BEH! I'm searching to find some of the articles I've read over the years about ketones and their superiority as a fuel for brain function. I will have to try Mercola.com, but here is an undetailed snippet of info...... From my own experience, the lower the carbs, the sharper my mind. Keto diets are recommended for kids who suffer seizures, as wekk as for incurable migrane sufferers. There is one diet called "the warrior" diet which advocates "fasting" all day, with small amounts of protein/fat or fresh fruits and veggies until the evening meals where you have a controlled "fest." Part of it's claims (and reported experiences) are a much sharper forcus, brain function and ability to conentrate. I've tried it... it works, brainwise. The idea of stuffing ourselves "to feed our brain" doesn't really hold water. Muscles - maybe, but the brain doesn't need or want food every couple of hours.
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Low Carb Diets Feed Your Brain
Did you know that Mother Nature meant well creating ketones? Did you know that their main purpose is to feed the brain?
Yes, that's true no matter how many times you've heard the opposite from dieticians and nutritionists. "This bags the question of why a diet presumed so dangerous for fat loss is being used clinically without problem" -- Lyle McDonald, "The Ketogenic Diet." The part concerning clinical use became clear when you consider the brain-feeding function of ketones.
Is the state of ketosis natural? See for yourself. Ketosis occurs when concentration of ketone bodies in the blood elevates above 0.2 (mmll/dl) - twice as high as a standard average diet causes. After exercise, it jumps up to 2 mmll/dl 20 times the "normal" level! Meanwhile, have you ever heard that exercise is dangerous because it causes kesotis? What's the matter with professional nutrition establishment?
Did you know that the two ketone bodies, acetoacetate and D-3-hydroxybutyrate, are the only freely soluble fats (lipids) the body can use? This very important fact explains a significant part of the ketosis mystery.
Ketosis is achieved by reducing carbohydrates to such a low level that the body is forced to use incompletely metabolised fats (ketone bodies) as fuel.
Ketone bodies function as :
- Brain fuel. The major role of ketone bodies is to supply an alternative (to glucose) fuel for the brain in situations where there are little or no carbohydrates available with food.
- Building blocks for brain tissue. Ketone bodies are precursors for the essential substance (acetyl-CoA) required in the synthesis of lipid (myelin) in the neural cells.
The mechanisms for both major functions are described in the tiniest details. It is well know how they act on the cellular and intracellular (mitochondrial) levels and how they can correct certain pathological states of the brain cells.
The concentration of ketone bodies in the blood at any time represents a balance between the rate of their production by the liver and the rate of their use by tissues.
What concentration is normal?
- Norm (normoketonaemia) is a concentration of total ketone bodies in blood below 0.2 mmol/l.
- Ketosis (hyperketonaemia) is concentrations above this level but below the ketoacidosis.
- Ketoacidosis are concentrations above 7 mmol/l.
Past Technical Mistake Leads to Modern Misconception
Historically, ketosis was associated with the pathology of diabetes, resulting in the view that ketone bodies were toxic waste products. It happened simply because the only available test at that time detected 3-hydroxybutyrate (which, in fact, is not a ketone body at all but here it doesn't matter) in diabetic urine. Acetone on the other hand is a ketone and is present in blood and urine when the plasma concentration of acetoacetate is elevated. The body gets rid of it through the lungs; this is where the sweet smell on the breath during ketosis comes from.
In 1967, the streamline health sciences developed a so-called enzymatic method of analysis of acetoacetate and 3-hydroxybutyrate, which led to the dramatic finding that the human brain, while in the condition of prolonged starvation, was able to use ketone bodies. This finding triggered a reversal of the negative opinion of ketosis as a pathological and dangerous condition -- well, almost.
Many, if not most, dieticians and nutritionists continue to warn dieters against the dangerous consequences of ketosis. Do you have any idea why?
Let us know your opinion!
Sources
1. Bach AC, Ingenbleek Y and Frey A (1996). "The Usefulness of Dietary Medium-Chain Triglycerides in Body Weight Control: Fact or Fancy?" Journal of Lipid Research 37:708-726.
2. Girard, J.R.; Ferrč, P.; Pčgorier, J.P.; and Duče, P.H. (1992). "Adaptations of Glucose and Fatty Acid Metabolism During Perinatal Period and Suckling-Weanling Transition," Physiological Reviews 72:507-562.
3. Krebs, H.A.; Woods, H.F.; and Alberti, K.G.M.M. (1975). "Hyperlactataemia and Lactic Acidosis," Essays in Medical Biochemistry 1:81-103.
4. McGarry, J.D. and Foster, D.W. (1980). "Regulation of Hepatic Fatty Acid Oxidation and Ketone Body Production," Annual Review of Biochemistry 49:395-420.
5. Nehlig, A. and de Vasconcelos, A.P. (1993) "Glucose and Ketone Body Utilization by the Brain of Neonatal Rats," Progress in Neurobiology 40:163-221.
6. Owen, O.E.; Morgan, A.P.; Kemp, H.G.; Sullivan, J.M.; Herrera, M.G.; and Cahill, G.F. (1967). "Brain Metabolism During Fasting," Journal of Clinical Investigation 46:1589-1595.
7. Page, M.A. and Williamson, D.H. (1971). "Enzymes of Ketone Body Utilization in the Human Brain," Lancet 2:66-68.
8. Porter, R. and Lawrenson, G. (eds) (1982). "Metabolic Acidosis." Ciba Foundation Symposium 87: London: Pitman.
9. Robinson, A.M. and Williamson, D.H. (1980). "Physiological Roles of Ketone Bodies as Substrates and Signals in Mammalian Tissues," Physiological Reviews 60:143-187.
10. Williamson, D.H. (1982). "The Production and Utilization of Ketone Bodies in the Neonate." In: Jones CT (ed). The Biochemical Development of the Fetus, pp 621-650. Amsterdam: Elsevier Biomedical.
11. Williamson, D.H. (1987). "Brain Substrates and the Effects of Nutrition," Proceedings of Nutrition Society 46:81-87.
12. Zammit, V.A. (1996). "Role of Insulin in Hepatic Fatty Acid Partitioning: Emerging Concepts," Biochemical Journal 314:1-14.
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