For the many victims of Parkinson's disease associated with the use of statin drugs, recent research from the Institute of Neurology, London sheds light on a possible mechanism. In "Neuroscience Letters" recently, Hargreaves and team published their studies of CoQ10 levels in blood and tissue from the brain regions of people with Parkinson's disease (PD).
Although abundant evidence exists of lowered CoQ10 levels in peripheral blood no studies have assessed the CoQ10 status of the PD brain prior to this.
Since the widespread use of statin drugs, cases of Parkinsonism have been noted to occur after the start of statin therapy. With the well-known side effect of statin therapy being substantial reductions in CoQ10 synthesis, one naturally must consider the possibility of statin causation in these statin associated PD cases.
Until now we have had only peripheral blood level to guide our thinking. Now with tissue CoQ10 levels coming from the very areas involved in Parkinson's disease, especially from the substantia nigra, the concept of statin causation is suggested.
One must realize that nearly every cell in our bodies has the capacity to synthesize certain vital biochemicals on demand. Just as glial cells of the brain synthesize brain cholesterol using its mevalonate pathway, so does this same mevalonate pathway allow for the synthesis of CoQ10, dolichols and other vital components for life.
In this study they investigated the CoQ10 status of the substantia nigra, cerebellum, cortex and striatum brain regions of both PD patients and age-matched controls. The results of this study indicate a significant reduction (p=0.007) in CoQ10 concentration in the cortex region of the brain. In conclusion, the results of this study indicate evidence that a deficit in brain CoQ10 status may be involved in the pathophysiology of Parkinson's.
Therefore statins, with their ability to block mevalonate pathway cholesterol synthesis, must also block the synthesis of CoQ10. The result is a number of side effects relating to the important role of CoQ10 in the function of our bodies.
Not only is CoQ10 a vital component of our energy producing oxidative phosphorylation (OXPHOS) system in each of our cells, it also has a major anti-oxidation role to neutralize the free radicals resulting from this OXPHOS reaction. Without this our mitochondrial mutation rate increases dramatically resulting in permanent functional change.
As a result, there is increasing evidence that impairment of mitochondrial function and oxidative damage secondary to CoQ10 deficiency are contributing factors to the
pathophysiology of Parkinson's disease.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor