Gerry,

You write:

"I currently take 34.5 g of Mucuna (40% levodopa) daily plus 45 g of tyrosine."

That's approximately 14g of levodopa per day, plus whatever may come from the tyrosine. This compares with for most people on C/L of under 1g (= 1000mg) per day.

I think it would be really useful to everyone if we understood why these numbers are so different.

For a start, you don't take carbidopa. Wikipedia states that [1]:

"Carbidopa reduces the amount of levodopa required to produce a given response by about 75% ..."

That reduces the comparable level from 14g to approximately 3g.

Are there any other corrections to make?

How do you avoid nausea with these amounts of levodopa?

Reference:

[1] https://en.wikipedia.org/wiki/Carbidopa

John

The doctors who have pioneered the protocol Gerry is on have a paper where they give the reasoning and mechanisms for how the nausea is controlled through administration of 5-htp instead of using Carbidopa. They also discuss other negative affects of Carbidopa and why it is not necessary for the use of treating parkinsons when using 5-htp, which allows for avoidance of side effects.

Here is an excerpt from the paper that may be of assistance in understanding how Carbidopa and 5-htp work.

"Through irreversible inhibition of AADC, carbidopa or benserazide compromises peripheral synthesis of serotonin and dopamine. This drug-induced inhibition of peripheral metabolism of l-dopa by AADC leaves more l-dopa unmetabolized and available to freely cross the blood–brain barrier into the central nervous system. As a result, when carbidopa or benserazide is administered, lower l-dopa daily intake values are required to achieve the same central nervous system results.4,6

It is documented that 5-HTP controls l-dopa-induced nausea, utilizing the same basic chemical mechanism as carbidopa and benserazide: AADC inhibition. Carbidopa and benserazide inhibition is irreversible while 5-HTP inhibition is reversible. The use of 5-HTP is superior, since under proper administration it is a nutrient that does not deplete systems or induce abnormal system functions when properly administered.1,7,35–37

If the goal of administering 5-HTP for the control of l-dopa-induced nausea is to have it function as a nutrient, this is not merely a simple substitution. It requires concomitant administration of l-dopa with 5-HTP, along with the “core nutrients”: l-tyrosine, a thiol (l-cysteine, glutathione, S-adenosyl methionine, or l-methionine), and cofactors (vitamin C, vitamin B6, and calcium carbonate). Administration of properly balanced core nutrients needs to be guided by organic cation-transporter type 2 functional status analysis, in order to achieve a balance that does not convert the nutrients into a drug."

Here is the paper - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4238750/

noone knows for sure what is in this particular mucana powder, much less how much l-dopa. one reason they might not put CARBIDOPA in it is that it would require a doctor's prescription and it's a relatively cheap drug. always the skeptic.

this whole discussion is ridiculous to me, a newbie posts on this board asking advice on a treatment almost nobody who posts on this board uses, GARRYW says he uses this treatment but has never tried carbidopa/levodopa so can't make a comparison, and then we have billbobby who doesn't have pd just happens to find this thread and is hyping the treatment and just reposts what's on the mfg's website. it's all taking place in a virtual reality. anyone can say this stuff works great but how do you prove it? honestly, for all the years this stuff has been on the market why is it still such a mystery if it was heads and shoulders better than C/L?

keep in mind that the brain only needs a tiny amount of l-dopa and if you take 100mg of l-dopa orally, less than 5mg actually gets into the brain. that's why you need to take such tiny amounts of agonists compared to l-dopa since almost all of it is available to the brain. 12mg of neupro is good for a day. so to me at least, i don't believe this mucana is 40% l-dopa.

Day 3 update.

The protocol does give relief of symptoms but only for 1-1.5hr max. Then the off effects seem to be worse than when on stalevo.

After alerting his Dr. She recommended him to up the intake of Mucuna d5 to 8 pills per dose. However still the effectiveness has only increased about half an hour to an hr.

On the second day he started developing dyskinesia in his legs which has been very uncomfortable for him. We left a message with his Dr. About this new condition.

So far this protocol has been very difficult for him but is hoping things will turn around when he gets the regimen dialed in.

The average time for how long it takes for a parkinsons patient to get narrowed in on the levels of the nutrients for symptomatic alleviation, as I have read in their studies/website, is around 3-6 months. So understand that it will take a while and at first while transferring from the meds to the amino acids side effects are rather pronounced while the transfer takes place.

”Novel observations reporting a group of 17 Parkinson’s disease patients led to identification of carbidopa-induced dyskinesias, which had not been documented prior to 2012.1 These patients had been ingesting prescribed concomitant l-dopa/carbidopa preparations for 1–7 years. Their drugs were continued as the core nutrients were started. The mean daily dosing value of l-dopa/carbidopa was 1,000 mg and 250 mg, respectively, at the initiation of the core nutrients. The mean duration of previous drug treatment was 3 years, 7 months. Onset of dyskinesias began within the first week of treatment when the core nutrients were added. Dyskinesias were generally described as facial twitching and head bobbing due to peripheral muscle-control problems within the neck and upper shoulders. When dyskinesias developed, the l-dopa/carbidopa was immediately discontinued and the nutritionally sourced l-dopa increased fivefold to compensate for the loss of the carbidopa effect on the central nervous system by blocking peripheral conversion of l-dopa to dopamine. This conversion to higher-dose l-dopa was monitored using the previously published pill-stop technique.37 Following this protocol, all patients achieved full resolution of dyskinesias within 4 days. This led to the hypothesis that the dyskinesias that resolved after applying the new protocol had been induced by the carbidopa and were not related to the l-dopa. There were no refractory dyskinesias experienced.”

Source - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4238750/

Some posting on this thread are in the stone ages. Are so close minded that they will never learn. Sometimes makes we wonder if they work for the drug companies.

why beat around the bush badboy, your're talking about me. considering i've tried iv. glutathione, low dose naltrexone, chelation therapy, and just about every supplement mentioned on this board including mucana it's pretty ridiculous saying i might work for a drug company, especially since i've been critical of the high costs of new pd drugs on this board and have stated many times i'm only taking C/L, noone is making a fortune on selling generic C/L.

If you want to have a rational discussion about the HINZ protocol and discuss the scientific merits of the papers of the papers presented by those making likely millions from selling their supplements i'll gladly participate. i'll start by saying these papers are written by people with a financial stake in this treatment and no independent researcher has ever duplicated their results. so you expect anyone to accept their findings without some reservations?

Everyone on this board is anonymous, there is noone verifying if a poster is being honest or dishonest, has pd or doesn't have pd, is working for a drug/supplement company or not. What I saw here was a newbie asking for advice on an unproven pd treatment, backed up by studies conducted by those with a vested interest on selling this treatment and none by independent researchers, which at least to me makes this research highly suspicious, a non-pder just by chance shows up on this board and starts hyping this treatment yet doesn't know anyone with pd who has used it much less has benefitted from it. The newbie starts the procedure and gets support from this non-pder who as far as i know knows noone who has pd. And you wonder why i'm just a little skeptical about motives here?

To repeat, if you want to debate each paper mentioned here and all the claims about the HINZ protocol, i'm more than willing. The purpose the this board i hope is not to blindly accept as fact everything posted here, especially when a treatment costs as much and is difficult to follow as the HINZ protocol, as controversial and when other members posts about the HINZ treatment complaining about the significant price increases in 40% MUCANA.
I find it just a little interesting that their treatment requires you buy this MUCANA from them, hey, isn't that something drug companies do? And jack up the prices?

I posted on this thread not because i have a knee jerk reaction against alternative treatments, i have a knee jerk reaction about some poor pd'er possibly getting ripped off and ending up worse.

So you are essentially saying that Im some shill trying to get others to invest in this treatment by hyping it up? The reasoning that Im posting in this thread and reposting what they have shown in peer-reviewed scientific papers is that if they are correct then that means they are able to successfully treat parkinsons disease while managing all the side effects normally associated with taking L-dopa and having no or slowed disease progression. It would be the best possible treatment for managing parkinsons. They have shown that a large portion of disease progression is not associated with direct progression of parkinsons itself but rather improper use of L-dopa/Carbidopa leading to a further relative nutritional deficiency of the following

”L-dopa may induce depletions of serotonin, thiols, l-tyrosine, and l-tryptophan, resulting in RNDs.”

”Carbidopa may induce depletions of peripheral serotonin, dopamine, norepinephrine, and epinephrine, along with system-wide depletion of niacin and vitamin B6, resulting in multiple system RNDs. Over 300 enzymes and proteins require vitamin B6 for normal function.”

All I am trying to do is post EVIDENCE for why it very possibily could work to try to show the fact that there is substantial evidence in support of the validity of this research/protocol.

I have known about their research for over a year now but only recently started on the protocol myself(for concussions) because I wanted to thoroughly understand how this works before investing in it. After thoroughly doing the research on it, I have came to understand what they have actually discovered and the significance behind it. They are able to treat any neurotransmitter related disease at a essentially 100% success rate(there are a few disease states that are more difficult to manage and take longer to correct). Diseases can be seen here - https://neurosupport.files.wordpress...lticolored.jpg

please, before ridiculing what I am saying on here, look into the science and the evidence for that science that they have published before immediately disregarding it as not correct. I can understand and respect skepticism but only if you have looked at both sides of the fence before presenting disbelief for what I am presenting. So please read their 19 studies on what they are doing before disregarding it.

In regards to a few of your statements.

The reason they dont use Carbidopa is this - ”The mechanism of action of the carbidopa and benserazide causes irreversible binding and inactivation of vitamin B6 throughout the body. The consequences of this action are enormous, interfering with over 300 enzyme and protein functions.”

So why use Carbidopa when they have discovered that 5-htp is able to do the exact same function as Carbidopa, while being far more effective, not causing inactivation of vit. B6, and not causing further deletion of neurotransmitters/thiols/co-factors.

In regards to how it is still a mystery is that it has not been on the market for that long. They have only really narrowed in on how to correctly treat parkinsons disease over the last 5 years. Also, how is it supposed to get known if everyone has the same reaction to it as you do? If everyone says well how does everyone not know about it if it is better and disregard it because of that, then there is no one in the first place to try it to say that it works.

For it to get known, people have to look at the science, understand it, and think beyond what they currently know regarding these diseases. What they have shown may go against what your current knowledge allows for, but the fact of the matter is that it works. And it works far better than anything currently available because it is correcting the problem, not creating more.

Sources - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4238750/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211847/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068871/