Sit Down Before Reading, A Memoir by Dave Bexfield
The concluding chapter of Sit Down Before Reading has been broken into four parts (1-4). The final section is tentatively scheduled to publish September 25, but may need to be delayed.
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.
Part 2
House of Horrors
All of us have biases whether we admit them or not. I’m typically pretty openminded, but when people start crowing about things unsupported by the evidence, or worse, the science, eyebrows raise along with deep-seeded biases. And nothing, nothing, brings out my prejudices like someone waxing on—and on and on and on—about some purportedly disease-busting diet. Think someone trying to exhaustively explain the undervalued benefits of Bitcoin over lunch, only instead they are extolling the benefits of a restrictive diet while you are trying, trying, to enjoy a green-chile cheeseburger, truffle fries, and a pint of microwbrewed IPA before ordering that fresh-baked gooey chocolate-chip cookie topped with a scoop of vanilla bean ice cream for dessert. And enlightening you with news that everything you love to eat is bad, helping you to slowly dig your own grave. (Of course it’s slow, I’d say under my breath, utensils make inefficient excavators. Good thing burgers and fries are finger food.)
I always ask, sometimes aloud but usually to myself, Where’s the beef? I want research with meat on the bone, not anecdotes, before I contemplate upending my diet, particularly one that excludes said meat. I’ve railed about the weak scientific support of these diets and supplements, from op-ed submissions to The New York Times (never published, now an appendix to this memoir) to lengthy blog posts on ActiveMSers. I went so far as to dedicate part of a chapter in this memoir to this source of ongoing frustration. I even remember the internal consternation when Confidant #2 (from Chapter 11) generously—prophetically?—gifted me a book on nutrition days after I revealed my 2006 MS diagnosis to him. (Bonus fact: he even played an essential role in my Breaking Bad project, the first time we had spoken in more than a decade.)
Diets grate on me, especially those that eliminate Cheetos, and I’m not shy about expressing my distaste. But notably with these rants, I begrudgingly typically included a disclaimer. That “I don’t know” if a diet could be an unexpected bridge to a remarkable remedy. Only that if it was, one had yet to surface in the research. I would leave unsaid that I remained extremely dubious at the prospect of a diet curing disease. A level of dubiousness not dissimilar to the way most view Lyme disease.
Ohhh….
“Any grand health gains would be looked at with extreme dubiousness.” Fudge. That was what my brain told me to look for in May of 2023.
There was a reason my trial of e-stim and antibiotics had yielded bupkis. No matter how much I wanted it to work, it was not the secret combination that I had hoped it would be. Repeated trials would continue to fail. When this depressing reality settled, I wish I had had a mirror to see in real time the blood drain from my face, the waxy pallor of a man finally facing the terror that has haunted his existence while living with a chronic disease.
The cure, unbelievably, must involve … diet. My personal house of horrors. And this amateur sleuth’s nightmare scenario. Worse, I had already written a tight draft of the maybe ending to this memoir, complete with a chapter title that hinted at what was to come, “The Shocking Conclusion,” a wink toward electrical stimulation. In that draft I had warned readers that unlike many of my bold proclamations in this book, I was uneasy about this one, referencing the potential that it could be “a steaming pile of malarky.” Which now, clearly, it was. Even my paper shredder got upset with me. You could take all the disasters mentioned in this memoir, from the Deepwater Horizon to the Hindenburg, roll them into one giant cluster doobie, light it up and smoke it, and you’d have your Chapter 52, renamed Dumpster Fire. Maybe I could still do that podcast I mentioned in jest last chapter, “Hook, Line & Sucker,” with me the sucker-in-chief?
How in the hell was I going to untangle a litany of dietary modifications, much less test them? I needed a coconut miracle.
Coconut Shell Paperweight - Original coconut on which the rescue message was inscribed by Kennedy to rescue the crew of the PT-109 and delivered by natives, Biuku Gasa and Eroni Kumana, of the Solomon Islands. Photo credit: jfklibrary.org; public domain.
On the night of August 1, 1943, the PT boat commanded by Lieutenant John F. Kennedy was sunk after being hit by a Japanese destroyer in Blackett Strait, south of Kolombangara in the Solomon Islands. Four days after they had been given up as lost, Kennedy and his surviving crew were discovered by Biuku Gasa and Eroni Kumana, two indigenous Solomon Islands scouts working for the Allies. Kennedy carved the message into this coconut husk that 11 crew members were still alive and passed it along to Gasa and Kumana, who carried the message to a nearby Australian coast watcher. The chance encounter with the islanders resulted in the rescue of PT-109's crew.
I had to start somewhere. Dr. Wahls isn’t the only one who has boasted about a diet curing her disease. There’s a sizeable smattering of breathless tales on the internet about the wonders of targeted food restrictions, and three close personal friends—all with suspected Lyme—have had wild success after lengthy elimination diets. But again, these are anecdotes. Anecdotes are all but anathema to scientists. I reasoned that if there were actionable clues tucked into recent diet research, my go-to doc on YouTube, Dr. Brandon Beaber, would have posted an informed opinion about them. (Coincidentally, he even dedicated an entire video to “Why Doctors Don’t Trust Anecdotal Evidence”.)
Among his 300+ streaming videos, there’s a corner reserved for nutrition. He even dedicated an entire playlist for the dozen videos he’s created concerning Dr Wahls and her diet/recovery. But one random video, an uncategorized one from April 10, grabbed my attention with its breathless title: “Does Ozempic Prevent MS?”
Unlike standard weight-loss drugs, the new classes of these drugs—Ozempic, Wegovy, Trulicity, and the like—lowered the risk of MS by a gobsmacking amount, as much as 85% lower than expected according to an April 2024 study. Even an older drug used to treat diabetes, metformin, shocked with a 61% reduction in risk. That sounds positively nuts. “I am highly, highly skeptical of the results of this study,” said Dr. Beaber with a cocked head. “One reason: it’s just too good to be true.”
"Disproportionality analysis illustrating the association between multiple sclerosis and weight loss-inducing drugs based on the data from the FDA Adverse Event Reporting System database. The reporting odds ratio represents the odds of a certain adverse event (in this case, ‘multiple sclerosis’) occurring with the drug of interest, compared to the odds of the same adverse event occurring with all other drugs in the database. An asterisk (*) denotes the presence of an inverse association, defined when the upper limit of the 95% CI for reporting odds ratio is less than 1. GLP-1, glucagon-like peptide-1; SGLT-2, sodium-glucose cotransporter-2." Shirani A, Cross AH, Stuve O. Exploring the association between weight loss-inducing medications and multiple sclerosis: insights from the FDA adverse event reporting system database. Ther Adv Neurol Disord. 2024 Apr 1;17:17562864241241383. doi: 10.1177/17562864241241383. PMID: 38566910.
Hiding in plain sight, grand gains, extreme dubiousness. Exactly what I was looking for. Even naltrexone made the list. Although not quite as effective as the others, a low-dose version, LDN, has been used off-label in the chronic disease community for decades. If I was four and hunting for Easter eggs, this surely meant I was past “getting warmer” and into “hot-hot” close. But now for the gauntlet of truth. These drugs would have to show promise not just in MS and autoimmune disease, but across a swath of illnesses, from mental disorders and dementia to long Covid and cancers. Its success outside of weight loss would be so widespread, so shocking, that it would be called a potential miracle drug. And one more thing: scientists would have no frigging clue as to why they are so effective across such a wide and diverse range of health conditions. Except that maybe it’s because they are “anti-inflammatory.”
“Ozempic and Mounjaro have another benefit: treating inflammation,” screams a headline. “We Know Where New Weight Loss Drugs Came From, but Not Why They Work” screams another from The New York Times. Months later, the paper upped the ante. “Ozempic and other drugs like it have proven powerful at regulating blood sugar and driving weight loss,” reads the opening paragraph. “Now, scientists are exploring whether they might be just as transformative in treating a wide range of other conditions, from addiction and liver disease to a common cause of infertility.”
That explorative dive into the efficacy of these drugs on myriad health issues has been described as one that could upend medicine.
Scientists believe the drugs are about to revolutionize several fields of medicine, such as cardiology and endocrinology. Researchers are also running dozens of trials to see whether they might help with Alzheimer’s, liver disease, polycystic ovary syndrome and even skin conditions. If these trials prove successful, the drugs may extend many lives by years, save billions in medical costs and divide public health into before-and-after epochs. A researcher studying these drugs told me he felt like the scientist who first discovered antibiotics.
“’Obesity first’ doctors say they start with one medication, to treat obesity, and often find other chronic diseases, like rheumatoid arthritis, simply vanish,” reads a June 18, 2024 piece in The New York Times. Dependence on alcohol appears to significantly wane. Polycystic ovary syndrome, a leading cause of infertility, is put into retreat. Cancer defenses are buttressed while cirrhosis and liver cancer risk drop. Cardiovascular events like heart attacks and stroke have dropped so much with their use that in March the Food and Drug Administration approved these diet drugs for those at risk, and a trial in kidney disease was so successful it had to be halted. These weight-loss drugs might even cure sleep apnea, a condition that affects an estimated 936 million worldwide. That shocking study landed June 21, 2024 in the New England Journal of Medicine, leading to headlines and an aftermath that I ominously predicted: “Can You Finally Throw Away Your CPAP Machine?” accompanied by the collapse of stock in businesses that manufacture them.
“The idea that a single drug that could target so many kinds of disease might sound too good to be true,” said the June 24 edition of the NYT Morning Briefing. That includes promise in Parkinson’s, reducing cravings and addictions, slowing Alzheimer’s, lowering smoking rates, and short-circuiting depression. “These drugs, called GLP-1s (glucagon-like peptide 1 receptor agonists), mystify even the scientists who study them. When I asked researchers how it was possible that Ozempic might help with cognitive issues and nonalcoholic fatty liver disease and opioid addiction, they gave the same answer: We don’t know!”
Researchers might not know why these drugs are so effective across such a wide range of illnesses, but I know. They are all treating Lyme disease, the disease my doubters have been insisting could not possibly be the root cause of so many illnesses. A single type of parasite doing so much damage was too unbelievably horrific to be true. Now that a single type of intervention appears to work for all those same illnesses, scientists are stuck in a similar state of disbelief, only they are now cautioning that such unbelievable success is too good to be true.
It's time to start believing. (Especially after the July 5, 2024 release of a 15-year study published in JAMA that “found that the patients who received GLP-1 agonists had a significantly lower risk of developing 10 out of 13 cancers studied, including kidney, pancreatic, esophageal, ovarian, liver and colorectal cancer.”)
A Miracle Diet?
Dr. Wahls didn’t cure her MS with Ozempic. My friends didn’t buck their Lyme disease with Wegovy or Trulicity or Victoza. Neither did all those diet/lifestyle peddlers who swamp the social media feeds of those struggling with chronic illnesses.
What’s going on? Those restrictive diets and lifestyle protocols must be mimicking aspects of the newest classes of weight-loss drugs, which work, in part, by helping the body to lower blood sugar. According to the Mayo Clinic, blood sugar is measured with an A1C (or HbA1c) test, which reflect “your average blood sugar level for the past two to three months,” measuring “what percentage of hemoglobin proteins in your blood are coated with sugar (glycated).”
So that leads to the million-dollar, er, billion/trillion-dollar question. What dietary and lifestyle changes can help reduce blood sugar?
“Controlling your blood sugar often involves limiting foods such as fruits, candy, and sweetened drinks that contain obvious sugar,” say health experts. “But starches such as bread and pasta also contain a lot of sugar in the form of carbohydrates — long, complex chains of sugars.”
Carbohydrates. They dominate Western diets. It’s not just desserts, select fruits, and breads and pastas that you must be wary of. Starchy vegetables like potatoes and corn are loaded with them. Then you have your other typical sides or fillers, like rice or beans, both bursting with carbs. Cereals and sweetened yogurts are problem areas, and forget about beer and cocktails. Many of our favorite snacks—chips, crackers, pretzels, popcorn, and processed foods in general, are laden with them. Even foods you think are healthier can be carb bombs, from gluten-free baked goods and low-fat salad dressings to fruit juice and milks (cow, almond, soy, etc.).
Carbs are like the actress Olivia Colman. Everywhere. Good luck avoiding them. You can’t—they are a significant energy source (carbs, not Ms. Colman). But you can limit them. Enter most diets.
Mediterranean, gluten-free, paleo, low-fat, the Zone, vegan, DASH, Ornish, even carnivore diets. They all limit, to an extent, carbs and sugars. But there are certain diets, like Atkins, where carb reduction is the focus with few restrictions on fats and proteins. The most popular of these currently, and conveniently one of the most studied, is the ketogenic diet: a low-carb, high-fat, often protein-rich diet.
In a nutshell, keto diets severely restrict carbs, which “typically serve as the main source of energy production in the body's tissues,” capping daily consumption to 50 grams or less, about what you would find in a typical bagel. When the body is depleted of glucose, it switches to an alternate energy source: ketones, which are created by converting fat. Burning fat stores when the body enters a state of “ketosis” typically results in weight loss, hence the reason for the diet’s popularity, despite its counterintuitive components. “Diet” and “high fat” are uncommon bedfellows, causing unease among many nutritionists and dieticians.
But there is something else decidedly unusual about ketogenic diets. They weren’t originally used for weight loss.
Recall two tenets from SHARDS: history harbors hints and answers await in the anomalies. In 1915, a professor of pediatrics from Johns Hopkins University School of Medicine started studying why fasting, which triggers ketosis, helped cure his nephew of epilepsy. The answer never became clear, but in 1921 a doctor from the Mayo Clinic, Russell Wilder, M.D., proposed a “nutritional treatment for epilepsy that tricks the body into believing it is fasting”—a ketogenic diet. It worked, and wildly well. For one type of epilepsy, more than half were cured in one trial, with a remarkable 80% showing significant improvement. But as pharmaceutical solutions were developed and patients were given a choice, popping a less-effective pill had more appeal than an overly restrictive diet, and going keto gradually lost favor as a treatment option.
Revisiting this history opens a long-forgotten, hidden gateway. I didn’t know that an entire class of epilepsy is thought to be autoimmune, labeled, appropriately, autoimmune epilepsy. Again, because I’ve linked all characteristics related to autoimmunity to Lyme disease, if my theory is correct, it can mean only one thing: ketogenic diets—and by extension, forms of intermittent fasting—must help treat the bacterial infection. Which, as unlikely as it sounds, at least passes the smell test upon closer inspection. Dr. Wahls’ paleo-based diets, her most restrictive—and the one she personally follows—combines elements of ketogenesis and fasting. Other successful “disease dieters” are almost certainly restricting carbs enough to mimic aspects of ketogenic and fasting diets, whether intentional or not.
Gulp. After all that over-the-top obnoxious chatter in the last chapter about me being a potential g-word and making the GMDOAT (Greatest Medical Discovery Of All Time), it would seem the time is nigh for the measuring stick of history to finally Tonya Harding my kneecaps, my triple salchow days in jeopardy. Either that, or I’m #GeniusAF.
As with the previous gauntlets of truth, it now all comes down to whether a keto/fasting diet is the shizzle, the bomb, the GOAT of diets, treating everything from autoimmune diseases and mental disorders to long Covid and cancers. If not, all my bonkers hypotheses are mercifully capped.
Choose your method of execution: Harding or Soprano.
Genius AF
If you’ve been reading this memoir since the beginning—wading through insane story after insane story, from me landing in The New York Times and collecting $500K after winning an epic row with my health insurer to Laura and I surviving the trauma of getting locked outside our hotel room butt naked right as my Viagra kicked in—you don’t have to be Nostradamus to predict how this is going to unfold. Getting capped isn’t happening unless you count the cap Sarah the astrophysicist promised to eat in Chapter 50 if I was right. (Good thing you can find edible ones on Etsy.)
The first mentions of ketogenic and fasting diets in my inbox—“the carb reduction [diet] reduces the glucose in your body [which] may reduce MS inflammation” while fasting “reduced MS inflammation and improved some symptoms”—popped up in 2019. Former newspaper reporter Ed Tobias, a member of ActiveMSers, had sent me a preview copy of his new book, We're Not Drunk, We Have MS: A toolkit for living with multiple sclerosis. I filed that away as an interesting tidbit and quickly moved along. The diet failed to make another appearance on my radar until early April in 2024, while writing the final chapters of this memoir, when a headline in The Washington Post gave me pause: “High-fat keto diet may help people with serious mental illness”.
I remember thinking that was odd. Really odd. By that point I was sure that Lyme disease was a significant contributor to many forms of mental illness. And yet an astonishing 79% of patients with schizophrenia and bipolar disease in the Stanford trial experienced “clinically meaningful improvement” after just four months of a keto diet. That brought up a flood of questions. How could a diet possibly fight a bacterial infection? Were there any other examples of this success in clinical research? Had it even been tested in multiple sclerosis?
”Ketogenic Diet Shows Major Benefits for Multiple Sclerosis” screamed the University of Virginia announcement from 2022, an announcement I apparently missed (or, quite possibly, ignored). “Patients with relapsing-remitting multiple sclerosis who adopted a high-fat, low-carbohydrate ketogenic diet saw significant improvements in their MS – including reductions in neurologic disability, fatigue and depression and heightened overall quality of life.” The improvements were sweeping and significant. According to the published research study, participants in the 6-month trial reported a “nearly 50% decline in self-reported fatigue and depression scores” and “significant improvements were noted in Expanded Disability Status Scale scores, 6-minute walk [times] and Nine-Hole Peg Tests [for dexterity].”
These results aren’t just surprising, they best every single one of the FDA-approved MS medications on the market. It’s well known in the chronic disease community that our meds don’t improve our health, that they merely slow the progression of our illnesses. But a cheap diet trumping our expensive drugs? Before the haters can hate, it was a rather small study and “more research is needed,” so Big Pharma CEOs can breathe a sigh of relief. Like there is a group out there that has pockets deep enough to pay for a larger research study on a non-money-making diet without the financial backing of a drug company, lol. As if. Bullet dodged, all Matrix like.
For there to be any risk to established medical practices, there would have to be a boatload of at least plausible evidence to support such nonsense that the ketogenic diet and intermittent fasting may be the shizzle. There would have to be so much that it would need to fill the most famous boat in history, the Titanic, for the mere suggestion of such a hairbrained hypothesis to be taken seriously.
Of course, among the pantheon of worst mistakes in history (referenced at the start of this chapter), the unsinkable Titanic, poorly captained by one Edward Smith, sits atop most lists for a reason.
History harbors hints for what causes many disasters. In the case of the RMS Titanic, “high speeds, a fatal wrong turn, weather conditions, a dismissed iceberg warning and lack of binoculars and lifeboats all contributed to one of the worst maritime tragedies.” Haste, human error, happenstance, and hubris. And that cliché about history, that it’s destined to repeat? It’s a cliché for a reason. Like Britney Spears in 2000, oops, it looks like we did it again, only instead of putting 2,240 lives at risk, multiple billions. Oops.
“A systematic review of 70 dietary studies revealed that … fasting and calorie restriction, in particular, were associated with improvement of rheumatoid arthritis activity,” found a 2021 study. The study found similar effects in psoriatic arthritis and ankylosing spondylitis. Myriad research papers, trials, case studies, and drama-filled reports concerning these diet interventions are tucked into the corners of all autoimmune diseases, peppering research study after research study. “Intermittent fasting: A promising dietary intervention for autoimmune diseases.” “Crohn’s disease successfully treated with the paleolithic ketogenic diet.” “The ketogenic diet modifies the immune system to combat different disease conditions.”
Different diseases. It’s not just flavors of autoimmunity. Ketogenic diets have shown “promising therapeutic potential in Alzheimer’s disease, Parkinson’s disease … and migraine.” The diet currently is being “used in clinical practice for … non-neurological conditions, including heart disease, diabetes, obesity, autism, glioblastoma and cancers.” Yes, cancers, and the acclaimed Cedars-Sinai is investigating the powerful role of intermittent fasting after they noticed their patients on these diet regimens often did better.
But wait, there’s more.
“Can a low-carb, anti-inflammatory diet be the answer to long COVID woes?” wonder medical professionals. Researchers aim to find out after case studies report patients are eliminating long Covid with both the keto diet and intermittent fasting. There’s even a push to investigate the diet in mental illnesses involving diet, after cases of severe anorexia resolved after carbohydrate restriction. And like the newest weight-loss drugs, these low-carb interventions appear to dampen addictive behavior and help treat substance abuse. A January headline from NPR’s “All Things Considered” perhaps expresses it best. “Patients say keto helps with their mental illness. Science is racing to understand why.”
Enter every panicked “what’s happening?!?” meme on the internet, from Poltergeist to The Office.
How can it be remotely possible that a single class of weight-loss drugs and a single type of dietary intervention can influence so many difficult-if-not-impossible-to-treat health conditions—health conditions I’ve repeatedly tied to Lyme disease throughout this memoir? How??? HOW?!
Scientists have spitballed so many theories that they’ve become soggy from all the phlegm and sputum. It must be altering the gut microbiome. Or contributing to “specific cellular pathways in mediating neuroprotective effects.” Or it’s spurring energy supply restoration. Or it’s inducing anti-inflammatory pathways. Or it’s reducing oxidative stress. Or it’s altering epigenetic mechanisms.
Translation: they have no effing clue.
It’s none of those. Per Occam’s razor, often the simplest answer is the right one. And it couldn’t get much simpler.
Part 3
Laying Siege
Dating back to 3000 BC, one of the first recognized military tactics deployed by early civilizations was the now-classic siege. “A siege occurs when an attacker encounters a city or fortress that cannot be easily taken by a quick assault, and which refuses to surrender,” explains Wikipedia. “Sieges involve surrounding the target to block provision of supplies and reinforcement or escape of troops.”
By far, sieges are most associated with the Middle Ages and their imposing castles. With the relatively rudimentary weaponry of medieval times, castles made for nearly impenetrable fortresses. Defenders could effectively blunt most forms of attack, relying on thick stone walls and high perches to thwart and repel advances. But lengthy sieges routinely presented a unique problem that even the most battle-hardened and prepared fortresses struggled to overcome. Access to food.
Historically, sieges have been quite effective in warfare, as opponents wear down the opposition by slowly strangling access to desperately needed, increasingly dwindling, resources. The consequences can be devastating, as more than one million Russians, mostly civilians, died of starvation in the infamous WWII Siege of Leningrad by the Nazis. “People ate everything from wallpaper paste to shoe leather to supplement their meager bread rations, and some even resorted to cannibalism.”
“Residents of Leningrad queueing up for water”. People in besieged Leningrad taking water from shell-holes. Location: Nevsky Prospect, between Gostiny Dvor (the long building on the left) and Ostrovsky Square. Photo credit: Boris Kudoyarov, 1 Dec1941. Wikipedia Commons: RIA Novosti
What do you think spirochetes, the microscopic corkscrew bacteria behind Lyme disease, need to survive? Where do they get their energy? “It appears that this bacterium is unable to synthesize amino acids, nucleotides, fatty acids, or most other cellular building blocks,” say researchers. “The present metabolic studies determined that B. burgdorferi is capable of utilizing only a small number of different carbohydrates as energy sources.”
Specifically, sugars, or glucose, derived from carbs. This buffet of carbohydrates circulates in the blood like floating miniature boats at a tired sushi restaurant, and “B. burgdorferi uses those nutrients to increase metabolism and rapidly replicate.”
Marauding spirochetes have overrun the traditional defenses of immune systems and established residence in the body, rendering their myriad tactics to repel and evict the raiders moot. They appear to have taken over the castle with no plans to relinquish their conquest, setting up a stout defense. Except in an unexpected twist, these drugs and diets that reduce blood sugar are all effectively laying siege, denying the bacteria critical food rations. The shapeshifting, stealthy bacteria with the indestructibility of the T-1000 Terminator has a weakness.
There’s another unexpected wrinkle.
Our body’s immune system already uses a form of siege warfare to eliminate unwanted intruders. “Iron is an essential trace element for humans and other vertebrate hosts, as well as for their microbial invaders,” explains UCLA professor Tomas Ganz, PhD, MD, in a 2010 paper. “Within hours of infection in humans and other vertebrates, concentrations of iron in extracellular fluid and plasma dramatically decrease,” a process called hypoferremia, which starves interlopers of the essential nutrient. As a defense mechanism, our bodies become temporarily anemic.
But Lyme is different, really different. Our body’s ingenious “iron curtain” defense is powerless against B. burgdorferi. “The bacterium that causes Lyme disease substitutes manganese for iron in its diet,” found a study conducted by Johns Hopkins University Bloomberg School of Public Health. “The pathogen is the first known organism to live without iron.” Instead, researchers discovered that “to cause disease, Borrelia burgdorferi requires unusually high levels of manganese,” a stunning development. “The manganese mechanism may be a chink in the bacterium’s armor that humans can exploit,” said Hopkins’ study researcher Valerie Culotta.
Dr. Culotta was righter than she could have possibly imagined, as some of us humans already are exploiting that weakness. By accident.
While manganese is an essential nutritional element for human diets, “absorption of manganese from a meal decreases as the meal's iron content increases.” What kinds of meals are rich in iron? Those laden with meat, fish, poultry, and eggs, protein cornerstones of ketogenic and fasting diets.
And then there’s this head-smacker that just plunked into my lap: your gender affects how well your body absorbs and retains manganese. “Men generally absorb less manganese than women, which may be related to the fact that men usually have higher iron stores than women,” reports an overview of the element by Oregon State University. “Iron deficiency has also been shown to increase the risk of manganese accumulation in the brain.”
Now everything crystallizes. Castles, armor, sieges, starvation, all of it.
It appears I’ve stumbled upon yet another hallelujah booyah (HB). But I’m afraid this HB might be an even bigger bombshell than anticipated.
To understand the level of excitement coursing through my body, imagine if I could run, it was the spring of 1983, and I was 10 miles south of my Los Ranchos de Albuquerque home, on the basketball court in the Pit after shockingly winning the NCAA championship in an unforgettable upset. That’s me, at this moment, frantically looking for hugs like the legendary NC State coach Jimmy Valvano.
According to the U.S. Department of Health and Human Services, “women are more likely than men to have an iron deficiency because they lose blood during menstruation, [while] pregnancy and childbirth can also cause iron deficiency,” leading to the agency’s concern with females between the ages 12-49. New research published in JAMA is confirming—and terrifying. “More than a third of young women in the United States — nearly 39 percent of those ages 12 to 21 — have an iron deficiency.” What ominously pairs with chronically low iron?
“Patients with chronic inflammatory disorders, autoimmune diseases, and infections often present with anemia, namely anemia of inflammation (AI),” reports a 2023 research article. “AI is a very frequent clinical condition affecting globally more than a billion people with chronic inflammatory disorders, such as chronic kidney disease, heart failure, and inflammatory bowel disease.”
Our bodies are desperately trying to fight off these bacterial invaders the best way they know how, cutting off supplies of iron. But when it comes to Borrelia burgdorferi, it’s as effective as restricting the amount of salad a hungry T-rex can eat. In fact, it’s making matters worse.
Less iron translates into more manganese, the mineral Lyme spirochetes require to survive. To understand what this means to your health, manganese is first absorbed in the small intestine before it is shuttled off to other areas of the body. “Most of the mineral is stored in bone, with smaller amounts in the liver, brain, kidneys, and pancreas.”
Left: Pure (99.97 %+) iron chips, electrolytically refined, as well as a high purity (99.9999 % = 6N) 1 cm3 iron cube for comparison; Alchemist-hp, 24 April 2010. Right: Pure (99.99 %) manganese chips, electrolytically refined, typical view of on air oxidized surface, as well as a high purity (99.99 % = 4N) 1 cm3 manganese cube for comparison; Alchemist-hp,
31 October 2010.
It’s all making sense—those spirochetes are drilling for manganese. And in the process, causing unspeakable damage to the environment better known as the human body. Neurological diseases and brain disorders, chronic kidney conditions, chronic liver disease and cancers, a vast range of sickness related to irritable bowel syndrome, and pancreatic illnesses including forms of diabetes, all the result of a solitary spirochetal quest.
Boys and girls have similar levels of manganese throughout childhood and adolescence, explaining why type 1 diabetes, which tends to appear in children 4-7 years old and then from 10-14, is equally prevalent in both sexes. Birth defects I’ve connected to Lyme, e.g., Down syndrome and cystic fibrosis, are divided equally among genders. The same is true of IBS, as “girls and boys are equally affected by the disorder.” But once women begin menstruating, their reserves of manganese become far more robust than those of men. And spirochetes can hardly wait, munching on manganese before it even leaves the intestines to storage centers.
“In the past couple of years, a TikTok trend has emerged in which women share what it’s like living with chronic stomach issues, including irritable bowel syndrome (IBS)—a condition that affects the stomach and intestine and can cause cramping, abdominal pain, bloating, diarrhea, and constipation,” reports Fortune magazine. “These women are raising awareness—the tag #HotGirlsWithIBS has over 112 million views on TikTok—while also normalizing the health issue.”
"TikTok is full of posts about gut health and digestive issues, ranging from mild gluten and lactose intolerance to severe Crohn’s disease and other forms of inflammatory bowel disease." TikTok compilation credit: Hyacinth Empinado/STAT, in the STAT article "From social media to pink billboards, it's suddenly "hot" to discuss gut diseases," by Isabella Cueto.
How cute, how quaint, say gaslighting medical providers, who “are seeing a pattern of more and younger people wanting to deal with their gastrointestinal distress,” yet doctors “suspect anxiety related to increased isolation during the pandemic is playing a big role in the increase in visits,” reports an August 2024 article from the Associated Press.
Silly girls. And then those girls grow up to be women. And guess what’s waiting in adulthood?
Women are up to 10 times more likely to have autoimmune liver disease than men. Women “have a greater risk of developing dementia during their lifetime… [and] around twice as many women have Alzheimer’s disease—the most common type of dementia—compared to men. Chronic kidney disease is more common in women. And pancreatic cancer rates are rising fastest in women, particularly young women, according to a 2023 study.
It appears that the mystifying gender gulf—the one tilting decidedly to the female persuasion in autoimmune disease and so many other illnesses—finally has a sensical answer. (Unsurprisingly, my not-so-confident “hunch” concerning the Xist gene in Chapter 48 was off.) The risk of iron deficiency in men (and with it an increase in manganese) doesn’t rise until they approach their mid-60s. This helps explain why “most men start experiencing severe complications when they hit their late 50s to mid-60s,” as cancer rates and heart complications, and myriad other health issues, increase precipitously.
But women? There is an unmistakable bullseye on their backs, particularly during those years when they are menstruating, those same prime years when autoimmune diseases are most likely to strike. In the futile struggle to protect itself, human evolution is even getting involved. A study released by Harvard in late May of 2024 confirmed that “the average age at menarche—the first menstrual period—has been decreasing among younger generations in the U.S.” As autoimmune diseases have soared in the last 50 years, it’s no coincidence that “studies have shown trends towards earlier menarche over the past five decades.” With their coveted stores of manganese, vulnerable female immune systems are trying to kickstart iron depletion, its most reliable defense mechanism against bacterial invaders, and the result has been the earlier and earlier arrival of a woman’s first period. It won’t matter.
We now know the bacteria’s modus operandi. B. burgdorferi’s quest for manganese is central to its survival and proliferation. And to achieve this goal, Lyme spirochetes have adopted a relentless drill-baby-drill approach to access reservoirs of the trace element in their hosts. In response, the body fruitlessly tries to restrict the bacteria’s access to the wrong trace element, iron. The result?
Unfathomable carnage of human health.
No, no, no, it couldn’t be that easy. For all of this to be true, scientists would have to witness low iron levels in all the conditions I’ve linked to Lyme. “Anemia of chronic disease happens when you have an autoimmune disease or other illness lasts longer than three months and that causes inflammation,” says the Cleveland Clinic, listing some of the conditions that may cause anemia. Cancer. Chronic kidney disease. Heart failure. Autoimmune diseases, including rheumatoid arthritis, lupus, vasculitis, sarcoidosis, inflammatory bowel disease, and irritable bowel syndrome. What about mental disorders?
“Research suggests a connection between low iron levels and symptoms of depression, anxiety, and schizophrenia.”. It’s bad. “Anemia relates to a 34% increase in dementia risk, and 41% for Alzheimer’s disease,” found another study. “The prevalence of dementia is expected to increase threefold over the next decades, with the largest increases predicted in the countries where the prevalence of anemia is highest.”
Researchers, though, are puzzled.
“Little is known about the relationship between iron deficiency and autoimmune disease,” says a 2019 study by Taiwanese scientists, which found a “meaningful association between iron deficiency anemia (IDA) and later autoimmune disease development.” After analyzing the data, clear trends emerged. “Among patients with IDA, female patients and patients with the simultaneous chronic diseases of allergic rhinitis, urticaria, cancer, chronic obstructive pulmonary disease (COPD), hyperlipidemia, or hypertension had a significantly higher risk of autoimmune disease. The risk of autoimmune disease was considerably higher within the 2 years after an IDA diagnosis.”
Our last hurdle involves long Covid. Sure enough, “new research has shown that people with long COVID may have a higher risk of low iron levels.” University of Cambridge researchers discovered that “people who developed long COVID had more problems regulating iron levels, which was noticeable as soon as two weeks after they had COVID-19.”
Of course, we now know that as iron levels drop, manganese levels rise, to the overjoyed glee of Lyme spirochetes. I gotta feeling it looks something like an unmoored sea of ecstatic Minions preparing to party like there’s no tomorrow.
Changing levels of manganese—“difficult to assess and not routinely measured in clinical practice,” according to the NIH—have been implicated in a broad range of health conditions, from a wide variety of cancers to mental disorders to neurological diseases. “Associations have been observed between Mn accumulation and neurodegenerative diseases such as… Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis,” reports a 2023 study. It’s also been “connected with susceptibility to neurodegenerative diseases, fertility, and infectious diseases… including metabolic diseases, such as type 2 diabetes mellitus/insulin resistance, osteoporosis, obesity, atherosclerosis, and non-alcoholic fatty liver disease.”
Obesity? Does Lyme also have its claws in our never-ending fight against weight gain? That would mean being overweight has little to do with willpower and everything to do with an untreated disease. That would mean a full rewrite of our understanding of diet and nutrition.
Science, stop meddling with our biases!
Upending Nutrition
I hadn’t investigated the connection between autoimmune disease and obesity. Um.
“Obesity may be associated with an increased risk of several autoimmune diseases, such as asthma, hypothyroidism, psoriasis, rheumatoid arthritis, and type 1 diabetes,” says one 2023 study. “Compelling epidemiological evidence reveals a strong association between being overweight or obese and the risk of developing autoimmune diseases,” says another from 2023. “Emerging data identify a key role for chronic inflammation in mediating obesity related disease states and reveal higher incidence of autoimmune disease development,” says a third from 2022. And then there was a 2023 study that tied it all together—iron, glucose, fat metabolism and obesity. Researchers have known about the iron-obesity link for more than 50 years, dating back to the 1960s.
Children and adolescents with overweight and obesity are twice as likely to be iron deficient, with prevalence of iron deficiency increasing with body mass index (BMI). Pregnant women with obesity have impaired iron absorption in late pregnancy, and their offspring have reduced iron stores aged six months. Adults with obesity are also at higher risk for iron deficiency.
These inflamed bodies are frantically trying to fight off infection by cutting off iron. No wonder the newest diet drugs are having such a dramatic effect in the overweight community. Many of these patients have Lyme disease. They’re sick. And they are finally getting appropriate treatment.
It also looks like we can put a fork in the battle-of-the-bulge diet wars, which will almost certainly earn me prized real estate on the dartboards of diet influencers worldwide. This could easily be the topic of an entire volume of books, but from my perch, our diets—basically the whole lot of them, from paleo to Mediterranean to anti-inflammatory—are all limiting carbohydrates in one way or another, slowing down Lyme disease with varying degrees of success. The most effective diets simply restrict the most carbs, the most popular being the easiest to follow.
That’s it.
Given the ubiquity of Lyme in society, it makes total and complete sense that “the rise in overweigh and obesity has paralleled the increase in the incidence of immune-mediated inflammatory diseases,” according to a 2023 Lancet study. Even so, nutritionists and dieticians naturally flinch at diets that are clogged with fat like ketogenic diets, as do researchers. When faced with a clear paradox—“despite the fact that the high-fat Arctic diet may sound like a heart attack waiting to happen, the Inuit tend to have low rates of heart disease and diabetes”—it’s a struggle to comprehend what is happening.
I’ve shown that the “it-must-be-the-genes” knee-jerk reasoning is not merely deeply flawed, it’s just wrong, like so many other medical theories I’ve dismantled in this memoir. It’s convenient to blame the Western diet for our ills, the endless buckets of deep-fried shrimp (at least before Red Lobster’s bankruptcy) and slabs of death-by-chocolate cake, yet an iron-clad connection has been as elusive as the Loch Ness Monster. For good reason. Neither exists (sorry, Nessie fans).
Western diets aren't causing autoimmune disease, nor are they triggering cancer, autism, long Covid, Alzheimer's, or almost any other health condition, including Lyme disease. Ah, but like dry timber in a parched forest, those carb-laden diets are largely responsible for fueling the relatively recent worldwide crush of illness, not starting the fire. (So, partial credit?)
But, but, but what about eating our fruits and veggies, cutting back on salt, upping our fiber intake, and limiting sugars and alcohol?? What about following federally recommended dietary guidelines?
The foods and beverages that people consume have a profound impact on their health. The scientific connection between food and health has been well documented for many decades, with substantial and increasingly robust evidence showing that a healthy lifestyle—including following a healthy dietary pattern—can help people achieve and maintain good health and reduce the risk of chronic diseases throughout all stages of the lifespan.
Common sense. Eminently logical. A nutritional slam dunk. We also need to “eat clean” and avoid heavily processed and genetically modified foods, right? After all, you are what you eat. Is what we’ve been told, repeatedly. Just one wee, tiny problem. (By now, I expect scientists are in agreement that they don’t like it when I find wee, tiny problems in their research.) None of these sweeping claims about nutrition are exactly backed by science. “Well-documented” and “increasingly robust” evidence isn’t as supportive as you think.
Nutritional theories, such as red meat causes cancer, are “based almost entirely on a type of research method called nutrition epidemiology, which is just untested theories, essentially, guesswork,” said Harvard-educated nutrition specialist Dr. Georgia Ede in an interview. That’s one reason coffee is good for you one week, and then practically rat poison another. The same is true of diets. Without a clear medical reason to do so, eliminating fat, dairy or gluten from a diet has such weak empirical support that doctors have started pushing back, even against the recommendations of behemoths like the American Heart Association.
In a near 10-year-old piece from The New York Times, “How the Sugar Industry Shifted the Blame to Fat,” the opening sentence spells out what happened. “The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show.” Three Harvard scientists got $50 grand each from a sugar trade group to get a journal article published in the New England Journal of Medicine that would minimize “the link between sugar and heart health and cast aspersions on the role of saturated fat.”
A year after that NYT piece, in 2017, the book The Case Against Sugar hit bookshelves. “Bad science and the processed-food industry have colluded to make fat public enemy No. 1 — all the while neglecting carbohydrates, especially the highly processed and easily digested kind,” reads the NYT review of Gary Taub’s investigative work. “The rising belief that dietary fat consumption was the cause of obesity and heart disease — which had been written about sporadically for decades — suddenly coalesced into fact, shifting the public’s attention away from sugar.”
It worked, and astonishingly well. Everyone was taught that saturated fats cause high cholesterol and heart disease, that choosing fat-free or low-fat is always preferable for health reasons. In 2017 a contingent of physicians finally had had enough and penned a scathing rebuke of the popular dogma surrounding nutrition.
Despite popular belief among doctors and the public, the conceptual model of dietary saturated fat clogging a pipe is just plain wrong. A landmark systematic review and meta-analysis of observational studies showed no association between saturated fat consumption and (1) all-cause mortality, (2) coronary heart disease (CHD), (3) CHD mortality, (4) ischemic stroke or (5) type 2 diabetes in healthy adults. Similarly in the secondary prevention of CHD there is no benefit from reduced fat, including saturated fat, on myocardial infarction, cardiovascular or all-cause mortality.
It gets worse. This team of cardiologists “contend that the ‘fat free’ movement caused higher intakes of carbohydrate foods, including sugar,” a catastrophic dietary change that we now know is inadvertently supercharging undetected cases of Lyme. In paper after paper, doctors from all walks are screaming to be heard, that “the development of the diet-heart hypothesis in the mid twentieth century led to faulty but long-held beliefs that dietary intake of saturated fat led to heart disease.” That “numerous meta-analyses and systematic reviews of both the historical and current literature reveals that the diet-heart hypothesis was not, and still is not, supported by the evidence.” That “there appears to be no consistent benefit to all-cause or cardiovascular disease mortality from the reduction of dietary saturated fat.” That saturated fat unexpectedly has “an inverse relationship with obesity-related type 2 diabetes.” Unheard screams, mirroring those from the Lyme community.
A dietician friend of mine is similarly exasperated. She has long mused that people without celiac disease are doing themselves no favors by embarking on gluten-free diets, a feeling reinforced by the research. And for the life of her, “anti-inflammatory” diets make little sense, because nutrition doesn’t work that way, despite the unsupported advice from leading centers, like Johns Hopkins and Harvard, which warn us that many of the “major diseases that plague us — including cancer, heart disease, diabetes, arthritis, depression, and Alzheimer's — have been linked to chronic inflammation.” And they know this how? “Many experimental studies have shown that components of foods or beverages may have anti-inflammatory effects,” said Dr. Frank Hu, professor of nutrition and epidemiology in the Department of Nutrition at the Harvard School of Public Health.
Alright. (Pause, deep breaths, maintain composure.) So, “components” of diet “may” tamp down chronic inflammation. Geez. Evidence-based nutrition is fuzzy, and frustrating. Shades of grey are the rule—and everyone in the field knows it. So, let’s make it black and white. WHAT THE HELL DO YOU THINK IS CAUSING CHRONIC INFLAMMATION, CYTOKINE STORMS, AND THE ENDLESS REVOLT OF OUR BODIES AS IF THEY WERE UNDER REPEATED ATTACK?!
What matters most about what you consume is one, single factor: whether you have Lyme disease, particularly active Lyme disease.
Sacrilege! The U.S. government says that “diet-related chronic diseases, such as cardiovascular disease, type 2 diabetes, obesity, and some types of cancer, are very prevalent among Americans and pose a major public health problem … [and that] more than half of adults have one or more diet-related chronic diseases.”
“Diet-related chronic diseases” is a euphemism for Lyme disease, just as “autoimmune diseases” are cases of misdiagnosed variations of Lyme disease. Diet matters tremendously if you are infected with B. burgdorferi spirochetes—and shockingly not as much as you’d think if you aren’t. The proof lies, as always, in the science.
Consider Japan and their cuisine and contrast it with nations that feast on staples of the Western diet. Japanese are generally thin, have some of the longest life expectancies in the world, and have low rates of heart disease, cancers, and autoimmune disorders. The country is even “worlds apart” on mortality rates from Covid. The connection would appear to be crystal clear—wherever you see obesity, disease and sickness follow—suggesting that the secret sauce to their good health is diet, yet every competent scientist knows that correlation does not imply causation. And the Japanese diet isn’t profoundly healthier than others. “As delicious as it is, Japanese food has plenty of carbohydrates and fats that can easily scare away the health-conscious types.” What the heck?
Once again, answers await in the anomalies. Since the days of Aristotle and Plato, we have been seeking meaning about the aging process, the philosophers in agreement that they “do not appreciate old age in general” and that it denigrates “not only physical conditions but also intellectual capacity of the soul.” But not always, which has piqued the curiosity of scientists. “For a little over a decade, scientists have been studying a subset of people they call ‘super-agers,’” reports a recent article in The New York Times. “These individuals are age 80 and up, but they have the memory ability of a person 20 to 30 years younger.” Instead of focusing on common health issues of old age such as dementia, researchers took a different approach with this somewhat rare group. What is their secret to living long and healthy lives?
The June 2024 study out of Spain the Times referenced pointed to less brain atrophy and minimal signs of Alzheimer’s compared to others the same age, supporting past research. But substantial differences between the lifestyles of super-agers and “normals” were hard to tease out. Really, head-scratchingly hard. They didn’t exercise more, researchers told the paper. “There were no differences between the groups in terms of their diets, the amount of sleep they got, their professional backgrounds or their alcohol and tobacco use.” A similar study on super-agers out of Chicago found the same thing. “Some exercised regularly, but some never had; some stuck to a Mediterranean diet, others subsisted off TV dinners; and a few of them still smoked cigarettes.”
If it’s not diet or exercise driving better health, what-o-what could it be? “Super-agers probably have ‘some sort of lucky predisposition or some resistance mechanism in the brain that’s on the molecular level that we don’t understand yet,’ possibly related to their genes,” posited researchers.
Or not.
Look closer. The super-agers also boasted some “slightly better” health markers, markers easy to brush off as TMI. Sure, they (unsurprisingly) performed a bit better on mobility tests, but they also “showed lower prevalence of hypertension and glucose disorders than typical older adults.” High blood pressure, a widespread problem that is thought to be a byproduct of poor lifestyle choices—eating unhealthily, not exercising enough, too much stress—and glucose, aka high-octane spirochete fuel.
This select group of super-agers shares a single common bond, and it’s not exercising daily or squeezing out maximum nutrients from heart-healthy meals. They all appear to be Lyme free, a conclusion that scientists have been tantalizingly close to realizing for years.
Our Colombian expert Dr. Juan-Manuel Anaya, who originally reported on the too-similar-to-be-a-coincidence likeness between autoimmune diseases in 2010 (the “autoimmune tautology” referenced in Chapter 48), observed a similar strange paradox in his latest 2024 research.
Autoimmune diseases (ADs) are one of the groups of chronic illnesses that impose a significant burden of disease and health costs worldwide. Age is a crucial risk factor for the onset of ADs. Theoretically, it is inferred that with organic and immune system aging, the loss of immune tolerance and specificity of immune activity becomes more intense, the probability of autoimmunity is increasing. However, there is a group of individuals whose prevalence of ADs is very low or non-existent, despite the biological aging.
Centenarians. If you manage to live to see 100 candles on your birthday cake, surely some squeaked into the triple digits stringing along an autoimmune disease or two. But no, Anaya and his team of researchers discovered. There was a distinct “absence of ADs in centenarians,” a finding that defies statistical odds. (Curious cases of seemingly defying long odds have been a recurring theme of this memoir.)
Really? Good health in old age relies chiefly on the absence of active Lyme disease? Diets, genes, and chance don’t much matter? Our fourth SHARDs tenet reminds us that reliable research repeats, so we should see evidence of this health paradox in other studies. And we do.
“Despite the claim that chance plays an important role in the achievement of exceptional longevity, it has repeatedly been shown that already earlier in life, centenarians are a selected group with fewer disabilities, comorbidities, hospitalizations, and better cognitive function compared to non-centenarians.” Enter into evidence a mammoth study from late 2023, one that investigated blood biomarkers of Swedes with such exceptional longevity. Researchers sifted through 44,000 records to see what separated the super-agers from their peers. Wanna guess what they discovered was the secret sauce to aging gracefully?
“Higher levels of total cholesterol and iron and lower levels of glucose,” write the study’s authors, emphasizing “higher” and “lower” with italics (the bolding of cholesterol, iron, and glucose is my handiwork). They also pointed to other distinct markers: those related to lower inflammation, improved liver and kidney function, and lack of signs of anemia—all markers tied directly to the presence, specifically the lack thereof, of Lyme disease. If there were any dietary trends that influence longevity—for instance, people who ate more plants and eschewed red meat lived two years longer on average—they absolutely should have surfaced in these centenarian studies. They didn’t.
Mystery solved. Science has spoken. The whole concept of dieting seems to be, at best, misguided, and some popular diets may even inadvertently amplify the health risks associated with Lyme. Counterintuitively, while generally quite healthy in many respects, “veganism has been associated with adverse health outcomes, namely, nervous, skeletal, and immune system impairments, hematological disorders, as well as mental health problems,” reported a 2023 study, all symptoms that scream of Lyme’s involvement. And now we have a good idea as to why that may be. “Vegetarians have a high prevalence of depleted iron stores,” reports another study. “A higher proportion of vegetarians, compared to nonvegetarians, had iron deficiency anemia. This is especially true for premenopausal vegetarian women.” Vegetarian and vegan diets are unquestionably great for Mother Earth and fabulous for animals, but without proper iron supplementation, could provide spirochetes with a coveted manganese feast.
If you are still struggling to wrap your head around this upending of nutrition, and I imagine a great many of you are, let’s try using our box-out technique introduced two chapters ago to help it all make sense. The three distinct groups referenced above all have experienced uncommonly low rates of disease: the Inuit before 1950, centenarians, and the Japanese. That means all three, theoretically, possess the answer to good health. And that answer is??
Genetics! Except, no. In 2018, scientists analyzed over 54 million records on Ancestry.com to find the genetic secret to longevity and came away shocked. “The heritability of life span, a hot research topic for decades, is considerably less than widely thought,” researchers discovered, finding that “genes accounted for well under 7 percent of people’s life span, versus the 20 to 30 percent of most previous estimates.” The best predictor of a life span? Spouses. “They were more similar than the life spans of sisters and brothers. Since spouses share relatively few DNA variants, that suggested a strong influence of non-genetic factors that they do share.” Other studies back this finding, so much so that it’s an open secret among geneticists. It’s definitely not “good genes” driving better health.
Diet then! Except, again, no. A 2020 study aimed to separate genetics from diet by examining Japanese Americans, “who are genetically identical to the native Japanese people, but have experienced rapid and intense Westernization in terms of their lifestyles” and compared them to native Japanese. It wasn’t pretty. The authors concluded “that native Japanese people must continue the Japanese lifestyle, and that Japanese Americans should adopt the Japanese lifestyle as a preventive measure against the onset of metabolic and atherosclerotic diseases.” Makes sense, but our three disparate “disease-lite” groups all indulge in not-so-pristine diets. The Inuit: high fat and protein, few carbohydrates, and a dearth of fresh fruits and vegetables. The Japanese: high carb and plenty of fats. Centenarians: a grab bag of fun that may or may not include TV dinners on your lap in front of the tube while watching Matlock reruns. None are particularly healthy on paper, yet collectively this group has astonishingly low rates of heart disease, cancer, and other maladies despite seemingly self-destructive food choices. It’s definitely not the end result of a “healthy diet.”
Avoiding modern toxins! Maybe? Except, nah. Sure, the Inuit in the early 1900s didn’t have to worry about forever chemicals and myriad other newly developed carcinogens, but centenarians have been microwaving their food in plastic leftover containers for more than 40 years and the Japanese have more cell phones than people. Not that cell phones cause brain cancer or any other health issue (that we know of), but Japan has near equal exposure to modern ick that Americans have, and they are far healthier. It’s definitely not deft toxin avoidance.
So, luck? Statistical burps? That’s what we are left with: the scientific equivalent of fat chance. I suppose one could make that case for reaching the ripe age of 100, but to attribute the luck of the Irish to an entire island nation in the Pacific with 167 million residents seems like a statistical improbability of the highest order. It’s not simply good fortune.
What matters most about what you consume is one, single factor: whether you have Lyme disease, particularly active Lyme disease.
What does this all mean? I’m going to try to relay the consequences with the most subdued amount of giddiness that I can muster—get rid of your Lyme disease and the science appears to imply that you may be able to eat or drink pretty much whatever the hell you want (in moderation). THAT’S UTTER INSANITY, your brain is barking, as kids worldwide celebrate any reason to not eat Brussels sprouts. How could nutrition science be in such conflict, then? Upon closer inspection, it’s not, and the research is still valid. Most diet studies are infected with patients who have been literally infected with Lyme, which, in turn, drives our nutritional guidelines. The problem isn’t so much with faulty science or incompetent scientists, it’s faulty data. Our food pyramids are made of malleable sandstone, as evidence suggests that the secret key to good health is jettisoning those unwanted, spiral-shaped bacterial deviants.
Yahoo!
But about that “getting rid of Lyme” stuff… uh, I’ve got the worst kind of news. Sobering news. Until new spirochete-busting medications are developed, trialed, and released—a process that will take time, likely multiple years even at Operation Warp Speed levels—most known efforts to rid your body of entrenched spirochetes are doomed to fail.
This is a good time to remind scientists of what Chinese general, strategist, and philosopher Sun Tzu advised in his opus The Art of War. “If you know the enemy and know yourself, you need not fear the result of a hundred battles. If you know yourself but not the enemy, for every victory gained you will also suffer a defeat. If you know neither the enemy nor yourself, you will succumb in every battle.”
How can it be that a masterful collective of scientists can develop a pandemic-busting vaccine in record speed to save humanity, yet for years, decades, even centuries, generations of brilliant scientists have been in a frustrating stalemate with countless other health conditions and chronic illnesses, a history checkered with few cures and underwhelming treatments? Goose eggs in the autoimmune disease arena, thought to number over 100 maladies. Diddly in the realm of chronic disease, too many to list. Jack squat in the suffocating theater of mental illness, from dementia to bipolar disorder to autism. Cures in the cancer department restricted to a meager handful.
It makes no sense, violating the first rule of SHARDs. Are scientists of today and yesteryear a contingent of over-educated, incompetent dunderheads barely equipped with the number of brain cells necessary to properly button up a white coat? Or do they just not know the enemy?
The few types of cancers that they do have on the run—cervical cancer, lung cancer, and stomach cancer, for example—have known causes in many cases (human papillomavirus, cigarette smoking, and the spirochete helicobacter pylori, respectively). When scientists know the enemy, from Covid to HIV, it’s game over, as Tzu predicted. But when the enemy is unknown, treatments flip from curative to symptom management and crossed fingers, a mixed bag of victories and defeats.
The war these scientists think they have been fighting is 100% unwinnable. There will never, ever be a single cure for an autoimmune disease. Same with most cases of mental illness. Long Covid will persist longer, as in forever. Moon shots to cure many common forms of cancer, no matter how many hundreds of millions (billions?) plowed into the effort, will largely fail.
But what about those new semaglutide weight-loss medications, ketogenic diets and fasting?
There’s a sneaky, overlooked reason most diets crash and burn over time. Vanquishing Lyme falls into the same category. To avoid looking like the English trying to storm that French castle in that scene from Monty Python and the Holy Grail, smarter tactics must be deployed, using all that you’ve learned over these many pages.
If you know thy enemy, the outcome of 100 battles is preordained.
It’s time to be fearless.
Due to late-breaking developments, Part 4 and the conclusion of Sit Down Before Reading has been delayed. The new publication date for the final installment is now early fall, estimated to be September 25. After two-and-a-half years of research and writing, the finale of SDBR needs to be as accurate and as up to date as possible. Thanks for your understanding.
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