Hi gang. Sorry for the long post but something has happened that has somewhat surprised me and I need both to share to provide others with information, offer - whilst not an apology - at least make an admission - and lastly ask for advice. Here goes:
Dxed 5 years ago. Started on Azilect and then added 8mg of Requip and I still take these in the morning. 3 years ago added 300mg of Madopar per day but only stayed on this for a couple of months. I'd read about dyskinesia and also heard that Mucuna offered the same relief but didn't cause dyskinesia. I maintained a single 25/125 Madopar for some reason and took it in the morning along with the Az and Requip. The rest of the day was just Mucuna.
Now the only Mucuna that seemed to offer any serious relief was the 98% version. I took 1/8 of a teaspoon along with some green tea. It worked soooooooooo well. I didn't really understand why others pledged an allegiance to normal pharmaceuticals. And no dyskinesia! What could be better?
That was until two days ago I am definitely developing this. It's not 'peak dose' phenomenon but irritatingly appears to be lasting for the duration of the levadopa cycle. It's happening both with the Madopar but also when I take the Mucuna. This wasn't what I signed up for! It's pretty mild but is an obvious concern and is widespread (arm jerks, then head goes, then leg etc).
So an admission to those of you that claimed it was the same as lab stuff (Winnie, Julie Grace et al). Seemingly, you are right. The argument is that the carbidopa causes the dyskinesia but surely my single 25/125 can't have done that damage?
And I don't know where to go from here. Any advice would be very welcome. Its hard and confusing when one's 'plan' goes wrong and that was the direction one had planned to go with for the foreseeable future. Do I keep up with the Mucuna or just revert to the Madopar? At least the latter is free in the UK!
Regards to you all and beware all you guys on 99% Mucuna. It's probably not the harmless elixir we all perceive it to be.
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jeeves19
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Firstly, very sorry that you are going through this and thank you for sharing.
Secondly, we've been through this recently. A few things:
1. Very high concentration (98,99,100 etc) ldopa supplements are NOT 'mucuna' any more than pure nicotine is 'tobacco' or pure caffeine is 'coffee'. See my thread here about this:
3. There's no shortage of discussion about dyskinesia/MC on this board but the latest (good) science suggests that disease duration is the key variable, *not* how much ldopa you've ingested in your life. Jefferyn has made some good comments about this (don't remember when).
At the risk of being controversial, I'd raise this with your Neuro, and be upfront about what youve been doing with the ldopa supplement.
The dyskenesias are a function of the dopamine supplementation - not levadopa (or carbidopa) per se
My Dad can get dyskenesia if EITHER his sinemet intake is too high OR his Dopamine agonist is too high.
Levadopa in Mucuna is the same (identical) as in pharmaceuticals. If your mucuna tablets are genuinely 99% levadopa they are identical to sinemet without carbidopa
Carbidopa is not the problem itself - that is , it is as much or little of a problem as the benserazide in Madopar, or the green tea. All of them are decarboxylase inhibitors. That is, they all help more of the levadopa not get converted by the rest of your metabolism, and therefore make it to the brain
So, I think, mucuna "works" by giving the possibility of adding dopamine in smaller increments. If you take a mucuna tablet you might just take an extra 60mg of levadopa. If you take a sinemet 12.5/50 - thats the equivalent of 250mg levadopa. If you were 150mg short of the trigger level for dyskenesia the sinemet pushes you over it, while the mucuna stays below it
And Madopar 125 is 25/100 - the equivalent of 500mg of levadopa (and has benserazide -not carbidopa)
That's not to say Carbidopa can't cause other issues, but it's relationship to dyskenesia is just that it lets more levadopa becomes dopamine in the brain, and its excess dopamine in the brain that causes the dyskensias
But you have confirmed that levadopa is the same wherever it comes from. C9H11NO4
This is the correct story I think. It does matter that the mucuna and LDopa are different as manufactured or collected, concentrated and purified (all distinct and consequential aspects), but practically as or more immediately significant for the person I think is that over time WE change in several ways, partly due to disease progression and partly due to the presence of the LDopa that we didn't produce but that was introduced from outside, because its presence causes physical changes and may include changes in "receptor regulation," receptor positioning, receptor activity, and the like, where the presence of a substance starts (sometimes several) feedback mechanism that, in different locations to different extents even, alters the number of naturally occurring receptors or cells or cell parts involved with producing and signaling the neurotransmitter amount or mix.
Your brain may think that, since there is ample LDopa or simply more cells producing it or using it, that there are too many actual cells or too much production, and may thus curtail actual production, so that now when withdrawn or being taken up or depleted (consumed, changed to waste product), you now "fall off a cliff" until you get more from outside...this is one single illustration of mechanisms that abound throughout your nerve and endocrine systems. It's as if, walking on a floor told the floor how much lift it needed to give you to keep you on the floor, then someone with cables picked you up, the floor noticed that there was less weight on it, and weakened the floor to keep all the signals in equilibrium. Then the cables let you back down on the floor and it is not ready and you crash through it. They call this a "negative feedback loop." (Another more directly scientific name is "receptor down-regulation.") Such changes can cause all sorts of consequences, including needing more and more, or responding less and less, or introducing side effects of various sorts. It's a well known, widespread principle of brain signaling and functioning development all up and down the age range.
One way that can work is that you can be highly sensitive to a very refined or concentrated amount of the active ingredient.
So smoothing out by reducing the amounts, or introducing more gradually, or selecting a less concentrated or less highly refined version, and schedules or timing, and gradually building to a more sustainable, less highly sloped, encounter, reducing the dips and peaks, trying to get to a smoother climb, longer and more stable peak, and smoother more gradual falloff, may be the thing to try.
Hi WinnieThe Poo. Would you kindly clarify what you mean . "If you take a sinemet 12.5/50 - thats the equivalent of 250 mg levadopa." I am confused because isn't that 50 mg. levodopa? Do you mean it's the equivalent of 250 levodopa from Mucuna? In a raw unprocessed Mucuna powder of 4-7% levodopa, what would it take to get to 250 mg. levodopa? Please forgive my ignorance - I am a relative newbie to Mucuna therapy
Levadopa once absorbed into the bloodstream is decarboxylated into dopamine by the metabolism. Some of that happens in the brain - where its wanted. Most of it is converted in the rest of the body where its not wanted. Dopamine can't cross the blood brain barrier, so dopamine decarboxylated in the general metabolism won't reach the brain, and can cause unwanted issues like nausea, hypertension, glaucoma and others.
Sinemet 12.5/50 contains 12.5mg carbidopa and 50mg levadopa. Carbidopa (like Benserazide in Madopar) is a DDCI (dopa decarboxylase inhibitor) , which when used in a 1:4 ratio with levadopa greatly inhibits decarboxylation into dopamine. Like dopamine, carbidopa can't cross the blood brain barrier. So it stops dopamine being made in the rest of the body but not in the brain.
As a result more levadopa makes it to the brain. The prescribing advice given, is that on switching from levadopa to carbidopa only 1/5th the amount of levadopa is needed. Put another way, the rule of thumb is that 5 times as much levadopa in the bloodstream gets to the brain when it is taken with carbidopa.
So in terms of dopamine delivered in the brain, as opposed to wasted in the rest of the body 50 mg of levadopa in sinemet is equivalent to 250mg pure levadopa (and with less adverse affects of unwanted dopamine in the general metabolism)
If you assume 5% ldopa whole macuna powder you would need 5 grams to be the equivalent levadopa in the brain.
Thank you so much WinnieThe Poo. Very grateful for your patience and detailed reply. So it seems that 5% ldopa whole macuna powder 5 grams (or 1 teaspoon of the powder) would equal the levodopa from a 12.5/50 Sinemet. And 10 grams (or 2 tsp mucuna powder) would equal levodopa from a 25/100 Sinemet tablet. WHEW. These conversions and calculations make make my non-math mind spin. I can start slowly with one or two teaspoons per dose of good quality mucuna like Banyan and see if my gait and arm swing improve. Many thanks.
I don't know know if it will help (and I still think your first port of call should be your neuro), but if I was going to do it, I'd read the studies where they are positive about MP. Bin the ones where they don't provide enough info about the mucuna formulation they use, and then attempt to replicate the mucuna formulation and dose from one of the remaining ones.
Warning: you may have to ingest a fair amount of it. After all, the plant is max 9% ldopa.
I agree with Chris, again. (I've been of the impression that dyskinesia is caused by too much levodopa and sometimes when the blood sermon level is on its way up and sometimes when it's on its way down.) It's everything else in the plant except the levodopa that makes it act faster, last longer, and with less dyskinesia than C/L. Which is to say, what's valuable about Mucuna P is not the levodopa, but the rest of the plant.
Apparently, the rest of the plant does a better job than carbidopa.
Hi, I know this study and I don't know how reliable it is. Dr. Maldonado asserts that Mucuna does not produce dyskinesia and apparently it doesn't seem correct.
There are a number of studies that conclude that, whilst mucuna (note: not 99 percent ldopa extracts, but actual mucuna) offers some advantages over CL, less dyskinesia is not one of them.
That has certainly been our experience. For the last four years my husband has relied on 1 Tablespoon Mucuna POWDER (stirred into water) taken approximately once every 3 hours through the day, and it has given him far fewer side effects than the Sinemet and Stalevo he took for the previous 11 or so years. They never worked as well or as consistently for him as the Mucuna has. In fact they lost effectiveness completely 4 years ago. He does have some dyskinesias now and other effects of Parkinson's Disease, but when he first started taking Mucuna powder the downward trend of his PD symptoms reversed and steadied for a number of years. Now he drools quite a bit, struggles a little more mentally, falls more often (usually saved by wearing knee pads), and his walking has deteriorated to the point where he uses a disability scooter to get around outdoors. But he was diagnosed 16 years ago in 2004, and at age 73 he still does not feel defeated. He is currently assembling a multi-gym that was delivered to us in 79 pieces, so he's doing alright, thanks mainly to Mucuna powder.
We’ve corresponded before Healthseeker. What I like about the 98% is that it only requires 1/8 of a teaspoon. I hated the taste of the full tablespoon stuff! But I’m thinking of return to the ‘brown’ stuff as I sense it has other properties in it. Do you use just this or add some Madopar:Sinemet to it? Also, what do you do to make it drinkable?! Thanks
Hello jeeves19. When you mention the "brown stuff" I wonder if you were trying the 'roasted' mucuna bean powder. My husband always takes the grey Mucuna powder, ground from uncooked Mucuna beans. We were hesitant to try the brown mucuna because heating can destroy nutrients. I don't know if or how cooking affects levodopa, but any loss of nutrient value might be significant.
Also, although a Tablespoon of grey Mucuna powder works for my husband, you might need a whole lot less. If I were you I'd start off with a quarter teaspoon or so and if that works, note how long before it begins to wear off, before taking more. We spent months experimenting and charting everything before we found the quantity and timing that suited my husband best.
He actually doesn't mind the taste of the grey Mucuna powder mixed in water, but you could just as easily mix it with your favourite fresh juice (e.g. pineapple, orange, cranberry, grape) or other cold drink. I've heard that Mucuna mixes well with cocoa, so you might devise a chocolate Mucuna drink, perhaps sweetened with some Mannitol.
Oh yes, and he takes one Stalevo (levodopa, carbidopa and entacapone) first thing in the morning and one in the afternoon, independent of the Mucuna. The levodopa in the Stalevo does nothing for him, but we think the carbidopa helps the levodopa in the Mucuna cross his blood brain barrier, and the entacapone inhibits the end-of-dose 'wearing-off' symptoms. If he doesn't take these two doses of Stalevo, he finds the effects of the Mucuna wear off quicker.
Detox Trading here in the UK. Good prices, consistent organic quality and they supply in up to 5 kg bags. Here's a link - detoxtrading.co.uk/product/...
Thanks. And what about nearness to food? Does he have a certain window whereby he has to take it away from this? I'd be curious to know what timings he has decided upon re. ingestion.
I get biphasic dyskinesia at any dose of levodopa - even just 50mg. I get peak dyskinesia at anything over 300mg a day. I got dyskinesia 3.5 years in and 2 years in to taking C/L at super low dose (about 150-200mg a day). Only thing that stopped it for me was brain surgery. Mucuna for me had worse side effects than C/L. Dyskinesia is dopamine dysfunction in the pallidothalamic tract(PTT) IMHO and from Dr. Jeanmonod's research. I no longer have a PTT on my right side and no more dyskinesia in my left body.
I have been using mucuna 99% for 3.5 years and no problems so far. I have read that the less processed mucuna can be more effective for some folks, I'm thinking of adding that to the mucuna I take now to see if the elements will aid what I'm already doing, have to find the right one tho, and would lower the more concentrated mucuna. Have found no info on what the synthetic Levodopa is made from, what I take is from Mucuna. I know everyone is different and finding the right combo can be tricky. I like not having to have a prescription and paying extra $$$$ and still have my Dr keeping an eye on things.
Obviously the water out of your tap contains impurities which are different from the impurities in a bottle of Evian and those mixes are noticeably different.
But if you boil tap water and condense the steam on a cold surface and produce pure 99% distilled water it is identical to the distilled water made from Evian
You should have taken undergrad college Chemistry. Water contains "some" elements of H2O and exists in 3 forms 1) solid, 2) liquid and 3) sweet gas.
Without repeating "in the weeds" chemistry, it is false to say water is simply H2O unless we are talking in very broad, non-scientific terms. The same holds true for your other comments on salt and L-Dopa in MP.
Almost all chemical analysis and experiment deals with water not as an individuated molecule but in macroscopic quantities.
Therefore, Even if you'll get a ratio of hydrogen to oxygen that's roughly 2:1 in a fluid like water but it does not have the macroscopic properties (pH, boiling point, etc.) of water then we DO NOT HAVE WATER but a mixture of hydrogen and oxygen molecules in their elemental form.
Why don't you tell us what the differences are between the ldopa found in 99% ldopa supplements and the ldopa found in prescription parkinsons medication?
L-Dopa found in prescriptions always has a 99.9% or higher purity level and is graded as "prescription grade".
L-Dopa found in supplements is almost always "food grade" with purity level anywhere between 90% to 95%. Seldom above it regardless of "claims" due to inferior processing.
It is important to differentiate purity with concentration and vice versa.
For MP supplements, MP seeds in nature are about 4-5% L-Dopa when ground and analyzed... then they are extracted to varying degrees and quality. You will never see a batch # or be able to track back.
Pharmaceutical L-Dopa is basically synthetically derived and is trackable unless it is a phony pharmaceutical.
We have been over this issue several times in previous posts which you should read.
Simplistically and to save my time, ask them (Nutrivita) for a authenticate and current 2020 COA from an American or EU lab re: a batch # you can track. Don't hold your breath while waiting with the others who had the same question months ago and are still waiting. They all thought like you.
Nutrivita is Good bulk supplement company, but not a pharma by any stretch of the imagination.
KN95 masks made in"America" are classic examples of deceptive claims in order to sell Chinese non-approved masks to gullible Americans who are clueless. Analogous to the Chinese chem business.
Riddle me this. Why does Sigma-Archer charge $670 for 100 grams or $1,800 for 500 grams of 3-(3,4-Dihydroxyphenyl)-L-alanine, L-3-Hydroxytyrosine, L-DOPA versus $113 for 500 grams from Nutrivita?
"Simplistically and to save my time, ask them (Nutrivita) for a authenticate and current 2020 COA from an American or EU lab re: a batch # you can track...
...Why does Sigma-Archer (sic) charge $670 for 100 grams or $1,800 for 500 grams of 3-(3,4-Dihydroxyphenyl)-L-alanine, L-3-Hydroxytyrosine, L-DOPA versus $113 for 500 grams from Nutrivita?"
I sent a PM. Some answers to your specific questions.
#1 2020 COA is a current year FULL "Certificate of Analysis" whose contents can and do vary by lab but all must follow FDA guidelines...and always contains info related to the LOT # and various heavy metal impurities (think of an accounting audit). My assumption here is that your supplier is not selling you "dated" chems. If so, you would need the lot# and batch # to make a request which may mean a COA generated in 2018 or earlier.
The appropriate COA for the chem used in manufacturer should be available upon request. If it is not available, lab analysis PROBABLY was never done or does not support the supplier's claims (i.e.non compliance with cGMP and FDA) or was not done by an accredited lab.
As an example, I find it amusing that some PwP buy bulk cannabis without a relevant COA. They have absolutely no clue as to the Total CBD Equivalents. Yuk! Total denial.
#2 It is very expensive (anywhere from $100 for a simple spec to about $2,000 and up for a complex spec) to retain a good lab to do an analysis of your chemical unless you are buying and distributing in bulk (kilogram size). Do not confuse these costs with the cost of blood testing for heavy metals.
Now you know why most supplement companies don't provide COAs on a "current basis" for any of their products claiming to be "pharmaceutical" grade.
This says less about the 99% product and more about you.
Some people never get dyskinesia even though they take CL. Some get it after a decade. Some after like 2 years. It's all very individual. My mother had a good 11 years on CL before getting any of it. Hikoi reports a similar experience.
Just a thought, but have you tried B1 recently? I know you’ve tried it from time to time without feeling it made any difference. Isn’t it supposed to stop dyskinesia though? Might it be worth trying again?
It seems to take a fairly good daily dose and then may take 3-6 months to show much effect, going back to the vast efforts by Dr. Costantini. Look around for the passages in this website, or someone else has the exact place for the summaries. Worth your time.
So sorry to hear about your difficulties with dosing, my husband has found it an absolute minefield and has had his share of unpleasant dyskinesia as his dose of Modopar was slightly increased. He too was dx 5 years ago and he always felt the Modapar didn’t help with symptoms as much as he would like. After 4 years he was taking 4 x 25/100 per day but didn’t want to increase dose as dyskinesia was getting worse. Changed Neuro and he added in Rasagiline which did make him feel a little more mobile then made the dyskinesia much worse.
He did think about Mucuna but on reading about dosing it did seem difficult and somewhat scary to do it without help.
After a couple of weeks he had cut down on these Rasagiline pills due to dyskinesia Asked the Neuro and he added in Amantadine which was like a miracle for these dyskinesias.
He still experiences them some times but this combination has allowed him to decrease the Modapar by a half dose a day and since lock down in U.K. has walked between 2 and 4 miles a day.
Not sure where you are in the U.K. but my husband is under the hospital for Neurological diseases in Queens Square under Professor Paul Jarman and we are really pleased we changed to his care.
Would you drop me a quick line if and when it stops working for him? I’d be interested to see how it pans out as we’re similar in disease years. Thanks
It seems to me that you are over medicated. I am not sure that the drugs you are taking play well together. Have you checked this out with your neurologist.
Dyskinesia, dystonia, etc are all due to meds (ie. L/C) not disease and probably to nutritional deficiency induced by long term intake of levodopa that competes with other amino-acids creating shortage (see Dr Hinz and his Amino Acid Therapy)
Mucuna 98% is like levodopa without the benefit of the rest of the plant that are antioxidants, neuro-protective, etc etc. (i.e 100 mg of mucuna 98% of levodopa are approx. the same of 200 mg with 49% levodopa) Carbidopa from L/C meds increases the effectiveness but side effects are the same because some metabolites of the levodopa have a long half life in the blood so tend to accumulate in your body (muscles, tissues, fat) and when the body is full then you see the side effects of medication.
So IMMO (supported by my neuro and my experience) you have to clean up your body as much as you can,
Short term and immediate actions are: sauna, aerobic exercise (cardio-fast walking), intermittent fasting, bumper but best is fast with drug withdrawal, from 3 to 7 days (but may be dangerous).
In the 70' they use to do a 7 days fasting with drug holiday (withdrawal) in hospital (depending on your conditions). It is dangerous if you are addicted to levodopa, and requires medical supervision.
Any other solutions that doesn't sensibly decreases L/C risk to be only temporary.
"Dyskinesia, dystonia, etc are all due to meds (ie. L/C) not disease and probably to nutritional deficiency induced by long term intake of levodopa that competes with other amino-acids creating shortage (see Dr Hinz and his Amino Acid Therapy)"
This is not correct at all. Dystonia is frequently a very early PD symptom and it very regularly precedes *any* levodopa intake, never mind "long term levodopa intake". This is uncontroversial.
Dyskinesia may be *induced* by high dopamine levels brought on by CL and other PD meds but PD progression is the primary determinant of when it will occur, not how much levodopa youve consumed over your life or how long you've been taking it (refer the African study).
Hinz says all sorts of things (as does Janice whatsherface).
They're all in here in the same proportions as dr hinz's own brand! I used to take 2 a day with mucuna and add cysteine or nac. Not the cheapest stuff but it's a good product.
it is not an opinion but my experience and my neuro's with 40 years of clinical experience with natural remedies and fasting. Since DX 13 years ago, I've followed the uncontroversial conventional medicine for 8 years getting only worst and worst. Every problem was managed with meds dosing or addition. Every meds was bringing its side effects to be managed soon or later with other meds and so on. A never ending bad loop for me.
I was not myself and in a miserable status with Impulse Control Disorders, Uncontrollable Insomnia and Sleep Attacks, progressive non-motor symptoms, etc etc
I lost my job and i was told the truth and i had to face it.
I was 10% of the man i was 8 years before and this was evidently the disease progression. I discovered by myself that this was not true.
If s.one takes insuline every day, then he develops diabetes; if an healthy person takes anti-PD meds at normal dosage, he develops a drug induced PD.
I discovered the meaning of Impulse Control Disorders and understood they were caused by meds. discovered Janice book and read it. it was inspirational and changed my mind and saved my life. Then in 4 months i gradually removed the three non-L/C meds i was taking (amantadine, neupro, entacapone and stilnox) and most of the non-motor symptoms progressively vanished. L/C meds had to be increased to compensate.
I changed eating regimen to be more healthy and lost 8 kg in 3 months (from 80 to 72 kg) naturally without effort and then stopped.
In april 2015 I was taking 800/1000 mg L/C (from 300 mg) to be on for 24 hours; after four months I was gradually losing sfintere control (involuntary farting and shouting, urgency to urinate), and increasing head bobbing, freezing, strong stuttering, grimaces, strong sleep disorders and so on.
My usual neuro said it was the disease and to return to previous therapy but i didn't want to return to previous status. Looked fora new neuro and during a chelation session heard about a new one (my current one).
First visit he told me that the problem was too much L/C and put me thru 6 days fasting with meds reduction (2 days with 200 mg, 2 days without meds - 0 mg and 2 days with 200 mg).
It has not been an easy process, but the a.m. problems disappeared in these 6 days.
Nothing to do with the disease. Now my stuttering goes with meds and is an indicator i use for therapy control.
Periodically i go thru a 12 hours of cleanup without meds nor food (in OFF status) and every dyskinesia i have disappear . For sure I'm off and slow and in miserable condition but it helps lot.
The fact that you have been through a lengthy and complicated experience to find what works best for you doesnt mean its ok for you to spread misinformation. For example, the blanket claim that dystonia is not caused by PD (and is only caused by meds) is incorrect. Its false. Whoever told you this was mistaken. You might as well say that PD doesnt cause tremor or bradykinesia.
"The fact that you have been through a lengthy and complicated experience to find what works best for you doesnt mean" - that I've not the holy truth in my pocket (i'm ok with this)
" its ok for you to spread misinformation". (i'm not ok with this)
I'm not spreading misinformation because there is no evidence (i've not found any) that never-medicated PwP develops dystonia. While more and more cases are reported of PwP diminishing side effects of meds, including dystonia, reducing meds.
Levodopa make s.one move if taken in the right quantity, but if too much have the opposite effects, it blocks and slows down movements
Dr Parkinson described 3 main motor-symptoms: tremor, bradykinesia and rigidity.
He didn't described any kind of dyskinesia or dystonia. These were added later on together with many others, but always on medicated people.
PD is a very slow disease, that takes years or decades to manifest ... what happens "overnight" (good or bad) is not caused by the disease but by meds or (rarely) by food.
Unfortunately most doctors are instructed to believe that the body is faulty and their meds are safe and ok, causing no side effects. This is not correct. The body has incredible self-repair capacity, that is overwhelmed by toxins and stress (ie. wrong lifestyle, stress, bad food, over-medications, lack of movement)
As many other diseases, i believe that PD is a malfunction due to the tentative of the body to manage a (nutritional / amino-acid) deficiency / unbalance, due to the above causes, progressively limiting the functions affected by the shortage to save resources and increase survival and life.
This is not what western medicine affirms but also western medicine has not the holy truth and has shown (too) many gaps and to be auto-centric and self referenced more then open to analyze data objectively and neutrally.
I don't want (neither hope) to change anyone's mind but i'm also free to say what i believe in good faith and honesty.
"I'm not spreading misinformation because there is no evidence (i've not found any) that never-medicated PwP develops dystonia. "
There's plenty. It's not even a question. It is a common symptom pre-diagnosis. If you choose to ignore it because you prefer to blame pretty much every PD symptom on meds, then fine, but that doesn't change the facts.
1. "Dystonia is also more common in younger people with Parkinson’s, in people who are younger than 40 or 50, for example. It may even be the first symptom of the disease. Sometimes people with young or early-onset Parkinson’s first notice dystonia during exercise and then later develop other symptoms of Parkinson’s, like tremor or stiffness, that leads to the diagnosis.
Nikki was diagnosed with Parkinson’s at the age of 35 after noticing her toes curling and her foot aching. "
Thank you Hidden and all the others for your interesting comments. (this is what makes this forum so good and valuable)
But I have an objection.
The fact that a disease responds to levodopa doesn't mean it is PD (for example, the lethargic encephalitis in the movie Awakenings).
I've read that there may be the possibility that a number of Patients who have been diagnosed with PD, were having another movement disorder and, after taking L/C meds, later on developed a full drug induced PD.
in any case it is true that long term use of L/C causes a number of side effects, that are commonly associated with disease progression, but in my opinion often are not because they diminish or even disappear with L/C reduction or withdrawal (assuming to be able to withstand)
I had dystonia before taking any medication and I had it when I went completely off all meds for a year. I also have it now when I am in my “off” state. I don’t take meds at night so I am in an off state every night. I take c/l during the day and have dyskinesia almost constantly at a relatively low dose, which is why I don’t take meds at night. My dyskinesia stops after 3-4 hours after my last daily c/l dose.
I don't take l/c during night (with strong insomnia) also to clean up the body from some of the toxic metabolites of the meds.
They are hard nights, where my body probably uses the residual levodopa stocked during the previous day, with limited mobility.
I've noticed that during these nights i sometime have dystonia (the fingers of my left foot curl ) and high blood pressure, due to lack of dopamine, while during the day I have dyskinesia due to overmedication (the fingers of my right foot moves up an down without my permission - i've to concentrate to stop them)
in my point of view, since the dystonia increases during the night, with the decrease of the residual meds, and dyskinesia increases (with other side effects) with meds, and none of them was present at diagnosis, they are drug related.
As long as you acknowledge that others (Hikoi and me, for example) did have dystonia prior to taking any medication, so although dystonia can be a result of medication that is not the only case. Many members here, including those not on meds, have described foot curling as an early symptom.
Yes, me. I had dystonia at least 1 year prior to any kind of external tremor or bradykinesia. I didn't get diagnosed until after all that had set in (I had a pretty good idea as to what it all was due to family history and was in no rush to get it comfirmed). Obviously I didn't take any meds prior to dx.
Parkinson's wasn't perfect. He didn't know everything, and why would he have? It was the 1800s lol. Did he mention anosmia? REM sleep disorder? Constipation? Apathy? depression? Speech issues? Mild cognitive impairment? Dementia? Swallowing difficulties?
ok, that is evidently my mistake. i'll review with my neuro my believes based on this witnesses.
Great forum. i've collected more info and answers here in two days than elsewhere in years.
I remain then with one question:
how can we explain then when dyskinesia and dystonia vary with meds, i.e. increase with meds increase and decrease hours after drug withdrawal - and body clean up?
If i remember well Mr. Parkinson noted constipation and sleep disorders in the problems common to all patients.
You are still but a sample of one in an extremely variable and complex disease among an extremely variable and complex population (including many different genotypes and unique genetic changes in every individual after conception) in extremely variable and complex environments, embedded in a language that at times is inescapably variable or indistinct and nonstandard in a fair number of its terms and usages, across a quite large population of individuals. Your experience simply can't be used to reliably generalize the way you have done.
The nomenclature of PD symptoms is often misunderstood given the complex nature of the phenomena involved. To say that drug-induced, peak-dose dyskinesia often manifests as dystonia, as often experienced by more advanced patients.
And I quote:
“Dystonia is the second most common form of LID (Levodopa‐induced dyskinesia) presenting as sustained muscle contractions. It occurs either in pure form or in combination with the chorea, in the latter case manifesting as twisting of the leg on walking or the arm being pulled behind the back. Dystonia accounts for greater disability than chorea. “Off” time dystonias are usually painful.”
The study of dystonia gives an interesting idea between the relationship of dopamine with exercise and I quote "Dopa-responsive dystonia (DRD), also known as Segawa's disease, is another form of dystonia that can have a genetic cause. Individuals with DRD typically experience onset during childhood and have progressive difficulty with walking. Symptoms characteristically fluctuate and are worse late in the day and after exercise. ".
Maybe ldopa is consumed by the body with exercise?
it may be that dystonia is a movement disorder (may be due to a shortage of dopamine, localized or not) that responds to levodopa treatment.
Unfortunately current dosages of levodopa may be too much and causes drug induced PD.
Dr Hinz says that dyskinesia is a nutritional amnio acid deficiency induced by too much levodopa that competes with the other amino-acids reducing the absorption and creating a neuro transmitters unbalance. His protocol aims to resolve this unbalance with oral integration.
The fact that a disease responds to levodopa doesn't mean it is PD (for example, the lethargic encephalitis in the movie Awakenings). I've heard thet there may be the possibility that a number of Patients who have been diagnosed with PD, were having another movement disorder and, after taking L/C meds, later on developed a drug induced PD.
I, like many others who have shared, experienced dystonia as a very early symptom of PD. In my case, many years prior to even starting sinimet. So to say that dystonia is brought on only as a consequence of taking C/L cannot be true. No clinical trial can discount that this actually happened to me.
I had early onset PD at the age of 47, and I have read of many cases where dystonia is a common early symptom of persons with early onset.
The fact that a disease responds to levodopa doesn't mean it is PD (for example, the lethargic encephalitis in the movie Awakenings).
I've heard that there may be the possibility that a number of Patients who have been diagnosed with PD, were having another movement disorder and, after taking L/C meds, later on developed a full drug induced PD.
in any case it is true that long term use of L/C causes a number of side effects, that are commonly associated with disease progression, but in my opinion often are not because they diminish or even disappear with L/C reduction or withdrawal (assuming to be able to withstand)
A good guide to fasting is dr fungs book, the obesity code. I personally take my meds at 6am, no food with it. Just a cup of black coffee for breakfast and lunch, then at 6pm eat anything you want except wheat and dairy. The book explains how this activates the cells garbage disposal and actually starts to clear up tangled proteins like alpha synuclean.
So how are you doing generally with this pain in the ass disease Bass? Still working? I’m so sick right now but bizarrely am trying to form a 50s rock n roll band. Addicted to levadopa and rock! 😴
Thanks for asking! Im still working. Been doing a little better, always tweaking my regimen. Some things that seemed to help me were doubling my Lithium Orotate to 10mg per day, fasting 4 days a week, cutting out wheat and dairy, adding more exercise (whatever I can do). Thewierd thing about exercise for me is that when I lift (dumbells) iin the morning, I get extra shaky. Dr says Im using up all my dopamine. I dont believe it, I dont have any dopamine to begin with!
I recently impulse-bought a HELLACIOUS Mesa Boogie Basis M2000 bass amp on ebay, I love it! Needs a trip to the shop, though, one of the switches is broken off. Also found some dudes interested in jamming on some metal, hopefully soon!
Im getting into amp sims recently. Hard to work sympathetically with your laptop and there are often challenges but it's an area i keep exploring. Try Native Instruments plugins. Pricey but some nice sounds that save you having to buy real amplifiers
One of my good friends makes the best amp sims out there. Look up StudioDevil. FUN FACT - he was invited over to Edward VanHalens studio where he and Eddie modeled EVH's Marshall Plexi that he recorded all those early albums with! They went through the circuitry bit by bit and modeled the whole thing. He has tons of great amps and cabinets in his simulator. heres a link to the basic free version. Try it out!
Nice one Bass. I am thankful to have seen 'the man' in 78 when they came over and supported Sabbath. People were still shouting for VH when The Sabbs started their set!
both, because during fasting body detox processes are from 3 to 5 times more intense and if you can it is better to avoid toxins from meds. I also recommend: if you are not able to evacuate without meds, because your bowel movements are weak, i can suggest too take only the doses necessary to evacuate two times in 24 hours to avoid long lasting of stool inside your gut or take a laxative to help movements.
after the second evacuation your gut will be pretty empty and you can "enjoy" the rest of your fast and drug holiday.
If you are able to stay one week without meds, then you will notice also an increase of the efficacy of the meds, so first new dose after fast should come after two days from gradual restart of light food intake and be 1/4 of the usual dose. Then adapt based on result and duration, because otherwise dyskinesia will come back very soon.
remember that your microbiota after 3 days fasting is less than 50% of the normal one and after 7 days it is no more than 20%. Therefore gradual restart of eating is as much important as fasting and takes the same days (7 days fasting and 7 days of gradual return to normal food intake). wrong food restart can vanish benefits creating a weak microbiota that can create problems to liver.
fasting is a potent process but also is not a game; document yourself or look for expert support before proceeding.
if you like you can consider glutathione IM or IV during fasting / drug holiday, or also bicarbonate or vitamin C IV to help detox process. But pls ask your doctor for medical advise.
I did a 10 day water fast many years ago before I got PD. In those days I had 'bottle'. Unsure if I have the same levels of discipline as those days. But thanks for the interesting information.
Life after DBS isn't perfect, but it's about 98% medication free! I'm hiking, biking, swimming and walking without meds and I couldn't be happier about that. It's been a year now. Still working out the programming kinks, but only every 3 months. My only regret was not doing it sooner. I waited until I felt like there was no choice. Hope you're doing well!
dyskinesia is related to levodopa intake. mucuna (if not in risible 5) adds some nutritional elements that make levodopa peak less potent and may reduce it in the medium or long term
Well, the evidence coming in suggests that MP can be associated with if not “cause” dyskinesia. That’s not good news. I’m on year 4 of MP, 1.2g per day L-Dopa equivalent. I recently started taking 1/2 Sinemet 25-100 per MP dose. That’s for the Carbidopa. The small amount of Carbidopa in just 1/2 of a yellow pill seems to greatly enhances the MP absorption. So essentially my dose is what would be Sinemet 12.5 - 300. So far I’ve had no dyskinesia, which I’m beginning to think has more to do with progression than anything else. If I had a suggestion for you Jeeves it would be take a brief L-Dopa vacation, as long as you can tolerate. Maybe just munch on fava beans for a week. Then go back to MP at a lower dose, with increased enzyme inhibitors. I regularly use green tea and grapefruit juice. I’ve never tried Azilect, but it might be worth a shot. Good luck with it and hope this helps -JG
Jeeves, I would echo some of the experiences of reedboat. I restricted my intake of Sinimet from day one and for 8 following years thinking that it would prevent the onset of dyskinesa. I even stopped taking sinimet and all other rx meds completely for year and taking mucuna (as a part of the Hinz protocol). And I still developed dyskinesa.
I have concluded the following based my experiences:
1) Limiting C/L drugs did not prevent my eventual onset of dyskenisia.
2) Taking Mucuna instead of C/L drugs did not prevent my eventual onset of dyskenisia.
3) I firmly believe that dyskenisia is brought on by the progression of the disease, and is not related to carbidopa or levodopa use, regardless of whether the sources are synthetic or natural. I used both.
4) Sorry to not sugar coat it, but there is nothing you could have done to avoid it, and now that you have started to experience it, it will be with you indefinitely and will become one more symptom that you will now have to manage on an ongoing basis. Sorry.
5) Others have said that "the other elements of the naturally occurring mucuna" can have beneficial effects like assisting with the absorption of the Levedopa from the mucuna across the blood brain barrier. This has not been my experience at all. Under the Hinz protocol, (after purging with system of all rx meds over a period of several months), I ingested increasing levels of 40% mucuna up to 32grams per day! Trying to get my brain to absorb enough levodopa from it. But even at those very high levels, enough was not crossing my bbb, and each 8gram dose would last less than 3hrs. Fast track to now, my current intake of mucuna is 0.4grams of 98% Mucuna per dose, which when taken with 1/2 a sinimet (25/100) twice per day for the Carbidopa, gives me approx 4 hrs of on time X 4 times per day.
Just a disclaimer, these are my experiences, my conclusions, and my reality. I share as additional information that you can use or not, in charting your own course. Best of luck.
You're welcome. I think that sharing ones own personal experiences is what makes this resource so valuable. No medical advice just actual experiences. Good luck.
From my experiences with my support groups, I tend to agree with your personal observations. Unfortunately, your current dose protocol will probably change over time as the need for more Sinemet probably changes.
I agree. But I am trying some things to hopefully help to control the need over time. The dynamic nature of this disease means you can't ever stay in one place. Thank you for sharing. It is much appreciated.
This is very helpful, thanks for sharing. I ended up with this ratio by trail and error. I came off of everything for about 2 weeks, and restarted with the lowest doses of sinimet (1/2 of one 25/100mg), (which was meant only to supply carbidopa and not necessarily for the levodopa) and mucuna (as the main source of levodopa), fully intending to ramp up as needed. Turns out that this was all I needed so I'm here for now. Thanks again and good luck.
in fact i was quite sensible to B6 supplementation.
I'm looking for some theory behind. My question is: which is the perfect ratio (in average)?
How much mg (or mole) of levodopa goes with 1 mg (or mole) carbidopa?
S.one could say: don't care. just take much mucuna and regulate carbidopa accordingly. Unfortunately levodopa and carbidopa absorption both vary and you may and up with double excess with the known effects of the overmedication.
I agree with you. There are numerous documented cases of PWP who get dyskinesia in the absence of any levodopa. And, there are numerous documented cases of PWP who take levodopa (regardless of the source) for an indefinite period and never get dyskinesia.
I am going to go with Simon Stott of The Science of Parkinson’s fame and if, you like me, think him the final word on the matter, you might find this a worthy blog because it makes several interesting points some of which contradict a number of things said in this thread.
More important among them, short-term use of MP does come with fewer dyskinesias.
“Interestingly, the low dose of Mucuna pruriens showed similar motor response with fewer dyskinesias than normal L-dopa treatment, while the high dose of Mucuna pruriens provided an even greater improvement in motor features at 90 and 180 minutes, resulting in a longer ON period with less dyskinesias. In addition, the high dose of Mucuna pruriens resulted in less complications when compared with normal L-dopa treatment (both with and without dopa-decarboxylase inhibitors).”
If I might add one more controversy to this thread, Dr. Stott also mentions the infamous sub-Saharan African study and, low and behold, the study actually shows that the delay of levodopa therapy is accompanied by a delay in the onset of dyskinesia.
“The Ghanians delayed start of levodopa therapy on average 4.2 years and the Italians delay levodopa therapy on average 2.4 years.”
“The motor fluctuations were similar in the two populations, with a slightly lower risk of dyskinesias in Ghanaians.”
As reflected in the chart in the study, dyskinesia showed up in the Ghanaians after 7 years and in the Italians after 6.5 years -- while the study does not conclude one follows the other it does allow for the possibility that a longer delay of levodopa therapy might result in a longer delay of dyskinesia. And further underscoring the delay of dyskinesia was the feature that most of the Ghanaians who developed dyskinesia were younger.
However, Simon concludes with a recommendation against taking MP with conventional L-dopa therapy.
“Can I take my prescribed L-dopa treatment AND mucuna pruriens?
“If I had PD I would definitely NOT be supplementing my normal L-dopa treatment regime with any supplements that contain mucuna pruriens extract (certainly not without discussing it with my clinician first).”
This is for one simple reason: high levels of L-dopa (in the lab at least) does bring on abnormal involuntary movements (or dyskinesias) a lot quicker than low levels of L-dopa.
Supplementation of normal L-dopa treatment regimes with mucuna pruriens could significantly increase the level of L-dopa that the body is receiving, raising the risk of developing side effects like dyskinesias. While the short term benefits may be pleasing, the long term picture could be more troublesome as a result of this approach.
To be fair, this is simply speculation as we have no idea what the combination of the two treatments will do. But it is better to be safe than sorry.
So what does it all mean?
There is a large market providing mucuna pruriens-containing supplements, but as this post has indicated caution should be taken when considering their use as the preparation of the beans can significantly impact the amount of L-dopa (and nasty by-products of the process) in the final product."
IMMO, levodopa from MP should replace levodopa from drugs, not add to it otherwise overmedication occurs and the side effects. benefits of using mucuna are in the other hundreds of nutritional elements that comes with it.
I would like to first say that I admire and respect your standing in this community, and for how selflessly you share your vast knowledge to all.
In continuing the discourse, one question about...
"As reflected in the chart in the study, dyskinesia showed up in the Ghanaians after 7 years and in the Italians after 6.5 years -- while the study does not conclude one follows the other it does allow for the possibility that a longer delay of levodopa therapy might result in a longer delay of dyskinesia. And further underscoring the delay of dyskinesia was the feature that most of the Ghanaians who developed dyskinesia were younger. Perhaps, for example, delaying the levodopa therapy for 8 years might delay the onset of dyskinesia by a full year and I’ll take what I can get."
Given that everyone progresses at a different rate, might this be a factor of ones predisposition? I have seen a pwp wheelchair bound after one year, and others perfectly mobile after 15 years. How reliable is the 1 year difference?
Thank you for your kind words, but there's lota and lots of people on this forum whose knowledge is far more vast than mine. Mine is puny by comparison to some.
I'm just speculating above.
Yes, of course, everyone progresses at a different level, but I was addressing a slightly separate issue which is often a point of disagreement on the forum, that being, whether or not the delay of a levodopa therapy delays the onset of dyskinesia and within the very study that is cited to prove that delaying the therapy does not delay the onset of dyskinesia, the cohort which delayed the initiation of levodopa therapy was accompanied by a delayed onset of dyskinesia.
Hi Bepo, With the 40% Mucuna, how much L-tyrosine and 5-HTP does he take? Does he take those with each dose of Mucuna? I have been taking 5HTP only once at night but perhaps would be good to take with each dose of Mucuna? Thanks!
In my experiences the more I exercised the less present dyskinesias were present. And also I learnt to contiously 'break' the dyskinesia when I get them.
Everyone talks about supplementing or taking a pill to counteract symptoms, when you go back to basics the way to deal with it is already there...best of all it's free.
The more you encourage neuroplasticity to occur, the better your symptoms will be managed.
I did experience dyskinesia and have only used mucuna from nutrivita although I think it was because of slight overdosing for the reason that the twisting wore off as the dose wore off. I don’t know exactly what worked but it went away I can tell you I do take high dose thiamine and Dr. C said B1 will ultimately get rid of dyskinesia. I’ve recently taken ChrisWf’s heads up and started taking daybreaks from everything. That’s working well for me. But I experienced dyskinesia for three weeks on and off over three years ago and haven’t since
Hi Jeeves, sorry to hear about the dyskinesia, it’s the worst symptom I’ve experienced yet. I was taking 4 grams a day, 2 in the morning and 2 in the afternoon for about two years, but for the past year or so have cut down to 2 grams a day. And yes I take a complete break from everything including supplements and mucuna from nutrivita. I was genuinely surprised that the symptoms like tremor which is my most marked were not that bad as a matter of fact they were easier than when I take the drugs. Hope this helps.
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I am definitely developing this. It's not 'peak dose' phenomenon but irritatingly appears to be lasting for the duration of the levadopa cycle. It's happening both with the Madopar but also when I take the Mucuna. This wasn't what I signed up for! It's pretty mild but is an obvious concern and is widespread (arm jerks, then head goes, then leg etc).
Looking for people who have phased out Carbidopa/Levodopa in favor of an all-mucuna program
Mucuna Pruriens
Dyskinesia 
Madopar vs Sinemet (& mucuna)
Parkinsons Medication
