The influence of ketogenic therapy on the 5 R's of radiobiology.
Level 5 - mechanism / opinion, no new human data
Narrative review of biological mechanisms and preclinical hypotheses without new empirical data
PubMed 28905672 · doi:10.1080/09553002.2017.1380330
What was done
This narrative review synthesized preclinical evidence and theoretical mechanisms regarding how ketogenic therapy (ketogenic diets and short-term fasting) affects the five classic radiobiological determinants of treatment outcome: reoxygenation, DNA repair, radiosensitivity, cell cycle redistribution, and repopulation.
What was found
The abstract reports no numerical findings or pooled effect estimates. It outlines mechanistic rationale: shifting metabolism away from glycolysis toward mitochondrial respiration increases reactive oxygen species and impairs ATP synthesis in cancer cells, while elevated ketone bodies (notably beta-hydroxybutyrate as an endogenous class-I histone deacetylase inhibitor) and reduced glucose induce differential stress resistance, protecting normal cells while sensitizing tumors to radiation damage.
Why it matters
It establishes a conceptual framework for using dietary metabolic interventions as a low-cost, non-toxic adjuvant to potentially increase the therapeutic ratio of radiotherapy in solid tumors.
Limits
The paper is a non-systematic narrative review based primarily on preclinical models and theoretical mechanisms without controlled human clinical outcome data or quantitative analysis.
Cited by
- context Being in a state of ketosis can act as an adjuvant therapy by enhancing chemotherapy's cancer-killing effects while protecting healthy cells.