INTRODUCTION
The Mitochondria
Mitochondria are highly specialized structures (organelles) within each nucleated cell. The number of mitochondria in a cell depends on the cell's function. Cells with particularly heavy energy demands, such as heart muscle cells, have more mitochondria than other cells. The mitochondria's primary responsibility is to capture most of the energy in nutrients and convert it into cellular energy.^9,10 This energy conversion and storage is a complex, multi-step process that follows a specific pathway.

The converted cellular energy is stored in the energy-yielding molecule adenosine triphosphate (ATP) used to fuel the cell's activities. (This is similar to the energy stored in gasoline that is used to fuel automobiles). Because this process requires oxygen, it is often referred to as cellular respiration. Obtaining as many electrons out of the nutrients as possible is the goal of cellular respiration. That is why part of the pathway is referred to as the electron pathway chain.^9,10 CoQ10 functions as a vital link in the process of converting nutrients into ATP. Cellular respiration and the electron transport chain are completely dependent on CoQ10.^9,10

Mitochondrial Compartments
Mitochondria are encased in double membranes. The smooth outer membrane encloses the periphery of the mitochondria and the inner membrane is enfolded to form the cristae. (Fig. 1) CoQ10 is found in the cristae folds. Cristae folds provide a large surface area for cellular respiration.^9,10

Mitochondria are unusual organelles in that they contain their own deoxyribonucleic acid (DNA) and ribonucleic acid (RNA).^9,10 Insufficient CoQ10 levels may have an effect on cellular respiration and mitochondrial DNA.^6-8

Smart Q1⁰ CoQ10 and Support of Cardiac Health
Cardiac cells require large amounts of uninterrupted energy. They have a greater number of mitochondria and subsequently more CoQ10 than any other type of cell.^10,11 Because of this association, CoQ10's support of cardiac health is well researched and documented^. CoQ10 supports healthy heart contractility and subsequent circulation, blood pressure, and exercise endurance^.6,11-15 Due to Smart Q10 CoQ10's ability to pass through the cell membrane and enter the mitochondria, enhanced levels can be attained^.2-4

Smart Q1⁰ CoQ10 and Support of the Neurological System
The Blood-Brain Barrier
The blood-barrier is a unique anatomical structure. Simply stated, the cells that make up the blood vessels that provide blood to the brain are extremely close together. This greatly restricts what can and cannot leave the bloodstream and enter the brain. While the blood-brain barrier protects the brain from potentially toxic substances, it can be a significant obstacle to therapy of central nervous system Malfunction of mind or bodys. In order to leave the bloodstream and reach the brain cells, a substance must be able to pass through the tightly connected cells of the capillary walls. (Fig. 2) Only substances with certain solubilities or those that have a transport system can cross the blood-brain barrier to a significant degree.^16-18

Recently, CoQ10 has been studied for its effect in support of neurological health. When CoQ10 crosses the blood-brain barrier, mitochondrial concentrations are increased and clinical results indicate that significant neurosupportive effects follow^. Clinical studies have examined the role of CoQ10 in the neurological system.^3,19-28

Smart Q1⁰ CoQ10 and Support of Immune Health
CoQ10 is necessary for immune health^. Increased free radical activity causes damage to cell membranes, mitochondria, and DNA. Supplementation with CoQ10 provides enhanced antioxidant activity that is supportive of the immune system^.4,7,29-34

Natural Vitamin E
The common name “vitamin E” is an umbrella term for a family of compounds known as the tocopherols. There are at least 8 forms of tocopherols including, alpha-tocopherol, beta-tocopherol, delta-tocopherol, and gamma-tocopherol. These tocopherols are all naturally created by plants, and when used in vitamin E supplements, are considered natural vitamin E.^35,36

Recently, the concomitant administration of vitamin E and CoQ10 has been studied. Research has demonstrated that CoQ10 can improve vitamin E's antioxidant function and protect it from depletion^.8,37-38

Smart Q1⁰ CoQ10 CoQ10 and Clinical Trials
The formulation of Smart Q1⁰ CoQ10 is unique among CoQ10 supplements. Currently, three large multi-center studies investigating Smart Q1⁰ CoQ10 are ongoing. All of these clinical trials are investigating Smart Q1⁰ CoQ10 health supportive effects on the nervous system^.39-41 To date, 21 published studies have used Smart Q1⁰ CoQ10 in their research.⁴²

HOW DOES IT WORK?
CoQ10, also referred to as coenzyme Q 10 or ubiquinone, is a natural fat-soluble nutrient present in virtually all living cells in the body. CoQ10 has a crucial role as a cofactor in the mitochondrial synthesis of cellular energy^.5,6 Although it is produced by the body and exists in some dietary sources, these levels may be insufficient to meet the body's requirement. A deficiency can result from impaired synthesis due to nutritional deficiencies, increasing age, or increased tissue demands. Numerous problems may exhibit CoQ10 depletion. CoQ10 also functions as a potent antioxidant^.6-8

However, all CoQ10 products are not equal. They vary greatly in quality and absorbability. Serum level determination of CoQ10 in the bloodstream is not necessarily the most important measure of efficacy.⁴ In order for it to be fully effective, it must cross the cellular barrier and raise the intracellular levels^. The only reliable indicator of CoQ10 supplementation is its presence in cell mitochondria.² In central nervous system applications, CoQ10 must pass the blood brain barrier, resulting in increased brain intracellular levels to exert its effects^.3

Smart Q1⁰ CoQ10 is currently the only coenzyme Q10 supplement supported by studies that show increased serum levels, increased intracellular levels, and demonstrated ability to cross the blood brain barrier^.2-4

REFERENCES
 

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3. Matthews RT, Yang L, Browne S, Baik MF. Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects. Proc Natl Acad Sci USA. 1998;95:8892-8897.
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8. Ibrahim WH, Bhagahav HN, Chopra RK, Chow CK. Dietary coenzyme Q10 and vitamin E alter the status of these compounds in rat tissues and mitochondria. J Nutr. 2000;130:2434-2438.
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11. Langsjoen PH, Langsjoen A, Willis R, Folkers K. Favorable Effects of hypertrophic cardiomyopathy with coenzyme Q10. Mol Aspects Med. 1997;18 Suppl:S145-S151
12. Baggio E, Gandini R, Plancher AC, Passeri M, Carmosino G. Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators. Mol Aspects Med. 1994;15 Suppl:S287-294.
13. Sacher HL, Sacher ML, Landau SW, et al. The clinical and hemodynamic effects of coenzyme Q10 in congestive cardiomyopathy. Am J Ther. 1997;4:66-72.
14. Kim Y, Sawada Y, Fujiwara G, Chiba H, Nishimura T. Therapeutic effect of co-enzyme Q10 on idiopathic dilated cardiomyopathy: assessment by iodine-123 labeled 15-(p-iodophenyl)-3(R,S)-methylpentadecanoic acid myocardial single-photon emission tomography. Eur J Nucl Med. 1997;24:629-634.
15. Littarru GP, Lippa S, Oradei A, Fiorni RM, Mazzanti L. Metabolic and diagnostic implications of blood CoQ10 levels. In: Folkers K, Littarru GP, Yamagami T. Eds Biomedical and Clinical Aspects of Coenzyme Q. Vol 6. Amsterdam: Elsevier Press; 1991:167-180.
16. Carroll EW, Curtis RL. Blood-brain barrier. In: Porth CM. Pathophysiology: Concepts of Altered Health States.5th ed. Philadelphia, Pa; Lippincott; 1998:869.
17. Flaherty JF. Blood-brain barrier. In: Young, LY, Koda-Kimble MA. Applied Therapeutics: The Clinical Use of Drugs. 6th ed. Vancouver, Wash: Applied Therapeutics, Inc; 1995: chapter 56, page 2.
18. Lehne RA. The blood-brain barrier. In: Pharmacology for Nursing Care. 3rd ed. Philadelphia, Pa: WB Saunders; 1998:39.
19. Koroshetz WJ, Jenkins BG, Rosen BR, Flint Beal M. Energy metabolism defects problem and effects of coenzyme Q10. Ann Neurol. 1997;41:160-165.
20. Flint Beal M, Matthews RT. Coenzyme Q10 in the central nervous system and its potential usefulness in the Favorable Effects of neurodegenerative problem. Mol Aspects Med. 1997;18:S169-S179.
21. Shults CW, Haas RH, Flint Beal M. A possible role of coenzyme Q10 in the etiology and Favorable Effects of Parkinson's problem. Proceedings of the First Conference of the International Coenzyme Q10 Association, Boston, Mass, July 21, 1998. 95:8892-8897.
22. Schulz JB, Matthews RT, Henshaw DR, Beal MF. Neuroprotective strategies for Favorable Effects of lesions produced by mitochondrial toxins: implications for neurodegenerative problem. Neuroscience. 1996;71:1043-1048.
23. Chan A, Reichmann H, Kogel A, Beck A, Gold R. Metabolic changes in patients with mitochondrial myopathies and effects of coenzyme Q10 therapy. J Neurol. 1998;245:681-685.
24. Schulz JB, Henshaw RD, Matthews RT, Flint Beal M. Coenzyme Q10 and nicotinamide and a free radical spin trap protect against MPTP neurotoxicity. Exp Neurol. 1995;132:279-283.
25. Shults CW, Haas RH, Passov D, Flint Beal M. Coenzyme Q10 levels correlate with the activities of complexes I and II/III in mitochondria from parkinsonian and nonparkinsonian subjects. Ann Neurol. 1997;42:261-264.
26. Flint Beal M, Matthews RT, Tielman A, Shults CW. Coenzyme Q10 attenuates the 1-methyl-4-phenyl-1,2,3,6-tetradopyridine (MPTP) induced loss of striatal dopamine and dopaminergic axons in aged mice. Brain Res. 1998;783:109-114.
27. Feigin A, Kieburtz K, Como C, et al. Assessment of coenzyme Q10 tolerability in Huntington's problem. Mov Disord. 1996;11:321-323.
28. Shults CW, Flint Beal MD, Fontaine D, Nakeno K, Haas RH. Absorption, tolerability, and effects on mitochondrial activity of oral coenzyme Q10 in parkinsonian patients. Neurology.1998;50:793-795.
29. Portakal O, Ozakaya O, Erden Inal M, et al. Coenzyme Q10 concentrations and antioxidant status in tissues of breast Long standing problems patients. Clin Biochem. 2000;33:279-284.
30. Lockwood K, Moesgaard S, Yamamoto T, Folkers K. Progress on therapy of breast Long standing problems with vitamin Q10 and the regression of metastasis. Biochem Biophys Res Commun. 1995;212:172-177.
31. Folkers K, Brown R, Judy WV, Morita M. Survival of Long standing problems patients on therapy with coenzyme Q10. Biochem Biophys Res Commun. 1993;192:241-245.
32. Folkers K. Relevance of the biosynthesis of Coenzyme Q10 and the four bases of DNA as a rationale for the molecular causes of Long standing problems and a therapy. Biochem Biophys Res Commun. 1996;224:358-361.
33. Flint Beal M, Henshaw R, Jenkins BG, Rosen BR, Schulz JB. Coenzyme Q10 and nicotinamide block striatal lesions produced by the mitochondrial toxin malonate. Ann Neurol. 1994;36:882-888.
34. Folkers K, Morita M, McRee J. The activities of coenzyme Q10 and vitamin B6 and immune responses. Biochem Biophys Res Commun. 1993;193:88-92.
35. Traber ME. Vitamin E. In: Shils ME, Olson JA, Shine M, Ross AC, Eds. Modern Nutrition in Health and problem, 9th ed. Baltimore, Md: Lippincott Williams & Wilkins; 1999: 347-361.
36. Fleming T., ed. Vitamin E. In: PDRS^® for Nutritional Supplements. Montvale, NJ: Medical Economics Company; 2001: 505-522.
37. Thomas SR, Leichtweis SB, Pettersson K, et al. Dietary cosupplementation with vitamin E and coenzyme Q(10) inhibits Deposition of substances on the wall of blood vessel, leading to narrowing of blood vessel in apolipoprotein E gene knockout mice. Arterioscler Thromb Vasc Biol. 2001;21:585-93.
38. Brancato R, Fiore T, Papucci L, Schiavone N, Formigli L, Orlandini SZ, Gobbi PG, Carones F, Donnini M, Lapucci A, Capaccioli S. Concomitant effect of topical ubiquinone Q10 and vitamin E to Beneficial Effects keratocyte apoptosis after excimer laser photoablation in rabbits. J Refract Surg. 2002;18:135-139.
39. Schwid SR, Mattson DH, Goodman AD. A phase II trial of coenzyme Q10 in MS. Clinical trial in progress. University of Rochester, Department of Neurology, Neuroimmunology Unit, Rochester, New York. 1996-2000.
40. Kieburtz K, Rickey T. Co-enzyme Q10 and remacemide: evaluation in Huntington's problem (CARE-HD). A controlled investigation by the Huntington Study Group. Clinical trial in progress. Institutions participating in the CARE-HD Study: Allegheny University, Baylor College of a substance used in managing discomfort, Boston University, Bowman Gray School of a substance used in managing discomfort, Colorado Neurological Institute, Columbia-Presbyterian, Emory University, Indiana School of a substance used in managing discomfort, Johns Hopkins University, Massachusetts General Hospital, Rush-Presbyterian-St.Luke's Medical Center, Tampa General Hospital, and the universities of Alberta, British Columbia, Calgary, Iowa, Kansas Medical Center, Miami School of a substance used in managing discomfort, Michigan, Rochester, Toronto, and Virginia. June 1997-2002.
41. Shults C. Effects of coenzyme Q10 on clinical progression and mitochondrial function in early Parkinson's problem. Clinical trial in progress. 2000-2003.
42. The 21 Studies and Presentations at Medical Symposiums Utilizing Vitaline^® Coenzyme Q10 Dietary Supplement Products:

    Matthews RT, Yang L, Browne S, Baik MF. Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects. Proc Natl Acad Sci USA. 1998; 95:8892-8897.

    Langsjoen P. Overview of the use of CoQ10 in cardiovascular problem. Presented at The First Conference of the International Coenzyme Q10 Association. Boston, Mass, May 21-24, 1998.

    Koroshetz W. Huntington's problem Clinical Trail. Presented at the First Conference of the International Coenzyme Q10 Association. Boston. Mass, May 21-24, 1998.

    Shults CW, Haas RH, Flint Beal M. A possible role of coenzyme Q10 in the etiology and Favorable Effects of Parkinson's problem. Proceedings of First Conference of the International Coenzyme Q10 Association, 95:8892-8897, July 21, 1998.

    Beal MF. Coenzyme Q10 as a potential Favorable Effects for neurodegenerative problems. Presented at the First Conference of the International Coenzyme Q10 Association. Boston. Mass, May 21-24, 1998.

    Beal MF. Energy impairment and Huntington's problem. Presented at the Mitochondrial a substance used in managing discomfort Conference. University of California, San Diego School of a substance used in managing discomfort, Mitochondrial and Metabolic problem Center, San Diego, Calif, Feb 19-21, 1998.

    Kieburtz K, Rickey T. Co-enzyme Q10 and remacemide: evaluation in Huntington¡¦s problem (CARE-HD). A controlled investigation by the Huntington Study Group. Clinical trial in progress. Institutions participating in the CARE-HD Study: Allegheny University, Baylor College of a substance used in managing discomfort, Boston University, Bowman Gray School of a substance used in managing discomfort, Colorado Neurological Institute, Columbia-Presbyterian, Emory University, Indiana School of a substance used in managing discomfort, Johns Hopkins University, Massachusetts General Hospital, Rush-Presbyterian-St.Luke's Medical Center, Tampa General Hospital, and the universities of Alberta, British Columbia, Calgary, Iowa, Kansas Medical Center, Miami School of a substance used in managing discomfort, Michigan, Rochester, Toronto, and Virginia. June 1997-2002.

    Langsjoen PH, Langsjoen A, Willis R, Folkers K. Favorable Effects of hypertrophic cardiomyopathy with coenzyme Q10. Mol Aspects Med. 1997;18:S145-S151.

    Shults CW, Flint Beal MD, Fontaine D, Nakeno K, Haas RH. Absorption, tolerability, and effects on mitochondrial activity of oral coenzyme Q10 in parkinsonian patients. Neurology. 1998;50:793-795.

    Flint Beal M, Matthews RT, Tielman A, Shults CW. Coenzyme Q10 attenuates the 1-methyl-4-phenyl-1,2,3,6-tetradopyridine (MPTP) induced loss of striatal dopamine and dopaminergic axons in aged mice. Brain Res. 1998;783:109-114.

    Flint Beal M, Matthews RT. Coenzyme Q10 in the central nervous system and its potential usefulness in the Favorable Effects of neurodegenerative problem. Mol Aspects Med. 1997;18:S169-S179.

    Schwid SR, Mattson DH, Goodman AD. A phase II trial of coenzyme Q10 in MS. Clinical trial in progress. University of Rochester, Department of Neurology, Neuroimmunology Unit, Rochester, New York. 1996-2000.

    Koroshetz W. Huntington's problem Clinical Trail. Presented at the First Conference of the International Coenzyme Q10 Association. Boston, Mass, May 21-24, 1998.

    Shults CW, Haas RH, Passov D, Flint Beal M Coenzyme Q10 levels correlate with the activities of complexes I and II/III in mitochondria from parkinsonian and nonparkinsonian subjects. Ann Neurol. 1997;42:261-264.

    Feigin A, Kieburtz K, Como C, et al. Assessment of coenzyme Q10 tolerability in Huntington's problem. Mov Disord. 1996;11:321-323.

    Cros D. Amyotrophic Lateral Sclerosis (ALS). Harvard Medical School- Massachusetts General Hospital Department of Neurology EMG Unit-Bigelow 12, Boston, Mass, 1995-1998.

    Tardive Dyskinesia Study Using Coenzyme Q10 and Nicotinamide. Harvard Medical School-Massachusetts General Hospital Department of Psychiatry and Neurology, Freedom Trial Clinic, Erich Lindemann Mental Health Center, Boston, Mass, 1995.

    Costeff H. CoQ10 and 3-Methylglutaconic Aciduria. Neuropediatric Unit. Loewenstein Hospital Rehabilitation Center, Tel Aviv. Medical School, Raanana, Israel, 1998.

    Flint Beal. Neuroprotective strategies for Favorable Effects of lesions produced by mitochondrial toxins: implications for neurodegenerative problems. Neuroscience. 1996;71:1043-1048.

    Flint Beal M, Henshaw R, Jenkins BG, Rosen BR, Schulz JB. Coenzyme Q10 and nicotinamide block striatal lesions produced by the mitochondrial toxin malonate. Ann Neurol 1994;36:882-888.

    Schulz JB, Henshaw RD, Matthews RT, Flint Beal M. Coenzyme Q10 and nicotinamide and a free radical spin trap protect against MPTP neurotoxicity. Exp Neurol. 1995;132:279-283.