# Tyramine
**Tyramine** (4-hydroxyphenethylamine; also called para-tyramine, mydrial, or uteramin) is a naturally occurring monoamine compound and trace amine produced by decarboxylation of the amino acid tyrosine.[1](https://pubchem.ncbi.nlm.nih.gov/compound/5610) It is found in fermented, aged, and ripened protein-rich foods, acts as an indirect sympathomimetic that promotes the release of noradrenaline, and is the cause of the hypertensive "cheese effect" seen when tyramine-rich foods are eaten by people taking monoamine oxidase inhibitors (MAOIs).[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC6831736/) • [3](https://pmc.ncbi.nlm.nih.gov/articles/PMC1760741/)
| Key fact | Detail |
|---|---|
| Identity | 4-(2-aminoethyl)phenol; molecular formula C8H11NO; molecular weight 137.18 g/mol; CAS 51-67-2[1](https://pubchem.ncbi.nlm.nih.gov/compound/5610) |
| Origin | Formed by decarboxylation of tyrosine, both endogenously and by bacterial tyrosine decarboxylase (TDC) enzymes in food[1](https://pubchem.ncbi.nlm.nih.gov/compound/5610) • [4](https://pubmed.ncbi.nlm.nih.gov/22369263/) |
| Classification | A trace amine, present at much lower concentrations in the central nervous system than the classical biogenic amines[5](https://pubmed.ncbi.nlm.nih.gov/27092049/) |
| Main receptor | An endogenous agonist of trace amine-associated receptor 1 (TAAR1), a G protein-coupled receptor that couples to Gαs and stimulates cAMP production[5](https://pubmed.ncbi.nlm.nih.gov/27092049/) • [6](https://pmc.ncbi.nlm.nih.gov/articles/PMC4820462/) |
| Metabolism | Inactivated mainly by monoamine oxidase (MAO-A and MAO-B); trace amine half-lives are on the order of 30 seconds[7](https://pmc.ncbi.nlm.nih.gov/articles/PMC2014643/) |
| Food risk with MAOIs | With MAO inhibition, roughly 6 to 10 mg of tyramine can trigger a mild pressor reaction and 10 to 25 mg a severe reaction[8](https://www.fao.org/fileadmin/user_upload/agns/pdf/FAO-WHO_Expert_Meeting_Histamine.pdf) |
| Typical food levels | In beer, tyramine formation ranged from 8 to almost 30 mg/L in one study, tracking lactic acid bacteria counts[9](https://pubmed.ncbi.nlm.nih.gov/31159007/) |
## Chemistry and biosynthesis
Tyramine is a primary amino compound, formally obtained by decarboxylation of tyrosine, with the IUPAC name 4-(2-aminoethyl)phenol.[1](https://pubchem.ncbi.nlm.nih.gov/compound/5610) It is listed by ChEBI as a neurotransmitter, a cholinesterase inhibitor, and a metabolite of humans, mice, and *Escherichia coli*.[1](https://pubchem.ncbi.nlm.nih.gov/compound/5610)
In food, tyramine is generated by decarboxylation of free tyrosine through tyrosine decarboxylase (TDC) enzymes derived from bacteria present in the food.[4](https://pubmed.ncbi.nlm.nih.gov/22369263/) Bacterial TDC enzymes have been unequivocally identified and characterized only in [Gram-positive bacteria](https://www.edgepedia.org/gram-positive-bacteria), especially lactic acid bacteria, and the pyridoxal phosphate-dependent genes encoding them (*tyrDC*) appear in a similar genetic organization across several species, suggesting a common origin in a single mobile genetic element.[4](https://pubmed.ncbi.nlm.nih.gov/22369263/) The same enzymes can decarboxylate phenylalanine to produce 2-phenylethylamine.[4](https://pubmed.ncbi.nlm.nih.gov/22369263/) Formation depends on the availability of tyrosine in the food, the presence of tyramine-producing bacteria, environmental pH, and salt content, and any food containing free tyrosine is subject to tyramine formation under poor sanitation, temperature abuse, or extended storage.[10](https://pubmed.ncbi.nlm.nih.gov/30165672/) • [4](https://pubmed.ncbi.nlm.nih.gov/22369263/) Even within a species such as *Enterococcus faecalis* or *E. faecium*, decarboxylating potential varies greatly between strains, so food safety implications are strain-dependent.[11](https://pubmed.ncbi.nlm.nih.gov/25914676/)
## Occurrence in food
Fermentation provides a particularly good source of tyramine in human nutrition, and the diet is the primary source of physiologically relevant tyramine concentrations in humans.[10](https://pubmed.ncbi.nlm.nih.gov/30165672/) Foods that have undergone aging contain relatively large amounts, including aged cheeses, sausages, salami, sauerkraut, and tap beer.[12](https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/021641S008_MedR_P1.pdf) Most foods contain negligible amounts or no tyramine, while a few products may contain large amounts.[13](https://www.accessdata.fda.gov/drugsatfda_docs/label/2006/021708s000_021336s000lbl.pdf)
Quantitative work illustrates how production conditions control levels. In a study of beer brewing, tyramine formation varied from 8 to almost 30 mg/L and showed a significant positive relationship with lactic acid bacteria counts: counts below 4 × 103 CFU/mL produced little tyramine, counts of 1 × 104 to 1 × 105 CFU/mL corresponded to 5 to 15 mg/L, and counts above 1 × 105 CFU/mL corresponded to 15 to 25 mg/L. The bacteria isolated were *Pediococcus* species, and washing brewer's yeast with phosphoric acid reduced tyramine levels in the final product.[9](https://pubmed.ncbi.nlm.nih.gov/31159007/) Modern food production and hygiene standards have produced large reductions in tyramine concentrations in most foodstuffs and beverages, including many cheeses.[14](https://pmc.ncbi.nlm.nih.gov/articles/PMC9172554/)
## Physiology and receptors
Tyramine belongs to the trace amines, a group of endogenous amines classically comprising β-phenylethylamine, p-tyramine, tryptamine, p-octopamine, and some of their metabolites, named for their low tissue levels in mammals.[15](https://pubmed.ncbi.nlm.nih.gov/29941461/) In rat brain, whole-tissue p-tyramine concentrations have been estimated at 1 to 102 nM, varying between brain regions, and trace amines are metabolized rapidly, with half-lives on the order of 30 seconds.[7](https://pmc.ncbi.nlm.nih.gov/articles/PMC2014643/) Unlike most trace amines, p-tyramine appears to be stored in synaptic vesicles.[7](https://pmc.ncbi.nlm.nih.gov/articles/PMC2014643/)
The discovery in 2001 of the trace amine-associated receptor 1 (TAAR1), independently by the groups of Borowsky and of Bunzow, gave tyramine a defined molecular target: the receptor stimulates cAMP production when exposed to p-tyramine or β-phenylethylamine.[7](https://pmc.ncbi.nlm.nih.gov/articles/PMC2014643/) Among the trace amines, β-phenylethylamine and tyramine are the most potent activators of TAAR1, with β-phenylethylamine more potent at human and mouse TAAR1 and the reverse at rat TAAR1.[6](https://pmc.ncbi.nlm.nih.gov/articles/PMC4820462/) TAAR1 acts in the brain as a rheostat of dopaminergic, glutamatergic, and serotonergic neurotransmission, and in the periphery it regulates nutrient-induced hormone secretion.[15](https://pubmed.ncbi.nlm.nih.gov/29941461/) Tyramine also acts independently of TAAR1 in some settings; in mouse midbrain dopamine neurons, tyramine and β-phenylethylamine reversibly reduced D2 autoreceptor-mediated G-protein-gated inwardly rectifying K+ channel currents by acting at sites other than TAAR1.[6](https://pmc.ncbi.nlm.nih.gov/articles/PMC4820462/)
## The tyramine pressor response and the cheese effect
Tyramine functions as an indirect sympathomimetic by promoting the release of noradrenaline from synaptic vesicles, producing a measurable rise in blood pressure known as the tyramine pressor response.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC6831736/) Normally, dietary tyramine is extensively inactivated on first pass by MAO in the gut wall and then the liver; MAO-A is the predominant peripheral isoform and about 90% of intestinal MAO is the A isoform.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC1760741/) • [16](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515917/) When MAO-A is inhibited, greatly increased amounts of tyramine enter the systemic circulation and then adrenergic neurons, raising noradrenaline release and blood pressure.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC1760741/)
This potentiation is the "cheese effect" or "cheese reaction", first recognized as a pressor effect of dietary origin in patients taking non-selective MAOIs such as phenelzine and [tranylcypromine](https://www.edgepedia.org/tranylcypromine).[16](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515917/) • [2](https://pmc.ncbi.nlm.nih.gov/articles/PMC6831736/) In combination with an MAOI, an intake of approximately 10 to 25 mg of tyramine is required for a severe reaction compared with 6 to 10 mg for a mild reaction.[8](https://www.fao.org/fileadmin/user_upload/agns/pdf/FAO-WHO_Expert_Meeting_Histamine.pdf) The crisis can include headache, migraine, nausea, vomiting, and, in severe cases, end-organ damage, intracerebral hemorrhage, and death.[2](https://pmc.ncbi.nlm.nih.gov/articles/PMC6831736/) The consistent observation of this reaction with the selective MAO-A inhibitor clorgyline forced its abandonment as an antidepressant.[3](https://pmc.ncbi.nlm.nih.gov/articles/PMC1760741/)
## Tyramine and MAO-B inhibitor drugs
Selective MAO-B inhibitors used in [Parkinson's disease](https://www.edgepedia.org/parkinsons-disease) carry much less tyramine risk at therapeutic doses because they spare the MAO-A that metabolizes dietary tyramine.[16](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515917/) Tyramine challenge studies quantify this with the tyramine sensitivity factor (TSF), the ratio of tyramine doses needed to raise systolic blood pressure by a set amount before and after the drug; a TSF above 2 is often considered clinically relevant.[17](https://pmc.ncbi.nlm.nih.gov/articles/PMC9881082/) At indicated doses, selegiline up to 10 mg/day shows TSF values of 1.75 to 3.12, rasagiline up to 1 mg/day a TSF of 2, and safinamide up to 100 mg/day a TSF of 2.15.[17](https://pmc.ncbi.nlm.nih.gov/articles/PMC9881082/) Selectivity is lost dose-dependently at higher doses: selegiline above 20 mg/day and rasagiline above 2 mg/day also inhibit MAO-A, and "cheese effect" symptoms such as headache with marked blood pressure elevation, palpitations, and nausea have been reported with selegiline at 20 to 30 mg.[17](https://pmc.ncbi.nlm.nih.gov/articles/PMC9881082/) • [18](https://pmc.ncbi.nlm.nih.gov/articles/PMC3514092/) [Safinamide](https://www.edgepedia.org/safinamide) showed no significant TSF changes even at supratherapeutic doses of 300 to 350 mg.[17](https://pmc.ncbi.nlm.nih.gov/articles/PMC9881082/) In the rasagiline clinical development program, no hypertensive crisis occurred at 1 mg daily, where most patients did not follow dietary tyramine restriction, though postmarketing reports of markedly elevated blood pressure after tyramine-rich meals exist.[19](https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/201971Orig1s000lbl.pdf) Dietary tyramine restriction is not necessary for all patients on MAO-B inhibitors, but is advised at higher doses.[17](https://pmc.ncbi.nlm.nih.gov/articles/PMC9881082/)
## Other health associations
Beyond the hypertensive effect, dietary tyramine intake has been associated with migraine headaches in select populations, with the mechanism linked to tyramine's role as a neurotransmitter.[8](https://www.fao.org/fileadmin/user_upload/agns/pdf/FAO-WHO_Expert_Meeting_Histamine.pdf) At pico- to nanomolar concentrations, tyramine can influence a range of physiological mechanisms, exhibiting neuromodulatory properties as well as cardiovascular and immunological effects.[10](https://pubmed.ncbi.nlm.nih.gov/30165672/) Trace amine signaling, including tyramine's, has been studied in neuropsychiatric disorders such as attention-deficit hyperactivity disorder, major depressive disorder, and schizophrenia, and dietary trace amines can activate human TAAR1 in primary intestinal epithelial cells, though no receptor-mediated mechanism for tyramine acting on polarized gut epithelia has been confirmed.[20](https://pmc.ncbi.nlm.nih.gov/articles/PMC11448870/)
## References
1. [Tyramine, CID 5610, PubChem](https://pubchem.ncbi.nlm.nih.gov/compound/5610)
2. [Highly Variable Pharmacokinetics of Tyramine in Humans and Polymorphisms in OCT1, CYP2D6, and MAO-A, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC6831736/)
3. [Monoamine oxidase: isoforms and inhibitors in Parkinson's disease and depressive illness, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC1760741/)
4. [Tyramine and phenylethylamine biosynthesis by food bacteria, PubMed](https://pubmed.ncbi.nlm.nih.gov/22369263/)
5. [Trace Amines and the Trace Amine-Associated Receptor 1: Pharmacology, Neurochemistry, and Clinical Implications, PubMed](https://pubmed.ncbi.nlm.nih.gov/27092049/)
6. [Trace Amines and the Trace Amine-Associated Receptor 1, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC4820462/)
7. [Trace amine-associated receptors and their ligands, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC2014643/)
8. [FAO/WHO Expert Meeting on histamine and other biogenic amines, section 2.2.3 Tyramine](https://www.fao.org/fileadmin/user_upload/agns/pdf/FAO-WHO_Expert_Meeting_Histamine.pdf)
9. [Biogenic Amine Changes Related to Lactic Acid Bacteria During Brewing, PubMed](https://pubmed.ncbi.nlm.nih.gov/31159007/)
10. [Food sources and biomolecular targets of tyramine, PubMed](https://pubmed.ncbi.nlm.nih.gov/30165672/)
11. [Tyrosine decarboxylase activity of enterococci, PubMed](https://pubmed.ncbi.nlm.nih.gov/25914676/)
12. [FDA medical review, rasagiline (Azilect) NDA 021641/S008](https://www.accessdata.fda.gov/drugsatfda_docs/nda/2009/021641S008_MedR_P1.pdf)
13. [FDA label, EMSAM (selegiline transdermal system)](https://www.accessdata.fda.gov/drugsatfda_docs/label/2006/021708s000_021336s000lbl.pdf)
14. [The Prescriber's Guide to the MAOI Diet, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC9172554/)
15. [Trace Amines and Their Receptors, PubMed](https://pubmed.ncbi.nlm.nih.gov/29941461/)
16. [Rasagiline in treatment of Parkinson's disease, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC2515917/)
17. [How to Optimize the Effectiveness and Safety of Parkinson's Disease Therapy, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC9881082/)
18. [Drug therapy in patients with Parkinson's disease, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC3514092/)
19. [FDA label, rasagiline tablets (2017)](https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/201971Orig1s000lbl.pdf)
20. [Actions of Trace Amines in the Brain-Gut-Microbiome Axis via TAAR1, PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC11448870/)
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*Topic: Encyclopedia › Physical world and mathematics › Chemistry › Organic substances › Amines and nitrogen functional groups › Psychoactive amine substance families › Endogenous trace amines and catecholamines › Phenethylamine-derived trace amines*
*Initially written Sep 17, 2026 · Reviewed: Oct 15, 2026 · Edited: Oct 15, 2026 · Last review: Oct 15, 2026*
*Copyright 2026 EdgeChat AI, a subsidiary of Biostate AI.*
License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license