MCAS, Motion Sickness, and Me: A Genetic Perspective
Exploring the Role of COMT, MTHFR, and Histamine Pathways in Chronic Symptoms
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A Lifelong Symptom in Disguise
I recently found myself on a plane, battling the familiar waves of motion sickness. As I sat there, trying to steady my senses, I realized something: this wasn’t new. Motion sickness has been my unwelcome travel companion for as long as I can remember. But it wasn’t until I was diagnosed with Mast Cell Activation Syndrome (MCAS) after a severe bout of COVID that I began to piece together the deeper story.
Initially, I thought MCAS was a new condition—an unfortunate souvenir of long COVID. But as I delved deeper into my health history and analyzed my pre-COVID DNA data, I discovered that this condition had likely been lurking in my genetics all along. And, surprisingly, it tied back to my lifelong struggles with motion sickness.
The Science of Motion Sickness
Motion sickness occurs when there’s a disconnect between the sensory signals your brain receives. For example, when you’re reading in a moving car, your inner ear senses motion, but your eyes stay fixed on the page. This mismatch can lead to nausea, dizziness, and even vomiting. It’s a phenomenon that involves the brain, inner ear, and nervous system.
But why are some people more prone to motion sickness than others? Emerging research suggests that genetics and underlying health conditions play a significant role. For individuals like me, with MCAS and a specific genetic profile, the connection becomes even more intriguing.
The Genetic Connection: COMT and MTHFR
The COMT (Catechol-O-Methyltransferase) and MTHFR (Methylenetetrahydrofolate Reductase) genes are key players in how our bodies process stress, inflammation, and neurotransmitters. Here’s a closer look at their roles:
COMT: This gene regulates the breakdown of catecholamines like dopamine, epinephrine, and norepinephrine. Variants in the COMT gene can lead to slower processing of these chemicals, which may heighten sensitivity to stress and sensory input—both of which can exacerbate motion sickness. (mine is slow)
MTHFR: This gene affects how the body processes folate, which is crucial for DNA repair, neurotransmitter production, and detoxification. Variants in MTHFR can contribute to higher levels of inflammation and impaired detox pathways, which are commonly seen in MCAS patients. Interestingly, MTHFR variants may also influence vestibular signaling—the body's ability to maintain balance and interpret motion—potentially making individuals more susceptible to symptoms like dizziness and nausea. I have two copies (+/+) which means I’m homozygous. That doesn’t mean that I had a 100% likelihood of developing it — but the odds were not in my favor.
Both COMT and MTHFR variants are linked to heightened histamine responses and neuroinflammation, two factors that can play a role in motion sickness.
Did you know that Bonine (Meclizine), a popular over-the-counter remedy for motion sickness, is actually an antihistamine? This connection underscores how histamine pathways—a key factor in MCAS—can also affect vestibular function and motion sickness, providing a fascinating overlap between genetics, chronic illness, and everyday solutions.
MCAS and Motion Sickness: A Hidden Link
MCAS, a condition where mast cells release excessive amounts of histamine and other inflammatory mediators, can intensify sensory sensitivities and inflammation. These factors overlap with the triggers and symptoms of motion sickness:
Histamine Overload: Histamine is a key player in nausea and vomiting, which are central symptoms of both motion sickness and MCAS flares.
Nervous System Dysregulation: Chronic inflammation from MCAS can affect the vagus nerve, which plays a crucial role in calming the body and preventing nausea.
Sensory Sensitivities: Individuals with MCAS often report heightened reactions to environmental stimuli, making them more prone to motion sickness.
How Genetics Helped Me Understand
By running an analysis of my pre-COVID DNA data, I identified variants in both COMT and MTHFR that shed light on my lifelong motion sickness. This discovery helped me see motion sickness not as an isolated symptom but as part of a larger picture tied to MCAS and my genetic blueprint.
Since uncovering this connection, I’ve taken steps to manage both motion sickness and MCAS more effectively. Understanding my genetics has allowed me to:
Tailor My Supplements: Supporting methylation pathways with appropriate B vitamins (like methylfolate) has made a noticeable difference.
Address Histamine Sensitivity: Using antihistamines and mast cell stabilizers before travel has helped mitigate symptoms.
Strengthen My Nervous System: Practices like vagus nerve stimulation and mindfulness exercises have reduced my overall sensitivity to triggers.
Practical Tips for Managing Motion Sickness and MCAS
For those who suspect a similar connection, here are some steps to explore:
Analyze Your DNA: Platforms like 23andMe + genetic analysis tools can help identify COMT and MTHFR variants. (interested in this? lmk in the comments if you want a step-by-step on how to do this)
Prepare for Travel: Use antihistamines, stay hydrated, and consider ginger supplements or acupressure bands for nausea.
Support Nervous System Health: Incorporate vagus nerve exercises, such as deep breathing and cold exposure, into your routine.
Work with a Specialist: A functional medicine practitioner can guide you in managing MCAS and addressing genetic factors.
The Bigger Picture
My experience with motion sickness has been a reminder that our symptoms often hold deeper stories. By connecting the dots between genetics, chronic illness, and neurobiology, I’ve gained not only a better understanding of my health but also a sense of empowerment.
For anyone navigating similar challenges, know this: your body’s quirks and patterns are worth exploring. They might just lead you to unexpected insights and solutions.
A study you may find interesting:
Hromatka, B. S., Tung, J. Y., Kiefer, A. K., Do, C. B., Hinds, D. A., & Eriksson, N. (2015). Genetic variants associated with motion sickness point to roles for inner ear development, neurological processes and glucose homeostasis. Human molecular genetics, 24(9), 2700–2708. https://doi.org/10.1093/hmg/ddv028
Interesting on MTHFR; I have one good gene and one mutated gene for that. My last brain scan showed subpar activity in my cerebellum, which controls mobility. I’ve been challenged with that my entire life; now I know I am clinically clumsy!
how do you get tested for mthfr?