I've been doing a lot of research on this for my Dad, I've actually got him
started on a fava bean diet, he started this morning.  There are postings at
http://james.parkinsons.org.uk/, if you look in the search engine for Fava,
you bring up a lot, there is also something called mucuna, that I'm going to
try next.  My Dad absolutely refuses to go to the dr, so I'm desperately
trying all of this stuff, I've had responses from people who say they work,
to mixed results.

Here is a copy of a research doc:

Dietary Factors in the Management of Parkinson's Disease

P.A. Kempster, M.D., M.R.C.P. (U.K.), F.R.A.C.P.
and
M. L. Wahlqvist, M.D., F.R.A.C.P.

 Dr. Kempster is with the Departments of Neurosciences and
Medicine and Dr. Wahlqvist is with the Department of Medicine.
Monash Medical Centre, 246 Clayton Rd., Clayton 3168. Melbourne.
Australia.

ABSTRACT

 Oral administration of L-dopa is currently the most effective
way to treat the cerebral dopamine deficiency which causes
Parkinson's disease. Unfortunately, many patients with advanced
Parkinson's disease develop an unstable pattern of response to
L-dopa because of fluctuating delivery of the drug to the brain.
Diet contributes to this problem through Its adverse effects on
L-dopa pharmacokinetics. This article reviews dietary strategies
to improve responsiveness to pharmaceutical L-dopa treatment and
the potential use of food as a source of L-dopa. Nutritional
factors concerning weight loss and energy balance in Parkinson's
disease are also discussed. A set of dietary guidelines is
developed to assist clinical nutritionists and neurologists in
the practical management of patients with Parkinson's disease.
Nutrition Reviews 1994;52,2:51-58 Feb 1994

INTRODUCTION

 Parkinson's disease is caused by idiopathic progressive
degeneration of pigmented neurons in the substantia nigra region
of the brainstem. These neurons use the neuro-transmitter
dopamine and innervate the motor portions of the basal ganglia,
in particular the caudate nucleus and putamen. Although the
precise role of the substantia nigra in normal motor control is
uncertain, the deficiency of dopamine that results from
degenerative changes in this region leads to a disturbance
of motor function manifested clinically as Parkinsonism.

 Following a series of improvements in the understanding of
brain catecholamine neurochemistry in the l950s,
levo-dihydoxy-phenylalanine (L-dopa), the amino acid precursor
of dopamine, was first used to treat Parkinson's disease. The
effectiveness of this drug soon became clear, with dramatic
improvement in many previously severely disabled patients.[1]
However, further experience exposed certain complications of
long-term L-dopa treatment. In some cases, the pattern of
response to L-dopa became unstable and was further marred by the
development of periodic involuntary movements.[2,3]

 L-Dopa medication is now. usually initiated in patients with
relatively mild Parkinson's disease early in the course of the
illness. Modern treatment combines L-dopa with a peripheral
decarboxylase enzyme inhibitor (carbidopa or benserazide) to
minimize conversion of L-dopa to dopamine outside the nervous
system. In most cases, motor symptoms improve and a stable and
satisfactory response continues for the next few years. With
further disease progression, many patients begin to experience
fluctuation of response to L-dopa, and drug-induced dyskinetic
involuntary movements may then accompany the beneficial effects
of the medication. Significant motor fluctuations develop at a
rate of about l0% per treatment year.[4] In their most severe
form, motor fluctuations produce, the "on-off" syndrome.[5]
Patients with this affliction swing between severe Parkinsonian
disability ("off' phases) and relative improvement of motor
fluctuation which restores mobility at the expense of
involuntary movements ("on" phases). Capricious and abrupt
fluctuation between these states occurs many times a day. The
fact that patients cannot predict when sudden loss of
independent mobility will occur is in itself a major cause of
disability in this syndrome.

 The pharmacokinetic properties of L-dopa lead to fluctuating
blood levels, generating fluctuation of motor function in
susceptible patients.[6] The drug has a relatively short
half-life because of enzymic catabolism. and dietary intake is
apt to interfere with its absorption and transport within the
body. Fluctuating delivery of L-dopa to the brain does not seem
to matter early in the disease course. However, disease
progression brings increasing dependence on pharmacological
dopamine receptor stimulation. Severe motor fluctuations are
generally seen in patients who retain a capacity to respond well
to L-dopa but have lost most of their endogenous dopamine
production because of nigral cell loss. A precipitous decline in
motor functions thus occurs each time that the supply of
exogenous L-dopa to the brain lapses.

-----------------------------------------------------------

Table 1. Dietary Factors Which Affect Clinical Response to
L-Dopa Medication

1.  Timing of L-dopa doses in relation to mealtime.

2.  Effects of food on gastric emptying

    Energy content of food

    Meal size

    Food viscosity

3.  Competition between dietary neutral amino and L-dopa for
absorption across the intestinal mucosa.

4.  Competition between circulating neutral amino acids and
L-dopa for active transport across the blood-brain
barrier.

-----------------------------------------------------------

 Despite a number of refinements to pharmacological treatment in
recent years, L-dopa remains the most physiological and
effective method to stimulate the central dopamine receptors and
is the mainstay of treatment for most Parkinsonian patients.
Some dopamine receptor agonist drugs have a longer and more
stable duration of action but cannot match the potent clinical
effects of L-dopa. The complication of fluctuating motor
response to L-dopa is therefore one of the major problems in the
long-term care of patients who have Parkinson's disease. Because
food intake contributes to the vagaries of L-dopa
pharmacokinetics, diet is an important influence on the
effectiveness of pharmacological treatment.

 Other nutritional factors such as food toxicants[7] and dietary
antioxidants[8] may eventually be shown to play a role in the
etiology or progression of Parkinson's disease. However, this
review will concentrate on aspects of clinical nutrition that
relate to the practical management of Parkinson's disease.

DIETARY INFLUENCES ON L-DOPA PHARMOCOKINETICS

 L-Dopa is normally present as an intermediate metabolite in
neurons which produce catecholamine neurotransmitters (dopamine,
noradrenaline, adrenaline). It is synthesized by the enzyme
tyrosine hydroxylase from the diet-derived aromatic amino acid
tyrosine. Brain tyrosine hydroxylase is confined to dopaminergic
and noradrenergic neurons, has a high affinity for its substrate
tyrosine, and its activity is regulated by the rate of neuronal
firing.[9,10]

Administration of tyrosine to Parkinsonian patients may increase
dopamine synthesis and turnover in the central nervous
system,[11] but there is no evidence of any clinical benefit
from treatment with tyrosine. Phenylalanine is an indirect amino
acid precursor of L-dopa but has no clinical effect on
Parkinsonism.[12] A normal diet contains little L-dopa.[13] and
the small amount of circulating L-dopa in normal subjects
probably emanates from synthetic activity in peripheral
sympathetic neurons and the adrenal medulla.[14]

 To exert its action In Parkinson's disease, L-dopa must he
absorbed from the gastrointestinal tract into the bloodstream,
cross the blood-brain barrier, and then be enzymatically
converted to dopamine within the brain to interact with striatal
dopamine receptors. Intake of food. particularly protein, can
interfere with this process at a number of levels. Single oral
doses of L-dopa, when administered in the fasting state, produce
efficient and reliable absorption of L-dopa, which corresponds
to predictable and relatively prolonged motor responses even in
patients with the most erratic pattern of response to their
usual oral L-dopa medication.[15]

 Patients are often advised to take L-dopa doses with meals. By
reducing L-dopa absorption, food may reduce side effects such as
nausea on first exposure to medication containing L-dopa.
However once motor fluctuations have developed after prolonged
treatment, food is usually a hindrance to the bioavailability
and clinical effectiveness of L-dopa.

 L-Dopa is optimally absorbed from the duodenum and proximal
jejunum.[16] The drug is not absorbed across gastric mucosa,[17]
but oral doses are dependent on gastric emptying for access to
absorption sites. The rate of gastric emptying is chiefly
determined by the energy content of food and is inversely
proportional to the energy density of meal.[18] Thus fat will
retard gastric emptying to greater degree than either protein or
carbohydrate. Low gastric acidity slows emptying [19] although
routine administration of antacids to Parkinsonian patients does
not improve L-dopa absorption.[20] Some types of dietary fiber
increase food viscosity and slow gastric emptying.[21] The
gastric mucosa contains the enzyme dopa decarboxylase,[22] which
will catalyze unwanted conversion of L-dopa to dopamine,
reducing the amount of L-dopa available for subsequent
absorption from doses affected by delayed gastric emptying.

 When L-dopa is administered by naso-duodenal tube[23] or to
subjects who have previously had a gastrectomy,[19] absorption
is very rapid and efficient. Effects on gastric emptying are
probably largely responsible for the observation that when
L-dopa given with food, the rise in plasma concentration is
reduced, delayed and unpredictable as compared with
fasting.[24,25]

 On reaching the proximal small gut, L-dopa crosses the mucosal
barrier by a stereospecific, saturable active transport
mechanism shared by large neutral amino acids such as
phenylalanine, tyrosine, tryptophan, leucine, isoleucine,
valine, methionine, and histidine.[26] Dietary protein can thus
lead to competition for these active carrier sites. Once L-dopa
molecules have reached the bloodstream, access to the brain is
dependent on similar active amino acid transport across the
blood-brain barrier for which it must compete with other
circulating neutral amino acids.[27]

 Intravenous infusion of L-dopa at a constant rate can produce
stable and sustained motor responses in patients with motor
fluctuations. When oral protein or neutral amino acid loads are
then administered, a transient loss of response occurs without
change in blood L-dopa concentration, indicating a block to
L-dopa passage into the brain through competition for transport
across the blood-brain barrier.[24] Constant rate intraduodenal
infusion also produces efficient L-dopa absorption, stable
L-dopa blood level, and sustained clinical responses in fasting
patients. With oral administration of protein, the relative
importance of competition by dietary neutral amino acids at gut
and blood-brain barrier levels can be compared. Oral protein
causes a loss of clinical response to L-dopa without affecting
blood concentration: this indicates that the major site of
interference between L-dopa and amino acid active transport is
at the blood-brain barrier.[28] Experimental data regarding the
equilibrium constant for active transport of large neutral amino
acids also agree with this observation. In gut, as in most
tissues, the equilibrium constant is considerably higher than
physiological concentrations of neutral amino acids However, the
constant for brain capillary endothelial cells (which form the
physiological blood-brain-barrier) is about 10 times less than
for other tissues and approaches the sum of postprandial plasma
concentrations of large neutral amino acids.[29]

 Unpredictability is a major feature of severe motor
fluctuations. Although patients experience the fluctuations
every day, the timing of dramatic changes in motor disability
and the amount of "on" and "off" time per day are never the same
despite constant pharmacological treatment. Erratic L-dopa
absorption due to the influence of food on gastric emptying[30]
and the dissociation between L-dopa plasma concentration and
clinical effect because of dietary neutral amino acids in the
bloodstream[31] appear to be the chief factors generating the
unpredictable element of motor fluctuations.

-----------------------------------------------------------

Table 2. Practical Dietary Guidelines for Parkinsonian
    Patients

DIETARY ADVICE RELEVANT TO ALL PATIENTS WITH PARKINSON'S DISEASE

Take L-dopa doses with food when starting treatment.

Energy intake at upper limit of age-related energy
requirement (probably greater than 30 kcal/kg of ideal
weight), particularly if patient is below ideal weight or   has
a history of weight loss.

Calcium intake above recommended dietary allowance of 500
mg/day.

Supplementation with dietary fiber and adequate fluid intake
to prevent or reduce constipation.


PATIENTS WITH FLUCTUATING RESPONSE TO L-DOPA

Take oral L-dopa doses at least 30 minutes before meal times
to minimize effects of postprandial gastric emptying.

Protein intake not to exceed recommended dietary allowance
and evenly distributed throughout the day.

Trial of protein redistribution diet for patients with
  refractory motor fluctuations.

  Careful monitoring of weight and nutrition by a clinical
  nutritionist or dietitian.

  Return to standard diet if significant clinical benefit
  does not occur within 2 weeks.

  Supplement calcium intake if necessary.



Judicious use of broad beans in season or frozen alternative
  (pods and legumes cooked gently and consumed together) in
  substitution for protein-rich foods.

-----------------------------------------------------------

DIETARY STRATEGIES TO IMPROVE THE RESPONSE TO L-DOPA TREATMENT

 Most patients with Parkinsonian motor fluctuations are able to
observe effects of food intake on motor function, and many
remark spontaneously that meals tend to cause shortening or
failure of response to L-dopa tablet doses. Parkinsonian
patients are also particularly amenable to dietary modification
strategies. In many situations in medical practice, dietary
modification is an important aspect of treatment, but from a
patient's perspective, changes in life-long dietary habits are
required for an  abstract goal of improved general health at
some future time. For patients suffering from Parkinsonian motor
fluctuations, interference between food and response to
medication contributes to disability on an hour-to-hour basis,
and any response to dietary therapy is likely to be immediate.
In practice, Parkinsonian patients will often accept quite
drastic dietary changes and some will institute their own
empirical modifications of diet.

 Manipulation of protein intake has been the most widely studied
dietary strategy. Various protein-restriction diets have been
evaluated with clinical and pharmacokinetic
measurements.[31-36] Most studies agree that a high protein
intake inhibits the effectiveness of L-dopa treatment and that
the benefits of reduced protein intake are mediated through
reduction in circulating neutral amino acid concentration rather
than increased L-dopa absorption.[31,35,36] Carter et al. found
that protein restricted to the recommended dietary allowance
(RDA) level of 0.8 g/kg/day allowed a better response to L-dopa
than a usual protein intake of 1.6 g/kg/day.[35] However, the
most effective dietary strategy involves redistribution of
protein intake.[31] This requires protein to be virtually
excluded in food taken during the day (protein content
restricted to 7 g) with daily protein requirement being made up
in a high-protein evening meal. Carter et al compared various
diets in a group of fluctuating patients on standard oral L-dopa
medication. While taking an average American amount of protein
in their diet, these patients were "on" for 51% of the waking
day. When protein intake was reduced to the RDA level, "on" time
increased to 61% and when a protein redistribution diet was
taken, patients remained "on" for 71% of the time.[35] The
protein redistribution diet requires considerable reorganization
of mealtimes, and patients have to accept a period of loss of
response to medication following the higher-protein evening
meal. Nevertheless, with appropriate dietary guidance and
encouragement, the majority of patients are able to comply with
the diet. About 60% of patients report improvement in control of
motor symptoms and a more stable response to L-dopa, usually
within a few days.[34] The diet offers no benefit to patients
who do not fluctuate because of poor responsiveness to
L-dopa.[34]

 Long-term experience with the protein redistribution diet
suggests that 70% of patients who gain an initial advantage will
use the diet for 12 months or more.[37] A study of the
nutritional status in patients restricting daytime protein
intake for 2 months showed that significant reduction in the
intake of protein, calcium, phosphorus, iron, riboflavin, and
niacin occurred.[38] However, only calcium intake fell to below
the RDA level, probably because of a restriction on the intake
of dairy products. Body weight and serum prealbumin
concentration did not change significantly. Although dietary
protein redistribution is an effective long-term treatment in
some patients, careful monitoring of nutrition is required. This
is of particular importance when the usual diet is marginally
adequate and when patients are at risk for osteoporosis.

 Manipulation of dietary components other than protein has been
studied less extensively. Carbohydrate loads, by stimulating
insulin secretion, reduce circulating amino acid levels.[39]
This may be the explanation for the observation that the
effectiveness of oral L-dopa doses is enhanced by glucose
loading.[40] Berry et al administered balanced
carbohydrate:protein  (ratio  =  5)  meals  to Parkinsonian
patients and found that plasma neutral amino acid levels did not
change.[41] They suggested that the effect of carbohydrate in
lowering amino acid concentration could cancel out the rise
following a moderate protein load and that a balanced dietary
intake may be as effective as protein restriction/redistribution.

 Limiting or redistributing protein intake may minimize
competitive inhibition of transmembrane passage of L-dopa into
the brain but may not be the best way to influence other forms
of dietary interference with the action of L-dopa, particularly
the effects of food on gastric emptying. Redistribution of the
dietary energy content or adjustment of the fiber-type and
viscosity of meals may allow more efficient access of L-dopa
medication to absorption sites. These forms of dietary
manipulation have not been systematically evaluated in
Parkinson's disease. Meal size will also affect the time taken
for gastric emptying. Small snacks taken with L-dopa medication
do not significantly interfere with the clinical response to the
drug.[42] However, dividing daily dietary intake into multiple
small feedings rather than three standard meals does not improve
the effectiveness of treatment.[33]

DIETARY SOURCES OF L-DOPA

 Food can also be a source of L-dopa. In 1913, Guggenheim first
isolated dihydroxyphenylalanine in its levorotatory form after
extracting it from Vicia faba beans.[43] He was also first to
demonstrate a pharmacological action of L-dopa when he ingested
some of his bean extract and became nauseated. He found the bean
pods to be a richer source of L-dopa than the beans.

 There are anecdotal reports that patients with Parkinson's
disease will benefit from meals of broad beans, and that
response to Vicia faba may even be better than conventional
L-dopa medication in some cases.[44] Recent studies have
established the dose-response and L-dopa absorption
characteristics of Vicia faba.[45,46] There is sufficient L-dopa
in broad bean pods to be pharmacologically active in Parkinson's
disease. The beans are a natural food which contains L-dopa in a
physicochemical form different from that of tablet formulations
and may thus have some use in the management of Parkinsonian
motor fluctuations.

 In our single-dose studies[46], we evaluated patients with
pronounced "on-off" motor oscillations. Clear and unequivocal
responses to L-dopa doses occur in such cases and their
magnitude and time course can be accurately quantified by serial
objective motor assessments. Simple meals of broad bean pod
mixture were prepared by microwave cooking and homogenization
and were administered with carbidopa. In five of six patients
studied, Vicia faba meals produced motor improvement accompanied
by dyskinetic involuntary movements in the absence of other
dopamine receptor-stimulating pharmacological agents. Motor
responses following V. faba ingestion were generally equivalent
to but no better than responses to conventional oral L-dopa
doses, suggesting that the motor benefits of Vicia faba can be
attributed to their L-dopa content alone, rather than to other
pharmacologically active naturally occurring substances.

 We measured the L-dopa recovery at 0.25% per weight of Vicia
faba pods. (Guggenheim, who used stoichiometric methods to
measure the L-dopa content of a sample of fresh bean pods,
obtained an identical result,[41]) Thus a 100-g serving of Vicia
faba pods contains about 250 mg of L-dopa, equivalent to the
L-dopa content of one of the standard pharmaceutical
formulations. Our pharmacokinetic measurements were consistent
with ingestion of L-dopa doses of that order of magnitude
although plasma L-dopa concentration following V. faba doses was
more variable than for tablet doses after fasting. Prolonged
freezing did not lead to clinically significant degradation of
the L-dopa content of Vicia faba, Figure 1 shows a comparison of
motor response and plasma L-dopa concentration following
standard L-dopa/carbidopa and broad bean pod doses in a patient
with pronounced motor fluctuations. The magnitude of response
(difference between "off" and "on" states) is almost identical.
The V faba meal produces a longer response which seems to be
explained by a larger L-dopa dose and higher plasma
concentration, The post-dose rate of rise and decay of plasma
L-dopa level in our studies was similar to standard L-dopa
preparations; V. faba meals did not have the properties of a
slow release L-dopa preparation.[47]

 Most of the L-dopa contained in V, faba exists in a free-form
in the bean pods although small quantities of dopa glucoside can
be detected in both legumes and pods.[48] L-dopa also occurs
naturally in significant quantities in several other leguminous
species. It is present in the Georgia velvet bean (Stizolobium
deeringianum)[49] and the legumes and seeds of the Indian
medicinal plant Mucuna pruriens.[50] The L-dopa yield per weight
of the latter plant is considerably greater than from Vicia faba.

 Natural sources of L-dopa cannot compete with tablet
formulations for convenience and predictable bioavailability.
However, V faba does have some potential advantages in reducing
the interaction between oral L-dopa medication and diet. Rather
than simply restricting oral protein intake, a diet that
substitutes V. faba for other foods which contain protein, in
conjunction with conventional L-dopa/decarboxylase inhibitor
medication, may have a stabilizing effect on motor fluctuations
and reduce food-induced "off" phases. Vicia faba is a relatively
rich protein source (if both legumes and pods are ingested),[51]
which has a positive effect on both plasma L-dopa concentration
and motor function.

 Lack of availability of pharmaceutical L-dopa/decarboxylase
inhibitor drugs is a major limitation to the management of
Parkinson's disease in developing countries. Vicia faba is
widely grown in some regions of the world and is inexpensive,
both as a nutritional substance and as a pharmacological
treatment. Vicia faba or one of the other L-dopa containing
plant species could be used where standard pharmacological
treatment is not available or is in short supply. Higher doses
of L-dopa are required when a decarboxylase enzyme inhibitor is
not administered. However, the early phase of L-dopa treatment
in the l960s and l970s demonstrated that high-dose L-dopa was
effective in Parkinson's disease despite some side effects
because of excessive peripheral conversion of L-dopa to
dopamine.[1]

WEIGHT LOSS AND ENERGY BALANCE

 Weight loss is a common symptom in Parkinson's disease. James
Parkinson mentioned cachexia as part of the first description of
the disorder.[52] Two anthropometric surveys of Parkinsonian
patients have shown that mean body mass is significantly lower
than for age-matched controls. In one study, females were
predominantly affected,[53] while in the other, weight loss
affected both sexes with evidence of protein/calorie depletion
in men and energy subnutrition in women.[54] Weight loss often
occurs in phases during the disease course, followed by periods
of stabilization of weight. Sometimes, weight loss can be so
rapid and severe that investigation for underlying malignancy is
carried out.[55] Many patients with advanced disease and severe
motor fluctuations have low body weight and deficient body fat
stores. Alterations in both energy input and output occur in
Parkinson's disease and may contribute to weight loss.

ENERGY INPUT

 Reduction in food intake may contribute to negative energy
balance. Nausea and anorexia can occur in relation to most
anti-Parkinsonian medications including L-dopa and dopamine
receptor agonist drugs. Depression and cognitive impairment are
both common in Parkinson's disease and may reduce apetite.
Olfactory sensation has been shown to be reduced. and this might
affect taste and desire for food.[56] The degenerative changes
of Parkinson's disease result in a 60% reduction of dopamine
content in the hypothalamus,[57] and hypothalamic Lewy bodies
(neuronal intracellular inclusion bodies which are the
pathological hallmark of Parkinson's disease) may also be
found.[58] In theory these changes could impair the central
weight and appetite control mechanisms.

 Disturbances of motor function affecting mastication and
swallowing are common in Parkinson's disease and will impair the
ingestion of food if severe. However, a recent study comparing
body weight of patients with Parkinson's disease and
Steele-Richardson syndrome (a separate extrapyramidal
degenerative disease entity) found that body weight was slightly
lower in Parkinson's disease. The fact that Steele-Richardson
syndrome usually causes greater impairment of bulbar muscle
function than Parkinson's disease suggests that bulbar
involvement is not the chief cause of weight loss.

ENERGY OUTPUT

 The motor disability of Parkinson's disease impairs mobility
and may reduce the level of physical activity. Yet in some
situations, energy consumption by skeletal muscle may be
increased. Involuntary motor activity due to tremor or L-dopa
induced dyskinesia are the most obvious examples of this.
Extrapyramidal rigidity (increased resting muscle tone) and
dystonia (sustained abnormal limb or truncal postures due to
abnormal cocontraction of agonist and antagonist muscle groups)
may also increase muscle energy use. Resting energy expenditure,
as measured by oxygen consumption, is increased in Parkinsonian
patients.[60,61] Levis et al. measured energy expenditure before
and after L-dopa doses and found that both increased muscle tone
in "off" phases and involuntary movements in "on" phases could
increase oxygen consumption.[61]

 One of the major evolutionary influences on the development of
motor control in animals is the requirement that essential motor
activity be performed with minimum expenditure of energy. The
motor system achieves this goal through appropriate selection of
agonist and antagonist muscle groups and by coordinating
contraction of these muscles. The basal ganglia play a central
role in this process, which occurs "automatically" as part of
every voluntary movement and which is disturbed in various basal
ganglia disease states. In Parkinson's disease, the basic
pattern of muscle selection and activation for movement is
preserved, but insufficient muscular activity is recruited for a
specific task.[62] For a movement to continue, additional cycles
of motor recruitment are required. Control of complex,
simultaneous, or sequential movements is impaired to an even
greater degree.[63] One consequence of these abnormalities of
the organization of movement may be a loss of efficiency of
energy consumption. Thus, for a given level of physical
activity, a patient with Parkinson's disease may expend more
energy than a normal subject.

CONCLUSION

 The 20th century has seen the progressive development of the
scientific basis of an expanding discipline of clinical
nutrition, scarcely articulated until recently.[64] The
progression has been from micronutrients and deficiency disease,
to macronutrients and chronic noncommunicable disease, to an
interest in nonnutrients in food of biological importance and
how they modulate the expression of disease and provide
opportunities for management.

 The present interest in food as a source of L-dopa stems from
embryonic knowledge obtained early this century and now has to
be reconciled with other nutritional factors which affect motor
function and response to pharmacological therapy in Parkinson's
disease.



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52.     Parkinson J. An essay on the shaking palsy. London:
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> -----Original Message-----
> From: BRowley368 [SMTP:[log in to unmask]]
> Sent: Friday, April 03, 1998 7:51 AM
> To:   Multiple recipients of list PARKINSN
> Subject:      Faba beans
>
> Hello all,
>
> My dad has a question about Broad beans (Vicia Faba).
>
> I know there has been a little bit of discussion about "Fava" but here are
> dad's question.  Have there been any definitive studies done on the use of
> broad beans as a source of dopamine? Are they being grown anywhere in the
> world on a commercial basis for their dopamine?
>
> Thanks
>
> Bonnie
> daughter of Jim 76/2