| First, check the warburg hypothesis: https://en.m.wikipedia.org/wiki/Warburg_hypothesis Cancer cells rely much more on glycolysis than oxidative phosphorylation (respiration, basically breaking down sugar with oxygen). You get a net of two molecules of ATP from glycolysis compared to 30 or so from respiration, so you can expect that cancer cells need much more sugar than normal cells just to survive.
https://en.m.wikipedia.org/wiki/Cellular_respiration Second, glucose competes with dehydroascorbate (DHA, oxidized vitamin c) for glut1/3 transporters. DHA gets transported into cells (in particular RBC's) to be reduced back to the anti-oxidant form by glutathione: ascorbate. Then that ascorbate molecule can remain in the cell acting as an antioxidant or be pumped back out of the cell to the blood, etc. If DHA doesn't make it into a cell quickly it gets hydrolyzed and excreted and you lose that molecule of vitamin c. So chronically lower blood sugar is expected to conserve your vitamin c and allow higher ascorbate levels, especially within your cells. This can have all sorts of beneficial effects. Strengthened collagen makes it easier for a tissue to heal/encapsulate the cancer and harder for it to metastasize, quenching free radicals can prevent damage to surrounding tissue, etc. But also, cancer cells accumulate more iron than normal cells: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5983609/ Ascorbate can also reduce Fe3+ iron to the Fe2+ form. That Fe2+ iron can then undergo the fenton reaction to form free radicals: https://link.springer.com/article/10.1007%2FBF03033342 Those free radicals can go onto to kill the (high iron) cancer cells. For this reason vitamin C kills almost all cancer cell lines in vitro at doses that do not harm normal cells: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2516281/ |