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Re: The Dangers of Megadosing Vitamin C

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Hveragerthi Views: 29,378
Published: 12 years ago
This is a reply to # 1,531,495

Re: The Dangers of Megadosing Vitamin C


I am curious if you have any research to back your claims.  The only study I could find directly on buffered vitamin C showed it reduced, but not eliminated oxalic acid.  And this study is suspect since they specifically named a brand name of buffered C, which leads me to believe that the study was funded by the manufacturer.  Other than that I found nothing showing the buffered C "dissolves" the oxalates.  Here are a few of the studies that came up under the search terms:


J Nutr. 2005 Jul;135(7):1673-7.

Ascorbate increases human oxaluria and kidney stone risk.

Massey LK, Liebman M, Kynast-Gales SA.

Department of Food Science and Human Nutrition, Washington State University, Spokane, WA, USA.

Currently, the recommended upper limit for ascorbic acid (AA) intake is 2000 mg/d. However, because AA is endogenously converted to oxalate and appears to increase the absorption of dietary oxalate, supplementation may increase the risk of kidney stones. The effect of AA supplementation on urinary oxalate was studied in a randomized, crossover, controlled design in which subjects consumed a controlled diet in a university metabolic unit. Stoneformers (n = 29; SF) and age- and gender-matched non-stoneformers (n = 19; NSF) consumed 1000 mg AA twice each day with each morning and evening meal for 6 d (treatment A), and no AA for 6 d (treatment N) in random order. After 5 d of adaptation to a low-oxalate diet, participants lived for 24 h in a metabolic unit, during which they were given 136 mg oxalate, including 18 mg 13C2 oxalic acid, 2 h before breakfast; they then consumed a controlled very low-oxalate diet for 24 h. Of the 48 participants, 19 (12 stoneformers, 7 non-stoneformers) were identified as responders, defined by an increase in 24-h total oxalate excretion > 10% after treatment A compared with N. Responders had a greater 24-h Tiselius Risk Index (TRI) with AA supplementation (1.10 +/- 0.66 treatment A vs. 0.76 +/- 0.42 treatment N) because of a 31% increase in the percentage of oxalate absorption (10.5 +/- 3.2% treatment A vs. 8.0 +/- 2.4% treatment N) and a 39% increase in endogenous oxalate synthesis with treatment A than during treatment N (544 +/- 131 A vs. 391 +/- 71 micromol/d N). The 1000 mg AA twice each day increased urinary oxalate and TRI for calcium oxalate kidney stones in 40% of participants, both stoneformers and non-stoneformers.


Effect of supplemental ascorbate and orange juice on urinary oxalate



The relationship between ascorbate intake, in supplemental form and naturally occurring in orange juice, and urinary oxalate was assessed in 6 healthy individuals. An experimental model which allowed a differentiation between endogenously- and exogenously-derived urinary oxalate was used. Twenty-four hour urine samples were collected the last day of baseline, supplemental ascorbate, and orange juice treatment periods. Oxalate load tests were administered the day following each experimental treatment. Oxalate loads consisted of 175 mg unlabeled and 18 mg 1, 2-13C2 oxalic acid. The orange juice treatment was associated with higher urinary excretion of endogenously-derived oxalate, citrate, and calcium, and a higher urinary pH. Since these urinary changes were not observed during the supplemental ascorbate period, the two sources of ascorbate differentially affected key urinary components which are related to calcium oxalate nephrolithiasis.


Stability of ascorbate in urine: relevance to analyses for ascorbate and oxalate.

Chalmers AH, Cowley DM, McWhinney BC.

Erratum in:

        Clin Chem 1986 Feb;32(2):390.

Ascorbate is unstable in urine at room temperature at pH values ranging from 1 to 12. At pH 7 and above, oxalate is generated in amounts directly proportional to the ascorbate concentration. In 12 different urines, adjusted to pH 12 and incubated for 20 h at room temperature, there was a significant correlation between the amount of oxalate formed and the initial ascorbate concentration (r = 0.97, p less than 0.01). The mean (+/- SD) concentration of oxalate (1.32 +/- 0.70 mmol/L) formed during this period approximated the initial ascorbate concentration (1.57 +/- 1.09 mmol/L). Disodium EDTA, 10 mmol/L final concentration, stabilizes ascorbate in urine and inhibits its conversion to oxalate at pH values of 4.4 to 7.0 during a 24-h period. We therefore propose that urine specimens for ascorbate and oxalate analyses be collected with disodium EDTA present such as to give about this final concentration.



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