How MCAS is diagnosed: tryptase, the 24-hour urine tests and the criteria

Short answer

MCAS is diagnosed on three things at once: episodic symptoms in two or more organ systems, a measured rise in a mast cell chemical during an episode, and improvement on mediator-blocking drugs. The usual proof is serum tryptase drawn within hours of a flare, above your own baseline by 20% plus 2 ng/mL (1, 3).

If you have already been told your tryptase was normal so this is probably stress or anxiety, that is not a closed case and you are not imagining things. A single baseline tryptase is the wrong test to settle the question: the criteria ask for a rise during an episode compared with your own calm-day number, and the sample has to be taken inside a window measured in hours (1, 9). In a 2024 survey of 130 people with confirmed or suspected MCAS run by the UK charity Mast Cell Action, 97% had been living with symptoms for two years or more, the average age at diagnosis was 43, and 61% were dissatisfied or very dissatisfied with how they were diagnosed (19). The path is genuinely hard, and most of the difficulty is in the testing, not in you.

Note: this article explains what guidelines and research say about getting to a diagnosis and is not medical advice, and it is not a guide to treatment. Your clinician decides which tests fit you and how to read them. Call 911 and use epinephrine if you have it for signs of anaphylaxis: hives or a red itchy rash, a swollen throat or swollen areas of the body, wheezing, trouble breathing or coughing, a hoarse voice, trouble swallowing, chest tightness, vomiting, diarrhea or stomach cramping, passing out, or a feeling of impending doom. A severe reaction can happen with no skin symptoms at all. The AAAAI says to use epinephrine and call 911 rather than take an antihistamine first and wait to see whether it improves (18).

This page is only about the road to a diagnosis. For what the condition feels like day to day, we have a separate guide to MCAS symptoms, and a general overview of mast cell activation syndrome.

What are the criteria for an MCAS diagnosis?

Three criteria have to be met together, and the sticking point is almost always the second one. The set in widest clinical use was proposed by an international group led by Peter Valent in 2012, refined since, and is usually called the consensus-1 or Vienna criteria (4, 3).

Alongside the criteria sits a classification, because MCAS is a label for a mechanism rather than a single disease (3, 10):

• Primary (clonal) MCAS — the criteria are met and abnormal, clonal mast cells are found, usually carrying a KIT D816V mutation. Mastocytosis sits here, as does monoclonal MCAS, where there are clonal markers but not enough to call it mastocytosis.

• Secondary MCAS — normal mast cells set off by something identifiable, most often an IgE allergy, a drug, an infection or insect venom.

• Idiopathic MCAS — the criteria are met, clonal disease and allergy have been looked for and not found.

• Mixed or combined — features of more than one, including primary plus secondary, and the version where hereditary alpha tryptasemia is also present.

That classification matters at the testing stage because it decides what else gets ordered: a KIT D816V blood test, sometimes a bone marrow biopsy, and allergy testing are all about sorting which box you are in, not about proving MCAS itself.

The second set of criteria, and why your doctor may not use it

There is a competing set, published in 2020 by Lawrence Afrin, Gerhard Molderings and colleagues and called the global "consensus-2" (5). It is built differently: one major criterion plus at least one minor criterion, with no better explanation available.

That last row is the whole argument in one line, and the gap is more than a hundredfold. Most US allergists and immunologists work from consensus-1; the AAAAI's own work group report is a variation on it (1, 2). We come back to the dispute, and to what it means for you in an exam room, further down.

Why is my tryptase normal if I have MCAS?

Because a normal baseline tryptase was never meant to rule MCAS in or out — the criteria ask for a change during an episode, and most people never get that sample taken. Theo Gülen, writing in Current Allergy and Asthma Reports in January 2024, puts it plainly: "a normal sBT level does not exclude MCAS, whereas a high sBT alone is not an indication or criterion of MCAS" (7).

Tryptase is an enzyme stored in mast cell granules. When mast cells degranulate in a big way, it spills into the blood. Two numbers matter, and they are different tests of the same substance:

• Baseline serum tryptase (sBT) — drawn on a calm day, or at least 24 hours after all symptoms of an episode have resolved (1, 9). Mayo Clinic Laboratories reports a reference range below 11.5 ng/mL, and notes that published upper limits in healthy populations have ranged from 8.2 to 15 ng/mL (12).

• Acute serum tryptase (sAT) — drawn during or just after an episode.

The 20% + 2 rule, worked through

The threshold is written as sAT > (1.2 × sBT) + 2 ng/mL. In words: the episode sample has to be at least 20% above your own baseline, and then another 2 ng/mL on top (1, 3). The Mast Cell Disease Society gives the arithmetic with a baseline of 8 ng/mL: (8 × 1.2) + 2 = 11.6, so the episode sample has to clear 11.6 ng/mL (9).

• 3 ng/mL — 5.6 ng/mL

• 5 ng/mL — 8.0 ng/mL

• 8 ng/mL — 11.6 ng/mL

• 11.5 ng/mL — 15.8 ng/mL

• 15 ng/mL — 20.0 ng/mL

Two things fall out of that table. First, at a low baseline the bar is low in absolute terms — which is the point of the "+ 2," since it stops ordinary day-to-day wobble from counting. Second, the higher your baseline, the bigger the absolute jump you need, which is exactly the problem hereditary alpha tryptasemia creates, below.

The window: hours, not days

This is where most testing fails. Tryptase rises about 30 to 60 minutes after onset and then falls with a half-life of roughly two hours (12, 7).

The sources differ at the edges, and that difference is honest rather than sloppy — how long the level stays up depends on how high it went. What they agree on is that a sample taken the following week tells you nothing about the episode. Mayo also warns that tryptase can look normal in someone with genuine acute mast cell activation if the blood is drawn more than 12 hours afterwards, and that some people rise above their own baseline after anaphylaxis while never crossing 11.5 ng/mL at all — which is precisely why the comparison is with your own number and not with the lab's range (12).

One handling detail worth knowing, because it can quietly ruin a sample: tryptase degrades fast in the presence of red blood cells, so the serum has to be separated promptly (12).

What this means in practice

The realistic plan is to agree the test in advance, while you are well, so it can be run when a bad episode happens rather than being thought of afterwards. The AAAAI advises working with a local allergist precisely so that emergency and lab staff know to order and complete these tests on time, since they are not standard labs (2). If you go to an emergency department during a severe reaction, a tryptase drawn there is one of the most valuable pieces of evidence you will ever get — it is also the one most often missed.

What do the 24-hour urine tests actually measure?

They measure the breakdown products of three other mast cell chemicals, which survive long enough to be collected over a day — unlike histamine itself, which disappears too quickly to measure usefully (1, 14).

• N-methylhistamine — What it is a metabolite of: Histamine; Mayo reference value (adults): 19–143 mcg/g creatinine (over 16 years) (14); What raises it besides mast cells: A very histamine-rich diet (about 30%), MAO inhibitors (13)

• 2,3-dinor-11β-prostaglandin F2α — What it is a metabolite of: Prostaglandin D2; Mayo reference value (adults): <1802 pg/mg creatinine (15); What raises it besides mast cells: Angioedema, widespread hives, myeloproliferative disease (15)

• Leukotriene E4 — What it is a metabolite of: Cysteinyl leukotrienes; Mayo reference value (adults): ≤104 pg/mg creatinine (16); What raises it besides mast cells: Asthma, aspirin-exacerbated respiratory disease, eosinophilic pneumonia, atopic dermatitis, Crohn's disease, rheumatoid arthritis (16)

In the US these are often ordered together as a single mast cell mediator panel on one 24-hour collection, alongside urine creatinine, which is what the results are normalised to (13). Mayo's own internal study put the three of them together at 90% sensitivity for detecting systemic mastocytosis — note that is mastocytosis, a different and much better-defined condition, not MCAS (15).

Opinions on how much weight to give them differ. The AAAAI's 2019 work group report says N-methylhistamine has shown little clinical utility for MCAS on its own and is better read as supporting evidence next to other mediators, while 11β-PGF2α was the most frequently raised baseline mediator in one MCAS cohort (1). An AAAAI Ask the Expert answer from Javier Chinen, posted against a question dated August 6, 2025, calls urinary markers supplementary to tryptase and notes that experts still argue about how big a rise counts — a minimum of 30% over baseline is suggested, but not firmly validated (17).

Timing again, and why the jug has to be cold

The 24-hour collection is not a background measurement. Mayo instructs that collection should begin within a few hours of symptom onset (16). For people whose symptoms come in short bursts, a random (spot) urine taken right after an episode is often preferred over a full 24 hours, because a day's worth of urine dilutes a one-hour spike (14).

Handling matters as much as timing. Mayo's mast cell mediator panel asks for no preservative with the sample frozen, and says any preservative or temperature control has to be applied within four hours of finishing the collection (13). Mast Cell Action's testing resource for clinicians tells patients to use a clean, preservative- and acid-free container, keep it refrigerated before and throughout, collect each fresh sample separately and chill it before adding it to the main container, and transport it cold (20). The Mast Cell Disease Society records a case where an unrefrigerated 24-hour urine came back falsely negative and was positive when repeated and handled properly (9). If the instructions you get at the lab desk are thinner than that, ask.

Medicines and food that change the answer

This is the part most often skipped, and it is the reason a lot of "negative" results are not really negative. Mayo's patient preparation for the mast cell mediator panel, where medically feasible, is specific (13):

• MAO inhibitors, aminoguanidine — Stop before collection: 3 weeks (Mayo's N-methylhistamine page says 2 weeks for MAOIs); Effect on the result: Falsely raises N-methylhistamine (13, 14)

• Aspirin — Stop before collection: 2 weeks; Effect on the result: Falsely lowers the prostaglandin metabolite (13, 15)

• NSAIDs (ibuprofen, naproxen and similar) — Stop before collection: 72 hours; Effect on the result: Falsely lowers the prostaglandin metabolite (13)

• Zileuton (Zyflo) — Stop before collection: 48 hours; Effect on the result: Lowers leukotriene E4 (13, 16)

• A very histamine-rich diet — Stop before collection: Discuss with the ordering clinician; Effect on the result: Raises N-methylhistamine by around 30%, most of all on a spot sample after a histamine-heavy meal; an average North American diet has no effect (13, 14)

• Diamine oxidase inhibitors — Stop before collection: Ask; Effect on the result: Lower N-methylhistamine (14)

• N-acetylcysteine at antidote doses — Stop before collection: Ask; Effect on the result: Can falsely lower the creatinine the result is divided by (14)

"Where medically feasible" is doing real work in that list. Nobody should stop a prescribed medicine to pass a test — that is a decision for the clinician who prescribed it, and for aspirin in particular it may not be safe to stop at all. The point is to have the conversation before the jug is handed over, not after the result comes back low.

Two more honest caveats, both from the labs themselves. A normal leukotriene E4 does not rule out mast cell disease (16). And a raised prostaglandin metabolite is not specific to mast cells, so it means something only next to matching symptoms (15). If your food reactions look more like a digestive-enzyme problem than a mast cell one, histamine intolerance is a separate explanation worth reading about.

Hereditary alpha tryptasemia: when a high tryptase is not MCAS

A raised baseline tryptase is far more often a common inherited trait than a sign of mast cell disease. Hereditary alpha tryptasemia (HαT) is caused by having one or more extra copies of TPSAB1, the gene for alpha-tryptase. It is inherited in an autosomal dominant way — one extra copy from one parent is enough — and The Mast Cell Disease Society describes it as affecting around 5% of the populations studied (11).

The numbers that matter for anyone holding a lab slip:

• About 6% of Western populations have a baseline tryptase above 11.4 ng/mL, and HαT accounts for a little over 90% of those cases. Significant kidney disease accounts for about 7%, and clonal conditions such as mastocytosis for the rest (11).

• Mayo puts HαT at roughly 4% to 7.5% of the Western population and calls it the most common cause of a raised baseline tryptase. Most carriers have no mast cell symptoms at all (12).

• Baseline tryptase in HαT is generally above 8 ng/mL (11).

HαT is confirmed by tryptase genotyping using droplet digital PCR, which counts gene copies — ordinary sequencing usually cannot (11). The AAAAI work group report lists testing for increased TPSAB1 alpha-tryptase copy number alongside KIT testing in the MCAS workup (1).

Here is why it tangles the diagnosis in both directions. A high baseline tryptase can look like proof of a mast cell problem when it is just genetics — and the consensus-1 group is firm that a raised baseline tryptase on its own is not a criterion, and that HαT carriers do not show hyperactive mast cells or raised urinary mediators unless they also have mastocytosis (3). In the other direction, a higher baseline raises the absolute bar of the 20% + 2 rule, so a real episode has to produce a bigger jump to count. HαT and MCAS can also coexist, and The Mast Cell Disease Society lists "HαT + MCAS" as its own category (10).

HαT has its own associations worth mentioning to a clinician: flushing, itching and recurrent hives, IBS-like abdominal pain and bloating, anaphylaxis especially to stinging insects, joint hypermobility and retained baby teeth, and symptoms of autonomic dysfunction (11). If that cluster sounds familiar, the diagnostic paths for POTS and for Ehlers-Danlos syndromes and hypermobility run alongside this one and are often walked at the same time.

Ruling things out: KIT D816V, bone marrow and the lookalikes

Most of an MCAS workup is spent excluding other explanations, and that is a feature of the criteria rather than a delay. The AAAAI's sequence runs roughly like this (2):

1. A blood test for the KIT D816V mutation, to look for clonal mast cell disease. A negative result is not 100% reliable, so a scoring system is used alongside it.

2. If clonal disease is still suspected, a bone marrow biopsy and aspirate.

3. A negative bone marrow then establishes idiopathic MCAS, once the three criteria are met.

Consensus-1 adds that bone marrow investigation is not recommended when KIT D816V is absent and there are no other features of a myeloid neoplasm (3) — useful if you are being pushed toward a marrow biopsy without a clear reason.

Several common conditions produce overlapping symptoms and get looked at along the way. Chronic spontaneous urticaria explains most long-running hives. Dermatographia, where skin welts when scratched, and cholinergic urticaria, where heat and sweating bring on small itchy bumps, are both mast-cell-mediated but are their own diagnoses, not MCAS. Carcinoid tumours, pheochromocytoma, hereditary angioedema and thyroid disease sit on the same differential list for episodic flushing and blood pressure swings, which is why a workup can feel like it is wandering off topic when it is not.

Treatment is a separate subject and not covered here; the drug trial that forms criterion three is run and interpreted by the clinician making the diagnosis.

Why is MCAS diagnosis so controversial?

Because two expert groups disagree about how common the condition is, by a factor of more than a hundred, and a patient standing between them can get opposite answers from two reasonable doctors.

The consensus-1 position. Gülen, Akin, Valent and 25 co-authors argued in The Journal of Allergy and Clinical Immunology: In Practice in November 2021 that looser criteria label people whose many non-specific symptoms — fatigue, pain, endometriosis — have no established link to mast cells, that overdiagnosis delays the correct diagnosis, and that it exposes people to drugs they do not need (3). The strongest empirical support for that view is a 2024 study of 703 consecutive adults referred for suspected mast cell disorders: only 31 met criteria for idiopathic MCAS, a prevalence of 4.4%, rising to 27% among those with unprovoked anaphylaxis (8).

The consensus-2 position. Afrin, Molderings and colleagues argued in 2020, and again in Diagnosis in June 2026, that the strict criteria define the condition out of existence for most of the people who have it: that recurrent anaphylaxis is uncommon in MCAS rather than typical, that mediator rises are often too subtle to clear a lab's normal range, that a truly asymptomatic baseline is rarely attainable in someone who is never fully well, and that clinicians routinely exclude MCAS on one normal baseline tryptase without ever testing during an attack (5, 6). On the 20% + 2 rule specifically, they say it appears to have been asserted without evidence and that they cannot accept it as a gold standard (5). They also note that no published study or case report has yet demonstrated overdiagnosis or harm from it (6).

Both of those last two paragraphs are each side describing the argument, so read them as positions, not as settled findings. What is not in dispute is the clinical reality underneath: the criteria demand a measurement taken inside a narrow window during an unpredictable event, and the measurement is often not taken.

What it means for you. Three practical consequences.

• Which criteria your clinician uses determines whether you get the diagnosis, so it is fair to ask which set they work from. In the US, most allergists and immunologists use consensus-1 or the AAAAI variant.

• A consensus-1 clinician declining the label is not calling you a liar. They are saying that this specific evidence has not been produced — which is a statement about the test record, not about your symptoms.

• The Mast Cell Disease Society, which is not a fringe body, supports a clinical diagnosis with ongoing treatment when other conditions have been thoroughly excluded, symptoms affect two or more organ systems at once, there is a response to anti-mediator therapy, and the person is monitored with periodic repeat mediator testing (9). "Not proven yet, keep testing during flares" is a legitimate place to be, and it is different from "nothing is wrong."

What a realistic testing sequence looks like

No two workups are identical, and your clinician sets the order. Roughly, though:

• Before anything — What is typically done: Write the episode history: date, what happened, what came before, how long it lasted, which organ systems; Timing that matters: Ongoing — this is what criterion one is built from (7)

• Baseline bloods — What is typically done: Serum tryptase on a calm day; Timing that matters: At least 24 hours after any reaction (1, 9)

• Agree the plan — What is typically done: A standing order or written instruction for acute tryptase, so a lab will draw it during a flare; Timing that matters: Arranged while you are well (2)

• During an episode — What is typically done: Serum tryptase; and/or start a urine collection; Timing that matters: Tryptase within about 30 minutes to 2 hours of onset, informative out to 4–6 hours; urine started within a few hours (1, 16)

• Afterwards — What is typically done: Repeat baseline tryptase to show the return; Timing that matters: At least 24 hours after symptoms resolve (12)

• Sorting the category — What is typically done: KIT D816V blood test; TPSAB1 copy number for HαT; allergy testing; bone marrow only if indicated; Timing that matters: After, or alongside, mediator testing (1, 2)

• Criterion three — What is typically done: A clinician-run trial of mediator-blocking treatment, with the response documented; Timing that matters: Decided and interpreted by your clinician (3)

If the first round is negative and your history is still suggestive, repeating the mediator tests while you are symptomatic is the standard next move, not an admission of defeat (20, 9).

Living with MCAS testing: the questions people ask next

My episodes happen at 3am. How am I supposed to get a tryptase drawn in the window?

This is the single hardest part of the whole process, and it is worth planning for rather than hoping. Three approaches people use with their clinicians: a standing lab order kept on file so an urgent-care or emergency department can draw it without a new referral; an agreement that any emergency-department visit for a reaction includes a tryptase; and, for episodes with a somewhat predictable trigger, timing a clinic visit so a draw is possible. For urine, a chilled, preservative-free container kept at home means a collection can start within the few hours the labs ask for (16, 20). Your clinician decides what is workable where you live.

Do I have to stop my antihistamines before testing?

Not for the reasons people usually assume, and not on your own. The published patient-preparation lists for the mast cell mediator panel name MAO inhibitors, aspirin, NSAIDs and zileuton — H1 and H2 antihistamines are not on them (13). Where antihistamines do matter is criterion three, the treatment-response criterion, and for that your clinician needs to see what happens on and off them, which is a decision they make. Never stop a prescribed medicine to prepare for a test without asking the person who prescribed it.

My tryptase went up but not by 20% plus 2. Does that mean nothing?

It is not nothing, and it is not a diagnosis either. Under consensus-1 the rise has to clear the threshold to count as criterion two (3); Mayo notes that some people rise above their own baseline after anaphylaxis without ever crossing the lab's normal range (12). A sub-threshold rise is a reason to test again during a worse episode, and to check whether the sample timing, the baseline value and the sample handling were all right. Bring the actual numbers and the draw times, not just the "normal" flag.

Can I order these tests myself from a direct-to-consumer lab?

Some of them are orderable without a doctor in parts of the US, and doing so is usually a poor use of money. These tests are interpreted as a pair — an episode value against your own baseline, with the clock times attached — and a single number arriving with no context is exactly what is already misleading people. The AAAAI's advice is to work with a local allergist so the tests get ordered and completed on time (2).

How long should this take, and what if nobody will test me?

Longer than it should. In Mast Cell Action's 2024 survey, 97% of respondents had symptoms for two years or more before the survey, average age at diagnosis was 43, and 46% of diagnoses were made by an allergist or immunologist (19). If you are stuck, the usual next step is a referral to an allergist-immunologist with an interest in mast cell disease, and bringing a dated episode log rather than a general description of feeling unwell.

Does a diagnosis of MCAS change anything practical?

It changes what gets prescribed, what gets watched, and what emergency staff do when you arrive. It does not change what you are experiencing now, which is why "not diagnosed yet" and "nothing is wrong" are not the same sentence. People often also want to know what the label covers day to day, which is the subject of our guide to MCAS symptoms.

How to bring this up with your doctor

First, the red flags that come before any of this. Call 911 and use epinephrine if you have been prescribed it for signs of anaphylaxis: hives or a red itchy rash, a swollen throat or swollen areas of the body, wheezing, trouble breathing or coughing, a hoarse voice, trouble swallowing, chest tightness, vomiting, diarrhea or stomach cramping, passing out, or a feeling of impending doom. A severe reaction can happen without any skin symptoms. Do not take an antihistamine first and wait to see whether it gets better (18).

Bring a log, not a story. The single most useful thing you can hand over is a dated list: when each episode started, what happened in the hour before it, which organ systems were involved, how long it lasted, and what you took. Criterion one is built out of exactly that information, and a clinician reading dates is in a different frame of mind from one listening to a summary (7).

What to say. "I have episodes affecting at least two systems at once — [name them]. I would like to find out whether mast cell activation is involved. Can we get a baseline tryptase now, and set up a way to get an acute tryptase drawn inside the window next time this happens?"

What to ask.

• "Which MCAS criteria do you work from?"

• "What is my baseline tryptase, as a number?"

• "Can we put a standing order in place so an acute tryptase gets drawn during a flare?"

• "Should we test TPSAB1 copy number for hereditary alpha tryptasemia, and KIT D816V?"

• "Which of my current medicines could affect the urine results, and is it safe to pause any of them?"

• "If the first round is negative, what is the plan for repeating it while I am symptomatic?"

Ask for the numbers, not the verdict. Request a copy of the results with the values, the reference ranges and the collection times. "Normal" on a report tells you nothing about whether the sample was drawn in the window.

If you have been told it is anxiety. You can hold both things at once: anxiety is real and treatable, and it is also not a test result. A reasonable reply is, "I would like that considered, and I would also like a baseline tryptase and a plan for an acute sample, so we have the measurement either way." If a clinician will not test and will not refer, a second opinion from an allergist-immunologist is a normal step, not an escalation.

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How Welltory helps — and what it cannot do

The limits first. Welltory is a general wellness product, not a medical device. It does not diagnose, detect, predict, monitor, prevent or treat any condition, and it cannot identify MCAS, mast cell activation, or anaphylaxis. Nothing in the app is a mediator test, and nothing in it substitutes for one. Per Welltory's own help documentation, measurements may be less accurate for people under 18 and during pregnancy (21).

Why a dated log is the one place an app genuinely fits here. The whole diagnosis rests on episodes, and the test has to be taken inside a window after an episode starts. That makes two unglamorous things valuable: knowing when an episode actually began, and having a record you did not reconstruct from memory three weeks later.

You tag the event; the app records the rest the same way every day. Add a tag from the plus sign at the top of the feed — "flush, 40 min", "ER visit", "tryptase drawn 1:20pm". Resting heart rate, heart rate variability, stress minutes, Battery and sleep are recorded the same way every day, so when you look back at a bad night you are comparing it with your own ordinary nights rather than with a population average. Battery and stress minutes need iOS with an Apple Watch or Oura.

My Patterns, over months, shows what your tagged events have in common. My Patterns collects tags from flagged stress and rest stretches on iOS with an Apple Watch or Oura, and patterns start appearing at roughly seven tagged events in a month — so a couple of episodes will not produce one. Anything it surfaces is an association, not a cause, and it is a prompt for a conversation rather than an answer.

A record you can hand over. The Journal (Premium) keeps your measurements, tags and notes together, and the web app exports a CSV (Dashboard → choose a chart → Export). Walking into an appointment with "here are eleven dated episodes over four months, with times" is a materially different conversation from "it happens a lot."

The same red flags apply here, in the same type size. Hives, throat swelling, trouble breathing, wheezing, passing out or a feeling of impending doom means epinephrine if you have it and 911, whatever any app is showing (18).

How we made it

Made with AI tools, then edited and fact-checked by the Welltory team. See our Editorial & AI policy.

Sources were chosen in this order: the two published consensus criteria sets and the peer-reviewed exchange between them, the AAAAI Mast Cell Disorders Committee work group report, patient-facing guidance from The Mast Cell Disease Society, and US reference-laboratory test documentation for the practical details of timing, handling and interference. Every URL was checked. Where sources disagree — the acute tryptase window is the clearest example — we show the range rather than pick one number.

We did not include a chart drawn from Welltory data. Welltory holds no mast cell mediator measurements and no verified MCAS cohort, so any chart would be decoration rather than evidence.

Jane Smorodnikova, co-founder of Welltory, built the methodology behind how we read physiological data.

Written by Tatsiana Yashyna.

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