How Does It Work?:
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Krebs Cycle Chelates - Enzymatic Therapy


Supplies a scientifically balanced combination of minerals for heart health
Krebs Cycle Chelates
Packaging  100 Tabs
SKU No. 7751 33%
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Prod. No. 2581
MSRP $16.95
Our Price: $11.33
UPC Code: 763948077519
 
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Bullet Krebs Cycle Chelates Description
This supplement is a scientifically balanced combination of major and trace minerals, including boron, chelated to the Krebs cycle intermediates. The Krebs cycle intermediates are a unique chain of five organic acids: citrate, fumarate, malate, succinate, and alpha ketoglutarate.

Benefits

 •  Easily absorbed mineral supplement.

Key Features  

 •  Vegetarian formula.
 •  Includes five Krebs Cycle intermediates of each mineral: citrate, fumarate, malate, succinate, alpha ketoglutarate.
 
 Krebs Cycle Chelates Suggested Use
Four tablets daily.
 
 Krebs Cycle Chelates Ingredients/Supplement Facts
Supplement Facts
Serving Size: 4 Tablets

Ingredients Amount %DV

Calcium (as CFMSA chelate) 600 mg 60 %
Iron (as CFMSA chelate) 5 mg 28 %
Iodine (from marine organic minerals) 100 mcg 67 %
Magnesium (as CFMSA chelate) 400 mg 100 %
Zinc (as CFMSA chelate) 15 mg 100 %
Selenium (as CFMSA chelate) 75 mcg 107 %
Copper (as CFMSA chelate) 1 mg 50 %
Manganese (as CFMSA chelate) 2 mg 100 %
Chromium (as CFMSA chelate) 100 mcg 83 %
Molybdenum (as CFMSA chelate) 25 mcg 33 %
Sodium 10 mg <1 %
Potassium (as CFMSA chelate) 99 mg 3 %
Boron (as CFMSA chelate) 4 mg †
Vanadium (as CFMSA chelate) 50 mcg †

Other Ingredients: cellulose, modified cellulose gum, stearic acid, silicon dioxide, magnesium stearate, modified cellulose, and maltodextrin.
Contains No: sugar, yeast, wheat, gluten, soy, dairy products, artificial coloring, artificial flavoring and preservatives. This product contains natural ingredients; color variations are normal.

†: Daily value not established.
 
 Krebs Cycle Chelates Additional Information

How Does It Work?:
Background
The Krebs cycle, also known as the citric acid cycle or the tricarboxylic acid (TCA) cycle, was first identified by Hans Adolf Krebs in 1937. The Krebs cycle consists of a series of enzymatic reactions, which use oxygen to convert carbohydrates, proteins, and fats into carbon dioxide and water. The cycle is also responsible for the generation of cellular energy in the form of adenosine triphosphate (ATP). ATP is a nucleotide utilized to transport energy for cell metabolism. Each turn of the cycle generates one molecule of ATP and two molecules of carbon dioxide (CO2). The Krebs cycle takes place within the mitochondria, distinct organelles found inside every cell and commonly referred to as the “energy powerhouse”.1

The Krebs cycle consists of 8 critical steps involving the creation of 5 intermediate compounds:

  1. Acetyl coenzyme A (acetyl CoA), a product of glycolysis (the first step in the breakdown of glucose), is one of the starting components of the Krebs cycle. The acetic acid subunit of acetyl CoA is combined with oxaloacetate to form citrate. The coenzyme subunit of acetyl CoA is released by hydrolysis (a reaction with water) to combine with another acetic acid molecule and begin the Krebs cycle again. 1

     
  2. Citrate is converted into its isomer isocitrate. Isomers are molecules possessing the same chemical formula, but different structural configurations.1

     
  3. Isocitrate is oxidized to form the second intermediate, alpha-ketoglutarate. During this reaction, carbon dioxide (CO2) is released and nicotinamide adenine dinucleotide (NAD+), an important coenzyme and carrier of electrons in the electron transport chain, is reduced to NADH. This transfer of electrons is critical to the generation of cellular energy.1

     
  4. Alpha-ketoglutarate is oxidized to succinyl coenzyme A (succinyl CoA). A second molecule of CO2 is released and another molecule of NADH is formed.1

     
  5. A water (H2O) molecule donates its hydrogen atoms to the coenzyme A subunit of succinyl CoA. Then, a free-floating phosphate group (-PO4) displaces coenzyme A and forms a bond with the succinyl complex. The phosphate is then transferred to a molecule of adenosine diphosphate (ADP) to produce an energy molecule of adenosine triphosphate (ATP). It leaves behind one molecule of succinate.1

     
  6. Succinate is oxidized by a molecule of flavin adenine dinucleotide (FAD), another compound necessary for the transfer or electrons and generation of energy within the cell. The intermediate fumarate is formed and FADH, the reduced form of FAD, is released.1

     
  7. Fumarate is hydrolyzed (by water) to form the final intermediate, malate.1

     
  8. Malate is oxidized by NAD+ to regenerate the Krebs cycle starting component, oxaloacetate. Another molecule of NADH is formed. Oxaloacetate is then free to combine with acetyl CoA and begin the Krebs cycle again.1



The Krebs cycle intermediates include the five organic acids: citrate, alpha ketoglutarate, succinate, fumarate, and malate. Research suggests that minerals chelated (bound) to these intermediates, like those found in Krebs Cycle Chelates, have several advantages over other mineral forms.

Krebs cycle intermediates are readily absorbed and utilized by the body. These complexes are more easily ionized than other mineral forms. This ability to dissociate (break apart into positive cations and negative anions) increases the amount of ionized minerals available for uptake by the body. Krebs cycle intermediates are also very stable over the broad pH range found in the gastrointestinal tract. As a result, the net absorption of mineral cations is far greater with Krebs cycle intermediates than with other mineral complexes.1

Supplementation with Krebs cycle chelated-minerals is often used to enhance the mitochondrial production of cellular energy.†2 Sustainable energy is especially important in tissues requiring high levels of energy, such as the heart, arteries, and veins.†3

The following table details the benefits of each ingredient found in Krebs Cycle Chelates:

 

Ingredient Benefit
Calcium Calcium is an essential mineral for heart health and an important regulator of the Krebs cycle.† Inside the mitochondria, calcium activates several enzymes involved in Krebs cycle reactions, including pyruvate dehydrogenase, isocitrate dehydrogenase and oxoglutarate dehydrogenase.† Research indicates that calcium can increase the rate of Krebs cycle reactions in heart mitochondria.† An increase in calcium can drive reactions toward completion, leading to a net increase in energy production.†4 Calcium has also been well researched for its role in healthy heart function.† The mineral allows actin and myosin, two proteins found in muscles, to interact properly during contraction.† Through this cellular process, calcium directs the pacemaker activity and the excitation-contraction movement of the pumping heart.†5
Iron Another mineral essential to human health, iron plays a pivotal role in energy metabolism and healthy red blood cell production.† Most of the body's iron is stored in red blood cells.6 Supplementation has been shown to not only enhance energy levels, but also improve lipid profiles.†7 Research indicates that optimal iron levels are necessary to keep the heart functioning properly.†8
Iodine Iodine is a trace element utilized by the thyroid gland to synthesize thyroid hormones, which regulate basal metabolic rate.†6 Plasma thyroid hormone levels have been critically linked to effective cardiac function.† Optimal hormone levels promote healthy systolic intervals and a healthy heart rate.†9
Magnesium Involved in the synthesis of deoxyribonucleic acid (DNA) and ribonucleic acid (RNA), magnesium is essential to all living organisms.† Magnesium ions are also required as cofactors by certain enzymes, including those which utilize ATP.6 Like calcium, magnesium plays an important role in the excitation and contractions of the heart.†10 Clinical research has shown that magnesium promotes healthy heart rhythms.†11
Zinc Zinc is an important component in enzymes, including carbonic anhydrase and peptidase, which are involved in carbon dioxide metabolism and protein digestion, respectively.†6 Clinical research has documented a significant direct correlation between zinc and aortic valve health.†12 Several clinical trials have shown that zinc supplementation plays a critical role in cardiovascular health.†11, 12, 13
Selenium Selenium is an essential trace element. Because of its functions as an antioxidant and enzyme catalyst, selenium has been well documented for its cardio-protective effects.†14
Copper Copper is another essential trace mineral and important component of coenzymes involved in the electron transport chain.†6 Research has shown that copper provides significant support for healthy heart muscles.†15, 16, 17
Manganese Several manganese-activated enzymes play crucial roles in the metabolism of carbohydrates and amino acids.†6 Manganese is also involved in the regulation of the pathway of activity in the cardiac mitochondria and possesses cardiac antioxidant properties as well.†18, 19
Chromium An essential trace mineral necessary for the proper use of dietary sugars and other carbohydrates by optimizing the production and effects of insulin.†6
Molybdenum A catalyst in the break down of fats and cholesterol.† Molybdenum also functions as a cofactor for three enzymes, which contribute to the antioxidant capacity of the blood.†20, 21 Molybdenum concentration has been linked to healthy vasoconstriction in experimental models.†22
Potassium Potassium is the most abundant cation (positive ion) found inside the cells of the body. It is involved in the regulation of the action potential in cardiac cells.† Through this cellular process, potassium promotes healthy muscle contraction and rhythm.†23
Boron Boron is an essential trace element involved in mineral metabolism.† Research suggests supplementation may protect arterial health.†24
Vanadium Vanadium supports healthy energy metabolism in heart cells.† This essential trace mineral has also been shown to enhance cardiovascular function.*25 Vanadium also adds support to sodium and potassium transport in red blood cells.†26, 27

References:
 

  1. Lehninger AL, Nelson DL, Cox MM. The Citric Acid Cycle. In: Principles of Biochemistry, 2nd ed. New York City, NY: Worth Publishers; 1993:446-74.
  2. Marconi C Sassi G The effect of an alpha-ketoglutarate-pyridoxine complex on human maximal aerobic and anaerobic performance. Eur J Appli Phys. 1982;49(3):307-17.
  3. Wiesner RJ et al The anaerobic heart: succinate formation and mechanical performance. Exp Biol. 1986;45(1):55-64.
  4. Wan B, LaNoue KF, Cheung JY, Scaduto RC Jr. Regulation of citric acid cycle by calcium. J Biol Chem. 1989 Aug 15;264(23):13430-9.
  5. Schaffer SW, Tan BH. Effect of calcium depletion and calcium paradox on myocardial energy metabolism. Can J Physiol Pharmacol. 1985 Nov;63(11):1384-91.
  6. Tortora GJ, Grabowski SR. Principles of Anatomy and Physiology. 8th ed. New York, NY. Harper and Row. 1996:837-838.
  7. Ece A, Yigitoglu MR, Vurgun N, Guven H, Iscan A. Serum lipid and lipoprotein profile in children with iron deficiency anemia. Pediatr Int. 1999 Apr;41(2):168-73.
  8. Beck-da-Silva L, Rohde LE, Pereira-Barretto AC, de Albuquerque D, Bocchi E, Vilas-Boas F, Moura LZ, Montera MW, Rassi S, Clausell N. Rationale and design of the IRON-HF study: a randomized trial to assess the effects of iron supplementation in heart failure patients with anemia. J Card Fail. 2007 Feb;13(1):14-7.
  9. Galloe AM, Rolff M, Nordin H, Ladefoged SD, Mogensen NB. Cardiac performance and thyroid function. The correlation between systolic time intervals, heart rate and thyroid hormone levels. Dan Med Bull. 1993 Sep;40(4):492-5.
  10. Michailova AP, Belik ME, McCulloch AD. Effects of magnesium on cardiac excitation-contraction coupling. J Am Coll Nutr. 2004 Oct;23(5):514S-517S.
  11. Pansin P, Wathanavaha A, Tosukhowong P, et al. Magnesium and zinc status in survivors of sudden unexplained death syndrome in northeast Thailand. Southest Asian J Trop Med Public Health. 2002;1:172-9.
  12. Tohno S, Tohno Y, Moriwake Y, et al. Compositional changes of the aortic valve similar to the artery with aging. Biol Trace Elem Res. 2002;1-3:83-93.
  13. Bhaskar M, Madhuri E, Abdul Latheef SA, Subramanyam G. Influence of zinc on cardiac and serum biochemical parameters in rabbits. Indian J Exp Biol. 2001;11:1170-2.
  14. Alissa EM, Bahijri SM, Ferns GA. The controversy surrounding selenium and cardiovascular disease: a review of the evidence. Med Sci Monit. 2003;1:RA9-18.
  15. Elsherif L, Ortines RV, Saari JT, Kang YJ. Congestive heart failure in copper deficient mice. Exp Biol Med (Maywood). 2003;7:811-17.
  16. Medeiros DM, Wildman RE. Newer findings on a unified perspective of copper restriction and cardiomyopathy. Exp Biol Med. 1997;215:299-313.
  17. Heller LJ, Mohrman DE, Prohaska JR. Decreased passive stiffness of cardiac myocytes and cardiac tissue from copper deficient rat hearts. Am J Physiol Heart Physiol.2000;8:H1840-H1847.
  18. Fleming T., ed. Manganese In: PDRฎ for Nutritional Supplements. Montvale, NJ: Medical Economics Company; 2001: 296-298.
  19. Naya FJ, Black BL, Wu H, et al. Mitochondrial deficiency and cardiac sudden death in mice lacking the MEF2A transcription factor. Natur Med. 2002;11:1303-09.
  20. Fleming T., ed. Molybdenum In: PDRฎ for Nutritional Supplements. Montvale, NJ: Medical Economics Company; 2001: 308-311.
  21. Mendel RR. The role of the molybdenum cofactor in humans. BioFactors. 2000;11:147-148.
  22. Liu DL, Yan M, Chua YL, Chen C, Lim YL. Effects of molybdenum, silicon and nickel on alpha1-adrenoceptor induced constriction of rat isolated aorta. Clin Exp Pharmacol Physiol. 2002;5-6:395-98.
  23. Rowland E, Krikler DM. Potassium supplementation in the treatment of ventricular arrhythmias. Acta Med Scand Suppl. 1981;647:95-100.
  24. Samman S, Naghii MR, Lyons Wall PM, Verus AP. The nutritional and metabolic effects of boron in humans and animals. Biol Trace Elem Res. 1998 Winter;66(1-3):227-35.
  25. Noda C, Masuda T, Sato K, Ikeda K, Shimohama T, Matsuyama N, Izumi T. Vanadate improves cardiac function and myocardial energy metabolism in diabetic rat hearts. Jpn Heart J. 2003 Sep;44(5):745-57.
  26. Barceloux DG. Vanadium. J Toxicol Clin Toxicol. 1999;2:265-78.
  27. Carmignani M, Volpe AR, Masci O, et al. Vanadate as factor of cardiovascular regulation by interactions with the catecholamine and nitric oxide systems. Biol Trace Elem Res. 1996;1:1-12.
 
 Krebs Cycle Chelates Warning
Accidental overdose of iron-containing products is a leading cause of fatal poisoning in children under 6. Keep this product out of reach of children. In case of accidental overdose, call your physician or poison control center immediately.
 

Enzymatic Therapy - Krebs Cycle Chelates  100 Tabs

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