Mast Cell Activation Syndrome Resource Page

The following is a mast cell summary put together for and from my own research. It is not meant to be medical advice, but rather an aggregation of resources and my own ‘self-experimentation’ results. I’m sharing it here as many fellow CSF leakers have asked what I learned and how I’ve tamped down on huge reactions since going into anaphylaxis during my last round of blood patching. These issues arose following diagnostics for my spinal CSF leak, and worsened as treatment occurred. Following severe anaphylaxis to fibrin glue patching in early 2018, my mast cells have been dysfunctional, and I have been working on managing it since.

For reference, prior to starting the regimen below, I had 24/7 searing and burning pain in my skin, adrenaline dumps at night that kept me up until 5am with heart racing, shaking with cold and low blood pressure, hives, heart racing, gastro-intestinal distress, and many instances of anaphylaxis following certain foods or smells. Since using the protocol I’ve listed out below, those have all disappeared, save for occasional reactions to new foods or smells. The skin burning disappearing was especially a relief, as is my ability to sleep again.

I update this page often, and welcome corrections or additional research – please use the contact page on the menu bar above to send me an email. 

Written: August 30, 2019
Last updated: March 7, 2021

Mast Cell Activation Syndrome: Table of Contents

1. Basics of Mast Cell Dysfunction
2. Symptoms and Triggers of Mast Cell Dysfunction
3. Treating Mast Cell Activation Naturally
4. Treating Mast Cell Activation Pharmaceutically
5. Mast Cells and Pain
6. Mast Cells and Inflammation
7. Mast Cells and Celiac Disease
8. Mast Cells and Ehlers Danlos Syndrome (EDS)
9. Mast Cells, Jet Lag, and Chronotherapy
10. Unconventional Treatments for Mast Cell Dysfunction
11. Books to Read


Mast cells are immune system cells that live in the bone marrow and in body tissues, internal and external, such as the gastrointestinal tract, the lining of the airway, and the skin. Everyone has mast cells in their body, and they play many complex and critical roles in keeping us healthy. The positive roles that they play include protecting us from infection, and helping our body by participating in the inflammatory process. However, mast cells are also involved in allergic reactions, from the tiny swelling that appears after a mosquito bite to a life threatening, full-blown anaphylaxis.

-The Mastocytosis Society of the United States (TMS)

Mast cells are “sentinels” of the immune system, a type of white blood cell that helps control the immune processes in the body. They are resident immune cells, because they reside in tissues and not in our bloodstream. They reside in tissues all over the body, from the connective tissue, to endothelial cells, to epithelial cells, and even the brain.

They’re important – we need them! – but balance is key, as with many body systems. When the mast cells are hyperactive, they can lead to systemic problems, as set forth below.

What is mast cell degranulation?

The mast cells are filled with tiny granules, as you can see in the screenshot of the video below. When they get “angry,” a process known as degranulation, they dump up to 200 different signalling chemicals – called mediators – into the blood stream. Those mediators are inflammatory, so the degranulation process kicks up a cascade of other processes in the body.

We don’t want to eliminate the mast cell’s ability to degranulate. That degranulation response is part of the body’s natural defence when it senses invaders, and it’s also part of what helps keep us safe and healthy when things go wrong.

The problem is that mast cell activation syndromes result when that normal defence response goes off the rails, meaning the mast cells mount a defence for innocuous things that would not otherwise be a threat. The immune system now thinks things that would not deserve an ATTACK! response for a ‘normal’ immune system now do.

A mast cell and a mast cell following activation-induced degranulation

Resting mast cell vs. an activated one. Source.

Essentially, the normal mast cell process is altered and the mast cells are trained to degranulate to a variety of triggers, including excipients in medication, stress, and more. I go into the types of triggers below.

Below is a short video showing what happens when mast cells degranulate:

Mast cells exist in organs and tissue throughout the body, and mediate allergic, immune, and inflammatory reactions.

Angry mast cells can lead to feelings of increased anxiety

They also increase anxiety, via their mediator release, huge inflammatory response to that release, and high levels of histamine in the body. A Psychology Today article even called for examining patients for mast cell dysfunction when they present with anxiety, depression, or brain fog, noting:

When patients consult their primary care doctor with many seemingly random dramatic complaints affecting unrelated organ symptoms, which often feature prominent psychiatric symptoms, they are often thought to be suffering from a psychosomatic condition and told “its all in your head.” They may be sent home with a prescription for an antidepressant or anti-anxiety medication, which not only is experienced as invalidating but does not address the root cause of their symptoms. Identifying MCAS as the source of symptoms has important treatment implications and can speed recovery.

Furthermore, a 2017 case study entitled “Mast cell activation disorder masquerading as a nervous breakdown,” notes that a patient who presented with severe psychiatric symptoms was actually found to have MCAS, and his neuro-psych symptoms dissipated once the mast cells were stabilized. That same paper states that “although rare, some patients can present with minor neurocognitive disturbances as well as frank psychotic behaviors.”

Anecdotally, several mast cell patients I’ve spoken with have said their anxiety levels plummeted once the mast cells were stabilized, including several who had a “feeling of doom” that accompanied extreme anxiety.


Mast cells and pain

Mast cells and pain. Source: EMBRN


Mast cell activation syndrome should not be confused with mastocytosis, or histamine intolerance.

The former is usually a lifelong issue that gets worse with trauma, triggers, diseases, etc. The latter can occur at childhood or adulthood, and often with a sudden onset.

Histamine intolerance can be a subset of mast cell diseases, or potentially a standalone issue with a specific root cause. Mast cell diseases are transcend histamine alone, as you can see in the section about meditators below — histamine is one of 200 meditators that dump into the bloodstream when mast cells degranulate.

If your issue is histamine intolerance and not a mast cell issue, see Dr. Joneja’s PDF primer about it here.

All mast cell diseases are caused by the proliferation and accumulation of trained/altered mast cells or the inappropriate release of mast cell mediators, creating symptoms in multiple organ systems.

But there are different subsets of mast cell activation disorders. The focus on this page is mast cell activation disorder (MCAS), which is when the mast cells are hyperactive and degranulate easily/too frequently). An April 2020 study estimates that “this disease that could affect up to 17% of the population on a spectrum from very mild to debilitating symptoms. MCAS is often either misdiagnosed or the diagnosis is greatly delayed due to a lack of provider awareness.”

There’s also mastocytosis, where a patient has too many mast cells and they are often also trigger-happy. Mastocytosis is often confirmed with a bone marrow biopsy that looks for a KIT-gene mutation.

The Mastocytosis Society has a chart for the different types of systemic mastocytosis, and this chart does not include other varients such as Cutaneous Mastocytosis, Mast Cell Sarcoma, nor does it include the newer Hereditary Alpha Tryptasemia.

Varients of Systemic Mastocytosis from TMS

The three major forms of mast cell diseases are mastocytosis, mast cell activation syndrome (MCAS), and Hereditary Alpha tryptasemia (HAT). Mast cell diseases can cause tremendous suffering and disability due to symptomatology from daily mast cell mediator release, and/or symptoms arising from infiltration and accumulation of mast cells in major organ systems. Although systemic mastocytosis is a rare disease, those suffering with MCAS have recently been increasingly recognized and diagnosed. As a result, patients with MCAS appear to represent a growing proportion of the mast cell disease patient population. It is important to note that the process of mast cell activation can occur in anyone, even without a mast cell disease, as well as in patients with both mastocytosis and MCAS.
– The Mastocytosis Society, Overview page

The way I describe the difference to friends and family: MCAS involves inappropriate mast cell degranulation (angry mast cells) and mastocytosis involves extra mast cells that proliferate from the bone marrow and they may also be angry – sometimes a double whammy.

This image below from a January 2020 study “Mast Cells: Fascinating but Still Elusive after 140 Years from Their Discovery,” is also a helpful pictorial demonstration of the many conditions that can arise when mast cells are dysfunctional.

conditions related to mast cells

This figure shows the wide variety of conditions where mast cells have been implicated.

From the study, with full citations here:

This figure schematically illustrates the wide spectrum of pathophysiological conditions in which mast cells and their mediators have been implicated. For several decades mast cells were considered to play mainly proinflammatory roles in several allergic disorders, such as bronchial asthma, allergic rhinitis, urticaria, food allergy, anaphylaxis, atopic dermatitis, and angioedema.

During the last years, it became evident that mast cells represent an important cell during bacterial, fungal, viral, and helminth infections. Elegant studies have demonstrated that mast cell-derived mediators can play protective roles against several venoms. Mast cells and their mediators can be involved in several aspects of tumor initiation and growth, presumably through the production of several angiogenic and lymphangiogenic factors. Systemic mastocytosis is a clonal disease associated with a somatic gain-of-function KIT mutation. Mast cells, strategically located in different sections of the human heart and atherosclerotic plaque, are involved in different phases of atherosclerosis and myocardial infarction. These cells can be involved in several autoimmune disorders, such as rheumatoid arthritis, coeliac disease, multiple sclerosis, and bullous dermatoses.

Mast cell–nerve communications are involved in stress, pain, pruritus, and in inflammatory bowel diseases.

A. Good overview posts about MCAS:

  • This thorough symptom list, Clinical Manifestations of Mast Cell Activation Syndrome By Organ Systems, by Dr. Lawrence Afrin and Dr. Tania Dempsey.
  • Jill Carnahan’s overview of mast cell activation, When Histamine Goes Haywire, here.
  • Hoffman Center: MCAS, When The Immune System Runs Rampant, here. Their MCAS questionnaire here.
  • This PDF from the Mastocytosis Society, that differentiates between mastocytosis, cutaneous masto issues, and mast cell activation syndrome. (Link is to PDF in my Dropbox where you can download to your computer)
  • The video below “Living With Mast Cell Activation Syndrome” from Dr. Maitland, presented at the Ehlers Danlos Global Learning Conference in 2018.

B. Technical explanation of mast cells / mediators in the body

There’s a lot of science discussing the association between mast cells and nerves in most tissues, including studies that suggest the mast cells are constantly providing information to the nervous system. Mast cells are also widely distributed in both connective tissue and mucosal surfaces, and interact with their environment locally in very different ways. They’ve got a load of different functions, too – they’re thought to play a major role in resistance to infection, and are involved in inflammation and the tissue repair that follows initial inflammation during an injury. They also are involved in hair follicles!

And that’s just the tip of the iceberg. They’re involved in so much of the body’s processes that patients go to different specialists with seemingly no commonalities within their symptom profile — only to later find out that the mast cells, located all over the body, are the culprit.

Mast cells are capable of the synthesis of a large number of pro- and anti-inflammatory mediators, including cytokines, growth factors and products of arachidonic acid metabolism. Pre-stored mediators, such as histamine, serine proteases, proteoglycans, sulphatases, and tumour necrosis factor (TNF), are released within minutes after degranulation of the cell.”
Full study/explanation of mediators in Significance of Conversation between Mast Cells and Nerves.

Mast cells increase their numbers in specific site in the body by proliferation, increased recruitment, increased survival, and increased rate of maturation from its progenitors. Mast cells are implicated in brain injuries, neuropsychiatric disorders, stress, neuroinflammation, and neurodegeneration. Source: Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer’s Disease Pathogenesis.

C. Additional publications about mast cell activation

Good resources page from Dr. Theoharides, the “Mast cell master” behind Neuroprotek supplements. Great starting point for mast cell questions/studies. Page is here.


mast cell activation symptoms and effects in the body
A. What are the symptoms of mast cell dysfunction?

Because mast cells exist in so much of the body’s tissues and systems, when they degranulate a large range of symptoms throughout the body may occur.

  • Flushing of the face, neck, and chest Itching, +/- rash
  • Hives, skin rashes – see TMS’ “visual guide to skin lesions” for more, here.
  • Atopic dermatitis and eczema (see here, and here.)
  • Angioedema (swelling)
  • Nasal itching and congestion
  • Wheezing and shortness of breath
  • Throat itching and swelling
  • Headaches
  • Brain fog and cognitive dysfunction, accompanied with anxiety or depression
  • Diarrhea, nausea, vomiting, abdominal pain, bloating, gastroesophageal reflux disease (GERD)
  • Bone/muscle pain, osteosclerosis, osteopenia, osteoporosis
  • Light-headedness, syncope/fainting
  • Rapid heart rate, chest pain
  • Low blood pressure, high blood pressure at the start of a reaction
  • of a reaction, blood pressure instability
  • Uterine cramps or bleeding
  • Tinnitus / ear ringing
  • Dermatographism (can write on your skin leaving a red welt where you traced something with fingernail or blunt object – more here.)
  • Edema (fluid accumulation in different parts of body)
  • Decreased wound healing
  • Interstitial cystitis
  • Deterioration in dentin and teeth
  • Often liver enzymes that are wonky (High bilirubin, elevated liver enzymes, and high cholesterol)
  • Brain fog
  • Coagulation issues and blood disorders (Clots, deep vein thrombosis, easy bruising, heavy periods, nosebleeds and/or cuts that won’t seal up easily)

Mast cell mediator that is degranulated, plus possible effects:

Histamine: Flushing, itching, diarrhea, hypotension, panic attacks/anxiety
Leukotrienes: Shortness of breath
Prostaglandins: Flushing, bone pain, brain fog, cramping
Tryptase: Osteoporosis, skin lesions
Interleukins: Fatigue, weight loss, enlarged lymph nodes
Heparin: Osteoporosis, problems with clotting/ bleeding
Tumor Necrosis Factor-α: Fatigue, headaches, body aches

B. What are the triggers for mast cell degranulation?

Triggers for mast cell degranulation are across the map, from food to activity to environmental exposure and trauma. It’s difficult to imagine just how such disparate and seemingly innocuous things (vibration?!) can degranulate mast cells, but here we are.

The list below is cobbled together from the The Mastocytosis Society, the Canadian Mastocytosis Society, and blogs:

  • Exercise Heat, cold or sudden temperature changes
  • Sun/sunlight
  • Fatigue
  • Stress
    • Emotional (trauma, loss, abandonment)
    • Physical (including pain, accidents, and medical procedures. For medical procedures, see this 2019 PDF guide to bring to hospital with you that discusses mast cell disorders, plus stages of anaphylaxis and triggers.)
    • Environmental (weather changes, pollution, pollen, pet dander, mold, gas leaks)
  • Food or beverages higher in histamine. See diet lists below under TREATING MCAS for more details. A big problem for people trying to get well is that many of the “no” list for histamine is actually recommended heavily for autoimmune diets – eg. fermented foods/natural probiotics, spinach, etc which will all make MCAS symptoms worse.
    • Yeast
    • Alcohol
    • Dairy (especially fermented dairy like kefir, blue cheeses, or aged dairy like Parmesan cheese)
    • Gluten
    • Fermented foods (especially sauerkraut, kombucha, miso, kimchi, fish sauce, and soy sauce – anything that gives food a wonderful umami taste, basically)
    • Cured and smoked meats and fish
    • Shellfish
    • Citrus fruits
    • Vinegars
    • Leftovers (I can tolerate dinner food the next day at lunch but that’s it. Usually, I will just freeze it right away and defrost to eat, so it stops the aging/histamine degradation process.
    • Berries, especially strawberries
    • Spinach
    • Chocolate other than pure dark chocolate
    • Tomatoes
    • Some food additives (see here for more)
  • A surprising amount of medications (most opioids, NSAIDs, antibiotics and some local anesthetics – a longer list is here)
  • Contrast dyes used in MRIs, CTs etc
  • Mechanical irritation (rubbing/chafing)
  • Friction
  • Vibration
  • Natural odours (strong natural scents like essential oils, environmental smells)
  • Chemical odours (cleaning products, for example)
  • Perfume
  • Infections (viral, bacterial or fungal infections can make MCAS worse and should be addressed carefully with help of your doctor.)
  • Venom (bees, wasps, spiders, snakes, etc.)
  • Diesel fuel (smell)
  • For some, sunlight (!!)

Viruses (like COVID-19) can also trigger mast cell activation

I’m including this because we’re seeing a lot of write ups about long-COVID, and the impacts on the body. Some mast cell docs believe that part of long-COVID is due to dysfunctional mast cells. In a September 2020 study from doctors Afrin, Weinstock, and Molderings, the conclusion notes:

The prevalence of MCAS is similar to that of severe cases within the Covid-19-infected population. Much of Covid-19’s hyperinflammation is concordant with manners of inflammation which MC activation can drive. Drugs with activity against MCs or their mediators have preliminarily been observed to be helpful in Covid-19 patients. None of the authors’ treated MCAS patients with Covid-19 suffered severe infection, let alone mortality.

And we already know that mast cells can go haywire from a variety of viruses. For example, what kicked everything off for me was getting dengue fever from a mosquito on my travels. There are quite a few studies looking at the role of mast cells in dengue infections, including one that notes:

Immune cells called mast cells can hinder rather than help the body’s response to dengue virus, which suggests that mast cell products could be used as biomarkers to identify severe forms of the disease.

mast cells and viruses like dengue fever

“The response of mast cells to dengue virus can be beneficial or detrimental. When a mosquito injects dengue virus (brown hexagons) into the skin, the viruses are detected by specific antibodies (green) or unidentified receptors (blue) on the surface of resting (i.e., non-activated) mast cells. These can then trigger an anti-viral response (left) by releasing the contents of their granules (degranulation) and by upregulating intracellular anti-viral molecules (RIG-I and MDA5). The activated mast cells also secrete signaling molecules called chemokines, which recruit other immune cells including natural killer cells (NK), natural killer T cells (NKT) and T cells, which help to clear the virus. However, if local control mechanisms fail, the virus will enter the bloodstream and be carried to other organs (right). This activates the mast cells in these organs so that they undergo degranulation, releasing ready-made proteases such as chymase and tryptase, and synthesizing inflammatory mediators (leukotrienes and vascular endothelial cell growth factor [VEGF]). These increase the permeability of capillaries, leading to vascular leakage. Mast cells in these organs can also be activated by endogenous inflammatory mediators (such as C3a and C5a) that help the body to remove pathogens. Blocking mast cells (or their mediators) with drugs such as cromolyn, ketotifen and montelukast reduces pathogenic vascular leakage, but might also hamper viral clearance. Anti-mast cell therapy could thus be a double-edged sword.”

As the caption to the (ADORABLE) image notes, mast cells can be a double-edged sword in viruses, because we want them to do their job and clear out a virus, but when they are dysfunctional, they overdo it. (And in non-MCAS patients, trying to tamp down on the response may, the study notes, prevent them from doing their job in clearing the virus altogether.

As with the the COVID-19 study above, studies relating to influenza also note that tamping down on mast cell activation can be beneficial. A study “Mast Cell-Induced Lung Injury in Mice Infected with H5N1 Influenza Virus” in mice notes,

“A combination of ketotifen and the neuraminidase inhibitor oseltamivir protected 100% of the mice from death postinfection. In conclusion, our data suggest that mast cells play a crucial role in the early stages of H5N1 influenza virus infection and provide a new approach to combat highly pathogenic influenza virus infection.”

So, all this to say: if you have a virus like COVID-19, dengue fever, influenza, and more, this too can be a trigger to activate mast cells. And treating mast cell activation can thus potentially mitigate severity of viruses, though we wouldn’t want to overshoot (at least in dengue). As more research comes out, especially with respect to COVID-19, I will update this section.


** This is just what has worked for me so far and is not medical advice. Mast cell doctors (see the overview links above) do say to embark on a full H1/H2 blockade, every 12 hours.

A. Reducing Histamine and Stabilizing the Mast Cells Naturally

A note on eliminating triggers. This is not only environmental (I had to switch shampoos and soaps and much more to all-natural products as my skin would burn when I used ‘normal’ ones), but also eating a lower histamine diet to ensure lower circulating levels of histamine in the body.

Note that for many vibration is a trigger, so car rides, electric toothbrushes, and more can degranulate. For me personally, any concentrated oils are an issue. I used a serum on my hands every night before bed and had huge histamine issues/adrenaline dump at midnight until I realized that it was the serum – it had mint oil in it, which for me is now a trigger. That’s how sensitive things are for some, even when least expected.

  • Some medications are also degranulators or histamine liberators. See this list from the Canadian Mastocytosis Society here.
  • How food is processed / ingested can affect your reaction, so you may react one day but not another. The way that a food is processed can change how much of an IgE reaction a person has to it.
  • A note about IgG vs. IgE reactions: There’s often confusion about testing for food allergies or allergies using IgG and IgE testing. They are related to the functioning of mast cells, but not an accurate test for mast cell activation. Mast cells have receptors for both IgE or IgG on them, and both types of antibodies can result in higher histamine levels or higher levels of other meditators, as well as triggering degranulation itself. IgG reactions the calmer of the two, though they are still capable of producing anaphylaxis-like symptoms. These antibodies are common not only for pathogens we are affected by, but also food issues when we have issues with GI permeability (leaky gut and more). IgE reactions, in contrast, are usually sharp and immediate — like when we are stung by something we are allergic to. It’s a fast-paced degranulation response by the sentinels of the immune system to try and protect from something significant. While not part of MCAS testing per se, they can be useful. It’s important to use IgG antigen testing if you are testing IgG, and then phase out those foods for several months to see if that makes a big difference, then try to reintroduce with nutritionist support.

B. Diets that can can help lower overall histamine burden 

Few mast cell patients I’ve spoken with eat a normal diet. As a former food/travel writer, this part is hard. I joke that I’m the worst food writer ever, but the truth is after wrapping my head around celiac disease 20 years ago, cutting things out strictly and systematically is not new to me. I just didn’t ever think I’d have to cut out so much!

Some diet plans from around the web:

  • Low Histamine- Swiss Sighi lists
    • Elimination diet recommendations here.
    • Food lists for histamine: long PDF of graded histamine levels in foods/additives, etc here.
  • Low Histamine – Alison Vickery:
    • DIET PDF from Allison Vickery. She uses a functional approach that combines naturopathic and allopathic medicine, and cites her sources fully.
    • You can find her mast cell posts here.
  • Beyond low histamine: some people with Ehlers Danlos variations or auto-immune issues such as Crohns or colitis also have trouble digesting foods beyond the low histamine varieties. See this page about those additional restrictions, including a low histamine diet suggestion list for people who need to mindful of other categoris.
    • These categories include lectins, oxalates, salicylates, sulfur, and FODMAPs, which – depending on the body — can affect MCAS as well. Note that if oxalates are an issue, higher-doses of Vitamin C will be a problem. It is important to keep track of data related to food and supplements to ensure you can pin down triggers.
    • Lectins are proteins found in some plants, and preliminary research suggests that they may activate mast cells also. For a low-lectin diet list, see here.
    • Oxalates are found in Vitamin C, which is an issue as high-dose vitamin C is helpful for mast cell stabilization, and for collagen synthesis.
  • Speaking of FODMAPS: a low FODMAP diet can also reduce circulating histamine.
  • Some helpful apps for mobile use: Baliza is a German company that has developed several apps that are useful for the low histamine diet, and both are updated as new data and studies come out.
    • Food Intolerances: The app is very thorough and allows you to sort by different food intolerances or allergies. Includes measurements for histamine, fructose, sorbitol, gluten, lactose, and FODMAPs.
      Apple here; Play store here.
    • OxiPur: Measures foods by oxalate and soluble oxalate, searchable, sortable by food category, and includes some measurements related to oxalate content, like calcium in each food. Apple only, here.
    • Histamine Info: App that uses the Sighi list above, and is updated frequently. Apple only, here.

C. Supplements that can help treat mast cell activation 

(Studies supporting why I take each of these products are below.)

  • DAO Umbrellux: A DAO enzyme made from porcine sources, taken 15 minutes prior to meals. I’ve tried many different DAO formulations and this is the only one that seems to work for me and not cause additional reactions.
  • Vitamin C Nutribiotic Ascorbic Acid Powder (non-gmo, pharmaceutical grade)
  • Vitamin C Nutribiotic Sodium Ascorbate (non-gmo, pharmaceutical grade). There is some evidence that sodium ascorbate also helps the extracellular matrix, so I include that in my supplements / total Vitamin C count.
  • Camu Camu, organic and freeze dried. My preferred vehicle for vitamin C.
  • Non-GMO MicroIngredients Quercetin from Sephora Japonica buds If you prefer capsules, Jarrow Formulas Quercetin, Cardiovascular Support, 500 mg. Quercetin should be taken with fat to help it absorb. A more bioavailable version of Quercetin is the Thorne Quercetin Phyotsome. The phytosome formulation, in this case bound with sunflower lecithin, helps the quercetin absorb better.
  • Zeolite: Functional doctors believe that zeolate can help clear histamine from the body. Zeolite is also used as a binder for metals for some.
  • NasalChrom: Useful for seasonal-type allergies, food reactions that include nose running/itching in face. Sodium cromlyn is a mast cell stabilizer.
  • Zatidor eye drops: These are ketotifen fumerate, potent mast cell stabilizer – if you can’t access pills or compounded ketotifen, eye drops may help with oral symptoms considerably.
  • PEA: Palmitoylethanolamide, pure and from a reputable source. Two companies I trust are PeaCure and Vitalitus. When choosing a brand, it is important to make sure the supplement has been micronized to small diameters; this is the form the studies used that showed it was effective. PeaCure is the smallest diameter (they are ultra-micronized), and Vitalitus is micronized to less than 5 micrometers, and are a good second option.
  • Magnesium LThreonate is the type of magnesium I use. Doublewood’s brand has caused no reactions, and is available in USA and Canada.
  • Jarrow Formulas Curcumin 95, Provides Antioxidant Support, 500 mg, (don’t buy with black pepper extract – mast cell degranulator!)
  • LutiMax luteolin plus Rutin powder (NOTE- not Lutein! Must be luteolin. Another option for luteolin, rutin, and quercetin is Neuroprotek –  this is Dr. Theoharides supplement from his Algonot company, and profits fund further studies)
  • Mirica® – Pea (Palmitoylethanolamide) and Luteolin – Natural Pain Relief – Made with OptiPEA® from The Netherlands, if you wanted to combine the two (Luteolin and PEA). I don’t do so, but it’s an option. The PEA is micronized, not ultra-micronized.
  • Amazing Herbs Premium Black Seed Oil, Organic and Cold Pressed.
  • Vital Nutrients Vitamin E 400 (with Mixed Tocopherols) (NOT soy free) OR, Healthy Origins Tocomin SupraBio (Tocotrienols) 50 mg –  if like me you don’t just want one of the tocopherol but rather tocotrienols too. (Soy free. 1 in AM and 1 in PM)

** Note that the links above for Amazon are affiliate links, as with the others on Legal Nomads (see the footer for more), where I get a 4% commission on some purchases.


  • H1 twice a day, 10am and 10pm (Zyrtec)
  • MicroIngredients pure powdered Quercetin – 1 scoop 500mg, 1x a day
  • Quercetin phytosome – 2 capsules with dinner
  • PEA (PeaCure or Vitalitus brand), 1x AM, 1x with lunch
  • Vitamin C 1-3g per day (camu-camu is what I use most)
  • Luteolin/Rutin powder – 1 scoop (150mg of each in 1 scoop) before bed
  • DAO, 1x with lunch and 1x with dinner
  • Magnesium L-Threonate – 2 capsules in late afternoon
  • 1 Vitamin E with lunch and 1 with dinner
  • 1 Vitamin D (1000mg) in AM

D. Studies that support using natural mast cell stabilizers

  • Brain “fog,” inflammation and obesity: key aspects of neuropsychiatric disorders improved by luteolin. (Study – Brain “fog,” inflammation and obesity: key aspects of neuropsychiatric disorders improved by luteolin). The same study also notes that luteolin protects against histamine release from mast cells
  • Palmitoylethanolamide  (works on the endocannabanoid system)
    • “The ability of PEA to control MC degranulation, via a CB1 ⁄ CB2 independent mechanism, has paved the way for its therapeutic use in both animals and humans. The PEA-mediated stabilisation of MCs has proven to be useful in the treatment of atopic and irritative dermatitis. In conclusion, we can hypothesise that cannabinomimetic compounds, including PEA and its congeners, act to control MC activation and degranulation early during the inflammatory response, thus leading to a swift resolution and preventing the development of chronic inflammatory disease.” (Study)
    • Palmitoylethanolamide is a potent mast cell stabilizer and pain reliever (Glia and mast cells as targets for palmitoylethanolamide, an anti-inflammatory and neuroprotective lipid mediator – study)
    • For those with other issues a potent neuroinflammation reducer too, acting synergistically within the endocannabenoid system. Overview /meta analysis, and neuroinflammation study: N-Palmitoylethanolamine and Neuroinflammation: a Novel Therapeutic Strategy of Resolution.
    • And luteolin PLUS Palmitoylethanolamide = even more stabilization. Study: PEA and luteolin synergistically reduce mast cell-mediated toxicity and elicit neuroprotection in cell-based models of brain ischemia. (This is the Mirica product above)
  • Binders, including zeolite, mentioned as a help for mopping up histamine here, and a specific post about how zeolite binds histamines here. See also Study – Histamine-binding capacities of different natural zeolites: a comparative study.
  • Rosae multiflora fructus extract stops mast cell release of histamine (rat study – Rosae Multiflorae Fructus Hot Water Extract Inhibits a Murine Allergic Asthma Via the Suppression of Th2 Cytokine Production and Histamine Release from Mast Cells – Study
  • Quercetin
    • Blocks histamine release due to chemotherapy drug. Study – Quercetin ameliorates paclitaxel-induced neuropathic pain by stabilizing mast cells, and subsequently blocking PKCε-dependent activation of TRPV1.
    • Quercetin also generally works for a wide range of allergies. Quercetin and Its Anti-Allergic Immune Response – study.
    • Quercetin works better than sodium cromlyn for stabilizing mast cells in certain conditions. Study: Quercetin Is More Effective than Cromolyn in Blocking Human Mast Cell Cytokine Release and Inhibits Contact Dermatitis and Photosensitivity in Humans.
    • Quercetin phytosome increases availability and allows for more meditator stabilization and cytokine blocking. Study: “Significant improvements in both in vitro solubility and oral absorption (in terms of both exposure and maximum concentration achieved) by healthy volunteers in a human clinical study were obtained with the Quercetin Phytosome formulation as compared to unformulated quercetin.”
  • Cannabinoid receptor agonists suppress mast cell release of histamine Study – Selective Cannabinoid Receptor-1 Agonists Regulate Mast Cell Activation in an Oxazolone-Induced Atopic Dermatitis Model. Also in the study “Cannabinomimetic Control of Mast Cell Mediator Release: New Perspective in Chronic Inflammation,”
  • Curcumin (tumeric) also acts as an antihistamine, and has been found to decrease mediator release by mast cells, when activated:
    • Anti-inflammatory effect of curcumin on mast cell-mediated allergic responses in ovalbumin-induced allergic rhinitis mouse (study)
    • Lipopolysaccharide (LPS) exposure differently affects allergic asthma exacerbations and its amelioration by intranasal curcumin in mice. (study)
    • Curcumin Ingestion Inhibits Mastocytosis and Suppresses Intestinal Anaphylaxis in a Murine Model of Food Allergy. (study)
    • Inhibitory eff ects of curcumin on passive cutaneous anaphylactoid response and compound 48/80-induced mast cell activation (study)
  • Vitamin C: Helps stabilize mast cells
    • Alison Vickery’s post about how Vitamin C can help increase DAO in the body, which then mops up histamine from food.
    • Article: The relationship between Vitamin C, Mast Cells and Inflammation:
      In the light of these studies, we found that vitamin C relieves most of the symptoms of diseases that involve activation of MCs and we can conclude that further research on the role of vitamin C and MCs is needed.”
    • Article: Vitamin C Revisited: “In critically ill patients, future research should focus on the use of short-term high-dose intravenous vitamin C as a resuscitation drug, to intervene as early as possible in the oxidant cascade in order to optimize macrocirculation and microcirculation and limit cellular injury.”
  • Nigella sativa (black cumin seed) blocks mast cell degranulation in rats (A study – “Effects of Nigella sativa seeds and certain species of fungi extracts on number and activation of dural mast cells in rats.”)
  • Probiotics that may help:
    • Lactobacillus G/G: study
    • Not a great site, but lists probiotics that trigger histamine release vs. those that are safe: here.
  • Vitamin E has been found to decrease mast cell degranulation in some studies. (study)


  • Study of Natural Mast Cell Stabilizers: a) chart (excerpt below) or, b) full study.

Natural mast cell stabilizers



Generally:  an H1/H2 “blockade”, taken every 12 hours. Plus mast cell stabilizers and occasionally pain medication.

  • H1 blockers (Suggested to leave Benadryl for emergencies) – eg. Zyrtec, Xyzal, Claritin, Allegra, hydroxyzine, doxepin, loratadine, fexofenadine.
  • H2 blockers Pepcid, Zantac, Tagamet, famotidine
  • Leukitriene inhibitors: Montelukast/Singulair
  • Prescription mast cell stabilizers (NOTE: these are not full mast cell stabilizers as they do not block cytokine release, but have some mast cell stabilizing properties and mast cell doctors prescribe them as stabilizers often.)
    • Cromolyn sodium
    • Ketotifen (oral, compounded and by prescription in the United States. Teva makes a ketotifen oral tablet called Zatiden in Canada and other countries. Ketotifen oral tablets are also over the counter in many countries such as Mexico, Myanmar, India, and more. Zatidor eye drops are ketotifen as well, but fumarate form)

See the study Pharmacological treatment options for mast cell activation disease, as well as the suggestions in the Hoffman article from the overview section, here.

Further, the Mastocytosis Society has a list of pharmaceutical treatments that are common in mast cell disorders here.


too much histamine due to mast cell dysfunction

[Image source]

A. Pain and mast cell activation, generally
(includes tables with treatment options)

(Source: “A Practical Guide for Treatment of Pain in Patients with Systemic Mast Cell Activation Disease”)

Throughout the entire pain communication network, mast cells are the gatekeepers of pain. Mast cells can communicate with neurons, glia cells, microglia, and vascular endothelial cells through mediators. They influence brain functions directly through histamine. Pain alone can thus increase mast cell degranulation. Mast cells and the nervous system influence each other’s responses through mediators and cytokines. In the periphery mediators can stimulate receptors, resulting in pain. This stimulates mast cell activation creating a feedback loop, resulting in neurogenic inflammation. Mast cells can recruit other immune cells, which release more mediators, boosting inflammation.

Extreme mast cell activation causes inappropriate mediator release and reactivity, causing an enormous range of reactions in all tissues and systems. Classical analgesics, most narcotics and nonsteroidal anti-inflammatory drugs (NSAIDS), can trigger MCAD and thus can be ineffective. (See chart 1 “TABLE 4” below)

Pain in Mast Cell Activation Disorders

Source: study.

Pain perception in mast cell dysfunction should be treated by addressing the mast cell mediator-related causes. But pain is also one of the biggest mast cell triggers – so lowering pain levels is important. Mast cell stabilizers, avoiding inflammatory foods, meditation: these have all helped and may help before stronger drug therapy if that’s what you prefer — especially since neuropathic pain is so hard to treat. (Personally, I went from 24/7 burning pain all over my body to none, unless I consume/am around something that angers mast cells.)

Neuropathic pain poorly (if at all) responsive to classical drug management in the case of mast cell activation, as shown in the table below. Moreoever, some of those drugs may worsen the severity of symptoms by further increasing mast cell activity.

Drug management of MCAS/MCAD

Source: study.

B. Mast cells and fibromyalgia / pain: 2019 study

A 2019 study concludes that mast cells are key players of neuroendocrine and painful disorders, including fibromyalgia, and that inhibiting mast cells would be a useful tool in treating fibromyalgia.

 Natural molecules could include the flavonoids, luteolin and tetramethoxyluteolin, alone or in combination with other substances selected to reduce stress Other natural molecules could include palmitoylethanolamide, which apparently inhibits neuro-inflammation and reduces pain.” Source: “Mast Cells, Neuroinflammation and Pain in Fibromyalgia Syndrome

C. Mast cells and IBS (Irritable Bowel Syndrome)

A 2021 study in Nature entitled “Local immune response to food antigens drives meal-induced abdominal pain” concludes that researchers have identified the biological mechanism that they think may explain why some people experience abdominal pain when they eat certain foods. The studies, from KU Leuven, were carried out in mice and in humans and point to local mast cell activation. This local immune response includes the release of histamine and other mediators (as set forth in this resource page) which lead to pain and discomfort. The researches feel that the findings could pave the way to the development of more efficient treatments for IBS and other food intolerances, and are currently pursuing a larger clinical trial of antihistamine treatments.

An open access piece that accompanies the study, called “Food for thought about the immune drivers of gut pain”, notes that while debilitating gut pain is common, the underlying cause is often unclear. This new mast cell study points to a localized immune response that cause normally innocuous foods to be perceived as harmful, leading to persistent pain.

mast cells, histamine, and IBS

An immune response to harmless food causes pain. The 2021 study reveals “a previously unknown cause of gut pain. a, Immune cells in the gut, including mast cells, which contain histamine molecules, don’t usually target food or microorganisms that normally reside there (commensal bacteria). If mice are infected with the bacterium Citrobacter rodentium, immune cells respond when the gut barrier breaks down (gut cells lose their connectivity), and food and bacteria leave the gut lumen and enter the body. Immune cells target C. rodentium by releasing defence molecules, and also target the harmless food present by producing antibodies that recognize it. Pain occurs as a result of the infection. b, After infection, repair of the gut barrier begins. Mast cells become primed to respond by moving near to neurons and expressing a receptor (generated on the basis of the antibody made previously) that recognizes a fragment of the food called an antigen. c, On subsequent ingestion of the food, mast cells recognize it and release histamine through a process called degranulation. Histamine binds to a receptor on sensory neurons, activating them and causing pain.” Source: Nature.

The article notes that

People with IBS had more mast cells in close proximity to nerve fibres compared with healthy individuals, suggesting more-effective transfer of information between the mast cells and nerve endings of the sensory neurons.

And suggests that as a result of the data provided by this study, treatments for IBS may in the future include:

  • improving the gut permeability to reduce gut access to the intestinal immune system (what healing ‘leaky gut’ focuses on);
  • targeting IgE antibodies that are specific to the food substance of interest;
  • reducing mast-cell degranulation (the topic of this page!);
  • targeting the specific molecules released by mast cells; and
  • blocking the colonic sensory nerves that transmit information and cause pain.


(This is why low inflammation + low histamine diets are useful)

  • Dr Theoharides believes CRH stimulates the mast cells in the hypothalamus (and elsewhere) to produce something called vascular endothelial growth factor (VEGF), which then increases the permeability of the blood-brain barrier (BBB). That leaky BBB then allows more immune cell (e.g. mast cell) and perhaps pathogen infiltration into the brain and bingo, you have inflammation. Source: Could the Brain’s Mast Cells Be Causing Chronic Fatigue Syndrome (ME/CFS)?.
  • Mast cells and neuroinflammation: Mast cells are both sensors and effectors communicating between the nervous, vascular, and immune systems. In the brain, they live in the “brain side” of the blood-brain-barrier, and there they interact with astrocytes, microglia, and blood vessels via their mediators and chemicals. They are first responders in the body, catalyzing reactions, amplifying responses in the body, and also recruiting OTHER immune responses once they’re activated. When dysregulated, this contributes to neuroinflammation. See also the next study.

    “Mast cells both promote deleterious outcomes in brain function and contribute to normative behavioral functioning, particularly cognition and emotion. Mast cells may play a key role in treating systemic inflammation or blockade of signaling pathways from the periphery to the brain.”
    Source: Mast Cells and Neuroinflammation“.

  • An enhanced interaction between mast cells and nerves can lead to neurogenic inflammation. Inflammatory models have shown a significant increase in the number of mast cells, resulting in the increased release of inflammatory mediators on degranulation.

    “Inflammatory mast cell mediators may modulate sensory nerves through the activation of receptors on nerve terminals. […] Thus, mast cell activation can result in an increase in the excitability of sensory nerves and the production and secretion of neuropeptides.”
    Source: Significance of Conversation between Mast Cells and Nerves

  • Mast cells play a crucial role in the peripheral inflammation as well as in neuroinflammation due to brain injuries, stress, depression, and PTSD. Therefore, mast cells activation in brain injury, stress, and PTSD may accelerate the pathogenesis of neuroinflammatory and neurodegenerative diseases including Alzheimer’s disease. Mast cells in brain injuries, stress, and PTSD may promote the pathogenesis of Alzheimer’s disease. “We suggest that inhibition of mast cells activation and brain cells associated inflammatory pathways in the brain injuries, stress, and PTSD can be explored as a new therapeutic target to delay or prevent the pathogenesis and severity of Alzheimer’s disease.” Source: Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer’s Disease Pathogenesis
  • Another study from April 2019 called Mast Cells in Neurodegenerative Disease notes that neuroinflammation is well-established now as a primary pathological component of diseases such as multiple sclerosis, and is gaining acceptance as an underlying component of most, if not all, neurodegenerative diseases. Before, studies focused on the glial cells of the central nervous system, but now researches are looking at mast cells as well, since mast cells affect both their microenvironment and neighbouring cells including T cells, astrocytes, microglia, and neurons. And they can also disrupt and change the permeability of the blood brain barrier, which “has the potential for dramatically altering the neuroinflammatory state,” per the study.
  • Mast cell disorders: From infancy to maturity: “Mast cells are also establishing a new‐found importance in severe asthma, and in remodeling of blood vessels in cancer and atherosclerotic vascular disease. Furthermore, recent evidence suggests that mast cells sense changes in oxygen tension, particularly in neonates, and that subsequent degranulation may contribute to common lung, eye, and brain diseases of prematurity classically associated with hypoxic insults.” This article is a review of mast cell disorders and chronic inflammatory conditions that involve mast cell dysfunction.


  • Mast cells associated with onset of celiac [study]. “We provide a description of the progressive stages of Celiac Disease, in which mast cells are the hallmark of the inflammatory process. Thus the view of Celiac Disease, should be revised, and the contribution of mast cells in the onset and progression of Celiac Disease, should be reconsidered in developing new therapeutic approaches.”
  • Intestinal mast cell involvement with celiac disease [study].
  • A review of studies that investigate the role of mast cells in the pathogenesis of coeliac disease, showing that these cells increase in number during the progression of the disease and contribute to define a pro-inflammatory microenvironment. [study] “In conclusion, it can be assumed that mast cells represent one of the main players of the intestinal damage in the onset of Celiac Disease. Hence, the pathogenesis of Celiac Disease disease should be revised and the contribution of mast cells in the onset and progression of the disease should be considered in the planning of new therapeutic approaches.”


Part of what led me to write this page was the staggering prevalence of mast cell issues within the leaker community. That community is primarily made up of “long haul” leakers like me, people with connective tissue dysfunction or some other genetic and/or pathogenetic reason that the body isn’t able to seal and heal the dura robustly, even with intervention.

It turns out that continuous mast cell degranulation can affect the connective tissue adversely, and for patients with connective tissue disorders that’s a double whammy. When mast cell degranulation happens it not only releases histamine but also proteases, which are enzymes that lead to the breakdown of proteins into smaller polypeptides or single amino acids. Since mast cells live all over the body in tissues, this can affect the integrity of that tissue over time.

EDS is a genetic connective tissue disorder caused by defects in collagen or other proteins that are part of the extracellular matrix (ECM). The ECM is a network that holds tissues together, so when mast cell degranulation comes in and breaks down that network, it can lead to permeability of, say, the gut lining — but also per studies lead to additional tissue laxity and/or hypermobility symptoms.

So mast cell disease can go beyond “just” the symptoms day to day but also the effects on the whole body’s connective tissue, especially if you have a pre-existing genetic disorder.

  • Several investigators have noted a possible link between EDS and MCAD, primarily patients with the hypermobility type of EDS.” – this study examines whether the fact that mast cells live in connective tissue, combined with the “wonky” connective tissue of EDSers means that mast cell activation is more common because of the changes in structure of connective tissue in primarily hEDS patients. Full study hereby Doctor Maitland and Doctor Afrin.
  • After being recruited to connective tissues, mast cells go through more change when they are influenced by surrounding cells. And many mast cells live in our connective tissues. This study looks into how dysregulation of the mast cells occurs in connective tissue disorders.


The circadian clock modulates a multitude of human conditions including asthma and allergy although the cellular mechanisms regulating the clock are still under investigation. Mast cells, which serve as key effector cells in allergic disease were shown to be under control of the SCN and to have a circadian expression and release of their mediators in response to activation.

For more see my long article about jet lag, mast cells, and immune cellswhich includes a thorough jet lag protocol to minimize the circadian rhythm disruption when you travel.

COVID-19 and Chronotherapy

Increasingly, scientists are looking to the circadian rhythm of the body to help manage the diseases of the present, and the treatments of the future.

“When we saw the controversy surrounding the use of ibuprofen, we wanted to fully understand why this drug was beneficial to some people, but having negative effects on others,” said Harry Karmouty-Quintana of University of Texas Health. In a report published in the British Journal of Pharmacology called The case for chronotherapy in Covid‐19‐induced acute respiratory distress syndrome, Harry’s team suggests providing anti-inflammatory medicine at specific times of the day, which would impact the body’s response to the medication without interfering with its fight against COVID-19.

“We hypothesize that the intrinsic circadian clock of the lung and the immune system may regulate individual components of CRS, and thus, chronotherapy may be used to effectively manage ARDS in COVID‐19 patients,” notes the study – which dovetails well with the sections on mast cells, below. We know mast cells have their own circadian rhythm, and that they release cytokines when they degranulate (release inflammatory substances into the blood). It follows, per Harry’s team, that administering medication based on the schedule of that inflammatory flood could optimize the body’s attempts to heal.

Per the conclusion:

“This would mean that afternoon is the preferred time window for drug administration whereas intake at night should be avoided. This is particularly important when administering immune modulators where a single dose is usually given. Furthermore, the goal of chronotherapy in COVID‐19 is to avoid reaching steady‐state drug levels; as in the case of anti‐inflammatory therapy, these would dampen the inflammatory response directed towards the virus.”

Based on what doctors know about the circadian clock of immune cells, they think that time timing of anti-inflammatory agents are important. This is because the immune cells release cell signals associated with negative effects to the body during the mid-to-late afternoon, but release antiviral molecules during the night and into the early morning. A “therapeutic window” for medication would give the medication an opportunity tamp down on inflammation that harms, while also allowing immune cells to produce the inflammatory molecules needed to fight the virus at night.


  • Breathing: pranayama, Butyeko:
    • Treatment of mast cells with carbon dioxide suppresses degranulation via a novel mechanism involving repression of increased intracellular calcium levels. [Study breathing increases Co2]
    • Evidence-Based Role of Hypercapnia and Exhalation Phase in Vagus Nerve Stimulation: Insights into Hypercapnic Yoga Breathing Exercises [Study article – “Research has shown that vagal stimulation helps you not only in controlling the health of your organs and tissues, but it also determines the growth of your stem cells which, in turn, help body in repairing and replacing damaged cells”]
  • Meditation:
    • A comparison of mindfulness-based stress reduction and an active control in modulation of neurogenic inflammation [study]
    • Meditation and vacation effects have an impact on disease-associated molecular phenotypes [study]
  • Self-hypnosis
  • Removing triggers (emotionally and physically)
  • EMDR / trauma therapy or somatic experiencing therapy
  • Intermittent fasting. Not recommended to try multi-day water fasts, as histamine levels start rising again with too much fasting. However, restricting eating to an 8-hour or 6-hour window does seem to benefit. More on types of IF here.


The two most helpful books I’ve read about mast cells are:

  • Mast Cells United: A Holistic Approach to Mast Cell Activation Syndrome, by Amber Walker The title notes that it’s a holistic approach, and I suppose this simply shows how non-holistic other approaches are because the treatment she uses includes antihistamines, ketotifen, cromlyn and other medication that are not simply holistic/flavonoids. But from worldwide travels to essentially being completely bedbound and incapacitated indefinitely, she has put together a remarkably thorough book. She’s in the medical field, though not a doctor, so the perspective as patient is also invaluable.
    • See this study article for the tryptase requirement, one Afrin, Castells, and other doctors disagree with as being too strict/exclusionary. Afrin’s measures for useful diagnostic markers are heparin, prostaglandin D2, histamine and chromogranin A.
    • And also see this response from Drs Afrin and Dempsey, about why tryptase shouldn’t be a gold start of diagnostics for MCAS, below:

Is an elevated tryptase level a reliable marker of mast cell activation syndrome?

In our combined clinical experience now across many thousands of MCAS patients, we (Dr. Dempsey and Dr. Afrin) have not seen a rise in tryptase to be a reliable marker of mast cell activation.  Again, a persistently elevated tryptase may be a reliable marker of an increased number of mast cells in a person, and a clear, brief spike in the tryptase level over some lower, stable baseline level of tryptase probably represents a brief flare of mast cell activation, but such a spike it is not a reliable marker of mast cell activation.  In fact, it appears that mast cells can become activated via so many different routes, releasing so many different mediators under different circumstances, that it is difficult to imagine how a spike (by any amount) in just one mast cell mediator could be a truly reliable marker of mast cell activation detectable in most activation events in most people.  We have even seen many patients whose tryptase levels have gone *down* during events of flagrant mast cell activation, such as anaphylaxis.  And we have seen that in patients whose symptoms are suggestive of mast cell activation, it almost always is the case that elevated levels of mast-cell-specific mediators other than tryptase can be found in the blood and/or urine.

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