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American Journal of Clinical Nutrition, Vol 22, 535-548, Copyright © 1969 by The American Society for Clinical Nutrition, Inc.
1 Department of Internal Medicine, University of Iowa, Iowa City, Iowa 52240
Six apparently healthy men from the Iowa State Penitentiary volunteered for metabolic studies of human scurvy. They were hospitalized on the metabolic ward and given a diet totally devoid of vitamin C but adequate in all other essential nutrients. Although two of the prisoners escaped, the remaining four developed clinical signs of scurvy; follicular hyperkeratosis of the thighs, buttocks, calves, and the posterior aspects of the arms; swollen bleeding gums; perifollicular hemorrhages and congested follicles; and conjunctival hemorrhages. Biochemically there was virtually complete disappearance of ascorbic acid from the blood and urine, although an interfering substance gave erratic results once deficiency occurred.
Carbon-14 labeled l-ascorbic acid was used to estimate the pool size in these subjects and to measure the rate of catabolism of this vitamin. These results are reported elsewhere (6)
Blood counts, numerous biochemical measurements, the rate of wound healing, and physiologic tests including electrocardiograms, electroencephalograms, basal-metabolism rates, and blood coagulation studies, showed no abnormalities as a result of induced scurvy.
It is estimated that clinical symptoms began to appear when the total body pool had decreased to approximately 300 mg and when the rate of catabolism of vitamin C had fallen to less than 2.5 mg daily.
The present studies do not provide sufficient evidence to estimate the optimal daily allowance of ascorbic acid, nor do they answer the question of what enzymatic roles are supplied by ascorbic acid, but they are in close accord with the British Sheffield study (4) in which a supplement of 10 mg ascorbic acid daily was found to cure and to prevent clinical scurvy.
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