2647 replies to this topic

[kurt9]

I've largely answered my own question here. I am using both Cantrophenoxine (Lipofuscin removal) and Rosmarinic Acid (an attempt at AGE crosslink removal) for 2 months PRIOR, then waiting an additional month before doing this stem cell/senolytic protocol. That way I separate them out so that the two do not interfere with each other and potentially cause problems. I'll see what happens.

 

Would it be reasonable to say that the stem cell/senolytic protocol can aid in or be a form of ECM turnover process? Given that every cell in our bodies come from a stem cell and that this would presumably include the fibroblasts, that renewing one's fibroblasts ought to assist in ECM turnover, thus helping to reduce or eliminate AGE crosslinks.

[Kelvin]

I've largely answered my own question here. I am using both Cantrophenoxine (Lipofuscin removal) and Rosmarinic Acid (an attempt at AGE crosslink removal) for 2 months PRIOR, then waiting an additional month before doing this stem cell/senolytic protocol. That way I separate them out so that the two do not interfere with each other and potentially cause problems. I'll see what happens.

 

Would it be reasonable to say that the stem cell/senolytic protocol can aid in or be a form of ECM turnover process? Given that every cell in our bodies come from a stem cell and that this would presumably include the fibroblasts, that renewing one's fibroblasts ought to assist in ECM turnover, thus helping to reduce or eliminate AGE crosslinks.

 

I've not seen anything that can improve the extracellular matrix besides the elastin precursor, tropoelastin.  But tropoelastin is mainly applied to the skin and wouldn't help the ECM across the entire body.

 

Good information on rosmarinic acid.

 

You can also use NMN periodically (probably with the old mito protocol, or NMN by itself) to reduce AGEs since it is a proven AGEs reducing agent.

[Kelvin]

Interesting. What other effects did you notice from the C60 protocol? 

 

Reduced need for sleep.

 

Prior to using C60 I went from not being rested after 8.5 hours of sleep to being able to get by with just 6 hours, even finding it difficult to sleep longer than 6.5 hours unless I had been sleep deprived for a number of days in a row.

Edited by Kelvin, 21 February 2026 - 08:48 PM.

[Blu]

What is the consensus on decent C60 oil sources in EU, as of today?

[bullGenteel]

I am planning to buy some more c60. I did reread a older thread with trunbuckle and some other users here.

I thought I should post because I thought of buying the nano technology brand mentioned in this thread recently. Then I recalled him saying 99.95% with some oxidants may be better than 99.99%. Maybe the original rat study used 99.95%. Kentvar in the same thread said something along the lines that 99.99% crystallized to much with supporting references.

The brand Kelvin shared is 99.99% I think? Just as another aside I always bought fish oil in a liquid bottle. Some user's suggested gel caps can still allow some oxidizing to occur. But the gel caps would be convenient and they could be frozen upon purchase.

I know there is the telomere thread by questforlife that has critical questioning about senyiotics, so I skip that portion of this protocol. I have already had a bad experience with senyiotics. Thpugh partially rescued senscient cells seems promising but likely will still be weakened cells with more antioxidants stress similarly to older cells due to shorter telomeres, until that can be addressed fully.

[Kelvin]

Turnbuckle was speculating about 99.95% purity being better only because he thought it would blend more easily in oil than 99.99% C60 powder would.

 

Turnbuckle also said he blends his own C60 in oil, but he has extensive training and experience in laboratory work.

 

Most people will be better off just buying a good brand off-the-shelf like the one I recommended, especially since C60 is highly sensitive to light which means to blend it properly without spoiling C60 you would need to do it in special laboratory lighting conditions (which I assume Turnbuckle has the equipment to do on his own).

[stephen_b]

Turnbuckle post on LinkedIn 2 months ago.
 

https://www.linkedin...dischler-yae3e/

[nadaepeu]

https://www.nature.c...255-025-01421-8

Abstract: Nicotinamide adenine dinucleotide (NAD(H)) and its phosphorylated form NADP(H) are vitamin B3-derived redox cofactors essential for numerous metabolic reactions and protein modifications. Various health conditions are associated with disturbances in NAD+ homeostasis. To restore NAD+ levels, the main biosynthetic pathways have been targeted, with nicotinamide (Nam), nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) being the most prominent boosters. However, while many preclinical studies have examined the effects of these precursors, a direct comparison in humans is lacking, and recent rodent research suggests that the NAD+-boosting effects of NR and NMN may depend on their microbial conversion to nicotinic acid (NA), a mechanism not yet confirmed in humans. Here we show in a randomized, open-label, placebo-controlled study in 65 healthy participants that 14 days of supplementation with NR and NMN, but not Nam, comparably increases circulatory NAD+ concentrations in healthy adults. Unlike the chronic effect, only Nam acutely and transiently affects the whole-blood NAD+ metabolome. Using ex vivo fermentation with human microbiota, we identify that NR and NMN give rise to NA and specifically enhance microbial growth and metabolism. We further demonstrate ex vivo in whole blood that NA is a potent NAD+ booster, while NMN, NR and Nam are not. Ultimately, we propose a gut-dependent model for the modes of action of the three NAD+ precursors with NR and NMN elevating circulatory NAD+ via the Preiss–Handler pathway, while rapidly absorbed Nam acutely affects NAD+ levels via the salvage pathway. Overall, these results indicate a dual effect of NR and NMN and their microbially produced metabolite NA: a sustained increase in systemic NAD+ levels and a potent modulator of gut health. ClinicalTrials.gov identifier: