LCFC#4: You never forget your first (shock)
Plus: The anxiety of runaway heart rhythms
“What the f*ck was that?”
I’d just jumped on a friend’s back and wrapped myself around him for a piggyback ride into the Pacific Ocean.
Then BOOM! There was a sharp jolt to my chest.
He swung me around, his eyes wide. “Are there electric eels in here?”
“No. . . . It was me.”
For four years after the insertion of my ICD (implantable cardioverter defibrillator), I’d told myself that the doctors had misdiagnosed me. I’d felt fine after the cut below my collarbone healed. I could run, swim, hike, no shortness of breath, no dizziness, no fast heart rates, no passing out. I traveled to Spain, France, England, Mexico, Canada and the Czech Republic.
I’d switched jobs, moving from North Carolina to Washington D.C. to New York City. I made to-do lists dozens of Post-its long and kept pushing, mindlessly.
I was “fine,” I said.
Then, my personal paddles of life, that defibrillator in my chest, gave its first kick. The wall of denial I’d built to fortify my fragile sense of self dissolved. Feeling impatient and unsafe in my own body, I fled the Big Apple for the seemingly greener grass of South Carolina and the comfort of my sister’s home. Surely there my broken heart couldn’t hurt me.
Weeks after settling in, there was a BOOM! while I was running (no more running). Then, one and another in the middle of the night. (I blamed it on lightning bolts that flashed right before, and I didn’t sleep for a week, maybe longer.)
A shock-tuplet came weeks later while visiting North Carolina. Up a few flights of stairs, and BOOM! BOOM! … BOOM! (Obviously it was the stairs. Denial is a sly adversary).
The shocks, of course, made me squeal in pain. The shocks are why I loathe the word shock and avoid using it trivially, if I can.
The seconds, minutes or hours before a shock were the cruelest, though. There was always a tightness in my stomach, a clenching in my chest. Heart racing. Breathlessness. Then a restlessness, a tension, a need to hide, that heightened until the jolt knocked my heart back to normal — a rap on the knuckles for bad behavior.
Friends would ask if I’d been anxious first, then the shock came. Take away the anxiety and the shocks would stop? It didn’t work that way. Trust me, I’d tried. Instead, I’d explain, I’d feel the physical characteristics of a racing heart first, then tense up and writhe — typically on the floor, like a fish out of water. All I could do was wait for the searing jolt (or jolts) that would bring relief.
It was so hard to believe that the physical sensations induced anxiety that I’d question whether what I remembered was right.
Finally, a sliver of validation came last week when a colleague at work shared new research that shows that artificially increasing a mouse’s heart rate raises the animal’s anxiety levels.1
Yep, I bet it does. I feel that. I mean I’ve literally felt that.
Little did I know that what I had felt and talked about with friends was a long-debated research question: What comes first — an emotion, then a physical sensation, or a physical sensation, then an emotion?
In the recent mouse study, the physical sensation — the animals’ increased heart rate — came first, then the emotion — anxiety, assessed by the animals’ behavior. Looking at the mice’s brains, the scientists doing the study identified a region, associated with awareness of bodily sensations, that became more active when the animals had higher heart rates and were acting anxious.
What’s fascinating is that when the researchers turned off cells in that brain region, the mice stopped acting anxious even though their hearts were beating fast, up to 900 times a minute.2 (The fastest human heart rate recorded to date, as best I can find, is 600 beats per minute, as fast as an unaltered mouse’s.)
And there’s more. Consider this sentence from the paper: “Patients with panic disorder and agoraphobia are more likely to have mitral valve prolapse or clinical symptoms similar to paroxysmal supraventricular tachycardia.” Bottom line: There’s an association between heart issues and anxiety disorders.3 This study tugs at the very fabric of that body-brain connection.
The new work, if validated and further explored, could have implications for understanding human emotion and possibly treating anxiety-related disorders.
But there are caveats with the research. First, the study was done in mice; applicability to humans, if it exists, is a long way off. And second, the research only looked at acute anxiety.
I note the second caveat because I experienced both highly acute anxiety (before a shock), and also chronic anxiety (not addressed in the study), which is exhausting and was for me for years. Every situation — the joys and trivialities of life, going to the beach, dating, grocery shopping, driving, visiting friends, even walking my dog — became laden with angst, a fear that I’d lose control of my body, that I’d be helpless, that I’d need a stranger to save me.
How does chronic anxiety fit into this line of research on body-brain connections? I don’t know — at least not yet.
The researchers used gene editing and light, specifically a technique called optogenetics, to manipulate the mice’s heart rate and cells in the animals’ brains.
Science News, where I work, will have a more in-depth report on this new paper soon. I’ll share the news story in my next newsletter.
A possible topic for a future newsletter?