If you attended high school most days, you might have learned that atoms are made of protons, electrons and neutrons, having charges that are positive, negative or neutral, in that order. If the charges get out of balance, the atom is either negatively or positively charged. The switch between one type of charge and the other allows electrons to move from one atom to the next. It’s this flow of electrons that we call electricity and is the energy that controls everything about the body. This is the source of the signals that allow us to grab the doorknob or turn the ignition switch, or even to think about what to have for dinner. Instead of flowing along a continuous wire, as happens in the house, these signals jump from one cell to the next—and they do it fast.
The potassium inside a cell and the sodium outside have a lot to do with our electrical capacity. At rest, a cell has more negatively charged potassium inside than positively charged sodium. As the negatives and positives are attracted to each other, they cross the barrier between them—the cell membrane—through a gate, and create electricity in order to initiate a movement, thought or biological function. This impulse triggers the gate on the neighboring cell, then on the next one, the next one. This is how the sinoatrial (SA) node of the heart (its pacemaker) tells it to contract and how your eye tells your brain what you just saw. One of the interesting, though admittedly still painful, facets of life happens when you hit a finger with a hammer. The pain message travels through a sensory nerve to the brain in a fraction of a second, and then the brain associates the assault with discomfort before it tells you to move your finger away from the site of injury. Even though you realize what just happened, it takes a brief moment before the throbbing starts. All this is based on electrical activity. This might happen at 250 miles an hour, much slower than the 180,000 miles per second speed of electricity along a wire.
Our cells—more than 60 trillion—work hard every day to multiply themselves, digest nutrients, remove wastes and make energy from something called ATP. Inside each cell are little power plants called mitochondria, the number depending on the job of the cell. An eyelid will not have as many mitochondria as a bicep. ATP is made inside a mitochondrion, where Co-Enzyme Q 10 directs the function of the electron transport chain by collecting and transferring electrons along the chain. In its reduced form, where it gains an electron, CoQ10 acts as an antioxidant, effectively recycling vitamin E and possibly having an anti-atherogenic effect (Turunen, 2002).
Although often ignored by conventional medicine, it is important to note that CoQ10 shares a metabolic pathway with cholesterol and that stores diminish with age, whether by decreased synthesis or by increased requirements, or even by the elevated lipid peroxidation that accompanies aging. If we regulate cholesterol with a statin drug, we also regulate the manufacture of CoQ10; hence the need for supplementation to maintain the electrical grid. In the first double-blinded study ever that examined CoQ10 in cardiac interventions, it was discovered that enzyme supplementation in heart failure patients reduced hospital admissions and death by improving cardiac function through enhancement of the respiratory chain at doses of 100 mg three times a day (Mortensen, 2013).
Allopathic medicine rarely looks into the micronutrient deficiencies that either foretell or cause impaired function of the heart’s electrical circuits. Its therapeutic options are confined to treating symptoms. Cellular—or membrane—medicine recognizes the important components of the energy formation cycle. Patients who suffered congestive heart myopathies had shown remarkable responses to CoQ10 therapy when assiduously administered in a faithful regimen (Langsjoen, 1985). If such was the case decades ago, why has there been so little publicity? New York Heart Association (NYHA) class IV heart failure defines almost complete cardiac insufficiency. Patients who were expected to die within two years under conventional therapy did not because it was recognized that CoQ10 is indispensable in mitochondrial bioenergetics (Langsjoen, 1988).
Absorption of supplemental CoQ10 on an empty stomach is poor, with more than sixty percent excreted in feces. It improves when taken with foods having a considerable lipid profile. In the presence of bile detergents lipids are broken into very small particles, thus increasing their surface area and subsequent susceptibility to the lipase enzymes that digest fats. Now, especially in the company of phosphatidylcholine, these particles are absorbed by intestinal mucosa and passed into the bloodstream. It takes about three weeks of faithful supplementation to attain maximum serum concentrations.
As with most integrative modalities, ongoing studies are welcome, but suffer lack of funding because they interfere with the profits garnered by pharmaceuticals. The number of eligible heart transplant patients surpasses the available number of donors. On the bright side, CoQ10 has a beneficial effect on these persons by virtue of providing a pharmacological bridge that offers an improvement in functional status and quality of life (Berman, 2004), including ejection fraction (Fotino, 2013).
For a long time, medicine has sought a means to return flexibility to the cardiovascular system that has succumbed to the ravages of time and insult, such as smoking, excessive sugar intake, and diets that promote advanced glycation endproducts. Patients suffering NYHA class III CHF who received supplemental CoQ10 at 100 mg tid, experienced improvement in left ventricular contractility and ejection fraction after only four weeks (Belardinelli, 2005), indicating the plausibility of such a protocol.
Studies may be clouded by anticipated outcomes, the bias of which may be directedby expectations of funding bodies. In too may instances, Eurasian investigatorsfind more successes than North Americans. The bottom line appears that low CoQ10concentrations are predictive of adverse CHF events, leaving one to understandthe rationale for intervention with the supplement. Endogenous manufacture ofCoQ10 requires sufficient vitamin B6 for biosynthesis. Most of us consume lessthan 10 mg of CoQ10 a day from dietary sources, leaving plenty of room for supplementation,even if we lack a pathology. The last thing we need is a power failure.
Abe, K., Matsuo, Y., Kadekawa, J., Inoue, S., and Yanagihara, T. Effect of coenzyme Q10 in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS): evaluation by noninvasive tissue oximetry. J Neurol.Sci. 1-1-1999;162(1):65-68.
Baggio, E., Gandini, R., Plancher, A. C., Passeri, M., and Carmosino, G. Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure (interim analysis). The CoQ10 Drug Surveillance Investigators. Clin Investig. 1993;71(8 Suppl):S145-S149.
Bargossi, A. M., Grossi, G., Fiorella, P. L., Gaddi, A., Di Giulio, R., and Battino, M. Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors. Mol.Aspects Med 1994;15 Suppl:s187-s193.
Belaia, O. L., Kalmykova, V. I., Ivanova, L. A., and Kochergina, L. G.
Belardinelli R, Muçaj A, Lacalaprice F, Solenghi M, Principi F, Tiano L, Littarru GP. Coenzyme Q10 improves contractility of dysfunctional myocardium in chronic heart failure. Biofactors. 2005;25(1-4):137-45.
Belardinelli R, Muçaj A, Lacalaprice F, Solenghi M, Seddaiu G, Principi F, Tiano L, Littarru GP. Coenzyme Q10 and exercise training in chronic heart failure. Eur Heart J. 2006 Nov;27(22):2675-81.
Berman M, Erman A, Ben-Gal T, Dvir D, Georghiou GP, Stamler A, Vered Y, Vidne BA, Aravot D. Coenzyme Q10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study. Clin Cardiol. 2004 May;27(5):295-9.
Chen, R. S., Huang, C. C., and Chu, N. S. Coenzyme Q10 treatment in mitochondrial encephalomyopathies. Short-term double-blind, crossover study. Eur.Neurol. 1997;37(4):212-218.
Choe, J. Y., Combs, A. B., and Folkers, K. Prevention by coenzyme Q10 of the electrocardiographic changes induced by adriamycin in rats. Res Commun Chem Pathol Pharmacol 1979;23(1):199-202.
Crane FL. Biochemical functions of coenzyme Q10. J Am Coll Nutr. 2001 Dec;20(6):591-8.
Folkers K, Vadhanavikit S, Mortensen SA. Biochemical rationale and myocardial tissue data on the effective therapy of cardiomyopathy with coenzyme Q10. Proc Natl Acad Sci U S A. 1985 Feb;82(3):901-4.
Folkers, K., Morita, M., and McRee, J., Jr. The activities of coenzyme Q10 and vitamin B6 for immune responses. Biochem Biophys.Res Commun. 5-28-1993;193(1):88-92.
Folkers, K. Heart failure is a dominant deficiency of coenzyme Q10 and challenges for future clinical research on CoQ10. Clin Investig 1993;71(8 Suppl):S51-S54
Fotino AD, Thompson-Paul AM, Bazzano LA. Effect of coenzyme Q₁₀ supplementation on heart failure: a meta-analysis. Am J Clin Nutr. 2013 Feb;97(2):268-75.
Gottlieb, S. S., Khatta, M., and Fisher, M. L. Coenzyme Q10 and Congestive Heart Failure. Ann.Intern.Med 11-7-2000;133(9):745-746.
Hofman-Bang, C., Rehnqvist, N., Swedberg, K., Wiklund, I., and Astrom, H. Coenzyme Q10 as an adjunctive in the treatment of chronic congestive heart failure. The Q10 Study Group. J Card Fail. 1995;1(2):101-107.
Keogh A, Fenton S, Leslie C, Aboyoun C, Macdonald P, Zhao YC, Bailey M, Rosenfeldt F. Randomised double-blind, placebo-controlled trial of coenzyme Q, therapy in class II and III systolic heart failure. Heart Lung Circ. 2003;12(3):135-41.
Laaksonen, R., Ojala, J. P., Tikkanen, M. J., and Himberg, J. J. Serum ubiquinone concentrations after short- and long-term treatment with HMG-CoA reductase inhibitors. Eur.J Clin Pharmacol. 1994;46(4):313-317.
Langsjoen PH, Vadhanavikit S, Folkers K. Response of patients in classes III and IV of cardiomyopathy to therapy in a blind and crossover trial with coenzyme Q10. Proc Natl Acad Sci U S A. 1985 Jun;82(12):4240-4.
Langsjoen PH, Folkers K, Lyson K, Muratsu K, Lyson T, Langsjoen P. Effective and safe therapy with coenzyme Q10 for cardiomyopathy. Klin Wochenschr. 1988 Jul 1;66(13):583-90.
Langsjoen PH, Langsjoen AM. Supplemental ubiquinol in patients with advanced congestive heart failure. Biofactors. 2008;32(1-4):119-28.
Molyneux SL, Florkowski CM, George PM, Pilbrow AP, Frampton CM, Lever M, Richards AM. Coenzyme Q10: an independent predictor of mortality in chronic heart failure. J Am Coll Cardiol. 2008 Oct 28;52(18):1435-41
Mortensen SA. Overview on coenzyme Q10 as adjunctive therapy in chronic heart failure. Rationale, design and end-points of "Q-symbio"--a multinational trial. Biofactors. 2003;18(1-4):79-89.
SA Mortensen, A Kumar, P Dolliner, KJ Filipiak, D Pella, U Alehagen, G Steurer, GP Littarru, F Rosenfeldt The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure. Results from the Q-SYMBIO study European Journal of Heart Failure ( 2013 ) 15 ( S1 ), S20
Sander S, Coleman CI, Patel AA, Kluger J, White CM. The impact of coenzyme Q10 on systolic function in patients with chronic heart failure. J Card Fail. 2006 Aug;12(6):464-72.
Sinatra ST. Refractory congestive heart failure successfully managed with high dose coenzyme Q10 administration. Mol Aspects Med. 1997;18 Suppl:S299-305.
Turunen M, Wehlin L, Sjöberg M, Lundahl J, Dallner G, Brismar K, Sindelar PJ. beta2-Integrin and lipid modifications indicate a non-antioxidant mechanism for the anti-atherogenic effect of dietary coenzyme Q10. Biochem Biophys Res Commun. 2002 Aug 16;296(2):255-60.
*These statements have not been evaluated by the FDA. These products are not intended to treat, diagnose, cure, or prevent any disease.