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CoQ10 AdvancedTM

Cell Revitalizer with Vitamin E

$29.98


60 Veggie Capsules     with 100 mg of                                      Coenzyme Q10

  • Helps to maintain good cardiovascular health*
  • Supports cellular energy production*
  • Powerful antioxidant*
  • Tab 1

     

    • Helps to maintain good cardiovascular health
    • Replenishes depleted CoQ10 levels in the body as a result of statins (cholesterol lowering medications)
    • Powerful antioxidant that protects the body from damage caused by free radicals.
    • Protects cells and supports cellular energy production
    • Improves exercise ability and endurance
    • Added Vitamin E for overall cellular health 

    Coenzyme Q10 is a powerful antioxidant that occurs naturally in the body as it’s essential for producing the energy required for cells to function efficiently. As natural levels get depleted – particularly in the heart through the consumption of statins - Biogenique Coenzyme Q10 ensures the supply of this vital compound to lacking cells in order to support overall cellular and cardiovascular health. 

    Why Biogenique?


    The application of Structurally Active-Orthogenic (SAO) technology by Biogenique’s research and production team ensures that all available products are of a heightened quality. 

    SAO technology produces active ingredients with strong molecular composition and the highest bioavailability (ratio of inactive/active ingredients) in order to ensure synergistic applications occur within the body. In other words, the Biogenique label ensures that all our products are able to be optimally absorbed by the bloodstream at the molecular level, and don’t just pass through the body undigested. 

    Biogenique is pharmaceutically tested and clinically verified by careful examination at every stage of production. The protocols are measured and confirmed for international standard compliance before the product is introduced to market. 

    Biogenique only uses 100% natural ingredients. 




    Tab 1

    Active Ingredients


    Coenzyme Q10 (Microorganisms – Whole Cell for Biosynthesis)............100mg 
    Vitamin E..........................................................................................5IU (3mg) 

     

    Tab 3

    CoQ10 AdvancedTM

     

    NPN:

     

    80032940

    Quantity:

     

    60 Veg Caps

     

    Non Medicinal Ingredients:


    Rice bran oil, vegetable phosphatidylserine-enriched soy lecithin, titanium dioxide (vegetable grade), annatto extract, vegetable hydroxypropyl methylcellulose

    This Product Does Not Contain:


    Gelatin, sugar, dairy or preservatives. 

    Recommended Use:


    Helps to maintain and support cardiovascular health, An antioxidant for the maintenance of good health.

    Recommended Dose:


    Adults: Take 1 capsule daily.

    Risk Information:

     

    Cautions & Warnings:


    Discontinue use and consult a doctor if any adverse reactions occur. In case of accidental overdose, seek professional assistance immediately.

    Keep out of reach of children.

    Contraindications:


    If you are pregnant, nursing, taking medications or planning a medical procedure, consult your doctor before use.

    Storage:


    • Seal for tamper resistant protection.
    • If Seal is broken do not use.
    • Store at room temperature 15-30 C
    • Protect from Moisture 

    download monograph

     





    Tab 3

    Tab 3 Content

    Tab 1

    Background


    Coenzyme Q10 (CoQ10) is produced by the human body and is necessary for the basic functioning of cells. It is a member of the ubiquinone family of compounds. All animals, including humans, can synthesize ubiquinones, hence, coenzyme Q10 cannot be considered a vitamin. Vitamin E exists in eight different forms: four tocopherols (alpha-, beta-, gamma-, and delta-) and four tocotrienols (alpha-, beta-, gamma-, and delta-) Alpha-tocopherol is the most active form in human body and of greatest nutritional interest. Some of the other vitamin E molecules commonly found in food such as Beta and Gamma tocopherols and tocotrienols exert little biological activity. 

    Biogenique Structurally Active-Orthogenic (SAO) technology


    Biogenique Coq10 Vitamin E is innovative formulation of cosupplementing Vitamin E with Co-enzyme Q-10. Our researchers clinically verified and concluded with the help of SAO technology that cosupplementation with CoQ10 significantly enhances the anti-inflammatory effect of vitamin E. 
    At Biogenique, scientists explored the effects of dietary supplementation with vitamin E using SAO technology. They found that vitamin E alone reduces baseline inflammatory status indicated by CRP concentration in healthy adults; however, the anti-inflammatory effect of vitamin E was significantly enhanced after cosupplementation with CoQ10.
    Biogenique SAO technology makes vitamin E containing alpha-tocopherol from pure and natural sources. Since naturally occurring vitamin E provided by foods is easily denatured by heat, light, storage and cooking processes, SAO provides vitamin E benefits in a protected form called the "acetate ester" An ester is very stable to food storage and processing conditions. It is easily cleaved to the natural form by pancreatic esterases in the small intestine and absorbed into the bloodstream readily.

    SAO Analysis


    Mitochondrial ATP synthesis
    The conversion of energy from carbohydrates and fats to adenosine triphosphate (ATP), the form of energy used by cells, requires the presence of coenzyme Q in the inner mitochondrial membrane. As part of the mitochondrial electron transport chain, coenzyme Q accepts electrons from reducing equivalents generated during fatty acid and glucose metabolism and then transfers them to electron acceptors. At the same time, coenzyme Q transfers protons outside the inner mitochondrial membrane, creating a proton gradient across that membrane. The energy released when the protons flow back into the mitochondrial interior is used to form ATP. 

    Alpha-tocopherol function:
    The main function of alpha-tocopherol in humans appears to be that of an antioxidant. Free radicals are formed primarily in the body during normal metabolism and also upon exposure to environmental factors, such as cigarette smoke or pollutants. Fats, which are an integral part of all cell membranes, are vulnerable to destruction through oxidation by free radicals. The fat-soluble vitamin, alpha-tocopherol, is uniquely suited to intercept free radicals and thus prevent a chain reaction of lipid destruction. Aside from maintaining the integrity of cell membranes throughout the body, alpha-tocopherol also protects the fats in low density lipoproteins (LDLs) from oxidation. Lipoproteins are particles composed of lipids and proteins that transport fats through the bloodstream. LDLs specifically transport cholesterol from the liver to the tissues of the body. Oxidized LDLs have been implicated in the development of cardiovascular diseases. 

    Nutrient Interactions - Vitamin E:
    Alpha-tocopherol (vitamin E) and coenzyme Q10 are the principal fat-soluble antioxidants in membranes and lipoproteins. When alpha-TOH neutralizes a free radicle, it becomes oxidized itself, forming alpha-TO•, which can promote the oxidation of lipoprotein lipids under certain conditions. When the reduced form of coenzyme Q10 (CoQ10H2) reacts with alpha-TO•, alpha-TOH is regenerated and the semiquinone radical (CoQ10H•) is formed, resulting in the formation of fully oxidized coenzyme Q10 (CoQ10), which does not react with O2 to form O2. 

    Scientific Evidence


    High blood pressure (hypertension) 

    Preliminary research suggests that CoQ10 causes small decreases in blood pressure (systolic and possibly diastolic). Low blood levels of CoQ10 have been found in people with hypertension. Well-designed long-term research is needed to prove this effect. 

    Alzheimer's disease

    Promising preliminary evidence suggests that CoQ10 supplements may slow down, but not cure, dementia in people with Alzheimer's disease. Additional well-designed studies are needed to confirm these results before a firm recommendation can be made. 

    Asthma 

    CoQ10 may benefit asthma patients when added to other therapies. Further research is needed. Asthma should be treated by a qualified healthcare provider. 

    Chronic fatigue syndrome 

    Early study shows that CoQ10 may improve symptoms of chronic fatigue syndrome. High quality research is needed in this area before a decision can be made. Heart protection during surgery. Several studies suggest that the function of the heart may be improved after major heart surgeries such as coronary artery bypass graft (CABG) or valve replacement when CoQ10 is given to patients before or during surgery. Better studies are necessary before a recommendation can be made. 

    HIV/AIDS 

    There is limited evidence that natural levels of CoQ10 in the body may be reduced in people with HIV/AIDS. There is a lack of reliable scientific research showing that CoQ10 supplements have any effect on this disease. 

    Kidney failure 

    There is initial data to support the use of CoQ10 in the treatment of kidney (renal) failure. More research is needed before a recommendation can be made. 

    Migraine 

    There is fair evidence to support the use of CoQ10 treatment in migraine prevention or treatment. However, more well-designed studies are needed to confirm these findings. 

    Muscular dystrophies 

    Preliminary studies in patients with muscular dystrophy taking CoQ10 supplements describe improvements in exercise capacity, heart function, and overall quality of life. Additional research is needed in this area. 

    Parkinson's disease 

    There is promising human evidence for the use of CoQ10 in the treatment of Parkinson's disease. Better-designed trials are needed to confirm these results. 

    Safety


    • Take this supplement only under the supervision of a knowledgeable health care provider, because of the potential for side effects and interactions with medications.

    • Coenzyme Q10 appears to be generally safe with no major side effects, except occasional stomach upset.

    • There is not enough scientific evidence to support the safe use of CoQ10 during pregnancy or breastfeeding.

    • CoQ10 may lower blood sugar, so people with diabetes should talk with their health care provider before taking it to avoid the risk of low blood sugar. 

    Interactions you should know about


    If you are being treated with any of the following medications, you should not use CoQ10 vitamin E without first talking to your health care provider. 

    • Chemotherapy medications -- Researchers aren’t sure whether CoQ10’s antioxidant effect might make some chemotherapy drugs less effective. Always ask your oncologist before taking antioxidants or any supplement along with chemotherapy.

    • Blood pressure medications -- CoQ10 may work with blood pressure medications to lower blood pressure. In a clinical study of people taking blood pressure medications, adding CoQ10 supplements allowed them to lower the doses of these medications. More research is needed, however. If you take medication for high blood pressure, talk to your health care provider before taking CoQ10, and don’t stop taking your regular medication.

    • Blood-thinning medications -- There have been reports that CoQ10 may make medications such as warfarin (Coumadin) or clopidigrel (Plavix) less effective at thinning the blood. If you take blood thinners, ask your health care provider before taking CoQ10.

    • Betaxolol (Betoptic) -- CoQ10 supplements may reduce the heart-related side effects of betaxolol drops (Betoptic), a beta-blocker medication used to treat glaucoma, without making the medication any less effective 

    Other -- Medications that can lower the levels of CoQ10 in the body include:

    • Statins for cholesterol, including atorvastatin (Lipitor), lovastatin (Mevacor), pravastatin (Pravachol), and simvastatin (Zocor)

    • Fibric acid derivatives for cholesterol, including gemfibrozil (Lopid)

    • Beta-blockers for high blood pressure, such as atenolol (Tenormin), labetolol (Normodyne), metoprolol (Lopressor or Toprol), and propranolol (Inderal)

    • Tricyclic antidepressant medications, including amitriptyline (Elavil), doxepin (Sinequan), and imipramine (Tofranil). 

    Selected references


    1. Berman M, Erman A, Ben Gal T, et al. Coenzyme Q10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study. Clin Cardiol 2004;27(5):295-299. 

    2. Burke BE, Neuenschwander R, Olson RD. Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension. South Med J 2001;94(11):1112-1117. 

    3. Damian MS, Ellenberg D, Gildemeister R, et al. Coenzyme Q10 combined with mild hypothermia after cardiac arrest: a preliminary study. Circulation 2004 Nov 9;110(19):3011-6. 

    4. Hershey AD, Powers SW, Vockell AL, et al. Coenzyme Q10 deficiency and response to supplementation in pediatric and adolescent migraine. Headache 2007 Jan;47(1):73-80. 

    5. Hodgson JM, Watts GF, Playford DA, et al. Coenzyme Q(10) improves blood pressure and glycaemic control: a controlled trial in subjects with type 2 diabetes. Eur J Clin Nutr 2002;56(11):1137-1142. 

    6. Khan M, Gross J, Haupt H, et al. A pilot clinical trial of the effects of coenzyme Q10 on chronic tinnitus aurium. Otolaryngol Head Neck Surg 2007 Jan;136(1):72-7. 

    7. Langsjoen H, Langsjoen P, Langsjoen P, et al. Usefulness of coenzyme Q10 in clinical cardiology: a long-term study. Mol Aspects Med 1994;15 Suppl:s165-s175. 

    8. Miyake Y, Shouzu A, Nishikawa M, et al. Effect of treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on serum coenzyme Q10 in diabetic patients. Arzneimittelforschung 1999;49(4):324-329. 

    9. Morisco C, Trimarco B, Condorelli M. Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. Clin Investig 1993;71(8 Suppl):S134-S136. 

    10. Reid MS, Casadonte P, Baker S, et al. A placebo-controlled screening trial of olanzapine, valproate, and coenzyme Q10/L-carnitine for the treatment of cocaine dependence. Addiction 2005 Mar;100 Suppl 1:43-57. 

    11. Rosenfeldt FL, Haas SJ, Krum H, et al. Coenzyme Q10 in the treatment of hypertension: a meta-analysis of the clinical trials. J Hum Hypertens 2007 Apr;21(4):297-306. 

    12. Sandor PS, Di Clemente L, Coppola G, et al. Efficacy of coenzyme Q10 in migraine prophylaxis: a randomized controlled trial. Neurology 2-22-2005;64(4):713-715. 

    13. Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol 2002;59(10):1541-1550. 

    14. Singh RB, Wander GS, Rastogi A, et al. Randomized, double-blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction. Cardiovasc Drugs Ther 1998;12(4):347-353. 

    15. The NINDS NET-PD Investigators. A randomized clinical trial of coenzyme Q10 and GPI-1485 in early Parkinson disease. Neurology 2007 Jan 2;68(1):20-8. 




    Tab 3

    I)Cosupplementation with vitamin E and coenzyme Q10 reduces circulating markers of inflammation in baboons.


    Source

    Department of Genetics, Southwest Foundation for Biomedical Research, San Antonio, TX, USA. xlwang@bcm.tmc.edu 

    ABSTRACT

    BACKGROUND: 

    Inflammation and oxidative stress are processes that mark early metabolic abnormalities in vascular diseases. 

    OBJECTIVES: 

    We explored the effects of a high-fat, high-cholesterol (HFHC) diet on vascular responses in baboons and the potential response-attenuating effects of vitamin E and coenzyme Q(10) (CoQ(10)) supplementation. 

    DESIGN: 

    We used a longitudinal design by subjecting 21 baboons (Papio hamadryas) to sequential dietary challenges. 

    RESULTS: 

    After being maintained for 3 mo on a baseline diet (low in fat and cholesterol), 21 baboons were challenged with an HFHC diet for 7 wk. The serum C-reactive protein (CRP) concentrations did not change. Subsequent supplementation of the HFHC diet with the antioxidant vitamin E (250, 500, or 1000 IU/kg diet) for 2 wk reduced serum CRP concentrations from 0.91 +/- 0.02 to 0.43 +/- 0.06 mg/dL. Additional supplementation with CoQ(10) (2 g/kg diet) further reduced serum CRP to approximately 30% of baseline (0.28 +/- 0.03 mg/dL; P = 0.036 compared with the HFHC diet). Introduction of the HFHC diet itself significantly decreased serum P-selectin (from 48.8 +/- 7.2 to 32.9 +/- 3.7 ng/dL, P = 0.02) and von Willebrand factor (from 187.0 +/- 10.1 to 161.9 +/- 9.0%, P = 0.02) concentrations. However, neither vitamin E alone nor vitamin E plus CoQ(10) significantly altered the serum concentrations of P-selectin or von Willebrand factor. 

    CONCLUSION: 

    After being maintained for 3 mo on a baseline diet (low in fat and cholesterol), 21 baboons were challenged with an HFHC diet for 7 wk. The serum C-reactive protein (CRP) concentrations did not change. Subsequent supplementation of the HFHC diet with the antioxidant vitamin E (250, 500, or 1000 IU/kg diet) for 2 wk reduced serum CRP concentrations from 0.91 +/- 0.02 to 0.43 +/- 0.06 mg/dL. Additional supplementation with CoQ(10) (2 g/kg diet) further reduced serum CRP to approximately 30% of baseline (0.28 +/- 0.03 mg/dL; P = 0.036 compared with the HFHC diet). Introduction of the HFHC diet itself significantly decreased serum P-selectin (from 48.8 +/- 7.2 to 32.9 +/- 3.7 ng/dL, P = 0.02) and von Willebrand factor (from 187.0 +/- 10.1 to 161.9 +/- 9.0%, P = 0.02) concentrations. However, neither vitamin E alone nor vitamin E plus CoQ(10) significantly altered the serum concentrations of P-selectin or von Willebrand factor. 

    II)The effect of CoQ10 and vitamin E on serum total sialic acid, lipid-bound sialic acid, some trace elements and minerals in rats induced with doxorubicin:


    Source

    This study was designed to evaluate the effect of CoQ10 and vitamin E on serum total sialic acid (TSA), lipid bound sialic acid (LSA) and some elements in rat administered doxorubicin (DXR). Cu levels were increased in the group treated with DXR + vitamin E in comparison with DXR (p<0.05) and CoQ10 groups (p = 0.001). Furthermore, copper levels were increased in the group treated with DXR + CoQ10 in comparison with CoQ10 group (p < 0.05). Zn levels were decreased in the group treated with DXR + vitamin E in comparison with CoQ10 group (p < 0.05). Mg levels were decreased in subjects treated with DXR + vitamin E in comparison with the control group values (p < 0.05). Particularly, the observed increase in Cu levels in rats from DXR + vitamin E group might be due to the decrease of vitamin E. However, the oxidative damage could be as a result of DXR occurence and may be helpful to clinicians in chemotherapy using anthracycline. 

    III)Effects of lifestyle on plasma levels of the IGF system and the antioxidants coenzyme Q10 and vitamin E in Kenyan rural and urban populations. Kenyatta University, School of Applied Human Sciences, Department of Exercise Recreation and Sports Science, Nairobi, Kenya.


    OBJECTIVE: 

    Overnight fasting blood plasma insulin-like growth factor-I (IGF-I), insulin-like growth factor binding protein-1 (IGFBP-1), coenzyme Q10, (CoQ) vitamin E and plasma lipids were compared between a semi-nomadic Samburu population and relatively urbanized cohorts from Nairobi, Kenya. 

    RESEARCH DESIGN AND METHODS: 

    143 middle aged subjects without known diabetes were included. IGF-I and IGFBP-1 were analyzed by RIA, and CoQ and vitamin E by HPLC. Plasma lipid levels were analyzed by standard laboratory methods routinely used in the clinics. 

    RESULTS: 

    The age adjusted IGF-I serum levels were low in the Samburu male and female populations, ranging from 0 to -4 IGFSD-score (SDS), and a minor part of the investigated population reaching as low as -5 and -7 SDS. The Nairobi cohorts showed significantly higher values reaching from -2.5 to +1 SDS (P<0.0001). The nomadic Samburu population showed fasting IGFBP-1 values ranging from 30-100 μg/l, while that of the urbanized Nairobi cohorts was considerably lower (25-60 μg/l) (P<0.0001). CoQ concentrations of the Nairobi cohorts were 1.5-2.0 nmol/ml similar to the levels found in several European countries. The Samburu population on the other hand showed extremely high CoQ values ranging from 2 to 9 nmol/ml (P<0.0001). Vitamin E levels of the Nairobi group were low (5-20 nmol/ml), but the Samburu population had even lower levels ranging from 3 to 15 nmol/ml (P<0.0001). Plasma lipid levels such as cholesterol, triglycerides, LDL/HDL, ApoB/ApoA ratios as well as BMI and weight were significantly higher in the Nairobi population (P<0.0001). 

    CONCLUSION: 

    Low IGF-I and high IGFBP-1 levels of the Samburu cohorts indicate malnutrition. High lipid levels of the Nairobi cohorts indicate that these groups have several risk factors for cardiovascular diseases and diabetes type2. 

    IV) Supplementation with α-lipoic acid, CoQ10, and vitamin E augments running performance and mitochondrial function in female mice.


    Source

    Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada. 

    ABSTRACT

    Antioxidant supplements are widely consumed by the general public; however, their effects of on exercise performance are controversial. The aim of this study was to examine the effects of an antioxidant cocktail (α-lipoic acid, vitamin E and coenzyme Q10) on exercise performance, muscle function and training adaptations in mice. C57Bl/J6 mice were placed on antioxidant supplement or placebo-control diets (n?=?36/group) and divided into trained (8 wks treadmill running) (n?=?12/group) and untrained groups (n?=?24/group). Antioxidant supplementation had no effect on the running performance of trained mice nor did it affect training adaptations; however, untrained female mice that received antioxidants performed significantly better than placebo-control mice (p ≤ 0.05). Furthermore, antioxidant-supplemented females (untrained) showed elevated respiratory capacity in freshly excised muscle fibers (quadriceps femoris) (p ≤ 0.05), reduced oxidative damage to muscle proteins (p ≤ 0.05), and increased expression of mitochondrial proteins (p ≤ 0.05) compared to placebo-controls. These changes were attributed to increased expression of proliferator-activated receptor gamma coactivator 1α (PGC-1α) (p ≤ 0.05) via activation of AMP-activated protein kinase (AMPK) (p ≤ 0.05) by antioxidant supplementation. Overall, these results indicate that this antioxidant supplement exerts gender specific effects; augmenting performance and mitochondrial function in untrained females, but does not attenuate training adaptations. 

     







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