Parkinson's Research

Almost every herb page on this site has to be honest about thin evidence. This one does not. Mucuna pruriens in Parkinson’s disease is the single best-evidenced herbal intervention in neurology — not because the herb is magical, but because the velvet bean contains real levodopa, the same molecule that has been the cornerstone of Parkinson’s treatment since the 1960s. It has been tested in double-blind randomised crossover trials, published in Neurology and the Journal of Neurology, Neurosurgery and Psychiatry, with pharmacokinetic blood sampling and blinded motor scoring. That is a level of rigour almost no botanical ever receives.

And here is the thing that page after page on the internet gets wrong: the strength of that evidence is exactly why Mucuna is not a “natural alternative” you can quietly swap in for your prescription. It works because it is a drug. Drugs that work have doses, interactions, withdrawal effects and side effects, and levodopa — from any source — has all four.

This article walks through what the trials actually found, in order, with the numbers the abstracts actually report — including the part patients are almost never told: why Mucuna makes far more people nauseous than Sinemet does, and why that has a precise, completely predictable chemical explanation.

Table of Contents

  1. Why This Evidence Is Different
  2. Kampavata: the Ayurvedic Record
  3. What Is Actually in the Bean
  4. The 1995 HP-200 Multicenter Trial
  5. Katzenschlager 2004: the Double-Blind Crossover
  6. The 2017 Neurology Randomized Trial
  7. The 16-Week Daily-Use Study
  8. The Carbidopa Problem
  9. Seed Powder Versus Capsules
  10. The Access Argument
  11. What a Real Dose Looks Like
  12. The Neuroprotection Question
  13. Safety and Side Effects
  14. What Mucuna Does Not Do
  15. Key Research Papers
  16. Connections
  17. Featured Videos

Why This Evidence Is Different

When a herb is studied, the usual story is a handful of small open-label studies, some cell-culture work, and a review that makes the whole thing sound more settled than it is. Mucuna is genuinely not that, and the reason explains everything else on this page. Levodopa — L-3,4-dihydroxyphenylalanine — is an ordinary amino acid derivative that the velvet bean makes in quantity in its seeds. It is not a “Mucuna compound” that resembles levodopa. It is levodopa: the molecule in the bean and the molecule in a Sinemet tablet are identical.

That lets Mucuna trials do something almost no herbal trial can — measure the active drug in the patient’s blood, plot its concentration over four hours, and correlate it with a blinded motor score. You are not guessing at a mechanism; you are watching a known drug enter the bloodstream from an unusual delivery vehicle.

It also means the honest framing is not “does the herb work?” — of course it does, it contains the drug — but three much sharper questions:

Kampavata: the Ayurvedic Record

Long before levodopa was synthesised, Ayurvedic physicians in India described a disorder called Kampavata — a tremor illness classified among the Vata rogas, the neurological diseases — and treated it with Atmagupta, the Sanskrit name for Mucuna pruriens.

The scholarly source for this is a short but frequently cited 1990 paper in Movement Disorders by Bala V. Manyam, a neurologist at Southern Illinois University, titled Paralysis agitans and levodopa in “Ayurveda”: ancient Indian medical treatise. Manyam made two points that are still quoted three decades later. The first is the pharmacological one: an ancient system independently landed on the one plant in its pharmacopoeia that contains the drug modern medicine would eventually isolate. The second is subtler and rather beautiful — if paralysis agitans existed before the industrial revolution, then environmental-toxin theories of Parkinson’s need to account for naturally occurring compounds with worldwide distribution, not only industrial ones.

A note on the “4,500 years” figure. You will see this number everywhere, including on the hub page that links here, and it is a reasonable shorthand for the traditional dating of the Ayurvedic corpus. But it is a claim about a tradition, not a finding any of the clinical papers below verified. Textual dating of the Ayurvedic samhitas is genuinely contested among historians, with estimates spanning well over a millennium. What is solid and citable is Manyam’s narrower point: the classical texts describe a tremor disorder and name this plant as its treatment. That is remarkable enough without needing a precise number attached.

Tradition is not evidence of efficacy — the site says this on every herb page and it is still true here. What tradition is good for is telling you where to look. In this case it pointed researchers at exactly the right bean.

What Is Actually in the Bean

The number that governs everything practical about Mucuna is its levodopa content.

The best measurement comes from Cassani and colleagues, who in 2016 analysed 25 Mucuna samples collected from Africa, Latin America and Asia and published the results in the Journal of the Neurological Sciences. Their findings:

That third point is the single most practically important line in the whole Mucuna literature and it almost never gets repeated. If you boil the beans, you have thrown most of the medicine away. In the trials, the preparation is roasted seed powder — and roasting matters for a separate reason too, because raw Mucuna seeds carry antinutritional compounds that traditional preparation is designed to reduce.

Levodopa is also chemically fragile in ways that matter for storage. Pulikkalpura and colleagues published a dedicated 2015 paper in Scientific Reports on levodopa in Mucuna pruriens and its degradation. The practical upshot for anyone keeping powder at home: levodopa oxidises. Powder that has gone brown, damp or stale is not the same product as the powder that was assayed at 5.3%, and there is no way to tell by looking how much is left.

Why the bean is not only levodopa

There is a persistent and genuinely unresolved thread in this literature suggesting Mucuna does something its levodopa content alone does not explain. Manyam, Dhanasekaran and Hare fed rats the Mucuna-derived preparation HP-200 for 52 weeks at 2.5, 5.0 or 10.0 g/kg/day and measured monoamine neurotransmitters across four brain regions. The result was odd: a significant effect on dopamine content in the cortex, but no significant effect on dopamine, its metabolites, norepinephrine or serotonin in the nigrostriatal tract — the very pathway that degenerates in Parkinson’s. The authors’ own conclusion was that the antiparkinsonian effect “may be due to components other than levodopa, or that it has a levodopa-enhancing effect.”

Take that as an open question, not a selling point: it is a rat study, it is twenty years old, and “we could not explain the effect” is not the same as “we found a second active compound.” But it is a real anomaly, published by the same group that ran the first human trial.

The 1995 HP-200 Multicenter Trial

The modern clinical story starts here. In 1995 the Journal of Alternative and Complementary Medicine published the results of a multicenter trial of HP-200, a Mucuna-derived powder, run by a group publishing collectively as the HP-200 in Parkinson’s Disease Study Group.

What they did:

What they found: statistically significant reductions in both Hoehn and Yahr stage and UPDRS scores from baseline to week 12 (p < 0.0001). The mean dose needed for optimal symptom control was 6 ± 3 sachets per day — which, at 7.5 g each, is roughly 45 g of powder daily, a genuinely large quantity of material. Adverse effects were described as mild and mainly gastrointestinal, with no abnormalities in laboratory testing.

Now the caveat, and it is a big one. This was an open study — no placebo arm, no blinding, no randomisation. In Parkinson’s specifically that is a serious limitation rather than a technicality, because the placebo response in Parkinson’s trials is unusually strong and has been shown in imaging studies to involve genuine dopamine release. An unblinded 12-week improvement in a disease with a famously large placebo response is a promising signal and nothing more. What 1995 really established was tolerability at scale: sixty patients took a great deal of Mucuna powder for three months without laboratory abnormalities. That is what made the controlled work worth funding.

Katzenschlager 2004: the Double-Blind Crossover

Nine years later, a team at the National Hospital for Neurology and Neurosurgery in London — Regina Katzenschlager working with Andrew Lees, one of the most senior Parkinson’s clinicians in the UK — published the study that changed how this bean is discussed. It ran in the Journal of Neurology, Neurosurgery and Psychiatry in December 2004.

The design was small but tight:

The results, which are the numbers everyone quotes

Compared with standard levodopa/carbidopa, the 30 g Mucuna preparation produced:

The faster onset was mirrored by shorter latency to peak plasma levodopa — so the clinical effect and the blood chemistry told the same story, which is exactly what you want to see.

How to read this honestly. The headline “Mucuna beats Sinemet” is not what happened. Look at the doses. The 30 g Mucuna arm delivered roughly 1,500 mg of levodopa (at ~5% content) against 200 mg in the comparator tablet. Higher peak levels and a bigger AUC from seven-and-a-half times the levodopa is not a surprise. What is genuinely interesting is that all that extra levodopa did not produce more dyskinesia — and that the onset was faster, which is not merely a dose effect and points at something about how the powder is absorbed. The authors were careful in their own conclusion, calling only for a randomised, controlled study of long-term efficacy and tolerability. Which is precisely what came next.

The 2017 Neurology Randomized Trial

Roberto Cilia and colleagues at the Parkinson Institute in Milan, working with a neurology clinic in Santa Cruz, Bolivia, published in Neurology — the journal of the American Academy of Neurology, and about as mainstream as this field gets — on 1 August 2017. The paper is Mucuna pruriens in Parkinson disease: A double-blind, randomized, controlled, crossover study.

Their stated purpose is unusually direct, and it frames the whole modern research programme: to find out whether Mucuna “may be used as alternative source of levodopa for indigent individuals with Parkinson disease who cannot afford long-term therapy with marketed levodopa preparations.”

The design was the most thorough yet — 18 patients with advanced Parkinson’s, each receiving six different single-dose treatments in randomised order:

  1. Dispersible levodopa 3.5 mg/kg plus benserazide (a decarboxylase inhibitor) — the reference treatment.
  2. High-dose Mucuna, 17.5 mg/kg levodopa-equivalent.
  3. Low-dose Mucuna, 12.5 mg/kg.
  4. Pharmaceutical levodopa without any decarboxylase inhibitor, 17.5 mg/kg — the control that isolates the carbidopa question.
  5. Mucuna plus benserazide, 3.5 mg/kg.
  6. Placebo.

The Mucuna was powder from roasted seeds obtained without any pharmacologic processing — deliberately, because the whole point was to test something a person in a low-income setting could actually make. Outcomes were change in motor response at 90 and 180 minutes and duration of the on state, plus adverse events, blood pressure, heart rate and dyskinesia severity.

What they found

The authors’ conclusion: single-dose Mucuna met all noninferiority efficacy and safety outcome measures against dispersible levodopa/benserazide, and high-dose Mucuna behaved like levodopa alone at the same dose but with a more favourable tolerability profile. The trial is registered as NCT02680977.

Note the dose ratio, because it is the key to the whole page. The high-dose Mucuna arm was 17.5 mg/kg against 3.5 mg/kg in the reference arm — five times the levodopa. That is not a flaw in the trial; it is the trial correctly compensating for the missing carbidopa. Cassani’s pharmacokinetic work concluded that without a decarboxylase inhibitor, Mucuna provides clinical benefit only when its levodopa content is at least 3.5-fold the standard levodopa-plus-inhibitor dose. The 2017 trial dosed accordingly, and it worked.

The 16-Week Daily-Use Study

This is the study that most Mucuna advocacy leaves out, and it is the most useful one on the page.

A single dose in a clinic is not treatment. Parkinson’s is a disease you medicate every few hours for the rest of your life. So the same Milan–Bolivia group ran the follow-up: Daily intake of Mucuna pruriens in advanced Parkinson’s disease: A 16-week, noninferiority, randomized, crossover, pilot study, published in Parkinsonism & Related Disorders in April 2018.

Fourteen patients with motor fluctuations and dyskinesias took Mucuna powder from roasted seeds and marketed levodopa/carbidopa, in randomised order, crossover, across 16 weeks. Outcomes were quality of life, motor and non-motor symptoms, and time with good mobility without troublesome dyskinesias, plus tolerability, adverse events, laboratory indices and ECG.

The result

Seven of the fourteen patients — 50% — stopped Mucuna early. Four because of gastrointestinal side effects. Three because their motor performance progressively worsened. Nobody discontinued during the levodopa/carbidopa phase.

In the patients who could tolerate it, the clinical response to Mucuna was similar to levodopa/carbidopa on all efficacy measures. So the drug worked. It was the delivery that people could not live with.

The authors are explicit about why, and their explanation is the intellectual centre of this entire article: the tolerability problem was “as one could expect by the relatively rapid switch from LD/CD to levodopa alone in advanced PD.” Taking Mucuna instead of levodopa/carbidopa means taking levodopa without carbidopa. Everything else follows from that.

There is a hopeful footnote. The patients who dropped out entered a study extension using Mucuna supernatant water — the liquid from the soaked or cooked preparation rather than the whole powder — for a median of 16 weeks, and that was well tolerated. It suggests the gastrointestinal problem may be partly the bulk plant material rather than the levodopa itself. It is a small uncontrolled extension of a 14-person pilot, so hold it loosely, but it points somewhere sensible.

The conclusion the authors drew is the correct one and worth quoting in spirit: larger parallel-group studies are needed to work out the right formulation, the right titration schedule and the right maintenance dose to minimise side effects long-term. That work has not been done. Anyone telling you Mucuna is a proven long-term replacement for levodopa/carbidopa is describing a study that does not exist.

The Carbidopa Problem

If you read nothing else on this page, read this section. It explains the nausea, it explains the dose ratio, and it explains why Mucuna is not simply “natural Sinemet.”

Levodopa has to reach the brain to work. It is the precursor your neurons convert into dopamine. But the enzyme that performs that conversion — aromatic L-amino acid decarboxylase, also called dopa decarboxylase — is not confined to the brain. It is abundant in the gut wall, the liver, the kidneys and the bloodstream.

So plain levodopa, swallowed on its own, gets converted to dopamine before it ever crosses the blood-brain barrier. Two things follow, and both are bad:

Carbidopa exists solely to prevent this. It blocks dopa decarboxylase but does not itself cross into the brain, so it shuts down peripheral conversion while leaving brain conversion untouched. Benserazide, used in Europe, does the same job. This is the entire reason your prescription says levodopa/carbidopa and not just levodopa — and it was one of the most important refinements in the history of Parkinson’s treatment. Before decarboxylase inhibitors, levodopa was tolerable for far fewer patients.

Mucuna contains no carbidopa. No amount of processing puts it there. Every gram of levodopa you take as seed powder is unprotected levodopa.

This single fact explains all of the following, and they now stop looking like separate findings:

There is one genuine consolation. Less levodopa reaching the brain per dose, and a different absorption profile, may be exactly why Mucuna produced fewer dyskinesias in both the 2017 trial and the animal work. Contin and colleagues made precisely this argument in Clinical Neuropharmacology in 2015: impaired bioavailability without a decarboxylase inhibitor “might explain the suggested lower dyskinetic potential of Mucuna compared with standard LD formulations.” The weakness and the benefit are the same property viewed from two sides.

Seed Powder Versus Capsules

Almost every Mucuna product sold in health-food shops and online is a standardised extract in capsules, typically labelled “15% L-dopa” or “98% L-dopa.” Every clinical trial described above used roasted whole seed powder. These are not the same product, and there is direct evidence that the difference matters.

Contin and colleagues studied two Parkinson’s patients who were already self-prescribing commercial Mucuna capsules alongside their standard levodopa. Each was challenged, after a 12-hour washout, with 100 mg levodopa as a standard tablet with carbidopa or benserazide, versus 100 mg of levodopa from Mucuna capsules — and the capsule content was independently assayed to confirm it really did contain 100 mg.

The bioavailability results were stark:

This is two patients, and it should not be over-read. But the direction is unambiguous and the mechanism is understood: a milligram of levodopa from a capsule is not a milligram of levodopa from a tablet, because the tablet comes with carbidopa and the capsule does not.

Practical consequences for anyone buying Mucuna

If someone is going to use Mucuna anyway, the trial-supported form is roasted seed powder, from a supplier who publishes third-party levodopa assays for the specific batch. That is a small set of suppliers.

The Access Argument

Everything above is framed as a comparison, as though a patient were choosing between Mucuna and a prescription. For a very large number of people with Parkinson’s, there is no choice to make, because there is no prescription available.

Fothergill-Misbah and colleagues — a group spanning Newcastle University, a Parkinson’s support group in Nairobi, a Catholic hospital in Sogakope, Ghana, and the Milan Parkinson Institute — laid this out in Parkinsonism & Related Disorders in 2020, in a paper asking directly whether Mucuna could be the answer to Parkinson’s management in sub-Saharan Africa and other low-income countries.

Their argument:

Their conclusion is carefully hedged — Mucuna “could potentially be part of the answer” — and that hedging is earned, not timid. Note that the same research group ran the 16-week study that found a 50% dropout rate. They are not naive about the difficulties; they simply think the comparison for these patients is not Mucuna versus Sinemet. It is Mucuna versus nothing at all.

This reframes the risk calculation completely, and it is why the Cassani paper spent effort on a low-cost preparation method using locally grown seeds, and why the 2017 trial insisted on roasted seed powder “obtained without any pharmacologic processing.” A treatment that requires a pharmaceutical supply chain is no treatment at all for someone who cannot reach one.

If you are reading this in a country where levodopa/carbidopa is available and affordable, this argument does not apply to you. It is an argument about access, not about superiority. Using it to justify substituting Mucuna for a prescription you could simply fill inverts its entire meaning.

What a Real Dose Looks Like

Nothing in this section is a recommendation. It is here because people ask, and because vague answers lead to worse decisions than honest arithmetic. Mucuna dosing in Parkinson’s should be supervised by the neurologist managing the case, alongside the prescribed medication — not instead of it.

Working from the verified trial numbers:

Two things should jump out.

First, these are large quantities of plant material. Twenty to forty-five grams of bean powder daily is a meaningful volume of food, and it is exactly why the adverse events are gastrointestinal. This is nothing like a capsule of an adaptogen taken with breakfast.

Second, look at the gap between this and what is on the shelf. A typical commercial Mucuna capsule delivers a few hundred milligrams of extract. Reaching a trial-level levodopa dose from ordinary capsules would mean swallowing an implausible number of them — and the Contin data say that even then the absorbed dose would fall short. Most people taking commercial Mucuna capsules for Parkinson’s are taking a small fraction of any dose that has ever been shown to work. That is worth knowing in both directions: it limits the benefit, and it also means much of the marketed product is unlikely to do a great deal either way.

On cost

Prices vary enormously by country and the access papers argue economics structurally rather than in figures, so no prices are quoted here. The structural point is what matters: Mucuna is a legume that grows in the tropics and can be prepared by roasting and grinding, while branded levodopa requires manufacturing, regulatory approval, import and distribution. Where a household can grow or buy beans locally but cannot reach a pharmacy, that difference is the whole argument. Where a pharmacy is reachable, imported “standardised” capsules are frequently more expensive per effective dose than generic levodopa/carbidopa — a point the wellness marketing never raises.

The Neuroprotection Question

A recurring and appealing claim is that Mucuna does not merely mask symptoms but protects the dying neurons. The evidence for that is entirely preclinical. It is real work, it is interesting, and it has not been shown in a single human being.

What exists:

How much weight should this carry for a decision about your own treatment? Very little. The history of neuroprotection in Parkinson’s is a graveyard of compounds that protected rodent neurons beautifully and did nothing measurable in patients. Rodent models are induced by toxins over days; human Parkinson’s develops over decades through mechanisms still not fully understood, and that gap has defeated far better-funded candidates than this one.

The Lieu finding of intrinsic decarboxylase-inhibitor-like activity in the water extract does deserve follow-up, because it connects directly to the supernatant-water observation from the 2018 human study. Two independent lines pointing at the water fraction is a real lead — for researchers, not a reason to change what you swallow.

Safety and Side Effects

Mucuna is levodopa. Its safety profile is levodopa’s safety profile, minus the protection carbidopa provides, plus whatever the plant matrix contributes.

Common, expected and dose-related

The serious report on the record

In 1990 The Lancet published a report by Infante and colleagues titled Outbreak of acute toxic psychosis attributed to Mucuna pruriens. It is a short report and it is old, but it belongs on this page: a plant containing a potent dopaminergic drug can, in some circumstances, cause acute psychiatric harm. Anyone who tells you Mucuna is safe because it is natural should be shown this citation.

Interactions that matter

The raw seed

Raw Mucuna seeds contain antinutritional compounds, and the plant’s pods are covered in the spicules that give it the folk name “cowitch” and cause intense itching on contact. Traditional preparation — roasting, soaking, grinding — exists for good reasons. This is not a bean to experiment with straight off the vine.

What Mucuna Does Not Do

This section is deliberately blunt, because the rest of the page is genuinely positive and that positivity is easy to over-read.

Mucuna does not replace prescribed levodopa/carbidopa, and it does not replace neurological care. The best long-term evidence available — the 16-week crossover study — found that half the patients could not stay on it, while none had trouble staying on their prescription. That is the headline result of the only study that tested daily use, and no study since has overturned it.

Never stop or reduce prescribed Parkinson’s medication abruptly. This is not routine caution. Abrupt withdrawal of dopaminergic medication can cause severe, sudden deterioration in mobility and swallowing, and in rare cases a life-threatening reaction resembling neuroleptic malignant syndrome, with rigidity, fever and altered consciousness. Every change to a Parkinson’s regimen is tapered, and it is tapered by the person managing your case. If you want to try Mucuna, that is a conversation to have with your neurologist — who will want to know the batch, the assayed levodopa content, and the timing relative to your existing doses.

Mucuna does not come with carbidopa, and it never will. That is not a defect that a better brand fixes. It is the chemistry. More nausea per unit of clinical benefit is the price, permanently, because peripheral decarboxylation is unblocked.

Mucuna has not been shown to slow the disease in humans. The neuroprotection work is entirely in rodents.

Mucuna does not solve the problems levodopa creates over decades. Motor fluctuations, wearing-off and dyskinesia arise substantially from the progressive loss of dopamine neurons able to buffer a pulsatile dose, and a different levodopa source does not change that trajectory — though it may, on the controlled evidence, be gentler on the dyskinesia side of it.

And Mucuna is not a reason to skip the rest of Parkinson’s care. Physiotherapy, high-intensity exercise, speech and swallow therapy, sleep and constipation management, depression screening and fall prevention do at least as much for daily life as any medication adjustment. None are optional, and none come in a jar.

Key Research Papers

Every citation below was verified against the PubMed record before publication. Where a number is quoted in this article, it comes from the abstract of the paper cited.

  1. HP-200 in Parkinson’s Disease Study Group. An alternative medicine treatment for Parkinson’s disease: results of a multicenter clinical trial. Journal of Alternative and Complementary Medicine, 1995;1(3):249–55. PMID: 9395621 — the 60-patient, 12-week open trial.
  2. Katzenschlager R, Evans A, Manson A, Patsalos PN, Ratnaraj N, Watt H, Timmermann L, Van der Giessen R, Lees AJ. Mucuna pruriens in Parkinson’s disease: a double blind clinical and pharmacological study. Journal of Neurology, Neurosurgery and Psychiatry, 2004;75(12):1672–7. PMID: 15548480 — faster onset, longer on-time, full pharmacokinetics.
  3. Cilia R, Laguna J, Cassani E, Cereda E, Pozzi NG, Isaias IU, Contin M, Barichella M, Pezzoli G. Mucuna pruriens in Parkinson disease: A double-blind, randomized, controlled, crossover study. Neurology, 2017;89(5):432–438. PMID: 28679598 — the six-arm noninferiority trial.
  4. Cilia R, Laguna J, Cassani E, Cereda E, Raspini B, Barichella M, Pezzoli G. Daily intake of Mucuna pruriens in advanced Parkinson’s disease: A 16-week, noninferiority, randomized, crossover, pilot study. Parkinsonism & Related Disorders, 2018;49:60–66. PMID: 29352722 — the daily-use study, and the 50% dropout finding.
  5. Cassani E, Cilia R, Laguna J, Barichella M, Contin M, Cereda E, Isaias IU, Sparvoli F, Akpalu A, Budu KO, Scarpa MT, Pezzoli G. Mucuna pruriens for Parkinson’s disease: Low-cost preparation method, laboratory measures and pharmacokinetics profile. Journal of the Neurological Sciences, 2016;365:175–80. PMID: 27206902 — 25 samples assayed; the 5.29% figure and the boiling loss.
  6. Contin M, Lopane G, Passini A, Poli F, Iannello C, Guarino M. Mucuna pruriens in Parkinson Disease: A Kinetic-Dynamic Comparison With Levodopa Standard Formulations. Clinical Neuropharmacology, 2015;38(5):201–3. PMID: 26366963 — commercial capsules versus tablets, same nominal dose.
  7. Fothergill-Misbah N, Maroo H, Cham M, Pezzoli G, Walker R, Cilia R. Could Mucuna pruriens be the answer to Parkinson’s disease management in sub-Saharan Africa and other low-income countries worldwide? Parkinsonism & Related Disorders, 2020;73:3–7. PMID: 32179240 — the access argument, stated by the people making it.
  8. Manyam BV. Paralysis agitans and levodopa in “Ayurveda”: ancient Indian medical treatise. Movement Disorders, 1990;5(1):47–8. PMID: 2404203 — Kampavata and Atmagupta, the historical anchor.
  9. Manyam BV, Dhanasekaran M, Hare TA. Effect of antiparkinson drug HP-200 (Mucuna pruriens) on the central monoaminergic neurotransmitters. Phytotherapy Research, 2004;18(2):97–101. PMID: 15022157 — the 52-week rat study and its unexplained result.
  10. Lieu CA, Kunselman AR, Manyam BV, Venkiteswaran K, Subramanian T. A water extract of Mucuna pruriens provides long-term amelioration of parkinsonism with reduced risk for dyskinesias. Parkinsonism & Related Disorders, 2010;16(7):458–65. PMID: 20570206 — rodent; the intrinsic decarboxylase-inhibitor hypothesis.
  11. Pulikkalpura H, Kurup R, Mathew PJ, Baby S. Levodopa in Mucuna pruriens and its degradation. Scientific Reports, 2015;5:11078. PMID: 26058043 — why storage and preparation change the dose.
  12. Infante ME, Perez AM, Simao MR, Manda F, Baquete EF, Fernandes AM, Cliff JL. Outbreak of acute toxic psychosis attributed to Mucuna pruriens. The Lancet, 1990;336(8723):1129. PMID: 1978001 — the serious adverse report on the record.
  13. Lampariello LR, Cortelazzo A, Guerranti R, Sticozzi C, Valacchi G. The Magic Velvet Bean of Mucuna pruriens. Journal of Traditional and Complementary Medicine, 2012;2(4):331–9. PMID: 24716148 — general review of the plant.
  14. Dhanasekaran M, Tharakan B, Manyam BV. Antiparkinson drug — Mucuna pruriens shows antioxidant and metal chelating activity. Phytotherapy Research, 2008;22(1):6–11. PMID: 18064727
  15. Tharakan B, Dhanasekaran M, Mize-Berge J, Manyam BV. Anti-Parkinson botanical Mucuna pruriens prevents levodopa induced plasmid and genomic DNA damage. Phytotherapy Research, 2007;21(12):1124–6. PMID: 17622977
  16. Kasture S, Pontis S, Pinna A, Schintu N, Spina L, Longoni R, Simola N, Ballero M, Morelli M. Assessment of symptomatic and neuroprotective efficacy of Mucuna pruriens seed extract in rodent model of Parkinson’s disease. Neurotoxicity Research, 2009;15(2):111–22. PMID: 19384573 — rodent only.
  17. Rai SN, Birla H, Singh SS, Zahra W, Patil RR, Jadhav JP, Gedda MR, Singh SP. Mucuna pruriens Protects against MPTP Intoxicated Neuroinflammation in Parkinson’s Disease through NF-κB/pAKT Signaling Pathways. Frontiers in Aging Neuroscience, 2017;9:421. PMID: 29311905 — mouse model.
  18. Yadav SK, Prakash J, Chouhan S, Singh SP. Mucuna pruriens seed extract reduces oxidative stress in nigrostriatal tissue and improves neurobehavioral activity in paraquat-induced Parkinsonian mouse model. Neurochemistry International, 2013;62(8):1039–47. PMID: 23562769 — mouse model.

Live PubMed searches

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  3. Levodopa, carbidopa and peripheral decarboxylase inhibition
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