I have not found fatigue, anemia, and allergies due to VITC induced copper deficiency documented anywhere. The copper defeciency scare seems to be rumour perpetuated phenomenon based on weak hypothesizes or on in vitro research wich in many cases with VITC does not hold true in vivo. Yet, this supposition is enough to negate the numerous proven immune enhancing attributes of VITC. Also, she claims it was the high doses of AA that may have had sideffects-when she switched to lower dose natural then things were better. This is not an argument of natural VITC vs. AA but of higher dose vs lesser dose.
"Although vitamin C supplements have produced copper deficiency in laboratory animals, the effect of vitamin C supplements on copper nutritional status in humans is less clear. Two small studies in healthy young adult men indicate that the oxidase activity of ceruloplasmin may be impaired by relatively high doses of supplemental vitamin C. In one study, vitamin C supplementation of 1,500 mg/day for 2 months resulted in a significant decline in ceruloplasmin oxidase activity (7). In the other study, supplements of 605 mg of vitamin C/day for 3 weeks resulted in decreased ceruloplasmin oxidase activity, although copper absorption did not decline (8). Neither of these studies found vitamin C supplementation to adversely affect copper nutritional status." http://lpi.oregonstate.edu/infocenter/m ... index.html
Influence of ascorbic acid supplementation on copper status in young adult men.
Finley EB, Cerklewski FL.
The influence of ascorbic acid supplementation on the copper status of young adult men was investigated. Subjects consuming self-selected diets took 500 mg of ascorbic acid with each meal (1500 mg/day) for 64 days. Blood samples were obtained at 0, 28, 52, and 64 days in order to determine serum copper and serum ceruloplasmin. Each subject thus served as his own control. Analyses were repeated 20 days after the ascorbic acid supplement was terminated. Serum ceruloplasmin activity was significantly reduced (p less than 0.01) at every data point throughout the ascorbic acid supplementation period. A similar but nonsignificant trend was observed for serum copper. Furthermore there was a significant increase (p less than 0.01) in serum copper concentration 20 days after the supplementation period. Although observed effects occurred within physiological ranges of normal values, this study confirms that a high ascorbic acid intake is antagonistic to copper status of men as has been demonstrated in laboratory animals.
PMID: 6837490 [PubMed - indexed for MEDLINE]
Effect of varying ascorbic acid intakes on copper absorption and ceruloplasmin levels of young men.
Jacob RA, Skala JH, Omaye ST, Turnlund JR.
Western Human Nutrition Research Center, U.S. Department of Agriculture, Presidio of San Francisco, CA 94129.
Intestinal copper absorption and blood measures of copper status were studied in healthy young men receiving varying intakes of ascorbic acid (AA) over 14 wk in a live-in nutrition suite. Copper absorption and retention were assessed by measuring absorption of a stable isotope of copper and total fecal copper during four AA intake periods: 2 wk x 65 mg AA/d, 4 wk x 5 mg/d, 3 wk x 605 mg/d and 4 wk x 5 mg/d. Measures of copper status were serum copper and serum ceruloplasmin determined by both enzymatic and immunochemical methods. Copper absorption, copper retention, total serum copper and the serum level of ceruloplasmin protein were not affected significantly by the changes in AA intake; however, the oxidase activity of serum ceruloplasmin was decreased an average of 21% during the high (605 mg/d) AA intake period. The results suggest that in adult men moderate supplemental intakes of AA reduce ceruloplasmin oxidase activity specifically but do not depress intestinal copper absorption or overall body copper status.
PMID: 3694287 [PubMed - indexed for MEDLINE]