Does IV/C (SA) cause bladder damage in rats?

[ofonorow]

Hello,

I have taken larges doses of IV Sodium Ascorbate in the past. As much as 80 grams a day with amazing results. Improved vision, and a cataract that disappeared almost overnight and is still gone over 2 years later.

I have considered another round of it for a prostate issue. However I saw a report of a study where sodium ascorbate caused bladder damage in rats. I do not know what the dose level was, but I am concerned as I now have a bladder issue that has appeared.

I am curious if you have any information about ascorbate and the bladder.

Thanks,
Ralph G

If you could find that report, we would love to research it I have never heard this, and it sounds like something contrived to discourage people from trying IV/C for cancer. Only sodium ascorbate (not ascorbic acid) is the form of vitamin C that should be used IV. Since Klenner, there are few to no reports of serious side effects. As safe or safer than water.

[ofonorow]

Hi,

It was on ehow.com in an article titled "The disadvantages of Sodium Ascorbate"

Here is the link:

http://www.ehow.com/list_5993860_disadvantages-sodium-ascorbate.html

I wish there were more references because I don't find many facts in that article.

I will research more.

[ofonorow]

sciencelab.com is a manufacturer of chemical and laboratory equipment. I could not find the reference mentioned. If anyone can, please post.

Now looking in Pubmed and/or google/scholr for the Nebraska study mentioned in an Oxford press.

have to pay for full article, but this result is for sodium ascorbate in food - not IV.
Effect of sodium ascorbate on tumor induction in rats treated with morpholine and sodium nitrite, and with nitrosomorpholine
http://www.sciencedirect.com/science/article/pii/S0304383576800183

Summary
Groups of male MRC Wistar rats were treated for 2 years either with morpholine (10 g/kg food) together with sodium nitrite (3 g/l drinking water) or with N-nitrosomorpholine (NM, 0.15 g/l drinking water). In both cases, a group of rats was given sodium ascorbate (22.7 g/kg food) in addition to these treatments. When ascorbate was present, the liver tumors induced by morpholine and nitrite showed a 1.7-fold longer induction period, a slightly lower incidence, and an absence of metastases in the lungs, indicating that ascorbate had inhibited the in vivo formation of NM. Ascorbate did not affect liver tumor induction by the preformed NM. The group treated with morpholine, nitrite, and ascorbate had a 54% incidence of forestomach tumors, including an 18% incidence of squamous cell carcinomas, possibly because ascorbate promoted NM action in this organ.

Claims to be a repeat of the above experiment, but again, sodium ascorbate was administered in food, not iV.

Liver and Forestomach Tumors and Other Forestomach Lesions in Rats Treated With Morpholine and Sodium Nitrite, With and Without Sodium Ascorbate
http://jnci.oxfordjournals.org/content/71/1/81.short

Abstract

Administration to rats of ascorbate with morpholine and nitrite was previously shown to inhibit the liver tumor production and to enhance the induction of forestomach tumors, as compared to treatment with morpholine and nitrite. In a repetition of this experiment, 10 g morpholine/kg in the diet and 2 g sodium nitrite/liter in the drinking water were administered for life to male MRC-Wistar rats without (group 1) or with (group 2) 22.7 g sodium ascorbate/kg in the diet. Group 3 was untreated. Group 2 showed a lower liver tumor incidence with a longer latency than group 1, indicating a 78% inhibition by ascorbate of in vivo N-nitrosomorpholine (NMOR) formation. The incidence of forestomach papillomas was 3% in group 1, 38% in group 2, and 8% in group 3. The difference between groups 1 and 2 was not significant due to the shorter life-span of group 1. Group 1 and especially group 2 had more forestomach hyperplasia and hyperkeratosis than group 3. Ascorbate might have enhanced induction of these lesions because of an action synergistic with that of NMOR. However, it is most likely that the lowered NMOR dose and concomitantly increased survival produced by the ascorbate were solely responsible for the increased incidence of forestomach papillomas and other lesions in group 2.

Again, same group - and sodium ascorbate was given orally (along with another chemical to offset alkalinity?

Tumorigenicity of Sodium Ascorbate in Male Rats1
http://cancerres.aacrjournals.org/content/58/12/2557.short

Abstract

Sodium ascorbate, like other sodium salts such as saccharin, glutamate, and bicarbonate, produces urinary alterations when fed at high doses to rats, which results in mild superficial urothelial cytotoxicity and regeneration but not tumors in a standard 2-year bioassay. Sodium saccharin was shown to produce a low incidence of bladder tumors in rats if administered in a two-generation bioassay. In the present study, we evaluated sodium ascorbate in a two-generation bioassay that involved feeding to the male and female parental F344 rats for 4 weeks before mating, feeding the dams during gestation and lactation, and then feeding the weaned (at 28 days of age) male F1 generation rats for the remainder of their lifetime (up to 128 weeks of the experiment). Dietary levels of 1.0, 5.0, and 7.0% sodium ascorbate were tested. At 5.0 and 7.0% sodium ascorbate, there was an increase in urinary bladder urothelial papillary and nodular hyperplasia and the induction of a few papillomas and carcinomas. There was a dose-responsive increase in renal pelvic calcification and hyperplasia and inhibition of the aging nephropathy of rats even at the level of 1% sodium ascorbate. Because the short-term urothelial effects of sodium ascorbate in rats are inhibited by treatments producing urinary acidification to pH < 6.0, we coadministered high doses of long-term NH4Cl to groups of rats with 5.0 or 7.0% sodium ascorbate to evaluate the long-term effects. The combination of 7.0% sodium ascorbate plus 2.78% NH4Cl in the diet was toxic, and the group was terminated early during the course of the experiment. The group fed 5.0% sodium ascorbate plus 2.04% NH4Cl showed complete inhibition of the urothelial effects of sodium ascorbate and significant inhibition of its renal effects. We also demonstrated the presence of a calcium phosphate-containing urinary precipitate in rats fed sodium ascorbate at all doses, in a dose-responsive manner. The formation of the precipitate was inhibited by coadministration with NH4Cl. The proliferative effects of sodium ascorbate on the male rat urinary tract in this study are similar to those seen with sodium saccharin when administered in a two-generation bioassay. Mechanistic information suggests that this is a high-dose, rat-specific phenomenon.

[ofonorow]

Lets analyze that ehow.com article written by Jonathan Lister.

Skin Effects
Sodium ascorbate taken at high doses can have adverse effects on the skin. These side effects may range from small skin irritations such as rashes, itching, and hives to swelling in the face, lips, or tongue. If the latter condition occurs, consumption should stop immediately, and a trip to the emergency room is in order, as it may be a symptom of digitalis, a potentially fatal skin condition.

Sounds serious, i.e. "fatal." If this were true, it is impossible that this would not be a known side effect of IV/C - almost always administered as sodium ascorbate. If anyone can connect digitalis and sodium ascorbate, please provide the reference.

Pain and Respiratory Problems
In injectable form, too much sodium ascorbate may cause pain throughout the body. This is most often displayed in chest pain or burning sensations, bone pain, and difficulty breathing. Sodium ascorbate in an injection has a much more immediate effect on the body than when consumed orally, and the supplement should not be overused.

Again, sounds serious and authoritative - yet, unheard of in our experience. I would appreciate any references.

Damage to Internal Organs
According to sciencelab.com, prolonged exposure to sodium ascorbate at high levels may cause problems with internal organs. The compound may develop toxic interactions with the kidneys, upper respiratory tract (as mentioned above), and the gastrointestinal tract. This claim is backed up by a 1995 study published by the Oxford University Press. This study, conducted by doctors at the University of Nebraska's medical center, found that prolonged exposure to sodium ascorbate caused significant damage to the urinary bladder of male rats.

This warning is based on the previous cited studies from the Univ. of Nebraska. If people can get into these papers, and it is true that there were differences in the urinary bladders between the two groups (with and without sodium ascorbate) please let us know.

[Saw]

In addition vitamin C supplementation was shown to inhibit skin, nose, tracheal, lung, and kidney carcinogenesis, to either not influence or enhance skin, mammary gland, and colon carcinogenesis, and to enhance urinary bladder carcinogenesis, when given as sodium ascorbate, but not when given as ascorbic acid.

http://www.ncbi.nlm.nih.gov/pubmed/3540970

[ofonorow]

I could find no skin condition called "digitalis" and only an allergic reaction to the drug of that name,
Digitalis allergy with demonstrable antibody
http://www.sciencedirect.com/science/article/pii/0021870754900131

Also, if anyone can get into this Univ. of Neb papers, and see what the results were in groups receiving and not receiving sodium ascorbate re: the bladder, I would appreciate it.

[ofonorow]

I did find this from Japan regarding sodium ascorbate and bladder cancer in rats
http://tpx.sagepub.com/content/33/7/766.full

Lack of Urinary Bladder Carcinogenicity of Sodium L-Ascorbate in Human c-Ha-ras Proto-Oncogene Transgenic Rats

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Moreover, the total bladder tumor incidences, including papillomas, did not differ statistically (with Na-AsA, 37.0%; without Na-AsA, 30.8%). No bladder tumor was detected in Non-tg rats. Various kinds of other lesions in various organs were noted in Tg rats treated with or without Na-AsA treatment, but no intergroup differences were evident. In conclusion, Na-AsA did not show tumorigenicity in highly bladder-cancer-susceptible transgenic Hras128 rats. These results suggest that Na-AsA is a pure promoter but not a complete carcinogen in rats.