331 replies to this topic

[stephen_b]

See this post. It has to do with surface area comparisons.

[Turnbuckle]

It's difficult to understand how taking an anti-oxidant for six months would extend your lifespan by 30 months. It might explain six months or less, but not 30. Now if you propose certain superpowers for C60--that some of it sticks around forever with almost homeopathic effectiveness, then you'd also expect one dose to be sufficient for years. Beyond that, you also have to explain how an anti-oxidant can grow hair and make scars disappear, which isn't among the known effects of anti-oxidants.

C60 is fat soluble. Fat soluble chemicals can stay in the system for a very long time, even years or decades.

Here is a recent paper showing C60 injected into rats decays in most organs by a factor of about 2 over 4 weeks. So in one year there would be .01% of the original dose left. On the other hand, if a rat took it every day for ten days, they'd have 9 times the initial dose in their system. And after a long time of taking a daily dose, this would build up to more than 40 times the daily dose. Except for the spleen, where the dose would build up much faster. Not to say that the old C60 is still effective, of course. Niner, for instance, saw a measurable decline in exercise reps after stopping for a short time.

[hav]

I burn about 2900 calories per day
http://www.self.com/...Level=3&submit=

The calorie proportional does would then be 2900 * .0070833 = 20.5 mg per day.

Does this seem like a reasonable way to calculate dose?

I guess a huge missing variable, is how quickly does the human body filter out the C60 from the blood.
One should adjust the previous calculation for the relative speed at which the humans and rats remove the C60 from the blood.

And in answer to how long I have been doing this, I have been taking this does since about October.

Not sure that when you burn up calories, you are burning up any c60. I think the energy required to break up c60 exceeds that of any natural body processes. Also, if taken in lipid solution, clearance from the bloodstream would not be a measure of clearance from the body. Theory is that primary distribution of c60/oo is via the lymphatic system and that it is stored in fatty cellular membranes. As previously discussed here, my guess is that the c60/oo probably only gets cleared when the cell housing it dies, and maybe not even then if the fatty membranes get recycled.

Howard

Edited by hav, 02 January 2013 - 06:29 PM.

[hav]

Here is a recent paper showing C60 injected into rats decays in most organs by a factor of about 2 over 4 weeks. So in one year there would be .01% of the original dose left. On the other hand, if a rat took it every day for ten days, they'd have 9 times the initial dose in their system. And after a long time of taking a daily dose, this would build up to more than 40 times the daily dose. Except for the spleen, where the dose would build up much faster. Not to say that the old C60 is still effective, of course. Niner, for instance, saw a measurable decline in exercise reps after stopping for a short time.

Any idea what they injected? c60 in solution or suspension? In water or oil? Don't have access to the full-text, myself.

Howard

[Turnbuckle]

Here is a recent paper showing C60 injected into rats decays in most organs by a factor of about 2 over 4 weeks. So in one year there would be .01% of the original dose left. On the other hand, if a rat took it every day for ten days, they'd have 9 times the initial dose in their system. And after a long time of taking a daily dose, this would build up to more than 40 times the daily dose. Except for the spleen, where the dose would build up much faster. Not to say that the old C60 is still effective, of course. Niner, for instance, saw a measurable decline in exercise reps after stopping for a short time.

Any idea what they injected? c60 in solution or suspension? In water or oil? Don't have access to the full-text, myself.

Howard

According to the Baati paper, liposomes were used as a carrier for unmodified C60, which they didn't think was best for studying the pharmokinetics. But they too found the highest levels of C60 in the spleen, so high that it precipitated there.

[hav]

Here is a recent paper showing C60 injected into rats decays in most organs by a factor of about 2 over 4 weeks. So in one year there would be .01% of the original dose left. On the other hand, if a rat took it every day for ten days, they'd have 9 times the initial dose in their system. And after a long time of taking a daily dose, this would build up to more than 40 times the daily dose. Except for the spleen, where the dose would build up much faster. Not to say that the old C60 is still effective, of course. Niner, for instance, saw a measurable decline in exercise reps after stopping for a short time.

I was able to find an even more recent 2012 study involving one of the same participants, Reiji Kubota, Here he used c60 dissolved in corn oil and delivered via gavage but used the same lc/ms method to detect c60 in the organs... and found none at all:

Sub-acute oral toxicity study with fullerene C60 in rats.

Using liquid chromatography-tandem mass spectrometry, fullerene C60 were not detected in the liver, spleen or kidney at the end of the administration period and also at the end of the recovery period. In conclusion, the present study revealed no toxicological effects of fullerene C60; however, the slight increases in liver and spleen weights after the 14-day recovery period may be because of the influence of fullerene C60 oral administration. In the future, it will be necessary to conduct a long-term examination because the effects of fullerene C60 cannot be ruled out.

I'm thinking that injecting c60 may have a pretty different impact on the organs compared to taking it orally.

Howard

[Turnbuckle]

Here is a recent paper showing C60 injected into rats decays in most organs by a factor of about 2 over 4 weeks. So in one year there would be .01% of the original dose left. On the other hand, if a rat took it every day for ten days, they'd have 9 times the initial dose in their system. And after a long time of taking a daily dose, this would build up to more than 40 times the daily dose. Except for the spleen, where the dose would build up much faster. Not to say that the old C60 is still effective, of course. Niner, for instance, saw a measurable decline in exercise reps after stopping for a short time.

I was able to find an even more recent 2012 study involving one of the same participants, Reiji Kubota, Here he used c60 dissolved in corn oil and delivered via gavage but used the same lc/ms method to detect c60 in the organs... and found none at all:

Sub-acute oral toxicity study with fullerene C60 in rats.

Using liquid chromatography-tandem mass spectrometry, fullerene C60 were not detected in the liver, spleen or kidney at the end of the administration period and also at the end of the recovery period. In conclusion, the present study revealed no toxicological effects of fullerene C60; however, the slight increases in liver and spleen weights after the 14-day recovery period may be because of the influence of fullerene C60 oral administration. In the future, it will be necessary to conduct a long-term examination because the effects of fullerene C60 cannot be ruled out.

I'm thinking that injecting c60 may have a pretty different impact on the organs compared to taking it orally.

Howard

It's not entirely clear that they knew what they were doing, as they had residue in the oil even at the .1mg/ml level.

[niner]

It's not entirely clear that they knew what they were doing, as they had residue in the oil even at the .1mg/ml level.

Yeah, I don't think there's much of anything we can take from the Takahashi et al. corn oil sludge paper, other than that it shows that macroscopic particulate c60 comes out in the mouse poop. That part at least suggests to me that filtration of c60-oo preparations is optional.

[niner]

It's difficult to understand how taking an anti-oxidant for six months would extend your lifespan by 30 months. It might explain six months or less, but not 30. Now if you propose certain superpowers for C60--that some of it sticks around forever with almost homeopathic effectiveness, then you'd also expect one dose to be sufficient for years. Beyond that, you also have to explain how an anti-oxidant can grow hair and make scars disappear, which isn't among the known effects of anti-oxidants.

C60 is fat soluble. Fat soluble chemicals can stay in the system for a very long time, even years or decades.

Here is a recent paper showing C60 injected into rats decays in most organs by a factor of about 2 over 4 weeks. So in one year there would be .01% of the original dose left. On the other hand, if a rat took it every day for ten days, they'd have 9 times the initial dose in their system. And after a long time of taking a daily dose, this would build up to more than 40 times the daily dose. Except for the spleen, where the dose would build up much faster. Not to say that the old C60 is still effective, of course. Niner, for instance, saw a measurable decline in exercise reps after stopping for a short time.

There's a couple different factors at play. One is the rate at which c60-oo leaves the system. There's plenty of precedent for very hydrophobic substance taking a very long time to leave, particularly if they aren't susceptible to oxidation and conjugation with hydrophilic moieties, which is the way we get rid of most xenobiotics. Dioxin would be an example of this. The c60-fatty acid adduct has another reason to stay in the body, which is that it will have one or two polar head groups with a very hydrophobic tail (or middle) that will make it energetically harder to remove it from a membrane, compared to pristine c60 or the various hydrophilic analogs. c60 is going to be inherently resistant to the usual forms of xenobiotic metabolism, as it doesn't provide much of a handle for the oxidative enzymes. No one has yet run the experiment that would accurately characterize the pharmacokinetics of c60-oo in its "long tail" slow decay mode. Baati looked at the initial rapid clearance phase only. At any rate, it's safe to say that it takes a long time for c60-oo to leave the lipid compartment.

The other major factor involved in this issue is the level of c60 needed to achieve various aims. It looks like different phenomena require different levels of c60. For example, as we recently saw in Baati, a 4mg/kg oral dose in a rat was not enough to eliminate effects of a CCl4 challenge, but a 4mg/kg i.p. dose was enough. I found that the amelioration of muscle fatigue fell off pretty quickly, but even after waiting 6 weeks, I still had enough on board to get rid of the symptoms of postural hypotension that used to bother me. Baati's rats got pretty huge doses, particularly in the first week, but they continued getting dosed for 6-7 months. They had plenty of time to get good and saturated. Could it be that the life extension effect requires only a very small c60 level? Maybe. We need to explain about a two year life extension. Can long clearance kinetics and very high antioxidant potency explain it? If the liposomal preparation of pristine c60 mentioned above had a half life of one month, I think we could make a good case for a six week half life for c60-oo in the long clearance phase. That would be 17 half lives in two years, and 2**17 = 131,072. If over the course of the entire experiment, the rats received a total dose that was 131,072-fold higher than the amount needed to maintain the life-extension effect for a brief time, then that would explain it. Considering the huge total dose and the high potency of c60-oo, I don't think the ratio of 131k is out of the question.

What if there's something else going on besides an antioxidant effect? Regarding the hair-growing and other effects we've seen, we know that a shift from glycolysis to oxidative phosphorylation is required for stem cell differentiation, so it's not a huge leap to think that a compound that impacts mitochondrial efficiency the way c60-oo does might have an effect here. We just had a thread resurface that talked about hyperbaric oxygen treatments, which are apparently quite good at mobilizing stem cells. Could these be related phenomena? Maybe. Are stem cells involved in the life extension effect? That wouldn't surprise me, and might provide part of an explanation for a persistent effect.

As far as never having seen such effects from antioxidants in the past, first I would say that there has never been an antioxidant like c60-oo. c60-oo is very likely to be highly localized to the mitochondria, where antioxidants are really needed, because that's where the superoxide factory is. c60 acts catalytically, rather than getting chemically burned out, and is extremely potent against radicals. (The "radical sponge") In fact we have seen some of the effects observed with C60 from other antioxidants, such as NAC. It's been shown to be effective against muscle fatigue, and also to induce the kinds of weird autonomic effects when first dosed (e.g. sweating, odd peripheral sensations) that a number of c60 users reported.

[Chupo]

Regarding the the oral dosage of c60oo not being as effective, could it be because rats lack a gallbladder?

[DeadMeat]

Here is a recent paper showing C60 injected into rats decays in most organs by a factor of about 2 over 4 weeks. So in one year there would be .01% of the original dose left. On the other hand, if a rat took it every day for ten days, they'd have 9 times the initial dose in their system. And after a long time of taking a daily dose, this would build up to more than 40 times the daily dose. Except for the spleen, where the dose would build up much faster. Not to say that the old C60 is still effective, of course. Niner, for instance, saw a measurable decline in exercise reps after stopping for a short time.

Any idea what they injected? c60 in solution or suspension? In water or oil? Don't have access to the full-text, myself.

Howard

According to the Baati paper, liposomes were used as a carrier for unmodified C60, which they didn't think was best for studying the pharmokinetics. But they too found the highest levels of C60 in the spleen, so high that it precipitated there.

Interesting, but with the injected liposomes they had the same problem of large C60 particle size.

In this study, C60-liposome was suspended in the administration solution, and the C60 was an unmodified form. Hence, the difference in the biodistribution of C60 between previous studies and this study might be attributable to differences in physical properties, the particle size distribution of C60 in the administration solution, and/or period after completion of the injections. Compared with previous studies, the C60 particle size in the administration solution for this study seems large (particle size: >100 nm, particle size was obtained from measuring of diluted administration solution by Zetasizer Nano, Malvern Instruments Ltd.) because the C60 water solubility is low. We considered that C60 injected in the tail vein could be filtered by lung capillary vessels and accumulate in the lungs prior to being distributed to other tissues. C60 not being detected in the blood indicates that clearance of C60 from the blood by filtration might effectively occur in the lungs.

Attached Files

•  C60aggregatesLipoiv2011.pdf   406.03KB   8 downloads

[mikey]

I think the increase in the rats life span can be explained with the oxidative theory of aging. I also think that the rats probably died because they ran out of C60 and once again became victims to oxidative aging.

It's difficult to understand how taking an anti-oxidant for six months would extend your lifespan by 30 months. It might explain six months or less, but not 30. Now if you propose certain superpowers for C60--that some of it sticks around forever with almost homeopathic effectiveness, then you'd also expect one dose to be sufficient for years. Beyond that, you also have to explain how an anti-oxidant can grow hair and make scars disappear, which isn't among the known effects of anti-oxidants.

Will all due respect, it seems that antioxidants do improve hair growth - as has been experienced by myself and a doctor friend by taking Tocomin Suprabio tocotrienols. The theoretical reason that hair becomes dysfunctional and grows poorly is because oxidative damage to hair follicles is poorly controlled as we age. http://www.ncbi.nlm....ubmed/10965354

Nutritional deficiencies probably have a role in this, too.

The published eight month study of Tocomin showed better than 34% average increase in hair count, logically because these tocotrienols control the effect of oxidation on hair follicles, allowing follicles to function normally.

We don't lose follicles. They just become dysfunctional.

As well, as I've said before, after about 18 months my hair darkened a couple of shades, probably because the tocotrienols also reduced the oxidative effect of hydrogen peroxide, which is thought to lighten hair from grey to white as we age and our bodies don't control hydrogen peroxide as well.

As well, when I read the (H(2)O(2) study by Wood (above) I began taking 3,000 mg of methionine a day under the notion that it might improve the darkening that has been happening.

As to whether antioxidants can participate in scars fading, it might be that the right antioxidants reduce oxidative stress enough that the body's natural healing mechanisms can function. I haven't investigated this in the literature, but it seems possible.

Edited by mikey, 02 January 2013 - 11:58 PM.

[motorcitykid]

As I sit here staring at my first 100ml bottle of C60 (cheshire cat grin) which arrived UPS only moments ago, I wonder how much, how often?

Has there been a consensus reached on the rat to human dosing ratio? From initial dose to weekly and monthly thereafter? Suggestions?

[niner]

Regarding the the oral dosage of c60oo not being as effective, could it be because rats lack a gallbladder?

Good point. Although most rats are omnivorous, in that they'll eat most anything if they're hungry, isn't their diet in nature mostly low fat plant matter? If they aren't meant to eat fat, maybe the oral route (for lipid formulations) is poor in rats, but better in people. This could be an argument that the human "equivalent" dose of c60-oo might be even less than we think, compared to rats.

[Kevnzworld]

Mikey wrote :
" As well, when I read the (H(2)O(2) study by Wood (above) I began taking 3,000 mg of methionine a day under the notion that it might improve the darkening that has been happening. "

Given that methionine restriction (MR ) has been shown to increase lifespan, wouldn't this be a heavy price to pay for potentially darkening hair color?
Quote : Both in vitro and in vivo studies have indicated that the anti-aging properties of MR may be mediated, in part, by reductions in oxidative stress driven by decreased production of reactive oxygen species (ROS). Overall, these data indicate MR as an important new tool for anti-aging research with potential clinical implications.

http://www.mendeley....n-aging-cancer/

[Turnbuckle]

Mikey wrote :
" As well, when I read the (H(2)O(2) study by Wood (above) I began taking 3,000 mg of methionine a day under the notion that it might improve the darkening that has been happening. "

Given that methionine restriction (MR ) has been shown to increase lifespan, wouldn't this be a heavy price to pay for potentially darkening hair color?
Quote : Both in vitro and in vivo studies have indicated that the anti-aging properties of MR may be mediated, in part, by reductions in oxidative stress driven by decreased production of reactive oxygen species (ROS). Overall, these data indicate MR as an important new tool for anti-aging research with potential clinical implications.

http://www.mendeley....n-aging-cancer/

It would seem so. Three grams of anything every day is a lot unless you're also taking it for other reasons. Color out of a box is simpler and probably cheaper too.

[stephen_b]

Given that methionine restriction (MR ) has been shown to increase lifespan, wouldn't this be a heavy price to pay for potentially darkening hair color?

I was about to post the same thing.

[hav]

Interesting, but with the injected liposomes they had the same problem of large C60 particle size.

In this study, C60-liposome was suspended in the administration solution, and the C60 was an unmodified form. Hence, the difference in the biodistribution of C60 between previous studies and this study might be attributable to differences in physical properties, the particle size distribution of C60 in the administration solution, and/or period after completion of the injections. Compared with previous studies, the C60 particle size in the administration solution for this study seems large (particle size: >100 nm, particle size was obtained from measuring of diluted administration solution by Zetasizer Nano, Malvern Instruments Ltd.) because the C60 water solubility is low. We considered that C60 injected in the tail vein could be filtered by lung capillary vessels and accumulate in the lungs prior to being distributed to other tissues. C60 not being detected in the blood indicates that clearance of C60 from the blood by filtration might effectively occur in the lungs.

Thanks for the full-text of that study. The solution of c60, toluene, and chloroform they injected those poor rats with sounds nasty. I wonder if the solution stability is so low that the c60 precipitates out into the bloodstream shortly after injection thus bringing organ filtration into play. Something that obviously doesn't happen with c60 dissolved into oil and taken orally.

Howard

[mikey]

Mikey wrote :
" As well, when I read the (H(2)O(2) study by Wood (above) I began taking 3,000 mg of methionine a day under the notion that it might improve the darkening that has been happening. "

Given that methionine restriction (MR ) has been shown to increase lifespan, wouldn't this be a heavy price to pay for potentially darkening hair color?
Quote : Both in vitro and in vivo studies have indicated that the anti-aging properties of MR may be mediated, in part, by reductions in oxidative stress driven by decreased production of reactive oxygen species (ROS). Overall, these data indicate MR as an important new tool for anti-aging research with potential clinical implications.

http://www.mendeley....n-aging-cancer/

Sounds like I just quit taking extra methionine!
Thank you.

Mikey wrote :
" As well, when I read the (H(2)O(2) study by Wood (above) I began taking 3,000 mg of methionine a day under the notion that it might improve the darkening that has been happening. "

Given that methionine restriction (MR ) has been shown to increase lifespan, wouldn't this be a heavy price to pay for potentially darkening hair color?
Quote : Both in vitro and in vivo studies have indicated that the anti-aging properties of MR may be mediated, in part, by reductions in oxidative stress driven by decreased production of reactive oxygen species (ROS). Overall, these data indicate MR as an important new tool for anti-aging research with potential clinical implications.

http://www.mendeley....n-aging-cancer/

It would seem so. Three grams of anything every day is a lot unless you're also taking it for other reasons. Color out of a box is simpler and probably cheaper too.

No cancerous colors from boxes! I'd rather let my experiments be "natural."

The tocotrienols have done most of it, anyway. But I'm grateful to Kevnzworld for shining a light on methionine!

Edited by mikey, 03 January 2013 - 11:29 PM.

[ClarkSims]

I am starting a new thread about the H2O2 and gray hair study.

I have reread it a few times, and I still don't understand it.
I just looked up Tyrosinase, and it appears to me that they have it backwards. They should be restricting methionine, not supplementing it.

[smithx]

If Lifelength knows your self reported age, and still says that they see your telomeres as those of a 70 year old, I'd see a few possibilities:

- If they are trying to sell some regimen to reverse your supposed aged status, that would be a motive for falsely reporting too high a telomeric age

- They may have mixed up the samples or done the tests incorrectly

- If neither of those two apply, I'd believe them at least as much as anyone else, because they are likely to have angry customers if they give them bad news, and doing so nonetheless implies some sort of integrity.

Well, Lifelength claims they are the only company who measures short telomeres, but they're the company that said I was 70 years old.

They're fighting me, with me thinking that since they seemed to have lost my test for two months that they ended up giving me someone else's test. I mean, the other two companies said I was 59.

So, Lifelength appears to be way, way off with their shortest telomere test.

Are they giving you the actual results, or just telling you an age?

With their Beverly Hills doctor, basically just taking a lot of time telling me I'm 70.

[YOLF]

Could it be that you've just acclimated to a new you? Were you dosing daily or intermittent?

And also a case of longer is not better as more people have reported that the effects fade with continuous use than not.

You can add me to the list of people who observed initial benefits that faded away to roughly baseline after continuous use (couple months of 2.4mg daily).

[anagram]

perhaps c60 oxidizes Fe from 2+ to 3+, stopping the fenton reaction. if this were the case then the changes in c60's apparent benefit may just be dependent on bodily concentration of iron. other radioprotectants like hyroxylamines do the same thing, oxidizing iron is key to everything. the excellent efficacy of c60 and ntBHA(a hydroxylamine) may also be due in part to they're weird unrecognizable structures to cells, cells cannot metabolize these compounds so they stay in mitochondria for a long time.
I think that a lot of in vivo antioxidants are antioxidants simply because the body cannot do much with them. take for example Piracetam, Astaxanthin, methylene blue, Aspirin, all anti glycation drugs, Guanadine, Metformin, anything, they are all xenobiotic and have a potent effect on mitochondria and lipid per oxidation. I also suspect that c60 is interpreted as a small nano bacteria, reminding cells to produce nitric oxide and ferritin, which would confer a lot of the benefits that c60 appears to have.
I am a little scared of the fact that c60 treated rats all died at the same time, but perhaps if c60 make cells over produce ferritin in an attempt to get rid of iron to kill off nano bacteria, but over time the ferritin builds up to intolerable levels and kills the good cells.

[ClarkSims]

This is the first I have heard of the Fenton reaction, and of the Fenton reaction in mitochondria. I found several papers
about it


The Role of Reactive Oxygen Species in Mitochondrial Permeability ...


www-04.all-portland.net/bsr/017/0043/0170043.pdf


Hydroxyl radical is produced via the Fenton reaction in submitochondrial particles under oxidative stress: implications for diseases associated with iron accumulation

http://www.ncbi.nlm....pubmed/19490751

Thanks for pointing this out. It is very interesting.

As far as the rats all dying at the same time, I think it is because they ran out of C60 at the same time. They were only given one period of large exposure several years earlier, and eventually all the mitochondrial C60 was exhausted when those mitochondria died.

This discussion brought to mind, another way that C60 could act as an antioxidant. It could be the acceptor of all the unwanted electrons from the electron transport chain, which otherwise would form reactive oxygen species. This would prevent their formation all together.

[trance]

I believe it was reported that the last couple of rats were euthanized, actually. Probably close to the same time.

[Turnbuckle]

I believe it was reported that the last couple of rats were euthanized, actually. Probably close to the same time.

I think this is right, they were euthanized, and the paper was remiss in not saying that. In any case, squaring the curve is what you expect when you've pushed lifespan to the limit and cured every disease, as in curve E, below.

Attached Files

•  lifespan.gif   8.56KB   12 downloads

[Fred_CALICO]

@anagram : Your references to publications?

Why and astaxanthin is a xenobiotic?
Humans ingest for millennia! Degrading enzymes should be in our genomes? Is not it?

Edited by sell58, 23 January 2013 - 05:33 PM.

[niner]

@anagram : Your references to publications?

Why and astaxanthin is a xenobiotic?
Humans ingest for millennia! Degrading enzymes should be in our genomes? Is not it?

Any substance that is foreign to the body is called xenobiotic. That's the definition of the word. Of course there are enzymes that degrade it. We have an entire system of enzymes, collectively known as the xenobiotic metabolism system, that has evolved to deal with the various molecules we encounter in the world.

[Fred_CALICO]

I do not think the anagram meant that way. I would like a response from Anagram.
On the other hand, it is interresting to see that the definitions are not the same in the U.S. and in France.

http://en.wikipedia....wiki/Xenobiotic
A xenobiotic is a chemical which is found in an organism but which is not normally produced or expected to be present in it. It can also cover substances which are present in much higher concentrations than are usual. Specifically, drugs such as antibiotics are xenobiotics in humans because the human body does not produce them itself, nor are they part of a normal diet.


http://fr.wikipedia....ki/Xénobiotique

A xenobiotic (originally, the term comes from xénobiose, ancient Greek ξενος "foreign" and βιος "life") is a substance that is foreign to the body ALIVE1.
In general, a xenobiotic is a chemical molecule can be toxic and polluting within organizations, including low concentrations2 see very low (eg pesticides, drugs).
This toxicity is sometimes explained by the "inadequacy" of organisms that have never encountered this substance during their evolution by natural discharges related to immunity, endocrine disrupting activities of xenobiotic or for toxicological reasons (toxicity "intrinsic" the xenobiotic or its ability to act synergistically with another polluant3 or infectious factor).

[niner]

I do not think the anagram meant that way. I would like a response from Anagram.
On the other hand, it is interresting to see that the definitions are not the same in the U.S. and in France.

You deserve an answer from anagram, I agree. US and French definitions are not really different. "foreign to the body" and "not normally produced or expected to be present in it" are essentially the same thing. US and French toxicologists certainly use the term in an identical way. The definition from the English wiki is a little screwy, IMHO. I'm not sure that a compound needs to be "found in an organism" to be called xenobiotic. Does that mean a compound isn't xenobiotic until you put it in the body? I don't see the point of that, and no other definition I've seen describes it that way.