www.tomlevymd.com

[Guest guest]

Thank you very much for posting these on vitamin C. I have taken as much as

30 grams a day orally without reaching bowel tolerance.....

Vitamin C is in my primary arsenal.

mjh

[Guest guest]

CHAPTER 3

THE ULTIMATE ANTIDOTE

" Science commits suicide when it adopts a creed. "

Huxley

Overview

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

(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

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

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.

Endotoxin

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 ( 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.