Definition: Parkinson’s disease is a common neurological condition afflicting about 1
percent of men and women over the age of seventy. In
Parkinson’s disease, a small region in the brain, called the substantia nigra, begins
to deteriorate. The neurons of the substantia nigra use the brain chemical dopamine.
With the loss of dopamine, tremors begin and movement slows. Despite current drug
therapies, Parkinson’s disease remains a progressive and incurable condition. Many
patients with Parkinson’s disease may also suffer from age related cognitive decline
or have some of the symptoms of Alzheimer’s disease.
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interpretation by Ray Sahelian, M.D.
Treatment Strategies for Parkinson’s disease
The nutritional treatment for Parkinson’s disease is still an uncharted
territory. The most promising approach appears to be the use of antioxidants to slow the
oxidation and damage to the substantia nigra. It’s possible that additional
nutritional approaches may be found in the future. Those who exercise regularly
early in their adult life have a lower risk of Parkinson's disease.
Over the past few decades, doctors have made
important advances in the treatment of Parkinson’s disease with pharmaceutical
medicines. Yet, several nutritional treatment strategies exist which should be explored further.
Improving the Antioxidant System
Of all the nutritional treatments available for Parkinson’s disease,
antioxidants appear to be the most promising choices to prevent or slow the progression of
this condition. Individuals whose diets include plenty of healthy foods containing
antioxidants are less likely to develop Parkinson’s disease. Patients should consume
foods, such as fruits and vegetables, that contain glutathione or can help produce it. Cyanohydroxybutene, a chemical found in broccoli, cauliflower, Brussels sprouts and
cabbage, is also thought to increase glutathione levels. High intake of dairy products may
lead to a higher incidence of Parkinson's disease.
The following antioxidants may be helpful in
addition to standard pharmaceutical therapy. Please use low dosages initially
until you learn how each supplement works for you before upping the dose. Also,
combining supplements and medicines can sometimes have a stimulating effect.
Learn how each supplement works by itself before adding another one.
Mucuna Pruriens
is an herb to seriously consider for Parkinson's disease. Mucuna pruriens has been
successfully used in India for centuries. Mucuna may work as an antioxidant and
also as a dopamine provider. We know little about the ideal
dosage of mucuna to treat Parkinson's disease. We have interesting anecdotes at
the bottom of the page regarding the use of mucuna pruriens by individuals with
Parkinson's disease.
Selenium is an antioxidant that can help increase levels of glutathione. A dose of 50 to 100 micrograms a day can be taken with any meal. Selenium is also normally found in multivitamin and mineral pills.
Melatonin is the sleep hormone with antioxidant abilities. A dose of 0.3 to 1 mg can be taken one or three hours before bed for those with insomnia. Tolerance can develop with regular use and since we don’t know the long-term effects of nightly use, it’s best to limit the frequency of use of melatonin to once or twice a week. In the 1980s, some individuals taking a synthetic drug called MPTP developed symptoms similar to Parkinson’s disease. It was determined that MPTP causes an oxidative destruction of substantia nigra neurons. Interestingly, a study with rats has determined that the administration of melatonin is able to almost completely prevent the neurotoxicity from MPP, a toxin very similar to MPTP. The rats on melatonin and MPP did not get symptoms of Parkinson’s disease while the controls on MPP alone did.
Withania somnifera, also known as ashwagandha, was found in a rodent study to be helpful for tardive dyskinesia symptoms although it is not known whether ashwagandha would be helpul in dyskinesia due to L-DOPA induce dyskinesia.
Providing Dopamine Precursors
L-dopa, the immediate precursor to
dopamine, is a nutrient available by
prescription. L-dopa (often combined with carbidopa) is the most commonly used medicine to
treat Parkinson’s disease. It is possible that the use of L-dopa for prolonged
periods causes oxidation and toxicity to brain cells. If this turns out to be true, it
would further justify the recommendations that antioxidants be added to standard
Parkinson’s disease therapy. There is, as of yet, no clinical proof that taking
antioxidant supplements help those with Parkinson’s disease live longer but all
indications point to the possibility that the course of the disease can be slowed by
providing adequate antioxidant support.
Tyrosine is an amino acid that can be converted
into L-dopa. But there is no reason to take tyrosine if L-dopa is available. Another way
to increase dopamine levels is with the use of B vitamins, particularly
NADH. Preliminary
studies have shown some benefit with NADH in the therapy of PD. Although more research is
needed, for the time being, it would seem reasonable to add NADH at a dose of 2.5 mg. NADH
can be taken every other morning on an empty stomach. NADH may also help regenerate the
antioxidant glutathione which could be beneficial. Be careful when you add NADH when you
are already taking L-dopa or other medicines that treat Parkinson’s disease, since
the effects could be cumulative. The long-term effectiveness of NADH in patients with
Parkinson’s disease is currently not known. Taking between one to three times the RDA
for the B vitamins seems to be a reasonable option.
Blocking Dopamine Breakdown
Dopamine is broken down in the brain by an enzyme called monoamine oxidase
(MAO). When the activity of MAO is inhibited, dopamine stays around longer and this
benefits those with Parkinson’s disease. Several drugs are available that block the
activity of MAO. Selegiline is the most effective and the one used most commonly. The
prescribed dosage is 5 mg a day.
No nutrients are currently known that prevent
the breakdown of dopamine. However, a study conducted on rats at the College of Humanities
and Sciences, Beijing Union University, in Beijing, China, indicates that the Chinese
herbs codonopsis and astragalus can inhibit MAO type B and increase the activity of the
antioxidant SOD. We don’t have any human trials to determine whether these two herbs
would benefit patients with Parkinson’s disease. Although selegiline is a very helpful medicine, high doses
may increase the risk of heart irregularities.
Additional Nutrients to Consider
Some of the following nutrients may not be directly involved in making more
dopamine, but could well improve general cognitive abilities. Many patients who have
Parkinson’s disease, especially the elderly, have age related cognitive decline.
You may also consider drinking less milk (see below).
Fish oils at 500 to 1,000 mg a day of EPA/DHA with meals. The role of fish oils
in Parkinson’s disease is not known, but they can generally improve overall brain health.
Gingko biloba at 40 mg most days with breakfast or lunch. This herb has antioxidant
properties and helps improve memory and alertness.
Replacing hormones in patients with Parkinson’s disease may be an additional option. Whether
pregnenolone,
DHEA, or other hormones are helpful in Parkinson’s
disease is currently not known. Long term use of high doses of
hormones has side
effects.
It’s quite likely that the proper use of natural supplements can reduce the necessary dose of L-dopa, selegiline, and other drugs currently used to treat Parkinson’s disease, or help slow down the progression of the condition. There’s still a great deal we need to learn about the nutritional treatment of Parkinson’s disease.
Cause of Parkinson Disease
Although Parkinson’s disease can
occur from viral infections or exposure to environmental toxins, such as pesticides
(gardeners and farmers are more prone to Parkinson's disease), the
causes of the majority of cases are not well known. Scientists suspect that oxidative
damage to neurons in the substantia nigra could well be one of the major causes,
particularly due to the depletion of the antioxidant glutathione.
People who sustain
substantial head injuries face an increased risk of developing Parkinson’s
disease years later. This has been shown in more than one study, therefore, it
is safe to assume that head injury, such as in boxing, is a cause of
Parkinson's disease.
Parkinson Disease Symptom
Individuals with Parkinson’s disease have tremor of the hands, rigidity,
poor balance, and mild intellectual deterioration. The tremor is most apparent
at rest and is less severe with movement.
Parkinson's Disease
Diagnosis
It is difficult to diagnose Parkinson's disease in the early stages.
Early on, PD is diagnosed almost primarily by its symptoms, and studies indicate
that physicians make an incorrect initial diagnosis of Parkinson's disease in
between 10% and 40% of cases. Blood tests are not helpful for diagnosis.
Common medicines used in
Parkinson's disease to improve prognosis
There are basically three types of Parkinson's disease drugs that are commonly prescribed for
patients with Parkinson’s disease. First, doctors prescribe dopamine precursor
medication,
such as L-dopa, which converts into dopamine. A second medication type is using drugs
that block the breakdown of dopamine. A common medicine used for this purpose is selegiline (also known as deprenyl). And third, drugs are provided that
influence dopamine receptors directly. The two most commonly prescribed are bromocriptine
and pergolide. Researchers from the
Mayo Clinic say that in some cases, patients taking pergolide (Permax) may experience
damage to heart valves. In some cases, patients taking cabergoline may
experience damage to heart valves. High cumulative doses of and long-term
treatment with cabergoline ( Dostinex ) are risk factors for the development of
valvulopathy.
A Mayo Clinic study published in July 2005 Archives of
Neurology describes Parkinson’s patients who developed a gambling problem while
taking Mirapex or similar drugs.
Dopamine agonists may trigger sudden uncontrollable
sleepiness in about one in five patients.
New Parkinson's Drug
In June, 2006 FDA approved Azilect (rasagiline) for the treatment of
Parkinson's disease. Axilect is a monoamine oxidase type--B (MAO-B) inhibitor
that blocks the breakdown of dopamine, a chemical that sends information to the
parts of the brain that control movement and coordination. Azilect was approved
for use as an initial single drug therapy in early Parkinson's disease, and as
an addition to levodopa in more advanced patients. Levodopa is a standard
treatment for Parkinson's disease.
Parkinson's disease statistics
Prevalance of Parkinson's Disease: 1 million people.
Famous people with Parkinson's
disease
Muhammad Ali, president Harry Truman, Michael Fox.
Parkinson's Disease
Research Update
Eating food rich in vitamin E may help protect against Parkinson's
disease. A review of eight studies that looked into whether vitamins C and E and
beta carotene had an impact on the odds of developing Parkinson's disease showed
that a moderate intake of vitamin E lowered the risk. Neither vitamin C nor beta
carotene seemed to have a protective effect against the illness. The researchers
said they did not know whether vitamin E supplements would have any benefits.
Parkinson's disease is a chronic, irreversible neurodegenerative disease that
affects 1 percent of people over the age of 65 worldwide. In the United States
alone at least 500,000 people suffer from the illness. Parkinson's disease
occurs when brain cells that produce a chemical called dopamine malfunction and
die. Symptoms include tremors, stiffness, slow movement and poor coordination
and balance. The scientists, who looked at relevant Parkinson's disease studies
from 1966 to March 2005, said more research is needed to confirm their findings.
Vitamin E is an antioxidant that protects cells from damage. Foods rich in the
vitamin include nuts, seeds, wheat germ, spinach and other green leafy
vegetables.
Gardeners should wear protective clothing
when using pesticides, say scientists who have concluded in a new study that the
chemicals can increase the risk of Parkinson's disease. Researchers at the
University of Aberdeen in Scotland have discovered that the more pesticides
gardeners are exposed to, the more likely they are to develop the degenerative
brain disease.
The results reinforce the need for amateur gardeners and farmers alike to wear
protective equipment when spraying pesticides. Anthony Seaton and his team in
Aberdeen interviewed 767 Parkinson's sufferers and 1,989 healthy people about
risk factors for the disease, including their use of pesticides. They found that
people with the illness were more likely to have used pesticides. Amateur
gardeners were 9 percent more likely to suffer from the disease than
non-pesticide users. Farmers were 43 percent more likely.
Consumption of milk and calcium in midlife
and the future risk of Parkinson disease
Neurology 2005;64:1047-1051
Objective: To examine the relation between milk and calcium intake in midlife
and the risk of Parkinson disease (PD). Conclusions: Findings suggest that milk
intake is associated with an increased risk of Parkinson disease. Whether
observed effects are mediated through nutrients other than calcium or through
neurotoxic contaminants warrants further study.
Levodopa and the progression of Parkinson's disease.
N Engl J Med. 2004 Dec 9;351(24):2498-508.
Despite the known benefit of levodopa in reducing the symptoms of Parkinson's
disease, concern has been expressed that its use might hasten neurodegeneration.
This study assessed the effect of levodopa on the rate of progression of
Parkinson's disease. CONCLUSIONS: The clinical data suggest that levodopa either
slows the progression of Parkinson's disease or has a prolonged effect on the
symptoms of the disease. In contrast, the neuroimaging data suggest either that
levodopa accelerates the loss of nigrostriatal dopamine nerve terminals or that
its pharmacologic effects modify the dopamine transporter. The potential
long-term effects of levodopa on Parkinson's disease remain uncertain.
Is levodopa toxic?
J Neurol. 2004 Sep;251 Suppl 6:VI/44-6.
The objective of this workshop was to review and discuss the debate on
neurotoxicity of levodopa in the treatment of Parkinson's disease with
consideration of preclinical and clinical findings. We concluded that in
particular preclinical outcomes of in vitro models of neurodegeneration describe
neurotoxic effects of levodopa, whereas trials in animal models provided
controversial results. To date, clinical trials in Parkinson's disease patients
showed no convincing proof of direct neurotoxic effects of levodopa on
progression of neurodegeneration with various applied functional imaging
techniques particularly with specific radiotracers for nigral dopaminergic
neurotransmission. However, the controversy on neurotoxicity of levodopa only
partially considered indirect mechanisms, i. e. levodopa-associated homocysteine
elevation. But there is accumulating evidence that this long-term side effect of
chronic levodopa administration dose dependently individually contributes to
progression of neurodegeneration due to increased release of neurotoxins,
induction of oxidative stress and mitochondrial dysfunction according to results
of in vitro and animal trials and to at least peripheral neuronal degeneration
and increased risk for onset of atherosclerosis-related disorders according to
clinical trials in Parkinson's disease patients. From this point of view we
demand that future research on the efficacy and putative neurotoxicity of
antiparkinsonian compounds should also consider putative toxic long-term effects
of drug administration and should look for putative peripheral biomarkers and
individual, environmental or nutritative risk factors in order to establish a
preventive therapy, i. e. folic acid administration in the case of levodopa-associated
homocysteine elevation.
Middle-aged men who drink a glass or two of milk each day may be increasing their risk of developing Parkinson's disease later in life. The ingredient or possible contaminant in milk responsible for this effect is unclear, but the current findings suggest it's not the calcium. The new findings, which appear in the medical journal Neurology, support those of an earlier report linking high consumption of dairy products with an elevated risk of Parkinson's disease among men, but not women.
Pre-treatment with R-lipoic acid alleviates the effects of GSH depletion in
PC12 cells: implications for Parkinson's disease therapy.
Neurotoxicology. 2002 Oct;23(4-5):479-86.
Oxidative stress is believed to play a key role in the degeneration of
dopaminergic neurons in the substantia nigra (SN) of Parkinson's disease (Parkinson's
disease)
patients. An important biochemical feature of Parkinson's disease is a significant early
depletion in levels of the thiol antioxidant compound glutathione (GSH) which
may lead to the generation of reactive oxygen species (ROS), mitochondrial
dysfunction, and ultimately to subsequent neuronal cell death. In earlier work
from our laboratory, we demonstrated that depletion of GSH in dopaminergic PC12
cells affects mitochondrial integrity and specifically impairs the activity of
mitochondrial complex I. Here we report that pre-treatment of PC12 cells with R-lipoic
acid acts to prevent depletion of GSH content and preserves the mitochondrial
complex I activity which normally is impaired as a consequence of GSH loss.
Although symptoms of Parkinson's disease
often improve when the drug levodopa is given, brain scan results suggest that
the drug hastens progression of the disease, according to a report in The New
England Journal of Medicine. Given these conflicting findings, the long-term
effects of levodopa on the disease remain unclear. The researchers evaluated 361
patients with early Parkinson's disease who were treated with levodopa at one of
three doses or with inactive placebo for 40 weeks. The main outcome measure was
the extent to which symptoms worsened during treatment, but a subgroup of
patients was also evaluated with brain scans. Parkinson's symptoms worsened to a
lesser extent in patients who received levodopa, at any dose, than in those who
received placebo. In contrast, brain scanning in 116 patients showed that
patients treated with levodopa lost more critical nerve cells than those who
received placebo.
Dr. Sahelian comments: perhaps
levodopa acts as an oxidant, damaging nerve cells.
Neuroprotective effect of Ginkgo biloba L. extract in a
rat model of Parkinson disease.
Phytother Res. 2004 Aug;18(8):663-6.
The neuroprotective effects of a standardized extract of Ginkgo biloba L. (EGb
761) were investigated on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in
the nigrostriatal dopaminergic system of the rat brain. Rats were given a week
of pretreatment with daily administrations of Ginkgo biloba. Unilateral striatal
injection of 6-OHDA was followed by treatment with Ginkgo biloba for a week.
Serial measurement of contralateral forepaw adjusting steps revealed a
progressive deficit in motor activity. At 8 weeks after 6-OHDA lesion the number
of contralateral forepaw adjusting steps was significantly higher in rats that
were treated with high doses of Ginkgo biloba (100 mg/kg daily) than in those
treated with low doses (50 mg/kg) or with the vehicle. Dopamine neuron loss in
the substantia nigra and a depletion in striatal dopamine corresponded with
behavioural deficit. These data suggest that the neuroprotective effects of
Ginkgo biloba reduce the behavioural deficit in 6-OHDA lesions in rat and also
indicates a possible role for the extract in the treatment of Parkinson's
disease.
Pilot trial of high dosages of
coenzyme Q10 in patients with Parkinson's disease.
Exp Neurol. 2004 Aug;188(2):491-4.
The safety and tolerability of high dosages of coenzyme Q10 were studied in 17
patients with Parkinson's disease (PD) in an open label study. The subjects
received an escalating dosage of coenzyme Q10--1200, 1800, 2400, and 3000 mg/day
with a stable dosage of vitamin E (alpha-tocopherol) 1200 IU/day. The plasma
level of coenzyme Q10 was measured at each dosage. Thirteen of the subjects
achieved the maximal dosage, and adverse events were typically considered to be
unrelated to coenzyme Q10. The plasma level reached a plateau at the 2400 mg/day
dosage and did not increase further at the 3000 mg/day dosage. Our data suggest
that in future studies of coenzyme Q10 in PD, a dosage of 2400 mg/day (with
vitamin E/alpha-tocopherol 1200 IU/day) is an appropriate highest dosage to be
studied.
Triple-blind, placebo-controlled trial of
Ginkgo biloba in sexual dysfunction due to antidepressant drugs.
Hum Psychopharmacol. 2004 Sep 20
A triple-blind (investigator, patient, statistician), randomized,
placebo-controlled, trial of Ginkgo biloba 240 mg daily was carried out.
Following a 1-week control, ginkgo biloba was given to 24 patients with sexual
impairment due to antidepressant drugs. Efficacy analysis was carried out on
eight males and five females on placebo and six males and five females on
Ginkgo, completing the full 12 weeks of treatment. A validated, sex
(gender)-orientated questionnaire was recorded at - 1, 0, 1, 3, 6, 9 and 12
weeks, and a non-blind follow-up for a further 6-weeks on Ginkgo. Hamilton
anxiety and depression ratings were made at 0, 6 and 12 weeks and simple global
assessments of alertness and memory. There were some spectacular individual
responses in both groups, but no statistically significant differences, and no
differences in side-effects.
In patients with early Parkinson's disease, selegiline and other drugs in a class called monoamine oxidase type B inhibitors are cheap and effective treatments that reduce disability and the need for levodopa, researcher report in the British Medical Journal. Their study findings also show that the drugs are not associated with increased mortality, as had been reported in an earlier study.
Heart valve disease appears to be relatively common in Parkinson's disease patients treated with pergolide (Permax). Evidence suggests that the degree of damage correlates with lifetime dose of the drug, but the effects may be reversible. Pergolide belongs to a class of drugs called dopamine agonists. It is derived from ergot, a substance obtained from plants, and works by acting in place of dopamine, a natural substance in the brain needed to control movement.
Oxidative stress to dopaminergic neurons as models of Parkinson
disease.
Gille G.Veterinary University of Vienna, Veterinarplatz 1, A-1210 Vienna,
Austria.
Ann N Y Acad Sci. 2004 Jun;1018:533-40.
The effects of exogenous toxins (MPP(+), rotenone) and potentially neurotoxic
properties of levodopa (L-DOPA) on the survival rate of dopaminergic neurons in
dissociated primary culture are presented. Dopamine agonists show a capacity to
counteract MPP(+)-toxicity. Moreover, a preserving potential of the antioxidant
and bioenergetic coenzyme Q(10) (CoQ(10)) on the activities of tyrosine
hydroxylase (TH), complexes I and II of the respiratory chain, and hexokinase
activity in striatal slice cultures against MPP(+) is demonstrated. Parkinson's
disease and exercise.
Effect of anti-parkinson drug HP-200 (Mucuna pruriens) on the central
monoaminergic neurotransmitters.
Manyam BV, Dhanasekaran M, Hare TA.Texas A & M University System Health Science
Center College of Medicine, Temple, TX
Phytother Res. 2004 Feb;18(2):97-101
HP-200, which contains Mucuna pruriens endocarp, has been shown to be
effective in the treatment of Parkinson's disease. Mucuna pruriens endocarp -
not a new treatment for parkinson's disease - has
also been shown to be more effective compared to synthetic levodopa in an animal
model of Parkinson's disease. The present study was designed to elucidate the
long-term effect of Mucuna pruriens endocarp in HP-200 on monoaminergic
neurotransmitters and its metabolite in various regions of the rat brain. HP-200
at a dose of 2.5, 5.0 or 10.0 g/kg/day was mixed with rat chow and fed daily ad
lib to Sprague-Dawley rats (n = 6 for each group) for 52 weeks. Controls (n = 6)
received no drug. Random assignment was made for doses and control. The rats
were sacrificed at the end of 52 weeks and the neurotransmitters were analyzed
in the cortex, hippocampus, substantia nigra and striatum. Oral administration
of Mucuna pruriens endocarp in the form of HP-200 had a significant effect on
dopamine content in the cortex with no significant effect on levodopa,
norepinephrine or dopamine, serotonin, and their metabolites- HVA, DOPAC and
5-HIAA in the nigrostriatal tract. The failure of Mucuna pruriens endocarp to
significantly affect dopamine metabolism in the striatonigral tract along with
its ability to improve Parkinsonian symptoms in the 6-hydorxydopamine animal
model and humans may suggest that its anti-parkinson effect may be due to
components other than levodopa or that it has an levodopa enhancing effect. The
pathophysiology of Parkinson's disease.
Epidemiology and treatment of Parkinson
disease in India.
Parkinsonism Relat Disord. 2003 Aug;9 Suppl 2:S105-9.
Parkinson's disease has a low prevalence in India except in the small Parsi
community where Bharucha et al. found a high prevalence. Although early onset
Parkinson disease and familial cases have been described from India, no
genetic mutations have as yet been identified. Parkinson's disease has been
known in India since ancient days and the powder of Mucuna Pruriens seeds was
used for its treatment. The present day management of Parkinson's disease in
India is similar to that in the other countries. Unfortunately, lack of
awareness, limitation of human resources and cost factors deny the benefits of
therapy to many patients. End stage Parkinson's disease.
Curcumin has strong antioxidant properties. Curcumin is derived from turmeric.
Parkinson's disease fact : the four most popular parkinsonian neurotoxins are 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, and paraquat.
Degenerative
Parkinson's disease emails
Q. Is Parkinson's disease hereditary?
A. Parkinson's disease is both hereditary and due to
environmental factors.
Q. I was diagnosed with parkensons
disease approx. one year ago, the neurologist put me on carbidopa, as that was
the only thing medicaid would pay for; I vommited repeatedly after each dose.
Losing so much weight it became dangerous and the Dr. discussed hospitalization.
He finally decided to simply treat the pain I experience and stopped the other
treatment. At whits end my brother went to the local health food store and began
researching sources of dopamine, Finding a product, mucuna pruriens, formulated
by Dr. Sahelian. ,I started on two capsules a day when I first got up, within
just six days I could sign my name again and hold a fork to my mouth and
in just over a week was able to hold 90% still. I continue to take two a day and
am still experiencing progress and am experiencing the return of memories and
mental functions. I have and continue to recomend the mucuna product to others
who are also experiencing
progress.
A. Wow, this is an amazing testimonial. We do suggest
using the lowest mucuna dose that works and perhaps it is a good idea to have
your doctor monitor your progress.
A second email
received in June, 2006 -
I wanted to write and tell you my progress, I
was diagnosed with parkinsons disease. The Dr. tried several medications that
were specifically to supply dopamine, My body repelled each of the medications
and left at whits end the Dr. decided to treat the severe pain with percocet;
Disturbed at that my brother went to our health food store,( Good Earth,
Bradenton, Fl. ) and did a search with
the staff, They found your product, I started mucuna on April 22, 2006, Within
days I was able to write my own name and was able to remember things. Steadily I
have continued to make progress To this date July 7th. 2006. At first I took two
a day before breakfast, But I experienced a recent set back, As my memory got a
bit worse, I decided to take three a day, My memory is already getting
better and tomorrow I will start taking two again. I am only 40 years old but my
Dr. said since
my father had Parkinsons I was a prime candidate for it AND That a psychological
medicine I was on Risperdal, had sped up the progress and caused it to hit me
much earlier than normal. I have informed my my neurologist that I am on mucuna
and he was releaved to see the extreme progress. He took down all the
information and said he would monitor my progress and told me that the increase
I had taken was fine but to decrease it as soon as possible. and will probally
contact you himself. But he was releaved at my success. and was fine with the
macuna and would investigate it, And watch my progress to possibly try it with
other patients. PLEASE share this letter to Dr. Sahelian, confirm with him that
my Dr. is very excited and intrigued with what he sees. He will monitor me. I am
steadily getting better( except for a brief healing crisis) and I am thrilled to
be coming out of this dark cave Parkinsons puts you in.
Third email received December 2006 - I have been trying to keeo you
all posted as to my progress with my Parkinsons disease and mucuna pruriens. I
want you to know that I can walk steady the pain has even eased up and last but
NOT least my tremors have slowed down fro a 10 to q 3. I fully believe in mucuna
pruriens, please feel free to use my testamonials in any ads or articles
as proof. dear THANK YOU WITH ALL MY HEART.
Q. Is Parkinson's Disease associated with
dementia?
A. There can be an overlap between
dementia and Parkinson's
disease.
Q. What's an early sign or symptom of
Parkinson's disease?
A. Shaking or tremor is an early symptom of Parkinson's
disease. Progression leads to trembling in arms, legs, jaw, and rigidity or
stiffness of the limbs.
Q. Is there a cure for Parkinson's
disease?
A. At this time there is no cure for Parkinson's
disease. Stem cells
may perhaps offer help in the future.
Q. Does a history of Parkinson's disease
in the family increase my risk?
A. I don't know, this is a good question.
Q. My local Parkinson's Disease foundation
in New York does not know about mucuna for PD.
A. Mucuna is not well known yet and little human
research is available in the Western medicine field but hopefully it will be
studied more thoroughly to see if it helps in this condition.
Q. I just wanted to mention that I
appreciate the Parkinson's disease info you have presented here.
A. Thank you.
Q. Is excess exercise a cause for
Parkinson's disease?
A. Not unless the exercise is boxing and you get
repeatedly thumped in the head.
Q. Is diarrhea or chronic loose stools a
symptom of Parkinson's disease?
A. Gastrointestinal difficulties are not associated
with or are rarely a Parkinson's disease symptom.