Tyramine

Tyramine at a Glance

Tyramine is a trace amine — a simple biogenic amine made by removing the carboxyl group from the amino acid tyrosine. It occurs at low levels in the human body, is produced in quantity by the bacteria that ferment food, and turns up in trace amounts in a scattering of plants, including several herbs here.

On its own it is a nuisance molecule, not a medicine. It has no therapeutic use, and in a healthy person eating ordinary food it barely exists as a systemic drug at all: monoamine oxidase A (MAO-A) in the gut wall and liver destroys almost all of it before it reaches the circulation — in one 88-volunteer study, 76.8% of a 400 mg oral dose came back in urine as the MAO metabolite 4-hydroxyphenylacetic acid ^{13Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}.

That first-pass barrier is the whole story. Remove it — with a monoamine-oxidase inhibitor — and the same amine that a cheese sandwich delivers harmlessly becomes capable of a hypertensive crisis. This is the “cheese effect”, and it is the reason tyramine matters to a herbal database at all: the traditional contraindication between MAOI drugs and tyramine-bearing herbs rests entirely on this molecule.

The Cheese Effect

In the early 1960s, patients taking the first monoamine-oxidase-inhibitor antidepressants began presenting with sudden, severe headaches and blood-pressure spikes. The link to food — and specifically to aged cheese — was worked out and then demonstrated experimentally, establishing tyramine as the pressor agent responsible ^{2Reference 2Blackwell B et al. · 1967Hypertensive interactions between monoamine oxidase inhibitors and foodstuffsView study →}.

The mechanism is a removed safety margin rather than a new drug action:

• Normally, dietary tyramine is almost entirely deaminated by MAO-A in the intestinal mucosa and liver before it reaches the systemic circulation ^{5,13Reference 5Finberg JP · 2011ReviewSelective inhibitors of monoamine oxidase type B and the “cheese effect”View study →Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}. What little gets through is cleared within minutes — the elimination half-life is roughly 0.5 hours ^{14Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}.
• Under MAO inhibition, that barrier is gone. Tyramine reaches sympathetic nerve terminals intact, is taken up, and dumps stored noradrenaline into the synapse in one uncontrolled burst — the pressor response, and at the extreme, hypertensive crisis with headache, and in rare historical cases intracranial haemorrhage and death ^{3,5Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 5Finberg JP · 2011ReviewSelective inhibitors of monoamine oxidase type B and the “cheese effect”View study →}.

Two things about this story are routinely got wrong.

First, it is a dose–response, not a switch. The blood-pressure rise is graded and proportional to how much tyramine gets through; there is no threshold below which nothing happens and above which crisis is certain ^{4Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →}. Sensitivity also varies substantially between individuals, which is why a fixed food list is a poor substitute for judgement ^{3,4Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →}.

Second, the classic restricted-food lists are decades out of date. A review of more than 150 recent analyses found that changes in food production — defined starter cultures, hygiene regulation, shorter or better-controlled ripening — have cut tyramine sharply in most foods, and that even many “matured” cheeses are now safe in normal portions ^{3Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →}. Cheese was historically the only food associated with documented fatalities; the modern picture is a small number of genuinely risky items rather than a long list of forbidden ones ^{3,4Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →}.

How Tyramine Raises Blood Pressure

Tyramine is the textbook indirectly acting sympathomimetic. It does not activate adrenergic receptors itself. Instead it is a substrate for the noradrenaline transporter, enters the sympathetic nerve terminal, is taken up into synaptic vesicles by the vesicular monoamine transporter, and displaces stored noradrenaline, which then leaks out into the synapse by reverse transport. The vasoconstriction and rise in blood pressure are the released noradrenaline’s, not tyramine’s ^{7Reference 7Broadley KJ · 2010The vascular effects of trace amines and amphetaminesView study →}.

That has been the standard account for over fifty years, and for the systemic pressor response it holds. But it is not the complete mechanism, and the page should say so. Two developments complicate it:

• TAAR1 and the trace-amine receptors. In 2001 a family of G-protein-coupled receptors activated by tyramine, β-phenylethylamine, tryptamine and octopamine was cloned from human and rodent tissue — the trace amine-associated receptors ^{9,10Reference 9Borowsky B et al. · 2001Trace amines: identification of a family of mammalian G protein-coupled receptorsView study →Reference 10Bunzow JR et al. · 2001AnimalAmphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptorView study →}. Tyramine is one of the endogenous agonists at TAAR1, which is expressed in brain monoaminergic regions and in peripheral tissues including blood vessels ^{7,11Reference 7Broadley KJ · 2010The vascular effects of trace amines and amphetaminesView study →Reference 11Berry MD et al. · 2017Pharmacology of human trace amine-associated receptors: therapeutic opportunities and challengesView study →}. This gives trace amines a receptor of their own rather than a purely borrowed pharmacology.
• Direct vascular constriction. In isolated porcine coronary artery, p-tyramine caused concentration-dependent vasoconstriction that was unaffected by endothelium removal or by adrenoceptor, histamine, dopamine or 5-HT receptor antagonists — i.e. in that preparation it was not acting indirectly at all, and the authors attributed the effect to phenylethylamine-specific (TAAR-like) receptors ^{8Reference 8Herbert AA et al. · 2008Dietary trace amine-dependent vasoconstriction in porcine coronary arteryView study →}.

The honest summary: the clinically important pressor response — the one MAOI patients are warned about — is the classical indirect noradrenaline-release mechanism, and that is what the human challenge data track. A direct TAAR-mediated vascular component is real in vitro but its contribution in intact humans is unquantified ^{7,8Reference 7Broadley KJ · 2010The vascular effects of trace amines and amphetaminesView study →Reference 8Herbert AA et al. · 2008Dietary trace amine-dependent vasoconstriction in porcine coronary arteryView study →}.

The Tyramine Pressor Dose

Because tyramine’s effect is graded, the literature quantifies it with a pressor-dose challenge: give escalating oral or intravenous tyramine and find the dose that raises systolic blood pressure by a defined amount — conventionally 30 mmHg. Comparing that dose before and during a drug gives a clean multiplier for how much the drug potentiates dietary tyramine. This is the standard by which every MAO inhibitor’s dietary risk has been characterised ^{5,15Reference 5Finberg JP · 2011ReviewSelective inhibitors of monoamine oxidase type B and the “cheese effect”View study →Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →}.

The results separate the drug classes sharply:

Drug / class	Effect on the oral tyramine pressor dose	Practical reading
Tranylcypromine (irreversible, non-selective)	20–40× potentiation of oral tyramine 15,16Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →Reference 16Berlin I et al. · 1989Determination and comparison of the pressor effect of tyramine during long-term moclobemide and tranylcypromine treatment in healthy volunteersView study →	Full dietary caution; the classic “MAOI diet” 4,23Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →Reference 23Ulrich S et al. · 2017ReviewTranylcypromine in mind (Part I): review of pharmacologyView study →
Phenelzine, isocarboxazid (irreversible, non-selective)	Same class effect; dietary restriction applies 4Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →	Full dietary caution
Oral selegiline, ≥20 mg/day	Pressor sensitivity clearly enhanced; MAO-B selectivity is lost at this dose 17Reference 17Schulz R et al. · 1989Tyramine kinetics and pressor sensitivity during monoamine oxidase inhibition by selegilineView study →	Treat as a non-selective MAOI
Moclobemide (reversible, MAO-A-selective)	~4× left shift of the oral dose–pressor curve; ~10× less than tranylcypromine; no rise below 80 mg oral tyramine 15Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →	Ingesting under ~100 mg tyramine unlikely to be clinically relevant 15Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →
Rasagiline 0.5–2 mg/day (MAO-B-selective)	50–75 mg tyramine challenges produced no clinically significant reactions in 110 Parkinson’s patients 20Reference 20deMarcaida JA et al. · 2006Effects of tyramine administration in Parkinson’s disease patients treated with selective MAO-B inhibitor rasagilineView study →	No specific dietary tyramine restriction 20Reference 20deMarcaida JA et al. · 2006Effects of tyramine administration in Parkinson’s disease patients treated with selective MAO-B inhibitor rasagilineView study →
Safinamide (MAO-B-selective)	No meaningful pressor potentiation in a randomised double-blind challenge 21Reference 21Marquet A et al. · 2012RCTThe effect of safinamide, a novel drug for Parkinson’s disease, on pressor response to oral tyramine: a randomized, double-blind, clinical trialView study →	No specific restriction
Selegiline transdermal 6 mg/24 h	~400 mg of tyramine eaten as aged cheese produced no pressor effect at steady state 18,19Reference 18Blob LF et al. · 2007Effects of a tyramine-enriched meal on blood pressure response in healthy male volunteers treated with selegiline transdermal system 6 mg/24 hourView study →Reference 19Barrett JS et al. · 1997Pressor response to tyramine after single 24-hour application of a selegiline transdermal system in healthy malesView study →	Bypassing the gut preserves the intestinal MAO-A barrier 18Reference 18Blob LF et al. · 2007Effects of a tyramine-enriched meal on blood pressure response in healthy male volunteers treated with selegiline transdermal system 6 mg/24 hourView study →
Linezolid (antibiotic, weak reversible MAOI)	Modest potentiation of the intravenous tyramine pressor response 22Reference 22Cantarini MV et al. · 2004Effect of oral linezolid on the pressor response to intravenous tyramineView study →	Real but minor; the tyramine caution follows the MAOI property, not the drug class label

Two structural lessons fall out of that table. Selectivity matters — MAO-A is the isoform that guards the gut, so selective MAO-B inhibition can be achieved without a cheese effect, while MAO-A inhibition (or non-selective inhibition) produces one ^{5,6Reference 5Finberg JP · 2011ReviewSelective inhibitors of monoamine oxidase type B and the “cheese effect”View study →Reference 6Finberg JP · 2014Update on the pharmacology of selective inhibitors of MAO-A and MAO-B: focus on modulation of CNS monoamine neurotransmitter releaseView study →}. Route matters — the transdermal selegiline result is the cleanest demonstration that the barrier being protected is intestinal, not central ^{18Reference 18Blob LF et al. · 2007Effects of a tyramine-enriched meal on blood pressure response in healthy male volunteers treated with selegiline transdermal system 6 mg/24 hourView study →}.

Meals matter too, and by a surprising amount: the same 200 mg dose taken with food gives 53% lower systemic exposure and 72% lower peak concentration than taken fasted, because absorption is slowed and spread out across a working MAO-A barrier ^{14Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}. Roughly twice as much tyramine is needed with a meal to produce the same effect ^{14Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}.

Dietary Sources That Actually Matter

Tyramine in food is a microbial product: bacteria with tyrosine decarboxylase convert free tyrosine into tyramine during ripening, fermentation or spoilage. The amount therefore tracks proteolysis and microbial load, not the food category — which is exactly why category-level restriction lists mislead ^{3,4,28Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →Reference 28Natrella G et al. · 2024ReviewA comprehensive review on the biogenic amines in cheeses: their origin, chemical characteristics, hazard and reduction strategiesView study →}.

Direct analyses have repeatedly found that most “forbidden” foods carry little. Using the conventional 6 mg-per-serving cut-off for MAOI patients ^{25Reference 25Shulman KI · 1999Refining the MAOI diet: tyramine content of pizzas and soy productsView study →}:

Food	Measured tyramine	Verdict
Chicken liver, aged 9 days	63.84 mg per 30 g 24Reference 24Walker SE et al. · 1996Tyramine content of previously restricted foods in monoamine oxidase inhibitor dietsView study →	Genuinely dangerous
Air-dried sausage	above 6 mg per 30 g serving 24Reference 24Walker SE et al. · 1996Tyramine content of previously restricted foods in monoamine oxidase inhibitor dietsView study →	Restrict
Sauerkraut	7.75 mg per 250 g 24Reference 24Walker SE et al. · 1996Tyramine content of previously restricted foods in monoamine oxidase inhibitor dietsView study →	Restrict
Soy sauce	0.941 mg/mL 24Reference 24Walker SE et al. · 1996Tyramine content of previously restricted foods in monoamine oxidase inhibitor dietsView study →	Restrict — small volumes add up
Tofu stored a week	clinically significant levels 25Reference 25Shulman KI · 1999Refining the MAOI diet: tyramine content of pizzas and soy productsView study →	Restrict
Commercial chain pizza (incl. double pepperoni, double cheese)	no significant tyramine 25Reference 25Shulman KI · 1999Refining the MAOI diet: tyramine content of pizzas and soy productsView study →	Safe
Most modern cheeses in normal portions	reduced by starter cultures and hygiene standards 3Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →	Usually safe; aged/gourmet varieties are the exception

Risk-assessment work on dry fermented sausages puts numbers on the residual hazard: mean exposure was 6.2 mg per meal, the risk to healthy consumers was negligible, but the probability of a person on a classic MAOI exceeding the 6 mg safe threshold from that food alone was 34% ^{26Reference 26Latorre-Moratalla ML et al. · 2017Tyramine and histamine risk assessment related to consumption of dry fermented sausages by the Spanish populationView study →}. Broader surveys of fermented foods and cheeses reach the same shape of conclusion — a minority of high-amine products carrying most of the risk ^{27,28Reference 27Saha Turna N et al. · 2024ReviewA review of biogenic amines in fermented foods: occurrence and health effectsView study →Reference 28Natrella G et al. · 2024ReviewA comprehensive review on the biogenic amines in cheeses: their origin, chemical characteristics, hazard and reduction strategiesView study →}.

The obsolete lists (bananas, avocado, yeast spreads in ordinary amounts, chocolate, most beers) largely reflect either historically higher-amine products or confusion with other biogenic amines; the sensible modern instruction is to avoid a short list of aged, cured and fermented items rather than to police the whole diet ^{3,4Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →}.

Tyramine in Herbs

This is the compound-unique material — the reason tyramine is in a herbal database rather than a food-safety one.

Tyramine occurs, generally in trace amounts, across a scattered set of plant families. Within this database it is a listed constituent of:

• Broom (Cytisus scoparius) — the original herbal case. Mid-century Belgian work characterised broom’s vasoconstrictor amines, tyramine among them ^{34Reference 34Jaminet F · 1953Jaminet F (1953). [Biochemical study of broom herb (Sarothamnus scoparius L.). I. Its vasoconstrictor amines]. Journal de Pharmacie de Belgique. https://pubmed.ncbi.nlm.nih.gov/13053399/View study →}, and the flowering tops carry it alongside hydroxytyramine (dopamine) and the quinolizidine alkaloids sparteine and cytisine. Broom’s pharmacopoeial contraindication with MAO inhibitors traces directly to this amine content — it is pharmacological inference, not a demonstrated clinical interaction.
• Common reed (Phragmites australis) — carries tyramine together with N-methyltyramine and N,N-dimethyltyramine (hordenine) and β-carboline MAO inhibitors (harman, harmine, harmaline) in the same plant, which is the least comfortable combination in the set.
• Peyote and San Pedro — trace tyramine accompanies mescaline and hordenine in the mescaline cacti; the San Pedro alkaloid survey also reports 3-methoxytyramine at around 0.01% of dry stem ^{35Reference 35Ogunbodede O et al. · 2010New mescaline concentrations from 14 taxa/cultivars of Echinopsis spp. (Cactaceae) (“San Pedro”) and their relevance to shamanic practiceView study →}.
• Shepherd’s purse (Capsella bursa-pastoris) — mid-century work traced the herb’s “physiologically active substances” to its biogenic amines ^{36Reference 36Kuroda K · 1968Physiologically active substance in Capsella bursa-pastorisView study →}, and tyramine sits alongside choline and acetylcholine in its constituent list. It is also the reason the herb’s traditional “mild antihypertensive” framing is internally awkward: tyramine is a pressor amine.
• Tick trefoil (Desmodium spp.) — listed with tyramine, N,N-dimethyltyramine and hordenine.
• Acacia — species-dependent. Phenethylamines are unequivocally confirmed in Australian Acacia, while reports for southern African Vachellia/Senegalia rest on tentative or anecdotal data and are not reliable ^{37Reference 37Sadgrove NJ · 2022Rumors of psychedelics, psychotropics and related derivatives in Vachellia and Senegalia in contrast with verified records in Australian AcaciaView study →}. This is a genus where the amine claim must be attached to a species, not to the genus.

The herb-level implication is narrower than it looks. No quantitative tyramine figure has been published for any of these herbs, and the amounts described are trace. A cup of infusion is not a portion of nine-day-old chicken liver. The realistic concern is not that a tyramine-bearing herb will spike blood pressure on its own but that (a) it adds to dietary tyramine load in someone on an irreversible MAOI, and (b) in plants like common reed, Syrian rue and the ayahuasca vine, MAO-inhibiting β-carbolines and tyramine-type amines occur in the same preparation or the same brew — the herb supplies both halves of the interaction.

Related tyramine derivatives appear widely enough in plants to have their own entries here: the phenolic amides N-trans-p-caffeoyltyramine and N-benzoyltyramine, the positional isomer meta-tyramine, and the N-methylated series running from N-methyltyramine through hordenine to candicine, which is well characterised in Citrus ^{38Reference 38Servillo L et al. · 2014N-methylated derivatives of tyramine in citrus genus plants: identification of N,N,N-trimethyltyramine (candicine)View study →}. These are chemically related but pharmacologically distinct — an amide-bound tyramine is not free tyramine and does not carry the pressor liability.

What It's Used For

Tyramine has no therapeutic application, so the evidence below is about what it does, not what it treats. The strongest data by far are human pressor-challenge studies; everything else is preclinical.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Note that a high score here means “well demonstrated”, not “beneficial”: the best-evidenced entry is an adverse interaction.

01The pressor response under MAO inhibitionProven82%Human challenge trials across every MAOI class + documented clinical crises ^{2,3,5,15,20Reference 2Blackwell B et al. · 1967Hypertensive interactions between monoamine oxidase inhibitors and foodstuffsView study →Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 5Finberg JP · 2011ReviewSelective inhibitors of monoamine oxidase type B and the “cheese effect”View study →Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →Reference 20deMarcaida JA et al. · 2006Effects of tyramine administration in Parkinson’s disease patients treated with selective MAO-B inhibitor rasagilineView study →}

02Indirect sympathomimetic pressor effect (no MAOI)Promising66%Dose-ranging human PK/PD, n=88 at 400 mg oral ^{13,14Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}

03Probe drug for MAO-A activityShaky42%Established methodology; genotype study found no strong heritable variation ^{13,17Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →Reference 17Schulz R et al. · 1989Tyramine kinetics and pressor sensitivity during monoamine oxidase inhibition by selegilineView study →}

04TAAR1 and trace-amine neuromodulationShaky38%Cloned human/rodent receptors, in-vitro + rodent pharmacology; no human outcome ^{9,10,11,12Reference 9Borowsky B et al. · 2001Trace amines: identification of a family of mammalian G protein-coupled receptorsView study →Reference 10Bunzow JR et al. · 2001AnimalAmphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptorView study →Reference 11Berry MD et al. · 2017Pharmacology of human trace amine-associated receptors: therapeutic opportunities and challengesView study →Reference 12Pei Y et al. · 2016Trace amines and the trace amine-associated receptor 1: pharmacology, neurochemistry, and clinical implicationsView study →}

05Migraine and headache triggerShaky20%Observational and self-report; provocation evidence weak ^{29,30Reference 29Martin VT · 2016Diet and headache: part 1View study →Reference 30Jansen SC et al. · 2003ReviewIntolerance to dietary biogenic amines: a reviewView study →}

06Gut-microbial tyramine and intestinal signallingShaky18%Single mouse/organoid study line, 2024 ^{31,32Reference 31Li C et al. · 2024Enterococcus-derived tyramine hijacks α2A-adrenergic receptor in intestinal stem cells to exacerbate colitisView study →Reference 32Maini Rekdal V et al. · 2019Discovery and inhibition of an interspecies gut bacterial pathway for levodopa metabolismView study →}

Mechanisms

The load-bearing row is MAO-A. Almost everything distinctive about tyramine’s pharmacology is a consequence of how thoroughly that one enzyme normally destroys it.

Pharmacokinetics

Tyramine’s pharmacokinetics are the reason the compound is interesting, so they deserve the weight.

Absorption and first pass. Tyramine is absorbed readily from the gut, but almost none of it survives. MAO-A in the intestinal mucosa and then in the liver deaminates it on first pass, so oral bioavailability of the free amine is very low and highly dependent on how fast the dose arrives. Quantitatively: after 400 mg orally in 88 volunteers, 76.8% of the dose was recovered in urine as 4-hydroxyphenylacetic acid (4-HPAA), the MAO metabolite, confirming oxidative deamination as the dominant pathway; mean AUC was 3.74 min·µg/mL and apparent oral clearance a very high 107 L/min ^{13Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}. An independent 200 mg study gave apparent oral clearance of 135 ± 55 L/min and peak serum tyramine of 37.7 ± 26 ng/mL fasted ^{14Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}.

Half-life. Short — about 0.53 hours (roughly 32 minutes) after an oral dose in fasted subjects, with peak concentrations between 20 minutes and 1 hour ^{14Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}. A tyramine pressor episode is therefore sharp and self-limiting rather than prolonged.

The food effect is large and practically important. The same 200 mg dose taken with a meal produced 53% lower AUC and 72% lower Cmax than the fasted dose, with peak concentration delayed and prolonged ^{14Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}. Challenge studies independently find that roughly twice the tyramine is needed with food to produce an equivalent pressor response ^{14,15Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →}. Slower delivery lets the MAO-A barrier keep up.

What MAO inhibition changes. Inhibiting MAO does not just raise tyramine exposure; it redirects metabolism. On selegiline 20 mg/day the 4-HPAA share of recovered material fell from 86% to 64% while conjugated tyramine rose from 13% to 35% — conjugation partially compensating for the lost deamination ^{17Reference 17Schulz R et al. · 1989Tyramine kinetics and pressor sensitivity during monoamine oxidase inhibition by selegilineView study →}. Under moclobemide, peak plasma tyramine after an oral dose rose 2.6-fold, and a 2.5-fold lower plasma concentration produced the same blood-pressure rise, indicating both increased exposure and increased sensitivity ^{15Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →}.

What does not explain the variability. Given the size of the interindividual differences in pressor sensitivity, the obvious hypothesis was genetic. It failed: functionally relevant polymorphisms in OCT1, CYP2D6 (including poor and ultra-rapid metaboliser genotypes) and MAO-A had no significant effect on tyramine pharmacokinetics, metabolism to 4-HPAA, or pressor response ^{13Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}. Systemic 4-HPAA exposure varied only up to threefold, arguing against the existence of ultra-low or ultra-high peripheral MAO-A phenotypes ^{13Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}. The variability is real but its source is unidentified.

Clinical Trials

There are no trials of tyramine as a treatment, because it is not one. The human clinical literature consists almost entirely of tyramine-challenge studies run as safety pharmacology for MAO-inhibitor drugs — a well-populated, methodologically consistent body of work spanning tranylcypromine, moclobemide, selegiline (oral and transdermal), rasagiline, safinamide and linezolid ^{15,17,18,20,21,22Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →Reference 17Schulz R et al. · 1989Tyramine kinetics and pressor sensitivity during monoamine oxidase inhibition by selegilineView study →Reference 18Blob LF et al. · 2007Effects of a tyramine-enriched meal on blood pressure response in healthy male volunteers treated with selegiline transdermal system 6 mg/24 hourView study →Reference 20deMarcaida JA et al. · 2006Effects of tyramine administration in Parkinson’s disease patients treated with selective MAO-B inhibitor rasagilineView study →Reference 21Marquet A et al. · 2012RCTThe effect of safinamide, a novel drug for Parkinson’s disease, on pressor response to oral tyramine: a randomized, double-blind, clinical trialView study →Reference 22Cantarini MV et al. · 2004Effect of oral linezolid on the pressor response to intravenous tyramineView study →}.

Last checked: July 2026.

Isolate vs. Plant Studies

Unusually for this database, essentially all the evidence is isolate evidence — and that is a strength for the pharmacology and a weakness for the herbal question.

Every human dataset here used pure tyramine: encapsulated doses of 50–400 mg, intravenous infusions, or a tyramine-enriched meal built from analysed aged cheese ^{13,14,15,18,20Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →Reference 18Blob LF et al. · 2007Effects of a tyramine-enriched meal on blood pressure response in healthy male volunteers treated with selegiline transdermal system 6 mg/24 hourView study →Reference 20deMarcaida JA et al. · 2006Effects of tyramine administration in Parkinson’s disease patients treated with selective MAO-B inhibitor rasagilineView study →}. That is why the dose–response is so cleanly characterised. There is no ambiguity about what was administered.

The plant side is the opposite. Tyramine’s occurrence in broom, common reed, tick trefoil, shepherd’s purse and the mescaline cacti is reported qualitatively only ^{34,35,36Reference 34Jaminet F · 1953Jaminet F (1953). [Biochemical study of broom herb (Sarothamnus scoparius L.). I. Its vasoconstrictor amines]. Journal de Pharmacie de Belgique. https://pubmed.ncbi.nlm.nih.gov/13053399/View study →Reference 35Ogunbodede O et al. · 2010New mescaline concentrations from 14 taxa/cultivars of Echinopsis spp. (Cactaceae) (“San Pedro”) and their relevance to shamanic practiceView study →Reference 36Kuroda K · 1968Physiologically active substance in Capsella bursa-pastorisView study →} — no herb here has a published tyramine concentration. So the herb-level caution is a two-step inference: this plant contains tyramine (documented), and tyramine plus an MAOI is dangerous (documented) — but the bridging quantity is unknown. No study has administered a tyramine-containing herb to a person on an MAO inhibitor.

The food literature sits in between: measured concentrations in real matrices ^{24,25,26,28Reference 24Walker SE et al. · 1996Tyramine content of previously restricted foods in monoamine oxidase inhibitor dietsView study →Reference 25Shulman KI · 1999Refining the MAOI diet: tyramine content of pizzas and soy productsView study →Reference 26Latorre-Moratalla ML et al. · 2017Tyramine and histamine risk assessment related to consumption of dry fermented sausages by the Spanish populationView study →Reference 28Natrella G et al. · 2024ReviewA comprehensive review on the biogenic amines in cheeses: their origin, chemical characteristics, hazard and reduction strategiesView study →}, but with enormous within-category variation that makes any single figure a poor predictor of the next sample ^{4,28Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →Reference 28Natrella G et al. · 2024ReviewA comprehensive review on the biogenic amines in cheeses: their origin, chemical characteristics, hazard and reduction strategiesView study →}.

Prevalence in Nature

Tyramine is one of the most widely distributed simple amines in biology, appearing wherever tyrosine is decarboxylated — in plants, in bacteria, and endogenously in animals.

In plants it occurs at trace levels across scattered families: Fabaceae (broom, tick trefoil), Poaceae (common reed), Brassicaceae (shepherd’s purse), Cactaceae (peyote, San Pedro) and species-dependent occurrences in Acacia ^{34,35,36,37Reference 34Jaminet F · 1953Jaminet F (1953). [Biochemical study of broom herb (Sarothamnus scoparius L.). I. Its vasoconstrictor amines]. Journal de Pharmacie de Belgique. https://pubmed.ncbi.nlm.nih.gov/13053399/View study →Reference 35Ogunbodede O et al. · 2010New mescaline concentrations from 14 taxa/cultivars of Echinopsis spp. (Cactaceae) (“San Pedro”) and their relevance to shamanic practiceView study →Reference 36Kuroda K · 1968Physiologically active substance in Capsella bursa-pastorisView study →Reference 37Sadgrove NJ · 2022Rumors of psychedelics, psychotropics and related derivatives in Vachellia and Senegalia in contrast with verified records in Australian AcaciaView study →}. It is more often present as a biosynthetic waypoint than as an end product — the precursor to the N-methylated series (N-methyltyramine → hordenine → candicine, well characterised in Citrus ^{38Reference 38Servillo L et al. · 2014N-methylated derivatives of tyramine in citrus genus plants: identification of N,N,N-trimethyltyramine (candicine)View study →}), to the hydroxycinnamic acid amides, and, via hydroxylation, to dopamine and the benzylisoquinoline alkaloids. Free tyramine concentrations in medicinal herbs have not been quantified.

In microbes it is a fermentation product. Lactic-acid bacteria, enterococci and various contaminants carry tyrosine decarboxylase and generate tyramine during cheese ripening, sausage fermentation, soy fermentation and spoilage — which is why levels track microbial ecology and hygiene rather than the raw ingredient ^{27,28,32Reference 27Saha Turna N et al. · 2024ReviewA review of biogenic amines in fermented foods: occurrence and health effectsView study →Reference 28Natrella G et al. · 2024ReviewA comprehensive review on the biogenic amines in cheeses: their origin, chemical characteristics, hazard and reduction strategiesView study →Reference 32Maini Rekdal V et al. · 2019Discovery and inhibition of an interspecies gut bacterial pathway for levodopa metabolismView study →}.

In animals, including humans, tyramine is a genuine endogenous trace amine, present in the nervous system at nanomolar concentrations alongside β-phenylethylamine, tryptamine and octopamine, with TAAR1 as a dedicated receptor ^{9,12Reference 9Borowsky B et al. · 2001Trace amines: identification of a family of mammalian G protein-coupled receptorsView study →Reference 12Pei Y et al. · 2016Trace amines and the trace amine-associated receptor 1: pharmacology, neurochemistry, and clinical implicationsView study →}. Gut bacteria add a second, non-dietary internal source ^{31,32Reference 31Li C et al. · 2024Enterococcus-derived tyramine hijacks α2A-adrenergic receptor in intestinal stem cells to exacerbate colitisView study →Reference 32Maini Rekdal V et al. · 2019Discovery and inhibition of an interspecies gut bacterial pathway for levodopa metabolismView study →}.

Its Role in Plants

In plants, tyramine is primarily a defence intermediate. Tyrosine decarboxylase (TyDC) converts tyrosine to tyramine, and tyramine hydroxycinnamoyltransferase (THT) then conjugates it with hydroxycinnamoyl-CoA esters to form hydroxycinnamic acid amides — feruloyl- and coumaroyltyramine and relatives — which are deposited into the cell wall to reinforce it against pathogens and wounding.

The pathway is inducible and the two enzymes are jointly rate-limiting: in transgenic tobacco, elevating TyDC and THT levels increased wound-induced accumulation of tyramine-derived hydroxycinnamic acid amides ^{33Reference 33Hagel JM · 2005Elevated tyrosine decarboxylase and tyramine hydroxycinnamoyltransferase levels increase wound-induced tyramine-derived hydroxycinnamic acid amide accumulation in transgenic tobacco leavesView study →}. Free tyramine is thus best understood as a short-lived metabolic pool feeding a structural defence response, not as a stored secondary metabolite — which is consistent with how little of it is found free in most tissues.

Several of those amides are themselves database entries with their own pharmacology, including N-trans-p-caffeoyltyramine and N-benzoyltyramine.

These are plant-biology functions and carry no implication for human pharmacology.

Discovery & Synthesis

Tyramine was first isolated in 1909 by George Barger and George Walpole, who identified it among the pressor principles of putrefying meat — a provenance that fits the molecule rather well ^{1Reference 1Barger G · 1909Isolation of the pressor principles of putrid meatView study →}. It was characterised around the same period in ergot and in cheese, and its name derives from tyrosine, itself named from the Greek tyros, “cheese”, because tyrosine was first obtained from casein. The etymological coincidence with the “cheese effect” is genuine but accidental: the naming predates the 1960s clinical discovery by half a century.

The pharmacological story arrived in two waves. The 1909–1930s work established tyramine as a sympathomimetic pressor amine. Then in the 1960s, with MAO-inhibitor antidepressants in wide use, the cheese reaction was recognised and traced experimentally to dietary tyramine ^{2Reference 2Blackwell B et al. · 1967Hypertensive interactions between monoamine oxidase inhibitors and foodstuffsView study →} — turning a laboratory curiosity into one of the best-known drug–food interactions in medicine.

Synthesis and manufacture. Tyramine is a structurally trivial molecule and is made synthetically for research use — the obvious routes are decarboxylation of tyrosine and reduction of the corresponding nitrile or oxime. It is not manufactured as a drug, has no commercial extraction industry, and the specific historical first synthesis is not well documented in the accessible literature. The tyramine that matters to people is made by bacteria in food, not in a factory.

Patents: not yet researched.

Toxicity & Safety

Tyramine carries a moderate flag, and the reason is entirely conditional. On its own, in a person with functioning monoamine oxidase, it is one of the least consequential compounds here — over three-quarters of an oral dose is destroyed before it does anything ^{13Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}. Combined with an MAO inhibitor, it is capable of a hypertensive crisis. The badge reflects the interaction, not the molecule.

Safety at a Glance

⚠️ Moderate toxicityDrug interactions

• MAOI + tyramine = hypertensive crisis. With an irreversible non-selective MAOI (phenelzine, tranylcypromine, isocarboxazid) or high-dose oral selegiline, dietary tyramine is potentiated 20–40-fold and can cause severe headache and a dangerous blood-pressure spike; historically, fatalities ^{2,3,15Reference 2Blackwell B et al. · 1967Hypertensive interactions between monoamine oxidase inhibitors and foodstuffsView study →Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →}.
• The 6 mg-per-meal line. For someone on a classic MAOI, roughly 6 mg of tyramine in a single meal is the conventional safety threshold — a level that aged chicken liver, air-dried sausage, sauerkraut, soy sauce and some aged cheeses can exceed on their own ^{24,25,26Reference 24Walker SE et al. · 1996Tyramine content of previously restricted foods in monoamine oxidase inhibitor dietsView study →Reference 25Shulman KI · 1999Refining the MAOI diet: tyramine content of pizzas and soy productsView study →Reference 26Latorre-Moratalla ML et al. · 2017Tyramine and histamine risk assessment related to consumption of dry fermented sausages by the Spanish populationView study →}.
• Herbal MAO inhibitors count. The β-carbolines in Syrian rue, ayahuasca vine and common reed inhibit MAO-A; the same dietary rules apply while they are active, and common reed carries both halves of the interaction in one plant.
• Sensitivity varies severalfold between individuals and is not predicted by MAO-A, OCT1 or CYP2D6 genotype ^{3,13Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}. Fixed food lists are a poor substitute for individual judgement ^{4Reference 4Van den Eynde V et al. · 2022The prescriber’s guide to the MAOI diet — thinking through tyramine troublesView study →}.
• Selective and reversible inhibitors are lower risk, not no risk. Rasagiline, safinamide and transdermal selegiline showed no clinically significant tyramine reaction in challenge studies ^{18,20,21Reference 18Blob LF et al. · 2007Effects of a tyramine-enriched meal on blood pressure response in healthy male volunteers treated with selegiline transdermal system 6 mg/24 hourView study →Reference 20deMarcaida JA et al. · 2006Effects of tyramine administration in Parkinson’s disease patients treated with selective MAO-B inhibitor rasagilineView study →Reference 21Marquet A et al. · 2012RCTThe effect of safinamide, a novel drug for Parkinson’s disease, on pressor response to oral tyramine: a randomized, double-blind, clinical trialView study →}; moclobemide potentiates about fourfold ^{15Reference 15Korn A et al. · 1988Tyramine pressor effect in man: studies with moclobemide, a novel, reversible monoamine oxidase inhibitorView study →}; linezolid modestly ^{22Reference 22Cantarini MV et al. · 2004Effect of oral linezolid on the pressor response to intravenous tyramineView study →}. Dose and selectivity both matter — oral selegiline loses its MAO-B selectivity above 20 mg/day ^{17Reference 17Schulz R et al. · 1989Tyramine kinetics and pressor sensitivity during monoamine oxidase inhibition by selegilineView study →}.
• Herb-level tyramine is unquantified. No database herb has a published tyramine figure; the MAOI contraindication on those pages is pharmacological inference, not measured exposure.
• Not a concern for people not taking an MAO inhibitor. Intestinal and hepatic MAO-A clear it almost completely; half-life ~0.5 h; the modern food supply carries far less tyramine than the classic restriction lists assume ^{3,13,14Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}.

Full Safety & Interactions Detail

The interaction, named precisely. The enzyme is monoamine oxidase A, and the site that matters is the intestinal mucosa and liver, not the brain. Anything that inhibits MAO-A — irreversibly (phenelzine, tranylcypromine, isocarboxazid), or reversibly (moclobemide), or non-selectively at higher doses (oral selegiline ≥20 mg/day ^{17Reference 17Schulz R et al. · 1989Tyramine kinetics and pressor sensitivity during monoamine oxidase inhibition by selegilineView study →}), or incidentally as a secondary property (the antibiotic linezolid ^{22Reference 22Cantarini MV et al. · 2004Effect of oral linezolid on the pressor response to intravenous tyramineView study →}) — raises tyramine’s systemic exposure and its pressor effect. Selective MAO-B inhibitors at therapeutic doses (rasagiline 0.5–2 mg/day, safinamide) do not, and challenge studies support prescribing them without a tyramine diet ^{20,21Reference 20deMarcaida JA et al. · 2006Effects of tyramine administration in Parkinson’s disease patients treated with selective MAO-B inhibitor rasagilineView study →Reference 21Marquet A et al. · 2012RCTThe effect of safinamide, a novel drug for Parkinson’s disease, on pressor response to oral tyramine: a randomized, double-blind, clinical trialView study →}. Transdermal selegiline is the instructive case: by bypassing the gut it leaves the intestinal MAO-A barrier intact, and ~400 mg of tyramine eaten as aged cheese produced no pressor response at steady state ^{18,19Reference 18Blob LF et al. · 2007Effects of a tyramine-enriched meal on blood pressure response in healthy male volunteers treated with selegiline transdermal system 6 mg/24 hourView study →Reference 19Barrett JS et al. · 1997Pressor response to tyramine after single 24-hour application of a selegiline transdermal system in healthy malesView study →}.

What a reaction looks like. Abrupt severe (often occipital) headache, a sharp systolic rise, palpitations, sweating, nausea; in severe historical cases, intracranial haemorrhage. It is short-lived, tracking tyramine’s ~30-minute half-life ^{14Reference 14VanDenBerg CM et al. · 2003Tyramine pharmacokinetics and reduced bioavailability with foodView study →}. Modern reviews argue that the treatment has historically caused iatrogenic harm — over-aggressive blood-pressure lowering — more often than the reaction itself now does ^{3Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →}.

Proportion, honestly. The modern literature is considerably less alarmist than the 1970s food lists. Most cheeses in normal portions, commercial pizza, and the great majority of everyday foods do not contain problematic tyramine ^{3,25Reference 3Gillman PK · 2018A reassessment of the safety profile of monoamine oxidase inhibitors: elucidating tired old tyramine mythsView study →Reference 25Shulman KI · 1999Refining the MAOI diet: tyramine content of pizzas and soy productsView study →}; the risk concentrates in a short list of aged, air-dried, spoiled and fermented items ^{24,26,27,28Reference 24Walker SE et al. · 1996Tyramine content of previously restricted foods in monoamine oxidase inhibitor dietsView study →Reference 26Latorre-Moratalla ML et al. · 2017Tyramine and histamine risk assessment related to consumption of dry fermented sausages by the Spanish populationView study →Reference 27Saha Turna N et al. · 2024ReviewA review of biogenic amines in fermented foods: occurrence and health effectsView study →Reference 28Natrella G et al. · 2024ReviewA comprehensive review on the biogenic amines in cheeses: their origin, chemical characteristics, hazard and reduction strategiesView study →}. Risk assessment of dry fermented sausages found negligible risk to the general population but a 34% chance of an MAOI patient exceeding the 6 mg threshold from that food alone ^{26Reference 26Latorre-Moratalla ML et al. · 2017Tyramine and histamine risk assessment related to consumption of dry fermented sausages by the Spanish populationView study →}.

Other biogenic amines travel with it. Foods high in tyramine are often high in histamine, and histamine intolerance is a separate condition with a much lower tolerable intake ^{26,30Reference 26Latorre-Moratalla ML et al. · 2017Tyramine and histamine risk assessment related to consumption of dry fermented sausages by the Spanish populationView study →Reference 30Jansen SC et al. · 2003ReviewIntolerance to dietary biogenic amines: a reviewView study →}. Symptoms attributed to “tyramine sensitivity” in people not on MAOIs frequently belong to histamine or to other amines, and the evidence for dietary-amine intolerance in general is weaker than its popularity suggests ^{30Reference 30Jansen SC et al. · 2003ReviewIntolerance to dietary biogenic amines: a reviewView study →}.

Migraine. Tyramine’s status as a migraine trigger is traditional rather than demonstrated; the trigger with the strongest provocation evidence in the dietary literature is caffeine withdrawal and MSG, not tyramine ^{29Reference 29Martin VT · 2016Diet and headache: part 1View study →}. Individuals who reliably identify a trigger food are worth taking seriously; the general claim is not well supported.

Reproductive note (prose only). No dedicated reproductive- or developmental-toxicity dataset exists for isolated tyramine; the compound has not been assessed for genotoxicity or repeat-dose toxicity as a pure substance in the modern regulatory sense. Pregnancy and lactation decisions belong to the herb or product page where intake is decided, not to this molecule page.

What is not known. Interactions here are limited to the monoamine-oxidase axis and the pressor pharmacology. Tyramine has not been characterised as a CYP or P-glycoprotein substrate/inhibitor of consequence, and the one pharmacogenetic study to look found no effect of CYP2D6 or OCT1 genotype on its handling ^{13Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →}.

Dosage

There is no dose of tyramine. It is not a medicine, not a supplement, and nothing here should be read as an intake target. The figures below are the doses used in research, recorded because they give the only quantitative sense of scale available.

For orientation: the 6 mg-per-meal MAOI threshold is about 1/65th of the 400 mg dose used to study tyramine pharmacology in unmedicated volunteers ^{13,26Reference 13Rafehi M et al. · 2019Highly variable pharmacokinetics of tyramine in humans and polymorphisms in OCT1, CYP2D6, and MAO-AView study →Reference 26Latorre-Moratalla ML et al. · 2017Tyramine and histamine risk assessment related to consumption of dry fermented sausages by the Spanish populationView study →} — the gap between the two numbers is precisely the protection that MAO-A provides.

Herbal exposure is unquantified. No tyramine figure has been published for broom, common reed, tick trefoil, shepherd’s purse or the mescaline cacti, and the reported amounts are described as trace. These are doses studied in research and a clinical safety threshold — not a personal recommendation.

References

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