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Health News - Parkinson's
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Also see: Should Parkinson's Disease Patients Take CoenzymeQ10?

Vitamin E May Reduce Risk of Parkinson's

October, 2002

Consuming foods high in vitamin E could reduce the risk of developing Parkinson's disease, says a study published in the Oct. 22, 2002 issue of Neurology, a journal of the American Academy of Neurology.

Researchers examined the effects of consuming not only vitamin E, but also vitamin C and carotenoids, both from food and dietary supplements. The study was led by Dr. Shumin Zhang, assistant professor of epidemiology and medicine at Harvard School of Public Health in Boston.

"Vitamin E is a strong antioxidant, so vitamin E could protect the cells from oxidative stress, so potentially, vitamin E can reduce the risk of Parkinson's disease," Zhang said.

Zhang and colleagues looked at the records of 76,890 women from the Nurses' Health Study and 47,331 men from the Health Professionals Follow-Up Study and analyzed the dietary habits and medical status of the study participants. The two studies were established nearly two decades ago to follow the lifestyles of thousands of people on a long-term basis with the goal of studying information that could further medical science.

By 1998, there were 371 cases of Parkinson's disease, a debilitating disease caused by an imbalance in brain chemicals. There were 161 cases among the women's group and 210 among the men. The illness is characterized by loss of motor skills that can trigger body tremors.

Researchers found taking standard vitamin supplements had no effect on Parkinson's disease. However, those who routinely consumed a greater amount of foods rich in vitamin E, such as nuts, did appear to have a lower risk.

Although it cannot as yet be determined how much vitamin E is necessary, Zhang said including sufficient levels of vitamin E in a balanced diet is a good start.

Vitamin E has been looked at in Parkinson's disease before and also in another degenerative disease that attacks the brain, Alzheimer's, explained Dr. Burton Scott, a neurologist and assistant professor of clinical neurology at Duke University Medical Center in Durham, N.C. Previous studies have found vitamin E tablets to have no effect on Parkinson's, but foods high in vitamin E may be a different story, Scott said.

"The vitamin E [alpha-tocopherol found in most multivitamins] may not be the main player in what's having the effect," Scott told UPI. Instead, it could be the action of the whole food that's contributing to this benefit. Likewise, it may not be the d-alpha tocopherol form of vitamin E commonly found in Vitamin E supplements that creates the beneficial effect, but a combination of various forms of vitamin E tocopherols and tocotrienols, such as d-Beta, d-Gamma, d-Delta, as well as d-Alpha.

At present, about 1 million people in the United States have Parkinson's disease, Scott said. Former U.S. Attorney General Janet Reno, boxer Muhammad Ali, Pope John Paul II and actor Michael J. Fox all have this illness.

Also see: Vitamin E Update: Gamma-tocopherol, Not Alpha­-tocopherol, Inhibits Cancer Cell Growth

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CoenzymeQ10 fights Parkinson's Disease

October, 2002

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 CoenzymeQ10, 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. 

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.

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.

Shults and his team found Parkinson's patients are low in CoQ10. The biochemical 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. 

The 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 Q10 already fared significantly better than did other volunteers. Lower doses also slowed the progression of Parkinson's, though much less effectively.

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," Clifford Shults, a neurologist the University of California in San Diego, explained.

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

Also see: Should Parkinson's Disease Patients Also Take CoenzymeQ10?

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Folic Acid May Protect the Brain from Parkinson's

Individuals with Parkinson's disease have been shown to have low levels of serum folic acid, and studies with mice have led researchers to believe that a deficiency in the vitamin may render the brain more susceptible to Parkinson's disease. 

In a study conducted by researchers at the National Institute on Aging, folic acid protected mice from the development of Parkinson-like symptoms when given MPTP, a drug known to produce these symptoms. The research, published in the January 2002 issue of Journal of Neurochemistry, involved the administration of MPTP to mice whose diets included folate and to mice whose diets were deficient. The deficient mice developed elevated homocysteine levels in the brain and serum, inducing DNA damage to dopamine-producing cells in the substantia nigra section of the brain. This leads to cell death in this region of the brain, causing the disordered movements characteristic of Parkinson's disease. Mice who received adequate levels of folate are more able to repair DNA damage, and therefore demonstrated only mild Parkinson's symptoms when administered MPTP.

National Institute of Aging Laboratory of Neurosciences chief, Mark Mattson PhD, commented, "This is the first direct evidence that folic acid may have a key role in protecting adult nerve cells against age-related disease. It is clear from this study that a deficiency of this vitamin is associated with increased toxin-induced damage to the dopamine-producing neurons in the mouse brain."

Dr Mattson suggests that ensuring an adequate intake of folic acid by dietary means or by consuming supplements could help to protect the brain from Parkinson's and other neurodegenerative diseases.

The incidence of Parkinson's disease increases with age. Symptoms of the disease include tremor or trembling, slowness of movement, rigidity of the limbs and trunk, and impaired balance and coordination.

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NADH -- a new therapeutic approach to Parkinson's disease. Comparison of NADH by oral and intravenous application.

The reduced coenzyme - nicotinamide adenine dinucleotide (NADH) - has been used as medication in 885 parkinsonian patients in an open label trial. About half of the patients received NADH by intravenous infusion, the other half received NADH orally by capsules. In about 80% of the patients a beneficial clinical effect was observed: 19.3% of the patients showed a very good (30-50%) improvement of disability, 58.8% a moderate (10-30%) improvement. 21.8% did not respond to NADH. 

Statistical analysis of the improvement in correlation with the disability prior to treatment, the duration of the disease and the age of the patients revealed the following results: All these 3 parameters have a significant although weak influence on the improvement. The disability before the treatment has a positive regression coefficient (t value < 0.01). The duration of the disease has a negative regression coefficient (< 0.01) and so has the age a negative regression coefficient (t value < 0.05). 

In other words, younger patients and patients with a shorter duration of disease have a better chance to gain a marked improvement by taking NADH than older patients and patients with longer duration of the disease.

The orally applied form of NADH yielded an overall improvement in the disability which was comparable to that of the intravenous applied form.

Birkmayer JG, Vrecko C, Volc D, Birkmayer W.

Birkmayer-Institut fur Parkinsontherapie Vienna, Austria.

Source: Acta Neurol Scand Suppl. 1993;146:32-5.

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Coenzyme1 - NADH - improves the disability of parkinson's patients

Coenzyme1, also called nicotinamide adenine dinucleotide (NADH), has been used in an open label trial as novel medication in 34 patients with Parkinson's disease, using an intravenous administration technique. In all patients a beneficial clinical effect was observed. 21 patients (61.7%) showed a very good (better than 30%) improvement of disability, 13 patients (38.3%) a moderate (up to 30%) improvement. Concomitant with the improvement of the disability, the urine level of homovanillic acid (HVA) increased significantly in all patients (in some patients by more than a 100%). The daily "on phases" of the patients could be increased from 2 up to 9 hours in the individual patients by NADH administration.

Birkmayer W, Birkmayer GJ, Vrecko K, Mlekusch W, Paletta B, Ott E.

Birkmayer-Institut fur Parkinsontherapie, Vienna, Austria.

Source 1: Journal of Neural Transm Park Dis Dement Sect. 1989;1(4):297-302.

Source 2: Ann Clin Lab Sci. 1989 Jan-Feb;19(1):38-43.

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