Vitamin C deficiency effects

VITAMIN C IN HEALTH AND DISEASE

Tissue saturation of vitamin C occurs in humans at intakes of about 100 mg/day; higher intakes can result in elevated concentrations of the vitamin in extracellular fluids (plasma, connective tissue fluid, humors of the eye) where pharmacologic action of this antioxidant vitamin may be possible. Accordingly, vitamin C intakes greater than those required to prevent scurvy have been considered for a variety of health purposes. Many of the clinical studies in which supranutritional doses of vitamin C have been found to be of some benefit have compared treated subjects with controls who did not have tissue saturation with respect to the vitamin. Such studies therefore cannot indicate whether the effects of the vitamin C treatments were due simply to achieving tissue saturation or to pharmacologic actions of the vitamin in extracellular fluids. Thus, while there appear to be benefits associated with increasing vitamin C intakes to levels that effect tissue saturation, the evidence in support of benefits of vitamin C doses above that level is not clear.

Vitamin C deficiency effects


Immunity and Inflammation

Ascorbic acid has been found to affect immune function in several ways. It has been shown to modulate T cell gene expression, specifically affecting genes involved with signaling, carbohydrate metabolism, apoptosis, transcription, and immune function.  It can stimulate the production of interferons, the proteins that protect cells against viral attack. It can stimulate the positive chemotactic and proliferative responses of neutrophils. It can protect against free radical-mediated protein inactivation associated with the oxidative burst of neutrophils. It can stimulate the synthesis of humoral thymus factor and antibodies of the IgG and IgM classes. Some studies have found massive oral doses of the vitamin (10 g/day) to enhance delayed-type hypersensitivity responses in humans, although somewhat lower doses (2 g/day) have shown no such effects.

Common Cold

The most widely publicized use of so-called megadoses of vitamin C are in prophylaxis and treatment of the common cold. Large doses (1 g) of vitamin C have been advocated for prophylaxis and treatment of the common cold, a use that was first proposed some 25 years ago by Irwin Stone and the Nobel laureate Dr Linus Pauling.  Since that time, many controlled clinical studies have been conducted to test that hypothesis . Whereas many of these have yielded positive results, until recently few have been appropriately designed, with respect to blinding, controls, treatment randomization, and statistical power, to make such conclusions unequivocal. In general, most results have indicated only small positive effects in reducing the incidence, shortening the duration, and ameliorating the symptoms of the common cold.

Heliobacter pylori

Randomized trials have shown that vitamin C supplementation can reduce seropositivity for H. pylori and protect against the progression of gastric atrophy in seropositive patients.  This appears to be related to reduced risk of gastric cancer, for which H. pylori is a risk factor.

Herpes

Topical application of ascorbic acid reduced the duration of lesions as well as viral shedding in patients with Herpes simplex virus infections.

Other Infections

Ten of 14 randomized controlled trials found apparent reductions in incidence,  and 8 of 10 found apparent reductions in severity, of infections other than colds. Nevertheless, the results of studies of vitamin C and infections have been inconsistent. Some studies with scorbutic guinea pigs, fishes, and rhesus monkeys have shown vitamin C deficiency to decrease resistance to infections, but several studies have yielded negative results.

Cardiovascular Health

The antioxidant characteristics of ascorbic acid allow it to have an anti-atherogenic function in reducing the oxidation of low-density lipoproteins (LDLs), a key early event leading to atherosclerosis.86 Being rich in both cholesterol and polyunsaturated fatty acids (PUFAs), LDLs are susceptible to lipid peroxidation by the oxidative attack of reactive oxygen species. Research has shown that oxidized LDLs stimulate the recruitment, in the subendothelial space of the vessel wall, of monocyte-macrophages that can take up the oxidized particles via scavenger receptors  to form the lipid-containing foam cells found in the early stages of atherogenesis.

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