Research: LYNCH and colleagues, Whi

Listed in Issue 28


LYNCH and colleagues, Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts USA review (165 references) the current scientific knowledge regarding the role of vitamin C in the prevention of atherosclerosis and its associated clinical conditions. @r:Reliable evidence from animal studies demonstrates that vitamin C can retard the progression of experimental atherosclerosis. The majority of these studies were however performed either in guinea pigs, using vitamin C depletion, or in cholesterol-fed rabbits, using vitamin C supplementation. Both these animal models have their limitations, because guinea pigs are neither a well-established nor well-studied model for atherosclerosis, and rabbits develop atherosclerosis at high serum beta-VLDL cholesterol levels, in addition to being capable of vitamin C synthesis. Humans, in contrast, develop atherosclerosis spontaneously and readily at moderately elevated serum LDL cholesterol levels and have lost the ability to synthesise vitamin C. Therefore, although the animal studies described are quite promising and suggestive of the anti-atherogenic effect of vitamin C, this research needs to be expanded to primates before more definitive conclusions may be drawn. Similarly, the current evidence from epidemiological studies regarding the role of vitamin C in the prevention of CVD is inconclusive. Some studies indicate a very strong correlation between increased vitamin C intake and incidence of CVD events, while other studies show no correlation. Studies regarding CVD risk factors demonstrate that vitamin C may moderately decrease total serum cholesterol levels, increase HDL levels and exert a hypotensive effect. These findings are most interesting and should be followed up vigorously in basic research studies to elucidate biological mechanisms. Additionally, large placebo-controlled, double-blind, randomised trials of vitamin C supplementation (without simultaneous supplementation with vitamin E) are needed, in populations with a wide range of vitamin C body levels, in order to confirm or refute a role for vitamin C in the prevention of CVD. However, no such trials are being conducted. The possible mechanisms by which vitamin C may affect the development of atherosclerosis and the onset of acute coronary events include effects upon arterial wall integrity related to biosynthesis of collagen and GAGs, altered cholesterol metabolism mediated by vitamin C-dependent conversion of cholesterol to bile acids, and effects upon triglyceride levels via modulation of lipoprotein lipase activity. Another intriguing possible mechanism for the anti-atherogenic effect of vitamin C is the prevention of atherogenic, oxidative modification of LDL. Many in vitro studies have shown that vitamin C strongly inhibits LDL oxidation by a variety of mechanism. The potential effects of vitamin C upon platelet function and EDRF metabolism are particularly fascinating, as they may have widespread consequences in the prevention of atherosclerotic lesion development and acute clinical events. Therefore, both metabolic and antioxidant functions may contribute to the possible reduction of CVD risk by vitamin C.






Lynch SM et al. Ascorbic acid and atherosclerotic cardiovascular disease. Subcell Biochem (25): 331-67. 1996.


Alas, there is never perfection in scientific research, especially regarding vitamin C. No matter how many fantastic studies have been performed, in vitro, in animals and with human trials, there are flaws and limitations with the design, the populations or animal hosts used. However, despite the list of limitations listed, the authors have produced a strong list of how vitamin C retards and/or prevents atherosclerosis, as well as a list of possible mechanisms for vitamin C's anti-atherogenic effects. @i:67

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