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LETTER TO THE EDITOR |
Molecular and Clinical Nutrition Section
Bldg 10, Room 4D52 –MSC 1372
National Institutes of Health
Bethesda, MD 20892-1372
E-mail: markl{at}intra.niddk.nih.gov
Dear Sir:
Concerning our recent article in the Journal (1), Bähr et al wrote that we considered oral and intravenous vitamin C supplementation in the context of paracrine vitamin C function in the adrenal gland. The statement by Bähr et al takes what we wrote out of context. We did not consider supplementation but, rather, discussed supplementation only in the context of the data we presented.
Our results showed a rapid adrenal vitamin C secretory burst after ACTH stimulation in humans that resulted in adrenal venous vitamin C concentrations 4-fold peripheral values (1). Although we suggested several possibilities, it is not known why adrenocorticotrophic hormone produces the release of adrenal vitamin C. Adrenal vein vitamin C concentrations reached during ACTH-stimulated vitamin C secretion may be similar to those attained by oral pharmacologic vitamin C intake in humans. Specifically, such pharmacologic intake is 2–3-g doses taken at intervals of several hours, which are expected to produce plasma concentrations of 
200 µmol/L (2). We noted that such high oral intake of vitamin C perhaps could either simulate or interfere with paracrine signaling by vitamin C in the adrenal vein. However, nowhere in our report did we advocate pharmacologic doses, either oral or intravenous, of vitamin C. Consistent physiologic intake of vitamin C–rich foods will produce plasma concentrations of 80–90 µmol/L. Consumption of vitamin C–rich foods, meaning fruit and vegetables, is associated with health benefits. It is not known whether such health benefits can be produced only by consuming vitamin C. For health benefits, we have advocated, and we continue to advocate, the consumption of 5–9 daily servings of varied fruit and vegetables—not vitamin C supplements.
Bähr et al described their animal and cell studies of vitamin C deprivation in guinea pigs and reported their conclusions about aldosterone secretion (3) (4). Plasma values of these animals were stated to be 10 µmol/L. These numbers were likely to be much lower because of overestimation, a problem especially at low plasma values when spectrophotometric assays are used for measuring (5). The adrenal glands of these animals had their vitamin C content reduced by 95%. By comparison, in healthy humans with steady state plasma concentrations of 6–7 µmol/L, accumulated vitamin C in circulating white blood cells is reduced by only 50–60%, not 95% (6). Despite the assertion of Bähr et al to the contrary, the animals they described were extremely deficient in vitamin C, given that their adrenals had only 5% of the normal vitamin C content. In guinea pigs with vitamin C deficiency, cortisol secretion is increased, in keeping with the stress of a systemic illness (7-9). Thus, it may be difficult to disentangle the effect of low adrenal vitamin C concentration on adrenal steroid (cortisol, aldosterone, or both) secretion from that of a pituitary-adrenal response to the stress of scurvy or possibly even to the stress of a prescorbutic state. For all of these reasons, the guinea pig depletion experiments of Bähr et al cannot be used as justification either for or against advising vitamin C supplementation in humans. Selective adrenal gland vitamin C deficiency, such as that obtained by creation of conditional knockouts of adrenal sodium–dependent vitamin C transporter 2, may enable future study of the role of vitamin C in adrenal steroid hormone secretion.
Bähr et al raised the possibility that vitamin C may serve to protect adrenal glands from reactive oxygen species produced by lipid peroxidation; this role is among the many possible functions of adrenal vitamin C, as others have also recognized and as we wrote in our article. Whereas ascorbate's function as an antioxidant seems both plausible and attractive, such action remains unproven in vivo (10).
ACKNOWLEDGMENTS
Neither of the authors had a personal or financial conflict of interest.
REFERENCES
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