Coenzyme Q10 (CoQ10): Help for Broken Hearts

Coenzyme Q10 (CoQ10): Help for Broken Hearts

According to the American Heart Association, more than 71 million Americans—about  one in three—suffer from one or more types of heart disease.  Every 35 seconds, someone dies from it.1

The term “heart disease” covers a broad spectrum of conditions that affect blood and oxygen flow to and from the heart.  But you may see other names such as coronary heart disease (CHD), cardiovascular disease (CVD), congestive heart failure (CHF), myocardial infarction (MI), and coronary artery disease (CAD).

There are also many conditions that are frequently associated with heart disease such as high blood pressure, high cholesterol, atherosclerosis, stroke, peripheral artery disease, and many others.

The Ever-Ready Energizers

Coenzyme Q10, a vitamin-like compound found in the center of the cell known as the mitochondria, produces adenosine triphosphate (ATP) which helps every cell in the body produce the energy needed for maintenance and growth.  ATP also helps enzymes produce protein needed by the body to digest food and perform other biological processes such as protecting the heart and skeletal muscles.

In addition, coenzyme Q10 (CoQ10) works as an antioxidant to destroy cell-damaging free radicals—those oxidized molecules caused by overexposure to the sun, radiation, cigarette smoke, environmental contaminants, and air pollution.  Free radicals not only alter cell membranes, mutate DNA, and cause cell death, but they are also a major contributor to many age-related health issues.

Coenzyme Q10 is often found in organ meats (liver, kidney, heart), beef, soy oil, sardines, mackerel, and peanuts, so it is possible to get enough coenzyme Q10 from the diet.  However, manufacturing CoQ10 in the body requires adequate levels of eight vitamins, several trace minerals, and the amino acid tyrosine. A deficiency in any one of these vital nutrients can hinder the body’s production of coenzyme Q10.

And coenzyme Q10 naturally decreases with age.  The body reaches peak levels of coenzyme Q10 at around age 20.  By the age of 40, the body has 40% less coenzyme Q10 than at age 20 and by 70, the body has 60% less coenzyme Q10.2

While research suggests that coenzyme Q10 may benefit immune function, diabetes, fertility, memory and fatigue disorders, periodontal disease, macular degeneration, and cancer, most research focuses on the beneficial effects of coenzyme Q10 in relation to heart disease.

The Heart of the Matter

There’s much research on the effectiveness of coenzyme Q10 for reducing cardiovascular risk.


  • Indian researchers administered coenzyme Q10 or a placebo to rabbits fed a diet high in trans fats.  Coenzyme Q10 reduced markers of oxidative damage and artherosclerosis.3

Congestive heart failure (CHF)

  • Researchers at the University of Kentucky found limited evidence that coenzyme Q10 may benefit oxidative stress and depressed coenzyme Q10 levels common in CHF patients.4
  • Coenzyme Q10 helps CHF patients increase cardiac output and reduce stroke volume.5
  • A CHF patient in Brazil, given 150 mg per day of coenzyme Q10, experienced gradual improvement in left ventricle function with decreased systolic function three months after supplementation ended.6


  • Australian researchers have found that coenzyme Q10 may help reduce both systolic and diastolic blood pressure.7
  • Another study indicated that coenzyme Q10 offers significant and consistent benefits for hypertension.8
  • UCLA researchers concluded that coenzyme Q10 can be a potent tool in the prevention of hypertension and hyperlipidemia.9

Know Your Statins

Unfortunately, the drugs often prescribed to help regulate cholesterol can also deplete the body of necessary coenzyme Q10.

Statins (also known as HMG-CoA reductase inhibitors) such as atorvastatin, rosuvastatin, pravastatin, simvastatin, lovastatin, and fluvastatin sold under the trade names Lipitor®, Crestor®, Pravachol®, Zocor®, Mevacor®, and Lescol® lower cholesterol by reducing the body’s production of HMG-CoA reductase, an enzyme needed to produce cholesterol.

But this process is not selective.  Not only do statin drugs block cholesterol production, they also block the production of coenzyme Q10 creating a deficiency that, at a minimum, lowers immunity and helps produce the side effects associated with statin drugs.  One study showed that patients taking lovastatin had lower total and LDL cholesterol levels, but reported higher incidences of fatigue.10

The potential side effects of coenzyme Q10 deficiency, however, can be more serious.  A study conducted at Columbia University found that subjects taking atorvastatin for 30 days showed a significant decrease in coenzyme Q10 levels after just 14 days, causing the researchers to suggest that “widespread inhibition of CoQ10 synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.”11

Finally, in May 2002, Dr. Julian Whitaker filed petitions with the U.S. Food and Drug Administration (FDA) calling for black box warnings on all statin drugs, similar to the warnings used in Canada for statins.12  The petitions state that coenzyme Q10 depletion, as a result of statin drug use, can put patients at risk for impaired myocardial function, liver dysfunction, and myopathies including cardiomyopathy and congestive heart failure.  The FDA has yet to act.

While the longer term implications of coenzyme Q10 deficiency are serious, using LDL cholesterol as the primary (and often only) predictor of heart disease—as set out in the National Institutes of Health’s Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults—may be entirely inappropriate for a number of reasons, according to cardiologist Stephen T. Sinatra, MD, FACC.13  They include:

  • The report suggested a threefold increase in the number of Americans given prescriptions for statin drugs—a move that would increase sales of statins by about 20 percent annually.
  • The oxidation of LDL cholesterol remains a hypothesis for heart disease, yet cholesterol levels continue to drive treatment.
  • Research on omega-3 fatty acids shows improved survival rates for those with cardiovascular disease, independent of cholesterol levels, lending support for reducing inflammation as a way to improve cardiovascular mortality.
  • Statins may play a role in intervention and treatment because of their anti-inflammatory properties—not their cholesterol-lowering properties.  In fact, one study indicated that about half of myocardial infarction patients have normal LDL cholesterol levels and C-reactive protein may be a better predictor for atherosclerosis.15
  • Compared to patients taking statin drugs, untreated subjects with normal C-reactive protein levels did not have an increased risk of recurrent cardiac events while those whose C-reactive protein levels were elevated had significant risk of fatal coronary events regardless of their LDL cholesterol levels.

According to Dr. Sinatra, the report rejects other potentially more accurate predictors of cardiovascular disease including C-reactive protein and homocysteine levels—both measures of internal inflammation.  

Dr. Kilmer McCully, a leading expert on heart disease and the first to claim that elevated homocysteine levels are a prime risk factor for cardiovascular disease, shares this view.  “This approach to prevention is entirely misguided and based on an outmoded hypothesis of causation,” he says.  “Treatment of cholesterol elevation and dyslipidemia is merely addressing a symptom and not the cause of the disease.”14

Putting Coenzyme Q10 to Work

Coenzyme Q10 has been approved in Japan since 1974 for use in heart failure.16  Research in the U.S. is ongoing and shows promise for improving symptoms associated with macular degeneration, migraine, cancer, neurodegenerative diseases, hearing loss, muscular degeneration, male fertility, complications from diabetes, and more.

Cited Sources:

1) “Heart Disease and Stroke Statistics: 2006 Update,” American Heart Association
Accessed Feb. 2006

2) “Benefits of coenzyme Q10,” New Straits Times, 7/31/2005.

3) Singh RB, et al. “Effect of coenzyme Q10 on experimental atherosclerosis and chemical composition and quality of atheroma in rabbits.” Atherosclerosis, 146, 2:275-282, 2000.

4) Weant KA & Smith KM. “The role of coenzyme Q10 in heart failure.” Annals of Pharmacotherapy, 39, 9:1522-1526, 2005.

5) Tran MT, et al. “Role of coenzyme Q10 in chronic heart failure, angina and hypertension.” Pharmacotherapy, 21, 7:797-806, 2001.

6) Salles JE, et al. “Myocardial dysfunction in mitochondrial diabetes treated with coenzyme Q10.” Diabetes Research in Clinical Practice, 10/24/2005.
7) Rosenfeldt F, et al. “Systematic review of effect of coenzyme Q10 in physical exercise, hypertension and heart failure.” Biofactors, 18, 1-4:91-100, 2003.

8) Houston MC. “The role of vascular biology, nutrition and Nutraceuticals in the prevention and treatment of hypertension.” JANA, S1:5-71, 2002.

9) Sarter B. “Coenzyme Q10 and cardiovascular disease: a review.” Journal of Cardiovascular Nursing, 16, 4:9-20, 2002.

10) Singh RB, et al. “Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction.” Molecular Cellular Biochemistry, 246, 1-2:75-82, 2003.

11) Rundek T, et al. “Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke.” Arch Neurology, 61:889-892, 2004.

12) “Dr. Julian M. Whitaker petitions FDA to include coenzyme Q10 use recommendation in all statin drug labeling.” Townsend Letter for Doctors and Patients, 8/1/2002.

13) Sinatra ST, MD. “Is cholesterol lowering with statins the gold standard for treating patients with cardiovascular risk and disease?” (editorial), Southern Medical Journal, 3/1/2003.

14) Challem J. “A Prescription for Alarm.” Nutrition Science News, 9/1/2001.

15) Ridker PM, Stampfer JM, & Rifai N. “Novel risk factors for systemic atherosclerosis: A comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease.” JAMA, 285:2481-2485, 2001.

16) “Coenzyme Q10,”
Accessed Feb. 2006

Leave a Reply