A person from my work left an interesting article from a DR. Levy on my desk at work. It claims that he treated a women with chronic lyme with an IV drip of Vitamin C and now she is cured! Has anyone ever heard of such a thing or tried it?
-------------------- Amy Holloway Posts: 255 | From Michigan | Registered: Oct 2005
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I had many, many IV Vit C drips that also included other ingredients. I am well today, but I do not contribute that to IV Vit C drips. It took many, many other modalities to get me well, the drip being just one of about a hundred.
I've just read the studies of vitamin c on polio and heart disease. Both done by reputable doctors, one a noble prize winning doc. I'm fairly convinced that this "vitamin" along with helping bodily functions contains antimicrobial capabilities. Of course it's nonpatentable and cheap so there is not alot of studies on the benefits. There is quite a few on the "dangers". (same ol song and dance)
Always a good place to get started. I'll be adding megadoses of C to my protocal very soon to see what happens. happy little guinea pig am I
Posts: 731 | From Humble,TX | Registered: Feb 2005
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I'm headed in for #15 IV vitC today. They help many things as GIGI says but they do no cure anything. What ascorbic acid does is nuetralize and convert toxins to more readily disseminated compounds that the body can handle.
I have had a very highbacteria load that causes herxes and increased sx when I try to get rough with antibiotics. The Vit C at 50 grams IV or more goes a long ways to help the body get rid of this toxic load.
-------------------- "In spite of the ever increasing cost of living, it remains quite popular" S. Shackel Posts: 87 | From walla walla wa | Registered: Dec 2005
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IMO this is nothing more than voodoo medicine...
Vit C can also prevent absorption of some abx's as well.
-------------------- I am not a doctor...opinions expressed are from personal experiences only and should never be viewed as coming from a healthcare provider. zman Posts: 2527 | From safety harbor florida(origin Cleve., Ohio | Registered: Jan 2004
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I'm still not convinced vit C has no antimicrobial properties. Very little on the subject either way.
Helicobacter pylori infection in humans is associated with chronic type B gastritis, peptic ulcer disease, and gastric carcinoma. A high intake of carotenoids and vitamin C has been proposed to prevent development of gastric malignancies. The aim of this study was to explore if the microalga Haematococcus pluvialis rich in the carotenoid astaxanthin and vitamin C can inhibit experimental H. pylori infection in a BALB/cA mouse model. Six-week-old BALB/cA mice were infected with the mouse-passaged H. pylori strain 119/95. At 2 weeks postinoculation mice were treated orally once daily for 10 days (i) with different doses of algal meal rich in astaxanthin (0.4, 2, and 4 g/kg of body weight, with the astaxanthin content at 10, 50, and 100 mg/kg, respectively), (ii) with a control meal (algal meal without astaxanthin, 4 g/kg), or (iii) with vitamin C (400 mg/kg). Five mice from each group were sacrificed 1 day after the cessation of treatment, and the other five animals were sacrificed 10 days after the cessation of treatment. Culture of H. pylori and determination of the inflammation score of the gastric mucosae were used to determine the outcome of the treatment. Mice treated with astaxanthin-rich algal meal or vitamin C showed significantly lower colonization levels and lower inflammation scores than those of untreated or control-meal-treated animals at 1 day and 10 days after the cessation of treatment. Lipid peroxidation was significantly decreased in mice treated with the astaxanthin-rich algal meal and vitamin C compared with that of animals not treated or treated with the control meal. Both astaxanthin-rich algal meal and vitamin C showed an inhibitory effect on H. pylori growth in vitro. In conclusion, antioxidants may be a new strategy for treating H. pylori infection in humans.
He regards total dental cleanup as essential as well.
THE ULTIMATE ANTIDOTE
"Science commits suicide when it adopts a creed."
Vitamin C has demonstrated the ability to neutralize a wide variety of toxic substances, many of which are completely unrelated chemically. Frequently, vitamin C directly interacts chemically with a given toxin to render it less toxic or nontoxic. This is known as a chemical antidote effect. However, vitamin C can also act as a physiological antidote to a toxin or poison. Such an antidote effect can result when vitamin C helps to undo or repair the damage caused by a certain toxin without having to directly interact with the toxin (Nowak et al., 2000). In Chapter 2 it has already been demonstrated that vitamin C is superbly effective in either neutralizing or negating the effects of a number of chemically different and extremely potent endotoxins and exotoxins, which are produced as by-products of microbial growth. Furthermore, when the toxin is a chemotherapy drug, vitamin C quite often will promote the anticancer actions of that drug without increasing the drug-induced toxic effects. In mice with liver tumors, Taper et al. (1987) showed that the combination of vitamin C with another vitamin was able to increase the therapeutic effectiveness of six different cytotoxic drugs without increasing their undesirable toxic side effects.
Some toxic substances have also been documented to have cancer-causing effects. Many of these toxins can be demonstrated to increase the consumption of vitamin C. This is one important piece of evidence implying that vitamin C plays a role in the neutralization of toxins. Calabrese (1985) published a significant partial list of toxins that lowered vitamin C levels and whose toxicity or cancer-causing effects were modified by vitamin C. While not nearly exhaustive, this list serves to underscore the versatility of vitamin C in lessening or eliminating the toxicity of chemically diverse substances. Calabrese listed the following:
1. Some chlorinated hydrocarbon insecticides and organophosphate insecticides 2. Toxic elements: arsenic, cadmium, chromium, cobalt, copper, cyanide, fluoride, lead, mercury, selenium, silica, and tellurium 3. Industrial hydrocarbons: benzanthrone, benzene, chloroform, glycerol, hydrazine, polychlorinated biphenyls, trinitrotoluene, and vinyl chloride 4. Gaseous pollutants: carbon monoxide and ozone
It is important to supplement vitamin C even if it is only to normalize the body's vitamin C status. However, supplementation is also essential because depletion of vitamin C levels in the face of toxicity indicates that toxins are being neutralized as a result of vitamin C's metabolic breakdown in the body. A given chemical toxin can make the body's ability to cope with other challenges all the more difficult by lowering the vitamin C level in the course of its detoxification. In the extreme, however, large enough doses of such a chemical toxin can rapidly produce a toxin-induced scurvy, which is a state that can kill the patient in short order even if the chemical toxin presence is self-limited and not continuous. In this chapter you will see that a large amount of evidence exists to indicate that the toxin-induced lowering of vitamin C levels actually indicates that available vitamin C is working to neutralize as much toxin as possible. The depleted vitamin C status of the body merits prompt supplementation for no reason other than the fact that it is depleted, reliably weakening the immune system and potentially exposing the body to other medical problems.
Although many toxins have been shown to decrease vitamin C levels in the non-vitamin C-producing human, the opposite effect is typically seen in a vitamin C-producing animal. As long as the amount of toxin is not so large as to immediately overwhelm the vitamin C-producing capacity of the animal, vitamin C levels will reliably rise when toxic challenges present themselves. This allows all toxin challenges of a lesser degree to be "automatically" neutralized by the increased vitamin C production in such an animal. Longenecker et al. (1939) and Longenecker et al. (1940) noted that the vitamin C-producing rat responded with an increased formation of vitamin C to a large number of organic compounds generally considered to be toxic. Conney et al. (1961) also noted a number of drugs "possessing completely unrelated chemical and pharmacological properties" would "stimulate markedly" the excretion of vitamin C in rats, indicating an increased liver production of vitamin C to the toxic challenges posed by these drugs. The list of drugs that Conney et al. found would stimulate vitamin C synthesis, metabolic breakdown, and excretion included the following:
1. Hypnotics: chloretone and barbital 2. Analgesics: aminopyrine and antipyrine 3. Muscle relaxants: orphenadrine and meprobamate 4. Antirheumatics: phenylbutazone and oxyphenbutazone 5. Uricosuric agent: sulfinpyrazone 6. Antihistaminics: diphenhydramine and chlorcyclizine 7. Carcinogenic hydrocarbons: 3-methylcholanthrene and 3,4-benzpyrene
It is not really important whether you are familiar with any of the drugs just mentioned above. What is important is that vitamin C appears to be a natural detoxifying agent to neutralize these drugs along with many other toxins, or drugs perceived by the body as toxic. It is also important to realize that vitamin C is effective in detoxifying a wide array of dissimilar and diverse toxins.
In addition to the direct antioxidant effects that vitamin C has on so many toxins, which reduces them to less toxic or nontoxic metabolites, it is important to realize that vitamin C has another important effect in the mechanism of drug detoxification. Vitamin C also appears to stimulate the activity of several drug-metabolizing enzymes in the liver (Zannoni et al., 1987). Schvartsman (1983) asserted that the action of vitamin C in stimulating the enzymatic system of the liver "may thus constitute the main justification for increasing its use in the therapy of intoxications." It has long been known that one of the main functions of the liver is to detoxify toxins, and increased vitamin C appears to directly stimulate this activity in addition to its direct antioxidant action on a given toxin.
This chapter will deal with the documented effects of vitamin C on specific toxic agents. Although vitamin C can often offer complete cures or absolute protection for many different types of poisoning, little of this information has reached any of the medical textbooks, and many people worldwide continue to suffer and die needlessly from such intoxications since modern medicine still has no effective treatment for them. Furthermore, even when a given toxin cannot be neutralized or eliminated by vitamin C, the damage inflicted by such toxins can almost always be significantly repaired by the administration of adequate doses of vitamin C. Almost all toxins precipitate varying amounts of damage by generating large amounts of tissue-damaging and enzyme-damaging free radicals. Antioxidant therapy, headed by vitamin C, remains the best way to deal with an onslaught of free radicals.
Although there are many antioxidants available to help deal with the excess free radicals seen in different medical conditions and intoxications, it is important to understand that all antioxidants are not created equal and do not have equal potency. Challem and Taylor (1998) pointed out that the human body cannot completely compensate for a lack of vitamin C with its own internally produced antioxidants, such as superoxide dismutase and uric acid. To be sure, the antioxidants as a group will attempt to compensate for the lack of some by an increased activity of others. However, vitamin C is probably the only antioxidant that cannot be completely and safely eliminated from the diet by the substitution of any of the other antioxidants, regardless of their doses or the combination used. Frei et al. (1989) and Frei et al. (1990) pointed out that vitamin C is the only antioxidant in the blood plasma that can offer complete protection for circulating blood fats (lipids) from metabolic breakdown (peroxidation). They also asserted that vitamin C is the most effective antioxidant in human blood plasma, offering blood lipoproteins complete protection against the oxidative damage that can be caused by activated white blood cells.
SPECIFIC TOXINS AND VITAMIN C
As most people know, alcohol in excess is clearly a toxin. The toxicity level of smaller amounts continues to be debated. As with so many other toxins, the liver is the main site of alcohol neutralization/metabolism when a toxic dose of alcohol is encountered.
Susick and Zannoni (1987) looked at the effects of vitamin C on the consequences of acute alcohol consumption in humans. Vitamin C or a placebo was given to 20 male subjects for two weeks prior to alcohol consumption. The subjects who received the vitamin C demonstrated improved motor coordination and color discrimination, which is evidence of a lessened alcohol toxicity. The vitamin C also resulted in a "significant enhancement" in the elimination of alcohol from the blood. Klenner (1971) asserted that 40,000 mg of vitamin C given intravenously along with vitamin B1 will "neutralize" the effects of alcohol in an intoxicated person. Klenner also asserted that the same treatment would "save the life" of a person unfortunate enough to drink a significant amount of alcohol after taking Antibuse (disulfiram). This drug, used to make alcoholics feel sick after drinking in order to break their habit, can also kill. It prevents alcohol from being completely metabolized, which results in high concentrations of acetaldehyde in the body. Vitamin C detoxifies the acetaldehyde (see below, this section).
Meagher et al. (1999) showed that alcohol ingestion in healthy humans increases oxidative stress as indicated by an increase in the products of lipid peroxidation (LPO). They also showed that the same abnormal laboratory indicators of oxidative stress were already significantly elevated in patients with alcohol-induced hepatitis or chronic liver disease in the absence of additional acute alcohol intake. Finally, they were able to show that vitamin C was able to reduce abnormal elevations of oxidative stress in patients who already had chronic alcoholic liver disease. They concluded that oxidative stress, which was significantly lowered by vitamin C, preceded and contributed to the evolution of alcoholic liver disease. Zhou and Chen (2001) were able to show that alcohol abusers demonstrated lower blood levels of antioxidant enzymes and antioxidants, including vitamin C. They suggested that chronic oxidative damage in alcoholics should be treated chronically with antioxidant supplementation that included vitamin C to minimize long-term oxidative damage to the body. A similar recommendation was made by Marotta et al. (2001), who also concluded that an "effective antioxidant supplementation" regimen was able to decrease laboratory evidence of increased oxidative stress. Furthermore, such supplementation should be especially properly dosed, as the diuretic (increased urine-forming) property of alcohol ingestion is associated with a further substantial loss of vitamin C in the urine (Faizallah et al., 1986). This means that alcoholics both metabolize vitamin C more quickly and flush it out more quickly in the urine, mandating vigilant supplementation in order to minimize the long-term toxic damage of alcohol.
Lesser consumptions of alcohol appear to be associated with lesser utilizations of vitamin C and other antioxidants. In 11 "apparently healthy" subjects the blood levels of vitamin C were reduced by approximately 12% to 15% after a course of "moderate" alcohol consumption over a total time period of 12 weeks (van der Gaag et al., 2000). Interestingly, at the levels of alcohol ingested, the mild drops in vitamin C levels were seen with beer and "spirits" drinking, but not with red wine. Even the slight drop in vitamin C levels is evidence that alcohol may very well be toxic at any dose.
One of the primary breakdown products of alcohol (ethanol) is acetaldehyde, another toxic substance (Cohen, 1977). Vitamin C appears to play a direct role in both the initial breakdown of any non-excreted ethanol to acetaldehyde (Giles and Meggiorini, 1983; Susick and Zannoni, 1984), and in the improved detoxification of the acetaldehyde through the increased and more stable binding of acetaldehyde to blood proteins (Tuma et al., 1984).
Wickramasinghe and Hasan (1992) looked at the toxic effects that the serum of alcohol drinkers had on lymphocytes outside of the body. They believed the toxicity was due to the presence of unstable acetaldehyde-protein complexes, allowing the acetaldehyde to break free and poison the lymphocytes. Vitamin C was able to reduce this cytotoxic effect, further justifying its use in alcohol toxicity. In seven healthy volunteers Wickramasinghe and Hasan (1994) showed that only 1,000 mg of vitamin C daily for three days prior to an acute alcohol consumption decreased the associated acetaldehyde-mediated toxicity that resulted from that ingestion. Krasner et al. (1974) were able to show that there was a direct correlation between the level of vitamin C in the white blood cells and the rate of clearance of ethanol from the blood. Sprince et al. (1975) and Sprince et al. (1979) looked at acetaldehyde-induced toxicity in rats. They found that vitamin C could offer significant protection against the toxic symptoms of acetaldehyde and the ultimate lethality of the acetaldehyde. O'Neill and Rahwan (1976) also showed that vitamin C resulted in a "statistically significant reduction in acetaldehyde-induced toxicity" when given to mice exposed to symptom-inducing amounts of acetaldehyde. Moldowan and Acholonu (1982) found that a dose of vitamin C given to mice 90 minutes before an otherwise fatal injection of acetaldehyde reduced the mortality rate. Also looking at mice, Tamura et al. (1969) demonstrated that vitamin C, along with glucose and cysteine, had a clear antidotal effect in blocking the otherwise lethal effect of acetaldehyde given to mice.
Navasumrit et al. (2000) also showed in mice that alcohol increased the generation of free radicals and the frequency of damage to DNA. A pretreatment regimen with vitamin C lessened the increase in alcohol-induced oxidative stress, and the otherwise increased frequency of DNA damage was prevented. Suresh et al. (2000) looked at the effects of a large vitamin C dose on alcohol-induced toxicity in rats. The dose was 200 mg per 100 g body weight, which would equate to 140,000 mg of vitamin C for a 150-pound person. The vitamin C clearly reduced alcohol-induced toxicity, as reflected in decreased triglyceride and liver enzyme levels relative to the rats given alcohol (ethanol) alone. In mice, Busnel and Lehmann (1980) examined the motor (muscle) disturbances in swimming behavior induced by alcohol. This was effectively a laboratory test equivalent to a human's drunken walk. They found that fairly large doses of vitamin C (125 and 500 mg/kg body weight) completely prevented alcohol-induced abnormal swimming behavior, while a smaller dose of vitamin C (62.5 mg/kg) had no significant effect. A 500 mg/kg dose would amount to 35,000 mg of vitamin C for a 150-pound person, while the lowest dose would amount to slightly less than 4,400 mg of vitamin C for the same person. This study of Busnel and Lehmann is another clear example of how important the proper dose of vitamin C is in treating any toxic condition, whether in animal or man. It also shows how a suboptimal dose may have little or no effect on a given toxin or toxic clinical effect.
A significant amount of research has also been done regarding the effects of vitamin C on alcohol toxicity in guinea pigs. Yunice et al. (1984) found that administration of vitamin C was clearly effective in accelerating the clearance of infused ethanol from the blood of guinea pigs. Yunice and Lindeman (1977) were also able to show that vitamin C could completely prevent the lethal effects of an acute alcohol dosage that would otherwise kill 68% of the mice recipients. Ginter and Zloch (1999) were able to demonstrate that guinea pigs receiving the most vitamin C over a 5-week pretreatment period metabolized alcohol much more quickly than guinea pigs on minimal amounts. Yunice et al. also showed that greater amounts of supplemented vitamin C were able to help ethanol-treated guinea pigs gain weight compared to ethanol-treated animals receiving significantly less vitamin C. The concentrations of vitamin C were noted to be lower in the liver, kidney, and adrenal glands in the ethanol-treated animals relative to control animals, which indicated the increased utilization of vitamin C by the toxicity of the ethanol. Suresh et al. (1999) also found that alcohol administration lowered tissue levels of vitamin C in guinea pigs.
Ginter et al. (1998) gave guinea pigs diets with no added vitamin C, "medium" amounts of vitamin C, or "high" amounts of vitamin C for a five-week period. Just prior to sacrificing the animals, an injection of ethanol calculated to result in short-term acute intoxication was given. As a model of chronic alcohol abuse, several other groups of guinea pigs with differing vitamin C intakes were given lesser alcohol doses every week prior to being sacrificed. Relative to unsupplemented animals, guinea pigs with the highest tissue vitamin C concentrations had "significantly decreased" levels of ethanol and acetaldehyde in the liver and brain. They also had lower liver enzyme levels and lower cholesterol levels. The authors concluded that the administration of "large amounts" of vitamin C appears to accelerate the metabolism of both ethanol and acetaldehyde, while reducing some of their adverse health effects.
Suresh et al. (1999a) looked at the effects of a "mega dose" of vitamin C on increased LPO induced by alcohol in guinea pigs. They found that the supplementation of vitamin C to the alcohol-fed animals decreased laboratory findings of oxidative stress and reduced the levels of increased enzyme activity toxically induced by the alcohol. Susick and Zannoni (1987a) maintained guinea pigs on differing doses of vitamin C. They gave a dose of ethanol that raised the SGOT (a liver enzyme) 12-fold in animals that had liver vitamin C levels below 16 mg/100 g of liver weight. However, the same dose of ethanol given to animals that had liver vitamin C levels above this threshold had a "marked reduction" (60%) in the ethanol-induced increase in SGOT. Suresh et al. (1997) looked at the alcohol-induced increase in blood fats (hyperlipidemia) in guinea pigs and found that vitamin C significantly reduced this increase. Susick et al. (1986) were also able to demonstrate that enough vitamin C had a significant protective effect against the toxic effects of chronic alcohol consumption in guinea pigs.
Acute and chronic alcohol consumption in humans takes a serious toll in both morbidity and mortality. Zannoni et al. (1987) wrote a review article clearly demonstrating that adequately dosed vitamin C is the best way to detoxify alcohol, prevent future alcohol-induced damage, and repair past alcohol-induced damage. Pawan (1968) provides an example of a study contesting the ability of vitamin C to accelerate the ethanol clearance rate in man. As is so often the case, however, the vitamin C dosage is tiny. Pawan reported that 600 mg of vitamin C given acutely had no influence on ethanol clearance rates. It is unlikely that 600 mg of vitamin C could seriously affect the clinical status of virtually any form of significant toxicity in an adult human, unless some of the symptoms related to a toxin-induced scurvy. The cumulative research on ethanol and vitamin C indicates that vitamin C can definitely lessen much of the damage done to the body by alcohol, especially in the liver. Furthermore, studies looking at acute alcohol exposure and vitamin C indicate that a high dosing of vitamin C, rather than hot coffee and forced ambulation, is the best and quickest way to metabolize alcohol and sober someone up. Obviously, the best way to deal with transporting an acutely intoxicated individual is through the use of a designated driver.
Barbiturates have long been used for hypnotic or anesthesia applications. Phenobarbital is a type of barbiturate that has long been used in the management of epilepsy. Excess barbiturates in the body result in depression of the central nervous system.
Klenner (1971) reported dramatic success in reversing acute barbiturate toxicity with vitamin C. A patient who had ingested 2,640 mg of talbutal, an intermediate-acting oral barbiturate, presented to Klenner in the emergency room with a blood pressure of 60/0. By blood pressure standards, this is barely alive. Klenner gave 12,000 mg of vitamin C with a 50 cc syringe by intravenous push, followed by a slower infusion of vitamin C by vein. Within only 10 minutes the patient's blood pressure was up to 100/60. The patient woke up three hours later and completely recovered, having received a total of 125,000 mg of vitamin C over a 12-hour period.
Klenner also reported on another patient with a secobarbital barbiturate overdose. The patient awoke after 42,000 mg of vitamin C was "given by vein as fast as a 20 gauge needle could carry the flow." Ultimately this patient received 75,000 mg of vitamin C by vein and 30,000 mg by mouth over a 24-hour period. Klenner asserted that the success of his vitamin C protocol "in no less than 15 cases of barbiturate poisoning" indicated that "no death should occur" in this condition. Klenner (1974), in discussing the dramatic effects of vitamin C on barbiturate poisoning (and carbon monoxide poisoning), commented that "the results are so dramatic that it borders on malpractice to deny this therapy."
In dogs and mice, Kao et al. (1965) were able to show that a "large dosage" of injected vitamin C helped to reverse the barbiturate-induced depression of the central nervous system. They found that the vitamin C in this situation improved the blood pressure and breathing in acutely intoxicated animals.
Carbon monoxide poisoning operates by a similar mechanism to methemoglobinemia, which is discussed in a later section. Carbon monoxide binds much more tightly to hemoglobin than oxygen, resulting in a loss of oxygen-carrying capacity for all of the hemoglobin bound to carbon monoxide rather than oxygen. When enough carbon monoxide is bound in the blood, the rapidly increasing oxygen debt in all of the body's tissues ultimately causes death.
Klenner (1971) reported a dramatic success in a case of probable carbon monoxide poisoning. On a cold day an unconscious patient was brought to Klenner's office, and the history was that the person had been found in the cab of his truck with the engine running and the windows closed. Assuming carbon monoxide poisoning, Klenner promptly gave 12,000 mg of vitamin C in a 50 cc syringe by intravenous push through a 20 gauge needle. The patient was awake within 10 minutes and wondering why he was at the doctor's office. He returned to work within 45 minutes.
Klenner (1974) made a further suggestion regarding carbon monoxide poisoning. He noted that victims of house fires, particularly children, frequently die as a result of carbon monoxide poisoning. He suggested that treating patients with any form of smoke inhalation with vitamin C at a dose of 500 mg/kg body weight will immediately negate the toxic effects of the carbon monoxide. Klenner stated that this is an especially desirable intervention to apply early after smoke exposure since some symptoms of "smoke poisoning" can be delayed up to 48 hours.
Although Klenner's observations on the effects of vitamin C on carbon monoxide poisoning are the only ones that I found in the literature, they are still quite dramatic. The clinician should have no doubt that intravenous vitamin C should be generously administered in the treatment of carbon monoxide poisoning, as vitamin C appears to be the clear treatment of choice for this condition.
An endotoxin is one of the toxins associated with the outer membranes of certain bacteria and is released only when the bacteria are disrupted or killed. Endotoxins are not secreted and are generally less toxic than exotoxins, which are secreted as a consequence of microbial metabolism rather than microbial death. De la Fuente and Victor (2001) showed that vitamin C was one of the antioxidants that could protect mouse lymphocytes from endotoxin-induced oxidative stress. Cadenas et al. (1998) showed that increased dietary vitamin C could protect against the endotoxin-induced oxidative injury to guinea pig liver proteins. They also showed that vitamin C inhibited the endotoxin-induced increase in markers of oxidative stress outside of the guinea pig. Rojas et al. (1996) found that endotoxic shock in guinea pigs totally depleted the heart tissue of vitamin C, although vitamin E levels were not affected. They found that vitamin C supplementation completely blocked the elevation of a certain laboratory indicator of increased oxidative stress in the heart. These authors concluded that vitamin C in the heart is a target substance metabolized by enough endotoxin, and vitamin C can have a protective effect against endotoxin-induced free radical damage in the heart tissue. This is especially interesting in light of data linking heart disease to periodontal (gum) disease (Katz et al., 2001; Abou-Raya et al., 2002; Teng et al., 2002), periodontal disease with the presence of endotoxin (Aleo et al., 1974), and increased levels of vitamin C with a lessened incidence of heart disease (Khaw et al., 2001; Simon et al., 2001).
LaLonde et al. (1997) studied rats subjected to excessive liver oxidant stress resulting from third-degree burns. Although a 20% burn did not produce animal death, the addition of endotoxin caused many of the burned animals to die. This was associated with a further decline in laboratory evidence of liver antioxidant defenses. Vitamin C was the antioxidant most depleted in the liver, and its administration along with several other antioxidants prevented animal death.
Endotoxin can have other significant toxic effects. Dwenger et al. (1994) administered endotoxin intravenously to sheep while monitoring a number of laboratory parameters. The administration of vitamin C intravenously before endotoxin was given helped to protect against the elevated lung blood pressures seen with endotoxin alone. Benito and Bosch (1997) found that guinea pigs maintained on low dietary vitamin C were very sensitive to endotoxin. These guinea pigs had no detectable vitamin C in their lungs, and their levels of vitamin E were significantly decreased as well. The researchers concluded that supplemental vitamin C was important in the protection of the lungs against oxidative injury associated with the presence of endotoxin. Similarly, Fuller et al. (1971) were able to show that guinea pigs maintained on minimal vitamin C were very susceptible to shock induced by endotoxin. In the animals that died, the tissue damage was most pronounced in the lungs and heart.
Victor et al. (2002) found that immune cells challenged with endotoxin had lower levels of vitamin C. Victor et al. (2000) looked at the effects of giving vitamin C to mice with endotoxin-induced shock on the function of macrophages, important immune cells. They found that enough vitamin C could essentially normalize macrophage function in the face of substantial endotoxin. Aleo and Padh (1985) looked at fibroblasts, a specialized cell type known to be especially sensitive to the toxicity of endotoxin. They found that endotoxin directly inhibited the uptake of vitamin C by the fibroblasts in a dose-dependent manner. The more endotoxin was present, the less vitamin C ended up inside the cells, where it is needed. This inhibition of vitamin C uptake by endotoxin was similarly demonstrated in adrenal gland cells (Garcia and Municio, 1990). This vitamin C uptake inhibition is particularly significant since it suggests that one of the especially negative effects of endotoxin is to keep adequate amounts of vitamin C from getting into the cells. Such a finding also indicates that achieving a certain level of vitamin C in the blood does not assure its delivery in adequate amounts to some of the tissues when enough endotoxin is already present. In fact, Shaw et al. (1966) found that vitamin C at a dose of only 200 mg/kg body weight did not reduce the lethal effects of a certain dose of endotoxin given to rats. As with so many other toxins and infections, an inadequate or suboptimal dose of vitamin C often has no discernible effect on the clinical outcome. Aleo (1980) also concluded that vitamin C was able to help protect against the endotoxin-induced depression of cell growth. This is a function that is vital to "the recovery and regeneration of connective tissues subjected to the disease process."
The details in the above studies documenting the effectiveness of vitamin C in treating illnesses provoked by bacteria-generated endotoxins serve to demonstrate once again why vitamin C is the ideal agent to be used in nearly all infectious diseases. Vitamin C has already been shown to be highly effective in the treatment of nearly every infectious disease investigated (see Chapter 2). Many advanced infections have their own related toxins and/or toxic effects, and vitamin C appears to be the ideal agent for treating both the infection and associated toxin.
Posts: 654 | Registered: Oct 2003
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Member # 259
My gosh, how I do despise stupid talk like this - whoever you are - Zee! I have heard the word before from others on this board. People like you make me want to shut down my computer and never again type another word on this board.
Vitamin C, without which we do not live very long, is also a superior
Detoxifying Agent for the Brain
Metals are usually locked into the brain cells, after they have been oxidized (= lose their electron(s) of the outer orbits) by the intracellular enzyme catalase. In this form they are firmly bound to proteins or peptides.
Vitamin C delivers a free electron to the intracellular environment. Metal ions become reduced and return to this metallic form. For example, mercury returns from its Hg+ or Hg++ back to Hg0. In this form mercury becomes a gas at room temperature and crosses cell membranes and tissue with no problem. It can therefore leave the cell and get in contact with extracellular proteins, where it loses its electrons again.
From here it is easier for the body to eliminate Hg by usiong the sulfhydryl-group containing amino acids, peptides or proteins (such as glutathione or cysteine) or by using porphyrin-compounds. Hg can be exchanged in the mucous membrane of the gut into vegetable fiber residues inside the fecal matter, etc.
Intravenous Vitamin C is far superior to oral Vitamin C in accomplishing this task.
Of course there are more detox agents for the brain -- Vit C is just one of them and as you can see, it needs other agents to take on additional tasks to finish the job.
Interestingly, Jarosz et al. (11) reported that a high daily dose of vitamin C for 4 weeks (5 g per day) given to H. pylori-infected patients with chronic gastritis resulted in apparent H. pylori eradication in 30% of treated patients. In those patients the highly significant rise in total vitamin C concentration in the gastric juice persisted for at least 4 weeks posttreatment. Vitamin C not only seems to be an antioxidant and a free radical scavenger (17, 21, 26) but also shows antimicrobial activity against H. pylori both in vitro and in a Mongolian gerbil infection model (39).
I think I will discuss and bring it up at the doctors office and now start him on a vitamin C supplement for a while. I don't think it will hurt at this time.
-------------------- Amy Holloway Posts: 255 | From Michigan | Registered: Oct 2005
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I did over 100 of these and it did nothing except cost a bunch of $$. The Vit C in excess can cause problems, esp. with insulin and your own body's response. I'd say small amounts are ok, like 10 grams, and mixed with B vitamins and minerals like Mag sulfate, but the high dose C is no good based on years of experience.
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>>> The Vit C in excess can cause problems, esp. with insulin and your own body's response.
=="Body needs are so great that so called minimal daily requirements must be ignored. A genetic error is the probable cause for our inability to manufacture ascorbic acid, thus requiring exogenous sources of vitamin C"
Found this hope it's usefull. As to why? Absorbtion problems? dunno.
* Klenner, The Journal of Applied Nutrition, 1953
``Vitamin C response when taken by mouth is not predictable... [it is] reported that the scorbutic state could develop even though the patient was taking large doses of vitamin C by mouth ... one of our daughters several years ago ... had contracted chicken-pox. Vitamin C was started on this child ... In spite of the fact that she was given 24 grams every 24 hours there was no interruption in the progress of the disease. Itching was intense. One gram administered intravenously stopped the itch within 30 minutes and she went on to peaceful sleep for the next eight hours. Although feeling fine, a second injection was given at this time, following which there were no new macules and recovery was fast and uneventful. In the past few years we have noted that in chicken-pox when massive injections are employed there [are] no repeating waves of macules, and the usual seven to nine days required for crusting is reduced to less than twenty-four hours.''
Posts: 731 | From Humble,TX | Registered: Feb 2005
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quote:Originally posted by lymie tony z: IMO this is nothing more than voodoo medicine...
Vit C can also prevent absorption of some abx's as well.
I know that xinc can prevent absorbtion of some abx (doxy, for example). Some formulations do combine vit C and zinc. But I never read of or heard before this, of vit C itself causing problems with abx absorption.
That being said, I did try some mega-vit C with lyme. Orally, though; not iv. Maybe I didn't give it long enough (could it have been like a "herx"?), but it seemed to make things slightly worse, if anything-- so I assumed maybe lyme, unlike common colds, was not susceptible to C; maybe spirochetes even liked it, I thought. I did continue to take some C, just not constant super-high doses. It's hard to know what to try, but since succeses have been reported, seems it's worth giving it a try. Be very cautious with i.v. anything, though-- you must have really pure stuff, formulated for iv use, and follow all the cautions you would with other iv stuff. DaveS
Posts: 4567 | From ithaca, NY, usa | Registered: Nov 2000
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Really interesting site about studies done in the 50's with references
One example ``An active case of tuberculosis was treated ... [with] vitamin C intravenously ... with 500 mg. orally [plus] citrus juices. From the start the temperature was reduced and maintained at normal. The cough and expectoration have completely ceased, and a gain in weight of nearly ten pounds has been recorded.
Just wanted to add another thumbs up for IV Vit C. I have had loads of them, and I really think they have made a big difference in clearing lyme pathogens. I get a BIG herx from the IV, and have to sometimes take a break from the weekly dose to slow down the herx, but I really think it has helped to "turn on" immune activity, particularly in my central nervous system.
Vitamin C has already been extensively and unequivocally documented to readily cure a wide range of infectious diseases, including many viral syndromes considered incurable even today (Stone, 1972; Smith, 1988, Levy, 2002). In reviewing a great amount of this information, it becomes apparent that for most infectious diseases, especially viral ones, the only clinical failures of vitamin C appear to occur when a large enough amount of vitamin C cannot be effectively delivered to the invading microorganisms.
With this in mind, then, a more effective dosing and/or delivery system of vitamin C to the various tissues of the body should further improve the clinical efficacy of this agent. In cancer, Riordan et al. (1995) demonstrated the likelihood that vitamin C was an effective anti-tumor therapy as long as high enough concentrations of it could be achieved inside the tumor(s). These researchers also concluded that oral vitamin C supplementation was unlikely to produce blood levels of vitamin C high enough to have a direct killing effect on a given tumor. Later, in studying a certain line of cancer cells and the ability of vitamin C to kill those cancer cells, Casciari et al. (2001) elegantly demonstrated this point. They showed that the rapid intravenous infusion of vitamin C as sodium ascorbate in combination with alpha lipoic acid was effective in reaching vitamin C levels that were toxic to the cancer cells. They also showed that a fat soluble analogue of vitamin C, phenyl-ascorbate, was able to kill cancer cells effectively at a dose roughly three times lower than seen with unaltered vitamin C.
All of the conclusions reached by Casciari et al. noted above support the proposed concept that most clinical failures of vitamin C for infections or other medical conditions relate to inadequate delivery. They administered as much as 60,000 mg of vitamin C over an 80-minute period, a very sizable dose and a fairly rapid administration by most standards of current usage. Yet such a large and rapidly administered infusion of vitamin C will not always be clinically effective. This still does not mean that the vitamin C might not be the optimal treatment for a given condition.
At the Colorado Integrative Medical Center (www.coloradomedicalcenter.com) in Denver, CO, we are starting to use a unique form of vitamin C therapy known as pulsed intravenous vitamin C (PIVC) therapy. First and foremost, this therapy utilizes the principle that the more rapidly a given dose of any nutrient or medication is given, the higher the peak blood level of that substance will be. This very rapid delivery of vitamin C was first reported to be both safe and highly effective by Klenner (1971). In acute barbiturate overdose Klenner gave as much as 42,000 mg of vitamin C "by vein as fast as a 20 gauge needle could carry the flow." This dose awoke the patient and began the reversal of the barbiturate toxicity without causing any side effects of note. Klenner safely administered IV push vitamin C on multiple occasions, often on very critically ill patients, with great clinical success and no reported toxicity.
The concept of PIVC is to get acute blood levels of vitamin C as high as possible. By simple diffusion physiology, an acute doubling or tripling of the blood vitamin C levels will temporarily allow an acute doubling or tripling of the amount of vitamin C that normally diffuses into perfused tissues via the gradient that is present at the baseline concentration. The temporary blood levels achieved can be substantial. If Casciari et al. can get a certain high blood level from infusing 60,000 mg of vitamin C over 80 minutes, then an IV push of 20,000 mg of vitamin C over 2 minutes can be expected to temporarily increase the peak blood concentration by 10-fold or more over the rapid intravenous infusion. This amount has already been administered safely on multiple occasions.
A physiological effect of such a rapid administration of vitamin C appears to occasionally induce an acute hypoglycemia. Sylvest (1942) found that a majority of people given intravenous vitamin C showed a clear lowering of blood sugar. This effect is possibly due to a significant reflex release of insulin from the pancreas. Such a conclusion is directly supported by the work of Cheng et al. (1989), who found that vitamin C injected into rats "produced a dose-dependent and marked hypoglycaemic effect after intravenous injection." They also found that the hypoglycemic effect was maximal at five minutes after injection, coinciding with an increase in the plasma insulin concentration. Vitamin C is a very similar molecule to glucose, and a rapid spike of vitamin C released into the blood likely can induce the same reflex insulin spike that is seen in a glucose tolerance test, where a large dose of glucose is given to evaluate how quickly and effectively one can restore glucose levels to normal by inducing insulin release. Clinically, this hypoglycemic effect has been the most notable in patients who are ingesting little food and drink, and in those patients who are generally sickest, as in advanced neurological conditions. In such patients just an infusion of vitamin C can cause hypoglycemia as well, not requiring the rapid IV push. Such patients may need a bolus of 50% glucose to rapidly reverse the low blood sugar, as it has been noted to occur even when the carrier IV fluid is 5% dextrose (sugar) in water. However, the IV push does seem to more reliably cause the hypoglycemic symptoms, which fits with the animal literature cited above.
This vitamin C-induced hypoglycemia should prove to be a very desirable effect clinically, however. Severe hypoglycemia has already been safely and deliberately induced in a protocol that has been in existence for over 70 years now. Known as insulin potentiation therapy (www.iptq.org), intravenous insulin (roughly 20 to 40 units) is given rapidly to induce hypoglycemia. As hypoglycemia becomes manifest, minidoses of cancer chemotherapeutic agents are administered. Such small doses, in the presence of insulin-induced hypoglycemia, appear to be facilitated in their transport across the cell membrane pathways such that the drugs reach killing concentrations inside cancer cells at much lower dosage levels. Traditional chemotherapy can often be given without causing the otherwise inevitable loss of hair seen with the much larger doses.
Vitamin C and glucose actually directly compete with each other for insulin-mediated transport into the various cells of the body (Washko et al., 1991; Cunningham, 1998). Increased intracellular access should prove to be a major leap forward in the effective treatment of most diseases already known to be responsive to vitamin C, and in likely quite a few more diseases that just need more effective dosing of vitamin C to show a positive response. Proprietary protocols being developed at the Colorado Integrative Medical Center are using such "Vitamin C-Enabled Intracellular Nutrition" (VEIN) methodologies.
A side effect associated with high doses of vitamin C, along with other nutrients given intravenously, and sometimes associated with concomitant hyperbaric oxygen therapy, has been noted at our facility. On three occasions patients have complained of bilateral mid-back discomfort. When this has been reported, further intravenous nutrients are discontinued, oral hydration and intravenous hydration are initiated, and oral or intravenous furosemide is given. This has resolved the discomfort in all circumstances. No associated abnormal laboratory findings have been seen to result. It is hypothesized that when the solute load gets high enough in the blood perfusing the kidney, a dehydrating effect is acutely inflicted on the kidney cells, causing the pain/discomfort reflex. Neglected, more serious complications could occur. However, the regimen just outlined takes care of such situations fairly promptly. Furthermore, such a side effect can actually give the health care practitioner a practical point beyond which further intravenous nutrition should not be pushed acutely.
Anecdotally, I have had the occasion to clinically cure a case of acute Lyme disease with three days of intravenous vitamin C therapy. Whether this is readily repeatable, or whether a chronic case of Lyme disease would respond as well remains to be seen. At the Colorado Integrative Medical Center we are now initiating a combination of therapies including those mentioned in this newsletter to see precisely how much success we can have on a regular basis with this particular disease. We are presently accepting new patients at this time who have this condition and are looking for another treatment option.
Contact Information: Colorado Integrative Medical Center 1260 South Parker Road Denver, CO 80231 Toll-free: 866-750-2121 FAX: 303-750-4992 Ask for Darren Green, office manager
Casciari, J., N. Riordan, T. Schmidt, X. Meng, J. Jackson, and H. Riordan. (2001) Cytotoxicity of ascorbate, lipoic acid, and other antioxidants in hollow fibre in vitro tumours. British Journal of Cancer 84(11):1544-1550. Cheng, J., S. Hsieh-Chen, and C. Tsai. (1989) L-Ascorbic acid produces hypoglycaemia and hyperinsulinaemia in anaesthetized rats. The Journal of Pharmacy and Pharmacology 41(5):345-346. Cunningham, J. (1998) The glucose/insulin system and vitamin C: implications in insulin-dependent diabetes mellitus. Journal of the American College of Nutrition 17(2):105-108. Klenner, F. (1971) Observations on the dose and administration of ascorbic acid when employed beyond the range of a vitamin in human pathology. Journal of Applied Nutrition 23(3&4):61-88. Levy, T. (2002) Vitamin C, Infectious Diseases, and Toxins: Curing the Incurable. Philadelphia, PA: Xlibris Corporation. (www.xlibris.com) Riordan, N., H. Riordan, X. Meng, Y. Li, and J. Jackson. (1995) Intravenous ascorbate as a tumor cytotoxic chemotherapeutic agent. Medical Hypotheses 44(3):207-213. Smith, L. (1988) The Clinical Experiences of Frederick R. Klenner, M.D.: Clinical Guide to the Use of Vitamin C. Portland, OR: Life Sciences Press. Stone, I. (1972) The Healing Factor: "Vitamin C" Against Disease. New York, NY: Grosset & Dunlap. Sylvest, O. (1942) The effect of ascorbic acid on the carbohydrate metabolism. Acta Medica Scandinavica 110:183-196. Washko, P., D. Rotrosen, and M. Levine. (1991) Ascorbic acid in human neutrophils. The American Journal of Clinical Nutrition 54(6 Suppl):1221S-1227S.
Copyright 2003 by Thomas E. Levy, M.D., J.D. All Rights Reserved; Reproduction Permitted only with Acknowledgement and of the Entire Document
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Cancer: Why intravenous vitamin C may be the next big thing Thirty years ago cancer researchers thought they might be on to something big. Their ambitious theory: Vitamin C in high doses might kill cancer cells.
The problem was absorption. When vitamin C is taken orally, the intestines can absorb only so much. When the saturation point is reached, further mega-doses are meaningless. Absorption isn't an issue when C is administered intravenously, but apparently the technology wasn't developed enough in the 1970s to assess the effects of intravenous vitamin C on cancer cells.
Three decades later, scientists at the US National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) took up the cold case and made a startling discovery.
Intravenous vitamin C is readily absorbed Could there actually come a time when intravenous chemotherapy is supplemented with, or in some cases replaced by intravenous vitamin C?
By mainstream medicine standards we're a long way from such a day, but we're a little bit closer thanks to NIDDK researchers who published a new vitamin C study earlier this month in the Proceedings of the US National Academy of Sciences.
While studying recommended daily intake levels of vitamin C, the NIDDK team realised that intravenous administration of C solved the absorption problem of oral intake. Lead researcher, Dr Mark Levine told HealthDay News that 10 grams of intravenous C prompts blood levels of the vitamin that are more than 25 times higher than that achieved when C is administered orally.
This is where researchers reopened the case that was discontinued in the 70s.
When 10 types of cancer cells and four types of normal cells were exposed to a vitamin C dose of less than four millimoles (easily obtainable intravenously), in five of the cancer cell types, about half of the cells were either killed or apoptosis (cell "suicide") occurred. Also, C exposure almost completely halted the growth of surviving cells.
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All of this would be for nothing, of course, if any damage was done to the normal cells tested, but these cells were completely unaffected.
Levine and his NIDDK team can't explain what mechanisms produced these results, but theorised that the high concentration of C prompted the formation of hydrogen peroxide (HP), which is known to kill cells. In this case the healthy cells may have repaired any HP damage, while the cancer cells may have been more vulnerable.
C's huge healing potential Writing in the Proceedings of the National Academy of Sciences, the NIDDK researchers concluded: "These findings give plausibility to IV ascorbic acid in cancer treatment, and have unexpected implications for treatment of infections where hydrogen peroxide may be beneficial."
"Plausibility" means we still have a long way to go down the research path before anyone can unconditionally state that high doses of intravenous vitamin C can fight cancer. But the last part of that quote indicates a potential for high doses of intravenous C as a multi-purpose treatment.
US HSI Panellist Dr Allan Spreen had this to say about the pioneering efforts of Fredrick R. Klenner, who did intravenous C research many decades ago:
"Dr Fred Klenner was using intravenous ascorbic acid (vitamin C) against viruses, serious bacteria and even toxins such as snakebites as early as the 1930s. His patient records showed amazing successes, witnessed by hospital personnel, while most outsiders (who refused to review his data) labelled him a quack. Those who did, such as Drs. Jungeblut and Zwerner, Otani, Ormerod, and others, all came away impressed that his work was both accurate and therapeutic. He treated diphtheria, whooping cough and tetanus, and in the middle of a polio epidemic in North Carolina he was considered to have 'cured' 60 out of 60 cases of infantile polio."
Could C by IV turn out to be the "wonder drug" of the 21st Century? You can be sure I'll report to you on any further studies.
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Posts: 654 | Registered: Oct 2003
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Frequent Contributor (1K+ posts)
Member # 3662
Well i am looking...
Vit C is readly absorbed in the stomach. When a certain threshold is reached it is excreted by the kidneys. This is known as fact.
I think it is a lot cheaper to take the Vit C orally in increasing dose and watch for it in the urine. Once you have reached that point increased doses will not do anything as it all spills out.
On the other hand, IV vit C provides a much higher peak dose as it takes time to be eliminated by the kidneys. During that time there are a number of oxidation and enzimatic reactions that can occur in the blood. These likely do not occur via the oral route so there may be something else happening during that time. BUT if this is the case, then it is not the effect of ascorbic acid (vit C) in the normal physilogical sense it is more a chemical reaction that is occuring between the blood, tissue and the ascorbic acid, and there can be a lot.
There is also the matter of how the ph is adjusted to make it infusable via IV. Pure ascorbic acid cannot be infused directly. So how this is done also may have some bearing.
So as far as the the use of vitamin C IV vs oral form as far as the "vitamin" aspect goes I still remain unconvinced that there is a diference. As a chemotherapy agent, I would say , yes there is a possible difference.These two methods are however not the same and the long term (and short term) effects are in no way known nor understood.
So as far as I am concerned, I would categorize vitamin C IV in the same group as peroxide infusions.. some like them some don't but I would not do it, at least until there is some explanation as to why it might work.
Posts: 1184 | From north america | Registered: Feb 2003
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Personally I take a small dose of Salt/vit C. He wants to promote his own supplement. Not sure about it.
Issue No. 9 June, 2005
The Many Faces of Vitamin C
A question that has been presented to me numerous times since the publication of my book, Curing the Incurable: Vitamin C, Infectious Diseases, and Toxins, is "What kind of vitamin C should I take, and why?" It is a very good question, indeed, as the variable effects on both short-term and long-term clinical outcomes can be dramatic.
It should first be emphasized that all of the forms of vitamin C share the characteristic of having a positively-charged cation and a negatively-charged anion in the dissolved form. Ascorbic acid is the hydrogen ion with the ascorbate anion; sodium ascorbate is the sodium ion with the ascorbate anion; calcium ascorbate is the calcium ion with the ascorbate anion; and so on. It is now readily apparent that all forms of vitamin C share the characteristic of having the ascorbate anion. In fact, it is the ascorbate anion that is the electron-donating, clinically active portion of all vitamin C preparations. However, the companion cations can have significant biological impacts as well, and this needs to be considered when choosing the best forms of supplementation for both short-term and long-term needs.
The lion's share of all forms of vitamin C come as mineral ascorbates. The most common mineral ascorbates used in vitamin C supplementation include the following:
Sodium ascorbate is probably the best and certainly the least expensive of the mineral ascorbates for regular supplementation at relatively high doses (six grams or more daily). Many doctors and patients fear the regular dosing of sodium, however, due to the long- standing medical admonition to minimize sodium intake, especially for hypertension and cardiac failure patients. Indeed, sodium chloride (table salt) has long been known to facilitate fluid retention (increased plasma volume), a state that directly aggravates hypertension and heart failure. However, it appears that only sodium really results in significant fluid retention when administered with the chloride anion. Sodium when given with the anions citrate, ascorbate, or bicarbonate does not appear to adversely affect hypertension or to increase blood volume. Because of these findings, it has been directly suggested that the concept of "sodium-dependent" hypertension should be changed to "sodium chloride-dependent" hypertension (Kurtz and Morris, 1983; Kurtz et al., 1987). Anecdotally, I have never found multi-gram doses of sodium ascorbate to adversely affect blood pressure or blood volume status. However, since there always appear to be exceptions to every rule in biology, anyone who notices elevated blood pressures or ankle edema after high doses of sodium ascorbate would probably be well-advised to supplement with a different form of vitamin C.
Calcium ascorbate is currently a very popular form of vitamin C supplementation. In addition to being directly labeled as calcium ascorbate, this form of vitamin C is also marketed as an "ester" form of vitamin C or a "buffered" form of vitamin C. Much of the popularity of this form of vitamin C comes from the fact that many people are looking for extra sources of calcium on a daily basis in addition to taking their vitamin C. With some minor variability, these products typically deliver approximately 100 mg of calcium for every 800 to 900 mg of ascorbate given. Also, the 100 mg or so of calcium with each gram of product usually has a very high degree of absorption when compared to other common forms of calcium supplementation, such as calcium chloride or calcium bicarbonate (Tsugawa et al., 1999).
However, the calcium-delivering properties of calcium ascorbate are precisely the best reasons for avoiding this product. Although it appears from the early work of Weston A. Price, D.D.S. that acutely raising the ionic calcium levels in the blood can greatly improve the acute phases of healing in damaged tissues, this does not address what the long-term consequences of calcium administration may entail. In fact, it appears that the bulk of the scientific data supports the concept that the vast majority of the older population is massively overdosed on calcium and legitimately suffering from calcium toxicity. We continue to be stressed with warnings of increased risk of osteoporosis while the data clearly shows that most deaths in patients with osteoporosis relate to the vascular system and not the bones (Kruger and Horrobin, 1997). Furthermore, excess calcium in the coronary arteries, one marker of long-term calcium overdosage, is also directly correlated to increased risk of heart attack (Raggi et al., 2003), increased incidence of chronic degenerative disease (Arad et al., 2001; Christian et al., 2003; Kiryu et al., 2003; Wong et al., 2003), and increased degree of overall "all-cause mortality" (Shaw et al., 2003).
So, if you are a older chronic calcium supplement taker, just be aware that there are negatives to this practice. The chance of dying from an osteoporotic fracture doesn't remotely approach the chances of dying from a heart attack, cancer, or another chronic degenerative disease. Furthermore, it is far from clear that the traditional treatment approach to osteoporosis significantly affects the likelihood of a subsequent fracture. The scientific evidence, however, is very clear that supplemental calcium often fuels the progression of atherosclerosis, with the expected increased chance of heart attack.
If the above does not convince you that supplemental calcium, with very rare exceptions, should be completely avoided, at least start tracking your calcium accumulations. The coronary artery CAT scan should show no calcium. Check it. Your heart should not be calcifying. Check your ECHOcardiogram. Hair analysis should not show excess calcium. Check it. If any or all of these tests are positive for calcium, you should be especially concerned about dumping still more supplemental calcium into your blood and body on a daily basis.
Magnesium ascorbate is another significant mineral ascorbate. Unlike the other mineral ascorbates (except for sodium ascorbate) it is very difficult to overdose on this form of ascorbate. This is because the magnesium cation is very bioavailable and very effective in reversing the damage done by excess calcium, a condition shared by most older individuals. Bioavailable magnesium (as ascorbate or as magnesium- amino acid chelates; NOT the commonly taken magnesium oxide form) is very effective in mobilizing abnormally deposited calcium throughout the body. As such, it is one of the most effective (and still least utilized) treatments available for osteoporosis.
While there is nothing wrong with taking large amounts of magnesium ascorbate, it is more economical to take large doses of bioavailable magnesium and sodium ascorbate separately to obtain the optimal effects of both these supplements.
Potassium, manganese, zinc, molybdenum, and chromium ascorbates are additional mineral ascorbates. All of the cations are desirable as supplements, but they can be easily be overdosed if they are used to deliver multi-gram doses of ascorbate.
Ascorbyl palmitate is another form of vitamin C that is somewhat unique in that it has both water-soluble and fat-soluble qualities. It is touted by some as a superior delivery form of vitamin C as ascorbate into the body. This has not really been clearly proven, and even if it were, ascorbyl palmitate would be a very expensive way to provide daily multi-gram doses of ascorbate. The fat-soluble qualities of ascorbyl palmitate do make it a good form of vitamin C to include in various skin creams and other dermatological preparations.
Liposomes were first proposed as a unique drug delivery system approximately 35 years ago (Bangham, 1995; Gregoriadis, 1995). One of the primary reasons for utilizing a liposome-encapsulation delivery system is to assure a near complete absorption of the encapsulated nutrient or drug into the bloodstream. The physical qualities of the liposome also eliminate the need for digestive activity before absorption.
Anecdotally speaking, I have taken a liposome-encapsulated form of ascorbate and found that it is virtually impossible to induce the "C- flush" effect that can be seen with large enough doses of the mineral ascorbates, most commonly sodium ascorbate and calcium ascorbate. Furthermore, it appears that the enhanced absorption along with the phospholipid dose absorbed at the same time has uniquely positive clinical benefits.
My Current Recommendations
For the reasons mentioned above, I never recommend the regular ingestion of vitamin C as calcium ascorbate. The remaining mineral ascorbates are acceptable forms of vitamin C supplementation, but one can risk overdosing the cations if multi-gram doses of these forms of vitamin C are taken, with the exceptions of the sodium and magnesium ascorbates.
For regular daily supplementation, sodium ascorbate is an economical, well-tolerated form of vitamin C. While many wish to avoid the "C- flush" effect, it appears to be a very good way to keep the gut relatively detoxified and clean. For those wishing to have a near- complete absorption of their vitamin C dose, the liposome- encapsulated form of vitamin C is optimal.
For acute infectious and toxic states, I still recommend getting intravenous sodium ascorbate, usually at doses of 50 grams or more over several hours for most individuals. However, I would also recommend adding the liposome-encapsulated form of vitamin C orally at the same time. If the intravenous sodium ascorbate is not available, I recommend taking sodium ascorbate to bowel tolerance, and then taking the liposome-encapsulated form of vitamin C, several grams hourly, guided by symptoms and clinical response to determine subsequent dosing.
Arad, Y., D. Newstein, F. Cadet, M. Roth, and A. Guerci (2001) Association of multiple risk factors and insulin resistance with increased prevalence of asymptomatic coronary artery disease by an electron-beam computed tomographic study. Arteriosclerosis, Thrombosis, and Vascular Biology 21(12):2051-2058. Bangham, A. (1995) Surrogate cells or Trojan horses. The discovery of liposomes. Bioessays 17(12):1081-1088. Christian, R., D. Dumesic, T. Behrenbeck, A. Oberg, P. Sheedy, and L. Fitzpatrick (2003) Prevalence and predictors of coronary artery calcification in women with polycystic ovary syndrome. The Journal of Clinical Endocrinology & Metabolism 88(6):2562-2568. Gregoriadis, G. (1995) Engineering liposomes for drug delivery: progress and problems. Trends in Biotechnology 13(12):527-537. Kiryu, S., V. Raptopoulos, J. Baptista, and H. Hatabu (2003) Increased prevalence of coronary artery calcification in patients with suspected pulmonary embolism. Academic Radiology 10(8):840-845. Kruger, M. and D. Horrobin (1997) Calcium metabolism, osteoporosis and essential fatty acids: a review. Progress in Lipid Research 36(2- 3):131-151. Kurtz, T. and R. Morris, Jr. (1983) Dietary chloride as a determinant of "sodium-dependent" hypertension. Science 222(4628):1139-1141. Kurtz, T., H. Al-Bander, and R. Morris, Jr. (1987) "Salt-sensitive" essential hypertension in men. Is the sodium ion alone important? The New England Journal of Medicine 317(17):1043-1048. Raggi, P., B. Cooil, L. Shaw, J. Aboulhson, J. Takasu, M. Budoff, and T. Callister (2003) Progression of coronary calcium on serial electron beam tomographic scanning is greater in patients with future myocardial infarction. The American Journal of Cardiology 92(7):827- 829. Shaw, L., P. Raggi, E. Schisterman, D. Berman, and T. Callister (2003) Prognostic value of cardiac risk factors and coronary artery calcium screening for all-cause mortality. Radiology 228(3):826-833. Tsugawa, N., T. Yamabe, A. Takeuchi, M. Kamao, K. Nakagawa, K. Nishijima, and T. Okano (1999) Intestinal absorption of calcium from calcium ascorbate in rats. Journal of Bone and Mineral Metabolism 17 (1):30-36. Wong, N., M. Sciammarella, D. Polk, A. Gallagher, L. Miranda-Peats, B. Whitcomb, R. Hachamovitch, J. Friedman, S. Hayes, and D. Berman (2003) The metabolic syndrome, diabetes, and subclinical atherosclerosis assessed by coronary calcium. Journal of the American College of Cardiology 41(9):1547-1553.
Copyright 2005 by Thomas E. Levy, MD, JD All Rights Reserved; Reproduction Permitted only with Acknowledgement and of the Entire Document
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