For those who love sinemet please consider this as info only......I do not necessarily subscribe to all of these notions (but I subscribe to some)......

The activation of cancerous cells by carbidopa is of great concern and is alluded to in many ref's such as the Physicians Desk Ref (PDR) under the vagaries of "may" cause etc.. by the manufacturer themselves. Fact: PWP are at increased risk for cancer.....ask for refs and ill load you up with a year of reading Prof Papers ie: med journ pubs.all reputable such as ......Oxford....Columbia etc. just for example.. I rarely if ever cite from "University of Timbuktu"......no offense to Timbuktuians intended! And try to keep my cites within the past 3-5 yr's with a few exceptions where there appears to be a lack of research/progress in betwixt surges of interest/investigation......

Gilbert JA, Frederick LM, Ames MM (November 2000). "The aromatic-L-amino acid decarboxylase inhibitor carbidopa is selectively cytotoxic to human pulmonary carcinoid and small cell lung carcinoma cells". Clinical Cancer Research. 6 (11): 4365–72. PMID 11106255

Is natural dopamine better than Sinemet?

Thursday July 18, 2013


Mucuna pruriens or cowhage seeds are a natural source of Levodopa and its use to treat Parkinson’s symptoms can be traced over 4500 years ago when it was first used by Indian physicians practicing traditional Ayurvedic medicine. The benefit of cowhage seeds is due to the fact that these seeds contain 3-4% levodopa, the standard medical treatment for Parkinson’s. Interest in Mucuna pruriens has grown especially amongst individuals searching for a natural treatment.

Because cowhage seeds contain the dopamine precursor levodopa, clinical studies have been preformed to study its use in Parkinson’s disease. One study showed that Mucuna helped Parkinson’s patients with on-off fluctuations and dyskinesia[1]. Motor symptoms improvement was faster with Mucuna 30 grams (Phytrix, manufacturer) than carbidopa/levodopa 50/200. However only eight patient’s were studied and more research needs to be done.

At present, there is no recommended dose as further clinical trials are needed.

The following general principles must be understood when investigating the use of Mucuna pruriens:

1. The proposed active compound, levodopa, found in these seeds is chemically the same as that in standard medicine. Mucuna, therefore, can have the same side effects that are seen with levodopa.

2. Mucuna pruriens seeds, like other natural substances, are made up of more than just levodopa. Proposed benefits could be due to other biologically active compounds not yet determined that are present in the seed. Although these compounds may add benefit they can also have additional side effects and drug interactions.

3. Supplements are not regulated by the FDA so any single brand may not have the purity or strength claimed on the manufacturing label. Supplements are big business and you may not always be buying what you think you are buying. Toxic side effects from impurities in supplements have been observed. Look for supplements with the label ‘USP verified’ to insure potency, purity and bioavailability is appropriate.

4. Natural supplements can interact with you medicines. Talk to your healthcare provider before beginning a supplement.

5. The amount of levodopa present in beans can vary dramatically from on bean to the next based on age, where it is grown, etc; so it may be difficult to standardized a dosage.

Other names for Mucuna pruriens are: velvet bean and cowhage seed.

As always, it is important that you talk with your healthcare provider before changing your medical therapy.

Monique L. Giroux, MDMonique L. Giroux, MD
Guest Blogger, Former Medical Director of NWPF

I recommend from personal experience starting at a standardized dose of 150mg L-Dopa from 1000 mg velvet bean extract.........and transferring that dose to the 25/100 Carb levo that you are currently at....etc.....I am not a Dr. and this is my experience only and can be reinforced by other individuals on this forum should they choose to do so......

Carbidopa, an inhibitor of aromatic amino acid decarboxylation, is a white, crystalline compound, slightly soluble in water, with a molecular weight of 244.3. It is designated chemically as (—)-L-α-hydrazino-α-methyl-β-(3,4-dihydroxybenzene) propanoic acid monohydrate. Its empirical formula is C10H14N2O4•H2O. Used in tandem with L-DOPA (also known as levodopa, a dopamine precursor converted in the body to dopamine), it increases the plasma half-life of levodopa from 50 minutes to 1½ hours. CarbiDOPA cannot cross the blood–brain barrier, so it inhibits only peripheral DDC. It thus prevents the conversion of L-DOPA to dopamine peripherally. This reduces the side effects caused by dopamine on the periphery, as well as increasing the concentration of L-DOPA and dopamine in the brain.

The combination of carbidopa/levodopa carries the brand names of Kinson,Sinemet, Pharmacopa and Atamet; while Stalevo is a combination with entacapone, which enhances the bioavailability of carbidopa and levodopa.

Carbidopa is most commonly used as a method to inhibit the activity of dopamine decarboxylase. This is an enzyme that breaks down L-Dopa in the periphery and converts it to dopamine. This results in the newly formed dopamine being unable to cross the blood–brain barrier and the effectiveness of L-Dopa treatments is greatly decreased. Carbidopa reduces the amount of levodopa required to produce a given response by about 75% and, when administered with levodopa, increases both plasma levels and the plasma half-life of levodopa, and decreases plasma and urinary dopamine and homovanillic acid. Elimination half-life of levodopa in the presence of carbidopa is about 1.5 hours. Following SINEMET CR, the apparent half-life of levodopa may be prolonged because of continuous absorption. This is extremely useful in the treatment of Parkinsons disease symptoms because the amount of levodopa administered to the patient can be greatly reduced. This reduction in dosage is extremely useful due to the side effects that may occur from an overdose of L-Dopa within the body.

Carbidopa is also used in combination with 5-HTP, a naturally occurring amino acid which is a precursor to the neurotransmitter serotonin and an intermediate in tryptophan metabolism. Carbidopa prevents 5-HTP's metabolism in the liver and the resulting elevated levels of serotonin in the blood. Research shows that co-administration of 5-HTP and carbidopa greatly increases plasma 5-HTP levels. Several cases of scleroderma-like illness have been reported in patients using carbidopa and 5-HTP.[2] In Europe, 5-HTP is prescribed with carbidopa to prevent the conversion of 5-HTP into serotonin until it reaches the brain
(Gilbert JA, Frederick LM, Ames MM (November 2000). "The aromatic-L-amino acid decarboxylase inhibitor carbidopa is selectively cytotoxic to human pulmonary carcinoid and small cell lung carcinoma cells". Clinical Cancer Research. 6 (11): 4365–72. PMID 11106255.
2.http://www.truestarhealth.com/Notes/1339004.html
3.Sletzinger, M.; Chemerda, J. M.; Bollinger, F. W. (1963). "Potent Decarboxylase Inhibitors. Analogs of Methyldopa1". Journal of Medicinal Chemistry. 6 (2): 101. doi

Karady, Sandor; Ly, Manuel G.; Pines, Seemon H.; Sletzinger, Meyer (1971). "Synthesis of D- and L-.alpha.-(3,4-dihydroxybenzyl)-.alpha.-hydrazinopropionic acid via resolution". The Journal of Organic Chemistry. 36 (14): 1946. doi:10.1021/jo00813a023.
5. Karady, Sandor; Ly, Manuel G.; Pines, Seemon H.; Sletzinger, Meyer (1971). "Synthesis of L-.alpha.-(3,4-dihydroxybenzyl)-.alpha.-hydrazinopropionic acid from optically active precursors by N-homologization". The Journal of Organic Chemistry. 36 (14): 1949.

L Dopa or Levodopa, how to increase brain chemical, dihydroxyphenylalanine
December 19 2015 by Ray Sahelian, M.D.



L dopa, dihydroxyphenylalanine, is the most effective symptomatic agent in the treatment of Parkinson's disease and the "gold standard" against which new agents are compared. More than 30 years after its development, levodopa is still the most effective treatment for the symptomatic control of Parkinson's disease. Although a number of therapies have been developed in an attempt to improve Parkinson's disease management, such as dopaminergic agonists and inhibitors of COMT and MAO-B, most patients still depend on levodopa alone because of its superior ability to control PD symptoms.

The issue of toxicity has been raised by in vitro studies suggesting that levodopa might be toxic to dopaminergic neurons, but this has not yet been proven. A more pressing concern regarding levodopa is its association with the development of motor complications after long-term use.

More than 50% of Parkinson's disease patients treated with L-dopa develop L-dopa-induced dyskinesias in the long term. Some patients exhibit severe dyskinesias soon after starting low doses of L-dopa, whereas other patients remain free of this disabling complication despite treatment with L-dopa. Avoiding or delaying the appearance of l dopa induced dyskinesia is one of the main objectives of the management of PD.

Formation of L Dopa
Phenylalanine amino acid > Tyrosine amino acid > L-Dopa > Dopamine > Norepinephrine > Epinephrine.

Natural Supplements with L Dopa
Mucuna pruriens is an herb that contains a small percentage of natural L Dopa. Mucuna pruriens is available without a prescription. For more information on mucuna pruriens and levodopa, click on the link provided.

Q n A

Q: I have mucuna extract 99 percent l dopa from a company I use here in the UK but can you please tell me something. I realise pure l dopa which I have can release hgh etc and good moods. but do I have to use mucuna powder for testosterone raising or will my pure l dopa raise testosterone as well? I'm really confused what is the benefit of mucuna extract 99 percent compared to just mucuna powder (seeds) untouched? And will I benefit from them both in the same way or dies 99 percent extract wipe out all the other mucuna ingredients?
A:Much depends on how each company prepares their l dopa extract from the herb. Ther e could be differences between companies, and there is no guarantee that the product would be 99 percent pure. As a general rule, it is quite likely that many of the other substances in the mucuna herb would be removed and they contribute to many of the health benefits of this herbal product. Rather than focusing on elevating testosterone levels, one has to evaluate what exactly do they wish to benefit from taking either the l dopa 99 percent product or mucuna. There are a number of other herbs and supplements that influence mood and sex drive.



Q: Is the product "Mucuna Pruriens extract of 200 mg 15%" equal to 30 mg of L-Dopa? If so, I will go back to the website to purchase.
A: It has 30 mg l dopa but this herb has many other substances in it that have various effects and benefits so it cannot be simply compared to L dopa medication.



Hawaii J Med Public Health. 2013. Case of levodopa toxicity from ingestion of Mucuna gigantea. Hawai'i is home to 1000 native species of flowering plants. Mucuna gigantea is one such Hawaiian species which has been studied as affordable sustenance and as a cover crop in developing countries. Mucuna gigantea and other Mucuna species (spp.) in general, are known to contain natural levodopa and its utility in the treatment of Parkinson's Disease has also been evaluated. Levodopa is converted in the periphery into dopamine which can then act on dopamine receptors to cause nausea, vomiting, arrhythmias, and hypotension. We describe a case in which a patient presents with abdominal pain, nausea, and vomiting after legume ingestion. The bean was ultimately identified as Mucuna gigantea and the patient was diagnosed with levodopa-induced gastrointestinal toxicity from consumption of the legume. A literature review was conducted using the database search engines, Biological Abstracts and PubMed, with a broad combination of keywords of which include "mucuna, "gigantean," "levodopa," "l-dopa," "toxicity," and the association between Mucuna gigantea ingestion and levodopa toxicity is discussed. These findings expand the differential diagnosis of abdominal pain associated with nausea and vomiting in the correct clinical context.



Antioxidants and L Dopa
It is possible that the use of certain antioxidants could slow the progression of Parkinson's disease, or mitigate the potential side effects from l dopa.

Side effects of levodopa
Chronic treatment is associated with motor complications that marred the clinical benefit of levodopa. These problems and experimental data in cell cultures indicating a neurotoxic effect of levodopa have led to the idea of delaying the introduction of levodopa treatment for as long as possible to avoid the side effects of L dopa.
However, after an initial period of dramatic benefit, several limitations become apparent including, "dopa resistant" motor symptoms (postural abnormalities, freezing episodes, speech impairment), "dopa resistant" non-motor signs (autonomic dysfunction, mood and cognitive impairment, etc), and/or drug related side effects (especially psychosis, motor fluctuations, and dyskinesias). They can be very disabling and difficult to treat. Though mechanisms underlying motor complications are only partially understood, recent work has revealed the importance of pulsatile stimulation of postsynaptic dopamine receptors and the disease severity. As a result of intermittent stimulation there occurs a cascade of changes in cell signalling leading to upregulation of the N-methyl-D-aspartate subtype of gamma-aminobutryric acid-ergic neurones. Modified preparations of levodopa (controlled release preparations, liquid levodopa), catecholamine-o-methyltransferase inhibitors, dopamine agonists, amantidine, and various neurosurgical approaches have been used in the prevention and/or treatment of motor complications.

Levodopa treatment
Levodopa remains the mainstay treatment for Parkinson's disease. There remain two areas of controversy: (1) whether levodopa is toxic, and (2) whether levodopa directly causes motor complications. Levodopa is toxic to cultured dopamine neurons, and this may be a problem in PD where there is evidence of oxidative stress in the nigra. However, there is little firm evidence to suggest that levodopa is toxic in vivo or in PD. Clinical trials have not clarified this situation. Levodopa is also associated with motor complications. Increasing evidence suggests that they are related, at least in part, to the short half-life of the drug (and its potential to induce pulsatile stimulation of dopamine receptors) rather than to specific properties of the molecule.

Curr Neuropharmacol. 2015. Revisiting the Medical Management of Parkinson's Disease: Levodopa versus Dopamine Agonist. The optimal treatment for Parkinson's disease has been debated for decades. The introduction of levodopa (LD) treatment is frequently delayed because of theoretical concerns about its toxicity or the risk of drug-induced motor complications. These concerns have resulted in "LD phobia" with clinicians selecting dopamine agonist (DA) over LD as initial therapy.

Mov Disord. 2013. The history of parkinsonism: descriptions in ancient Indian medical literature. The clinical syndrome of parkinsonism was identified in ancient India even before the period of Christ and was treated methodically. The earliest reference to bradykinesia dates to 600 bc. Evidences prove that as early as 300 bc, Charaka proposed a coherent picture of parkinsonism by describing tremor, rigidity, bradykinesia, and gait disturbances as its components. The scenario was further developed by Madhava, Vagbhata, and Dalhana all through history. The 15th-century classic "Bhasava rajyam" introduced the term kampavata, which may be regarded as an ayurvedic analogue of parkinsonism. The pathogenesis of kampavata centered on the concept of imbalance in the vata factor, which controls psychomotor activities. The essential element in therapy was the administration of powdered seed of Mucuna pruriens, or atmagupta, which as per reports, contains 4%-6% of levodopa.

Clin Neuropharmacol. 2016. Levodopa and Other Pharmacologic Interventions in Ischemic and Traumatic Optic Neuropathies and Amblyopia. The visual impairment in traumatic and ischemic optic neuropathy and amblyopia may be permanent. Hence, lots of efforts have been focused on neuroprotection. Dopamine is one of the suggested neuroprotective agents. Besides its important role in the brain, dopamine is found in various cell types of the retina, and is claimed to play a neuromodulator and neurotransmitter role there. The dopamine D1 receptor is the most highly expressed subtype of dopamine receptors, and its activation has been shown to be potentially neuroprotective against oxidative-stress damage in retinal neurons. Levodopa, a precursor of dopamine, can easily breach the blood-brain and blood-retinal barriers, and exerts effective dopaminergic responses in the brain and retina. This article summarizes and discusses the use of levodopa and other pharmacologic agents in the treatment of 3 groups of visual pathway disorders that primarily involve neuronal systems: ischemic optic neuropathy, traumatic optic neuropathy, and amblyopia.

Patients taking L-dopa for any reason are much less likely to develop age-related macular degeneration. If they do, they develop the disease much later in life than those not taking L-dopa; Nov. 9, 2015, American Journal of Medicine.

Levodopa Addition Medication
Zelapar (selegiline HCl, Valeant) Orally Disintegrating Tablets, a monoamine oxidase-B (MAO-B) inhibitor, was approved in 2006 as a once-daily adjunct therapy for Parkinson's disease patients being treated with levodopa / carbidopa who exhibit deterioration in the quality of their response to this therapy.

When it comes to which drug works best for patients with newly diagnosed Parkinson's disease, older may still be better. Research published June 10, 2014 in The Lancet finds that the dopamine drug levodopa still outperforms newer medications for the long-term care of people newly diagnosed with Parkinson's. In the largest-ever trial of Parkinson's disease treatment, levodopa offered patients better mobility and a higher quality of life than the two main alternatives -- drugs called dopamine agonists and monoamine oxidase type B (MAO-B) inhibitors.

Levodopa Carbidopa

Levodopa and carbidopa are used for the treatment of Parkinson's disease. Levodopa can be used alone, but adding carbidopa lowers the amount of levodopa that is required and may reduce some of the levodopa side effects such as nausea and vomiting. Carbidopa is a medication (called a decarboxylase inhibitor) that, when taken with levodopa, helps prevent the levodopa from converting to dopamine outside the brain. The combination of carbidopa and levodopa allows more levodopa to get to the brain. The levodopa carbidopa combination decreases side effects caused by increased dopamine levels outside the brain by reducing the supply of “free” dopamine outside the brain. Most people take levodopa and carbidopa together, rather than levodopa by itself.

L Dopa or Levodopa research
Proc Natl Acad Sci U S A. 2013. Single dose of L-dopa makes extinction memories context-independent and prevents the return of fear. Traumatic events can engender persistent excessive fear responses to trauma reminders that may return even after successful treatment. Extinction, the laboratory analog of behavior therapy, does not erase conditioned fear memories but generates competing, fear-inhibitory "extinction memories" that, however, are tied to the context in which extinction occurred. Accordingly, a dominance of fear over extinction memory expression--and, thus, return of fear--is often observed if extinguished fear stimuli are encountered outside the extinction (therapy) context. We show that postextinction administration of the dopamine precursor L-dopa makes extinction memories context-independent, thus strongly reducing the return of fear in both mice and humans. Reduced fear is accompanied by decreased amygdala and enhanced ventromedial prefrontal cortex activation in both species. In humans, ventromedial prefrontal cortex activity is predicted by enhanced resting-state functional coupling of the area with the dopaminergic midbrain during the postextinction consolidation phase. Our data suggest that dopamine-dependent boosting of extinction memory consolidation is a promising avenue to improving anxiety therapy.


Q. A while back you presented an article concerning Mucuna Pruriens as a potential natural source of L-dopa (precursor to dopamine). In order for L-dopa to efficiently cross the blood brain barrier however, measures must be taken so that it doesn’t get absorbed into the periphery (gut). The traditional way to do this is to administer the L-dopa along with a peripheral DDC (dopamine decarboxylase) inhibitor such as carbidopa as well as with a COMT (Catechol-O-methyl transferase) inhibitor. I have read that green tea extract can act as a natural COMT inhibitor but have never heard of any natural substances that can act as a DDC inhibitor. Are there any natural substances that can improve the efficiency of the Mucuna Pruriens by increasing the amount of L-dopa that crosses the blood brain barrier?
A. You ask a good question regarding L Dopa and decarboxylase inhibitor, but we have not come across such research yet, but we will keep our eyes open.


Q. What do you think of Coq10 supplement taken the same day as L dopa.
A. I have not seen any studies combining the two, There could be overstimulation.


Q. On the subject of: Parkinson' s Disease- Natural Treatment Options and Parkinson's Disease Information, I read on your website that "Perhaps levodopa acts as an oxidant, damaging nerve cells" and also that Mucuna may work as an antioxidant. Since Mucuna Pruriens contains levodopa which is an oxidant, then Mucuna is also an oxidant, Right? How do we know whether a herb or a drug is an antioxidant or not?
A. Only a small percent of mucuna pruriens is L dopa, the rest are other substances that have antioxidant protection whereas L dopa, the pharmaceutical drug, is 100 percent L dopa. Each herb has to be individually studied to determine whether it has antioxidant properties.


Q. I love your site and the information you provide, and have purchased some very helpful supplements from Physician Formulas. I know that those suffering from Parkinson's who take Dopamine find that it works well at first, but begins to be less effective over time. Is it possible this could happen with L-Dopa from mucuna pruriens, or does the fact it comes from a natural source that the body converts to Dopamine reduce the chance of loss of effectiveness over time? As an "aging" male of 56, soon to be 57 (though I'm pretty healthy and fit & certainly don't feel "old"!), I'm aware that my hormone levels are probably declining, and decided to try L-Dopa to boost natural levels of testosterone to aid in muscle-building, but now I've become concerned whether long-term use could actually leave me WORSE off - is that possible? Thank you for your time, and keep up the great work you do to help all of us out here get a handle on our own health - I'm a firm believer in "natural" cures & that we shouldn't just leave it all to our family doctors and prescription drugs.
A. This is a good question. Unfortunately we are not aware of long term human studies with mucuna pruriens to determine what kind of effect it has on dopamine receptors in the brain or other influences on brain tissue. We suspect that mucuna pruriens does not have a similar effect as does L dopa. But, to be sure, we often suggest taking breaks from the use of supplements, which could be a day or two off a week, a few days off each month, and a week or two off every 3 months. (L Dopa or Levodopa, how to increase brain chemical, dihydroxyphenylalanine
December 19 2015 by Ray Sahelian, M.D. )

happy investigating

BP