Just a quick aside:
George cited this study in the comments of the last but one post:
Metformin inhibits mitochondrial complex I of cancer cells to reduce tumorigenesis
While I think it is possible that metformin might inhibit mtG3Pdh at levels below those which inhibit complex I, the complex I effect may well still be equally real.
He goes on to say:
"Remodelling the ETC - I like that. The idea of the ETC as a modular assembly that will be reconfigured as the substrate balance shifts. Directly by the effects of the substrates on its outputs".
Remodelling the ETC using RET from FADH2 inputs might be antineoplastic too ie, less complex I would then be available for whatever ox phos the cancer is capable of…
Now: What normal food will generate the highest FADH2 input to the ETC per unit NADH? Correct, stearic acid will.
So what does stearic acid do to breast cancer cells in culture?
Stearate preferentially induces apoptosis in human breast cancer cells
Does it work in a rodent model?
Dietary stearate reduces human breast cancer metastasis burden in athymic nude mice
Do people with breast cancer have low stearate levels in their cell membranes?
Erythrocyte membrane fatty acid composition in cancer patients
Does stearate-driven RET down regulate complex I availability in cancer cells which are partially dependent of glucose derived NADH oxidation via said complex I? And so kill them?