Before the Lyme Disease Vaccine Rolls Out, We Should Probably Talk About The Science™

Symptoms that look like everything, tests that confirm nothing, and a story that became fact

Before the Lyme disease vaccine rolls out, we should probably talk about The Science™. Not the headlines, not the fear campaigns. The actual data. Because once you peel that back, it gets messy with a quickness..

I started looking at this because someone sent this clip to me from Instagram. Here is a screenshot:

It’s interesting that Instagram is allowing many videos like this one to circulate now, but that’s a different discussion for a different day. Let’s take a look at the Lyme disease situation!

A quick google search, and I was immediately thrust into the warm, familiar arms of epidemic fear mongering. The headlines didn’t disappoint, replete with a dark image of an enormous tick, crawling across a blood stained map of the United States … which the tick could easily traverse in just a few steps, considering it is roughly half the size of the entire country 😂.

🔻The Growing Epidemic Hiding in Plain Sight

BY GRANT MERCER
APRIL 3, 2026

OMG…Honey They Shrunk The Country!!

And the fear mongering isn’t just aimed at general population, the Big Smarties are getting it too 👇

Lucky for everyone, Pfizer has an almighty vaccine on the way.

The return of the Lyme vaccine: VLA15 and beyond

After a long gap without a human Lyme vaccine, the pipeline is no longer theoretical. In a recent Sermo survey, 70% of physicians support wider use of a Lyme disease vaccine (31% strongly support, 39% support with careful safety monitoring). Another 25% of physicians are unsure and need more data.

The leading Lyme vaccine candidate is VLA15, developed by Pfizer and Valneva. It is a multivalent OspA-based vaccine being evaluated in the Phase 3 VALOR trial (NCT05477524).

• VALOR is a large efficacy, safety, and immunogenicity study in participants aged 5+ in endemic regions.

• Company reporting and independent clinical commentary point to Phase 3 outcomes anticipated in the first half of 2026, with regulatory submissions to follow if results are positive.

• The regimen is positioned as a multivalent primary series with a booster strategy aligned to seasonal risk timing, which will matter for real-world uptake and scheduling.

The trial wasn’t considered successful, but they’re going to submit it for approval anyway. Who cares!

Vaccine for Lyme disease shows promise in clinical trial amid rise in tick bites

• Updated: Mar. 31, 2026, 10:10 a.m.

• |Published: Mar. 31, 2026, 10:05 a.m.

And we have some monoclonals on the way as well … phew!

Alrighty, so far we have:

• Fear mongering ✅

• Injections on the way ✅

But wait … how do you know if you have Lyme disease???? You might think that’s easy to answer. ✋ Um, whoa. Not so fast.

But wait, all of those symptoms could be MS…

Or Fibromyalgia…

Apparently Lyme is an imposter, and can dress itself up like a number of different diseases. Even the tell-tale rash.

Oh my gosh, this means that Lyme can’t be clinically diagnosed! As in, a doctor cannot see a patient and differentiate Lyme disease from other diseases just by looking at a patient. Because the symptoms can really be anything, making diagnosis way less straightforward than people assume.

So what to do?!?!? A TEST, of course.

Ah yes, this is sounding more familiar by the second. Lyme is an imposter and a shapeshifter, just like many other infections we have looked at. See here, here, here, and here.

You know I had to look up the primary paper on Lyme, and boy it did not disappoint with its flexible science and indulgent conclusions.

As you know, our first stop is always the Methods section.

(see below)

Below:

My goodness.

“Were obtained from adults with Lyme disease of recent onset.”

Ok guys…

This is the foundational paper for Lyme disease - the one that first identified the bacterium (Borrelia burgdorferi) that allegedly “causes” Lyme disease.

Which means there was no precedent for Lyme disease when this paper was written. So what is it? A collection of symptoms for which there cannot be a differential diagnosis (because that same collection of symptoms exists for a number of other diseases, ie MS, fibromyalgia, mononucleosis, etc, etc).

The ONLY way to diagnose Lyme disease would be to find the thing that all of these symptomatic people have in common that is DIFFERENT from other people experiencing similar symptoms.

Let’s see what they found.

Please read that again.

👉 “Of 142 specimens from 56 patients, 3 yielded spirochetes.”

WELL … if that’s not a clear signal, I guess I just don’t know what is.

Y’all.

In this foundational paper, after weeks of growing blood and urine and spinal fluids in a cess pool of other biological and chemical ingredients, they found a thing (bacterium) present in 3 out of 56 samples.

That means 53 of the samples (95%) DIDN’T HAVE THE BACTERIA. But in a remarkable feat of “scientific” gymnastics, they concluded that the bacteria was causing the disease!

O

M

G

I mean, that’s a remarkably weak signal from which to come to a definitive conclusion.

In fact, a reasonable person could just as easily interpret that as evidence pointing away from a single, consistent infectious cause… especially given how broad and overlapping the symptoms are. But what do I know.

Anywhooooo….

At the end of the day, it was concluded that Borrelia burgdorferi is the cause of Lyme disease, and that’s how they came to it.

Okie dokie.

Laboratory testing

CDC recommends the use of FDA-cleared antibody tests for laboratory diagnosis of Lyme disease. As with antibody tests for other infectious diseases, the accuracy of these tests depends upon how long you’ve been infected. Antibody tests may appear falsely negative during the first few weeks of infection, typically when a patient has an erythema migrans rash, but FDA-cleared assays have good sensitivity after 4-6 weeks have passed. Once your blood tests positive for antibodies, it will likely continue to do so for months to years, even when the bacteria are no longer present.

I’m not going to rehash fuckery I’ve already hashed, however if you would like to take a look at antibody assay tests, you can start with the Elisa plate, which is one of the FDA approved tests for Lyme disease confirmation.

ELISA Plate

👇This is an ELISA plate*. It is commonly used in Signal Sorcery to “show” antibodies and determine things…

Here is a list of what is commonly used in an ELISA assay plate:

1. Blocking Solution

This supposedly prevents “sticky” background noise by covering unused surfaces 🤣
Common blockers:

• Bovine Serum Albumin (BSA)

• Casein (milk protein)

• Gelatin

• Non-fat dry milk

• Synthetic blocking buffers

2. Sample

• Serum, plasma, cell culture supernatant, or other biological fluid containing the unknown antibodies or antigens.

3. Detection Antibody (secondary antibody)

Usually enzyme-linked (conjugated)

• Common enzyme conjugates:

  • Horseradish Peroxidase (HRP)

  • Alkaline Phosphatase (AP)

4. Wash Buffer

(“removes” unbound stuff between steps 😂)

• PBS + Tween-20 (PBST)

• Tris-buffered saline + Tween (TBST)

5. Substrate / Chromogen

(reacts with the enzyme to make a visible color)

• For HRP: TMB (3,3′,5,5′-tetramethylbenzidine) → turns blue/yellow

• For AP: pNPP (p-nitrophenyl phosphate) → turns yellow

6. Stop Solution

• Stops the reaction at a specific time so color doesn’t keep developing.

  • Sulfuric acid (H₂SO₄)

  • Hydrochloric acid (HCl)

  • Sodium hydroxide (NaOH)

Well that’s a lot of ingredients…to show the antibodies.

Great news! They are going to add in some AI for good measure. Perfect.

Next-generation testing for Lyme disease

The next wave of Lyme diagnostics is trying to solve two problems that standard workflows handle poorly:

1. Detecting infection earlier than antibody kinetics allows

2. Distinguishing active infection from past exposure

In late 2025, researchers at Dartmouth Hitchcock Medical Center presented a droplet digital PCR (ddPCR) approach to identify Borrelia DNA more rapidly and reliably than serology alone, addressing the common clinical scenario in which antibody testing reflects prior exposure rather than current infection. If this class of testing scales, it could shrink the “uncertain early window” where clinicians are forced to choose between watchful waiting and treatment under uncertainty.

AI is also being applied to Lyme testing and interpretation workflows, including pattern recognition across multi-assay data and clinical features to reduce missed cases and improve decision support.

Oh my goodness … what was that? Can you please say it again in my good ear?

“However, the typical test — called two-tier serology — detects early Lyme accurately only 30% of the time.”

I’m going to pause here so you can let that sink in.

“…detects early Lyme accurately only 30% of the time.”

Thirty percent.

Can we just revisit the foundational paper please?!?!? The one where Willy Bergdorfer found the Borrelia burgdorferi bacterium and named it after himself. Specifically the part where 95% of the samples didn’t have the bacterium that supposedly causes this collection of symptoms.

Hey! Here’s a thought, maybe it’s not a lack of AI problem. Or a testing problem. Maybe it’s actually not a Borrelia burgdorferi problem at all.

You may or may not know you were bitten.
You may or may not develop a rash… and if you do, it may look like anything.
You may have symptoms, or you may not.
You may test positive, even though you’re not sick.
You may test negative, even if you’re sick af.

At some point, it starts to feel like we’re forcing a square peg through a round hole, folks.

I’ll end by clarifying that I am not saying that people don’t have these symptoms. I am not saying that they don’t suffer terribly. I am not saying that people don’t get sick with a collection of symptoms that are very similar to the ones described (or not similar at all).

I am saying that when The Science™ gymnastics start to look like Cirque de Soleil, it might be time to reevaluate some stuff. And I think we are there.

Just a reminder that I don’t have to provide an explanation for the origin of this collection of symptoms to say that the foundational paper is bullshit. Nor do I need a fully formed alternative to see a house of cards when I’m looking at one.

If I had to guess, and this is purely conjecture, I’d say the reality is messy. It’s multifactorial, inconsistent, and not the result of one single objective cause … or even the same objective cause across the board.

This is an unsatisfying answer, and one that The Science™ simply doesn’t tolerate. Somewhere along the way Big Science™ got incredibly uncomfortable saying, “we just don’t know,” or even worse, “we were wrong”.

That sucks. And it’s a problem.

Because the beauty of science, the entire point actually, is flexibility… but not in the goal posts. In the ability to update, revise, and (gasp) even abandon prior conclusions when faced with new evidence.

Instead of evolving and seeking to actually understand anything, methods get molded, bent, and reshaped to justify conclusions that were decided in advance. That’s not fucking science. It’s continuing to build the same busted house of cards. It’s bullshit dressed up as rigor and labeled science.

And the further we go down this road…nodding along, agreeing that the emperor is wearing beautiful clothes…the further we drift from ever actually figuring anything out.

I snort laughed while making this. If you laughed too, thank you.

🤣

Thanks for hanging out. I love you guys.

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