Heart disease is the biggest killer in the Western world, and more of us are dying of it every year. And yet, doctors think they’ve got it licked. That’s because they believe they know not only what causes it, but also how to treat it. All we have to do, they say, is cut fat from our diet, or take statin drugs. If we get heart disease, drugs or surgery will take care of it.
But there’s growing evidence there could be a vastly simpler solution – vitamin C.
Since the 1950s, the vitamin C-heart disease connection has been quietly bubbling away beneath the surface, but it could now be about to break through in an explosion of research. Indeed, this inexpensive vitamin appears to be central to the whole question of why we get heart disease – and then perhaps how to cure it.
The term ‘heart disease’ is a misnomer, as the problem is not so much the pumping organ itself, but the arteries that feed it. If these become narrowed, blood flow to the heart is restricted, making it malfunction. At best, it will cause pain (angina), at worst, a heart attack. The conventional medical view used to be that atherosclerosis (narrowing arteries) was an inevitable result of ageing, but that shoulder-shrugging attitude has now been replaced with finger-wagging. Today, coronary artery disease is considered to be almost wholly the fault of the sufferer’s lifestyle – smoking, lack of exercise and, above all, a high fat diet.
The logic behind the ‘fat causes atherosclerosis’ theory is simple. Arteries become narrowed by deposits of cholesterol on their inner walls; fat contains cholesterol, ergo, fat causes atherosclerosis. The idea is so entrenched in the medical mind that the proposition is no longer a theory, but established fact.
But the theory is manifestly wrong.
Flawed fat findings
Ancel Keys is credited with first postulating the ‘fat causes heart disease’ thesis in the 1950s. In what is now referred to as the ‘six countries study’, he examined the fat intake of six countries – the populations of which led to a bias in his results – and allegedly demonstrated a clear correlation between mortality from coronary heart disease and fat consumption (J Mt Sinai Hosp NY, 1953; 20: 118-39).
In the later ‘Seven Countries’ study, Keys put the blame solely on saturated fats but, by then, his earlier conclusions had been firmly taken on board by government and embraced by industry, which could offer low-fat processed foods to prevent heart disease.
Industry has also ignored the evidence that saturated fats don’t clog arteries (J Clin Epidemiol, 1998; 51: 443-60). In addition, the well-known Framingham study, which has followed a Massachusetts population for decades, has uncovered the precise reverse of the accepted theory: the greater the intake of saturated fat and cholesterol, the lower the blood cholesterol (Fallon S et al. Comments on the Report of the 2005 Dietary Guidelines Advisory Committee. 27 September 2004).
Evidence from the animal kingdom is yet another reason to ditch the ‘fat causes atherosclerosis’ theory. Even though domestic animals eat a diet every bit as fat-laden as people, they don’t get atherosclerosis – a fact well known to vets 50 years ago (Smith HA, Jones TC. Veterinary Pathology. Philadelphia: Lea &. Febiger, 1957).
Drs Rath and Pauling
It took 40 years for reason to emerge, when young unknown German doctor Matthias Rath joined forces with old, highly celebrated scientist Linus Pauling.
Rath was part of a group of researchers who had discovered that the major culprit in cholesterol was lipoprotein(a) [Lp(a)], an especially ‘sticky’ molecule that incorporates itself into the collagen found in artery walls, thereby causing athero-sclerosis. Pauling and Rath’s first breakthrough was to realise that atherosclerosis is not a disease, but possibly the body’s way of repairing or bolstering weak or damaged arteries (Proc Natl Acad Sci USA, 1990; 87: 6204-7).
Their next great insight was that animals don’t get atherosclerosis because they possess an enzyme that converts glucose into vitamin C in their liver.
To test this theory, Rath and Pauling used one of the few animals that, like humans, cannot make its own vitamin C – the guinea pig. These animals were all given an identical high-fat diet, but some also received 40 mg/day of vitamin C (the equivalent to 5 g/day for a human). Five weeks later, the animals lacking vitamin C had developed severe atherosclerosis, whereas those taking vitamin C were totally clear (Proc Natl Acad Sci USA, 1990; 87: 9388-90). The finding that vitamin C stimulates the production of collagen provided the final clinching piece of evidence (Biochem Cell Biol, 1990; 68: 1166-73).
Rath and Pauling arrived at two totally revolutionary conclusions: (1) Self-made vitamin C maintains healthy arteries in animals, virtually no matter the diet, by bolstering arterial collagen; (2) If deprived of vitamin C, the body uses the lipoprotein in cholesterol to repair damaged arteries.
Thus, atherosclerosis in humans and guinea pigs is due to vitamin C deficiency. In short, heart disease is “chronic scurvy” (Proc Natl Acad Sci USA, 1990; 87: 6204-7).
Predictably, despite Pauling’s preeminence as the ‘father of modern chemistry’, the medical profession dismissed his extraordinary radical ideas out of hand.
Yet, within a few years, the supporting evidence began to surface. In 1992, a major study of over 11,000 Americans showed that those with the highest intakes of vitamin C had almost half the rate of heart disease (Epidemiology, 1992; 3: 194-202). Although some subsequent studies failed to find any benefit from vitamin C, on balance, the latest evidence appears to vindicate Pauling’s thesis. Most recently, data from nearly 300,000 people show conclusively that an intake of 700 mg/day or more of vitamin C reduces the risk of heart disease by 25 per cent (Am J Clin Nutr, 2004; 80: 1508-20).
But there’s a puzzle. According to Pauling’s theory, no one taking enough vitamin C should get heart disease at all. So, why should the risk be reduced by only a quarter with 700 mg/day of the vitamin – a massive 10 times the RDA?
The answer appears to be that even this huge dose is inadequate (see box above).
Here again, the clue comes from animals, which naturally produce huge amounts of vitamin C. A 70-kg goat makes about 13,000 mg (13 g) of vitamin C every day, a large dog about 2.5 g/day. The Committee on Animal Nutrition has also shown that monkeys (which, like us, can’t produce their own vitamin C) need around 55 mg/kg body weight/day of vitamin C for optimal health. In human terms, this means an average 70-kg person needs to take nearly 4 g/day.
It’s even possible that very high-dose vitamin C might actually reverse heart disease. Curiously, the only trials to test this theory were done 50 years ago by Canadian physician Dr G.C. Willis.
Willis was an atherosclerosis expert and had pioneered angiography (the now widespread method of photographing arteries using X-rays). What he saw convinced him that the conventional explanation for atherosclerosis was wrong – so wrong that even a plumber could see it.
If the condition was due to a build-up of cholesterol in the blood, the narrowest arteries should be the first affected, just as sludge builds up more quickly in narrow water pipes. In fact, the opposite is true in the body – the biggest arteries tend to fur up first.
Willis made the crucial observation that atherosclerosis mainly occurs in the vessels near the heart, but what was so special about them? Although wide and apparently strong, it was their very proximity to the heart that was the problem, he concluded. The sheer pumping force of the heart put those vessels under constant mechanical stress, thus weakening them. So, furring of the arteries may not be a pathological deposition of fat, he suggested, but a means of artificially thickening the arteries to prevent damage (Can Med Assoc J, 1953; 69: 17-22).
Arguably, Willis should have been given a Nobel for his findings because, 30 years later, Drs Michael Brown and Joseph Goldstein were awarded the 1985 Nobel Prize in Medicine for the discovery that atherosclerotic plaques are deposit-ed in response to injury of the blood vessel wall.
But Willis went even further when he discovered the key role of vitamin C. He knew that guinea pigs were the only animals to get heart disease and, like Pauling, made the vitamin C connection (J Exp Med, 1956; 103: 199-205). He tested vitamin C on his more severe heart-disease patients, giving them what was then a high dose of 1.5 g/day. What he got was the first – and, so far, only – evidence that vitamin C can reverse heart disease when, in nearly a third of his patients, the atherosclerosis began to disappear (Can Med Assoc J, 1957; 77: 106-8).
Curiously, no one has ever tried to repeat this groundbreaking study, not even Pauling himself – who declared, with characteristic hubris, that the vitamin C-heart disease connection was so self-evident that it didn’t need clinical trials to prove it.
One recent convert to the benefits of vitamin C is British optometrist Dr Sidney Bush, who stumbled upon the connection while treating eye infections in contact-lens patients.
After prescribing vitamin C to prevent eye infections, on examining his patients, he noticed that the fine retinal blood vessels at the back of the eye, which are often clouded in mild atherosclerosis, were gradually beginning to clear. Bush found that the effective dosage was high – up to 10 g/day.
But the lesson for heart disease is clear. Says Bush, “Our discovery is a virtually perfect surrogate outcome predictor of coronary heart disease.”
As good as statins
Clearly, more research is needed to confirm whether vitamin C can reverse heart disease. But given the current EU campaign against high-dose supplements, such research is apparently unlikely.
However, there does appear to be a recent and growing interest in the role of vitamin C in heart disease within the bastions of conventional medicine. A number of new studies are contributory: one has found that vitamin C works similarly to statins, the drugs of choice for heart disease (Eur J Clin Nutr, 2005; 59: 978-81); another discovered that vitamin C inhibits oxidation of cholesterol (J Agric Food Chem, 2004; 52: 6818-23), and a third found that it can reduce atrial fibrillation (heart flutters), a potentially fatal condition related to atherosclerosis (Med Sci Monit, 2003; 9: RA225-9).
These recent studies are the first glimmers of a remarkable possibility: that the number-one killer in the West can be overcome by a vitamin.