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Chapter 48: Hallelujah Booyah

Updated: Jun 5

school children in South Africa in 1993

In 1993, Laura and I arrived on the shores of South Africa. We were among the students on the floating university Semester at Sea, and our visit to Cape Town was a fleeting four days. But in those four days, all of us felt determined to be world changers. Apartheid was in its final throes, and we were going to do whatever possible to accelerate its demise. And then, before we disembarked the ship, guest professor Charles Villa-Vicencio took to the microphone. He was the director of the Truth and Reconciliation Commission, which organized the public hearings on the atrocities committed during apartheid. An energized student, Scott, asked the professor what we could do to help, specifically.

I don't think there's a damn thing you can do in four days. And it may even be a little bit arrogant to try to do anything in four days. Black people have been engaged in a titanic struggle for 350 years. Nelson Mandela has been in jail for 27 years. Others of us have been in jail. We've done everything we conceivably can. No bunch of students are going to change the country in four days. I hope you will go, Scott, and you will take the shoes from your feet and that you will know that you are standing on somebody's holy ground. Where blood has been shed. Where people have died. Where people will continue to shed their blood and they will continue to die. And I hope that you would use these four days to be sensitive to that situation and to talk to as many people as you can.

[Video by Carl Wikman, who passed in 2023.]

That evening we attended a welcome reception at the University of the Western Cape, an all-black university. At first it was the standard buffet and get-to-know-you talk, but then our personally assigned student guide, Butcher, had an idea: to sneak out of the banquet and tour the campus like renegades. We soon found ourselves as surprise guests of honor at a makeshift party in a dorm room. Bottles of warm beer, originally tucked under the coffee table as a courtesy upon our arrival, were brought out of hiding and shared.

Following the advice of Dr. Villa-Vicencio, I sat down and talked with one student extensively. I asked him questions and then listened. And then listened some more. Then, it was time to go. He reached out to shake my hand and made it a point to look me directly in my eyes when he spoke.

"Thank you." His grip tightened. "You are the first white person in my 20 years that I have ever had a conversation with."

Dave in a dorm room in South Africa in 1993

A single handshake that, in an instant, irrevocably changed two worlds. I learned so much that day. I also learned that I had—and still have—much, much more to learn about struggle, humanity, life. I’ve told this same story many times, and it is as applicable for this moment as any. And it starts with a single life lesson: listening. What a concept, listening. If only the scientists, researchers, and doctors had just listened to patients. That something was wrong. That something was very, very wrong.

If only they had listened. If only.

As we peer up, the towering building blocks of modern medicine are unexpectedly swaying. Our understanding of chronic disease, mental illness, cancers, vaccination, and so much more is not only being challenged, but also being wholly rewritten, the settled science of the past now a faint shadow, smeared and riddled with bits of spent pink eraser.

Today, in a twist no one saw coming including myself, Lyme disease has become the most researched illness in human history—by far, and it’s not even close—despite scientists being unaware that they had been investigating the tickborne illness all along. Yet within these studies are the answers to countless conundrums that have dumbfounded the medical profession since Hippocrates. I am only beginning to grasp the enormity of this reality.

The research into autoimmune diseases alone is intensely revealing, unlocking mysteries with keys thought forever undiscoverable. Since it appears that most, if not all, autoimmune diseases are mislabeled cases of Lyme disease, any health condition that has a significant correlation to them must then be intimately connected to a form of Lyme or a related coinfection. The result can only be described as a researcher’s Holy Grail, leading scientists directly into nests of groundbreaking revelations resulting in an unprecedented number of celebratory epiphanies, or, informally, hallelujah booyahs (HBs for short).

A little housekeeping is required before we start. First, I’d take a quick selfie to mark the occasion, as when this chapter concludes, you’ll probably want to take another for comparison. (I’d also recommend you fix up your hair, avoid clothing that might reflect poorly on your sense of fashion, and stare into the camera with an appropriate expression, e.g., curious wonder, skeptical puzzlement, eager anticipation, dismissive bitterness because someone is making you read this.) Next, grab a pillow and place it on the floor in front of you. This, obviously, is to protect your jaw when it drops. Now, please get properly seated as instructed by the title of this memoir—it’s time to begin.

With the flair of a carnival barker, I call on you to pick a condition, any condition! And since we lack the capacity to do this in real time, let’s say I heard someone yell out Down syndrome, which is “a genetic condition where a person is born with an extra copy of chromosome 21.” Clearly it couldn’t be from a tick bite because, as Lady Gaga says, they were born this way. But why were they born that way? The CDC says, “no one knows for sure why Down syndrome occurs or how many different factors play a role.” Let’s unravel that birth defect mystery. Does autoimmunity play any sort of role?

“You can say that people with Down syndrome are the largest human population with a predisposition to autoimmune disorders,” said Joaquín Espinosa, PhD, director of the Linda Crnic Institute for Down Syndrome at the Colorado University Anschutz Medical Campus in a 2018 interview. Okay, I think that qualifies as an unequivocal “yes.” In fact, Italian researchers in 2021 stated that “autoimmunity represents a well-known complication of Down syndrome: it is estimated that people affected by this disease present a risk four to six times higher than the normal population to develop autoimmune diseases such as celiac disease, type 1 diabetes mellitus, and hypo- or hyperthyroidism.” The risk of celiac disease is up to ten times higher than compared to the general population.

dominoes falling

A domino falls. If Lyme disease is masquerading as various forms of autoimmune conditions, it follows that people with Down syndrome are getting blitzed by Borrelia burgdorferi spirochetes. But how did the bacteria get there? Scientists have noted a telling, damning link.

“The occurrence of familial aggregation of autoimmune disorders is well known, and the relatives in such families often form autoantibodies,” say researchers in a study that looked at the role of heredity in Down syndrome. “We were not surprised when 50% of children with Down syndrome from families harbouring an autoimmune disorder had antibodies.” Scientists have long believed that these autoantibodies “can cause autoimmune diseases, and, increasingly, autoimmunity has been found to be associated with a wide range of diseases, such as cancer, infectious disease (e.g. such as COVID-19), cardiovascular disease and neurodegenerative disease,” said a 2022 study, conveniently reaffirming my solidifying theory of Lyme’s favorite stomping grounds. They even, forebodingly, identified those potentially carrying the dormant-for-now spirochete. “However, autoantibodies are also found in healthy populations, albeit usually not in high levels and, for the most part, do not cause damage or attack the host.”

Awash in unprecedented levels of autoimmune disease, Down syndrome, therefore, must be largely, or exclusively, triggered by spirochetes passed down from a parent infected with Lyme disease. There is no other plausible means of transmission. It’s a hallelujah booyah! But not just any HB, a dam-busting HB with monumental consequences that portends to rewrite the understanding of how Lyme disease is transmitted.


It has long been confirmed that Lyme disease can be passed down in utero. Even the CDC acknowledges this, partially lifting the distracting fog surrounding transmission. The national public health agency of the U.S., tasked with protecting the health of citizens, however, has long insisted that it is “rare,” yet stories abound on the internet of congenital Lyme disease. Like the November 2023 piece by Kristina Bauer, who, living with undiagnosed Lyme for 30 years, passed it down to her four children. It took seven years for their health to return. But it’s not just stories, there are entire movements trying to raise awareness of how the disease can spread during pregnancy, like Mothers Against Lyme.

Are parents infected with Lyme disease, many misdiagnosed with an autoimmune condition, routinely passing the bacterial infection down to their children?

Studies have analyzed in depth the curious trend of autoimmune diseases clustering in families. In 2013, a group of Colombian scientists tried, conducting a meta-analysis looking at 44 studies. “Familial autoimmunity was found in all the autoimmune diseases investigated,” reported the researchers. “The results found in this work support aggregation of diverse autoimmune diseases (that is, familial autoimmunity) and the view of a common origin for autoimmune diseases (that is, the autoimmune tautology).” What is the theory behind this “tautology”? A 2010 paper from Dr. Juan-Manuel Anaya, who coined the phrase and was a co-author on the above meta study, explains.

Although autoimmune diseases exhibit contrasting epidemiological features, pathology, and clinical manifestations, three lines of evidence demonstrate that these diseases share similar immunogenetic mechanisms (that is, autoimmune tautology). First, clinical evidence highlights the co-occurrence of distinct autoimmune diseases within an individual (that is, polyautoimmunity) and within members of a nuclear family (that is, familial autoimmunity). Second, physiopathologic evidence indicates that the pathologic mechanisms may be similar among autoimmune diseases. Lastly, genetic evidence shows that autoimmune phenotypes might represent pleiotropic outcomes of the interaction of non-specific disease genes.

There were simply too many coincidental parallels between these chronic diseases for it to be mere chance, leading Anaya and these researchers to that stunning conclusion: that there is a common origin for autoimmune diseases. Right away I started nodding and doing my Matthew McConaughey impression—it’s another HB, alright, alright, alright! (I will now use this unique opportunity to finally tell one of my groan-inducing McConaughey jokes. Why did the actor give up on his dream of becoming a professional NASCAR driver? His racecar only turned alright, alright, alright. I’d share more, but I’ll spare you the pain.)

Future studies don’t just support Anaya’s hypothesis, they all but confirm it.

A 2020 study looked at pregnancy loss in relation to autoimmune disease and found an unmissable connection, not just with parents, but with first-degree relatives afflicted with autoimmunity. The researchers confirmed that, “women with family history of autoimmunity had higher risk of pregnancy loss” and that their findings suggest a “possible shared mechanism of miscarriage and predisposition to autoimmunity.”

A 2021 Norwegian study looked at the health of more than 1.3 million children, 3,575 of them with cerebral palsy, as well as the health of the mothers and fathers. “Mothers with any autoimmune disease had a 40% increased risk of CP in their offspring,” an unmistakable connection to Lyme. A 2022 French meta-analysis discovered a link between a father's or mother's autoimmune disease and their children's risk of developing certain neurodevelopmental disorders (autism spectrum disorder and attention-deficit/hyperactivity disorder).

But it was an October 2023 study that removes all doubt of a connection, finding that a mother or father with an autoimmune disease notably increases the risk that their children will develop an autoimmune condition, the risk rising even more if both parents are affected. “This study demonstrated broadly how autoimmune diseases pass from parents to infants of both genders and separately quantified the maternal and paternal contributions to disease,” concluded the researchers.

Replace “autoimmune” with “Lyme” and let that sink in. If a mother or father has Lyme disease, the risk that their child will develop Lyme soars. The research into the parental influence on autoimmunity, birth defects, and mental disorders is hold-onto-your-hat, mind-bendingly illuminating. Lyme disease varieties must be spread without hikes in the woods or visits to grandmas in New Jersey. Spirochetes are being passed along by infected mothers, and fathers are at least somewhat complicit. When years or decades later, some of those children develop the same autoimmune condition as Mom or Dad, it’s considered to “run in the family.” That’s why so many autoimmune diseases (re: Lyme) appear to have a “hereditary” component. It’s another hallelujah booyah!

3 generations of family together

Three generations: Grandma, Dad, and baby Dave

The reason that so many people with Lyme don't remember a tick bite is because there likely never was one. Living in or traveling to an endemic area is not a required precursor to getting infected. Additionally, this also explains why some healthy-as-a-horse people experience medical issues suddenly out of the blue—potentially the aftermath of a recent tick bite—while others recall dealing with myriad unexplained health issues from their earliest memories. Once again, cue Lady Gaga: They were born that way.

Now the loose hereditary link in autoimmune disease makes perfect sense. Of course identical twins are most at risk of developing the same condition—because the pair likely come from the same infected placenta, which is where Lyme, it appears, is passed to the unborn. Among identical twins, 70% share the same placenta. But since Lyme presents so differently, odds that it would produce the same autoimmune disease in other family members plummet, explaining why it is less likely to occur among fraternal twins and traditional siblings, and why the connection drops further with parents. And what if a parent’s parent was infected? If grandma had Lyme, she likely would have unknowingly passed along the spirochetes to her children, meaning that aunts and uncles could also be potential carriers, ensuring the disease’s grip and spread.

The calculus of how Lyme disease spreads now completely changes, as countless stubborn inconsistencies and mysteries surrounding the disease fall aside, along with an armada of newly toppled dominoes. Ever since its discovery, Lyme disease has been synonymous with ticks. IT’S NOT SPREAD PRIMARILY BY TICKS!

The “tickborne” illness is only sometimes introduced that way to a human host, flipping the defining adjective attached to the disease. It is instead frequently spread by infected mothers, who pass the stealthy spirochetes down to their children, with their daughters then passing it down to their children, and on and on. But mothers, unknowingly, are getting a huge assist from members of the opposite sex.

The fears raised in a 2014 study, which found Borrelia spirochetes in semen and vaginal secretions of Lyme disease patients, justifies the alarm raised by concerned researchers a few years ago. “It does not matter how controversial the idea of vector-free spirochete transmission might seem in the beginning,” warn the study’s authors. “As long as evidence of sexual transmission of Borrelia burgdorferi both between vertebrate hosts and between tick vectors exists, this question must be addressed.”

Naively, scientific studies have been addressing it. “Some chronic illnesses such as diabetes mellitus, coronary heart disease, stroke, depression, and dementia are shared between couples,” reported an October 2023 study. “For example, one’s diabetes mellitus can increase the risk of diabetes by up to 40% in his or her spouse. An individual’s dementia, stroke, or depression can also increase the risks of them in his or her spouse.” But they’ve never suspected sexual transmission, no, never. It’s gotta be something else. “The spousal concordance of chronic illnesses may be due to shared environmental and behavioral characteristics.”

It’s everywhere you look. Couples must be doing something together that is exposing them to risk. Are they bathing in the same contaminated swimming holes used by estrogen-enriched pregnant cows? Regularly biking around manufacturing plants that belch residue from burning recalled products acquired at steep discounts from dollar stores? Dining together at restaurants that serve Westernized foods and overuse inorganic cleaning products? It boggles the mind—what-oh-what could spouses be doing together?

“First-degree relatives and spouses of individuals with celiac disease are at increased risk of nonceliac autoimmune disease,” found a 2015 study, which saw a rise in cases of Crohn's disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, and ulcerative colitis” in close family members. Since spouses aren’t “blood” relatives, the environment always gets the blame.

Authors of a 2020 Swedish study nearly fell out of their chairs when they unexpectedly discovered the spousal connection in their research. “The surprising finding in this nation-wide family study on medically diagnosed patients was the high risk for autoimmune hepatitis (6.0) between spouses, which exceed the risk between siblings, suggesting the existence of strong environmental risk factors.” A 2015 study looking at lupus all but confirmed that autoimmune diseases ran in families, but also concluded that the environment had to play a role, “because spouses only share the family environment.” What else could it be?

Once again, a masterful deke that has faked out scientists. Let’s get out Occam’s razor for yet another trim. It’s not the environment that is causing partners to fall ill at inordinately high rates. Women are infecting men. Men are infecting women. And women are passing along spirochetes to their children.

Lyme disease has been spreading this way for thousands and thousands of years, surging and receding like the tides. Medical experts from the world’s best-regarded institutions got it all wrong. No wonder scientists have concluded that there is a genetic component to so many diseases, but that the connection had been too fuzzy to be the sole contributor. No wonder scientists blame an out-of-whack immune system, but the presence of suggestive markers like autoantibodies has been maddeningly inconclusive. And no wonder scientists have insisted that there must be an environmental factor, but could never make conclusive heads or tails of the inconsistent geographic spread of diseases.

No effing wonder.

An HB Palooza

There’s so much more to be realized from this transmission revelation, meaning the HBs are poised to just keep rolling. To better understand how Lyme disease variants have been spreading stealthily over the years, it helps to refer to one of the tenets of SHARDs: history harbors hints.

The past is flooded with references to Lyme disease, only it wasn’t called Lyme because even though the town was founded in 1665, the realization that ticks help spread the disease wasn’t made for another 300+ years. People in the 1700s simply called it “the pox,” which UK researchers, as recently as 2020, had attributed to a rash of syphilis cases mingled with other sexually transmitted infections.

After analyzing hospital records, researchers concluded that an eye-popping 1-in-5 Londoners were infected with this pox and “fouled,” a number even they admitted seemed outrageously high. And odd, as far more women were afflicted. But what else could it be, they wondered, spinning enough convoluted theories—the women of the time were prostituting themselves in droves—to make a throw that could blanket the entire British Isles. Adjust the magnification power on the microscope, though, and those strange numbers—a 20% infection rate driven by women—line up perfectly with Lyme disease.

Syphilis and Lyme are both diseases featuring a spirochete, Treponema pallidum and Borrelia burgdorferi, respectively. While syphilis typically presents with a sore in the genital area or around the mouth (which tends to appear 10-90 days after infection), both otherwise produce remarkably similar and devastating symptoms, particularly when left untreated. Syphilis, though, is rather easy to identify through a reliable trio of tests and treatment is usually successful if the disease is caught early.

Left: Electron micrograph of Treponema pallidum on cultures of cotton-tail rabbit epithelium cells (Sf1Ep). Treponema pallidum is the causative agent of syphilis. In the United States, over 35,600 cases of syphilis were reported by health officials in 1999. 26 January 2006; CDC (public domain). Right: Under a high magnification, this digitally colorized scanning electron microscopic (SEM) image depicts three, Gram-negative, anaerobic, Borrelia burgdorferi bacteria, which had been derived from a pure culture. This pathogenic organism is responsible for causing the illness, Lyme disease, a zoonotic, vector-borne, ailment, transmitted to humans by way of a tick bite. 31 December 2011; CDC (public domain).

But there is another key, Darwinian difference between the infections fatally overlooked by the medical community. Syphilis has only been traced back centuries, at most a few thousand years. The sexually transmitted disease is such an immature marauder that, according to the CDC, “approximately 40% of babies born to women with untreated syphilis can be stillborn or die from the infection as a newborn.” Routinely killing offspring, potential future carriers of the spirochete, isn’t conducive to spreading mayhem.

Lyme disease? It’s been evolving for tens of millions of years and far predates humanity, refining its plundering to an exacting science. Over time, the bacterial parasite has learned how to evade the immune system and hide when threatened, how to efficiently disable—but not regularly kill—its host, and how to spread without raising suspicions. But the two diseases share enough commonalities that one can glean telltale patterns that unmask the far more experienced plunderer.

First, even though scientists have yet to catch up in the confirmation department, let’s reasonably assume that both diseases, essentially kissing cousins, spread similarly: maternally and sexually. All evidence points that direction for Lyme; ticks are merely an add-on bonus when it comes to transmission.

Next, pay specific attention to when and how syphilis spreads, with odds of transmission ranging from under 10% for asymptomatic mothers to a frightening 60-100% for those with an active infection. It would stand to reason that Lyme could have a similar transmission pattern. If someone is actively experiencing symptoms—for example, enough to warrant the diagnosis of an autoimmune disease—the risk of transmission to an unborn child or sexual partner would be elevated, and exceedingly high if in the middle of a flare. Either way, it’s not a given that it would be passed down in utero or to a partner, but the likelihood of maternal-to-fetal transmission alone would far outstrip the likelihood of contracting the disease from a tick bite.

Now add in the latency factor. Syphilis often shows its stripes quickly, but Lyme is notorious for lying dormant for extended periods of time—decades are not uncommon. With the exception of obviously apparent birth defects that appear immediately, years may pass before a disturbance to the immune system rousts the spirochete from its slumber.

So, all told, what does this information tell us about Lyme and its co-conspirators? Any spread from infected, asymptomatic carriers would be difficult, if not impossible, to track. Dormant disease doesn’t appear to regularly transmit, and even if it did, it would likely remain in its dormant state. Without far more accurate testing, there is no way of identifying carriers. But those who have autoimmune disease? That we can track, and it is sublimely revealing.

Stalking the Stalker

Let’s recap. Lyme disease primarily is being spread two ways: by sex and in utero. Ticks, those blood-sucking arachnids, are essentially distracting noise, their numbers relatively inconsequential in this epidemic. When a couple has sexual relations and one is infected, the other is at risk of acquiring the bacterial infection. Then, when infected women get pregnant and have children, their sons or daughters are at equal risk of acquiring the spirochetal disease. They grow up have sex with future partners, and Lyme menacingly continues to spread. This part is straightforward.

Given the maternal and sexual transmission of Lyme, we now know that ticks aren’t strangely more attracted to females and their unique pheromones, yet there is no question that women are on the front lines of this growing epidemic. “Women account for an estimated—and astonishing—78 percent of people who have [autoimmune] disorders,” reads a 2021 article in Scientific American, noting that “autoimmune diseases are now the fifth-leading cause of death in women younger than 65.” The gender disparity has flummoxed researchers for more than 50 years.

Quote from Scientific American journal article

Then, mere months ago, scientists out of Stanford University made a breakthrough, reporting in a February 2024 study “that a molecule known as Xist may be driving female-biased autoimmunity.” The study’s senior author Dr. Howard Chang told Medical New Today that, “doctors and scientists have wondered for decades about the female prevalence of autoimmune diseases. Sex hormones, different chromosome counts, and other factors like pregnancy were invoked. This research shows that a single female specific RNA is a major driver – a novel explanation to a longstanding mystery.”

Perhaps. Now let’s add a game-changing curveball. Another reason why females increasingly get the short end of the stick, so to speak, may be perhaps a bit too literal.

“Surveys across the world find that men typically report about twice as many lifetime partners as women,” stated 2018 research on the subject. The CDC came up with a more modest median of 4.3 opposite-sex partners for women, 6.3 opposite-sex partners for men (for those between the ages of 25-49). Even pushing aside the inherent braggadocio of the male gender and unfulfilled fantasies of threesomes, men, quantifiably, have more partners. Maybe not a lot more, but more. Just a single extra female partner per male should affect the disease’s gender disparity.

I tried to get clarity on this by asking popular artificial intelligence programs to break down how this would affect the disease’s spread over generations, the first time I had turned to AI for assistance with this memoir. And got anything but clarity. At first, I got a hard “no-can-do, Dave,” as if I was scheming to unleash a plague on humanity. After tacking to a more innocuous scenario—how might a disease that turns your body green (called Lime disease, natch) spread with a set of parameters—I got some answers that paralleled my hypothesis. With each passing generation, “the percentage of females with Lime disease increases steadily due to both in-utero transmission and the possibility of sexual transmission from green fathers (previously infected males).”

Confirmation! …or hallucination? I also got AI articulate nonsense, hardly reassuring. Mapping the spread of Lyme over generations, considering the plethora of potential variables, is a task for far more accurate and tailored computer models that I don’t have access to. But my hunch is that it will help explain the gender disparity in autoimmune conditions observed by scientists over time, particularly when combined with the research on Xist.

Regardless, the transmission revelation now gives us a desperately needed, sensical, why-didn’t-we-figure-this-out-sooner explanation for the influence of race or ethnicity on health conditions.

Dave as Poirot with fingers in the air

Isolation Immunity

It’s no longer a mysterious “genetic predisposition” that any one community is more susceptible than another to contract a certain disease, e.g., Blacks and lupus or Native Americans and rheumatoid arthritis. This new, deeply revealing finding says it’s more about the family unit and how often people of various racial or ethnic backgrounds intermarry or have children with those of other populations. If Native Americans have been afflicted with RA going back a hundred years or more, that flavor of Lyme disease chiefly gets spread around in their communities, the arthritic-leading version of the disease getting passed down to future generations.

The mysterious veil surrounding the Inuit, indigenous people of the Arctic, and their surprising resistance to autoimmune diseases, cardiac issues, and most types of cancer, has been lifted as well. (Unsurprisingly, other isolated communities around the world appear to enjoy similar protections.) It’s not because of their genes, their seafood heavy diets, or how their bodies react to the extremely cold environments they live in. And it’s certainly not because of their vitamin D levels, a common, nauseating source of blame in the autoimmune world. It’s primarily their isolation, and, critically, that their isolation is in areas largely devoid of ticks carrying Lyme disease, in this instance due to temperatures inhospitable to the arachnids.

We even get epidemiological answers as to how variations of Lyme spread geographically. Take lupus. In the United States, the presence of the disease is counterintuitively modest in tick areas, with a larger footprint in the South. Even more curious: it disproportionally affects Black individuals. Why? Again, history harbors hints.

The slave trade in America was in high gear during the 17th and 18th centuries. Slaves were brought over primarily from West Central Africa. What else is in that region of Africa? Ticks, specifically ticks infected with Lyme and similar nasty diseases. A 14-year study researching malaria found that upwards of 25 percent of the residents in one Senegal village had been infected with Lyme, mirroring the results found in rural villages in neighboring countries. “It's a significant rate of incidence for a sickness that affects all age groups," said zoologist George Diatta of Dakar in an interview. "Only malaria and the flu are as frequent, and we estimate that, like other endemic sicknesses, Lyme disease is a serious public health problem."

Unlike the never-ending puzzlement surrounding Jimmy Hoffa’s final resting place, the confounding mysteries of lupus now have a gobsmacking explanation. The lupus version of Lyme was likely first introduced to the United States in the 1600s by enslaved Black men and women, gradually spreading over generations disproportionately in African American communities. Not coincidentally, today cases of lupus drench the Caribbean, Brazil, the United Kingdom, and the United Arab Emirates, well known major markets for the slave trade centuries ago. Overlaying the two maps—areas with the highest concentrations of lupus compared to the largest hubs of the slave trade—will take your breath away, as the similarities are unmistakable.

African Slave Trade map

Map of both intercontinental and transatlantic slave trade in Africa; 15 Feb 2021. Image credit: KuroNekoNiyah (Wikipedia).

Researchers in the UK unknowingly confirmed the connection in a 2001 Lancet study when they hypothesized that “the high prevalence of [lupus] in recent migrants from west Africa suggests that the disease is not rare in west Africa, and that there is a genetic basis for the high risk of [lupus] in people of west African descent compared with other groups.” London was a “major slaving center,” which likely is the reason behind the high prevalence of lupus in the area today compared to other regions in Europe.

Oh, oh, those sporadic outbreaks of disease—clusters of neurodegenerative diseases that rise up in isolated communities and then inexplicably slowly fade—now are more explicable as well. As families intermarry, Borrelia burgdorferi spreads, but only for so long. The sickest don’t have children and healthy offspring (at least in that moment) opt to move on to pastures perceived safer, away from villages with unusually high rates of disease.

Then there are the “sickly” families, where illness prominently spills into generations—grandparents, parents, and their children—with an assortment of autoimmune diseases, cancers, mental disorders, and chronic conditions. They all follow the same pattern, and if you look closer, you’ll discover that it is common for these clusters to originate in areas endemic to Lyme. Tick bite or inherited, it doesn’t matter. The disease is so ubiquitous in those regions that when families grow, odds soar that Borrelia burgdorferi is circulating broadly in these communities. It’s all but inescapable. If the mother is infected, she likely will inadvertently pass her spirochetal infection to her kids, who then grow and marry that sweetheart down the street, ensuring that the pattern repeats with the grating consistency of a skipping record.

The potential amount of scientific discovery from these hallelujah booyahs to answer the to-date unanswerable is exhausting.

More Answers

Tragically, autoimmune diseases and birth defects are far from the only illnesses passed down from a parent infected with Lyme disease. If an expectant mother has an autoimmune disease, the risks notably rise that her future children also may experience a medley of mental health issues. A huge 2022 Denmark study reviewed over 2 million single births—2.26% were born to mothers diagnosed with an autoimmune condition—to look for any association with mental disorders. They didn’t have to look very hard.

Prenatal exposure to most common specific autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, and psoriasis, was associated with a significantly increased overall risk of mental disorders in offspring. … In particular, children of mothers with autoimmune diseases diagnosed before delivery were more likely to develop a wide range of neurodevelopmental disorders (eg, intellectual disability, childhood autism, and ADHD), organic disorders, obsessive-compulsive disorder, schizophrenia, and mood disorders.

My mother-in-law had rheumatoid arthritis and debilitating migraines. Brian, my brother-in-law, has schizoaffective disorder and a host of health issues—balance and coordination issues, fatigue, and more. Gulp. I think I may be experiencing my own hallelujah booyah, only with far, far less enthusiasm. This was one discovery I did not anticipate making, ever.

I’m trying to catch my breath. And failing.

Dave sitting in a wheelchair

Armchair researchers, as well as those with white coats and PhDs, can continue to use the connection with autoimmune diseases to investigate the likelihood that Lyme disease is playing a part in any illness, birth defect, or health condition. Take Alzheimer’s disease. When dusting for fingerprints at that health crime scene, scientists have found damning evidence of the elusive spirochete’s involvement, supporting past research that dates back decades. Researchers have even noted that the brains of Alzheimer’s patients have signs of pre-inflammation, suggesting an infectious cause. “Based on our past 30 years of research, we no longer think of Alzheimer's as primarily a disease of the brain,” said Dr. Donald Weaver, an expert in the field practicing at the Krembil Brain Institute out of Toronto. “Rather, we believe that Alzheimer's is principally a disorder of the immune system within the brain.” An autoimmune disease.

I peeked at the connection of autoimmune diseases to other conditions, and, uhh, I could dedicate an entire chapter to each one with enough evidence that would swamp even the most hardened skeptic. For example, amyotrophic lateral sclerosis is littered with suspicious connections, with ties to everything from multiple sclerosis and type 1 diabetes to Behcet disease and ulcerative colitis. Some researchers think there’s no real connection between autoimmune disorders and ALS, blaming the perceived link on “shared biology or environmental confounders.” Oh those confounders, leading the authors of another ALS study to punt when they shockingly discovered an unexplainable one. “The high spouse correlation will be a challenge to environmental epidemiology of ALS.”

Challenge accepted. It’s another HB moment, only one that also saves countless buckets of ice. These clues all point in one direction: Lou Gehrig’s disease is an aggressive variety of Lyme, and it can be sexually transmitted, which is the reason that spouses are at elevated risk. (Fun fact, Lou Gehrig had a second home in Lyme, CT, and enjoyed gardening. Thankfully, his wife Eleanor lived to 79, apparently with no significant health issues.)

Let’s briefly, very briefly, look at a few other conditions to see if Lyme disease is in play. This connection doesn’t mean that Lyme is the sole driver or trigger of a condition, but odds are high that the infection is playing an outsized, perhaps even dominant, role.

Parkinson's disease, likely. Urological cancer, likely. Stroke, likely. Autism, likely (pssst, it’s not vaccines). Lung cancer not attributed to inhaling carcinogens, likely. Chronic kidney disease, likely. Anorexia and other eating disorders, likely. Pulmonary fibrosis, likely. Obstructive sleep apnea, likely. Migraine, likely. Cardiovascular disease, likely. COPD, the fourth leading cause of death worldwide, likely. Hypertension, affecting nearly half the population, likely, so likely that some scientists believe it is an autoimmune disease. Have fun looking into more connections as you burrow into this goldmine of a rabbit hole.

You could also reverse engineer Lyme’s impact by using the likelihood of developing an autoimmune disease after an immune-altering event. We’ve already established that this commonly occurs after an illness (and occasionally after a vaccination). If you already have a burbling case of Lyme and come down with a serious viral infection—one that acts as a forest fire, waking Lyme from its extended naptime—you will see a spike in rates of autoimmune disease. Always. Take HIV. Like Covid and viral pandemics before it, getting infected with HIV packs a wallop of a punch. That’s why a 2020 Canadian study “found that people living with HIV were more than twice as likely to suffer from autoimmune diseases” than their HIV-negative counterparts.

Pregnant woman
Pregnant woman at a WIC clinic in Virginia; photo credit: Ken Hammond/USDA, 13 Nov 2002 (public domain)

Other reliable triggers include stress and trauma. One would think those would be hard to gauge and quantify given that they are typically so variable and unpredictable, but you would be wrong. Pregnancy, specifically the act of childbirth, falls into the eminently predictable. For many women, that is the most traumatic experience they’ll ever have, which means autoimmune diseases, or relapses if one already exists, should spike after childbirth. A 2011 study investigated and, yup, “the results did suggest an association between pregnancy and the risk of subsequent maternal autoimmune disease, with increased risks noted after caesarean section and decreased risks after abortion.”

That would also then seemingly explain many cases of postpartum depression, right? The trauma of giving birth awakens dormant Lyme, newly activated Lyme triggers depression, mom gets diagnosed with postpartum depression. A 2018 study confirms this hallelujah booyah, as it reported that “patients with PPD had a significantly higher risk of subsequent autoimmune diseases, specifically, increased risks of pernicious anemia, rheumatoid arthritis, and Graves’ disease.” A timely December 2023 article in The Washington Post backs up this hypothesis 100%. At least researchers appear to be on the right track.

The focus on the link between immune health and postpartum depression is part of a seismic change happening in the study of psychiatric illnesses. Scientists around the world are finding that underlying autoimmune and inflammatory processes can have a profound impact on the brain and may be more common than previously believed in patients with a variety of neuropsychiatric conditions, including major depression.

Cytokines should be involved, and they are, as researchers found that “increased inflammatory cytokines in the blood were associated with increased risk for severe and suicidal PPD.” But just the stress of caring for a newborn could be enough to wake up Lyme and trigger PPD in some people, meaning fathers and even adoptive parents would be at risk. And sure enough, they are.

Disruption of sleep and elevated stress — which are common in mothers nurturing a newborn — also are known to impact the immune system and increase inflammation. The link between stress and the immune system may also help explain why parents who do not directly experience pregnancy and childbirth can develop PPD. About 1 in 10 fathers develop PPD, as do some parents who adopt.

The trauma triggers explain even more. Like every unexplainable war syndrome: shell shock syndrome, Gulf War Syndrome, even mysterious syndromes where the soldier never saw combat. “A Secret War, Strange New Wounds, and Silence From the Pentagon,” screams a headline in the November 5, 2023 issue of The New York Times. “A few gun-crew members were eventually given diagnoses of P.T.S.D., but to the crews that didn’t make much sense,” reads the article, as the gunners never saw the enemy. They did, however, fire tens of thousands of chest-thumping rounds of high-explosive shells. Could it be causing traumatic brain injuries? A logical guess, but there is another potential culprit. Thump enough, and Lyme goes wakey wake.

Sound science is supposed to make sense, and the resulting symptoms back up the reality that they are from the reemerged and now active bacterial infection. The aftermath is always disturbingly the same. Psychosis, suicides, heart issues, digestive problems, crushing fatigue. A 2005 study tried to put it all into perspective, cataloging typical symptoms: “fatigue, weakness, sleep difficulties, headache, muscle ache and joint pain, problems with memory, attention and concentration, nausea and other gastro-intestinal symptoms, anxiety, depression, irritability, palpitations, shortness of breath, dizziness, sore throat and dry mouth,” researchers report. “Despite popular claims to the contrary, no simple biomedical etiology has been discovered to account for these disorders, hence the term “medically unexplained.”

Does all of this sound strikingly familiar to another disease that until now has been impossible to explain? How about another HB!

Sickness Spreads

There is another health concern commonly linked with autoimmune disease, one that generates a wince-inducing hallelujah booyah. Cancer.

A 2012 study looked into the link between cancer and autoimmune diseases, and the researchers expected to find that the cancers were the result of the powerful cytotoxic treatments often used to tame many of these autoimmune conditions, like mitoxantrone for multiple sclerosis, thought to occasionally instigate blood cancers. Except they discovered that’s not the case. “Not all multiple sclerosis patients treated with mitoxantrone develop secondary leukemia while others develop leukemia without mitoxantrone exposure. Therefore, patient related factors seem to play a fundamental role in the pathogenesis.” It’s a known problem, as blood cancers and autoimmune disease frequently tag team, found a 2014 study. “Many of 33 studied autoimmune diseases … especially when diagnosed at younger ages, were associated with higher risk of non-Hodgkin lymphoma.”

It's not just blood cancers. It’s also a range of urological cancers, like bladder and prostate. “The risk of urological cancer was increased after all autoimmune diseases,” said researchers after analyzing a large Swedish health database in 2013. Other studies have found an association between autoimmune disease and kidney cancer, brain cancer, lung cancer, and more, while other studies have found that the children of parents with autoimmune diseases are more susceptible to cancer, particularly blood cancers in childhood. It gets more damning.

A soon-to-be-published June 2024 study out of the U.S. and sponsored by the NIH unequivocally fingers the mother directly, all but confirming the most common transmission of Lyme: “Maternal autoimmune disease was associated with increased childhood cancer risk” as “autoimmune diseases (all types) were positively associated with all childhood cancers combined.”

Those poor kids. Childhood cancer survivors are then faced with, yup, a soaring risk of developing one or more autoimmune diseases of their own. Worse, while that risk peaks within 5 years of their cancer diagnosis, it never goes away, persisting “up to 30 years later for most conditions, and up to 50 years later for some conditions.” Those sneaky, hibernating spirochetes ruin every party.

Study after study after study confirm, reconfirm, and reconfirm again that there is “a pervasive, largely positive association between … autoimmune and inflammatory diseases and subsequent cancer development.” Researchers repeatedly have been sounding the alarm about the suspicious connection between the two seemingly unrelated conditions.

Dear God. What, then, are the cancers most associated with autoimmune disease? My AI assistants produced a consensus. For women: breast cancer, ovarian cancer, lung cancer, gastrointestinal tumors, non-melanoma skin cancer, bladder cancer, and non-Hodgkin’s lymphoma. For men: bladder cancer, prostate cancer, kidney cancer, lung cancer, and non-Hodgkin’s lymphoma. Lastly, in children who have had cancer, these types of cancer are most linked to developing an autoimmune disorder later in life: leukemia, Hodgkin’s lymphoma, kidney cancer, and central nervous system tumors. All exactly as predicted—no need to summon Nostradamus—and the consequences are beyond enormous.

Chart of cancers associated with autoimmune disease

No, no, no, that can’t be. That just can’t be.

That means that even if we add Covid-19 to the cancer calculus, it should support the autoimmune/cancer connection because reliable research repeats (or perhaps, more appropriately, rational reasoning repeats). To refresh your memory from two chapters ago, Covid awakens dormant Lyme. After a couple cups of coffee, now active Lyme gets diagnosed as “Long Covid.” Then, in time, Lyme triggers cancer in a select group of patients.

F*** me. It’s the same. It’s always the same.

Researchers studying people diagnosed with Covid, both hospitalized and not, found that the risk of developing cancer “was significantly higher for particular types of cancer: renal (kidney), hematological (blood), colon, and lung. Focusing on blood cancers alone, scientists noted that the hospitalized COVID-19 group had a significantly greater likelihood of being diagnosed with leukemia, myeloma, or non-Hodgkin lymphoma compared with the controls.”

Since the introduction of Covid, “cancers such as colorectal, pancreatic, breast, thyroid, uterine and skin related” also have been rising in young adults, say experts. Again, researchers don’t know why. More research is needed, they always stress, even though “it may take years to establish a clear association between COVID-19 and cancer progression.”

Years?! People are dying—now, right now. So let’s cement the Lyme-cancer link once and for all, and head back north to the frozen tundra, home to the Inuit—the indigenous group mostly residing in northern Canada and parts of Alaska and Greenland—who for generations enjoyed virtually nonexistent rates of autoimmune disease and many cancers. It’s nothing short of an epidemiological bonanza.

A 2008 study in The Lancet tried to make sense of the unique health trajectory of this population. “Although malignant diseases were believed to be almost non-existent in Inuit populations during the beginning of the 20th century, the increasing life expectancy within these populations showed a distinct pattern, characterised by a high risk of Epstein-Barr virus-associated carcinomas of the nasopharynx and salivary glands, and a low risk of tumours common in white populations, including cancer of the prostate, testis, and haemopoietic system.”

Well, well, well. Remember from the previous chapter how researchers were convinced EBV was at the root of multiple sclerosis? If that were the case, MS would have been found in this population, where EBV was clearly circulating. But nope, as another what-causes-[insert autoimmune disease here] hypothesis collapses under the weight of a single study published more than 15 years ago. Other than a handful of EBV-fueled cancers, the Inuit in the early 1900s looked to have a unique superpower: pristine immune systems protecting them from countless maladies. What changed?

To justify health issues that began emerging in the 1950s, researchers then, predictably, jumped on the Western-influence bandwagon. “During the second half of the 20th century, Inuit societies underwent major changes in lifestyle and living conditions, and the risk of lifestyle-associated tumours, especially cancers of the lung, colon, and breast, increased considerably after changes in smoking, diet, and reproductive factors.”

Other research reflexively blamed similar trends. “In Canadian [Inuit] no case of diabetes mellitus has yet been reported in the traditional-living central and eastern Arctic regions,” reported a 1981 book on the emergence of Western diseases in the Inuit population, although rates of type 1 diabetes were on the uptick in other less remote regions. Colorectal cancer, once rare, was experiencing a notable rise as well, and “in earlier periods breast cancer was extremely rare, reported almost as non-existent, among both Canadian, Alaskan and Greenland [Inuit].” Ditto cancer of the uterus. Before 1967, lung cancer in Canadian Inuit was only found in women, as they “tended day and night lamps which emitted much heavy sooty smoke from the seal and fish oils.”

Inupiat Eskimo family portrait

A family portrait of an Inupiat Eskimo mother, father, and son by Edward S. Curtis, retouched March 2013. Public domain.

A health utopia—with virtually zero cases of diabetes, colon cancer, breast cancer, and unexplained lung cancer—does a 180. Despite scant evidence of cause and effect and the noticeable absence of Chick-fil-As on the tundra, the fingers of researchers, reflexively, all pointed to fast food, Lucky Strikes, and estrogen thrust upon the indigenous group by the seepage of Western society. Because what else could it possibly be?

It only gets more incriminatory. A 2008 epidemiology study examined the unique Inuit cancer pattern and the influence of migration. “Compared to Inuit never living in Denmark, Inuit migrating to Denmark had more than 3 times higher relative risk of prostate cancer, nonmelanoma skin cancer, cutaneous malignant melanoma and bladder cancer. Increased risks were also observed for cancers of the mouth, brain, breast, rectum, stomach, colon and for leukemia.” A 2015 study found that in recent years “the increase is particularly marked for lung, colorectal and female breast cancers.”

Breast cancer. It took me two years and the final chapters of SDBR to fully confirm, in the waning days of March 2024, that the fingerprints of Lyme’s involvement in the most common cancer among women are absolutely everywhere, all the way down to an environmental trigger and its steady rise in subsequent generations, as reported by an oft-cited 2004 study on trends in breast cancer.

Studies of migrants provided the first solid evidence that environmental (rather than genetic) determinants were responsible for most of the observed international and inter-ethnic differences in breast cancer incidence: comparisons of breast cancer risk in (low-risk) Asian populations migrating to the (high-risk) USA and their offspring revealed major increases in risk between successive generations, and increases in risk were observed in populations from European countries with relatively low incidence (Italy and Poland) after migration to Australia, particularly if the migration took place in childhood.

As a consequence of changing exposures to reproductive and nutrition-related determinants over time, women are at increasingly high risk of breast cancer, with incidence rates increasing in most countries and regions of the world in the past few decades. The most rapid rises are seen in developing countries, where breast cancer risk has historically been low relative to industrialised countries. Increasing trends in developing areas are often considered the result of the 'westernisation' of lifestyles….

Westernization of lifestyles, how quaint. Even the mistaken assumptions scientists continue to make are woeful retreads of tired hypotheses. Again, sound science is supposed to make sense. This smacks of the debunked, once widely accepted hypothesis that spicy food caused ulcers, only on a scale that is difficult to comprehend. (As stated earlier, we now know a spirochete causes ulcers, occasionally triggering stomach cancer.) The only way it could get any worse is if medical researchers had found that doxycycline had some unexpectedly positive effects on breast cancer. And that these anti-cancer effects were backed up by a fat stack of promising studies brimming with potential for future, confirming research.

Okay, it gets worse.

Researchers have been trying to pinpoint the broad-spectrum antibiotic’s unique powers for years. Doxycycline has long been used for stubborn cases of acne, urinary tract infections, and a host of other conditions, including those quite serious. When not directly treating an active infection, its surprising success has been attributed to its “anti-inflammatory” properties. Doxycycline is even being recommended by the CDC to be used to prevent sexually transmitted infections in select, high-risk groups. Now that it has been found to also treat forms of cancer, its growing list of benefits have expanded to include “anticancer” properties.

An anti-inflammatory, anti-STI, anticancer, miracle drug. But, most importantly, doxycycline is anti-Lyme.

When it comes to breast cancer, in particular, doxycycline alone is unlikely to be the silver bullet. But it is an unquestionable step in the right direction to potentially prevent a cancer that appears to be often, if not largely, fueled by a bacterial infection, leading to a poignant reflection from one researcher who found the antibiotic influenced the recurrence of breast cancer. “Since doxycycline first became clinically available in 1967, its anticancer activity has been right under our nose, for more than 50 years.”

I myself can barely comprehend what I have discovered—after all these hallelujah booyahs, my world is spiraling just like yours. So many of my friends and family have been impacted by just this one type of cancer. And then… Laura’s grandmother had breast cancer, Laura’s mother died of breast cancer, Laura herself has long been considered high risk with a target on her back, er, chest. Because it “runs in the family.”

Dave in front of the Nobel Museum

Despite the overwhelming mountain of evidence that unbelievably continues to grow higher, I imagine most of you reading this are struggling to make sense of it all. It couldn’t possibly be this bad, could it? It’s unfathomable that scientists could have gotten it so wrong and for so many years. And then, all this carnage was discovered by Dave, the goofy, writerly, non-scientist with scant medical credentials? Sure, he’s been talking about winning the Nobel Prize since the earliest pages of his memoir, boasting about making the greatest medical discovery in history, but it’s just Dave. It cannot compute.

I understand, I do. Yet virtually every single related published study I’ve found—on Lyme, on autoimmune disease, on mental illness, on long Covid, on vaccines, on cancers, on so many illnesses—back up my hypotheses. So, so many studies, from the positively mundane to the most damning, like the recent 2023 study that detected Borrelia burgdorferi “in various types of breast cancer.”

Typically, with any hypothesis, there are significant roadblocks that need to be addressed and resolved before it can merit serious consideration. Dr. Marshall, the Australian Nobel Prize winner who discovered that spirochetes were causing stomach cancer (not stress or spicy foods, the popular belief at the time), has long stressed to his fellow researchers the importance of trying to break your own cherished theories. His advice has been invaluable in this endeavor.

As you look back on my journey of discovery through chapters past, you’ll see that I’ve sunk more than a few of my own overly confident assumptions. Instead of trying to discredit evidence that conflicted with my findings, I repeatedly dispatched once promising theories to fates more akin to cement-shoe-wearing rival mobsters going for an unfortunate dip in the Hudson. What’s left is what you’re reading. I haven’t been able to break it, and I’ve been trying like hell to do just that. I invite others to do the same. Debate, scrutinize, all-out eviscerate. If you can’t succeed, that’s the mark of the soundest of science. But if any of you still can’t believe in the science, allow me to remind you of a rule astrophysicist Neil deGrasse Tyson turns to when facing detractors and disbelievers.

“The good thing about science is that it's true whether or not you believe in it.”

Researchers need to be reminded of this now more than ever. Despite the absolute best of intentions, scientists sometimes get it wrong. It was just reported in April that it appears astronomers may have discovered a major flaw in their understanding of dark energy, a level of wrong that now requires a complete reset of theories related to how the universe was thought to end. Shit happens. Only now, with this particular parasitic infection and its smarmy buddies, we are in that nightmare situation all-too familiar to Peace Corps volunteers, the one I retold back in Chapter 5: Neck deep in a slurry of urine and feces, the walls of the makeshift latrine too slick to escape.

To get out of this Lyme disease and coinfection hellscape, tangled with bias and preconceptions, medical experts will need to stay composed and breathe. They’ll need to be fearless. And even if they could never imagine what is unfolding in their wildest dreams, they’ll need to believe, and quickly. Because there is one scenario that buckles the knees due to fear at the very possibility that it could come to pass.

It’s at the doorstep, the doorknob is turning, and it’s about to step into the foyer. It’s unavoidable and unmissable.

That reckoning I foretold so many pages ago?

It’s here.

door handle turning


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