Following the identification of ascorbic acid as the “antiscorbutic factor,” human volunteers attempted to induce scurvy in themselves by subsisting on a vitamin C-free diet. J. Menshing, in Germany, ate a virtually vitamin C-free diet for 100 days; his blood vitamin C fell to zero but there were no discernible signs of scurvy. H. Rietschel and H. Schick repeated the experiment, extending the period of deprivation to 160 days but again without the appearance of any overt signs of scurvy (Rietschel and Mensching 1939). J. H. Cran-don, in the United States, deprived himself of vitamin C and noted the appearance of the first recognizable signs of scurvy after some 5 months (Crandon, Lund, and Dill 1940).
However, the first controlled study designed to produce scurvy in humans was undertaken at Sheffield in England during the latter stages of the Second World War and published in 1953 (eight years after the conclusion of the work) as Medical Research Council Special Report (Medical Research Council 1953).Twenty young volunteers (aged 21 to 34) took part in the experiment; anecdotal reports indicate that they were conscientious objectors to military service, although, understandably perhaps, this information was not included in the official report of the study.
All participants were placed on a vitamin C-free diet. Ten received no supplements; seven were given 10 mg ascorbic acid daily; and three received 70 mg ascorbic acid daily. The general picture to emerge was that the classical signs of scurvy (hyperkeratotic follicles, gum lesions, impaired wound healing - in that order) were experienced by those in the deficient group but not by either of the supplemented groups.
The hair follicle changes occurred after 17 weeks of deprivation and the gum changes after 26 weeks - somewhat later than the corresponding period calculated by Barnes in 1864. The difference presumably reflected differences in the subjects’ vitamin C status at the beginning of the deprivation period. Furthermore, a supplement of 10 mg ascorbic acid was sufficient to restore the scorbutic subjects to normal health.
The report recommended that “in order to arrive at a figure for a daily allowance which covers individual variations and includes a safety margin, it is suggested that the minimum protective dose of 10 mg be trebled” (Medical Research Council 1953:145). For 40 years the United Kingdom Recommended Daily Allowance for vitamin C remained at 30 mg, and the experimental evidence for this amount was the single “Sheffield Study” of 1944 - a study that, in terms of sex and age alone, it may be argued, was based on a completely unrepresentative population group.
A similar investigation, but with fewer participants, was reported from the United States in 1969.The subjects in this instance were prisoners who “bought” remission periods by subjecting themselves to scurvy. The signs of deficiency appeared somewhat earlier than in the “Sheffield Study” - skin lesions in 8 to 13 weeks and gum changes in 11 to 19 weeks (Hodges et al. 1971). Both the Sheffield and the U. S. projects included wide-ranging physiological and pathological examinations, and further projects of this nature are unlikely to add very much to our clinical knowledge of the condition.
There remain, of course, peripheral problems that are of some academic interest but of little practical significance, such as the identification of further species unable to synthesize ascorbic acid and, therefore, susceptible to scurvy - and the mirror image of this, the search for a mutant form of guinea pigs resistant to scurvy. One of the more interesting current problems centers on the apparent refractiveness of the elderly to scurvy; it has been shown that persons over 80 years of age may have extremely low blood levels of ascorbic acid without the emergence of any of the expected clinical features (Hughes 1981: 60).