by Duane Graveline, MD, MPH
The oxygen concentration in the air we breath is 20.9%. At first there was no atmospheric oxygen on our planet, then came photosynthetic bacteria, slowly adding oxygen to the atmosphere. Only after passage of eons was the oxygen level sufficient to support multi-cellular organisms and, finally, humans.
We are entirely dependent upon oxygen for energy production, yet oxygen, the magic substance of life, is also very toxic. Paradoxically, oxygen is both friend and foe.
Most of us are unfamiliar with its toxic role. As a former USAF flight surgeon, I early on recognized the toxicity of oxygen in studying the consequences of breathing high concentrations of oxygen for long time periods.
As a vital friend, oxygen is the final acceptor of the energy electrons derived from the food we eat. Food is the source of energy, but it is not biologically useful until it is converted into a form that our cells can use.
Electrons are the medium of energy exchange for every living thing. Our mitochondria contain the electron transport chain, passing electrons from food along from one receptor to another until, combined with oxygen, water is formed and ATP (Adenosine triphosphate - the energy currency for cells ) results.
As a formidable foe, oxygen, so abundant and vital to mitochondrial function, is inevitably transformed during metabolism into highly reactive intermediates called reactive oxygen species (ROS). This is a natural, daily part of deriving energy from foods but it is also where the toxic damage begins. Our mitochondria are the primary focus of this kind of damage.
Ordinarily we have several very effective anti-oxidant systems, such as coenzyme Q10, defending us against oxidative attack by ROS but their effectiveness falls off with age and state of health.
It is these reactive products, in excess of our ability to correct them, that are the direct cause of damage to adjacent proteins, enzymes, lipids and DNA strands. The result: mitochondrial mutations, aging and chronic diseases of all kinds, including progressive muscle weakness, an abnormal enlargement and deterioration of the heart muscle, movement problems, and cognitive dysfunction, to name but a few.
What these conditions have in common is one or more defects in mitochondrial DNA, resulting in fewer or abnormal proteins being produced that are critical for proper mitochondrial function. Accordingly, mitochondrial function in the affected tissue, be it skeletal or heart muscle, the brain, or the optic nerve, and often throughout the entire body, is dramatically impaired.
Introduce a statin drug and the entire energy equation shifts into excess ROS production, for when a statin is started, tissue CoQ10 is reduced very substantially ( some estimate as much as 50% ).
No longer can anti-oxidation systems keep pace with the ROS demand, resulting in the formation of excess mitochondrial mutations.
As if this were not sufficient to cause havoc in our DNA, statins also deplete dolichols having the responsibility, among other things, of overseeing the synthesis of glycoproteins known as glycohydrolases, vital to the daily task of detection and correction of DNA errors.
Not only do we produce more damage but we become less able to correct this damage when on statins. The reason for this special effect of all statin drugs is that they are all reductase inhibitors, and since the vulnerable reductase biochemical step is at the very beginning of the mevalonate pathway, statins inevitably block this pathway.
That is the path the pharmaceutical industry has chosen to decrease cholesterol synthesis and it works. Unfortunately, cholesterol is not the only vital substance synthesized by the mevalonate pathway - CoQ10, dolichols, Rho, nuclear factor kappa B and normal phosphorylation also use this same pathway.
The consequences of blocking these vital substances are formidable on the basis of what we already know but we are only just beginning to learn the full spectrum of adverse reactions.
In a manner of speaking we have all been guinea pigs for the drug companies. Even cholesterol, the ultimate target for statin development, has vital functions previously unknown. Not only is it essential for memory function but cholesterol plays a key role in cell messaging and identification and controls the so-called lipid rafting function of cell transmissions. Not bad for 'public health enemy number one.'
To the normal source of mitochondrial mutations associated with aging and chronic disease are added the dire consequences of mevalonate blockade by statins.
When doctors tell their concerned patients about their muscle aches and pains after being on a statin, "You have to expect this kind of thing now, you are over fifty," they unknowingly are coming very close to the truth, for the statin drugs, in a manner of speaking, are causing premature aging.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Updated April 2016