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Alternative methods to extend telomeres

Started by QuestforLife , Sep 04 2018 03:18 PM

telomeres nad nampt ampk resveratrol allicin methylene blue nmn sirtuins statin

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#1111 Castiel

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Posted 17 September 2025 - 01:49 PM

Forgot to mention the near identical to resveratrol molecule pterostilbene is showing strong antiaging effects in topical skin treatment.

High dose oral pterostilbene adversely affects cholesterol, but topical can achieve high dose without such effects afaik

Scientists test an anti-aging cream that actually works
"Pterostilbene cream improved wrinkles, skin firmness, collagen, and pore size far better than a control emulsion. The results highlight pterostilbene as a promising natural ingredient for next-generation anti-aging skincare."
https://www.scienced...50914205851.htm

Informative x 2

#1112 QuestforLife

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Posted 17 September 2025 - 02:38 PM

I heard somewhere that telomere elongation can only occur during replication stage. Not sure if true and if this affects telomerase activation.

Yes, that's true, cells have to be in s-phase for the telomere to be accessible (*).

But like so many things in biology it may not be an absolute rule. And this is where short telomeres being more easy to elongate come in, because the end is more accessible.

The telomere end is completely accessible during DNA-replication, as it has been unrolled. And it is completely inaccessible when folded up and tucked in. But in-between these two states there are situations where the telomere end has some accessibility, and this is enhanced with a short telomere because it is more difficult to tuck it in.

This is the proposed mechanism behind rejuvenation of old people using telomerase activators that are not strong enough to lengthen telomeres back to youthful length, but may be strong enough to take you back some of the way, or rather maintain an equilibrium point at some greater length than would otherwise be the case, with greater mortality than is optimal, but lower than it would otherwise have been.

It is virtually impossible to say how many years this might give you, or how much extra health span. But Bill Andrews is 73 and an endurance runner. He doesn't look young. And doesn't look to be getting any younger. But the does look much better than most his age.

(*) It may be a mechanism for inhibiting telomerase activation as well, i.e. short telomeres have one telomerase blocking mechanism removed, but this is not confirmed.

Edited by QuestforLife, 17 September 2025 - 02:40 PM.

Good Point x 2

#1113 Castiel

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Posted 18 September 2025 - 06:04 PM

Im still surprised asking chatgpt shows lack of lifespan telomerase experiments in vitro or in vivo for pterostilbene.

Given resveratrol effects and pterostilbene topical effects. It seems like a common sense conclusion is pterostilbene may be able to achieve similar easier.

Pterostilbene raises ldl at high dose, but the high doses would only be needed for a few weeks or months assuming it is as effective as resveratrol at activating telomerase. Given higher bioavailability and longer half life.

One would think someone would test pterostilbene for this in animals or at least in cells.

Good Point x 1

#1114 QuestforLife

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Posted 19 September 2025 - 11:49 AM

Both resveratrol and pterostilbene are two-faced, they seem to inhibit or activate telomerase depending on dose and cell type. As far as I'm concerned, no one has yet figured out what their mechanism of action is, precisely. To me they always seemed like poisons that in certain circumstances end up being hormetic.

Good Point x 2
Agree x 1

#1115 Castiel

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Posted 01 October 2025 - 02:18 PM

A recent article commenting on topical pterostilbene

https://www.popularm...-age-your-face/

It seems rejuvenating effects are observed if cells are exposed to high enough dose for long enough

like x 1

#1116 QuestforLife

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Posted 08 October 2025 - 11:25 AM

Summary of ‘Alternative Methods to Extend Telomeres’ Sept 2018 to Oct 2025

Early work on NAD+

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/#entry857309

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-2#entry868202

SIRT4

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-3#entry870174

Loss of NAD+ because of telomere shortening

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-13#entry900015

Work on Statin-Sartan protocol

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/#entry862269

link between ROCK inhibitors and telomerase

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/#entry864097

possible link with senolytics

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/#entry864534

using ROCK and mTOR inhibitors to reprogram brain cancer cells into normal neurons

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/#entry865160

How ROCK inhibitors block differentiation

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-4#entry878635

Feedback on protocol

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-5#entry881808

Summary of ROCK inhibition action on cells

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-6#entry883118

Attempts to come up with alternatives to statin and sartans

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-7#entry884915

Diagram of interventions

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-8#entry885663

Paper linking up ROCK and ECM

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-8#entry885731

ROCK and tgf-b

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-8#entry886244

Mean and Max lifespan extension with a ROCK inhibitor

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-10#entry896988

Work on telomerase activators and other important telomere papers

Royal Jelly

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-2#entry866228

Review of various activators

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-4#entry875566

Asiaticoside

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-5#entry880274

Some other telomeres studies

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-7#entry884556

Effect of antioxidant on telomere shortening in the bone marrow

https://www.longecity.org/forum/topic/102169-alternative-methods-to-extend-telomeres/page-8#entry885539

#1117 dlewis1453

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Posted 09 October 2025 - 03:21 PM

Great compilation QuestForLife! Thanks for all the time you spend meticulously documenting your research and sharing your results with us. I've been very busy with life in 2025 and haven't had much time to post, but I still eagerly read all of your updates.

I'm curious if you are still using stearic acid as a fat burning agent? I'm considering starting a cocoa butter protocol to try to burn fat and gain muscle at the same time.

#1118 QuestforLife

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Posted 11 October 2025 - 11:08 AM

I'm curious if you are still using stearic acid as a fat burning agent? I'm considering starting a cocoa butter protocol to try to burn fat and gain muscle at the same time.

The answer is no. I haven't used Stearic acid for some time.

I now only use DHM to encourage fusion and also - the bounce back from glucose to fat burning you get when you use niacin. I find that metabolic health is the easiest and most effective longevity level to pull, and this can be done effectively with niacin.

Good Point x 1

#1119 Castiel

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Posted 11 December 2025 - 05:03 PM

Consulted with gpt and it believes the resveratrol study showing human cell rejuvenation was through alt mechanisms not through telomerase activation, given the cells involved don't express telomerase. So if resveratrol can activate alt at high doses in normal aged cells, it is conceivable other compounds may also activate alt and lengthen telomeres.

#1120 Advocatus Diaboli

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Posted 12 December 2025 - 06:46 AM

Re: Post 1119

Edited note--the formatted table in point 3, below, was damaged when inserting into this post.

DeepSeek says:

Conclusion

"It is conceivable and probable that certain compounds—particularly those that degrade ATRX, inhibit DNA repair, or modulate recombination—could create cellular conditions that permit or promote the ALT pathway in susceptible cells. However, this would be a dangerous and undesirable effect for healthy tissue, akin to promoting carcinogenesis.

The more relevant and active field is discovering compounds that lengthen telomeres via telomerase activation or slow their attrition, and separately, discovering compounds that specifically kill ALT-dependent cancer cells by inhibiting the pathway.

If your interest is in healthy aging, the focus should be on the former (telomerase/telomere maintenance), not on the cancer-associated ALT pathway."

The full answer to the prompt (taken from post 1119) "is conceivable other compounds may also activate alt and lengthen telomeres." is:

Excellent and sophisticated question. This ventures into cutting-edge molecular biology and aging research. The short answer is:

Yes, it is highly conceivable, and there is active research in this area. However, the relationship is complex, nuanced, and importantly, activating the ALT pathway is generally not a desired goal for healthy aging.

Let's break this down.

1. Understanding ALT vs. Telomerase

First, a crucial distinction:

Telomerase is the enzyme that naturally maintains telomeres in stem cells, germ cells, and, problematically, in ~85-90% of cancers. It adds telomeric DNA directly.
ALT (Alternative Lengthening of Telomeres) is a recombination-based mechanism used by ~10-15% of cancers (common in sarcomas, glioblastomas, and certain carcinomas) and some immortalized cell lines to maintain their telomeres without telomerase. It is characterized by heterogeneous telomere lengths, telomeric DNA copying between chromosomes, and special structures called ALT-associated PML bodies (APBs).

2. Could Compounds "Activate" ALT in Normal Cells?

This is the core of your question. In theory, yes, but with major caveats.

The Trigger: ALT activation in cancer usually occurs after the cell has already become cancerous and has lost normal cell cycle controls (often via p53 and Rb pathway inactivation). It is a survival mechanism for those rogue cells.
Hypothetical Pathway: A compound could, in principle, induce the conditions that favor ALT by:
1. Severely disrupting normal telomere maintenance (e.g., chronically inhibiting telomerase in a cell that relies on it).
2. Inducing DNA damage and recombination at telomeres (e.g., through compounds that cause telomere-specific oxidative stress or replication stress).
3. Dysregulating the proteins that suppress ALT in normal cells (e.g., proteins involved in the ATRX/DAXX chromatin remodeling complex, whose loss is a hallmark of ALT-positive cancers).
The Reality: Deliberately inducing ALT in a normal, healthy cell would likely be highly mutagenic and carcinogenic. You would be pushing the cell toward a cancer-associated, genetically unstable state.

3. Compounds That May Indirectly Influence Telomere Length or ALT Status

Research has identified substances that affect telomere biology, some of which might tip the balance in cells already on the cusp of using ALT. None are straightforward "ALT activators" for therapy.

Compound/Class Proposed Mechanism Effect on Telomeres Relevance to ALT Cereblon Modulators (e.g., some immunomodulatory drugs) Degrade proteins like ATRX (a major ALT suppressor). Could potentially induce ALT-like features in cells where ATRX is degraded. Direct. This is a prime example of a compound that could theoretically enable ALT by removing a key blocker. DNA Damage Response (DDR) Inhibitors (e.g., ATR inhibitors) Impair the cell's ability to repair DNA, including at telomeres. Cause telomere dysfunction and replication stress. Indirect. Could create the genomic instability that promotes recombination-based telomere maintenance (ALT). Recombination Modulators Affect homologous recombination (HR) pathways. Could either promote or inhibit telomeric recombination. Direct. Modulating HR is at the heart of the ALT mechanism. Oxidative Stress Agents Increase reactive oxygen species (ROS). Cause telomere shortening and damage, potentially triggering a crisis. Indirect. Could be a first step in forcing a cell to seek an alternative survival mechanism like ALT. G-quadruplex Stabilizers (e.g., BIBR1532, Telomestatin) Stabilize the G-quadruplex structures in telomeric DNA, blocking telomerase. Initially shorten telomeres; in cells without telomerase, can trigger crisis. Indirect. By inhibiting telomerase, they might select for the outgrowth of any pre-existing ALT cells in a population.

4. The Therapeutic Paradox & Future Directions

The intense research focus is not on activating ALT, but on targeting and inhibiting it to kill ALT-positive cancers.

ALT Inhibitors are being sought to treat the cancers that rely on this pathway. Potential targets include proteins essential for ALT (e.g., BLM, MUS81, SLX4, PML) or the unique chromatin state of ALT telomeres.
For Healthy Aging: The goal is telomere maintenance, not ALT activation. Research here focuses on mild telomerase activators (e.g., TA-65, a cycloastragenol derivative), lifestyle factors (diet, exercise, stress reduction), and other compounds (astragalus extracts, marine omega-3s) that may slow attrition through antioxidant or anti-inflammatory effects.

Conclusion

It is conceivable and probable that certain compounds—particularly those that degrade ATRX, inhibit DNA repair, or modulate recombination—could create cellular conditions that permit or promote the ALT pathway in susceptible cells. However, this would be a dangerous and undesirable effect for healthy tissue, akin to promoting carcinogenesis.

If your interest is in healthy aging, the focus should be on the former (telomerase/telomere maintenance), not on the cancer-associated ALT pathway.

Edited by Advocatus Diaboli, 12 December 2025 - 06:48 AM.

#1121 QuestforLife

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Posted 12 December 2025 - 12:39 PM

Consulted with gpt and it believes the resveratrol study showing human cell rejuvenation was through alt mechanisms not through telomerase activation, given the cells involved don't express telomerase. So if resveratrol can activate alt at high doses in normal aged cells, it is conceivable other compounds may also activate alt and lengthen telomeres.

Bear in mind that cells in vitro are exposed to atmospheric oxygen levels as opposed to the much lower levels found in the body. Therefore, they will experience much higher oxidative stress in vitro. Under those conditions it is possible that resveratrol becomes a pro-oxidant, and given the molecule has an affinity for DNA, and that telomere DNA is highly susceptible to oxidative stress due to its prevalence of guanosine, I find it likely that in some conditions resveratrol can either contribute to the breaking off of bits of telomere, or exploit those existing conditions due to its affinity for DNA to potentially lead to recombination.

I have spoke before about combining resveratrol with copper to promote a healthy form of oxidative stress and it seems this approach is gaining traction now for the treatment of brain cancer, where the oxidative stress destroys the cell free chromatin particles that cancer spews into tissues and the blood stream.

I should add, I advise caution if any readers are thinking of using this protocol long-term, as elevated oxidative stress will oxidize cholesterol in your bloodstream. In my case I have normal blood pressure and low inflammation, so this did not do me too much harm, but I do have borderline high cholesterol, and over a year or so this protocol did lead to the occurrence of Xanthelasma; others might not be as lucky.

#1122 bullGenteel

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Posted 13 December 2025 - 09:05 AM

I am on the end of a trial of your herbal statin/startin protocol. This is I guess my third attempt. I feel yhe results are postive overall. I was gonna suggest reservatrol/copper as much more helpful compared to no reversatrol in the protocil. My understanding from your work is that it enhances the sirt 4 activity to arrest cellular growth to promote repair. I am only 10 days or so in, but feel it is helping overall more so my last time I did not use reversatrol.

I know when I took nicotine for a month or so. I remember I felt fine till a few weeks in. I didn't get any muscele soreness contributed to vasoconstriction. It may have been glucose related because I just a little felt off. I did have some varicose veins that showed up later though in just one small area around an injured ankle. I dont think I had symptoms of vasoconstriction perhaps because I was taking reservatrol/copper. I must have taken that for a couple of months. I was only taking 30mg reversatrol but every 4 hours or so.

I feel subjectively better, in this latest round of your protocol, taking reversatrol. The reversatrol is known to lower blood pressure to relax the walls of blood vessels somehow. I was gonna ask your opinion if reverstrol could be combined with your original statin/startin protocol. But I had a feeling it could have negative interactions since if the medications are a blood pressure med and cholesterol med. I never got around to trying those meds but the reversatrol has seemed to enhance your herbal statins protocol for me. I know that as well I was underfunctioning around this time, and it was likely due to mitochondria woes. I did feel a lot better after I addressed this.

I do have higher inflammation from a couple injuries and neuro inflammation. It may be more considered to limit reversatrol use only with the herbal statin/startin protocol a few times a year. I would likely think I would be farther along if I were better at self managing my recovery. I was a skatterbrain before I do make some moderate setbacks at times this last year. I do feel weary about experimenting for a prolonged period. I felt safer when I followed a stricter keto diet and took anti-inflmmatories. I guess some users have followed a similar stack for decade or so workout much problems and Linus pauling loved to 93. I think I will do some tests with a doctor for some problems that can creep up.

I was dreaming up an idea to make a post about a theoretical semi-permanent cure for OCD. I can get some overly ambitious notions. I wouldn't try it, ever perhaps; certainly not, till I have made much more headway in recovering from a brain injury. It was a similar line of thinking, I cherry picked it from Turnbuckles stem cell thread with the user Kelvin using 5htp to circulate stem cells that ended up downregylating serotonin receptors. I have modified his work to seemingly help myself with recovery without the negative serotonin complications. Nicotine receptors are presupposed to upregulate from agonistic means. But it could interact with adrenaline/ neroepinehriene and dopamine. Even blood pressure but I wondered if something in kind like Reversatrol could counter blood pressure. It would probably just be a novel theoretical assumption for a what if requested query of users. I have scored an imbalanced IQ scores before, so I may have cool sounding ideas that are not feasible in implementation in actual fact. It may be wishful thinking I like to think the nicotine lozenges I used had some semi-lasting OCD allevation by upregulating receptors, but I'm not sure.

I am just an experimentor with nothing to add to the science. My stronger skills are just in reading. I should say sorry to hear about your troubles with reverstrol. I similarly have normal blood pressure and have at times been tested as high normal cholesterol and other times fine. I seem to remember you mentioning you would only take reversatrol for a couple weeks per month or somewhere along those time lines. Or did I mistake that claim with another in your thread? Was that enough use consistent to have negative effects I wonder? I guess it is all part and parcel with experimenting. I guess minor cosmetic corrections are called for. I can say I did recall fafner55 used trelahose to dissolve skin tags or blemishes of some kind. The supplements is indicated for high lipids. I don't excel at science or medicine as I say. I am not really capable of working out science on my own to come up with any high level solutions. I appreciate user's such as your self who share well constructed theories as something I can look into for myself.

#1123 QuestforLife

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Posted 13 December 2025 - 10:56 AM

I guess it is all part and parcel with experimenting.

Exactly. I never take large does of resveratrol, those with copper are very small. I do still believe in the Cu+Res combo but like many things we have to be cautious and get dosing just right.

Thanks for the tip on trelahose, I will look into it.

#1124 bullGenteel

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Posted 14 December 2025 - 04:11 AM

For sure no problem, I hope fafner55 thread could help you, Im sure if it's posible you have a better chance than most based off your contributions here. Fafner55 has some interesting protocols. Like I said I can read well enough but not really skilled enpugh to develop any protocols. I suspect your protocol here would be best for handling senscient cell removal rather than not taking into account cell becoming less stem like as we age. I liked your ideas and your proposals. I had one bad experience with senscient cell removal. If I had been better organized I may may have been further along in this last year of looking at brain injury treatment I still really appreciate your work. I saw a research article about larger cell losing stemness which could account for alzhimers.

I thought fafner's trelahose experiment was interesting but he said he felt overall better, subjective results from regular fasting and it seemed a little to superficial for me to just to remove some blemishes. Plus I don't trust myself to make physically experiment, I even struggle with probitoic yougart sometimes. If it turns out his work comes in handy for correcting a wayward venture in biohackong than that is part and parcel too.

Talking about being careful about doses and keeping stacks minimal to avoid unintended consequences. I got scared when I had a lot of skin tags show up after doing your protocol. I am pretty sure I stupidly combined high dose chondriton too close to the protocol -or during it I don't recall. Off top of my head chondirton can build up cells it is used with glucosamine. Cholesterol, diabetes and poor circulation might be correlated with skin tags. But AI is suffers heavily from confirmation bias as not being able to vet research. A quick query and colon poops might be correlated with cholesterol. Perhaps reversatrol played some part. I suffer ocd and hypochodry. But I should get my colon checked. I don't have excessive digestion issues. I did intake some questional probiotic batches.

I know the skin tags stopped appearing when I cut out telemere enhancers and if I recall reversatrol and especially chondriton. I clued into that and overuse of telemeres and chondriton were suspect to me. I got a biopsy done and it was negative for any malignancy. It was a little scary. I am not the most carefully organized person. I think I may be slowly improving. I wasn't ever a very organized person but a concussion can magnify problem areas I suppose.

I suspect reversatrol at my low dose wasn't enough to fully offset vasoconstriction if it did anything. I didn't feel much symptoms but I wasn't exercising much. I got a little bit of varicose veins appeared.

Keep us informed if it can be useful if any of us have lipid issues like I may have experienced some minor issues too, although perhaps from combining a needless variable with chondriton.

#1125 bullGenteel

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Posted 14 December 2025 - 11:31 PM

I should say I don't think this protocol necessarily lead to excessive moles or skin tags. I was thinking of posting before but I thought it was just my stupidity not following the guidelines or warning in this thread. I judge my behavior in considerstuon I am recovering from a brain injury.

It was about 6 or 7 months ago. I know I extended the rox/loc inhibitors protocol for like 5 weeks or so up from 3. Then I ended up taking telomere enhancing supplements for like 3 months straight. I had worried for a while that I had previously used c60 and did repairs to cells that may have had shortened telomeres induced by my injuries. I worri3d i had healed cells wirh short telomeres. I thought I could remedy that mistake by taking telomere agents daily. Sorry for all the excessive personal info. I get in the mode of wishful thinking problem solving, inplace of following the actual logical framework that actually works. I had read your advice that the best time to extend telomeres is with the progentor stage after the protocol. I believe you warned that telomere extension should also be cycled I am assume to prevent some excessive growth, bengin or otherwise, as well as to conserve stem cells and give stem cell pools a chance to recover.

I also took reversatrol, high dose chondriton and nicotine during this time, except for during the 5 weeks of the protocol I didnt take nicotine. I took astralgus root daily, if I recall. I have considered taking astralgus root for a few days a week. You mentioned it may be easiest to lengthen already short telomeres because of the curled tail or something along that line. That may be safer way for myself to correct some degree the shorter telomeres I amy have in damaged cells resulting from my injuries from the accident

. I also did a few days of senyiotics which had some ill effects. Winging it and lowered inhibition and poorer decision making can make up the presentation of a concussion, but I am improving in this area.

Moles do run in my family. I inherited this from one of my parents. Said parent is at retirement age and neither parents have had cancer but my parent did have moles removed at one time or two out of preventive concerns. I was born with a mole or birthmark too.

I read colon polyps can start out as benign but I don not have any symptoms of such. I did do an extended fast so that may help. I also have done one more round of your protocol and never experienced any more skin tags or moles. None of my moles have grown or changed shape since I stopped taking excessive telomere enhancers, nicotine and chondriton. Maybe I sould try a trelahose protocol as well in near future.

Just thought I would add this info, since I think I didnt follow precautions properly for this protocol 6 months ago, but I belive I am being smarter at following the protocol properly now. I probably push too many protocols stem cell and this one. I will try to limit the schedule I do.

I did decide to skip the c60 I would normally use for the growth phase in this protocol. I have planned to just use
Growth promotors and fusion perhaps with low dose roc/lox inhibitors.

Edited by bullGenteel, 14 December 2025 - 11:59 PM.

#1126 QuestforLife

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Posted 16 December 2025 - 06:37 PM

I should say I don't think this protocol necessarily lead to excessive moles or skin tags. I was thinking of posting before but I thought it was just my stupidity not following the guidelines or warning in this thread. I judge my behavior in considerstuon I am recovering from a brain injury.

I wouldn't be too hard on yourself. Self-experimenters makes mistakes, that is just the nature of the game.

Often the key is in the dose and the timing. Often you can get the benefits but not the harm by backing off on the dose or taking breaks as soon as side effects start.

Edited by QuestforLife, 16 December 2025 - 06:37 PM.

#1127 bullGenteel

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Posted 17 December 2025 - 08:33 AM

I am slowly working on myself. I tend to have a bit of an inferiority complex for my personality. Sorry if I am oversharing a little. It is just a little more amplified with having had a brain injury and I also have an imbalanced IQ. It is a little challenging to balance self growth and rehabilitation but I meant to do some of this work before I had an accident 10 plus years ago.

The past 6 months I have been mostly down on myself or just the circumstances. The mishap was that I felt so much better halfway through this protocol on my attempt back then. Sorry for personal info, probably couldn't be helped but the last 6 months I felt a major setback with even small goals and to be my best around friends and family. I guess I had troubles due to both an imbalanced IQ and brain injury. I didnt fully organize the amount supplies of reversatrol and boswellia I would need. It is safe to just say it overwhelms me to work through this whole protocol. I struggled to fully wrap my head around some modifications made to the mitchodria protocol thread.

I simply ran out of reverstrol and I replaced it with a cheap drugstore brand with grapseed extract. I just hoped it was a low enough dose of senyiotic and that it wouldn't do much. I think I have more rigid thinking and poor decisions making that is slow to improve. After 3 days I got a really bad headache. I even vaguely thought I should jump on fusion to perhaps some how save the situation by replacing sensceint/damaged cell lost. But I can't cope with making big changes like that too quickly since I am a very slow thinker and have OCD and hypochondria. Before the reversatrol/grapeseed I saw a lot of improvement. I was remembering multiple appointments with out aids and remembering to bring everything I needed for any task I had. I could jog without getting a mild throb in my ankle and very little to no stiffness afterwards.

That all went away after my headache. I felt the same or a little worse than before the protocol. Partly I amy have felt worse was I wasn't adequately optimizing my mitochondria. But I definately lost a lot of the gains. I did an extended fast that may have helped just a little.

I do feel some, but not as great of improvements from currently doing thisn protocol. I wish I could have asked more questions. Having an imbalanced IQ I find it hard to explain myself and hard to learn from others unless something just clicks for me right away. So there probably wasn't a whole lot different I could have done this last year.

I do wonder if the gains I had meant to make before and now with this protocol may be short term and temporary. I have trouble wrapping my head around more complex ideas that aren't simple, linear cause and effect seems easiest for me to grasp.

I think I gathered that for your protocol to be successful I need to dedifferentiate somatic cells into progentor cells than, while they are on a progentor like state, encourage cell division. I get kinda stuck on how I am finding success by limiting any growth/fusion agents and mtor. I guess this will result in temporary benefits when the progentor like cells revert back to somatic cells in a couple weeks. So, I may have for that brief time have the most stem like cells possible through my strict attempt to reduce growth and differentiation but it won't last.

I wonder, if I am explaining myself adequately enough, I could get some gyidance. I think you gave me guidance last time I posted 6 months ago. I hope to be better at asking questions and understanding this time around. Could I just take some fusion or mtor promotors a couple days a week for 2 weeks? I have taken roc/lox inhibitors for 2 weeks to hopefully revert cells to progentor like state. Then keep taking the roc/lox inhibitors. Then after a week take some hyperfusion agents, minus any c60, along with low dose roc/lox inhibitors I could try?

I get stuck in my approach to break down the protocol into sepearate redifferntiation and growth stages. Sorry I struggle with logical problem solving. Is the redifferention to progentor cells needs to be addressed simultaneously with promoting division and telomere elongation? I just dont want to spend this month on this protocol for it not to be attempted as correctly as I am possible for me to manage to do.

I am curious if my setback I caused wirh senyitoics might be remedied with this protocol and for others who had any bad experience with senyiotics. It may be wishful thinking. But atleast I feel I still have potential to recover more even if a little bit of that potential was lost. I will still be ahead either way and thankful and hopeful because I am able to see improvements, despite some setbacks.

Sorry, l'll try to not clutter people threads with my back story so much.

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Also tagged with one or more of these keywords: telomeres, nad, nampt, ampk, resveratrol, allicin, methylene blue, nmn, sirtuins, statin

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