| Product Description |
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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
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Easily absorbed mineral supplement. |
Key Features
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Vegetarian formula. |
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Includes five Krebs Cycle intermediates of
each mineral: citrate, fumarate, malate, succinate, alpha ketoglutarate. |
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| Suggested Use
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| Four tablets daily.
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| Ingredients/Supplement Facts
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| 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 |
† |
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| 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.
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| Additional Information |
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| 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:
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
Citrate is converted into its isomer isocitrate. Isomers are molecules
possessing the same chemical formula, but different structural configurations.1
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
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
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
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
Fumarate is hydrolyzed (by water) to form the final intermediate,
malate.1
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:
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.
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.
Wiesner RJ et al The anaerobic heart: succinate formation and mechanical
performance. Exp Biol. 1986;45(1):55-64.
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.
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.
Tortora GJ, Grabowski SR. Principles of Anatomy and Physiology. 8th
ed. New York, NY. Harper and Row. 1996:837-838.
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.
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.
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.
Michailova AP, Belik ME, McCulloch AD. Effects of magnesium on cardiac
excitation-contraction coupling. J Am Coll Nutr. 2004
Oct;23(5):514S-517S.
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.
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.
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.
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.
Elsherif L, Ortines RV, Saari JT, Kang YJ. Congestive heart failure in
copper deficient mice. Exp Biol Med (Maywood). 2003;7:811-17.
Medeiros DM, Wildman RE. Newer findings on a unified perspective of copper
restriction and cardiomyopathy. Exp Biol Med. 1997;215:299-313.
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.
Fleming T., ed. Manganese In: PDR® for Nutritional Supplements.
Montvale, NJ: Medical Economics Company; 2001: 296-298.
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.
Fleming T., ed. Molybdenum In: PDR® for Nutritional Supplements.
Montvale, NJ: Medical Economics Company; 2001: 308-311.
Mendel RR. The role of the molybdenum cofactor in humans. BioFactors.
2000;11:147-148.
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.
Rowland E, Krikler DM. Potassium supplementation in the treatment of
ventricular arrhythmias. Acta Med Scand Suppl. 1981;647:95-100.
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.
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.
Barceloux DG. Vanadium. J Toxicol Clin Toxicol. 1999;2:265-78.
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.
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Warning! Read carefully before using Krebs Cycle Chelates |
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| 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.
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