A final possibility is that the megadoses of vitamin C induced some redistribution of body iron stores that masked an actual increase in total body iron. In patients with
iron overload and secondary
ascorbic acid deficiency, parenteral ascorbic acid promotes iron release from the reticuloendothelial cell,
26,
27 which is the immediate precursor compartment for circulating ferritin. There was a tendency for serum ferritin levels to fall in iron-replete subjects during the early part of the study (
Fig 3), which is consistent with some redistribution from reticuloendothelial stores. However, our subjects were neither iron loaded nor ascorbic acid depleted. Furthermore, we have been unable to demonstrate any acute effects on serum iron or serum ferritin levels when normal subjects are given 500 mg ascorbic acid three times daily for 14 days (
Fig 3). A final point is that some initial redistribution of body iron stores would not obscure a long-term effect on serum ferritin levels.