Vol. 4 • Issue 4 • Page 41
When it comes to cardiovascular disease, statistics paint a grim picture. More than 260,000 Americans die every day from the disease and its complications.1Equally troubling is that more than 70 million Americans live with known risk factors that precede these fatalities.1
Although early preventive measures can turn the tide against this killer, heart disease remains the No. 1 cause of death in the United States.2Clearly, we need better strategies to treat this condition, aside from the traditional statins, stints and bypass surgery.
Fortunately, we may very well have found it with coenzyme Q10 (CoQ10 or ubiquinone), a novel vitamin-like compound that can improve the heart's adaptation to degeneration.3,4In fact, in severe cases of heart dysfunction, this substance is even more effective when used with other conventional agents.5,6
Coenzyme Q10 was first identified by physician Fred Crane in 1957 and had been investigated for its ability to help mitochondrial cells create energy.7Over the last 50 years, scores of scientific studies have documented CoQ10's ability to protect the myocardium from biochemical and histological damage arising from various ischemic-related events.8Early trials with animals showed that hearts had less edema, as well as less cell membrane disturbance, mitochondrial lysis and disarrangement of myofibrils after ischemia and reperfusion.9,10 Additionally, scientists found this compound could help restore blood flow back to the heart after ischemia. Current, well designed studies show that CoQ10 plays a key role in the heart's innate physiological function, energizing, sustaining and regenerating its bioenergetic pathways and vigilance.11
What is CoQ10?
Coenzyme Q10 is found in every cell of the body and the mitochondria, hence its designation ubiquinone, coined from the Latin word ubique, meaning everywhere. Mitochondria are tiny organs found in the cytosol part of cells, known as the powerhouse. The cytosol produces adenosine triphosphate (ATP) which stores, supports and recycles energy.12
Ninety percent of the body's physiological needs depend on CoQ10, since it allows the mitochondria to convert food metabolites into ATP. Without the jumpstart of CoQ10, there's no energy to sustain life. This dynamic compound also neutralizes organic substances so that free radicals can't damage cellular structures, including DNA.13Micro-organisms have CoQ as 6, 7 or 9 isoprenoid units (CoQ6, CoQ7, CoQ9). Mammalian CoQ is of the 10-unit isoprenoid type, which gives way to its distinction and its application. The isoprenoid units may have similar functions, but because of the nature of their germane, they can show differences in some properties, such as the various control mechanisms in a given cell. In retrospect, the structure of all CoQ molecules resembles a head with a tail. The tail can have up to 12 repeating units. The human body manufactures only one type of CoQ-a tail of 10 repeated units for which it's named.14
The Heart's Workhorse
In many cells found in muscles such as the biceps, 200 mitochondria circulate per cell. However, in a heart cell, more than 5,000 mitochondria proliferate per cell.15Stephen Sinatra, MD, FACC, FACN, CNS, a board-certified cardiologist, found that CoQ10's energy-producing ability is crucial when the heart is starving for oxygen. His data demonstrate that survival rates improve over placebo when CoQ10 is administered in the middle of a heart attack.15
The majority of the published scientific literature on CoQ10 has focused on congestive heart failure. But the compound also can improve various aspects of cardiac function. This is a direct result of the early collaborative work of Karl Folkers, Gian Paolo Littarru and Denton Cooley.16Recently, researchers in the division of cardiology at the department of medicine of Northwestern University reported that CoQ10 normalized the actions of the left ventricular ejection fraction.17This elucidated both the signs and symptoms of persistent and severe heart failure. The male and female patients (mean age 54 years) in this study suffered from idiopathic dilated cardiomyopathy, having evidence of myocardial viability.18,19
The concept of myocardial viability is based on the fact that severely damaged hearts (myocardium infarction) in patients can be improved after coronary vascularization, which restores the flow of oxygen, nutrients and/or blood to the heart.20In practical terms, CoQ10 can restore normal metabolic function to a heart starved for oxygen, energy and vital nutrients, thus reinitiating the innate revascularization processes.
Re-Oxygenation after Hypoxia
CoQ10 also can re-energize or quickly re-oxygenate heart muscle tissue after episodes of hypoxia.21 lso known as anoxia, hypoxia can occur from insufficient circulation of blood, red blood cells or dysfunctional blood flow from heart failure. Hypoxia also can occur when adequate amounts of oxygen don't reach the blood in the lungs.
When the partial pressure of oxygen (PO2) drops below 8.0 KPa (60mmHg), respiratory failure occurs.22This can cause a decrease in the contractile force of the heart, a drop in myocardial high-energy phosphates, as well as the release of ATP metabolites and creatine phosphokinase.23Creatine phosphokinase is the enzyme found mainly in the heart, brain and skeletal muscle. Elevation of this enzyme in the blood emanating from the heart is a biomarker of damaged heart muscle and/or the occurrence of a heart attack.24
Mounting evidence shows CoQ10 can impede the breakdown of specific constituents, substrates or spare metabolic agents that can be salvaged for the resynthesis of ATP.25When CoQ10 is administered in cases of congestive heart failure, ATP is restored, thus re-initiating the cardiac contractile force of the heart.25
The Statin Controversy
The efficiency of statin drugs to treat patients suffering from hypercholesterolemia cannot be disputed.26Many studies indicate that statins not only lower the risk of vascular events, but they also improve symptoms of peripheral arterial disease. In addition, they exert beneficial pleiotropic effects on hemostasis, as well as improve blood vessel function, inflammation and renal function.27-29
However, researchers have found a definitive link between statin drug use and CoQ10 depletion. This is of vital concern becauseCoQ10 plays a major role in igniting mitochondrial energy production. A statin-induced deficiency may directly cause diseases of muscle tissue, known as myopathy.30
Nine observational studies and six randomized controlled investigations show that statin therapy can reduce plasmal serum CoQ10 levels by 16 percent to 54 percent. Researchers believe this may be directly related to the drop in LDL levels caused by statins. Paradoxically, LDL cholesterol is one of the substances that transports CoQ10 throughout the body.30Current data suggest that millions of people being treated with 3-hydroxy-3 methylglutaryl Coenzyme A (HMG-CoA) reductase inhibitors, such as lovastatin, simyastatin and pravastatin, may be experiencing reductions in CoQ10 levels.31This is because the enzyme is critical to convert HMG-CoA to mevalonic acid, which is one of the first steps involved in the biosynthesis of cholesterol.
Mevalonic acid, however, is a precursor of CoQ10 and is also required for ubiquinone synthesis. The problem here is that CoQ10 uses the same biosynthetic pathway of cholesterol.32Because of this innate physiological roadblock, CoQ10 levels in plasmal serum tend to decline. As mentioned earlier, that decline can range from 16 percent to 54 percent.30
Peter H. Langsjoen, MD, FACC, is one of today's most eminent CoQ10 researchers. Citing data from his research, he states that heart muscle function weakens when CoQ10 levels begin to decline from statin drug therapy.33This diastolic dysfunction occurs because the relaxing phase or filling phase of the cardiac cycle is disrupted. After the heart muscle contracts, an enormous amount of cellular energy is needed to recalibrate calcium gradients in heart tissue so that muscle fibers can repose.34
If the diastolic phase is severely altered, the risk of developing congestive heart failure increases. Data indicate, however, that CoQ10 can recharge cardiac muscle tissues and strengthen muscle contractions, thus renunciating the above events.35Additionally, Dr. Langsjoen confirmed the hypothesis that CoQ10 could improve statin drug-related side effects and cardiomyopathy.36
Testing the Hypothesis
To assess possible side effects of statins (myalgia, fatigue, dyspnea, memory loss and peripheral neuropathy), researchers discontinued statin therapy and administered 240 mg/day of CoQ10 to patients, who were followed for 12 months. Several findings are noteworthy. Fatigue decreased from 84 percent to 16 percent; myalgia, from 64 percent to 6 percent; dyspnea, from 58 percent to 12 percent; memory loss, from 8 percent to 4 percent; and peripheral neuropathy, from 10 percent to 2 percent.36
The results of this study strongly suggest that statin-related side effects, including statin cardiomyopathy, may be more common than prior published reports showed. These findings also reflect a strong indication that the combination of discontinuing statin therapy, coupled with aggressive CoQ10 therapy, can substantially improve adverse statin-induced complications safely and effectively.37
In a related study at Stony Brook University, researchers found that CoQ10 reduced muscle pain linked to statin use. Because statins inhibit the endogenous synthesis of CoQ10 and block mitochondrial energy production in muscle tissue, muscle weakness or soreness often surfaces. In this double-blinded treatment protocol, researchers used 100 mg/day of CoQ10 for 30 days. Muscle pain decreased by 40 percent and pain interference with daily activities decreased by 38 percent.38These results indicate that CoQ10 may be a viable treatment option when making the decision to stop statin therapy.
As physicians, be aware of this drug-nutrient interaction and become vigilant to the possibility that statin drugs can interfere with skeletal muscle myocardial bioenergetics.37To this end, many forward thinking cardiologists are suggesting that patients on statin drugs take CoQ10.31
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CoQ10 and Heart Failure
Definitive evidence shows that CoQ10 can improve heart bioenergetic pathways in patients with end-stage heart failure.39To assess whether CoQ10 could improve the pharmacological bridge from heart failure to heart transplantation, researchers at Rabin Medical Center in Israel administered 60 mg U/day of CoQ10 or a placebo randomly to patients for three months. Twenty-seven patients completed the study and continued to receive their regular regimen of medications.38The study group showed dramatic improvements in the six-minute walk test and a reduction in labored breathing and fatigue.
These researchers concluded that CoQ10 can serve as a valuable adjunct to normal pharmacologic protocols to treat patients with end-stage heart failure.39In heart failure patients, a marked decline of CoQ10 exists, and the severity of that decline is associated with the severity of heart failure, according to cardiologists at the Heart Centre at the Copenhagen University Hospital in Denmark.
These researchers also cite that numerous double-blinded, placebo-controlled trials with CoQ10 have shown statistically significant improvements in various clinical parameters, such as exercise capacity, reduced cardiovascular morbidity and decreased hospitilization.40Based on the collective data, CoQ10 appears to be devoid of any serious side effects and can improve quality of life for patients, even those in the most problematic stage of heart disease.
The Right Dose
The exact dose of CoQ10 to produce a favorable effect on varying degrees of severely dysfunctional hearts is still being investigated. But the general consensus is that that 2.5 ug/ml appears to serve as the critical starting maintenance point.
Researchers contend that 100 mg to 300 mg of CoQ10 in ubiquinol form will have a positive impact in patients with congestive heart failure. In its ubiquinone form, CoQ10 doses can range from 100 mg to 600 mg daily. With dose ranges of 450 mg of ubiquinone, blood levels of CoQ10 have generally hovered at 2.2 mcg/ml.32At the same dose level of ubiquinol, blood ranges have increased to 8.5 mcg/ml. Data indicate that patients suffering from severe heart failure need to maintain levels of 4 mcg/ml of CoQ10 to have a therapeutic impact.36In its metabolized or reduced form, CoQ10 is the most effective and quickest way to sustain proposed therapeutic blood levels.36
For general preventive measures as a daily supplement, I recommend dose rangesfrom 30 mg to 100 mg daily in ubiquinol form. Higher daily dose ranges may be warranted for the following conditions:
• Blood sugar control (100 mg/2 times a day)
• Cancer and aids (390 mg/day or 40 mgkg bw/day)
• Elevated cholesterol levels (100 mg/2 times a day)
• Hypertension (225 mg/day)
• Muscular dystrophy (100 mg to 150 mg/day)
• Neurodegeneration (1,200 mg/day)
• Periodontal disease (50 mg/day)
• Sickle cell anemia (3 mg/kg/day) 42-49
ata from around the world show that CoQ10 is a strong and viable agent to preserve and maintain proper heart function. From all indications, its role as a possible noninvasive treatment, when used early or with conventional therapy, can improve quality of life for many patients. It also can enhance the lives of those looking to establish or augment known preventive protocols. n
For a list of references, go to www.advanceweb.com/healthyaging and click on the references toolbar.
George L. Redmon, PhD, ND, is a leading expert on nutritional supplements, herbal botanicals and holistic health care. Dr. Redmon has authored six books on alternative ways to manage arthritis, chronic fatigue, sexual dysfunction, obesity and prostate disturbances.
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