Sit Down Before Reading, A Memoir by Dave Bexfield
The concluding chapter of Sit Down Before Reading has been broken into five parts (1-5).
Part 1
Many of the world’s greatest medical discoveries were accidents, flukes, sheer luck. Penicillin, the pacemaker, the Pap smear, X-rays, insulin, the existence of allergies, Viagra, vaccinations, even Valium, which was originally created to be a fabric dye. “For all you would-be Nobel Prize-winners, remember the one trait that tied all these lucky strikers together: open-mindedness,” intones the narrator in a 2001 broadcast of PBS’s NOVA. “As the American physicist Joseph Henry once noted, ‘The seeds of great discoveries are constantly floating around us, but they only take root in minds well prepared to receive them.’”
You are going to need that open mind, one yawning as wide as you can possibly make it. Despite my best efforts to rationalize all that has happened over these 52 chapters of Sit Down Before Reading, I honestly can’t. After living with what I thought was multiple sclerosis for 17 years, I never should have discovered in the fall of 2021 that I had been misdiagnosed, that it had been Lyme disease all along. You know what happened next. To figure out how such a mistake could have possibly happened, I buried myself in research and started writing this medical memoir, publishing each chapter in near real time at www.SitDownBeforeReading.com. In the process, I uncovered shocking evidence that I was not a rare outlier as I had initially thought. I had company. Gobs and gobs of company.
What you are about to read isn’t so much the confluence of good fortune, but forces that defy explanation. The conclusion of this memoir, after two-and-a-half years of innumerable false starts and barren rabbit holes, continues that trend. It will challenge you one final time.
I know, I know! You, along with even my wife, are up to HERE, hand gesturing to neck, with my challenges. First it was my over-the-top proclamation that all autoimmune diseases are just variants of Lyme disease. Then I blamed most cases of mental illness, from schizophrenia and bipolar disorder to severe depression and PTSD, on the bacterial infection. When I added long Covid to the mix, boldly claiming it was the result of dormant Lyme getting activated, readers nearly revolted. I stirred that pot even more, putting severe adverse reactions to vaccinations—from Guillain Barre to autism—squarely on Lyme, triggered by the (usually safe) immune system disruption. Then, when you thought it couldn’t get any worse, I tossed in birth defects, a bundle of serious conditions like strokes and Parkinson’s, as well as a frightening share of cancers, fingering Lyme as the primary suspect behind them all.
“This theory cannot possibly be correct,” wrote a deeply skeptical, now-retired chemist. His multiple sclerosis diagnosis decades ago, his skin cancer, his ischemic stroke in 2012, it just couldn’t all be the result of undetected, untreated Lyme disease.
Despite the cavalcade of evidence I’ve presented on the previous pages, for most it’s still too much to be believed. The human brain just cannot compute the magnitude of my claims, that such overwhelming carnage could largely be the result of a single, microscopic culprit. And that scientists—scientists we’ve put our trust in by the bucketloads—totally missed it.
How could that conceivably be? How did we get here? Seriously, how the hell could this happen?
When a series of perfect storms violently collide, they form what I call an immaculate storm. They tend to manifest quietly, innocently. This storm of storms, the world’s most catastrophic horror story, began to develop in the early 1900s, when doctors and medical researchers tried grappling with rising sickness and disease. Despite repeated evidence of spirochetal involvement in diseases such as multiple sclerosis, researchers dismissed the findings, blaming poor analysis and mistaken interpretations (the tiny bacteria observed under high-powered microscopes were probably just “scratches in the glass”). This led to the first of three fatal assumptions in the scientific community.
Without a convincing suspect to blame for these similar illnesses, scientists in the mid-1950s coalesced around a novel, counter-intuitive hypothesis, one that bucked Darwin’s theory: that the body must be attacking itself. The theory of autoimmunity was birthed, and gradually took hold, eventually converting the doubters. It was a eureka moment, and soon doctors were scrambling to identify and diagnose people with a new class of disease, the newfound conditions often named after the lucky discoverer who got there first. It was thought to be a golden era of medical advancement.
Not twenty years later, the second fatal assumption was made.
In the mid-1970s, children in Lyme, Connecticut, were falling alarmingly ill with a condition that looked remarkably similar to rheumatoid arthritis. Scientists reasoned that it was just too coincidental for it to all be RA, especially afflicting those at such a young age. Eventually, in November of 1981, medical entomologist Willy Burgdorfer, Ph.D., made his fateful discovery, that deer ticks were the causative agent spreading this disease. Lyme disease and the spirochete Dr. Burgdorfer discovered, Borrelia burgdorferi, were cemented in history. After the celebratory backslaps, instead of taking a refreshed view of illnesses past that eerily resembled the bacterial infection, scientists neglected to revisit their own work. By that point the theory of autoimmune disease was considered settled science, even though misdiagnoses were woefully common and treatments were universally middling. Besides, if you looked close enough, scientists thought they could tell the difference between Lyme and autoimmune disease. After all, they had developed a test that they deemed was accurate-ish.
The third fatal assumption surfaced almost immediately, swallowing any contradictory theories with the efficiency of Biblical whales or black holes: that Lyme disease was exclusively a tickborne illness.
Armed with the belief that the bacteria were spread to humans chiefly by ticks, and specifically only blacklegged deer ticks, scientists felt secure in swatting away any convoluted notions that autoimmune diseases or other illnesses could be attributed to Lyme. Epidemiologists embraced and seconded that thinking, as researchers and doctors alike all but parroted O.J. Simpson attorney Johnnie Cochran. If there’s not a tick, it’s another form of ick. Don’t worry, the scientists all said. If it’s not endemic, it’s not an epidemic.
This sealed the unrelenting and unchecked spread of the disease leading to today’s crisis. Who possibly could have predicted that a spirochete, a corkscrew parasite with the unique ability to propel itself through liquid substances, could be spread through sexual contact or passed down from mother to unborn child? Just because that’s primarily the way syphilis and its spirochetes spread, it was much too big of a leap for scientists to apply that method of transmission to another spirochetal bacteria with similar properties. And yet that is indeed, as I discovered, how Lyme disease primarily spreads, which I broke down in detail in Chapter 48: Hallelujah Booyah. And it’s been spreading that way in mammals for tens of thousands of years, far predating humanity.
By eliminating Lyme disease right away as a suspect in myriad illnesses because of the lack of a clear tick connection, scientists unwittingly have repeatedly sabotaged their own research. Once I figured out their let’s-contradict-Darwin autoimmune disease blunder, maxing out the blunder scale when considering history’s other biggest mistakes, everything else fell neatly into place. Any illness, disease, or health condition with close ties to autoimmune disease—an extensive list that includes mental illness, long Covid, birth defects, cancers, and a host of chronic conditions—meant that Lyme, therefore, must be involved in at least some, if not most, of those cases.
Hold on one darn-tootin’ minute, scientists will protest. If B. burgdorferi can’t be detected, a diagnosis of Lyme must be rejected. That’s been the prevailing thought since testing for the disease began in 1984. If only it were that simple. It is well known that the Lyme spirochete is legendary for its virulence and its ability to hide and evade the immune system, employing a range of tactics, including the deployment of “don’t eat me” proteins. Despite enormous technical advances over the years, scientists still struggle mightily to consistently detect the bacteria.
Think of black holes. The idea first surfaced in the late 1700s, Albert Einstein predicted their existence in 1916, the term was coined in 1967, but it wasn’t until “astronomers using the Event Horizon Telescope (EHT) — an international collaboration that networked eight ground-based radio telescopes into a single Earth-size dish — captured an image of a black hole for the first time.” That discovery occurred on May 21, 2019. It took 103 years from Einstein’s prediction to get visible confirmation. Just because scientists cannot yet see wriggling Borrelia burgdorferi spirochetes right now doesn’t mean they’re not there. They’re there, we just don’t have a way to see them reliably yet. When will we get that visual reassurance? Using history as a guide, add 103 years to Willy’s 1981 discovery and we could be looking at 2084 before science fully catches up. Good thing there’s a reliable and convenient way to “see” the spirochetes using existing blood tests.
Wait, what?
The Elusive Test
When I boldly (or obnoxiously) proclaimed that Lyme disease was at the root not only of all autoimmune disease, but also a panoply of illness, people started unsubscribing from my MS website ActiveMSers in droves, dozens a week, often spiked with digging parting shots. “You used to be funny.” Ouch. People can bark that it’s outrageous and far too speculative to connect all sorts of illnesses to Lyme, but science would beg to differ. When you look closer and flush away biases, you’ll discover that such obstinate disbelief is not supported by the data. Once again, scientists and wanna-be scientists alike are tripped up by the science. This intricate puzzle snaps together properly only one way.
If Lyme is indeed the source of “autoimmune” issues, that would mean that all tests used to detect autoimmunity instead would be detecting the presence of the bacterial infection. A popular clue doctors use to help diagnose autoimmune disease is the existence of autoantibodies in the blood. Scientists first discovered autoantibodies in the late 1940s (in lupus and rheumatoid arthritis) during the autoimmune renaissance, but their presence, maddeningly, wasn’t the defining disease marker scientists had hoped it would be.
Class, why would that be? Anyone, anyone?
Because they are found too frequently, leading to today’s consensus in the research community that “autoantibodies play a pivotal role in the pathogenesis of many diseases and that autoantibodies mediate both systemic inflammation and tissue injury.” Understandably, that discovery has ginned up excitement in brain research, as a 2021 study stated matter-of-factly that “the realization that autoantibodies can contribute to dysfunction of the brain has brought about a paradigm shift in neurological diseases over the past decade.”
That paradigm shift has prophetically stretched far beyond the confines of expectations… to every illness in this memoir linked to Lyme disease. The presence of autoantibodies—there are many types, and more are still being discovered—is a clear sign that one or more varieties of Lyme disease is in play. Could it be the long-sought identifier for Lyme that scientists have craved?
Autoantibodies are routinely found in schizophrenia and bipolar disorder, a bevy of chronic illnesses, birth defects, even long Covid, with their presence tied to severity. A study released in late June of 2024 is particularly telling. “Autoantibodies have long been eyed in Long Covid, with various studies finding them enduring in patients’ blood,” so scientists injected the blood of long Covid patients into mice, and presto, those mice came down with a cascade of symptoms similar to those found in the patients. The experiment’s results mirrored the results from a similar 2021 study on fibromyalgia, so researchers feel they are onto something for long Covid. Maybe. “But their role has been ambiguous in the syndrome, partly because so many different types show up in patients.”
Let us not forget cancer. “Autoantibodies are classically associated with autoimmune diseases, where they are an integral part of diagnostic panels,” stated a 2021 study. “However, recent evidence is accumulating on the presence of autoantibodies … in many types of cancer.” Readers of this memoir should know those cancers well, as they litter previous pages, with Lyme disease a primary suspect. Central nervous system cancers, colon cancers, pancreatic cancer, liver cancer, thyroid cancer, breast cancer, ovarian cancer, bladder cancer, prostate cancer, lymphomas, melanomas, and others, including lung cancer. Thankfully the news isn’t entirely dreadful. There are many other causes of cancer, like smoking, and if my theory concerning autoantibodies is correct, having them bodes well for survival found a 2023 study. “The presence of autoantibodies is an independent indicator of good prognosis in patients with lung cancer.” (The parasite, apparently, is learning not to kill its host too quickly. I imagine these spirochetes were caught off guard and unprepared when the life expectancy of humans, stable for eons in the 30s, suddenly doubled and then some in the 1900s.)
But there is one autoantibody wrinkle that has thoroughly flummoxed scientists.
“Thousands of studies over the past decade have investigated autoantibodies as potential biomarkers for disease risk assessment, diagnosis, and prognosis,” reports a 2022 study. Except, hmm, something wasn’t quite right. “Given the prevalence we observed for these common autoantibodies in healthy individuals, in some cases exceeding a quarter of all individuals, they will be frequently encountered in such studies and may confound them as false positives.”
Those individuals aren’t healthy, and those aren’t false positives. What those researchers discovered in “healthy” individuals: a desperately needed marker to identify lurking Lyme disease festering in people who appear well. They might get odd rashes from time to time, maybe. Or regularly tweak something they don’t remember tweaking. Perhaps they have innocuous symptoms that get brushed aside as part of life—snoring, flaking skin, constipation, an achy lower back. When Lyme disease remains mostly dormant, it’s easy to overlook, especially if symptoms fade after six months. It might not surface for many years, biding its time until one’s immune system weakens in old age, presenting as dementia or a stroke or heart disease or cancer. So sad, bum luck, bad genes, unavoidable, people will say. At least [name TBD] lived a full life.
Because cases of Lyme disease present so wildly differently, no wonder autoantibodies are such a fuzzy, misunderstood marker. And now the numbers are finally adding up and making sense. The 2022 meta-analysis that estimated that nearly 15% of the world’s population had antibodies to Lyme disease—suggesting a current or recent infection in 1.2 billion inhabitants of our planet—was off. By at least a billion or two. Add in all the suspected missed cases identified in past chapters as well as those asymptomatic, and the true toll of the menacing bacterial parasite, given its relentless ability to spread sexually, congenitally, and through ticks, is closer to a more realistic 3 billion.
A third of everyone living on Earth, infected. And even that may be an underestimate.
It doesn’t have to be that way. Those seeds of great discovery, those floating around us, physicist Joseph Henry foretold in our first paragraph of this final chapter? There’s one floater that we’ve been shooing away for millennia, with the frustrated annoyance of dealing with a pesky gnat.
The elusive building block necessary to achieve a cure for Lyme disease.
Accidents Happen
Several summers ago, Rob the outdoorsman (the same Rob who discovered his own case of Lyme with my assistance, recapped in Chapter 42) was scaling wild-caught salmon in our backyard. He had experience scaling salmon, as he had lived in Alaska (and probably caught them with his bare hands while under the watchful eyes of grizzlies), and felt that doing the messy task outdoors would prevent wallpapering our kitchen with fish bits. Turns out, our kitchen décor’s loss was an unmitigated win for the raccoons living in our neighborhood.
That night, after bathing in the backyard grass to celebrate their unexpected Alaskan windfall, the raccoons took the wicked bender of a party to our roof. At 2:30 in the morning. Laura is typically asleep at 2:30 a.m. But it’s damn hard to sleep with literal party animals cavorting feet above your head. So, in our sleepless haze, we hatched a brilliant plan to rid the pests: turn on and off the porch light. Aggressively. (Don’t ask. Clicking the light switch hard, with intention, felt productive.) But instead of scaring them, the lights had the opposite effect, as if we had just turned on an open-for-business disco ball. “Oh, lookie, that must be where the party’s at, Bob!” is what one raccoon almost certainly squeaked to another before crashing the affair.
Time for Plan B. Scare the bejesus out of them. “Open the door,” I told Laura. The house alarm!? What about our neighbors? The fact that it was 2:35 a.m.? What was I thinking? “I think the raccoons are tearing up the liner on our roof to turn it into a nest so they can fornicate and have babies, ensuring a generation of future rabble rousers will return home to their place of birth. Like salmon.” She opened the door.
WOO-WOO-WOO-WOO. The urban pests scattered. Peace was secured. Until, of course, the next night.
Given that setting off the house alarm nightly was an unsustainable solution, it was time for Plan C. I went into my rodent toolbox of tricks and tried one that had worked on small children. Sound effects of barking dogs through our outdoor speakers. (Again, don’t ask.) The raccoons seemed bemused, as dogs lack the wherewithal to bound onto roofs to give chase and, generally, also prefer sleeping during ungodly hours of the night. Then I had another idea.
Sampa The Great, the Zambian singer, rapper, and songwriter, has a song—Bona—that uncomfortably rattles our walls with fierce, booming bass. Instead of cranking the outdoor tunes, what if I just shook the house from the inside with thumping subwoofers? I cued Bona. And turned it up to 11 as the bass dropped. If the music hadn’t been so deafening, we would have heard those raccoons exiting stage left faster than that time the NFL’s Baltimore Colts scampered for Indy in the wee hours of March 28-29, 1984. Those masked little buggers may not have heard the music, but they no doubt felt the music. Problem solved. They’ve never returned.
To understand the relevance of this, we must embrace the alternative, uproot any simmering biases, and head to Iowa, circa 2007.
Since the dawn of humanity, people have fallen sick to disease. And since the dawn of humanity, people have fallen prey to the siren call of cures. Actual snake oil for arthritis, heroin for coughs, vibrators for female hysteria conveniently applied to the pelvic region. (There were a lot of women in the early 1900s suffering from hysteria, apparently.) MS alone has been an ideal proving ground for eccentric elixirs, as people have “tried to ameliorate MS with leeches, quinine, foxglove, tobacco, hemlock, valerian, coffee, tea, being suspended above the ground, vertically, for four minutes at a time, and being wrapped in sheets sprayed with cold water.” But by far, the most popular tonics through time, regardless of illness, have been supplements and diets.
Who can forget the cabbage and urine diet that swept through Roman times, promising to dispatch everything from warts and ulcers to dysentery and drunkenness? If you ate your cabbage—and drank the pee of others who ate lots of cabbage—relief certainly was in your future. As crazy as this sounds in the 2020s, guess what’s a new, popular diet fad again? Cabbage soup! Urine cannot be far behind. Arsenic diet pills were popular in the 1800s until the whole poisoning/death issue, and the tapeworm diet craze in the early 1900s, in retrospect, seems rather ill conceived as a weight-loss technique given that it required the voluntary ingestion of tapeworms.
When it comes to Lyme disease, there are countless “protocols” to follow that purportedly will help dislodge pesky spirochetes hidden in myriad chasms of your body. You’ll find supplements that promise to drive them out of their protective cysts and dissolve their biofilms, the shields that prevent antibiotics from doing damage. Capsules of oregano oil or other herbs as a substitute for antibiotics. These all could have some influence on the disease, perhaps even a significant effect, although few herbal remedies have been studied clinically. It’s primarily a guessing game.
Then you have a range of diets, so many diets, that eliminate foods that may (or may not) fuel Lyme disease—sugar, gluten, alcohol, dairy, processed foods, caffeine, aged cheese, even broccoli. The list is longer than a 6-year-old’s wish-list for presents from Santa. What’s truly bad to ingest if you have a bacterial infection? Again, it’s hold your breath and hope that you hit the lotto as scientific trials, if they even exist, are routinely inconclusive. Anecdotes are plentiful; objective evidence is noticeably absent.
Multiple sclerosis, predictably, has its own alternative diet religion with fiercely loyal—and vocal—followers. Eat this, avoid that, seek this, shun that. But like the diets for Lyme, the magic sauce has been elusive. An Australian multiple sclerosis study published in the waning days of 2023 “found that neither dairy nor gluten intake was associated with disease activity or quality of life” despite two years of patients diligently avoiding pizza and other glutenous, cheesy, dairy laden foods. Regardless, the hunt for relief by diet modification continues. But there is one restrictive diet that has grabbed a firm handhold among ardent amateur alchemists in the field of disease diets: The Wahls Protocol.
Photos courtesy Dr. Terry Wahls
The book of the same name is arguably the most famous and popular of all MS books ever published. Developed by Dr. Terry Wahls, the cover alone makes bold claims: “A radical new way to treat all chronic autoimmune conditions—how I beat progressive MS using Paleo principles and functional medicine.” On the homepage of Dr. Wahls’ website, her jaw-dropping recovery is stated as plainly as the Iowa plains where she practices: “Dr. Terry Wahls was dependent on a tilt-recline wheelchair for four years until she reclaimed her health using a diet and lifestyle program she designed specifically to restore her cellular health—she now pedals her bike to work each day.”
Her incomparable, wild success has generally divided people into two camps: true believers who are prepared to put on matching Nikes, and cynics convinced she is a charlatan preying on desperate patients. Unsurprisingly, her 2011 TED Talk has drawn some 4 million views… and a warning. “Note from TED: This talk, which features health advice based on a personal narrative, has been flagged as potentially outside TED’s curatorial guidelines. Viewer discretion advised.” So, is Dr. Wahls blowing smoke or blowing up the landscape of how to treat chronic disease?
The answer might shock you.
The Last Epiphany
In the early morning hours of May 8, 2023, my brain did that thing, like it did when it reached previous epiphanies. The experience is so unnerving, bursting with untold promise, that the dates get etched into permanent memories—the day I cracked the secrets of intellectual property, the day I figured out my health issues, the day I realized that Lyme disease fueled long Covid. The first time I was fully aware that it had happened, my Breaking Brain/Breaking Bad moment, you’ll recall from our previous chapter that I told Laura that from that day forward, our lives were going to profoundly change. At the time, she thought I had a screw loose. She was right, of course, but so was I.
At about 1:30 a.m. that May day in ‘23, my brain was back in that breathtaking forest, a tangle of unrealized potential. But this deep dive into my grey matter felt different; I was aware enough to direct its focus. Could it get any closer to treatment answers for my chronic Lyme, answers that had beguiled doctors since the days the disease was discovered? I recall laughing to myself at the absurdity of the request, almost wanting to apologize to my brain for wasting its time on what certainly was going to be a futile endeavor. Other than a few antibiotics, I knew little about treating Lyme. There was zero chance for a eureka moment. Sorry, sorry. I tried rolling over and going back to sleep—never mind brain, goodnight moon—but the appeal had been made, and a minute or two later (maybe?) it spit out an unexpected nugget. I sat up in bed.
“A cure for chronic Lyme already exists.” (I said that part aloud so my doubting ears could hear.) Ohhhkay. So, while new, more targeted antibiotics would be enormously helpful, it’s not mandatory? Great, thanx. And??? What the hell is it?
Minutes later (I think, time is fuzzy during these moments), I got more clarity. The answer lies in plain sight, only researchers can’t see it.
Huh? A potential Holy Grail of health is disguised with comical Groucho glasses? Not exactly, said my brain. More than likely, telltale clues would be found in a small trial, probably for an autoimmune disease, that may have generated initial excitement, but then for a variety of reasons, was ultimately discredited and dismissed. Perhaps because it couldn’t be replicated by other researchers. Or funding was absent to conduct further, confirming trials.
The answer then got refined further. While reviewing trials was going to be helpful, individual case studies held even more promise. Those would be the hardest to prove and would meet the most skepticism. It’s highly likely that scientists overlooked critical signs or mistakenly attributed patient improvements to wrong elements of a treatment. Any grand health gains would be looked at with extreme dubiousness.
Being primarily familiar with multiple sclerosis research, I immediately thought of two studies that cleared those bars. CCSVI, the angioplasty procedure to improve blood flow by opening blocked or narrowed veins, generated huge press until the study’s success couldn’t be replicated by other centers. As there is a clear venous component to Lyme disease, and I consistently felt stronger temporarily after taking Viagra, I could see why the procedure worked, at least temporarily. Certainly, there could be something there there, particularly considering the success ED medications have on preventing Alzheimer’s in both men and women. The other study? Dr. Wahls’ stunning turnaround.
Since Dr. Wahls miraculously rose from her wheelchair in 2007, the University of Iowa physician has been dutifully trying to prove that her “cure” was no fluke, repeatedly studying aspects of her diet in more than a half dozen clinical trials. She has expended an overwhelming amount of energy trying to scientifically prove her case, typically not the sign of a conniving conwoman, yet her trials continuously fail to overwhelm. Complaints of fatigue often slide for people on her protocol, a routinely difficult symptom to accurately gauge objectively, yet blatant curative signs—people getting out of wheelchairs or ditching their walkers—are noticeably absent. What’s going on?
photos courtesy Dr. Terry Wahls
Dr. Wahls, a fifth generation Iowan, first noticed facial discomfort while she was studying for her MD at the University of Iowa, brought on typically by stress. The discomfort turned to severe jolts of pain, “like electrical jolts of pain.” The following year she lost eyesight in her left eye after rollerblading on a hot August afternoon, yet it took 15 years to finally get diagnosed. An official diagnosis meant that for the first time, Dr. Wahls could take medications appropriate for her condition. They all failed and her health continued to crater. “At my nadir in 2007, I’d spent four years in a reclined wheelchair,” said Dr. Wahls. “My face pains were relentlessly worse, difficult to turn off. It was very clear. I was looking at becoming bedridden, demented, probably having continuous intractable trigeminal neuralgia.” It had turned so fierce that she had changed her living will. If the ravages of her disease prevented her from swallowing, she instructed her physicians not to provide tube feedings or IV fluids so that she could “maintain that control if my life got that grim at the end.”
Then she had an flash of inspiration, burying herself in nutrition research, uncovering studies on “the impact of micronutrients on brain function and structure,” she writes in 2007 research that led her “to add sulfur amino acids, kelp (iodine), resveratrol (flavonoids), and vitamin D to my daily regimen.” She then eliminated gluten, dairy, and eggs, making vast changes to her diet—in essence a modified paleolithic/ketogenic diet—while reducing her “toxic load” and boosting her physical and mental therapies, before incorporating yet another wrinkle to her rehab mission: electrical stimulation of muscle.
Two months after starting my e-stim and intensive nutrition, I could again sit in a standard desk chair without being exhausted—for the first time in years. At three months, I could walk between exam rooms in the clinic. At five months, I could walk to the clinic, and at seven months, I could bicycle around the block. A year after starting e-stim and intensive nutrition, I was able to bicycle 18 miles, and the following year I rode a horse on a trail ride in the Canadian Rockies. (source)
She was, for all intents and purposes, cured. Her path as an MS trailblazer was secured. How in the world did she do it? Likely the way countless researchers throughout history have made scientific breakthroughs—by total accident supported by a series of timely coincidences and sheer good fortune.
Serendipity
Dr. Wahls’s original case study, “Neuromuscular electrical stimulation and dietary interventions to reduce oxidative stress in a secondary progressive multiple sclerosis patient leads to marked gains in function: a case report” published in Cases Journal in 2009, details her experimental process and remarkable recovery. It’s deeply revealing.
There are three primary potential mechanisms of action: her diet, her supplements/medication, and her electrical stimulation. Within each of the three are mountains of variables, an everything-but-the-kitchen-sink approach. The study of her diet alone is hugely problematic due to the number of variables (a challenge with most diet studies)—now we must multiply that by three. Is it the combination of all three, two of the three, or a novel application of a single one that led to her recovery? It would appear to be a sucker’s bet to glean any helpful clues from the trio of therapies, but by following our SHARDs doctrine and employing our box-out technique, we may just have a puncher’s—and kicker’s—chance. (See New Mexican Holly Holm v. Rhonda Rousey, Nov. 14, 2015. Fun fact, the former UFC champion was briefly Laura’s cardio kickbox instructor. Oh, and she swung by our house to say hello the other day. Because crazy follows us.)
First, look at Dr. Wahls’s overtly restrictive diet—and pay close attention to the presumed mechanisms of action through, among an avalanche of theories, “enhanced responsiveness to neurotrophins, perhaps increasing dendritic sprouting and myelin generation.” Whew. Now ignore all that for the moment. There is so much dizzying food manipulation in her case, let’s temporarily box out that variable.
The same is true of most of her supplements and medications, each element potentially doing something… or nothing at all. But there is one intriguing drug that stands out in stark contrast to the others: minocycline, an antibiotic, specifically an antibiotic in the same family as Lyme-busting doxycycline. Now we’re cooking!
We’ve boxed out diet and everything but minocycline. That leaves e-stim. Could the accidental combination of e-stim and antibiotics be a potential long-sought elixir to intractable, untreated Lyme disease? On the surface that sounds laughably outrageous, but there is precedent. Both e-stim and the archaic Rife machine produce electrical currents that max out at the equivalent of a 9-volt battery, and Lyme patients—often on antibiotics—swear by the 1930s invention despite having no clue how it works.
Vibrations didn’t kill my rooftop partygoers, but they definitely shook them out of their comfort zone. What if the continuous pulses of electrical stimulation are doing the same thing to spirochetes—zapping them so that they leave their protective burrows of cysts and microfilms? Forcing them to reenter the bloodstream, where an army of antibiotics is actively circulating to dispatch the bacterial invaders?
Last year, when I told Randall the actuary of my theory, my helpful volunteer dating back to Chapter 31 politely suggested that I “keep it in my back pocket” for a future book. Or never. (Misdiagnosed with MS, he continues to improve after treatment for Lyme.) Point taken, but if my brain did land on a final epiphany, I reasoned that maybe I shouldn’t ignore it. At the same time, there was also a very real chance that my vibration theory was a bunch of hoo-ha over a steaming pile of malarky. With so little existing research to support the theory, the e-stim/antibiotic approach was admittedly flimsy in terms of SHARDs, but if it was successful in my case, there at least would be evidence of reproducibility.
After six months of painstaking tweaking and experimentation, I got my answer.
It couldn’t be. It just couldn’t be.
My worst fears were realized. I could avoid it no longer—I had to confront my personal nightmare.
