Mongolia is on top of the charts regarding death from liver and other cancers and from heart decease. So I very much doubt that keto-diet has a protection against cancer.
On the other hand the life expectancy both absolute and conditional at a particular age of Mongolians either matches or within 2-3 years of that of Indians who eat mostly vegetarian diet. So if Mongolian have high prevalence of cancers, then they must have less prevalences of other deceases. So if keto diet has any protection, then it is against those other deceases, but not for cancer and heart ones.
> In KDs, the 4:1 ratio of high fat to low carbohydrates mimics the metabolic effects of starvation (Figure 2). These diets slow cancer by inhibiting insulin/IGF and downstream intracellular signaling pathways, such as phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR). Ketogenic diets also amplify adenosine monophosphate—activated protein kinase (AMPK), which inhibits aerobic glycolysis and suppresses tumor proliferation, invasion, and migration. Mouse models of metastatic cancer show that exogenous ketones themselves have direct cytotoxic effects on tumor viability.5 β-hydroxybutyrate can modify chromatin by binding to and thereby inhibiting histone deacetylase, ultimately repressing transcription and curbing cancer cell proliferation (Figure 1).
[0]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6375425/
This same article also mentions that a ketogenic diet can promote weight gain in cancer patients, which is a concern because frequently such patients lose weight as a result of both their disease and the treatment for it.
Although not a scientific paper, there is some suggestion in [1] that both fasting and keto can have benefits in terms of making chemotherapy both more tolerable and effective. The suggestion here is that driving down insulin and blood sugar may be the mechanism, which seems naively to mean it effectively "starves out" the cancer. Note however that both keto and fasting act on the insulin/IGF, AMPK and mTOR pathways, so there is a moderately large web of cellular/biological interactions to untangle here.
As a side note, the insulin/IGF, AMPK, and mTOR pathways are frequently implicated in animal studies of general longevity as well. We don't know the extent to which this stuff transfers over to humans, but, if you're a mouse, we can extend your life dramatically by playing around with these metabolic pathways.
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[0]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6375425/
[1]: https://www.curetoday.com/view/early-evidence-shows-fasting-...
The paper starts with the fact that tumor acidosis promotes disease progression through a stimulation of fatty acid metabolism in cancer cells.
Instead of blocking fatty acids, they test a hypothesis that excess uptake of specific fatty acid could have antitumor effects.
I forget how they measure it in animals but I believe it results in animals no longer being among the living.
https://tim.blog/2018/06/05/the-tim-ferriss-show-transcripts...
I would examine if keto / severe calorie restriction kills more precancerous and cancerous cells through stress.
It's probably best to start calorie restriction before acquiring cancer to keep the population of precancerous down.
As you usually loose weight on keto, maybe that explains the protective effect?
One of the primary hypotheses behind chemotherapy is to halt all cell division to let stress kill off more cancerous cells than healthy ones. The idea being that cancerous cells are more fragile than healthy ones, even though they proliferate faster and don't execute programmed cell death themselves as readily.