Is atherosclerosis really a symptom of scurvy?

Part 2: Drs Rath and Pauling

In the late 1980s, a young unknown German doctor named Matthias Rath joined forces with the double Nobel Prize Laureat, Linus Pauling. Together they formulated a new hypothesis. Rath had been one of the researchers who discovered that the major culprit in cholesterol was a substance called lipoprotein(a) (Lp(a)). Lipoprotein(a) is a particularly 'sticky' molecule which incorporates itself into the collagen found in artery walls. Rath and Pauling's first breakthrough was to realise that atherosclerosis is not a disease in itself, but the body's way of repairing weak or damaged arteries [1].

They then theorised that the reason carnivorous animals don't get atherosclerosis, despite eating a protein-rich and high-fat diet, was because they possessed an enzyme that converted glucose into vitamin C in their liver. To test this theory, Rath and Pauling used the guinea pig which is one of the few animals that, like humans, cannot make its own vitamin C.

The guinea pigs were fed a high-fat diet. But some also received a 40 mg/day of vitamin C supplement. results were clear and convincing. At the end of the study, the arteries of the guinea pigs fed the vitamin C were in a perfectly healthy condition; on the other hand, those lacking vitamin C had developed severe atherosclerosis.[2]

Rath's and Pauling's conclusions

From the results of their study findings Rath and pauling concluded that:

  • Self-made vitamin C maintains healthy arteries in animals, virtually no matter the diet, by bolstering arterial collagen;
  • If deprived of vitamin C, the body uses the lipoprotein in cholesterol to repair damaged arteries.

The hypothesis, then, is that atherosclerosis in humans is due to vitamin C deficiency; simply a form of chronic scurvy.[1]

However, you won't be surprised to learn that, despite Pauling's preeminence as the 'father of modern chemistry', this radical idea was dismissed out of hand by the medical profession.


1.Rath M, Pauling L. Hypothesis: lipoprotein(a) is a surrogate for ascorbate. Proc Natl Acad Sci U S A. 1990; 87: 6204-7.
2. Rath M, Pauling L. Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. Proc Natl Acad Sci USA, 1990; 87: 9388-90

Part 1: Introduction | Part 2: Rath & Pauling | Part 3: Supporting evidence | Part 4: Reversing CHD | Part 5: Better than statins

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Last updated: December 9, 2011