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fermer ce livreScurvy and its Prevention and Control in Major Emergencies (WHO; 1999; 70 pages)
Afficher le documentAcknowledgements
Afficher le documentScurvy: definition
ouvrir ce répertoire et afficher son contenuIntroduction
ouvrir ce répertoire et afficher son contenuScurvy
ouvrir ce répertoire et afficher son contenuVitamin C
fermer ce répertoireRecommended Daily Allowance (RDA)
Afficher le documentProblem of calculating RDA for vitamin C
Afficher le documentMinimum or optimum requirements
Afficher le documentFactors affecting vitamin C reserves
Afficher le documentMegadoses
Afficher le documentHypervitaminosis/vitamin C toxicity
Afficher le documentSupplementation frequency
ouvrir ce répertoire et afficher son contenuSources of vitamin C
ouvrir ce répertoire et afficher son contenuStrategies to prevent scurvy in large refugee populations
Afficher le documentCosts
ouvrir ce répertoire et afficher son contenuConclusions and recommendations
Afficher le documentReferences
Afficher le documentAnnex 1
Afficher le documentAnnex 2
Afficher le documentAnnex 3
Afficher le documentBack Cover
 

Hypervitaminosis/vitamin C toxicity

It is not known to what extent routine ingestion of very high doses of vitamin C seriously impairs health in a lasting way. Occasional large intakes of vitamin C may cause stomach cramps, nausea, and diarrhoea in some fasting subjects but have no long-term adverse effects. Several mechanisms prevent excessively high concentrations of ascorbic acid in blood plasma (Hodges, 1980). Only a certain amount of vitamin C can be absorbed, and if more is ingested it will be excreted in the faeces. The second line of defence is the kidneys, which excrete excess amounts. A third protective mechanism is that food generally contains small amounts of the vitamin. The frequency of reported toxic manifestations is very low relative to the number of persons routinely ingesting large doses (Olson & Hodges, 1987).

It has been specifically proposed that megadoses of vitamin C increase oxalate production (thereby increasing the formation of renal stones); competitively inhibit renal reabsorption of uric acid; enhance the destruction of vitamin B12 in the gut; intensify the enteric absorption of non-haem iron, thus leading to iron overload; result in mutagenic effects; and increase vitamin C catabolism that would persist after returning to lower intakes of the vitamin (Combs, 1992). These and other possible effects of high doses have been reviewed by Hornig and Moser (1981) and Rivers (1989), who conclude that ingestion of even massive amounts of vitamin C (up to 10 g/day) does not usually constitute a health risk for humans. Nevertheless, large doses are contra- indicated in cases of renal insufficiency, chronic haemodialysis, unusual forms of iron overload, and in oxalate stone formers.

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