The multiplicity of metabolic functions that vitamin C performs gives
rise to three distinct therapeutic applications for ascorbate. The first
is the prevention of scurvy, with doses up to 65 mg daily. The second is
the augmentation of vitamin C metabolic functions with doses ranging from
1 to 20 grams per day. This dose allows significant quantites of ascorbate
to be invested in suport of hydroxylation reactions, connective-tissue
integrity, antioxidant defenses, immune responsiveness and adrenal sufficiency.
The third is the delivery of reducing power, in doses ranging from 30 grams
to 200 grams or more per 24 hours. Under the highly oxidizing conditions
typical of most infectious diseases, the generation of DHA (dehydroascorbate)
exceeds the availability of NADH and other endogenous reducing agents.
Under such conditions, high dosages of vitamin C are largely destroyed.
Due to the marked instability of DHA, accumulated DHA is irreversibly
hydrolyzed into diketo-L-gulonic acid, which is in turn either oxidized
into L-threonic and oxalic acids or decarboxylated onto various 5-carbon
carbohydrates.
The top figure illustrates the normal balance between oxidation of ascorbate and reduction of DHA. In this situation, DHA is quickly reduced to ascorbate before significant hydrolization of DHA can take place. Vitamin C is conserved.
In the middle figure, a high rate of oxidation typical of infection is illustrated. In this situation, DHA accumulates because its production exceeds the reducing capacity of the organism. The accumulated DHA undergoes hydrolysis which ultimately diminishes the ascorbate pool. Dr. Cathcart calls this scenario acute induced scurvy and it has been reported by Kolinkerinos to be a common occurrance in Australian aboriginal infants following vaccination.
The bottom figure illustrates how supplemental ascorbate maintains the ascorbate pool in the face of high ascorbate oxidation and rapid DHA hydrolysis. SWFAdapted from: Robert F. Cathcart, The third face of vitamin C. Journal of Orthomolecular Medicine 7(4): 197-200, 1992.