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Monoamine Oxidase Inhibitors (MAOIs) are the original modern antidepressants1, and often the most effective. Being old and a pain in the ass keeps them from being prescribed more often. MAOIs I know about that are available as medications (or other products) of some sort:
- Aurorix / Manerix (moclobemide) - Not approved for use in the US, but available throughout the world.
- Emsam (selegiline transdermal system)
- Marplan (isocarboxazid)
- Nardil (phenelzine)
- Parnate (tranylcypromine)
- pirlindole / pirasidol / Пиразидол / Нормазидол (Normazidol) - Not approved in the US. Probably limited to former Soviet states and maybe elsewhere in former Communist countries. I’ve found info about it on sites in Russia and Ukraine, as well as Hungary.
- amphetamine - No, really.
- Just actual amphetamines like Adderall, not other stimulants like Ritalin (methylphenidate) or Provigil (modafinil).
- How much you need to take before there’s any effect on MAO-A (and, maybe, MAO-B) that does more than boost how well amphetamine works, is subject to debate.
- And while amphetamine and amphetamine-containing drugs as ADs was a standard way of treating depression back in the 1930s through 1950s, it is now way off-label most places, and highly discouraged in the US and many other countries.
- As in you’re down to opioids - good luck with that - aromatherapy, and VNS is looking like a good idea highly discouraged.
- Eldepryl (selegiline oral) and Azilect (rasagiline) are MAOIs that primarily affect dopamine and are used as add-ons to levodopa to treat Parkinson’s. Depression is a common side effect2, especially when used alone, but at higher dosages Eldepryl (selegiline oral) is effective as an AD. Why does the selegiline patch work as an AD at a low dosage when the pills don’t? I explain that a bit further down.
- Zyvox (linezolid) is an antibiotic used to kill nasty bacteria resistant to the popular antibiotics (MRSA, e.g.). It has side effects similar to the MAOI ADs, and carries the same food restrictions and drug-drug interaction warnings. It is being investigated as an AD and is currently in the decades-away stage of testing3.
- furazolidone is another antibiotic used to treat nasty bacteria and protozoa, such as those that cause cholera and other conditions that could make you literally shit yourself to death. It’s no longer available in the US, but can be found in some countries where you run the risk of shitting yourself to death.
- Matulane (procarbazine) - Well, it’s not like you’d want to eat much of anything when you’re on chemo for lymphoma, right? Because life doesn’t suck enough when you have cancer, there’s an anti-cancer med that’s also an MAOI, so you have to pick which med you want to take if you’re already on an MAOI for MDD and/or an .4
- Tobacco? The data are mixed regarding tobacco, tobacco products, and nicotine as MAOIs. The science seems to be supporting the hypothesis that tobacco smoke is a fairly selective inhibitor of MAO-B. So patches, snuff, chew (ick!), gum and other non-smoke tobacco or nicotine products probably won’t give you any AD, anti-anxiety, or
- This study on smoking cessation tracked MAO-B plasma levels along with nicotine to check if people actually quit smoking using the RIMA Aurorix / Manerix (moclobemide). It shows a noticeable, but not necessarily significant increase in how much MAO-B people have after they stop smoking.
- This study found different brands of cigarettes had different effects on MAO-B and amounts of substances with MAO-inhibiting properties, indicating it depended on additives, processing, etc.
- This imaging study of humans found MAO-A was reduced by a whopping 28% in smokers, and notes the 40% reduction in MAO-B is probably why smokers are less likely to get Parkinson’s.
- Seriously, smoking prevents, delays, or mitigates the effects of Parkinson Disease (PD). As long as you started smoking before you started shaking and twitching. Don’t believe me? How about these NIH-funded studies5:
- Relationship between length of time smoking and Parkinson Disease
- Smoking duration, intensity, and risk of PD
- How protective are coffee, alcohol, and cigarettes?
- Finally there’s methylene blue, a truly fascinating substance. It was the very first fully-synthetic drug, as well as the very first fully-synthetic antidepressant6. While currently not used as an AD it has numerous uses:
- As a dye for medical and industrial purposes
- An antibiotic to prevent and treat UTIs, mainly in the elderly
- It was one of the original cures for malaria
- Like all old-school malaria treatments, it’s making a comeback.
- Prevention and treatment of ifosfamide-induced neurotoxicity
- Treating vasoplegia
- These days its main medical use, aside from dyeing your balls blue prior to surgery7, is that for which it still has FDA approval: being the primary - i.e. pretty much only - treatment for severe methemoglobinemia - a blood disorder that prevents your blood from delivering oxygen to your brain and everywhere else you need oxygen (i.e. everywhere else).
- One of the symptoms of methemoglobinemia is your skin turns blue.
- Methylene blue dyes stuff blue.
- Extra neat-o points for something that would turn your skin blue if you touched it8 returns blue skin to its normal color.
MAOIs come in different flavors based upon three factors:
- How tightly they bind to MAO.
- This is described as “reversible” - the bond dissolves relatively quickly and MAO goes back to doing its job in a matter of days, or “irreversible” where MAO is constantly inhibited for 10 - 20 days after you stop taking the drug.
- Irreversible MAOIs require the two-week “washout” before starting new meds to avoid potentially harmful, even life-threatening drug-drug interactions.
- The food restrictions also stay in place for two weeks.
- Irreversible MAOIs are generally more effective than reversible.
- Of course they are! They’re more difficult to deal with.
- Which type of MAO they target.
- The two I know of are MAO-A and MAO-B.
- MAO-A metabolizes serotonin, norepinephrine, dopamine, and tyramine9.
- It does this in your brain, gut, liver, and skin10.
- MAO-B metabolizes dopamine, phenylethylamine, and tyramine.
- If you have a lot of it someplace it will make a dent in any serotonin and norepinephrine that happens to be lying around.
- MAO-B works in your brain and blood.
- Because of where it works, and that it doesn’t affect tyramine as much as MAO-A does, MAOIs that target only MAO-B don’t have the dietary restrictions that other MAOIs do.
- Their selectivity.
MAOIs are typically grouped by binding then selectivity. Based on that we get:
- Non-Selective (affecting both MAO-A and MAO-B)
- Selective for MAO-B
- Azilect (rasagiline) - Used as ADs by people and their doctors who are getting desperate.
- I’m not sure if using Azilect (rasagiline) for anything except as an add-on for levodopa is really an option.
- Unlike the dopamine-agonist class of Parkinson’s meds (Mirapex (Pramipexole), Requip (Ropinirole), e.g.) which are used as ADs, levodopa is far more likely to cause depression than fix it.
- As with all crazy meds, I wouldn’t completely rule it out if you’re running low on options.
- Stahl will throw it at treatment-resistant depression11.
- Because the depression thing may not be entirely its fault (see below).
- As of this writing all Reversible MAOI ADs on the market are Selective for MAO-A (RIMAs)
- And all the ones approved as ADs are not approved for use in the US.
- Aurorix / Manerix (moclobemide)
- pirlindole / pirasidol
- toloxatone - assuming it’s still on the market anywhere.
- amphetamine-based medications
- Although the data are contradictory regarding amphetamine’s selectivity and potency as an MAOI.
- Everyone agrees it’s reversible and it inhibits MAO-A.
- There’s some debate regarding the extent of its effect on MAO-A.
- As well as its effect, if any, on MAO-B.
- Once again: as effective as they can be, amphetamine-based medications are waaaay down the list of meds to treat MDD for numerous reasons.
- Zyvox (linezolid), although for now that matters most regarding drug-drug interactions with any crazy meds you’re taking.
- methylene blue is the only reversible, non-selective MAOI I’m aware of. At least, its active metabolite is. My money is on a gene therapy for depression becoming real before Azure B - actual name used for the methylene blue in question - being developed into a drug that makes it to the US market.
To grossly oversimplify things, MAOIs create an effect similar to , they just go about it in a different way. They don’t inhibit, or slow down the transportation mechanism, but monoamine oxidase - the chemical primarily responsible for metabolizing (breaking down) the monoamine class of neurotransmitters for reuse, recycling, or waste disposal9. This causes a build-up in several monoamine neurotransmitters. Which ones and to what extent, both within and on the surface of a neuron, depends on which type12 of MAOI you use. Just as there are different receptors for all the different neurotransmitters, there are multiple types of MAO that break them down. The most popular MAOIs on the market interfere with (inhibit) the action that affects the big three flavors of brain juices thought to have the most affect on depression: serotonin, norepinephrine, and dopamine. They also affect the amino acid neurotransmitter tyramine, too much of which can result in assorted cardiovascular and related problems. The foods you can’t eat when taking some13 MAOIs are all rich in tyramine. MAO-A inhibitors are effectively similar to SNRIs, since MAO-B also metabolizes dopamine. So they’re good for as well as MDD. Those that inhibit MAO-B affect phenylethylamine (PEA), which is an interesting neurotransmitter that, when it comes to mood disorders, Stahl, Julien, Preskorn, and most everyone else seems to ignore14. Since the way selective MAO-B inhibitors work, MAO-A would keep munching dopamine, and PEA supposedly isn’t involved in mood, how do they work as ADs? Stahl thinks it has something to do with MAO-B metabolizing protoxins15 into the toxins that are a contributory factor to Parkinson’s. So why is the Emsam Patch (selegiline transdermal system) an effective AD when Eldepryl (selegiline oral) and Azilect (rasagiline) make you more depressed? First of all Stahl writes that the patch affects MAO-A in your brain but not in your gut, which is why the patch is a great AD without dietary issues at the lower dosages. But why is Emsam a not-that-selective MAOI? My guess: it’s a matter of efficacy, and bioavailability. Rasagiline works well enough to boost levodopa’s efficacy and no more, while selegiline inhibits so much MAO-B that MAO-A will leave behind lots of dopamine, and even serotonin and norepinephrine will be affected. And selegiline may not be all that selective after all. Oh, and metabolizing to l-amphetamine and l-methamphetamine may have something to do with it. Supposedly you don’t get all that much meth, and it’s the levorotatory- enantiomers, not the more potent dextrorotatory- ones16, that are created in any event. But the bioavailability of selegiline in pills is such that it isn’t distributed well enough to affect serotonin, norepinephrine, and maybe PEA, enough to be an effective AD, while the selegiline in the patch is. Stahl thinks if you take enough Eldepryl (oral selegiline), it will effect MAO-A, and could be a half-decent AD. As for Eldepryl (selegiline oral) and Azilect (rasagiline) making you more depressed, I honestly think that’s a result of the Parkinson’s. While they could easily make you more depressed if you took them for depression (or some other off-label application), I think it would be less likely to happen if you didn’t have PD, because severe depression is a symptom of PD. As far as ADs go, Eldepryl (selegiline oral) and Azilect (rasagiline) should be pretty far down the list, but I don’t think they should be completely off the table. MAOIs do much more. I cover what that is in the articles about the individual drugs, as most of it is med-specific. But thing that’s obvious is MAOIs have anticholinergic properties, since they all have anticholinergic side effects.
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When taking an MAOI that inhibits MAO-A, or two of the three that are selective for MAO-B - Eldepryl (selegiline oral) or Azilect (rasagiline) - at high-enough dosages17, you may need to limit or completely avoid foods high in dopamine18 and the amino acid/neurotransmitter tyramine, which is chemically related to dopamine - they are both produced from tyrosine in your diet - and keeps your blood pressure up. Too much tyramine = too much blood pressure, which you don’t want. As for the Emsam Patch (selegiline transdermal system), you don’t need to be so careful with what you eat because 1) patches deliver the drug directly to your blood avoiding all the MAO enzymes in your digestive system, and 2) there’s not a lot of MAO-B in your gut in any event. Foods to avoid or limit:
- Any food you think might be spoiled.
- If it’s questionable, there’s no question. Toss it.
- Aged & moldy cheeses (Cheddar, Stilton, bleu/blue, Swiss, Camembert, pretty much most of the good ones).
- Aged, smoked, or otherwise cured meats and fish (dry sausages, salami, corned beef, ham, lox, kippers).
- I can’t get a fix on bacon.
- One or two slices should be OK.
- Just don’t pig out on it.
- Fermented vegetables (kim chee, sauerkraut) and soy products (shoyu and tamari (soy sauces), tofu, miso, and natto).
- Broad beans & related legumes (fava beans, snow peas) - these are rich in dopamine, not tyramine. Contrary to what the wikipedia article on tyramine would have you believe.
- Meat extracts (bouillon, broth, canned/bottled soups and gravies, beef tea, Marmite).
- Assorted condiments (Fish sauce, Vegemite).
- Sourdough bread.
- Banana peels
- Who the hell would eat banana peels?
- If you have to ask, you’ve never been to anywhere where people have far more imagination & adventure than cash, and are willing to make (and eat) something like stewed green bananas19.
- All of one person taking an MAOI has died from eating stewed green bananas, but from their death we learned banana peels are full of tyramine.
- Ripe banana pulp contains 7 mcg/gram of tyramine compared to a peel which contains 65 mcg/gram of tyramine and 700 mcg/gram of dopamine.
- Go Science!
- Chianti, tap or otherwise unpasteurized beer (i.e. beer that is worth drinking), Absinthe20 and Absinthe flavor-maskers like Vermouth and Pernod.
- Hey, at least you can drink some (i.e. small amounts) of alcohol.
- Hell, you can even have a shot of real booze, like vodka or gin!
- The data are contradictory but mostly bad about really good real booze, like Lagavulin and other actual whiskies, or actual gins (i.e. not crap like Beefeater).
- Ironically, some alcohol-free beer could be more of a problem than shitty beer like Budweiser!21
- Too much alcohol of any kind will result in amphetamine-like effects that eventually lead to a full-on hypertensive crisis (see below).
RIMAs, because they are reversible, are supposed to have less of an effect on tyramine. I don’t know how that works - although the best guess I’ve read is because they barley inhibit enough MAO-A to be effective for depression, and don’t inhibit MAO-B, you shouldn’t build up enough tyramine to get into trouble. Fortunately for me people taking a RIMA like Aurorix / Manerix (moclobemide) are still advised to avoid high-tyramine foods, so I don’t have to go any further than that.
For a good collection on what you can’t eat and, more importantly, what you can, and how much of it, along with recipes to give you an idea of what a low-tyramine diet looks like, download a copy of Kathrynne Holden’s Meal Ideas and Menus: Avoiding High-tyramine Foods Made Easy. Another excellent resource is the University of Pittsburgh Medical Center’s MAOI diet facts - where foods are grouped into three categories: eat all you want, limit, and avoid. For an especially paranoid list of foods and other things you can’t consume, along with how much tyramine some of them have, see this page on Dr. Bob’s site.
Food sensitivity is highly variable with the combination of a person’s genetics, medication, and, especially with artisan/small-scale cheeses, cured meats and fermented products, the fermentation, curing, etc. process. Why? Because the tyramine content will be highly variable, as this letter from Kikkoman® will demonstrate. For example: soy sauce that comes in a packet shouldn’t be a problem, mainly because that isn’t real soy sauce22. In any event it means if you screw up and eat something you shouldn’t, it may not kill you. Actually, it probably won’t kill you. Most people (as many as three out of four) can have some23 of the forbidden foods without any problems. Think about it, people were taking Marsilid (iproniazid) and Marplan for TB and depression for a decade in the 1950s and 1960s before it killed someone. Do you think they were all avoiding Stilton, Marmite and kippers in the UK? Before there were warnings about doing so? Or Americans in the late 1950s & early 1960s were not eating corned beef or ham & Swiss sandwiches, salami, sauerkraut and the like daily? Or that people from both countries were not drinking beer on tap? Even if their doctors told them not to drink? People probably had bad, but not fatal reactions, and as many of the foods on the list contribute to high blood pressure anyway, a GP probably prescribed a
fun-free tasteless low-fat, low-salt, booze-free diet before stepping it up to another med. Because who ever heard of such a thing like foods messing with modern drugs?
Stahl thinks the dietary risks are overblown, as did others before him. The first deaths from tyramine-induced hypertensive crisis happened when high blood pressure and heart attacks were all the medical industry thought about, and thus imprinting “MAOIs + tyramine- or L-dopa-rich food = dead!”, so it makes sense that the tyramine/L-dopa problem is blown all out of proportion. Can more of the proscribed foods be consumed in moderation? While I think they probably can, I’ll still come down on the side of paranoia caution, and recommend avoiding old cheese and banana peels. But chocolate and sourdough bread? I’m fairly certain those are safe to eat in reasonable quantities. And small amounts of real soy sauce are probably safe. The safest course of action is to avoid whatever is on the piece of paper your doctor or pharmacist hands you. But it’s like food allergies/sensitivities. You won’t know if you have a “see a peanut and die” or “eat more than a few and need to spench” level of sensitivity until you try something.
No matter what your genetic make up is, you can still have too much dopamine and/or tyramine24. What happens if you end up with too much? The Cheese Effect/Reaction/Syndrome. I’m not making up that name25. It starts with a really bad headache. If you continue to accumulate tyramine (you can’t stop eating Reuben sandwiches with a nice pint of Guinness, e.g.) you’ll find yourself in a full-on hypertensive crisis (your blood pressure suddenly shot up to 180/120). In addition to the severe headache, the symptoms of a hypertensive crisis include:
- Neck stiffness or soreness
- Dilated pupils and sensitivity to light (photophobia)
- Blurred vision
- Confusion & anxiety
- Irregular heartbeat (palpitations, tachycardia or bradycardia)
- Shortness of breath
- Constricting chest pain
If those seem similar to the symptoms of a heart attack, you’re right. That’s because a hypertensive crisis can escalate to a heart attack and kill you. So you’ll have to find something else instead of fava beans and a good Chianti the next time you want to have a friend for dinner. After you stop taking an irreversible MAOI you still need to stay on a low-tyramine diet for at least two weeks, three to play it safe, after your last dose.
If you thought the dietary restrictions were a pain, get ready for all the drug-drug interactions! Drugs.com’s drug interactions checker has 470 major drug-drug interactions for Parnate (tranylcypromine), which is two fewer than amitriptyline (265) and warfarin (207) combined26. Most of the drug-drug interactions fall into two groups, those that can cause a hypertensive crisis as described above, and those that cause . Symptoms of serotonin syndrome include:
- Agitation or restlessness
- Dilated pupils
- Rapid heart rate
- High blood pressure
- Loss of muscle coordination or twitching muscles
- Muscle rigidity
- Heavy sweating
- Goose bumps
Anyone showing the following symptoms is in serious trouble. As in potentially life-threatening trouble:
- High fever
- Irregular heartbeat
While taking any other AD is pretty much considered off-limits when taking an MAOI, Stahl thinks you can get away with some TCAs, if both the MAOI and TCA are taken at low dosages and plasma levels are checked frequently. He also considers the same to be true for combining low dosages of MAOI with one of: an amphetamine, Ritalin (methylphenidate), or even tramadol for people are left with no other options. As in they failed ECT no other options. If you’re taking an MAOI, it’s a good idea to get a MedicAlert ID with that information on it in case you’re not able to tell anyone that you are when you really, really need to27. As with the drug-food interactions, you need to avoid taking all the meds that can kill you for two to three weeks after you stop taking an MAOI.
On top of all that, they must have some atrocious side effects, right? What else do they do? Make you lose all of your hair? Lose all interest in sex? Grow ears on your chest?
Actually, MAOIs side effects are pretty much the same as other ADs.
Surprisingly, for meds that have an intense positive effect on the “Big Three” neurotransmitters (serotonin, norepinephrine, and dopamine) involved in the monoamine hypothesis of depression (AKA the chemical imbalance theory), they tend to be less likely to make someone who is bipolar bouncing-off-the-ceiling manic than any other AD. The ones that affect dopamine (i.e. not the RIMAs) tend to offset most of the sexual side effects increasing serotonin causes, and increasing norepinephrine often enhances women’s libidos and/or sexual response. Boosting serotonin has annoying side effects (weight gain, sexual side effects) that are compensated for with more dopamine. Boosting norepinephrine, though, can have some nasty side effects, like an irregular heartbeat (arrhythmia), and
your the med’s choice of too low or too high blood pressure. If you think the former isn’t a problem, you haven’t had the experience of actually passing out and hitting the floor after standing up too quickly28.
Irreversible MAOIs have anticholinergic side effects:
- Anorexia (weight loss)
- Blurry vision
- Muscle weakness
- Sedation - exacerbating the effect from increasing serotonin
- Stasis of urine (fancy doctorese for urinary retention, or: sitting/standing there and nothing happens for what seems like half an hour)
- Sweating - exacerbating the effects of increased norepinephrine and dopamine
- Weight loss instead of weight gain * Not all side effects are bad.
- Conversely, can be bug, not feature, for some people.
MAOIs, especially Parnate (tranylcypromine), make nicotine more addictive. So if you use tobacco products, vape, or anything else with nicotine and are thinking about quitting, you should do so before starting an MAOI. MAOIs also have the potential for a discontinuation syndrome similar to SSRIs & SNRIs. Oddly enough it’s more likely to happen with irreversible MAOIs, where the reduction of serotonin and norepinephrine is a gradual process after you stop taking the med, than it is with a RIMA. This is probably because the irreversible MAOIs are doing more than just inhibiting MAO.
Before SSRIs hit the market, “poop out” was defined by some people who took MAOIs for longer than a year, even though blood platelet inhibition - which is the closest thing, short of an expensive PET or SPECT scan, to monitoring for therapeutic blood levels you get for MAOIs - was unchanged. Adding other meds - options are discussed in the articles for each med - usually don’t help, but raising the dosage often will. And while some people can tolerate dosages above the recommended limit, you can take only so much of any med. Once tachyphylaxis happens, the odds are raising the dosage is delaying the inevitable. As with SSRIs you can try the other MAOIs available to you, but the results will probably be the same. This seems to be much less of a problem with Aurorix / Manerix (moclobemide) and the Emsam Patch (selegiline transdermal system) than Marplan (isocarboxazid), Nardil (phenelzine), and Parnate (tranylcypromine). I don’t have any data about pirlindole / pirasidol. Since amphetamines rarely poop out and tobacco keeps its antidepressant and anxiolytic effects for decades29, I guess this problem has more to do either with the chemical structures of the older MAOIs, and/or they are just too freaking potent, than with MAO inhibition in general.
With potentially lethal drug-drug and drug-food interactions that can last for three weeks after you stop taking it, and a good chance they’ll stop working after only a year, who the hell wants to take these ancient meds30? If you’re reading this book for someone who is too depressed to do so for themself, my money is on that person. If you go to all the psych med rating and review sites, support group sites, and sites that aren’t about meds or conditions, but have a lot of people who are crazy and discuss meds anyway, you’ll find that the MAOIs consistently rate higher than all other ADs. Especially for forms of depression, anxiety, and the ever-popular combination of anxiety and depression, that don’t respond to anything else, in people who took one med after another that barely worked, didn’t work, or stopped working. After going through all that, a year or three of relief might be worth it before the waaaaay-off-label treatments and/or ECT.
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- Stahl, Stephen M. Stahl’s Essential Psychopharmacology: Neuroscientific Basis and Practical Applications (Essential Psychopharmacology Series) Fourth edition. Cambridge University Press 2013. ISBN: 978–1107686465
- Stahl, Stephen M. Prescriber’s Guide: Stahl’s Essential Psychopharmacology (Essential Psychopharmacology Series) Fifth edition. Cambridge University Press 2014. ISBN: 978–1107675025
- Virani, Adil S., K. Bezchlibnyk-Butler, and J. Jeffries Clinical Handbook of Psychotropic Drugs 20th edition. Hogrefe & Huber Publishers 1 July, 2013. ISBN: 978–0889374515
- Julien, Robert M. Ph.D, Claire D. Advokat, and Joseph Comaty Primer of Drug Action: A comprehensive guide to the actions, uses, and side effects of psychoactive drugs 12th edition. Worth Publishers 2011. ISBN: 978–1429233439
- Schatzberg, Alan F., Jonathan O. Cole, and Charles Debattista Manual of Clinical Psychopharmacology 7th Edition 2010–04–29. American Psychiatric Publishing, Inc. ISBN: 978–1585623778.
- Mosby’s Drug Consult 2007 (Generic Prescription Physician’s Reference Book Series) An imprint of Elsevier 2007. ISBN: 978–0323040587.
- Krantz, John C. Jr. and C. Jelleff Carr Pharmacological Principles of Medical Practice Fifth edition. Williams & Wilkins 1961. LCC Card Number: 58–6565.
- Ramsay, Rona R., and Dominic JB Hunter. “Interactions of D-amphetamine with the active site of monoamine oxidase-A.” InflammoPharmacology11.2 (2003): 127–133. Free full text at ResearchGate
- Kupiec, Thomas C., and Arvind K. Chaturvedi. “Stereochemical determination of selegiline metabolites in postmortem biological specimens.” FEDERAL AVIATION ADMINISTRATION OKLAHOMA CITY OK CIVIL AEROMEDICAL INST, 1997.
- Reynolds, G. P., J. D. Elsworth, K. Blau, M. Sandler, A. J. Lees, and G. M. Stern. “Deprenyl is metabolized to methamphetamine and amphetamine in man.” British journal of clinical pharmacology 6, no. 6 (1978): 542–544.
- Stahl, Stephen M. and Angela Felker. “Monoamine Oxidase Inhibitors: A Modern Guide to an Unrequited Class of Antidepressants.” CNS Spectrums 13 (2008): 647. Free full text at ResearchGate
- Schirmer, R. Heiner, Heike Adler, Marcus Pickhardt, and Eckhard Mandelkow. “Lest we forget you—methylene blue….” Neurobiology of aging 32, no. 12 (2011): 2325-e7. Free full text at Max Planck Research Unit for Structural Molecular Biology
- Sandler, M, M A Reveley, and V Glover. “Human Platelet Monoamine Oxidase Activity in Health and Disease: A Review.” Journal of Clinical Pathology 34.3 (1981): 292–302.
- Targum, Steven D. “Identification and Treatment of Antidepressant Tachyphylaxis.” Innovations in Clinical Neuroscience 11.3–4 (2014): 24–28.
- Mann, J. John. “Loss of antidepressant effect with long-term monoamine oxidase inhibitor treatment without loss of monoamine oxidase inhibition.” Journal of clinical psychopharmacology 3.6 (1983): 363–365.
- Jefferson, James W. “Who put the tyramine in Mrs. Murphy’s fava bean?.” The Journal of clinical psychiatry 69.8 (2008): 1–478.
- Grady, Meghan M., and Stephen M. Stahl. “Practical guide for prescribing MAOIs: debunking myths and removing barriers.” CNS spectrums 17.01 (2012): 2–10. Free full text at onlinedigeditions.com
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They were treating people for tuberculosis with an early version of Marplan - iproniazid - in the US in the early 1950s. The ur-version of both meds - isoniazid - was developed in Germany in 1912, and could have been treating TB for a long-ass time. Too bad no one paid any attention to it. Methylene blue has been around since the 19th century. The now-discontinued iproniazid was on the market as the first modern antidepressant in 1952. It was causing people's livers to explode, and that problem happened more often with its original use - the treatment of tuberculosis. The usual mix of poor med compliance and bacterial evolution meant ever-increasing dosages were required. The drug-food interactions were problems with iproniazid mainly at the higher dosages, much like selective MAOIs.
“Antidepressants” in that they are a brand new class of drugs, and not one repurposed to treat mental illness, as amphetamines, opiates, and barbiturates (originally, and still to this day, used as antiepileptic drugs) were.
"Class" because methylene blue was just one drug - as isoniazid was ignored - and one drug by itself is only a class in the world of.
2 Far more common than when any AD exacerbates depression. You can usually file that under “makes symptoms worse”, which is a potential side effect of every drug on the planet, and not just crazy meds. Aspirin can make your headache worse and possibly make it more likely for you to have a heart attack, which is one reason why you shouldn't just start chewing Baby Bayer every day without talking to a doctor first.
3 I.e. they've been feeding it to depressed rats (http://www.ncbi.nlm.nih.gov/pubmed/21624345) and anxious mice (http://www.ncbi.nlm.nih.gov/pubmed/23021974) and so far like what they see.
Unlike other antibiotics that can make you go batshit manic, even if you aren't bipolar, at least they know why that happens with Zyvox (linezolid). With Cipro who the hell knows why? My guess is it has something to do with the recently-discovered immune system pathways into the brain. Whatever the reason, if it means an entirely new class of ADs that work on in a truly novel way, I'm all for it.
4 If I found myself in that situation I'd just say, "Fuck it." And would, indeed, fuck it by flying to Phuket and maxing out my credit cards on Lagavulin and hookers.
5 Do I ever love that the US government funded studies in the 21st century about the neuroprotective effects of tobacco smoking regarding PD. Eventually someone thought, "Wait a minute. We shouldn't be doing that. We have to show that smoking is 100% bad, not 99% bad!" So they funded this study at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206154/. The results? If it's really easy to quit smoking you might already have PD. Even in your 30s. Oooops!!!! That's what happens when you use science to justify an absolutist position. While the results didn't match what they set out to do, they still tried to bury the previous studies by putting neuroprotective in quotes and ignoring the evidence that tobacco smoke is an MAO-B inhibitor and focused entirely on its effects on ACH. Because dopamine has absolutely nothing to do with PD, right?
6 Although this was before the FDA existed and there was such a thing as approvals. Hence it technically wasn't the first real AD. But laudanum, morphine, and cocaine where prescribed as ADs before Methylene blue. Are those are the old-fashioned, natural remedies we should be trying? Ask Jim Cruise or Tom Carrey. Those guys seem to know all there is to know about medicine.
7 No, really, that's what it's used for. See for yourself at: http://online.liebertpub.com/doi/abs/10.1089/1092642041255504?journalCode=lap. Methylene blue gives you blue balls. It's used on other endocrine glands as well.
8 Don't try that at home. Touching the sort of methylene blue you can buy on Amazon or at a hobby shop isn't a good idea as it isn't the same pretty blue as you'd get when you go in for surgery. Plus: the kind used to dye stuff is irritating to skin. And you probably don't want to use methylene blue as a hobby dye if you are using an MAOI, just in case you do touch it, as you can absorb it through your skin.
9 Technically when a substance is transformed by enzymes for another use, like breaking down food for energy, but not transformed into an active metabolite that does whatever the parent substance also does, or is supposed to do, it's called catabolism.
When neurotransmitters, etc. are broken down by MAO they're being catabolized, not metabolized, because your brain is getting energy from the transformation. Once they've done their job as messengers, neurotransmitters are food. I use metabolize in this article because, other than your brain getting some energy out of the conversion, and the resulting substance sometimes being another neurotransmitter (dopamine becomes norepinephrine, e.g.) instead of a metabolite that gets passed to your bloodstream on its way to getting flushed, there's no real difference between the catabolism and metabolism of a neurotransmitter, and consistency of terminology seems more important. If you want to be more precise, take a college course.
10 There's also MAO-A in semen, so anyone who has had the misfortune of using a blacklight in a motel room knows just how fucking long this list can get.
11 But what won't he throw at TRD? I swear, practically every med in his Prescriber's Guide has TRD listed as an off-label use.
12 In the US that's 3 out of (depending how you count) 4 or 5.
13 In the US “some” means “most”.
14 Probably for good reason. I can find a lot of papers on it, but nowhere near as many as I thought there would be. There are still a hell of a lot more published on phenylethylamine's association with mood disorders (the PEA Hypothesis) than the pharmacokinetics and binding profiles of all the TCAs combined, and everyone accepts those numbers as gospel. One test on a couple of rats to get the binding profile for dosulepin? Works for wikipedia, most researchers, and the whole damn interwebs!
But I can understand why legitimate psychopharmacologists wouldn't want to touch it. Phenylethylamine is a trace amine, so it doesn't take much to tweak it one way or the other. You need to be extremely careful, because another aspect of the PEA Hypothesis is that too much of it contributes to schizophrenia. Another problem, aside from phenylethylamine and its precursor L-phenylalanine being readily available as supplements, is that phenylethylamine is an ingredient in some DIY amphetamine recipes.
15 As with prodrugs, a protoxin is something that gets metabolized from an inert substance into an active one, in this case a toxin.
16 You're going to have to wait for me to go into the pharmacological detail on the differences between the two, so you're on your own for now. Briefly: the d-enantiomer of amphetamine is way more potent than the l-enantiomer But that isn't the case with every drug. Levorotary and dextrorotary merely describe how the molecules twist polarized light you shine through them. Really.
17 I don't know what that dosage is, sorry. As those meds are used as add-ons to meds for Parkinson's, it's unlikely you need to worry about it. I hope.
18 It's usually the precursor L-dopa that's in food, but dopamine is just L-dopa with a few atoms stripped off of it. And, yes, many people can eat their way out of mild-to-moderate depression by eating many of the foods people who take MAOIs should avoid. I lived on a diet rich in broad beans and fermented foods, especially fermented soy products, for a long time and had way more problems with mania and seizures than I did with depression, and that was before I ever heard or read the word "dopamine," let alone knew about how it could trigger mania and lower my seizure threshold through the floor. If your depression is mild enough to treat with food, why the hell are you reading this site?
19 I honestly wouldn't eat it myself. Unless a woman from a part of the world were such a dish is common were to cook it just for me. I'll try all sorts of weird food (the extremely delicious durian, e.g.), but for some things I'll need more encouragement.
20 It should be a given that anyone with any form of brain cooties should never, ever go near a bottle of Absinthe. Leave that for people who, for whatever stupid reason, want to feel what it's like to be crazy. Take it from the guy who made his own when it was still illegal.
Liqueurs like Vermouth and Pernod started out as ingredients of Absinthe, added to mask the incredibly vile taste of wormwood extract distilate.
21 Probably because the only decent near-beers, like Kaliber, are brewed and distributed like real beer.
22 Since moving to East Jesus Montana, where Dinty Moore is considered gourmet chow, my standards have lowered considerably in the last 10 years. Nevertheless I still remember what it's like to be an insufferable food snob prior to developing allergies to everything I used to eat. Like all such people deserve. Any soy sauce that isn't fermented with koji in a wooden vat - OK the vats don't need to be made of wood, that gives you an idea of much of a food snob I used to be, but fermented with koji, or the Japanese equivalent of sourdough - which is well over 90% of the 'soy sauce' sold in the world and everything you'll find in a packet, isn't really tamari or shoyu, and is probably safe to consume in reasonable amounts if you're on an MAOI.
I once worked at Kikkoman® on a death march project installing software I knew wouldn't work and everyone there knew wouldn't work. Why did they buy it? Because Kikkoman® HQ in Japan had an arrangement with the Japanese-based owners of the company for which I worked, that's why. To make things worse they were in the middle of moving their head office from SF to Atlanta. Anyway, I can verify that Kikkoman® was brewed the traditional way 30 years ago and tasted like the real thing the last time I had some about 15 years ago. So it's unlikely they're lying on their website or in that letter, and is the only real soy sauce you're going to find in most American grocery stores (like the one closest to where I live - if you consider 16 miles "close" - in a town with a population hovering around 1,000), thus need to be careful about if you're taking an MAOI.
They may have been / still be dicks when it comes to managing the company, but they don't mess around with their core product.
23 "Some" being defined as either a subset of the foods, a small amount of all of them, or a small amount of a subset of them. There's no way of telling in advance.
24 Theoretically you could get too much without taking an MAOI, especially if you were whatever phenotype that was the MAO equivalent of a poor metabolizer.
25 The Cheese Effect/Reaction/Syndrome got its names from the early days of MAOIs when people taking them consistently got headaches, and, with higher dosages of the drugs and/or greater intake of cheese, more severe symptoms.
26 I was tempted to build an interactions list of all three meds, but didn't. I'm afraid doing so might break something.
27 I think it's a good idea for anyone with brain cooties to get a MedicAlert ID - from the MedicAlert Foundation (http://www.medicalert.org/), as every First Responder in North America has them on speed dial. You never know when you won't be able to communicate and someone should know why you aren't cooperating when you look conscious.
28 I think watching it happen to someone else is worse. Especially that one time you don't catch them.
29 Or for however long you live.
30 Even by antiepileptic drug standards - the first truly effective one is from the 1850s - I think a class of meds with its first member created in 1890 counts as ancient.
Monoanime Oxidase Inhibitor (MAOI) Antidepressants by Jerod Poore is copyright © 2010 Jerod Poore
|Last modified on Thursday, 05 May, 2016 at 17:39:24 by JerodPoore||Page Author: Jerod Poore||Date created: 26 November 2010|
All drug names are the trademarks of someone else. Look on the appropriate PI sheets or ask Google who the owners are. The way pharmaceutical companies buy each other and swap products like Monopoly™ real estate, the ownership of any trademarks may have changed without my noticing.
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Almost all of the material on this site is by Jerod Poore and is copyright © 2003, 2004, 2005, 2006, 2007, 2008, 2009, 2010, 2011, 2012, 2013, 2014, 2015, and 2016 Jerod Poore. Except, of course, the PI sheets - those are the property of the drug companies who developed the drugs the sheets are about - and any documents that are written by other people which may be posted to this site will remain the property of the original authors. You cannot reproduce this page or any other material on this site outside of the boundaries of fair use copying without the express permission of the copyright holder. That’s usually me, so just ask first. That means if want to print out a few pages to take to your doctor, therapist, counselor, support group, non-understanding family members or something like that - then that’s OK to just do. Go for it! Please. As long as you include this copyright notice and something along the lines of following disclaimer, I’m usually cool with it.
All rights reserved. No warranty is expressed or implied in this information. Consult one or more doctors and/or pharmacists before taking, or changing how you take any neurological and/or psychiatric medication. Your mileage may vary. What happened to us won’t necessarily happen to you. If you still have questions about a medication or condition that were not answered on any of the pages you read, please ask them on Crazy Talk: the Crazymeds Forum.
The information on Crazymeds pertains to and is intended for adults. While some information about children and adolescents is occasionally presented (e.g. US FDA approvals), pediatric-specific data such as dosages, side effects, off-label applications, etc. are rarely included in the articles on drugs or discussed on the forum. If you are looking for information regarding meds for children you’ll have to go somewhere else. Plus we are big pottymouths and talk about S-E-X a lot.
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Nobody on this site is a doctor, a therapist, or a pharmacist. We don’t portray them either here or on TV. Only doctors can diagnose and treat an illness. While it’s not as bad as it used to be, some doctors still get pissed off by patients who know too much about medications, so tread lightly when and where appropriate. Diagnosing yourself from a website is like defending yourself in court, you suddenly have a fool for a doctor. Don’t be a cyberchondriac, thinking you have every disease you see a website about, or that you’ll get every side effect from every medication1. Self-prescribing is as dangerous as buying meds from fraudulent online pharmacies that promise you medications without prescriptions.
All information on this site has been obtained from the medications’ product information / summary of product characteristic (PI/SPC) sheets and/or medication guides - which is all you get from sites like WebMD, RxList,
NAMBLA NAMI, etc., the sources that are referenced throughout the site, our personal experience and the experiences family, friends, and what people have reported on various reputable sites all over teh intergoogles. As such the information presented here is not intended as a substitute for real medical advice from your real doctor, just a compliment to it. You should never, ever, replace what a real doctor tells you with something from a website on the Internet. The farthest you should ever take it is getting a second opinion from another real doctor. Educate yourself - always read the PI/SPC sheet or medication guide/patient information leaflet (PIL) that comes with your medications and never ever throw them away. OK, you can throw away duplicate copies, but keep at least one, as that’s your proof of purchase of having taken a med in case a doctor doubts your medical history. Plus they take up less space than a bottle, although keeping one inside of a pill bottle is even better.
Crazymeds is not responsible for the content of sites we provide links to. We like them, or they’re paid advertisements, or they’re something else we think you should read to help you make an informed decision about a particular med. Sometimes they’re more than one of those things. But what’s on those sites is their business, not ours.
Crazymeds is optimized for ridiculously large screens and browsers that don’t block ads. I use Firefox and Chrome, running under Windows 72. On a computer that sits on top of my desk. With a 23 inch monitor. Hey, at least you can make the text larger or smaller by clicking on the + or - buttons in the upper right hand corner. If you have Java enabled. Like 99% of the websites on the planet, Crazymeds is hosted on domain running an open source operating system with a variety of open source applications, including the software used to display what you’ve been reading. As such Crazymeds is not responsible for whatever weird shit your browser does or does not do when you read this site3.
Crazymeds now uses a secure server, but it is not so secure that you can discuss anything having to do with nuclear power facilities, air traffic control systems, aircraft navigation systems, weapons control systems, or any other system requiring failsafe operation whose failure could lead to injury, death or environmental damage. Just so you know. So if you’re mentally interesting and have a job that deals with that sort of thing, talk about said job elsewhere. Otherwise feel free to discuss your meds and brain cooties.
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1 While there are plenty of books to help you with hypochondria, for some reason there’s not much in the way of websites. Then again, staying off of the Internet is a large part of curing/managing the disorder.
2 Remember kids, Microsloth operating systems are like TOS Star Trek movies with in that every other one sucks way, way more. With TOS Star Trek movies you don’t want to bother watching the odd-numbered ones. With Microsloth OS you don’t want to buy and install the even-numbered ones. Anyone who remembers ME and Vista knows what I mean.
3 Have I mentioned how open source operating systems for commercial applications is one of the dumbest ideas in the history of dumb ideas?* I don’t even need my big-ass rant any more. Heartbleed has made my case for me. And that’s just the one that got all the media attention. The very nature of an open source operating system makes security as much of an illusion as anonymity on teh Intergoogles. Before you flip out too much: the domain Crazymeds is hosted on uses a version of SSL that is not affected by the Heartbleed bug. That’s one of the many reasons why I pay a lot of money and keep this site on Lunarpages.
* Yes, I know I’m using open source browsers. I also test the site using the now-defunct IE and Safari browsers. Their popularity - and superiority - killed IE and Safari, so that’s why I rely on the open source browsers. It’s like brand vs. generic meds. Sometimes the generic is better than the brand.