It was 2008. I was living in Beijing. I’d just changed house, moving into a room that had opened up in an apartment a friend was renting. Because I’d been in Africa for two months, I moved in sight unseen. It was a very old building in a very old hutong. In that neighborhood was a rhythm of life that was rapidly disappearing and probably now gone entirely. I loved it. Moving to that apartment, however, would turn out to be the most serious mistake I have ever made in my life.
The room smelled faintly like a damp, old towel. At first, I didn’t pay it much attention. Someone had actually left some old towels in the closet. “That must be it,” I thought. I stuffed them in a plastic bag and threw them away. A few days later, the smell had still not dissipated, so I emptied out the entire closet. I opened up every window so the January air could waft the smell away. “Mission accomplished,” I thought.
A few days later, the smell was still there. I had no idea where it was coming from, but it was driving me crazy. I isolated it to the back of the bedroom closet and decided maybe if I just kept the door closed, it would be okay. Over time, the smell only seemed to grow stronger. Then one night, it became overpowering. I took a hammer to the drywall. It cracked and fell away in chunks. Behind the drywall it was pitch black, mold (likely Stachybotrys chartarum) spreading in every direction.
I should have moved out that night, but I was a broke freelance writer just out of college, and I had no idea how dangerous mold can be. So I did not move out. I simply closed the closet door and resolved never to use it again.
A couple of weeks went by. I started forgetting things, losing things. I had a hard time concentrating. Then one day, as I was laying in bed, reading, I started to fall asleep. No Jen, you’re not falling sleep, you’re passing out. I had a premonition. It was like a faint voice in my head. Get out Jen. Get out now. Get out of this room now, or you will die. I got up, walked four steps out of my bedroom and into the kitchen, then collapsed on the floor, unconscious.
I don’t know if it was minutes later or hours later, I woke up on the kitchen floor. A thick, black snot was oozing out of my nose. I moved out that night and, still not knowing any better, brought all of my possessions with me.
A biochemist friend of mine explained, “We all breathe in thousands of mold spores a day.” Most kinds of mold are harmless to most people most of the time. The dose makes the poison. But also, the type makes the poison: we were not meant to be exposed to the kind of mold ecologies that can grow on dry wall medium in water-damaged buildings.
It’s important to understand my situation is not common: I was exposed to massive amounts of black mold over a period of only a few weeks. Most people affected by black mold are exposed to much lower doses over a much longer period of time. They may never link the gradual illness or the acute downfall that comes months or years later to a mold exposure. And even though my exposure was severe and obvious, I did not immediately make the link. From my exposure in 2008 until my viral onset in 2011, I was more or less perfectly healthy. My acute myalgic encephalomyelitis (ME) onset would not come until three years later, in 2011. It would take me another three years after that to understand the significance of mold in my illness, after reading a transcript of presentation given by Julie Rehmeyer to the Santa Fe Institute and after having a conversation with Erik Johnson on the shores of Lake Tahoe in Incline Village, Nevada. (Julie went on to write a fascinating, compelling book Through the Shadowlands: A Science Writer’s Odyssey into an Illness Science Doesn’t Understand.” Read it to learn more about her scientific and personal journey with mold avoidance.) What I learned from them and from Lisa Petrison set me on a journey to Moab, Utah in search of “good air.”
That journey is a whole book, a whole film unto its own. The “tent scene” in Unrest is just a small glimpse of what really happened. In brief: I spent three years living in tents in my backyard in Princeton from April, when the temperatures became tolerable, until October, when the leaves fell from the trees and formed damp mounds on the grass, rendering me alternately screaming or immobile until I’d leave to spend the winter in some western desert. Much of the time I was making Unrest, I was conditionally homeless.
Before mold avoidance, I was almost completely bedbound, able to eat only three or four foods. After, I experienced a remission of nearly all my food sensitivities, greater cognitive and physical capacity, and an improvement in some of my ME symptoms (see the table at the end of this article for more detail). But it was not an easy life. The cost of avoidance is the temporary increase in sensitivities. The slightest exposures could now cause extreme cognitive and physical symptoms. And then there was all that laundry…
“Moldies” have fought very hard to be heard in our community and some people with viral onset ME are skeptical that they and people who are mold sensitive (or chemically sensitive for that matter) share the same same illness. As with many other competing paradigms and theories within our community, I don’t think it’s necessarily a case of “either/or.” We as patients fight over the validity of our triggers when (and this is the argument I will be building toward over the course of these “Onset” posts), it may well be a case of “some of the above.” For some, it may be genes + a virus or genes + a toxic exposure. For others, toxic exposures + a virus. For the very unlucky, a toxic exposure, a concussion, a pregnancy, and a virus.
What I believe connects all of my apparently disparate triggers, and perhaps the triggers involved in some patients’ cases, is connective tissue. I am nearly certain that the mechanism underlying my ME symptoms was craniocervical instability (CCI) because those symptoms, which began after my acute viral onset, lifted instantly and completely first, with invasive cranial traction, and second, when I woke up in recovery after my craniocervical fusion surgery. In non-genetic, non-traumatic cases of CCI (i.e., where the bone is intact), it is believed that the cause is lax ligaments. In other words, damage to the connective tissues in the neck. I hypothesized in my last piece that the inflammatory response to an acute infection damaged the ligaments in my craniocervical junction and caused my CCI. However, that is not a normal response to a virus. Why did I have such a strong immune response to an infection that might in another person not even cause any symptoms? Why could I not heal? I think my mold exposure in 2008 set the stage.
First, it’s possible that mold can directly damage connective tissue. While viruses can trigger an increase in collagen-degrading enzymes as a consequence of the host’s inflammatory response, black mold can directly release collagen-degrading enzymes.
However, there is a second reason why I think mold mattered. I believe it is what triggered my mast cell activation syndrome (MCAS), a condition where mast cells overreact to environmental triggers and release excessive amounts of chemical mediators including histamine, cytokines, proteases and heparin. Mast cells are resident in connective tissues and are usually found at barriers: close to small blood vessels, in the mucosal membranes of the nose and gut, along the blood-cerebrospinal fluid barrier in the human brain. They are important in inflammation and allergic reactions, including anaphylaxis. There’s still a lot we don’t know about MCAS, much less its relationship to connective tissue and connective tissue disorders. However, MCAS has been associated with Ehlers-Danlos Syndrome (EDS), a connective tissue disorder, via some genetic evidence as well as clinical observation. A growing number of ME/CFS physicians believe MCAS may underly the food, odor and environmental sensitivities found in (many, not all) people with ME.
When I moved from Beijing to Cambridge, MA to begin my Ph.D in 2008, a few months after fleeing that mold-ridden apartment, I became, for a time, extremely attuned to mold. It did not trigger the neurological symptoms or histamine flushing I would develop years later, but I could smell mildew in bathrooms and in old buildings and in wet towels. It was abnormal and overpowering. Gradually, I started developing intolerances to foods that had never bothered me before. Eventually, I became sensitive to alcohol. It’s possible these were all symptoms of early MCAS.
If there is a link between excessive mast cell activation and collagen degradation, it may be via tryptase. Tryptase is a protein produced by mast cells and is a marker of both mast cell activation and anaphylaxis. Tryptase activates metalloproteinases (those collagen degrading enzymes I discussed in my last article) and it has been associated with cartilage breakdown in osteoarthritis. It has also been found to be elevated in the blood not only of people with MCAS but also in people with Q fever and in a mouse model of viral myocarditis.
In sum, mold exposure and viral infection may well both contribute to an increase of tryptase, MMPs and other collagen-degrading factors and thus, weak connective tissue. This might happen directly or via chronic mast cell activation. (Mold may also have immunosuppressive effects.)
In my case, I think of the virus I caught in 2011 and my massive inflammatory response to it as the straw that broke the camel’s back (or more accurately, if my assumptions are correct, my neck). It’s what tipped me over into symptomatic craniocervical instability. My massive mold exposure in 2008 set the stage, perhaps by directly causing some initial connective tissue damage, perhaps by triggering MCAS, perhaps by altering my immune response to viruses in some other way.
A month before my viral infection, I moved into Omar’s apartment in Cambridge. We used to joke that my illness was “the Omar effect.” Years later, I learned that the summer before I moved in, the roof had leaked and water fell through the ceiling and into Omar’s unit, causing major water damage.
To be continued in Onset: Part III (Connections)
Read all the posts in my CCI + tethered cord series
Read this disclaimer. Crucially, surgery carries risks and it’s important to remember that in medicine, the same exact symptoms can have multiple, different causes. We have no idea how prevalent CCI is in our community and there’s been no research into its relationship with ME. We do know that it is more common among patients with EDS.