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Re: +++ MAO-A or B ? Gerovital (procaine) selectivity

Posted by Marty on July 3, 2008, at 15:14:48

In reply to Re: +++ MAO-A or B ? Gerovital (procaine) selectivity Marty, posted by SLS on July 3, 2008, at 5:34:15

> I feel strongly that MAO-A is the main player in mood disorders.

If you mean that inhibiting MAO-A helps more people in depression, then I agree. But I don't think MAO-A or MAO-B is part of the causation in most people and in most mood disorders. That said I'M 100% SURE some people (a VERY SMALL % of ALL the people complaining about depression issues) has some poor MAO in terms of Quality in some and in terms of Quantity in others. And even some mixes : too much MAO (quantity) because of poor quality of MAO (quality). Now that begins to be fun to figure out what it means and for which system it does. Everything goes.


> Investigations into the gene activity that expresses MAO-A in depressed subjects has been demonstrated to be reduced. Results of genotyping have recently implicated the promoter region of the X-chromosomal MAOA gene (MAOA-uVNTR) as being underexpressed.

If you means PARTS of the code is underexpressed then I see the point. BUT if it means the WHOLE code that would mean LESS MAO-A which doesn't support your idea that most depressed people benefit mostly from MAO-A inhibition. I found genetic medical literature to be much more a bitch to read than most pure neurological/psychopharmaceutical literatures.. difficult to interpret.


> Moclobemide is a great example of how a selective inhibitor of MAO-A can produce a robust remission of depression, even if only transiently. I would assign the reason for the tachyphylaxis that is commonly seen with moclobemide as its being reversible.

This conclusion don't look very scientific to me (even if I have the same gut feeling as you BTW) because there's not many RIMA to compare and so correlation is kind of difficult : "All the MAOIs works better than this loner RIMA (Moclobemide). Conclusion: RIMA sucks, MAOIs rules and the difference between the 2 being the REVERSABILITY, we propose that REVERSABILITY is the culprit and thus stinks." XD .. I sometimes wish we could publish our own amateurish paper on pubmed.


> My guess is that there is indeed some MAO-A inhibition with selegiline at the dosages necessary to treat depression. I would want to research that a bit before calling this a fact.

Selegiline (Deprenyl, EMSAM) does inhibit MAO-A at higher dose while only inhibiting MAO-B at lower. And, yes, this is why the infamous Tyramine diet kicks in at higher dosage: because of the MAO-A in the gut.

The risk of tyramine reaction increases with dosage. Investigators warn of this when discussing hypertensive crisis, such that it is recommended to not ingest tyramine at any dosage above the minimum of 6mg/24hr. This would be an indicator that selegiline inhibits MAO-A in the gut.


> I wouldn't be afraid of MAO-A inhibitors. Just be afraid of moclobemide.

Moclobemide has been develop in Canada and my pdoc is one of the guys who worked on it.. and he's damn proud of it. I wish I knew before I told him how it's "been the WORST of EVERY ~30 meds I tried in my life! ...." lol

/\/\arty


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poster:Marty thread:836966
URL: http://www.dr-bob.org/babble/20080626/msgs/837863.html