Marina Titova

Why I’m not preparing my kids for college

“Since your kids don’t go to school, how will they get into college…

Read more

a month ago · 102 likes · 49 comments · Marina Titova

Subscribe now

And April 2026 draws to a close….🤪

I love you guys.

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.

Subscribe now

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.

🤣

Thanks for hanging out. I love you guys.

The cholesterol racket apparently knows no bounds and simply will not stop until we have everyone, including children, on a cholesterol lowering drug. The enormity of this ridiculousness cannot be overstated. But the beat goes on. If you would like to know more about this topic I encourage you to read the work of Malcolm Kendrick here and (here). Stephan Thomas has a good synopsis of Kendrick’s work here.

Here we go…

March 13, 2026 Updated 3:11 p.m. ET

People at risk of heart disease should start trying to lower their cholesterol as early as age 30 and continue into old age. They should also be getting their cholesterol levels lower than many doctors had previously recommended.

That is the new guidance released Friday by the American Heart Association, the American College of Cardiology and nine other professional organizations.

Before reading any further than the first sentences, I clicked on the “new guidance” hyperlink , which brought me here:

And before reading the new guidelines, I clicked the “Author Info & Affiliations” tab found after the committee member names.

This landed at Appendix 1, which is conveniently buried deep within the document.

The table lists each member of the guideline writing committee, and documents whether they had any financial or professional relationships with healthcare companies or organizations (yep, those companies whose products are affected by the guideline recommendations.).

Spoiler alert…there were relations.

Note👇

* = Significant relationship

Appendix 1. Writing Committee Relationships With Industry and Other Entities

Next up is Appendix 2. This section lists the physicians and organizations that reviewed the guideline before publication and discloses any financial relationships they reported with healthcare companies.

The companies appearing in these disclosures are typically the same pharmaceutical manufacturers whose drugs are discussed in the guideline … particularly those producing cholesterol lowering therapies like statins or lipid lowering agents.

Appendix 2. Peer Review Committee Relationships With Industry and Other Entities

To be crystal clear… the documents above list the financial relationships (conflicts of interest) of both the individuals who wrote the guidelines and the reviewers who evaluated them. These disclosures identify any consulting work, research funding, advisory roles, or other professional ties those individuals have had with pharmaceutical companies whose drugs or products are addressed within the guidelines themselves.

From my estimation, and as I have documented many times previously, there is a very clear pattern that has emerged across the medical-pharma-industrial complex that looks like this:

And this familiar pattern was certainly evident the last time the ACC/AHA cholesterol guidelines were updated in 2018. The industry response following those guidelines was almost immediate. This is when add-on cholesterol drugs (ezetimibe and PCSK9 inhibitors) became all the rage. The authors bellyached within the document about the price of PCSK9 inhibitors, which at the time were considered pricey. They said “JUMP PHARMA”, and within months, the manufacturers said “HOW HIGH???” Amgen cut the list price of Repatha by about 60%, and Sanofi/Regeneron followed with Praluent. Once the price point decreased, the market expanded, and new drugs came down the pipeline … prescribing increased, and combination lipid therapy became the norm.

The conflict of interest picture was not as overt as we sometimes see, but it wasn’t exactly covert either. The 2018 guideline’s writing committee reported no relevant financial relationships during the development window, including the chair. But the peer-review appendix sings a different song. Several reviewers disclosed consulting, research funding, or advisory relationships with companies that manufacture cholesterol drugs… you know, like Amgen, Sanofi, Regeneron, Merck, Pfizer, and Esperion. More importantly, the evidence base driving the guidelines came heavily from industry funded trials such as FOURIER and ODYSSEY OUTCOMES. In other words, the guidelines were technically written without direct pharmaceutical industry funding … but The Science™ propping those guidelines up was absolutely industry funded.

For example:

Let’s take a small detour and look at just one example from that table, Dr. James L. Januzzi Jr., a cardiologist at Massachusetts General Hospital and Harvard Medical School. His disclosure entry lists consulting roles with several diagnostics companies and participation in research or trial oversight roles connected to multiple pharmaceutical firms.

Here is Dr Januzzi on OpenPayments.gov.

Academic experts who conduct the clinical trials, publish the evidence, and advise professional societies on treatment recommendations often swim in broader research waters that are heavily funded by the pharmaceutical industry whose products those guidelines ultimately evaluate.

Aaaaaand the result was predictable in 2018. Industry funded the trials → the trials shaped the guidelines → the guidelines directed the therapeutical approach → the market followed … and lots of people got very rich.

So what do you think the new 2026 guidelines look like?

From The NY Times article Friday:

If the new guideline were widely followed, especially by younger people who could end up with a lifetime of lower LDL levels, there could be a big effect, cardiologists say.

The group recommends starting to test for levels of LDL cholesterol — the “bad” cholesterol — during childhood, at around age 10. Doing so could identify the one in 250 people with a genetic condition that leads to extremely high cholesterol levels. They would need to be immediately prescribed a cholesterol-lowering drug.

Earlier testing! And more testing!

Well OF COURSE that’s the answer!!! Hey, I bet the next guidelines will advise to start testing fetuses in utero! I mean, shit, let’s get a vaccine going in the pipeline. And we can start taking cholesterol boosters every other quarter with the covid shit shots - I mean, I think we could probably call them something more appropriate though. Cholesterol booster probably wouldn’t sell. Cholesterol dimmer kinda hits … 🤣

What else do the new guidelines say?

NYT continues…

The guideline also says people should not rely on supplements to lower their LDL. A clinical trial, run by Dr. Nissen, tested six supplements. Five of them — fish oil, cinnamon, turmeric, plant sterols and red yeast rice — were no better than a placebo. The sixth — garlic in pill form — actually raised LDL levels.

Let’s just take a little look at the SPORT clinical trial, cited as evidence for discouraging the use of things other than pharmaceuticals.

Comparative Effects of Low-Dose Rosuvastatin, Placebo, and Dietary Supplements on Lipids and Inflammatory Biomarkers

Authors: Luke J. Laffin, Dennis Bruemmer, Michelle Garcia, Danielle M. Brennan, Ellen McErlean, Douglas S. Jacoby, Erin D. Michos, Paul M Ridker, Tracy Y. Wang, Karol E. Watson, Howard G. Hutchinson, and Steven E. Nissen

First of all, let’s have a round of applause for Gina Kolata of the New York Times and her journalistic prowess 👏. Excellent job parroting the narrative without doing any sort of digging that might resemble investigation.

👇Here’s what that would look like.

Subscribe now

A total of 190 participants completed the study, which means a scant 25 people were in each cohort. Just in case you are unfamiliar with clinical trials, these numbers are quite small, making it highly sensitive to baseline imbalances. For example, while 3.5% of participants were current smokers, none were assigned to the Rosuvastatin arm. 33% were former smokers, but who cares. Apparently nobody, because that wasn’t even noted in the table.

With the scant 25 person sample size, even just a few unevenly distributed risk factors (like 1 or 2 smokers) could influence outcomes. Speaking of outcomes…we are, of course, in surrogate endpoint land, not actual clinical outcome land. I mean, with that stunning 28 day trial length, designed to detect large statin-like effects over a very short time period. Really, any possibility of slower metabolic changes from supplements being detected is statistically almost impossible with such small groups and short follow-up. This trial was set up to show some Real Science™. So there’s that.

Also this:

Patients taking 1 of the studied supplements before trial enrollment were allowed to participate if they discontinued for 4 weeks before enrollment.

Some supplements have longer physiological effects than 4 weeks, especially those that influence lipid metabolism.

For example, red yeast rice. It contains monacolin K, which is chemically identical to lovastatin, and the LDL-lowering effects can last at least several weeks after discontinuation. Or fish oil, a commonly used supplement, has omega-3s that incorporate into cell membranes. These effects can last months.

So if someone had been taking a supplement long-term, a 4 week washout might not fully eliminate its biological effects. But whatever, who cares.

Now let’s look at the disclosures, of which there are many …

Funding Support and Author Disclosures

This trial was funded by AstraZeneca Pharmaceuticals. Dr Laffin has been a consultant and/or served on steering committees for Medtronic, Lilly, Mineralys Therapeutics, AstraZeneca, and Crispr Therapeutics; has received research funding from AstraZeneca; and has ownership interest in LucidAct Health and Gordy Health. Dr Bruemmer has been a consultant and served on a steering committee for Esperion. Dr Jacoby has been a consultant and served on a steering committee for AstraZeneca. Dr Michos has been a consultant and/or served on steering committees for AstraZeneca, Bayer, Boehringer Ingelheim, Esperion, Novartis, Novo Nordisk, and Pfizer; and has received research funding from the American Heart Association and the National Institutes of Health. Dr Ridker has been a consultant and/or served on steering committees for Agepha, AstraZeneca, Civi Biopharm, Flame Inc, Health Outlook, IQVIA, Janssen Pharmaceuticals, Novartis, Novo Nordisk, Omeicos, and Sirnanomics; and has received research funding from Amarin, Kowa Pharmaceuticals, the National Heart, Lung, and Blood Institute, and Novartis. Dr Wang has been a consultant and/or served on steering committees for AstraZeneca and Novartis; and has received research funding from Abbott Laboratories, Artivion, Boston Scientific, Bristol Myers Squibb, and Chiesi. Dr Watson has been a consultant and/or served on steering committees for Amari, Amgen, Boehringer Ingelheim, Esperion, Novartis, and Lilly; and has been a speaker for Boehringer Ingelheim. Dr Hutchinson is an employee of AstraZeneca. Dr Nissen has received institutional research funding from AbbVie, AstraZeneca, Amgen, Bristol Myers Squibb, Cerenis, Eli Lilly, Esperion, Medtronic, MyoKardia, Novartis, Pfizer, The Medicines Company, Silence Therapeutics, Takeda, and Orexigen; and is an unpaid consultant for Respira, Alnylam, Beren Therapeutics, Prolaio, TenSixteen Bio, Altimmune, MetroBiotech, and Intercept. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Well isn’t it so weird that the study funded by the company that makes a cholesterol drug, comparing that cholesterol drug to inexpensive supplements, where 75% of the authors were financially tied to companies that make cholesterol medications, notably the one funding the trial … found that the cholesterol drug is best.

Dr. Laffin all the way to the bank.

And I love the last sentence, ”All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.” 👏🤗

All 3 other authors. 😂

Of course there were plenty of companies represented in the disclosure document that also make lucrative cholesterol drugs.

I encourage you to look into the work of Ben Goldacre. His book, Bad Pharma: How Drug Companies Mislead Doctors and Harm Patients, is about the pharmaceutical industry, its relationship with the medical profession, and the extent to which it controls academic research into its own products.

For example, in a “2007 journal article published in PLOS Medicine, researchers studied every published trial on statins, drugs prescribed to reduce cholesterol levels. In the 192 trials they looked at, industry-funded trials were 20 times more likely to produce results that favoured the drug”. (source)

Have a look at this paper, published in JAMA (2003):

Scope and Impact of Financial Conflicts of Interest in Biomedical Research

Conclusions: Financial relationships among industry, scientific investigators, and academic institutions are widespread. Conflicts of interest arising from these ties can influence biomedical research in important ways.

Check out this bullshit, published by The Lancet this year.

Assessment of adverse effects attributed to statin therapy in product labels: a meta-analysis of double-blind randomised controlled trials

I’ll summarize:

💁🏻‍♀️ Cherry picked data held by the CTT group that they won’t share with anyone ever, finds that statin adverse effects are all in your head and maybe drug companies should consider changing their labels so you don’t create a confirmation bias situation … you know, for all those people imagining side effects. 🫨

And the beat goes on.

Pharmaceutical companies just continue to market their drugs through thinly veiled propaganda, delivered by salesmen in white coats, heralded as experts and revered as The Science™.

And apparently nobody is ever going to notice this in any meaningful way. Certainly not the New York Times 😂.