Ketone production only occurs when blood insulin levels are very low, which naturally happens in a low carb diet that includes very low glycemic load foods.
Not exact matches
A reduction in TG levels also did not cause hepatic steatosis (Figure 3, A and B) or increase the
production of
ketone bodies (Figure 3C), and at most had
only a modest effect on circulating nonesterified free fatty acid (NEFA) levels (Figure 3D).
So yeah, not those but I — I also think, and get back to the ADHD question, there needs to be a big emphasis on not
only systemic inflammation but supporting lipid metabolism through things like fatty supplementation, you know, Omega 3s, medium - chain triglyceride, even get good
ketone production.
If you are sticking long enough to a ketogenic diet the
production of the different types of keton bodies will change: the serum and urine volume of acetoacetate (the
only ketone detected by ketostix) is significantly reduced, according to Phinney and Volek, you will have more Hydroxybutyrate in your serum - and thereby in your urine.
Not
only do
ketones inhibit the
production of antioxidants, they also break down these little bastards!!
Fortunately, similar occurrences happen during overnight fasts and intermittent fasts as well with
only downside of a slightly lower rate of
ketone production.
In contrast, fat - derived
ketone bodies produce
only NADH, which increases the redox span of the coenzyme Q couple and reduces
production of ROS.
Further, the
production of acetoacyl CoA, a substrate of
ketone body formation, can occur
only in the liver and thus does not apply to skeletal muscle metabolism.
Utilizing
only fat stores for energy can be sustained for a while, but eventually the
ketone production secondary to fat breakdown makes patients very sick.