Godot, I just saw your post. I will address it later
alecnevsky, you understand it right. High levels of FFAs prevent skeletal muscles from utilizing glucose. This is not something new. Thus the recommendation for people with metabolic syndrome is to loose weight and go on a low fat diet. Both of these measures will lower FFAs concentrations and improve glucose metabolism.
Regarding the brain function, in the period during the adaptation, while glucose is still low and ketones are not quite high, it's normal to feel brainfogged, irritable and weak.
And I don't think that a ketogenic diet will lead to the brain getting 75% of its energy from ketones. This happens during a fast, after ~3+ weeks of starvation, when the
sustained level of beta-hydroxybutyrate reaches 5-7 mMol/L. Maybe a
therapeutic ketogenic diet will give you a sustained level of ketones this high -? The numbers I saw were in 3-4 mMol/L range and the Atkins diet types stay at around 2.
The other thing, discussed in this thread above (Jimmy Moore's graphs), is that on a diet, the level of ketones goes up and down, reflecting the fat content of the last meal, while on a fast the levels rise steadily. When they reach their max, that's when the brain switches to getting 75% of its energy demands from ketones.
If you look at the graph (Cahill
http://www.med.upenn...08-9Lazar-1.pdf page 8), note how the level of beta-OHB rises steeply until day 10 (that's when, on average, the beginners' brains switch to ~30% of ketones). Then from day 10 to day 17 the level of beta-OHB rises slower. Why? The liver keeps producing ketones at the same rate and their concentration builds up steadily. The slower rising rate after day 10 reflects the fact that the brain began using beta-OHB. If it did not, the graph would keep on rising at the same rate.
Note that the adaptation to ketosis, as far as utilization of beta-OHB by the brain is concerned, occurs in stages: the concentration of beta-OHB must reach a certain level and be sustained for a while, which triggers a qualitative change in brain metabolism. Subjectively, this is perceived as malaise (brainfog + weakness) which appears from nowhere and grows -- and then clears quite suddenly.
Note that eventually the graph of beta-OHB flattens out (here it happens past day 30, but this is a compound graph with data collected from mostly obese people fasting for the first time in their lives, which means that the stages of adaptation are delayed).
The flattening of the graph reflects the fact that eventually the utilization of ketones by the brain matches their production rate by the liver. I believe that's when the 75% number is reached.
I hope that now you understand why the adaptation to starvation requires that skeletal muscles ignore both ketones and glucose. This is what allows the level of ketones to rise. As for glucose, this graph does not show it, but in my own experience, which is in line with the studies which I would have to find, each time the brain steps up its beta-OHB consumption, the blood level of glucose rises somewhat. Again, this is easy to understand: the levels of fuels in the blood, ruffly = their production - utilization.
This is what goes on during starvation the metabolism of which a ketogenic diet tries to emulate. How exactly it works out on a diet, I'm not sure, except that all the stages are significantly delayed and certain levels are never reached.
Re carbs on a diet, the main purpose is to provide glucose so that endogenous protein would not be catabolized for its production. The excess triggers a rise in insulin and lowers the level of ketosis. As long as the level of FFAs is high, the skeletal muscle will not utilize it, and it will take a while for it to go to baseline. But you can check it for yourself with a blood glucose meter.
Edited by xEva, 31 March 2013 - 10:18 PM.