That's not applicable here, Nate.
Stem cell self-renewal with C60
#181
Posted 28 May 2018 - 02:59 PM
#182
Posted 28 May 2018 - 05:39 PM
Ah you're not trying to go for fission here? Not sure what you're going for in terms of how exactly that would induce apoptosis of senescent cells. Also I thought the mechanism of action on fission might be increasing NAD+ levels by inhibiting CD38 but maybe not. My main concern here though was, as Michael put it, that phenolics are extensively metabolized into unabsorbable and/or biologically inactive metabolites in the intestines and liver, and so apigenin is fairly difficult to get into your system. Also, I thought inositol inhibited apoptosis. See:
https://www.tandfonl....4161/auto.4077
Edited by Nate-2004, 28 May 2018 - 05:40 PM.
#183
Posted 29 May 2018 - 11:27 AM
You are like a Johnny Appleseed of confusion, Nate. If you don't know what is going on, please refrain from making comments, and please stop reposting Michael's posts that don't apply. He might know what he's talking about, but you obviously do not.
Edited by Turnbuckle, 29 May 2018 - 11:29 AM.
#184
Posted 29 May 2018 - 01:20 PM
The only reason I continue reiterating the point about apigenin's lack of bioavailability is that people keep perpetuating the implication that it's effective orally in vivo, in mice or humans, regardless of what they're claiming the purpose is. I'm not trying to waste people's time I'm trying to save people's time and more importantly, money.
I don't see how this doesn't apply here, because you're taking it orally. I may not know as much as you or Michael, I have learned much from the both of you and others on this forum, but I'm not confused here. My only question to you earlier was a question of how you are dealing with the problem of its bioavailability.
Edited by Nate-2004, 29 May 2018 - 01:25 PM.
#185
Posted 29 May 2018 - 02:18 PM
The only reason I continue reiterating the point about apigenin's lack of bioavailability is that people keep perpetuating the implication that it's effective orally in vivo, in mice or humans, regardless of what they're claiming the purpose is. I'm not trying to waste people's time I'm trying to save people's time and more importantly, money.
I don't see how this doesn't apply here, because you're taking it orally. I may not know as much as you or Michael, I have learned much from the both of you and others on this forum, but I'm not confused here. My only question to you earlier was a question of how you are dealing with the problem of its bioavailability.
I don't think you are trying to be helpful at all. I think you are addicted to posting and don't care if you are wasting people's time and cluttering up threads. As for apigenin's bioavailability, you are misinformed. The availability from parsley may be low, but I'm not using parsley--
Given that dietary flavones are ingested predominantly as glycosides, their fate is determined by how and where they are absorbed, metabolized, transported, and excreted. The absorption of orally delivered flavone O-glycosides and aglycones has been the subject of many animal studies, particularly in rats. Most of these rat studies show that apigenin, luteolin, and their simple glucosides are absorbed quickly. The time of maximum plasma concentration (Tmax)3 was generally ≤1 h, with a maximum plasma concentration (Cmax) of 1–100 μmol/L (97–100), depending on the dose and the type of food coconsumed (food matrix).
https://www.ncbi.nlm...les/PMC5421117/
The metabolism of apigenin, a weak estrogenic flavonoid phytochemical, was investigated in the rat. After a single oral administration of radiolabeled apigenin, 51.0% of radioactivity was recovered in urine, 12.0% in feces, 1.2% in the blood, 0.4% in the kidneys, 9.4% in the intestine, 1.2% in the liver, and 24.8% in the rest of the body within 10 days.
https://www.ncbi.nlm...pubmed/15466493
Which means that at least 88% was absorbed. In a human trial, the absorption was rapid and far greater than with parsley. And as the paper says, most of the apigenin was apparently changed in the body and thus not excreted in the urine as apigenin per se--
The results showed thatthere was a quick urinary excretion after 1 h for both luteolinand apigenin, which might be attributed to their fast absorptionfrom the gastrointestinal tract, due to rapid hydrolysis of bothluteolin and apigenin glycosides by the enzymes of intestinalbacteria [5]. The fraction of the oral dose excreted in urine wasonly 2.30% for luteolin and 6.09% for apigenin within 12 h,respectively. The results suggested that sulfuric acid/glucuronicacid conjugates of luteolin and apigenin only represent smallpart of metabolites [13], other possible metabolites or potentialstorage tissues (blood, liver, kidney, intestines, and bodyresidues, etc.) need to be identified. However, the experimentalresults showed the accumulative excretion amounts of apigeninwere more than that of luteolin (Fig. 2A). Fig. 2B showed thecumulative urinary excretion of luteolin and apigenin decreasedat 2 h and increased once again during 5–6 h which suggestedabsorption of both could occur via an enterohepatic pathway[14]. Our results were different from those observed in humanvolunteer after parsley ingestion: within 24 h following ingestion,only 0.58% of apigenin was recovered in urine samples
Edited by Turnbuckle, 29 May 2018 - 02:29 PM.
#186
Posted 29 May 2018 - 02:28 PM
The P53 gene is important for ...
Maybe Artemisinin would have some value here?
It is widely studied for selective cancer cells cytotoxicity. Researchers found that cytotoxicity connected with its action on heme, but maybe, in the end, it translates to p53 expression.
https://www.ncbi.nlm...pubmed/24078446
https://www.ncbi.nlm...pubmed/25755006
http://www.jbc.org/c.../6587.full.html
Its quite controversial compound as it increases ROS in mitochondria. Fortunately, it's mostly specific to bacteria mitos, that's how its antiprotozoal and antimicrobial properties arise. Though its probably a case when dose makes a poison so overdoing Art could be unwise.
#187
Posted 29 May 2018 - 05:33 PM
Maybe Artemisinin would have some value here?
It is widely studied for selective cancer cells cytotoxicity. Researchers found that cytotoxicity connected with its action on heme, but maybe, in the end, it translates to p53 expression.
https://www.ncbi.nlm...pubmed/24078446
https://www.ncbi.nlm...pubmed/25755006
http://www.jbc.org/c.../6587.full.html
Its quite controversial compound as it increases ROS in mitochondria. Fortunately, it's mostly specific to bacteria mitos, that's how its antiprotozoal and antimicrobial properties arise. Though its probably a case when dose makes a poison so overdoing Art could be unwise.
Bacteria don't have mitochondria, but the protozoa that cause malaria do, and this drug targets their mitochondria while not substantially affecting mammalian mitochondria--
we found strikingly rapid and dramatic reactive oxygen species (ROS) production is induced with artemisinin in isolated yeast and malarial but not mammalian mitochondria
http://journals.plos...al.pone.0009582
Though as you indicated, it might be a bit dangerous.
As for IP6 and resveratrol I proposed for my senescence protocol, turns out there is a product that combines them--Longevinex--which was found to be beneficial in a very small human trial.
Longevinex® (L/RV) is a low dose hormetic over-the-counter (OTC) oral resveratrol (RV) based matrix of red wine solids, vitamin D3 and inositol hexaphosphate (IP6)...These three cases demonstrate that application of epigenetics has long-term efficacy against AMD retinal disease, when the retinal specialist has exhausted other therapeutic modalities.
https://www.ncbi.nlm...les/PMC4210925/
The paper uses the buzzword epigenetics, but I couldn't find where they've shown epigenetics to have anything to do with it. If the benefits instead resulted from removal of senescent cells, then combining it with fission ought to make it work much faster. Another paper speculates on the connection between senescence and macular degeneration--
Cellular Senescence in Age-Related Macular Degeneration: Can Autophagy and DNA Damage Response Play a Role?
We hypothesize that under some circumstances, RPE (retinal pigment epithelium) senescence may contribute to or/and precede irreversible pathological events in the retina specific for AMD (Age-Related Macular Degeneration), such as RPE loss and inflammation.
https://www.ncbi.nlm...les/PMC5687149/
Edited by Turnbuckle, 29 May 2018 - 05:51 PM.
#188
Posted 29 May 2018 - 06:22 PM
Stem cell self-renewal protocol, update 2
"And later, if feeling fatigue, 5 g L-Threonine + tablespoon of olive oil"
I'm adding taurine to that as well -- 5 grams or more. The combination of taurine, threonine and olive oil seems to work better than anything for removing the post protocol fatigue that occasionally develops hours later. I will also look into finding a better oil, as it seems unlikely that olive oil would happen to the best.
Taurine is important to stem cell nutrition and stimulates poliferation--
Taurine plays an important role in brain development, including neuronal proliferation, stem cell proliferation, and differentiation, via several mechanisms. Taurine can be directly used in clinical applications to improve brain development because it has no toxic effects on humans.
https://www.ncbi.nlm...pubmed/26906683
#189
Posted 29 May 2018 - 07:19 PM
As for IP6 and resveratrol I proposed for my senescence protocol, turns out there is a product that combines them--Longevinex
It seems that Longevinex has been revised and now includes more ingredients:
Ingredients
- Trans resveratrol
- Quercetin
- Rice bran IP6
- Vitamin D3
- Green tea (ECGC)
- Chlorogenic acid
- Nucleotides
- Beta cyclodextrin
Do you think taking the new full set to be beneficial or Resv+IP6 is the heavyweight combo that does the most of the senescent clearance and the rest are just "nice to have"?
Edited by aribadabar, 29 May 2018 - 07:23 PM.
#190
Posted 29 May 2018 - 08:07 PM
It seems that Longevinex has been revised and now includes more ingredients:
Do you think taking the new full set to be beneficial or Resv+IP6 is the heavyweight combo that does the most of the senescent clearance and the rest are just "nice to have"?
First, their purpose isn't elimination of senescent cells, and second, I've always suspected manufacturers of adding things to make to make it difficult for consumers to save money by buying the ingredients. In any case, quercetin seems iffy as a senolytic, so I wouldn't use it.
#191
Posted 29 May 2018 - 10:23 PM
As mitotic cells reach the end of their lives they slow down their dividing time almost as if they don't want to step any closer to the cliff.
Just look at this paper on methylene blue and in Fig 10 how substantially it extends the culture time to senescence and number of doublings of IMR90 cells.
https://www.scienced...213231715001159
Ironically this is the opposite of what we want to do at this point. At the risk of being facetious maybe we should all go out and get drunk, smoke a few cigars and eat some fast food? In short, we want to do ourselves some damage! (But not to our stem cells).
#192
Posted 30 May 2018 - 09:27 AM
Ironically this is the opposite of what we want to do at this point. At the risk of being facetious maybe we should all go out and get drunk, smoke a few cigars and eat some fast food? In short, we want to do ourselves some damage! (But not to our stem cells).
Stem cells say: Don't worry, be happy!
MB is an interesting substance, and after the work with MB and tau in the brain, other researchers looked at what else it might do, and found that it increases adult neural stem cell (ANSC) motility--
We further investigated the potential effect of MBon another ANSC functional property, their migratoryactivity (Fig. 2). Migration assays using Boydenchambers revealed that exposure of ANSC to 100 nMMB for a period of 6 h resulted in an approximately7-fold increase in the number of migrated cells(37.27 ± 15.15) in comparison to ANSC grown inDMEM (control, 5.12 ± 5.7).
#193
Posted 01 June 2018 - 10:36 AM
Thus if you take C60 from one of the online vendors and hope to live longer as the rats did, you probably won’t. In fact, by using up stem cells through asymmetric division, you may be robbing your future health to get an immediate but temporary benefit. This was not apparent with the rat trial as rats don’t live long enough for it to make a difference.
This comment threw me a little. Am I wrong in thinking the intention of the protocol in this thread is to produce a sustainable c60 life extension approach?
Edited by Fanatik, 01 June 2018 - 10:38 AM.
#194
Posted 01 June 2018 - 01:44 PM
This comment threw me a little. Am I wrong in thinking the intention of the protocol in this thread is to produce a sustainable c60 life extension approach?
Go back to the first post in this thread, where this is explained. The goal is to bias for symmetric division and self-renewal, whereas the uniformed use of C60 will likely produce asymmetric division and depletion of the stem cell pool.
#195
Posted 02 June 2018 - 01:52 AM
https://www.ncbi.nlm...les/PMC2864748/
Nutraceuticals Synergistically Promote Proliferation of Human Stem Cells
http://sci-hub.tw/10...scd.2006.15.118
#196
Posted 03 June 2018 - 11:33 PM
feedback on third round of this protocol using mitoq instead of pqq, no Potassium nitrate, no L-Selenocysteine, no Only Trace Minerals.also using 0.05ng of gfd11 per week
first day total crash slept all day and also slept late at night but it was like positive sleeping when you need to recover from sleep deprivation
second day good energy but less than usual when swimming
third day good normal energy
BP never goes over 120 or 84 now
vision keeps improving
skin keeps plumping up
wrinkles less and less visible
4th round:
very high energy all days, skin incredible, vision....i have mild infection/irritation from goggles anti fog spray so i can t judge this, BP has normalized to 106/74 since 3 days and hope it ll stay there
i am doing this protocol every weekend 3 days in a row, is this ok?
the other days i resume my usual supplements
Stem cell self-renewal protocol, update 2
The following looks complicated with a lot of supplements. But the core protocol requires just 2 things — stearic acid and C60. The basic idea is to put mitochondria into fusion with stearic acid, then to stimulate stem cells into symmetric division with C60. Mitochondrial morphology (fusion vs fission) biases division to either symmetric or asymmetric division. We want symmetric division for self-renewal and expansion of the stem cell pool — one stem cell becoming two. Then with the next treatment two becomes four, and so on in a compound interest fashion. Everything else is to protect stem cell telomeres and to make the process more efficient. The timing is based on cellular processes that run at different rates.
Time 0 (morning on empty stomach) —
Core brand Liposomal Glutathione — .5 g
Astragalus root extract powder — 5 g, in fruit juice, and/or Cycloastragenol — 10 mg
Optional —
L-Selenocysteine — 400 µg
One cap of LEF brand “Only Trace Minerals.”
Time 1:00 —
Stearic acid — 10 g, in brownie or hot chocolate (post #7)
Time 2:00 —
TUDCA — 500 mg
PQQ — 40 mg
Jiaogulan — 800 mg (or LEF brand AMPK activator)
L-Threonine — 5 g
Optional—
ALA — 600 mg
Taurine — 5 g
NAC — 600 mg
Time 3:00 —
C60 — 1 teaspoon of .6 mg/ml in oil, 3 mg C60
Vitamin C — 2 g
Optional —
Potassium nitrate — 300 mg
Gym at Time 3:30
And later, if feeling fatigue, 5 g L-Threonine + tablespoon of olive oil
I typically use all the options.
Suggested schedule —
Three days in a row, then a break of two or more days.
Notes —
C60
The fullerene C60 dissolved in oil is known to be an excellent antioxidant, and also has the ability to stimulate stem cells. The mechanism vis-à-vis stem cells has not appeared in published research, but I believe it is a physical feature of C60—that once attracted to the mitochondria for whatever reason, it has the right size and shape to plug UCP2 pores. These pores act as a governor on the ATP output by allowing protons to escape. Stem cell mitochondria are covered up with these pores, and thus function mostly by glycolysis rather than by oxidative processes. UCP2 pores are known to disappear before a stem cell begins dividing, and C60 appears to mimic that step by blocking the pores.
Thus if you take C60 from one of the online vendors and hope to live longer as the rats did, you probably won’t. In fact, by using up stem cells through asymmetric division, you may be robbing your future health to get an immediate but temporary benefit. This was not apparent with the rat trial as rats don’t live long enough for it to make a difference.
Stearic acid
Fusion was the missing factor all along. Stearic acts almost like a hormone, driving mitochondria into fusion, and fusion itself biases stem cells to self-renewal.
Supplements to lengthen telomeres include antioxidants to reduce telomere shortening and supplements that stimulate telomerase. Since none are known to do the job completely, I’ve included a number of them —
Glutathione
Astragalus root extract
Cycloastragenol
TUDCA
ALA
NAC
Vitamin C
L-Selenocysteine
Supplements to increase mitochondrial biogenesis and efficiency—
PQQ
Trace minerals
C60
Supplements that support stem cell nutrition—
L-Threonine
Taurine
Supplements that stimulate stem cells proliferation—
C60
TUDCA
Supplements that stimulate muscle stem cells (satellite cells)—
Potassium nitrate (forms NO)
NAC + Taurine (forms H2S)
These work with exercise
Glutathione
I used Core brand Liposomal Glutathione for bioavailability. Optionally you could break open a cap or two of ordinary reduced glutathione, mix it in a little water and take it on an empty stomach, lying on your left side for 10-15 minutes for gastric absorption.
How to take
L-Threonine, taurine and NAC can be mixed into fruit juice. Mix dry powders first for best dispersion of NAC (which is rather corrosive). Stearic acid in brownies or hot chocolate on an empty stomach speeds up the digestion and absorption. Digestion of raw stearic acid powder or flakes (which does not melt at body temp) will likely take a long and variable amount of time. Imagine digesting candle wax.
Edited by lost69, 03 June 2018 - 11:36 PM.
#197
Posted 04 June 2018 - 10:30 AM
feedback on third round of this protocol using mitoq instead of pqq, no Potassium nitrate, no L-Selenocysteine, no Only Trace Minerals.also using 0.05ng of gfd11 per weekfirst day total crash slept all day and also slept late at night but it was like positive sleeping when you need to recover from sleep deprivationsecond day good energy but less than usual when swimmingthird day good normal energy
I've experienced this as well--fatigue that begins about four hours afterward and may last a few hours, but never to this degree. The first couple of times I just couldn't stay awake, and then discovered more threonine, taurine, and a slug of olive oil would help. But I still get it, just not as severe. In fact yesterday, after adding silymarin to the protocol, I didn't get it at all. Fatigue seems to be common with stem cell treatments and can be long term for some. Here it seems to be very short, possibly because the stem cells are appearing where they belong and where they already were. But it's still mysterious why it should happen at all.
Edited by Turnbuckle, 04 June 2018 - 10:31 AM.
#198
Posted 04 June 2018 - 11:19 AM
Supplement for fusion: C18:0 — stearic acid.
Regulation of mitochondrial morphology and function by Stearoylation of TfR1
“We find that animal cells are poised to respond to both increases and decreases in C18:0 levels, with increased C18:0 dietary intake boosting mitochondrial fusion in vivo.”
Instead of pure form of stearic acid, Can cocoa butter be the substitute for stearic acid along with C60 in your protocol?
Or, Can just high percentage of dark chocolate be the substitute for stearic acid?
Edited by Graviton, 04 June 2018 - 11:20 AM.
#199
Posted 04 June 2018 - 11:46 AM
forgot to mention blood tests, they are all in the optiaml range like 10-20 years ago, blood glucose 78 (norm 70-100) and it was 84-94 since 2010, creatinine from 1.1 to 0.99 (max 1.3) which is good because i have to take a drug which is toxic to kidneys and creatinine was only moving upwards year by year, iron almost normal and it was abnormal all my life (family genetics probably).
the only thing that moved to less optimal is ast-alt from 22-16 to 27-32 not a big deal max norm range for men is 30.by the way when we have liver working too much we easily get this type of fatigue/sleep maybe it comes from there and silymarin is particularly active on liver.i usually take silymarin everyday except during the protocol, i ll take it next time and then recheck liver
I've experienced this as well--fatigue that begins about four hours afterward and may last a few hours, but never to this degree. The first couple of times I just couldn't stay awake, and then discovered more threonine, taurine, and a slug of olive oil would help. But I still get it, just not as severe. In fact yesterday, after adding silymarin to the protocol, I didn't get it at all. Fatigue seems to be common with stem cell treatments and can be long term for some. Here it seems to be very short, possibly because the stem cells are appearing where they belong and where they already were. But it's still mysterious why it should happen at all.
#200
Posted 04 June 2018 - 11:57 AM
Instead of pure form of stearic acid, Can cocoa butter be the substitute for stearic acid along with C60 in your protocol?
Or, Can just high percentage of dark chocolate be the substitute for stearic acid?
Get stearic acid. It's readily available in the US and cheap. For instance -- https://www.amazon.c...s/dp/B0050LKJ6Y
#201
Posted 10 June 2018 - 10:01 PM
Edited by Turnbuckle, 10 June 2018 - 10:08 PM.
#202
Posted 10 June 2018 - 10:56 PM
Results of the SC protocol after three months (approximately 30 treatments)—Hand eye coordination: Better than when I played little league as a kid. I’ve also seen an improvement in throwing with my non-dominant hand.Mental: I’m perceiving subtle problems in written materials I’d thought were perfect, instantly seeing how to improve them.Knees: I’ve had pains in both for years, and a feeling of swelling and instability in one and occasionally both. These problems steadily lessened and now are gone. A sharp pain in one knee that was like an ice pick when I knelt on it is gone. This had plagued me for 15 years, but now I can kneel on stone with no problem.Skin: Becoming steadily tighter and smoother. No age wrinkles on face. No broken capillaries evident (likely due in part to getting more sun). Skin pinch test on neck has gone from 3 seconds to 1.Morphology: Fat is disappearing, muscle mass increasing. (I will be reporting on a method of dramatically increasing weight loss in the next few days.)Stamina: Much increased.Appetite: Reduced.Feet: The most incontrovertible effect of C60 is shoe size. This had been stable for 40 years, but in 2012 began inching up coincident with my first use of C60, ultimately producing an average increase of ¼ size/year. After I started this stem-cell protocol 3 months ago it has accelerated at what may be 4 times that rate. (Hopefully it will stop before I run out of common shoe sizes.)Hair: Quality seems better. Straighter and healthier looking. Bald spot that had filled in back in 2012 then receded again now has new hair, but has a way to go.Hearing: No official test, but I no longer have trouble hearing others in noisy environments.Balance: Improved.Vision: Hard to say as it was fine to begin with. No change in prescription.Height: No change since starting this protocol. One inch gain since first use of C60 in 2012.Hands: No change compared to a cast of one hand from 30 years ago. A messed up flexor tendon sheath in one palm that had been getting worse for years has been restored. I can’t even tell which one it was.Hypertension: Still have to use medication, but it has stabilized so I don’t have to check it as often.Epigenetic age: I had this tested before I began and will test it again after one year.
Do you expect your epigenetic age getting older or younger after your method?
Edited by Graviton, 10 June 2018 - 10:58 PM.
#203
Posted 10 June 2018 - 11:49 PM
Do you expect your epigenetic age getting older or younger after your method?
I expect it to decrease, and I set out the reasons here--
https://www.longecit...ing-the-clocks/
#204
Posted 11 June 2018 - 10:25 PM
I injured my right knee in 2017-09 jumping down a few feet off a rock while hiking. It was injured to the extent that climbing stairs was painful and slow. This injury showed no sign of healing until after a second treatment of a modified Turnbuckle protocol. Today the pain is nonexistent and it feels nearly completely healed. While I can’t be certain, in the absence of other factors it seems likely that these treatments contributed to healing this injury.
I took 2 tsp stearic acid twice/day and 1 tsp C60 in HCT oil once/day for three days beginning May 25 and June 1. On the other days I took no supplements or medications.
#205
Posted 13 June 2018 - 12:55 AM
Feet: The most incontrovertible effect of C60 is shoe size. This had been stable for 40 years, but in 2012 began inching up coincident with my first use of C60, ultimately producing an average increase of ¼ size/year. After I started this stem-cell protocol 3 months ago it has accelerated at what may be 4 times that rate. (Hopefully it will stop before I run out of common shoe sizes.)
I'm a ballet dancer by trade, and through years of massive overuse and abuse I've mangled up my sad feet. They're horrible. But I've learned a zillion things about feet -- they're amazing, 26 bones, 33 joints, more than a hundred tendons, muscles ligaments, fascia...
But with age feet flatten and appear to grow -- that is, their supporting ligaments and tendons lose elasticity. Arches drop as the tendons along the lengths of the soles elongate through time and loss and just living life. We also lose the fat pads cushioning the bottom of the feet. But your feet probably do not literally grow because of your protocol -- I'm guessing tissue has degenerated and ligaments have become looser.
Evidence is clear that as we age 100% of us will experience "foot growth." This isn't healthy, though, it's a sign of escalating damages we want to slow, stop, and reverse. We don't want bigger feet; we want stronger, more flexible feet. Be kind to them -- but you've gotta work your feet just like every other limb you'd like to keep with age -- but observing their inevitable expansion probably isn't a sign of good foot health.
#206
Posted 13 June 2018 - 10:22 AM
Evidence is clear that as we age 100% of us will experience "foot growth." This isn't healthy, though, it's a sign of escalating damages we want to slow, stop, and reverse. We don't want bigger feet; we want stronger, more flexible feet. Be kind to them -- but you've gotta work your feet just like every other limb you'd like to keep with age -- but observing their inevitable expansion probably isn't a sign of good foot health.
You need to supply a reference for this assertion if you're implying that it could possibly explain the growth I've seen. I haven't found any research on it after a very superficial search on pubmed, but some sites say that feet do not grow (only becoming damaged, as with collapsing arches), while this site claims the following--
By some estimates, feet grow as much as a half size every decade after age 40...
As much as half a size every decade, it says, but coincident with my first use of C60 six years ago, my feet began to grow at a rate of 2.5 sizes per decade--five times that. And in the past three months of this stem cell protocol it has increased dramatically over that rate. So this is far out of any expected range, and far from representing damage, as I haven't had any foot pain since this began in 2012, while before that it was very common. Back then some shoe brands would leave me almost crippled, but that is no longer the case. My feet are much healthier today than before, and my formerly flat feet now show a decided arch.
Edited by Turnbuckle, 13 June 2018 - 10:38 AM.
#207
Posted 13 June 2018 - 03:27 PM
Thank you for documenting and sharing your personal self-experimentation, it's fascinating and beneficial for all. A helpful public service! Much of it loses me, of course, but this bit of anecdotal benefit claim observed jumped out at me:
I'm a ballet dancer by trade, and through years of massive overuse and abuse I've mangled up my sad feet. They're horrible. But I've learned a zillion things about feet -- they're amazing, 26 bones, 33 joints, more than a hundred tendons, muscles ligaments, fascia...
But with age feet flatten and appear to grow -- that is, their supporting ligaments and tendons lose elasticity. Arches drop as the tendons along the lengths of the soles elongate through time and loss and just living life. We also lose the fat pads cushioning the bottom of the feet. But your feet probably do not literally grow because of your protocol -- I'm guessing tissue has degenerated and ligaments have become looser.
Evidence is clear that as we age 100% of us will experience "foot growth." This isn't healthy, though, it's a sign of escalating damages we want to slow, stop, and reverse. We don't want bigger feet; we want stronger, more flexible feet. Be kind to them -- but you've gotta work your feet just like every other limb you'd like to keep with age -- but observing their inevitable expansion probably isn't a sign of good foot health.
Thank you. I was not aware of that. I previously thought foot growth was good. As I am medically trained, I know that the growth plate closed after 17-18 years of age on average. That's why I thought increase in height with C60OO would be impossible unless the growth plate not longer got closed with the treatment. Bigger feet may mean tendons & ligaments becoming more lax as per the following article.
health.clevelandclinic.org/shoes-getting-tight-feet-change-size-time
#208
Posted 14 June 2018 - 09:20 AM
Hi Turnbuckle
I've been doing some thinking about symmetric and asymmetric stem cell division and it's occurred to me how vital symmetric division is in maintaining the telomere length of stem cells and hence their ability to maintain sufficient cells in various tissues.
Every time a cell divides one cell gets the longer telomere strand and one cell gets the shorter one. These each serve as the template for the other strand to be made by DNA polymerases in the new cells; in each case the new strand will be shorter than its template due to the 'end replication problem'. This means one of the new cells will end up with the same telomere length as its progenitor and one will end up with a shorter one.
www.ncbi.nlm.nih.gov/pubmed/10787419
This means that a single stem cell forms the top of an expanding pyramid of cells and that the length of a stem cell’s telomere controls the size of somatic cell pool that can be supported by that one stem cell (in this simplified example with just one stem cell).
So the loss of a somatic cell, especially one with a shorter telomere is no big deal, as it can be replaced by the cell above it in the pyramid; you’ll always get a perfectly good replacement cell in both cases. But if you lose the stem cell at the top of the pyramid, you’ve permanently lost one cell from the pool (in this simplified example) that can’t ever be replaced from within that tissue. As stem cells can make more than one tissue type you’ve also lost the ability to support another tissue with that stem cell, should you need it due to the loss we’ve just described.
So where does symmetric and asymmetric division come in? Well there was a theory called the immortal strand hypothesis, where the stem cell kept the pristine strand (with the long telomere) and gave the other strand to the differentiated cell. But this looks like it isn’t true; the stem cell cannot control which strand it ends up with.
https://www.ncbi.nlm...pubmed/25700960
So if this is true, it means there is a 50% chance that each time a stem cell divides asymmetrically it will end up with the shorter strand, giving the long strand to the somatic cell. This means that the pool of cells it can now support is smaller (in any tissue it supports). Over time one can see how both the loss of stem cells through attrition, and their gradual loss of telomeres in asymmetric division, means that the number of cells in tissue goes down, and the body has to hold onto senescent cells for longer.
But if a stem cell divides symmetrically, one of the offspring stem cells will always preserve its telomere and be able to maintain the same number of offspring cells as its progenitor, and there will also be another stem cell produced; so even if the pristine stem cell is lost, you’ll have another one that is almost as good.
#209
Posted 14 June 2018 - 10:48 AM
So where does symmetric and asymmetric division come in? Well there was a theory called the immortal strand hypothesis, where the stem cell kept the pristine strand (with the long telomere) and gave the other strand to the differentiated cell. But this looks like it isn’t true; the stem cell cannot control which strand it ends up with.
https://www.ncbi.nlm...pubmed/25700960
So if this is true, it means there is a 50% chance that each time a stem cell divides asymmetrically it will end up with the shorter strand, giving the long strand to the somatic cell. This means that the pool of cells it can now support is smaller (in any tissue it supports). Over time one can see how both the loss of stem cells through attrition, and their gradual loss of telomeres in asymmetric division, means that the number of cells in tissue goes down, and the body has to hold onto senescent cells for longer.
But if a stem cell divides symmetrically, one of the offspring stem cells will always preserve its telomere and be able to maintain the same number of offspring cells as its progenitor, and there will also be another stem cell produced; so even if the pristine stem cell is lost, you’ll have another one that is almost as good.
Isn't it the purpose of telomerase to keep the telomeres of stem cells at the correct length, thus granting it immortality? Your link is not directed to telomeres, in fact, but to genetic damage to the stem cell genome. From that article, there appears to be no mechanism for selecting which is the better (less mutated) DNA strand or which has the longer telomeres (though telomeres are not mentioned), and given that telomerase should restore the latter, there would be no purpose to it anyway.
More important to maintaining stemness is the condition of the mitochondria. When stem cells divide asymmetrically, they segregate bad mitochondria to the somatic daughter cell while keeping the good ones in the stem daughter cell--
It has also been observed that in asymmetric division, old mitochondria, which are central metabolic organelles, are segregated to the daughter cell fated to cell differentiation, whereas in symmetric division, young and old mitochondria are equally distributed between both daughter cells.
https://www.ncbi.nlm...les/PMC5055439/
Thus a cycle of asymmetric and symmetric divisions would keep the stem cell pool topped off and eliminate their load of bad mitochondria. This protocol addresses the symmetric division, with the asymmetric division allowed to proceed as needed by the body.
Another consideration to stem cell vitality is the number of mitochondria and their activity. Stem cells are kept stem cells by the lack of mitochondrial activity, and failure of mitophagy will allow the numbers to build, possibly eliminating stemness.
Autophagy maintains the metabolism and function of young and old (hematopoietic) stem cells
With age, hematopoietic stem cells (HSCs) lose their ability to regenerate the blood system, and promote disease development. Autophagy is associated with health and longevity, and is critical for protecting HSCs from metabolic stress. Here, we show that loss of autophagy in HSCs causes accumulation of mitochondria and an activated metabolic state, which drives accelerated myeloid differentiation mainly through epigenetic deregulations, and impairs HSC self-renewal activity and regenerative potential...Our results demonstrate that autophagy actively suppresses HSC metabolism by clearing active, healthy mitochondria to maintain quiescence and stemness, and becomes increasingly necessary with age to preserve the regenerative capacity of old HSCs.
https://www.ncbi.nlm...les/PMC5344718/
And this suggests something else--that maybe this protocol shouldn't have PQQ or any supplements that promote biogenesis. Because fewer mitochondria in a stem cell appears to be better.
#210
Posted 14 June 2018 - 12:28 PM
Isn't it the purpose of telomerase to keep the telomeres of stem cells at the correct length, thus granting it immortality? Your link is not directed to telomeres, in fact, but to genetic damage to the stem cell genome.
I've never seen any evidence stem cells (other than embryonic stem cells) can re-elongate their telomeres. At best some residual telomerase activity can slow the rate of loss.
I'm aware the second paper is about mutations, but it makes my point the stem cell can't pick and chose between strands. But in any case I was being overly simplistic, as there are 46 chromosomes per cell and the daughter cells will have a mix and match of long and short strands to replicate from. Nevertheless it is the shortest telomere amongst all the 46 chromosomes that limits division, and there is evidence that certain chromosomes have the shortest ones consistently:
https://www.ncbi.nlm...pubmed/16804004
So I think my point stands that asymmetric division will in the long run be bad for the telomere length of stem cells; symmetric division by contrast will leave you with one stem cell as good as its progenitor.
Everything else you're say I agree with - I wonder if there is anything else we can do to apart from fusion to encourage the maintenance of stemness? Perhaps something to inhibit glucose metabolism?
Edited by QuestforLife, 14 June 2018 - 12:30 PM.
Also tagged with one or more of these keywords: c60, stem cells, mitochondria, fusion, stearic acid, aging, hydroxytyrosol, olive oil, mct oil, proliferation
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