Understanding why MCAS (Mast Cell Activation Syndrome) triggers do what they do:
by Russell Johnston, February 20, 2019

Long ponderings about the nature of MCAS and its triggers have led me to the following theoretical understanding. This view is unique to me, so far as I know, so take it with a grain of salt. But it’s a view that’s very consistent with a lot of what we know, and have known for a long time about poisons and learned associations for emesis(vomiting) (and other reactions to poison.) Please note — because we are talking about MCAS, we are talking about reactions that are NOT IgE reactions. In other words, not the classical allergies that everyone is familiar with. Perhaps not even reactions involving histamine (there’s more than one pathway.)

(You can substitute “cold,” “mangoes,” or whatever your individual MCAS triggers are the place of the word “mosquito.” below.)

Let’s say a mosquito bite seems to be a trigger of MCAS attacks for you.

The sight or sound from a mosquito *could* be what’s triggering MCAS and edema, etc. (There’s really nothing that can’t form a secondary/learned reaction and become a trigger.) That’s not very likely, of course. But heat and cold, and the smell of a food you know you react to are more common examples of mere cues (experiences/sensory information) that convince your brain poison is coming soon, causing an MCAS response, even though nothing bad has happened yet (or will, in most cases.) These triggers sparking a reaction can be entirely internal — within your body — as well, and not necessarily anything you’ve consciously sensed, or could sense.

Much more likely is that the substances the mosquito injects to dilute your blood, or stray cells from the mosquito, would trigger a small local reaction, first. The local reaction would be via dendrites and/or mast cells, I believe. But if you then also had an “MCAS attack,” that would happen subsequent to the bite, employing mast cells in various parts of your body, in a preventative reaction that is spurious — as if you were about to be subject to a whole lot of poison. But you aren’t.

The local reaction is a primary reaction to an actual toxin in that small area. The general MCAS reaction is secondary. It’s been “learned” by association, somehow, from previous MCAS attacks that happened to coincide with a mosquito bite or bites a few hours — or less — earlier that same day. Perhaps you got carsick (a primary trigger) after getting bitten by mosquitoes not long before you got in the car, a few times in a row. Given that MCAS has our reactions on a “hair-trigger,” that might be all it takes to form a secondary trigger, and therefore a secondary reaction in the form of MCAS attacks after future mosquito bites, even when you don’t get into a car that day.

Secondary reactions “trained” by the presence (or illusion) of a poison can come and go and can be to any environmental or internal cue at all. The secondary reactions to mere cues exist because toxins are so dangerous, therefore the body wants to prepare in advance for a toxic assault if it possibly can; seconds might matter. If you have the health condition MCAS, there doesn’t seem to be any real danger, yet the same “panics” in advance of or in the absence of poison happen.

Let me give an example from clinical poisoning experiments with animals. The animals were given a novel food, then — up to hours later — an odorless and tasteless poison. They got sick. A week later, introducing the food again caused a reaction similar to the animal being poisoned (because it was trying to defend itself from poison that wasn’t in fact there with degranulation by mast cells, etc.) No actual threat was present, nothing had harmed any part of their bodies. Even so, a reaction — just as in MCAS — happened just as if they’d been poisoned. A secondary trigger for degranulation had been formed (learned.) If the food was given repeatedly, however, this association was slowly unlearned. Again, it’s a form of protection for our bodies to anticipate poisons and marshal our defenses early, because toxins can kill or cause permanent nerve damage so quickly.

Some secondary triggers are more likely to form than others, however.

The more unusual a cue is, the more likely your brain/innate immune system is to single it out and associate it with an MCAS attack (apparent poisoning) happening for some other reason.

Foods are also particularly likely to be associated, too, creating a new MCAS trigger — since this is a common way poisons get into us.

Therefore, eating an unusual food or new food on the same day that you’re doing something that you know is likely to give you MCAS problems is a bad idea. If you know sunlight strongly triggers MCAS for you, say, then don’t eat things you don’t commonly eat on the same sunny day you went out shopping. Wait a day, and eat them then.

I hope to talk about my quest for remission number three in another post — suffice to say that getting back so many foods to eat loosened my previously strict food rules a lot; which led me into a series of non-MCAS autoimmune reactions that have stolen maybe six months from me by now. I think I’m now back on track, still eating far more kinds of food, but with more rigid controls when I add any food to my diet, now.

Next article in this series:
“True Allergy” vs “Intolerance”

Previous article:

Cannabis for allergies, etc — there’s a risk re viruses;
(and this might be true of antihistamines, too.)

Full list of my medical articles:

I've read at least the abstracts of (far) more than 250,000 peer-reviewed medical articles, I studied the history and philosophy of science at University.

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Russell Irvin Johnston

I've read at least the abstracts of (far) more than 250,000 peer-reviewed medical articles, I studied the history and philosophy of science at University.