By Duane Graveline, M.D., M.P.H.
CoQ10 (ubiquinone) is arguably our most important essential nutrient. Its role in energy production is to make possible the transfer of electrons from one protein complex to another within the inner membrane of our mitochondria in the formation of ATP.
The adult human body pool of this substance has been reported to be 2 grams and requires replacement of about 0.5 grams per day. This must be supplied by endogenous synthesis or dietary intake. Synthesis decreases progressively in humans above age 21 and the average ubiquinone content of the western diet is less than 5 mg/day. Thus, CoQ10 supplementation appears to be the only way for older people to obtain their daily need of this important nutrient.
Nearly 50 million people will be taking statin drugs this year in the United States alone. Most of these people will be over 50 years of age. Few of them will be on supplemental CoQ10. Simple logic dictates that the impact of lack of CoQ10 bio-availability on mitochondrial energy production will be profound as we age.
Because of the extremely high-energy demands of the heart, this organ is usually the first to feel CoQ10 depletion as cardiomyopathy and congestive heart failure. The importance of mitochondrial function in meeting the energy needs of the heart has been emphasized recently because of the increasing tendency for congestive heart failure (CHF) in statin drug users.
Peter Langsjoen, a well-known cardiologist, has published a series of excellent articles on this subject and reviewed the prevalence of statin associated CHF in many controlled studies, reporting on the prompt response of CHF to supplemental CoQ10 or reductions in statin dosage.
My investigations these past 8 years into the mechanism of action of the statin class of drugs has come at the same time the research community has been directing its attention to the effects of mitochondrial mutations on aging.
Natural aging is associated with progressive reduction in bioavailability of CoQ10 in the energy equation and also to the powerful anti-oxidant role of CoQ10. Interesting how many of the side effects of statins are those of premature aging along with its host of infirmities.
Ubiquinone in a slightly altered form known as ubiquinol is found in all membranes where it has a vital function in maintaining membrane integrity. Liver inflammation, with breakdown of liver cells releasing their enzymes into the blood stream and thereby serving as a marker of statin damage, is likely due, at least in part, to loss of cell wall integrity.
Ubiquinone is also vital to the formation of elastin and collagen formation. Tendon and ligament inflammation and rupture are frequently reported in the elderly and it is likely that the mechanism of this predisposition to damage is related to some as yet unknown compromise of ubiquonine's role in connective tissue formation.
There is another thoroughly documented role for CoQ10 just as important as mitochondrial energy production and cell wall integrity. That is its role within the mitochondria as a powerful anti-oxidant, with a free radical quenching ability some 50 times greater than that of vitamin E.
Without adequate stores of CoQ10 and lacking the repair mechanisms common to nuclear DNA, irreversible oxidative damage to mitochondria DNA results from buildup of superoxide and hydroxyl radicals.
We must remember that our mitochondria are in immediate contact with oxygen, front line warriors so to speak in the struggle to obtain life-giving oxygen without sustaining excessive oxidative damage. The inevitable result of excessive free radical accumulation is an increase in the rate of mitochondrial mutations.
It is only in the past few years that researchers have discovered the cumulative effect of somatic mitochondrial mutations and their direct impact on aging.
Our mitochondria already have a mutation rate some 4-5 times greater that that of nuclear DNA. Remember, our mitochondria despite their role and ubiquitous nature are originally alien to our cells.
Somehow, a stray mitochondrium was incorporated into one of our cells eons ago and the result was so favorable to both organisms, this mitochondrial equipped eukaryotic cell has created most of subsequent life as we know it.
Mitochondria have this distinct character that gives them both their own DNA and their own mutation rate, which, incidentally, now is the darling of anthropological researchers on our origins, migrations and the like.
With this high mutation rate, they are very sensitive to excess free radicals, the chemically very active products of oxidation. So in cases of insufficient CoQ10, we have less anti-oxidation resources to fight this free radical formation and the result is chaos in the structure of our mitochondria, leading to mutations.
The end result is less ATP and altered function in high energy tissues - brain, heart, eyes, kidney and muscles.
CoQ10 supplementation should be the first place we look for mitochondrial maintenance and repair.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Updated November 2015