Technical Data
Description
Vitaline® Chewable CoQ10 wafers contain coenzyme Q10 emulsified in vitamin E and mixed tocopherols and is formulated with Micosolle®, a proprietary excipient.
1 Clinical studies have demonstrated that this process enhances the absorption of CoQ10.
2-4
Two different methods can be used for the production of coenzyme Q10. One method is natural and the other is synthetic. The natural process utilizes living organisms and is referred to as a “biological fermentation/extraction process.” Coenzyme Q10 can also be synthesized by a chemical process, which produces a similar, but distinctly different product that contains chemical compounds not found in the natural form. Vitaline® Chewable CoQ10 contains the natural form of coenzyme Q10.1
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
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. 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
Vitaline® Chewable 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 Vitaline® CoQ10's ability to pass through the cell membrane and enter the mitochondria, enhanced levels can be attained.†2-4
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 disorders. 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. 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
Vitaline® Chewable 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
Vitaline® Chewable CoQ10's Ability to Enter Mitochondria and Cross the Blood-Brain Barrier†
CoQ10 is a large, fat-soluble molecule. When CoQ10 is manufactured with Micosolle®, it allows the molecule to change shape and become more flexible. The CoQ10 can then enter the cellular mitochondria and cross the blood-brain barrier.†1
Through special processing techniques, Vitaline® CoQ10 may be absorbed by the lymphatic system. This allows the CoQ10 to initially bypass the liver, resulting in increased absorption potential.1 Vitaline® CoQ10is the only form of CoQ10 with published studies demonstrating that it can cross the blood brain barrier.†2-4
Vitaline® Chewable CoQ10 and Clinical Trials
The formulation of Vitaline® Chewable CoQ10 is unique among CoQ10 supplements. Currently, three large multi-center studies investigating Vitaline® CoQ10 are ongoing. All of these clinical trials are investigating Vitaline® CoQ10 health supportive effects on the nervous system.†35-37 To date, 21 published studies have used Vitaline® CoQ10 in their research.38
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 diseases 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
Vitaline® Chewable 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
Recommendations
As a dietary supplement, take 1-2 chewable wafers daily or as directed by a physician or health care professional. Refer to label for complete instructions
Precautions
The safety of CoQ10 has been evaluated. Dosages in studies have ranged from 100 mg every day to 1200 mg per day. To date, no toxicities have been reported. Occasional gastric upset may occur.
12,13 Taking
Vitaline® Chewable CoQ10 wafers with meals usually alleviates this rare upset.
1How Is It Supplied?
Vitaline® Chewable CoQ10 wafers 60 mg
(16006,16056) 60 wafers in a bottle.
Vitaline® Chewable CoQ10 wafers 100 mg
(16103, 16133) 30 wafers in a bottle.
Vitaline® Chewable CoQ10 wafers 200 mg
(16153, 16173) 30 wafers in a bottle.
Storage Recommendations
Store at controlled room temperature, 59° to 86°F (15° to 30°C).
References
1. Meese J. President. Vitaline Corporation. Personal communication (verbal). October 20, 2000.
2. Nakmura T, Sanma M, Himeno M, Kato K. Transfer of exogenous coenzyme Q10 to the inner membrane of heart mitochondria in rats. In: Folkers K, Yamamura Y, eds. Biomedical and Clinical Aspects of Coenzyme Q. Vol 6. Amsterdam: Elsevier Press; 1980;3-14.
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.
4. Joliet P, Simon N, Barre J, et al. Plasma coenzyme Q 10 concentrations in breast cancer: prognosis and therapeutic consequences. Int J Clin Pharmacol Ther. 1998;36:506-509.
5. Mitchell P. The vital protonmotive of coenzyme Q. In: Folkers K, Littarru GP, Yamagami T. Eds. Biochemical and Clinical Aspects of Coenzyme Q. Vol 6. Amsterdam: Elsevier Press; 1991:3-10.
6. Sinatra ST, DeMarco J. Free radicals, oxidative stress, oxidized low density lipoprotein (LDL) and the heart: antioxidants and other strategies to limit cardiovascular damage. Conn Med. 1995;59:579-588.
7. Ravaglia G, Forti P, Maioli F, et al. Effect of micronutrients on natural killer cell immune function in healthy free-living subjects aged >/=90y. Am J Clin Nutr. 2000:71:590-598.
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.
9. Porth CM, Carroll EW. Mitochondria. In: Porth CM. Pathophysiology: Concepts of Altered Health States. 5th ed. Philadelphia, Pa; Lippincott; 1998:8-9.
10. Guyton AC, Hall JE. Mitochondria. In: Textbook of Medical Physiology. 9th ed. Philadelphia, Pa: WB Saunders; 1996:16-17.
11. Langsjoen PH, Langsjoen A, Willis R, Folkers K. Treatment 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 disease 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 treatment of neurodegenerative disease. 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 treatment of Parkinson's disease. 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 treatment of lesions produced by mitochondrial toxins: implications for neurodegenerative disease. 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 disease. 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 cancer patients. Clin Biochem. 2000;33:279-284.
30. Lockwood K, Moesgaard S, Yamamoto T, Folkers K. Progress on therapy of breast cancer 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 cancer 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 cancer 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. 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.
36. Kieburtz K, Rickey T. Co-enzyme Q10 and remacemide: evaluation in Huntington's disease (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 Medicine, Boston University, Bowman Gray School of Medicine, Colorado Neurological Institute, Columbia-Presbyterian, Emory University, Indiana School of Medicine, 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 Medicine, Michigan, Rochester, Toronto, and Virginia. June 1997-2002.
37. Shults C. Effects of coenzyme Q10 on clinical progression and mitochondrial function in early Parkinson's disease. Clinical trial in progress. 2000-2003.
38. The 21 Studies and Presentations at Medical Symposiums Utilizing Vitaline® Coenzyme Q10 Dietary Supplement Products:
39. 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.
40. Langsjoen P. Overview of the use of CoQ10 in cardiovascular disease. Presented at The First Conference of the International Coenzyme Q10 Association. Boston, Mass, May 21-24, 1998.
41. Koroshetz W. Huntington's Disease Clinical Trail. Presented at the First Conference of the International Coenzyme Q10 Association. Boston. Mass, May 21-24, 1998.
42. Shults CW, Haas RH, Flint Beal M. A possible role of coenzyme Q10 in the etiology and treatment of Parkinson's disease. Proceedings of First Conference of the International Coenzyme Q10 Association, 95:8892-8897, July 21, 1998.
43. Beal MF. Coenzyme Q10 as a potential treatment for neurodegenerative diseases. Presented at the First Conference of the International Coenzyme Q10 Association. Boston. Mass, May 21-24, 1998.
44. Beal MF. Energy impairment and Huntington's disease. Presented at the Mitochondrial Medicine Conference. University of California, San Diego School of Medicine, Mitochondrial and Metabolic Disease Center, San Diego, Calif, Feb 19-21, 1998.
45. Kieburtz K, Rickey T. Co-enzyme Q10 and remacemide: evaluation in Huntington's disease (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 Medicine, Boston University, Bowman Gray School of Medicine, Colorado Neurological Institute, Columbia-Presbyterian, Emory University, Indiana School of Medicine, 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 Medicine, Michigan, Rochester, Toronto, and Virginia. June 1997-2002.
46. Langsjoen PH, Langsjoen A, Willis R, Folkers K. Treatment of hypertrophic cardiomyopathy with coenzyme Q10. Mol Aspects Med. 1997;18:S145-S151.
47. 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.
48. 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.
49. Flint Beal M, Matthews RT. Coenzyme Q10 in the central nervous system and its potential usefulness in the treatment of neurodegenerative disease. Mol Aspects Med. 1997;18:S169-S179.
50. 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.
51. Koroshetz W. Huntington's Disease Clinical Trail. Presented at the First Conference of the International Coenzyme Q10 Association. Boston, Mass, May 21-24, 1998.
52. 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.
53. Feigin A, Kieburtz K, Como C, et al. Assessment of coenzyme Q10 tolerability in Huntington's disease. Mov Disord. 1996;11:321-323.
54. Cros D. Amyotrophic Lateral Sclerosis (ALS). Harvard Medical School- Massachusetts General Hospital Department of Neurology EMG Unit-Bigelow 12, Boston, Mass, 1995-1998.
55. 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.
56. Costeff H. CoQ10 and 3-Methylglutaconic Aciduria. Neuropediatric Unit. Loewenstein Hospital Rehabilitation Center, Tel Aviv. Medical School, Raanana, Israel, 1998.
57. Flint Beal. Neuroprotective strategies for treatment of lesions produced by mitochondrial toxins: implications for neurodegenerative diseases. Neuroscience. 1996;71:1043-1048.
58. 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.
59. 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.