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American Journal of Clinical Nutrition, Vol 24, 432-443, Copyright © 1971 by The American Society for Clinical Nutrition, Inc.
1 From the Department of Internal Medicine, University Hospitals, University of Iowa, Iowa City, Iowa 52240, and the U.S. Army Medical Research and Nutrition Laboratory, Fitzsimons General Hospital, Denver, Colorado 80240
Six healthy volunteers from the Iowa State Penitentiary at Fort Madison, Iowa, participated in studies of human scurvy. They were hospitalized on the Metabolic Ward of University Hospitals in Iowa City, Iowa, and fed a diet totally devoid of vitamin C.
One of the men withdrew from the study because of personal reasons. The remaining five subjects developed clinical scurvy in 84 to 97 days, manifested by signs and symptoms of fatigue, hemorrhagic phenomena, swollen joints, swollen bleeding gums, follicular hyperkeratosis, muscular aches and pains, and emotional changes.
Urinary ascorbic acid rapidly declined to undetectable levels early in the course of depletion and blood levels progressively became too low to measure accurately. Serum protein abnormalities appeared that consisted primarily of a decrease in albumin and an increase in alpha-2 and gamma globulins. Other changes occurred in serum lipids.
Radioisotopic studies indicated progressive depletion of the body pools during the depletion phase of the study and repletion in proportion to the amount of ascorbic acid administered daily. This study confirms and extends the observations made in our earlier study that the full clinical syndrome does not appear until the normal body pool has been depleted to less than 300 mg.
The minimal amount of ascorbic acid necessary to prevent or cure scurvy appears to be slightly less than 10 mg daily. Once again our observations are in accord with those of the British Medical Research Council. Estimates of the optimal intake of ascorbic acid must be made on the basis of these data plus a knowledge of the biological and physiological variables of mankind.
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