Vitamin C and Copper Status

What is vitamin C? Is there such a thing as a vitamin C complex? Why do so many people now believe in the complex?

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Post Number:#1  Post by desolation » Fri Jan 05, 2007 1:36 pm

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." ... 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]

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Post Number:#2  Post by DanSco » Thu Jan 11, 2007 5:53 pm

I have both Sally Fallon's cookbook and Mary Enig's Fats book. I consider them to be excellent books even though I know that they are not 100% correct.( very few things are!).
This may be headed a little off-topic, but I'll ask the obvious question: What is ceruloplasmin oxidase activity? If I have too little or too much of it, how does my health change?

Note: I am not a doctor nor do I pretend to be one on the internet. Do not duplicate what I do without a pat on the head from your doctor and a note from your mommy.

Posts: 42
Joined: Wed Aug 30, 2006 11:34 am

Post Number:#3  Post by desolation » Fri Jan 12, 2007 12:36 am

"A blue copper-binding serum oxidase that is deficient in Wilson's disease and that may catalyze the conversion of ferrous iron in tissues to ferric iron. The main copper-containing protein in plasma."

"Copper, largely tied up as protein, enters the stomach, and there and in the upper intestine [Sachs, et al] [Underwood p70], the proteins other than those entering from the bile [Owen] are degraded (bile proteins are degraded in infant rats when glucocorticoids are low [Mistillis & Mearrick] ), thus making the bile the means of excretion for adults [Sarkar p246]. Loss in sweat is usually negligible [Underwood p74} as are losses in urine [Evans 1973b p547]. The copper is moved across cell walls possibly associated with certain amino acids [Neumann PZ & Silverberg M] [Sarka p236]. It may be alpha aminoisobuteric acid which is involved since this amino acid behaves the opposite of other amino acids from cortisol [Chambers, et al]. The copper moves past a metallothionein barrier inside the cells [Cohen, et al] into the serum. Both copper and zinc increase the metallothionein barrier [Oestreicher & Cousins]. The serum carries it, largely complexed to albumin and histidine [Frieden 1980 p104], to the liver. The liver rapidly [Peisach, et al p482] removes it and stores it until such time as unknown hormones (which probably do not include cortisol in any direct way) cause the liver to release ceruloplasmin (which protein contains copper) to bring copper to the target cells [Frieden] for general purposes, as well as unbound copper when under stress. Adrenaline (epinephrine) stimulates ceruloplasmin release 150% [Weiner and Cousins] as well as free copper and may be the stress hormone for copper [Evans 1973b p556, 557]. Cortisol does not directly mobilize copper in stress. I suspect the immune peptide hormones may be used to stimulate copper for immunity but I have no data. The ceruloplasmin transporter is destroyed by the target cells, which includes those that make bile proteins for copper excretion. Ceruloplasmin has a half-life of 130 hours [Sternlieb]."

"Ceruloplasmin may function as an antioxidant in two different ways. Free copper and iron ions are powerful catalysts of free radical damage. By binding copper, ceruloplasmin prevents free copper ions from catalyzing oxidative damage. The ferroxidase activity of ceruloplasmin (oxidation of ferrous iron) facilitates iron loading onto its transport protein, transferrin, and may prevent free ferrous ions (Fe2+) from participating in harmful free radical generating reactions."

"Serum copper largely reflects serum ceruloplasmin, and is not a sensitive indicator of copper nutritional status. Serum ceruloplasmin levels are known to increase by 50% or more under certain conditions of physical stress, such as trauma, inflammation, or disease. Because over 90% of serum copper is carried in ceruloplasmin, elevated serum copper may simply be a marker of the inflammation that accompanies atherosclerosis."

My initial guess would be to note that as we see in the final paragraph above, vitc is also increased during times of stress, thereby counteracting the affect of stress and hence lowering ceruloplasim, inflammation, atherosclerosis, etc. As we know from the studies previously posted, though ceruloplasim is decreased-there is no copper deficiency.

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