CHAPTER 3 (the first part)


"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.


Alcohol (Ethanol)

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

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.