CoQ10

Levels of CoQ10 decline with age.  Most people at age 40 have only 64 percent of the CoQ10 levels they had at age 20, and by age 80, levels usually decline to 36 percent of a 20-yearolds coQ10 status.  There are other factors that can cause deficiencies.  Among these are statin drugs prescribed to lower serum cholesterol; conversely, people with high cholesterol levels often have low levels of CoQ10.  Other prescription drugs including beta blockers, may lower CoQ10 status, and there can be an antagonistic relationship between CoQ10 status and warfarin, a prescription anticoagulant.   Although CoQ10 occurs naturally in the body, several other nutrients are necessary to produce it, including vitamin C and several of the B vitamin complex. In foods, the best source of CoQ10 are wheat germ, soy, spinach, broccoli, meats, fish vegetable oils, and rice bran.  Additionally, exercise raises heart levels of CoQ10 in the heart and other muscles.

 

CoQ10, ATP, and Energy Production 

CoQ10 is an important component in the mitochondrial electron transport system, and therefore in the making of adenosine triphosphate, or ATP.  ATP serves as the major energy source for the cells; in fact, the cells would cease to function without it.  It follows therefore that CoQ10 is most heavily concentrated in muscles and organs that produce a great deal of energy, such as the heart, liver kidney and pancreas.

 

CoQ10, Antioxidants

A fat-soluble antioxidant, CoQ10 can also regenerate other antioxidants.  Deficiencies of coQ10 have been observed in several disease states.  Many of them are related to the function of the heart, such as congestive heart failure (CHF), cardiomyopathy, hypertension, and chronic obstructive pulmonary disease.  CoQ10 has also been shown to be deficient in people suffering from AIDS, periodontal disease, and cancer.

CoQ10 and Cardio Health

Coenzyme Q10 (CoQ10) serves as an energy transporter in the mitochondria and also as an antioxidant.  In Power Aging, Gary Null wrote, “I believe if every American took between 100 and 300 mg of (CoQ10) a day, and if people with cardiovascular disease took between 330 to 500mg of this wonder-nutrient daily, we could be saving hundreds of thousands of lives a year.”  Null also called CoQ10 “a superstar in protecting the heart.” In his book, The Total Guide to a Healthy Heart, cardiologist Dr. Seth J. Baum wrote that CoQ10 can help lower blood pressure and can help treat congestive heart failure.

 
A six-year study by scientists at the University of Texas found that people being treated for congestive heart failure who took CoQ10 in addition to conventional therapy had a 75 percent chance of survival after three years.  Patients who underwent therapy alone had only a 25 percent survival rate.

 
At the Lancisi Heart Institute in Italy, researchers sought to determine whether oral coQ10 supplementation may improve cardiocirculatory efficiency and endothelial function in patients with congestive heart failure (CHF).  They studied 23 patients with a mean age of 59, using a double-blind, placebo-controlled cross over design.

 

Patients were assigned to each the following treatments: oral CoQ10 10 (100mg tid), CoQ10 plus supervised exercise training (ET)  (60 percent of Peak VO2, five times a week), placebo, and placebo plus ET.  Each phase lasted four weeks.  Both peak VO2 and endothelium dependent dilation of the brachial artery (EDDBA) improved significantly after CoQ10 and after ET as compared with placebo.  They concluded that CoQ10 supplementation improves functional capacity, endothelial function, and left ventricle contractility in CHF without any side effects.  The combination of CoQ10 and ET resulted in higher plasma CoQ10 levels and more  pronounced effects on all these parameters.  [Berardinelli R Mucaj A, Lacalaprice F Solenghi M, Seddaui G, Principi F, Tiano L Littarru GP.

Coenzyme Q10 and exercise training in chronic heart failure.  Eur Heart J. 2006Aug 1; [Epub ahead of print]

 

The same researchers in 2005 published a study investigating whether oral CoQ10 supplementation could improve cardiocirculatory efficiency in patients with CHF.  They studied 21 patients in New York Heart Association (NYHA class II and III with stable CHF secondary to ischemic heart disease (ejection fraction 37 +/- 7%), using a double-blind, placebo controlled crossover design.  Patients were assigned to either 100 mg daily of oral CoQ10 or placebo for four weeks.  In the group receiving coQ10, the systolic wall thickening score index was improved both at rest and peak dobutamine stress echo, while left ventricular ejection fraction improved significantly. [Berardinelli R Mucaj A, Lacalaprice F Solenghi M, Seddaui G, Principi F, Tiano L Littarru GP.   Coenzyme Q-{10} improves contractility of dysfunctional myocardium in chronic heart failure.  Biofactors. 2005; 25 (1-4 ) : 137-45.]

 

Researchers at the University of Connecticut School of Pharmacy conducted a meta-analysis of trials conducted between 1966 and 2005, studying CoQ10 in heart failure to evaluate the impact of coQ10 therapy on ejection fraction and cardiac output.  Of the 11 trials identified, 10 evaluated cardiac output.  Doses ranged from 60 to 200 mg/day with treatment periods ranging from 6 months.  There was a 3.7 percent net improvement in ejection fraction, with a more profound effect among patients not receiving angiotensin-converting enzyme inhibitors.  Cardiac output increased an average of0.28 L/minute.  “CoQ10 enhances systolic function in chronic heart failure, but its effectiveness may be reduced with concomitant use of currant standard therapies,” the researchers concluded. [Sander S, Coleman Cl, Patel AA, Kluger J, WhiteCM.  The Impact of coenzyme Q10 on systolic function in patients with chronic heart failure.  J. Card Fail. 2006 Aug; 12 (6): 464-72]

 

After being maintained for three months on a baseline diet (low in fat and cholesterol),  21 baboons were given a high fat, high cholesterol (HFHC) diet for seven weeks.  Their serum C- reactive protein(CRP) concentrations did not change.  Subsequent supplementation of HFHC diet with antioxidant vitamin E (250, 500, or 1000IU/kg diet) for two weeks reduced serum CRP concentrations from 0.91± 0.02 to 0.43± 0.06 mg/dL.  Additional supplementation with CoQ10 reduces circulating markers of inflammation in baboons.  Am J Clin Nutr. 2004 September; 80(3): 649-655.]

 

With earlier clinical trials suggesting that CoQ10 supplementation might afford myocardial protection during cardiac surgery, researchers at Baker Heart

Research Institute in Melbourne, Australia sought to measure the effect of CoQ10 on mitochondrial function; to test the effect of CoQ10 in protecting cardiac myocardium against a standard reoxygentation stress in vitro; and to determine whether CoQ10 therapy improves

recovery of the heart after cardiac surgery.  Patients undergoing elective cardiac surgery were randomized to receive oral CoQ10 (300 mg/day) or placebo for two weeks prior to surgery.

 

The authors’ findings indicated that preoperative oral CoQ10 therapy in patients undergoing cardiac surgery increases myocardial and cardiac myocardial tolerance to in vitro-hypoxia-reoxygentation stress. [Rosenfeldt F, Marasco S, Lyon W, Wowk M, Sheeran F, Bailey M, Esmore D, Davis B, Pick A, Rabinov M, Smith J, Nagley P, Pepe S. Coenzyme Q10 therapy before cardiac surgery improves mitochondrial function and in vitro contractility of myocardial tissue.  J Thorac Cardiovasc Surg. 2005 Jan; 129(1):25-32.]

 

Researchers at the Heart Failure Institute of the Advocate Christ Medical Center in Oak Lawn, IL. Evaluated left ventricular diastolic function with Doppler echocardiography before and after statin therapy.  Statin therapy worsened diastolic parameters in most patients, while CoQ10 supplementation in patients with worsening diastolic function with statin therapy improved parameters  of diastolic function. [Silver MA, Langston PH, Sabot S, Patel H, Salinger A. Effect of atorvastatin on left ventricular diastolic  function and ability of coenzyme Q10 to reverse that dysfunction.  Am J Cardiol. 2004 Nov 15; 94(10):1306-10]

 

CoQ10 and Brain Health

A study from the national Academy of Sciences showed that short-term supplementation with moderate amounts of CoQ10 “produced profound anti-aging effects on the brain,”

In a study, CoQ10 levels in Parkinson’s patients were 35 percent lower than a control group of the same age.  According to the University of Maryland Medical Center, “studies of women with breast cancer suggest that CoQ10 supplements (in addition to conventional treatment a nutritional regimen including other antioxidants and essential fatty acids0 may shrink tumors, reduce pain associated with the condition, and cause partial remission in some individuals.”

 
Researchers at the University of North Dakota School of Medicine looked at regional distraction of CoQ10 and mitochondrial complex-1 activity in the brains control-(C57BL/6), metallothionein knock out-metallothionein transgenic, and homozygous weaver mutant mice; and human dopaminergic (SK-N-SH) cells to determine the neuroprotective potential of CoQ10 in Parkinson’s disease.  Complex-1 activity as well as CoQ10 were significantly higher in the cerebral cortex as compared to the stadium in all the genotypes examined.  Complex-1 activity and coenzyme Q10 were significantly reduced in weaver mutant mice and metallothionein knock out mice, but were significantly increased in metallothionein transgenic mice. 
 

Administration of coenzyme Q10 increased complex-1 activity, and partially improved motoric performance, in weaver mutant mice.  Direct exposure of rotenone also reduced coenzyme Q10,complex-1 activity was attenuated by CoQ10 treatment, suggesting that complex-1 may be down-regulated due to depletion of CoQ10 in the brain.  The researchers concluded, “Metallothionein-included CoQ10 synthesis may provide neuroprotection by augmenting mitochondrial complex-1 activity in Parkinson’s disease.” [Sharma SK, El Rafaey H, Ebadi M. Complex-1 activity and 18F-DOPA uptake in genetically engineered mouse model of Parkinson’s disease and the neuroprotective role of coenzyme Q10.  Brain Res Bull. 2006 Jun 15; 70(1):22-32.]

 

Earlier, the team had determined the neuroprotective role of CoQ10 in   apoptosis in cultured human dopaminergic (SKN-SH) neurons, in metallothionein gene-manipulated mice, and in alpha-synuclein knockout (alpha- synko) mice, to determine a possible therapeutic and anti-inflammatory potential for CoQ10 in Parkinson’s.  They concluded that glutathione and metallothionein synthesis might be included as an attempt to combat iron-induced oxidative stress, while exogenous administration of CoQ10mediated neuroprotection in PD.[Kooncumchoo P, Sharma S, Porter J, Govitraapong P, Ebadi M. Coenzyme Q(10) provides neuroprotection in iron-induced apoptosis in dopaminergic neurons. J Mol Neurosci. 2006;28(2):125:-41]

 

In the department of neurology at the University Hospitals of Leicester in the U.K., researchers began with two premises proven in clinical trials: that therapeutic hypothermia can improve survival after cardiopulmonary resuscitation (CPR), and that CoQ10 has shown a protective  effect in neurodegenerative disorders.  They investigated whether combining hypothermia with CoQ10 after out-of hospital cardiac arrest provided additional benefit.  Forty-nine patients were randomly assigned to either hypothermia plus CoQ10 or hypothermia plus placebo after CPR.  Hypothermia with a core temperature of 35 degrees c was instituted for 24 hours.  Liquid coQ10 or placebo was administered through a nasogastric tube for five days.  Age, sex, premorbidity, cause of arrest, conditions of CPR, and degree of hypoxia were similar in both groups; no side effects of CoQ10 were identified.

 

Three month survival in the CoQ10 group was 68 percent, while it was 29 percent, in the placebo group.  Nine coQ10 patients' verses five placebo patients survived with a Glasgow Outcome Scale of 4 or 5.  Mean serum S100 protein- a marker of cerebral damage-24 hours after CPR was significantly lower in the CoQ10 group.  The authors concluded that combining coQ10 with mild hypothermia immediately after CPR appears to improve survival and may improve neurological outcome in survivors.  [Damian MS, Ellenberg D. Gildemeister R, Lauermann J, Simonis G, Sauter W, Georgi  C. Coenzyme Q10 combined with mild hypothermia after cardiac arrest: a preliminary study.  Circulation. 2004 Nov 9; 110(19):3011-6.]

 

In a family with ataxia (an inability to control voluntary muscle movements and CoQ10 deficiency, analysis of genome-wide microsatelite markers suggested linkage of the disease to  chromosome 9p13 and led to identification of an aprataxin gene (APTX) mutation that causes ataxia occulomotor apraxia (AOA1[MIM606350]).  The authors suggested that CoQ10 deficiency may contribute to the pathogenesis of AOA1.  [Quinzii CM, Kattah AG, Naini A, Akman HO, Moothat VK, DiMauro S, Hirano M. Coenzyme Q deficiency and cerebellar ataxia associated with an aprataxin mutation .  Neurology. 2005 Feb 8; 64(3): 539-41.]

 

            CoQ10 supplementation ahs also been studied for its possible role in a variety of other health concerns ranging from diabetes to liver disease, complications from drug addiction, and irritable bowel syndrome.