29 replies to this topic

[zorba990]

Would like to start a thread about the use of C60 as a fish oil preservative:
http://www.iherb.com...-oz-500-ml/2796

Thought is 1/2 gram ultra pure C60 in above container, blow off with argon close and shake. Keep refrigerated and agitate once a day for a couple of weeks. When the oil is clear maybe send in somewhere for oxidative analysis?

[Junk Master]

That would be fascinating. Great idea.

[zorba990]

That would be fascinating. Great idea.

This was just mentioned in the Lou Gehrig's thread, so I can't take credit for the idea. I think it would be an interesting experiment. I imagine someone could probably get a grant to study C60 olive oil as a fish food additive...I guess it's on its way into the food and water supply regardless...

[HappyPhysicist]

Zorba,

Thanks so much for starting this thread! I just got done mixing 0.5 gram of C60 into 500 mL of Now Foods Omega 3 Fish Oil.

I am beginning to suspect that fish oil is an even better solvent than olive oil. When I mix the same amount of C60 into olive oil, I always get a visible C60 residue in the jar. This is one of the reasons I switched to 0.5 gram of C60 per 1000 mL of olive oil. But I would still get some C60 residue even with that concentration.

Now with my 0.5 gram in 500 mL (i.e. 1 gram per liter) in fish oil I get no residue at all! This is only after 3 days of mixing.

The color final product is very similar to olive oil, i.e., it looks like red wine when I shine an incandescent bulb on it from the back of the jar looking at the front of the jar.

The original color of Fish oil is golden, kind of like urine. This is very similar in color to the Tunisian olive oil I have used.

Another advantage is that it filters very fast. With olive oil it is a 'drip, drip, drip' through the filter, but with fish oil it is a very small stream through the filter.

Thanks,

Ben

[Turnbuckle]

Long-term intake of fish oil increases oxidative stress and decreases lifespan in senescence-accelerated mice.

The SAMP8 mice fed fish oil did not have a longer maximum lifespan and had a shorter average lifespan than mice fed safflower oil. To examine the mechanism underlying these results, the effects on oxidative stress of long-term ingestion of fish oil were also examined. SAMP8 mice fed fish oil for 28 wk showed strong oxidative stress that caused hyperoxidation of membrane phospholipids and a diminished antioxidant defense system due to a decrease in tocopherol compared with mice fed safflower oil.

Source: http://www.ncbi.nlm....pubmed/20621447

[HappyPhysicist]

I have a correction. Now that my fish oil is done filtering. I do indeed see some C60 residue. A little less than olive oil, but not significantly less. I can usually see it when I pour the olive oil into the filter. When I poured the fish oil into the filter I didn't see it. But once it was done filtering there was C60 residue visible.

[zorba990]

Long-term intake of fish oil increases oxidative stress and decreases lifespan in senescence-accelerated mice.

The SAMP8 mice fed fish oil did not have a longer maximum lifespan and had a shorter average lifespan than mice fed safflower oil. To examine the mechanism underlying these results, the effects on oxidative stress of long-term ingestion of fish oil were also examined. SAMP8 mice fed fish oil for 28 wk showed strong oxidative stress that caused hyperoxidation of membrane phospholipids and a diminished antioxidant defense system due to a decrease in tocopherol compared with mice fed safflower oil.

Source: http://www.ncbi.nlm....pubmed/20621447

That study actually seems to clarify the problematic mechanism as using up tocopherol. Like taking R-ALA with ALCAR, it seems one should increase full spectrum vitamin E with increase unsaturated fatty acid ingestion.

Also, the mice were "senescence-accelerated" which doesn't seems like a fair test. I really find it quite interesting that many of the thousands of tocopherol studies that were readily available on Pubmed 10 years ago no longer seem to show up.

[HappyPhysicist]

My rational for using fish oil is the higher omega-3 to omega-6 ratio. Supposedly Omega 3 is 'anti-inflammatory' while omega-6 is 'pro-inflammory'.

Edited by HappyPhysicist, 01 August 2012 - 06:04 PM.

[Turnbuckle]

Long-term intake of fish oil increases oxidative stress and decreases lifespan in senescence-accelerated mice.

The SAMP8 mice fed fish oil did not have a longer maximum lifespan and had a shorter average lifespan than mice fed safflower oil. To examine the mechanism underlying these results, the effects on oxidative stress of long-term ingestion of fish oil were also examined. SAMP8 mice fed fish oil for 28 wk showed strong oxidative stress that caused hyperoxidation of membrane phospholipids and a diminished antioxidant defense system due to a decrease in tocopherol compared with mice fed safflower oil.

Source: http://www.ncbi.nlm....pubmed/20621447

That study actually seems to clarify the problematic mechanism as using up tocopherol. Like taking R-ALA with ALCAR, it seems one should increase full spectrum vitamin E with increase unsaturated fatty acid ingestion.

Also, the mice were "senescence-accelerated" which doesn't seems like a fair test. I really find it quite interesting that many of the thousands of tocopherol studies that were readily available on Pubmed 10 years ago no longer seem to show up.

There were thousands? Really?

Here's one that covers more than 50 (and a 1/4 million people)--

The current analysis reexamines the relationship between supplemental vitamin E and all-cause mortality. All randomized, controlled trials testing the treatment effect of vitamin E supplementation in adults for at least one year were sought. MEDLINE, the Cochrane Library, and Biological Abstracts databases were searched using the terms "vitamin E," "alpha-tocopherol," "antioxidants," "clinical trial," and "controlled trial" for studies published through April 2010; results were limited to English, German, or Spanish language articles. Studies were also obtained through reference mining. All randomized controlled trials using vitamin E, with a supplementation period of at least one year, to prevent or treat disease in adults were identified and abstracted independently by two raters. Mortality data from trials with a supplementation period of at least one year were pooled. The selected trials (n = 57) were published between 1988 and 2009. Sample sizes range from 28 to 39,876 (median = 423), yielding 246,371 subjects and 29,295 all-cause deaths. Duration of supplementation for the 57 trials range from one to 10.1 years (median = 2.6 years). A random effects meta-analysis produce an overall risk ratio of 1.00 (95% confidence interval: 0.98, 1.02); additional analyses suggest no relationship between dose and risk of mortality. Based on the present meta-analysis, supplementation with vitamin E appears to have no effect on all-cause mortality at doses up to 5,500 IU/d.

http://www.ncbi.nlm....pubmed/21235492

Another study said this about omega 3 & 6:

Our findings further suggest that the life span of Wistar rats is not affected even if the ratio of dietary n-6/n-3 changes from 1 to 16.

http://www.ncbi.nlm....pubmed/19926924

Edited by Turnbuckle, 01 August 2012 - 06:16 PM.

[zorba990]

http://orthomolecula...05n01.shtml is an interesting read.

Edit: fixed broken link

Edited by niner, 02 August 2012 - 12:48 AM.

[niner]

Here is my canonical collection of links regarding high dose fish oil, which I'm not crazy about.

[zorba990]

One of the problems I have with the "fish Oil is bad for you" or "Omega 3's are bad for you" is that the Omega 3 content of the game meat we were likely to have evolved on was likely to be high.

http://www.bisonbasi...d_finished.html

I'm basing this on the assumption that the wild game we ate did not graze on grain but grasses, which were more plentiful.
So our membranes not containing these fatty acids in at least 4:1 ratio or higher would be a rare condition, and not one that our body systems were adapted to.

Fish Oil seems to lower inflammation, improve blood fatty acid profiles, and be somewhat anti-tumor
http://www.ncbi.nlm..../pubmed/8569432

So with all these benefits against the primary causes of death what's a little oxidation between friends?
Especially when we know that increasing tocopherol consumption (which was probably high in game meat as well at some point) will protect membranes?
http://www.rollinghi...igher-vitamin-e

How much full spectrum vitamin E is needed for how much Omega-3 is another matter, and one that should probably be investigated. But since Vitamin E shows little toxicity I currently err on high side since my consumption of grassed meat is lower that I would like due to cost issues (Vitamin E plus fish oil is cheaper even with full spectrum high quality tocopherols and good carlson fish oil).

[niner]

One of the problems I have with the "fish Oil is bad for you" or "Omega 3's are bad for you" is that the Omega 3 content of the game meat we were likely to have evolved on was likely to be high.

http://www.bisonbasi...d_finished.html

I'm basing this on the assumption that the wild game we ate did not graze on grain but grasses, which were more plentiful.
So our membranes not containing these fatty acids in at least 4:1 ratio or higher would be a rare condition, and not one that our body systems were adapted to.

Fish Oil seems to lower inflammation, improve blood fatty acid profiles, and be somewhat anti-tumor
http://www.ncbi.nlm..../pubmed/8569432

At nutritiondata.com, which at least seams like an unbiased source, in that they don't sell any particular food items, "game meat" bison, which sounds like it must be grass fed by definition, has a decent n-6:n-3 ratio of 3.7 if you trim off all the fat, so you're just eating visibly lean meat. However, the omega 3 fatty acids it contains are PUFA (2, 3, or 4 double bonds, with none of it in the HUFA (highly unsaturated FA) form, like EPA and DHA. Further, per ounce, you get less than a tenth of a gram of PUFAs of all kinds, so the fat from this particular form of game meat has a very low oxidation risk, being mostly SAFA and MUFA. The oxidation risk of a given fatty acid increases exponentially with each added double bond, so there is no comparison between game meets and fish oil, which has five (EPA) and six (DHA) double bonds.

If you eat the fat, grass fed bison has a worse 6:3 ratio. They said that a 3oz serving of cooked ground meat contained 38.2mg n-3 and 266mg n-6. That's a 6:3 ratio of 7. Still a very low PUFA level, though, and no HUFA.

In reasonable doses, fish oil is anti-inflammatory and a great thing. Here's the anti-tumor link you posted:

Lipids. 1995 Nov;30(11):1035-45.
Dietary menhaden oil enhances mitomycin C antitumor activity toward human mammary carcinoma MX-1.
Shao Y, Pardini L, Pardini RS.

Allie M. Lee Laboratory for Cancer Research, Department of Biochemistry, University of Nevada, Reno 89557, USA.

In the present study, we investigated the effects of high levels of dietary fish oil on the growth of MX-1 human mammary carcinoma and its response to mitomycin C (MC) treatment in athymic mice. We found that high levels of dietary fish oil (20% menhaden oil + 5% corn oil, w/w) compared to a control diet (5% corn oil, w/w) not only lowered the tumor growth rate, but also increased the tumor response to MC treatment. We also found that high levels of dietary fish oil significantly increased the activities of tumor xanthine oxidase and DT-diaphorase, which are proposed to be involved in the bioreductive activation of MC. Since menhaden oil is highly unsaturated, its intake caused a significant increase in the degree of fatty acid unsaturation in tumor membrane phospholipids. This alteration in tumor membrane phospholipids made the tumor more susceptible to oxidative stress, as indicated by the increased levels of both endogenous lipid peroxidation and protein oxidation after feeding the host animals the menhaden oil diet. In addition, the tumor antioxidant enzyme activities, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPOx), and glutathione S-transferase peroxidase (GSTPx), were all significantly enhanced by feeding a diet high in fish oil. MC treatment caused further increases in tumor lipid peroxidation and protein oxidation, as well as in the activities of CAT, SOD, GPOx, and GSTPx, suggesting that MC causes oxidative stress in this tumor model which is exacerbated by feeding a diet high in menhaden oil. Thus, feeding a diet rich in menhaden oil decreased the growth of human mammary carcinoma MX-1, increased its responsiveness to MC, and increased its susceptibility to endogenous and MC-induced oxidative stress, and increased the tumor activities of two enzymes proposed to be involved in the bioactivation of MC, that is, DT-diaphorase and xanthine oxidase. These findings support a role of these two enzymes in the bioactivating of MC and indicate that the type of dietary fat may be important in tumor response to therapy.

PMID: 8569432

In this paper, fish oil is kind of a chemotherapy agent, damaging all cells, but helping the mitomycin C (toxin) to selectively kill tumor cells by raising the level of oxidative stress. I'd say that was an argument for high dose fish oil if you're also undergoing mitomycin C chemotherapy, but otherwise, it looks like a negative.

Fish oil is great in low doses; I take 2 grams a day of a typical (non-concentrated) fish oil. I just don't think that the available data supports megadosing it.

[zorba990]

There is the suggestion, here,
http://paleohacks.co...f-heart-disease
that maybe even ALL UFA's should be greatly reduced or avoided due to this membrane issue.
Suggestiong,
Worrying about whether the oil itself is oxidized before you eat it is irrelevant if your lipoproteins are becoming oxidized as a result of PUFA-constructed membranes and PUFA transported in the VLDL as triglycerides.

However, if this is true then why did the Olive Oil only group of the ooC60 study have an extended lifespan? Those were pretty large oil doses.
Is there something in the Olive Oil that is so membrane protective as to negate the issue? Os is the membrane becoming more subject to oxidation not really an issue?

[niner]

However, if this is true then why did the Olive Oil only group of the ooC60 study have an extended lifespan? Those were pretty large oil doses.
Is there something in the Olive Oil that is so membrane protective as to negate the issue? Os is the membrane becoming more subject to oxidation not really an issue?

Olive oil is not a problem because it's mostly monounsaturated, with the next most common component saturated, and finally a little bit of a di-unsaturated fatty acid. The oxidizibility of a fatty acid increases exponentially with the number of double bonds. Olive oil doesn't present much oxidation risk because of its low double bond count. Fish oil, on the other hand, has either 5 (EPA) or 6 (DHA) double bonds, and is extremely oxidation prone.

[mikey]

Long-term intake of fish oil increases oxidative stress and decreases lifespan in senescence-accelerated mice.

The SAMP8 mice fed fish oil did not have a longer maximum lifespan and had a shorter average lifespan than mice fed safflower oil. To examine the mechanism underlying these results, the effects on oxidative stress of long-term ingestion of fish oil were also examined. SAMP8 mice fed fish oil for 28 wk showed strong oxidative stress that caused hyperoxidation of membrane phospholipids and a diminished antioxidant defense system due to a decrease in tocopherol compared with mice fed safflower oil.

Source: http://www.ncbi.nlm....pubmed/20621447

I wonder if the full text would tell if the fish oil was the triglyceride form or ethyl ester. It being EE might explain this negative effect.

[niner]

I wonder if the full text would tell if the fish oil was the triglyceride form or ethyl ester. It being EE might explain this negative effect.

Whether or not it was EE might have some effect on bioavailability, but the oxidation problem resides in the highly unsaturated part of the molecule, which is the same in either form. It probably wouldn't make much difference.

[mikey]

I wonder if the full text would tell if the fish oil was the triglyceride form or ethyl ester. It being EE might explain this negative effect.

Whether or not it was EE might have some effect on bioavailability, but the oxidation problem resides in the highly unsaturated part of the molecule, which is the same in either form. It probably wouldn't make much difference.

This page says that EE can be more subject to oxidation in re-synthesis to TG.
"Without a glycerol or monoglyceride substrate TG re-synthesis is delayed, suggesting that transport to the blood is more efficient in natural TG fish oils in comparison to EEs. Furthermore, this delay of TG re-synthesis in EE fish oils could cause an increase in free fatty acids and subsequent oxidation of those free fatty acids."

Then it says:
Ethyl ester fish oils are less stable, and readily oxidize

Omega-3 fatty acids in the form of EEs are much less stable than those in the natural TG form and readily oxidize. The oxidation kinetics of DHA as an EE or as a TG was assessed by measuring the concentration of oxygen found in the head space of a reaction vessel with both TG and EE forms¹⁷. The EE form of DHA was more reactive, and quickly oxidized, demonstrating that EEs are far less stable and can more readily produce harmful oxidation products¹⁷. Furthermore, the stability of phospholipid, triglyceride and EEs containing DHA has been assessed¹⁸. After a ten-week oxidation period, the EE DHA oil decayed 33 % more rapidly¹⁸.

Ethyl ester fish oil safety
During the digestive process, EEs are converted back to TGs by intestinal enterocytes1 which, results in the release of ethanol. Although the amount of ethanol released in a typical dose of fish oil is small, those with sensitivities to alcohol or those who are alcoholics should refrain from the consumption of EEs. Young children may also be more vulnerable to the toxic effects of ethanol even in small quantities. The exact amount of ethanol released from the EE fish oil is dependent on the exact profile of the fatty acids. For a typical 60 % omega-3 EE concentrate the amount of ethanol would be approximately 15 % by weight (see Figure 1). Additional concern exists regarding whether a small portion of EE
is absorbed directly into the body¹⁹. Unlike TGs, the presence of EEs in the body has been found to potentiate cytotoxicity¹⁹. Several in vitro studies using purified lysosomes²⁰, purified mitochondria¹⁹ or intact Hep G2 cells²² have provided evidence for toxicity of EEs. Studies in animals have shown that ethanol released into the liver and pancreas can result in severe organ damage²³. Post mortem organ analysis has demonstrated that EEs are toxic mediators of ethanol induced cellular injury²⁴, and have been shown to induce pancreatic injuries when infused in vivo into rats²⁵. It is possible that efficient EE digestion in the GI tract could prevent toxicity³, but until further studies carefully examine EE oxidation, the potential for direct uptake of EEs, or EE absorption into the circulation via the stomach, EEs should be consumed with caution.

[zorba990]

I ran into this and thought it was interesting in the context of large fish oil doses.
http://www.ncbi.nlm....pubmed/12951900
One thing that is very interesting the enormous vitamin E doses given. 10,000mg / kg! Wow that is unreal!
(I thought the 2000-3000iu a day that Colgan recommended for Athletes was a lot)

[niner]

I ran into this and thought it was interesting in the context of large fish oil doses.
http://www.ncbi.nlm....pubmed/12951900
One thing that is very interesting the enormous vitamin E doses given. 10,000mg / kg! Wow that is unreal!
(I thought the 2000-3000iu a day that Colgan recommended for Athletes was a lot)

It looks like that's 10,000mg/kg of food, not of body weight. That would be 1% of food by weight, which is still a hell of a lot. I don't know how much rats eat, but they ususally weigh around half a kilo.

[cbohrson]

Is it possible that the C60 could stay localized to the fish oil even after consumption, and counter the oxidation effects which presumably shortened the lives of mice? I'm imagining insoluble EPA/DHA droplets carrying C60 through the body's aqueous medium. C60 and EPA/DHA are hydrophobic enough that they'd generally stay together. I don't know enough about the transport of EPA/DHA through the body to actually assess this idea, however.

It'd be nice if you could get the anti-inflammatory benefits without having to worry about the oxidation issue, obviously.

[Jerramy]

I was just about to post a general query on this topic; I'm glad I did a search first. Learned a ton of stuff.

So the C60 aside (which I still need to get my hands on some), can fish oil be replaced by olive oil in my regimen? I'm finding that the fish oil really helps with my dry skin, and was under the assumption that it was protecting my body from damage (not the other way around). Olive oil is more available and stable, so if I could just use that instead in my diet, and that was somehow better, it would be a win-win situation. Or is there benefit in taking both?

The study showed that large doses of olive oil significantly extended rat lifespan. Has the same been shown for humans?

[niner]

I was just about to post a general query on this topic; I'm glad I did a search first. Learned a ton of stuff.

So the C60 aside (which I still need to get my hands on some), can fish oil be replaced by olive oil in my regimen? I'm finding that the fish oil really helps with my dry skin, and was under the assumption that it was protecting my body from damage (not the other way around). Olive oil is more available and stable, so if I could just use that instead in my diet, and that was somehow better, it would be a win-win situation. Or is there benefit in taking both?

The study showed that large doses of olive oil significantly extended rat lifespan. Has the same been shown for humans?

I wish everyone did a search first. Thanks for that. The fish oil not only can be replaced, it should be replaced. The original rat experiment that showed the amazing life extension was done using olive oil, not fish oil. There is no experimental evidence that I know of involving a C60-fish oil adduct. For all we know, it could shorten lifespans instead of lengthening them. We just don't know. There is a benefit in taking fish oil by itself in modest quantities; it contains essential fatty acids. This has been extensively demonstrated. And finally, yes, Olive oil has been shown to dose-dependently reduce mortality in humans. There was a recent paper involving the Spanish cohort of the very large EPIC database. The top quartile for olive oil consumption was two tablespoons per day (or more), and this was associated with a significant 26% reduction in risk of overall mortality. Baati's paper raises some interesting questions about the dosing strategy for olive oil use. How do occasional large doses of olive oil early in life lead to such a large life extension? In humans, would that strategy be better than daily dosing? How does lipid metabolism and response to olive oil polyphenols in Wistar rats compare to humans?

[Jerramy]

I guess there's nothing but to try it. No fish oil, half tablespoon of olive oil, twice a day.
Goal of non-chapped skin.

If all goes well, I'll report back in a week. If not, I'll try to report back anyway.
And if it kills me, you'll never know...

[d4shing]

Looks like it killed Jerramy. Has anyone else tried C60/fish oil?

[HappyPhysicist]

I tried it and it didn't kill me. Didn't help my ALS either. It appeared that C60 has a lower solubility in fish oil.

[niner]

I tried it and it didn't kill me. Didn't help my ALS either. It appeared that C60 has a lower solubility in fish oil.

Hey, HP! Nice to hear from you. How are you feeling these days?

[HappyPhysicist]

To be honest, like shit.

I tried the C60 for about 6 months but my progression continued right on schedule. It might still do wonders for longevity, it certainly didn't make me any worse.

[niner]

Sorry to hear that. I hope for the best, and hope that you keep looking at all possible treatments.

[free10]

To be honest, like shit.

I tried the C60 for about 6 months but my progression continued right on schedule. It might still do wonders for longevity, it certainly didn't make me any worse.

Feeling like shit means you are alive which is a start. Kind of strange the C60 was of little help as I thought it might be at least of some help. So I thought maybe hydergine and came up with this

http://www.lef.org/p.../abstr-008.html

Then I thought of a few TA65 users and how that might help. Here is a person with MS



or Parkinson's



Just a few thoughts