Life Extension Magazine February 2003
Should Parkinson's patients take CoQ10?
Neurologist M. Flint Beal and colleagues at the Massachusetts General Hospital and Harvard Medical School has spent years proving that coenzyme Q10 has neuro-protective properties that may help diseases such as Parkinson's and Huntington's. Dr. Beal has a growing body of research to support his hypothesis.12 Earlier research had established that patients with early, untreated Parkinson's disease have reduced activities of the electron transport complexes I and II/III in mitochondria from platelets, which seems to be attributable to the Parkinson's disease process.13 For example, results indicated that complex II/III activity was reduced by 20% in Parkinson's disease compared with age-/sex-matched controls.
In a later study, oral supplementation with coenzyme Q10 in one-year old mice attenuated MPTP (1-methyl-4-phenyl-1,2,3,tetrahydropyridine) mediated neurotoxicity, which has been shown to cause a parkinsonian syndrome in test animals.14 The researchers put four groups of one-year-old male mice on either a standard diet or a diet supplemented with coenzyme Q10 for five weeks. At four weeks, one of the standard diet groups and one of the supplemented groups were treated with MPTP. Striatal dopamine concentrations and dopaminergic axon density were reduced in both MPTP-treated groups, but they were much higher, 37% and 62%, respectively, in the group first treated with coenzyme Q10 and then MPTP compared to the group treated with MPTP alone.
Beal's team also demonstrated in middle-aged and old-aged rats, that coenzyme Q10 administration could restore levels of the nutrient to those of younger rats. The results showed that coenzyme Q10 levels rose by 10% to 40% in the mitochondria of the cerebral cortex region of the brain.14 What many people don't understand is that increasing serum or tissue levels of a nutrient through oral administration doesn't necessarily translate into some measurable disease-fighting or anti-aging benefit. That's what made this study's findings so promising. They showed that two months of supplementation resulted not only in replenished coenzyme Q10 levels in the brain and the brain mitochondria, but also in a significant increase of 29% in mitochondrial energy expenditure in the brain. Moreover, topping up coenzyme Q10 levels helped counter the neurodegenerative effects of an experimental neurotoxin administered to the dopamine-producing (striatal) region of the brain in the test rats.
The same study also showed that coenzyme Q10 might help other neurodegenerative diseases, such as Huntington's and amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease). The researchers found that the administration of coenzyme Q10 could restore concentrations, prevent nerve-cell degeneration, and extend survival in transgenic mice bred with a familial form of ALS genes.
Meanwhile, a pilot study showed that energy production in the central nervous system and muscle of Huntington's disease patients is impaired. But two or more months of coenzyme Q10 supplementation at 360 milligrams per day resulted in significant improvements in biochemical markers of energy production in 83% of patients.
Additional research findings suggest that coenzyme Q10 supplementation may also help various forms of ataxia, particularly cases that show a decreased level of coenzyme Q10 in their muscles. For example, UK scientists at the University of Oxford found marked improvements in mitochondrial defects among Friedreich's ataxia (FA) patients, which involve a deficiency of a mitochondrial protein called frataxin. Six months of antioxidant treatment with coenzyme Q10 (400 milligrams/day) and vitamin E (2100 IU/day) in 10 Friedreich's Ataxia patients resulted in a 178% increase in the cardiac phosphocreatine to ATP ratio and 139% increase in the maximum rate of skeletal muscle mitochondrial ATP production. These results were observed after only three months of treatment, and were sustained after the six month study was completed.15
In another example, a study of six patients with hereditary ataxia revealed baseline coenzyme Q10 levels that were 70% below normal.16 However, following daily supplementation with coenzyme Q10, ranging from 300 milligrams to 3,000 milligrams, all of them had improved strength, ataxia and fewer seizures, and some were even able to walk. After a year of supplementation, patient scores on an ataxia symptom scale improved by an average of 25%.
Despite the hail of good news regarding the usefulness of coenzyme Q10 for Parkinson's and other neurodegenerative diseases, the mood among researchers is one of cautious optimism. For example, even Shults, lead author of the latest study, suggests that, before recommending coenzyme Q10 supplementation for Parkinson's disease patients, he would like to conduct a larger study, one that will more definitively determine coenzyme Q10's effects, especially in high doses. That upcoming study will likely involve about 400 patients taking doses of over 1200 milligrams per day for a longer study period.
Meanwhile, the National Institute of Neurological Disorders and Stroke, which helped fund the study, said that findings were "very promising," but called it premature to recommend coenzyme Q10 to Parkinson's patients until a larger trial is done. Scientists are also concerned about the purity of commercial CoQ10 supplements (i.e. how much coenzyme Q10 is actually in a product?), and what risks may exist as far as side effects, drug interactions and other contraindications. These scientists believe that more data is necessary in order to establish safe and effective doses of coenzyme Q10 for neurodegenerative diseases.
While the ideal or most effective dose cited in the latest study is 1200 milligrams daily, that's five times the upper dose consumed for prevention purposes. There is, however, strong historical data regarding the safety of congestive heart failure patients taking about 300 milligrams a day of coenzyme Q10 and those suffering from Huntington's disease using 600 mg/day.
Why Parkinson's patients can't wait
Parkinson's disease is a progressive degenerative brain disorder that is currently incurable. Patients suffer increasing debilitating complications as the disease progresses. Today's therapies only mitigate the agonizing symptoms-they do not slow the rate of deterioration.
Even when treatments such as "Deep Brain Stimulation" become widely available, the benefits may only be partial. It is thus imperative for Parkinson's patients to protect as many dopamine-producing neurons as possible. The latest study indicates that high-dose coenzyme Q10 does just that.
While this is the first human study using coenzyme Q10 to treat Parkinson's disease, it was based on a large body of previously published research. For instance, a year 1998 study published in the Proceedings of the National Academy of Sciences17 concluded that "CoQ10 can exert neuroprotective effects that might be useful in the treatment of neurodegenerative diseases."
Parkinson's patients don't have the option of waiting for mainstream medicine to reach a consensus about coenzyme Q10. There are, however, sensible approaches that Parkinson's patients can follow to reduce any possible risk of taking high-dose coenzyme Q10.
For example, many healthy Life Extension members have been taking 300 mg a day and higher of coenzyme Q10 without encountering adverse effects. A Parkinson's patient may consider starting at 300 mg a day and then increasing to 600 mg two weeks later. If any prescription drugs are being taken, it is important to make sure this high dose of coenzyme Q10 will not create the need for a dosing adjustment. For instance, if Coumadin is being used, the weekly or bi-weekly coagulation blood tests that Coumadin patients are supposed to have can determine if additional Coumadin is needed.
After taking 600 mg a day of coenzyme Q10 for two weeks, a Parkinson's patient may want to increase the dose to 900 mg a day, and again make sure there is no prescription drug interference. After the 900mg/day dose has been established as being safe, the Parkinson's patient can increase the dose of coenzyme Q10 to 1200 mg a day. For maximum absorption into the bloodstream, always take coenzyme Q10 supplements with the fattiest meal of the day. Notify your doctors that you are taking this high dose of coenzyme Q10 so that they can monitor the effects of other drugs you are taking. It should be noted that while this cautious approach is prudent, Parkinson's patients participating in the most recent study were started at 1200 mg a day of CoQ10 with no significant side effects reported.
It is important to remember that coenzyme Q10 does not reverse Parkinson's disease, nor does it alleviate symptoms. The only effect that has been shown is that it slows disease progression. Parkinson's patients will still need to take medications to alleviate symptoms.
What has intrigued scientists the most is that coenzyme Q10 may help prevent common neurodegenerative diseases. If this turns out to be true, then healthy people may want to consume a higher dose of coenzyme Q10, perhaps as much as 300 mg a day.
Considering that initial studies from Japan showed as little as 30 mg a day of coenzyme Q10 was effective in the treatment of congestive heart failure, the fact that much higher doses do not produce side effects demonstrates the safety of this natural agent.
The body synthesizes abundant quantities of coenzyme Q10 in youth, but aging and the use of certain drugs (statins) causes a precipitous reduction in coenzyme Q10 production. This decline in coenzyme Q10 correlates with the many degenerative diseases that aging humans confront, including Parkinson's.
In response to this new study showing that 1200 mg a day of coenzyme Q10 slowed the progression of Parkinson's disease by 44%, commercial supplement companies are expected to bring out higher-potency CoQ10 capsules.
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