What the new NEJM study of the mRNA flu jab really tells us

The flu trial became the experiment the COVID era vaccines never ran: what happens when you give the "platform" alone.

Introduction

In my last essay I argued that pharmacists and formulation scientists were sidelined, leading to models that treated LNPs as passive “fat bubbles.” Pfizer’s own mRNA flu trial has now provided an unexpected experiment: the same platform, minus the spike. What has emerged verifies much of my (and Genervter Bürger) work and many of my previous substack posts…. and now a renal signal that I believe only a drug-like amphiphilic systems could explain.

When Pfizer’s long-delayed mRNA influenza vaccine trial data for those >65yo finally appeared on clinicaltrials.gov, it should have been front-page news. Instead, it slipped quietly online without a press release, no investor call. This is what we call, a tell.

What those tables revealed wasn’t just a failed trial, but a clue to the central problem of the mRNA project: even without spike, the inflammatory signature persists.

Alex Berensen clued me in with his substack post.

VERY URGENT: Pfizer's mRNA flu shot failed its pivotal clinical trial in adults 65 and older

And he noted a very important fact.

HOLY TOLEDO.

BUT, what was actually published in the NEJM were the results of the trial for 18-64 yo as you can see here¹.

There results were lauded as you can image from the usual folk. For instance CIDRAP (Center for Infectious Disease Research and Policy²), who I used to follow and think was solid…(*shakes head*) had this to say about the trial. Predictably, the coverage was celebratory.

BUT, the data on those 65 and older wasn’t published. (is this shades of the Vioxx scandal?) as Marianne Demasi discusses in her blog³

Major journal under fire for omitting Pfizer’s failed flu data in seniors

Those Over 65 were pretty healthy

Lets look at the inclusion and exclusion criteria of these patients who were older and in the trial which you can find at clinicaltrial.gov for trial NCT05540522⁴

Surprise!! The over-65 participants in Pfizer’s study weren’t frail nursing-home residents; they were by design HEALTHY retirees.

No cardiovascular disease, no heart failure, no chronic disease, even a lab result was enough to kick you out of the trial. And for sure, no one with any kind of kidney damage.

Etc etc. But yet, as Alex Berenson notes, the kidney and respiratory signal was unmistakable.

Here are the kidneys. Left is the mRNA vaccine, right is the traditional flu jab

THIS IS SERIOUS, folks.

It is a big red flag when the vaccine causes all these kidney issues in the healthiest segment of an age group that is most of risk for kidney damage or decline. You don’t want to give anything that increases the risk of kidney damage in this population. I spent decades dosing and monitoring aminoglycosides and seeing this signature jump out of Pfizer’s tables was déjà vu.

I’m not going to talk about the respiratory signal just yet. Maybe later in another post. But it likely due to the same mechanisms as the kidney damage.

Reactogenicity Profile vs. Conventional Flu Vaccine

Overall, Pfizer’s own data shows about a sixfold greater incidence of MODERATE to pretty SEVERE local and severe reactions (fevers OVER 39 from a vaccine??!! and severe fatigue like you can’t get out of bed???). I guess that means IT IS WORKING, right?

But this looks identical to the COVID-19 mRNA shots:

Fatigue, lymphadeopathy, fevers, pain.

Even after you remove the spike protein, the pattern remains the same. Here is the data from the NEJM paper for the 18-64yo.

This means it is those pesky LNPS, not the resulting antigen that defines much of the reactogenic profile. I don’t think anyone says that the flu antigen is “toxic.”

The LNP as the Active Ingredient

The LNPs are NOT INERT FAT BUBBLES. They are ionizable cationic amphiphiles (CADs) that flip to a positive charge under acidic pH in endosomes, bind the mRNA electrostatically, fuse with cell membranes, then revert to neutral. This pH sensitivity means it is pharmacologically active.

CADs share structural similarities with known lysosomotric compounds like chloroquine, or some SSRI antidepressants, or like amiodarone, or what I am concerned right now in this post, aminoglycosides. These molecules are charged at one end (the tertiary amine in the ionizable lipid) and fat soluable at the other end (the lipid tails).

This means they accumulate in lysosomes (the garbage and recycling centres in the cell), and trigger phospholipidosis and affect mitochondrial lipid turnover. The liver and kidneys are prime targets.

I don’t think this kidney injury is mysterious. It is classic amphiphilic behaviour, like aminoglycosides and it is coming from the LNPs.

This article was seminal for me.⁵

These toxicologists suggest kidney phospholipidosis as well as hepatic phospholipidosis is possible with LNPs. Could the results we see with this mRNA flu jab show this possibility? We KNOW the COVID-19 shot results in kidney damage.⁶ And John Beadoin has documented this for some time now.

Timing characteristics of the epidemic of acute kidney injury involved deaths

Cationic amphiphiles have a known toxicological signature:

1. Membrane destabilization: They insert into mitochondrial and endosomal membranes, altering permeability ( our first preprint goes into this in detail).

2. Lysosomal accumulation: They form lamellar inclusions (myeloid bodies) classic markers of phospholipidosis. Here are some examples.⁷ BTW vacuoles were reported in the rat toxicology studies.

   

   Fig. 1. (A) Lamellar body. (B) Fusion of two lamellar bodies inside the hepatocyte (∗ collagen fibres in the space of disse). (C) Hyperplasia of the endoplasmic reticulum during phospholipidosis. (D) Phagocytosis of lamellar bodies by Kupffer cells in the sinusoidal space. (E) Several lamellar bodies are located intracellular inside a hepatocyte that displays a high grade of vacuolization. (F) A Kupffer cell loaded with lipid droplets close to a disintegrated hepatocyte on the bottom of the picture. (G) In contrast, lipid droplets characterizing the steatosis.

3. Complement activation (CARPA): They trigger rapid immune cascades that explain the fevers and chills post‑injection which I have discussed previously.

4. Organ deposition: Biodistribution studies show high uptake in liver, spleen, kidney, GI tract, and ovaries and likely sequester in adipose tissue.

Nephrotoxicity fits perfectly within this pharmacologic pattern. A kidney is essentially a lipid‑handling bioreactor with extraordinary perfusion. When you expose it repeatedly to amphiphilic cations and subtle tubular damage follows. That is what the influenza trial’s renal signal hints at to me. And this is very similar to what we see with another amphiphilic drug: aminoglycosides like gentimicin, tobramycin and the like. Drugs I am very familiar with, dosing and monitoring in my hospital career.

Platform-Wide Lessons

mRNA technology is advertised as plug‑and‑play: swap spike for hemagglutinin, RSV F‑protein, or cytomegalovirus antigens and the “platform” remains the same. The Pfizer influenza results reveal the fatal flaw in that logic. When the plug changes but the adverse pattern doesn’t, the “platform” is the real pharmacological actor.

The mRNA influenza data confirms what I and Genervter Bürger have been saying for quite some time. The mRNA platform toxicity is not limited to spike, it may even be that the spike protein is just an accelerator of the damage done by the LNPs. This influenza trial is the best trial so far where one can hypothesize what the LNPs by themselves might be able to do.

We cover that in our first pre-print which takes about the mechanistic aspects of the LNPs and how they echo CAD-like properties.⁸ Over 1000 views and 900 downloads!

Then we followed up with Falko’s (Genervter Bürger) masterful explanation of what happens from a systems biology perspective with the LNPs. And it is not pretty.⁹ We have submitted this paper this week.

This is NOT an antigen problem. It is material and formulation science hidden under immunological branding. As we discussed in our preprints, the LNPs are ACTIVE PHARMACOLOGICAL COMPOUNDS, not excipients and should be classified as such. They are basically pharmacological detergents, scrubbing the cell membranes like steel wool (well you get the idea). And the resulting organelle trafficking and membrane restructuring following this CAD-like endocytic processes. This triggers downstream signaling cascades causing dysregulation of cellular communication, stress response, and energy balance. And we think it can be long-lasting.

Critics often lump everything under the phrase “ the mRNA platform” which implies that the modified synthetic RNA molecule itself is triggering inflammation. But Kari Karikó’s and Weissman’s Nobel Prize in 2023 was awarded for resolving that problem. They achieved it by substituting naturally occurring nucleotide analogs, specifically pseudouridine for uridine and making the RNA immunologically silent to innate sensors like TLR7 and TLR8. They made the mRNA stop acting like the viral RNA that it was.

So when we see the same constellation of inflammatory symptoms such as lymphadenopathy, fatigue, fevers, and even organ-level inflammation showing up whether or not the encoded protein is spike, the logical culprit isn’t the mRNA itself. It’s the lipid nanoparticle format with its cationic lipids, and the innate immune activation and signal transduction effects that these cause directly in the body. Together with the dsDNA, dsRNA, endotoxins and other impurities they cant or wont get rid of. (and that is another story)

BioNTech (and Pfizer) Know

In a paper Dr David Wiseman brought to my attention, the problems of the LNPs have been noted.¹⁰

Note: The authors Jorge Herrero and Heinrich Haas work for BionTech SE in Mainz Germany.

This language from a manufacturer signals that maybe the regulators have been talking to them. Published the day before the NEJM study. No coincidences.

Conclusion

A serious scientific culture would stop and ask whether this LNP technology should be repurposed for chronic or annual dosing in vaccines at all. We would also recognize what these LNPs represent, and stop thinking of them as simply “fat bubbles.” I think the LNPs are nephrotoxic and studies to show this possibility should be undertaken.

Regulators instead continue labeling these lipids as “inactive ingredients,” instead of doing the rigorous pharmacokinetic and carcinogenicity evaluations required for small‑molecule drugs. Or for gene therapy for that matter.

Even though Pfizer (and Moderna!) maybe getting some heat in the background, the regulatory sleight of hand must end.

Thanks for reading. And as always, continue to pray the rosary.

Addendum

I believe there are enough signals here, that there is enough justification to run the basic CAD-risk assays¹¹ that should have been done from the start. At minimum, regulators should require:
1) phospholipidosis screens in human kidney cells with CAD controls (like impiramine!);
2) lysosomal-trapping and pH-partitioning studies to quantify ionizable-lipid accumulation;
3) electron microscropic ultrastructure of kidney and liver tissue looking for multilamellar bodies (as shown above);
4) biodistribution studies tracking the lipids (each of them individually and their breakdown or metabolites), and determine actual half-lives and distributions in humans; and
5) transcriptomic/proteomic profiling to detect the classic CAD stress signature.

These are standard toxicology tests for any cationic amphiphilic compound. We have 70 yrs of pharmacology for these drugs. The fact they were never done for vaccine ionizable lipids is precisely why these kidney findings matter: they point directly at an unexamined mechanism sitting in the blind spot of the platform.

1. https://www.nejm.org/doi/pdf/10.1056/NEJMoa2416779

2. https://www.cidrap.umn.edu/influenza-vaccines/experimental-mrna-flu-vaccine-shows-superior-efficacy-against-symptomatic

3. Major journal under fire for omitting Pfizer’s failed flu data in seniors

4. https://www.clinicaltrials.gov/study/NCT05540522?tab=results#outcome-measures

5. https://www.sciencedirect.com/science/article/abs/pii/S0378427423002242?via%3Dihub

6. https://www.sciencedirect.com/science/article/pii/S0002962925000011

7. https://www.sciencedirect.com/science/article/pii/S0014579306010325

8. https://zenodo.org/records/17342544

9. https://www.preprints.org/manuscript/202511.0517

10. https://pubs.acs.org/doi/10.1021/acs.biomac.5c01219

11. https://www.sciencedirect.com/science/article/abs/pii/S0887233315000156