Vitamin C (ascorbic acid) is an important water soluble antioxidant in humans. In this role, vitamin C interacts primarily with glutathione and vitamin E to protect the cell from oxidative stress. Vitamin C can by synthesised in most mammals, but humans must obtain their vitamin C from the diet as they do not possess the necessary L-gulonolactone enzyme. As a result insufficient dietary intakes of vitamin C lead to a series of metabolic disorders that manifest themselves as serious disease. Such disorders include tissue fragility, capillary haemorrhages, and delayed wound healing, the manifestation of which is termed scurvy. Although a deficiency of vitamin C is fatal within weeks, it is increasingly being recognised that chronic low intakes of vitamin C above the threshold for an outright deficiency may lead to sub-clinical symptoms that only manifest in disease over much longer time scales. Such insufficient vitamin C intakes have been suggested to play a role in the development of cardiovascular disease.
For example, the association between leukocyte vitamin C levels and cardiovascular disease have been investigated. One group of researchers measured the leukocyte vitamin C concentrations in patients with and without coronary artery disease1. The results showed that those patients with coronary atherosclerosis had vitamin C leukocyte levels that were significantly lower compared to subjects without coronary atherosclerosis. There was also a significant inverse associations between the levels of ascorbic acid and the abnormality observed in the coronary arteriograms in smokers. Therefore it appears that the vitamin C concentrations in leukocytes are correlated with certain subtypes of cardiovascular disease. The role of vitamin C in cardiovascular disease is well reported in the specialist nutritional literature. It was Linus Pauling that popularised the idea that vitamin C insufficiency may be a driver of cardiovascular disease, which he explained as being related to changes in lipoprotein(a) (here).
Certainly the structural changes seen in the aorta of scorbutic subject resembles some of the physiological changes that occur during the development of cardiovascular disease. In particular, endothelial proliferation accompanied by intimal thickening as well as a high degree of metachromasia (changes in staining colour) in the ground substance have been found in experimental animals deprived of vitamin C. Structural changes also occur in the liver with vitamin C deficiency, and this may contribute to the higher levels of cholesterol, nonesterified fatty acids, cholesterol esters and phospholipids that occur with vitamin C deficiency, all of which are reversed on repletion with the vitamin. The elevated cholesterol levels may also result because the conversion of cholesterol to bile acids is mediated by cytochrome P450, which is synthesised in the present of vitamin C. The efficacy of vitamin C to lower plasma cholesterol levels adds weight to the role of vitamin C in cardiovascular disease.
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