[aquario]

I noticed in an article about mucuna that it contains elements of a tryptamine compound identical to one found in certain Amazonian rain forest plants used to make ayahuasca. Tryptamines are potent neurotransmitters and neuromodulators (serotonin and melatonin are tryptamines). As someone who lived through the ‘60’s (and who did inhale), I’ve wondered what, if any, beneficial effects revisiting some of those older plant medicines might have in parkinson’s. Anybody out there have any experience positive or negative? Other well-known tryptamines are psilocybin, ibogaine, and dimethyltriptamine.

Jon

[reverett123]

Just kidding, of course. I missed most of the Sixties. But, let me tell you about the Seventies sometime

But seriously folks....
There is at least one of our number with some experience in the South American jungles but I will leave it to her to speak on that. Generally positive, though.

As for myself, I have been "respectable" for so darned long that I wouldn't know where to buy a pack of rolling papers. I'm afraid that I would have to turn to nieces and nephews. Now, ain't that weird?, as Brother Dave Gardner would have said. We were taught to beware the dirty old man selling pot to us kids. Now my only chance to find some smoke would involve the wee tykes smuggling contraband. Once again the Universe shows its sense of humor.

But, I digress , I can say that cannabis helps with the stress element but not with dyskenisia for me. This data indicates the advisability of further research and several grants of large sums of tax dollars. We prefer PayPal

And, to close this tiny cluster of little "in" jokes, remember-
Mucuna will get you through times of no money
better than money will get you through times of no mucuna.

Originally Posted by aquario

I noticed in an article about mucuna that it contains elements of a tryptamine compound identical to one found in certain Amazonian rain forest plants used to make ayahuasca. Tryptamines are potent neurotransmitters and neuromodulators (serotonin and melatonin are tryptamines). As someone who lived through the ‘60’s (and who did inhale), I’ve wondered what, if any, beneficial effects revisiting some of those older plant medicines might have in parkinson’s. Anybody out there have any experience positive or negative? Other well-known tryptamines are psilocybin, ibogaine, and dimethyltriptamine.

Jon

[aquario]

Geez, Rick, I don’t have enough hair left to have dreads, so you’re unlikely to recognize me (though I’ve finally learned to like reggae as an alternative to inhaling). As to South American jungles, it would be interesting to find out what the incidence of parkinson’s is in tribes which use ayahuasca ceremonially (and regularly). It just seems to me that such powerful neuro-transmitters as the entire tryptamine family might have some interesting consequences for pwp’s. Whether those consequences are beneficial or not was the purpose behind me throwing this thread into the mix.

Anecdotally, it’s interesting that Albert Hofmann who was the chemist who specialized in tryptamine variants, who first discovered lsd, as well as the first person to synthesize psilocybin, and who took these substances many times both in laboratory settings and in situ, lived to 102 – finally departing this past spring. So much for the brain damage that psychedelics were supposed to cause.)

ps: Brother Dave Gardner?? I think I must have seen you at the Earth Wind & Fire concert.

[ol'cs]

a "tryptamine", specifically an "aromatic ring hydroxylated tryptamine", more specifically the "5-hydroxytryptamine (serotonin;commonly abreviated as 5-HT)" is the natural (made inside the body from the amino acid tryptophan [(similar to dopamine being made from the amino acid L-Dopa)], that we get in our diet) ligand that is the neurotransmitter of the "serotonin pump". When 5-HT is present in the proper concentrations, and acting just the right way at the various serotonin receptor subtypes, this has a great effect on keeping a "healthy" mood in people. Low concentrations and other factors delimited to 5-HT is one of the root causes of clinical depression.
But there is a very great difference, when these tryptamines are dimethyated on the terminal nitrogen atom of the ethylamino side chain on the "indole" aromatic (aromatic in the chemical sense, nothing to do with odor) nucleus of this molecule.
As "nitrogen unsubstituted" (non-methylated) molecules, tryptamines act to regulate the serotonin system that affects and controls ,in part, our moods. As "N-methylated" tryptamines, the molecule has very different effects on the mind. These "N-methylated" tryptamines, are now potent hallucinogenics, for instance, 5-hydroxy-NN-dimethyltryptamine is "psilocin", the active metabolite of hallucinogenic "magic" mushrooms. This has been explained as the fact that this molecule resembles 5-HT, but acts mostly at the 5-HT2 receptor, creating an imbalance in the action of normal 5-HT receptor workings, throwing a real "monkey wrench" into the working of the serotonin transporter system. Other NN-dimethylated tryptamines that are hallucinogenic are dimethyltryptamine (DMT) and various indole ring hydroxylated and methoxylated NN-dimethyltryptamines, found in the "cane toad poison" and certain south american vines of the "banisteriopsis" family (yopo snuff).
There are very small amounts of these tryptamines produced by many genera of plants, few, including mucuna, produce enough of them to be hallucinogenic, so you only have a few sources of potent NN-dmt's in nature.
So don't worry about hallucinogenics in your mucuna product. Concern yourself with the fact that there are no natural peripheral decarboxylase inhibitors in mucuna, so mucuna is more likely to give you dyskinesia.

[imark3000]

'Concern yourself with the fact that there are no natural peripheral decarboxylase inhibitors in mucuna, so mucuna is more likely to give you dyskinesia.'
i don't get this bit? absence of decarboxylase inhibitors means less l-dopa make to the brain ..and less damage and dyskinesia.

[ol'cs]

Drugs like Carbidopa prevent L-Dopa from being deactivated outside the brain, so that there is a higher concentration of L-Dopa in the bloodstream. A higher concentration of l-Dopa in the bloodstream means that there is more L-Dopa available to cross the blood-brain barrier into the brain. Once in the brain, we rely on the same decarboxylase enzymes to produce dopamine from L-Dopa.
Decarboxylation of L-dopa to dopamine outside the brain is a bad thing because dopamine is a cardiostimulant, and we don't want that side effect.

[olsen]

Originally Posted by aquario

I’ve wondered what, if any, beneficial effects revisiting some of those older plant medicines might have in parkinson’s. Anybody out there have any experience positive or negative? Other well-known tryptamines are psilocybin, ibogaine, and dimethyltriptamine.

Jon

Noticed the mention of "ibogaine". I continue to be intrigued by the report that the use of Ibogaine increases GDNF. and with the notation above that Ibogaine is a known tryptamine. Madelyn

(http://www.sciencedaily.com/releases...0609170806.htm
"...The research by scientists at theUCSF-affiliatedErnest Gallo Clinic and Research Center builds on their earlier work. In 2005, they reported the first hints that increased levels of this brain protein, known as GDNF, cut down alcohol consumption. The new study established how quickly the effect kicks in, and shows for the first time that the chemical blocks relapse and does not interfere with normal cravings. The research also pinpointed the brain site where GDNF acts to control drinking...


http://neurotalk.psychcentral.com/sh...d.php?p=307040


...The scientists confirmed in a cell model that Ibogaine stimulated GDNF activity. Finally, they showed that a known inhibitor of GDNF blocked Ibogaine's ability to decrease alcohol craving in the rats, suggesting a direct link between Ibogaine's desirable actions and GDNF.

'If we can alter the GDNF pathway, we may well have a new treatment against alcohol and drug addiction without the unwanted side effects of Ibogaine,' Ron said

[imark3000]

Originally Posted by ol'cs

Drugs like Carbidopa prevent L-Dopa from being deactivated outside the brain, so that there is a higher concentration of L-Dopa in the bloodstream. A higher concentration of l-Dopa in the bloodstream means that there is more L-Dopa available to cross the blood-brain barrier into the brain. Once in the brain, we rely on the same decarboxylase enzymes to produce dopamine from L-Dopa.
Decarboxylation of L-dopa to dopamine outside the brain is a bad thing because dopamine is a cardiostimulant, and we don't want that side effect.

I agree, that is if you take too much mucuna you may have side effects due to its presence outside the brain but these side effects do not include dyskinesia. I believe.

[Ibken]

Originally Posted by imark3000

I agree, that is if you take too much mucuna you may have side effects due to its presence outside the brain but these side effects do not include dyskinesia. I believe.

I've been using mucuna since mid '05 , both w/ sinemet and without. sometimes with just carbidopa (lodosyn) and I have - and still do - experienced what i call dyskinesia as a result. It manifests during both the 'on'' period - 1st 30 miin or so after taking it - and when it begins to ''wear off' about an hour or more. What i'm calling dyskinesia is initially a sudden involuntary muscular walking up on my toes. Then an outward stretching out of my left leg and foot, followed by a twisting - writhing action of the ankle - then more toe walking, etc and I'm 'on'. There is some sort of blockage in my left leg that seems to be the reason for these strange movements... and it must be getting worse wiith time, as this so--called dyskinesia diddn't happpen early on. Read MJF's description of what he experienced after taking l-dopa. The off dysk is worse, painful left ankle twisting, can't walk - have to go lie down.

Maybe those w/out such a block don't expperience this ''resistance" effect? One more reason for white rats to cage in clusters, yes, learning from each other!

Hard to talk about such things, when we don't really know what means what!

ibby

[imark3000]

my words : " I agree, that is if you take too much mucuna you may have side effects due to its presence outside the brain but these side effects do not include dyskinesia. I believe"
Note that I was refering to side effects of L-dopa of mucuna outside the brain ...
As for L-dopa reaching the brain, yes it may cause dyskinesia. But unlike sinemet, only a small part of the l-dopa in mucuna (when taken by itself) makes it across bbb and the rest is absorbed by the body. The benifits are less so is the harm.