Strong as an Oak: Finding Answers in Mast Cell Diseases

My mother always said I was a healthy child; “strong as an oak,” just like her. That story made sense at the time, especially compared to my father, who had asthma and an involved  family history of autoimmune and immune deficiency disorders.

But as an adult, my body tells a very different story.

Today, I live with a long list of diagnoses: Sjögren’s disease with significant neurological involvement, Hashimoto’s thyroiditis, autoimmune atrophic gastritis, and hypermobile Ehlers-Danlos syndrome. Yet even these do not fully explain my symptoms. Many of them have been dismissed with a familiar refrain: your immune system is just overactive.

Looking back, there were early signs that something wasn’t quite right. As a teenager, I would wake with a swollen face. Hours spent around chlorine left me struggling to breathe. Once, hairspray on my neck triggered years of weeping sores that resembled scalp psoriasis, only to disappear as mysteriously as they began.

At the time, none of it added up.

It wasn’t until a few years ago that I learned the difference between true IgE-mediated allergies and mast cell activation. That distinction changed how I understood not only my own symptoms, but my father’s as well. What had long been labeled as asthma—unpredictable, triggered by almost anything, sometimes beginning after a single bite of food—looked, in retrospect, more like mast cell–driven reactions than classic asthma.

Around five years ago, my own symptoms became harder to ignore. It started with episodes of facial flushing, sometimes linked to alcohol consumption, often seemingly random. Over time, patterns emerged. Sunlight, synthetic fragrances, cleaning chemicals like bleach, wildfire smoke, and even emotional stress could trigger reactions. A burning bladder became a warning sign that something was off. Exposure could set off a cascade: a racing heart, migraine, nausea, flushing, dizziness.

At the same time, I began experiencing fatigue, joint pain, and muscle aches. When I started losing my eyebrow hair, I suspected an autoimmune condition, likely thyroid-related. That instinct was correct, but it was only the beginning.

After contracting COVID-19 in 2023, my health deteriorated rapidly. Within weeks, I developed severe, persistent allergy symptoms and elevated eosinophils on routine lab work. That led me to an allergist, where further testing revealed a tryptase level of 15. My doctor noted that if it approached 20, a bone marrow biopsy might be necessary to evaluate for systemic mastocytosis.

But another possibility made more sense given my history.

Because of my father’s symptoms, I began to suspect hereditary alpha tryptasemia (HaT). I requested genetic testing and it came back positive. With that result, and my clinical presentation, I met the criteria for mast cell activation syndrome (MCAS). For the first time, a significant piece of the puzzle fell into place.

Starting cromolyn sodium was a turning point. My energy improved, and many reactions became more manageable. But not every intervention went smoothly. When I began allergy immunotherapy, I had concerns about whether it was appropriate given mast cell activation. Those concerns proved warranted.

During one session, I went into anaphylaxis: my blood pressure spiking, my skin flushing bright red before I lost consciousness. It was the first time I had experienced a full anaphylactic reaction, and it was a stark reminder of how reactive my system had become.

It reinforced something I had been learning throughout this process: my body often recognizes danger before medicine has a name for it. I now carry an epinephrine auto-injector everywhere I go.

As someone who works in patient advocacy and health policy, I understood early that answers would not come quickly. I approached my care the way I approach policy problems: by gathering evidence, asking targeted questions, and pushing for next steps even when the path forward was unclear. Just as importantly, I had to learn to tolerate uncertainty and accept “good enough” answers when definitive ones weren’t available.

Understanding hereditary alpha tryptasemia has given me a framework, and although not a complete explanation, a foundation to work with. It has helped me see my symptoms not as isolated problems, but as part of a broader pattern of immune dysregulation involving mast cells and beyond.

We are still early in understanding these conditions. Research into HaT and mast cell activation is evolving, and much remains unknown. But for patients like me, even partial answers can be transformative. They shape how we interpret our symptoms, how we pursue care, and how we advocate for ourselves.