BACKGROUND:Neurodegenerative diseases are characterised by damage to nerve cells. They include Alzheimer's, Parkinson's and Huntington's diseases, and amyotrophic lateral sclerosis (ALS). Each has somewhat different symptoms, but they are related in having a significant impact on mental health. They also have similar underlying defects that involve mitochondria and oxidant levels.
Mitochondria are the “power houses” of all cells. Coenzyme Q10, also called CoQ10 or ubiquinone, is required for mitochondria to work properly and is an antioxidant. People normally produce enough CoQ10, but can get small amounts from foods such as oily fish, liver and whole grains.
Numerous claims have been made about the benefits of CoQ10 supplementation. These initially focused on improving energy levels and treating heart failure. With the connection made between neurodegenerative diseases and mitochondria, attention has focused on using CoQ10 to prevent or treat these disorders.
The link between CoQ10 and Parkinson’s disease was made through a tragic chance discovery. In 1982, six young adults from Southern California were diagnosed with Parkinson’s disease. The real-life CSI-like story identified the cause as a contaminant in an illegal “designer drug” they had all used. This story is documented in The Case of the Frozen Addicts.
The contaminant was called MPTP and has since become an important tool in research on Parkinson’s. Part of what was discovered is that MPTP has its damaging effects within the mitochondria in the same processes that require CoQ10. This led to much interest in whether supplemental CoQ10 could prevent or treat the mitochondrial damage that underlies this group of neurological disorders.
EVIDENCE FROM STUDIES
CoQ10 was shown to slow down the damaging effects of MPTP given to rats. Other animal research produced promising results with other neurodegenerative diseases. Then 80 patients in the early stages of Parkinson’s were enrolled in a randomised, double-blind study. Those taking 1200mg CoQ10 had significantly slower deterioration over 16 months. But a larger study (with 131 patients) found no significant differences between those taking CoQ10 or a placebo. Other trials have found that while patients’ CoQ10 levels are increased with supplements, symptoms did not improve.
To provide more clear-cut evidence, the US National Institutes of Health funded the largest controlled trial in this area, of 600 people with Parkinson’s. The study was terminated after an interim analysis showed that it would be futile to continue. The conclusion was that CoQ10 provided no benefits to Parkinson’s patients.
Huntington’s disease also involves mitochondrial defects, but their precise role is unclear. A randomised controlled trial with more than 300 Huntington’s disease patients found some beneficial effects from CoQ10 compared to placebo. But the differences between the groups were small and not statistically significant. This study used a daily 600mg dose and further research has focused on whether higher doses are safe in patients with Huntington’s. Results suggested that 2,400mg/day is safe.
PROBLEMATIC ASPECTS
CoQ10 has been found to be safe in clinical trials. The most common adverse effects are gastrointestinal, affecting less than one per cent of people. The most common symptoms are nausea, diarrhoea or heartburn.
RECOMMENDATIONS
CoQ10 is a powerful antioxidant, so supplements may be generally beneficial. People normally produce sufficient CoQ10, although some have a rare genetic disorder where CoQ10 production is insufficient. CoQ10 supplements benefit such patients, but the underlying connection between neurodegenerative diseases, mitochondria and CoQ10 is suggestive. Clinical trials have not provided clear evidence of benefit, especially for those with Parkinson’s disease. Whether CoQ10 will be beneficial for those with other neurodegenerative diseases remains to be seen.
Dónal O’Mathúna has a PhD in pharmacy, researching herbal remedies, and an MA in bioethics, and is a senior lecturer in the School of Nursing Human Sciences at DCU
