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Should Parkinson's Disease Patients Take CoenzymeQ10?
 


[Potential Parkinson's Disease Treatments]
[Significantly Delay the Progression of Parkinson's Disease]
[Other Parkinson's Disease Related Studies that Support these Results]
[CoQ10 Benefits Diseases Related to Parkinson's Disease]
[Research Progresses Methodically]
[Should a Parkinson's Patient Wait 5-10 years for Conclusive Data?]
[References]
[
Latest News - CoenzymeQ10 fights Parkinson's Disease]

Parkinson's disease is a degenerative disorder that afflicts more than 1 million Americans with muscle stiffness, trembling, slowed movement and poor balance. It appears to kill nerve cells in a brain region known as the substantia nigra, which produces dopamine, a biochemical key in physical movement.  As Parkinson’s disease progresses, an accelerated rate of cell death occurs, resulting in even less dopamine being produced and more pronounced complications. 

Standard recognized medical treatments available today only address symptoms.  These therapies don’t protect against the underlying pathologies in Parkinson’s disease, specifically the death of dopamine-producing neurons (brain cells).  Drugs such as L-Dopa provide dopamine to the brain and temporarily alleviate symptoms.  These drugs, however, do not slow the advance of the disease.  At advanced stages, the drugs do not work and complications become severe. 

Medical researchers are trying to determine why some people develop Parkinson’s disease while others do not.  One reason they are exploring is that low CoenzymeQ10 levels may make people more susceptible to Parkinson’s.  CoenzymeQ10 is naturally formed in the human body.  It is crucial in production of energy at the cellular level.  As people age, they naturally produce less CoQ10, which helps explain the increased risk of Parkinson’s disease with age. 1

In a 2002 Parkinson’s disease study, Yale researchers evaluated one of the dopamine transport characteristics of subjects ranging in age from 18 to 88.  They found that the striatal dopamine transporters, a marker of brain degeneration characteristic of Parkinson’s disease decreased as people got older.  The number of these Parkinson’s disease markers decreased by 46%, when comparing the oldest to the youngest subjects in the study.  This reflects a 6.6% decrease per decade of life.  This normal loss of dopamine transporters occurs faster in patients with Parkinson’s disease.  Some researchers are studying whether this age-related factor in Parkinson’s disease is caused by the known decrease in CoenzymeQ10 as people age, or by otherwise reduced levels of CoQ10 in some people.2

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Potential Parkinson’s Disease Treatments

Several potential therapies that might reverse the course of Parkinson’s disease are under investigation.  Stem-cell therapy has received the most publicity because it is easier to understand.  With this potential Parkinson’s disease therapy, the brain is repopulated with the dopamine-producing cells that are destroyed by Parkinson’s.  In this study, dopamine neurons derived from embryonic stem cells function in an animal model of Parkinson’s disease. 3

Another potential Parkinson’s disease therapy involves the surgical implanting of electrons in the brain to stimulate nerve impulses in the subthalmic nucleus.  A study published in Surgical Neurology in 2002 on this technique called “deep brain stimulation,” showed significant improvement in all motor function tests in 36 advanced Parkinson’s patients.  These Parkinson's patients were able to reduce their use of the drug L-Dopa by an average of 53%, with daily off-times reduced by 35%.  Deep brain stimulation therapy reportedly also reduced Dyskinesia, which is an impairment of voluntary muscle movement. 4,5

Altering the genes in brain cells responsible for causing motor abnormalities in Parkinson’s patients in another alternative being explored.  A gene transfer technique used in rat studies could be used to protect dopamine producing neurons and minimize the Parkinson’s disease symptoms.  The scientists who published this study in Science in 2002 indicated that this gene transfer method which showed benefits in rats should be beneficial for humans with Parkinson’s disease.6

By implanting a pump in the chest, and using a new drug-delivery method that sends proteins deep into the substantia nigra region of the brain, scientists at the University of Kentucky are having some success treating Parkinson’s disease.  These 10 Parkinson’s patients are undergoing glial cell line-derived neurophic factor (GDNF) delivery to the section of the brain where dopamine is produced.  So far, GDNF seems to both shield healthy brain cells from Parkinson’s disease and cause damaged cells to regenerate.  After just a few months of the treatment, the researchers are reporting evidence of improvement in Parkinson’s disease symptoms.  A similar trial is being conducted in England, where they report improved muscle control in all five Parkinson’s patients after a month of treatment. 

These experiments indicate a possible cure for Parkinson’s disease is on the horizon.  But Parkinson’s sufferers ask what can be done today to slow the progression of their disease or avoid the need for brain implants or chest implants, gene or stem cell therapy? 

More researchers are looking at CoenzymeQ10 as a potential Parkinson’s disease treatment.  Since CoQ10 acts as a critical energy carrier in mitochondrial electron transport, it also functions as an antioxidant to inhibit lipid peroxidation that kills dopamine producing neurons.7 

Coenzyme Q10 has been found to be useful as a neuroprotective agent for diseases marked by mitochondrial dysfunction.  This includes Huntington’s chorea, Fredreich’s ataxia, ALS (Lou Gehrig’s disease), and Parkinson’s disease.  CoQ10 is being studied as a potential treatment for early Parkinson’s disease, as well as in combination with another drug as a potential treatment for Huntington’s disease.8 

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Significantly Delay the Progression of Parkinson’s Disease

A nutritional supplement called CoenzymeQ10 can significantly delay the progression of Parkinson’s disease, slowing the degeneration of brain cells, a UC San Diego-led team reports.  Results of a new nationwide clinical trial show that Coenzyme Q10, a vitamin-like chemical, may be the first treatment that can fight the relentless degeneration caused by Parkinson's disease.  This may prolong the period that Parkinson’s patients can carry on normal daily activities. 9

Parkinson's disease patients who took a substance known as CoenzymeQ10 performed 44 percent better on exams for Parkinson's disease symptoms for intellectual and physical function than study volunteers who did not receive CoQ10.

In 1997, Dr. Clifford Shults and his University of California, San Diego team found Parkinson's disease patients are low in Coenzme Q10.  They found an average 35% lower level of CoQ10 in the mitochondria of Parkinson's disease patients than in the control group of similar aged people. At this time, Shults and team hypothesized: “The cause of Parkinson’s disease is unknown, however evidence suggests that mitochondrial dysfunction and oxygen free radicals may be involved in its pathogenesis.  The dual function of CoenzymeQ10 as a constituent of the mitochondrial electron transport chain and a potent antioxidant suggest that it has the potential to slow the progression of Parkinson’s disease.” 10

Coenzyme Q10 is made naturally in the body and is a coenzyme, aiding in metabolic processes as do vitamins.  In particular, CoQ10 helps the cellular mitochondria which produce energy for the cells of the body. 

In the Parkinson’s study reported in 2002, investigators studied 80 volunteers at 10 medical centers across the nation, and over the course of 16 months randomly gave patients four daily doses of wafers containing either zero, 300, 600 or 1,200 milligrams of CoQ10. Eight months into the study, patients receiving the highest doses of CoQ10 already fared significantly better than did other volunteers. Lower doses also slowed the progression of Parkinson's disease, though much less effectively.

The actual test results were based on the Unified Parkinson’s Disease Rating Scale (UPDRS), which is designed to measure Parkinson’s disease progression.  The lower the UPDRS scores, the better the performance.  Results showed a UPDRS score increased by 11.99 for the placebo group, 8.81 for the 300-mg /day group, 10.82 for the 600 mg/day group, and the lowest score of 6.69 for the 1200 mg/day group.  This reflects 44% less mental and physical disability for the 1200mg/day Parkinson’s patient group than the placebo group.  The test evaluated Parkinson’s patients’ basic motor skills, mental status, mood and behavior and the ability to perform daily living activities.  The Parkinson’s patients in the 1200 mg/day group were better able to function, and maintained greater independence for a longer time. 

Dr. Shults emphasized the disease "never stopped progressing," still the more CoQ10 a patient received, the slower the progression.

In comparison, existing treatments for Parkinson's disease, such as the drug levodopa, decrease in effectiveness over time.

In the future, researchers wish to see whether CoQ10 actually prevents damage to nerve cells in a larger study with hundreds of patients, perhaps with even larger doses of the nutritional supplement.

"This is a preliminary study that needs to be confirmed in larger populations before I can recommend people spend $1,500 to $2,500 a year on something that isn't proven to work," Dr. Clifford Shults, the lead researcher, explained.

The scientists presented their findings at the American Neurological Association's October 2002 annual meeting in New York City. The research also will appear in the Archives of Neurology.

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Other Parkinson’s Disease Studies that Support These Results

Researchers at Harvard Medical School and the Massachusetts General Hospital have provided corroborating results.  Led by neurologist M. Flint Beal, they have spent years proving that CoenzymeQ10 has neuro-protective properties that may help people with diseases such as Parkinson’s disease and Huntington’s disease. 

Dr. Beal’s team’s early studies established that Parkinson’s patients had reduced activities of the electron transport complexes in mitochondria.11   Later studies demonstrated that oral supplementation with CoenzymeQ10 in 1-year old mice yielded 37% and 62% higher levels of striatal dopamine concentrations.8   The Harvard team also demonstrated that Coenzyme Q10 oral administration in middle-age and old-aged rats could restore levels of the nutrient to that of younger rats. 

The importance of this research is two-fold.  The Harvard team demonstrated that CoenzymeQ10 supplements taken orally could replenish levels of Coenzyme Q10 in the brain mitochondria.  The Coenzyme Q10 was not destroyed in the digestive tract.  And secondly, increasing CoenzymeQ10 levels orally helped counter the neurodegenerative effects of reductions due to aging. 

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Coenzyme Q10 Benefits Diseases Related to Parkinson’s Disease

The Harvard studies also showed that Coenzyme Q10 might help other neurodegenerative diseases, such as Huntington’s and ALS (Lou Gehrig’s disease).  These studies demonstrated that oral administration of CoenzymeQ10 could restore concentrations in the brain, prevent nerve-cell degeneration, and extend survival in mice bred with a form of ALS genes.8

Research Progresses Methodically

Cautious optimism describes the mood among Parkinson’s researchers.  They know that theirs is a painstaking process.  For example, having established that the highest level of Coenzyme Q10 – 1200 mg/day – in the 2002 Parkinson’s disease study was the most beneficial, researchers must now exceed that level to yet find the optimum level.  Dr. Shults has expressed a desire to conduct a longer and larger study of Coenzyme Q10 effectiveness for Parkinson’s disease – searching for the optimal dosage, more definitively determine the effects, and establish any side effects from long-term, high-dosage use. 

The National Institute of Neurological Disorders and Stoke, which funded the 2002 Parkinson’s disease study, proclaimed the results very promising.  They called it premature to recommend CoenzymeQ10 to Parkinson’s patients until a larger trial is done.  General concerns include a question of side effects, drug interactions and other contraindications. 

While there were no reported side effects to Parkinson’s disease patients taking any dosage of CoenzymeQ10 during the 16-month UC San Diego study, the highest 1,200 mg/day dosage is five times the currently recommended upper dose for Parkinson’s disease prevention purposes.  There is, however, strong historical safety data from congestive heart failure patients taking doses of 300 mg/day Coenzyme Q10, and from those taking 600 mg/day for Huntington’s disease. 

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Should a Parkinson’s Patient Wait 5 – 10 Years for Conclusive Data?

Parkinson’s disease is a progressive degenerative brain disorder.  It is currently incurable.  Today’s treatments only lessen the agonizing symptoms – they do not slow the deterioration. 

Having electrodes implanted in one’s brain in treatments such as Deep Brain Stimulation is not something to look forward to.  Even so, when this becomes available, benefits of this type of Parkinson's disease treatment may not reverse the Parkinson's disease back to the patient’s condition today.  Thus, a Parkinson’s patient should protect as many dopamine-producing neurons as possible.  The UC – San Diego study indicates that high-dose Coenzyme Q10 does just that.  For the first time in medical history, a human study has shown that the progression of Parkinson’s disease can be slowed by 44% when patients consume 1200 mg CoenzymeQ10 per day.

While this Parkinson’s disease study has not yet been duplicated, it was based on a large body of peer-reviewed Parkinson's disease and neurotransmitter studies already published.  In addition to the studies previously mentioned, a 1998 Parkinson’s disease study published in the Proceedings of the National Academy of Sciences demonstrated that Coenzyme Q10 administration increased brain mitochondrial concentrations and exerts a neuro-protective effect, which may be useful in the treatment of neurodegenerative diseases such as Parkinson’s disease.12

A larger-scale, longer-term Parkinson's disease study as Dr. Shults recommends, will likely take time to obtain funding, then obtain volunteers, then proceed through the maybe 3-year treatment period, write the study results, then peer reviews, and finally publication in a respected journal. 

During that time, a Parkinson’s disease patient might want to consult with their physician about beginning a treatment of CoenzymeQ10.  There are approaches that Parkinson’s patients can follow to reduce any possible risk of taking high-dose Coenzyme Q10. 

These safety measures may include, gradually increasing dosage of CoQ10 from 300 mg/day to 600 mg/day, then 900 mg/day, finally to 1200 mg/day after establishing no adverse affects after a couple of weeks at each level. 

Any medications that the Parkinson’s disease patient is taking should be monitored by the prescribing physician to ensure that the effect of the medication does not change with increased consumption of CoQ10, thus requiring a dosing adjustment of the medication. 

It should be noted that while a cautious approach is prudent, the Parkinson’s disease patients in the UC – San Diego study were started on either 300, 600, 900, or 1200 mg of CoenzymeQ10 daily, with no significant side effects reported for any group. 

While Coenzyme Q10 was shown to reduce the progression of Parkinson’s disease, it neither reverses the disease, nor reduces symptoms which have already appeared.  So, it is important for the Parkinson’s patient who chooses to use CoenzymeQ10 to continue any medication that they are already taking. 

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References

  1. Kalen A, et al. Age-related changes in the lipid compositions of rat and human tissues. Lipids, July 1, 1989; 24(7): 579-84.
  2. Van Dyck CH, Age-related decline in dopamine transporters: analysis of striatal subregions, nonlinear effects and hemispheric asymmetries. Am J Geriatr Psychiatry 2002, Jan-Feb;10(1):36-43
  3. Kim JH, et al. Dopamine neurons derived from embryonic stem cells function in an animal model of parkinson’s disease.  Nature, advance online publication, 2002, June 20 DOI: 10.1038/nature00900.
  4. Vesper J, et al. Results of chronic subthalamic nucleus stimulation for Parkinson’s disease: a 1-year follow-up study.  Surg Neurol 2002 May;57(5):306-11; discussion 311-3.
  5. Malhi GS, et al. Novel physical treatments for the management of neuropsychiatric disorders. J Psychosom Res 2002 Aug;53(2):709-19.
  6. Luo J, et al. Subthalmac GAD gene therapy in a parkinson’s disease rat model.  Science 2002 Oct 11;298(5592):425-9.
  7. Albano CB, et al. Distribution of CoenzymeQ10 homologues in brain. Neurochem Res 2002 May;27(5):359-68.
  8. Beal MF. CoenzymeQ10 as a possible treatment for neurodegenerative diseases.  Free Racid Res 2002 Apr;26(4):455-60.
  9. Shults CW et al. Effects of CoenzymeQ10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol 202 Oct;59(10):1541-50.
  10. Shults CW, et al. CoenzymeQ10 levels correlate with the activities of complexes I and II/III in mitochondria from parkinsonian and non- parkinsonian subjects. Ann Neurol 1997 Aug;42(2):261-4.
  11. Beal MF, et al. CoenzymeQ10 attenuates the 1-methyl-4-phenyl-1,2,3,tetrahydropyridine (MPTP) induced loss of striatal dopamine and dopaminergic axons in aged mice. Brain Res. 1998 Feb 2;783(1):109-14.
  12. Matthews RT, et al. CoenzymeQ10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects. Proc Natl Acad Sci USA 1998 Jul 21;95(15):8892-7.

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