Edward sent me this paper. I think I did already have a copy on my hard drive but you can't really start to make head nor tail of what is really going on until you have a handle on F:N ratio and the physiological role for superoxide. I'd completely forgotten about the paper.
For those people who think humans are in some way different from rats, here's Fig 1 from the paper on humans eating either a saturated fat ketogenic diet or a polyunsaturated fat ketogenic diet, just for 5 days:
Look at the glucose, lowest in the PUFA group, look at the ketones, highest in the PUFA group, look at the insulin sensitivity, waaaay higher in the PUFA group. Rat or human, makes no odds. PUFA fail to generate superoxide in mitochondria. Is this good or bad?
The whole point of a ketogenic diet (epilepsy excepted) is to induce starvation-appropriate physiological insulin resistance. What is the point of setting up a ketogenic diet which does not have the ability to convert from running on glucose to running on fat?
Aside: Why might anyone want to run their metabolism on FFAs? Superoxide. I want more mitochondria to supply spare ETC capacity, to minimise the sort of levels of free radicals which wipe out mitochondria when the pressure is on. Physiological superoxide signals for mitochondrial biogenesis, without all of that tedious exercise to do the same job on a mixed diet. End aside.
Now it is just possible to argue that chronically reduced insulin may render adipocytes immune to the insulin sensitising effects of PUFA. Maybe. The obese mice of the next Protons post are on a mixed PUFA-carb diet to assist their "ballooning" experience. High insulin plus insulin hypersensitive adipocytes gives obesity. Perhaps the combination of low insulin with distendable adipocytes is OK if the insulin levels are low enough. Volunteers queue over there please.
But we are still in a situation where FFAs are high, yet glucose can still enter cells. What does this do to cellular ATP status? The whole point of insulin resistance is to avoid cellular caloric overload, full stop. If you load liver cells with PUFA and add in glucose the end result, by whatever mechanism, is cirrhosis. Perhaps other tissues fare better. Am I about to try it?
No thank you.
And for a real giggle you can see exactly what sort of utter crap made up the high PUFA diet, just read Table 1. "Imitation" if the first word of the first "food"!