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Coenzyme Q10 Supplementation Improves Outcomes In Early Parkinson’s Disease

 James Meschino DC, MS, ROHP

 In the October (2002) edition of Archives of Neurology, Clifford Shults et al, presented the findings of a clinical trial, which demonstrated that patients with early-stage Parkinson’s disease, who were give Coenzyme Q10 (CoQ10) supplementation for 16 months, showed significantly less impairment than did patients given the placebo.  The efficacy of treatment was readily apparent by the eight month, and the study showed that patients given the highest dose of CoQ10 had the best overall results.  The test doses of CoQ10 were 300, 600, and 1,200 mg per day.  The side effects of CoQ10 at these high doses were mostly mild and included back pain, headaches, and dizziness. Researchers indicate that the administration of CoQ10 is not aimed only at symptomatic relief, but rather addresses the underlying biochemical disorder(s) associated with the development of the disease. (1) The results indicate that follow-up research at perhaps even higher doses should proceed “pretty aggressively”, said Bernard Ravina of the National Institute of Neurological Disorders and Stroke, which funded the study.  (2)

In 1999, C. Shults and R. Haas first noted that Parkinson’s disease patients had reduced activity of complex I of the electron transfer chain in the area of the brain affected by Parkinson’s disease (substantia nigra, but not other areas of the brain) and in their blood platelets.  In blood platelets, the level of mitochondrial CoQ10 in Parkinson’s disease patients was shown to be approximately 141.8 ng/mgl protein on average, compared to the age/sex-matched control group of non-Parkinson disease patients, whose average CoQ10 level was 216.3 ng/mg protein.

The electron transfer chain within the mitochondrial membrane is the region in which ATP energy is produced from the aerobic metabolism of the macronutrients, carbohydrates, fat, and protein.  In oxidative phosphorylation, the hydrogen atoms stripped off from these macronutrients in the Kreb’s cycle are transferred to the cytochrome system within the mitochondrial membrane by NAD and FAD, which are derived from the B-vitamins niacin and riboflavin, respectively.  As the hydrogen electrons are shuttled down the cytochrome chain (similar to traveling down a staircase) from a high level of energy to lower levels of energy, the energy difference between each of the two steps is given off as free energy, which can be used to re-couple ADP with phosphate to form more ATP.  Like all other tissues, the substanita nigra of the brain requires an adequate supply of ATP energy in order to survive and function normally.  Within the mitochondrial membrane, CoQ10 acts as a hydrogen electron shuttle that literally escorts the hydrogen electrons from one cytochrome to the next cytochrome (from one step in the staircase to the next).  It specifically functions as an electron acceptor for complex I and complex II within the mitochondrial membrane.  As such, a decline in CoQ10 levels within the mitochondrial membrane results in a decreased ability to synthesize ATP, resulting in development of the type of cellular dysfunction, and cell death, found in Parkinson’s disease. Animal studies clearly show that CoQ10 supplementation protects mice from the development of Parkinson’s disease by the neurotoxin MPTP, which is known to produce Parkinson’s disease in the mice model.  (3)

A number of researchers now indicate that a significant aspect of the genetic component of Parkinson’s disease is an inability to synthesize adequate amounts of CoQ10, and that supplementation with CoQ10 can compensate for this genetic defect and potentially halt the onset or further progression of the disease.

  1. Shults et al previously showed that Parkinson’s disease patients could absorb supplemental CoQ10 with a trend towards increasing complex I activity within the mitochondrial membrane, and in theory, reverse the underlying defect in Parkinson’s disease by facilitating more optimal synthesis of ATP energy within the mitochondria of the substantia nigra. (3) These previous investigations led to the clinical trial reported in the October (2002) edition of The Archives of Neurology, which was the first placebo-controlled study to show that CoQ10 supplementation can halt the progression of early-stage Parkinson’s disease in human subjects. However, this study involved only 80 subjects in total (40 in the CoQ10 group and 40 in the placebo group). The impressive finding of the study has paved the way for larger studies to follow that should more clearly establish the degree to which CoQ10 supplementation may be useful as a treatment for this disease and possibly as a preventive agent in high-risk populations (e.g., those displaying low levels of CoQ10 synthesis upon genetic testing of CoQ10 synthetic enzymes).  (1,2)

It is also noteworthy that CoQ10 is a fat-soluble antioxidant, which scavenges free radicals within the mitochondrial membrane.  Oxidative stress (free radical damage) has also been shown to contribute to the cellular dysfunction, and cell death, seen in Parkinson’s disease.  Animal studies demonstrate that CoQ10 supplementation can prevent the damage induced by various neurotoxins that are known to produce Parkinson’s disease, Amyotrophic Lateral Sclerosis, and Huntington’s disease.  This preventive effect has been shown to involve the antioxidant properties of CoQ10 acting as a vital fat-soluble free radical scavenger within the mitochondrial membrane – a place where a great deal of oxygen free radicals are created each moment of our lives during aerobic energy production. (3,4)

It is also compelling to note that Parkinson’s disease primarily afflicts individuals over the age of 50, which correlates with the phase in life when most people experience an age-related decline in CoQ10 synthesis to some degree.  This appears to be due to a genetically controlled program, which produces a decline in the activity of CoQ10 synthetic enzymes as we age.  This age-related decline in CoQ10 synthesis has been associated with an increased risk of congestive heart failure (due to reduced ATP synthesis by the heart muscle), and some studies show that CoQ10 supplementation has been effective in reversing this condition in a significant number of congestive heart disease patients and in patients with other cardiomyopathies.  (5,6,7,8,9,10) Many anti-aging experts suggest that all adults should take at least 60 mg per day of CoQ10 as an anti-aging, disease prevention supplement once over the age of 45 or 50.  Support for this argument appears to be strengthened by the recent study involving Parkinson’s disease patients, as Parkinson’s disease afflicts one million people, many of whom are over the age of 50, but the incidence of the disease in younger people is increasing at an alarming rate, according to the American Parkinson’s Disease Association. (11)

Shults, (M.D.) C.W. et al. Effects of Coenzyme Q10 in Early Parkinson Disease. Archives of Neurology; Vol.59, No.10: October 2002.

  1. Study: Dietary supplement may slow Parkinson’s.
  2. Shults, Clifford W, Haas, Richard H. A possible role of coenzyme Q10 in the etiology and treatment of Parkinson’s disease. Biofactors, 1999, Vol.9, Issue 2-4; p.267
  3. Beal, M.F. Coenzyme Q10 as a possible treatment for neurodegenerative diseases. Free Radical Research. April 2002; 36(4): pp.455-60
  4. Folkers, K. Heart failure is a dominant deficiency of Co-enzyme Q10 and challenges for future clinical research on Co Q10. Clinical Investigator 1993; 71 (& suppl): S51-54
  5. LiHarru, G.P., Ho, L and Folkers, K. Deficiency of Co-enzyme Q10 in human heart disease. Part II. Int J Vit Nutr Res 42, 413, 1972
  6. Folkers, K. et al. Biochemical rationale and myocardial tissue data on the effective therapy of cardiomyopathy with Co-enzyme Q10. Proc Natl Acad Sci 82, 901, 1985
  7. Kitamua, N., et al. Myocardial tissue level of Co-enzyme Q10 in patients with cardiac failure in: Biomedical and Clinical Aspects of Co-enzyme Q10, Vol. 4 (Folkers, K. and Yamamura, Y eds.) Elsevier Science Publ. Amsterdam, 1984, pp. 243-252
  8. Langsjoen, H., et al. Usefulness of Co-enzyme Q10 in clinical cardiology: A long-term study. Mol Aspects Med 15 (suppl), S165-175, 1994
  9. Greenberg, S. Co-enzyme Q10: a new drug for cardiovascular disease. J Clin Pharm 1990; 30, 7: 596-608
  10. Sahelian, Ray. Supplements for Parkinson’s Disease? Better Nutrition. October 2000; Vol.62, Issue 10: p.24


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