Coenzyme Q10 - The Spark of Life

As an anti-oxidant to quench free radicals, CoQ10 is the number one favorite choice. Not only does the body produce it, but supplementing with it offers many protective and restorative benefits.

Co Q10 has 90 atoms of hydrogen per molecule to donate, compared for example, to another popular antioxidant ECGC which only has 12 atoms to donate. This doesn’t mean using other antioxidants isn’t useful or appropriate. It just means that we need to consider CoQ10 as the leader. Especially, since Coenzyme Q10 is so critical for cellular energy production…and once again, especially important for afibbers.

Why don’t we see more emphasis on Coenzyme Q10?
In the book, Energy and Defense, written 16 years ago by recognized world authority on Coenzyme Q10, Gian Palo Littarru, PhD, observes in his concluding statements:

…” There is an undeniable gap these days in the transfer of new knowledge on the molecular basis of disease from biochemistry to the practicing physician.

Professor Karl Folkers, who studied CoQ10 for the past 35 years, opened an important scientific meeting in 1990, quoting an old proverb of Voltaire “Nature is more powerful than education; time will develop everything.” And he continued, “CoQ10 is nature, knowledge is education, whether relevant or not, time beyond 33 years will internationally and broadly establish CoQ10 in medicine.”(22)

Well, here we are, 21 years after that meeting and the importance of Coenzyme Q10 has still not “arrived” in mainstream medicine. As you are (hopefully) aware by now from the many references on this topic, the fundamental, crucial requirement for Coenzyme Q10 in our body is not a new discovery. CoQ10’s function has been known for over 50 years.

Dr. Perrone, from the Oxidative Stress post, commented that until a drug company comes up with a patent on an antioxidant, we won’t be hearing much about a/o benefits, but if and when they ever do figure out how to patent one, you can be sure, we’ll be hearing a lot about the benefits of using anti-oxidants and in this case, specifically, CoQ10.

It seems incredible that so few of us with heart problems, such as Lone Atrial Fibrillation, energy issues, muscle weakness and pain, cancer, diabetes, autoimmune disorders, neurological disorders… are not automatically tested for CoQ10 blood levels the very first time we describe our complaints. Sadly, the majority of patients and doctors remain clueless about the CoQ10 connection.

Especially disturbing is the fact that virtually everyone is tested for cholesterol levels and most often, prescribed a statin at the very hint of an opportunity to do so, but once again, CoQ10 is never prescribed along with the statin to help protect mitochondrial DNA from statin damage.

This post is not about the adverse effects of statins but rather it is adjunctive to the Oxidative Stress report emphasizing the crucial value of Coenzyme Q10 as powerful antioxidant.(1)

That said, however, anyone who has taken a statin drug or is currently on a statin, should sit up and take notice because statins block CoQ10 production along with other important hormones. Included at the end in the Reading and Resources section are several clips related to various reports and findings about adverse effects of statin drug use. Because of the ongoing prevalence of prescribing statin drugs, these cautions can’t be ignored, so no CoQ10 review would be complete without including the caveats so one can make informed decisions.

Even if your physician is not informed about the importance of CoQ10, that doesn’t mean you should be.

Jackie

COQ10: ESSENTIAL FOR ENERGY
Coenzyme Q10 is an essential nutrient that enables the body to turn food into energy. CoQ 10’s role is similar to that of a spark plug in a car engine. Just as the car cannot function without the initial spark, the body cannot function without Coenzyme Q10.

CoQ10 is essential for heart health, immune function and overall wellness. It has been found useful in treating congestive Heart Failure, cardiomyopathy, periodontal disease and neurological disorders including Parkinson’s along with cancer, diabetes and autoimmune disorders.

Natural CoQ levels do decline with age and although CoQ is found in all plant and animal sources, optimal doses cannot be achieved through typical diets. Organ meats are the richest source of CoQ10 but few eat these foods regularly. Therefore, supplementation is needed to achieve optimal CoQ10 levels.

There are numerous books written about CoQ10. Many heart-health books and guides include chapters specific for supplementing with CoQ10. The heart has the highest number of mitochondria so would naturally have the highest concentration of CoQ10 and, therefore, the highest requirement as well.

It is especially important for anyone taking statin drugs such as Lipitor, Atorvastatin, Zocor, Simvastatin, Pravachol, Pravastatin, Lovastatin, Mevacor, Fulvastatin, Leschol, Crestor, Rosuvastatin to understand the need to supplement sufficiently with Coenzyme Q10 because statin drugs block the production of this enzyme right along with cholesterol. For that reason, muscle and heart energy production is also blocked and can cause multiple problems that seem to be ignored either by ignorance or choice for some patients. Statin-induced cardiomyopathy has been discussed in studies by cardiologist, Peter Langsjoen, MD(2) and by now, most people are familiar with the mitochondrial DNA damage and subsequent physical problems from statin use in former astronaut and NASA physician, Duane Graveline, MD.(3)

REVIEW OF COENZYME Q10
Reiterating for emphasis and continuing to elaborate, this following segment is from The Strategy (4) for readers who have not yet visited that Observational Report:

Coenzyme Q10 is called “The Spark of Life” in Dr. Sinatra’s book(5) Chapter 4. Without CoQ10, we can’t survive. As cellular levels of CoQ10 fall, so does general health. Not only is CoQ a powerful antioxidant providing protection from free-radical (oxidative stress damage), but CoQ’s role in cellular energy production is of paramount importance. CoQ transports electrons to the mitochondria where energy is used to generate ATP thereby making fuel for every cellular function.
(Heart cells have the highest concentration of mitochondria-about 5000 in each heart cell compared to an average of about 70 in a biceps muscle for instance).

In the mitochondria of each cell, CoQ provides the spark that initiates the energy process. When there is a CoQ deficiency, the cellular “engine” misfires and may fail or die…leading to a failing heart, or immune system and the inevitable weakening of defense again disease and aging… [and relevant to this discussion – the energy for the ATP to maintain the Na/K pump and the requisite tissue compliance factor that supports the prolonged refractory period and therefore NSR.]

Dr. Sinatra calls CoQ10 “fertilizer” for heart." He says, “With a fertilizer like CoQ to fortify the mitochondria, it makes sense to treat or fortify an energy-starved heart composed of thousands of mitochondria. This makes the cardiac cell pulsate and you get more mileage out of the cell, especially in an ischemic cell.”

CoQ also acts to reduce artery damage and plaque formation via its antioxidant action. It also has a remarkable affinity to protect heart cells that are deficient in oxygen. This is of major important in the tissue compliance factor. As a powerful antioxidant, CoQ helps diminish the detrimental effects of free-radical damage or oxidative stress. Certainly, an influencing factor for afib according to studies.

CoQ10 prolongs the action potential and we know that is what helps maintain NSR. Dr. Sinatra notes studies using CoQ10 (60 mg/day) reduced incidence of premature ventricular contractions (PVCs). Other studies indicate CoQ shortened the QT interval reflecting membrane stabilization in heart attack patients. [This now ties in with the voltage issue Erling has introduced in CR Session #72. The dots are now connected.]

CoQ10 researcher William V. Judy, PhD,(21) said this in his teleconference on Coenzyme Q10: “Co Q is responsible for conduction of the impulse down that nerve into the AV node, the SA node and is important for membrane stabilization. Remember when the heart contracts, sodium rushes in, calcium rushes in – there is a long plateau of the action potential, then potassium rushes out and so forth, but that final stabilization where the membrane becomes stable – requires the sodium/potassium ATP pump which is energy driven and if you have CoQ deficiency in a small locus then you have instable membranes which lead to heart dysfunctions.(21)

Q. The body makes CoQ. How large of an impact is endogenous CoQ?
A. We have looked for years for an endocrine mechanism- we know that thyroid controls metabolism – maybe some control over thyroxine over metabolism and there, over CoQ, but we know the major stimulus for CoQ synthesis is the demand for energy and oxygen at the cellular level. People who exercise produce more CoQ than those who are sedentary. Athletes produce a tremendous amount of CoQ where non-athletes have maybe half that. So we really think that exercise is the promoter of CoQ synthesis. When people stop on a daily basis their CoQ levels decrease rapidly.

CoQ is peak in the body at age 21. The levels decrease gradually and at the age of 65 most people are 45-50% low. Fortunately, there are people who are above that – maybe 12% of the population have high levels and they age very slowly, never sick and live well in their tenth decades.

Then we have a group that has early deficiencies of CoQ in early 40’s and mid 50’s and have early aging and have early age –related degenerated diseases – have high medical bills

Pharmaceutical Issues:
We know about the CoQ10 and statin drugs; many other interactions interfere with pharmaceuticals. The book by Ross Pelton, “Pharmaceuticals that Interfere with Energy Synthesis” says: – we know of a hundred pharmaceuticals, especially the beta blockers, the diabetic drugs, antidepressants, cardiac drugs, statins, that interfere either with CoQ synthesis or the CoQ in the electron transport system to produce energy. This is why the most common clinical symptom complaint among people who are on a lot of drugs is, “Doctor where is my energy? I have no energy.” Often it is the drugs and the amount of drugs interfering with nutrition. And CoQ – by all means—is nutrition On the other hand, we know very little interaction between CoQ and drugs except for one thing -- CoQ raises metabolism and therefore may increase metabolism of certain drugs in the body.

Note: AF patients on warfarin/Coumadin are often told to avoid Coenzyme Q10 as there is a warfarin interference.
Dr. Judy says: It’s been shown in England (St. Mary’s Hospital) that neither Co10 nor vitamin E interferes with the clotting processes. We have hundreds of patients on Coumadin who have taken CoQ for 20 years and have no blood clotting problems

Professor Gian Paolo Littarru(22) is recognized as the foremost Coenzyme Q10 researcher today. He observes that CoQ10 levels decline with age, peaking in heart tissue at ages 19-21and declining continually. In the brain, tissue levels peak at age 45 and then decline.

He also notes that because of the high antioxidant properties, CoQ concentrations in LDL is prophylactic in the formation of atherosclerosis.

Important Aside:
Statins block Coenzyme Q10 production.
Not for this discussion, but serious consideration should continue along the lines of questioning the wisdom of prescribing statins for the majority of the population as a “preventive” drug….given the preceding information about the importance of CoQ.


REFINING THE INFORMATION
It becomes important to recognize that not all supplement forms of CoQ10 are readily absorbed. In the previous posts reviewing the current research by Dr. Judy, he discusses the bioavailability issues. The old ubiquinone forms (especially the dry powder) typically needed to be taken with a fat-containing meal. The improved formulations incorporate nano-particles in a lipid that facilitate transport to the target tissue. (6)


UBIQUINOL FORM OF COENZYME Q10
The Ubiquinol form becomes useful in people over the age of 40 since a conversion problem seems to be very prevalent. Some practitioners prefer giving a combo-dose of both the nano-particle Ubiquinone and the Ubiquinol converted form.

[My personal experience from experimenting to generate energy and stamina for weak muscles is that I didn’t achieve that goal even with 400 mg of nano-particle Ubiquinone. Success came when I adjusted intake to 400 ubiquinol and 200 nano-particle ubiquinone for six weeks. After about two weeks, it seemed too good to be true, so I stopped the ubiquinol briefly. The symptoms returned, so I resumed the 600 combo dosing. After six weeks and because I was so much more comfortable, I opted to take only 100 nano-particle ubiquione and dropped to 200 mg ubiquinolas ‘maintenance’ because the ubiquinol form is expensive, but for me, well worth it. I found it stabilized my heart as well. A lab test last year indicated I was just under 4 – probably still too low. Jackie]

The body uses two forms of CoQ10. Ubiquinone is the better known form, also known as the oxidized form, used primarily for energy production in the electron transport energy cycle inside the cell.

Ubiquinol is the active, reduced, antioxidant form of CoQ10. Ubiquinol plays a primary role of decreasing oxidative damage caused by lipid peroxidation within mitochondria. According to research, plasma ubiquinol is decreased in patients with elevated cholesterol (hyperlipidemia).

There is evidence that suggests that the ability to convert ubiquinone to ubiquinol may diminish with age, resulting in diminished protection against oxidative stress and reduced energy levels. Ubiquinol may provide a strong initial stage defense against cellular oxidative damage and requires supplementing to maintain optimum health.

Researchers at East Texas Medical Center found that patients with advanced congestive heart failure taking high doses of ubiquinone CoQ10 were not able to achieve adequate improvements in blood serum CoQ10 levels. When switched to ubiquinol, blood CoQ10 levels improved dramatically with a consequential improvement in clinical symptoms and left ventricular function. It is also being studied for its effects on TNF alpha, and therefore, inflammation.(7)

The Ubiquinol reduced, active form has much current information on the Internet for further research if you decide to use it. Check the Ubiquinol form of Jarrow QH-Absorb at Hans’ web vitamin link.


DOSING: It’s best to take CoQ in the morning with some fat.
If working with higher doses, it’s better to split the dose, taking half in the morning and half in the early afternoon around 2 pm. If you take it later, it may be too energizing later on in the day. Serum levels reach peak concentrations in 6 hours with the more absorbable forms.

The studies by cardiologist Peter J. Langsjoen, MD, indicate success in reversing cardiomyopathy with doses “averaging 580 mg/day of ubiquinol (450-900 mg/day).”(2)

Nutritionist Tony Perrone, PhD (in the Oxidative Stress report), indicates he uses a range of dosing depending on the disease he is treating. In the case of auto-immune disorders, it is not uncommon to start with doses of 1200mg twice a day of the dry-powder, CoQ mixed with fat for absorption and reports good results.

He says, “CoQ10 has been studied in humans to some extent for safety and all of these studies that I reviewed on PubMed and other data bases have shown a very good safety profile with GI upset being the most serious side effect that I’ve seen in the literature…I’ve not seen it in practice.” In humans dosing up to 5000 mg a day in Parkinson’s, Alzheimer’s, heart disease and cancer in humans have been used safely. He doesn’t go over 5,000 nor does he suggest it, but thinks even more would probably be safe. The cost would be the limitation long before one reaches high dosing.

TESTING
As stated in The Oxidative Stress Report – Dr. Perrone advises using Lab Corp for the testing because their higher upper range. When he tests, he says he is looking for a serum blood level of at least 6 and probably closer to 10 in a therapeutic environment.

[Note: As with magnesium, though, …”The plasma/serum CoQ(10) level is influenced by a number of physiological factors and, therefore, has limited value as a means of assessing intracellular CoQ(10) status.” (8)
So it may be reasonable to assume just as with magnesium, if serum CoQ levels are low, most likely, IC CoQ will also be low…especially taking into consideration the higher needs of very active people, those over 40 due to absorption/conversion issues and the elderly and obviously anyone suffering from heart issues, muscle weakness, periodontal disease, neurological and auto-immune disorders.

However Dr. Littarru(22) says that CoQ10 blood levels have definite metabolic and diagnostic implications. (Since he’s the world’s expert, I trust his data and experience.)

Additionally, it is known that CoQ absorption may be inhibited by Candida overgrowth or other sources of intestinal inflammation. Jackie]

References for Self-Study
Obviously, this is a huge topic. Rather than make a long post even longer, following are various related links of interest. Depending on how motivated you are, it’s worth knowing all you can about the need for optimal Coenzyme Q10 – considering it is truly,”The Spark of Life.”

Happy reading!

Jackie


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 Suppl41-50. 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 Suppl78-88.

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.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]
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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 Suppl137-44 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

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