Vitamin C is essential for the production of collagen and other connective tissue components in the body. Most animals synthesize their own vitamin C according to needs. However, about 40 million years ago this ability was lost in our human ancestors as a result of a genetic mutation. Therefore, we have to obtain vitamin C from our diet or through nutritional supplements.

Dr. Rath introduced the groundbreaking concept of a “Scurvy-vitamin C-heart disease-connection” over two decades ago. According to this concept, heart disease is an early form of scurvy, a condition that increases the needs for biological repair of weakened arterial walls due to impaired collagen synthesis in the body. As a consequence, cholesterol transporting molecules, such as, LDL and Lp(a) deposit in the vascular walls as reinforcing factors, but at the same time contribute to a buildup of atherosclerotic plaques increasing the risk of heart attack or stroke.

The connection between vitamin C and atherosclerosis was confirmed in a scientific experiment in guinea pigs that, similar to humans, cannot produce their own vitamin C¹. We observed that guinea pigs that were fed a five-week diet deprived of vitamin C developed atherosclerotic deposits in the arterial tree accompanied by damage to the inner lining of the artery wall specifically at areas closer to the heart at the site of maximum mechanical stress. However, animals supplemented with vitamin C did not show any significant structural changes in their blood vessels. This study confirmed that the invariable consequence of ascorbate deficiency is loosening of the connective tissue and the loss of the protective barrier in artery walls.

Another important feature of human metabolism is its ability to produce a specific lipoprotein - lipoprotein(a) - which is absent in animal species. Dr. Rath proposed that the appearance of Lp(a) at the time of a loss of vitamin C production had offered significant advantage to the ancestors of man². The Lp(a) can act as a physiological surrogate to compensate for the vitamin C deficiency by protecting the integrity of blood vessel walls. In order to avoid the fatal consequences of extreme ascorbate depletion, such as hemorrhagic bleeding, our body increases the concentration of specific “repair” factors including Lp(a), fibrinogen, etc. These temporary “repair” factors can compensate for the connective tissue impairment, but if vitamin C insufficiency continues, this repair process overshoots resulting in atherosclerotic build up leading to heart attacks and stroke.

Recently, we confirmed the vitamin C-Lp(a)-heart disease connection using our unique animal model which mimics human metabolism in respect to its two critical aspects: inability to synthesize vitamin C (Gulo^-/-) and internal synthesis of human Lp(a) (Lp(a)⁺). We observed that {Gulo^-/-;Lp(a)⁺}mice fed a diet low in vitamin C have a high level of Lp(a) deposits in the vascular walls, develop atherosclerotic plaques and have increased blood levels of Lp(a) compared to animals supplemented with high doses of vitamin C^3.

While our study confirms that vitamin C is essential to maintain healthy blood vessels and reduce atherosclerosis, the Dr. Rath Research Institute has also clinically proven that vitamin C is not the only nutrient critical in maintaining a healthy cardiovascular system. We have established that vitamin C, in combination with the amino acids lysine, proline and other specific nutrients, is critical for maintaining healthy arteries and the cardiovascular system.

Ref:

1. 1.M. Rath, L. Pauling, Proc. Nati. Acad. Sci. USA Vol. 87, pp. 6204-6207, 1990
2. 2.M. Rath, L. Pauling; Journal of Orthomolecular Medicine 1991, 6:125-134
3. 3.J. Cha, A. Niedzwiecki, M. Rath; Am J Cardiovasc Dis 2015;5(1):53-62