“Experimental Human Scurvy”, 1940-09-05 ():
[historical background] A normal active adult placed himself on a vitamin C-free diet supplemented by the other known vitamins for a period of 6 months. The findings in this state of pure vitamin C deficiency [scurvy], that is, in the absence of factors such as multiple avitaminoses, infection, growth or other stress, were as follows:
132 days of a diet totally deficient in vitamin C were required for the first abnormal clinical signs—hyperkeratotic papules—to appear; 161 days were necessary for the appearance of the perifollicular hemorrhages of scurvy.
The plasma-ascorbic acid level was zero for 13 weeks before the first evidence of clinical scurvy was manifest. It is not necessarily, therefore, a good index of the vitamin C status of the individual.
The vitamin level in the white-cell-platelet layer of the centrifuged blood was a good index of the vitamin C status of the subject. This level fell to zero shortly before the appearance of clinical scurvy.
Adequate wound healing occurred after the plasma-ascorbic acid had been zero for 44 days and when the white-cell-platelet ascorbic acid level was 4 mg. per 100 cc. [see pg5/6, pg9/10]
With total vitamin C deficiency, failure of wound healing occurred. The tissues under these circumstances showed microscopically a lack of intercellular substance. Parenteral vitamin C alone brought about good healing, and considerable intercellular substance appeared within 10 days.
Hyperkeratotic papules containing ingrown hairs appeared over the buttocks and posterior aspects of the legs as a result of vitamin C deficiency; indeed, they may be the first sign of such a deficiency.
There were no gross changes in the gums or teeth (with good pre-existing oral hygiene). Although the mouth was grossly negative, x-ray films of the teeth showed interruptions of the lamina dura in early acute scurvy. Such an x-ray picture may be one of the better diagnostic criteria in early scurvy.
Vitamin C deficiency did not produce anemia.
After prolonged vitamin C deficiency there was inability to perform aerobic work, although the capacity for anaerobic work was undiminished. After a period of aerobic work in the scorbutic state the rate of disappearance of the blood lactate was abnormally slow.
During a 6-month period of total deficiency and after a month of clinical scurvy the blood complement titer was still normal. Over this period there was no evidence of lowered resistance to infection.
The Göthlin, Dalldorf and Rümpel-Leeds tests were negative, even in the presence of frank scurvy. These tests must therefore be poor indices of subclinical scurvy, even though they may in some cases produce petechiae which are cleared up by ascorbic acid therapy.
With severe vitamin C deficiency there was a fall in the blood pressure.
There was a lowering of the total phosphorus content of striated muscle, with an increase in the phosphagen phosphorus.
All the signs and symptoms of scurvy rapidly disappeared following the intravenous injection of ascorbic acid.
When the state of deficiency was complete the plasma-ascorbic acid level fell to zero in 5 hours after injection of 1 gm. of the vitamin.
Although the blood became completely saturated (as measured by plasma saturation curves and white-cell-platelet levels) after 3–4 gm of ascorbic acid had been given intravenously, the tissues were not completely saturated at this time, since the urinary output of ascorbic acid was still well below maximal over a 6-hour period.
[A remarkable n = 1 self-experiment with extensive quantified data, which helps establish important things about disease like how lack of vitamin C intrinsically disables wound healing—results which ordinary scientific methods would struggle to establish with just animal experiments or correlational methods.]
View PDF: