If I may play devil's advocate on that hypothesis. The mechanism that allows the liver to produce sufficient ketones is low(er) insulin. Therefore it must be the same mechanism that somehow stops working, i.e. high(er) insulin. All things being equal (same diet throughout especially), using my paradigm, I can deduce that somehow there's a condition that prevents the liver from working as it should and this condition likely shuts down insulin receptors at the liver, and this condition manifests at some point and stays. This condition would also be accompanied by higher BG, not much but measurable (something like 100mg/dl vs 80mg/dl); failure to lose fat or even fat gain; other things related to energy status like fatigue and such; hunger/cravings. Basically this condition would mimic all the symptoms of a high-carb diet, but without the carbs, since it would disrupt the same thing a high-carb diet disrupts: liver insulin receptors primarily.

Bear in mind that's just how I see it, not necessarily how it actually works.

To stay on topic, at the risk of harping on with my idea of as-of-yet unknown medical condition, if it's possible a condition mimics all the symptoms of a high-carb diet, then it's even more true that reversing type 2 diabetes starts with ignoring the guidelines. Because then, once we've addressed diet and find the disease does not improve, we've discovered the existence of a genuine medical condition which we must address with something other than diet alone. Sarah's talk didn't go that far likely because she's working from the premise of the old flawed paradigm.