285 replies to this topic

[Turnbuckle]

 

Well it looks like I need to buy a spectrometer, and start taking measurements.  Do you have any suggestions on which machine I should buy?  I obviously want something that will save the data to usb stick, or other electronic form, that I can save, analyze and share.

 

 

 

I bought one for work more than twenty years ago but never used it myself. It was several thousand. Here's one that is ten times less ($399) and measures into the UV and IR spectrum as well as the visible. Likely there are others available.

[Graviton]

 

One of the things we look for when ascribing a biological effect to a molecule is dose response.  We expect to see a larger effect with a larger dose.  Here you found no effect from a much larger dose of C70, but saw a large effect when taking a very small dose. 

 

 

 

 

 

I didn't compare the large dose with the small dose directly. The large dose wasn't twice a day, nor did the small dose cause a problem only once a day. If C70 has a relatively short residence time in the ER (as reported) then a brief interference with protein folding would have only a minor influence on the cell, as cells surely have a reserve. But if C70 is present all the time by taking it twice a day for some days, a problem could easily develop when some cells ran low on vital proteins and began malfunctioning. However I never felt a pain like the one I had in my neck, and it was actually quite scary. I'm quite aware that this is an anecdotal report and could have some other cause, nevertheless I have no interest in repeating it. If any other self-experimenter wants to try it, I would be very interested in hearing the results. Such an experiment should not require the C70-rich extract I used. SV oil is made with 99.5% C60 with the balance mostly C70 (roughly 93% of the non-C60 fraction if in the same proportion as the extract), thus a dose of 15 mg mixed fullerenes should deliver the same 70 micrograms of C70. If one took that twice a day for three or four days, that would provide the C70 dosing that likely caused the problem.

 

For the suppliers using 99.95% purity, the same experiment would require 150 mg twice a day--roughly half a liter of oil solution a day.

 

Other nanoparticles are known to induce ER stress to the point of killing the cell--

 

Titanium Dioxide Nanoparticles Induce Endoplasmic Reticulum Stress-Mediated Autophagic Cell Death via Mitochondria-Associated Endoplasmic Reticulum Membrane Disruption in Normal Lung Cells.

 

Gold nanoparticles induce apoptosis, endoplasmic reticulum stress events and cleavage of cytoskeletal proteins in human neutrophils.

 

Silver nanoparticles activate endoplasmic reticulum stress signaling pathway in cell and mouse models: The role in toxicity evaluation.

 

Can I see the related papers or evidences that C70oo(or not fatty acid adduct C70) getting into ER cause a problem/problems in a long run?

Also, I would like to know the rationales and how C70 can affect protein foldings in ER. (beside personal experiences)

 

As niner said, if C70oo lasts with a long half life in ER, then does it mean homeostasis acts as a good thing or a bad thing?

[Turnbuckle]

Can I see the related papers or evidences that C70oo(or not fatty acid adduct C70) getting into ER cause a problem/problems in a long run?

 

Also, I would like to know the rationales and how C70 can affect protein foldings in ER. (beside personal experiences)

 

As niner said, if C70oo lasts with a long half life in ER, then does it mean homeostasis acts as a good thing or a bad thing?

 

There are no such papers. My experience with twice daily dosing of a mix of C60 and C70 is unique as no one else has tried it to my knowledge. So I looked around for some possible explanation and found the paper shown below. The C70 in that research was different. Rather than having adducts from olive oil, the researchers conjugated it with Texas red. It was not found to stay in the ER but to move to different parts of the cell at different times. If C70 with random olive oil adducts did this, it would explain why I only saw negative results by taking it twice a day--

We show C70-TR are non-specifically endocytosed into MC where they are shuttled throughout the cytoplasm, lysosomes, mitochondria, and into endoplasmic reticulum at different times...

 

In conclusion, we have identified the ER as a primary organelle for 70-carbon based fullerene derivatives localization in human MC as opposed to previous publications which show 60-carbon based fullerenes localize to the mitochondria This localization may help explain how the fullerenes exhibit their inhibitory activity through blunting of calcium and ROS spikes leading to subsequent reduction in histamine deganulation and cytokine production.

 

http://www.ncbi.nlm....les/PMC2888797/

 

As for C70 interfering with protein folding, I only said it might, as that is one function of the ER. The above paper suggests a different mechanism for another observed effect, but doesn't have proof of that either. Their suggestion sounds much like that of the titanium nanoparticle paper--

 

Our results showed that TiO2-NP induced endoplasmic reticulum (ER) stress in the cells and disrupted the mitochondria-associated endoplasmic reticulum membranes (MAMs) and calcium ion balance, thereby increasing autophagy.

 

Titanium Dioxide Nanoparticles Induce Endoplasmic Reticulum Stress-Mediated Autophagic Cell Death via Mitochondria-Associated Endoplasmic Reticulum Membrane Disruption in Normal Lung Cells.

 

ER stress is shown in the silver nanoparticle paper, at sufficient doses--

 

In the present study, endoplasmic reticulum (ER) stress was used as a sensitive and early biomarker to evaluate the toxic potential of AgNPs in three different human cell lines in vitro and in vivo in mice...The adverse effects of exposure to AgNPs may be avoided by rational use within the safe dose.

 

http://www.ncbi.nlm....pubmed/26024651

 

And also in the gold NP paper, but apparently to a lesser degree. At least one study has been made of the toxicity of gold NPs vs size, and size turns out to be very important--

 

---------------------

The cytotoxicity of TPPMS/TPPTS-modified gold nanoparticles depended primarily on their size and not on ligand chemistry. Particles 1–2 nm in size were highly toxic and both smaller gold compounds (Tauredon) and larger 15-nm gold colloids were comparatively nontoxic, irrespective of the cell type tested. Differences in the kind of cell death pathway (apoptosis versus necrosis) were consistently observed. This finding suggests different uptake kinetics and/or cellular target specificities even for similarly sized gold nanoparticles. Most likely nanoparticle toxicity follows endocytosis, but it is entirely possible that the toxicity may stem from interactions at the cell membrane, even though the particles are also endocytosed.

 

http://www.virlab.vi...les - Small.pdf

---------------------

 

The toxicity goes down to .8 nm at least, and the size of bare C60 particles in solution is given as .6 to .8 nm. C70 should only be slightly larger. This paper doesn't give the cause of the toxicity, but likely it is the same ER stress as above, so one should be wary of fullerenes that localize there.

Edited by Turnbuckle, 25 August 2016 - 12:36 PM.

[ta5]

We don't know enough to say whether it's safe to take C60oo at all.

 

Kmoody's hypothesis now is that there was something wrong with the SES C60oo, but it's not proven that any difference between it and what Baati prepared is responsible for the tumor growth.

 

Baati used SES C60 (the pure C60 powder) in the original study, but prepared it himself, in the dark. It was then stored in the dark.

 

Kmoody's lab purchased SES-prepared C60oo, which may or may not have used Baati's method, may or may not have been prepared in the dark and may or may not have been stored in the dark.

 

Kmoody then prepared their own batch of C60oo using Baati's method and found a difference between that at the SES C60oo.

 

But we still don't know if the difference is significant or if dark preparation and storage makes C60oo safe or not.

 

 

Totally agree. I stopped taking C60oo when I first learned about the tumor growth in the Grohn study in this post back in May.

 

I'm eagerly waiting for more information about the safety of the different commercial oils before I take it again. It might help if we had more details about how the different oils are produced and stored. The lack of analysis, information, and openness from the producers bothers me. 

[Daniel Cooper]

So much murkiness in this situation that I don't see getting resolved any time soon.

 

I'm curious, how many of you were taking C60oo but now have stopped due to this information, and how many of you have continued?

 

Also, if you were taking C60oo but discontinued, how long of a period after stopping would it take for you to relax a bit about the danger?

 

 

 

[sthira]

...We are doing a full toxicology work-up now, but those results will not be completed until a few months at least. We do intend to publish them in a peer review journal.

Since posted in June, any news from the quiet lands of c60?

We are assessing at least half a dozen different vehicles for C60 other than pure olive oil. We have PK/PD pilot data on these and are moving into efficacy and toxicity metrics. These results will be published when we have concluded these studies.

[Captain Obvious]

"I'm curious, how many of you were taking C60oo but now have stopped due to this information, and how many of you have continued?"

Since I believe it was not a peer-reviewed study, it hasn't been replicated and the researchers might have a business interest, it hasn't influenced my consumption of C60. That said, it still is a xenobiotic and should be approached as such.

Edited by Captain Obvious, 03 January 2017 - 09:36 PM.

[lost69]

i did not stop and only use carbonoliveoil.com and i do it myself when i have time.as many other reported i did not feel the same effects from other vendors at all

 

i keep macrophages/immune system activated by anti cancer compounds just as a prevention tool

[Daniel Cooper]

i did not stop and only use carbonoliveoil.com and i do it myself when i have time.as many other reported i did not feel the same effects from other vendors at all

 

i keep macrophages/immune system activated by anti cancer compounds just as a prevention tool

 

 

Not sure if this is the proper venue but I'd be interested in what anti-cancer compounds you are using.

[lost69]

 

i did not stop and only use carbonoliveoil.com and i do it myself when i have time.as many other reported i did not feel the same effects from other vendors at all

 

i keep macrophages/immune system activated by anti cancer compounds just as a prevention tool

 

 

Not sure if this is the proper venue but I'd be interested in what anti-cancer compounds you are using.

 

 

sent a PM

[Maikel Alves]

Well, some months ago I decided to mix two brands of c60 and it killed me completely. I feel tired everyday. I already checked hormonal levels and tried other stimulants but nothing see to work.
I just sleep more and my body behave as adrenal or thiroyd fatigue. Some advice?

I have some cancer historic in my family and I will start some exams after this threat

[zorba990]

"I'm curious, how many of you were taking C60oo but now have stopped due to this information, and how many of you have continued?"

Since I believe it was not a peer-reviewed study, it hasn't been replicated and the researchers might have a business interest, it hasn't influenced my consumption of C60. That said, it still is a xenobiotic and should be approached as such.

I stopped taking it. I went through several start and stop periods with several months between. Each time restarting my kidneys felt stressed. No blood work ever showed any issue, but I decided to wait it out a bit. I feel fine currently.

[samstersam]

 

I stopped taking it. I went through several start and stop periods with several months between. Each time restarting my kidneys felt stressed. No blood work ever showed any issue, but I decided to wait it out a bit. I feel fine currently.

 

 

How does it feel when your "kidneys are stressed?"

 

Do you have renal problems?

Edited by samstersam, 07 February 2017 - 03:20 AM.

[zorba990]

I stopped taking it. I went through several start and stop periods with several months between. Each time restarting my kidneys felt stressed. No blood work ever showed any issue, but I decided to wait it out a bit. I feel fine currently.

How does it feel when your "kidneys are stressed?"

Do you have renal problems?

Dull ache in the kidney area. I don't have any renal problems, but it's happened each time I started c60oo again. It goes away a week or two after stopping use. It does not happen with olive oil itself or any other supplement. Even dehydration doesn't seem to cause anything similar. Urine output is not changed but the ache is there and annoying enough that combined with the aforementioned study, gives me some pause about continuing to use it for the time being.

[Empiricus]

 

 

I stopped taking it. I went through several start and stop periods with several months between. Each time restarting my kidneys felt stressed. No blood work ever showed any issue, but I decided to wait it out a bit. I feel fine currently.

How does it feel when your "kidneys are stressed?"

Do you have renal problems?

Dull ache in the kidney area. I don't have any renal problems, but it's happened each time I started c60oo again. It goes away a week or two after stopping use. It does not happen with olive oil itself or any other supplement. Even dehydration doesn't seem to cause anything similar. Urine output is not changed but the ache is there and annoying enough that combined with the aforementioned study, gives me some pause about continuing to use it for the time being.

 

 

I have also experienced the dull ache in the lower back that a number of c60 users have reported and attributed to possible kidney injury.  

 

First episode of back pain began when I started taking higher doses (5-6 ml) of a commercial product once a week for a month (up from 1-3 ml) in Dec and Jan of 2015.  During this period I was also taking high doses of nicotinamide.  Second episode of back pain -- somewhat worse lower back pains-- began when I mixed c60 with olive leaf extract and then HT (hydroxytyrosol) enriched c60 around March-April 2016.   A third episode of back pains -- persistent and more severe back pain accompanied by nausea -- developed after I took HT enriched c60 in late June 2016.  Around the same time I picked a handful of olive leaves off a wild olive tree and ate them raw.  I'm now wondering if the olive leaves weren't the main culprit... 

 

* * * * *

 

Several studies show HT is protective of kidneys, but I also came across this study: 

 

Toxicity of Olive Leaves (Olea europaea L.) In Wistar Albino Rats

 

Sawsan A. Omer, M.A. Elobeid, M.H. Elamin, Z.K. Hassan, P. Virk, M.H. Daghestani, E.M. Al-Olayan, Nadia A. Al-Eisa and Z.M. Almarhoon

 

The aim of this study was to evaluate the effect of Olive Leaf Extracts (OLE) on the haematology and biochemistry as well as on the liver and kidney of rats fed on the extracts for 6 weeks. Thirty Wistar albino rats were divided into five groups, Group 1 fed regular diet without OLE (control group), group 2 (fed 0.2% ole), group 3 (fed 0.4% ole), group 4 (fed 0.7% OLE) and group 5 (fed 0.9% OLE) for 6 weeks. Serum concentrations of Alkaline Phosphatase (ALP), Lactate Dehydrogenase (LDH), Total Bilirubin (TBil) and cholesterol, glucose, triglycerides as well as hematological profiles were determined in the present study for each group of rats. There was a significant increase in the serum levels of ALP and total bilirubin in groups 3 and 4 and 5 compared to the control group. There was also significant decrease in the serum triglyceride, glucose and cholesterol in test groups as compared to the control group. The haematological profile showed significant decrease in the values of red blood cell counts, haemoglobin and packed cell volume of the animals in group 5. Microscopically both liver and kidneys showed histological alterations in the form of fatty cytoplasmic vacuolation, necrosis of the hepatocytes and a slight hemorrhage was recorded in the kidneys of the experimental animals especially those fed 0.9% olive leaf extract. The olive leaves extract should be handled with care in arts and other animals and special attention should be paid when using OLE for longer periods of time and at higher doses as it may result in an undesirable effect on liver and kidneys as it has been shown in the present study.

 

http://scialert.net/...175.1182&org=10

 

* * * * * 

 

The third episode of pain in my lower back persisted month after month.  This time, the back pain was accompanied by three other symptoms: nausea and fatigue, a metallic taste in my mouth in the mornings and urine that was beige in color and foamier than usual.   Because these resemble symptoms of kidney disease, I had kidney tests done on 3 occasions.  Each time, the results came back normal.  Nevertheless, I read that the kidney tests don't show anything unless your kidney function is lower than 25%, so there can be damage that doesn't show on tests.

 

In September 2016 stopped the paleo-like diet I had been experimenting with and put myself on a kidney diet. I discovered that I was able to control the symptoms by lowering my intake of phosphorous -- one of the main things you limit on a kidney diet.  I discovered certain foods caused extreme back pain. Milk consumption made the pain worse (dairy is high in phosphorous).  The absolute worst was goat cheese.  Even a modest amount set off the back pain every time.  Turns out goat cheese is the cheese highest in phosphorous. 

 

So I persisted with my kidney diet, but the pain and nausea would come back at me with a vengeance if I didn't strictly adhere to it.  The diet didn’t fix the problem, but only made it so I didn’t experience extreme bouts of back pain and nausea. 

 

* * * * *

 

As it happened, I had gone off NR in June 2016.  A two-week experiment with NR had left me feeling great, but with pain in the soles of my feet.  This pain persisted even after I stopped the NR.  That led me avoid consuming any NR for 3 months until mid October.  That’s when I decided (1) the back pain and nausea issue (which seemed to be c60 related) was a lot more serious than the foot pain (which I assumed to be NR related); and (2) that the two symptoms were likely not related.  

 

So in October I started taking 150 mg of NR once a day.   

 

Then in November I decided to take massive doses of NR, in hopes it might help the apparent kidney problem.  I took about 1,000 to 1,500 mg/day for 6 days. By the end of the week, I experienced a marked reduction in my back pain for the first time since June. The other associated symptoms also became reduced.  I found I was able to eat dairy and other high-phosphorous foods -- even goat cheese -- without getting any of the usual back pain and nausea symptoms.

   

For the rest of Nov-Dec-Jan I have been taking 250-325mg of NR.  Sometimes I would mega-dose for a couple days.  The back pain and the associated symptoms are now barely detectable.  I no longer experience the debilitating bouts of back pain accompanied by nausea and fatigue that had afflicted me throughout the summer and fall.  

 

* * * * *

 

My last dose of c60 was the one I took in late June 2016 that appeared to have precipitated the 3rd episode of back pain.  

 

The soles-of-feet pain that had prompted me to stop taking NR didn't get any worse after I resumed NR in late October.  I would say the pain diminished somewhat.  Inexplicably, consuming a teaspoon of baking soda seems to make the soles-of-feet pain worse.  

Edited by Empiricus, 09 February 2017 - 04:03 AM.

[Turnbuckle]

During this period I was also taking high doses of nicotinamide...

 

 

 

 

I don't recommend taking NAD+ supplements with C60. Best to allow a day's washout between them. See this post, and this subsequent post.

[Journey2016]

This is my current stack...

Trying to raise NAD levels for addiction

[BioFreak]

I think I got some bad news. I talked to kmoody:

 

 

All vendor vessels were insufficient to stop by-product formation. We did not test all vendor products for increasing tumor formation, but the presence of the by-products does increase tumor formation in our assays, so presumably most/all of them have the potential to promote tumor formation or exacerbate growth. The by-products appear to be epoxides but we have not confirmed exact structure by MS yet. The cause of death is unknown because we did not do histopathology.

You can mention that this is our current thinking but studies are ongoing.

 

My theory on this is:

 

C60 only acts as a buffer, taking on, and later giving away electrons. During storage in the bottle, without any additional antioxidants, c60 soaks up any free radicals. However those free radicals are not indefinitely locked in the c60 molecule. This means, once other chemicals form during storage, they might possess enough force to pull out the electrons and creating something thats not beneficial at all. Within the body this might be of no concern because antioxidants would readily clear out the electrons from c60, however, without any replenishing of antioxidants there is room for the electrons to be used in formation of harmful chemicals. The problem with this, is that the concentration of those chemicals in the bottle rises to a point where it could be harmful.

 

Maybe adding antioxidants would prevent this from happening, by trapping the electrons in meaningful numbers from c60 before any other chemicals can do so. Another way would be finding out how those epoxides form, if they are indeed the problem. Once we know how this happens we may be able to stop formation of those.

 

This is all under the assumption that c60 indeed would not be forming epoxides in the human body due to an active antioxidant system readily depleting electrons from c60. In this case, the beneficial action of c60 would be simply to act as an free radical buffer, to store those in times of high production, and releasing them once the bodies antioxidant system has again more antioxidants flowing around then needed.

 

I've long stopped taking c60 due to kmoodys study and I would advise you to do so too.

 

Let's look at the bright side:

If it is really epoxides forming in c60oo, and if those were the reason for cancer in the study, we won't need lengthy animal experiments to address this issue. All we would need is:

1. proof that epoxides are forming in amounts that can cause cancer in those test animals (or if its not epoxides find what else is being formed)

2. reproduce the formation of epoxides in c60oo

3. add antioxidants to fresh c60oo using the same protocol used in 3. and see if epoxides form again, if no, yay, storage solution found (we now just need to find out how long it can be stored), if no, find another way to stop epoxide formation...

 

And only then, start again with animal experiments.

[kmoody]

Let's look at the bright side:

If it is really epoxides forming in c60oo, and if those were the reason for cancer in the study, we won't need lengthy animal experiments to address this issue. All we would need is:

1. proof that epoxides are forming in amounts that can cause cancer in those test animals (or if its not epoxides find what else is being formed)

2. reproduce the formation of epoxides in c60oo

3. add antioxidants to fresh c60oo using the same protocol used in 3. and see if epoxides form again, if no, yay, storage solution found (we now just need to find out how long it can be stored), if no, find another way to stop epoxide formation...

 

And only then, start again with animal experiments.

 

Agreed, but easier said than done. When we tried to force generate epoxides by light exposure the resulting formulation was acutely lethal in the test animals. So the question becomes whether or not it is worth optimizing the "perfect" dose that causes/exacerbates cancer. We are preferring a different course of study, trying to identify alternative formulations that preserve the efficacy but are resistant to epoxide formation. At some point we probably will need to do a dose response to determine how much contaminant is necessary to actually be toxic. Its just a messy (and expensive) series of studies to run.

[ambivalent]

All vendor vessels were insufficient to stop by-product formation.​

 

​​I understood goodandcheap passed your quality control Kelsey, have you tested subsequently and found them to fail?

[stephen_b]

Agreed, but easier said than done. When we tried to force generate epoxides by light exposure the resulting formulation was acutely lethal in the test animals. So the question becomes whether or not it is worth optimizing the "perfect" dose that causes/exacerbates cancer. We are preferring a different course of study, trying to identify alternative formulations that preserve the efficacy but are resistant to epoxide formation. At some point we probably will need to do a dose response to determine how much contaminant is necessary to actually be toxic. Its just a messy (and expensive) series of studies to run.

 

 

Can you speak to the mechanism of epoxide formation? Would refined monounsaturated oil or a different oil avoid this happening?

[Captain Obvious]

Exactly what are these studies and where are they available for scrutiny?

Since there only dozen of peer-reviewed studies related to C60 on pubmed, none of which show toxicity or mutagenesis of C60 fullerenes (one showed DNA damage for C60 and nanotubes, which are known to be toxic), IMHO the strongest evidence so far is the Baati study which as I recall showed LESS cancer incidence and prolonged lifespan in rats.  

If we want to take anecdotal reports as evidence, there is plenty of that here, mostly positive.

Edited by Captain Obvious, 14 February 2017 - 10:17 AM.

[Turnbuckle]

 

 

 

 

Agreed, but easier said than done. When we tried to force generate epoxides by light exposure the resulting formulation was acutely lethal in the test animals. So the question becomes whether or not it is worth optimizing the "perfect" dose that causes/exacerbates cancer. We are preferring a different course of study, trying to identify alternative formulations that preserve the efficacy but are resistant to epoxide formation. At some point we probably will need to do a dose response to determine how much contaminant is necessary to actually be toxic. Its just a messy (and expensive) series of studies to run.

 

 

 

I understand "acutely lethal" to mean that one dose of irradiated C60-EVOO  caused cancer that killed the animals. Is that right? And if  epoxides really are the problem (and not some constituent of olive oil), those would still form in vivo in humans, given that we aren't wearing fur coats all the time like rats. Thus C60 would never be safe and skin cancers ought to be common among those exposed by any route. 

Edited by Turnbuckle, 14 February 2017 - 12:32 PM.

[BioFreak]

 

Let's look at the bright side:

If it is really epoxides forming in c60oo, and if those were the reason for cancer in the study, we won't need lengthy animal experiments to address this issue. All we would need is:

1. proof that epoxides are forming in amounts that can cause cancer in those test animals (or if its not epoxides find what else is being formed)

2. reproduce the formation of epoxides in c60oo

3. add antioxidants to fresh c60oo using the same protocol used in 3. and see if epoxides form again, if no, yay, storage solution found (we now just need to find out how long it can be stored), if no, find another way to stop epoxide formation...

 

And only then, start again with animal experiments.

 

Agreed, but easier said than done. When we tried to force generate epoxides by light exposure the resulting formulation was acutely lethal in the test animals. So the question becomes whether or not it is worth optimizing the "perfect" dose that causes/exacerbates cancer. We are preferring a different course of study, trying to identify alternative formulations that preserve the efficacy but are resistant to epoxide formation. At some point we probably will need to do a dose response to determine how much contaminant is necessary to actually be toxic. Its just a messy (and expensive) series of studies to run.

 

 

You're right, and I didn't mean to test different doses of epoxides. After all, it would be pointless to know which dose of epoxides "just" causes non-acutely lethal cancer. We already know epoxides are harmful, so the way to go is to try to prevent epoxide formation at all, or for a long enough shelf life of the product. Awesome that you are already onto that. Did you test adding antioxidants (such as Vitamin e would be my first choice since it is being used in fish oil to protect it), and did you get less epoxides? Or does the antioxidant route show little promise? Did any substance class yet show inhibition of epoxide formation at any level?

 

Kmoody, I must say you work in an awesome lab. I'd love to work there and find answers to those questions...

[Turnbuckle]

We already know epoxides are harmful...

 

 

How do you know? Can you point to research proving that statement?

[BioFreak]

 

We already know epoxides are harmful...

 

 

How do you know? Can you point to research proving that statement?

 

 

quick google search:
https://www.ncbi.nlm...008750/?page=16

 

https://en.wikipedia.../Epoxide#Safety

 

If I'm wrong (I haven't done much research) then you are free to correct me. Right now epoxides are the main suspect in kmoodys lab and I trust their judgement.

[Turnbuckle]

 

 

We already know epoxides are harmful...

 

 

How do you know? Can you point to research proving that statement?

 

 

quick google search:
https://www.ncbi.nlm...008750/?page=16

 

https://en.wikipedia.../Epoxide#Safety

 

If I'm wrong (I haven't done much research) then you are free to correct me. Right now epoxides are the main suspect in kmoodys lab and I trust their judgement.

 

 

 

C60 epoxides appear to be more powerful anti-oxidants than pristine C60--

 

 

The introduction of pin-up oxygen on C60, such as in the oxidized fullerenes C60O and C60On, induced noticeable increase in the antioxidant activity as compared to pristine C60. The water-soluble inclusion complexes of fullerenes C60O and C60On reacted with linoleic acid peroxyl radical 1.7 and 2.4 times faster, respectively.

 

https://www.ncbi.nlm...les/PMC3244865/

 

 

 

 

 

So just because C60 epoxides were present in commercial samples of C60EVOO that caused cancer doesn't mean that the epoxide itself was responsible. It could just be a marker for an oxidized oil vehicle, and the actual cause could be adducts derived from the oil.

[BioFreak]

http://pubs.acs.org/....1021/jo9915527

 

c60 itself can become part of a molecule that is an epoxide, in theory. Yikes...

[BioFreak]

 

C60 epoxides appear to be more powerful anti-oxidants than pristine C60--

 

 

The introduction of pin-up oxygen on C60, such as in the oxidized fullerenes C60O and C60On, induced noticeable increase in the antioxidant activity as compared to pristine C60. The water-soluble inclusion complexes of fullerenes C60O and C60On reacted with linoleic acid peroxyl radical 1.7 and 2.4 times faster, respectively.

 

https://www.ncbi.nlm...les/PMC3244865/

 

 

 

 

 

So just because C60 epoxides were present in commercial samples of C60EVOO that caused cancer doesn't mean that the epoxide itself was responsible. It could just be a marker for an oxidized oil vehicle, and the actual cause could be adducts derived from the oil.

 

 

Well it seems like there are different kinds of epoxides with different properties, it could be that c60 is part of a newly generated epoxide molecule, or it could be that c60 is only taking part in the formation of epoxides without becoming part of the epoxide. So the properties those epoxides have depend on what kind of epoxides exactly are produced.

 

Their lab is pretty focused on epoxides right now. Maybe they have evidence we don't know about yet that justifies their focus. I'd bet epoxides are the main chemical that was detectable in the samples, and the highest amount in those samples exposed to extra sunlight(aka increasing with light dosage=main correlation) that was lethal. In their shoes, I`d first go after the substance that had the highest dose dependent correlation with lethality in both the first samples and the extra light exposed samples. And work down from there if it does not prove to be the lethal compound.
 

Because of the lethality of those extra light exposed samples, any changes in lethality by adding different compounds should be evident in a petri dish, meaning at this stage there should be no need for animal tests. Once there is a formulation that has low lethality, one could simply check the original samples, and the new formula, and check what molecules are lower or missing. If there are still epoxides but another substance has dropped a lot, that'd be a hint... Until then, I don't see anything wrong with their approach to focus on a) epoxides and b) reducing lethality. Even if they are wrong, this type of analysis should show the correlation between other substances in the sample and lethality. And you have to start somewhere...

[kmoody]

I understand "acutely lethal" to mean that one dose of irradiated C60-EVOO  caused cancer that killed the animals. Is that right? And if  epoxides really are the problem (and not some constituent of olive oil), those would still form in vivo in humans, given that we aren't wearing fur coats all the time like rats. Thus C60 would never be safe and skin cancers ought to be common among those exposed by any route. 

 

No. The animals died of within 1-3 days of toxicity from excessively light exposed C60-EVOO, an outcome we did not expect. Because we did not expect it, we were gearing all our study endpoints to look at tumor burden and were unfortunately unable to do anything useful in terms of determining cause of death.

 

Exactly what are these studies and where are they available for scrutiny? 

If we want to take anecdotal reports as evidence, there is plenty of that here, mostly positive.

 

We are in the process of drafting what we have available for publication. Because we observed the potential for significant toxic effects from a compound we know people are consuming, we elected to prematurely release anecdotes of our ongoing studies to inform users on this forum. The peer reviewed stuff is following but unfortunately takes time to properly compile and get reviewed.

 

I would venture a guess that no one that has made anecdotal reports here has done so much as check the concentration of C60 in what they are ingesting, so although we are still putting everything together properly for peer-review and your scrutiny, I think we warrant a bit more consideration than just another anecdotal report, especially given the significance of the apparent findings. The burden of proof to warn about possible toxic effects is lower than burden of proof for positive effects. I would rather make these concerns known as soon as we have a reasonable basis to suspect problems.

 

 

Can you speak to the mechanism of epoxide formation? Would refined monounsaturated oil or a different oil avoid this happening?

 

This is outside of my wheelhouse, but I will be bringing on additional chemists after our next funding round that may be able to provide insight to this.