It was like peeling off an electrified suit.
That’s exactly how I described what it was like when I first began removing triggers and adding the right medicines.
I never knew a time when my nerves weren’t hypersensitive. It affected me from head to toe, all the time, day and night. My eyes, ears, skin, and everywhere else both inside and out had nerves firing off, causing all sorts of symptoms from ringing in my ears to visual anomalies and sunlight sensitivity to numbness and tingling.
I still get nearly all of them when I am triggered, but they quiet right back down as soon as my mast cells go back to sleep again, thankfully.
Some symptoms are just annoying, like constant twitches or twinges. Some are excruciatingly painful, like the random stabbing pain. I call the stabbing pain “the invisible ice pick guy” because it hurts so bad and comes on so quickly it feels like I’m being stabbed to death.
I knew it was a problem but I never knew why I was sooo sensitive and of course my doctors had no answers. Sometimes even a hug hurt and forget being tickled. It was excruciating! My son, who has also been dx’d with MCAD has the same problems.
It finally all made sense once I learned about the mast cell and how it directly affects our nervous system:
They are scattered throughout the connective tissues of the body, especially beneath the surface of the skin, near blood vessels and lymphatic vessels, within nerves, throughout the respiratory system, and in the digestive and urinary tracts.
Here are a few different articles detailing the relationship between mast cells and our nervous system:
Mast cells are well known as versatile cells capable of releasing and producing a variety of inflammatory mediators upon activation and are often found in close proximity of neurons. In addition, inflammation leads to local activation of neurons resulting in the release neuropeptides, which also play an important immune modulatory role by stimulation of immune cells. In intestinal disorders like inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS), the number of mast cells is known to be much higher than in the normal intestine.
Moreover, both these disorders are also reported to be associated with alterations in neuropeptide content and in neural innervation. Mutual association between mast cells and enteric nerves has been demonstrated to be increased in pathophysiological conditions and contribute to spreading and amplification of the response in IBD and IBS. In this review the focus lies on studies appointed to the direct interaction between mast cells and nerves in IBD, IBS, and animal models for these disorders so far.
Mast cells are important first responders in protective pain responses that provoke withdrawal from intense, noxious environmental stimuli, in part because of their sentinel location in tissue-environment interfaces. In chronic pain disorders, the proximity of mast cells to nerves potentiates critical molecular cross-talk between these two cell types that results in their synergistic contribution to the initiation and propagation of long-term changes in pain responses via intricate signal networks of neurotransmitters, cytokines and adhesion molecules.
Both in rodent models of inflammatory pain and chronic pain disorders, as well as in increasing evidence from the clinic, it is abundantly clear that understanding the mast cell-mediated mechanisms underlying protective and maladaptive pain cascades will lead to improved understanding of mast cell biology as well as the development of novel, targeted therapies for the treatment and management of debilitating pain conditions.
In humans, lesions of contact eczema or atopic dermatitis can exhibit increases in epidermal nerves, but the mechanism resulting in such nerve elongation are not fully understood. We found that contact hypersensitivity reactions to oxazolone in mice were associated with significant increases in the length of nerves in the epidermis and dermis. Using genetically mast cell-deficient c-kit mutant mice selectively repaired of their dermal mast cell deficiency with either wild-type or tumor necrosis factor (TNF)-deficient mast cells, we found that mast cells, and mast cell-derived TNF, significantly contributed to the elongation of epidermal and dermal PGP 9.5+ nerves and dermal CGRP+ nerves, as well as to the inflammation observed at sites of contact hypersensitivity in response to oxazolone.
Moreover, the percentage of mast cells in close proximity to dermal PGP 9.5+ nerve fibers was significantly higher in wild-type mice and in c-kit mutant mice repaired of their dermal mast cell deficiency by the adoptive transfer of wild-type mast cells than in TNF-deficient mice or in TNF−/− mast cell-engrafted c-kit mutant mice. These observations show that mast cells, and mast cell-derived TNF, can promote the elongation of cutaneous nerve fibers during contact hypersensitivity in the mouse.
There are many more studies out there about the mast cell and the nervous system, but you get the idea.
Yep, it really can be that simple.
Well, sort of. It’s actually a very, very complex disease and it’s a full time job keeping symptoms at bay and avoiding triggers takes monumental effort so I shouldn’t ever use the word simple.
Doable is a better word. It’s definitely doable.