C60 experiments @ home
#511
Posted 03 June 2012 - 01:16 AM
#512
Posted 03 June 2012 - 03:29 AM
I see that some are using .8gr pr liter, would 1 gr per liter be alright? It would make dosing a lot easier.
I don't think there's anything particularly magical about that dose, it's just what they used in the paper, and people are tending to follow that protocol. I don't see why you couldn't load the olive oil up to the limit of saturation, as long as you keep the same dose of fullerene, but I'm sure some would disagree. At any rate, I really can't see any problem with 1g/liter.
#513
Posted 03 June 2012 - 06:23 AM
This is a big red flag or my purpose of using C60/OO. ALS is thought to be an autoimmune disease and so any substance that stimulates the immune system would be bad. Moreover, a recent discovery by researchers in Ireland showed that for at least a subset of ALS patients of Irish or Scottish decent, a possible cause of ALS is a lack of angiogenesis (growth of new blood cells). The hypothesized mechanism is that when motor neurons die (they die at a rate of about 1%/year in healthy individuals), they secrete angiongenin, which encourages blood vessels to take their place to nourish the remaining motor neurons. In certain types of ALS, this doesn't happen and the dead motor neurons prevent nutrients from reaching the remaining neurons, leading to a cascade effect, and the rate at which we lose motor neurons grows and increases form 1% to 10 or 30%, causing death in just a few years.
ALS has been called 'anti-cancer' by one astute forum poster. In many cases what is bad for cancer is good for ALS and vice versa.
So if C60 is suppressing angiogenesis, that will suppress cancer by keeping microscopic cancers from every growing beyond a few cells, but may exacerbate ALS.
So, If i suddenly take a turn for the worse, this might be good news for everyone else.
Ben... If I understand your post, I think there might be a misunderstanding...
TNF (and IL-6) are Immune System Cytokines that are implicated in promoting angiogenesis... And what that study I posted shows is that C60 increases TNF significantly... hence, killing off tumors and other pathogens... What auto-immune diseases are about is that TNF and other Immune System Killer Cytokines don't know when to stop... So C60 could be a good thing for you because it triggers TNF.
But, frankly, what you're experiencing is way beyond my scope of knowledge.. I haven't spent any time looking at ALS.
Do you know if you have the form of ALS discovered by the folks in Ireland. Can you post a link to get us started on the research trail. I'm willing to spend time on this if you give me some study leads...
Positive thoughts headed your way Ben!
-----------------------
P.S... Turnbuckle... About that "reset effect" of C60... Since my post about TNF on Friday evening, I've been thinking that the explosion of Cytokines by the Immune System on initial C60 exposure is part of the "reset". C60 puts the immune system into overdrive while it exists in the body, especially the spleen (see my post from Friday evening), promoting the tumor, even small tumor, killing work of Cytokines like TNF...
More posts on the way about this...
Edited by wccaguy, 03 June 2012 - 06:27 AM.
#514
Posted 03 June 2012 - 06:41 AM
Studies about TNF are now permissible to play in this game. The game called the C60-Olive Oil-LifeExtension-Explanation game. Actually, at the risk of overreaching again, as you've seen I sometimes do, let me sharpen the spear... just to be provocative and get more juices flowing...
If the first study linked to below is taken seriously... any Explanation that doesn't account for the paradoxical role of TNF is obviously deficient...
Because of the sharpness of that spear, I post the complete study abstract again...
Publications concerning the mechanism of biological activity, especially the immunological mechanism of C60(OH)20 nanoparticles, are relatively limited. However, the structure and characteristics of this carbon allotrope have been widely investigated. In this paper, we have demonstrated that water-soluble C60(OH)20 nanoparticles have an efficient anti-tumor activity in vivo, and show specific immunomodulatory effects to the immune cells, such as T cells and macrophages, both in vivo and in vitro. For example, C60(OH)20 nanoparticles can increase the production of T-helper cell type 1 (Th1) cytokines (IL-2, IFN- γ and TNF-α), and decrease the production of Th2 cytokines (IL-4, IL-5 and IL-6) in serum samples.On the other hand, C60(OH)20 nanoparticles show almost no adverse effect to the viability of immune cells in vitro but stimulate the immune cells to release more cytokines, in particular TNF- α, which plays a key role in the cellular immune process to help eliminate abnormal cells. TNF- α production increased almost three-fold in treated T lymphocytes and macrophages. Accordingly, we conclude that C60(OH)20 nanoparticles have an efficient anti-tumor activity and this effect is associated with an increased CD4+/CD8+ lymphocyte ratio and the enhancement of TNF- α production. The data suggest that C60(OH)20 nanoparticles can improve the immune response to help to scavenge and kill tumor cells.
It's now legitimate to play "TNF study cards" in this game... Wow! That amounts to thousands more cards that can be played...
The problem with TNF is that, like some other Immune System Cytokines, once the danger to health (infection, virus, etc.) is killed off, the Cytokines "hang around" and do damage to our systems. That's what "auto-immune diseases" are all about. The Cytokines do their cell killing work and then aren't shut down. Here's a short abstract about this paradoxical role of the "Cytokines" that focuses on TNF..
Tumor necrosis factor (TNF) is a cytokine with well known anticancer properties and is being utilized as anticancer agent for the treatment of patients with locally advanced solid tumors. However, TNF role in cancer biology is debated. In fact, in spite of the wealth of evidence supporting its antitumor activity, the cascade of molecular events underlying TNF-mediated tumor regression observed in vivo is still incompletely elucidated. Furthermore, some preclinical findings suggest that TNF may even promote cancer development and progression. With this work we intend to summarize the molecular biology of TNF (with particular regard to its tumor-related activities) and review the experimental and clinical evidence currently available describing the complex and sometime apparently conflicting relationship between this cytokine, cancer biology and antitumor therapy. We also propose a model to explain the dual effect of TNF based on the exposure time and cytokine levels reached within the tumor microenvironment. Finally, we overview recent research findings that might lead to new ways for exploiting the anticancer potential of TNF in the clinical setting.
Aubrey de Grey gets at this point in the first 2.5 minutes of this Youtube video posted posted just last month...
Turnbuckle... Could it be that "the C60 reset" is this explosion of Cytokines released by the Immune System upon C60 invasion that kills off tumors, large and small? (Remember... Baati said most remaining C60s were in the spleen and that Tracey2007 said that the spleen was the source of Immune System Cytokines.) I earlier posted a youtube video of a TED Talk by William Li entitled something like Can We Eat To Starve Cancer. You'll recall he said that we have small tumors in our bodies, almost all never becoming dangerous... until we age and get older? But suppose you ingest C60 and even those small tumors William Li talked about were killed off by the C60 triggered Cytokine (e.g., TNF) explosion? I dunno... This is making more and more sense to me...
Of course, the tumor killers de Grey refers to are the Cytokines, like TNF. And, again, once they've done their work, they need to be killed off and/or suppressed themselves. And you already know where I'm headed with this post, right?
Edited by wccaguy, 03 June 2012 - 07:17 AM.
#515
Posted 03 June 2012 - 10:21 AM
#516
Posted 03 June 2012 - 11:19 AM
Ben... If I understand your post, I think there might be a misunderstanding...
TNF (and IL-6) are Immune System Cytokines that are implicated in promoting angiogenesis... And what that study I posted shows is that C60 increases TNF significantly... hence, killing off tumors and other pathogens... What auto-immune diseases are about is that TNF and other Immune System Killer Cytokines don't know when to stop... So C60 could be a good thing for you because it triggers TNF.
But, frankly, what you're experiencing is way beyond my scope of knowledge.. I haven't spent any time looking at ALS.
Do you know if you have the form of ALS discovered by the folks in Ireland. Can you post a link to get us started on the research trail. I'm willing to spend time on this if you give me some study leads...
Positive thoughts headed your way Ben!
-----------------------
P.S... Turnbuckle... About that "reset effect" of C60... Since my post about TNF on Friday evening, I've been thinking that the explosion of Cytokines by the Immune System on initial C60 exposure is part of the "reset". C60 puts the immune system into overdrive while it exists in the body, especially the spleen (see my post from Friday evening), promoting the tumor, even small tumor, killing work of Cytokines like TNF...
More posts on the way about this...
wccagauy
Thank you for addressing one of Ben's concerns regarding C60/OO's possible effect in stimulating the immune system (by significantly increasing the pro-inflammatory cytokines such as TNF) and it's effect in ALS. I am also an ALS sufferer, currently waiting 2 more days for my C60(99.9%) to completely dissolve in Olive Oil before I centrifuge and filter it. The hope is, much like Ben mentioned, to stop or at least significantly slow down the disease progression. I will report my response to C60 as soon as I start using it.
I would be grateful if any of you guys can further look into whether C60/OO could really have a detrimental effect for ALS sufferers through stimulating the immune system. Below is the link to one of the studies of C3 (water soluble derivative of C60) in G93A (ALS model) mice showing no detrimental effect, only a modest benefit of 10 days disease onset delay and even more modest life extension of 8 days:
http://www.thebronxp...om/Articles/10.)%20%20PNAS-1997.pdf
The hope is that C60 dissolved in Olive Oil will have a significantly more positive impact.
My intention is not to hijack this wonderful thread towards ALS so apologies to those with that impression.
Thanks in advance.
Edited by Spider_, 03 June 2012 - 11:40 AM.
#517
Posted 03 June 2012 - 01:25 PM
Interesting. If C60oo really works (to be confirmed), I doubt it is through a sort of graft versus host disease though. I look at my mice, it is as if they had not taken C60oo...
A few things...
First, we don't know if the tripling of TNF found in rats given the C60(OH)20 solution also occurs in the C60/Olive Oil solution. Finding out whether it does or not would be a great and quick experiment to do. The rest of my comments assume that TNF is raised with the C60/Olive Oil potion as was the case in the C60(OH)20 solution.
Second, the question of how long C60 clearance takes is more important now. If the C60s are essentially cleared from the system within a few hours, as the study authors said it was, then, one wouldn't expect a massive Host Defense related Immune System attack due to lingering C60 in the body. On the other hand, if C60 persists in the body as some people have argued, then the raising of TNF and other Cytokines must be generally suppressed for the Immune System Host Defense mechanism not to result in Auto-Immune diseases. (And, so far, it appears that auto-immune diseases do NOT occur in the C60/Olive Oil treated rats.)
An ironic twist... It could be that C60 persistence in the body only works without triggering an overdone Immune Response because of the continuing dose of Olive Oil which triggers the CAIP. Without the Vagus-CAIP-HRV nexus at work, it's the clearance of C60 (and hence the lowering of TNF) that avoids Auto-immune diseases. Here's a study, among many, about this, emphasizing again the dual role of TNF and other Immune Cytokines.
Role of TNF/TNFR in autoimmunity: specific TNF receptor blockade may be advantageous to anti-TNF treatments
Third, I wonder about whether "the reset effect" that Turnbuckle first conceptualized has, not only to do with the greater release of TNF, but also the CAIP is reset somehow. Suppose, during animal development, the Immune modulating response of the Vagus Nerve had been compromised (perhaps in the gut because the CCK receptors for Olive Oil had been damaged). Suppose then that the increased TNF cytokine attack unleased by the Immune System response to C60 quickly undid the damage (as quickly as occurred for Turnbuckle after his first dose).
The benefit of those two "reset effects" would be powerful indeed...
- the killing off of large and even small tumors by the initial TNF Explosion
- a strengthened capability of the CAIP to suppress TNF in the future because of an overactive Immune Response in the future.
At first glance this may seem like "out of left field" speculation. And none of this can be proven. But, in fact, that speculation can Explain most, if not all, the evidence we have on the table. If I've not remembered some specific C60/Olive Oil potion effect, please remind me. I'm not trying to exclude anything.
- Initial TNF Explosion because of C60 invasion... study link documented
- TNF is expressed by the Immune System to kill off pathogens.... study link documented
- But the non-C60 rats are the ones who die of tumors... study link documented
- C60 rats must have had their tumors killed off by Immune Cytokines.... an implication of Baati
- Following C60/Olive Oil dosing, low TNF level phenomenon are then observed over time...
- tumors in the C60 rats begin to appear much later(?).... Baati? how did the C60 rats die?
- Turnbuckle's reported hair growth.... I will provide a low TNF/hair loss study link
- Turnbuckle's reported improved growth.... I will provide a low TNF/improved skin study link
- Multiple reports of improved aerobic/muscle performance... Study link to be provided as above
----------------------
These are the initial seeds of a Falsifiable, Hard to Vary Explanation of what occurred in Baati and in the human experience we know about.
Those people doing C60/Olive Oil dosing, please continue to share your experience so we can ensure the conversation about Explanations is consistent with observations....
Edited by wccaguy, 03 June 2012 - 01:39 PM.
#518
Posted 03 June 2012 - 01:30 PM
Perhaps the C60's SOD mimetic effect trumps its detrimental shifting of T helper cells into the Th1 inflammatory mode, kind of like the way an immunosuppressant like rapamycin can paradoxically be used to treat cancer because its strong mtor inhibition seems to outweigh its presumedly detrimental immunosupression. So these C60 compounds could still be beneficial for ALS, though you might want to consider augmenting it with a substance capable of shifting the balance back in favor of Th2 and its associated anti-inflammatory cytokines.wccagauy
Thank you for addressing one of Ben's concerns regarding C60/OO's possible effect in stimulating the immune system (by significantly increasing the pro-inflammatory cytokines such as TNF) and it's effect in ALS. I am also an ALS sufferer, currently waiting 2 more days for my C60(99.9%) to completely dissolve in Olive Oil before I centrifuge and filter it. The hope is, much like Ben mentioned, to stop or at least significantly slow down the disease progression. I will report my response to C60 as soon as I start using it.
I would be grateful if any of you guys can further look into whether C60/OO could really have a detrimental effect for ALS sufferers through stimulating the immune system. Below is the link to one of the studies of C3 (water soluble derivative of C60) in G93A (ALS model) mice showing no detrimental effect, only a modest benefit of 10 days disease onset delay and even more modest life extension of 8 days:
http://www.thebronxp...om/Articles/10.)%20%20PNAS-1997.pdf
The hope is that C60 dissolved in Olive Oil will have a significantly more positive impact.
My intention is not to hijack this wonderful thread towards ALS so apologies to those with that impression.
Thanks in advance.
#519
Posted 03 June 2012 - 02:19 PM
We have two theories of ageing here to consider - the mitochondrial theory of ageing, and oxidation.
Notice now that the C60-Olive Oil-LifeExtension-Explanation game has now fundamentally changed. The TNF study changes it...
First, because the Immune System Cytokine TNF is now implicated (and TNF grows tumors) I'd also argue that the Vagus-CAIP-HRV nexus ideas are going to have to play a part of any explanation (1) because TNF suppression is required and (2) because Olive Oil Stimulates the Vagus.
Second, the game is now 3 Dimensional. With Immune System TNF Cytokines being implicated, It's no longer possible to argue for the credibility of an Explanation that is Single Dimensional, as in, "it's all about mitochondria resetting" or "it's all about inhibiting oxidation." Once the implications of the TNF study are absorbed, arguing for a Single Dimensional Explanation is going to feel like so last Friday...
The Single Dimensional Explanations are sinking ships...
For my part, I'm abandoning the Vagus-CAIP-HRV ship I've been enjoying the float on. It's leaking like a sieve and I'd prefer not to go down with it. Elements of Immune System, Inflammation, CAIP, and Oxidation theories of aging are all going to need to play a role. I'm going to see about expanding the reach of what I think about.
Notice how the TNF study means that credible Explanations are now going to need to explain more than just how the C60/Olive Oil potion effects what's going on within cells. Whole systems and body functions are implicated now... I don't even know what the right word to use to name them is. That's how far behind I am...
Notice how the Mitochondria Reset Explanation is now a more difficult case to make. The case for some kind of reset occurring was strong. But what is that reset? Well, maybe the Mitochondria. It made sense. But with TNF explosions taking place after C60 ingestion, there's another kind of reset that also makes sense and a variable clearly triggering resets (TNF) has been found to occur after C60 ingestion.
And as noted up thread, those arguing for C60 persistence are going to have to explain how it doesn't lead to persistent, unhealthy Auto-Immune TNF attack.
----------------
I didn't anticipate that this Explanation Game would "go 3D" this early... But I did anticipate that it would at some point...
When radical life extension is a reality, all the scientifically credible schools of thought about aging will be be able to point to actual evidence and say "see, I told ya so."
I'm in to play...
http://www.youtube.com/watch?v=77RtB2CUtok
Edited by wccaguy, 03 June 2012 - 02:28 PM.
#520
Posted 03 June 2012 - 02:20 PM
With a low carb diet you should be ok. Carbs are the weight gainers, not fats.
This is extremely bad advice for most people. I wish this urban legend would die a well-deserved death.
There is a genetic factor you must consider, which 23andme has documented. About 1/3 of the population will not gain weight if they get over 30% of their calories from saturated fat, and will gain weight if they eat too many carbs. Paleo diet works for these folks. About a third of the population does not gain weight if they get more than 30% of their diet from mono-saturated fat, such as olive oil. Mediterranean diet works for these folks. The remainder will gain weight if more than 30% of their calories come from any kind of fat. Ornish diet anyone? As long as adequate calories are consumed, the weight gain occurs if one is eating contrary to one's genetic characteristics, even if one is not consuming excessive calories.
Except perhaps for the 30% us who are genetically paleo people, complex carbs are not likely to be detrimental; it's simple sugars that cause problems, especially fructose as found in corn syrup and in table sugar which are found in virtually all processed food (sucrose is a di-sacharide, half fructose and half glucose.) By the 23andme test, I am type 3, and I do gain weight if I eat high fat. I tried paleo, and went to the next belt loop. Recently I've eliminated sugar, all deserts and fructose corn syrup and by extension nearly everything you can buy in a can or a package. I do well with complex carbs (glycemic index is not a good measure here.) I don't gain weight with all the (non-factory made) bread, pasta, rice I want. I recognize this will make some people fat, but it works for me.
I am concerned that consuming as much olive oil as is being recommended will fatten me up (unless I burn an extra 4000 calories a day from exercise.) True, too, for most of reading this I'm sure. We know the dose used in mice, but not really how to scale to humans. One to one by body mass is unlikely to be necessary. The algorithms based on body mass to volume or to surface area are a starting point for toxicology studies, but that would I think put a dose at more like a few table spoons rather than near a cup of olive oil laced with C60. This amount is easily done with salad dressing and a pasta sauce, or on home-baked bread instead of butter. Just drinking the stuff is rather gross.
Edited by maxwatt, 03 June 2012 - 02:47 PM.
#521
Posted 03 June 2012 - 02:20 PM
I believe my levels of tnf-a where quite high in comparison with 'normal' levels. I asked the doc about it, but they said not to be concerned about tnf-a.
Should i be concerned if C60/OO pushes these levels higher than 3X the normal amount?
As soon as i get back to Miami, ill post the tnf-a test result, and what the folks at BioPhysical consider 'normal'.
Cheers
A
Circle me: https://profiles.goo...236572014252197
#522
Posted 03 June 2012 - 02:31 PM
It's amazing how often "the folks in white coats" have no idea what they're talking about.The Biophysical 250 i believe measures tnf-a. When i took the Biophysical i was only taking res (1-2 grams) and vitamins...
I believe my levels of tnf-a where quite high in comparison with 'normal' levels. I asked the doc about it, but they said not to be concerned about tnf-a.
Should i be concerned if C60/OO pushes these levels higher than 3X the normal amount?
As soon as i get back to Miami, ill post the tnf-a test result, and what the folks at BioPhysical consider 'normal'.
Cheers
A
Circle me: https://profiles.goo...236572014252197
No. Anthony... You don't have to be worried about Auto-Immune TNF attack... Well, not if you believe that the Vagus-CAIP-HRV nexus is important that is... Also, it's more of a concern if the C60s are cleared from the body. Baati et al says they were cleared. niner thinks not.
A point of evidence... Turnbuckle's experience tells us that his TNF levels must now be dramatically lower... His skin is better, hair growth returning, he and dog better exercise endurance... that can all be related to TNF reduction... I've promised study links about this. I haven't forgotten. I'll get to it by tomorrow morning...
------------
Anthony...
I've been thinking about you and an idea for a product I think you could easily sell and make money selling. (We want you to succeed.) Have you looked at that HRV literature I posted up thread?
I think you should add an HRV raising (Vagus/CAIP Stimulating/Activating) product to your product line. You know, TrackYourPlaque.com is selling HearMath's emWave2 PSR product for less than Amazon is selling it. I'll bet you could talk the HeartMath folks into having you selling it at a price comparable to what they're letting the TYP folks sell it for.
Heartmath's emWave2 is a truly terrific product... I found the literature of the CAIP because acetylcholine improved my ability to keep my HRV high (aka, per Heartmath called "coherence"). I couldn't explain how in the world that could be. So I went searching and that's how I found found Kevin Tracey's work. The CAIP suppresses TNF/raising HRV through acetylcholine release.
Edited by wccaguy, 03 June 2012 - 02:51 PM.
#523
Posted 03 June 2012 - 02:50 PM
Perhaps the C60's SOD mimetic effect trumps its detrimental shifting of T helper cells into the Th1 inflammatory mode, kind of like the way an immunosuppressant like rapamycin can paradoxically be used to treat cancer because its strong mtor inhibition seems to outweigh its presumedly detrimental immunosupression. So these C60 compounds could still be beneficial for ALS, though you might want to consider augmenting it with a substance capable of shifting the balance back in favor of Th2 and its associated anti-inflammatory cytokines.
This is my hope too. I am intending to try it in conjunction with WF10 aka. Immunokine (Tetrachlorodecaoxide) which is a chlorite containing immunomodulating drug that downregulates pro-inflammatory genes such as TNFalpha, Interleukin 1 beta, etc. It is an infusion medication that I have been taking for almost 9 months now that managed to slow down my disease progression significantly. For those who may be interested:
http://en.wikipedia....chlorodecaoxide
In conjunction with C60/OO it may be able to assist in keeping the shift over in the Th2 mode. We'll soon find out.
#524
Posted 03 June 2012 - 03:18 PM
I have a sister who suffers from multiple sclerosis and was struck by the many simularities among the various immunopathologies. In any event you might also look into bee venom to attenuate the TNF-a:This is my hope too. I am intending to try it in conjunction with WF10 aka. Immunokine (Tetrachlorodecaoxide) which is a chlorite containing immunomodulating drug that downregulates pro-inflammatory genes such as TNFalpha, Interleukin 1 beta, etc. It is an infusion medication that I have been taking for almost 9 months now that managed to slow down my disease progression significantly. For those who may be interested:
http://en.wikipedia....chlorodecaoxide
In conjunction with C60/OO it may be able to assist in keeping the shift over in the Th2 mode. We'll soon find out.
http://www.jneuroinf.../content/7/1/69
Bee venom attenuates neuroinflammatory events and extends survival in amyotrophic lateral sclerosis models
In order to determine whether BV suppressed neuroinflammation by inhibiting of the release of the pro-inflammatory cytokine TNF-α, we further examined the level of TNF-α by immunohistochemistry in BV- or saline-treated familial ALS mice. As expected, TNF-α immunoreactivity in hSOD1G93A mice was largely confined to the facial nucleus of the brain stem and motor neurons in the anterior horn of the spinal cord (Figure 5A,C, and5E). Interestingly, BV caused a significant 4-fold reduction in TNF-α immunoreactivity in both the brainstem and lumbar spinal cord (Figure5B,D, and<a href="http://www.jneuroinf...figure/F5">5F-H). These results suggest that BV treatment may be involved in an anti-neuroinflammatory responses that reduces motor neuron degeneration and prolongs the life span of hSOD1G93A transgenic mice at the symptomatic stage.
#525
Posted 03 June 2012 - 03:34 PM
This is my hope too. I am intending to try it in conjunction with WF10 aka. Immunokine (Tetrachlorodecaoxide) which is a chlorite containing immunomodulating drug that downregulates pro-inflammatory genes such as TNFalpha, Interleukin 1 beta, etc. It is an infusion medication that I have been taking for almost 9 months now that managed to slow down my disease progression significantly. For those who may be interested:
http://en.wikipedia....chlorodecaoxide
In conjunction with C60/OO it may be able to assist in keeping the shift over in the Th2 mode. We'll soon find out.
I am concerned, however, about something HappyPhysicist wrote, namely, that ALS has been called something like the reverse of cancer. I have no knowledge of what that means or the significance of that statement.
That said, if you are pursuing an Immune suppression approach and looking to inhibit TNF, you should be looking at 5-Lipoxygenase Inhibitors. 5-Lo is implicated in most of the most serious diseases, especially the auto-immune diseases. I created an FB page about those diseases and 5-LO. It's here. Boswellia (AKBA) is a profound inhibitor of 5-LO. I'd try it and Curcumin? first. Omega 3 and Vitamin D3 are essential front line strategies against against the 5-Lo/Leukotriene B4 Pathway...
Best wishes...
#526
Posted 03 June 2012 - 03:45 PM
Decreased heart rate variability in amyotrophic lateral sclerosis
There are a lot of studies about HRV and ALS. Do a google search about them. Because of the preponderance of that literature, I highly recommend getting an HRV Biofeedback Device. My favorite is Heartmath's emWave2. It's very cool. You can use it to train for Vagus Stimulation which, if you've been following my posts, you know it leads to increased HRV.
Doing the C60 experiment, then, also makes sense. Here's why, given the scare my post about TNF caused HappyPhysicist... Once the TNF Explosion is over, the C60 is cleared from your system (according to Baati, but a point which niner disputes and I respect niner a great deal).
Nevertheless, Turnbuckle's experience implies a profound reduction in TNF... By what means? We don't don't know... But we do know that one means TNF is reduced is through the Vagus-CAIP-HRV nexus... And your best hope should be that THAT is the explanation because, if it is, then you know your HRV ought to be higher.... Perhaps the C60, by means of the TNF explosion itself, improves the Vagus-CAIP system itself...
That said, you don't have to guess about how you're doing vis-a-vis HRV at any moment. You can tell where it is using devices like Heartmath's emWave2 device...
#527
Posted 03 June 2012 - 06:36 PM
<< Big Snip... Be sure to read maxwatt's post >>
A company I trust with a web store is Amphora http://www.amphoranueva.com/ . , Look for , Look for Chilean Picual Ultra, a "single variety, estate produced, early harvest, UP (certified ultra premium)....
max... Thanks for that great post about olive oil. I'm going to be staying 15 miles from this place in the SF Bay Area within a week. I think I'll spend some time at the store, ask some questions, etc. If there's anything I can do in person while I'm there, let me know... Thanks again!
#528
Posted 03 June 2012 - 06:48 PM
This is extremely bad advice for most people. I wish this urban legend would die a well-deserved death.
There is a genetic factor you must consider, which 23andme has documented.
I'm in the same boat as Maxwatt...and for those interested...the 23andMe data points...and it does hold true for me:
Response to Diet
Introduction
What you eat has a huge impact on your health, but how you respond to your diet is influenced by many factors. Researchers are learning that genetics plays a large role in how people perceive flavors and in their eating behaviors. Genetics also influences how your body metabolizes and uses different foods, perhaps helping to explain why some people can eat as much as they want and never gain weight while others can't seem to lose weight despite their best efforts.
Last Updated
January 19th, 2012
Gene/SNP Summaries
Effect of monounsaturated fat
Applicable Ethnicities: European
Marker: rs1801282
Several studies have shown that rs1801282 (also known as the Pro12Ala variant in the PPARG gene) influences whether an individual benefits from a diet high in monounsaturated fat. (This type of diet is often called a "Mediterranean"-style diet because olive oil is a good source of monounsaturated fat.) In people of European descent carrying at least one copy of the G version of rs1801282, increasing intake of just monounsaturated fat was associated with reductions in body mass index (BMI). In addition, a low fat diet led to an increase in waist circumference in people with the G version but a diet high in monounsaturated fat protected against this effect. The protection was even stronger in people with type 2 diabetes.
Who Genotype What It Means
GG A low fat diet may lead to increased waist circumference but a diet high in monounsaturated fat protects against increased waist circumference and may lead to
reductions in BMI.
CG A low fat diet may lead to increased waist circumference but a diet high in monounsaturated fat protects against increased waist circumference and may lead to
reductions in BMI.
Hebbeh CC A diet high in monounsaturated fat is not likely to have beneficial effects on BMI or waist circumference.
Citations
Razquin C et al. (2009). “The Mediterranean diet protects against waist circumference enlargement in 12Ala carriers for the PPARgamma gene: 2 years' follow-up of 774 subjects at high cardiovascular risk.” Br J Nutr 102(5):672-9.
Memisoglu A et al. (2003). “Interaction between a peroxisome proliferator-activated receptor gamma gene polymorphism and dietary fat intake in relation to body mass.” Hum Mol Genet 12(22):2923-9.
Effect of saturated fat on obesity risk
Applicable Ethnicities: European
Marker: rs5082
A study of about 3,500 people with mainly European ancestry showed that having two copies of the G version of rs5082 was associated with increased odds of obesity in those who ate a diet high in saturated fat. In people who consumed a diet low in saturated fat, rs5082 did not have an effect on risk of obesity.
Who Genotype What It Means
Hebbeh GG Increased odds of obesity on a high saturated fat diet. No increase in odds of obesity on a low saturated fat diet.
AG Typical odds of obesity on both a high and low saturated fat diet.
AA Typical odds of obesity on both a high and low saturated fat diet.
Citations
Corella D et al. (2009). “APOA2, dietary fat, and body mass index: replication of a gene-diet interaction in 3 independent populations. ” Arch Intern Med 169(20):1897-906.
Effect of fat intake on body mass index (BMI)
Applicable Ethnicities: European
Marker: rs662799
A study of more than 2,000 people of European descent found that among those who consumed more than 30% of their calories from fat, having two copies of the A version of rs662799 was associated with higher BMI compared to having one or no copies. The variant had no effect among those who consumed less than 30% of their calories from fat.
Who Genotype What It Means
Hebbeh AA A high fat diet (30% of calories from fat) is associated with higher BMI.
AG Dietary fat consumption is not associated with changes in BMI.
GG Dietary fat consumption is not associated with changes in BMI.
Citations
Corella D et al. (2007). “APOA5 gene variation modulates the effects of dietary fat intake on body mass index and obesity risk in the Framingham Heart Study.” J Mol Med 85(2):119-28.
The genotyping services of 23andMe are performed in LabCorp's CLIA-certified laboratory. The tests have not been cleared or approved by the FDA but have been analytically validated according to CLIA standards.
EDIT: sorry about the formatting.....but formatting can't seem to be fixed???
Edited by Hebbeh, 03 June 2012 - 06:49 PM.
#529
Posted 03 June 2012 - 07:18 PM
#530
Posted 03 June 2012 - 07:35 PM
.9 g/L is the saturation limit for olive oil.
For actual dissolution without reaction. This would be the purple solution. Over time, or much more rapidly if heated, the C60 reacts with the fatty acid esters in the olive oil. This is the dark red solution, according to Cataldo. This forms at room temperature when exposed to oxygen over a period of two weeks. I suspect these adducts are the active species. My understanding is that you can get a lot more C60 into the oil if it's in the adduct form.
#531
Posted 03 June 2012 - 09:29 PM
- The rat trial mentions 50 mg / 10 ml, which is 5 g/l
- Someone here just said 9 g/l
- Another study found a max. of 0.909 g/l
- I just purchased the study "Olive oil as a biocompatible solvent for pristine C60", and it claims that only a mere 3 to 6 microgram (μg) will dissolve, per milliliter (ml), depending on olive oil quality and temperature.
Say it's 5 μg / ml. That is just 5 mg/l, or a thousand times less than the rat trial claims.
Which study is wrong?
solubility.png 93.82KB 6 downloads
Edited by SarahVaughter, 03 June 2012 - 09:31 PM.
#532
Posted 03 June 2012 - 09:33 PM
I noticed that there is great confusion, both in the literature and in this thread, about how much C60 can be dissolved in olive oil:
- The rat trial mentions 50 mg / 10 ml, which is 5 g/l
- Someone here just said 9 g/l
- Another study found a max. of 0.909 g/l
- I just purchased the study "Olive oil as a biocompatible solvent for pristine C60", and it claims that only a mere 3 to 6 microgram (μg) will dissolve, per milliliter (ml), depending on olive oil quality and temperature.
Say it's 5 μg / ml. That is just 5 mg/l, or a thousand times less than the rat trial claims.
Which study is wrong?
solubility.png 93.82KB 6 downloads
Someone here said .9 g/l, not 9 g/l. You missed the decimal point. And the rat paper didn't say that 5 g/l actually all dissolved, as I recall.
Fifty mg of C60 were dissolved in 10 ml of olive oil by stirring for 2 weeks at
ambient temperature in the dark. The resulting mixture was centrifuged at 5.000 g for
1 h and the supernatant was filtered through a Millipore filter with 0.25 mm porosity.
That they pulled off the supernatant fluid suggests that there was undissolved material. Then they diluted it down to .8 mg/ml. So it's unclear what the actual solubility limit was. As for the chart, that is very strange. Most solids have higher solubility as the temperature goes up.
Edited by Turnbuckle, 03 June 2012 - 09:46 PM.
#533
Posted 03 June 2012 - 09:42 PM
Who has made the error of two orders of magnitude?
Edited by SarahVaughter, 03 June 2012 - 09:42 PM.
#534
Posted 03 June 2012 - 09:42 PM
The benefit of those two "reset effects" would be powerful indeed...
----------
- the killing off of large and even small tumors by the initial TNF Explosion
- a strengthened capability of the CAIP to suppress TNF in the future because of an overactive Immune Response in the future.
At first glance this may seem like "out of left field" speculation. And none of this can be proven. But, in fact, that speculation can Explain most, if not all, the evidence we have on the table. If I've not remembered some specific C60/Olive Oil potion effect, please remind me. I'm not trying to exclude anything.
- Initial TNF Explosion because of C60 invasion... study link documented
- TNF is expressed by the Immune System to kill off pathogens.... study link documented
- But the non-C60 rats are the ones who die of tumors... study link documented
- C60 rats must have had their tumors killed off by Immune Cytokines.... an implication of Baati
- Following C60/Olive Oil dosing, low TNF level phenomenon are then observed over time...
- tumors in the C60 rats begin to appear much later(?).... Baati? how did the C60 rats die?
- Turnbuckle's reported hair growth.... I will provide a low TNF/hair loss study link
- Turnbuckle's reported improved growth.... I will provide a low TNF/improved skin study link
- Multiple reports of improved aerobic/muscle performance... Study link to be provided as above
Question, my wife while being in pretty good health at 32 yrs old suffers from small tumors in her breast the doctors have diagnosed her with fibrocystic breast disease. FBD is a condition generally characterized by lumps that move freely in the breast tissue and vary in texture and size. Because FBD is a benign condition, it usually does not lead to breast cancer.
If the C60 does have the power to kill off these small tumors do you think this would be something she would benefit from?
Or would this be a way to test if C60 does have tumor killing properties? She has had this condition for the last 7 yrs and it is pretty painful I believe she would be able to tell pretty quickly if it was gone. She also has mild asthma and is excited to see if this will help in that area as well. I am going to help her log the effects as soon as we get some hopefully next week.
#535
Posted 03 June 2012 - 09:59 PM
According to that study, the max. concentration at room temp is 0.47 mg / ml.
The rat study claims 0.8 mg / ml was used.
solubility-c60.png 48.49KB 6 downloads
Note that they find a linear temp/solubility relationship, wheras the other study found an inverse one.
Every study I read so far has wildly different data for the solubility. Which one is correct?
Edited by SarahVaughter, 03 June 2012 - 10:02 PM.
#536
Posted 03 June 2012 - 10:05 PM
When fullerene C60 was dissolved in selected lipids (ethyl oleate, ethyl linoleate, linseed oil and castor oil) the spectrophotometric analysis shows that the oxidation is concentrated to C60 which is converted to an epoxide C60O. Thus, fullerene C60 displays antioxidant activity not only when dissolved in unsaturated lipids but also, more generally, when dissolved in unsaturated solvents subjected to autoxidation...
http://www.sciencedi...009308410000496
#537
Posted 03 June 2012 - 10:17 PM
Replace the vegetable oil with the olive oil mixture, bake it up, and have one brownie a day.
#538
Posted 03 June 2012 - 10:29 PM
We did a test with almond oil and that gets pink. But after ten days of mixing, our extra-virgin oil is still brown. The base oil is a rich yellow, so adding purple would yield brown. We tried mixing base EVOO with the pink C60 almond oil and the result is again light brown.
niner is saying that when we let the brown C60-EVOO solution stand, exposed to oygen, that it will turn pink? Can anyone confirm that this happened to their mixtures? We have eight stirrers in operation now and experimented with stirring exposed to the air and at higher temperatures, but brown is all we get.. We're not yet at two weeks though.
We also have an overhead stirrer, whipping along fericiously, and I imagine a lot of oxygen gets into the oil. Just as brown as the magnetically stirred oil in capped Erlenmeyers. We use 5 g / l.
If anyone obtained purple/pink, can they explain what oil they used and describe the production process? From what I read in this thread, the oil used that became purple was a very clear, non-cold pressed oil.
Edited by SarahVaughter, 03 June 2012 - 10:55 PM.
#539
Posted 03 June 2012 - 10:41 PM
Can anyone confirm their attained solution levels? Has anyone managed, for example. to fully dissolve 800 mg C60 into a liter of EVOO?
Edited by SarahVaughter, 03 June 2012 - 10:59 PM.
#540
Posted 03 June 2012 - 11:13 PM
Another thing I don't understand is how so many studies report a purple color, but since as to my knowledge, all extra virgin olive oil is yellowish or greenish, how can a purple color ever develop? Only bleached oils should be able to show a purple color, correct?
We did a test with almond oil and that gets pink. But after ten days of mixing, our extra-virgin oil is still brown. The base oil is a rich yellow, so adding purple would yield brown. We tried mixing base EVOO with the pink C60 almond oil and the result is again light brown.
niner is saying that when we let the brown C60-EVOO solution stand, exposed to oygen, that it will turn pink? Can anyone confirm that this happened to their mixtures? We have eight stirrers in operation now and experimented with stirring exposed to the air and at higher temperatures, but brown is all we get.. We're not yet at two weeks though.
We also have an overhead stirrer, whipping along fericiously, and I imagine a lot of oxygen gets into the oil. Just as brown as the magnetically stirred oil in capped Erlenmeyers. We use 5 g / l.
If anyone obtained purple/pink, can they explain what oil they used and describe the production process? From what I read in this thread, the oil used that became purple was a very clear, non-cold pressed oil.
I've found that an almond oil solution (.4 g/l), which was originally magenta, eventually turned whiskey colored. EVOO (.6 g/l) was always whiskey colored, and extra light OO (.6 g/l) was red/magenta, but has drifted toward a whiskey color with time, even though it's still much redder than the EVOO.
I might try vacuuming out the dissolved gasses prior to dissolving the C60 to see if this color drift is due to the formation of epoxides.
The ideal colors from Nano LLC:
Attached Files
Edited by Turnbuckle, 03 June 2012 - 11:46 PM.
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