Cancer risk in humans is very strongly tied to insulin resistance,

One old paper for a prospective study with a correlations about getting older? What could go wrong?

Although the experimental findings we have presented are relatively straight-forward, we can only speculate as to why a variety of age-related diseases might be linked to insulin resistance and/or hyperinsulinemia. In this context, it is worth noting that caloric restriction, in both invertebrates and mammals, leads to a decrease in age-related morbidities and enhanced life span, associated with enhanced insulin sensitivity, and lower glucose and insulin concentrations (33–37).

Aha, and the authors admit that it’s speculation.

It’s similar to the Vitamin D correlations. Are people with these chronic ‘Western’ diseases dying from Vitamin D deficit, or do people who work indoors, stand and sit a lot, drive everywhere and likely have on time to cook decent meals get these chronic diseases?

Here’s a different hypothesis:

Ketones and lactate “fuel” tumor growth and metastasis: Evidence that epithelial cancer cells use oxidative mitochondrial metabolism - PMC

Previously, we proposed a new model for understanding the “Warburg effect” in tumor metabolism. In this scheme, cancer-associated fibroblasts undergo aerobic glycolysis and the resulting energy-rich metabolites are then transferred to epithelial cancer cells, where they enter the TCA cycle, resulting in high ATP production via oxidative phosphorylation. We have termed this new paradigm “The Reverse Warburg Effect.” Here, we directly evaluate whether the end-products of aerobic glycolysis (3-hydroxy-butyrate and L-lactate) can stimulate tumor growth and metastasis, using MDA-MB-231 breast cancer xenografts as a model system. More specifically, we show that administration of 3-hydroxy-butyrate (a ketone body) increases tumor growth by ∼2.5-fold, without any measurable increases in tumor vascularization/angiogenesis. Both 3-hydroxy-butyrate and L-lactate functioned as chemo-attractants, stimulating the migration of epithelial cancer cells. Although L-lactate did not increase primary tumor growth, it stimulated the formation of lung metastases by ∼10-fold. Thus, we conclude that ketones and lactate fuel tumor growth and metastasis, providing functional evidence to support the “reverse Warburg effect.” Moreover, we discuss the possibility that it may be unwise to use lactate-containing i.v. solutions (such as lactated Ringer’s or Hartmann’s solution) in cancer patients, given the dramatic metastasis-promoting properties of L-lactate. Also, we provide evidence for the upregulation of oxidative mitochondrial metabolism and the TCA cycle in human breast cancer cells in vivo, via an informatics analysis of the existing raw transcriptional profiles of epithelial breast cancer cells and adjacent stromal cells. Lastly, our findings may explain why diabetic patients have an increased incidence of cancer, due to increased ketone production, and a tendency towards autophagy/mitophagy in their adipose tissue.

quote from the paper:

Thus, our current observations may also explain the close and emerging association between diabetes and cancer susceptibility.20 A number of elegant studies have been carried out in mouse animal models to assess this association and chemical induction of diabetes in rats with streptozocin is sufficient to enhance tumor growth.21 Similarly, acute fasting in rodent animal models is also sufficient to dramatically increase tumor growth.22 Both of these experimental conditions (diabetes and fasting/starvation) are known to be highly ketogenic and, thus, are consistent with our current hypothesis that ketone production fuels tumor growth. Finally, given our current findings that ketones increase tumor growth, cancer patients and their dieticians may want to re-consider the use of a “ketogenic diet” as a form of anti-cancer therapy.

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which the carnivore diet avoids (by not introducing glucose).

Are you aware of the phenomenon of “use it or lose it” ? It should be familiar to those interested in muscle building. Do you think that it doesn’t apply to the pancreas?

Lack of insulin production is a possible pathway for the pancreas atrophying:

Currently, in both type 1 and type 2 diabetes patients, the reduction of pancreas size might be accounted for by: (i) lack of insulin action on the exocrine pancreas resulting in tissue atrophy, as insulin is a potent growth factor for the exocrine pancreas (disruption of endocrine and exocrine relationship)

Which is to say that you’re not challenging the pancreas with glucose, and that may make the pancreas “weak”, which will be a surprise if you ever get out of ketosis.