The bio marker associated directly with heart failure stage is a fatty acid acylcarnitine which indicates that the heart cell and other muscles are "relatively" unable to metabolize fatty acids due to their mitochondrial energy weakened state.
Fasting and other activities that produce beta hydroxybutyrate improve cell mitochondria and their function inclusive of short, medium and long chain fatty acid metabolism requiring the CCA enzyme to allow mitochondrial metabolism of smaller carbon subunits or fragments. Beta hydroxybutyrate is already a short 2 carbon fragment that is processed mainly by the liver into the first used fuel and therefore is the preferred fuel of mitochondria.
How does exercise improve heart failure?
Why is high intensity interval exercise superior to endurance exercise which is superior to brief aerobic exercise?
EXERCISE related KETOSIS.
If one thinks of a pump handle well, beta hydroxybutyrate is the energy put in to prime the energy pump. It is an energy signal and also a supplement to augment cell function.
Having fuel or energy allows the cell to be primed and able to use longer chained fatty acids for metabolism.
The normal heart primarily uses fatty acids for energy.
The normal brain almost exclusively uses glucose for energy.
Both can use lactate and beta hydroxybutyrate as alternative energy sources.
Beta hydroxybutyrate is the preferred fuel of both.
Beta hydroxybutyrate increases BDNF and brain function.
Beta hydroxybutyrate increases muscle mass and function.
Ursolic acid increases cellular fatty acid metabolism and also produces beta hydroxybutyrate from the liver.
Diabetes is associated with inhibition of glucose metabolism and increased fatty acid intermediate metabolites such as acylcarnitine. In effect diabetic cells display insulin resistance with refusal to import more intracellular glucose but unexpectedly imports or manufactures more fatty acids. This results in marbling of muscle, fatty liver, fatty pancreas, fatty heart and their resulting dysfunctions, sarcopenia, steatohepatitis, beta cell dysfunction/diabetes, heart failure and increased bio marker of fatty acid metabolism dysfunction- acylcarnitine. This is a mild acquired form of carnitine-acylcarnitine deficiency physiology a severe inborn error of metabolism in newborns.
Affected newborns are unable to metabolize longer chain fatty acids and have seizures, irregular heart beat, low ketones, low blood sugar, fatty liver, cardiomyopathy. This is caused by genetic errors in the newborn. The obvious cause of this acquired physiology is OVER NUTRITION and the obvious treatment is INTERMITTENT FASTING or under nutrition from exogenous sources (food and calorie laden beverages.). Fat cells get larger and increase in number but fat cell storage is not the problem. Insulin resistance and abnormal energy signaling in lean body cells is the problem.
Insulin resistance leads to both elevated blood glucose as the cells resists intracellular transport of more toxic glucose while at the same time becoming saturated with elevated stored lipids and its lipotoxic cellular effects.
To improve the cells of the lean body one must metabolize via beta oxidation accumulated fatty acids and restore normal insulin sensitivity.
Within three days of fasting, insulin resistance is reduced by approximately 70%. Most of that occurs within 24 hours.
Once the acute insulin sensitivity dysfunction is decreased, 12 or more hours of fasting per day will maintain the improved insulin sensitivity.
Is it not obvious that avoiding insulin requiring foods will result in less energy storage as fat and further improve insulin sensitivity making the basal or fasting insulin rate fall?
(Eating fat does not significantly increase insulin, an energy storing hormone. Eating more fat, and therefore less carbohydrate, results in higher resting metabolic rates. Eg. Adding 10 grams of coconut oil to a measured normal diet resulted in a resting metabolic rate of 106% of baseline.)
What are the high glycemic foods that require the most insulin? Processed carbohydrates like flour, high fructose corn syrup and sugar are the most obvious.
Additionally, one cannot lose stored body fat unless one reduces insulin, an energy storing hormone. The breakdown of fat for burning is inhibited by insulin, an energy storing hormone.
The solution appears obvious and has been verified by circadian scientists, timed-restricted-feeding and its corollary timed-restricted-fasting. Fasting 12 or more hours reduces liver glycogen and restores insulin sensitivity. The effect of fasting is to reduce glycogen stored in the liver and muscles. When glucose level is below 100, the liver stores glucose first, as glycogen and fat, then glucose levels rise within the normal range of 100-140 stimulating the release of insulin and the muscles store glucose as glycogen and fat and fat cells store glucose as fat. Insulin is an integral part of energy storage. Fasting reduces insulin and depletes liver glycogen, and muscles use their stored energy until the next meal. If the fasting interval is extended, excess energy can be released from fat stores in fat cells but only if insulin, a storage hormone, is reduced. Normalizing insulin levels to the low range of normal is desirable.
If one reduces insulin and insulin resistance which allows fat burning, weight loss from calorie restriction does not slow down metabolism. Further high fat low carb diets are associated with increased metabolic rates. It has been noted by Dr. Jason Fung and possibly others that bariatric surgery is different from calorie restricted weight loss because basal metabolism is maintained AND that this result is due to fasting. He questions the need for surgery if fasting is the mechanism for fat loss and avoiding processed carbohydrates is the cause of insulin resistance, excess fat storage and obesity. At an even smaller fractal level, cellular metabolic health is promoted by circadian clock genes of metabolism. When the fast is broken by the first bite or consumption of calories the clock begins for the feed cycle.
Is there an optimum duration for the feed cycle? Probably until the liver and muscles have a full tank of stored fuel as glycogen and fat.
Is there an optimum duration for the fast cycle? Probably longer than the feed cycle due to the speed of refueling over speed of energy use and the abundance of stored calories in body fat. As the metabolically healthy adult is fat burning ketones after 12 hours indicating glycogen depletion from the liver, 12 hours is the lower limit.
Action: Low carb higher fat diet consumed within 4-12 hours, high intensity interval exercise, 12-16 hours of fasting with or without Ursolic acid 200 mgs three times daily and weekly resistance exercise.
Caveat: High cortisol high stress causes insulin resistance and thwarts effect of feed fast cycle to promote cellular metabolic health. Two minutes of slow paced breathing 5 seconds in and 5 seconds out for 2 minutes twice daily and or walking in nature and or 2 minutes of absolute silence using noise cancelling devices should reduce brain cortisol by stimulation of vagal nerve signals to the brain.
Net effect: Beta hydroxybutyrate levels increase and BDNF brain derived neurotrophic levels increase. The latter cannot be commercially measured but Elite Heart Rate Variability is a proxy measure. Healthy aging is associated with high for age Heart rate variability index.
Disclaimer: This information may not be suitable for individuals under medical care and treatment. It is always recommended to consult with your personal physician before making these changes.
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