CoQ10 participates in free radical and antioxidant reactions and is involved in the production of energy cells, especially heart cells. It is a powerful antioxidant and helps maintain a healthy heart. Because aging decreases the body’s ability to synthesize CoQ10, supplementation is necessary. It is estimated that 46% of the population over 40 and 75% of seniors may be CoQ10 deficient.
CoQ10, which is chemically similar to vitamins and functions much like one, is a vital catalyst the body needs for cellular energy.
The chewable CoQ10 tablet provides a faster delivery system that speeds nutrients directly into the bloodstream for fuller and quicker absorption.
- Increases strength of the heart even without exercise
- Better body efficiency improves weight loss results
- Protects against heart attacks
- Lowers high blood pressure
- Slows the aging process
- Increases energy for daily tasks
- Provides intense benefit to immune system
- Significant value for periodontal, or gum disease
- Helps to improve memory
- Defends against Alzheimer’s
- Easy to swallow – Great taste – Fast acting
1 chewable tablet should be taken in the morning on an empty stomach.
Coenzyme Q-10 is a necessary component of cellular energy production and respiration. CoQ-10 provides support to all cells of the body, and is especially supportive of tissues that require a lot of energy, such as the heart muscle, periodontal tissue, and the cells of the body~s natural defense system. CoQ-10 helps provide increased energy and exercise tolerance, as well as optimal nutritional support to the cardiovascular system. Chewable tablets increase delivery into the system. Lower levels of Coenzyme Q-10 may be evident in cardiovascular disease, particularly in congestive heart failure. Taking a CoQ-10 supplementmay also correct reduced blood levels of CoQ-10 that result from the use of HMG-Co A reductase inhibitors for the treatment of elevated cholesterol levels. CoQ-10 alsotreats gum disease and helps to maintain healthy gums and teeth, protects the nerves and may help slow Alzheimer’s or Parkinson’s disease, and may help prevent cancer and heart disease. It plays a role in slowing down age related degenerative changes.
Hargreaves IP. Ubiquinone: cholesterol~s reclusive cousin. Ann ClinBiochem. 2003 May;40 (Pt 3):207-18.
Department of Clinical Biochemistry, Neurometabolic Unit, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK. firstname.lastname@example.org
Coenzyme Q(10) is the predominant form of ubiquinone in man. CoQ(10) functions as an electron carrier in the mitochondrial respiratory chain as well as serving as an important intracellular antioxidant. Lowered blood and tissue concentrations of CoQ(10) have been reported in a number of diseases, although whether this deficiency is the cause or an effect of the disease remains largely unresolved. Some studies have reported lowered plasma CoQ(10) concentrations after statin drug treatment of hypercholesterolaemic patients. However, a deficiency in CoQ(10) status has yet to be demonstrated in patients experiencing the rare myotoxic side-effects of these drugs. Most clinical investigations assessing the therapeutic potential of CoQ(10) have focused on cardiovascular disease, specifically congestive heart failure. Although a number of studies have reported clinical improvement in congestive heart failure patients after CoQ(10) supplementation to standard therapy, concerns about the design of these studies coupled to the small number of patients involved have limited their acceptance. Assessment of CoQ(10) status is generally based on plasma measurements. As plasma concentrations are influenced by a number of physiological factors and may not represent cellular concentrations, platelets, lymphocytes and fibroblasts may provide suitable alternatives for these measurements.
Shults CW. Coenzyme Q10 in neurodegenerative diseases.Curr Med Chem. 2003 Oct;10(19):1917-21.
Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093-0662, USA. email@example.com
Coenzyme Q(10) (ubiquinone), which serves as the electron acceptor for complexes I and II of the mitochondrial electron transport chain and also acts as an antioxidant, has the potential to be a beneficial agent in neurodegenerative diseases in which there is impaired mitochondrial function and/or excessive oxidative damage. Substantial data have accumulated to implicate these processes in the pathogenesis in certain neurodegenerative disorders, including Parkinson~s disease, Huntington~s disease and Friedreich~s ataxia. Although no study to date has unequivocally demonstrated that coenzyme Q(10) can slow the progression of a neurodegenerative disease, recent clinical trials in these three disorders suggest that supplemental coenzyme Q(10) can slow the functional decline in these disorders, particularly Parkinson~s disease.
Winkler-Stuck K, Wiedemann FR, Wallesch CW, Kunz WS. Winkler-Stuck K, Wiedemann FR, Wallesch CW, Kunz WS.Effect of coenzyme Q10 on the mitochondrial function of skin fibroblasts from Parkinson patients. J Neurol Sci. 2004 May 15;220(1-2):41-8.
Klinik fur Neurologie der Otto-von-Guericke-Universitat Magdeburg, LeipzigerStrasse 44, 39120 Magdeburg, Germany.
Klinik fur Neurologie der Otto-von-Guericke-Universitat Magdeburg, LeipzigerStrasse 44, 39120 Magdeburg, Germany.Several lines of evidence suggest an impairment of mitochondrial function in the brain of patients with Parkinson~s Disease (PD). However, the presence of a detectable mitochondrial defect in extracerebral tissue of these patients remains a matter of dispute. Therefore, we investigated mitochondrial function in fibroblasts of 18 PD patients applying biochemical micromethods. Putative beneficial effects of coenzyme Q(10) (CoQ(10)), a potent antioxidant, on the mitochondrial function of skin fibroblast cultures were evaluated. Applying inhibitor titrations of the mitochondrial respiration to calculate flux control coefficients of respiratory chain complexes I and IV, we observed deficiencies of both complexes in cultivated skin fibroblasts of PD patients. Cultivation of fibroblasts in the presence of 5 microMCoQ(10) restored the activity of impaired respiratory chain complexes in the fibroblast cultures of 9 out of 18 PD patients. Our data support the presence of a generalized mitochondrial defect in at least a subgroup of patients with PD that can be partially ameliorated in vitro by coenzyme Q(10) treatment
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