Here is a copy of an article for my blog I used to write.
Is the common belief that if a little is good, then more must be better. Although, many substances that provide beneficial effects to the body can be harmful, or even deadly, in large amounts. Even water or oxygen can be harmful or deadly in high amounts, or in the right circumstances.
Megadosing of vitamin C was made famous by the Linus Pauling Institute, especially among cancer patients. The belief is that large amounts of vitamin C can boost the immune system, destroy pathogens, and protect the body from free radical damage safely because the excess vitamin C will be eliminated from the body. Although, the use of massive doses of vitamin C for therapy by the Linus Pauling Institute is done for very short periods of time, up to a week. Even though short term megadosing of vitamin C may cause problems in some people, the risk of adverse effects greatly increases with long term use of excessive amounts of the vitamin.
Vitamin C does boost the immune system, and in does protect the body from some free radical damage. And it is true that excess vitamin C can be eliminated from the body. The practice of vitamin C megadosing does present some safety issues.
A severe deficiency of vitamin C can lead to a disease known as scurvy. Symptoms of scurvy include connective tissue breakdown, causing bleeding, muscle weakness, impaired wound healing, and nervous system disorders. It is believed that megadosing of vitamin C for extended periods of time, then drastically reducing the dose or going off cold turkey may lead to a condition known as rebound scurvy. Rebound scurvy is believed to occur when the body continues to excrete large amounts of vitamin C when megadoses are no longer being supplemented. Although, very few cases of rebound scurvy have been reported, and information about the cases have not been well-documented.
Excessive vitamin C intake is also known to displace vitamin B12 from the body. Vitamin B12 is essential for the maturation of blood cells. Deficiencies of B12 lead to a problem known as macrocytic anemia. This condition leads to the formation of abnormally large red blood cells, with impaired ability to carry oxygen. Decreased oxygen levels may cause fatigue, muscle weakness, shortness of breath, and possibly heart arrhythmias.
Macrocytic anemia also leads to the formation of abnormally large white blood cells with altered nuclei. White blood cells are an important component of the immune system. Therefore, macrocytic anemia from B12 deficiency may impair immune function.
B12 deficiencies may cause nerve damage leading to nerve pain and numbness, or loss of some senses. Mental disturbances may also develop including depression, dementia, paranoia, irritability, and delirium.
Vitamin C is a water soluble compound, which can be easily flushed from the body. Although, vitamin C is a relatively unstable compound, and a portion of excess ingested vitamin C breaks down into oxalic acid in the body.
Oxalic acid is beneficial to the body as well as detrimental. As vitamin C breaks down in to oxalic acid, the oxalic acid actually serves as an antioxidant to the vitamin C helping to prevent oxidative destruction of the vitamin C. On the other hand, oxalic acid can bind with minerals forming insoluble oxalates. Of particular importance is calcium oxalate, which can form kidney stones. Studies have shown that oxalic stones, which make up 80% of kidney stones, only formed in people with kidney diseases, but not in healthy individuals at doses of 200mg daily. At 1,500mg daily intake there was only a tiny rise in the incidence of oxalic stone formation. It is believed that the insignificant rise is due to the fact that vitamin C is poorly absorbed by the body. Therefore, the higher levels of vitamin C are not being absorbed, and therefore are not converted in to oxalic acid.
Oxalic acid also binds with the electrolytes sodium and potassium, and the mineral magnesium. Among other functions of sodium and potassium is the regulation of heart rate. Magnesium serves a multitude of important functions including maintaining normal blood pressure, proper muscle function; including the heart, preventing muscle cramping, and insulin production.
Oxalic acid is an irritant to the urinary tract. Irritation of the urinary tract from oxalic acid can lead to urinary tract infections in sensitive individuals.
There is also concern that vitamin C may cause uric acid stones to form from excess excretion of uric acid. Acidification of the urine with vitamin C increases the ratio of uric acid to the more soluble sodium urate. For this reason, treatment of uric acid stones includes alkalinizing the urine with sodium bicarbonate (baking soda) or calcium citrate to increase sodium urate formation.
Excessive levels of vitamin C are contradicted in people suffering from kidney stones, gout, cirrhosis, kidney diseases, and certain other disorders.
Safety studies at doses of 200 to 1,500mg daily are conflicting. Safety studies of extremely high doses, up to 20,000 have not been done. Therefore I recommend not exceeding 2,000mg daily for healthy individuals. Normally, I recommend 500mg 3 times daily for most individuals. Slightly higher levels are recommended for smokers, individuals under a lot of stress, stimulant users; including caffeine (coffee, tea, guarana, kola nut, etc.), and those taking medications known to deplete vitamin C, such as Prednisone.
A major concern of taking excessive doses of vitamin C is the fact that large amounts of vitamin C can block copper absorption. Copper serves various functions in the body including production of the antioxidant, anti-inflammatory, and immune stimulating enzyme copper superoxide dismutase. Copper is essential for the formation of collagen and elastin, which give strength and elasticity to the tissues. Copper also plays a role in the formation of neurotransmitters for proper nerve function. As a factor in the production of melanin, copper helps to prevent graying of the hair. In addition, copper helps to maintain proper levels of blood lipids (fats), including cholesterol.
Decreased copper levels can lead to decreased collagen and elastin synthesis. This in turn leads to bone loss, blood vessel weakness, poor wound healing, gum disorders, tendon and ligament weakness, cartilage disorders, bruising, and wrinkles. Disorders such as emphysema and diverticulitis also involve loss of elastin in tissues.
The risk of heart disease increases with copper deficiencies. This is most likely due to weaker arterial walls, combined with increased inflammation, increased oxidative damage, and elevated cholesterol levels.
Vitamin C is often touted as an immune stimulant, although excessive levels may have the opposite effect. The enzyme copper superoxide dismutase (cu-SOD) produces hydrogen peroxide in response to infections. Hydrogen peroxide serves various functions, including activation of the immune system’s white blood cells. White blood cells fight infections, and cancer cells within the body. Therefore, declining levels of cu-SOD can have an adverse effect on the immune system.
Inflammation has been shown to be a major contributor to the formation of cancers. Another primary function of cu-SOD is to reduce inflammation. Copper therefore may play a crucial role in other inflammatory diseases as well, such as colitis, and arthritis.
As an antioxidant, cu-SOD helps protect cells from free radical damage. The body requires free radicals, such as hydrogen peroxide. Excessive levels of free radicals have been implicated in various diseases though, including cancer.
Hemoglobin requires copper for its production. Therefore, copper deficiencies can lead to anemia.
Copper is essential for the formation of thyroid hormones. Copper deficiencies lead to hypothyroidism, although excessive levels suppress thyroid function. This is especially true if zinc deficiencies are present since zinc promotes thyroid function. Note that excessive levels of zinc can over stimulate the thyroid.
As a cofactor in neurotransmitter production, copper deficiencies can lead to depression. High copper levels though have also been linked to depression, as well as schizophrenia, ADHD symptoms, and other neurological disorders.
The brain and spinal cord contain some of the highest levels of copper in the body. Copper is not only essential for the formation of neurotransmitters, but also for myelin, which insulates nerves so they do not “short circuit”.
Interestingly, the brain contains about 10 times the level of vitamin C as found in the blood. Vitamin C actually has to be oxidized to cross the blood-brain barrier. Oxidation converts the vitamin C in to dehydroascorbic acid, which allows it to be transported in to the brain through sugar receptors. There the dehydroascorbic acid is converted back in to ascorbic acid, commonly known as vitamin C. Here the vitamin C helps prevent damage to the myelin from free radicals, and aids in the conversion of dopamine to norepinephrine.
Copper is essential for the proper regulation of histamine throughout the body. High levels of histamine can lead to allergic responses, including asthma. In the brain, histamine plays roles in mood, behavior, libido, addictions, and sleep and wake cycles.
Despite all the benefits of copper, excess levels of copper can be dangerous. Copper supplementation is not recommended in most cases, although it should be combined with zinc if supplementing zinc. The common ratio of zinc to copper in supplements is 50mg zinc to 2mg copper. Women with excessive levels of estrogen would probably benefit more by taking zinc, but not copper. Estrogen increases copper levels, and zinc antagonizes copper helping to reduce the risk of copper toxicity.
Copper, which is displaced by excess vitamin C, is essential for the formation of hemoglobin, which carries oxygen to the tissues, and removes carbon dioxide. Iron is also essential for the formation of hemoglobin, and iron absorption is increased by vitamin C. This all brings up an interesting problem. If iron levels are increased by improved absorption from vitamin C, but hemoglobin cannot be formed due to lack of copper, what happens to all the iron being absorbed?
As with copper, and vitamin C, iron is essential for the body and serves various purposes. Although, as with copper and vitamin C, excess levels of iron can be dangerous. And since the body has no efficient way of ridding itself of excess iron, iron levels may easily build up to toxic levels.
As iron accumulates in the body it is primarily stored in organs and glands, where it can lead to organ failure and glandular damage. The heart, liver, and pancreas are at the greatest risk of damage and failure from iron overload.
Side effects of iron overload include heart disorders, diabetes, cirrhosis of the liver, adrenal insufficiency, hypothyroidism, parathyroid damage resulting in low blood calcium, pituitary gland dysfunction, atrophy of the testes and ovaries, nervous system damage and disorders, arthritic disorders, graying or bronzing of the skin, and decreased energy levels. Numerous microbes, and protozoa, thrive with high iron levels. These include Candida, Listeria, Chlamydia, Salmonella, Plasmodium, Staphylococcus, Streptococcus, Cryptococcus, Campylobacter, Pseudomonas, Helicobacter pylori Escherichia coli, and numerous others.
Iron overload is also known to increase the risk of various cancers including liver cancer, Kaposi's sarcoma, breast cancer, melanoma, and colon cancer. The increased risk of cancer is probably due to the increased activity of cancer pathogens. For example, human papilloma virus has been linked to several cancers including breast cancer. Human herpes virus type 8 has been linked to the viral form of Kaposi's sarcoma. Liver cancer has been linked to hepatitis viruses, and aflatoxins from the fungus Aspergillus
Arthritis may occur from iron overload due to two factors. Oxidative destruction can lead to join damage. In addition, certain forms of arthritis are triggered from pathogens. For example, rheumatoid arthritis has been linked to an infection with a form of Chlamydia bacteria.
Heart disease, due to iron overload, is generally believed to result from oxidative damage to the arterial lining, and to the heart muscle itself. There may be a secondary factor though. Scientists have found a link between Chlamydia bacteria and arterial sclerosis, which may lead to arrhythmias, angina, and heart attack.
Excess of levels of iron have also been found in the brains of Alzheimer's patients. As with the excessive aluminum levels found in the brains of Alzheimer's patients, that excessive iron levels have not been proven to be a cause of Alzheimer's. Although, it is hypothesized that the excessive level of iron may be causing oxidative damage to the brain, leading to Alzheimer's disease.
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:
http://www.ncbi.nlm.nih.gov/pubmed/15987848
J Nutr. 2005 Jul;135(7):1673-7.
Massey LK, Liebman M, Kynast-Gales SA.
Department of Food Science and Human Nutrition,
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.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TB1-3RGSPD8-M&...
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.
http://www.ncbi.nlm.nih.gov/pubmed/3930094?dopt=Abstract&holding=npg
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.
How far beyond a look at the Ksp's, alpha-1, and the beta expressions for calcium with the various anions involved do you think one needs to go ?
Again, I cannot find any studies to back your claims. Do they exist? And are the studies independent? Being that you are ignoring my request for studies I have to assume that they do not exist.
So if I cite it not, it doesn't exist !! LOL, that's a good one.
Maybe I should go over reading lessons while we are on chemistry lessons since I did not say that. What I pointed out is that if you cannot provide proof I have to ASSUME that it does not exist. This is hardly the same as does not exist. I can assume that you will not come back with more irrelevant information, but this does not mean you won't. I have spent many years dealing with people who like to play games claiming that there is proof of their claims and yet they never seem to come up with it because it does not exist. Or they send you off on wild goose chases by posting references that often they do not read and they don't quote the part of the study they are referring to so you have to wade through their references only to find out that the evidence to their claim does not exist. And they know most people will not waste their time doing this. So far you have fit the typical "I have no real evidence" type person I normally have to deal with. I can pull up all sorts of studies to contradict what you have posted, but I specifically wanted to see the proof of your claims, which I still don't see. You merely posted some titles to articles that you may or may not have even bothered reading yourself. Try posting the exact quotes from these sources that back what you are claiming so I know you actually read and understood them. Then we can go from there to see if there is any real basis for your claims.
One does not need studies for simple considerations such as the solubilities of simple organic salts !! This is the most basic chemistry, learned freshman year.
ROTFLMAO!!!!! If they were soluble salts in the solution then they would not have precipitated out as stones. By the way since when did calcium oxalate become considered a soluble salt? And you learned chemistry where?
http://en.wikipedia.org/wiki/Oxalic_acid
"Oxalic acid is the chemical compound with the formula C2O2(OH)2 or HOOCCOOH. This colourless solid is a relatively strong carboxylic acid, being about 3,000 times stronger than acetic acid. The dianion, known as oxalate, is a reducing agent as well as a ligand for metal cations. Many metal ions form insoluble precipitates with oxalate, a prominent example being calcium oxalate, the primary constituent of the most common kind of kidney stones."
"Try posting the exact quotes from these sources that back what you are claiming"
I'm not claiming anything, except that what I consider large doses of ascorbate do not in themselves cause kidney stones, as you've wrongfully asserted. I provided articles, but I'm not going to hold your hand and quote them. If you don't want to read them, I don't care !!
Actually you made several claims, that being one. But posting a bunch of titles to articles is hardly providing proof. Anyone can copy and paste a bunch of references from someone elses work, but this does not mean they read or understood the references themselves. In the time you have wasted here you could have easily quoted what you are referring to. The fact that you are refusing to do this just proves to me that you have not read them. And why would I go looking for copies of your references then have to dig through them to try and find what you are referring to, that is IF the evidence is even there to begin with? Several of these are books, which I definitely do not have time to read through to find someone's opinion when the studies show differently. Even your reference number 7 is "Ascorbate increases human oxaluria and kidney stone risk", which the title alone seems to say the opposite of what you claim.
You also claimed that ascorbate dissolves oxalates. Have seen no proof of this either.
And "that repeated short-term periods of lactic acidosis are more responsible for stones than ascorbate." This brings up two points. First of all is the question of why then don't athletes develop kidney stones on a regular basis from the repeated short-term periods of lactic acidosis? The lactic acidosis bouts are common in athletes, yet I have never seen any evidence that athletes are more prone to stones. So this is very contradictory to your claim.
Secondly the end of your sentence states "are more responsible for stones than ascorbate". "More responsible" indicates that ascorbates do in fact cause kidney stones, which again is contradictory to your statement earlier that ascorbates dissolve kidney stones.
Calcium oxalate itself is very insoluble in pure water, but you've neglected several competing equilibria. Its clear from your manner, that you're not interested in anything I have to offer.
Again as I pointed out if it is soluble as you claim then how does it form kidney stones? Simple question.
The articles I cited were written by PhD's. If you don't like it, good for you, but your argument isn't with me, regardless of your experience in dealing people you may believe are somehow like me, whoever you are. Why don't you take it up with the authors, show them that they are wrong, and then help these people by advancing knowledge - instead of wasting time ROFL.
Actually as your study number 7 shows and your own statement about ascorbates causing kidney stones, along with the research I have already seen already already prove my earlier point. So unless you show me proof to the contrary and contrary to your own claims then I see nothing wrong with my original article.