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Health
News - Parkinson's
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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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