331 replies to this topic

[pone11]

 

no purely antioxidant theory can explain enhanced longevity, hair regrowth, the disappearance of scars, or the boosting of stem cell injections. It has simply never happened before with any antioxidant.

An antioxidant has been shown to enhance longevity- Skulachev's mitochodrially-directed plastoquinones. The reason that most common antioxidants don't seem to do much is that they have lousy pharmacokinetics, don't localize where they are most needed, and require regeneration. c60-oo is unlike all the other antioxidants to date, other than the various c60 analogs that have also shown profound biological effects.

 

 

Are any plastoquinone derivatives (SkQs) commercially available?

[pone11]

 

 

It could be checked by measuring the methylation of the mtDNA before and after treatment. If correct, there would be less methylation afterward. This wouldn't be the only case of a drug acting this way. Procaine has been shown to increase the longevity of rats (with intermittent treatment) and bind to DNA where it acts as a methytransferase inhibitor.
 

Step aside from our recent discussion. Is it possible to do such test ? If it is expensive we could try to crowdfunding it here )

 

I see a number of sites that test for methylation of DNA, but I don't see any that specifically test for methylation of mtDNA. There probably hasn't been much commerical interest in it since people didn't even realize that mtDNA was methylated until recently.

 

 

I have always wanted to get a fatty acid composition test done on my mitochondrial membranes.  I have yet to find a commercial vendor who can isolate those membranes.

 

I did find vendors willing to report their fatty acid compositions, but only if I had someone else prepare the samples.

[pone11]

 

 

Exactly right. Rats and mice have much longer telomeres to begin with (5-10 times longer than humans), so if a rat lived twice as long due to some supplement, it is most likely not because the supplement had any effect on its telomeres. Thus a doubling of a rat's lifespan doesn't mean a human will see the same benefit. As noted below, you can knock out telomerase in mice with genetic manipulation and telomere shortening won't become at issue for their progeny for several generations.

 

 

Great points.   It was always a mystery to me why so many short-lived species have so many extra telomeres than long-lived species.    

 

My assumption has always been that many of these short-lived rodent species die quickly because of hugely unstable polyunsaturated fat compositions in their membranes.  With age they lose catalase and SOD activity, and increase free radicals, and this literally eats them alive because their cell membranes are so highly reactive.

 

There is an interesting study here that gets at these points:

http://www.ncbi.nlm....pubmed/18029129

 

The longest lived rodent lives 28 years and the above study abstract contains the very intriguing information that "DHA-containing phospholipids represent 27-57% of all phospholipids in mice but only 2-6% in naked mole-rats."   This is followed by " The lower level of DHA-containing phospholipids suggests a lower susceptibility to peroxidative damage in membranes of naked mole-rats compared to mice."    By the way, if anyone has access to full text on that study I would love to read it.

 

This is why the whole O3 and O6 issue is so important with humans too.   We live in a diet of processed foods where there is some insane ratio > 15:1 of Omega-6 to Omega-3, and the absolute levels of both fats in Western diets is quite high.   I take seriously the ideas of people like Ray Peat - and other biochemists - that these fats should make up the minimum possible percentage of calories in the diet.  But there are no good human studies that document what the optimum level should be.

[niner]

An extensive discussion of copper, SOD, and Alzheimer's Disease was split off into its own thread.  Please direct further copper-related discussion there, and try to keep this thread on the topic of C60.

[Logic]

Exactly right. Rats and mice have much longer telomeres to begin with (5-10 times longer than humans), so if a rat lived twice as long due to some supplement, it is most likely not because the supplement had any effect on its telomeres. Thus a doubling of a rat's lifespan doesn't mean a human will see the same benefit. As noted below, you can knock out telomerase in mice with genetic manipulation and telomere shortening won't become at issue for their progeny for several generations.
 
It is likely, therefore, that the enhancement of longevity is due to improved functioning of the mitochondria, and there is a lot of evidence for that, including the presence of C60 in the mitochondria but not in the nucleus.

I just want to remind everyone of the fact that telomeres shorten 100X faster in mice than in humans before the theory of C60oo at least affecting the rate of telomere attrition is completely discounted.

http://www.longecity...ndpost&p=617036

If I remember correctly there is continuous 'communication/feedback loops' between the mitochondria and nucleus.
I think it possible that C60oo may decrease the need for NAD+ in the mitos, leaving more for SIRT, PARP etc in the nucleus and elsewhere?
This would explain why some individuals already on C60oo that also tried Nicotinamide Riboside felt overstimulated or experienced no extra effect from NR on top of C60oo?

On the other hand C60oo may also be highly effective at stopping lipid peroxidation??

[Turnbuckle]

 

Exactly right. Rats and mice have much longer telomeres to begin with (5-10 times longer than humans), so if a rat lived twice as long due to some supplement, it is most likely not because the supplement had any effect on its telomeres. Thus a doubling of a rat's lifespan doesn't mean a human will see the same benefit. As noted below, you can knock out telomerase in mice with genetic manipulation and telomere shortening won't become at issue for their progeny for several generations.
 
It is likely, therefore, that the enhancement of longevity is due to improved functioning of the mitochondria, and there is a lot of evidence for that, including the presence of C60 in the mitochondria but not in the nucleus.

I just want to remind everyone of the fact that telomeres shorten 100X faster in mice than in humans before the theory of C60oo at least affecting the rate of telomere attrition is completely discounted.

http://www.longecity...ndpost&p=617036

If I remember correctly there is continuous 'communication/feedback loops' between the mitochondria and nucleus.
I think it possible that C60oo may decrease the need for NAD+ in the mitos, leaving more for SIRT, PARP etc in the nucleus and elsewhere?
This would explain why some individuals already on C60oo that also tried Nicotinamide Riboside felt overstimulated or experienced no extra effect from NR on top of C60oo?

On the other hand C60oo may also be highly effective at stopping lipid peroxidation??

 

 

I'm not sure what this paper is telling us. Even at the ends of their lives, the plots show that mice still have telomeres 8 times longer than humans. It also shows short telomeres getting longer at the same rate as the telomerase mice, and that the wild type lived just as long in the end. The benefit to mice from telomerase reverse transcriptase appeared to be primarily at middle age. Thus I'd say that telomere length is not determining mouse lifespan.

Edited by Turnbuckle, 02 January 2015 - 06:42 PM.

[sensei]

I found this paper:

 

"

Antioxidative fullerol promotes osteogenesis of human adipose-derived stem cells"

 

http://www.ncbi.nlm....les/PMC4149442/

 

 

 

And:

 

"Thus, fullerenes not

only accelerate the rate at which hair shafts grow but also

induce de novo synthesis of new hair follicles."

 

http://www.researchg...9db7e000000.pdf

 

 

I think these sort of effects may be the basis for the scar removal and hair re-growth some people see.  Perhaps it is a dosage issue.

[sensei]

I also found a citation that beta-cyclodextrin binds, stabilizes and removes lipofuscin

 

http://www.researchg...ment_epithelium

 

look at the molecular shape of cyclodextrin:

 

http://en.wikipedia....ki/Cyclodextrin

 

C₆₀ but not C₇₀ forms a 1:2 inclusion compound with cyclodextrin (CD)

 

http://en.wikipedia....enes_as_ligands

 

so 2 cyclodextrin molecules bind around each c60 molecule -- could be an actual process going on when c60 is ingested, or a novel method for lipofuscin removal

Edited by sensei, 05 January 2015 - 02:05 AM.

[tunt01]

X

[bosharpe]

Any new information on possible stem cell depletion from regular/intermittent use of C60oo? 

[Kalliste]

Depends. Did you read about the high dose MitoQ and interference with neural stem cell mtROS signaling-study?

[bosharpe]

No I didn't read that. I don't suppose you could post me a link?

[APBT]

No I didn't read that. I don't suppose you could post me a link?

 

http://www.longecity...scussion/page-4

[bosharpe]

Thanks for that. I will probably halt dosing C60oo for a while after reading this and other information on this thread. I don't want to do more harm than good to my body at my age (29). 

[sensei]

Thanks for that. I will probably halt dosing C60oo for a while after reading this and other information on this thread. I don't want to do more harm than good to my body at my age (29). 

 

 

Remember the dosage for the rats was 1.7 mg/kg each time they were gavaged.  - That equals 153 mg dose for me --I'm 90 kilos.

 

The Baati rats were given 24 doses

 

 

That is the equivalent of almost 4 grams -- on a mg/kg basis.

 

There is no meaningful evidence that would prompt one to scale the dose for C60.  

 

All I can go by is the visible changes in my hair color when taking the high doses I have taken.

 

 

I had taken a break of several months and some gray crept into my temples.  This leads me to believe that there is a significant transport capability in the human body to clear the C60 -- and that continual dosing is needed to reap all the benefits observed.

 

I only have the limited data set of my own experience -- however, I am back on ~ 20-30 mg daily.

 

Results lag administration by a few months based on previous observations. We should know if this round of C60 dosing reverses the gray at my temples in a month or two.

 

There may be a synergistic effect with lycium barbarum and astragalus.  However, the doses of those herbs was not significant at all -- and rather intermittent, and not always coincidental with the C60 administration.

 

I cannot discount an interaction however.

Edited by sensei, 10 July 2015 - 01:50 PM.

[Kalliste]

Yeah they got that nasty result with a very large dose. Although it's impossible to be sure, I suspect you could get something similar from C60 if you went up to something like a mg/kg or 2-5mg/kg dosages. It's nothing weird really.

Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.
 

[niner]

Remember the dosage for the rats was 1.7 mg/kg each time they were gavaged.  - That equals 153 mg dose for me --I'm 90 kilos.

 

The Baati rats were given 24 doses

 

That is the equivalent of almost 4 grams -- on a mg/kg basis.

 

Well, sorta.  It's usually considered appropriate to apply an allometric scaling to doses between different animals.  This interspecies scaling relates to differences in metabolic rate and other biological metrics.  The rat-to-human scaling factor is 1/6, so that 153 mg dose is 25.5 mg if you apply the scaling, and the total dose given to the rats is 4g/6 = 667 mg. 

[sensei]

 

Remember the dosage for the rats was 1.7 mg/kg each time they were gavaged.  - That equals 153 mg dose for me --I'm 90 kilos.

 

The Baati rats were given 24 doses

 

That is the equivalent of almost 4 grams -- on a mg/kg basis.

 

Well, sorta.  It's usually considered appropriate to apply an allometric scaling to doses between different animals.  This interspecies scaling relates to differences in metabolic rate and other biological metrics.  The rat-to-human scaling factor is 1/6, so that 153 mg dose is 25.5 mg if you apply the scaling, and the total dose given to the rats is 4g/6 = 667 mg. 

 

 

 

Yes, it is, when empirical evidence on clearance rates and metabolic effects on pharmacokinetics are available to support the scaling factor.

 

For C60, there is no body of comparable (interspecies) evidence, frankly there isn't much pharmacokinetic data regarding C60 in any species.  The Baati study is the only study to attempt to detail clearance rates of C60 (in rats), and they are non-linear IIRC.

 

Furthermore, C60 is not metabolized like normal drugs -- there is no enzymatic action by the liver, and no substantive evidence to determine even half-life.  C60 may be more analogous to mineral supplementation than administration of valium.

 

In the absence of compelling evidence one should take the data as one finds it, namely that 1.7 mg/kg given intermittently in doses over the course of ~ 20% of the organism's lifespan apparently causes increased longevity in mammals, and that doses of 4 mg/kg daily does not result in any observed acute nor chronic toxicity.  

Edited by sensei, 11 July 2015 - 01:41 AM.

[Turnbuckle]

An interesting paper that shows epigenetic changes lower mitochondrial energy production. However, these changes are to n-DNA, not mt-DNA, at least in this experiment--

 

Age-associated accumulation of somatic mutations in mitochondrial DNA (mtDNA) has been proposed to be responsible for the age-associated mitochondrial respiration defects found in elderly human subjects. We carried out reprogramming of human fibroblast lines derived from elderly subjects by generating their induced pluripotent stem cells (iPSCs), and examined another possibility, namely that these aging phenotypes are controlled not by mutations but by epigenetic regulation. Here, we show that reprogramming of elderly fibroblasts restores age-associated mitochondrial respiration defects, indicating that these aging phenotypes are reversible and are similar to differentiation phenotypes in that both are controlled by epigenetic regulation, not by mutations in either the nuclear or the mitochondrial genome. Microarray screening revealed that epigenetic downregulation of the nuclear-coded GCAT gene, which is involved in glycine production in mitochondria, is partly responsible for these aging phenotypes. Treatment of elderly fibroblasts with glycine effectively prevented the expression of these aging phenotypes.

 

Full text

 

 

 

Note the last line, which suggests that glycine supplementation might slow aging. Another paper has found this to be the case in mice, but attributes it to a different mechanism--

 

Dietary glycine supplementation mimics lifespan extension by dietary methionine restriction in Fisher 344 rats

 

If glycine restores mitochondrial energy production, then you'd expect it would be helpful also with dieting, and that seems to be the case--

 

Glycine supplementation during calorie restriction accelerates fat loss and protects against further muscle loss in obese mice.

 

 

Edited by Turnbuckle, 11 January 2016 - 12:23 PM.

[HighDesertWizard]

Glycine suppresses TNF-α-induced activation of NF-κB in differentiated 3T3-L1 adipocytes

 

Glycine regulates the production of pro-inflammatory cytokines in lean and monosodium glutamate-obese mice

 

NF-kB Cytokine Transcription Inhibition through various means has been shown in dozens of studies to significantly improve survival probability.

 

Here are survival curve snapshots from just a few of those studies.

 

turnbuckle... Are there a set of increased survival probability curves you can show us related to a mitochondria explanation of longevity? If yes, would you please point us to them?

 

Thanks!

 

[ EDIT: I forgot to mention that the study animals should be mammals. Thanks. ]

Edited by HighDesertWizard, 12 January 2016 - 03:01 AM.

[Turnbuckle]

 

turnbuckle... Are there a set of increased survival probability curves you can show us related to a mitochondria explanation of longevity? If yes, would you please point us to them?

 

 

I am aware of no such curves in unmodified mammals. That the Baati rats lived so much longer is widely believed to be the result of improved mitochondrial function and is consistent with evidence C60 localizes to mitochondria and with the experiences of people here taking it, though the mechanism is wide open and is the topic of this thread.

 

For those looking at mitochondria to extend lifespan, here is an interesting tool--

 

MitoAge: a database for comparative analysis of mitochondrial DNA, with a special focus on animal longevity.

 

Mitochondria are the only organelles in the animal cells that have their own genome. Due to a key role in energy production, generation of damaging factors (ROS, heat), and apoptosis, mitochondria and mtDNA in particular have long been considered one of the major players in the mechanisms of aging, longevity and age-related diseases. The rapidly increasing number of species with fully sequenced mtDNA, together with accumulated data on longevity records, provides a new fascinating basis for comparative analysis of the links between mtDNA features and animal longevity. To facilitate such analyses and to support the scientific community in carrying these out, we developed the MitoAge database containing calculated mtDNA compositional features of the entire mitochondrial genome, mtDNA coding (tRNA, rRNA, protein-coding genes) and non-coding (D-loop) regions, and codon usage/amino acids frequency for each protein-coding gene. MitoAge includes 922 species with fully sequenced mtDNA and maximum lifespan records. The database is available through the MitoAge website (www.mitoage.org or www.mitoage.info), which provides the necessary tools for searching, browsing, comparing and downloading the data sets of interest for selected taxonomic groups across the Kingdom Animalia. The MitoAge website assists in statistical analysis of different features of the mtDNA and their correlative links to longevity.

 

Edited by Turnbuckle, 12 January 2016 - 11:23 AM.

[stefan_001]

An old article...wondering whether this promotion faction is seen also in other tissues....

A novel promoting action of fullerene C60 on the chondrogenesis in rat embryonic limb bud cell culture system.
Tsuchiya T1, Yamakoshi YN, Miyata N.
Author information

Abstract
Fullerene C60 was solubilized with polyvinylpyrrolidone (PVP) in water, and the aqueous solution was applied to the rat limb bud cell differentiation system. By the incubation with various concentrations of C60 with poly(vinylpyrrolidone), cell differentiation was extremely promoted, up to the levels of a 3.2-fold increase of the controls. Although poly(vinylpyrrolidone) alone inhibited the cell differentiation in proportion to the concentration, the observed promoting action by C60 surpassed the action of poly(vinylpyrrolidone). This specific promoting action on the chondrogenesis is the novel significant activity of C60.
PMID: 7832801 [PubMed - indexed for MEDLINE]

[Turnbuckle]

By the incubation with various concentrations of C60 with poly(vinylpyrrolidone), cell differentiation was extremely promoted, up to the levels of a 3.2-fold increase of the controls. 

 

Fits with the anecdotal evidence that C60/EVOO stimulates stem cells.

[HighDesertWizard]

 

turnbuckle... Are there a set of increased survival probability curves you can show us related to a mitochondria explanation of longevity? If yes, would you please point us to them?

 
I am aware of no such curves in unmodified mammals. That the Baati rats lived so much longer is widely believed to be the result of improved mitochondrial function and is consistent with evidence C60 localizes to mitochondria and with the experiences of people here taking it, though the mechanism is wide open and is the topic of this thread.

 

 

turnbuckle... Appreciate your reply... I poke you because I respect you... Truly...

 

 

The most widely believed explanations of the Baati study longevity benefit have something in common. They ignore key evidence from the study itself. The evidence is ignored because the explanations themselves cannot account for it. By definition, it must be presumed to be irrelevant to the longevity benefit.

 

What is ignored?

• "C60 concentrations reached the limit of solubility in spleens"
• There is a picture showing Splenic Macrophages engulfing F-C60 crystals

Now, it's true that the animals showing spleen accumulation weren't the ones with the longevity benefit. They were killed early in the study. Nevertheless, kmoody has confirmed that F-C60 accumulates in the Spleen and in the Liver.

 

Has a study showed that the Splenic Macrophage data is irrelevant to the longevity and tumor inhibition benefit?  No...

 

Are there other studies demonstrating that Splenic Macrophages are important to increased survival odds and might be to cancer prevention?  Yes...

 

turnbuckle... You appear to take other studies showing F-C60 accumulating in mitochondria seriously while ignoring where the Baati study actually found F-C60 accumulating. Have I missed something? Does your preferred explanation address F-C60 accumulation in the spleen. If not, why have you presumed to ignore that evidence?

 

A few key findings--of many that exist--are relevant here. Lots of details to explore

• The organ Origins of Tumor Associated Macrophages have been identified and the study "positions the spleen as an important extramedullary site, which can continuously supply growing tumors with these [cancer promoting macrophage and neutraphil] cells."
• Kevin Tracey and his teams have determined that "Intact Splenic Signaling" is required for Lifespan Benefit upon lethal inflammation intervention. The focus of that beneficial Splenic Signaling is NF-kB Cytokine Transcription Inhibition. And it's that Inhibition that underlies the emerging demonstrations of survival benefit when NF-kB is inhibited.
• F-60-OH has been shown to inhibit NF-kB Nuclear Translocation and hence inhibit Cytokine Transcription. BTW, that study finding means that All the survival curves shown in this thread are Within Topic Scope in any discussion of the F-C60-OO lifespan benefit.

In 2012, Tracey and his teams published a diagram showing the key biological objects underlying the survival benefit they've uncovered and, in one way or another, are demonstrated empirically here. All the biological objects shown are relevant to the explanation of the F-C60-OO lifespan benefit. (To keep this short, I won't address the Olive Oil and Intestine evidence.)

 

I'm a software engineer and longevity science hobbyist. I'm working on a longer and more formal description of this mechanism. I could use some help, but I'm happy to do the work alone if that's what's necessary. In the meantime, I thought it a good idea to share a little about what I'm up to.

 

 

Edited by HighDesertWizard, 13 January 2016 - 04:55 AM.

[Turnbuckle]

I recall we've had this discussion about the spleen before, and it deserves its own thread as it is off topic to the present one. If you start one, you should post evidence that the absence of a spleen has some dramatic influence on life expectancy.

[Logic]

"...We have also identified oleuropein, a phenolic compound in
Olea europaea leaf extract, olive oil, and olives, as a
potent stimulator of proteasome activities in vitro. Human
primary fibroblasts treated with oleuropein were also more
resistant to oxidative stress and exhibited extended cellular
life span. We have suggested that oleuropein most
likely alters the conformation of 20S α -gated channels..."
http://www.tandfonli...762.2013.792926

 I wonder if C60oo might not be potentiating the above effect?
(The study is a goldmine of information on the whys and hows of decreasing AGEs and ALEs including the upregulation of 'built in' defence mechanisms)

[niner]

"...We have also identified oleuropein, a phenolic compound in
Olea europaea leaf extract, olive oil, and olives, as a
potent stimulator of proteasome activities in vitro.  [...]

 I wonder if C60oo might not be potentiating the above effect?

 

This would be a candidate for the benefits seen from the consumption of (relatively large amounts of) olive oil.  I doubt that it has much if anything to do with the effects we see from c60oo because the dose of oleuropein is so low.  For most of us, the dose of olive oil that we get from c60oo would put us in the lowest quartile of the study of the Spanish cohort from EPIC where olive oil health effects were seen. 

[Turnbuckle]

If the original hypotheses is correct and C60 demethylates mtDNA, this could impact cardiovascular disease (CVD) via platelets. Hypermethylated regions in platelet mitochondrial DNA have been found to be a marker for CVD, and may even be a cause—

 

 

In this study, we hypothesized that DNA methylation in platelet mitochondria is a potential contributor to CVD development through modulation of platelet activity. We examined platelet mtDNA methylation among healthy individuals and CVD patients, and we observed significantly higher mtDNA methylation of four genes in CVD patients . . .

 

The mitochondrial genome is known to retain a very low level of DNA methylation, and we observed low levels of platelet mtDNA methylation in healthy individuals, with higher mtDNA methylation in those with CVD. The observed changes were relatively small in magnitude, except for MT-CO1, [where we observed] an astounding difference (18.53%) . . .

 

 

http://clinicalepige...3148-015-0078-0

 

 

 

In fact, most of the healthy controls had zero methylation at that gene, while those with CVD had up to 29%. 

 

Other genes had elevated levels of methylation—MT-CO2, MT-CO3, and MT-TL1, though the difference and absolute amounts were less. Mutations in some of these genes are known to produce exercise intolerance and fatigue, so restoring their full activity would look much like the responses to C60, assuming muscle cells were similarly impacted. 

Edited by Turnbuckle, 14 January 2016 - 02:26 PM.

[Turnbuckle]

A link between Alzheimer's and Parkinson's and mitochondrial epigenetics--

 

Altered Mitochondrial DNA Methylation Pattern in Alzheimer Disease-Related Pathology and in Parkinson Disease.

 

Mitochondrial dysfunction is linked with the etiopathogenesis of Alzheimer disease and Parkinson disease. Mitochondria are intracellular organelles essential for cell viability and are characterized by the presence of the mitochondrial (mt)DNA. DNA methylation is a well-known epigenetic mechanism that regulates nuclear gene transcription. However, mtDNA methylation is not the subject of the same research attention. The present study shows the presence of mitochondrial 5-methylcytosine in CpG and non-CpG sites in the entorhinal cortex and substantia nigra of control human postmortem brains, using the 454 GS FLX Titanium pyrosequencer. Moreover, increased mitochondrial 5-methylcytosine levels are found in the D-loop region of mtDNA in the entorhinal cortex in brain samples with Alzheimer disease-related pathology (stages I to II and stages III to IV of Braak and Braak; n = 8) with respect to control cases. Interestingly, this region shows a dynamic pattern in the content of mitochondrial 5-methylcytosine in amyloid precursor protein/presenilin 1 mice along with Alzheimer disease pathology progression (3, 6, and 12 months of age). Finally, a loss of mitochondrial 5-methylcytosine levels in the D-loop region is found in the substantia nigra in Parkinson disease (n = 10) with respect to control cases. In summary, the present findings suggest mtDNA epigenetic modulation in human brain is vulnerable to neurodegenerative disease states.

 

http://www.ncbi.nlm....pubmed/26776077

 

 

In AZ, the brain regions affected are associated with memory and learning, among other things. In AZ, the mtDNA is hypermethylated in the D-loop region, while in Parkinson's it's the reverse. The D-loop is a section of the mtDNA that is triple stranded and heavily methylated (around 35%), and it seems unlikely that C60 could demethylate it by the method described in the OP.

 

Mitochondrial dysfunction in Parkinson's disease

 

Results revealed the presence in the sole L-strand of unconverted cytosines, thus indicating the existence of methylation in the D-loop ... In particular, all analysed clones showed identical methylation patterns, with the majority of the methylated cytosines located outside of CpG nucleotides. The global percentage of methylation (the percentage of methylated cytosines with respect to overall cytosine content of the analysed sequence) was around 35% ... 

 

http://www.sciencedi...925443909001963

 

 

[Nate-2004]

This is all very interesting. I don't have any hypothesis to add here but as a continuous user of C60OO I think perhaps I should change the dosing my regimens overall.

 

Perhaps something like 5 days on with my stack and then one or two weeks off.  So like ~14mg (20ml) C60OO, NR, Pterostilbene/Resveratrol and Honokiol from Mon-Fri one week and then pause for a week, then do it again. Then try every two weeks. This would certainly save money too, although I'd probably increase the dosage on NR to 1g per day. I'd probably also eat more anti-oxidant on those days as well. 

 

My reasoning is that some people are seeing benefits from continuous use while there is also sufficient reason not to use it continuously. There's also the hypothesis about fission and fusion. So I'd be using it daily but in short bursts with frequent, longer breaks.

 

Anecdotally speaking, as of yesterday, 6 days into C60OO dosing with my high quality homemade stuff and after a 2 week break, I've begun experiencing allergies again. My seasonal allergies went away for at least a couple of years now and I assume this was related to some kind of decline in the immune system over reactiveness. Now I'm sneezing after hanging out in the park and am getting a stuffy nose. Definitely allergies. This is self-reporting and anecdotal, perhaps my allergies never fully went away and I'm misremembering. It is spring after all and they aren't severe. It could be that I just forgot experiencing them slightly last spring. It has been a long time though and they used to be super bad all the way up until just 3 or 4 years ago, then they started going away.

 

Also I have experienced no change in the degree of Essential Tremor I've had since I was 12. The tremor got worse after I turned 36 and has since become worse over the past 6 years since then.  It's neurodegenerative and so I don't know if I should be expecting a change here or not. If it did decrease I would know because I could see it in a comparison of myself in video and in how well pictures turn out when I take them. 

 

Are there any updates on this hypothesis?

Edited by Nate-2004, 27 May 2016 - 04:01 PM.