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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
close this folderScurvy
close this folderSigns and symptoms
View the documentClassic scurvy
View the documentExperimental scurvy
View the documentMild vitamin C deficiency
View the documentScurvy in pregnant and lactating women and infants
View the documentDiagnosis of scurvy
open this folder and view contentsHistory of scurvy
open this folder and view contentsVitamin 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

Experimental scurvy

Several studies have been undertaken to determine the extent to which human scurvy, as seen clinically, can be explained purely by a deficiency of vitamin C in the diet. The English physician William Stark began a series of experiments on himself in the mid-1700s. During the first 12 weeks he lived on bread and water with a little sugar, at the end of which he was "dull and listless" with swollen gums that bled easily. For the next 3 weeks he consumed a more varied diet and recovered. Next, he returned to bread or flour with various supplements in turn-olive oil, butter, animal fat, a little cooked lean meat, and finally honey. He died about 6 months later, presumably of scurvy.

In 1939, John Crandon, a surgeon at Harvard Medical School, placed himself on a diet of bread, crackers, cheese, eggs, beer, pure chocolate, and sugar with supplements of yeast and all the known vitamins except vitamin C. From 6 weeks onwards no ascorbic acid could be detected in his blood plasma. After 12 weeks he began to feel fatigued. No clinical signs of deficiency developed until the 19th week when his skin became dry and rough and signs of hyperkeratosis began to appear. After 23 weeks small haemorrhages began to occur on his lower legs. He also had two self-inflicted wounds on his back. The first, made after 13 weeks on the diet, showed normal healing ten days later; while the second, made after 26 weeks, showed no sign of healing within ten days. Various tests showed rapid exhaustion. He was then given, by intravenous injection, 1 g of ascorbic acid each day for a week. A subjective improvement was noticed in the first 24 hours, and his second back wound healed rapidly within the following ten days.

During World War II an experiment was carried out in Sheffield, England, on volunteers who objected to military service. Their basic diet included milk, which was aerated for 30 minutes at 70°C with 1 ppm of copper added; and dried potato strips that were boiled in large volumes of water, left to stand in the water for 90 minutes, then mashed and kept hot for 30 minutes before being served. Daily vitamin C intake was less than 1 mg, although levels of other vitamins and iron were satisfactory (Hodges et al., 1971). After a variable period in which they received 50 mg supplementary ascorbic acid per day, ten of the volunteers received no more of the vitamin for 26-38 weeks. Ten others received either 10 mg or 70 mg per day. It took between 4 and 11 weeks for plasma levels of vitamin C to fall to undetectable levels. After 17 weeks, the subjects whose plasma level had fallen fastest showed some hyperkeratotic follicles on his upper arm; 4 weeks later, this was true of six of the ten subjects; and after 20 weeks in all ten, along with haemorrhaging in six. After 30 weeks without vitamin C, changes began to appear in the gums. By the 36th week, nine of the ten subjects had purplish, swollen, spongy and bleeding gums. After 26 weeks, wounds did not heal properly and subjects complained of pain and stiffness in their joints. In the 36th week, one subject, the day after heavy physical exercise, woke up with severe pain and difficult breathing. This was considered a cardiac attack due to scorbutic haemorrhage, which was also seen in another subject. Symptoms disappeared within 24 hours of receiving 1 g of vitamin C. The other members of the group were given a daily supplement of 10 mg vitamin C. All showed improvement after 2 weeks, their skin appeared normal after 8 weeks, and their gums were completely normal after 10-14 weeks. The group that received 10 mg vitamin C from the beginning of the trial developed no signs of deficiency, although vitamin C blood levels were at zero (Hodges et al., 1971).

Twenty years later another study was undertaken among prisoners in Iowa City, USA. For a hundred days, 4 male volunteers consumed a liquid purified diet composed of casein, sucrose, starch, oils, minerals, vitamins (other than C), and the amino acid cystine. The vitamin C content of the mixture was zero. Subjects were required to walk some 10 miles a day, and they maintained approximately constant weight on their 3000-calorie diet. Observations were similar to those seen in other studies except that signs appeared earlier-skin changes in 8-13 weeks and gum changes in 11-19 weeks. This was probably due to the fact that the diet contained absolutely no vitamin C. After 100 days, subjects were given doses of 6.5-34.5 mg vitamin C per day and all signs of scurvy disappeared (Hodges et al., 1969).

In 1953, the British Medical Research Council reviewed previous experimental studies and concluded that healthy men have stores of vitamin C sufficient to enable them to remain on deficient diets for periods ranging from 160-200 days without developing overt scurvy (Hodges et al., 1971). It was also stated that a daily dose of 10 mg of vitamin C was sufficient to prevent scurvy for as long as 424 days and that the same dose was enough to cure scurvy once it had appeared.

Experiments have shown that the onset of scurvy signals the development of serious consequences and that treatment should follow immediately. It is important to note that scurvy, as it appears today among refugees, is generally more severe and involves more systems than experimental scurvy. This is due to such factors as multiple deficiencies (e.g. anaemia), climatic extremes, a high level of physical activity, and associated infectious diseases. Otherwise, experimental and spontaneous scurvy are remarkably similar in clinical presentation.

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