• N&PD Moderators: Skorpio

Catechins and amphetamines

Timothy Leary

Bluelighter
Joined
Dec 5, 2009
Messages
61
I know that this is really playing with fire but I was wondering about the possibility of using green tea extract as a selective MAO-B inhibitor to potentate amphetamines. Chatechins are listed as selective MAO-B inhibitors in multiple places as is tea itself. I drink tea quite a lot, mostly those with high catechin contents (green and black) and have noticed a slight antidepressant effect with amphetamines. I was playing around with the idea of taking a green tea extract (they are labeled as 80-90 percent catechin, no caffiene)

How dangerous do you think this would be? I have 60 mg vyvanse capsules and could break one up and break up the the tea extract capsules. I also have several dopamine antagonists and sedatives, trazodone, olanzapine,
Quetiapine, and Isopropyl nitrite as a vasodialator. Any suggestions, or is this rediculously stupid even at very low dose titration
 
Tobacco smoke has mild MAO-B inhibiting properties, too, but there's still no problem with smoking while taking amphetamines. Only if you took some stronger MAO-inhibitors like tranylcypromine, would there be a possibility of a dangerous interaction.
 
tranyl is a MAO-A inhibitor, MAO-B inhibitors are relatively safe when combined with stimulants.
 
I thought that tranylcypromine inhibits both MAO-A and MAO-B unselectively... Ok, selegiline would be an example of a selective MAO-B inhibitor. I know that it would be less dangerous in combinations, and one of its metabolites is actually l-amphetamine... But the point is, unless more than 80% of MAO is inhibited, there is little potential for dangerous interactions.
 
^ I remember seeing a DEA's report on "future drugs of abuse" that listed one isomer of tranylcypromine as a potentially abusable psychostimulant... Reportedly the DA releasing effect is strong enough that some depression patients treated with tranyl actually experience euphoria and become (hypo-)manic. I personally doubt that anyone would abuse a drug with such dietary restrictions involved...
 
I had tried Amphetamine or Methamphetamine or MDMA with low doses of Deprenyl (Selegeline) many times, and had no problem. MAO-B inhibits seem to be safe with combo.

It is MAO-A inhibitors you have to be careful combining with stimulants. I tried Meclobemide with 1 tablet of MDMA a long time ago, and got away with it, so I stupidly tried a small amount Methamphetamine with Meclobemide 10 years ago, and some St. John wort, and it was one of the worst mistakes I have ever made. I felt horrible for many days afterward, and I always felt it took a few years off my life, and damaged my SNS system in the long term.

I tried it before I knew about BlueLight, and I wished I had of found Bluelight sooner to warn me not to do this.
 
Yeah, I have heard that MAO-A inhibitors are very contra-indicated with stims, they just pump up your epinephrine levels with none of the fun dopamine effects.

I think I'll pass on this, I don't really know how selective catechins are. selegiline will cross over to the A isoform at high dosages or if used for long periods. Besides I think just some tea would be fine by itself.
 
Ypu are seriously underestimating the human capacity for stupidity. People huff gas, share rigs, take datura...

Yeah I know... I did that kind of things(including huffing gas a couple of times) when I was still in high school. Now I mostly abuse alcohol and take other drugs only occasionally. What I meant was just that tranyl isn't likely to become a black market drug that people buy on the street to get high.
 
I had tried Amphetamine or Methamphetamine or MDMA with low doses of Deprenyl (Selegeline) many times, and had no problem. MAO-B inhibits seem to be safe with combo.

You've had no problem with this combo. I have had problems. I put on 1/16 of an 8 mg Emsam patch (so 500 mcg over a number of hours) and took 7.5 mg Adderall (sublingual) and within minutes I was ripping that cunt off my shoulder due to elevated HR (110 bpm resting), elevated BP (139/95) and a curious desire to drive a spiked bat through my forehead.

seniormoderator:Ebola? has a detailed thread on combining selegeline and amphetamine.

OP I believe (believe) EGCG is a very weak MAO (there's quantified data out there somewhere). It's also an aromatic amino acid decarboxylase inhibitor in case you're eating some DOPA or something. I seem to remember no adverse reaction with a 40% EGCG extract, but that's just me.
 
I was playing around with the idea of taking a green tea extract

Not a bad idea in principle. Not too long ago, I actually considered trying this myself, until the maximum bummer of 'negative results' promptly bitch-slapped all my enthusiasm for what looked damn good on paper:

http://www.ncbi.nlm.nih.gov/pubmed/16910171

Following acute ingestion of green tea by six human subjects, HPLC-MS2 analysis revealed that flavan-3-ol methyl, glucuronide and sulfate metabolites appeared in the bloodstream but did not pass through the blood-cerebrospinal fluid barrier. These observations emphasize the discrepancies between in vitro and in vivo evidence

I don't mean to shit all over a theoretically sound idea. Given the promising neuroprotective and (multiple) prodopaminergic properties of the tea gallocatechols in rats, the hype was well-deserved, but the discussion regarding those particular compounds' relevance to the human CNS should have been swiftly extinguished back in '06. Though I guess it's unsurprising that in cases such as these, profitable sales trump science, at least when it comes to issues of consumer awareness.

On the other hand, this isn't to say that there aren't viable and effective alternatives. A veritable slew of MAOs are to be found both within nature and without, many of them reversible and selective. Do a little digging, and I'm sure you'll come upon at least one MAOI-containing plant extract that sounds attractive to you. But keep in mind, if you were to find an MAO-B-selective inhibitor that would appear to suit your needs, you shouldn't expect too much from such a weak drug. Concerns regarding test-tube versus human in vivo evidence are of relevance here as well - confirmation of efficacy is considerably lacking for MAO-B inhibitors for just about every presumed 'indication' other than Parkinson's, for which they look moderately efficacious. Having subjected myself to multiple trials of selegiline with thoroughly underwhelming results, I was curious as to why the purported panacea exhibited nothing akin to the palpably dopaminergic qualities of the conventional pscyhostimulants. After some digging, I came upon this,

http://www.ncbi.nlm.nih.gov/pubmed/3030067

and a couple other studies that I'm too lazy to dig up at the moment.

The primate B isoform seems to be restricted near-entirely to the ganglial/cortical glia surrounding dopaminergic neurons, as contrasted with its much wider and more therapeutically/pharmacologically convenient distribution in the rat brain. Such a dearth of the enzyme in human nervous tissue suggests a very minor role in basal dopamine transmission in non-Parkinsonian humans, calling selegiline's/rasagiline's many associated claims into question. This rat-human discrepancy has understandably led to many exaggerated impressions of efficacy for MAO-B inhibitors within what amounts to 'in vivo in vitro' literature with regard to [human] clinical implications.

Again, your idea is good in theory, but having tried it myself with less-than-exciting results, I wouldn't exactly recommend it to a friend. I can only hope that it works well for you and that I stand as a true and unsubstantiated oddity among the throes of sincere selegiline enthusiasts. And to reiterate, if your goal is dopaminergic neuroprotection or restoration of motor activity, MAO-BIs are definitely for you; but using them for anything else could very likely be a waste of time and money.

+1 for no probs with selegiline & amphets...

Seconded (thirded?), provided that one adheres to the oft-mentioned 10mg oral limit
 
I wanted to find a natural MAO-B inhibitor a long time ago, couldn't get one (besides Selegiline which kinda stinks ) then i made a list on facebook of the stuff i found, i forgot/was too lazy to record the refs and stuff though. but at least its a list that somebody could research the affinities and/or somehow gain useful information







-methylene blue (NOT RECCOMENDED 4 human consumption....can cause vasoconstriction, nausea, oxygen deprivation, death) ( reversible MAO-A inhibitor, at higher doses also inhibits MAO-B).

-turmeric (active compound curcumin) ---[only when taken with piperine, a.k.a. black pepper, piperine slows down curcumin metabolism](reversibly inhibits MAO-A and MAO-B) "140 to 560 mg/kg for 14 days, were able to elicit dose-dependent relation of immobility reduction in the tail suspension test and the forced swimming test in mice. The effects of the extracts at the dose of 560 mg/kg were more potent than that of reference antidepressant fluoxetine. The extracts, at the dose of 140 mg/kg or above for 14 days, significantly inhibited the monoamine oxidize A (MAO) activity in mouse whole brain at a dose-dependent manner, however, oral administration of the extract only at a dose of 560 mg/kg produced observable MAO B inhibitory activity in animal brain"

-Geiparvarin, a substance in the Australian Willow, MAO-B inhibitor

-catechin / catechins, found in green Tea, and tons of other fruits/vegetables/random stuff, ..MAO-B inhibitor

-cats Claw (Uncaria tomentosa) contains Catechin, epicatechin, and other compounds, ..MAO-B inhibitor(s)

-harmaline (strong reversible inhibitor of MAO-A, questionable inhibition of MAO-B), found in Syrian Rue, Banisteriopsis Caapi and many other amazonian plants. can cause NAUSEA, anxiety, and hallucinations.

-passion flower (very weak, questionable efficacy, probably due to content of harmaline alkaloids)

-emodin, a substance in rhubarb stalks (not in leaves, the leaves are poisonous) ,... also found in Japanese Knotweed (inhibition of MAO-B, however emodin also increases estrogenic activity)

-coffee (most commonly exibits weak non-selective inhibition, due to harmaline alkaloids. highest levels of these alkaloid are found in ready to drink (instant) coffee)

-wild green oats (a.k.a. oats, but some differences exist) have been shown to have some inhibitory activity upon MAO-B enzymes. this is questionable, only a few studies have been done on it. however, oats have been proven to raise levels of free testosterone in the body, many studies have confirmed oats as having aphrodisiac properties.

-Syrian Rue, also Banisteriopsis Caapi, (contain harmaline alkaloids, very potent MAO-A inhibitor, can cause hallucinations, and vomiting)

-Kaempferol, a substance found in onions, teas, broccoli, strawberries, and tons of other stuff (google it) has been shown to have potent MAO-A inhibition.

-Apigenin, a citrus bioflavonoid, also found in several herbs including chamomile, parsley, thyme, celery, and mugwort, has shown potent MAO-A inhibitory activity. One micromole (uM) of apigenin inhibited 50% of mouse brain MAO.

-Piperine, the principal chemical responsible for spicyness in black pepper, has shown weak MAO-A and MAO-B inhibitory properties. However, piperine should be taken in caution, because it can significantly slow the metabolism of many drugs, causing body levels of the drug to increase greatly.....

-red yeast rice posesses potent MAO-A and MAO-B inhibitory properties.

-quercetin = MAO-A inhibition, weaker MAO-B inhibition.

-Maclura tricuspidata (active ingredient "gancaonin A") = potent MAO-B inhibition, lesser MAO-A inhibition

-red clover, containing Formononetin, strongly inhibited MAO-A and B.

-Sophora flavescens, a chinese plant, posesses strong inhibition of MAO-A and B, this plant also supresses substance P, and has a putative agonist activity at mu and kappa opioid receptors .
 
does anyone know at what dose Catechin or 98% Tea catechins extract would be an effective MAO-B inhibitor to potentiate phenethylamines?

BTW rhubarb contains MAO-B inhibitor as well.
 
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