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So I got my script for moclobemide, but unfortunately it's only 150mg for 3 days after which she'll increase me to 300mg then higher probably in the coming weeks. I only expect very mild effects from 150mg, similar in strength to rhodiola or St John's Wort.

The pharmacy near my house apparently don't have any moclobemide because it's "too old". Lame. Trying to find it somewhere else.

I expect it to make me more anxious for a while, but the psych woman told me she'd hand out a few benzos if it's bothering me. Looks like I will be getting anxious then...

Okay, I've now located some moclob. First impressions coming shortly...
 

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My Moclobemide starting dose was 600mg and I didn't feel anxious. I went up to 900-1200mg but it didn't really help me. At least I had no bad side effects from this drug.
 

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Discussion Starter #5
I dosed about 40 minutes ago. As expected, nothing dramatic has happened, but the worst of my anhedonia and dysphoria seems to have lessened. I'll increase to 300mg in a few days.

I'd say the serotonin and dopamine effects are pretty equal, and thankfully I'm not noticing any noradrenaline increase. I don't feel any more nervous than before. Music sounds a little better.

This one has potential...
 

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150mg Moclobemide can't affect dopamine levels - that's psychopharmacological. And do you really think you can exactly feel which drug affects which neurotransmitter systems in your brain? ;)
 

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Sure it can. Dopamine is broken down equally between MAO-A and B.
You still haven't got it that Moclobemide is a reversible, selective MAO-A inhibitor. Sure you can raise dopamine levels with it significantly... just overdose, then it's unselective. ;) If you take normal doses and inhibit something like 80% of MAO-A and 30% of MAO-B that's plenty enough to degrade dopamine. Not being able to strongly raise the levels of serotonin, norepinephrine and dopamine is the price one pays for not having to follow dietary restrictions.
 

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Discussion Starter #10
Maybe I need to start drinking kava again to get MAO-B blocked too. I hate selegiline so that is out of the question.

Update on moclobemide: I took another 150mg dose and I feel awful. Very much the same as when I started Prozac. I am thinking more and more that this "MAOI lite" is nothing better than an SNRI, only with the added bonus of many drug interactions. I am definitely getting some Valium tomorrow.
 

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Maybe I need to start drinking kava again to get MAO-B blocked too. I hate selegiline so that is out of the question.
If you take Moclobemide and block MAO-B sufficiently via overdose or another drug, you have to follow dietary restrictions and could take Nardil or Parnate instead.
 

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Discussion Starter #13
Yeah I am beginning to think one of the real MAOIs would better suit me. I'd try SSRI + Wellbutrin first though.
 

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But isn't tyramine destroyed by MAO-A?
And MAO-B. This article should give you a good understanding, but it's pretty long. ;)

On MAO-B and Tyramine Metabolism:

Dear Sir:The Spring issue (Volume 61, #1) of AJPE included an articleby Alsharif, Theesen and Roche on teaching medicinal chemistry. It was particularly interesting and innovative. I would like to pointout, however, that there was an error on page 59 in the section on MAO inhibitors. The authors state that MAO-B is the enzymeresponsible for metabolizing tyramine, and therefore a selective MAO-A inhibitor can be used to avoid the dietary restrictions.

Unless my pharmacology books and the PDR are wrong, I amunder the impression that MAO-A is found primarily in the gut and is the enzyme responsible for metabolizing tyramine, whereas MAO-B is found primarily in the brain and is not particularlyinvolved in metabolizing dietary tyramine. In support of this view, selegiline, a selective MAO-B inhibitor, is used successfully in Parkinson's disease without any dietary restrictions.

Maureen E. Bronson Wilkes University

More on MAO Dear Sir:We appreciate the comments regarding the error on page 59 of our paper, "Structurally Based Therapeutic Evaluation: A Therapeutic and Practical Approach to Teaching Medicinal Chem-istry." The following discussion evaluates the statement made by the reader and reviews the clinical use and safety of selective MAO-A and MAO-B inhibitors as it pertains to our article. Our statement on page 59 should have been written as: "The vasoactive phenethylamine tyramine, found in the cheese and wine of thislasagna dinner, is metabolized by MAO (MAO-A and MAO-B) and is accumulating in the presence of the enzyme inhibitor."

We would like to address the reader's statement as it pertains to our article. There are two different types of MAO: type A which preferentially deaminates catecholamines such as serotonin, epi-nephrine and norepinephrine and type B which preferentiallymetabolizes 2-phenylethylamine. MAO-A and MAO-B are both responsible for the metabolism of tyramine and dopamine. BothMAO-A and MAO-B are distributed in various age-related con-centrations throughout the human body, including the gut and brain. MAO-A has a higher concentration in the intestine thanMAO-B, while concentrations of MAO-B are higher than MAO-A in the brain. Furthermore, although the placenta contains pre-dominantly MAO-A, platelets and lymphocytes express predomi-nantly MAO-B, platelets and lymphocytes express predominantlyMAO-B.

In our article we state: "Of these, only (structure) 5 selectively inhibits MAO-A (halogen on the phenyl ring), which would still allow tyramine to be metabolized by MAO-B. The hypertensive crisis might have been avoided with 5." Antidepressant activity isassociated with selective inhibition of MAO-A and not with inhi-bition of MAO-B. The safety of the reversible inhibitors of MAO-A(RIMA), structure 5, is attributed to the ability of tyramine andother indirect-acting sympathomimetic amines to competitively displace the RIMA from their inhibiting site on MAO-A. The displaced MAO-A is then available to metabolize tyramine. There-fore, hazardous potentiation of pressor responses to dietary tyramine that accompanied MAO-A inhibition could be markedly attenuated by using reversible inhibitors of MAO-A. Further-more, when using a RIMA, an additional safety factor is provided because both MAO-A and MAO-B are available to metabolize tyramine.

We did not discuss the competitive displacement of reversible MAO-A inhibitors by tyramine in our article. However, a state-ment can be included to make the discussion more complete. "Of these, only 5 selectively and reversible inhibits MAO-A (halo-gen on the phenyl ring). The reversible nature of structure 5, isattributed to the ability of tyramine and other indirect-actingsympathomimetic amines to competitively displace structure 5 from its inhibiting site on MAO-A, thereby freeing MAO-A to joinMAO-B in the metabolism of tyramine. The hypertensive crisis might have been avoided with structure 5."
 

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interesting

Thanks for the article Medline. Very interesting.

Euphoria, I have been skeptical about moclobemide's use in treating SA, but you should give it a little time before you come to a final conclusion.

SSRI + Wellbutrin sounds like a good combo although I'm still a bit skeptical of the whole reuptake inhibition craze. I might try it though if I can convince my doc, but I am much more interested in trying Adderall at this point since I also have ADD. Plus I think it would be a more effective way of boosting the "big three" than bothering with Wellbutrin.

It seems like you want the benefits of a real MAOI without the drawbacks. There is one big difference though between these tactics and taking Nardil. You realize that nardil has an active metabolite that is GABAnergic right? I really believe this plays a big role in the effectiveness of nardil and that's why I have little excitement over other MAOI's like parnate which have no such action.
 

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Discussion Starter #16
Euphoria, I have been skeptical about moclobemide's use in treating SA, but you should give it a little time before you come to a final conclusion.
If anything I'll just use its mild anxiolytic effect to get myself a job so I can buy the stuff online that really works.

The way I see it, moclobemide's effects are mainly on serotonin because dopamine, noradrenaline and adrenaline are all metabolised by more than one enzyme (unlike serotonin). Dopamine has more catabolic enzymes than noradrenaline and adrenaline, so more adrenergic effects will be present than dopaminergic. In fact moclobemide seems the functional equivalent of Effexor with its weak NDRI properties and strong SRI.

SSRI + Wellbutrin sounds like a good combo although I'm still a bit skeptical of the whole reuptake inhibition craze. I might try it though if I can convince my doc, but I am much more interested in trying Adderall at this point since I also have ADD. Plus I think it would be a more effective way of boosting the "big three" than bothering with Wellbutrin.
As long as you get neurotransmitters in the synapse, it doesn't really matter what the mechanism is. I've heard good things about tyrosine for motivation and pleasure, and it's especially useful for stimulant crashes.

It seems like you want the benefits of a real MAOI without the drawbacks. There is one big difference though between these tactics and taking Nardil. You realize that nardil has an active metabolite that is GABAnergic right? I really believe this plays a big role in the effectiveness of nardil and that's why I have little excitement over other MAOI's like parnate which have no such action.
Oh, I'd never take an unselective MAOI again. Too many side-effects. I don't think GABA should be targeted for anxiety or depression, though it does work.
 

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Are you going to give it some more time? You might as well give it at least a week or two just for kicks =P It can't hurt.
 

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Moclobemide works fast in general, often within 1-2 weeks, but you need a therapeutic dose (300mg bid = 600mg). If it doesn't help within 3 weeks, increase the dose to 600mg in the morning and 300mg at midday and wait another 2 weeks. If it still doesn't help, throw it away.
 

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Yeah, that's the maximum dosage in every country ;). My psychiatrist told me Pdocs go above 600mg to 900mg (or even 1200mg) if necessary, because it can help, but it can not hurt. This strategy is especially useful when the patient showed a partial response to 600mg.
 
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