When there is insufficient ascorbate, then Lp(a) is intentionally synthesized – Lp(a) infiltrates the area of injury, together with other lipoproteins and repair substances, to form a “sticky” patch, which is liable to grow into plaque if the substitute function of Lp(a) is overused.

Human and non-human primates are pretty much the only animals that develop atherosclerosis (although rabbits and some other rodents can be forced to develop heart disease when fed a diet loaded with saturated fat and cholesterol, but the disease process is very different from that seen in humans).

Drs. Pauling and Rath proposed that Lp(a) is a surrogate for ascorbate in human and non-human primates (E.g. apes, monkeys, lemurs), the guinea pig and thefruit bat. Detectable amounts of Lp(a) are found almost exclusively in the blood of these species, which have lost the ability to make their own vitamin C, but rarely in the blood of animals that still produce their own vitamin C (the European hedgehog is one exception!).

Dr. Pauling’s hypothesis is that primates evolved Lp(a) to help them heal blood vessels which were more prone to injury because they had been weakened by poor collagen synthesis due to lack of vitamin C – i.e. Lp(a) was a quick survival response to injury for the short and dangerous lives of our paleolithic, hunter/gatherer ancestors;

Vitamin C dosages sufficient to correct our lack of C does not necessarily lower Lp(a) levels, but may simply keep blood vessel walls strong, preventing injuries that require the binding of Lp(a)

A small human trial run by Dr. Rath, people with high Lp(a) levels who supplemented with 9g of ascorbate for 14 weeks experienced an average 27% reduction in Lp(a) levels. However, a larger, controlled trial failed to confirm this result. The larger trial used only half of the dose of vitamin C used in Dr. Rath’s trial, so the result could just be due to a failure to use enough ascorbate. Lp(a) levels, which are mostly determined by your genes, may take a while to return to normal lower levels, or it may be that vitamin C doesn’t actually lower the level of Lp(a). The only conclusively proven ways to lower Lp(a) levels are niacin supplements (which can be taken in the form of inositol hexanicotinate).

If sufficient vitamin C is available to protect the vessel from injury and to participate in vascular repair, the need for Lp(a) is immaterial. Without adequate amounts of vitamin C, Lp(a) is a life-saver.

Guinea pig Experiments – Ascorbate (40 mg / kg of body weight per day) prevented the development of atherosclerotic lesions in the guinea pig and the accumulation of Lp(a) in the arterial wall. An analogous mechanism in humans is suggested because of the similarity between guinea pigs and humans with respect to both the lack of endogenous ascorbate production and the role of Lp(a) in human atherosclerosis. The guinea pig is the only rodent that does not synthesize its own vitamin C. In the 1950s, the Canadian cardiologist Dr. G. C. Willis demonstrated that guinea pigs on a diet lacking saturated fat or cholesterol develop lipid deposits in their arteries (identical to human atherosclerosis), if their diet is also low in vitamin C. Dr. Willis also found that this atherosclerosis could be reversed by high-dose vitamin C supplementation.

Pauling and Rath repeated and expanded Dr. Willis’ work, suggesting that:

The minimum amount of vitamin C required to prevent the development of atherosclerosis in a 70 kg (154#) human, is 2,800 mg of vitamin C /  day.