There are two primary energy sources for the body:
· Carbohydrates in the form of sugars (i.e. glucose) produce energy by glycolysis to make acetyl CoA for the citric acid cycle.
· Fats in the form of triglycerides produce energy by beta-oxidation to make acetyl CoA for the citric acid cycle.
Carbohydrates and fats are converted to energy in cellular organelles called mitochondria. Energy is produced by both glycolysis and the citric acid cycle. Environmental toxins can inhibit the production of energy from both carbohydrates and stored fats resulting in obesity. For instance aluminum at a concentration of some drinking water in the U.S. inhibits glycolysis.
Since development of the Bayer process for aluminum purification from bauxite in 1888, there has been a steady increase in the amount of aluminum humans ingest and accumulate. Aluminum, at levels found in some drinking water (108ppb,108mcg/liter, 4mcM), inhibits hexokinase, an enzyme that catalyzes the first step in carbohydrate metabolism (i.e. glycolysis)1. The biochemical response to the inhibition of glycolysis is the conversion of carbohydrates to fat as triglycerides comprised of long chain fatty acids2. This fat can be stored in adipose tissue or metabolized for energy. However, aluminum also inhibits the production of L-carnitine required for movement of long chain fatty acids in stored fat to the mitochondria for conversion to energy3-6. Therefore aluminum inhibits two key steps in metabolizing carbohydrates and fats for energy generation:
· Aluminum inhibits the first step of carbohydrate metabolism called glycolysis1. Inhibition of glycolysis promotes the conversion of carbohydrates to stored fats (e.g. lipogenesis)2.
· Aluminum inhibits the biosynthesis of L-carnitine3-6. L-carnitine is required for mobilizing stored fat as long chain triglycerides for mitochondrial energy production7.
The result of aluminum ingestion is therefore, more fat from carbohydrate, more fat being stored, and less fat being utilized for energy, resulting in obesity that does not respond to dieting.
Ketogenic Diet of Medium Chain Triglycerides for Coping with Aluminum Toxicity
Switching from a low fat – moderate carbohydrate diet to a high fat – low carbohydrate diet results in higher than normal levels of chemicals called ketones in the blood. For this reason the high fat diet is called a ketogenic diet. The source of fat on a ketogenic diet can be from plant and/or animal sources, such as canola oil, coconut oil, and/or beef tallow. All fats are primarily triglycerides comprised of fatty acids of varying chain length and unsaturation that are esterified to glycerol. These fatty acids are of three types:
· Long chain essential fatty acids (e.g. linoleic and alpha-linolenic acids)
· Long chain non-essential fatty acids (i.e. EPA and 22C DHA)
· Medium chain fatty acids (i.e. lauric acid found as 50% of coconut oil)
History of the Ketogenic Diet
The fact that the human body can switch from carbohydrates to triglycerides as its primary source of energy is called the “Schwatka Imperative”. This is named after Lieutenant Frederick Schwatka who volunteered for a 19 month 3,000 mile Arctic mission, taking with him only enough carbohydrate to last 10 months8. On June 15th of 1879 he ate his last hard bread and then it became imperative that his body switch to a diet of primarily fresh-killed reindeer meat with occasional fish. For the first two or three weeks on the ketogenic diet he felt “… an apparent weakness and inability to perform severe exertive, fatiguing journeys.” Then miraculously after two to three weeks on the ketogenic diet his strength and stamina returned to normal. For example, during the last two days of the expedition he hiked 75 miles.
Lieutenant Schwatka was looking for information on why the men of the Franklin Expedition perished in the Arctic a quarter century earlier. Schwatka was lucky he traveled ten years before the Bayer Process for aluminum purification from bauxite was developed in 1888. Since 1888 people in general have been dosed with ever increasing levels of aluminum that is impacting how their mitochondria generate energy.
Moderate Carbohydrate Diet with Supplements for Losing Weight and Aluminum
Johnston in 2006 compared 10 overweight people on a low fat and moderate carbohydrate diet with 9 overweight people on a ketogenic diet with high fat and low carbohydrate diet. The groups were fed diets providing the following percentages of energy:
Moderate Carbohydrate Diet: 30% fat – 40% carbohydrate – 30% protein
Ketogenic Diet: 60% fat – 5% carbohydrate – 35% protein
After eight weeks the moderate carbohydrate dieters lost more weight than the ketogenic dieters. The researchers concluded that the ketogenic diet did not offer any significant metabolic advantage over the moderate carbohydrate diet12.There are supplements of biochemicals naturally found in your body that taken daily will result in improved stored fat utilization and weight loss. These supplements are:
· Dissolved silica (a.k.a. OSA) for lowering your body-burden of aluminum13-15
· CoQ10 for improving your energy and cognition16
· PQQ for increasing mitochondrial biogenesis and cognition16-18
By lowering aluminum levels in your body, glycolysis and fat metabolism will return to normal. This coupled with new mitochondria will allow you to metabolize or “burn” stored fat resulting in dieting with weight loss.
There are also supplements of biochemicals naturally found in your body that will lower LDL and triglycerides, both of which are linked to an increased risk of vascular disease, such as stroke and heart attack:
· EPA (eicosapentaenoic acid) for reducing triglycerides by 5 to 10%19
· PA (palmitoleic acid) for reducing triglycerides by 15% and LDL by 8%20
· Vitamin D for reducing triglycerides by 23%21
Lowering triglycerides and LDL decreases the risk of vascular disease, heart attack, and stroke. For more details on these supplements see my book “Prevent Alzheimer’s, Autism, and Stroke”22.
Ketogenic Diet with Fat from Medium Chain Triglycerides
Medium chain triglycerides (MCT), as opposed to long chain (i.e. 18 carbon atoms) triglycerides (LCT), do not require L-carnitine for mobilization and conversion into energy by the mitochondria10. Therefore the metabolism of MCT is not inhibited by aluminum. Also the oxidative utilization (sum of digestion, absorption, and oxidation) of MCT can be 3 to 4 times greater than for LCT10. These results were obtained with animals preconditioned to survive, like Lieutenant Schwatka, on a ketogenic diet10. Therefore the modern equivalent of the “Schwatka Imperative” is to either:
· Remain obese while surviving on a diet of medium chain triglycerides or
· Lose some weight by decreasing aluminum accumulation and eating a moderate carbohydrate diet.
Many people are opting for the MCT diet, such as coconut oil, without lowering aluminum. This will provide more energy and improved cognition. Unfortunately it will not result in weight loss since aluminum is still inhibiting the mobilization and conversion of stored long chain fatty acids to energy. Also:·
MCT or Coconut oil does not contain essential fatty acids (e.g. linoleic and alpha-linolenic acid)
· Lauric acid, comprising 50% of coconut oil, increases LDL by 16% in humans and LDL is linked to vascular disease, such as stroke and heart attack11
References
1. Lai, J.C., and Blass, J.P.; Inhibition of brain glycolysis by aluminum; J. Neurochem.; Feb.; 42(2):438-46 (1984)
2. Mailloux, R.J., et al.; Hepatic response to aluminum toxicity: Dsylipidemia and liver diseases; Exper. Cell Res.; 317:2231-2238 (2011)
3. Gaballa, I.F., et al.; Dyslipidemia and disruption of L-carnitine in aluminm exposed workers; Egyptian J. Occup. Med.; 37(1):33-46 (2013)
4. Lemire, J., et al.; The disruption of L-carnitine metabolism by aluminum toxicity and oxidative stress promotes dyslipemia in human astrocytes and hepatic cells; Toxicol. Lett.; Jun.; 203(3):219-26 (2011)
5. Waly, M. I-A., et al.; Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal; Mol. Psychiatry; 9:358-70 (2004)
6. Waly, M. I-A., and Deth, R.; Neurodevelopmental toxins deplete glutathione and inhibit folate and vitamin B12-dependent methionine synthase activity – a link between oxidative stress and autism, FASEB J.; 22:894 1 (2008)
7. Fritz, I.B., Kaplan, E., Yue, K.T.; Specificity of carnitine action on fatty acid oxidation by heart muscle; Am. J. Physiol.; Jan.; 202:117-21 (1962)
8. Schwatka, F.; The Long Arctic Search; Stackpole, E.A., Editor; No. 44; The Marine Historical Association, Inc.; Mystic, CT (1965)
9. Beattie, O., and Geiger, J.; Frozen in time – The fate of the Franklin Expedition; Bloomsbury (2004)
10. Heo, K.N., et al.; Medium-chain fatty acids but not L-carnitine accelerate the kinetics of [14C]triacylglycerol utilization by colostrum-deprived newborn pigs; J. Nutr.; 132:1989-1994 (2002)
11. Tsai, Y.H., et al.; Mechanisms mediating lipoprotein responses to diets with medium chain triglyceride and lauric acid; Lipids; Sep.; 34(9):895-905 (1999)
12. Johnston, C.S., et al.; Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets; Am. J. Clin. Nutr.; 83:1055-61 (2006)
13. Edwardson, J.A., et al.; Effect of silicon on gastrointestinal absorption of aluminum; The Lancet; 342(8865):211-12 (1993)
14. Carlisle, E.M., and Curran, M.J.; Effect of dietary silicon and aluminum on silicon and aluminum levels in rat brain; Alzheimer Dis. Assoc. Disord.; 1(2):423-30 (2013)
15. Davenward, S,, et al.; Silicon-rich mineral water as a non-invasive test of the ‘aluminum hypothesis’ in Alzheimers disease; J. Alzheimer’s Dis.; 33(2):423-30 (2013)
16. Nakani, M., et al.; Effect of pyrroloquinoline quinone (PQQ) on mental status of middle-aged and elderly persons; Food Style; 21 13(7):50-3 (2009)
17. Chowanadisai, W., et al.; Pyrroloquinoline quinone stimulates mitochondrial biogenesis through cAMP response element-binding protein phosphorylation and increased PGC-1 alpha expression; J. Biol. Chem.; Jan.; 285(1):142-52 (2010)
18. Onyango, I.G., et al.; Regulation of neuron mitochondrial biogenesis and relevance to brain heath; Biochim Biophys Acta; jan.; 1802(1):228-34 (2010)
19. Bernstein, A.M., et al.; Purified palmitoleic acid for the reduction of high-sensitivity C-reactive protein and serum lipids: a double blinded, placebo controlled study; J.Clin. Lipidol.; 8(6):612-7 (2014)
20. Harris, W.S.; n-3 Fatty acids and serum lipoproteins: human studies; A. J. Clin. Nutr.; 65(suppl.):1645S-54S (1997)
21. Rejnmark, L., et al.; Simvastatin does not affect vitamin D status, but low vitamin D levels are associated with dyslipidemia; Results from a randomized, contolled trial: Internat. J. Endrocrin.; Article ID 957174 (2010)
22. Crouse, D.N.; Prevent Alzheimer’s, autism, and stroke, with 7 supplements, 7 life-style choices, and a dissolved mineral; Etiological Publishing (2016)
Dennis N Crouse, PhD Harvard, Scientist and Author