Sit Down Before Reading: A Memoir by Dave Bexfield
I remember clearly the last time that I played catch with Dad. It was the summer of 2006, soon after my multiple sclerosis diagnosis. We dug out our gloves and strolled down the street to the local high school’s ball field, talking about life, the uncertainty of the future, and—to escape the difficult answers about life and the uncertainty of the future—baseball. Would this be the Cubs’ year? What did I think about the new Washington Nationals? That Ryan Zimmerman could be a heckuva player. Did I know that his mother had MS?
Optic neuritis had recently done a number to my vision. Even with glasses, my frustrated optometrist couldn’t correct my eyesight much beyond the required legal limit to drive. Colors were gray and splotchy, my peripheral vision was wonky, and images appeared blurry if I could make them out at all. Heat exacerbated everything. This presented a problem, seeing as how baseballs are small. And hard. And they can chip a tooth, as Coach Bexfield discovered during one practice decades earlier. But we Bexfields are stubborn. We were going to play catch.
My dad, the coach of our Little League team (in yellow), me (front row, second from left) and my sister Karen (front row, fourth from right with bat).
For safety purposes, I held my left arm out far to the side, opened my glove, and told Dad to aim for the mitt. Just aim for the leather. And he did. For the next five minutes we played … chase. To think that just a year earlier at that same field I had hit my first, and only, over-the-fence home run, going so far as to run the bases while the bemused crowd of one watched on—my wife Laura, also the pitcher. But then! One, then two, then three tosses in a row found the worn pocket of my glove and we were playing catch, father and son, like old times.
That day my lifelong allegiance to the Cubbies—unrequited fandom passed down from my grandfather, who passed it down to my father—started to fade, migrating to another woebegone team, the Nats, and a new sports hero. The shift eventually made our family’s annual Christmas letter—themed that year appropriately around 2012’s end-of-the-world Mayan prophecy—shocking friends and family. Obviously the end of the world had to have been nigh. Dave abandoning the Cubs? The Dave who felt it wise to immortalize, in his college yearbook next to his senior photo, the sage quote, “Happiness is watching the Cubs win the World Series while holding Laura in my arms.” That Dave?
Mr. Zimmerman, a slick-fielding third baseman, went on to establish a slew of records for the DC ball club, eventually leading the team to a World Series ring in 2019 before retiring, dulling the tinge of pain I felt when the Cubs accomplished the feat in 2016. But his legacy extends far beyond the infield diamond and batter’s box. The same year I was diagnosed with MS, he established ziMS Foundation in honor of his mother, Cheryl, raising millions of dollars for research into the disease that rapidly disabled her after a 10-year quest to get diagnosed. In fact, Lyme disease was discussed as a distinct possibility in her case, but the tests repeatedly were negative. It had to then be MS, her doctors insisted. Today, the ravages of her disease have taken their toll.
My MS has progressed to the point that I can no longer care for myself and I rely on caregivers for all my daily needs. A typical day for me now includes: someone getting me up, someone giving me a shower, someone dressing me, someone brushing my teeth, someone fixing and feeding me breakfast, and doing everything else for me for the rest of the day. My current challenges are finding competent caregivers and surviving in a world which has little time or patience for the handicapped.
Cheryl’s future portended to be my future, a life wrecked by MS. Until. Until that fateful fall day in 2021 when I discovered that I had been misdiagnosed, that I instead had Lyme disease, that I’d gone through 17 years of failed treatments—7 disease modifying therapies, 5 clinical trials, and a stem cell transplant—all for naught. And that, critically, I had company, lots of company. As the first drops of IV antibiotics entered my bloodstream January 18, 2023—5 days before my 30th wedding anniversary, promise to my wife kept—I thought back to that day on the baseball field with Dad. He was only 62, just seven years older than I am now. I wonder how his arm is at 80. I wonder if we’ll get the chance to throw it around the horn again just because. I wonder.
When used promptly after infection, antibiotics are the only reliably known way to vanquish the spirochetes of neuroborreliosis, the neurological form of Lyme disease. But nearly two decades after an unnoticed blacklegged deer tick in the woods of Old Lyme, Connecticut, hitchhiked to Albuquerque on my scalp? I’d been using a wheelchair full-time for the last five years and was now unable to stand or take a single step on my own. There are scant case studies of people being treated so long after exposure. I had already been taking oral antibiotics, doxycycline, for more than a year with mixed results. But IV antibiotics had to work. They simply had to. What else could I do?
Everyone knows that antibiotics don’t change the trajectory of MS. Except when maybe they do. Obscure studies in obscure medical journals from years ago have hinted at their success, like the 2017 study “Trial of Minocycline in a Clinically Isolated Syndrome of Multiple Sclerosis” in the New England Journal of Medicine. Minocycline is commonly used to treat acne, like its sister drug doxycycline, and was chosen because of its anti-inflammatory properties and its ability to cross the blood-brain barrier. While not a traditional first-line treatment for Lyme disease, “minocycline is more highly lipid soluble than doxycycline and has excellent CSF penetration, making it potentially useful in treating Lyme neuroborreliosis.”
The randomized placebo-controlled Canadian study tested the treatment at 12 different MS clinics on 142 patients who had at least two brain lesions on MRI suggestive of MS—72 were assigned to the minocycline group (100 mg twice daily), 70 to the placebo group. Typically, about two out of three patients with early signs of MS go on to develop the disease. After six months, predictably, the risk of conversion to MS in the placebo group was 61%, mirroring other studies. But results from the minocycline group staggered the researchers and apparently impressed the editors of the most prestigious medical journal in the world: only 33.4% of patients developed multiple sclerosis and “all MRI outcomes at 6 months favored minocycline over placebo.” But researchers reported a complicating snag: the advantage by year two was decidedly unclear.
The benefit was also seen after one year of therapy, but not after two years, said chief author Dr. Luanne Metz of the University of Calgary’s Hotchkiss Brain Institute. “We did not have enough patients at 24 months to know whether the drug was still doing anything or not,” she told Reuters Health. Further tests would be ideal but paying for them will be difficult because no pharmaceutical company stands to make a lot of money from this use for the generic drug.
While the introduction of the antibiotic clearly “delayed” conversion to clinically definite MS in this study, so do disease modifying therapies for multiple sclerosis when given early in the disease course. On the surface, this means that the minocycline offered no overwhelming benefit above that expected from FDA-approved DMTs, had they been given for clinically isolated syndrome. And, conversely, if patients in the study did develop full-blown MS, remaining on the antibiotic or remaining untreated in the placebo group would have been unethical. As patients dropped out, the influencing power of the study faded. To date it has been referenced by fewer than three dozen other studies, a disappointing mark for a paper published in such a renowned journal.
Other than this lone NEJM study, have there been any other studies that have looked at MS and antibiotics? More than just a few. A quick search on Google Scholar for published research on multiple sclerosis and antibiotics revealed 60,700 results—doxycycline and MS alone produced 8,250 hits. Many combined antibiotics with existing MS therapies with varying degrees of success—in some cases astonishing, head-smacking success.
Take this revealing small research study published in JAMA Neurology in February 2008: Combination Therapy With Interferon Beta-1a and Doxycycline in Multiple Sclerosis, done at Louisiana State University Health Sciences Center in Shreveport, LA. The 15 patients in this trial had suffered significant disease breakthrough while taking Rebif, a common first-line therapy for multiple sclerosis. These patients were then given doxycycline in addition to the interferon for a total of four months. What happened next was nothing short of shocking.
After just those four short months, the number of brain lesions per patient dropped dramatically; more than 60% of the patients saw greater than a 25% reduction. And disability? A bonkers decrease. For perspective, it takes the average person with MS over two decades to progress from a 2.0 to a 4.0 on the MS disability scale (EDSS), and no MS drugs reliably reverse disability. Ever. But in this small, non-randomized targeted study of people failing Rebif—a beta interferon drug known to supercharge Lyme disease—the addition of doxycycline triggered a median decrease of 2.3 points, a shedding of disability so incredible that the participants could have auditioned for The Biggest Loser, MS edition.
This should have been a towering home run, one of those 450-footers that hit the upper deck or land on Waverly. Outcomes from these antibiotic-and-MS studies, though, have never been able to show any consistent form of effectiveness. Early results show promise, but the gains after the introduction of antibiotics don’t typically hold. There might be something there, researchers admit, but many of the studies didn’t have the scale, the placebo-controlled arm, or the patient randomness to reach any form of consensus that would justify prescribing antibiotic treatment over FDA-approved therapies for MS. And it’s destined to remain that way.
Instead of trying to analyze, parse, and scrutinize more of these antibiotic studies in MS and chew up an (estimated) 673 chapters, a brief text from Sam, a member of ActiveMSers, perhaps best sums up the overarching sentiment of practicing neurologists when it comes to the progressive neurological disease and antibiotics.
Hey! Asked my neuro about Lyme, nothing points in that direction for me. She told me it is a known fact that old neurological symptoms get better with antibiotics. But then return as soon as you stop with the antibiotics.
Wait, what? Loosely translated, “old neurological symptoms” is just another way of saying “existing MS symptoms,” as in, the current symptoms the patient is experiencing. And that those current symptoms get better with antibiotics. And that then, shockingly and without any explanation, these gains magically disappear … after the antibiotics are stopped.
People treated long after Lyme has been established and disseminated throughout the body face an uncertain future. That’s because if a standard course of antibiotics doesn’t clear up the infection, whelp, you are on your own.
Whether or not this is a “known fact” in neurologist circles, presumably without candlelit seances or chanting in tongues, my personal neurologist did bring up an interesting point the last time we spoke over a year ago. That antibiotics had, at times, made his patients feel even worse, as symptoms inexplicably revved up after receiving the bacteria-busting drugs.
Except it’s not inexplicable. It’s called a Jarisch Herxheimer reaction, the well-documented temporary reaction many Lyme disease patients experience when initiating antibiotics. And this is a huge, complicating factor. That’s because when patients sound the alarm, whether to their neuro or clinical trial coordinator, that they are suddenly going downhill, they are predictably pulled off their antibiotics and dropped from clinical trials to “prevent further harm.” Yet by apparently breaking down the spirochetes, thereby setting the manifestations of this reaction in motion, these antibiotics are doing the exact opposite of harming the patient. Another front colliding in the perfect storm, one of many.
Wait, wait, wait. MS can be confused for a host of other diseases, other look-alike mimics like neuromyelitis optica spectrum disorder or sarcoidosis, so how can I be so confident that these stealthy intruders aren’t infringing on Lyme’s parade? Easy. Other than Lyme disease, an infection, no known mimics of MS should respond positively to antibiotics. If any do, surprise surprise, that so-called mimic is more than likely a Lyme disease interloper… disguised as a mimic, disguised as MS. And please spare me the inevitable howls of “anti-inflammatory properties” of these antibiotics. Gains seen in these trials far outstrip any benefit from an anti-inflammatory bump.
Without the support of governmental resources to fund more robust trials and develop protocols to account for this seemingly negative—but temporary and predictable—reaction, any future investigations looking at MS and antibiotics appear certain to implode. But far worse, scientists are unknowingly forever dooming their own research. And because researchers can’t possibly imagine a scenario where Lyme disease has infiltrated the ranks of those diagnosed with MS, every single trial will meet a singular fate: some degree of failure. Trying to advance research then becomes a fruitless, impossible loop, with failure perpetually repeating itself, like those dudes on YouTube who purposefully entered a roundabout… circling for 24 hours. The only difference between these YouTuber’s never-ending traffic circle of doom and the roundabout MS researchers have been stuck in for decades? One faction was smart enough to eventually exit.
Long Lyme
Tragically, there is another group caught in a medical roundabout with seemingly no exit: those suffering from chronic or “long” Lyme. While the vast majority of those identified with early Lyme are cleared with a short course of antibiotics, an estimated 10% of people treated for Lyme disease with antibiotics see their symptoms return or linger, sometimes for years, even decades. And doctors don’t know why. A May 2023 study published in the Center for Disease Control and Prevention’s Emerging Infectious Diseases journal pinpointed an elevated immune system marker in the blood—interferon alpha—as a possible culprit, but research on the subject is in its infancy
When Lyme disease is caught later in the infection as it was in my case, clearing the spirochetes and the detritus they’ve left is vastly more challenging. People treated long after Lyme has been established and disseminated throughout the body face an uncertain future. That’s because if a standard course of antibiotics doesn’t clear up the infection, whelp, you are on your own. Antibiotics are not your salvation. Science and the CDC say so.
After being treated for Lyme disease, a minority of patients may still report non-specific symptoms, including persistent pain, joint and muscle aches, fatigue, impaired cognitive function, or unexplained numbness. These patients often show no evidence of active infection and may be diagnosed with post-treatment Lyme disease syndrome (PTLDS). Multiple clinical trials, funded by NIH and others, have shown no benefit to additional IV antibiotic treatment in patients with Lyme disease, although the interpretation of those results have been challenged by some.
I was absolutely determined to challenge those results—hell, I was going to be an exception to these flawed studies. Based on my earlier success with antibiotics, I knew that my body had the capacity to heal. When I started on treatment in the fall of 2021, I saw noticeable gains in the first couple of weeks before they leveled off. But just a month later, seemingly out of nowhere, they revved up again, as my health skyrocketed with a cascade of improvements. I went from being barely able to pedal my exercise recumbent bike to spinning for 20 minutes using solely leg power. Even my numbness decreased, just as Randall the actuary had described. It was incredible.
It turns out that I wasn’t alone in this attitude of defiance, not even in my quest to steer clear of the questionable. Ross Douthat, the New York Times columnist with Lyme disease who originally helped me all those months ago, wrote essentially those same words in his memoir, The Deep Places.
I became determined to be the exception to this pattern—the Lyme patient who didn't get tugged too far into the paranoid realm, the Lyme patient who experimented only with treatments that had some kind of clear basis in the material and quantifiable, the (male conservative New York Times columnist) Lyme patient whose account, once I was better, would be more convincing to skeptics influenced by sexism and wary of reality-television stars. Above all, I would be the exception to the pattern I kept seeing in all my reading, all my conversations: the Lyme patient who actually did get fully better, with no caveats or recurring complications, and who proved in my recovery both the reality and the treatability of the disease....
Mr. Douthat received IV antibiotics after extended courses of oral antibiotics failed to clear his infection. And he and all his determination remained sick, inevitably following the rule instead of bucking it. Similarly, my grand designs to be the model MS misdiagnosed patient—the one carrying the bright torch of recovery that others similarly misdiagnosed could follow to glorious recovery from their long-term Lyme—were likewise shredded. Apart from a behaving bladder and no more terrifying psychosis, those early gains had mostly evaporated by the time I started on IV antibiotics. After 30 days of infused ceftriaxone, the changes in my health were minimal to an outside observer. The biggest shift was in my maximum heart rate, which had been peaking in the low 120s. I could now get it into the upper 140s, lower 150s—a massive shift—but the windfall of improvements I had experienced earlier in those first few months of treatment were mostly absent.
For three more weeks, Laura patiently infused me with an extended course of hope, IV ceftriaxone, for a total of 52 days, hoping to change our luck. It didn’t matter. I was now officially a long hauler. A non-responder. Another person with treatment-resistant chronic Lyme. Now what? Mr. Douthat summed up my expected future in this passage.
Because every patient is different, every strain of borrelia and every mix of coinfections distinct, doctors urge sicker patients to embrace a medical version of FDR's “bold, persistent experimentation,” adding dietary changes and herbal regimens and Epsom salt baths and all kinds of supplements to whatever mix of antibiotics they prescribed … The dissenting view is that treatment for chronic Lyme isn't just a battle, but a long and grueling war.
The columnist struggled for five years to get his Lyme disease under control, veering far off the straight-and-narrow into the woo-woo of alternative medicine, going so far as try the Rife machine, a device invented a century ago by one Royal Raymond Rife. The inventor claimed that his "oscillating beam ray" device “could treat various ailments by ‘devitalizing disease organisms’ using radio waves.” Electronics Australia, once Australia's longest-running general electronics magazine (RIP 2000) found that machines like it produced “a tiny pulsed electrical current” of about 1 milliamp from essentially the power source of a nine-volt battery. Like many with Lyme disease, a desperate Mr. Douthat was up for trying anything for solace.
Was this my future? Strangely, inconceivably, and in more ways than I could have possibly imagined, it was. But before we get to that outrageous twist and others equally outrageous, let’s start with one that involves lower stakes, a single misdiagnosis case study.