Sit Down Before Reading: A Memoir by Dave Bexfield
The 39-year-old New York lawyer, standing 6’2” with an unmistakable level of authority and confidence, had been enjoying a well-deserved family vacation with his wife and children on an island off the coast of Maine when, after a day of uneventful fun (he had accidentally fallen into the icy waters of the surrounding bay a day earlier), he began to feel unwell. Chills, nausea, his lower back hurt. He opted to pass on dinner and tried to sleep through the shivering. By morning he had a fever and, odd, one of his legs felt weak. That night concern grew, as the weak leg became paralyzed and the other leg started to weaken—this was no normal summer cold as doctors had first presumed. The next day, both legs were inoperable, numb, his fever humming at 102° F. Pain and extreme sensitivity to touch soon arrived, as did bladder and bowel difficulties along with upper body weakness including facial palsy. His fever lasted nearly a week as doctors narrowed down a diagnosis. Except for the lack of a documented bullseye rash, all of his symptoms pointed to an aggressive case of Lyme disease. Purportedly an elevated white count in his cerebral spinal fluid, a marker for an acute infection, supported the diagnosis. Indeed, ten days earlier he had attended a Boy Scout jamboree at Bear Mountain State in Rockaway, New York, a stone’s throw from Westchester, a county in the state notorious for Lyme-carrying ticks. A likely scenario was that he had been bitten there before his symptoms developed on the small Canadian island Campobello, triggered by the icy plunge.
There was just one problem. Willy Burgdorfer, the scientist responsible for discovering Lyme disease, hadn’t been born yet. The year was 1921. Doctors in the ‘20s had other ideas for the cause of the man’s sudden issues. Maybe it was a blood clot in his lower spinal cord, theorized one doctor. No, his symptoms appeared to be caused by a lesion on his spinal cord, thought another. No, no, no, said a Dr. Robert Lovett, an expert in infantile paralysis. Even though it was a childhood disease and most became immune by age four, Dr. Lovett was convinced—despite the patient’s wife, Eleanor, “very strenuously” questioning the diagnosis—that his patient had an uncommonly rare case of adult-onset polio. His name: Franklin D. Roosevelt.
Many decades later, a team of scientists in 2003 relooked at his unusual case and, using a trio of diagnostic methods, came to a different conclusion: FDR instead likely had—with 99% certainty after Bayesian analysis—Guillain-Barré syndrome or GBS, as six of his eight symptoms aligned with the disorder. After receiving pushback, the team revisited their research in 2016 and stuck to their original finding.
His age, prolonged symmetric ascending paralysis, transient numbness, protracted dysaesthesia (pain on slight touch), facial paralysis, bladder and bowel dysfunction, and absence of meningismus are typical of Guillain-Barré syndrome and are inconsistent with paralytic poliomyelitis. FDR's prolonged fever was atypical for both diseases. Finally, permanent paralysis, though commoner in paralytic poliomyelitis [50%], is frequent in Guillain-Barré syndrome [15%].
Matching six of eight symptoms to a disease is good. But matching eight of eight is better. One clear outlier that doesn’t support a diagnosis of either polio or GBS is fever. Fever is a trademark symptom of a tickborne illness, a common early sign of Lyme disease. Unsurprisingly, Lyme also is well known to masquerade as Guillain-Barré, still fooling today’s physicians, and cases of it mimicking polio would certainly dot medical journals today had polio not been essentially eradicated. Another outlier: lower back pain, a side effect confirmed by an FDR historian and reported in The Washington Post. Back pain and Lyme disease are like Siegfried and Roy, famous partners. Research has concluded that “inflammatory back pain, even without radiculitis, may be related to Lyme disease in endemic areas.” (The irony that President Roosevelt and his wife are featured throughout this memoir—my photoshoot with his statue, Ms. Roosevelt’s praise for Dr. Ichelson’s discovery of spirochetes in the spinal fluid of MS patients, FDR’s dime for demonstration purposes to illustrate the tininess of ticks, even Mr. Douthat’s reference in his own memoir—is not lost on this author.)
Paul Sparrow, director of the Franklin D. Roosevelt Presidential Library and Museum, in Hyde Park, N.Y., told The Washington Post that, “I think polio changed FDR. I think polio changed America. I think FDR’s reaction to polio changed the world.” Replace those sentiments with what I would argue was most likely his proper diagnosis, Lyme disease, and then imagine what might have been. How my future, and the future of countless others, might have been rewritten.
As cases of misdiagnosed or undiagnosed Lyme disease rise like unwanted towering African termite mounds, it may help to reflect on life advice provided by FDR. “You gain strength, courage and confidence by every experience in which you really stop to look fear in the face. You are able to say to yourself, ‘I have lived through this horror. I can take the next thing that comes along.’… You must do the thing you think you cannot do.”
How does Lyme disease keep getting missed, overlooked, by the world’s leading researchers? Good science should be unassailable. Yet repeatedly, medical scientists appear comfortable, satisfied even, with close enough. In the FDR case study, 75% of his symptoms line up with Guillain-Barré syndrome. But 25% don’t. That’s a big, unexplainable blind spot that becomes eminently explainable if tickborne illnesses like Lyme are considered. My own misdiagnosis suffered the same fate. Although many of my initial symptoms mesh with multiple sclerosis, when I raised the alarm of a swollen knee and bizarre cardiac symptoms—symptoms that were not explainable with an MS diagnosis—doctors hit the snooze button.
Researchers have followed this same path with the “latitude gradient” theory, trying to put their square peg hypothesis of sunlight exposure and vitamin D deficiency into a round hole. It doesn’t fit. And when new evidence arises—incidence of MS is rising in northern Japan!—inevitable suggestions concerning the dreaded “Western diet” and the like get posited … and the subject gets dropped instead of inviting serious scrutiny as to why this might be happening. It doesn’t even require serious scrutiny, just a modicum, and access to an internet search engine. “In Japan, the vector tick is found in the mountainous area of the northern part of the mainland Honshu and Hokkaido,” says the country’s National Epidemiological Surveillance of Infectious Diseases (NESID). “In Hokkaido, it is found even in flatlands. Actually in Japan, the Lyme disease cases have been reported from these areas since it was first confirmed in 1986. The carrier rate of the tick is geographically variable and is in the range of 6.7-22%. Similar level of carrier rate was reported from Europe and Russia where B. garinii is endemic as in Japan.”
This readily available information suggests that MS isn’t rising in Japan. Lyme is. And its presence continues to hoodwink researchers worldwide. Even though it appears impossible to see, Lyme disease is rather easy to spot. It just requires having faith in the science, the equivalent of a PhD trust fall. The evidence will catch you. To properly convey what I am trying to say, I realized I needed help from a friend.
There are distinct advantages to running one of the world’s larger communities for a chronic disease. As founder of ActiveMSers.org, the not-for-profit website I started in 2006 to help others stay active with MS, I have had the pleasure of crossing paths with a wide range of people affected by the disease, or at least by a (mis?) diagnosis of the disease. I have an incredibly deep bench of resources with expertise in a kaleidoscope of professions—cookbook authors, professional photographers, jazz guitarists, wildlife conservationists, mother-in-laws of NFL stars, retired newsmen. You’ve met Randall the actuary. Now I’d like you to meet Sarah the astrophysicist. I reached out to Sarah for assistance in explaining how she and her colleagues gather evidence given all the unknowns swirling around the vastness of space. How they can “see” the unseeable. And how they, at times, can be blinded to the very stars twinkling right in front of their faces.
In science we often rely on reliable but not always perfect markers to trace something unseen. In astronomy, we see planets orbiting distant stars not directly, but by measuring the slight dimming or wobble of the host star. If our measurement of the star was wrong, then so was our assessment of the planet. This has happened before! We can be wrong and as Richard Feynman famously said, “Science is a way of trying not to fool yourself. The principle is that you must not fool yourself, and you are the easiest person to fool.” We have been fooled before and we will be fooled again. Over time, hopefully we get it right and I hope that the MS community gets this right and is not only seeing what we’ve been trained to see.
Dr. Barry Marshall, the Australian Nobel laureate who discovered that stomach ulcers are caused by a spirochete and not by stress or spicy food, advises researchers of all stripes to try to break their own cherished theories, upend their most prized hypotheses. If they can survive that personal, self-inflicted gauntlet, the odds improve that one day those ideas will be accepted into medical canon. To that I’ll expand on his sage try-to-break-it advice, a tenet for all scientific researchers I call SHARDs—essential bits of broken-down research that, when properly put together, produce an unbreakable, beautiful mosaic that can withstand the tightest scrutiny.
Sound science makes sense.
History harbors hints.
Answers await in the anomalies.
Reliable research is repeatable.
Dismantle or defend, don’t defer.
The first scientific bar to clear is theoretically the most straightforward, the equivalent of the smell test for spoiled food. The crux of any solid scientific finding must be grounded in logic. Ask yourself, does it all make sense. Not, does it mostly make sense … except for these outliers that we can’t rationally explain but c’mon, we’re close enough. If the hypothesis can’t Fosbury flop over the bar straight away, it’s nothing more than an overcooked slice of bread. Toast.
Next, it’s essential that researchers backtrack and investigate where the science has been, its history. Past research is revealing and can potentially expose far more than was understood at the time it was completed. Studies finished years, even decades ago, can harbor unrealized, essential clues. As proof, throughout this memoir you’ve unknowingly been passing over them. Over and over and over. An obscure study here, a casual mention there, an aside to an aside. I’ve been leaving a scrumptious trail of breadcrumbs, delicately seasoned with extra virgin olive oil, kosher sea salt, and select herbs, all lightly browned to perfection. (Like the puzzle surrounding Guinevere’s apples from Chapter 33, Sit Down Before Reading is both breezily easy to comprehend and maddeningly difficult to fully decipher.)
Then you have the reviled data abnormalities, the deviations in research that don’t add up. The one-offs. Embrace them—or rationally explain them. For it can be within those outliers where the grandest of discoveries lie waiting to be uncovered. Pass over them at your own peril.
Our penultimate edict is one that researchers are most familiar with. The only consistent and dependable way to defend research is to show that it is reproducible. Throughout this memoir you’ll notice that I’ve consistently cited past research to back up my discoveries. Do not mistake these repetitive references for a stutter or a hitch in my mental giddy-up. Without a budget to conduct my own original research, this is my proof—proof birthed often from the very research I’m ultimately dismantling.
And that takes us to the final rule in the SHARDs doctrine. I invite all readers, particularly those with degrees attached to their names, to strip down and try to take apart what I’ve written in these pages. Dismantle my research and Ginsu it into tiny digestible bits that you can enjoy with a nice glass of Chianti, fava beans optional. But if you can’t find fault with my conclusions, sitting back passively is unacceptable. Follow the lessons imparted by history—the decades it took before doctors accepted the idea of germs and handwashing, the years it took for ulcers to be recognized as an infection—and take action. Don’t defer this responsibility. Defend me. Now. Loudly.
Did you ever stop to wonder how I discovered that obscure Miami Beach speech by NIH neuroepidemiologist Dr. Kurland from 1962? There was no abstract summarizing his talk and it wasn’t referenced in any journal articles or newspaper stories. It was given over 60 years ago, a woefully dated span of multiple lifetimes in terms of medical research. How did I know to look for it? And how did I know the research was acutely relevant—from the revelation that cases of illness diagnosed as MS in South Africa were largely acquired in Europe to the showstopping spirochetal research of Dr. Ichelson?
The canon I’ve implored you to follow: SHARDs.
It started when I noticed that first glaring anomaly in the MS gradient theory, the obvious tilt of cases into the tick belt of the United States. None of the rationalizations made plausible sense as to why other areas of similar latitude were spared. But far more revealing? The fortuitous discovery of an outlier. A low latitude region—bathed in sunshine, warm sea breezes, and copious amounts of nature’s vitamin D—awash with abnormally high caseloads of multiple sclerosis.
Good science should be unassailable. Yet repeatedly, medical scientists appear comfortable, satisfied even, with close enough.
Good science may, at times, appear to bend, show cracks. Sure, it can evolve as more and better information becomes available. But it never truly breaks. Ever. By its very definition, solid science is unbreakable. Without a convincing explanation to justify its existence, this gradient outlier, this MS anomaly, would not only dismantle the “lack of sunlight” MS theory, it would outright destroy it. But how could Lyme disease, instead, be responsible for rising cases of MS when it’s not endemic in the zone I discovered? Indeed, blacklegged ticks—the vector responsible for disseminating Lyme disease—are wholly absent from the area. Doctors there never see the tickborne illness.
For my Lyme hypothesis to be correct, barring other yet-to-be realized modes of transmission, evidence had to exist that the disease was contracted after travel to an endemic region. Evidence had to exist that the disease exhibits some degree of latency to prevent doctors from making the connection. And evidence had to exist that the disease was routinely being misdiagnosed as something else.
I knew I had found a potential smoking gun. But for my research to be deemed reliable—and for it to clear the high bar of being repeatable—I needed to unearth another spent six-shooter with similar telltale wisps of gun smoke. With history being dreadfully predictable (see overlooked spirochetes, Dr. Marshall, a century of missteps), it was only a matter of time, and a lost weekend or two, before I’d land on Dr. Kurland’s talk. I already knew exactly what to look for—unexplained bumps in the gradient theory decades before Lyme was discovered—and any revelatory findings that had to have been summarily disregarded and dismissed.
Pack your bags. And your swimsuit. It’s time to take a medicine-upending, disease-busting, history-making trip to the elusive, undiscovered, epidemiological epicenter of undiagnosed Lyme disease masquerading as MS.