not be used to estimate a vitamin C requirement using the end-point of reduction of oxidative damage to DNA and chromosomes.
As summarized in Table 5-8, vitamin C has been shown to affect various components of the human immune response, including antimicrobial and natural killer cell activities, lymphocyte proliferation, chemotaxis, and delayed dermal sensitivity (DDS). Except for the metabolic unit study of Jacob et al. (1991) and the study of patients with furunculosis (Levy et al., 1996), the studies involved apparently healthy free-living populations supplemented with from 200 mg/day to 6 g/day of vitamin C in addition to dietary vitamin intake. Hence, the results relate largely to the pharmacological range of vitamin C intakes rather than the nutritional range of intakes usually provided from food alone.
As seen from analysis of Table 5-8, vitamin C supplementation resulted about equally in improved or little change in frequently used measures of immune function: lymphocyte proliferation, chemotaxis, and DDS response. The decrease in DDS during vitamin C depletion of men in a metabolic unit cannot be ascribed solely to changes in ascorbate status because the DDS did not increase again upon repletion for 4 weeks with 60 to 250 mg/day of the vitamin (Jacob et al., 1991). The only negative effect of intakes in the range of 600 to 10,000 mg/day was the decrease in ex vivo bactericidal activity found after apparently healthy men received 2,000 (but not 200) mg/day of the vitamin for 4 weeks (Shilotri and Bhat, 1977).
Few controlled studies of the effect of vitamin C intake on infectious episodes in humans have been reported, except for studies of the common cold (covered later under “Common Cold” in the section “Relationship of Vitamin C Intake to Chronic Disease”). Peters et al. (1993) reported a significantly decreased incidence of post-race upper respiratory infections in marathon runners receiving 600 mg/day of vitamin C compared to control runners taking a placebo.
Results from some studies show improvement in indices of immune function due to increased vitamin C intake, whereas other studies show no effect. The lack of effect may be due to the use of subject populations whose baseline vitamin C status is already adequate, because leukocytes saturate with vitamin C at a lower intake than is required to saturate plasma, about 100 mg/day (Levine et al., 1996a). Nevertheless, the existing data do not provide convincing evidence that supplemental vitamin C has a significant effect on