Talk:Monoamine oxidase inhibitor

I have two questions. Wellbutrin & tobacco

First, I'm wondering what interaction occurs if wellbutrin is combined with an MAOI?

I don't think bupropion interacts with irreversible or reversible MAOIs significantly, if at all. I would suggest, however, that if you're going to try it with one of the older MAOIs (phenelzine, tranylcypromine, isocarboxazid), you do so carefully, starting at a low dose of bupropion and monitoring your BP and pulse. 174.111.242.35 (talk)

Tobacco is listed as containing harmine. I know tobacco is used in ayahuasca recipes, but the tobacco page doesn't mention MAO-* or harmine, and the Harmal page doesn't mention tobacco.. where did this info come from?

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.

The truth is, which antidepressants are preferred and the order in which they are tried depends on the preferences of the individual practitioner: there's a general consensus about some things, but I don't think we should try to say what is preferred or what is an alternative to what, except maybe a general note that irreversible MAOIs are not generally considered as a first-line treatment because of the potential for interactions. (I think the weight gain which is extremely common with hydrazine MAOIs is a side effect whose importance is often overlooked, even though it has the potential to cause significant morbidity.) 174.111.242.35 (talk) 06:54, 17 May 2011 (UTC)

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.

Actually, the claimed Chianti interaction is the result of a single study from the 1970s that used methods for measuring tyramine levels that may not have been accurate. More recent studies since then have found low levels of tyramine in Chianti and other wines. I think we can safely say that wine does not cause any ine is safe, at least if consumed in moderation, and Chianti's "particularly bad reputation" is undeserved. Nonetheless, due to the failure to update old drug monographs, doctors are still telling patients not to drink not only Chianti, but wine in general, despite the lack of reliable evidence or relevant and well-documented case reports. Likewise, while it does contain phenethylamine, there aren't any case reports involving chocolate causing reactions (indeed, quite the contrary). A lot of the putative interactions listed in the PDR date to a time when there was a lot of anxiety (even hysteria) about MAOI-food interactions, and just about anything would be listed even if there was really no conclusive evidence. Such well-meaning attempts to "play it safe" on the part of physicians and pharm companies can be counterproductive, since patients who discover the harmlessness of chocolate or wine may then decide the dietary restrictions do not need to be taken seriously and assume that they can safely consume other items which may actually be dangerous, such as fava beans, aged cheeses, or Marmite.

Yeah, I thought of the MAOI interactions list in the PDR when I saw The Silence of the Lambs. :) Being a psychiatrist himself, Lecter would have been aware of these foods' reputation. (I don't know that human liver has ever been tested for tyramine levels.) 174.111.242.35 (talk) 06:54, 17 May 2011 (UTC)

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

Right, because Moclobemide is selective for MAO-A and the transdermal formulation bypasses the GI tract. 174.111.242.35 (talk) 11:17, 9 June 2011 (UTC)

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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.

Hyperpyrexia is associated with serotonin toxicity, whereas hypertensive crisis is thought to be due to the activity of sympathomimetic substances such as catecholamines. (There are some drugs, such as MDMA, that can cause both.) Only aged cheeses are a problem; most cheese today is processed rather than aged. Caffeine does not seem to cause interactions either, at least not in moderate amounts. Meat will not cause an interaction provided it is fresh and not aged or spoiled, although certain types of meat (notably liver) are more prone to spoilage. See above (re: Chianti) on wines. Most of the harmful interactions are with drugs, not foods. These interactions can occur with any of the older irreversible, nonselective MAOIs, not just tranylcypromine. 174.111.242.35 (talk) 06:54, 17 May 2011 (UTC)

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.)

I think MAOIs, including the older types, are generally preferred to ECT, due to such factors as potential amnestic effects of ECT, inavailability of ECT in some locales, time considerations (even outpatient ECT pretty much eats up a full day, particularly if the patient has to travel to a medical center in another town, and patients have to be accompanied by a family member or friend), and expense (especially for un(der)insured patients). ECT, on the other hand, may be chosen in cases of psychotic depression or when the patient is acutely suicidal and needs a treatment that will work rapidly. Also, a patient who achieves partial remission on MAOIs can have ECT without discontinuing the medication, and vice versa (so they're not necessarily alternatives in the sense of being mutually exclusive). 174.111.242.35 (talk) 06:54, 17 May 2011 (UTC)

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.

I don't have a source for this (I don't have access to my books right now, sorry!), but selegiline/deprenyl is metabolized into L-amphetamine and L-methamphetamine, extensively enough that it's possible for people on this medication to test positive for amphetamine on standard urine drug screens. 174.111.242.35 (talk) 11:17, 9 June 2011 (UTC)

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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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DXM

Removed the mention of DXM potentiation. AFAIK, this combination is extremely dangerous/lethal, and I have never heard of any potentiation of the desired effects. Correct me if I'm wrong :) --unsigned comment

You are most definitely NOT wrong. That combination has killed, with a not very large dose of DXM taken after Nardil. See http://www.inchem.org/documents/pims/pharm/pim179.htm#PartTitle:11.%20ILLUSTRATIVE%20CASES. I added DXM to the list of bad interactions. --Frank Lofaro Jr. 23:26, 4 January 2007 (UTC)

MDMA, DXM etc.

Some information should be added on the dangers and potentially lethal effects of combining MAOIs with these substances. Seretonin syndrome has occured, and been lethal when people have combined MAOIs with MDMA to either 'potentiate' the experience, with ignorance to the dangers (prescribed without education) or through adulteration.

See my addition, it addresses some of the points above which are a bit short on evidence base. Also see my additions to serotonin toxicity, serotonin syndrome, which answer the interaction issues with extensive references. But yes, MDMA with any MAOI is definitely risky, a short route to enriching undertakers. And yes, we need more headings and organisation. Perhaps someone can digest my extensive addition and suggest where to go from there, does the diet bit need moving? For those interested there is more information on my web site Ken Gillman 10:07, 24 September 2006 (UTC)

Shouldn't these go under the drug interactions section? Or even better, the last paragraph of the Dangers section could almost replace the drug interactions? Bobtheowl2 21:39, 28 February 2007 (UTC)

Unsourced

i have added an unsourced banner due to lack of sources.

hopefully enough people visit this page for it to have an effect. ....[goes off source hunting]Dylan2106 22:30, 28 March 2007 (UTC)

Shouldn't there be a warning?

Tobacco contains Harmal, a powerful monoamine oxidase inhibitors (MAOIs)

monoamine oxidase inhibitors (MAOIs)+tyramine =cheese syndrome

monoamine oxidase inhibitors (MAOIs)+ tryptophan=hyperserotonemia

Tyramine =foods that went through fermentation or decay. Foods containing considerable amounts of tyramine include fish, chocolate, alcoholic beverages, and fermented foods such as cheese, soy sauce and soy bean condiments, sauerkraut, processed meat, and red wine.

Tryptophan =chocolate, oats, bananas, dried dates, milk, yogurt, cottage cheese, red meat, eggs, fish, poultry, sesame, chickpeas, sunflower seeds, pumpkin seeds,spirulina and peanuts. It is found in turkey at a level typical of poultry in general.

List of foods containing tyramine

hum...since there are a lot of smokers, shouldn't there be a warning somewhere since these two syndromes are potentially lethal!!! --Wxyrty 21:29, 8 May 2007 (UTC)

If the levels of harmal in cigarrette smoke were high enough to cause an interaction, then smoking would be an effective antidepressant, which it is not. 88.105.156.188 13:41, 18 May 2007 (UTC)

This list of interactions appears to be based on outdated information. Practically all of the interactions you listed are not substantiated (no case reports and no reliable measurements of high tyramine levels; regarding tryptophan, only supplements are considered dangerous, generating frequent reactions), including: fish, chocolate, alcoholic drinks (except for draft beer and certain bottled beers - I will elaborate if you like), red wine, meat/fish (except if aged or spoiled), and all of the tryptophan-containing foods. Cheese is only a problem if it is aged; nowadays most cheeses are processed. 174.111.242.35 (talk) 08:08, 17 May 2011 (UTC)

aka oxidase inhibitor?

Are Monoamine oxidase inhibitors the only kind of oxidase inhibitor? That is, when someone uses the term "oxidase inhibitor," do they mean all and only the set of Monoamine oxidase inhibitors? Ling.Nut 13:46, 28 July 2007 (UTC)

Aha, never mind... thanks... Ling.Nut 13:51, 28 July 2007 (UTC)

I have a few questions if MAOI's provide more effective effects among people with certain mood, emotional or personality disorder like helping or used to treat it, like Dextroamphetamine, which is similar or close to that of Meth to name one, why dont they talk about that more as appose to the negative dont do drugs information. Alot of people out there need MAOI's to live normal lives. Why should they be looked down upon? Is this a government issue? —Preceding unsigned comment added by Vanity1 (talk • contribs) 15:30, 23 July 2008 (UTC)

Seriously, WIKIPEDIA is linking to drug buying sites

In the bottom (REFERENCES)

BLTC Research [1] (2006). "Rasagiline: a neuroprotective smart drug?". The Good Drug Guide. Retrieved on 2007-12-02. “At dosages above around 2 mg per day, rasagiline loses its selectivity for MAO type B and also inhibits MAO type A. An MAO-B selective regimen does not cause significant tyramine potentiation, the dreaded 'cheese effect' common to users of older unselective and irreversible MAOIs who eat tyramine-rich foods. Thus low-dosage rasagiline demands no special dietary restrictions.”

The "Rasagiline: a neuroprotective smart drug?" link go to ENP, a online pharmacy broker... I think it should be removed. —Preceding unsigned comment added by 85.80.193.230 (talk) 21:38, 31 July 2008 (UTC)

Indeed, there are many Wiki pages regarding so-called "research chemicals" that are written by companies who sell them and remain unedited by anyone with a more objective view. Thus, many of the pages referring to chemicals that may elicit desired psychoactivity (AKA street drugs albeit with legitimate potential for therapeutic and/or medical benefit) contain no information other than de facto advertising for their positive effects without citing information sources, potential interactions, or side effects. Oceanlab (talk) 17:14, 21 July 2012 (UTC)Oceanlab

need for mention of drug clinically

It would be very helpful to include an indication of what drugs among this class are in actual approved clinical use, in the English-speaking countries. Readers could then more easily identify those specific articles DGG ( talk ) 18:56, 19 December 2009 (UTC)

Emsam Dietary Restriction

Just a note. The MAOI dietary restriction is still in effect for the Emsam patch if prescribed at doses higher than 6 mg. From the prescribing information:

"EMSAM is an irreversible MAO inhibitor. As a class, these compounds have been associated with hypertensive crises caused by the ingestion of foods containing high amounts of tyramine. In its entirety, the data for EMSAM 6 mg/24 hours support the recommendation that a modified diet is not required at this dose. Due to the more limited data available for EMSAM 9 mg/24 hours and 12 mg/24 hours, patients receiving these doses should follow Dietary Modifications Required for Patients Taking EMSAM 9 mg/24 hours and 12 mg/24 hours. (See WARNINGS and PRECAUTIONS, Drug Interactions, Tyramine.)" - http://www.emsam.com/

If someone does not follow the Emsam link they may not see that information at the other article and may miss this information. Perhaps it would be helpful to add something like: "Dietary modifications for the lowest 6 mg dose is not necessary. MAOI food restrictions are still required for the 9 mg and 12 mg patches." Prescribing information: http://www.emsam.com/ Distributor product page: http://www.dey.com/products/ M MED11 (talk) 17:14, 18 July 2010 (UTC)

Piperine is not MAO-B selective.

Piperine is both a MAO-A and MAO-B inhibitor. http://www.ncbi.nlm.nih.gov/pubmed/15997146 —Preceding unsigned comment added by 70.248.192.104 (talk) 21:34, 30 November 2010 (UTC)

Dangers

Hyperserotonemia can occur without the ingestion of foods containing tryptophan. I know this to be true based on personal experience and I think it is irresponsible to suggest that serotonin toxicity occurs only when tryptophan is ingested. It should instead be noted that serotonin is a neurotransmitter derived from tryptophan, and that eating foods containing tryptophan can increase the likelihood of the syndrome occurring and/or accentuate the problem.

Also, Serotonin Toxicity or Serotonin Toxidrome are phrases which emphasize that it is a form of poisoning and give the reader an idea of the severity of the syndrome. The term "hyperserotonemia" suggests only an excess of serotonin and that it is a condition of the blood. As many people associate serotonin only or mostly with positive emotions, this could be misleading for readers who do not fully understand the function of serotonin or the dangers of extreme amounts it.

www.psychotropical.com is the website of one of the leading researchers on the topic. Hyperserotonemia does seem an acceptable term in this case, especially in combination with the link provided. I will not change anything unless someone agrees with me, but hopefully I have provided sufficient reasoning to support a little rewording around this section. --164.107.94.247 (talk) 09:30, 13 April 2011 (UTC)MHL

I've never heard it called "hypersorotonemia." At least in clinical use, the usual term seems to be "serotonin syndrome." I agree that the former is misleading, not only for the reason you give, but also because the syndrome is mediated primarily by serotonin in the CNS, not in the bloodstream in general. Whatever you end up calling it (I checked, BTW, and the Wikipedia article calls it serotonin syndrome), you should emphasize that it is severe and potentially fatal. Besides hyperpyrexia, patients suffering from serotonin syndrome can present with nausea/vomiting, dilated pupils, nystagmus, diarrhea, rapid breathing, shivering or chills, mental status changes (up to and including mania, psychosis, or coma), excessive sweating, ataxia, labile blood pressure, tremor, myoclonus, muscular rigidity, and seizures. (The signs and symptoms break down into three broad categories: autonomic, neuromuscular, and psychiatric.) 174.111.242.35 (talk) 15:54, 9 June 2011 (UTC)

Rhodiola?

Rhodiola Rosea is listed both as an MAOI and as a substance which should not be taken with an MAOI.

So Rhodiola Rosea should not be taken with itself? :D

Ppw0 (talk) 05:25, 2 May 2012 (UTC)

Berberine should be added to the list of reversible MAOIs, with preference for MAO-A and less pronounced interaction with MAO-B.

Hong-Fang Ji and Liang Shen (2011) "Berberine: A Potential Multipotent Natural Product to Combat Alzheimer’s Disease" Molecules 2011, 16, 6732-6740;

Hong-Fang Ji and Liang Shen (2012) "Molecular Basis of Inhibitory Activities of Berberine against Pathogenic Enzymes in Alzheimer's Disease" ScientificWorldJournal. 2012: 823201. Published online 2012 January 4.

Kong LD, Cheng CH, Tan RX. "Monoamine oxidase inhibitors from rhizoma of Coptis chinensis" Planta Med. 2001 Feb;67(1):74-6. Oceanlab (talk) 17:04, 21 July 2012 (UTC)OceanlabOceanlab (talk) 17:04, 21 July 2012 (UTC) (talk) 17:01, 21 July 2012 (UTC) note this is my first time adding to Wiki so my formatting may be disastrous.

St. John's Wort

I think SJW should be added to the list of herbal MAOIs. — Preceding unsigned comment added by 76.91.29.44 (talk) 07:04, 3 December 2012 (UTC)

The following ~150 page document probably has the most up-to-date info on St. John's Wort's mechanism of action:

St. John's Wort and Its Active Principles in Depression and Anxiety, W.E. Müller (Editor), 2005

^ Look for the DepositFiles link.

Add cacao to list of MAOIs?

Here's the info I'm going by:

http://i.imgur.com/UKNfYJK.gif

Tetrahydro-β-carbolines, Potential Neuroactive Alkaloids, in Chocolate and Cocoa. Tomas Herraiz, J. Agric. Food Chem., 2000, 48 (10), pp 4900–4904

Full paper: http://freakshare.com/files/cw8me933/Tetrahydro-Beta-carbolines---potential-neuroactive-alkaloids-in-chocolate-and-cocoa.pdf.html — Preceding unsigned comment added by 108.41.205.78 (talk) 18:38, 28 January 2013 (UTC)