http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3937164/
Phase I safety trial of intravenous ascorbic acid in patients with severe sepsis
Alpha A Fowler, III, Aamer A Syed, [...], and Ramesh Natarajan
Background
Parenterally administered ascorbic acid modulates sepsis-induced inflammation and coagulation in experimental animal models. The objective of this randomized, double-blind, placebo-controlled, phase I trial was to determine the safety of intravenously infused ascorbic acid in patients with severe sepsis.
Methods
Twenty-four patients with severe sepsis in the medical intensive care unit were randomized 1:1:1 to receive intravenous infusions every six hours for four days of ascorbic acid: Lo-AscA (50 mg/kg/24 h, n = 8), or Hi-AscA (200 mg/kg/24 h, n = 8), or Placebo (5% dextrose/water, n = 8). The primary end points were ascorbic acid safety and tolerability, assessed as treatment-related adverse-event frequency and severity. Patients were monitored for worsened arterial hypotension, tachycardia, hypernatremia, and nausea or vomiting. In addition Sequential Organ Failure Assessment (SOFA) scores and plasma levels of ascorbic acid, C-reactive protein, procalcitonin, and thrombomodulin were monitored.
Results
Mean plasma ascorbic acid levels at entry for the entire cohort were 17.9 ± 2.4 μM (normal range 50-70 μM). Ascorbic acid infusion rapidly and significantly increased plasma ascorbic acid levels. No adverse safety events were observed in ascorbic acid-infused patients. Patients receiving ascorbic acid exhibited prompt reductions in SOFA scores while placebo patients exhibited no such reduction. Ascorbic acid significantly reduced the proinflammatory biomarkers C-reactive protein and procalcitonin. Unlike placebo patients, thrombomodulin in ascorbic acid infused patients exhibited no significant rise, suggesting attenuation of vascular endothelial injury.
Conclusions
Intravenous ascorbic acid infusion was safe and well tolerated in this study and may positively impact the extent of multiple organ failure and biomarkers of inflammation and endothelial injury. this is exactly of what you stated before
1) All of the patients had abnormally low serum levels of vitamin C. Supplementing patients with nutrients that are pathologically low is not the same as loading them with abnormally high levels of those nutrients. There is a lot of precedent for replacing lost nutrients--usually, it consists of hydration with electrolyte replacement. Sometimes, this is coupled with symptomatic treatment.
2) As a reviewer of this study, I would express concern that the vitamin C replacement study pushed the serum concentration of ascorbate more than ten-fold higher than normal serum concentrations. 3) There is no reason to think that vitamin C has pharmaceutical activity beyond its role as an enzyme co-factor and its electron donor activity. If it does, in fact, have actual pharmaceutical activity, then mega-dosing on it is even more problematic than I have already discussed.
Keep in mind that the purpose of pharmaceutical agents is to disrupt metabolic pathways and processes. While there may be a valid reason to disrupt these activities when they enter a pathological state, there is absolutely no reason to interfere with them when they are functioning normally.
I seriously do not understand the desire to load up one's body with foreign chemicals (even when trace amounts of the chemicals are necessary for normal function). You delude yourself by thinking that since the chemical is "natural", it somehow cannot have adverse effects. Your body is meant to function within specific parameters, and your best bet to keep it functioning optimally is to eat a good balanced diet. Unless there is a specific medical reason to do otherwise, don't load your body up with abnormal levels of micronutrients, and don't abuse it with drugs.