks a ton !

 

PS: an extra question maybe but I think it's off topic. Did anyone manage to target some place in the body that needs repair ? I suffer from a ureteral stricture (e.g excess of scar tissue on the ureter), the only treatment is a reimplantation. Sounds like it's something C60 could theorically do but it's probably impossible to target it. That leads to the subquestion of "where does the C60 go first / what does it repair first "?

 

Thanks a TON !

Love,

Mr Blue

[Turnbuckle]

Did anyone manage to target some place in the body that needs repair ? I suffer from a ureteral stricture (e.g excess of scar tissue on the ureter), the only treatment is a reimplantation. Sounds like it's something C60 could theorically do but it's probably impossible to target it. That leads to the subquestion of "where does the C60 go first / what does it repair first "?

 

 

C60 doesn't directly repair anything. It hypothetically blocks UCP2 pores (through which protons are leaked) in quiescent SC mitochondria, thus waking up SCs to either differentiate or proliferate. Which path it takes is dependent on the mito morphology at that point. Mito fusion gets you proliferation and thus an increase in stem cells. After that, what is replaced will be dependent on cellular signalling. When cells die, they release signaling chemicals--paracrine factors--that tell stem cells to replace them. If too much damage is done, the result is the chaos of scarring, which can be irreversible. Insofar as it is not completely irreversible, this protocol will likely improve the outcome. I've had scars a few years old that completely disappeared. The age and size have a lot to do with it.

 

Does the body naturally renew the pool of stem cells after we stop C60 ? If not, could it be dangerous to take C60, reverse aging short term, and then maybe age a lot quicker later in life because we lack stem cells ? Another question, if applied topically (on the head for hair loss), will the stem cells from another part of the body "migrate" there ? (Probably a laughable question but I wanted to check). In other terms, do I use up my stem cell pools for my hair instead of using them for something more useful ?

 

 

There are around 200 cell types in the body, and most if not all have dedicated replacement cells stashed away in niches. These are multi-potent stem cells that can produce a limited number of cell types, depending on demand. These niches become depleted with aging. Recently it was discovered that there is also an embryonic cell type (VSEL) that is pluripotent and can serve as a backup to multi-potent stem cells. These pluripotent cells are immortal, at least in theory, so we may not have to worry about them. Still, I have suggested many times that this protocol is for geriatrics, as we don't know what the long term result will be. These pluripotent VSELs travel in the blood and are very small, so presumably they can get in anywhere. The problem is in the signalling. If you lose all the SCs in a hair root, for instance, there won't be any dying cells to release paracrine factors to tell those pluripotent cells what to do. Is it possible to apply such factors to the scalp? Possibly. But when a hair follicle is completely gone, it may be impossible to create a new one with supplements. Certain animals can do this, such a salamanders. They can create new limbs if needed. But we have lost that ability.

Edited by Turnbuckle, 05 August 2020 - 06:03 PM.

[eighthman]

Connected with Mr Blue, I do wonder about the relation between epigenetic age and stem cells.  It is encouraging to read about real physical changes reported in using this regimen.  My concern is that perhaps some areas are helped more than others in this, maybe connected to what is being actually measured in epigenetic tests.

 

For example, maybe the immune system is more accessible as to stem cell replacement than other things such as gray hair roots.  If so, that's still good w/covid and pneumonia hitting aged folks.

 

I appreciate this thread and the regimen. Just trying to figure it out.

[QuestforLife]

It might be preferable to use Vitamin C for that purpose.

 

 

It might help to add Vit C in addition to AKG; I doubt it would be effective alone as the in vitro study you point to used 100ug/ml.

 

From this study [1], Vit C serum levels were increased significantly (~38%) by 500mg vit C/day, but only to about 17ug/ml, less than a fifth of the required in vitro concentration. 

 

Perhaps we could do better with an lipsomal mix.

 

[1] https://www.tandfonl...4.2003.10719295

 

(Full text behind a paywall but can get it in the usual place)

 

 

Edited by QuestforLife, 06 August 2020 - 07:25 AM.

[QuestforLife]

The following article is pay only until Feb. of next year--

 

https://pubmed.ncbi....h.gov/31758373/

 

My hypothesis is that, insofar as SCs are somatic cell backups and VSELs are SC backups, the decline of VSELs is the root cause of aging, and that this C60/fusion protocol proliferates VSELs in vivo.

 

The paper you posted is quite remarkable, Turnbuckle.

 

I got my hands on the full text and have attached Figure 2. 

 

Look at the decline in VSELs by age 40 in both areas of the heart they looked at. You can see from this data why even the fittest hunter gatherers rarely live much beyond 40!

Attached Files

•  VSELs in the heart.png   351.09KB   4 downloads

[Turnbuckle]

The paper you posted is quite remarkable, Turnbuckle.

 

I got my hands on the full text and have attached Figure 2. 

 

Look at the decline in VSELs by age 40 in both areas of the heart they looked at. You can see from this data why even the fittest hunter gatherers rarely live much beyond 40!

 

 

After 40 it's all over. Just a long decline unto death. Thus the medical industry fights a thousand battles against aging, when there was one central source of it all along.

[QuestforLife]

After 40 it's all over. Just a long decline unto death. Thus the medical industry fights a thousand battles against aging, when there was one central source of it all along.

Looking at the falling VSEL numbers from age 9 to age 70, you'd only need about 5 doublings to restore the pool. Of course there woukd likely be some differentiation between rounds and also not all cells would respond to each stimulus. But it sounds achievable.

A note for those thinking about AKG. As it falls precipitously in the body after age 40, it may not be possible to reverse age under 40 using this supplement.

Edited by QuestforLife, 07 August 2020 - 04:43 PM.

[eighthman]

https://advances.sci...t/6/32/eaba1306

 

I appreciate that this regimen deals with aging paradoxes by reason of involving a cycle of change, not merely taking a pill, as is the custom in most fighting of aging.

[Turnbuckle]

https://advances.sci...t/6/32/eaba1306

 

I appreciate that this regimen deals with aging paradoxes by reason of involving a cycle of change, not merely taking a pill, as is the custom in most fighting of aging.

 

 

Methionine restriction has been shown to improve longevity in animals, and this is strange as méthionine is an antioxidant and is used by stem cells as a nutrient. Similarly, threonine is used by rodent pluripotent cells, and restricting it produces longer life. So what is going on? Why does feeding stem cells reduce longevity? My hypothesis is that dietary restriction conserves VSELs -- the very small embryonic like cells circulating in the blood that decline drastically with age. In humans their numbers fall off a cliff at around the age of 40. If you could restore the pool of VSELs, however, there would be no need to restrict méthionine (as long as you deal with its metabolite, homocysteine).

 

It is widely accepted that aging is related to decrease in rejuvenation/regeneration potential of several vital organs and tissues and could be explained by i) age related stem cell dysfunction, ii) accumulation of mutations in stem cell pool over a life-span and iii) shortening of the telomeres as result of decrease in telomerase activity. In this review we will present a hypothesis that aging could be also at least partially explained by an age-related decrease in number of pluripotent VSELs in adult tissues. We believe that this decrease in number of VSELs residing in adult tissues directly affects/impairs regenerative potential of organs as observed in advanced age.

https://www.ncbi.nlm...les/PMC3174085/

 

 

To appreciate the dramatic decline of VSELs with age, see the figure QuestforLife attached in post #1284.

Edited by Turnbuckle, 17 August 2020 - 12:18 PM.

[Turnbuckle]

A note for those thinking about AKG. As it falls precipitously in the body after age 40, it may not be possible to reverse age under 40 using this supplement.

 

Insofar as AKG acts through another mechanism -- such as by increasing methyltransferase in adult stem cells and transit amplifying cells -- it should reduce epigenetic age. 

[lost69]

Insofar as AKG acts through another mechanism -- such as by increasing methyltransferase in adult stem cells and transit amplifying cells -- it should reduce epigenetic age. 

 

i have used the stemcell renewal protocol as you suggested without the senolytic part for my acromion/clavicle bone oedema due to trauma, later i developped a very small osteonecrosis area on humeral head close to oedema parts.i showed everything to a good reumatologist/orthopedists/researcher and he said everything is healing well and no trouble even from the small osteonecrosis.he suggested recheck by 3 months but he is sure bone are ok already

 

do you suggest to keep the protocol without senolytic part until everything is healed complitely and also avoid mito fission/fusion (i never felt bad from mito fission even 1 week on fission)?

 

i am curious to see if the small osteonecrosis area on mri can be reversed and i was thinking to add AKG in renewal part or senolytic part due to its effect on bone remodelling too but i have too little knowledge to choose if it is best to use it on renewal or senolytic part.i'm 51yo and my dnage test of july should be ready soon so i have a baseline before adding changes and i have another test done about 2 years ago

 

thank you

Edited by lost69, 17 August 2020 - 11:57 PM.