There are several CoQ review posts, 2007, 2008 and 2011. The earlier post addresses coumadin interference concerns as stated by the CoQ research experts. Many of the significant and relevant details one needs to know about Coenzyme Q 10 are found there along with extensive research references...some of which follow.
At the lower doses, CoQ is not found to interfere with coumadin.
In cases of cardiomyopathy and heart failure, using high-dose CoQ has been found to be lifesaving.
Jackie
Coenzyme Q10 - Review of Relevant Details -
[
www.afibbers.org]
[
www.afibbers.org] -2008
CoQ10 - The Spark of Life
[
www.afibbers.org] - 2011
These reference links are included in this last report
REFERENCES
(1) Oxidative Stress – Cellular Damage Affects Everyone
[
www.afibbers.org]
(2) Statin-Induced Cardiomyopathy –
Peter H. Langsjoen, M.D., F.A.C.C. (Physician, Biochemist and Researcher.)
[
www.spacedoc.net]
(3) My Statin Story – Duane Graveline, M.D.
[
www.spacedoc.net]
(4) Observational Report: The Strategy – Metabolic Cardiology
[
www.afibbers.org]
(5) The Sinatra Solution: Metabolic Cardiology
Integrative Cardiologists Stephen T. Sinatra MD, FACC, CNS, CBT and James C. Roberts MD, FACC
(21) CoQ10 2005 teleconference with Dr. Judy and Designs for Health
Relevant notes: [
www.afibbers.org]
[
www.afibbers.org] update
(22) Energy and Defense
Littarru, G. P. Energy and Defense
1995 © C.E.S.I. Printed in Italy
pp 74 Reference study
Kalen, A Age related changes in the lipid composition of rat and human tissue. Lipids 24: 579- 584, 1989
Linnane, AW, Mitochondrial DNA mutations and the aging process: bioenergy and pharmacological intervention. Mutation Research 275 195-208, 1992
(6) Nano-particle Coenzyme Q10
[
www.ncbi.nlm.nih.gov]
[
www.ncbi.nlm.nih.gov]
[
www.lifeextensionvitamins.com]
Tischon Bio-Solve Q-gel patented reduced particle size
[
www.thefreelibrary.com]
(7) Supplemental ubiquinol in patients with advanced congestive heart failure.
Langsjoen PH, Langsjoen AM.
East Texas Medical Center and Trinity Mother Francis Hospital, TX, Biofactors. 2008;32(1-4):119-28.
Abstract
Patients with CHF, NYHA class IV, often fail to achieve adequate plasma CoQ10 levels on supplemental ubiquinone at dosages up to 900 mg/day. These patients often have plasma total CoQ10 levels of less than 2.5 microg/ml and have limited clinical improvement. It is postulated that the intestinal edema in these critically ill patients may impair CoQ10 absorption. We identified seven patients with advanced CHF (mean EF 22%) with sub-therapeutic plasma CoQ10 levels with mean level of 1.6 microg/ml on an average dose of 450 mg of ubiquinone daily (150-600 mg/day). All seven of these patients were changed to an average of 580 mg/day of ubiquinol (450-900 mg/day) with follow-up plasma CoQ10 levels, clinical status, and EF measurements by echocardiography. Mean plasma CoQ10 levels increased from 1.6 microg/ml (0.9-2.0 microg/ml) up to 6.5 microg/ml (2.6-9.3 microg/ml). Mean EF improved from 22% (10-35%) up to 39% (10-60%) and clinical improvement has been remarkable with NYHA class improving from a mean of IV to a mean of II (I to III). Ubiquinol has dramatically improved absorption in patients with severe heart failure and the improvement in plasma CoQ10 levels is correlated with both clinical improvement
[
www.ncbi.nlm.nih.gov]
(8) The effect of HMG-CoA reductase inhibitors on coenzyme Q10: possible biochemical/clinical implications.
Hargreaves IP, Duncan AJ, Heales SJ, Land JM.
Drug Saf. 2005;28(8):659-76 PMID: 16048353
UBIQUINOL STUDY REFERENCES
Bioenergetic and antioxidant properties of coenzyme Q10: recent developments.
Littarru GP, Tiano L.
Mol Biotechnol. 2007 Sep;37(1):31-7. Review.
PMID:17914161
Overview of the use of CoQ10 in cardiovascular disease.
Langsjoen PH, Langsjoen AM.
Biofactors. 1999;9(2-4):273-84. Review.
PMID:10416041
Reduced coenzyme Q10 supplementation decelerates senescence in SAMP1 mice.
Yan J, Fujii K, Yao J, Kishida H, Hosoe K, Sawashita J, Takeda T, Mori M, Higuchi K.
Exp Gerontol. 2006 Feb;41(2):130-40. Epub 2006 Jan 4.
PMID:16387461
Study on safety and bioavailability of ubiquinol (Kaneka QH) after single and 4-week multiple oral administration to healthy volunteers.
Hosoe K, Kitano M, Kishida H, Kubo H, Fujii K, Kitahara M.
Regul Toxicol Pharmacol. 2007 Feb;47(1):19-28. Epub 2006 Aug 21.
PMID:16919858[
COENZYME Q10 REFERENCES – for continued research
Biochemical functions of coenzyme Q10. Crane FL. J Am Coll Nutr. 2001 Dec;20(6):591-8.
Ubiquinol-10 is an effective lipid-soluble antioxidant at physiological concentrations. Frei B, Kim MC, Ames BN. Proc Natl Acad Sci U S A. 1990 Jun;87(12):4879-83.
Ubiquinol: an endogenous antioxidant in aerobic organisms. Ernster L, Forsmark-Andrée P. Clin Investig. 1993;71(8 Suppl)
60-5.
The antioxidant role of coenzyme Q. Bentinger M, Brismar K, Dallner G. Mitochondrion. 2007 Jun;7 Suppl
41-50. Epub 2007 Mar 16.
Ubiquinol-10 protects human low density lipoprotein more efficiently against lipid peroxidation than does alpha-tocopherol. Stocker R, Bowry VW, Frei B. Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1646-50.
The emerging role of coenzyme Q-10 in aging, neurodegeneration, cardiovascular disease, cancer and diabetes mellitus. Dhanasekaran M, Ren J. Curr Neurovasc Res. 2005 Dec;2(5):447-59.
Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation. Mohr D, Bowry VW, Stocker R. Biochim Biophys Acta. 1992 Jun 26;1126(3):247-54.
Plasma coenzyme Q10 response to oral ingestion of coenzyme Q10 formulations. Bhagavan HN, Chopra RK. Mitochondrion. 2007 Jun;7 Suppl
78-88.
Age-related changes in the lipid compositions of rat and human tissues. Kalén A, Appelkvist EL, Dallner G. Lipids. 1989 Jul;24(7):579-84.
Coenzyme Q10 in the human retina. Qu J, Kaufman Y, Washington I. Invest Ophthalmol Vis Sci. 2009 Apr;50(4):1814-8.
Coenzyme Q in cardiovascular disease. Singh RB, Niaz MA, Rastogi V, Rastogi SS. J Assoc Physicians India. 1998 Mar;46(3):299-306.
Perspectives on therapy of cardiovascular diseases with coenzyme Q10 (ubiquinone). Mortensen SA. Clin Investig. 1993;71(8 Suppl)
116-23.
Effects of coenzyme Q10 administration on pulmonary function and exercise performance in patients with chronic lung diseases. Fujimoto S, Kurihara N, Hirata K, Takeda T. Clin Investig. 1993;71(8 Suppl)
162-6.
A possible role of coenzyme Q10 in the etiology and treatment of Parkinson's disease. Shults CW, Haas RH, Beal MF. Biofactors. 1999;9(2-4):267-72.
Low plasma coenzyme Q10 levels as an independent prognostic factor for melanoma progression. Rusciani L, Proietti I, Rusciani A, Paradisi A, Sbordoni G, Alfano C, Panunzi S, De Gaetano A, Lippa S. J Am Acad Dermatol. 2006 Feb;54(2):234-41.
Study of CoQ10-enzymes in gingiva from patients with periodontal disease and evidence for a deficiency of coenzyme Q10. Nakamura R, Littarru GP, Folkers K, Wilkinson EG. Proc Natl Acad Sci U S A. 1974 Apr;71(4):1456-60.
Decreased levels of coenzyme Q(10) in patients with bronchial asthma. Gazdík F, Gvozdjáková A, Nádvorníková R, Repická L, Jahnová E, Kucharská J, Piják MR, Gazdíková K. Allergy. 2002 Sep;57(9):811-4.
Does coenzyme Q10 play a role in opposing oxidative stress in patients with age-related macular degeneration? Blasi MA, Bovina C, Carella G, Genova ML, Jansen AM, Lenaz G, Brancato R. Ophthalmologica. 2001 Jan-Feb;215(1):51-4.
Serum coenzyme Q10 levels in thyroid disorders. Ogura F, Morii H, Ohno M, Ueno T, Kitabatake S, Hamada N, Ito K. Horm Metab Res. 1980 Oct;12(10):537-40.
Biochemical deficiencies of coenzyme Q10 in HIV-infection and exploratory treatment. Folkers K, Langsjoen P, Nara Y, Muratsu K, Komorowski J, Richardson PC, Smith TH. Biochem Biophys Res Commun. 1988 Jun 16;153(2):888-96.
Human CoQ10 deficiencies. Quinzii CM, López LC, Naini A, DiMauro S, Hirano M. Biofactors. 2008;32(1-4):113-8.
Plasma ubiquinol-10 as a marker for disease: is the assay worthwhile? Kontush A, Schippling S, Spranger T, Beisiegel U. Biofactors. 1999;9(2-4):225-9.
Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study. Ghirlanda G, Oradei A, Manto A, Lippa S, Uccioli L, Caputo S, Greco AV, Littarru GP. J Clin Pharmacol. 1993 Mar;33(3):226-9.
Coenzyme Q10 and cardiovascular disease: a review. Sarter B. J Cardiovasc Nurs. 2002 Jul;16(4):9-20.
Relative bioavailability comparison of different coenzyme Q10 formulations with a novel delivery system. Liu ZX, Artmann C. Altern Ther Health Med. 2009 Mar-Apr;15(2):42-6.
Other suggested reading
[
www.kanekaqh.com]
www.coenzymeQ10.org
[
www.ncbi.nlm.nih.gov]
Sinatra, Passwater interview CoQ10, PLC
[
www.drpasswater.com]
[
www.drpasswater.com]
Collection of CoQ related articles thanks to Justine: [
www.coq10.co.nz]
CoQ10 is needed for basic cell functions in energy production.
CoQ10’s primary function is to shuttle electrons through the electron transport chain (ETC) in the mitochondrial inner membrane. This pathway is also referred to as the oxidative phosphorylation part of the central energy pathway. The electrons are received directly from succinate, or indirectly from several other substrates such as pyruvate, acyl-CoA, and alpha-ketoglutarate in the form of NADH. CoQ10 moves from one electron carrier complex to the next, ultimately delivering electrons, one at a time, in a never-ending cycle of oxidation and reduction (Figure 6).
While the electrons are delivered one at a time, they leave in pairs to form ATP and H20. If CoQ10 availability is not adequate the electrons will not be able to travel in pairs and single electrons will take another, less desirable, pathway that can lead to the generation of superoxide radicals. Optimal functioning of this pathway is critical for the fundamental energy generation that powers all cell functions. CoQ10 is also an antioxidant. Therapeutic approaches targeting mitochondrial disfunction and oxidative damage using CoQ10 hold great promise.19
[
www.metametrix.com]
Reports of interest - indicating statin therapy interferes with Coenzyme Q10 production and protection
CoQ10 Depletion.
The Achilles Heel of the Statin Crusade.
A Review of Published Animal and Human Trials
[
www.thincs.org]
(2003 presentation @ Weston Price Foundation)
Peter H. Langsjoen, M.D., F.A.C.C., Cardiovascular Diseases.
Research in Biomedical Aspects of Coenzyme Q10.
Doctors Dr., Tyler, Texas 75701,USA.
The depletion of the essential nutrient coenzyme Q10 (CoQ10) by the increasingly popular cholesterol lowering drugs, HMG-CoA reductase inhibitors (statins) has grown from a level of concern to one of alarm. With ever higher statin potencies and dosages, and with a steadily shrinking target LDL cholesterol, the prevalence and severity of CoQ10 deficiency is increasing noticeably to the physicians in the trenches of front line patient care. An estimated 36 million Americans are now candidates for statin drug therapy.
CoQ10 serves as the coenzyme for mitochondrial enzyme complexes I, II and III and is essential for mitochondrial ATP production. CoQ10 is also a clinically relevant fat-soluble antioxidant and is the only fat soluble antioxidant that is known to be synthesized de novo. It is found normally in the diet, predominantly in organ meats and is biosynthesized in all cells with peak capabilities in late teens and early twenties with a gradual age-related decline in blood and tissue CoQ10 levels after the age of 30 years.
Statin-induced CoQ10 depletion has been documented in 15 animal studies in six different animal species and has been shown to correlate with decreased ATP production, increased ischemia reperfusion injury, skeletal muscle injury and increased mortality.
There are 15 published trials on statin-induced CoQ10 depletion in humans. Of these 15 trials, nine were controlled trials, eight of which documented significant CoQ10 depletion. Statin-induced CoQ10 depletion has been shown to be associated with a fall in left ventricular function, an elevation of lactate to pyruvate ratio and an enhancement of LDL cholesterol oxidation. The current data on diastolic dysfunction further confirms the clinical importance of this drug-nutrient interaction.
Statin-induced CoQ10 depletion is well documented in animal and human studies with detrimental cardiac consequences in both animal models and human trials. Furthermore, this drug-induced nutrient deficiency is dose-related and more notable in settings of pre-existing CoQ10 deficiency such as in the elderly and in heart failure. Finally, statin-induced CoQ10 deficiency is completely preventable with supplemental CoQ10 with no adverse impact on the cholesterol lowering or anti-inflammatory properties of the statin drugs.
We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear. As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide-spread deficiency of a nutrient critically important for normal heart function.
Statins and Increased Coronary Artery Calcification
One study found an increase in progression of coronary artery calcification (CAC) to be significantly greater in patients receiving statins who had an MI compared with event-free subjects despite similar LDL control. Continued expansion of CAC may indicate failure of some patients to benefit from statin therapy and an increased risk of having cardiovascular events.(1)
[
www.ncbi.nlm.nih.gov]
Exercise failed to slow atherosclerosis progression in males taking statins
June 2004 [
www.theheart.org]
Statins not good for the elderly
The elderly are particularly vulnerable to the detrimental side effects of statins especially cognitive decline and muscle weakness (Golomb)
[
www.cmellc.com]
© 2005 Geriatric Times. All rights reserved.
Statin Adverse Effects: Implications for the Elderly
by Beatrice A. Golomb, M.D., Ph.D.
Russian Roulette
How do you know? Russian Roulette? A 39-year old woman died from a single dose of Crestor. Talk about winning the lottery in reverse! How do you know that if you take a statin, it might not happen to you? The odds are very low that you wouldn’t be affected…? But there is that nagging question…Are you a gambler?
[
www.cbsnews.com]
[
www.medicationsense.com]
[
www.newmediaexplorer.org] (Doug’s story - Life After Lipitor)
Once Upon a Time in the US Patent Office
…..the large pharmaceutical company Merck, applied for two patents… that included Coenzyme Q10 as a foil to the counteract the effects of myopathy associated with statins or HMG-CoA reductase Inhibitors.
This was 1989 and 1990.
You can read the full contents of these patents for yourself on the official United States Patent and Trademark Office web site (www.uspto.gov/). It is interesting to note that both of these patents were issued over twelve years ago (May and June of 1990) but that no use of the patented process of combining Coenzyme Q10 with HMG-COA Reductase Inhibitors (Statins) has yet been made or publicized.
The Patent numbers you will want to look up are: Patent Number: 4,933,165 Patent Number: 4,929,437
"What is claimed is:
1. A pharmaceutical composition comprising a pharmaceutical carrier and an effective antihypercholesterolemic amount of an HMG-CoA reductase inhibitor and an amount of Coenzyme Q.sub.10 effective to counteract HMG-CoA reductase inhibitor-associated skeletal muscle myopathy.
2. A composition of claim 1 in which the HMG-CoA reductase inhibitor is selected from: lovastatin, simvastatin, pravastatin and sodium-3,5-dihydroxy-7-[3-(4-fluorophenyl)-1-(methylethyl)-1H-Indole-2yl]- hept-6-enoate.
[
www.freepatentsonline.com]
[
www.freepatentsonline.com]
Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction.
Silver MA, Langsjoen PH, Szabo S, Patil H, Zelinger A.
Am J Cardiol. 2004 Nov 15;94(10):1306-10.
Statin therapy worsened diastolic parameters in most patients; coenzyme Q(10) supplementation in patients with worsening diastolic function with statin therapy improved parameters of diastolic function
Reduction of serum ubiquinol-10 and ubiquinone-10 levels by atorvastatin in hypercholesterolemic patients
Mabuchi H, Higashikata T, Kawashiri M, Katsuda S, Mizuno M, Nohara A, Inazu A, Koizumi J, Kobayashi J.
J Atheroscler Thromb. 2005;12(2):111-9.
All patients showed definite reductions of serum ubiquinol-10 and ubiquinone-10 levels, and mean levels of serum ubiquinol-10 and ubiquinone-10 levels decreased significantly from 0.81 +/- 0.21 to 0.46 +/- 0.10 microg/ml (p < 0.0001), and from 0.10 +/- 0.06 to 0.06 +/- 0.02 microg/ml (p = 0.0008), respectively.
Dose-related decrease of serum coenzyme Q10 during treatment with HMG-CoA reductase inhibitors
Mol Aspects Med. 1997;18 Suppl
137-44 Mortensen SA, Leth A
Although HMG-CoA reductase inhibitors are safe and effective within a limited time horizon, continued vigilance of a possible adverse consequence from coenzyme Q10 lowering seems important during long-term therapy.
The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications.
Langsjoen PH, Langsjoen AM.
East Texas Medical Center and Trinity Mother Francis Health System, Tyler, TX 75701
Biofactors 2003;18(14):101-11
The depletion of the essential nutrient CoQ10 by the increasingly popular cholesterol lowering drugs, HMG CoA reductase inhibitors (statins), has grown from a level of concern to one of alarm. With ever higher statin potencies and dosages, and with a steadily shrinking target LDL cholesterol, the prevalence and severity of CoQ10 deficiency is increasing noticeably.
An estimated 36 million Americans are now candidates for statin drug therapy. Statin-induced CoQ10 depletion is well documented in animal and human studies with detrimental cardiac consequences in both animal models and human trials.
This drug-induced nutrient deficiency is dose related and more notable in settings of pre-existing CoQ10 deficiency such as in the elderly and in heart failure. Statin-induced CoQ10 deficiency is completely preventable with supplemental CoQ10 with no adverse impact on the cholesterol lowering or anti-inflammatory properties of the statin drugs.
We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear.
As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide-spread deficiency of a nutrient critically important for normal heart function.
PMID: 14695925