Sit Down Before Reading: A Memoir by Dave Bexfield
I kept shaking my hands and stuffing them deeper into pockets, but they refused to warm. And strange, my fingers felt all pins and needles, numb. Yikes! They had also turned a ghastly shade of seasick white. But Laura and I were on land, and while it was a cool, wet day in the Colorado mountains, it was still late May in Silverton. We were there rooting on our good friend Lenny, who was participating in the popular Iron Horse bike ride that races the narrow-gauge steam train that regularly chugs up to the town from nearby Durango. His wife, who was with us at the finish line, looked at my Casper hands and knew right away what was wrong.
“That looks like Raynaud’s syndrome,” said Claudia of the condition that limits blood flow to the fingers and toes. “It’s typically triggered by cold or stress and is pretty common in ME/CFS.” She had been diagnosed with myalgic encephalomyelitis/chronic fatigue syndrome just two months earlier. It was totally new to me, as I never had any health issues. It was Memorial Day weekend of 2005. In months I would receive a suspected diagnosis of multiple sclerosis and would soon join Claudia in fighting a lifelong disability.
Until I stumbled on that list of autoimmune diseases commonly diagnosed along with rheumatoid arthritis, I had never considered that I, too, might be a victim of disease stacking—when doctors add medical conditions to your chart to explain new symptoms, missing the true culprit that underlies them all: Lyme disease. Compared to those with osteoarthritis, people with RA are 4.2 times more likely to get diagnosed with Raynaud’s (1.12% of those with RA as opposed to just 0.27% for OA). There technically are two types of Raynaud’s: one not linked to another underlying disease (Raynaud’s disease) and the rarer Raynaud’s phenomenon (also called secondary Raynaud’s), which is associated with other diseases (re: RA and the like) and could be more severe, even causing gangrene. By this definition I have the latter, as my last attack this past spring during a short 55-degree bike ride turned my gloved fingers not white or blue, but sickening, frostbite black. It was scary. Now it all makes sense.
According to the Cleveland Clinic, secondary Raynaud’s is a common dance partner with other autoimmune diseases. Those with connective tissue diseases are at higher risk—e.g., RA, Ehlers-Danlos Syndrome, Sjögren’s syndrome—with an incredible one third of all lupus sufferers two-stepping with Raynaud’s. But scleroderma? An astounding 90% of those patients are also affected by Raynaud’s. Research has even discovered that the constricting blood vessel disease can affect your heart.
It has been ominously consistent. How the same autoimmune and related health conditions keep cropping up in my research. And keep cropping up. And keep cropping up. As you might surmise, there is an inescapable reason.
You might want to pour another drink. Squeeze the hand of a loved one a bit tighter. Get a paper bag to prevent hyperventilating. This is hard for me, too. Most of the diseases mentioned throughout this memoir are diseases that friends of mine struggle with—and have struggled with for years, often decades. And many of these individuals have risen to be champions of their condition (or conditions), in some cases becoming leading advocates, dedicating their professional careers and personal lives to the cause. Books, podcasts, TED Talks, lectures, columns, videos, blogs, social media, and so much more. Many are emblazoned with defiant tattoos of their mission.
I started to grasp the breadth of autoimmune disease’s impact on society in 2016 when I was invited to attend my first HealtheVoices, the largest annual conference in the world for health advocates (sponsored by Janssen and Johnson & Johnson). There I met leaders from myriad disease communities, draped in frightening diagnoses I was only loosely familiar with at the time—lupus, rheumatoid arthritis, Sjögren’s syndrome, inflammatory bowel disease, type 1 diabetes, psoriasis, psoriatic arthritis, ankylosing spondylitis, chronic pain, celiac disease, and others. We all swiftly became friends, bonding over our similar struggles. Jen’s story was especially harrowing, getting diagnosed with stage 4 breast cancer at the age of 32 and receiving a double mastectomy. Only doctors later figured out, after several years of chemotherapy, that it was sarcoidosis, an autoimmune disease that can mimic cancer. How can I tell Jen that she appears to have been misdiagnosed twice, and how do I tell all my other dear colleagues that we may be far more alike than we could have ever possibly imagined?
For decades researchers have desperately tried to find commonalities within these diverse conditions to flush out details that could elucidate our understanding of autoimmune diseases. And they land repeatedly on the same findings as if they were all playing identical Bingo cards.
Similar unknown etiology.
Similar female preponderance.
Similar alarming rise of disease rates over the past 30 years.
Similar global hotspots (US, Canada, northern Europe).
Similar global warm spots (parts of southern Europe, Australia, South America).
Similar global cool spots (the Caribbean, large parts of Oceania, Southeast Asia).
Similar loose hereditary connections, where two or more family members present with the same autoimmune disease.
Similar familial autoimmunity, where a mix of autoimmune diseases frequently occur among family members.
Similar set of frequent symptoms such as fatigue, joint pain, weakness, rashes, vision problems, cognition issues, numbness, digestive difficulties.
Similar constellation of uncommon complications such as psychosis, heart issues (PoTS), lung issues, stroke, and more.
Similar laboratory markers in blood and cerebral spinal fluid (e.g., presence of antinuclear antibodies, elevated albumin serum), cytokines.
Similar noted complications with certain classes of antibiotics.
Similar immune suppressive treatments frequently used, from rituximab to high-dose steroids.
Similar recognition of the potential dangers of interferon beta therapy.
Similar trajectory of progression, complete with relapses followed by remittance.
Similar predisposition to acquiring other autoimmune diseases.
Even similar “genetic” signatures (more on that in a moment).
And there is one other ominous, foreboding similarity. They were all “discovered” before Lyme disease.
Claiming Dibs
When I started to pen this memoir, I originally was focused on convincing doubting doctors that I had Lyme disease, not multiple sclerosis, so that I could get appropriate treatment. That quickly evolved when I realized that there had to be others misdiagnosed like me, and I became determined to find out how many of us were out there and who they were. For months and months, I had presumed that the chief testing failure for Lyme disease was that it couldn’t detect a rare form of Lyme that resembled MS, Lyme encephalomyelitis. At the time I was firmly in the camp of doubters, that it was inconceivable, impossible, that Lyme disease instead was at the root of dozens of supposed autoimmune conditions. Scientists might swing and miss at times, but that would be next level whiffage, akin to Wile E. Coyote and his repeated ill-fated quests to dine on Road Runner.
Damn it all to hell, science! It kept repeating and repeating all obnoxious-like, as if it were a four-year-old boy trying to get the attention of his mother—Mom, Mom, Mom, Mom, Mom, Mom—despite her pleas, in a hushed voice, that she was on a very, very important phone call and did not want to be disturbed. Only later in my research, when the same autoimmune diseases kept making unexpected cameos in the scientific medical studies I was reviewing, did I even consider that the threat of misdiagnosis extended far beyond the confines of MS. For instance, I initially thought Puerto Rico, an odd outlier in Latin America with unexpectedly high rates of MS, was a brilliant discovery that would cement my leading hypothesis—that people acquire Lyme disease during travel to endemic areas only to be later diagnosed with MS. But it turns out, it wasn’t just cases of MS.
“Other unique environmental factors may also help explain the lower frequency of MS and other autoimmune disorders in Latin America,” reported a 2021 cover feature in the journal Practical Neurology. Again, other autoimmune diseases. The authors then regurgitated the same tired theories as to why less progressive, less advanced countries are spared. If it’s not the result of poor, inaccurate reporting, then it’s the sun. And the dirt. “Exposure to environmental pathogens such as parasites may have a protective effect, suppressing the development of MS, as suggested by the hygiene hypothesis. Other factors include vitamin D and sun exposure. These environmental factors may be different in Hispanic/Latinx individuals, in particular, those born in the US.”
There appears to be one ubiquitous environmental factor: an increased presence of ticks wherever you have been. And it doesn’t matter diddly-squat if you used too much hand sanitizer or slathered on too much sunscreen. If you’ve ever traveled to such an area, you are at risk. If you’ve ever lived in such an area, you are at higher risk. And if you’ve ever lived in such an area and spent your weekends camping in their favorite stomping grounds, you are at a significantly higher risk.
As I started to investigate autoimmune diseases other than RA, I began to feel sick, just sick. Celiac disease checks all the boxes for a Lyme mimic, too, from repeated observations of a “latitude gradient,” to a predictably weak “genetic” link, to an unusual prevalence of cases in Puerto Rico. A little blacklegged deer tick triggering a gluten allergy sounds ridiculous—until you read through the CDC’s July 2023 warning that Lone Star ticks are responsible for giving an estimated half million people in the US an equally unlikely gift… a severe allergy to meat.
I’ve tried to walk readers through the stages of misdiagnosis, and methodically work down from what is certain to be an initial reaction—impossible—to remotely possible. Then plausibly possible. And then progress, not too quickly, to uncomfortably possible, before descending to the inevitable: horrifyingly possible.
I’m sorry, folks. And I’m sorry to everyone who is going to be impacted by these revelations, including the physicians, the researchers, the nonprofit organizations, and even the pharmaceutical companies who have long supported patients of these diseases (and invested billions upon billions of dollars to treat them). I have countless friends in each of these arenas, all of whom are soon going to face a murky and uncertain future. I. Am. Sorry.
More than 350 million people worldwide are afflicted with one or more autoimmune diseases as they are defined today. And despite years and years of research, the cause of these diseases has been maddeningly elusive, treatments woefully mediocre, and cures noticeably absent.
I expect—nah, who am I kidding?—I know that there will be scores of fervent disbelievers no matter how much evidence I present. They’ll stick to trusting the doctors and the already published research over some rando health blogger and accidental memoirist named Dave, thank you very much. Okay.
But that barn door? It’s not just wide open—I’ve removed the hinges. And before this memoir concludes, I’ll be burning that entire barn down with more devastating evidence. (One might say Part IV is, ahem, a barnburner. Oh, Dave!) Those horses are never coming back. Not only because I've already provided the basic tools for an amateur researcher to reaffirm Lyme disease’s influence on any suspected autoimmune disease, but also because I’ll be stuffing that toolbox so full in the coming pages that virtually anyone suffering from Borrelia burgdorferi will get much-needed clarity as to the cause. They are going to demand answers. They are going to demand a proper diagnosis. They are going to demand helpful, meaningful treatment. And they are going to be loud—very, very loud.
I now realize that I got it all backward, beginning with the very first sentence of this memoir, "Zebra Found!” It turns out, I never found a zebra. It was a horse. And those animals that skittered away when I removed those barn doors? They were never horses to begin with. Look again. No, look closer. Do those equines have a single horn?
If you recall, in the parlance of medicine, a “zebra” is slang for a “surprising, often exotic, medical diagnosis when a more commonplace explanation is more likely.” For decades, in some cases a century or more, doctors have unwittingly been ignoring the horse—Lyme disease—and diagnosing patients with zebras. Except upon closer inspection, are those zebras actually mystical unicorns? Tragic cases of mistaken identity?
This is getting beyond disturbing. More than 350 million people worldwide are afflicted with one or more autoimmune diseases as they are defined today. They inflict real, often catastrophic damage. And despite years and years of research, the cause of these diseases has been maddeningly elusive, treatments woefully mediocre, and cures noticeably absent. Did scientists get it all wrong? Are they just variations of Lyme disease and closely related infections, many with unique names that honor the doctor or researcher who discovered said variation?
After more than a year of exhaustive research, that appears to be a distinct possibility. Grab that paper bag! Breathe in, breathe out. I know. It’s hard to stomach, much less fathom. Vector-borne infections—led by Lyme and bartonella, along with similar suspects—causing such a level of carnage. It couldn’t possibly be true, could it?
Before we answer that trillion-dollar question, it helps to understand how virtually all autoimmune diseases are diagnosed: by feel. Sure, laboratory findings, MRIs, and blood tests can help point your healthcare provider in the right direction, but it’s the amalgamation of these results crossed with a detailed review of symptoms, plus medical history, plus a physical examination that guide physicians. No test for any autoimmune disease is definitive. From rheumatologists to neurologists, the diagnostic troubles are the same: at best it’s an imperfect science, at worst it’s medicine’s most celebrated and consequential guessing game. It takes 4.5 years on average to even get a diagnosis, one that typically involves four doctors. The number of unanswered questions, from what causes these diseases to how to best treat and cure them, far outnumber the answers.
There’s a sinking reason scientists will struggle and ultimately fail to answer the pressing question I posed earlier. Where are they? Where are all those carriers of Lyme disease—an entire ocean of people who seemingly disappeared after sabretooth tiger hunts thousands of years ago only to spontaneously rise in the 1970s outside a sleepy Connecticut town like a Ridley Scott alien popping out of an astronaut’s chest?
By all accounts, these Lyme sufferers didn’t go anywhere. They’ve been here the whole time living amongst us.
The towering evidence points to the same horrifying conclusion: these patients, millions upon millions, may unwittingly make up the backbone of scores of original, groundbreaking research—the very research that has fueled the discovery, understanding, and interpretation of myriad autoimmune diseases. Autoimmune diseases that have, since their births, shared uncanny similarities with one another. In symptoms. In laboratory findings. In clinical presentations. In treatments. In etymology. In all of it. Doctors eagerly accepted this research and have been diagnosing Lyme patients—who have been increasingly swelling their waiting rooms as rates of autoimmune conditions inexplicably continue to rise—with the autoimmune disease from their textbooks that best fits with their symptoms. Meanwhile, researchers continue to furiously work to tease out the tiniest specks of evidence to solidify these now questionable diagnoses in painfully ironic attempts to prevent misdiagnoses.
Again, sound science is supposed to make sense. The mere idea of autoimmune disease—the body turning against itself—doesn't make a lick of sense. According to Charles Darwin’s theory of evolution, natural selection, essentially “survival of the fittest,” dictates that these sorts of health turncoats should have been weeded out quickly and decisively. Yet cases of “autoimmune diseases” have been rising alarmingly in recent decades, all but flagrantly mooning Darwin’s iconic theory complete with the caption “eat my shorts.” And then to compound their flawed reasoning, scientists latch on to theories to explain this rise that further defy Darwin, like lack of sunlight. Except for blockage due to apocalyptical asteroids or volcanic eruptions, the quantity of sunlight over millennia hasn’t changed appreciably, particularly in the last few decades. Sunlight is one of nature’s most reliable events. Why would slightly less vitamin D suddenly trigger a scourge of disease, but only since the days of Duran Duran?
Scientists have been struggling for years to bridge the paradoxical chasm between the existence of autoimmune diseases with Darwin’s signature theory. And in January of 2024, they thought they had finally figured it out, as major newspapers worldwide heralded the results of a potentially landmark study of ancient DNA that connected common genes thought to be associated with multiple sclerosis with the European migration of nomads herding cattle 5,000 years ago. An accompanying article in Nature reports that the Danish and UK researchers settled on a startling reason to explain the contradiction.
Surprisingly, one of the traits that seems to have had a strong evolutionary advantage is one associated with a predisposition to multiple sclerosis. This trait arrived in Europe with west-Asian pastoralists and became even more common in northern Europe over the subsequent millennia. Today, multiple sclerosis is a devastating disease caused by an overactive immune system attacking the nervous system. But that superpowered immune system, or genetic variants associated with it, could have helped ancient people to survive plagues and common pathogens.
Really? MS an evolutionary advantage? Really??
“That’s the best explanation we can come up with,” said co-author Dr. Eske Willerslev, a noted geneticist at the University of Cambridge, UK, who spearheaded the effort. Dr. Lars Fugger, an MS specialist at Oxford who assisted the team, explained to The New York Times, “that the disease may not have become common until recent decades,” apparently ignoring the obvious link of the rise of the disease to “Rio” and “Hungry Like the Wolf,” two of Duran Duran’s greatest hits. “In today’s environment, with less infectious disease than past centuries,” he told the Times, “a strong immune system becomes more likely to misfire, attacking its own body.”
How about we try a better explanation? Contrast their hypothesis with what we know about ticks. They’ve been around long before that asteroid hit 66 million years ago, as scientists found encased in amber a 99-million-year-old tick, a tiny nymph grasping a dinosaur feather. And ticks and their spirochetes don’t magically violate Darwin’s theory. Like humans, they evolve, and they have had a lot more time to fine tune their smarmy, destructive tendencies than humankind. Millions of years of evolution have taught the infectious bacteria how to evade the immune systems of their hosts with ruthless efficiency.
The body isn’t misfiring at all—it’s desperately trying to fight off invaders, invaders from the world’s most common infectious disease. And the proof is in the details. The unique ancient genetic variant the researchers discovered is HLA-DRB1*15:01, an antigen that is most commonly linked to modern day MS in genetic studies. Just one bone to pick, not unlike the 5,000-year-old bones used to extract DNA for their study. Nearly 20 years ago, researchers already connected 15:01 to another disease: Lyme, particularly more aggressive forms. More than a dozen other HLA-DRB1 variants have also been connected to Lyme, many the same variants the Danish researchers had hoped to use, according to the Times’ piece, “to trace the genetic roots of not only multiple sclerosis, but also diabetes, schizophrenia and many other modern illnesses” including Alzheimer’s.
For Christ’s sake.
For more than a century, the perfect storms of autoimmune disease have been colliding violently with each other, each one reinforcing one another, creating a devastating feedback loop in what can only be called an immaculate storm. With every “groundbreaking discovery,” it has grown stronger, effectively sinking any alternative theories before they can rise to the surface, its punishing seas swiftly drowning any voices that question science now deemed settled. Ross Douthat, The New York Times columnist who helped me grapple with my Lyme disease diagnosis all those months ago, noted this trend in medicine of groupthink swamping any contrarian evidence in a July 31, 2022, column. “A flood of research dollars and prescriptions going in the wrong direction, because everyone imitates everyone else, is the scientific equivalent of everybody making the same dress because that seems to be what the consumer wants … a hive mind in which dissent struggles to be heard.”
If we pull back the curtain to see just how such an immaculate storm formed, the source of its power appears shockingly pedestrian: nothing more than a club of opportunistic men in white coats, those who rushed to plant that first flagpole, pulling the levers. Just a group of doctors and researchers claiming dibs? That’s all?
I’m afraid so. Let’s merely reverse roles to see how easily it could happen. In 1927, Wilhem von Bexfield, inspired after returning from a trek in the Sahara Desert, made a remarkable discovery: that infections spread by ticks were the source of a panoply of strange symptoms. He deemed this new condition “lime disease,” partly as a dig to fellow researchers who he subsequently made green with envy. In its arthritic form, the most prevalent, these infections attack the lining of joints, causing pain, inflammation, and eventually, cartilage and bone damage. The disease could also harm the body’s internal organs such as the heart, lungs, and nervous system. To assist in diagnosis, Mr. von Bexfield created the Disease Assessment Factor Test, or DAFT, which measures certain proteins made by the immune system in the blood as well as specific antibodies.
Now, try to diagnose rheumatoid arthritis in a patient presenting with those symptoms, complete with an elevated level of DAFTness. Go ahead, try.
You can’t. It’s impossible. It will always, always, always be lime disease, as Mr. von Bexfield employs the exact same diagnostic measures used to diagnose modern-day RA. In this scenario, however, lime disease was discovered first and put on the mantle of settled science, effectively muscling out any alternative diagnosis. Now let’s take it a skosh further. If Mr. von Bexfield’s description of lime disease had included all known forms of the disease—producing everything from rashes to fatigue to wheat allergies—diagnosing most other supposed autoimmune disease would be equally impossible. After all, he claimed first dibs.
Lash yourself to the mast. As cherished theories in autoimmune disease implode, crushed under the weight of logic, it gets worse. Remember when I told you that on December 18, 2022, I awoke speechless after making an astounding discovery the night before? Our next twist turns us into the teeth of our immaculate storm and pits us face-to-face with the most pressing—and vexing—health issue of our time.
The immaculate storm rages on.