Talk:Monoamine oxidase inhibitor

I have cleaned up this article a bit, but it still needs a lot more work, like most of the neuropharmacology on wikipedia. I'm thinking the MAOI and MAO articles should be refactored into several articles, but I'm not sure what would be the correct way to divide them. I guess factors (articles) could be the biology and chemistry of MAO (MAO article), the clinical use of MAOIs (MAOI article), the recreational and religious use of MAOIs (MAOI_and_drugs article), a page on the safety of older MAOIs including dietary restriction guidelines (MAOI_safety), and perhaps a page on the newer developments (MAOI_news) such as RIMAs, transdermal deprenyl and so forth.

Research regarding MAOIs, particularly deprenyl, are turning up interesting things. Animal models indicate slowed aging due to reduced free-radical damage in dopaminergic cells, increased immune system efficiency, improved libido, etc..

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In my experience, and according to the label, moclobemide improves sleep. I presume this is because the MAO-A inhibition causes a pressor-effect on the serotonin-to-melatonin process, since that then becomes the only "place to go" for excess serotonin. Anyone have data to back this up?

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Shouldn't the following:

In the past they were prescribed for those resistant to tricyclic antidepressant therapy, but newer MAOIs are now used as an alternative to tricyclics.

read as, instead:

In the past they were prescribed for those resistant to tricyclic antidepressant therapy, but newer SSRIs are now used as an alternative to tricyclics. [change MAOI to SSRI]

Why? This depends entirely on the practicioner. Clinical trials show that e.g. moclobemide is as efficient as e.g. fluoxetine in treating major depression, and equally safe. (Even at 1200mg, the tyramine sensitivity is well within safe limits (TYR30 of 50mg+)). The newer MAOIs suffer from a bad reputation due to the previous generations of such drugs, as well as having arrived slightly later than the SSRIs, so doctors were already familiar with SSRIs. Also, in atypical depression, where neurotransmitters have typically been depleted (e.g. due to use of SSRIs), they are usually the most effective, even at low doses. Treatment refractory depression usually also improves with MAOIs.

And is this just sounds like too much of a Silence of the Lambs joke:

Examples of tyramine-containing foods include such common foods as liver, fava beans, Chianti and...

It is not a joke. Spoiled liver contains dangerous levels of tyramine. Fava beans (indeed any broad beans) contain levodopa. Many wines contain dangerous levels of tyramine, and Chianti has a particularly bad reputation in this regard. Tap beer can also pose a serious problem, due to inadequate cleaning. I imagine aspartame could be a problem too, since it can revert to phenylalanine, which would give much the same problem as chocolate.

None of these things should be a problem with moclobemide up to 1200mg, and transdermal deprenyl shows no increase in sensitivity.

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I know the retardation of neurotransmitters was probably the cause of the suicides, but what exactly was the cause of the suicides? This was never discussed in the article...

Antonio Away, on Depression Martin

Suicide is always a risk until significant remission occurs. Certain antidepressants, particularly those that alleviate anergia, will give you the extra energy you need to actually commit suicide. Unfortunately, the onset of this extra energy may sometimes be more rapid than the onset of actual antidepressant effect.

As for how, in the case of Tranylcypromine, a number of things (cheese, meat, wine, other alcohols, caffeine, drugs, etc..) can cause dose-unrelated hypertensive crises that end up with tachycardia or bradycardia, as well as intercranial bleeding. Also, an excessive rise in body temperature (hyperpyrexia) can occur, leading to coma and/or death.

It should be pointed out that this particular class of drugs appears to be generally considered an alternative to electroconvulsive therapy, not as an alternative to other drug regimens, due to the possibility of severe adverse reactions.

Actually, this is only true for the older generation drugs. Moclobemide has been shown to have no clinically relevant potentiation of tyramine if taken after the meal, rather than before it. And deprenyl is becoming available in transdermal form, which has no adverse effects at all (lower incidence than with placebo in all categories), apart from skin irritation under the patch. (Compliance is also typically higher with transdermal delivery, eliminating the typical problem of the patient not taking the medicine as prescribed.)

In many cases, you may want to consider such drugs as dextroamphetamine before trying out an MAOI. The role of dopamine in depression is seriously undervalued.

Again, not correct for RIMAs or non-oral delivery. And MAO-B inhibition (deprenyl or older MAOIs) are one of the few safe ways to increase dopamine activity, with the added benefit of preventing parkinson. Dex is not safe for long-term use, due to reduced neuroplasticity and other concerns.

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Here's a request I moved from Wikipedia:Requested pages page:

MAOI inhibitors and their specific brain functions, especially as pertains to interactions with other chemicals/medications.

Please expand or ignore as appropriate. --Heron 11:46, 24 Nov 2004 (UTC)

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