I reiterate: although I try to substantiate my convictions, I expose in this website my personal opinions about mucuna, which therefore are open to debate. Furthermore, I do not take responsibility for direct application of any treatment. Rather, patients must always consult their regular doctors before acting on any medical advice.
The guidelines I give here on the use of mucuna are always of a general nature, are indicative and should then be applied to the specific clinical situation of the individual patient. Under this premise, I will present some case studies.
Mucuna is a good supplementary treatment in some patients with Parkinson’s disease, but is not indicated in all cases.
This discrepancy might be due not only to possible side effects, which fortunately are usually few, but because it is not useful in certain stages of the disease.
In the majority of patients, mucuna must be combined (according to medical criteria) with other antiparkinsonian drugs. In some cases, especially at the beginning, this may be the only treatment.
It is advisable (under supervision) to add mucuna slowly while gradually decreasing the doses of Sinemet or other conventional antiparkinsonian drugs1.
The ultimate goal is for the patient to feel better as he takes fewer prescription drugs and suffers fewer side effects to boot. These are the findings of a review of extensive and detailed literature2.
Mucuna should not be used as a preventive treatment for Parkinson’s disease. Although it has fewer side effects than synthetic levodopa, mucuna is a “drug” and should not be used previous to the onset of the disease.
In a young person, diagnosed prior to the age of 60, orthodox treatment aims to delay as long as possible the use of levodopa (Sinemet, Madopar, Stalevo). Instead, it is currently used rasagiline (Azilect) or dopamine agonists such as pramipexole (Mirapex), rotigotine (Neupro patches) or ropinirole.
Later, when levodopa becomes necessary, the patient and his doctor can take into consideration the option of starting with mucuna because it causes less long term dyskinesia. It is a decision that must be shared by doctor and patient.
Although rasagiline and selegiline are MAO-B (incomplete), as a precaution it is preferable to stop taking them two weeks before starting the mucuna.
If the patient also received treatment with dopamine agonists the doctor may want to reduce those as well.
In any case, mucuna would be taken in very low doses (200 mg of formulas 15 %) at first, and then would gradually be increased.
When the symptoms first appear after age 70, the treatment strategy changes. Usually when Parkinson’s disease starts late it is more benign and treatment is simplified.
Moreover, in these older patients, the premise is to rule out the possibility of cardiac or other general problems, and to prevent any possible interactions with medications currently in use. At that age I would rather avoid dopamine agonists and by prescribing low doses of levodopa to gradually be increased.
If you opt for the mucuna, you must start with very low doses (200 mg formulas 15%) and then move up progressively. You can later try to improve the bioavailability of levodopa by adding some carbidopa.
Tablets containing only carbidopa (Lodosyn) are sold in some countries. In Spain carbidopa is not available independently. In these cases you can resort to adding Sinemet Plus (which has a higher proportion of carbidopa). We are providing 12.5 mg of carbidopa with half of a tablet. However, this tablet also contains 50 mg of synthetic levodopa thus it would be necessary to deduct a portion of the dose of mucuna (the equivalent of natural levodopa).
For example, you can start by adding half of a tablet of Sinemet Plus per 100-150 mg while removing one tablet of 800 mg Mucuna 15%, continuing the remaining medications.
In practice, almost all patients with Parkinson’s disease will be treated at some point in their lives with the synthetic levodopa in Sinemet, Madopar or Stalevo.
We found that some of our patients had not yet used these drugs. This is usually due to one of two factors: they are either in the early stages of the disease or, even if they have been diagnosed for months or years, they are young (under 60 years) and the doctor opted to delay the use of synthetic levodopa for fear of later complications (dyskinesia and others).
On the other hand patients may have been fortunate enough to have maintained a good functional capacity, and have not yet needed agonists or other antiparkinsonian drugs.
These patients who never used synthetic levodopa (Sinemet, Madopar or Stalevo) are potential candidates for testing the response to levodopa with natural extracts of mucuna seed.
In the course of the disease there is a specific time in which the doctor decides to start treating with levodopa (which is the most effective treatment). At that point, common sense suggests that the natural form of levodopa is a legitimate choice instead of the synthetic form.
Treatment should be started with seed extracts of mucuna in low-concentration formulas (15%) in small amounts. With these low doses the symptoms still may not have improved but we have established that mucuna is well tolerated. From there, we must increase dosage gradually according to patient response.
If a patient has been on a very low dose of Sinemet (or Madopar), 100 to 300 milligrams a day, for a short period of time, the doctor may consider gradually changing to mucuna extracts, other circumstances permitting.
The strategy is to gradually remove the synthetic levodopa while mucuna is added. But the problem is more complex for carbidopa (or benserazide) which is also contained in these tablets.
If the functional status of the patient is satisfactory and he is on a very low dose of Sinemet (or Madopar), it is even possible to dispense these drugs. It is worth enduring a short period of minor clinical deterioration, so that the patient is left without any drugs before starting mucuna.
Commonly, people who are taking synthetic levodopa (especially if the dose is medium or high) cannot do without it if it is reduced rapidly, not least because is associated with carbidopa (or benserazide).
In these cases one can use half a tablet of Sinemet 25/100 Plus (better than 25/250 Sinemet), to provide a bit of carbidopa (12.5 mg), since it includes some synthetic levodopa (50 mg) which logically should be considered in addition to the natural levodopa provided by mucuna.
At this point, a problem arises for the neurologist: mucuna levodopa is approximately three times more potent than the synthetic version, but that relationship changes when carbidopa is added to one or the other.
When you read the prospectuses of mucuna preparations you can see recommendations of dosage that apply only to patients who take simply mucuna. The laboratory assumes that you are not taking carbidopa. But if you take carbidopa (due to a combined treatment of mucuna with Sinemet), then the amount of product recommended will contain too much levodopa.
Another point of confusion comes from clinical trials comparing Sinemet and mucuna extracts containing just natural levodopa without carbidopa (although the plant can provide similar but unknown substances with a milder effect). They employ an amount of mucuna with relatively high doses of levodopa (without carbidopa) to compare the clinical efficacy of the latter with respect to Sinemet.
Last but not least, we must take into account the idiosyncrasies of the patient: some react to mucuna sooner or more effectively, others experience weak or delayed responses.
This issue is complex and cooperation between the patient the neurologist in a supportive atmosphere is essential, choosing the best strategy at this juncture is a true example of the art of medicine.
Fortunately, the experience does not show major problems despite the chaos usually surrounding mucuna: freely permitted online without a prescription, patients’ lack of knowledge, and the detachment most doctors feel regarding this topic. Under these conditions one would expect hundreds of medical complications to have been registered, and so far, I have heard of none.
In theory one could also replace some of the synthetic levodopa in Stalevo for the equivalent of mucuna levodopa (assuming that one would have to modify the proportions).
However, we would have to address all the issues raised in the previous section regarding Sinemet (because of its carbidopa content) along with the added problem of entacapone: since it inhibits COMT, the efficiency of mucuna levodopa is increased further, and the result is less predictable.
On the internet forums some of the most common complaints are discussed among those taking Stalevo along with the legume.
I have not heard of clinical studies comparing mucuna and Stalevo (levodopa + carbidopa + entacapone). So, while it is not as good, I suggest that if the patient and doctor agree, as a first step, Stalevo (at least some) would be replaced by the equivalent Sinemet and, as a second step, the issue could be addressed as detailed in the previous section.
With the exception of some particular cases, selegiline has been displaced by rasagiline, which has a similar but more specific action.
Both are inhibitors of MAO (monoamine oxidase) type B enzyme which, inter alia, results in more effective brain dopamine.
It seems also that rasagiline and selegiline are neuroprotective, and therefore recommended from the beginning of the illness, especially in young people. These drugs can bring about a slight amelioration of motor symptoms.
In later stages of the disease and in older patients the rasagiline (or selegiline) complicates treatment. Remarkably, it increases adverse effects (hypotension and dyskinesia) when combined with Stalevo (carbidopa + levodopa + entacapone) without providing clear advantages over a Stalevo-only treatment, and achieving little benefit in relation to a Sinemet-only therapy3.
Too many enzymes result inhibited: carbidopa restrains dopa-decarboxylase, entacapone slows down catechol-ortho-methyl-transferase, and rasagiline (or selegine) inactivates monoamine oxidase.
To make matters worse, sometimes this treatment is further associated with an antidepressant that prevents the reuptake of serotonin. In such cases complications are disseminated throughout the cerebral dopamine metabolism.
Common sense, or simple intuition, if you will, dictate my desire to flee from an artifice such as this.
Both selegiline and rasagiline are not absolute contraindications, and there is no firm theoretical basis to suspect this, but I suggest they be removed if one is planning to use mucuna.
In my opinion, the supposed benefits of combining mucuna with rasagiline and levodopa is mild and should be avoided, at least until further case studies are available.
In young patients it is customary to delay the initiation of levodopa (Sinemet or Madopar), using instead rasagiline (or selegiline). For the one to two years that patients are on this drug, they remain levodopa“virgins”.
As I mentioned before, it would be prudent to remove the Azilect (rasagiline) or Eldepryl (selegiline) before starting mucuna.
However, if patients are suddenly deprived for several days of a drug that had previously been useful, then they may complain of clinical deterioration during that period.
My proposal is to start testing the response to very low doses of “synthetic” levodopa combined with carbidopa (or benserazide): half of a tablet of Sinemet Plus (or a quarter of Madopar), equivalent to 50 mg of levodopa with its proportion of carbidopa (or benserazide).
Meanwhile, we must reduce the rasagiline (or selegiline) for several days before eliminating it.
Thus, on those days when patients are on half of a tablet of Sinemet Plus, their motor symptoms should not worsen, and, more importantly, we know how they tolerate “normal” levodopa.
An added advantage is that adverse effects are minimal or non-existent because carbidopa (or benserazide) eliminates peripheral cardiovascular and intestinal action.
As a second step, Sinemet (or Madopar) is replaced by low doses of mucuna as described in the corresponding section.
This group is large. Usually levodopa therapy is delayed in patients diagnosed before age 60, for fear of later complications. It is instead replaced with dopamine agonists that usually provide a good functional state for one to five years.
In general, if the daily amount of agonist is small, there would be minimal adverse effects to starting with mucuna. If the patient is already taking a medium or high amount of agonist, the neurologist should adjust the dose accordingly.
Patients treated with dopamine agonists have a tendency towards orthostatic hypotension which must be taken into account when adding levodopa, whether natural or synthetic.
The specific type of agonist is very important. Rotigotine (Neupro patches) is one of my favorite agonists. In theory, if there are no contraindications, and if under medical supervision, the patches can be combined with mucuna.
However, I have not yet found any publication that describes this association, perhaps this will be forthcoming in the near future.
Studies have been published describing patients treated with pramipexole (Mirapex) or Ropirinole who have received high doses of mucuna, and no significant adverse effects were observed.
Therefore it seems that in these patients previously treated with Mirapex or Ropirinole if mucuna were recommended, it could begin with low doses and slowly progress, always under the supervision of a neurologist.
In order to initiate the mucuna, the doctor may decide to slightly reduce the dose of agonist.
Amantadine was originally a medicine used to treat influenza. It also acts as a partial dopamine agonist with special features and which became fashionable as a treatment in some Parkinson’s patients who were unresponsive to other drugs. It is also assumed to be useful against dyskinesia.
In clinical trials patients treated with amantadine have received large doses of mucuna without encountering any significant adverse effects. However, if one is going to use mucuna, I recommend minimizing any substances that could interact with it.
Amantadine usually loses its effectiveness over time and it may be that the patient no longer needs the drug. If amantadine is not essential, it is preferable to remove it (gradually) before initiating mucuna.
I do not advise mucuna in combination with Stalevo and rasagiline, at least initially.
It is common sense to note that this combination blends many enzyme inhibitors: monoamine oxidase (rasagiline or selegiline), COMT catechol-ortho-methyl-transferase (entacapone) and decarboxylase (carbidopa).
All neurologists see patients that combine levodopa, carbidopa, entacapone and rasagiline, but this quartet usually produces more problems (100) than it solves. That is also my own experience and I avoid that situation when I can.
To test mucuna in these cases, I recommend first removing the rasagiline. As a second step you can follow the protocol that I have mentioned in the section on Stalevo.
There is no publication describing experiences with the use of mucuna in patients treated with apomorphine.
On the other hand, when a patient requires this drug (by injector pen or infusion pump) the disease is very advanced and the expectations of improvement with mucuna are minimal. I do not advise it.
Often, after many years of suffering from Parkinson’s disease, patients turn to velvet beans (or other supposedly miraculous techniques) searching for any remedy as a last resort. Those are precisely the cases where it is less desirable to use mucuna.
Once the disease is already very advanced, there are many other important drugs that cannot be removed from the treatment plan, and if the general condition of the patient is poor, this is not the time to do “experiments “.
In some specific cases, this can be tried using isolated doses of mucuna during the “off” periods, in an attempted “rescue” when there is little to lose. However, the physician must weigh the relationship between expected benefit and possible interactions.
Patients with multiple diagnoses or who are taking many medications should avoid mucuna.
There are some contrasting interactions as well as the possibility of other yet unknown effects.
I discourage the use of mucuna in these cases until more clinical trials are available.
This possibility makes sense. In patients who have had Parkinson’s disease for many years and have been taking various medications, the option of taking mucuna may be considered as an extra and occasional aid, when they begin to suffer the “off” period.
There was a patient comment to this effect on the forum, that I picked up in chapter 9, subsection About mucuna occasionally.
Synthetic levodopa in Sinemet is improved by carbidopa. This increases its clinical efficacy and prevents peripheral side effects (nausea, tachycardia).
Carbidopa further improves mucuna: it reduces the already mild side effects and makes it two or three times stronger.
This effect should be taken into account when a patient combines mucuna and Sinemet (or Madopar or Stalevo). These drugs contain carbidopa, which will also act with mucuna levodopa making it more effective (so it will be necessary to reduce the theoretical dose).
What happens if one is not taking Sinemet or other drugs? Then mucuna levodopa may be insufficient.
This group of patients is complaining that the mucuna “does nothing” and the reason is that levodopa is removed rapidly from the blood by the decarboxylase before it can reach the brain.
The solution: mucuna may be combined with carbidopa which in some countries is sold separately (this is called Lodosyn).
And what if you cannot buy Lodosyn? There is the option of taking half of a tablet of Sinemet Plus: 12.5 mg carbidopa including 50 mg of synthetic levodopa. This amount will be subtracted from the previous dose of levodopa from mucuna, bearing in mind that it will now be more potent.
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