Cholesterol and Vitamin C Deficiency Research
Abnormal levels and types of fats in the blood play a role in the development of atherosclerosis.
Known as Dyslipidemia, the most common type known to the public (and doctors) is the elevation of blood cholesterol levels. Cholesterol levels high enough result in the increased development of atherosclerosis, but such levels of cholesterol are not typically the initiators of the atherosclerotic process.
Instead, cholesterol is just one of a number of substances that will readily deposit in an area of the artery where atherosclerosis has already begun. Other types of blood fat, such as triglycerides, chylomicrons, and some lipoproteins, can also promote atherosclerosis when they exist in high enough concentrations in the blood.
Multiple trials have demonstrated that lowering the cholesterol level through medical, dietary, or surgical means decreases the incidence of coronary heart disease and the chance of death (heart attack) from it (Leren, 1970; Coronary Drug Project Research Group, 1975; Carlson et al., 1977; Lipid Research Clinics Pro gram, 1984; Frick et al., 1987; Dorr et al., 1978; Buchwald et al., 1990; Brophy et al., 2005).
Unfortunately, all this research on lowering cholesterol has caused medical professionals and the public to designate cholesterol elevation the primary, leading role as the cause of heart disease. Cholesterol only adds to the development of atherosclerosis after the process has been started by degenerative arterial changes taking place because of a deficiency in Vitamin C.
Simultaneously, as we will demonstrate, toxins left unneutralized due to a Vitamin C deficiency are also a primary reason why serum cholesterol levels are higher, with their greater likelihood of depositing in areas of developing atherosclerosis. Furthermore, the excess toxicity that is often associated with elevated cholesterol levels has its own direct and indirect effects in the causation of atherosclerosis.
Vitamin C deficiency can cause cholesterol accumulation in heart arteries even when cholesterol was not added to the diet.
Ginter (1978) found that Vitamin C deficiency alone in guinea pigs would result in the development of atherosclerosis. Under conditions of Vitamin C deficiency, he noted that cholesterol and triglycerides accumulated in the aorta, even without adding cholesterol to the diet. These changes were found to lead to a fairly classic picture of fully developed atherosclerosis. Willis (1953) had also documented that deficient dietary Vitamin C could be the sole reason for the development of atherosclerosis in guinea pigs. Willis asserted that the atherosclerotic lesions in the guinea pig, simply deprived of sufficient Vitamin C intake, appeared physically identical deficiency in form and structure to those lesions seen in human atherosclerosis. Willis also found that when the guinea pigs were fed increased amounts of cholesterol, injected Vitamin C demonstrated a protective effect against the development of atherosclerosis.
Similarly, Datey et al. (1968) found that Vitamin C administration reduced the incidence and severity of atherosclerosis in rabbits fed a diet high in cholesterol and hydrogenated fat. Ginter further noted that the simultaneous intake of additional cholesterol by the Vitamin C-deprived guinea pigs did accelerate the development of atherosclerosis. It would appear from this evidence that the arterial changes that result from Vitamin C deficiency make it easier for cholesterol and fats, whether elevated in the blood or not, to deposit in the blood vessel walls.
Administration of Vitamin C reduces incidence and severity of atherosclerosis in cholesterol-fed animals.
Duff (1935) noted that elevated cholesterol levels alone were unlikely to result in atherosclerosis. Rather, he proposed that “local alterations” in the blood vessel walls were necessary to allow the deposition of cholesterol there.
This predisposition for cholesterol deposition involves the chemistry of the basement membrane in which the endothelial cells of the artery are embedded. When enough Vitamin C is present, the basement membrane is well polymerized and gel-like, and when a significant Vitamin C deficiency is present, the basement is poorly polymerized and watery. A watery basement membrane, secondary to Vitamin C deficiency, appears necessary for any cholesterol or fat deposition to take place in this area of the blood vessel wall.
Cholesterol deposition in the arteries does not begin unless there Is a prior injury to the blood vessel.
Duff also noted that some form of injury to the blood vessel was needed to initiate cholesterol deposition. Whenever an area of the blood vessel is injured to any degree, this is usually accompanied by at least a localized deficiency of Vitamin C.
Willis and Fislunan (1955) found that localized depletions of Vitamin C were typically found in segments of arteries subjected to increased mechanical stress, which is a form of injury. This localized vita min C deficiency can then allow the early cholesterol deposition in atherosclerosis to proceed in a localized, focal manner in the affected basement membrane areas of the blood vessel wall.
Taylor et al. (1957) showed that a deliberate freezing injury to the artery in monkeys with high cholesterol levels appeared to “telescope into a few weeks” the development of atherosclerotic lesions that took several years to develop in humans. Although it was not measured, it would be reasonable to assume that the injured artery quickly became depleted of Vitamin C as well.
Even today many clinicians and researchers consider atherosclerosis to be a “one-way” or irreversible process. Multiple researchers have demonstrated otherwise. Without addressing the Vitamin C status, Taylor .et al. (1961) found that cholesterol and fats are taken up by the blood vessel walls when serum cholesterol levels exceed 250 mg% (milligrams per 100 milliliters), and that they are “apparently resorbed” back from the blood vessel walls when serum cholesterol levels are below 200 mg%.
Cholesterol deposits in blood vessels shown to be reabsorbed by blood when blood level of cholesterol is below 200.
Horlick and Katz (1949) were able to show that atherosclerotic lesions induced in chicks by excessive cholesterol feeding were noted to clearly regress when the cholesterol feeding was discontinued. Since the chick is one of the great majority of animals that synthesizes its own Vitamin C, internal Vitamin C production may well be accelerating the resolution of the arterial lesions. Horlick and Katz noted a range of responses, with some lesions showing less stainable fat but more fibrosis when cholesterol feeding was discontinued, indicating advanced atherosclerotic lesions would not completely resolve under such circumstances. However, they also noted some animals that demonstrated virtually a “complete remission” of the atherosclerotic changes, whether viewed grossly or microscopically.
Anitschkow (1928 and 1933), one of the first investigators to look at the response of arterial lesions to the cessation of cholesterol feeding (in rabbits), de scribed a gradual loss of lipids (fats) from atherosclerotic plaques. He also emphasized that the process was slow, noting that the evolution of a lipid-rich plaque into a plaque composed primarily of fibrous tissue took two to three years.
Interestingly, however, Horwitz and Katz noted that the rate of regression of lesions in the chicken was much greater than in the rabbit. This observation could possibly relate to the amounts of Vitamin C available during the healing period, as all animals that can make their own Vitamin C do not do so with equal efficiency. Undoubtedly, the amount of Vitamin C available to the blood vessel wall, how far advanced the atherosclerotic lesion is and how much circulating cholesterol and fats are present in the blood are all significant determinants as to both the reversibility of the lesion and the length of time needed to achieve that reversibility.
Wilens (1947) was also able to indirectly help to demonstrate the importance of lipid and cholesterol levels in the maintenance of atherosclerotic disease of the blood vessels. In autopsy examinations, he was able to demonstrate that there was a “high incidence of severe atherosclerosis” in obese individuals, who often have higher lipid and cholesterol levels. Conversely, with individuals who had been subjected to “protracted undernutrition” even moderate changes of atherosclerosis were “seldom observed”. Lipid and cholesterol levels will typically drop in such individuals.
While such a study does not address the role of Vitamin C in such undernourished individuals, it does indicate that starvation will tend to pull cholesterol and lipids back out of atherosclerotic plaques. This finding alone clearly demonstrates that atherosclerosis is not irreversible.
Indeed, in radioactive isotope research on the atherosclerotic lesions of rabbits, cholesterol already present in the lesions has been demonstrated to be subject to continuous turnover, far from a simple static, cumulative process (Newman and Zilversmit,1962).
Vitamin C retards penetration of cholesterol into blood vessels and increases release of cholesterol already present in those vessels.
Zaitsev et al. (1964) also looked at the movement of radioactively-tagged cholesterol in rabbits. They found that the effects of Vitamin C on atherosclerosis resulted in less cholesterol penetration into the blood vessel along with increased release of cholesterol al ready in the blood vessel.
NOTE: In order to fully appreciate much of the animal research on atherosclerosis, it is also critical to realize that animals can be induced to develop atherosclerosis by a mechanism and sequence not usually seen in humans. Lindsay and Chaikoff (1966) noted that atherosclerosis experimentally induced in animals without the assistance of a Vitamin C deficiency evolved quite differently from human atherosclerosis.
However, they also noted that the atherosclerotic changes in the blood vessels of certain primates having the disease naturally were “similar, if not identical” to those changes seen in man. Lindsay and Chaikoff also noted that the degree of cholesterol infiltration in the blood vessels of primates is generally less than that seen in man. These differences can be readily explained by the greater toxin loads generally faced by man, such as from dental sources (Huggins and Levy, 1999), with corresponding higher chronically circulating cholesterol levels.
This correlation between toxins and elevated cholesterol levels will be discussed later. Also, the primates as a group ingest much more Vitamin C in their diets than humans as a group. Furthermore, Lindsay and Chaikoff noted that the naturally occurring form of atherosclerosis in animals had substantial microscopic differences compared to the artificially induced forms of atherosclerosis provoked by various efforts to increase blood cholesterol and other blood fats.
Lindsay and Chaikoff also noted that the natural form of atherosclerosis was initiated by a degenerative change in the intima of the blood vessel wall, followed secondarily by a proliferative fibrotic reaction. In other words, the initial change, degeneration, is itself an arterial stress that results in the compensatory response of cellular proliferation and fibrosis. This is the same sequence of events seen with the chronic depletion of Vitamin C.
However, in the cholesterol-feeding forms of induced atherosclerosis, the “overdose” of cholesterol results ln immune cells (macrophages) in the blood vessel walls taking up the excess cholesterol. Since a high enough level of cholesterol seems to have its own toxicity (Ginter, 1975), this macrophage response is very possibly a compensatory immune-mediated response to lessen the acute toxicity of the excess cholesterol. After enough of these macrophages have taken up enough cholesterol, this excessive presence of stuffed macrophages is also interpreted by the body as another arterial stress, and a proliferation of cells with secondary fibrosis ca..t.J,.en result.
Mann et al. (1953) induced such lesions in cholesterol-fed monkeys. Basically, the abnormal amounts of cholesterol have to go somewhere, and the endothelial surfaces of the arterial walls are the first areas contacted. In fact, Shaffer (1970) noted that such cholesterol feeding to experimental animals is accompanied by “extreme” depositing of cholesterol and lipids throughout the body, not just in the blood vessels. And in Vitamin C-supplemented rabbits, Beetens et al., (1984) were able to demonstrate, after only a few weeks of a cholesterol rich diet, a clearly lessened degree of intimal thickening and lipid infiltration.
Animals fed high doses of cholesterol show rapid reductions of Vitamin C in plasma and cells.
High doses of cholesterol, in exerting the toxic effects described by Ginter (1975), appear to rapidly metabolize Vitamin C just like any other toxin or toxic effect. Dent et al. (1951) were able to demonstrate that feeding cholesterol to rabbits and other animal results in a drop in the Vitamin C levels in both plasma and cells. Booker et al. (1957) achieved a similar depression of the Vitamin C levels in rabbits and guinea pigs given a continual administration of cholesterol.
These findings seem to indicate that the technique of overfeeding cholesterol to laboratory animals also serves to promptly induce a Vitamin C deficiency as well. This rapidly induced Vitamin C deficiency allows the basement membrane behind the endothelial cells to allow or facilitate the deposition of the cholesterol and blood fat as the glycoproteins degenerate and the consistency becomes watery. In any event, the atherosclerosis that is eventually developed through either “natural” or artificial mechanisms is comparable enough that the results of animal atherosclerosis experimentation can generally be used to help understand human atherosclerosis.
Vitamin C interacts with and affects cholesterol metabolism in a number of ways. Turley et al. (1976) reviewed the literature and concluded that chronic but latent Vitamin C deficiency leads to increased blood levels of cholesterol. Ginter (1973) found that high levels of Vitamin C lower the cholesterol concentration in both the serum and the liver in guinea pigs. Sitaramayya and Ali (1962) also found that in both rats and guinea pigs the administration of Vitamin C prevented the cholesterol level in the blood from increasing after cholesterol feeding.
Ginter (1975a) and Ginter et al. (1971) also found in guinea pigs that low levels of Vitamin C reduce the rate of metabolic transformation of cholesterol into bile acids, its principal breakdown product, leading to in creased levels of cholesterol.
In rabbits, Sadava et al. (1982) were able to show that supplemental Vitamin C can protect against elevated blood cholesterol even when cholesterol is administered by injection to rabbits.
Banerjee and Singh (1958) found that scurvy-stricken guinea pigs had a significant increase in total body cholesterol levels, again reflecting the pivotal role of vitamin C in maintaining normal cholesterol metabolism. Maeda et al. (2000) similarly found that mice rendered unable to synthesize Vitamin C, effectively a “guinea pig equivalent,” demonstrated higher total cholesterol levels and lower HDL-cholesterol levels with lower plasma Vitamin C levels.
Relatively low daily doses of Vitamin C for 47 days significantly reduced cholesterol levels in humans tested.
Cholesterol levels and Vitamin C levels appear similarly related in man. Ginter et al. (1970) gave only 300 mg of Vitamin C daily for 47 days to a group of individuals over 40 years of age. A significant decrease in cholesterol levels was seen, and the effect was especially pronounced in individuals with cholesterol levels above 240 mg%. These individuals had an average drop of 34 mg% in their levels.
Ginter et al. (1977) later showed that 1,000 mg of Vitamin C daily for a full year had a comparable effect on cholesterol levels. Ginter et al. (1978) also looked at diabetic patients and found that 500 mg of Vitamin C daily over the course of a year resulted in striking cholesterol drops, ranging from 40 mg% to 100 mg% in a majority of the patients.
Another dietary fat, triglycerides, also showed a moderate decline with the Vitamin C administration given to Ginter’s patients just noted above. The metabolism of triglycerides is also subject to some regulation by Vitamin C.
Immediately after eating, the plasma will often be clouded by an increased content of triglycerides. Lipoprotein lipase (LPL), an enzyme also known as the clearing factor, serves to promptly metabolize these triglycerides and clear the clouded plasma.
Most patients taking 3,000 mg of Vitamin C/day increased LPL levels by 100% and decreased triglyceride levels by 50% to 70%.
Sokoloff et al. (1966) found that Vitamin C not only lowered the levels of cholesterol and triglycerides in rabbits and rats with high cholesterol levels, it also enhanced the activity of LPL (the clearing factor) while minimizing the development of atherosclerotic lesions. They also demonstrated that in 50 of 60 patients with increased cholesterol levels and I or heart disease 2,000 to 3,000 mg of Vitamin C daily increased the average LPL activity by 100% and decreased the average triglyceride level by 50% to 70%. As Weinhouse and Hirsch (1940) demonstrated that cholesterol is not the only fatty substance that accumulates in atherosclerotic plaques, it would seem that the favorable effects that Vitamin C has on the activity level of LPL also plays an integral role in minimizing or reversing the development of atherosclerotic lesions.
THE IMPORTANT TOXIN-FIGHTING ABILITIES OF CHOLESTEROL
Vitamin C also relates to cholesterol levels in the body in another extremely important although indirect fashion. The scientific literature reveals an abundance of evidence indicating that cholesterol serves as a primary neutralizer or inactivator of a wide array of toxic substances in both animal and human studies (Figueiredo et al., 2003; Park et al., 2005).
Alouf (1981 and 2000) reported the ability of cholesterol to neutralize a large number of different bacterial toxins capable of causing direct cellular damage. Chi et al. (1981) published data that indicated elevated serum cholesterols seemed to be a marker of, if not a direct response to, a variety of toxic exposures.
Cholesterol neutralizes a large number of bacterial toxins capable of causing direct cellular damage.
Watson and Kerr (1975) noted that the cell membrane-bound cholesterol in the arterial walls could not only bind bacterial toxins, it could also end up being a focus of reactive immune activity and act as one more agent promoting atherosclerotic damage.
Increased toxic pesticide exposures have been noted to correlate with increased cholesterol levels in the population of people exposed (Bloomer et al., 1977). Similarly, in rabbits exposed to lead, Tarugi et al. (1982) found a “striking elevation” of cholesterol to result. Yousef et al., (2003) showed that aflatoxin exposure increased cholesterol levels in rabbits, and that Vitamin C administration significantly lowered those cholesterol levels and clinically alleviated the harmful effects of the exposure.
Exposure to toxins and pesticides increases cholesterol levels.
Finally, Huggins and Levy (1999) have repeatedly observed significant drops in serum cholesterol levels in patients who have had mercury amalgams, root canals, and other sources of heavy metal and infective toxicity removed from their mouths.
Patients show significant serum cholesterol reductions after removal of dental toxicity.
Overall, then, it appears that one of cholesterol’s many functions in the body is that of a relatively nonspecific toxin neutralizer and/or inactivator. Because of this role, cholesterol levels appear to be routinely elevated in conditions of increased toxin exposure, representing another of the body’s compensatory mechanisms that, left unchecked, can cause its own significant harm by accelerating atherosclerosis.
The toxin-inactivating effects of cholesterol notwithstanding, Vitamin C still appears to be the ultimate toxin neutralizer and inactivator. When higher levels of Vitamin Care present to neutralize whatever toxins are present, cholesterol levels will not have to rise (and do not rise) in order to protect against those toxins. The cholesterol levels will end up remaining in the normal range. However, chronically low cholesterol levels generally leave much toxicity unneutralized even when Vitamin C intake would otherwise be adequate. In these cases, any compensatory increase in cholesterol will then be one of the body’s remaining best defense mechanisms against that toxicity, in the absence of more vigorously supplemented Vitamin C.
Therefore, in addition to high cholesterol levels promoting atherosclerosis by being available for direct deposition into the developing lesions, high cholesterols are also directly indicative that there are abnormally high levels of chronic toxin exposure. Such toxins will have their own direct effects on promoting atherosclerosis, as well as their indirect effects. This increased metabolism of Vitamin C can both maintain and worsen the Vitamin C deficiency that first initiated the atherosclerotic process.
Further evidence that cholesterol exerts this very important protective role against toxicity comes from studies that demonstrate an increased incidence of cancer or death from cancer in individuals with abnormally low cholesterol levels (Kark et al., 1980; Williams et al., 1981; Kagan et al., 1981; Stemmermann et al., 1981; Keys et al., 1985; Gerhardsson et al., 1986; Schatzkin et al., 1987; Knekt et al., 1988; Isles et al., 1989; Cowan et al., 1990).
Patients with abnormally low cholesterol levels have increased incidence of cancer and death from cancer.
More recently, it was demonstrated specifically that low levels of high density lipoprotein cholesterol (the “good” cholesterol) was significantly related to an increased risk of cancer (Mainous et al., 2005). One straightforward explanation for this correlation is that chronically low cholesterol levels leave significant chronic toxin exposures unneutralized, and cancer is but one of the consequences one would expect from such persistent toxicity. Furthermore, a number of the cholesterol-lowering trials that have demonstrated less heart deaths with lower cholesterol levels have shown almost equally significant increases in deaths from a number of other causes, including suicide, accidents, and violence (Golomb, 1998; Golomb et al., 2000).
Supporting this concept, Marcinko et al. (2005) showed that psychiatric patients with violent suicidal attempts had significantly lower cholesterol levels than patients with non-violent suicide attempts and the control subjects.
Psychiatric patients with violent suicidal attempts had significantly lower cholesterol levels.
Unneutralized chronic toxicity, such as from a heavy metal like mercury, commonly produces such clinical symptoms as depression, impaired nervous and muscular function, irritability, and emotional in stability. Depression from unneutralized toxicity can eventually result in suicide if the toxicity remains unaddressed, and the toxic effect continues to escalate.
Greater degrees of unneutralized toxicity will reliably lead to greater unchecked irritability and emotional instability, a condition that would facilitate a greater chance of violent suicide or death from violence. Similarly, progressive loss of muscle function and coordination can eventually result in fatal accidents, particularly in cars.
Cholesterol-lowering agents certainly appear to help stabilize the progression of or even help reverse atherosclerosis (Brown et al., 1990; Brown et al., 1993; Brown et al., 1993a; Brown et al., 1993b). However, they also leave the body with less protection from a continuous assault of environmental toxins, and susceptible individuals can end up dying from what might initially seem to be completely unrelated circumstances that do not “require” a logical explanation.
Interestingly, a similar clinical profile to that of mercury toxicity can result from almost any chronic, low-grade toxin exposure, although some toxins might have one or more other relatively unique clinical characteristics.
Virtually all toxins rapidly and significantly consume Vitamin C, and the resulting Vitamin C deficiency can make the effects of any toxins remaining in the body more significant, helping to give the common clinical picture of many different chronic toxin exposures, which is very similar to that described above for mercury toxicity.
In other words, all toxins can have direct toxic effects on target tissues, and they can indirectly result in many other nonspecific symptoms by virtue of the rapid consumption of the body’s Vitamin C stores. Furthermore, the rapid destruction of Vitamin C by toxins will make the subsequent exposure to new toxins of much greater clinical consequence.
Ginter (1975) points out another interesting relationship between Vitamin C and cholesterol. In rabbits and rats, which can synthesize Vitamin C (unlike the guinea pig), a forced high cholesterol diet results in the accumulation of Vitamin C in the liver and kidneys, with a dramatic increase in Vitamin C excreted in the urine. This forced ingestion of large amounts of cholesterol seems to indicate that the animals respond to this cholesterol dosing by making more Vitamin C.
Ginter (1975) suggests that this response to exceptionally high dietary cholesterol is like the response of any Vitamin C-synthesizing animal to a toxin. Ginter also points out that excessive cholesterol has toxic effects on the rodent liver. This observation helps to ex plain why increased dietary cholesterol reduces tissue levels of Vitamin C in guinea pigs (Ginter, 1970).
By whatever mechanism, high enough cholesterol doses are perceived by the organism as toxic, and Vitamin C stores are promptly depleted. High cholesterol levels apparently increase demands for Vitamin C because of the direct toxic effect of the high levels, as well as by the presence of the toxin(s) that the excess cholesterol is attempting to neutralize.
It would appear that elevated cholesterol levels can often routinely be normalized with the administration of Vitamin C, unless the amounts of toxicity are so overwhelming that ordinary doses of Vitamin C will not suffice and significant toxicity remains for the cholesterol to neutralize. Such extraordinary toxin exposures will be seen where there is a very large amount of industrial environmental toxin exposure, as from living downwind from a chemical factory.
Much more commonly, however, the toxic biproducts of anaerobic bacterial metabolism generated in root canal-treated teeth are overwhelming to the body and virtually impossible to completely neutralize on a regular basis around-the-clock. The degree of toxicity found with such anaerobic bacterial metabolism is akin to and on the same magnitude as that of botulism.
Botulism toxin is currently regarded as one of the most potent toxins ever discovered. Root canal-treated teeth will routinely produce toxicity in a manner very similar to that seen when the botulism bacteria are un wittingly admitted into an oxygen-deprived environment, as is seen when they are accidentally trapped in a vacuum-packed can of food. The subsequent loss of oxygen in the can makes otherwise harmless bacteria highly toxic. In the root canal-treated tooth, bacteria from the mouth also become highly toxic when they settle in the oxygen-deprived environment of this pulpless tooth, which happens routinely.
The consistent toxicity of root canals is well documented although not widely recognized or accepted.
The consistent toxicity of root canals is very well-documented, although not widely recognized or accepted (Meinig, 1996; Huggins and Levy, 1999; Kulacz and Levy, 2002). It is also a fact that is emotionally, although not scientifically, contested by the many dentists who routinely apply root canal treatments to their patients.
Willis et al. (1954) demonstrated that a majority of patients given only 500 mg of Vitamin C orally three times a day had objective evidence of regression of atherosclerotic narrowings on follow-up angiography (X-rays of dye injected into the blood vessels). This regression was seen after a Vitamin C administration period ranging from two to six months. A few patients showed no changes on follow-up, and a few patients showed detectable worsening of their arterial narrowings.
It is also very significant to note that any given patient showed the same changes in all lesions, i.e., improvement, worsening, or no change. No patient showed one lesion improving while another was narrowing further. These findings not only support the concept that Vitamin C alone can reverse atherosclerosis, they also indicate the need for an adequate dosage of Vitamin C to consistently achieve positive effects.
It is highly likely that the few patients who showed continued progression of their atherosclerotic lesions had ongoing toxin levels that 1,500 mg of vita min C daily was simply incapable of significantly neutralizing. Those who showed no progression would appear to have been taking just enough Vitamin C to neutralize daily toxicity without enough remaining to initiate significant vessel wall healing.
Any patient with a root canal-treated tooth, dead or infected tooth, or enough gum infection (periodontal disease) can be expected to have a daily toxin exposure that would be little affected or insignificantly neutralized by a dose of only 1,500 mg Vitamin C daily. Any disease secondary to that toxicity would be expected to proceed with little or no significant hindrance, just as witnessed by Willis in the few patients whose atherosclerosis continued to progress even with the supplemented Vitamin C.
Spittle (1971), after observing no recurrent heart attacks or strokes in 60 patients given from 1to 3 grams of Vitamin C daily over a 30-month period, asserted that atherosclerosis is likely “a long-term deficiency (or negative balance) of Vitamin C, which permits cholesterol levels to build up in the arterial system, and results in changes in other fractions of the fats.”
Repeating the studies of Willis and Spittle with a much higher oral dose of Vitamin C (say, 6,000 to 12,000 mg daily), along with periodic intravenous Vitamin C administrations and the proper removal of all root canal-treated teeth and other sources of dental toxicity would likely show even more dramatic clinical responses and lesion reversals in even a larger majority of the patients treated.
Cancer doctor finds that 98% of his patients had between two and ten “dead teeth” – most of which were root canal-treated teeth.
As noted earlier, more cancer is seen with lower cholesterol levels, which are indicative of higher unneutralized toxin levels. Issels (1999) specialized in the treatment of cancer, finding that 98% of his adult cancer patients had between two and ten “dead teeth.” Commonly, these were root canal-treated teeth, which Issels also considered to be dead and highly toxic. Such a high correlation between cancer and infective dental toxicity as typified by root canal-treated teeth is but one indication of how toxic such teeth can be, and of how difficult it is to maintain good health of any kind, cardiovascular or otherwise, as long as such teeth remain in the mouth.
Proper extraction of root canals and other infected teeth (with appropriate cleaning of the socket) is currently the only way to eliminate this very large source of chronic toxicity (Meinig, 1996; Levy and Huggins, 1996).