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close this bookScurvy and its Prevention and Control in Major Emergencies (WHO; 1999; 70 pages)
View the documentAcknowledgements
View the documentScurvy: definition
open this folder and view contentsIntroduction
open this folder and view contentsScurvy
close this folderVitamin C
View the documentDiscovery
close this folderProperties
View the documentChemistry
View the documentPhysiology
View the documentMetabolic functions
View the documentUse of vitamin C
open this folder and view contentsRecommended Daily Allowance (RDA)
open this folder and view contentsSources of vitamin C
open this folder and view contentsStrategies to prevent scurvy in large refugee populations
View the documentCosts
open this folder and view contentsConclusions and recommendations
View the documentReferences
View the documentAnnex 1
View the documentAnnex 2
View the documentAnnex 3
View the documentBack Cover


Vitamin C is readily absorbed from the gastrointestinal tract by an active transport mechanism, particularly at low intakes of the vitamin. Uptake by passive diffusion also occurs and is likely to be important at higher vitamin C intakes (Combs, 1992). A dose of less than 100 mg will be almost completely absorbed, whereas only about 70% of a dose of 180 mg is absorbed. When the dose is further increased to 1500 mg, only about half is absorbed, while at a level of 1.2g, only 16% is absorbed (see Table 7). The unabsorbed ascorbic acid remaining in the lumen of the bowel exerts an osmotic effect and can cause loose watery diarrhoea (Hodges, 1980). Absorption can be impaired in the aged and persons with excessive destruction or damage to the gastrointestinal tract.

Once L-ascorbic acid is absorbed, it is distributed throughout the body's water-soluble compartments. The metabolically active pool is approximately 1500 mg in healthy middle-aged men (Baker et al., 1971). In guinea pigs the concentration of this vitamin is highest in the adrenals, pancreas, salivary glands, testes, and brain (Hodges, 1980). There is no stable reserve of vitamin C; the major fractions are found in the liver and muscles by virtue of their relatively large mass (Combs, 1992). Excess of vitamin C is rapidly excreted largely in urine, but also to some extent in sweat and faeces. Thus, loss of vitamin C mainly occurs in the urine, which depend on body stores, intake and renal function (Marks, 1975). The first signs of scurvy are not seen until reserves are depleted to 300-400 mg.

A continuously low plasma vitamin C level (<0.1 mg/dl) can lead to scurvy. In humans, a plasma level of 0.4-1.4 mg/dl corresponds to a daily intake of 40 mg of vitamin C; with higher levels indicating saturation (Combs, 1992). Leucocyte vitamin C concentrations have a particular diagnostic value, as they reflect the levels found in tissues and are independent of plasma concentration. Leucocyte vitamin C concentrations are usually greater in women than men and decrease with age and some diseases (Combs, 1992). When body stores are depleted, administration of vitamin C results in storage until the tissues have been saturated, at which time urinary excretion increases. The difference between intake and excretion of the vitamin approximates the amount of vitamin utilized. The normal subject has been found to be capable of utilizing from 45 mg/day to 100 mg/day.

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