Vitamin C

Test-tube experiments in which vitamin C metabolites damaged DNA were recently reported, and another report involved thickening of the wall of the carotid artery in people taking supplemental vitamin C.

A lie gets half way around the world before the truth

has a chance to get its pants on.

Winston Churchill

These findings are absurd, but they were widely reported. However, we do not hear about them when they are refuted. A 1995 Hoffman LaRoche review which pronounced vitamin C safe included several studies in which up to 10 grams were taken each day for 3 years. The review concluded: “higher than RDA intakes of vitamin C have been associated with several indices of lowered cardiovascular disease risk including increases in HDL, and decreases in LDL oxidation, blood pressure and cardiovascular mortality.”

However, a 2004 study of the Third National Health and Nutrition Survey data found that vitamin C depletion and rank deficiency are actually widespread, affecting one person in 3:

a larger view …

This is incredible. The table shows that, for example, 17% of males aged 25 to 44 have a blood level less than 11μmol/L, which means that they are deficient in vitamin C and are in danger of developing scurvy. Scurvy! Now this is news – but who’s ever heard of it?

No wonder an analysis of the First National Health and Nutrition Survey data found a 42% and a 25% reduced risk of death for men and women respectively who got the most vitamin C from diet and supplements compared with those who got the least. A recent meta-analysis of 9 such studies found that those who took more then 700 mg of vitamin C per day were 25% less likely to develop CVD than those who got less.

Maybe someone should alert the American Heart Association.

Meanwhile, let us ponder what makes vitamin C so effective in the prevention of CVD. One of vitamin C’s most important functions is in the production of collagen, and this is the function that fails in scurvy, and is compromised in “vitamin C depletion.” The following section is technical, but the premise is simple: if vitamin C is in short supply, then collagen formed for repair of the arterial wall will be weak and vulnerable to oxidized cholesterol, mechanical stresses, homocysteine and other noxious influences in the bloodstream. Some have suggested that this is the fundamental cause of heart disease, and propose a simple strategy for relief. This strategy has been patented, experimentally tested and found to be effective, and is commercially available.

Collagen?

The illustration is from Michael Brown and Joseph Goldstein’s article “How LDL Receptors influence Cholesterol and Atherosclerosis” in the Scientific American magazine of November, 1984:

Brown and Goldstein received Nobel Prizes for elucidating the structure of the LDL cholesterol receptor, which is how cells get supplies of the cholesterol they need. Their premise that: “Damage to the thin layer of epithelial cells that lines an artery initiates plaque formation” is generally accepted. The epithelial cells line the intima, the inner wall of the artery, sealing the supporting middle of the wall away from the blood, and actively secreting substances such as prostacyclin and nitric oxide which modulate both the slipperiness of the blood and its tendency to clot, and the muscular tension in the wall of the artery which in turn regulates blood pressure.

How does the epithelial layer sustain damage? From homocysteine, a toxic amino acid which builds up in the blood if vitamin B6, folic acid or vitamin B12 are in short supply. By mechanical injury from the turbulence of the blood flow, or from the contraction of the heart muscle in the case of the coronary arteries. Or by infections with bacteria such as Chlamydia pneumoniae which was found in 55% of atherosclerotic plaques in this study (Emerging Infectious Diseases 1998, 4(4)) which raises C-Reactive Protein levels, a risk factor for heart disease. Or infection by nanobacteria, ubiquitous tiny organisms which form calcium overcoats, and which may be the cause of hardening of the arteries, and kidney stones and prostatitis besides. Calcium salts do cause inflammation (Circ Res 2005; 96:1248), and can be removed by chelation; and when chelating agents are given with tetracycline which kills the nanobacteria, there may be relief from heart symptoms such as angina. Or from oxidized cholesterol, caused by either insufficient antioxidants in the circulation, or acquired from food cooked in over-used cooking fat.

Or the damage may be caused by poorly-formed collagen which is not strong enough to support the endothelial cells. In this scenario, the epithelium is torn open as the poorly-formed collagen beneath breaks apart. This would explain why plaque is found at points of mechanical stress from turbulence in the bloodstream such as in the aorta and at bifurcations of the arteries, and from the mechanical stresses which flatten the coronary arteries with each heartbeat.

Collagen and mucin together form the ground substance which exists between the cells. Just as concrete reinforced with steel is tougher than its components, so do collagen and mucin together form the tough, composite “glue” which literally holds us together. Mucin binds water which gives a shock-absorbing texture to the ground substance, which is in a constant state of flux as it is degraded by enzymes and replaced with newly-synthesized material in the normal course of metabolism. Mucin is an old name for what are now called mucopolysccharides, or the glycosaminoglycans – for simplicity, let’s stick with mucin!

The collagens are the most common proteins in the body. They are found in the skin, in the bones (which are mineralized collagen), teeth, gums, tendons and ligaments, and give strength and elasticity to the blood vessel walls. Even the plasma of the blood is a form of collagen.

This stuff may be more familiar as glue, Jello and gelatin. When animal skins and bones are rendered into glue, the collagen they contain is hydrolysed (meaning water is added) so that it becomes more liquid. Then, as the glue dries, the water is removed and the cross links re-form (cross links are the links between the strands of collagen). With less rendering, the mucin survives and binds water to give Jello, or, if the water is removed, gelatin.

The presence of vitamin C triggers the synthesis of collagen in a dose-dependent fashion, meaning the more vitamin C, the more collagen is made. The process starts with mRNA copying the DNA template for the protein, forming pro-collagen. Then the pro-collagen is hydroxylated, which means the reaction in which an hydroxyl radical (-OH ) replaces hydrogen (-H ) in the synthesis of a molecule. Each hydroxylation reaction uses up one molecule of vitamin C. Here is an illustration of the process from a textbook of biochemistry:

We start inside the part of the cell devoted to protein synthesis, the rough endoplasmic reticulum. Here, pro-collagen is made from the RNA template and then hydroxlylated, which means -OH’s are added, and each -OH added consumes one molecule of vitamin C (unlike in vitamin C’s antioxidant function, where it is reversibly oxidized and lives to fight another day, hydroxylation irrevocably consumes the molecule). The pro-collagen passes through a pore called a ribosome into the cytoplasm of the cell (the many ribosomes on the surface of the endoplasmic reticulum give it a rough appearance, hence “rough endoplasmic reticulum”) where it is elaborated with sugars, and then it passes out of the cell into the intracellular space. Here, vitamin B6 acts as a co-enzyme for the copper-dependent enzyme lysyl oxidase which cross-links the pro-collagen strands to form collagen (Bird, TA et al, Lysyl oxidase: evidence that pyridoxal phosphate is a cofactor. Biochem Biophys Res Comm 1982; 108(3):1172-80). Further, the active form of B6, pyridoxal phosphate, has been found to be low in atherosclerosis. (Serfontain W et al, Plasma P5P level as risk index for coronary artery disease. Atherosclerosis 1985; 55:357-61). Weight for weight, strands of collagen are stronger than steel. As elastin, collagen gives the blood vessels the elastic resilience they need to cope with the pressure pulses of the heartbeat. Anything that interferes with collagen synthesis or repair – such as a shortage of vitamin B6 – will cause the arteries to deteriorate. (Levene CI et al, The aetiological role of maternal B6 deficiency in the development of atherosclerosis. Lancet 3/19/77; 1(8012):628-30

Hydoxylation takes place in step number 2, and each -OH costs one molecule of vitamin C. If vitamin C is in short supply, fewer –OH’s will be attached to the pro-collagen so that the cross-linking of the collagen fibers in step number 7 will be incomplete, and the collagen cannot attain its full strength.

Other deficiencies which affect this process include vitamin B6 deficiency which weakens the collagen because B6 is the co-factor for lysyl oxidase, which forms the cross-links in step number 7. One of the symptoms of B6 deficiency is edema, meaning that with too little collagen, mucin binds more water (like Jello). Low vitamin B6 therefore means fewer cross-links and weaker collagen. Too little thyroid hormone suppresses collagen synthesis and promotes mucin production in the arterial wall, weakening the composite material and causing an edema which is called myxedema in the severe deficiency state. The important thing here is that there are way more heart attacks in those who are low in vitamin C, vitamin B6, and thyroid hormone.

In scurvy, so little vitamin C is available that collagen synthesis fails and the circulatory system falls apart, so that half the victims die of internal bleeding. The other half die of infections, which underlines the importance of vitamin C in immune function. One of the most pernicious errors of assumption ever made is that enough vitamin C to avoid scurvy is enough vitamin C to maintain health. The RDA supplies enough vitamin C for some hydroxylation so that the collagen doesn’t fall apart, but not enough for the collagen to attain its full strength.

There is clear evidence of weak collagen in the widespread distribution of wrinkles, stretch marks, poor wound healing, gum disease, chronic back pain, high cholesterol, gallstones and cataracts, atherosclerosis and tooth decay.

Another requirement for vitamin C is in the production of bile. As with the synthesis of collagen, a molecule of vitamin C is used up in the hydroxylation of each molecule of cholesterol elaborated to form bile, which is essential for emulsifying fats during digestion. It follows that if vitamin C is in short supply we can’t excrete so much cholesterol, so we tend to develop gallstones and an elevated cholesterol level as a consequence. A second reason that cholesterol rises if vitamin C is in short supply is that vitamin C itself inhibits the enzyme HMG-Coenzyme A which is responsible for the production of cholesterol:

Since inhibition of HMG-CoA reductase occurs at physiological concentrations of ascorbic acid in the human leukocyte (0.2-1.72 mM), this vitamin may be important in the regulation of endogenous cholesterol synthesis in man.

Statin drugs are synthetic HMG CoenzymeA inhibitors, but vitamin C is a natural HMG CoenzymeA inhibitor, which is entirely without side-effects. Thus, a vitamin C deficiency raises the cholesterol level in the blood, and high-dose vitamin C supplementation lowers cholesterol levels in those whose levels are elevated (Gaby SK et al, eds, Vitamin Intake and Health: A Scientific Review. Marcel Dekker NY, 1991).

Vitamin C is concentrated to levels many times that in the blood in the specialized white blood cells of the immune system. Neutrophils actively take up oxidized vitamin C and recycle it into vitamin C once more until the concentration within the cell is 10 times that in the plasma. If bacteria are present, the neutrophil becomes “activated” and concentrates vitamin C a further thirty times. This protects the neutrophil while it uses oxidants to attack the bacteria. Immunity is severely degraded if the white cells cannot get enough vitamin C, and vitamin C is quickly depleted in even minor infections.

But to return to our torn collagen. In 1984, Brown and Goldstein wrote that: “the damaged endothelium becomes leaky and is penetrated by low-density lipoprotein (LDL) particles ...” Since then, in 1990, Mathias Rath and colleagues showed that the form of cholesterol which accumulates in plaque is not LDL, but rather lipoprotein(a), which consists of LDL attached to apoprotein(a). An apoprotein is the protein part of a lipoprotein, and a lipoprotein is a compound that carries fats and cholesterol, in the blood.

So lipoprotein(a) – Lp(a) – is the new LDL, the new “bad” cholesterol. Several studies have demonstrated that high Lp(a) increases the relative risk of heart trouble by 1.9 in men and 1.6 in women. Women who had both high Lp(a) and C-reactive protein had a whopping 3.67 time the odds of developing CHD. In a 1997 study, the mean level of Lp(a) for those with clean coronary arteries was 115 mmol/L, while those who had blockages in all three coronary arteries had a mean level of 305 mmol/L. However, perhaps because no drug is available which will lower Lp(a), remarkably little attention has been paid to this discovery.

There may be two reasons for the atherogenicity of Lp(a). First, it is similar enough to plasminogen that it inhibits the dissolving of clots. Second, it sticks to lysine and proline, the amino acids exposed when poorly-formed collagen tears open.

Linus Pauling’s take on this was that if we have enough vitamin C, collagen is made with it to repair damage to the arterial wall. If we don’t, we use lipoprotein(a) to repair the tear as it binds the exposed lysyl residues of the damaged collagen together, which is to say that Lp(a) is a surrogate for the missing vitamin C. But if the low-C state of affairs continues, plaque forms and thickens as white cells infiltrate the damaged area and the smooth muscle cells of the arterial wall proliferate, there is calcium infiltration (the -sclerosis part of atherosclerosis), and eventually the plaque ruptures and there is a heart attack.

Interestingly, plaque is found in every human population studied the world over. Even some of the young men in Barcelona, where the rate of heart attack is very low, have plaque. Amazingly, plaque is as prevalent in Japanese people, although their rate of heart attack is one sixth that of America. Plaque increases in both incidence and severity with age in most populations until it is practically universal. That this state of affairs has persisted for a long time is shown by the discovery of plaque in the arteries of Egyptian mummies, and the aphorism of the 17^th century physician Thomas Sydenham:

A man is as old as his arteries

But neither atheroma nor Lp(a) are found in creatures which make their own vitamin C. Man, the primates and a few other creatures such as the guinea pig are among the few creatures on the face of the Earth who do not make vitamin C from glucose in their livers. Only these creatures suffer plaque if they cannot obtain sufficient vitamin C, and only man among these suffers heart attacks. Pauling and Rath investigated the effect of depriving guinea pigs of vitamin C (who, like us, cannot make their own), and found Lp(a) in the plaque which formed in their arteries. Furthermore, feeding 40 mg/kg of vitamin C per day prevented plaque formation, and prevented accumulation of Lp(a) in the arterial wall. This is equivalent to about 3 grams per day for the average human.

This study confirms the results of Dr GC Willis of Canada, who researched the vitamin C content of the arterial walls of heart attack victims and those who suffered sudden deaths. He found little vitamin C in the aortas of the heart attack victims compared with those who suffered accidental death. He also induced atherosclerosis in guinea pigs by withholding vitamin C, and found quite profound vitamin C deficiency among the hospitalized elderly. Amazingly, Dr Willis published his research in 1955.

Pauling and Rath published their Unified Theory of Human Cardiovascular Disease in the Journal of Orthomolecular Medicine in 1992. Then Pauling had the inspiration that since Lp(a) was sticky for lysine, then lysine itself should protect against cholesterol deposition in the arterial wall. Lysine is essential amino acid, so that it is benign in any reasonable quantity. He found that the combination of vitamin C and lysine did indeed resolve angina pectoris in a human subject. Angina is like a cramp, a pain on exertion caused by reduced blood flow to the heart muscle because of plaque-narrowed coronary arteries. This man was taking aspirin, lovastatin, CoQ10, and 6 grams of vitamin C per day among other supplements, and had used up all his available leg veins in by-pass operations. However, in spite of employing every available medical remedy, his angina was worsening even with liberal nitroglycerin use:

In this predicament and with his history of restenosis, I suggested that he continue ascorbate and add 5 g of L lysine daily (ca., six times the lysine derived from dietary protein) to try to mitigate the atherosclerotic acitivity of Lp(a). After reading the 1990 Rath and Pauling reports and their manuscript titled "Solution to the puzzle of human cardiovascular disease", he began taking I g of lysine in early May 1991 and reached 5 g (in divided doses eight hours apart) by mid June. In mid July, his HDL was, as usual, a low 28 mg/dl. A low normal 0.9 mg/dl blood creatinine indicated that lysine could be increased, if needed. He could now walk the same two miles and do yard work without angina pain and wrote, "the effect of the lysine borders on the miraculous". By late August, he cut up a tree with a chain saw, and in early September started painting his house. By late September, possibly from over exertion, he again began to have angina symptoms during his walks, but after stopping strenuous work and increasing lysine to 6 g [calculated to provide a peak 280,000 molar excess in the blood over his then 6 mg/dl of Lp(a) to help compensate for the relatively high dissociation constant of lysine Lp(a)] these symptoms stopped entirely by mid October. His blood creatinine was still a normal 1.2 mg/dl. He attributes his newfound wellbeing to the addition of lysine to his other medications and vitamins. His wife and friends comment on his renewed vigor. (Pauling L, Case Report: Lysine/Ascorbate Related Amelioration of Angina Pectoris. J Ortho Med 1991, 6(3-4):144 46)

Pauling patented this treatment for heart disease, in the first such patent ever granted, and further patented the use of the technique for cleaning plaque from organs to be used in transplants.

Linus Pauling died on August 19, 1994, at the age of 93 years. He himself took 18 grams of vitamin C per day and died after a brief bout of prostate cancer, lucid to the end. This is in sharp contrast to many of his critics. Interestingly, Albert Szent-Györgyi (Saint George in Hungarian), who received a Nobel Prize for elucidating the vitamin C complex in 1937, took 1 gram of C each day, and also died at 93 years of age.

Discovery is seeing what everybody else has seen,

and thinking what nobody else has thought.

Albert Szent-Györgyi

Szent-Györgyi pointed out in his Nobel Prize acceptance speech that ascorbic acid by itself doesn’t resolve scurvy:

At the time that I had just detected the rich vitamin content of the paprika, I was asked by a colleague of mine for pure vitamin C. This colleague himself suffered from a serious haemorrhagic diathesis [meaning capillary bleeding as is found in scurvy]. Since I still did not have enough of this crystalline substance at my disposal then, I sent him paprikas. My colleague was cured. But later we tried in vain to obtain the same therapeutic effect with pure vitamin C. the ascorbic acid complex which includes vitamin P B the bioflavonoids B is necessary to do that.

Incredibly, by 1937, Szent-Gyögyi had deduced that the vitamin C complex (not just vitamin C) neutralizes the oxygen free radical (a term not yet invented!) in two stages:

Ascorbic acid oxidase oxidizes [ascorbic] acid with oxygen to reversible dehydro-ascorbic acid, whereby the oxygen unites with the two labile H-atoms from the acid to form hydrogen peroxide. This peroxide reacts with peroxidase and oxidizes a second molecule of ascorbic acid. Both these molecules of dehydro-ascorbic acid again take up hydrogen from the foodstuff .

But peroxidase does not oxidize ascorbic acid directly. I succeeded in showing that another substance is interposed between the two, which belongs to the large group of yellow, water-soluble Y plant dyes (flavone, flavonol, flavanone). Here the peroxidase oxidizes [the flavon, the bioflavonoid] which then oxidizes the ascorbic acid directly, taking up both its H-atoms. (ibid)

The significance of this is that a bioflavonoid such as the hesperidin (found in the white part of the orange rind), rutin, quercetin and so forth are needed for vitamin C to perform its antioxidant function, and they modulate the permeability of the capillaries – hence vitamin P. They are themselves potent antioxidents, and many also display metal binding activity, a property which may contribute to their antioxidant effects. So what we think of as vitamin C is actually ascorbic acid, a fraction of the vitamin C complex. Ascorbic acid does not cure scurvy, it is the vitamin C complex – ascorbic acid plus bioflavonoids - which cures scurvy.

Parenthetically, Ancel Keys retired to southern Italy, adopted the Mediterranean diet and died recently at 100 years of age. He found the diet of Crete to be profoundly protective against heart trouble during his misguided cholesterol studies, but used the much worse heart data from Corfu instead. The protective factor in Crete may the widely used herb purslane which raises the ω3:ω6 ratio of the diet:

The Lyon Heart Study was an intervention trial (first reported in 1993) in France that demonstrated that a diet resembling the Cretan diet, i.e. rich in plants and alpha-linolenic acid from canola oil, afforded better protection from the recurrence of myocardial infarction than the Step I American Heart Association prudent diet.

In the Cretan diet, the intake of alpha-linolenic acid is high due to the consumption of herbs, walnuts, seeds, snails, purslane, and lamb. The Lyon Heart Study is important because it provides the first clinical proof of a protective effect of the Mediterranean diet on cardiovascular disease. (Mediterranean diet)

Many others have noticed this. For example, this is from a website offering high-ω3 eggs:

Surprisingly, the men from Crete also had half the overall death rate as men from Italy, even though both groups of men were eating Mediterranean-style diets that were rich in olive oil, legumes, fruits, and vegetables. There was something unique about the Crete diet, but at that time, medical science was unable to pinpoint what it was.

The Missing Clue

Two decades later, one of the rinsing clues was provided: the traditional Crete diet has an ideal ratio of EFAs. This finding helped shed new light on the Crete diet because people from Crete eat large quantities of greens and wild plants, including purslane. Perhaps this hidden bounty of omega-3 fatty acids was one of the reasons for their superb health (9). Suspicions were confirmed by a landmark heart study conducted in France and known as the Lyon Diet Heart Study, where 302 heart attack survivors were assigned to a traditional heart diet, the “prudent” heart diet recommended by the American Heart Association (AHA). A similar group was assigned to a slightly modified version of the Crete diet. This new diet was based on Canola oil and olive oil, and it had a ratio of omega-6 to omega-3 fatty acids of 4 to 1, much lower than the AHA diet and the traditional Western diet. The diet was also lower in red meat and deli meats, but higher in fish, grains, fruits, and vegetables. Overall, it contained 35 percent fat, whereas the AHA diet is 30 percent.

The result of the study made medical history. Just four months into the clinical trial, the researchers discovered there had been significantly fewer deaths in the group on the modified Crete diet than on the AHA diet. (Christopher Eggs)

At this writing, the American Heart Association still offers its so-called prudent diet, and suggests ω3 supplements be used only by those at special risk. It is sobering to reflect on the numbers of lives lost because Keys ignored his own observation of the life-saving nature of the diet of Crete in favor of his cholesterol idea.

A Trial of Pauling’s Heart Disease Therapy

Mathias Rath went on to publish a trial of nutritional supplements including 2.7 grams of vitamin C and 450mg each of lysine and proline in people with heart disease in 1996. He demonstrated that early, small calcified plaques disappear entirely, and more extensive plaques grow at a decreasing rate. The study duration of one year was apparently too short for these plaques to cease growing and start shrinking as the early, small plaques had done, but that was clearly the trend:

Rath Trial …

The American Heart Association may never acknowledge this simple effective strategy, but it is available to those in need through Tower Heart Technologies.

Confirmation that vitamin C is effective against atherosclerosis comes from another source. Doctor of Optometry Sydney Bush published in a letter in the July, 2004, British Medical Journal that in the course of his usual practice of placing patients on vitamin C to prevent or treat contact lens problems, he had serendipitously discovered that high-dose vitamin C reversed arterial disease. Using a digital retinal camera, he saw that small aneurysms, bulging areas that indicate weak artery walls, in photographs of the retina resolve with supplementation. Bush believes that over 90% of patients with arterial disease can be improved with 3000 milligrams of vitamin C per day, but some need over 10,000mgs/day supplemented with extra vitamin E. Even hard calcifications, which look like a fine white line that runs down almost every artery of adults who have high cholesterol, disappeared over a two-year period of vitamin C supplementation.

Other observations suggest that vitamin C is protective against both atherosclerosis and heart attacks. For example, in a population of Finns, serum vitamin C below the threshold of deficiency elevated heart attack risk by 4 times. The researchers concluded:

To our knowledge, our current results are the first empirical evidence in humans to show that vitamin C deficiency, as measured by low plasma ascorbate concentration, is a risk factor for coronary heart disease. In our cohort plasma vitamin C concentration above the limit of deficiency was not associated with the risk of acute myocardial infarction. Thus, high intakes of vitamin C or vitamin C supplements would probably not reduce the risk of acute myocardial infarction. Our findings suggest, instead, that if a minimal necessary requirement of vitamin C is not met the risk of myocardial infarction is increased. (Nyyssönen K et al, Vitamin C deficiency and risk of myocardial infarction: prospective population study of men from eastern Finland. BMJ 1997; 314:634)

After Linus Pauling published How to Live Longer and Feel Better in 1979, vitamin C production climbed in America, but not in other Western countries. The incidence of heart disease has plateaued in America, but not in the other Western nations. A plausible explanation is that it is the increased intake of vitamin C supplements which caused the reduction of heart disease.

Using the Nurses Health Study data, Dr Walter C Willett of Harvard looked at vitamin C intake and risk of coronary heart disease in women. He concluded that vitamin C supplement use was associated with a lower risk of CHD (RR = 0.72; 95% CI 0.61 to 0.86). This means he found that the women who took supplemental vitamin C were, on average, 28% less likely to develop heart disease as the women who did not.

This is remarkably consistent with the results of a study of the Second National Health and Nutrition Survey which found a 21% to 25% decreased risk for heart death, and 25% to 29% decreased risk of all-cause mortality in people with normal to high serum vitamin C. The study’s conclusion was that “increasing the consumption of ascorbic acid ... could decrease the risk of death among Americans with low ascorbic acid intakes.” Among women in this population, the blood vitamin C level was associated with “protective” HDL cholesterol, which increased by 2 mg/dl for each 1 mg/dl increase in serum ascorbic acid level.

Linus Pauling said in his last interview:

I don’t know if there’s a need for a randomized, prospective double-blind study when you get evidence of this sort about the value of a large intake of vitamin C and also lysine for preventing the deposition of atherosclerotic plaques and preventing death from cardiovascular disease. I recommend that every person, every adult, take 3 grams of vitamin C a day and smaller amounts for children proportional to body weight. That every person who is at risk for one reason or another for cardiovascular disease take perhaps not only 6 grams of vitamin C per day but also 2 grams or more of lysine a day. Two grams may well be protective, but larger amounts might be needed for greater risk of cardiovascular disease.

Clearly, there is a huge difference between the 90mg RDA for vitamin C and the amount we can profit from. Consider that intravenous vitamin C in gram quantities cured even polio in the epidemic of the 1950s when it was administered by Dr Frederick Klenner. Dr Thomas Levy reviewed the literature in support of the proposition that vitamin C in sufficient quantity can cure all known bacterial and viral conditions if administered intravenously in his book Vitamin C, Infectious diseases and Toxins (Xlibris, 2002). This implies that we benefit from larger amounts when we’re sick, and this is confirmed by the fact that most creatures make their own in great quantities - the equivalent of many grams for a human - when they’re ill.

But although even steadfast nutritional conservatives acknowledge that illness depletes us of vitamin C, we don’t learn this from the author of the RDAs, the National Academy of Sciences, who cap the safe intake at 2 grams on the grounds that more may cause diarrhea – never mind that in sickness, Dr Robert Cathcart has established that this “bowel tolerance” increases (depending on the severity of the condition) up to hundreds of grams for life-threatening diseases such as AIDS. Nor do they share that man is the only creature to suffer from atherosclerosis. As we have seen, experimentation suggests that supplementing C to mimic the levels found in creatures that make their own causes atheroma to recede and perhaps eventually to disappear. It seems likely that with sufficient vitamin C in the diet, atherosclerosis might not occur.