Mucuna along with Sinemet for Parkinson

[tigrita]

I need a contact phone number to address my questions regarding taking Sinemet and Mucuna in capsules together for Parkinson Disease.

[HekateMoon]

Hi Tigrita. I take Madopar and Mucuna 50/50. I generally dont facilitate my phone number or anyone elses here but you can read dr Gonzalez Maldonado Parkinsonsvs Mucuna book and we can talk here if you wish. Regards Chelo

[slimweiss in reply to HekateMoon]

Same here as it relates to phone numbers. My husband has PD and takes Rytary 4 times a day. Since it's timed release it sometimes takes an hour for him to feel better. To bridge that gap he's been taking Mucuna. His neurologist says that it doesn't pass the BBB and so he's just wasting his money. Well, it makes him feel better so either it's a placebo affect or it actually is working. Either way he will continue to take it! He also does Zandopa which works well too,

[park_bear in reply to slimweiss]

The levodopa in Mucuna is the same as the levodopa in Rytary. No reason why one would get past the BBB and the other not.

[HekateMoon in reply to park_bear]

It needs the carbidopa but if you takes rytary some carbidopa remains in your system.

[slimweiss in reply to park_bear]

I wonder if it's ok to have my hubby take that while waiting for the Rytary to kick in. Seems to be working out ok so far but I've read that if you get too much c/l then your symptoms can be just as bad. It's like chasing the wind!!!

[park_bear in reply to slimweiss]

Rytary has a fast acting component so mucuna would not be any quicker.

[slimweiss in reply to park_bear]

Why does he feel badly for another hour after he has taken the Rytary? Seems like it takes an hour for him to start to feel better. If he takes a Mucuna pill, he starts to feel better quicker. Maybe it's because he's getting a higher dose of C/L.

[park_bear in reply to slimweiss]

Oh. Well then I bow to your experience. If it helps him to feel better then it is good.

[Godiv in reply to slimweiss]

I believe you. It takes Ritory quite a while for me also to kick in so I’ve been taking Sinemet as my “bridge.“ And for some reason it kicks in faster. So for some reason that sort of thing does work. But I’d love to switch that to Mucuna. Thinking that maybe the dyskinesia wouldn’t be as bad.

[HekateMoon in reply to slimweiss]

The carbidopa in sinemet or the. Bensezaride in madopar is still activating the levodopa in mucuna so some of it reaches the brain. Otherwise green tea acts as carbidopa. Read. Rafael Gonzalez Maldonado. Mucuna vs Parkinsons. He is a profesor of neurology in the university of Granada, Spain .

[park_bear in reply to HekateMoon]

Yes it is true that it needs the carbidopa or the Bensezaride, but to get past the gut rather than the blood brain barrier.

[Gcf51 in reply to park_bear]

I just googled Bensezaride, says not approved by fda. Does it do better at getting l=dopa pass the bacteria in your gut and keeping your body from changing to dopamine, resulting in a higher % making into the brain. I still wait at least 30min before after taking C/L to eat.

[park_bear in reply to Gcf51]

Bensezaride is approved for use in the UK. Some people seem to think it is better than carbidopa, but I have not studied it.

[WinnieThePoo in reply to Gcf51]

Neither carbidopa nor bensezaride have any effect on gut bacteria. They are ddci's. Dopamine decarboxylase inhibitors. They stop the metabolism of levadopa into dopamine once it is in the blood stream. They cannot pass the blood brain barrier so they stop decarboxylation in the rest of the body, but don't interfere with it in the brain. In simple terms they stop levadopa which has made it past the gut into the blood stream being wasted there (and causing side effects like nausea) and allow it all to pass into the brain where it is converted into dopamine

[Gcf51 in reply to WinnieThePoo]

I wonder what they put in timed released to help with gut problem????

[WinnieThePoo in reply to park_bear]

That's not true at all. Carbidopa and bensesaride are both ddci's. They act in the bloodstream, not the gut, to prevent the body's natural conversion of levadopa into dopamine. However, the ddci cannot cross the blood brain barrier, so they stop the body wastefully converting levadopa into dopamine where its not wanted (the bloodstream outside the brain) and leave the levadopa free to cross into the brain where it then is converted to dopamine. Levadopa can cross the blood brain barrier. DDCI'S and dopamine cannot

[park_bear in reply to WinnieThePoo]

Wrong again. The motivation for the development of Sinemet - which is a contraction of "sin emesis" - without nausea - was to prevent nausea induced by conversion of levodopa to dopamine in the gut by DDCs.

frontiersin.org/articles/10...

"When levodopa is administered orally, it is absorbed in the proximal small intestine, where it has to be actively transported from the lumen over the intestinal epithelial barrier into the blood stream. To prevent peripheral and intestinal levodopa metabolism by DOPA decarboxylase (DDC), peripheral DDC inhibitors, such as carbidopa, are co-administered with levodopa. "

movementdisorders.onlinelib...

"When l-dopa is given orally, there is almost complete absorption of the drug, and only 2% is eliminated unmodified in the feces; however, only approximately 30% of an oral dose of l-dopa, given alone, reaches the systemic circulation intact. Because of an extensive first-pass metabolism and rapid plasma clearing by decarboxylation to DA at the intestinal level and in the liver, only 1% of an oral dose of l-dopa enters the brain unmodified"

[WinnieThePoo in reply to park_bear]

go.drugbank.com/drugs/DB00190 read the mechanism of action

[park_bear in reply to WinnieThePoo]

Gosh, even your very own reference tells us the purpose of carbidopa is to prevent nausea: "An individual formulation containing solely carbidopa was generated to treat nausea"

Of course it prevents nausea by inhibiting the conversion to dopamine in the gut. That can also happen in other places as well but I never said otherwise.

[WinnieThePoo in reply to park_bear]

Yes. It's to prevent nausea. My Dad launched Sinemet in the UK. It has nothing to do with absorption in the gut. Your problem PB is that you read and quote verbosely a lot of scientific papers without understanding them

[park_bear in reply to WinnieThePoo]

Please explain to me your alternate understanding of "decarboxylation to DA at the intestinal level"

[WinnieThePoo in reply to park_bear]

The problem with these sorts of discussions is where to pick up the trail of mis-understanding. Hekate Moon kicked off by saying that "the carbidopa was still activating the levadopa..."

This is incorrect. DDCI's do not "activate" levadopa. They stop the body's decarboxylation of levadopa into dopamine, and they do that ONLY outside the brain, because they can't cross the blood brain barrier, so more of the levadopa that is in the bloodstream gets to the brain, and less is wasted in the rest of the body - where it tends to make people feel sick

Your reply was

"Yes it is true that it needs the carbidopa or the Bensezaride, but to get past the gut rather than the blood brain barrier."

That is not true. Carbidopa is not needed to help levadopa get past the gut. It is needed to stop it being converted into dopamine in the general bloodstream after it has been absorbed in the gut. Gut decarboxylation does occur - mainly due to bacteria, and the extent of that bacterial decarboxylation varies with the individuals microbiome composition, which is one of the reasons some people get such a poor response to Sinemet. But DDCI's like Carbidopa have a minimal if any effect on that. Their primary purpose and effect is to stop decarboxylation in the general bloodstream.

The basic principle is simple. Dopamine and DDCI's cannot cross the blood brain barrier. Levadopa can. So you can't administer dopamine direct, and any dopamine made outside the brain is wasted. DDCI's stop the waste and allow more dopamine to reach the brain. One of the consequences of that waste conversion of levadopa to dopamine outside the brain is nausea. But this is not caused by decarboxylation in the gut.

P166 of Erik Ahlskogs book - "The new Parkinsons Disease Treatment book" explains a bit. I quote

"1 Carbidopa/levadopa may be taken with non-protein food. Although the nausea does not originate from the stomach (it is due to stimulation of the brain nausea centre) food in the stomach may be helpful..."

So the issue isn't whether there might be a tiny bit of decarboxlation inhibition in the gut - it's whether your comments in the round, completely missed the point

[park_bear in reply to WinnieThePoo]

Peer-reviewed articles in medical journals are the proper primary source of information. Here is yet another one. This specifically addresses this subject and demonstrates yet again you are mistaken:

nature.com/articles/s41531-...

Mechanisms of peripheral levodopa resistance in Parkinson’s disease

"In the intestinal mucosa, AADC converts levodopa into dopamine. Although active in the intestine, AADC is also found in the circulation and in other organs, primarily the kidneys, liver and brain5.[Emphases added]"

Note the use of "also" with respect to the AADC that is found in circulation.

[JCRO in reply to park_bear]

PB, you are the cleverest and sanest contributor on here other than BOLT. Please try and ignore the responses of some. They know who they are. They contribute little and persistently snipe from safe little areas of knowledge. Clever they are not. Pleasant, not at all.

[WinnieThePoo in reply to park_bear]

Whatever. You know it all and it really doesn't matter to me. Carbidopa stops you feeling sick because it allows levadopa to get past the gut

Keep being right. It so becomes you 😂

[WinnieThePoo in reply to park_bear]

Mechanism of action

Carbidopa is an inhibitor of the DDC which in order, inhibits the peripheral metabolism of levodopa. 3 DDC is very important in the biosynthesis of L-tryptophan to serotonin and the modification of L-DOPA to dopamine.4

DDC can be found in the body periphery and in the blood-brain barrier.4 The action of carbidopa is focused on peripheral DDC as this drug cannot cross the blood-brain barrier.8 Hence, it will prevent the metabolism of levodopa in the periphery but it will not have any activity on the generation of dopamine in the brain.

go.drugbank.com/drugs/DB00190

[Gioc in reply to WinnieThePoo]

therefore this statement of yours above is wrong:

“One of the consequences of that waste conversion of levadopa to dopamine outside the brain is nausea.“

since nausea is regulated by the "stimulation of the brain nausea center".

I ask for a friend.

[park_bear in reply to Gioc]

Yes he is self-contradictory - since DDCIs do not get through the blood brain barrier, how are they supposed to reduce dopamine induced nausea if it originates in the brain?

[WinnieThePoo in reply to Gioc]

It's complicatedncbi.nlm.nih.gov/pmc/articl...

[Gioc in reply to WinnieThePoo]

It’s complicated? 😁and I quote your article:

”Nausea and vomiting are common gastrointestinali disorders that can be triggered by various emetic stimuli through the central and / or peripheral nervous system. Both nausea and vomiting are considered defense mechanisms when threatening toxins / drugs / bacteria / viruses / fungi enter the body via the enteral (e.g. gastrointestinal tract) or parenteral route, including blood, skin and respiratory systems. ".

It is just a question of the amount of levodopa. Sinemet (Sin emet: name composed of two words meaning “without vomiting”) with the addition of Carbidoba as DDCI allows you to use minor quantities of levodopa while maintaining the same therapeutic effects by reducing nausea.

Simple not complicated, the transformation into dopamine and the BBB are not involved, the amount of levodopa does.

[HekateMoon in reply to slimweiss]

Mucuna is a full plant. It has many neuroprotective properties that the synthetic does not. Main problem is with adjusting the dosage

[Juliegrace in reply to HekateMoon]

Some mucuna is the whole plant, but most of what people here refer to and take is processed and ends up being closer to the synthetic than not.

[ssrs in reply to slimweiss]

My husband does the same thing. He is on Sinemet but he takes the mucuna during the night when he feels that he needs it. His last Sinemet is at 6:00pm and the next dose at 6:00am.

[slimweiss]

3 years ago he was just on sinemet every 6 hours but then it dropped to him needing it every 5,4,3,2,1 hour! About a year or so ago he was switched to rytary which he takes every 4 hours - 8, 12, 4, 9 and then in the middle of the night he takes one Sinemet to get him through. He also takes tramadol for pain but I want to try PEA which seems like a much better option. Good luck with all of this. I don’t think I’ve ever had to deal with anything harder.

He fell getting out of bed last night. Now he has major pain in his back but can walk and get in and out of bed so hopefully nothing is broken. We’re not home either. Visiting our daughter in Florida and leaving tomorrow after being gone for a month. I’m sure that didn’t help. Sorry didn’t mean to go on and on!