Yes, my recent readings support the notion of cancer cells reverting to normal. So killing them as medicine would have us do (and not incidentally, at a large profit) is destroying cells that can take on a proper differentiated role in our body.

I used to be a keto-bro until I started reading and listening to Georgi Dinkov, Jay Feldman, and Mike Fave among others. Despite all I knew about how keto manages to work around all claimed reduced carb limitations, I couldn't put off the power of their arguments. I don't have a good enough handle on all of it yet to convince you, so I will take the honorable way out and bury you in references :-) Not to win an argument, just to make us both reconsider what we think we already know.

All are summaries from Georgi's blog of studies he comes across that support some aspect of his and Ray Peat's bioenergetic point of view.

Acidosis (Warburg Effect) drives cancer through increased fat oxidation (Randle Cycle):

Lactic acidosis arising from glycolysis is a major culprit. The increased acidosis blocks glucose oxidation and increases BOTH fatty acid oxidation (FAO) and fatty acid synthesis (FAS), further inhibiting the oxidation of glucose causing even greater rise of lactic acid. The study shows providing extra glucose can break the vicious circle.

The study also shows that the increased FAS activity seen in cancer is NOT fed by glucose, but by glutamine. And that cancer cells are apparently dependent on FAS for providing them with fuel to oxidize instead of lipids from the diet.

As the study showed one more time, cancer cells do NOT prefer glucose but fat, and most of that fat is synthesized de-novo from glutamine instead of being acquired from diet.

Achilles heel of cancer discovered – its lack of CO2

Study discusses fully stopping cancer growth with a patented CAIX inhibitor. Leaving out that vitamin B1 is a powerful CA inhibitor.

Cancer relies on fat as fuel due to high reductive stress

One of the few studies out there that not only links cancer with impaired OXPHOS, but demonstrates directly the role of reductive stress (exemplified by the NAD/NADH ratio) in cancer’s appetite for fats as fuel required for the cancer survival and proliferation/metastasis.

The study hypothesizes that limiting fat availability to cancer cells may be the best approach to curing it. Besides dietary restrictions, anti-lipolytic agents such as sugar, aspirin, niacinamide, vitamin E, insulin can be used to get down to baseline lipolysis.

Fatty acid oxidation – linking all illness (especially cancer) with stress and diet (fasting / low-carb)

This one is right up the ketogenic alley.

Cancer cells are the result of secondary and downstream effects of a deranged metabolism. Remove the deranging factor and the “cancer” cells likely revert to normal behavior/metabolism.

The study demonstrates that excessive fatty acid oxidation (i.e., β-oxidation) provides both the necessary and sufficient factor for initiation, growth and metastasizing of cancer.

Any activity or substance that shifts the so-called Randle Cycle in favor of FAO will likely lead to pathology, and the severity of that pathology can vary from mild elevations of blood glucose, to insulin resistance, to diabetes, and ultimately to CVD, liver disease, and even cancer depending on to what degree the Randle Cycle has been shifted in favor of FAO and for how long that state has persisted.

Increased fat oxidation (FAO) sufficient to cause senescence/aging/disease

Addresses the role of reduced glucose oxidation and increased fatty acid oxidation in cancer, among other diseases.

It is starting to look more and more plausible that aging/disease are nothing but symptoms of increasingly reduced glucose oxidation and increased FAO.

An interesting finding of the study is that saturated fats (SFA), despite being much preferable than PUFA for oxidation, are also capable of affecting the Randle Cycle and shifting the redox balance in favor of reduction.

Hope this gives you something to chew on, fren'.