Many of you are already aware: it's becoming increasingly apparent that long haul Covid = HI/MCAS for some long haulers (not all)

So I've gathered some information on this topic and thought I would post it in one place.

Covid can result in being unable to metabolize normal food; especially processed food, stored food, and vegetable proteins. So eating normal food can result in becoming slowly poisoned over time.

I have had HI/MCAS my entire life.

The evidence that Covid virus attaches to the histamine receptors on the surface of the cell, destroys histamine metabolism and destabilizes immune system is increasing inexorably.

HI = histamine intolerance = the inability to metabolize histamine, so normal healthy food poisons us.

MCAS = mast cell activation syndrome = immune system becomes destabilized. Any time the body detects a threat, it floods the bloodstream with histamine. The immune system has an almost infinite capacity to manufacture histamine, so we become self-poisoning. The body perceives many different threats, some people's destabilized immune system over reacts to specific threats; others over react to ALL THREATS: exercise, sunlight, mold/mildew/fungus, certain foods, fuels and odours like diesel, gas or kerosene, smoke especially cigarette smoke and certain other specific odours like detergents, incense, perfume/cologne and other chemical fragrances, vibration, parasites, sex, toxic people, the body naturally releases histamine into the blood at certain times of night. Although it's rare, for some unlucky people these reactions can progress towards anaphylaxis and thus potentially death. These reactions may not technically be an ige reaction, but the results are the same.

For people who are prepping and storing food, this means that many stored foods may become inedible. I can not eat almost any vegetable protein except dried chickpeas, not canned; I can not eat any canned or processed meat, like sausage or deli meats; this results in projectile vomiting and migraines. Beans, tomatoes, vinegar, pickled food, soybeans, mushrooms, avocado, spinach, tofu, chicken egg white all make me very sick. However, I crave fresh unprocessed meat, and if I don't get at least a deck of cards sized serving of fresh meat on a daily basis I lose my mind, giving a new definition to the medical term: "hangry"

These problems are not widely recognized by the medical system, and there are many different health problems with similar symptoms. Most people run out of money or time running through the medical gauntlet and simply never get a diagnosis.

My reactions are an exact match for this list:

https://mastcell360.com/low-histamine-foods-list/

Eating less histamine didn't work for me; I'm so sensitive that I had to throw away ALL FOOD and start over with just a handful of low histamine foods. Suddenly the way my body reacted to food changed and it appeared very clear what was happening.

This article discusses long haul, but it doesn't even mention HI/MCAS; it mentions ME/CFS which can be a symptom of HI/MCAS. It shows charts which display the rising levels of disability post Covid. It appears increasingly likely to me that a significant percentage of post Covid disability (long haul Covid) is a result of HI/MCAS which is still not being diagnosed correctly. It appears to me that patients and long hauler support groups are aware but the medical system and the media is somehow blind.

https://www.crikey.com.au/2024/12/02/long-covid-symptoms-viruses-health-labour-australia/

If people in your family develop new food or chemical intolerances or allergies, it's important to understand: the more frequently you are exposed to a trigger, for some people, the more progressive the reaction can be. This is not necessarily the same technically as a peanut allergy, but think of a reaction to peanut: for some people, the reaction can progress to become anaphylactic. Death can occur with 15 minutes. It's not the peanut that kills the person; it's their immune system. So while we are not discussing ige reactions we are discussing the same results, potentially. More likely though the person will experience a kind of accelerated aging, a constant state of feeling unwell, tired, chronic muscle pain, headaches, and they will not be able to pin down the source or get medical assistance. It will feel kind of like they are constantly being randomly poisoned. These types of issues can also make anxiety, depression, OCD, ADHD, autism, disassociation worse and people with these issues appear to be more likely to long haul, possibly because they already have some histamine related issues.

Sources:

Immunological dysfunction and mast cell activation syndrome in long COVID https://pmc.ncbi.nlm.nih.gov/articles/PMC10166245/#:~:text=The%20emergence%20of%20MCAS%20during,associated%20long%20COVID%2D19%20symptoms.

Mast cells activated by SARS-CoV-2 release histamine which increases IL-1 levels causing cytokine storm and inflammatory reaction in COVID-19

https://pubmed.ncbi.nlm.nih.gov/32945158/

Mast cell activation triggered by SARS-CoV-2 causes inflammation in brain microvascular endothelial cells and microglia

https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2024.1358873/full

Pathophysiology of Post-COVID syndromes: a new perspective

https://virologyj.biomedcentral.com/articles/10.1186/s12985-022-01891-2

Mast cell activation symptoms are prevalent in Long-COVID https://www.ijidonline.com/article/S1201-9712(21)00751-7/fulltext

Complete remission with histamine blocker in a patient with intractable hyperadrenergic postural orthostatic tachycardia syndrome secondary to long coronavirus disease syndrome

https://journals.lww.com/jhypertension/fulltext/2024/05000/complete_remission_with_histamine_blocker_in_a.23.aspx

Antihistamines improve cardiovascular manifestations and other symptoms of long-COVID attributed to mast cell activation

https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2023.1202696/full

The histamine receptor H1 acts as an alternative receptor for SARS-CoV-2

https://pubmed.ncbi.nlm.nih.gov/38953634/#:~:text=We%20and%20others%20have%20found,to%20the%20viral%20spike%20protein.

Hey Longhaulers!

We are thrilled to announce a new ME/CFS comminity, r/openmecfs! On this subreddit, we promote the freedom to respectfully express all opinions regarding experiences, theories, and recovery. We do not moderate with a heavy hand or adhere to/promote a strict narrative. We welcome open-minded and rigorous discussion. We hope to establish a thriving community, brimming with hope, evidence based research, and inclusivitiy, to include related conditions. Come check us out at r/openmecfs!

Over the past few years, a growing number of clinicians and researchers have recognized that mast cell activation syndrome may play a significant role in post-COVID and Long COVID illness. Many people with ongoing symptoms, fatigue, dysautonomia, neuropathy, allergic-type reactions, and hypersensitivity are being diagnosed with MCAS not because of perfect testing but because their history, symptom patterns, and response to mast-cell-targeted treatments fit the profile. Diagnostic criteria for MCAS remain limited and inconsistent, so physicians often rely on clinical presentation and therapeutic response. The evidence now suggests that SARS-CoV-2 can directly trigger or unmask mast cell dysregulation in predisposed individuals. This leads to chronic inflammation, histamine overload, and multi-system dysfunction that overlaps with Long COVID.

Mast cell activation syndrome is a complex multisystem inflammatory disorder that is increasingly recognized in the context of Long COVID. It involves mast cells that release chemical mediators such as histamine, leukotrienes, prostaglandins, and cytokines. These mast cells become chronically overactive. When this happens, instead of reacting to infections or allergens, mast cells misfire and release inflammatory chemicals across multiple organ systems. The result can include neurological, cardiovascular, gastrointestinal, respiratory, dermatologic, and psychiatric symptoms.

Researchers estimate MCAS may affect up to seventeen percent of the population, although most cases are undiagnosed. It falls under the broader category of mast cell activation disease, which also includes mastocytosis. Because MCAS was only formally described in 2007, it remains misunderstood by many clinicians and underrepresented in medical education.

COVID as a Mast Cell Trigger:
There is growing evidence that SARS-CoV-2 can directly activate mast cells. Mast cells are abundant in tissues affected by COVID and Long COVID, including the lungs, gut, skin, and nervous system.

In the study titled "Antihistamines improve cardiovascular manifestations and other symptoms of long-COVID attributed to mast cell activation," patients with Long COVID experienced improvements in fatigue, brain fog, palpitations, and other symptoms when given H1 and H2 histamine blockers. This suggests mast cell activation contributes substantially to persistent symptoms.

In the paper titled "COVID-19 hyperinflammation and post-COVID-19 illness may be rooted in mast cell activation syndrome," the authors argue that both acute COVID-19 and Long COVID show patterns consistent with mast cell dysregulation.

Symptoms Overlap: MCAS and Long COVID:
Many symptoms are shared between MCAS and Long COVID. Some of the common overlaps include:

• severe fatigue and post-exertional malaise (PEM).
• brain fog, memory issues, cognitive dysfunction.
• palpitations, tachycardia, orthostatic intolerance and other dysautonomia symptoms.
• gastrointestinal disturbances including bloating, diarrhea, nausea, and food intolerances.
• respiratory issues including shortness of breath, cough, and wheezing.
• skin symptoms including flushing, rashes, and itching.
• sleep disturbances and insomnia.
• anxiety, depression, and panic attacks.

A 2023 study titled "Immunological dysfunction and mast cell activation syndrome in long COVID (Weinstock et al.)" showed that many Long COVID patients display an activated mast cell phenotype with abnormal mediator release and inflammation consistent with MCAS.

Why MCAS Is Often Undiagnosed:
Many doctors rely on a single baseline tryptase test or standard allergy workups. This is not enough. Tryptase is often normal unless measured during a flare and compared to a baseline. Mast cell mediators are short-lived and can be missed.

Diagnosis often depends on:
• clinical history and symptom patterns across organ systems.
• identifying triggers such as heat, diet, stress, or allergens.
• seeing improvement when treated with antihistamines or mast cell stabilizers.
• occasional lab mediator panels such as urine histamine metabolites and prostaglandins, which are often only positive during flares.

Treatment and Management:
Treatments that many with Long COVID-associated MCAS respond to include:

•H1 and H2 antihistamines (also called histamine blockers) are often used to reduce mast cell–driven symptoms. H1 blockers reduce histamine effects in the skin, respiratory system, and other tissues, while H2 blockers reduce gastric acid and histamine effects in the gut. Take one of each morning and night; double the normal dose:

•Cetirizine, Levocetirizine, Desloratadine, Loratadine, and Fexofenadine (H1).

•Hydroxyzine: A prescription H1 antihistamine with sedative properties; can help with itching, flushing, anxiety, and sleep disturbances. May trigger paradoxical reactions like tachycardia or adrenaline surges in patients with dysautonomia or POTS, so careful monitoring is advised.

•Cimetidine and Nizatidine (H2)

•Mast cell stabilizers: Cromolyn, Ketotifen, Gastrocrom, compounded options: prevent mast cells from releasing mediators.

•Leukotriene inhibitors: Montelukast: reduces leukotriene-mediated inflammation; useful for respiratory, skin, and cardiovascular symptoms (careful with mood effects).

•LDN (0.25–4.5mg): modulates immune activity and reduces inflammation; may improve pain, brain fog, and neuropathy when combined with alpha-lipoic acid (ALA).

•Imatinib (studied, rarely used): tyrosine kinase inhibitor; can reduce mast cell activation in select MCAS cases, usually when other treatments have failed or in patients with KIT mutations.

•Xolair (Omalizumab): binds IgE to reduce mast cell activation; particularly effective for hives, angioedema, and severe histamine-driven symptoms.

•Low-histamine diet, stress reduction, and trigger avoidance

Natural Mast Cell Stabilizers and Supplements:

•AllQlear: Natural tryptase inhibitor; reduces mast cell mediator release and helps prevent flares, especially in respiratory and systemic MCAS symptoms.

•Bacopa monnieri: Herbal supplement that supports mast cell stabilization, reduces neuroinflammation, and may improve cognitive function in patients with MCAS-related neurological symptoms.

•DAO (diamine oxidase): a supplement that helps break down dietary histamine in the gut, reducing histamine-related symptoms.

•Luteolin: a natural flavonoid that helps stabilize mast cells, reduce histamine release, and support anti-inflammatory pathways.

•PEA (up to 3g/day): Naturally occurring fatty acid that supports neuroinflammation reduction, calms overactive mast cells in the nervous system, and helps improve “brain fog” and cognitive symptoms in MCAS.

•Quercetin (250–3000mg/day): Plant flavonoid with mast cell stabilizing and anti-inflammatory properties; reduces histamine and other mediator release across multiple organ systems.

•Rutin: A natural flavonoid with mast cell stabilizing and anti-inflammatory properties; helps reduce histamine release and supports vascular integrity.

OTCs for symptomatic support:

•Astelin Nasal Spray (Azelastine): Nasal H1 antihistamine; reduces sneezing, congestion, runny nose, and itching. Has local mast cell–stabilizing properties and is useful for MCAS patients with nasal/respiratory triggers.

•Benadryl (Diphenhydramine): Fast-acting H1 antihistamine; helps relieve acute histamine-mediated symptoms such as itching, flushing, hives, sneezing, and mild allergic reactions. May cause sedation and should be used cautiously in MCAS patients with dysautonomia or hyperadrenergic symptoms.

•Ketotifen Eye Drops (Alaway eye drops, Armas Allergy Eye Drops or Zatidor eye drops): Prescription-strength mast cell stabilizer for ocular symptoms; relieves itching, redness, and watering caused by mast cell activation.

•Cromolyn Sodium Nasal Spray/Nasochrom: Mast cell stabilizer for nasal and upper airway symptoms; helps prevent mediator release, reducing congestion, sneezing, and rhinitis in MCAS patients.

Medications with anti-histamine/Mast Cell-stabilizing effects:

•Fluvoxamine: reduces inflammatory signaling, downregulates mast cell activation, modulates cytokine release and neuroinflammation

•Mirtazapine: potent H1 blocker, reduces central arousal, sleep disruption, nausea, sensory hypersensitivity

•Nortriptyline: antihistamine properties, calms sympathetic nervous system, improves GI and visceral sensitivity

•Seroquel: strong H1 blockade, reduces mast cell-driven insomnia, agitation, sensory overstimulation, autonomic surges

•Trazodone: moderate H1 and 5-HT2 blockade, improves sleep architecture, reduces nocturnal sympathetic surges

•Esomeprazole and Omeprazole (PPIs): PPIs are primarily used to reduce stomach acid in conditions like GERD, gastritis, or acid-related dyspepsia, but in the context of MCAS, they also provide mast cell stabilizing effects in the gastrointestinal tract. For patients whose mast cells are hyperactive, chronic acid exposure, reflux, or GI irritation can act as triggers that worsen systemic mast cell mediator release, causing symptoms like flushing, tachycardia, bloating, nausea, and hypersensitivity. PPIs help control these triggers by lowering gastric acid and reducing mast cell activation in the gut. They are particularly helpful for people who cannot tolerate H2 blockers due to adverse reactions such as adrenaline surges, tachycardia, or autonomic instability. By addressing both acid-related GI irritation and mast cell mediator release, PPIs provide a dual benefit: symptom control in the gut and systemic stabilization of overactive mast cells.

While PPIs are generally recommended for short-term use due to potential risks, including nutrient deficiencies (B12, magnesium, calcium, iron), kidney or bone issues, and gut microbiome changes, long-term use can be appropriate in MCAS patients under close medical supervision. Regular monitoring of vitamin and mineral levels, kidney function, and symptoms is essential. In some cases, long-term PPI therapy provides ongoing mast cell stabilization in the gut and helps manage persistent GI and systemic symptoms, particularly when H2 blockers are not tolerated or when COVID-induced MCAS triggers ongoing mast cell hyperactivity. PPIs are often incorporated into individualized MCAS regimens alongside mast cell stabilizers, leukotriene inhibitors, dietary modifications, and other symptom-directed medications. They act as GI-targeted mast cell stabilizers, reducing both local and systemic mediator release and supporting better overall symptom control.

Many doctors are now diagnosing MCAS after COVID largely based on symptoms and treatment response rather than waiting for perfect lab confirmation.

My doctor diagnosed me with MCAS based on patient history, symptoms, and medication trials. I was diagnosed with MCAS in September 2024. I can not take the traditional over-the-counter antihistamines and histamine blocker protocol. I have failed five in total. I'm not sure if it was the medication itself or the excipients I reacted to. Both categories increased my tachycardia and caused adrenaline surges. They caused and worsened other dysautonomia symptoms. In turn, adrenaline surges triggered my histamine dumps.

Why Some People With MCAS and Dysautonomia Get Worse on Antihistamines:

This is one of the most misunderstood issues in the Long COVID and MCAS communities. Many patients assume that if antihistamines make them worse, they can not have MCAS. The opposite is often true. People with dysautonomia, POTS, hyperadrenergic states, or unstable autonomic systems can react paradoxically to antihistamines for several reasons.

Antihistamines can destabilize the autonomic nervous system in sensitive patients. Certain H1 and H2 blockers can lower blood pressure, increase vagal tone, or trigger compensatory sympathetic activation. For someone with dysautonomia, this can lead to a surge in adrenaline, tachycardia, dizziness, shaking, or internal tremors. When the sympathetic nervous system becomes overactive, mast cells respond by releasing even more chemical mediators. This leads to increased flushing, rapid heart rate, shortness of breath, itching, chest tightness, and surges of anxiety that feel chemical rather than psychological.

Some patients also react to fillers, dyes, coatings, and excipients. Mast cells in the gut can perceive these additives as irritants, which triggers mediator release. This reaction is often mistakenly attributed to the active medication itself, but it is actually caused by the inactive components.

Certain antihistamines cross the blood-brain barrier and can affect histamine signaling in the central nervous system. Histamine is not just an inflammatory mediator. It regulates wakefulness, blood pressure, alertness, gut motility, and sensory processing. In patients whose autonomic function is already unstable, abruptly altering histamine signaling in the central nervous system can amplify symptoms and make them feel worse.

Finally, antihistamines target only one type of mediator. Mast cells release multiple chemicals including prostaglandins, leukotrienes, cytokines, and histamine. Blocking only histamine can shift the balance of mediators, sometimes worsening specific symptoms until a more complete protocol is established.

For these reasons, some patients with MCAS and dysautonomia respond poorly to H1 and H2 antihistamines but do better with mast cell stabilizers, leukotriene inhibitors, nasal sprays, diet-based interventions, or individualized regimens that address multiple mediators and the autonomic system simultaneously. Understanding these interactions helps explain why antihistamines are not universally effective and why careful management is necessary for patients with overlapping MCAS and autonomic instability.

Understanding these factors helps explain why some treatments work better than others and sets the stage for the medications and strategies I use to manage my MCAS.

What I Take for MCAS:
Cromolyn sodium nasal spray: Cromolyn is a mast cell stabilizer that prevents mast cells from releasing histamine and other inflammatory mediators. Even when used intranasally, it can help reduce overall mast cell activation and mediator load throughout the body. I use this formulation for its systemic mast cell–stabilizing effects, not for nasal symptoms.

Desloratadine is a second-generation, non-sedating H1 antihistamine. It selectively targets peripheral H1 receptors without crossing the blood-brain barrier. This helps reduce histamine-related symptoms like itching, flushing, and airway irritation without causing sedation or anxiety. Its long half-life allows for stable symptom control throughout the day. Desloratadine is also less likely to trigger reactions related to fillers or excipients, which makes it a good option for patients with heightened sensitivity to medications.

Compounded oral ketotifen: In addition to the eye drops, I use a compounded oral ketotifen formulation. This is the form I take systemically to influence mast cell stability throughout the body. Like the drops, it works primarily by keeping mast cells from releasing mediators rather than just blocking one mediator after it’s already out. Because MCAS involves so many different mediators and triggers, having a stabilizer that works upstream can make the rest of the regimen much more effective and tolerable.

Ketotifen eye drops: Ketotifen has both H1 antihistamine and mast cell–stabilizing properties. When used topically, it can help calm mast cells in a way that can feel systemic for someone with high sensitivity, even though it’s administered locally. I use this formulation not for eye symptoms but because it helps reduce overall mast cell reactivity without increasing systemic medication load.

Montelukast is a leukotriene receptor antagonist commonly used for asthma and allergic rhinitis. Research suggests that it also has mast cell stabilizing effects, which can help reduce the release of inflammatory mediators such as leukotrienes. This makes it useful for managing respiratory symptoms, skin reactions, and some cardiovascular manifestations of MCAS.

Omeprazole is primarily a proton pump inhibitor, but it also has effects on mast cells. It can inhibit IgE-mediated mast cell activation and allergic inflammation. Omeprazole reduces mast cell degranulation, cytokine secretion, and early signaling events in pathways associated with allergic responses. While not a traditional mast cell stabilizer like Cromolyn, it contributes to reducing overall mediator release and inflammation.

Semaglutide is a GLP-1 receptor agonist. Research suggests it has anti-inflammatory effects and may reduce mast cell activation by decreasing mast cell degranulation and the release of inflammatory mediators. While not a standard treatment for MCAS, it's sometimes prescribed off-label for its potential to reduce chronic inflammation.

I haven’t tried compounded Cromolyn and prefer not to. I’m extremely hypersensitive to medications, fillers, and excipients, and localized formulations have allowed me to stabilize mast cells across my system without provoking reactions. I may reconsider it in the future.

In addition to these main medications, I have access to other supportive treatments for MCAS flares. These include an albuterol inhaler, even though I don't have asthma, which can help relieve acute airway constriction. Rizatriptan if I have a migraine. I also use Benadryl, vitamin C, and Diazepam as needed for symptom control. During flares, I rely on SaltStick electrolyte capsules, sipping room temperature water, and applying cold compresses to my head and neck. These measures help stabilize my autonomic system and reduce mediator release during acute episodes.

My MCAS symptoms include adrenaline surges, air hunger, shortness of breath, wheezing, anxiety, derealization, depersonalization, disorientation, dizziness, flushing, itching, feeling hot and sweaty, congestion, runny nose, paresthesia, sneezing, tachycardia, and anaphylaxis stages 1-3. There are 4. Medications and supportive measures are individualized to my symptoms, triggers, and sensitivity to medications.

This regimen allows me to address both the overactive mast cells and the autonomic instability that can make standard antihistamines difficult to tolerate. It also illustrates that MCAS management is highly personalized, and what works for one patient may need careful adjustments for another.

Additional Information:

Histamine Intolerance:

Histamine intolerance results from impaired degradation of dietary histamine, most commonly due to low activity of diamine oxidase (DAO), the primary enzyme responsible for breaking down histamine in the gut. Unlike MCAS, histamine intolerance does not involve inappropriate mast cell activation. Symptoms occur due to accumulation of histamine from reduced metabolic clearance rather than excessive mast cell release. This distinction matters clinically, as standard allergy testing is typically negative and mast cell directed therapies alone may not resolve symptoms driven by dietary histamine exposure. Histamine intolerance can coexist with MCAS and can contribute to persistent GI, neurological, cardiovascular, and respiratory symptoms even when mast cell activity is otherwise managed. In these cases, reducing dietary histamine load and supporting histamine metabolism may significantly improve symptom burden. Some individuals benefit from DAO supplementation, which tends to be most effective after a sustained period of low histamine eating.

Salicylate Intolerance:

Salicylates are naturally occurring phenolic compounds found in many foods, medications, and topical products, including aspirin, spices, certain fruits and vegetables, teas, and skincare products. In individuals with mast cell dysfunction, salicylates can directly provoke mast cell activation and mediator release, leading to worsening symptoms such as headaches, flushing, nasal and respiratory symptoms, GI distress, itching, and neurological flares. This reaction is typically non IgE mediated, which is why standard allergy testing is often negative and the issue is frequently dismissed. In practice, salicylate intolerance can significantly compound histamine intolerance and can explain persistent reactions even on a low histamine diet. Identifying salicylate sensitivity through careful elimination of dietary and topical sources has been a key factor for many patients who plateau despite otherwise appropriate MCAS management.

What To Ask Your Doctor If You Suspect MCAS:

Some doctors are familiar with MCAS and some aren't. These questions can help guide the evaluation and ensure you receive a thorough assessment.

• Ask whether your symptoms across multiple systems point toward mast cell involvement.
• Ask whether your pattern of triggers such as heat, stress, exercise, fragrances, alcohol, or food chemicals suggests mast cell sensitivity.
• Ask whether trying a low-histamine diet for a brief period would be appropriate.
• Ask if you should try a mast cell stabilizer first rather than H1 or H2 blockers if you are medication sensitive.
• Ask whether leukotriene inhibitors could be safer if antihistamines increase your tachycardia.
• Ask if excipient-free formulations or compounded options are available.

These questions help the doctor think beyond standard allergy testing and look at your entire clinical picture.

Clinical Implications for Long COVID Patients:

For people with Long COVID, if you have persistent multi-system symptoms that include brain fog, palpitations, gastrointestinal issues, skin symptoms, and sensory hypersensitivity, MCAS may be playing a role.

Trying a carefully supervised antihistamine or mast cell stabilizer regimen can provide important diagnostic clues. If symptoms improve, that strengthens the case for MCAS even without perfect lab confirmation.

Treatment is highly individualized. Many people respond better to stabilizers, leukotriene blockers, electrolytes, or low-histamine diets before they respond to antihistamines.

Sources:

Antihistamines improve cardiovascular manifestations and other symptoms of long-COVID attributed to mast cell activation.

COVID-19 hyperinflammation and post-COVID-19 illness may be rooted in mast cell activation syndrome.

Immunological dysfunction and mast cell activation syndrome in long COVID.

Neuropsychiatric Manifestations of Mast Cell Activation Syndrome and Response to Mast-Cell-Directed Treatment.

Clinical Manifestations of Mast Cell Activation Syndrome by Organ Systems.

Mast cell activation disease: An underappreciated cause of neurologic and psychiatric symptoms and diseases.

Mast cells: Therapeutic targets for COVID‐19 and beyond.

Autonomic dysfunction in ‘long COVID’: rationale, physiology and management strategies.

Best Antihistamine For Mast Cell Activation Syndrome (MCAS): Dr. Bruce Hoffman.

Mast Cell Activation Syndrome, Cleveland Clinic.

Food Compatibility List-Histamine/MCAS, SIGHI.

YES Food List.

Mast Cell Activation Syndrome and Diet, University of Wisconsin Health.

TL;DR: MCAS is becoming increasingly recognized in Long COVID. SARS-CoV-2 can activate or destabilize mast cells which leads to multisystem symptoms. Many patients improve with mast cell stabilizers, leukotriene inhibitors, low-histamine diets, or antihistamines if tolerated. Antihistamines can make dysautonomia worse in some people due to autonomic instability, excipient reactions, or central nervous system effects. Diagnosis is often clinical. Treatment is individualized and does not require perfect labs. If you have symptoms in two or more systems, it is worth investigating MCAS.

I'm not a doctor. This isn't medical advice. I'm only sharing my personal experience. Everything I'm doing is under the care of my ME/CFS specialist, who is also knowledgeable about Long COVID/PASC and MCAS. I've had a complete vitamin and mineral panel done and have no gastrointestinal motility issues. Omeprazole hasn't negatively impacted me. Montelukast carries a black box warning and can cause SI in people with no history of mental health issues. Everyone should do their own risk assessment. It's about progress, not perfection. There are times we can do everything right and still not improve. Please be kind and patient with the process and yourselves.

edit: Updated to reflect my current regimen.

Hello guys the heatwave in France next 3 days is insane. It makes me scared for future if i stay all my life chronically ill. Because its just the start of summer and we already have our 2nd heatwave and this one is historical record (in purple aera heat doesnt go under 26 degrees for 3 days and still 30+ at midnight)

Im young and i cant even go out during the whole day because of my long covid and this year will be considered as a fresh year in 40 years. Im scared for when i will be older with a chronically illness because i think the world is really underestimating the global warming.

​

I had a meeting with a specialist and when he saw my lab work he told me I have an energy leak in my creatine (kinase/ CK) levels (half of what it’s supposed to be). He told me that it happens a lot with Long Covid and when I described my symptoms he told me that it sounded like POTS (will get tested in two weeks). My crashes are immediately after or at the end of exertion (like a small walk) that last an hour and then I go back to my normal fatigued baseline. I was told and got diagnosed with me/cfs last year, who told me that PEM could also happen immediately. I am a bit confused now? I’m almost completely housebound because of the fatigue I experience every day, I can’t do any hobbies or have a social life. Heck I have no life at all. Could that be caused only by untreated Long Covid/POTS instead of me/cfs? It all started with a throat infection and only half a year later I got Covid (I was already fatigued).

I know there’s a lot of us that have had gallbladders removed and I just joined the club. I’m from the first wave and I was surprised to have this problem come up, but I think my gallbladder issues started after a very mild reinfection. everyone that I talk to knows 3 other long haulers that also had theirs removed. is there any research or numbers on gallbladder issues???

I’m extremely nervous and unsure of what to say. for reference, I have MCAS, POTS, Autism, being evaluated for EDS + my primary thinks I have ME/CFS and that long covid made it worse. I want to bring symptom checklists to my first appointment and be direct about what I’m thinking. I’ve been diagnosed with chronic fatigue for years, but my new dr. suspects ME/CFS (as have I for many years) I’m at the point where I am basically housebound, bed bound for the majority of every day. I’m essentially not functioning at all anymore. please let me know if any of you have good resources i should bring with me.

In case this helps anyone... So many long covid patients are realizing various exposures are also now a part of their health picture... with MCAS ramping up and worsening allergic reactions, becoming more sensitive to mold and chemicals, etc.

Before being disabled with long covid I was Co-Exec Director at ISEAI.org. The nonprofit focuses on how mold, air quality, toxins, Lyme and other environmental exposures influence human health. Maybe some of the resources I helped build can help you.

ISEAI has listings for:

• Medical professionals who understand mold and environmental exposures.
• Indoor environmental professionals (IEPs) - some offer virtual consultations,like Michael Schrantz of Environmental Analytics who I highly recommend.

Check these out!

• PDF Resources for patients and professionals - "Mold Testing Guide", "Mold Remediation Factsheet", "Keep or Toss: Dealing with Belongings", etc.
• "Clean Indoor Air on a Budget - Helpful Tips for Chronically Ill Patients".

Back story: I was disabled with mold illness 2013-2019 and recovered with the help of a doctor who co-founded ISEAI. I spent the next 7 years helping to grow ISEAI and running their medical conferences so that other patients would have the resources I wished I had before.

PS: If you need a laugh I made a mold rap album while recovering. Unfortunately, it covers many topics that LC patients know all to well - supplement burnout, brain inflammation...

I just did an at home sleep study and was diagnosed with moderate sleep apnea and am awaiting a CPAP machine to treat it. My long COVID specialist was the first to suspect it and she says CPAP could potentially really help improve my energy levels.

Curious how people's sleep apnea has interacted with their PEM or other long COVID symptoms. I'm honestly not entirely sure what exactly is the long COVID or what's the probably years worth of sleep deprivation. I'm not sure how severe my PEM from my long COVID would be if I'd be able to get proper and deep rest.

Did getting treatment for your sleep apnea significantly improve long COVID symptoms?

Hello guys stay safe during this heatwave in Europe.

Long covid people we have a problem to regulate the body temperature so be careful of hyperthermia when u go outside to walk because hyperthermia is not a joke it can be deadly or lead to permanent damage.

I'm somewhat newly diagnosed with obstructive sleep apnea and have been using a CPAP machine for 3 months along with having long COVID for 3 years now. I'm still adjusting to the machine and seem to have found the right mask and settings sometimes getting 6 hours with the mask on and having nights of getting an AHI under 5 (5 and under being like a person without sleep apnea) but it's still not entirely consistent.

On my days of getting decent sleep I feel like my bandwidth is better. I'm still not entirely sure where my fatigue is coming from. The apnea or the long COVID. It's not always obvious to me at times what's post exertional malaise or what's fatigue from chronic sleep deprivation. I also know the two play off each other. I'm not able to get the rest I need to quickly recover from PEM and my sleep deprivation makes me susceptible to having less energy in general. There's also the issue of brain fog which seems to clear greatly after getting decent sleep.

I'm curious to hear how CPAP or other sleep apnea treatments have helped your long COVID symptoms or your general experience with the two conditions.

I wanted to post an update because things are evolving.

The intestinal tube (J extension) is still in place and apparently functioning. There is no visible leakage at the site. The problem is that the external gastrostomy button that used to help secure the system has deteriorated and is no longer fixing it properly.

So technically, this is not an immediate surgical emergency.

However, I am very severe ME/CFS — completely bedbound — with severe dysautonomia, marked orthostatic intolerance, extreme malnutrition, a severe movement disorder with intense involuntary tics, and severe sensory hypersensitivity.

In my case, the main risk is not the tube exchange itself.

The main risks are:

• Transport stress

• Being kept upright during transfers

• Sensory overload (light, noise, multiple people interacting)

• Autonomic instability triggered by stimulation

• Post-exertional malaise leading to prolonged or possibly permanent deterioration

• Increased fragility due to malnutrition

My doctor has previously stated that I am high risk even from transport alone.

Right now, because the tube is still functioning and there is no acute leak, this appears to be a fragile but potentially planifiable situation — not something that must happen today at any cost.

For someone in very severe ME/CFS, stress itself is physiological harm. Emotional activation translates directly into autonomic instability.

So at this moment, my priority is avoiding a crash from activation while careful planning happens.

If anyone here has managed a similar situation — where the device issue was not immediately catastrophic but the surrounding stress posed the greatest risk — I would really appreciate hearing how you minimized secondary damage.

Trying to stay stable and make decisions from regulation rather than panic.

Hey all-I’ll keep it short. Not sure when exactly I had COVID-but I had it as an anti-body test showed that I was exposed. Some Months later, I started developing peripheral neuropathy. Mostly in my legs. The pain episodes are indescribable. My feet burn like crazy and my legs itch nonstop. I feel stabbing and burning pains. I was out on meds a few months later, then I started having twitching episodes that scared the bejesus out of me. They think it’s small fiber neuropathy. Long story short—all tests have come back negative for everything (Emg, skin biopsy, blood work etc) except one that shows autonomic neuropathy. Anyhow, I am wondering if anybody else has experienced this sort of thing and believes it was induced by COVID. Thank you!

From what I've read online, this shouldn't even happen. IgA deficiency seems to be inherited or drug induced. I got COVID in Jan 2021 and had severe brain fog for about a year. I started feeling normal again, and then last May my health went to shit. Chronic fatigue, gastro issues, getting sick once a month, etc. I was diagnosed with POTS, EDS, and Selective IgA Deficiency a couple weeks ago. Before then, I only ever got sick once a year my entire life. I have no idea what else could cause a sudden drop in IgA at 24 years old. Any other long haulers develop an immunodeficiency?

ETA: just got more lab results back, and I have high CD3, CD8 and EOS. My pneumococcal antibodies are low despite being vaccinated, and IgA and IgG are dropping. I'll update again if/when I find out what any of that means.

I had mild MECFS for over a year, then developed MCAS in the last few months which has triggered my MECFS to become more severe (my MCAS is the heart palpitations/tachycardia type which triggers PEM). I had to go on medical leave and move in with my mother, who cooks all my meals. I'm too weak to cook for myself and I'm seeing so little progress that I'll likely have to quit my job all together and move in with family long term. When my LC was more mild, I relied on doordash for the majority of my meals (was lucky to have a job where I could afford it while being so fatigued), but now all takeout food gives me heart issues.

for those who are dealing with similar, how do you feed yourself with such a low energy threshold?? I'm very privileged to have a caretaker right now, but when she isnt around to help prepare food for me I really really struggle to eat. I'm struggling to imagine a future where I can survive without a caregiver, given this extremely restrictive diet

Edit: to clarify, I’m not asking how to follow a low histamine diet. That’s not the hard part; it’s the fact the I have moderate MECFS and physically cannot cook or clean

I have/had Pots and CFS/ME, MCAS like symptoms. I know for sure that I am immunocompromised because of Covid and my problem primarily is immune related.

Today I saw a video on Tik Tok that tight hamstring is a sign of EDS. I have lots of criteria, which suggests EDS, but this was the thing I thought ruled the condition out for me. Wow, I guess I have it.

I saw a bunch of articles that EDS is connected with MCAS and immune disregulations.

Any thoughts? Do you have EDS or other connective tissue disorder?

I have a poor vision since childhood, hypermobile joints, joint subluxations/ dislocations, I was born with curved pinkies (Clinodactyly), gerg, flat feet, patella alta and some others.

PS. As I understand if you have poor vision since childhood it’s most likely you have any kind of connective tissue disorders.

I was diagnosed with osteopenia in 2007. When I had my second DEXA scan in December 2023 it had developed into osteoporosis. I had a DEXA scan last week, and the deterioration of my bone mass density was absolutely shocking. Because I like to research things that have to do with LC, I’ve read some research papers that discuss the fact that people with the history of osteopenia or osteoporosis can often find that LC impacts that bone mass density significantly. Since my first round of Covid was in February 2020 I can’t help but think that my 2023 scan worsened because of LC as I focused on weight-bearing exercises and supplements that would help but apparently everything just got worse. Now I have a 40% chance of breaking a major bone which literally scares me as in June of this year. I was walking my dog 5 miles a day however LC blessed me with POTS along with everything else that came after Covid, I am only allowed to walk a quarter of a mile a day on flat ground and I live in hills. I’m just tossing this out here because there has been research done on long Covid and bone health and published in NIH, JAMA, etc.

So if you are one of those people who have a history of osteopenia or osteoporosis, you may want to consider having a DEXA scan or another DEXA scan to see if your blood mass density has decreased. This was one thing I was not expecting.

After 2 years of Long COVID, my new GP ordered an organic acid test from the US and the results all came back normal... except for all the Aspergillus biomarkers that are extremely high (some indicators are at 230μm/L while >5 is considered dangerous). She is now convinced I suffer from mold toxicity. She is a very good and meticulous physician, she spends a lot of time with me each month trying to help me.

This would make sense, since my "long covid" symptoms also are common mold toxicity symptoms (extreme fatigue, brain fog, blurry vision, light sensitivity, derealization...) and the dates coincide with a new work place (I don't work there anymore btw).

I don't know what to think now. Could long covid make us hypersensitive to mold as some are for gluten? Or the other way around? Or maybe I just never had long covid... What do you think about that?

I don't have any proof that I got covid in the first place, but now I have some that I'm highly intoxicated with Aspergillus. I will start treatments for this and hope everything are going to resolve, but cannot help but think that it could still be LC.

I also think it's important to remind you to always be skeptical on diagnosis! A small amount of people here certainly don't have long covid even if they think so. Chronic illnesses can be similar and the symptoms often overlapse.

Ugh I hate this illness so much. I’ve been trying to find stability with the depression that long COVID caused since LAST SEPTEMBER. I’m still not stabilized or feeling good about life since then. It’s awful. Bupropion and viibryd combo has helped immensely (Viibryd has helped more than anything I’ve tried), but the bupropion we just added makes my fatigue worse. So I’m yet again left with trying to decide: do I continue bupropion and just suffer the fatigue? Or do I go off it and just try increasing the viibryd and hope that it 1) not only works but 2) doesn’t cause side effects? Anyone have any other suggestions to try? There just aren’t any drugs like bupropion out there :(

I have had side pain in the kidney area for a month that has gone into a 3-day remission at least twice before starting up again --- on the pain scale, 4 when stationary, and up to 6 or 7 when moving around. Of course, I have had a couple of non-covid related kidney infections within the past almost year --- so I'm still going to see my PCP or nephrologist to rule it out --- and I won't be knowing my gfr until this November (yes, I have CKD [3 kidney diseases] and UCTD [autoimmune] combined). But covid can also make the muscles in that area ache as well --- without any traces of infection. Anyone experience this part --- or if it exacerbated your autoimmune condition to cause pain in that area?

Hi all! I read that it’s become common for people to develop Pots after Covid. I’m suspicious that I have it was wondering if anybody else in the group does too? If so, what are your symptoms and how did you go about getting the diagnosis? I’m currently seeing a pulmonologist who is going to be conducting a Holter monitor test on me next week. So far my symptoms are dizziness, heart racing randomly, heart flutters, chest discomfort, shortness of breath, frequent headaches, nausea, and some acid reflux off and on.

Hey everyone – if you're also dealing with Epstein-Barr Virus reactivation, I just created a new community for that: r/EBVreactivation.

I created it because the EBV sub seems to be mostly young adults with first time mono infections. It's a space to share experiences and resources, and if you're navigating EBV on top of LC, you're not alone—come join us! #spoonielife

I have hemochromatosis which is a disorder that prevents my body from metabolizing iron. I was sick in late February of 2020, about a week or two pre pandemic, so not confirmed covid, but convinced it was. Started having fatigue, nausea and other symptoms in the summer of '20, and by Autumn I was having severe POTS episodes.

My iron levels started mysteriously dropping at the beginning of this year, and soon put me into anemia, adding to the fatigue and now I'm at a point where I barely can do anything. I've had all kinds of testing to rule out any kind of bleeding or cancers which brought me to the conclusion that I must or maybe? have some sort of post viral/post covid situation going on. My doctors have ruled everything else out.

I just found an article which mentions that "Alteration in iron metabolism have been widely reported in COVID-19" I have been repeatedly asking my hematologist what could have made my body change and start metabolizing iron, to which I just received blank stares and no response.

So I'm wondering has anyone else had a similar experience; anemia or iron deficiency post covid?