Mucuna Pruriens
 

Any one still takes this stuff or zadopa? In the old forum, some who took this stuff reported great experience after taking this stuff and curious to know if it can be a complete replacement of sinemet. Does it bring long term benefits (say neuron protective effect) or it bring the same evil (say dyskinesa) as sinemet? appreciate your sharing.

LING

mucuna
 

Ron Hutton and I both tried it in various forms a couple of years ago. My own experience was positive and I plan to get back to it. In fact, just yesterday I bought one of those little trays for filling capsules with mucuna in mind...

I tried it as raw powder, a standardized form called "Dopabean" by Solaray, and a strong concentrate by Herbalife. They all worked much like Sinemet. You had to do a little trial and error to get the dosage right, however.

I will probably reintroduce it in a few weeks. The reason I quit the powder was that it is an incredible staining agent. Black as can be and it does not come off. That's why I got the capsules. I can fill them outdoors.

Mucuna is a far more complex substance than levadopa. One thing that particularly interests me is that I was using dosages roughly equivalent to the Sinemet and getting similar results. But mucuna has no carbidopa to shield it from your body's enzymes. According to conventional wisdom, almost none should get to the brain. Yet it does.

Rick, where did you get this, please? I want to take my Zandopa and hate drinking it.

Rick, researchers surmise that mucuna contains a chemical that works like carbidopa. It's more effective that the same amount of L-Dopa via Sinemet.

This looks like a good deal:

http://www.athletes.com/store/now/cap.html

http://www.athletes.com/store/now/singlecaps.html

ZF-
 

I got mine at a local health food store for twelve bucks. Haven't tried it yet but looks very simple. Brand is "Cap M Quick"

Have you tried the Zandopa yet?

Thanks
 

Dear reverett123 & ZucchiniFlower,

Thanks for sharing! I have bought a couple bottles of Zandopa from India but is puzzled how to formulate the right dosage which can equate it with my current regime of sinemet:confused:. Any bright idea?

Besides, is there adverse effect/ side effect from taking Zandopa? say accelerating the deterioration of the disease...

LING

Here is a....
 

... good study done on extracts from mucuna species. It's a bit long, but for the chemically inclined good reading. Basically ,it refutes the presence of a peripheral decarboxylase inhibitor found in raw or boiled beans, so it cautions to go easy. Some samples contained little L-Dopa, others, up to 10%. Interestingly, in the raw bean (where the dopa content is greatest; cooking destroys it), tryptamine alkaloids were found in trace amounts (5-methoxy-NN, Dimethyltryptamine, also 5-hydroxy-tryptamine. These trippy halucinogens are not present in enough quantity to be biologically significant. It also states that if you have good stuff, it takes awhile to get used to the large amounts of L-Dopa that you will be taking without an inhibitor. So mucuna pruriens is stated to be of use for PWP in countries that are developing and sinemet is not usually available, but if I were to give my final analysis, I'd say stick to Sinemet (or Madopar).cs
http://www.cidicco.hn/newcidiccoengl...d%20Tebbet.pdf

mucuna
 

we have 2 acquaintances with PD who take both sinemet and mucuna (zandopa). their reasoning is to keep the dosage of sinemet as low as possible. since sinemet contains carbidopa, they do not worry about the peripheral effects of mucuna. carbidopa can be prescribed as a stand alone drug.

Rick, what size capsules did you get?

I tried Zandopa only once, a very small amount. I hated drinking it.

I found this in an old file:

Subject: Zandopa - Mucuna Beans Extract

Body: Hi Guys,
I have started using Zandopa, the Mucuna beans powder and I am getting
fantastic results. Zandopa has not been approved by the FDA in the US, but
has been approved in Canada & Europe.
The following are the benefits over Sinemet:
- The kick off time is extremely fast. Earlier with Syndopa (The Sinemet
generic) I used to take a minimum of 45 minutes and post prandial almost 1
hour. With Zandopa the kick off time is between 20 - 25 minutes and post
prandial around 35 - 40 mnts. It breaks the blood barrier faster, since
it's in a powder form and is taken mixed with water
- My dyskinesia has reduced a lot.
- The sick feeling I used to get after taking Syndopa 25/100 has
disappeared. Earlier, after taking Syndopa, I would 'freeze' for atleast
20 minutes, this does not happen now. Being a natural product, the
'chemical' afterfeel is not there.
- I was put on tablet of Syndopa 25/100, 5 times a day, I have replaced 3
of the doses with Zandopa.
- The recommended replacement dose is 2x7.5 gms for 1 syndopa 25/100. But
I find that 15 gms is too much and take just 7.5gms for one tablet.
-The only draw back is that being in powder form, taking it while I am at
work is inconvenient.
~Gautam

The Middle Way
 

I had a choice of 0, 00, and 000. Having nothing to go on, I chose the 00 figuring I would adjust.

more about Mucuna pruriens?
 

I was diagnosed about 16 months ago at age of 63. My main symptom is tremor and weak right hand. From day 1, the neurologist wanted to put me on sinemet but I refused. For the last year, I have been taking Mucuna powder. Started with one tea spoon then increased to 2 tea spoons daily. I take other supplements as well.
So far, so good and I still think I can do without chemical drugs.
Ofcourse I know I am in the begining but I am questioning the doctor's wisdom for early perscription of sinemet.
I honestly don't know if the mucuna is helping my Parkinson but I can assure you it has other health benifits :)
any body still taking the stuff??

Still on my list
 

In fact, I dusted off a bottle a couple of weeks ago and tried it one afternoon. Unfortunately (and it may have been that formulation) it got my bladder excited and I was up a lot that night. I decided to postpone in favor of retrying the dextromethorphan and will get back to it later.

Previous experience with it was positive. A little messy but otherwise I felt safer with it than Sinemet.

can mucuna replace sinemet all together?
and if not, why not?

comprehesive answer !??
 

The following article provides a comprehensive answer but in short : Most the L-dopa from the Mucuna will be absorbed by the body and only a small percentage reaches brain cells .. that is unless you have, like me, a blind faith in herbs .. (there is some research to support this blind faith as always :) )..


Ken Allan — Parkinson's Disease


Levodopa and Medicinal Beans
In the fall of 2005, on the PLWP2 (people living with PD) website, Peter Fox wrote about beans that contain levodopa. This was the first I had heard of it and I was delighted. It meant I could, if I chose, grow my own medication. The beans with levodopa are fava beans (broad beans), which will be easy for me to grow, and a tropical bean called mucuna, which will be more of a challenge. When I looked into the possibility of using these beans as medication, I soon realized it wouldn't just be a matter of adding them to my diet. There are considerations of timing and levodopa strength and the complication that levodopa is usually taken in conjuction with other drugs.

Levodopa (L-dopa) is the medicine of choice for relieving PD symptoms. This is because levodopa is a precursor for dopamine, the chemical messenger that is in short supply in PD. There are dopaminergic neurons, both in the brain and in other parts of the body, which manufacture, store and regulate the release of dopamine. In PD, the neurons of the substantia nigra have decreased in number to where they are unable to manufacture an adequate supply of dopamine. In the early stages of PD, levodopa medication relieves most, but not all, PD symptoms and does this with minimal side effects.

As PD progresses, with a further decrease in the number of dopaminergic neurons, dyskinesia becomes a common side effect of levodopa medication. Dyskinesia (random muscle contractions) occurs when the supply of dopamine from levodopa medication swamps the neurons, exceeding their ability to regulate the release of this chemical messenger.

There is no general agreement about when levodopa medication should begin. Some doctors recommend putting off the use of levodopa as long as possible. They feel that levodopa stresses our neurons which, in turn, leads to dyskinesia. By delaying until we really need it, we delay the onset of dyskinesia.

An alternate theory about levodopa use is that dyskinesia has nothing to do with the length of time that levodopa has been used. Rather it is purely a function of the number of remaining neurons, so we might as well start taking levodopa in the early stages of PD.

In fact, levodopa medication, by relieving the remaining dopaminergic neurons of one of their tasks (the production of dopamine), may slow the loss of neurons. This possibility received qualified support from a study done by Fahn et al called Levodopa and the progression of Parkinson's disease (N Eng J Med, 2004 Dec 9; 351(24): 2498-508). 361 patients with early PD were given levodopa (small, medium or large doses) or a placebo, with nobody knowing who was getting what. After 40 weeks, medication was stopped for two weeks and then standard movement tests were used to evaluate PD progress. The placebo group had the worst scores; the large dose levodopa group had the best scores. This would be a clear vote for early levodopa medication if the experimenters had not also done a new analytical test called neuroimaging which showed maximum PD progression for the large dose levodopa. In other words, the opposite result. Because neuroimaging is new, the experimenters were inclined to place more credence on the movement tests. But the contradictory results made them somewhat tentative in their conclusions.

Levodopa is not usually the first medication prescribed for PD. Dopamine agonists make message receptors more sensitive to chemical messengers, with the result that a smaller amount of dopamine is sufficient to transmit the message. Most neurologists start off new patients with a dopamine agonist and introduce levodopa later (the patient typically continues to take the dopamine agonist).

Dopamine, itself, cannot be taken as a drug for PD because it is unable to cross the blood brain barrier (BBB). The dopamine precursor, levodopa, can't cross the BBB either; at least, not on its own. But there are amino acid transporters that hang out at the BBB (like Charon at the river Styx) which are willing and able to ferry levodopa across. Willing, that is, unless you have eaten a protein rich meal at the same time as swallowing your pill. Then levodopa will have to compete with other amino acids for the services of the ferry. Once across the BBB, there are enzymes waiting which convert levodopa into dopamine.

But that's not the whole story: the enzymes which greet levodopa as it enters the brain have some identical twins in the bloodstream outside the brain. Levodopa which gets converted to dopamine in the peripheral bloodstream (that is, outside the brain) is of no use to the brain. The presence of these enzymes in the peripheral system means that for every molecule of levodopa that makes it to the BBB unchanged, there are many more that get converted to dopamine and get turned away. This creates a problem. You have to take a whack of levodopa in order for a sufficient dose to enter the brain. And then there's all that excess dopamine in the peripheral bloodstream looking for a home. Some of it can be used by your kidney; some can be used for regulating blood flow. The rest will cause nausea, vomiting and general unpleasantness.

Enter carbidopa. It acts as a bodyguard for levodopa, keeping enzymes at arms length. It does this well enough to allow five times as much levodopa to reach the brain. At the BBB, carbidopa gets turned away. This is convenient because once levodopa enters the brain we don't want carbidopa present to protect levodopa from the enzymes which will convert it to dopamine. When levodopa and carbidopa are taken together, a much higher percent of the levodopa reaches the rain. So the amount of levodopa taken can be reduced accordingly; this, in turn, prevents side effects by reducing the amount of excess dopamine in the peripheral bloodstream.

All levodopa pills come with enough carbidopa (or a similar drug) to protect the levodopa during its trip through our digestive system and bloodstream to the brain. Carbidopa is never 100% effective in its bodyguard action but it makes a big difference in the amount of levodopa that makes it to the brain.

Fava and mucuna beans do not appear to contain anything corresponding to carbidopa. From a medicinal point of view, the lack of carbidopa in the beans creates a problem. For an adequate dose of levodopa to reach the brain, a lot of beans have to be eaten. This is unhealthy, both because of the large amount of levodopa that gets converted to dopamine in the peripheral system and because beans typically contain small amounts of toxins. Bean toxins don't cause any difficulty if the beans are just eaten occasionally or in small amounts. But frequent meals of large helpings of beans would not be healthy.

In the USA, carbidopa is available by itself (under the trade name Lodosyn). Because it is a specialty item, it costs twice as much as a levodopa pill which has the same amount of carbidopa plus the levodopa. In Canada, Lodosyn is not an approved drug. So taking a Lodosyn pill with a small helping of beans is not an option.

At present, I have a prescription for 25 mg Carbidopa/ 100 mg Levodopa. Sometimes I just take the pill. But whenever convenient, which is most of the time, I break a pill in half and eat enough fava bean sprouts or mucuna bean powder to provide the other 50 mg levodopa. My assumption is that the bean levodopa will be able to piggy back on the carbidopa from the pill. Also, I know I am getting 50 mg levodopa from the pill so if my estimate of the levodopa content of the beans is a little off, the total error is less than it would be if I relied entirely on the beans. So far, this is working very well. But I'm in the early stages of PD and my system is more adaptable than it will be 10 years from now.

Vicia Faba and Mucuna Pruriens
These two bean species are the only plants known to contain significant amounts of levodopa. Despite having this in common, they are quite different in the way they distribute it. In fava, the seeds are the plant part with the least amount of levodopa (0.2% or less). In mucuna, the seeds are the plant part with the most levodopa (2.0% to 9.0%).

Leaves, stems, pods and blossoms of fava have 10 times more levodopa than seeds. The plant parts of mucuna have less than one tenth as much levodopa as the seeds. This affects the way we use these beans.

Mucuna has a long history of medicinal use in India where it was used to treat parkinsonian symptoms long before Dr. Parkinson gave his name to PD. The seeds are made into a powder which usually has about 4% levodopa.

Two similar clinical studies have been done with mucuna powder in place of carbidopa/levidopa pills. They are Manyam et al, An Alternative Medicine Treatment for Parkinson's Disease: Results of a Multicenter Clinical Trial (J of Alternative and Complimentary Med, 1995, Vol 1, No 3, p.249-55) and Katzenschlager et al, Mucuna Pruriens in Parkinson's Disease: a double blind clinical and pharmacological study (J Neurol Neurosurg Psychiatry 2004; 75: p.1672-1677). The patients in both studies did as well or better on mucuna powder as on carbidopa/levodopa pills This is remarkable to me because in order to have an effective dose of levodopa reach the brain (without the aid of carbidopa) the quantity of levodopa in the powder was five times what would have been given in a pill; and therefore there was much more excess dopamine in the bloodstream with the concommitant disposal problem.

Despite the success of mucuna powder in these tests, I am concerned about possible problems with consuming a large amount of bean powder on a long term basis. Katzenburger speculates that "it might be appropriate to administer mucuna preparation in combination with a peripheral dopa decarboxylase inhibitor [carbidopa] which may further improve tolerability and efficacy." This is the approach which, it seems to me, holds the most promise. So far, rats have been the main beneficiaries.

When mucuna was tested in conjunction with carbidopa, using rats (with induced parkinsonism), the results were quite impressive. This test was by Hussian et al. Their report was called Mucuna pruriens proves more effective than l-DOPA in Parkinson's disease animal model (Phytotherapy Research, 1998, Vol 11, Issue 6, p 419-423).

They gave carbidopa to the rats along with the mucuna to see if carbidopa has the same beneficial effect on mucuna derived levodopa as carbidopa has on manufactured levodopa. It did. In fact, carbidopa may have worked even better with the levodopa from mucuna than with levodopa in a pill. When the rats were put through some standard movement tests after being given equal amounts of levodopa, either manufactured or from mucuna, the rats who got the mucuna did better on the tests. Then the experimenters reduced the quantity of mucuna and found that half as much levodopa from mucuna produced the same benefit as a full measure of manufactured levodopa.

Their conclusion: "This study suggests that mucuna may contain unidentified antiparkinsonian compounds in addition to l-DOPA, or it may have adjuvants that enhance the efficacy of l-DOPA."

The combination of mucuna and carbidopa worked so well with rats that a similar trial with human subjects seems inevitable. If one exists, I have been unable to find it. The closest I have come is a mini-study in Turkey where PD patients ate fresh cooked favas in addition to their usual PD medication. Apaydin et al called their report Broad bean (Vicia faba)-A natural source of L-dopa-Prolongs "on" periods in patients with Parkinson's disease who have "on-off" fluctuations (Movement Disorders, 2001, Vol 15, Issue 1, p164-166).

Doctors at a clinic in Turkey received reports from their PD patients that when they ate favas in addition to their medication, they felt better. So the doctors recruited three patients willing to eat 250 gram portions (fresh cooked whole pods) on a regular basis, and to keep a detailed diary.

They were to continue on their usual carbidopa/levodopa medication so they had carbidopa in their system to guard the fava ingredients as well as to protect the levodopa in the pill.

Their conclusions: "We observed a beneficial effect of Vicia faba in our patients manifested by strikingly prolonged “on” time and shortened “off” time. We were surprised by the reported magnitude of our patients’ responses, given the fact that previous trials of higher doses of carbidopa/levodopa seemed to provide no further benefit. These observations are not readily explained by assuming that broad beans are simply a source of levodopa. For example, patient no. 2 was able to experience a sustained response from broad bean meals ingested on alternate days. Also, somewhat surprisingly, patient no. 3 experienced decreased dyskinesias with the addition of broad bean supplementation and reduction of carbidopa/levodopa therapy. This patient had previously failed to respond satisfactorily to carbidopa/levodopa adjustments which should have accomplished the same result if this was simply a levodopa effect."

"A placebo effect may have contributed in this unblinded trial, but the magnitude of the reported responses raises the possibility of other mechanisms. For example, the amino acid milieu generated from broad bean administration may favor the selective transport of levodopa across the blood–brain barrier. Alternatively, other products derived from broad bean may complement the antiparkinsonian effect. These results suggest that a controlled trial with close monitoring of the clinical response is warranted."

Some of the Turkish patients reported they did not get the same benefit when they cooked with dry beans. This might be due to the low levodopa content of dry fava beans. Or it might be that the cooking, which is usually much longer for dry beans than for fresh green beans, further degraded the small amount of levodopa in the beans.

This argues for growing your own fava beans and eating them as a green vegetable. Not so with mucuna. Since the dry bean is the best source of levodopa from mucuna, buying powder from a commercial source may as good as growing one's own. Especially considering the hardness of the seeds. I doubt that anything short of an industrial grinder would be able to turn these seeds into powder. When I got a few seeds for growing in my greenhouse, I tried soaking the seeds prior to planting. Not a drop penetrated the seed coat. So I tried scoring the seed coat with a sharp knife — it didn't make a mark. I got out my hacksaw, held the seed firmly with a pair of pliers, and made a light pass with the saw — I didn't want to damage the kernel — I needn't have worried — still no mark —this seed coat was roughly the same hardness as stainless steel. I got more aggressive with the saw and was able to cut through the seed coat. The seeds then took up water quite readily.

I will try growing mucuna but do not envision making my own powder, even if I am successful in growing the beans. A source for mucuna powder is:

Garry & Sun
550 E Plumb Lane,Suite 301/306
Reno, Nevada 89502
Website: Garry and Sun Natural Remedies

They import it from India where it is called kaunch powder.

One level teaspoon powder weighs 2.5 grams. Assuming 4% levodopa, that works out to 100 mg levodopa per teaspoon. How to deal with the powder? It is nearly tasteless so ½ teaspoon sprinkled on the peanut butter in a sandwich does not affect the flavour. If butter is softened, but not melted, mucuna powder will blend easily into the butter which can then be spread on bread, toast, biscuit. Levodopa is heat sensitive, so cooking with the powder is not recommended (when mucuna is being used as a food by regular folk, they cook the beans at some length to get rid of the levodopa).

Convenience is one of the main advantages of pills versus beans. Just remembering when to take medication is hard enough by itself. When that time comes it will, more often than not, be inconvenient to cook up some beans or measure out some mucuna powder, mix with butter and spread it on a slice of bread. One way around this is to mix powder with something edible ahead of time and have it divided into pieces with known amounts of levodopa.

If you are looking for a way to justify eating chocolate, heat a package of bakers chocolate just enough to make it soft. While the chocolate is warming up, blend 25 g (just over 3 tablespoons) mucuna powder into 2 tablespoons of soft butter. Blend this thoroughly into the soft chocolate until there is no colour variation. Spread on wax paper and, when it cools, cut into 20 equal pieces. Each piece will have roughly 50 mg levodopa.

I do something similar with Rice Krispie squares. This is a slightly altered version of the recipe which comes on every box of Rice Krispies:

1/2 cup butter
1/2 lb (225 g) mini marshmallows
3/8 cup (6 tblsp) mucuna powder
6 cups Rice Krispies
Note the doubling of the amount of butter — half goes with the melting marshmallows as usual (in a large pan on the lowest heat, stirred frequently); the other half is softened and blended into the mucuna powder. When the marshmallows have melted, stir in the butter-powder paste (quickly but thoroughly). Then stir in the (previously measured out) Rice Krispies. Spread out on wax paper and cut into the 30 equal pieces to give about 60 mg levodopa per square.

If you are going to experiment with mucuna powder, I recommend getting half your levodopa dose from a carbidopa/levodopa pill and half from the mucuna powder. My neurologist is okay with this, for me, but you should get the blessing of your own neurologist.

Levodopa in mucuna powder loses strength over time and it won't come with a strength rating, so you will not know, with any degree of precision, how much levodopa you are getting from the mucuna powder. However, one of the things I learned from reading the PLWP2 discussion board is that people with PD are remarkably well tuned in to their medication. After a few doses you will probably be able to judge (better than any measuring device) whether you should adjust the dose.

Fava beans are not quite so easy to deal with as mucuna, though there are many more options with fava. A warning note first. Before giving serious consideration to fava beans, find out if you have the genetically based problem called favism. This can be deadly if you have it and ignore it.

Favism is a hereditary abnormality in the activity of a red blood cell enzyme. This enzyme, glucose-6-phosphate dehydrogenase (G-6-PD), is essential for assuring a normal life span for red blood cells. This enzyme deficiency may provoke the sudden destruction of red blood cells and lead to hemolytic anemia with jaundice following the intake of fava beans. You can determine whether you are G-6-PD deficient by a simple blood test.

Assuming you get the green light for fava beans, the easiest form of the bean to obtain from commercial sources is the dry bean. I have eaten a few dry fava beans and found the mild nutty flavour quite agreeable. I don't recommend this, however — dry beans are quite hard and eating them this way would almost certainly lead to broken teeth. Also, they are low in levodopa so a powder made from them would be the least attractive option.

Fava beans come in two general types. The "major" vegetable type (also called broad bean), with a flat seed like a lima, is usually grown for fresh eating; tends to be large seeded, but not always. The "minor" field crop type (also called horsebean or ticbean), with a round seed like a chick pea, is more often grown for use as stock feed and for cooking from the dry bean.

Fava beans, like all beans, are rich in the amino acids phenylalanine and tyrosine which are precursors of levodopa. In the body, phenylalanine is converted into tyrosine. Tyrosine in turn is converted into levodopa, norepinephrine, and epinephrine, three key neurotransmitters. Tyrosine hydoxylase is the enzyme which converts tyrosine to levodopa.

It would appear that what distinguishes fava from other beans is that fava has a genetic blueprint for tyrosine hydroxylase. Because as soon as the bean seed starts to grow, levodopa content increases — presumably from the action of tyrosine hydroxylase on tyrosine.

One way to use dry beans of the minor type is to sprout them. Sprouting increases the levodopa content of the bean by a factor of five. My rule of thumb is that each sprouted fava bean contains two mg levodopa. The seed coat of a sprouted fava is rubbery and tasteless with negligible levodopa. When I am not rushed in the morning, I start my day with a half tablet of 25/100 carbidopa/levodopa plus 20 to 30 fava sprouts which I skin as I go.

While a powder from seeds is very low in levodopa, the dry seed is not the only potential source of powders. Simon de Boer, an organic farmer in South-Western Ontario, grew a field of favas and made powders from green leaves and pods dried in a low temperature dehydrator. Levodopa content of these powders is 1% to 2%. They can be used in the same way as mucuna powders.

Canned fava products are low in levodopa and of little interest, from a medicinal point of view.

Fresh green immature pods are one of the best sources of levodopa in fava. These are available from time to time from green grocers. The pod shell is much higher in levodopa than the green beans inside so edible pod varieties are best from a medicinal point of view. The trick with these pods is to not cook them any more than necessary and to eat them right away. Pods steamed for 15-20 minutes just lose 10% of their levodopa content. If set to one side and kept warm or allowed to cool slowly, they lose much of the remaining 90%.

Measuring Levodopa
When I grow 30 different varieties of fava in the summer of 2006, in addition to evaluating for flavour, I will be looking for the varieties highest in levodopa. To do this, I will have to measure levodopa content. I've been working on a kitchen chemistry method of measuring levodopa. This project has been a mixture of fun and frustration. So far, I have been able to determine the relative strengths of similar samples. That is, I can determine with confidence which fava seeds have the highest levodopa content. But when comparing fava seeds with fava pods or mucuna powders or with a standard 100 mg pill, it is harder to get repeatable results.

A kitchen chemistry method should be low tech and use chemicals which are not dangerous. The key chemical in this case is potassium iodate which under certain circumstances can be explosive. So it has to be handled with respect. Nevertheless, it is the form of iodine used in iodized salt, so if trace amounts got into our food, it would be more likely to do us good than to do us harm.

Levodopa reacts with potassium iodate, at pH 5, to form a reddish-orange compound. The intensity of the colour can be used to measure the amount of levodopa. When two samples are being compared, the one which is more intensely coloured is diluted until it is visually the same as the weaker one. The amount of dilution is used to calculate the relative strengths of the two samples. Relying on a visual determination of equal colour is less accurate than measuring with a spectrophotometer, but you can get surprisingly close when doing a visual comparison. The most significant errors with this method come from other factors.

A benefit from wrestling with the measuring problems is a better understanding of bean chemistry. The main difficulty I have encountered is that different sample types produce different shades of orange. Fava seeds produce a brownish orange, fava sprouts and pods are reddish orange, mucuna powder is a different shade of reddish orange and manufactured levodopa is yellow orange (though, with time, it gets more and more reddish). This makes comparing colour intensity very difficult. It also raises the question of what is being measured. Is it all levodopa? Does some of the colour come from chemical compounds which are closely related and biologically active in the same way as levodopa? Or is some of the colour coming from compounds which are unrelated to levodopa?

To answer this latter question, I checked a few other bean species and got no significant colour from them. This gives me confidence that any colour I get is probably from chemicals closely related to levodopa. Nevertheless, assigning a strength value is still difficult.

Another problem is that the colour shade and intensity are time dependent. The colour gradually becomes more intense and the colour shade gradually moves from yellow to red. To some degree this can be solved by measuring at a specific time after iodate addition.

Colour is also affected by pH. At first I tried adjusting pH using citric acid and pH paper. This worked reasonably well but required care and good judgement. And dilution changed the pH. I eventually settled on using a buffer.

There is also the problem of sample preparation so that all of the levodopa in the sample is dissolved and measured. In particular, if seeds are ground up for measuring purposes, there tends to be some variation in particle size; and seed chunks (as compared with fine powder) will be much slower to release their levodopa content into solution. Also, the prepared sample has to be filtered and any haze in the final sample interferes with strength determination.

The net result is a fairly large potential error in strength determinations. Probably on the order of 25%. In other words, if I measure a mucuna powder at 4%, it could be as high as 5% or as low as 3% — a huge error range from a scientific point of view; but these rough measurements still provide a useful guide for deciding how much to take as PD medication.



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

Lordy! And I thought I was wordy!
 

:D

I appreciate his research but have a problem or two with some of the conclusions.

First, although my data was lost when the old forum tanked, I do remember being perplexed by the fact that I did quite well with mucuna sans carbidopa. As I recall, I began my trial figuring a rough increase to compensate for the enzyme action and ended up very much over medicated.

Second, our bodies put a lot of resources into eliminating ldopa in the periphery and there is probably a reason. It might be better if the system was allowed to retain a regulatory power over it.

I do remember that it was a "smoother" drug with less motor problems. And it is a heck of a lot cheaper. A poor man could do a lot with mucuna and dextromethorphan and a bit of ginseng. I can see the state policeman now, "Now, boy, stop your twitching and explain to me why you've got a trunk full of cough syrup, dried roots, and funny beans!" :D

Hello, Mucuna IS a drug, herbal or not. It is used in India to treat PD, and clinical studies show it works 3 times better than sinemet. You are taking sinemet type drug, so I wonder why your surprised your neuro suggested sinemet.

Mucuna probably contains something similar to carbidopa, because the same amount of l-dopa in mucuna, compared with sinemet, resulted in three times better response. Carbidopa was not needed with mucuna.

It will probably cause dyskinesias, like sinemet, so don't take it and assume because it's natural, it has no long term side effects.

I agree BUT
 

Thank you ZucchiniFlower. I am not aware of resaerch which indicates that Mucuna contains Cabidopa. Additionally, the research I have seen (pls see below) requires 30 gm of mucuna to equate with 200/50 Ld/Cd.
I am taking 1 teaspoon (<5 gm) twice daily. I am assuming that only a small percentage of L-dopa reaches the brain (hence a very mild effect on symptoms too :( I think!).
Actually my dose does not exeed the tradtional Indian medicine recommendation for Medicinal Properties: Action:
Herb - anthelmintic, aphrodisiac, astringent, nervine, tonic, rejuvenative.
Seeds - antihelmintic, astringent, nervine tonic, and an aphrodisiac
Root - nervine tonic, diuretic
Below is relevant paper :

Mucuna pruriens in Parkinson's disease: a double blind clinical and pharmacological study.Katzenschlager R, Evans A, Manson A, Patsalos PN, Ratnaraj N, Watt H, Timmermann L, Van der Giessen R, Lees AJ.
National Hospital for Neurology and Neurosurgery, London, UK.

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.

PMID: 15548480 [PubMed - indexed for MEDLINE]

Hi Imark,

I didn't say mucuna contains carbidopa. It probably contains something that works in a similar way, because the mucuna is so effective. If one takes the same dose of L-dopa via mucuna or sinemet, mucuna does a better job.

Please do a search here for older threads regarding mucuna pruriens. There were many articles posted, including the one you posted (it definitely deserves a repost! :) Also experiences of patients using it.

It does seem to act faster, and sustains its action longer. From articles I read, the risk of dyskinesias remains. It seems that even though mucuna is more effective than sinemet, it doesn't increase dyskinesias compared to sinemet.

I'm going to try mucuna this month. I purchased a good, small, portable electric mixer to bring to work.

HP-200, a formulation made from the seed powder of Mucuna pruriens, contains among other constituents, about 4% L-DOPA. Same as Zandopa, which I purchased from India.

Research Article
Anti-parkinson botanical Mucuna pruriens prevents levodopa induced plasmid and genomic DNA damage

Abstract
Levodopa is considered the gold standard for the treatment of Parkinson's disease. However, a serious concern is dyskinesia and motor fluctuation that occurs after several years of use. In vitro experiments have shown that in the presence of divalent copper ions, levodopa may induce intense DNA damage. Mucuna pruriens cotyledon powder (MPCP) has shown anti-parkinson and neuroprotective effects in animal models of Parkinson's disease that is superior to synthetic levodopa. In the present study two different doses of MPCP protected both plasmid DNA and genomic DNA against levodopa and divalent copper-induced DNA strand scission and damage. It exhibited chelation of divalent copper ions in a dose-dependent manner. The copper chelating property may be one of the mechanisms by which MPCP exerts its protective effects on DNA.

Phytotherapy Research
Published Online: 11 Jul 2007

http://www3.interscience.wiley.com/c...TRY=1&SRETRY=0

I wonder if the anti-dyskinetic properties of mucuna powder has something to do with the pharmacokinetics of slow L-DOPA release in the small intestine. It may be something like sinemet CR without the carbidopa. A low, more continuous release into the blood circulation may provide just the right blood level to mostly get past the liver decarboxylase and through the BBB by normal amino acid transport.
Zucc, is one of the mucuna products you mentioned a liquid extract? If so, that would tend to shoot holes in this idea, since the L-DOPA would already be dissolved and probably be rapidly absorbed in the GI tract.

No, the Zandopa is a powder, and is usually ingested as a suspension. I think your idea has merit!

when I read this thread
 

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

more on mucuna
 

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?
 

:confused: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=

Raintree entry
 

Velvet Bean Plant Summary
Main Preparation Method: capsules or standardize extract

Main Actions (in order):
anti-Parkinson's, androgenic, aphrodisiac, hypoglycemic, anabolic

Main Uses:

1. for Parkinson's disease (contains natural L-dopa)
2. for impotency and erectile dysfunction
3. as an aphrodisiac and to increase testosterone
4. as a muscle builder and anabolic/androgenic aid to stimulate growth hormone
5. as a weight loss aid

Properties/Actions Documented by Research:
anabolic, androgenic, analgesic (pain-reliever), anti-inflammatory, anti-Parkinson's, antispasmodic, antivenin, aphrodisiac, febrifuge (reduces fever), hormonal, hypocholesterolemic (lowers cholesterol), hypoglycemic, immunomodulator, nervine (balances/calms nerves), neurasthenic (reduces nerve pain)

Other Properties/Actions Documented by Traditional Use:
antilithic (prevents or eliminates kidney stones), antiparasitic, cough suppressant, blood cleanser, carminative (expels gas), central nervous system stimulant, diuretic, hypotensive (lowers blood pressure), menstrual stimulant, uterine stimulant, vermifuge (expels worms)

Cautions: It contains L-dopa and has androgenic and hypoglycemic activity. See further cautions in next chapter.



much more at http://www.rain-tree.com/velvetbean.htm

finally got around to it
 

This afternoon I filled some capsules with mucuna and gave it a new try. I have been in a pattern of being "off" more and more in the evenings and lately even into the afternoons. Not a happy camper.

So this evening I substituted for my 7:00 feeding of 2X4 mg requip plus 1x200/25 sinemet CR a pair of capsules containing 1 gr of mucuna bean powder each.

I am very pleased because it is now 11:00 PM and I am anything but "off" and have done well all evening.

I do have a couple of questions- First, if mucuna is about five percent l-dopa as claimed, then have ingested 50 mg in each capsule for a total of 100 mg sans carbidopa. I shouldn't feel a thing. And second, the studies have used doses up to 30 grams and I am testing just 2! So what am I overlooking?

Tomorrow will be interesting. :)

This one's for you, juanhch :D

capsules vs raw powder
 

Hello :) :

I use raw powder assuming it has 4% L-dopa (one tea spoon twice daily) and I always thought it has little or no impact on my symptoms which are mild any way. What you are reporting is amazing but I am wondring if the capsule has higher L-dopa % as usually capsules contain 15 to 50 % L-dopa . Can you check this?

no, i capped it myself
 

from a bag of raw powder.

went to bed at 11;30 still on. up at 1:30 to the loo and was off. now just up at 8:00 and in a little better shape than usual.

just took 2 mucuna and 3 ginseng. if i am on before 9;00 am it willl be imrovement.

Please keep up the update
 

... with my best wishes that the +ve effects will continue ..

bad start
 

for the experiment. Day got out of control but I did figure out that one needs a lille more to start the day. I will do a better job tomorrow.

Rick, where did you get the raw powder? Is it Zandopa (HP200)? That's what they used in a clinical trial.
Thanks.


Research Article
Bioavailability of L-DOPA from HP-200 - a Formulation of Seed Powder of Mucuna pruriens (Bak): a Pharmacokinetic and Pharmacodynamic Study

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 (Cmax=1.56±0.163 g/mL) achieved at Tmax=83±16.09 min. The plasma half life was 102±2 min and the auc was determined as 6.508±0.421 g/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.

http://www3.interscience.wiley.com/c...22064/ABSTRACT

"Doses of HP-200 were started at 7.5 grams (which provided a standardized amount of levodopa), three times a day. Doses were then increased at weeks two and four to obtain the best response. The average daily dose by the end of the 12-week study was 45 grams of HP-200. Side effects were minimal. Those who had not taken levodopa medications prior to the study, tolerated HP-200 best."

I don't know when improvements were first seen and at what dose.

http://content.herbalgram.org/wholef...ew.asp?i=42085

COMPREHENSIVE REVIEW OF MUCUNA HERE (2007):

http://www.phcogrev.com/issue1/19.pdf

Article says mucuna contains NADH and COQ10 and it increased mitochondrial Complex 1 activity.

I'm using a generic raw bean powder
 

I looked at Zandopa and may try it later, but thought I would start out with the cheap stuff. Less than 20 bucks a pound. If I end up taking five grams a day (seems a reasonable figure at this point) then that's about three month's worth. Given that so many of us are struggling with fixed incomes, it would be good to have this option. And given the screwy world we live in, having a couple of pounds in the freezer could be a blessing. <Lord, that sentence would have once had an entirely different meaning. :D> Mucuna wil get you through times of no money better than money will get you through times of no mucuna.

You know, with the whole bean powder we may not be simply dealing with l-dopa alone. If HP-200 <"I bought one of those at Radio Shack years ago...."> is altered to increase l-dopa content there may be ingredients mssing.

about dose
 

Hello Zflower:
It is good if high dose up to 45 gm is safe (although the first link you posted did not work with me). I am trying to use minimum dose presently (3 tea spoons of raw powder daily) and will increase as needed. I have more faith in raw powder rather than extract hoping it has more goodies than present research tell :)
Hello Rick : You are doing very valuable experiment and I am sure many of us are following up with earnest and hope