Mitocharger™
Maintaining the Power Plant of Life
· Supports the health of mitochondria (power plants of the cell)
· Attacks a central theory of aging at it’s source
· Alleviates symptoms of Metabolic Syndrome and Type II Diabetes
· Enhances mitochondrial activity on six different levels
· Formulation design based on extensive research
The Importance of the Mitochondria
The cell is the basis of all life, and the mitochondrion is the power plant that keeps the cell operating. A simple but effective metaphor for what is one of the most significant and complex biochemical relationships known to science. Without mitochondria, cells simply do not produce the energy needed for the human body to function or even survive. It comes as little surprise, therefore, that any state of mitochondrial dysfunction can be associated with a host of metabolic conditions, including Type II Diabetes, Syndrome X and excessive free radical production.
Mitochondria , ATP
Mitochondria are bacteria-sized organelles, and thousands are located inside the membrane of each cell. The primary function of the mitochondria is to convert organic materials (originating mainly from the food we eat) into energy in the form of ATP (adenosine triphosphate – the immediate fuel of life). The rate at which the mitochondria perform this function is called the Basal Metabolic Rate (BMR), and an increased BMR leads to increased insulin sensitivity, which in turn leads to the greatest safeguard against a host of metabolic disorders, including the increasingly present Metabolic Syndrome, or Syndrome X.
The Vicious Cycle
Ironically, the mitochondria’s ability to produce ATP also results in the simultaneous production of other, unproductive metabolic by-products, particularly ROS (reactive oxygen species) free radicals.
SUPPLEMENT FACTS:
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18 0 Vegi-Caps |
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Serving Size: 6 Capsules Interactions/possible side effects: none known |
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R(+)-Lipoic acid : 150 mg Pregnancy/Nursing: avoid |
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Co-enzyme Q10: 100 mg Clinical Applications: support for mitochondrial dysfunction, |
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Rhodiola Rosea: 150 mg Type II diabetes; Syndrome X |
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Benfotiamine: 150 mg Complementary Products: Advanced B-Complex, Ortho-Core, R(+)-SR, Co-QPLUS |
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Oxaloacetic Acid: 100 mg D-Ribose, Magnesium Malate Renew |
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D-Uridine: 50 mg |
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Gynostemma Pentaphyllum: 100 mg |
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Acetyl-L-Carnitine: 1,500 mg |
The Mitochondrial Theory of Aging
The aforementioned ‘vicious cycle’ has become known as the Mitochondrial Theory of Aging. Even more insidiously, an inefficient mitochondrion generates more free radicals than an efficient one. This is because more fuel (in the form of glucose, amino acids and fatty acids) is required for each mitochondrion to produce the same amount of ATP, resulting in an increased ratio of ROS-to-ATP production. To complicate matters further, mitochondrial DNA (mtDNA) differs from the DNA of the nucleus and other organelles in that mtDNA has no enzymatic defense against oxidative stressors, self-generated or not. In-vivo studies have provided evidence for the Mitochondrial Theory of Aging so conclusive that one leading researcher summarized it this way: "It is generally accepted that oxidative mitochondrial decay is a major contributor to aging."[1]
Maintaining The Power Plant – With Cocktails
As we have seen, the relative clarity of the mitochondria’s role within human biochemistry is coupled with an inherent vulnerability that must be addressed if any attempt is to be made with regard to enhancing mitochondrial health. The process of addressing the elusive prerequisites to mitochondrial health is so intricate that entire professional medical societies have been established exclusively for its study. These include the Mitochondrial Research Society (Buffalo, N.Y.), the Mitochondrial Physiology Network (Innsbruck, Austria), and the United Mitochondrial Disease Foundation (Pittsburgh, PA), among others. Their efforts have helped to create a plethora of complex nutraceutical formulations designed to enhance mitochondrial function and health from every conceivable perspective. Below is an example of the categorical synopsis of their efforts.
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Strategy |
Theoretical Basis |
Example |
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1. Enzyme Bypass |
Provide energy beyond the site of the enzyme defect |
Succinate, Co-Enzyme Q10. |
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2. Anti-oxidants |
Reduce free radical damage to cell structures |
Vitamin E, C, lipoic acid. |
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3. Alternative energy |
Use an anaerobic system not requiring mitochondria |
Creatine Monohydrate, exogenous ATP. |
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4. Reduce lactate |
Reduce acidosis, more energy into the mitochondria |
Dichloroacetate, thiamine. |
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5. Strength exercise |
Improve strength, reduce number of mutant mtDNA |
Weights, isometrics. |
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6. Endurance exercise |
Improve endurance, reduce cardiovascular risks |
Jogging, cycling, walking. |
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7. Nucleotide precursors |
Prevent depletion of nucleotide pool (for DNA synthesis) |
Triacetyluridine, d-ribose, d-uridine |
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8. Vasodilation |
Prevent vascular spasm in MELAS stroke |
L-arginine, gynostemma pentaphyllum |
How It All Works
Enzyme Bypass: The theory here is to circumvent a defect along the mitochondrial Electron Transport Chain which produces ATP. This chain is initiated when electrons are transferred to a lipid-soluble carrier called a ubiquinone, which in turn crosses the cellular membrane. The supplemental form of ubiquinone is Co-Enzyme Q10 (Co-Q10), and studies have shown that it can expedite the Complex II phase of the Electron Transport Chain by up to 200%.[3]
Anti-oxidants: The universal anti-oxidant/free radical dichotomy certainly has mitochondrial applications as well, but the vulnerability of mtDNA alters the circumstances. Conventional anti-oxidants such as vitamins C and E are certainly useful, but the ideal mitochondrial anti-oxidant appears to be a-lipoic acid, or simply lipoic acid (preferably composed of the R(+)- enantiomer ). Lipoic acid is metabolized to its active form, diHydrolipoic acid (DHLA) inside the mitochondrion itself by the enzyme known as pyruvate dehydrogenase complex (PDH). This process, (and equally importantly, the dynamics of this process) produces intense biological activity, including the regeneration and recycling of vitamins C and E and enhanced insulin sensitivity.
Alternative Energy: This tactic involves the maximal utilization of a source of ATP that does not require any mitochondrial participation, thus augmenting overall ATP production without burdening dysfunctional or aging mitochondria. Both creatine monohydrate and the herb rhodiola rosea have demonstrated a capacity to increase ATP production, although the latter appears to do so by actually rejuvenating the mitchondria’s capacity to synthesis ATP.[4]
Reducing Lactate: The strategy here is to stimulate the enzyme pyruvate dehydrogenase – which is responsible for directing pyruvate into the mitochondria and away from lactate production. This can be done with the drug dichloroacetate as well as with vitamin B1 supplementation. The latter option has been made even more appealing by the development of benfotiamine, a lipid-soluble thiamin that is nearly 5 times more bio-available than conventional thiamin.
Nucleotide Precursors: Nucleotides are the structural units of DNA and RNA – including mtDNA and mtRNA. As mitochondrial dysfunction is closely associated with the depletion of nucleotides, maintaining a healthy nucleotide pool is paramount. Triacetyluridine, a chemoprotective drug that is a precursor of uridine (an RNA nucleotide), is believed to be capable of this. Naturally-derived uridine supplements have been studied for their ability to improve mitochondrial function in patients with HIV.[5]
Vasodilation: Vasodilation (the widening of the blood vessels due to relaxation of smooth muscle in the vessel wall) is linked to the mitochondria via the production of nitric oxide. The mitochondria are primary targets of nitric oxide, and even small amounts can regulate ATP synthesis. MELAS (or mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) is a mitochondrial disorder caused by mutations in the mtDNA of endothelial cells that lead to their dysfunction. Supplementation with L-arginine, a nitric oxide donor, has been shown to ameliorate the symptoms of MELAS. Other nitric oxide enhancers include citrulline malate and the highly efficient gynostemma pentaphyllum.
[1] Liu, J. et al (2002) Delaying brain mitochondrial decay and aging with mitochondrial antioxidants and metabolites. Ann NY Acad Sci 959: 133-66.
[2] Tarnopolsky MA, et al. Nutritional and exercise-based therapies in the treatment of mitochondrial disease. Curr Opin Clin Nutr Metab Care. 2002. Nov;5(6):619-29.
[3] Mazzio EA, Soliman KF. Effects of enhancing mitochondrial oxidative phosphorylation with reducing equivalents and ubiquinone on 1-methyl-4-phenylpyridinium toxicity and complex I-IV damage in neuroblastoma cells. Biochem Pharmacol. 2004. Mar 15;67(6):1167-84.
[4] Abidov M, et al. Effect of extracts from Rhodiola rosea and Rhodiola crenulata (Crassulaceae) roots on ATP content in mitochondria of skeletal muscles. Bull Exp Biol Med. 2003 Dec;136(6):585-7.
5 Banasch M, et al. Uridine supplementation enhances hepatic mitochondrial function in thymidine-analogue treated HIV-infected patients. AIDS. 2006 Jul 13;20(11):1554-6.