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  • N&PD Moderators: Skorpio

"24 Year Old Parnate Addict"

Yes tranylcypromine can be like amphetamine, but out of the MAOIs it's the one most likely to result in an A&E admission for hypertensive states, so be careful with it


I'm fairly certain that what you are referring to is the combination of selegiline and phenethylamine, which although doesn't 'convert' to methamp, for all intents and purposes acts in the same fashion as methamp.
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Selegeline's primary metabolite is L-methamphetamine (by removal of the N-propynyl group)
 
Parnate is the best unscheduled alternative for adderall,ritalin etc, WAY better than, say, wellbutrin or strattera.
 
Just DO NOT take PEA (phenylethylamine) in large doses ala (^the selegiline/PEA combo mentioned in a few threads above) with Tranylcypromine shows some preference to MAO-B but IS still inhibiting MAO-A.

To quote Permastoned from a previous thread:
MAO A has noradrenaline as a substrate, meaning metabolises it. Phenethylamine releases a large amount of noradrenaline into the synapse (moreso than dopamine). So if you inhibit MAO A, you can get a hypertensive crisis from when the levels of noradrenaline skyrocket, activating dem a1, a2, b1, b2, b3 receptors and pimpin dem hoes.
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Agreed tranylcypramine has some kind of stimulant (PEA analogue itself) BUT huge doses of PEA will just bolster that
 
lenses said:
MAOI's are interesting regardless. I'm thinking of investing in one and trying the above combo. Also as a vegan I don't have to worry as much about the whole food interaction thing.
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Yes you would. There are plenty of vegan foods that could lead to hypertensive crisis. Fava beans, brewer's yeast or soy sauce are some examples.
 
do tell!

Smyth said:
For selegiline you have to consume at least 30mg to get any positive mood lift.

I dont recommend this to beginners though.

I think I would prefer "trany" to this selegiline stuff, although ive still not tried it yet.
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I prefer Cisapride but to each his own!
 
As far as older, irreversible monoamine oxidase inhibitors go, them tranylcypromine at least isn't a hydrazine. Hydrazines tend to be toxic and also to make for suicide inhibitors of enzyme targets. Hydrazine itself is pretty noxious, there are certain fungi, much esteemed in finland and surrounding areas
commercially I mean, even sold in cans. But when improperly prepared, these fungi, the false morels and some of their allies; looks like a convoluted brown colored lump of ripped-out cerebellum, all covered in sulci and gyri, just like brain matter, only its stuck to a white stem.
yle
And chock full of a deadly poison, gyromitrin, that is, chemically something like N-formyl,ethylidenehydrazone gets metabolized to MMH (monomethylhydrazine) in-vivo, and it inactivates vitamin B6, causing massive scale GABA depletion, often seizures, delirium, psychosis, all the you'd expect from someone in DTs, whilst going through GHB withdrawal at the same time. Plus potential liver damage and all that business purely because its a hydrazine and hydrazines are nasty.
 
Sorry if this is off-topic.

How bad is parnate really about food interactions? I am desperately looking for something to bring back my positive emotions which left me when abusing dissociatives too much ... been on moclobemide before with no success at all, low-dose selegeline didn't work too but made me feel even more tense so I didn't want to increase dosage.

I mean, do you need to do straight diet? Or just be careful about some certain ingredients?
Is there even some peripherally acting drug one could take with it to aid with digesting the tyrosine?
 
This before anything: talk to your doctor about it, and go by what they say.

From a doctor whom I've spoken to, the food interactions were over-hyped. However, people did in fact die...

What I did is was very careful in the beginning, taking just a tiny amount of the relevant food, being very very careful about how much to consume. This is far from everyone's experience, just my own, but I didn't find any prohibitive food. Obviously steer clear of PEA, for sure. The same with other sympathomimetics, especially in the beginning.

I believe the thing to watch out for is a hypertensive crisis, which can lead to a stroke (time lost is brain lost). I may be wrong on this, but a hypertensive crisis is preceded by a painful headache in the back of the head. If that happens, I'm fairly certain that you need to go to a hospital.
 
Thanks for your reply, Ho-Chi-Minh :)

Somehow I think in such a case, you don't want to wait the time it needs for an ambulance to come over and the paramedics hopefully using the right antidote ...
It should be possible to carry such an emergency antidote as a nasal spray, shouldn't it? Something like clonidine, or maybe better an alpha- and beta blocker- or a benzodiazepine? What is the usual antidote for hypertensive crisis on MAO inhibitors?

When I was on moclobemide, I have tried to titrate d-amphetamine. I don't remember the exact dosages but let's say I started with 0.5mg sublingual, waited 15-30min, measured blood pressure and took another 0.5mg ... while the desired (dopaminergic) effects remained absent- well of course because it doesn't really block MAO-B - there was some stimulation and with maybe 2,5mg or so, blood pressure began to increase from ~120/80 to ~160/95 and an uncomfortable tense feeling set in.

Took (I don't really remember, 75mcg or 150mcg) clonidine sublingually and within minutes it faded away, blood pressure back to normal.

Don't know whether clonidine might work for real crisis too.
 
It seems like a most suitable drug, perhaps combined with tizanidine (the two seem to have some differences in spectrum of effects in vivo) such as tizanidine being a really potent hypotensive, enough with a few pills to knock someone senseless if they rise, from orthostatic hypotension. Its had me hit the deck before because of it. Clonidine, even at high doses seems to lack certain 'feeling' present with tizanidine.

Rather than targeting specific adrenergic (non auto-)receptors, with antagonists, reducing overall noradrenergic release sounds most sensible to me, although still one ought to go call for an ambulance afterwards, because it could come back), telling what has happened in the case of a hyprtensive crisis. I've used it before (clonidine under the tongue, oral tizanidine) whilst calling an ambulance after developing a sinus tachyarrhythmia of unknown origin. Didn't work to cardiovert the abnormal sinus rhythm but it did bring down the rampaging tachycardia, which was at the point my vision was fading to a pinpoint tunnel with black walls, and I thought I was going to pass out on the phone to the ER.


IMO 160/95 is getting into red alert territory, even in the ambulance they had their own guide chart, and that was near the top of 'in the red, emergency!'
 
I really can't make that call. From what I know, an adrenergic autoreceptor agonist seems to be in the right direction, at least. Lying down comfortably with the bare minimum amount of stimulation in one's surrounding might work well, too. I think lots of cold water might help. But in the end, I'm not qualified to recommend anything other than seeking emergency assistance.

This goes without saying, but you should be on board with whatever your doctor proclaims in this sort of scenario. If they say no, that means no. This is very risky business.
 
I was only making the suggestion for keeping in as best of one piece as possible whilst paramedics are already on their way, not to try and deal with it oneself.
 
I have run into patients who cannot live with out it with any quality of life and other (all other classes) have failed. They don't abuse it but that indicates to me the potential is there.

How many DRI derivatives have either been pulled before Phase IV or marketed and quickly withdrawn? They're not ever sold in the USA, and they blame Sibutramine for that, but that's an 5ht agonist not a DRI.
 
Does "it" in this instance mean Parnate, adrenergic autoreceptor ligands, sitimulants, or otherwise?...

I'm more concerned about Captagon being a Schedule I substance. It is broken down into theophylline and amphetamine--essentially caffeine and amp. in one.

There are quite a few examples of stimulants strangely being sanctioned to Schedule I status--stimulants that at least aren't significantly worse than those on the market, and which are quite less neurotoxic than Desoxyn. (like Pasalin)

I don't understand, though, why Tenuate and Fastin are only use for obesity, whereas I would think, at least in the case of the latter, that it is less abusable than amphetamine and methylphenidate-based medications.
 
Specifically Parnate at normal doses.

I suspect your answer is money. I also think about the most cardio-potential-disaster you can take with severe exogeous obesity is methamphetamine.
 
To wit the US was roundly against any DRI, SDRI, NDRI with any potency, reboxetine, mianserin until regranted a label as 6-aza (mirtazapine), doxulepin, amoxapine, really weird lists. Methysergide is schedule 1 now, like methqualone.

It's the patents I think.
 
modocmodoc said:
I have run into patients who cannot live with out it with any quality of life and other (all other classes) have failed. They don't abuse it but that indicates to me the potential is there.
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I disagree with the idea of patients being unable to function without it being indicative of any abuse potential; by your definition, insulin has abuse potential. I wouldn't say it's indicative at all of dependence (in the sense relating to addiction); unfortunately many diseases simply aren't curable, and the best that modern medicine can offer people suffering from those is medication that reduces the symptoms to a more tolerable level. IMHO, that does not make these people addicts.

modocmodoc said:
To wit the US was roundly against any DRI, SDRI, NDRI with any potency, reboxetine, mianserin until regranted a label as 6-aza (mirtazapine), doxulepin, amoxapine, really weird lists. Methysergide is schedule 1 now, like methqualone.

It's the patents I think.
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An astute observation. Aside from reboxetine - which is a dubious example because it doesn't fall into any of the categories you listed and clinical trials were pretty unfavourable - it's notable that most DRI/NDRI drugs were among the earlier drugs developed, hence the ones whose patents expired earliest (similar is true of MAOIs, barbiturates - like methaqualone which you mention - and a lot of tricyclics, which have all similarly fallen out of favour).
I not sure whether it wasn't just a typo, but your reference to SDRIs intrigues me. AFAIK there haven't been any drugs developed yet that are able to selectively target both the serotonin and dopamine transporters without also hitting the noradrenaline one. Did you have any examples of known SDRIs, even very old or obscure ones?
 
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