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Selegiline: MAO-B and MAO-A information/questions


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#1 Phreak

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Posted 26 April 2009 - 02:47 PM


Deprenyl [Selegiline HCl] is a irreversible selective MAO-B inhibitor (as I'm sure you all know :)) so it is pretty safe to mix with other drug. Obviously not all - in fact, some can have really, really bad reactions - but quite a few prescription medications are okay to take with it. Do you research, though, regarding dosage.
N.B. Irreversible does not mean that that the MAO-B inhibitory effects are permanent; rather that they may persist for up to 1-2 weeks following the last administration. It also means that Selegiline has a cumulative effect: whereas 5mg a day will still only "essentially" have selective MAO-B inhibitory effects, if taken daily for an extended period of time it will create a cumulative effect where the inhibition remains and so you are actually 'topping up' your dose, eventually leading to normal MAOI issues. Hence why, if you are taking Deprenyl as a Nootropic for motivation/concentration etc, as an anti-aging compound or as a supplement, it is recommended that you either take it EOD (Every Other Day) or 2-3 time a week, or taper your dose DOWN as you progress...

At low-doses, MAO-B inhibition has no (little?) serontonergic effects, which means that - in doses of about 5-10mg - is does no interfere with SSRI's or SNRI's. There may be a small amount of potentiation but nothing too big of a problem so long as you are careful (subjective report). Bear in mind that other drugs and supplements act as mild SSRI's, SNRI's (Tramadol is a fast-acting, short-lived SNRI - not something you'd expect), DARI's, NRI's, NDRI'S and MAOI's so make sure you do a quick browse before you go mixing - even with the herbal supplements. Off the top of my head I can think of some herbals that have these properties:

Cats Claw - lots of alkaloids that possess non-selective MAO-B inhibition
Kava Kava - a few MAO-B inhibiting alkaloids
Ayahuasca - MAOI
Kanna - SSRI properties
St. Johns Wort - strong MAOI
Liquorice Root - ^^ same as above
Yohimbe - weak MAOI
Passion Flower - small amounts of MAOI and SSRI alkaloids in some cases
Rhodiola Rosea - not direct an MAO-x if I remember correctly, but has something to do with 'balancing' MAO-x's. Would advise being looking this one up.

*** I may well be wrong about the above; I haven't cross-checked, I'm just remembering things I've seen written before. However, my point is that you need to be careful, BUT - due to Selegiline's specificity - if you are careful with how much, when and with what you take it with then you shouldn't run into any major problems. I've read of people taking 250mg Tramadol with 10mg Deprenyl; I've read of people taking 5mg Ritalin and 2.5mg Deprenyl; I've read of people taking small doses of PEA and Selegiline on a daily basis and, whilst probably not that good for you if done repeatedly, they were fine. I believe there is even a member on this forum whose takes 100-200mg Tramadol + 10mg Deprenyl + DLPA and even sometimes 5mg Adderall daily. You'd have to have quite a tolerance to deal with that, but it is an example that it's possible. It's only that though: an example, not a green light to push the boundaries. Probably the most dangerous issue with Selegiline and other drugs is hypertensive crisis. Hypertensive crisis IS a major issue, and you'll want to get yourself to a hospital immediately if you do something stupid and notice skin flushing and migraine-esque headaches, but no one here is that stupid...right? Numerous SSRI's plus high-doses of Selegiline also bear the risk of Serotonin Syndrome, but it's a lot harder to get than Wikipedia implies... ***

/completely unrelated information on Selegiline

________________________________________________________________________________
__________________


Annnyyywwwaaayy, more to the point:

I was just wondering at what point Selegiline becomes goes from a selective MAO-B inhibitor to a non-selective MAO-A inhibitor in these cases:

1) Dosage alone. 5-10mg is considered to only have MAO-B inhibitory effects, whereas...30mg (for example) would cause MAO-A inhibition. But where is the line? Assuming it is one's first time taking Selegiline, what dose would trigger its MAO-B effects, and what dose would trigger its MAO-A [more dangerous]?
2) How long does it take for the cumulative use of daily Selegiline to cross over into MAO-A territory? Using this example: 5mg a day, with food, everyday --> how long until you are getting MAO-A inhibitory effect?


I ask this because, in a previous thread, I got lots of helpful feedback from users (thanks again to those who gave me input :)) basically saying how my Nootropic stack was fine with Deprenyl, but I would need to watch out when it came to taking dopamine precursors or pro-drugs, such as L-Tyrosine, NALT, L-DOPA, DL-Phenylalanine and PEA alongside it, as this could seriously overload my CNS with Dopamine, have massive toxic effect and possibly kill me. Sound advice :) That being said, L-Tyrosine/NALT can be supplemented with Deprenyl in small doses quite effectively, but ONLY once I've got to know how I personally interact with Selegiline.
I've also seen logs for PEA + Selegiline having outstanding results on productivity and mental coherence, but - again - this is only for the experienced and becomes more a more recreational "high" on which one can do lots of work rather than a neuroprotecting-neuroenhancing stack.

Hmm, okay, this turned out more as a rambling statement than a question, but the bit in bold labeled (1) and (2) is what I am interested in. I have just started to factor in Deprenyl to my stack (at a dose of 2.5mg) and I want to make sure I'm being as safe as possible, whilst getting the most out of it.

I know a lot of people here think it's a load of crap and there are other, way more effective Nootropics out there, but I've tried quite a lot and this is one that I'm yet to try and (if it works) sounds right up my alley. So please, no replies like, "Deprenyl is shit. Here's what I take - xxxx - you should do the same." because that's not what I'm after (although if you have any constructive advice/criticisms then that is most welcome :)

I also have several other thread concerning Selegiline which all kind of tie in with this. I've just created one to do with chewing coca leaf (not cocaine) and Deprenyl, and a few others...


Thanks in advance
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#2 Phreak

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Posted 26 April 2009 - 04:02 PM

EDIT - This was the thread I meant to link to but I can't make changes to my original thread since it's been more than 10 minutes.

Coca leaf (Erythoxymum Coca) + low-dose Deprenyl for effective motivation

^^ Just more information + question on a potential combination.

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#3 bgwithadd

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Posted 26 April 2009 - 11:34 PM

The inhibition is pretty much permanent, actually. The MAO will usually get destroyed before it becomes active again which has a halflife of 40-60 days. The 1-2 weeks figure is because your brain will produce more over time.

PEA is the biggest danger with deprenyl, so long as you don't go over 10mg a day. There is some other obscure reaction, but it's with a more 'medical' drug not something people would take on their own, but you should research any drug before you take it. Coca leaf has tiny amount of cocaine and absorbs slowly so there should be no issue. You do get ramped up dopamine mixing deprenyl with other stuff whuch can keep you awake longer or potentially cause more serious problems but the key is to slowly add things in after taking deprenyl steadily for 2 weeks and see what you can tolerate (or even need). Deprenyl taken daily on its own is pretty powerful so don't assume you need to add in 50 other things to get results.

No one knows the exact line where MAO-A occurs or what the precentage is. Having some occurence doesn't mean that you are at lethal levels, though. People take MAO-A all the time, and only a handful of people have ever actually died. For a while I was taking 30mg a day with PEA, but even without PEA deprenyl is hard to tolerate because it increases histamine and metabolizes to l-amp and -methamp, both of which have unpleasant physical side effects, more so than the d isomers which are the ones that provide the biggest CNS/attention hit.
I don't think you'd really want to take more than mg a day, 10 at the outset. I found it very hard on my body PEA completely aside, worse than the adderall in many respects, though probably not so neurotoxic because it doesn't hammer the CNS in quite the same way. From health/longevity perspective, you are surely better off taking small dose like 1mg a day at most.

The only time I could see taking more is if you have very treatment resistant depression and you're desperate. In one study, about 80% (or was it 60%?) of treatment resistant depressives who did poor even on MAOIs were instantly cured by having 30mg of deprenyl + DLPA supp. The reason being its effect on PEA. It seems if your PEA levels are very low, it's just impossible to feel any kind of pleasure at all. Which makes sense because without it no matter what your dopamine or serotonin levels are they are not being utilized properly.

I would just do a search on deprenyl here or even go back through my posts and you will quickly learn pretty much all there is to know. (but at the same time, because you actually take anything it would be smart to make a post just in case you miss something. Most the supplements and even drugs are fairly benign but better safe then sorry.)

Edited by bgwithadd, 26 April 2009 - 11:38 PM.

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#4 Phreak

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Posted 28 April 2009 - 12:35 AM

That's some sound advice there, bgwithadd, thanks :p

I'm only going to ever be taking 2.5-5mg of Deprenyl a day so I'm okay there. However, what dose of PEA would go well with this without being too dangerous? I like the idea of 'motivational euphoria' - that's exactly what I'm after - so if you can recommend a decent PEA dose that'd be great.

Also, how long does PEA usually last for?

I was considering taking L-Tyrosine with Deprenyl after a few weeks getting used to the Deprenyl alone ---> which do you reckon is more effective? What I am looking for is a combination of Deprenyl & 'xxx' that will give me the most long-lasting "euphoria" (or feelings of intense well-being) but I'm not sure which is more effective:

L-Tyrosine; so I have more 'free' dopamine in my brain
(or)
PEA; so I have...PEA mixed with the MOA-B inhibition!

Which d'you reckon would be more effective and last the longest? I know that PEA is one I have to be more careful with, but are there any similar safety issues with L-Tyrosine?

EDIT - lol, I just remembered I saw something else you posted in one of my similar thread bgwithadd:
"First off - you will probably kill yourself taking PEA and deprenyl" (very reassuring :p), and, "If you take DLPA you will get an increase in PEA, endorphins, and dopamine. However, it's not the same as taking PEA directly because your brain won't just mindlessly shove PEA into your blood stream but will shut down production after a while."

Does this mean that DLPA, taken at a reasonable dose, is more effective than PEA directly because it's more of a 'controlled' intake?
With that being said, however, I can't find any evidence that DLPA causes an increase in PEA...? D'you have a source? Thanks.

Edited by Phreak, 28 April 2009 - 12:57 AM.


#5 yowza

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Posted 28 April 2009 - 03:28 AM

Isn't there a dosage in which you can take deprenyl without inhibiting MAOB?

There's a link here: http://www.eternitymedicine.com/english/04_eternity_medicine_products/Deprenyl/deprenyl_article.htm



Here's my interpretation:
In this article, it's mentioned that the actual mechanism of Deprenyl is that of a "Catecholamine Activity Enhancer" as opposed to an MAOB (the Catecholamine Activity Enhancement is what leads to the MAOB action at regular dosages, which is why this was the original theory for how this drug mainly worked). When taken at a therapeutic dosage, the MAOB inhibition occurs. However, if the dosage is taken below a certain level, would it be possible to avoid MAOB inhibition all together while getting the Catecholamine Enhancement benefit?

This also brings up the question of what kind of compounds could bring about this "Catecholamine Enhancement Levels" without causing downregulation or desensitizing receptors (the reason while many feel crappy once they stop taking a drug).

Here's the excerpt that caught my eye:

DEPRENYL: CATECHOLAMINE ACTIVITY ENHANCER
During the 1990s Knolls DPR research took a new direction. Working with rat brain stems, rabbit pulmonary and ear arteries, frog hearts and rats in shuttle boxes, Knoll discovered a new mode of action of DPR that he believes explains its widespread clinical utility. (2,16) Knoll discovered that DPR (and its cousin, PEA) are catecholamine activity enhancers (CAE). (Ed. - Dr Knoll explains this on his 2000 Monte Carlo Anti-Aging Conference Audio Cassette).

Catecholamines (CA) refers to the inter-related neurotransmitters dopamine (DA), noradrenalin (NA) and adrenalin. CAs are the transmitters for key activating brain circuits - the mesolimbic-cortical circuit (MLC) and the locus coeruleus (LC). The neurons of the MLC and LC project from the brain stem, through the mid-brain, to the cerebral cortex. They help to maintain focus, concentration, alertness and effortful attention. (17) DA is also the transmitter for a brainstem circuit - the nigrostriatal tract - which connects the substantia nigra and the striatum, a nerve tract that helps control bodily movement and which partially dies off and malfunctions in Parkinsons disease. (1)

When an electrical impulse travels down the length of a neuron - from the receiving dendrite, through the cell body, and down the transmitting axon - it triggers the release of packets of neurotransmitters into the synaptic gap. These transmitters hook onto receptors of the next neuron, triggering an electrical impulse which then travels down that neuron, causing yet another transmitter release. What Knoll and colleagues discovered through their highly technical experiments is that DPR and PEA act to more efficiently couple the release of neurotransmitters to the electrical impulse that triggers their release. (2,16)

In other words, DPR (and PEA) cause a larger release of transmitters in response to a given electrical impulse. Its like turning up the volume on CA nerve cell activity. And this may be clinically very useful in various contexts - such as Parkinsons disease and Alzheimers disease, where the nigrostriatal tract (PD) and MLC circuits (AD) under-function (1,17), as well as in depression, where they may be under-activity of both DA and NA neurons. (18,19)


Here's another excerpt that calculates the average amount needed for MAOB inhibition (this could vary if someone has genes that already downregulated the MAOB enzyme though I'm guessing):

Knoll has noted that the human MAO-B inhibiting DPR dose ranges from 0.05 to 0.20 mg/kg of bodyweight. (1) Thus, even in those wishing to use DPR at an effective MAO-B inhibiting dose, it should not be necessary to use more than 3-5 mg/day. Because DPR is a potent and irreversible MAO-B inhibitor, it may even turn out in many individuals that the suggested 1.5-2 mg/day life extension DPR dose may achieve MAO-B inhibition with long term use.


Based on the above a 185 pound male would weigh around 84 kg. If we were to take .05 and multiply by 84, we get 4.2 for someone weighing around 185 pounds to achieve MAOB inhibition. With steady state administration, as noted above, it would probably be less.

However, if below level amounts were taken sporadically (say 2-3 times a week), I wonder if one could achieve catecholamine enhancement with no MAOB inhibition. I know MAOB inhibition is what most people taking this drug want (so it would defeat the purpose) but this is an interesting concept for those that want catecholamine enhancement without the risk of receptor downregulation or desensitization.

This makes me wonder what other enhancement drugs are out there that could possibly fit solely under the CAE category...
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#6 bgwithadd

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Posted 29 April 2009 - 01:02 AM

Well, but is the deprenyl doing it just through PEA action? It seems like fantastic coincidence that it supposedly has same action to be honest. I think it's more likely at those doses it's hard to confirm brain levels than that it has some amazingly similar effect to something it also increases. Deprenyl itslef does not stay in the system very long but it's always had a 24 hour effect on me even when I skip a day or two.

#7 yowza

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Posted 29 April 2009 - 01:12 AM

Well, but is the deprenyl doing it just through PEA action? It seems like fantastic coincidence that it supposedly has same action to be honest. I think it's more likely at those doses it's hard to confirm brain levels than that it has some amazingly similar effect to something it also increases. Deprenyl itslef does not stay in the system very long but it's always had a 24 hour effect on me even when I skip a day or two.


What do you mean exactly? I'm a bit confused on what your trying to get at?

The CAE effect is explained best in the article I mentioned. The article will explain how the PEA effect is linked to the CAE activity that was discovered to be Deprenyl's mode of action at below therapeutic dosages.

#8 Phreak

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Posted 29 April 2009 - 10:26 AM

Just quickly:


I am now taking 500mg L-Tyrosine daily when I wake up (on a completely empty stomach). I then take 2.5mg Selegiline about 2-3 hours after. I am yet to notice a proper effect other than what might be a placebo from the Selegiline, but I have only been taking it for 4 days... Does it normally take longer to take effect?

Anyway, more importantly - my question:

I am thinking of taking DL-Phenylalanine with the Deprenyl, as it has a slight effect on PEA and is more 'controlled' than just taking a PEA supplement only. What dose do you reckon I should start at for the DLPA and at what time should I take it (e.g. with a meal, empty stomach, after/before the Deprenyl...?)

#9 john410

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Posted 05 October 2009 - 07:53 PM

I am now taking 500mg L-Tyrosine daily when I wake up (on a completely empty stomach). I then take 2.5mg Selegiline about 2-3 hours after. I am yet to notice a proper effect other than what might be a placebo from the Selegiline, but I have only been taking it for 4 days... Does it normally take longer to take effect?


Sorry to bump an old thread, but I couldn't find an answer to this using the search feature.

Thanks!

#10 ForeverYouthful

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Posted 05 October 2009 - 07:59 PM

In this thread I asked about He Shou Wu a.k.a. Fo-Ti. Some one said it was a selective MAO-B inhibitor. I'd like to know the implications of that. Thanks.

#11 brain

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Posted 06 October 2009 - 03:41 AM

what about the difference between liquid and pill forms? one study suggested that sublingual absorption increases selegiline concentrations five fold over oral (first pass) metabolism. if this holds true, taking 5 drops of selegiline citrate sublingually would actually amount to taking 25 mg in pill form, supposedly more than enough to begin to lose its selectivity. as little to any research has been done on the liquid selegiline formulations, i'm going to assume that the studies which measured MAO-A/B levels used the pill variety and as such were subjected to first pass metabolism. however, i've never heard of anyone actually having a hypertensive reaction on such a dosage of liquid selegiline - so i'm not sure exactly whats up here. it's possible that it still isn't enough to significantly inhibit MAO-A. if you look into the EMSAM patch (transdermal selegiline), you can notice that the doses of selegiline are much lower. 6, 9, and 12 mg per patch. this is apparently enough to inhibit MAO-A as well as B. any input is welcome.

side question: how efficient is sublingual absorption? if i place 5 drops of selegiline under my tongue and leave it there for a minute, what percentage of that is actually going to be absorbed?

Edited by brain, 06 October 2009 - 03:46 AM.


#12 heymazing

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Posted 21 January 2013 - 08:24 PM

but even without PEA deprenyl is hard to tolerate because it increases histamine and metabolizes to l-amp and -methamp, both of which have unpleasant physical side effects, more so than the d isomers which are the ones that provide the biggest CNS/attention hit.


My Gawd! Is this why I have had an outbreak of Eczema recently? I have added Deprenyl (Selegiline) to my regimen.

I have also moved to another country and started taking other nootropics (Alcar, Alpha Lipoic Acid & L-Carnosine) as well as MSM.

The only other thing I could think of is that I am eating more bananas here, which seems to be one of those allergy inducing fruits (although I never have been able to prove a direct correlation in myself, mainly because I never really used to eat them before coming here).

But out of that whole list: bananas, Alcar, ALA, L-Carnosine, MSM and Deprenyl (Selegiline)....Deprenyl would be the most likely culprit in bringing on an Eczema outbreak, wouldn't you say?

Sorry for bumping and ancient thread. This is very relevant to my current issue :)

Thanks in advance for all input.

#13 panhedonic

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Posted 15 February 2013 - 09:28 PM

Sorry I don't have an answer for you, but you might want to post what your Selegiline dosage is to get a proper answer from one of our pundits :)


but even without PEA deprenyl is hard to tolerate because it increases histamine and metabolizes to l-amp and -methamp, both of which have unpleasant physical side effects, more so than the d isomers which are the ones that provide the biggest CNS/attention hit.


My Gawd! Is this why I have had an outbreak of Eczema recently? I have added Deprenyl (Selegiline) to my regimen.

I have also moved to another country and started taking other nootropics (Alcar, Alpha Lipoic Acid & L-Carnosine) as well as MSM.

The only other thing I could think of is that I am eating more bananas here, which seems to be one of those allergy inducing fruits (although I never have been able to prove a direct correlation in myself, mainly because I never really used to eat them before coming here).

But out of that whole list: bananas, Alcar, ALA, L-Carnosine, MSM and Deprenyl (Selegiline)....Deprenyl would be the most likely culprit in bringing on an Eczema outbreak, wouldn't you say?

Sorry for bumping and ancient thread. This is very relevant to my current issue :)

Thanks in advance for all input.


I will also add to bumping this thread, only because it seems to be the right one to ask the question I asked before many times: Does sublingual selegiline really bump the dosage 5x? Where did that number actually come from? I take 5mg sublingual and I don't seem to have any notion that it works stronger than oral. (for 5 months now)

#14 heymazing

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Posted 16 February 2013 - 12:28 AM

I had just been using the regular recommended dose - 5 mg per day. But I pretty much answered my own question through testing, and it's a yes. Who knows for what reason, but whenever I take it my eczema starts to flare up by the end of the day..So I've left it in the bag recently. When my eczema goes away completely, I might take to it again!

Cuz I did quite like it :)

#15 brainslugged

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Posted 16 February 2013 - 08:00 AM

For a while I was taking 30mg a day with PEA, but even without PEA deprenyl is hard to tolerate because it increases histamine and metabolizes to l-amp and -methamp, both of which have unpleasant physical side effects, more so than the d isomers which are the ones that provide the biggest CNS/attention hit.


I have to take anti-histamines or else I get pain due to allergies.

Would something like cetirizine or even Vistaril would be okay to take alongside Selegiline?

#16 spermidine

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Posted 16 February 2013 - 08:53 PM

guys, wouldnt rasagiline be the more modern better non-toxic version of selegiline ? if so, why are you guys still discussing selegiline on here ?
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#17 jadamgo

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Posted 17 February 2013 - 09:37 PM

It's better for treating Parkinson's disease. It's definitely not better for treating clinical depression or anxiety. Is it better for life extension? That's unknown.
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#18 spermidine

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Posted 17 February 2013 - 09:51 PM

why wouldnt it be possible to help with depression ?

#19 jadamgo

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Posted 17 February 2013 - 10:08 PM

Because it has almost no MAO-A inhibiting ability, and MAO-B inhibition alone doesn't successfully treat depression. Boosting dopamine is nice, but rasagiline's dopamine boost isn't that strong. And while dopamine may be part of depression, it's just not the whole thing. Maybe rasagiline would work as an add-on to SSRIs or tricyclic antidepressants, but it won't do the job all by itself unless you're a strong placebo responder.
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#20 AOLministrator

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Posted 29 September 2014 - 05:19 PM

I have read things here that I don't quite believe and it seems I am not any more knowledgable than before ...

 

What I have been doing basically since 6 hours is to take one 5mg tablet selegiline every 1.5 hours and eat a bit of ripe cheese and tyrosine in between to see what it does. Also choline which arrived with that order and small amounts of piracetam that I take all the time...

 

Anyway, I am not having any blood pressure effects, although I measured something like 150/74 (highest I ever had since 7 years) once initially but I think it was just an error. I usually have 110/70 and 50 pulse because of high cardiovascular fitness. I don't want to take more because I will eat a rich meaty meal in a few hours and don't want to get any weird surprises. The choline just tastes *delicious* and I never had it before ... I feel like I have more energy (I basically have the adrenal gland "exhaustion" issues) but nothing really so dopaminergic, neither is it physical. Maybe just the choline, could still be placebo and such ...

 

 

 So, what can you say regarding the initial questions #1, #2?

 

 

Also I would like to know very practically and definitively, how much you can take on the first day without getting into dangerous territories and without considerable side-effects? Obviously what I am doing is overly cautious already, I could likely have started with 20mg and upped from there 5mg up to 40mg on day one while still eating all the cheese I can in between. I also think in the beginning it is a very good idea to always eat selegiline directly with ripe cheese because you would physically notice if and how it truly takes effect in direction of MAO-A (so no surprises later when upping and upping the dosage) and you also provide the fat needed for good bioavailability.

 

So ... I think it is working already though, my face/body feels a bit warmer especially in combination with the cheese but again blood pressure remains unchanged and the meter doesn't seem to be broken either. It is difficult to tell though by introspective, since it also metabolizes to amphetamine in small amounts and what not. Quite frankly though so far, I have had much 'harder' effects from just smoking cigarettes (including clear blood pressure changes after eating cheese supposedly from the MAOI action of tobacco) so I still think this cannot be it. I hope I can go with just 5mg on the long run but maybe that's even less than like smoking 10 cigarettes a day concerning MAOI so that would be a huge disappointment because I was hoping to get more in the realm of smoking 30-50 a day at no financial cost. If it turns out I need to eat 20-35mg a day just to get anywhere ... that would be quite pricey.

 

I still wonder though ... with cigarettes and cigarette withdrawal I always had this second component (which I very much assume to be the MAOI action). It only really took place after 76 hours approximately and subsided completely after 76-100 hours. Before I quit I was an extremely consistent chain smoker. I needed to keep a daily pensum of 27-32 cigarettes and I would even smoke 7 cigarettes in a row in the evening before sleep just to keep the daily value. I would sometimes forget smoking and then get concentration issues the day after. Half of it always was about keeping the level right. Above it was ok, below wasn't good. Can I have exactly that second component back with selegiline, or will it do no good? That is what I wonder.


Edited by Aolministrator, 29 September 2014 - 05:59 PM.


#21 VICREP

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Posted 30 September 2014 - 12:02 AM

I have been taking deprenyl for a couple months now. I have switched dosing from 1.25 mg , 5 days a week, to 2.5 mg 4-5 days per week. I'm taking it as a healthier, more long-term alternative to dextroamphetamine for ADD.

 

I honestly haven't noticed much of a difference. I'm guessing my does is way too low for significant changes to be noticed, but I'm very weary of dampening my dopaminergic system long term through overstimulation. Am I being to cautious? Should I try 5mg per day or am I likely to burn out as I did with dex?



#22 Area-1255

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Posted 30 September 2014 - 12:14 AM

Most of the side-effects from MAO inhibitors can be alleviated by strategic blockade of certain adrenergic and serotonergic receptors.

Alpha-1 blockade, alpha 2 blockade, serotonin 5-ht1a, 1b , 1d , 2a 2c and especially 5-HT3 (the serotonin nausea receptor and raises BP by this one)

Also, optimizing testosterone levels and nitric oxide production helps facilitate the positive benefits of mao inhibitors while alleviating tolerance and needing less.



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#23 juverulez

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Posted 21 November 2014 - 11:50 AM

how about alternating rasegeline with selegeline? 0.25 mg and 2.5 mg respectively, taken every other day.






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