Parkinson’s Disease

Parkinson’s disease results from damage to the nerves in the area of the brain
responsible for controlling muscle tension and movement. The damaged cells are the
ones needed to produce the neurotransmitter called dopamine. Thus, people with
Parkinson’s disease make inadequate amounts of dopamine. The disease progresses from
slight to severe tremors and produces a wide variety of symptoms. Depression and
dementia (including Alzheimer’s disease) often accompany Parkinson’s disease.

There is no cure for Parkinson’s, but symptoms are often improved by drug therapy. The
most commonly used drug is Sinemet®, which contains both levodopa and carbidopa.
Levodopa, or L-dopa, is the ―middle step‖ in the conversion of the amino acid L-
tyrosine into dopamine. L-dopa, but not dopamine itself, is able to move from the blood
stream to the brain. Carbidopa works by ensuring that more L-dopa is converted to
dopamine within the brain, where it is needed. Other drugs used include selegiline
(Eldepryl®, Deprenyl®), bromocriptine (Parlodel®), and amantadine (Symadine®,
Symmetrel®). All of these drugs can produce depletions or have significant interactions
with essential nutrients. Refer to the individual drug for information on its interactions
with supplements and herbs.

Dietary changes that may be helpful: Clinical studies have shown that one can
enhance the action of L-dopa and improve the symptoms of Parkinson’s disease by
consuming nearly all of the day’s protein intake at dinner, while keeping the protein
content of breakfast and lunch extremely low. This dietary approach is now a well-
accepted supportive therapy. However, it must be carefully monitored by a qualified
healthcare professional in order to avoid deficiencies of protein and certain vitamins and
minerals. Individuals wishing to use this dietary approach to Parkinson’s disease should
therefore consult a doctor.

Broad beans (Vicia faba) contain L-dopa. Anecdotal cases of symptomatic improvement
after broad bean consumption have been described in patients with Parkinson’s disease.
In one small clinical study, 250 grams (almost nine ounces) of cooked broad beans
produced a significant increase in L-dopa blood levels, which correlated with a
substantial improvement in motor performance lasting at least four hours in some of the
subjects. However, some people may have symptoms aggravated by broad bean

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consumption, and people taking medications like Sinemet and L-dopa should be aware
that broad bean consumption may increase L-dopa levels excessively. Therefore,
Parkinson’s disease patients should talk with a doctor before adding broad beans to their
diet.

Doctors recommend that Parkinson’s patients supplement with fiber and adequate fluid
intake to reduce constipation associated with this disease. See the discussion about
psyllium seed below in ―Herbs that may be helpful.‖

Lifestyle changes that may be helpful: People with Parkinson’s disease are at higher
than normal risk for osteoporosis and vitamin D deficiency. Regular weight-bearing
exercise, exposure to sunlight, and a variety of supplements and dietary changes may be
helpful in preventing osteoporosis.

Nutritional supplements that may be helpful: The relationship between Parkinson’s

disease, antioxidants in general, and vitamin E in particular, remains unclear. Some
preliminary studies have indicated that high dietary intakes of antioxidant nutrients,
especially vitamin E, are associated with a low risk of Parkinson’s disease, even though
Parkinson’s patients are not deficient in vitamin E. The correlation between protection
from Parkinson’s and dietary vitamin E may be not be due to the vitamin E itself,
however. Legumes (beans and peas) contain relatively high amounts of vitamin E.
Separate from their vitamin E content, legumes have been associated with low risk of
Parkinson’s disease. In other words, ―high vitamin E intake‖ may be a marker for diets
high in legumes, and legumes may protect against Parkinson’s disease for reasons as yet
undiscovered but unrelated to their vitamin E content.

Interest in the relationship between antioxidants and Parkinson’s disease led to a

preliminary trial using high amounts of vitamin C and vitamin E in early Parkinson’s
disease and to a large ten-year placebo-controlled study of high amounts of vitamin E
combined with the drug deprenyl. In the study combining vitamins C and E, patients
with early Parkinson’s disease given 750 mg of vitamin C and 800 IU of vitamin E four
times each day (totaling 3,000 mg of vitamin C and 3,200 IU of vitamin E per day) were
able to delay the need for drug therapy (L-dopa or selegiline) by an average of about two
and a half years, compared with a similar group of patients who were not taking the
vitamins. The ten-year placebo-controlled study using 2,000 IU of vitamin E per day
failed to show any benefit in slowing or improving the disease. The difference in the

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outcomes between these two studies might be due to the inclusion of vitamin C and/or
the higher amount of vitamin E used in the successful trial. However, the difference
might also be due to a better study design in the trial that found vitamin E to be
ineffective.

The amounts of vitamin E used in the above trials are very high, and for good reason.
Increasing the antioxidant levels in brain tissue is quite difficult to achieve. In fact, some
researchers have found that even very high intakes of vitamin E (4,000 IU per day) fail
to increase brain levels. Perhaps the lack of ability to increase vitamin E levels in the
brain has produced the poor results described in the report of the controlled trial.

Although vitamin B6 was reported many years ago in preliminary research to be helpful
in overcoming vitamin B6 deficiency and in improving clinical features of Parkinson’s
disease, it must not be used by patients taking L-dopa alone. Taking vitamin B6 with L-
dopa increases the conversion of L-dopa to dopamine outside the brain, thereby reducing
delivery of dopamine to the brain. However, vitamin B6 can be used in conjunction with
Sinemet or selegiline.

Preliminary studies have suggested that methionine (5 grams per day) may help treat
some symptoms of Parkinson’s disease. However, use of a related supplement, S-
adenosylmethionine (SAMe), may be detrimental in people with Parkinson’s disease.
SAMe is involved in ―methylation‖ reactions in the body. Animal studies indicate that
excessive methylation is associated with Parkinson’s disease, and SAMe has caused
Parkinson’s disease–like effects in animal studies. Both animal and human studies
indicate that increased methylation can cause the depletion of dopamine and block the
effects of L-dopa—changes that in theory should exacerbate symptoms of Parkinson’s
disease. Preliminary evidence indicates that SAMe may improve the emotional
depression and the impaired mental function that is often associated with Parkinson’s
disease. Nonetheless, many healthcare professionals recommend that patients with
Parkinson’s disease avoid supplementing with SAMe until more is known.

Drug therapy for Parkinson’s disease has been reported to deplete vitamin B3 in humans.
Vitamin B3 may be needed to decrease SAMe levels, and in so doing, may possibly help
people with Parkinson’s disease. However, the two main forms of vitamin B3, niacin
and niacinamide, when taken in combination with L-dopa, have demonstrated no benefit
in Parkinson’s disease patients. Nicotinamide adenine dinucleotide (NADH)—the active

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form of vitamin B3—is effective in raising the level of dopamine within the brain,
making it potentially useful in the treatment of people with Parkinson’s disease. In
preliminary research, NADH has been shown to reduce symptoms and improve brain
function in Parkinson’s patients. One researcher has recommended 5 mg taken twice per
day for Parkinson’s disease patients. Double-blind trials have yet to be conducted in
patients with Parkinson’s disease.

In a preliminary report, 5-hydroxytryptophan (5-HTP) used in combination with Sinemet,

improved the emotional depression that is often associated with Parkinson’s disease.
While 5-HTP may be helpful as a supplement to Sinemet treatment for Parkinson’s, 5-
HTP should never be used alone in Parkinson’s disease. 5-HTP is converted to serotonin
in the brain, and increasing serotonin without increasing dopamine can cause Parkinson's
symptoms, especially rigidity, to get worse. People taking selegiline should also not take
5-HTP without a physician’s supervision because this combination might raise serotonin
to excessively high levels.

L-tyrosine is the direct precursor to L-dopa. Theoretically, supplementing L-tyrosine

might be an alternative to L-dopa; however, L-tyrosine should not be taken with L-dopa
as it may interfere with the transport of L-dopa to the brain. One small preliminary study
demonstrated that some patients who supplemented with L-tyrosine (45 mg per pound of
body weight) for three years had better clinical results and fewer side effects than did
patients using L-dopa. However, that report needs to be confirmed in larger, better
controlled trials before doctors would consider recommending L-tyrosine as an
alternative to L-dopa.

In a small four-week trial, D-phenylalanine (100 to 250 mg twice daily) was shown to be
helpful in improving motor control and tremors in patients with Parkinson’s disease.
Before healthcare professionals act on the outcome of this report, it needs to be
confirmed in a larger, better controlled trial. D-phenylalanine should not be taken with
L-dopa as it may interfere with the transport of L-dopa to the brain. It should be noted
that L-phenylalanine, not its mirror image D-phenylalanine, is the amino acid that occurs
naturally in food and is essential in human nutrition. While D-phenylalanine is not
considered a nutrient, it can exert potentially beneficial effects on brain chemistry. Some
commercially available phenylalanine products contain a 50:50 mixture of D- and L-
phenylalanine (these products are known as D,L-phenylalanine, or DLPA). Individuals
with Parkinson’s disease should consult a physician before using DLPA.
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People with Parkinson’s disease treated with L-dopa have been reported to have reduced
levels of the neurotransmitter (chemical messenger) phosphatidylserine. In one trial,
supplementing with phosphatidylserine (100 mg three times daily) improved the mood
and mental function in patients with Parkinson’s disease, but exerted no beneficial
effects on muscle control. The phosphatidylserine used in this study was obtained from
cow brain. That product is not available in the United States, because of concern that an
extract of cow brain could cause ―mad cow‖ disease. The phosphatidylserine sold in the
United States is manufactured from plant sources, and there is reason to believe that its
effects are not entirely the same as those of cow-brain phosphatidylserine.

Vitamin D deficiency is common in Parkinson’s disease due to lack of sunlight exposure

and to the effects of reduced activity in Parkinson’s patients on calcium metabolism.
Low vitamin D levels in Parkinson’s disease have been reported to increase the risk of
hip fracture due to osteoporosis. This risk has been significantly reduced with the use of
synthetic activated vitamin D—a prescription drug. Whether the same effect could be
achieved with supplemental vitamin D remains unknown, though some doctors
recommend 400–1,000 IU vitamin D per day. Parkinson’s disease patients may wish to
discuss the use of synthetic activated vitamin D with a healthcare professional.

People with Parkinson’s disease have shown both decreased and increased levels of zinc
and copper. Both nutrients function in the antioxidant enzyme superoxide dismutase.
This enzyme tends to be low in the area of the brain involved in Parkinson’s disease.
Therefore, in theory, low levels of these trace minerals could leave the brain susceptible
to free radical damage. However, too much copper and zinc (as well as iron) can also act
as pro-oxidants, and all have been associated with an increased risk of developing
Parkinson’s disease in some preliminary research. Insufficient evidence currently exists
for either recommending supplementation with zinc and copper, or avoiding such
supplementation.

Herbs that may be helpful: In a one-year preliminary trial of 25 patients with

Parkinson’s disease and additional signs of Alzheimer’s disease, ginkgo biloba extract
(GBE) produced significant improvement in brain wave tracings. These improvements
were thought to signify improved brain metabolism. Further studies are needed to
confirm these preliminary findings. The typical recommendation for GBE is 40 to 80 mg
three times daily of a standardized extract containing 24% ginkgo heterosides.

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In preliminary research, an extract of Mucuna prurient (HP-200) was studied in 60
patients with Parkinson’s disease (26 patients were taking Sinemet before treatment with
HP-200 and the remaining 34 were not medicated). Statistically significant reductions in
symptom scores were seen from the beginning to the end of the 12-week study. The
amount used in the study was 7.5 grams of the extract (dissolved in water) three to six
times daily.

Other preliminary research has shown psyllium seed husks improve constipation and
colorectal function in patients with Parkinson’s disease and constipation. Typical
recommendation for psyllium seed husks is 3 to 5 grams taken at night with a one to two
glasses of fluid.

Checklist for Parkinson’s Disease

Ranking Nutritional Supplements Herbs

Other D-phenylalanine
5-HTP (with Sinemet)
L-tyrosine
Methionine
NADH
Phosphatidylserine
Vitamin B6 (with Sinemet or
selegiline)
Vitamin C and vitamin E (in
combination)
Vitamin D

NEWAYS PRODUCTS
Cascading Revenol; Ingenious; Maximol Solutions; Revenol;

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