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Abstract

Using an evolutionary genetic disease model, this review considers Vitamin C (VC) and its potential for treating COVID-19 (CV-19). The model’s validity rests on VC’s potent antioxidant property and the mutation sustained by the primate ancestor (est.) 61 MYA that left humans unable to produce VC. The result is humans cannot -by diet or oral supplementation- achieve plasma VC concentrations typical of vitamin C synthesizers. This may leave humans chronically vulnerable to infectious disease (hypoascorbemia). VC deficiency can become more acute during severe disease (anascorbemia) and, because of the relationship between disease severity and oxidative stress, can intensify the oxidative load and associated inflammation. During acute disease, oxidative stress becomes oxidative distress when highly reactive oxidants are produced at a rate faster than normal homeostatic mechanisms can quench them, such as with the inflammatory cytokine storm characteristic of severe CV-19. Cytokine storms directly underly the most severe complications of CV-19, e.g., acute respiratory distress syndrome (ARDS), sepsis, and multiple organ dysfunction syndrome (MODS). Infusions of VC into the plasma achieve concentrations that can exceed those of VC synthesizing species. At such concentrations, VC’s action as a non-rate limited antioxidant may lower the probability of a cytokine storm and the risk of tissue injury. I suggest that VC may prove a useful treatment in such contexts. In advance of the resulting ongoing clinical trials, this review will extrapolate a picture of VC’s potential therapeutic impact on the inflammatory cytokine storm and severe complications possible with CV-19.

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