especially the title with the last post being from Z flower ; i feel like I'm entering a garden and it is usually a calm thread and friendly

Absolutely OT.
paula

Thanks ZucchiniFlower. Pharam companies have no interest in Mucuna for obvious reasons nither the medical establishment, so we are left on our own with regard its use. The following link provides more information which I understand to mean that the anti PD benifits of mucuna may be due to costituents other than L-dopa. I will appreciate your comment

http://www.phcogrev.com/issue1/19.pdf
"Anti-Parkinson’s activity
Traditionally, M. pruriens has been used as a nerve tonic for
nervous system disorders. Because of the high concentration
of L-dopa in the seeds, it has been studied for its possible use
in Parkinson’s disease. Numerous in vivo studies also have
been conducted in rats and humans (28, 29). Hussain et al
proved that Mucuna pruriens is more effective than L-DOPA
in parkinson’s disease in animal model (30). Even L-Dopa free
fraction of seed showed significant antiparkinsonism activity
(31, 32). These studies state that at equivalent doses Mucuna
powder resembles L-DOPA with respect to modulation of
dopaminergic pathways, while the presence of other
constituents in contribute to improved antiparkinsonian
activity and greater tolerability in animals.
Clinical Research
HP-200, which is a first liquid levodopa contains Mucuna
pruriens endocarp, has been shown to be effective in the
treatment of Parkinson's disease. The long-term effect of
Mucuna pruriens endocarp in HP-200 on monoaminergic
neurotransmitters and its metabolite in various regions of the
rat brain was studied by Manyam et al. HP-200 at 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 antiparkinson
effect may be due to components other than levodopa or that
it has an levodopa enhancing effect (33). In a clinical trail,
Eight Parkinson’s disease patients with a short duration Ldopa
response and on period dyskinesias completed a
randomised, controlled, double blind crossover trial. Mucuna
preparation led to a considerably faster onset of effect,
reflected in shorter latencies to peak L-dopa plasma
concentrations. Peak L-dopa plasma concentrations were 110
% higher and the area under the plasma concentration v time
curve (area under curve) was 165.3% larger. No significant
differences in dyskinesias or tolerability occurred (34).
Hypoglycaemic and Hypocholesterolemic activity
M.C. Pant et al reported that Mucuna pruriens possesses
hypoglycemic and hypocholesterolemic effects in the normal
rats (35). The sugar level was lowered by 39% and the
cholesterol level was lowered by 61% with the rats fed with
Mucuna pruriens.

Imark, thanks so much for that articles. Mucuna has amazing properties and can do much more for us than Sinemet can, it seems.

That's fantastic. This is surprising:
I was happy to read:
I'm especially happy that is seems to be neuroprotective. An amazing find. I wonder when they first began using it for PD and how they stumbled on it. It's pathetic that the MDS at my health plan never even heard of it. But she gave her blessing, anyway, for me to take it. I just got a referrel for a new MDS.

In other articles the HP-200 was a powder. I didn't know they had a liquid formulation. I thought it was the same as Zandopa, a powder that you dissolve (or suspend) in water.

Bioavailability of L-DOPA from HP-200 : a formulation of seed powder of Mucuna pruriens (Bak) : a pharmacokinetic and pharmacodynamic study
Auteur(s) / Author(s)
MAHAJANI S. S. (1) ; DOSHI V. J. ; PARIKH K. M. (1) ; MANYAM B. V. ;
Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
(1) Divisions of Pharmacology, The Zandu Pharmaceutical Works Ltd., Bombay, INDE
Résumé / Abstract


HP-200, a formulation made from the seed powder of Mucuna pruriens, contains among other constituents, about 4% L-DOPA.

After five normal human volunteers were each given a single oral dose of 30 g of HP-200, plasma samples were obtained at 0, 20, 40, 60, 90, 120, 180, 240 and 360 min for assay of L-DOPA by HPLC technique using electrochemical detection. The supine systolic and diastolic blood pressures were recorded at each sampling time.

The results indicate that on oral administration, L-DOPA was absorbed from HP-200 with plasma peak levels (C[max]=1.56±0.163 μg/mL) achieved at T[max]=83±16.09 min. The plasma half life was 102±2 min and the auc was determined as 6.508±0.421 μg/h/mL.

The pharmacokinetic profile of HP-200 exhibited characteristics similar to formulations of synthetic L-DOPA, except for the lack of a sharp peak. HP-200, a new herbal formulation, appears to be suitable for the treatment of Parkinson's disease.


Revue / Journal Title
PTR. Phytotherapy research (PTR, Phytother. res.) ISSN 0951-418X
Source / Source
1996, vol. 10, no3, pp. 254-256 (7 ref.)

Published Online: 11 Oct 2004

Phytotherapy Research

Volume 18, Issue 9 , Pages 706 - 712
Research Article
Neuroprotective effects of the antiparkinson drug Mucuna pruriens
Bala V. Manyam 1 *, Muralikrishnan Dhanasekaran 1, Theodore A. Hare 2




Abstract
Mucuna pruriens possesses significantly higher antiparkinson activity compared with levodopa in the 6-hydroxydopamine (6-OHDA) lesioned rat model of Parkinson's disease. The present study evaluated the neurorestorative effect of Mucuna pruriens cotyledon powder on the nigrostriatal tract of 6-OHDA lesioned rats. Mucuna pruriens cotyledon powder significantly increased the brain mitochondrial complex-I activity but did not affect the total monoamine oxidase activity (in vitro).

Unlike synthetic levodopa treatment, Mucuna pruriens cotyledon powder treatment significantly restored the endogenous levodopa, dopamine, norepinephrine and serotonin content in the substantia nigra.

{previous article says:

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. } ??? I thought the substantia nigra was part of the nigrostriatal tract. I'm so confused.

Nicotine adenine dinucleotide (NADH) and coenzyme Q-10, that are shown to have a therapeutic benefit in Parkinson's disease, were present in the Mucuna pruriens cotyledon powder. Earlier studies showed that Mucuna pruriens treatment controls the symptoms of Parkinson's disease.

This additional finding of a neurorestorative benefit by Mucuna pruriens cotyledon powder on the degenerating dopaminergic neurons in the substantia nigra may be due to increased complex-I activity and the presence of NADH and coenzyme Q-10.

sorry this is a repost

Research Article
Efficacy and safety of herbal medicines for idiopathic Parkinson's disease: A systematic review

Volume 21, Issue 10, Pages 1709-1715

Published Online: 7 Jul 2006

Copyright © 2006 Movement Disorders Society

http://www3.interscience.wiley.com/c...2921/HTMLSTART

Article Text

Parkinson's disease (PD) is the second most common manifestation under the umbrella of neurodegenerative disorder family in the United States, with a prevalence of 100 to 200 per 100,000 persons older than 40 years of age.[1] Various pharmacological and surgical approaches have been developed to manage this common disease, but some of these approaches carry significant adverse effects. For example, the most commonly prescribed drug, levodopa (LD), is associated with dose-limiting motor and psychiatric side effects in 100% of young-onset patients[2] and 50% of other patients after 6 years of therapy.[3] Due to these limitations of conventional medicine, patients resort to complementary and alternative medicine (CAM). In the United States, 40% of all PD patients reported the use of at least one form of CAM for their illness,[4] whereas in the United Kingdom, 38.7% of patients used it solely for the treatment of their Parkinsonism.[5]

One of the most popular CAM modalities used is herbal medicine (HM). Some basic research on their mechanisms of actions have been performed. For example, Mucuna pruriens (MP) originated from Indian Ayurvedic medicine[6] has been found to possess significantly higher antiparkinsonian activity compared with synthetic L-dopa in the 6-hydroxdopamine (6-OHDA)- lesioned rat model of PD.[7] This superiority is proposed to be exerted by the combined actions of intrinsic L-dopa and neuroprotective substances (nicotine adenine dinucleotide [NADH] and coenzyme Q-10) in the herb.[8] In traditional Chinese medicine (TCM), various combinations of herbs are used to treat PD.[9] Recent research suggests that certain Chinese herbal compounds show neuroprotective effects in 6-OHDA-treated PC 12 model, which indicates that TCM herbs may offer a potential therapeutic strategy for various neurodegenerative diseases.[10] In addition, the use of cannabis among long-term LD users is also mentioned in the literature for its antidyskinetic function.[11] It is postulated that cannabis achieved such action by augmenting -aminobutyric acid (GABA)ergic transmission by means of the inhibition of GABA reuptake in the lateral part of the globus pallidus.[12]

Anecdotal evidence shows that some of these herbs offer beneficial effects,[13-15] but their use has also raised much concern as to their safety.[16-18] We conducted this systematic review to shed light on their efficacy, safety, and clinical applicability.

Herbal Medicine as a Monotherapy

Katzenschlager reported that MP seed powder and LD coadministered with carbidopa caused a similar degree of dyskinesia, as measured by Abnormal Involuntary Movement Scale and Goetz scales, but MP exhibited a more rapid onset of action and longer on time when compared to LD plus carbidopa. However, the best UPDRS rating during the on state did not differ significantly among the two therapies.

Carroll reached a conclusion that cannabis has no therapeutic effect on L-dopa-induced dyskinesia, as measured by Question 32-24 of the UPDRS and by other relevant outcome measures. In addition, no statistically significant improvements on overall UPDRS and PDQ-39 were observed.

Compared to Madopar, Tang noted that zhiyinxifeng granules showed a similar efficacy; while Guo reported a relatively higher efficacy of kanli decoction, both measured in terms of the improvement in the overall Webster scale scoring. However, flaws in design and statistical analysis in these two studies limited the reliability of their conclusions.

Adverse Events and Withdrawals

As a monotherapy, the adverse events of herbal medicines were reported in three studies (Katzenschlager, Carroll, and Tang). Katzenschlager reported a case of dropout due to short-lasting vomiting after the ingestion of 30 g of MP. Other side effects included transient nausea and mild dizziness. No observations on clinically relevant abnormalities in hematology and biochemistry were made.

....Only Katzenschlager used a firm diagnostic criteria (Queen Square Brain Bank Criteria[48]) for enrollment. ....

Worth a repost:

http://jnnp.bmj.com/cgi/content/full/75/12/1672

Journal of Neurology Neurosurgery and Psychiatry 2004;75:1672-1677

PAPER
Mucuna pruriens in Parkinson’s disease: a double blind clinical and pharmacological study
R Katzenschlager1,2, A Evans1, A Manson3, P N Patsalos4, N Ratnaraj4, H Watt5, L Timmermann6,



Background: The seed powder of the leguminous plant, Mucuna pruriens has long been used in traditional Ayurvedic Indian medicine for diseases including parkinsonism. We have assessed the clinical effects and levodopa (L-dopa) pharmacokinetics following two different doses of mucuna preparation and compared them with standard L-dopa/carbidopa (LD/CD).

Methods: Eight Parkinson’s disease patients with a short duration L-dopa response and on period dyskinesias completed a randomised, controlled, double blind crossover trial. Patients were challenged with single doses of 200/50 mg LD/CD, and 15 and 30 g of mucuna preparation in randomised order at weekly intervals.

L-Dopa pharmacokinetics were determined, and Unified Parkinson’s Disease Rating Scale and tapping speed were obtained at baseline and repeatedly during the 4 h following drug ingestion. Dyskinesias were assessed using modified AIMS and Goetz scales.

Results: Compared with standard LD/CD, the 30 g mucuna preparation led to a considerably faster onset of effect (34.6 v 68.5 min; p = 0.021), reflected in shorter latencies to peak L-dopa plasma concentrations.

Mean on time was 21.9% (37 min) longer with 30 g mucuna than with LD/CD (p = 0.021); peak L-dopa plasma concentrations were 110% higher and the area under the plasma concentration v time curve (area under curve) was 165.3% larger (p = 0.012). No significant differences in dyskinesias or tolerability occurred.

Conclusions: The rapid onset of action and longer on time without concomitant increase in dyskinesias on mucuna seed powder formulation suggest that this natural source of L-dopa might possess advantages over conventional L-dopa preparations in the long term management of PD. Assessment of long term efficacy and tolerability in a randomised, controlled study is warranted.


.....The two doses of the mucuna preparation were chosen to correspond to either 100 mg (one sachet containing 7.5 g, that is 500 mg of neat L-dopa) or 200 mg (two sachets together containing 1000 mg of neat L-dopa) of L-dopa in the presence of a decarboxylase inhibitor. This conversion factor was based on published studies comparing clinical and pharmacokinetic L-dopa effects with and without a decarboxylase inhibitor.

...Single dose challenges
Patients were admitted to hospital for an overnight stay on three occasions each separated by 1 week. Challenges were performed at exactly the same time in the morning in each patient, after withdrawal of all anti-parkinsonian medication from midnight, and patients took nothing by mouth with the exception of black tea or coffee and water. Patients were randomised to the order of the days on which they would receive the three trial medications:

* 200 mg L-dopa/50 mg decarboxylase inhibitor (carbidopa) as capsule formulation plus four sachets of placebo as a powder formulation closely resembling mucuna seed powder in consistency and flavour, dissolved in a glass of water, or:
* 15 g, that is, two sachets of mucuna seed powder (containing 500 mg of L-dopa) plus two sachets of placebo powder plus a placebo capsule identical in shape, colour, and taste to the LD/CD capsule, or:
* 30 g, that is, four sachets of mucuna seed powder (containing 1000 mg of L-dopa) plus a placebo capsule.

.....Nine patients (five women and four men) were enrolled in the study. One patient dropped out due to shortlasting vomiting following ingestion of the first study medication (30 g mucuna), which was considered to have reduced the amount available for absorption. Eight patients completed the study. Patients’ mean age was 62.2 years (range 50–72); mean disease duration was 12.4 years (range 7–17); and mean Hoehn and Yahr stage (when "off") was 3.5 (range 2.5–4). Patients took a mean daily L-dopa dose of 572 mg (range 200–1000 mg) prior to the trial. Other antiparkinsonian medications taken were amantadine in two (200 mg), pergolide in three (mean, 3.2 mg), and ropinirole (18 mg), cabergoline (6 mg), and pramipexole (1.4 mg) in one patient each.

Clinical assessments
Results and statistical significance of differences are shown in tables 1Go and 2Go. Duration of full on-time was 21.9% longer with the 30 g mucuna dose compared with LD/CD. Time from beginning of switching on to returning to a full off state was increased by 19.8% with 30 g mucuna but was 26.6% shorter with 15 g mucuna. The mucuna preparations reduced the latency from drug ingestion to achieving a full on-state: this was 33.4% or 23 min shorter with 15 g mucuna than with LD/CD, and 49% or 34 min shorter with 30 g mucuna. Similarly, time to beginning of switching on was reduced by 49% or 27 min with 15 g mucuna and by 57.9% or 31.6 min with 30 g mucuna. Best UPDRS motor scores and tapping speed when "on" did not differ significantly among the three study drugs.....

DISCUSSION:


Our study demonstrates that the seed powder formulation of M pruriens contains a considerable quantity of L-dopa which, at a dose of 30 g, is sufficient to consistently induce a sustained on-period in fluctuating PD patients with short duration L-dopa response. The quality of motor improvement was equivalent to that seen with synthetic LD/CD, but the onset of action, duration of effect, and pharmacokinetic profiles differed considerably.

The latency to clinical onset was significantly and markedly shorter with mucuna than with synthetic LD/CD. The duration of the on-period was significantly longer with 30 g mucuna than with LD/CD, with a mean difference of 37 min. The time from the beginning of a visible antiparkinsonian effect to returning to a full "off" was significantly longer with 30 g mucuna, providing an additional 46 min when patients were partially "on".

Compared to literature reports on dispersible L-dopa formulations, the latency to the onset of effect following mucuna in our study was within a similar range. However, the duration of on-time achieved with 30 g mucuna was considerably longer: the time patients spent in a full on-state was 204 min following 30 g mucuna, compared with 14819 and 97 min20 reported in two studies with dispersible L-dopa formulations.

These clinical findings were reflected in the pharmacokinetic profile of L-dopa concentrations, which showed a significantly higher peak plasma concentration with 30 g mucuna, occurring after a shorter latency Tmax. The difference in Tmax was significant with 15 g and only narrowly missed reaching significance with 30 g.

Peak L-dopa concentrations on mucuna were followed by a decline which was faster with 15 g mucuna but similar to LD/CD with 30 g mucuna, resulting in a significantly larger total AUC with 30 g mucuna.

These findings suggest that M pruriens formulations may actually have a higher bioavailability than standard L-dopa preparations. Although the latency to peak concentrations with LD/CD was rather long at 95.5 min, this is within the upper range of reported findings with standard L-dopa preparations.21,22 All reasonable and practical measures were taken to avoid dietary interferences. Drugs that could inhibit gastrointestinal absorption were excluded, and none of the patients had known malabsorption syndromes or other gastrointestinal conditions. However, all the patients had been on long term L-dopa therapy for many years prior to the study.

The most obvious differences between the mucuna preparation and the synthetic formulation used in this study were the administration of mucuna in the form of a suspension as opposed to a capsule, and the presence of a dopa decarboxylase inhibitor in the standard L-dopa preparation. Decarboxylase inhibitors mainly increase L-dopa plasma concentrations by blocking the peripheral degradation of L-dopa to dopamine, thus allowing more L-dopa to cross the blood–brain barrier. However, the gastrointestinal mucosa is a site for decarboxylation of oral L-dopa23 and decarboxylase inhibitors have been reported to enhance duodenal L-dopa absorption,24,25 presumably by inhibiting metabolic pathways such as aromatic dehydroxylation in the gut.22 Adding a decarboxylase inhibitor leads to considerably higher peak L-dopa concentrations.9,10,26 One study proposed a doubling of the bioavailability of oral L-dopa in the presence of a decarboxylase inhibitor, but this was based on findings with intravenously administered L-dopa.27 Studies investigating oral L-dopa invariably reported a reduction of exogenous L-dopa by 60–80%.10,11,13,28 The conversion factor of 1:5 chosen for the 30 g mucuna dose in relation to standard LD/CD (L-dopa reduction by 80%) is in the upper range of reported ratios. It is possible that the truly corresponding dose is slightly less than 30 g, but this does not seem sufficient to explain the large differences in pharmacokinetic and clinical findings.

The impact of decarboxylase inhibitors on latency to peak concentrations varies in the reported literature. This has been found to be either shorter,26 similar,10,12,29 or longer9 compared with L-dopa alone, and one study28 found a dose-dependent reduction in Tmax in the presence of CD. Although the delay to maximum plasma concentration of 95.5 min found in our study appears rather long, similar delays on standard release LD/decarboxylase inhibitor have been reported in the literature.27,28 There is no obvious explanation for this finding. All reasonable measures were taken to avoid interference by drugs or food, and none of the patients had evidence of malabsorption syndromes or other gastrointestinal conditions.

In view of previously reported experience with mucuna, our observations of much higher peak L-dopa concentrations and larger AUCs on mucuna are unexpected and surprising. A possible explanation may lie in the administration of mucuna as a suspension: L-dopa is mainly absorbed from the proximal small intestine, and delays in reaching the duodenum through the gastric valve are likely to occur more commonly with any form of coating than with dispersible formulations. This explains why dispersible L-dopa works more quickly than standard preparations. The latency to the onset of a clinical effect with dispersible L-dopa has been reported to be on average 26.820 or 27.9 min19 and is thus comparable to the mean latency of 34.6 min observed in our patients with 30 g mucuna.

Additives contained in the mucuna powder preparation may also have had an impact on absorption: the seed powder preparation used in this study was produced with the aim of achieving as standardised a composition as possible. The small amount of ascorbic acid, added for chemical stability,30 may potentially have enhanced intestinal absorption.31 Citric acid is also known to have some effect on L-dopa absorption,32 but the addition of a small amount of citric acid does not seem likely to be a sufficient explanation for such a marked difference in pharmacokinetics. Some other additives differed slightly from those found in the commonly used commercial Indian preparations, and further investigations into factors that may promote gastrointestinal absorption of the seed powder compound are warranted.

Decarboxylase inhibitors were shown to prolong L-dopa t1/2; to a moderate degree in most12,24,27 but not all9,33 studies. In contrast, our own data show a similar rate of decline of L-dopa plasma concentrations with 30 g mucuna and LD/CD. Although a small residual effect from patients’ on going carbidopa medication cannot be excluded due to its plasma t1/2; of 3 h, the similarity in the plasma concentration decline between LD/CD and 30 g mucuna raises the possibility of an additional active ingredient in the mucuna preparation with a blocking effect on L-dopa degradation. However, there is as yet no direct evidence of such active agents contained in the plant preparation.

The metabolite 3-OMD showed very similar AUC on mucuna and LD/CD, despite higher peak plasma concentrations of L-dopa with 30 g mucuna. This can largely be explained by the fact that in the absence of a decarboxylase inhibitor in the mucuna preparation, L-dopa was predominantly metabolised by decarboxylation, leading to smaller concentrations of 3-OMD.

The combination of rapid onset of action with long duration of effect appears to constitute a characteristic of this plant preparation. Previous limited pharmacokinetic reports with mucuna preparations suggested a lower bioavailability of mucuna with a somewhat slower increase and decline of L-dopa plasma concentrations and a lower peak.34 However, these comparisons were done with historical controls rather than in a controlled comparison. In contrast, our findings indicate that mucuna formulation may actually have a higher bioavailability than standard LD/CD which may not be explained by dose alone.

It is also noteworthy that despite larger mean L-dopa concentrations associated with 30 g mucuna, there were no significant differences in dyskinesia severity during the challenges. Although both the longer duration of effect and the larger AUC can in part be explained by higher maximum concentrations reached with 30 g mucuna,35 the differences are striking and raise the possibility of additional explanations.

Another aim of this study was to compare the clinical efficacy and tolerability of the two doses of the mucuna preparation. While a dose of 30 g of the mucuna preparation led to reliable and sustained antiparkinsonian effects in all patients, this did not always occur with the 15 g dose, and pharmacokinetic results clearly showed that L-dopa concentrations were considerably lower with the smaller dose.

Tolerability was comparable with all three study drugs. Adverse effects were mild and shortlasting, and the patient who dropped out from the study due to vomiting on 30 g mucuna fully recovered within a few minutes, and was prepared to stay in the trial. The assessment was discontinued, however, because part of the ingested drug was likely to have become unavailable for absorption.

Acute side effects of L-dopa such as nausea, vomiting, and orthostatic hypotension have been shown to be correlated with plasma concentrations9 and to occur less often in the presence of a decarboxylase inhibitor.9,36 In view of the significantly higher plasma concentrations reached with 30 g mucuna than LD/CD, it is encouraging that side effect profiles were similar in our study.

However, this lack of difference may have been partly due to the fact that tachyphylaxis and peripheral tolerance to dopamine receptor stimulation occur with chronic L-dopa administration, and different results may have been seen in de novo patients. It might be appropriate to administer mucuna preparation in combination with a peripheral dopa decarboxylase inhibitor which may further improve tolerability and efficacy.

The combination of M pruriens with domperidone, which blocks peripheral dopamine receptors, would also be expected to reduce peripheral adverse events. Domperidone was not used in this study because it has been shown to slightly improve L-dopa absorption.37

M pruriens grows widely throughout the tropics and is currently mostly planted to improve soil and provide animal feed, and to a smaller extent, for human consumption. It is believed the biological purpose of the L-dopa concentration is to protect the plant against insect attack. Mucuna contains larger amounts of L-dopa than any other known natural source.38,39 Further natural sources of L-dopa include other members of the mucuna genus, such as Stizolobium deeringianum,40 and Vicia fava (broad bean), in which L-dopa was identified in 1913.41 An open-label study of 250 g of cooked V fava compared with 100 mg synthetic LD/CD showed lower peak plasma concentrations following the bean meal, and pharmacokinetic profile and clinical effects very similar to synthetic L-dopa.42 In an uncontrolled study,38 one patient failed to switch on altogether following 150 g of V fava. Clinical benefit from longer term use has also been reported in an uncontrolled fashion.43 Although limited conclusions are possible in the absence of randomised, double blind investigations of V fava, there is no suggestion in the reported literature that it might share the pharmacokinetic properties of mucuna found in our study. Moreover, the use of V fava for the treatment of PD also has practical limitations: the much lower L-dopa content in V fava compared with mucuna requires the ingestion of bulky meals, and there is a risk of favism, a haemolytic anaemia which can occur in persons with a genetic deficiency of the enzyme glucose 6-phosphate dehydrogenase.

Recent animal data44 have suggested anti-lipid peroxidation effects of an alcohol extract of M pruriens. If confirmed in further studies, this raises the possibility of an additional beneficial role for mucuna.

Based on this preliminary pilot study in patients with PD and short duration L-dopa response, the 30 g M pruriens formulation seems to possess potential advantages over existing commercially available controlled release or dispersible formulations of L-dopa in that it combines a rapid onset of action with a slightly longer duration of therapeutic response compared with a dose of standard L-dopa calculated on the basis of the known quantity of L-dopa in mucuna using standard conversion ratios. No increase in dyskinesia severity or in peripheral dopaminergic adverse events was found on the mucuna preparation. Further analysis of the seeds’ content may reveal further explanations for the differences in the pharmacokinetic profiles found in this study. If these findings can be confirmed in larger and longer term studies, mucuna would seem to be a reasonable commercially viable alternative to standard L-dopa.

Is it just me, or does anyone else have a negative reaction to the name of the plant, Mucuna pruriens? It makes me think of "prurient mucus". I know that is totally irrational, but I must admit that it is a definite turn-off for me.

From a strictly objective, scientific perspective, however, M. pruriens appears to be a safe and effective source of anti-parkinson treatment. It is hard to argue with studies like those posted on this thread, as well as the centuries of safe, effective use in Ayurvedic medical practice.

I just may have to ignore my subjective bias and try it myself!

Robert

Robert, it's also called Velvet Bean. How's that for you?
It also has another name, cowage or something which I dislike.
Here it is: Cowage, Cowitch, Velvet Bean, Pica

It's also called:

(Bengal Bean, Buffalo Bean, Cow Itch, Cow-Itch, Cowage Velvetbean, Cowitch, Fogarate, Gratey, Hell Fire Bean, Itchy Bean, Mauritius Bean, Nescafe, Pica Pica, Pois Velu, Pois-Gratter, Purple Jade Vine, Velvet Bean)!!

THE FLOWERS ARE PRETTY PURPLE!
http://zipcodezoo.com/Plants/M/Mucuna_pruriens.asp

Cowage, Cowitch
[Velvet Bean]

Cowage, Cowitch
Click to enlarge

Mucuna pruriens (Cowage, Cowitch, Velvet Bean, Pica)

Mucuna pruriens, a member of the legume family, is a climbing plant that grows up to 30 ft. in length. Mucuna pruriens forms compound leaves that grow 4-10'' long and is composed of three leaflets. The pods of the Mucuna pruriens contain 2-5 per cluster and grow 2-3 inches long. Each pod contains 3-6 large black seeds. The pods have barbed hairs, also called trichomes, that cause an intense stinging irritation to the skin. (Thanks to whoever first soldiered on and got to the seeds.) It is a very prolific and hardy plant in the South.

The Mucuna plant has many traditional and medicinal usage including treating abdominal pain, cholera, diabetes, infertility, Parkinson’s disease, scorpion bites, snakebites, and toothache. Because of the large amount of Levo-dopa in the seed it is used for treating Parkinson’s disease.

http://plants.usda.gov/java/profile?...Print&photoID=