

By Duane Graveline, MD, MPH

Abundant research evidence now exists in the medical literature indicating that diminished mitochondrial function, through excess oxidation, occurs inevitably as we age and is a major factor in fatiguing illnesses.

This is a reflection of progressive loss of efficiency in the electron transport chain. This degradation appears to be naturally associated with the process of aging and is the primary mechanism in the fatigue of many chronic diseases.

One of the most important changes in tissues and cells that occurs during aging and chronic degenerative disease is accumulated oxidative damage due to cellular reactive oxygen species (ROS).

ROS are oxidative and free radical oxygen- and nitrogen-containing molecules, such as nitric oxide, oxygen and hydroxide radicals and other molecules. Critical targets of ROS are the genetic apparatus with its susceptibility to mutations and cellular membranes and in the latter case, oxidation can affect lipid fluidity, permeability and membrane function. Similar changes occur in fatiguing illnesses, such as chronic fatigue syndrome (CFS), where patients show increased susceptibility to oxidative stress.

The major consequence of excess oxidation is excess mitochondrial damage. Not only is the rate of damage increased as we age but our ability to identify and replace mitochondrial DNA defects degrades.

Another important change caused by accumulated ROS damage during aging and in fatigue is loss of electron transport function, and this appears to be directly related to mitochondrial membrane lipid oxidative change, which can induce permeability changes in mitochondria and loss of transmembrane potential and oxidative phosphorylation.

A major contributor to this excess accumulation of oxidative damage is Coenzyme Q10 deficiency, the principle anti-oxidant to mitochondrial function. Our ability to synthesize CoQ10 progressively falls with age and by midlife, most of us are completely dependent on external sources of this vital substance.

It is difficult to overstate the importance of this powerful anti-oxidant for in addition to its role as suppressor of ROS accumulation, it also is vital for cell wall integrity and is a necessary element of our electron transport system.

Every cell in the human body requires energy in the form of adenosine triphosphate, or ATP. No CoQ10 – no ATP, says it all. Few, if any, seniors have the CoQ10 adequacy of when they were 30. Supplementation is not only important for this group but critical for most.

The use of statin drugs greatly enhances this problem by two mechanisms. The first is by the inevitable inhibition of CoQ10 synthesis by this class of drugs. This is what reductase inhibitors do! To reduce cholesterol, statin drugs block the mevalonate pathway, critical to the synthesis of such vital substances as CoQ10 and dolichol.



