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  • Excessive vitamin C will probably lead to the non-recycling of its initial oxidized state, leading to further oxidation into unuseful molecules (oxalic acid). thus, vitamin C intake should match recycling capacity, which is dependent upon status of other antioxidants (antioxidant network) such as glutathione.
  • Higher vitamin C content in skin would probably mean long periods of inadequacy should probably be addressed with topical administration
  • Perhaps useful for diabetes
    • Is an aldose reductase inhibitor. Useful for preventing sorbitol accumulation in response to excess glucose uptake.
    • Blocks insuiln spike of glucose by competing with pancreatic uptake with glucose, reducing insulin response.
  • Don’t take large amounts prior to sun exposure (see Photocytotoxicity)
  • Vitamin C flushes, in that they are a result of saturated uptake and do not result in a proportionate vitamin C serum excess, and in that they cause motility starting at the small intestine (where other laxatives work at the large intestine), can be useful for rapidly removing intestinal contents.
  • Avoid consumption with fat (see nitrosamines)


  • Vitamin c in morning seems to pair with pregnenolone to increase rage and vigilance
  • all Vitamin C natural powder sources (amla, lemon) seem to cause inflammation
  • buffered vitamin c is nauseating
  • no noticed affect in shea butter on skin
  • vitamin c flush at 15g
  • vitamin c tolerable (without nausea) at 5g
    • seems to improve gut motility
  • Lipo Vitamin C, Mercola Brand: no apparent effect at normal dose. Seems to cause massive stomach upset at 6g.


Target of around 80mg/day (~1/2 drop, ~1/80 tsp) (Recent studies have shown that little unmetabolized ascorbate is excreted with dietary intakes up to about 80 mg/day and that renal excretion of ascorbate increases proportionately with higher intakes), perhaps 50mg by supplementation.

Avoid consumption with fat (see nitrosamines)


  • Dr Andrew Saul 2g every 6 mins gets a blood level comprable to IV. – helps with sickness
  • Dr Gonzales coworker says vitamin C does not mix well with pancreatic enzymes.

Add baking soda at 1:1 to create sodium ascorbate

Acute prooxidant effects of vitamin C in EDTA chelation therapy and long-term antioxidant benefits of therapy.
Hininger I1, Waters R, Osman M, Garrel C, Fernholz K, Roussel AM, Anderson RA.
Author information
Chelation therapy is thought to not only remove contaminating metals but also to decrease free radical production. EDTA chelation therapy, containing high doses of vitamin C as an antioxidant, is often used in the treatment of diseases such as diabetes and cardiovascular diseases but the effectiveness of this treatment may be variable and its efficacy has not been demonstrated conclusively. The objective of this work was to determine if the vitamin C added to standard chelation therapy cocktails was prooxidant. We administered a standard EDTA cocktail solution with or without 5 g of sodium ascorbate. One hour following the standard chelation therapy, there were highly significant prooxidant effects on lipids, proteins, and DNA associated with decreased activities of RBC glutathione peroxidase and superoxide dismutase while in the absence of sodium ascorbate, there were no acute signs of oxidative damage. After 16 sessions of standard chelation therapy, the acute prooxidant effects of vitamin C remained, but, even in the absence of nutrient supplements, there were beneficial long-term antioxidant effects of chelation therapy and plasma peroxide levels decreased. In conclusion, multiple sessions of EDTA chelation therapy protect lipids against oxidative damage. However, standard high amounts of vitamin C added to EDTA chelation solutions also display short term prooxidant effects. The added benefits of lower levels of vitamin C in chelation therapy need to be documented.

PMID: 15917185 DOI: 10.1016/j.freeradbiomed.2005.02.016
[Indexed for MEDLINE]
  • as might be expected, when vitamin C is added through IV in abundance, it disbalances the anti oxidant systems, using up glutathione, and thus causing pro-oxidant activity.
    • consequently, don’t take a lot of vitamin C through IV (probably limit to 1 gram)
    • however, the digestive system seems to account for this by causing a flush in the case of too much vitamin c


The biological functions of ascorbic acid are based on its ability to provide reducing equivalents for a variety of biochemical reactions.... both intra- and extracellularly (Englard and Seifter, 1986; Halliwell and Whiteman, 1997; Tsao, 1997).

Both the one- and the two-electron oxidation products of the vitamin are readily regenerated in vivo—chemically and enzymatically—by glutathione, nicotinamide adenine dinucleotide (NADH), and nicotinamide adenine dinucleotide phosphate (NAD-PH) dependent reductases (May et al., 1998; Park and Levine, 1996).

Vitamin C is known to be an electron donor for eight human enzymes. Three participate in collagen hydroxylation; two in carnitine biosynthesis; and three in hormone and amino acid biosynthesis.

Evidence also suggests that ascorbate plays a role in or influences collagen gene expression, cellular procollagen secretion, and the biosynthesis of other connective tissue components besides collagen, including elastin, fibronectin, proteoglycans, bone matrix, and elastin-associated fibrillin (Ronchetti et al., 1996). The primary physical symptoms of ascorbic acid's clinical deficiency disease, scurvy, which involves deterioration of elastic tissue, illustrate the important role of ascorbate in connective tissue synthesis.


The vitamin readily scavenges reactive oxygen species (ROS) and reactive nitrogen species (RNS) (e.g., hydroxyl, peroxyl, superoxide, peroxynitrite, and nitroxide radicals) as well as singlet oxygen and hypochlorite (Frei et al., 1989; Halliwell and Whiteman, 1997; Sies and Stahl, 1995)


Intestinal absorption of ascorbic acid occurs through a sodium-dependent active transport process that is saturable and dose dependent (Rumsey and Levine, 1998; Tsao, 1997). At low gastrointestinal ascorbate concentrations, active transport predominates, while simple diffusion occurs at high concentrations. Some 70 to 90 percent of usual dietary intakes of ascorbic acid (30 to 180 mg/day) are absorbed; however, absorption falls to about 50 percent or less with increasing doses above 1 g/day (Kallner et al., 1979). The bioavailabilities of the vitamin from foods and supplements are not significantly different (Johnston and Luo, 1994; Mangels et al., 1993).


Cellular transport of ascorbic acid and DHA is mediated by transporters that vary by cell type (Jacob, 1999; Tsao, 1997). DHA is the form of the vitamin that primarily crosses the membranes of blood and intestinal cells, after which it is reduced intracellularly to ascorbic acid.


Since the immediate oxidized forms of vitamin C are readily reduced back to ascorbic acid, relatively small amounts of the vitamin are lost through catabolism. The primary products of oxidation beyond DHA include oxalic and threonic acids, L -xylose, and ascorbate 2-sulfate (Jacob, 1999).


Recent studies have shown that little unmetabolized ascorbate is excreted with dietary intakes up to about 80 mg/day and that renal excretion of ascorbate increases proportionately with higher intakes


Data show little increase in plasma steady-state concentrations at intakes above 200 mg/day (Figure 5-3), and saturable intestinal absorption and renal tubular reabsorption data suggest that overload of ascorbic acid is unlikely in humans (Blanchard et al., 1997; Levine et al., 1996a). Possible adverse effects associated with very high intakes have been reviewed and include:
diarrhea and other gastrointestinal disturbances, increased oxalate excretion and kidney stone formation, increased uric acid excretion, pro-oxidant effects, systemic conditioning (“rebound scurvy”), increased iron absorption leading to iron overload, reduced vitamin B12 and copper status, increased oxygen demand, and erosion of dental enamel (Hornig and Moser, 1981; Rivers, 1987).


Most cells express two different transporter systems for vitamin C; a transporter system with absolute specificity for ascorbic acid and a second system that shows absolute specificity for dehydroascorbic acid. The dehydroascorbic acid transporters are members of the GLUT family of facilitative glucose transporters, of which at least three isoforms, GLUT1, GLUT3 and GLUT4, are dehydroascorbic acid transporters. Ascorbic acid is transported by the SVCT family of sodium-coupled transporters, with two isoforms molecularly cloned, the transporters SVCT1 y SVCT2, that show different functional properties and differential cell and tissue expression. In humans, the maintenance of a low daily requirement of vitamin C is attained through an efficient system for the recycling of the vitamin involving the two families of vitamin C transporters.



– once vitamin C is depleted, that’s when you start to see lipid oxidation
– vitamin C is the first anti-oxidant to be used/depleted
– oxidised vitamin C is non toxic

Megadose of vitamin C delays insulin response to a glucose challenge in normoglycemic adults
These effects might be partially explained by the competitive inhibition of glucose transfer into pancreatic β cells by high concentrations of circulating AA.

Blocks insuiln spike of glucose by competing with pancreatic uptake with glucose, reducing insulin response.

There is an important receptor called the Glut-1 receptor that activates in response to insulin to allow both glucose and vitamin C to enter the cell.


The glucose/insulin system and vitamin C: implications in insulin-dependent diabetes mellitus.
Cunningham JJ1.
Author information
The cellular uptake of vitamin C (ascorbic acid, ASC) is promoted by insulin and inhibited by hyperglycemia. If a rise in plasma ASC is uncoupled from insulin replacement in insulin-dependent diabetes mellitus (IDDM) then the degree of hyperglycemia could account for "tissue scurvy" in IDDM. Leukocyte ASC is lower in IDDMs compared with nondiabetics when vitamin C consumption is adequate and our data suggest that this is a variable component of the pathophysiology of IDDM. The complications of diabetes mellitus are believed to result from either the intracellular accumulation of sorbitol or the nonenzymatic glycoxidation of proteins or both. With respect to the abnormal cellular accumulation of sorbitol, vitamin C supplementation has been shown to be effective in several studies of adults with diabetes; the situation regarding the prevention of protein glycoxidations by supplementation is presently unclear. The roles of ASC as an aldose reductase inhibitor and a water soluble antioxidant in body fluids are potentially very important as adjuncts to tight glycemic control in the management of diabetes. Tissue saturation and maximal physiologic function in IDDM may require supplemental vitamin C intake.

PMID: 9550452
  • The complications of diabetes mellitus are believed to result from either the intracellular accumulation of sorbitol or the nonenzymatic glycoxidation of proteins or both
  • With respect to the abnormal cellular accumulation of sorbitol, vitamin C supplementation has been shown to be effective in several studies of adults with diabetes; the situation regarding the prevention of protein glycoxidations by supplementation is presently unclear
Vitamin C: an aldose reductase inhibitor that normalizes erythrocyte sorbitol in insulin-dependent diabetes mellitus.
Cunningham JJ1, Mearkle PL, Brown RG.
Author information
Diabetic hyperglycemia promotes sorbitol production from glucose via aldose reductase. Since the intracellular accumulation of sorbitol, or its sequelae, are postulated to contribute to the progression of chronic diabetic complications, aldose reductase inhibitors (ARI) offer therapeutic promise. Others have shown that vitamin C at pharmacologic doses decreases erythrocyte (RBC) sorbitol. We examined whether smaller, physiologic doses of vitamin C were also effective in individuals with insulin-dependent diabetes mellitus (IDDM) and whether vitamin C was an ARI in vitro.

Vitamin C supplements (100 or 600 mg) were taken daily for 58 days by young adults with IDDM and nondiabetic adults in an otherwise free-living design. Diabetic control was monitored by fasting plasma glucose, glycosylated hemoglobin, and glycosuria and was moderate to poor throughout the study. RBC sorbitol was measured at baseline and again at 30 and 58 days. Three-day dietary records and 24-hour urine collections were performed for each sampling day.

RBC sorbitol levels were significantly elevated in IDDMs, on average doubled, despite their more than adequate dietary intakes of vitamin C and normal plasma concentrations. Vitamin C supplementation at either dose normalized the RBC sorbitol in IDDMs within 30 days. This correction of sorbitol accumulation was independent of changes in diabetic control. Furthermore, our in vitro studies show that ascorbic acid inhibited aldose reductase activity.

Vitamin C supplementation is effective in reducing sorbitol accumulation in the erythrocytes of diabetics. Given its tissue distribution and low toxicity, we suggest a superiority for vitamin C over pharmaceutic ARIs.

PMID: 7963139

These effects are attributed to the osmotic effect of unabsorbed vitamin C passing through the intestine. Intestinal absorption of ascorbic acid occurs by a saturable process (Rumsey and Levine, 1998; Tsao, 1997). The remainder is not absorbed and is eliminated in the stool.

Fat and Vitamin C, Nitrosamines

  • Avoid mixing nitrites (found in preserved meats, or cycled vegetables (from stomach back to mouth)), vitamin c, fat, and high amine food: since this will cause a higher formation of nitrosamines, a cancerous subatance.
Nitrites, which are present in human saliva, and in certain preserved foodstuffs, may be converted to cancer causing compounds called nitrosamines. Nitrosamines are formed in acidic conditions, such as those afforded by stomach acid, but vitamin C inhibits their formation, by converting nitrite to nitric oxide.

Without fat, vitamin C curbed the levels of two nitrosamines by a factor of between five and 1000. And it completely eliminated the production of the other two.

But when 10% fat was added, vitamin C actually boosted the production of nitrosamines between 8 and 140-fold. Fat remains in the proximal stomach for some time after a meal and also makes up a substantial amount of the cells lining the stomach, say the authors.

Nitric oxide is formed when vitamin C reacts with nitrite in acid. However, the nitric oxide can diffuse into fat and then react with oxygen to form nitrosoamine generating chemicals.

The findings may be relevant to the recent observations that vitamin C supplements fail to reduce cancer risk, say the authors.

Nitrates in vegetables cycle back up into the mouth through salivary gland to become nitrites see files. This process start within 30 mins and lasts for longer than 7 hours – so the factor to consider is how long fat stays in the stomach. Gastric emptying of liquids is at 30 mins, and of solids 1-2 hours. So, vitamin C drinks probably clear within 1 hour, which would allow for consumption after a hour of taking, and perhaps, consumption of vitamin C drinks within 2.5 hours of eating fats. See “gastric emptying”

Nitrites are absorbed in the small intestine.


there is a narrow range of concentrations and exposure times where ascorbate exerts photoprotective effects, exceeding which leads to ascorbate-mediated increase in photocytotoxicity.
  • So one might want to avoid large doses of C before going out to the beach.


Turns into Dehydroascorbic acid (oxidized ascorbic acid)

Tomatoes cooked at 190.4 degrees Fahrenheit for 2 minutes lost about 10 percent of their Vitamin C content while those cooked for half an hour lost about 29 percent of this vitamin, as stated on Scientific American. However, the cooking method also affected how much vitamin C was lost, too. For instance, vegetables that were steamed or boiled lost between 22 and 34 percent of their vitamin C while microwaved or pressure-cooked veggies only lost about 10 percent of the vitamin C.

Starch iodine solution can show whether contians DHAA or AA . If AA is produce, solution will turn clear.


see files: topical-vs-ingestion-nutrients-09-00866.pdf

  • Normal skin contains high concentrations of vitamin C, which supports important and well-known functions, stimulating collagen synthesis and assisting in antioxidant protection against UV-induced photodamage
  • Recent studies suggest that encapsulation into a lipospheric form may assist with transport into the lower layers of the epidermis and could result in increased uptake [65,66,67]. However, the most pertinent issue for the efficacy of topical application is likely to be the plasma status of the individual: if plasma levels are saturated, then it appears that topical application does not increase skin vitamin C content
  • When plasma levels are low, some vitamin C can be delivered to the epidermal layer by topical application, although the efficacy of this is dependent on the formulation of the cream or serum used on the skin [51,52,53,54,55]. Vitamin C, as a water-soluble and charged molecule, is repelled by the physical barrier of the terminally differentiated epidermal cells. It is only when pH levels are below 4 and vitamin C is present as ascorbic acid that some penetration occurs [56], but whether this results in increased levels in the metabolically compromised stratum corneum is unknown. A great deal of effort has been put into the development of ascorbic acid derivatives for the purpose of topical application.

see files:

  • In fact, applying vitamin C to the skin is 20 times more effective than oral ingestion.11
  • So, even after stopping application, significant amounts of vitamin C will remain in the skin for up to three days.
  • Vitamin C’s skin-health benefits are largely attributed to its benefits in supporting healthy collagen.
Like most proteins, collagen consists of poly-peptide chains. But unlike most proteins, collagen is composed mainly of just three amino acids: glycine, hydroxyproline, and proline.

What makes collagen a kind of supermolecule, however, is its three-dimensional triple helix architecture. Three polypeptide chains alternating with one another are coiled in a left-handed helix to form a helical strand. Three of these helical strands then twist around on one another, like the strands of a rope, in a right-handed superhelix, to make up the complete molecule.

No wonder the tensile strength of collagen is greater than steel wire of the same weight. Understandably, the making of such a complex structure as collagen can only be accomplished in several steps. And vitamin C is involved in every one of them.

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