extreme excess dosages of vitamin C

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desolation
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extreme excess dosages of vitamin C

Post Number:#1  Post by desolation » Wed Sep 20, 2006 7:46 pm

Below is an expert I pasted from another forum detailing the supposed fallacy of high dose vitamin c. As I have recently been mega dosing with c I waas curious as to what any of you may think of the below study and reasoning.

"This is where the chemistry gets interesting.

I'll put the facts very simply and provide you the necessary documentation. You can put two and two together, and read the references provided, if you wish to assure yourself of the facts.

1. You need excessive peroxy nitrate potential, a result of excessive stress, high glucose concentrations, and a supply of iron.

2. Excess ascorbate then serves as shuttle of reducing equivalents, preventing peroxy nitrate free radical damage of membranes, in particular, red cell membranes. However, it has a little draw back, and that lies in the increase in non-heme Fe-catalyzed toxicity to cells. The first article hints as to how the formation of reducing equivalents from the free radical induced attack on glucose is paralleled and worsened by the presence of reducing equivalents or reducing equivalent chaparones (vitamin C, ascorbate).

The documentation:

Vitamin C as a reducing equivalent for treatment of disease:

http://www.doctoryourself.com/cathcart_thirdface.html

And a very nice little article in the Biochemical Journal that hints at free radical generation by non heme iron: Enhancement of iron toxicity in L929 cells by D-glucose: accelerated(re-)reduction. Ilka Lehnen-Beyel, Herbert De Groot, and Ursula Rauen. Biochem J. 2002 368(Pt 2): 517–526.

It has recently been shown that an increase in the cellular chelatable iron pool is sufficient to cause cell damage. To further characterize this kind of injury, we artificially enhanced the chelatable iron pool in L929 mouse fibroblasts using the highly membrane-permeable complex Fe(III)/8-hydroxyquinoline. This iron complex induced a significant oxygen-dependent loss of viability during an incubation period of 5 h. Surprisingly, the addition of L-glucose strongly enhanced this toxicity whereas no such effect was exerted by L-glucose and 2-deoxyglucose. The assumption that this increase in toxicity might be due to an enhanced availability of reducing equivalents formed during the metabolism of L-glucose was supported by NAD(P)H measurements which showed a 1.5-2-fold increase in the cellular NAD(P)H content upon addition of L-glucose. To assess the influence of this enhanced cellular reducing capacity on iron valence we established a new method to measure the reduction rate of iron based on the fluorescent iron(II) indicator PhenGreen SK. We could show that the rate of intracellular iron reduction was more than doubled in the presence of L-glucose. A similar acceleration was achieved by adding the reducing agents ascorbate and glutathione (the latter as membrane-permeable ethyl ester). Glutathione ethyl ester, as well as the thiol reagent N -acetylcysteine (NAC), also caused a toxicity increase comparable with L-glucose.

>These results suggest an enhancement of iron toxicity by L-glucose via an accelerated (re-)reduction of iron with NAD(P)H serving as central electron provider and ascorbate, glutathione or possibly NAD(P)H itself as final reducing agent.

And a second, earlier paper that explains the basis for the free radical (iron chelation and activation)
-----------------------------------------------------------------------------------------------
Iron bound to the lipophilic iron chelator, 8-hydroxyquinoline, causes DNA strand breakage in cultured lung cells. Leanderson P, Tagesson C. Carcinogenesis. 1996 17(3):545-50.

The formation of DNA-strand breaks was studied in cultured human lung cells (A 549) subjected to iron, either in the form of iron(III) citrate or in combination with the metal chelators ethylene diamine tetra-acetic acid (EDTA), nitrilo triacetic acid (NTA), or 8-hydroxyquinoline (8HQ). After 15 min exposure to 5 microM iron(III) citrate or iron chelate, the cellular levels of iron were found to be three times higher in cells subjected to iron-8HQ than in cells subjected to iron(III) citrate, iron-EDTA or iron-NTA.

--->Exposure to iron-8HQ caused extensive DNA-strand breakage, whereas no such breakage was found in cells exposed to iron-EDTA or iron-NTA. The DNA damage caused by iron-8HQ increased with time and dose, and DNA-strand breakage was clearly demonstrable in cells after 15 min exposure to as little as 0.1 microM iron-8HQ. Moreover, iron-8HQ was strongly toxic to the cells and inhibited their growth after exposure.

Along with the formation of DNA-strand breaks, the concentration of cellular malondialdehyde increased four-fold after exposure to iron-8HQ and two-fold after exposure to iron-EDTA or iron-NTA, suggesting that reactive oxygen metabolites might be involved in the toxic action. Moreover, both iron-EDTA and iron-NTA caused a considerable hydroxylation of deoxyguanosine (dG) residues in DNA in vitro, whereas iron(III) citrate and iron-8HQ only caused a minor hydroxylation of dG. This points to the possibility that iron-8HQ-mediated DNA-strand breakage in cells might be due to the action of a metal-bound oxyl radical formed from the iron-8HQ complex rather than to the formation of hydroxyl radicals.

---> Altogether, these findings indicate that iron bound to the lipophilic chelator, 8HQ, has strong toxic properties and that it may cause substantial DNA-strand breakage and lipid peroxidation in living cells.

================================================== ======
So what does this all mean?

On the one hand, in the healthy induhvidual who has a rigidly controlled dietary and exercise full nelson grip on glucose levels, activated iron damage to DNA and membranes might be minimized.

However, in the presence of significant ROS and perhaps elevated glucose as a result of stress and dietary induced hyperglycemia, it is NOT a good idea to consume extremely large doses of vitamin C.

The good bits: Modest doses of vitamin C have been shown to act synergistically with other reducing equivalent agents and prevent peroxynitrate lipid peroxidation in cell membranes.

The bad bits: most of us have less than stellar glucose control and have ROS issues that just might cause a world of hurt under the conditions of extreme excess dosages of vitamin C.

This fact is why Linus Paulings super vitamin C dosing strategy, whose lack of appliction is much lamented in the first citation, has been largely abandoned as a treatment by modern medical practitioners."
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Post Number:#2  Post by Dolev » Thu Sep 21, 2006 12:35 pm

That is not why "Linus Paulings super vitamin C dosing strategy ...has been largely abandoned as a treatment by modern medical practitioners."

More than that, you can't abandon something you never took possesion of.
Dolev

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Post Number:#3  Post by DanSco » Thu Sep 21, 2006 4:29 pm

It's time again to ponder the question that we always ask: If ascorbate is so bad, then why aren't all of the ascorbate producing animals in the world extinct?

I will agree that too much glucose or too much iron is bad. Do vitamin C tablets come loaded with iron and sugar?

Let me get this straight. In the first case they artificially increased the amount of iron in mouse cells and got iron toxicity. So why is it the ascorbate's fault, not the artificial amounts of iron?
Same in the second case. Here we see human lung cells in a petri dish bathed in iron solution. They found DNA strand breakage and again it's supposed to be because of ascorbate. When I get to the point in my life where my cells are in a petri dish, at that point I don't care if my DNA strands are broken!
-DanSco

Note: I am not a doctor nor do I pretend to be one on the internet. Do not duplicate what I do without a pat on the head from your doctor and a note from your mommy.

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Post Number:#4  Post by ofonorow » Fri Sep 22, 2006 7:18 am

DanSco - Bravo!

There is no Lethal Dose Level for vitamin C. Period. In other words, there is no dose which can kill a laboratory animal.
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Post Number:#5  Post by Dottore » Sun Sep 24, 2006 5:58 am

I agree. As Abram Hoffer says: Where are the bodies?
Dottore


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