From PsychonautWiki
Jump to: navigation, search

Monoamine oxidase inhibitors (also known as MAOIs) are a class of drugs which inhibit the activity of the monoamine oxidase enzyme family. They have a long history of use as medications prescribed for the treatment of depression and are particularly effective in treating atypical depression.[1] They are also used in the treatment of Parkinson's disease and several other disorders.[citation needed]

Mechanism of action

MAOIs act by inhibiting the activity of monoamine oxidase, preventing the breakdown of monoamine neurotransmitters and thereby increasing their availability. There are two isoforms of monoamine oxidase, MAO-A and MAO-B.

MAOA preferentially deaminates norepinephrine (NE), serotonin (5-HT) and epinephrine (E), while MAOB preferentially deaminates benzylamine and phenylethylamine (PEA). Dopamine (DA) and tyramine are equally catabolized by both forms of MAO.[2]


Further information: RIMA

The early MAOIs inhibit monoamine oxidase irreversibly, meaning they permanently deactivate it and the enzyme cannot function until it has been replaced by the body, which can take about two weeks. A few newer MAOIs, known as reversible inhibitors of monoamine oxidase A (RIMAs), are reversible. This means that they are able to detach from the enzyme to facilitate usual catabolism of the substrate.[citation needed]

Poly drug use


Skull and crossbones darktextred2.png

Check (also with independent research) if your MAOIs also inhibits other substances, most MAOIs are also cytochrome P450 inhibitors (and tyramine and a lot of substances are cytochrome P450 substrates) and some are acetylcholinesterase inhibitors (AChEIs) in addition for example!

Substances that inhibits the cytochrome P450 system’s ability to metabolize certain drugs, leading to an overall increase in processing times. When the CYP450 system is impacted in this way, it leads to higher levels of certain drugs in your system at one time. This can cause unwanted side effects, and sometimes, an overdose.


Tyramine causes hypertensive crises after MAO inhibition aka the "cheese effect" or "cheese crisis". Using a MAO inhibitor (MAOI), the intake of approximately 10 to 25 mg of tyramine is required for a severe reaction compared to 6 to 10 mg for a mild reaction.[3] Tyramine rich food should also be avoided by people prone to headache and migraine.

Psychoactive substances

Naturally occurring sources with tyramine.

Specie Tyramine (mg/gram of alive plant)[6]
L. williamsii 0.5 - 1
L. jourdaniana 0.6
L. diffusa 0.1
L. fricii 0.1
L. koehresii 0.1


Specific foods with high amounts of tyramine:[7][8][9]

  • Aged cheese (gouda, camembert, cheddar) -- Few cheeses (even. 'mature' cheeses) contain more than 25 mg of tyramine in 100 grams.[10] However, Stilton (a blue cheese) contains up to 217 mg tyramine per 100 grams.[7]
  • Aged, smoked or pickled meats
  • Aged or fermented soy and yeast products (soy sauce, teriyaki sauce, home baked yeast bread, sourdough bread)
  • Overripe fruits
  • High amounts of nuts

Tyramine formation has been associated with bacterial contamination of foods or temperature abuse conditions, but can also occur as a side effect of generally desired ripening processes.[8] Tyramine is a breakdown product of the amino acid L-tyrosine.

Psychoactive substances

The MAOIs are well-known for their numerous drug interactions, including the following kinds of substances:

  • Substances that are metabolized by monoamine oxidase, as they can be boosted by up to several-fold
  • Substances that increase serotonin, noradrenaline, or dopamine activity as too much of any of these neurotransmitters can result in severe acute consequences including serotonin syndrome, hypertensive crisis, and psychosis.
  • Long-term use with psychoactive substances that interact with MAOIs must be gradually discontinued to avoid discontinuation syndrome. Examples:
    • Cannabinoids: Cannabinoids are lipophilic. For example, THC has been detected in heavy cannabis users after 77 days of drug abstinence (Ellis et al., 1985).[11]
    • SSRIs: Because of the extended half-life of norfluoxetine, a minimum of 5 weeks should lapse between stopping fluoxetine (20 mg/day) and starting an MAOI. With higher doses the interval should be longer. For example, a serotonin syndrome was reported following a 6-weeks washout in a patient who had been given fluoxetine (80 mg/day).[12]

By chemicals

By pharmacolotherapy

  • Antibiotics
    • Linezolid
  • Essential nutrients
    • Choline
      • Certain cholinergics (see "Cholinergics")
  • Local and general anesthetic

List of MAOIs

Nonselective MAO-A and MAO-B inhibitors

  • Naturally occurring sources
Natural occuring source Chemical MAOI
Banisteriopsis caapi (ayahuasca, caapi or yagé) (−)-epicatechin[27] MAO-B
Banisteriopsis caapi (ayahuasca, caapi or yagé) (−)-procyanidins[27] MAO-B
Banisteriopsis caapi (ayahuasca, caapi or yagé) Harmaline[27] RIMA
Banisteriopsis caapi (ayahuasca, caapi or yagé) Harmine[27] MAO-A, MAO-B
Black pepper (Piper nigrum) Piperine[28] MAO-A, MAO-B
Cannabis, Cannabis extract MAO-A, MAO-B[29]
Cocoa bean (from Theobroma cacao) Caffeine[30] MAO-A, MAO-B[31]
Cocoa bean (from Theobroma cacao) Catechin[32][33] MAO-B[34]
Cocoa bean (from Theobroma cacao) Epicatechin[35][33] MAO-B[34]
Cocoa bean (from Theobroma cacao) Tetrahydro-beta-carbolines[36]
Coffee (Coffea arabica, Coffea canephora) Caffeine MAO-A, MAO-B[31]
Coffee (Coffea arabica, Coffea canephora) Harman[37] MAO-A
Coffee (Coffea arabica, Coffea canephora) Norharman[37] MAO-A
Liquorice/licorice (Glycyrrhiza Glabra) Isoliquiritigenin[38] MAO-A, MAO-B
Liquorice/licorice (Glycyrrhiza Glabra) Liquiritigenin[38] MAO-A, MAO-B
Long pepper (Piper longum) Piperine[28] MAO-A, MAO-B
Nutmeg (Myristica fragrans) Kaempferol[39] MAO-A
Nutmeg (Myristica fragrans) Myristicin MAO-A, MAO-B?[40]
Nutmeg (Myristica fragrans) Quercetin[41] MAO-A
Passionflower (Passiflora incarnata), weak MAOI Apigenin MAO-A
Passionflower (Passiflora incarnata), weak MAOI Harmine MAO-A, MAO-B
Passionflower (Passiflora incarnata), weak MAOI Kaempferol MAO-A
Passionflower (Passiflora incarnata), weak MAOI Quercetin MAO-A
Rhodiola rosea MAO-A, MAO-B[42]
Syrian rue (Peganum harmala) Desoxypeganine[43] MAO-A[44]
Syrian rue (Peganum harmala) Harmaline RIMA
Syrian rue (Peganum harmala) Harman MAO-A
Syrian rue (Peganum harmala) Harmine MAO-A, MAO-B
Tobacco 1,2,3,4-tetrahydro-b-carboline (THbC)[29] MAO-A, MAO-B
Tobacco 1,2,3,4-tetrahydroisoquinoline[29] MAO-A, MAO-B
Tobacco Harman[45] MAO-A
Tobacco Norharman[45] MAO-B
  • Psychedelics
  • Pharmaceuticals
    • Hydrazine (antidepressant)
      • Isocarboxazid (Marplan)
      • Nialamide (Niamid)
      • Phenelzine (Nardil, Nardelzine)
      • Hydracarbazine
    • Non-hydrazines
      • Tranylcypromine (Parnate, Jatrosom)

Selective MAO-A inhibitors

For safer MAO-A inhibitors, see RIMA.
  • Naturally occurring sources
    • Yohimbe (Pausinystalia johimbe): Yohimbine[47]
  • Psychedelics
  • Pharmaceuticals
    • Bifemelane (Alnert, Celeport) (available in Japan)
    • Isocarboxazid (common brand name Marplan)
    • Phenelzine (common brand name Nardil)
    • Pirlindole (Pirazidol) (available in Russia)
    • Tranylcypromine (common brand name Parnate)

Selective MAO-B inhibitors

  • Naturally occurring sources
    • Betel nut (Areca catechu): MAO-A inhibitor.[50][29]
    • Kava (Piper methysticum): Kava pyrones. The order of potency was desmethoxyyangonin > (+/-)-methysticin > yangonin > (+/-)-dihydromethysticin > (+/-)- dihydrokavain > (+/-)-kavain.[51]
    • Olives (Olea europaea), fresh, olive leaf extract: The selective MAO-B inhibitor hydroxytyrosol.[52]
  • Pharmaceuticals
    • Rasagiline (Azilect)
    • Selegiline (Deprenyl, Eldepryl, Emsam, Zelapar)
    • Safinamide (Xadago)


  • Naturally occurring sources
    • Mimosa tenuiflora: As there have been no MAO inhibitors detected in M. tenuiflora, there is ongoing interest into how yurema exerts its visionary effects.[53]

See also

External links


Question book-new.svg

This article does not cite enough references.

You can help by adding some.

  1. Cristancho, Mario. "Atypical Depression in the 21st Century: Diagnostic and Treatment Issues". Psychiatric Times. Retrieved 23 November 2013.
  5. Crosby, D.M.; McLaughlin, J.L. (Dec 1973). "Cactus Alkaloids. XIX Crystallization of Mescaline HCl and 3-Methoxytyramine HCl from Trichocereus panchanoi" (PDF). Lloydia and the Journal of Natural Products. 36 (4): 416–418. PMID 4773270. Retrieved 13 December 2013. 
  6. Grym, Rudolf (1997). Rod/Die Gattung Lophophora. Bratislava: Vydavateľstvo Roman Staník. ISBN 80-900933-9-6. (The book features an appendix on Lophophora chemistry by Dr Roman Štarha.)
  7. 7.0 7.1
  8. 8.0 8.1
  9. McCabe-Sellers BJ, Staggs CG, and Bogle ML. Tyramine in foods and monoamine oxidase inhibitor drugs: A crossroad where medicine, nutrition, pharmacy and food industry converge; J Food Comp Anal. 2006; 19:S58. |
  12. Principles and Practice of Psychopharmacotherapy, page 250
  13. 13.0 13.1
  15. 15.0 15.1 15.2
  18. Russo EB, Burnett A, Hall B, Parker KK (August 2005). "Agonistic properties of cannabidiol at 5-HT1a receptors". Neurochemical Research. 30 (8): 1037–43. doi:10.1007/s11064-005-6978-1. PMID 16258853. 
  19. Seeman P, Guan HC, Hirbec H (2009). "Dopamine D2High receptors stimulated by phencyclidines, lysergic acid diethylamide, salvinorin A, and modafinil". Synapse 63 (8): 698–704. doi:10.1002/syn.20647. Template:PMID.
  23. 23.0 23.1 23.2
  27. 27.0 27.1 27.2 27.3
  28. 28.0 28.1
  29. 29.0 29.1 29.2 29.3
  31. 31.0 31.1
  33. 33.0 33.1
  34. 34.0 34.1
  37. 37.0 37.1
  38. 38.0 38.1
  45. 45.0 45.1
  46. 46.0 46.1
  48. 48.0 48.1
  52.** Tea (Camellia sinensis), black tea, green tea, white tea, oolong tea: The selective MAO-B inhibitors catechin, and epicatechin /?tool=pmcentrez