Ascorbic Acid in Cancer Treatment: Let the Phoenix Fly.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanisms of action, pharmacokinetics, and existing preclinical and clinical literature without systematic review methodology.
PubMed 30174242 · doi:10.1016/j.ccell.2018.07.014
What was done
This paper reviews the historical trajectory, pharmacokinetics, mechanisms of action, and emerging preclinical and clinical evidence for vitamin C (ascorbic acid) as an anticancer agent. It specifically evaluates intravenous delivery dynamics and two primary mechanistic pathways: hydrogen peroxide generation leading to oxidative stress and ten-eleven translocation (TET) enzyme activation leading to DNA demethylation.
What was found
The abstract reports no empirical data, sample sizes, or quantitative statistical results. It outlines a mechanistic framework centered on intravenous pharmacokinetics achieving therapeutic levels, hydrogen peroxide-mediated cytotoxicity, and epigenetic regulation via TET enzymes.
Why it matters
It consolidates the biological rationale for using high-dose intravenous—rather than oral—ascorbate in oncology, providing mechanistic grounding for modern clinical trials.
Limits
The paper is a narrative review presenting no new clinical or experimental data. The abstract provides no systematic evaluation metrics, study selection methodology, or quantitative effect sizes for clinical efficacy.
Cited by
- supports Intravenous high-dose vitamin C acts as a pro-oxidant that generates hydrogen peroxide in blood and tissue to selectively kill cancer cells.