Why might ketogenic diets inhibit cancer growth and proliferation?

The principle effect of restricting carbohydrate (CHO) below 50 grams/day (or even better below 30 grams/day) is marked inhibition of insulin secretion by the pancreas. This is not a mystery. Glucose is the principle stimulus for pancreatic insulin secretion and sugars and starches digest mostly to glucose in the mouth, stomach and intestines. 

So since 90% or more of the CHO we eat are starches and sugars (it's hard for most of us to get more than 25 grams of fiber/day--fiber is also carbohydrate, but is much less insulinogenic) then restricting total CHO to less than 50 grams/day is an effective way to inhibit insulin, almost maximally. And maximal reduction of insulin is accompanied by manufacture of ketone bodies by the liver. 

And insulin is a hormone that stimulates cell growth. Cell growth is good when we're young and growing up, but too much insulin, stimulated by too much CHO in adults tends to make us grow sideways, as our fat cells expand with triacylglyerol manufactured from glucose---> glycerol  +   3 fatty acids linked to the glycerol molecule (hence triacylglycerol, where the acyl represents the fatty acyl linkage).

Receptors for insulin are on fat cells as well as muscle cells to signal them to take up glucose and fatty acids. 

But insulin receptors are also on cancer cells. And insulin stimulation of the insulin receptor on cancer cells causes them to grow and proliferate and to resist cell death. (More detail on this in a later section).

So reducing insulin secretion by a ketogenic diet of <50 grams of CHO/day does TWO things that can, in principle, inhibit some cancers:

a) It remarkably reduces insulin secretion. This in itself may inhibit some tumors because of the insulin receptor on their surface.

b) It causes ketosis: 

   1. We have shown in cell culture that ketone bodies inhibit cancers metabolically (more on this later).

   2. Ketone bodies have been shown by others to behave as histone deacetylase inhibitors (HDACi). HDACi's change the configuration of histones, proteins that coat DNA and help determine which genes are turned on or off. When HDACi's are administered, many cancers' growth/proliferation genes/proteins are turned off and programmed cell death (apoptosis) genes are turned on. In short HDACi's can slow cancer growth and cause cancer cell death.