Here is a very new study on the value of Co-enzyme Q10 in cellular energy production in the mitochondria (ref) (power plants of cells) of the heart:
"Atherosclerosis. 2011 Feb 17. [Epub ahead of print]
Dai YL, Luk TH, Yiu KH, Wang M, Yip PM, Lee SW, Li SW, Tam S, Fong B, Lau CP, Siu CW, Tse HF.
Cardiology Division, Department of Medicine, The University of Hong Kong, Hong Kong.
AIMS: Coronary artery disease (CAD) is associated with endothelial dysfunction and mitochondrial dysfunction (MD). The aim of this study was to investigate whether co-enzyme Q10 (CoQ) supplementation, which is an obligatory coenzyme in the mitochondrial respiratory transport chain, can reverse MD and improve endothelial function in patients with ischaemic left ventricular systolic dysfunction (LVSD).
METHODS AND RESULTS: We performed a randomized, double-blind, placebo-controlled trial to determine the effects of CoQ supplement (300mg/day, n=28) vs. placebo (controls, n=28) for 8weeks on brachial flow-mediated dilation (FMD) in patients with ischaemic LVSD(left ventricular ejection fraction <45%). Mitochondrial function was determined by plasma lactate/pyruvate ratio (LP ratio). After 8weeks, CoQ-treated patients had significant increases in plasma CoQ concentration (treatment effect 2.20μg/mL, P<0.001) and FMD (treatment effect 1.51%, P=0.03); and decrease in LP ratio (treatment effect -2.46, P=0.03) compared with controls. However, CoQ treatment did not alter nitroglycerin-mediated dilation, blood pressure, blood levels of fasting glucose, haemoglobin A1c, lipid profile, high-sensitivity C-reactive protein and oxidative stress as determined by serum superoxide dismutase and 8-isoprostane (all P>0.05). Furthermore, the reduction in LP ratio significantly correlated with improvement in FMD (r=-0.29, P=0.047).
CONCLUSION: In patients with ischaemic LVSD, 8weeks supplement of CoQ improved mitochondrial function and FMD; and the improvement of FMD correlated with the change in mitochondrial function, suggesting that CoQ improved endothelial function via reversal of mitochondrial dysfunction in patients with ischaemic LVSD." --end of copy
Copyright © 2011
CoQ10 also appears to have benefits in neurodegenerative conditions. ref ref
MITOCHONRIA Clarification
A few points about mitochondrial functions are necessary. Mitochondria produce energy for the host cell, such as muscles and nerves. ref In return, the cell uses some of that energy to protect the mitochonria against oxidation attacks. The waste products of energy production produce free radicals such as ROS, reactive oxygen species. Cellular antioxidants reduce the potentially damaging ROS to a safer form. Some ROS is used for beneficial functions. CoQ10 helps supply electrons for the energy process inside mitochondria plus also helps cells with antioxidant actions against radicals.
With age, both the number of mitochondria in cells and their level of energy production suffer reductions. A vital point here is that along with this reduction of energy comes a loss of protection against radicals since the cells have less energy for this function to supply the needed antioxidant elements. CoQ10 levels also reduce with age.
ROS are simply free radicals normally and naturally produced by energy production since oxygen is involved. While CoQ10 helps this energy process, it is the reduced number of mitochondria that jeopardizes health. CoQ10 needs to be balanced within certain levels. The best way to maintain mitochondrial numbers and energy production is by exercising to maintain (or build) muscle, or by calorie restriction. PQQ potentially has value to increase mitochondria too. There are some balance points for these processes that are still to be determined. Whether or not to supplement plus amounts for CoQ10 supplement are still all in debate. article Both too little and too much CoQ10 exhibit adverse effects.
CAUTION FOR STATIN DRUG CONSUMERS
Please read this article from FDA research. Article starts on second page. Here Are findings on CoQ10 production influence. Also included FDA precautions for Statins, but no CoQ10 link.
"The peer-reviewed scientific evidence supports the following findings:
1. Statins block the endogenous biosynthesis of both cholesterol and CoQlo by inhibiting the enzyme HMG CoA reductase, thus decreasing mevalonate, the precursor of both cholesterol and CoQi0.
2. CoQloisessentialformitochondrialATPproductionandisapotentlipidsolubleantioxidant present in cell membranes and carried in the blood by LDL. CoQl0 is biosynthesized in the body and available fiom dietary sources.
3. Statin-induceddecreasesinCoQloaremorethanjusthypotheticaldrug-nutrientinteractions. Good evidence exists of significant CoQlo depletion in humans and animals during statin therapy.
4. Scientificevidenceconfirmstheexistenceofdetrimentalcardiacconsequencesfromstatin- induced CoQlO deficiencies in man and animals.
Dr. Langsjoen’s curriculum vitae is attached.5. Statin-induced CoQl0 deficiency is dose related and the clinical consequences are notable most in the elderly and in settings of pre-existing congestive heart failure (CHF).
6. Statin-inducedCoQIOdeficiencycanbecompletelyreversedbysupplementalCoQl0.
7. Supplemental CoQl0 is safe and has no adverse effect on statin cholesterol-lowering or on statin anti-inflammatory effects.
8. We are in the midst of a congestive heart failure epidemic in the United States. Approximately 4.8 millions Americans are diagnosed with congestive heart failure. Half of those patients will die within 5 years. Each year, there are an estimated 400,000 new cases of CHF (Congestive Heart Failure Data Fact Sheet, www.nhlbi.nih.gov/health/public/heart/other).Although the causes of this epidemic are unknown, statin-induced CoQl0 deficiency has not been excluded as a possible contributing
factor.
9. All large-scale statin trials excluded patients with NYHA class I11 and IV heart failure such that the long term safety of statins in patients with heart failure has not been established."
NOTE: Increasing CoQ10 limits the oxidation of LDL cholesterol lipoproteins, a feat that vitamin E by itself might not accomplish. A heart disease study testing just vitamin E might not show much benefit compared to a study adding CoQ10 with vitamin E. ref ref
This next reference looked at the results of adding to the body vitamin E and CoQ10 for 5 days before taking LDL cholesterol cells out to test their ability to withstand metal oxidation. The pre-treated CoQ10 and vitamin E cells exhibited greater resistance to oxidation. The vitamin E only pre-treated LDL cholesterol cells actually showed less resistance to this type of oxidation at the vitamin E tested level, 1000mg. for 5 days. It appears at this level, the vitamin E acted like a pro-oxidant rather the as an anti-oxidant. Here is an explanation that shows vitamin E only effective against one of four possible oxidation processes. The CoQ10 level tested was 100 mg of ubiquinol, QH.