They’ll say: Oh, but that’s just the delivery system. Nonsense. That’s like saying the guy who kicks in your door and holds a syringe to your neck isn’t part of the assault, he’s just delivering the threat. The LNP is a pharmacological agent. It modulates the immune system, disrupts membranes, and induces inflammation all on its own, even when it’s carrying nothing. That was proven years ago.
The pharmaceutical companies knew it. The regulators knew it. The journals buried it.
This entire “payload” framing was sleight of hand, it kept your eyes on the mRNA so you wouldn’t ask too many questions about the shell. But the shell is a very big part of the story. Because you can’t outrun a system-wide immune trigger, and you sure as hell can’t undo what it does to kids, brains, hearts, or long-term inflammation cascades.
So again, the question no one in power wants you to ask:
It's a complicated PROCESS! Sigh! Thank you for emphasizing this. To me, it looks like a stochastic assembly and de-assembly -- the body will try to do something with it. And then, taking the parts, disseminating them, and in yet new cellular environments, they will get assembled and taken apart again. I don't know what it would take for this process to be terminated, and the various objects to be finally eliminated from the body. Do you have any indicators that this can happen? To me, it seems that the individual compounds are not something that Mother Nature needs and intends to have. Natural substances are recycled and, in this sense, never lost. No process can ever truly end. Even if one terminates, it affects countless others. So, your work reveals frustrating aspects of this LNP process that most don't appreciate. But it may be that even THAT is merely the tip of the iceberg :-(
Yes, but data is limited. We know the helper lipid is recycled, PEG lipid causes vacuoles. The ionizable lipid tertiary amine heads? Likely trapped in lysosomes. But not much data after 48hrs.
It may help understand the eventual cellular destination of these complexes. There are also some strange dark needle shaped deposits found inside cells.
You may wish to buy this book, which is a summary of Arne Burkhardt's histopathological work and has recently become available in English. With slides
Vaccinated – dead
Histopathological findings following COVID-19 vaccination
It's a memorial publication for the late Professor Arne Burkhardt containing all of the important pathology slides showing the vaccine-produced spike protein and all of damage being caused by it in the vascular system and organs such as the heart, spleen, liver, brain, lung, thyroid gland, adrenal gland, kidney, urinary bladder, testicles, prostate, pancreas, peripheral nerves, and skeletal muscles.
"A picture is worth a thousand words." These photos prove that the Covid jabs are destructive to the entire body.
The atlas is aimed primarily at pathologists, but also at physicians from other specialities and non-medical professionals interested in the topic. On the one hand, the impressive histological images are presented in order to sensitise colleagues working in routine pathology and forensic medicine to these completely new findings and to draw attention to the changes typical of mRNA injections. On the other hand, corresponding case descriptions are included which document the tragic circumstances and the manifold suffering of people after these injections.
Very interesting. Thank you! I’d be looking for vacuoles, staining for lipids. I wonder if they did any cryo-EM? That’ll show phospholipidosis and would prove my theory of LNPs as CADs
Long ago I learned in basic biochemistry, charge and shape are everything. There is not a model in the world that can adequately describe what is going on in these complexes, both before and after injection. The manufacturing was far too inconsistent to state anything reliable about what was in a given vial of final product, and handling until injection also variable. Then as you clearly explained, within any human, ( we are not un-complex cloned entities, who live in totally controlled environments ) the possibilities for these ADME complexes to change, reform etc. are nearly endless, thus the neat little diagrams are merely theories, that were never proven. Ultimately we live and function upon realties not theories. Thanks for another enlightening article.
Perhaps sometimes reading more than just selective spike/modRNA literature could solve some already discussed issues?:
What did we describe in the first paper?: Non-heterogeneous, intrinsic entropy in each individual LNP due to the formulation and ratios. We therefore correctly conclude that a colloidal particle system is not predictable.
And what did we write about DSPC recycling and bioavailability?:
"5.5. How Does 1,2-distearoyl-sn-glycero-3-phosphocholine (DSPC) Affect the PI Cycle?
In the context of the recycling processes and membrane organization, another aspect that has received little attention is the phospholipid, 1,2-distearoyl-sn-glycero-3-phosphocholine (DSPC) [255,256], which is used as an auxiliary lipid in LNPs. DSPC (also known as 18:0/18:0) has two saturated stearic acid chains. While structurally similar to the phospholipids naturally found in cell membranes, DSPCs are more tightly packed, more rigid, and more thermally stable [257] than the typical 18:0/18:1 and 18:1/18:1 phospholipids found in eukaryotic membranes [234,258]. It has a high gel-liquid transition temperature (Tm approx. 55°C), which confers it with unusual rigidity [259]. It is a natural phospholipid, primarily found in human pulmonary surfactant [260].
This raises the question of how DSPC affects the PI-cycle, as it is known that PCs are recycled into various phospholipids, including PI. Phospholipase D, which converts PCs into phosphatidic acid (PA), plays an essential role in this process [261,262,263]. PA is converted into CDP-diacylglycerol (CDP-DAG) by CDP-DAG synthase, a key step in channeling PA into the biosynthesis of PI and other phospholipids [264,265]. CDP-DAG subsequently serves as the immediate precursor for phosphatidylinositols, synthesized by PI synthase at the endoplasmic reticulum, forming the core PI scaffold [265,266].
To the best of our knowledge, it remains uncharacterized how DSPC is degraded and whether it can interfere with membrane physiology beyond the process of transfection through recycling. After 24 hours, most DSPC primarily accumulates in the liver, spleen, heart, kidney, and lung, indicating that these organs' plasma membranes take up the lipid [267]. This confirms DSPC's tissue delivery and retention. However, it is known that liposomes composed of phospholipids such as DSPC can strikingly alter membrane structure, as previously discussed in the review by Lonez et al. [223]. The exact cellular mechanism in vivo remains poorly characterized. Studies indicate that DSPC-containing liposomes can undergo hydrolytic and oxidative degradation, producing phospholipid-derived products that may alter membrane structure and stability in unpredictable ways [268,269].
Although not yet demonstrated in vivo, it is conceivable that lipid nanoparticles may interfere with autophagic lysosome reformation (ALR) [270,271], a process essential for sustaining lysosomal homeostasis and autophagic flux [272,273]. Since ALR depends on phosphoinositide transitions [274] and clathrin-mediated membrane remodeling [275], the insertion of ionizable lipids into these organelles could compromise the delicate balance of lysosomal recycling. Such perturbations may not only disturb autophagic flux but could also contribute to organ-specific toxicities observed with LNPs [107]."
So the role of DSPC in lipid nanoparticle bioactivity and PI-cycle interactions is not overlooked. It was explicitly analyzed in our work, including potential downstream effects on membrane physiology and organ-specific accumulation. There is a difference between ignoring and dwelling on old ways of thinking and reading attentively and rethinking, because the literature and plausibility have long been discussed.
Will have to read about CARPA. Meanwhile, I wonder if LNP reaction resembles fat embolism reaction which occurs when long bone fractures leak bone marrow into blood stream
Hi Dr Benoit. Thanks for commenting. Happy to see you! Yes, the fat embolism has some overlap (have seen one case and they are SCARY). LNPs and fat embolism are both supramolecular assemblies (so no “mg” amount) and have size dependent vascular effects. Both have non-classical pharmacology or emergent behaviour. But fat embolism are comprised of neutral lipids and cause sheer stress while the LNPs are charged (neutral only at neutral pH) and because they are ionizable amphiphiles cause membrane destabilization, complement activation and down stream effects.
Regarding CARPA. I have a theory there was a LOT of CARPA occuring but was misclassified as immune related stress response. If you’re interested I have a post on this. Was even thinking of writing a paper but I’ve been out of clinical for too long. https://mariagutschi.substack.com/p/carpa-isrr-or-anaphylaxis
LNP is a supramolecular assembly of amphiphilic* molecules that self-organize into nanoscale structures capable of encapsulating nucleic acids (e.g., modRNA or siRNA). They self-assemble AROUND the modRNA.
No. It was supposed to. If it ever was self- organizing or has always been driven by any kind of emf, redlight, bluelight is an ongoing discussion.
Yes, it was supposed to. Based on physical chemistry principles. How else do you make a colloid system? What happens inside the body is now just being worked out. But there are transient increases in cholesterol post jab
Why should I care about any of this? mRNA poisons are never gonna be on my list of things to try. They are useless for anything but destroying the body. I don't do vaccines or drugs or even OTC. Why would I?
The body does not require any of these poisons to live healthy or repair itself. After 6 years, we still don't know much about mRNA poisons other than they are meant to maim and murder. They, like all vaccines and drugs are invented to support the false religion of germ theory.
If you’re genuinely not interested in the topic, the logical question is: why comment at all?
There are documented cases of people with adverse effects, and there are also well-described biological mechanisms (e.g. LNP biodistribution, immune activation, membrane interactions) that warrant discussion regardless of personal lifestyle choices.
You don’t need to take vaccines, drugs, or anything else, but dismissing ongoing scientific questions by calling everything “poison” and rejecting germ theory altogether is not an argument, it’s a belief system.
If a topic doesn’t concern you, scrolling past it is always an option.
Or in terms that even guys hopefully can follow with nothing more than stupid relegious fanatism in the mind:
Commenting on a topic just to declare that you don’t believe in it is like entering a discussion on rocket engineering only to say you don’t believe rockets work.
That may be your personal belief, but it doesn’t add anything to the discussion.
all the time. Shedding is really exosomes and multivescicles acting in a parcrine manner. Other than Bansal et al, we havent had much data on exosomes etc documented. What exactly are inside, how long they are present etc etc, how they are transferred all needs to be worked out. I'm still trying to figure out the beginning, lol.
They’ll say: Oh, but that’s just the delivery system. Nonsense. That’s like saying the guy who kicks in your door and holds a syringe to your neck isn’t part of the assault, he’s just delivering the threat. The LNP is a pharmacological agent. It modulates the immune system, disrupts membranes, and induces inflammation all on its own, even when it’s carrying nothing. That was proven years ago.
The pharmaceutical companies knew it. The regulators knew it. The journals buried it.
This entire “payload” framing was sleight of hand, it kept your eyes on the mRNA so you wouldn’t ask too many questions about the shell. But the shell is a very big part of the story. Because you can’t outrun a system-wide immune trigger, and you sure as hell can’t undo what it does to kids, brains, hearts, or long-term inflammation cascades.
So again, the question no one in power wants you to ask:
When does the drug begin?
It's a complicated PROCESS! Sigh! Thank you for emphasizing this. To me, it looks like a stochastic assembly and de-assembly -- the body will try to do something with it. And then, taking the parts, disseminating them, and in yet new cellular environments, they will get assembled and taken apart again. I don't know what it would take for this process to be terminated, and the various objects to be finally eliminated from the body. Do you have any indicators that this can happen? To me, it seems that the individual compounds are not something that Mother Nature needs and intends to have. Natural substances are recycled and, in this sense, never lost. No process can ever truly end. Even if one terminates, it affects countless others. So, your work reveals frustrating aspects of this LNP process that most don't appreciate. But it may be that even THAT is merely the tip of the iceberg :-(
Yes, but data is limited. We know the helper lipid is recycled, PEG lipid causes vacuoles. The ionizable lipid tertiary amine heads? Likely trapped in lysosomes. But not much data after 48hrs.
Yes. Think of 1% oxidized cholesterol due to impurities. Think of some covalent bonds. The entire structure is a single entropic system.
Maria, I suppose you have a copy of this book?
https://eticamedia.eu/en/product/vaccinated-dead/
It may help understand the eventual cellular destination of these complexes. There are also some strange dark needle shaped deposits found inside cells.
You may wish to buy this book, which is a summary of Arne Burkhardt's histopathological work and has recently become available in English. With slides
Vaccinated – dead
Histopathological findings following COVID-19 vaccination
Ute Krüger · Walter Lang
https://www.histo-atlas.com/files/Reading-sample.pdf
It's a memorial publication for the late Professor Arne Burkhardt containing all of the important pathology slides showing the vaccine-produced spike protein and all of damage being caused by it in the vascular system and organs such as the heart, spleen, liver, brain, lung, thyroid gland, adrenal gland, kidney, urinary bladder, testicles, prostate, pancreas, peripheral nerves, and skeletal muscles.
"A picture is worth a thousand words." These photos prove that the Covid jabs are destructive to the entire body.
The atlas is aimed primarily at pathologists, but also at physicians from other specialities and non-medical professionals interested in the topic. On the one hand, the impressive histological images are presented in order to sensitise colleagues working in routine pathology and forensic medicine to these completely new findings and to draw attention to the changes typical of mRNA injections. On the other hand, corresponding case descriptions are included which document the tragic circumstances and the manifold suffering of people after these injections.
Very interesting. Thank you! I’d be looking for vacuoles, staining for lipids. I wonder if they did any cryo-EM? That’ll show phospholipidosis and would prove my theory of LNPs as CADs
" biology interacts with assemblies, not individual ingredient lists."
YES!!! This has been bothering me for a while. We simply cannot continue to ignore the complexity of biological systems.
Long ago I learned in basic biochemistry, charge and shape are everything. There is not a model in the world that can adequately describe what is going on in these complexes, both before and after injection. The manufacturing was far too inconsistent to state anything reliable about what was in a given vial of final product, and handling until injection also variable. Then as you clearly explained, within any human, ( we are not un-complex cloned entities, who live in totally controlled environments ) the possibilities for these ADME complexes to change, reform etc. are nearly endless, thus the neat little diagrams are merely theories, that were never proven. Ultimately we live and function upon realties not theories. Thanks for another enlightening article.
Yes, plus the physical chemistry of the LNPs often overlooked by biologists, virologists, immunologists. Thank for a great comment.
The role od dscp is mostly overlooked https://drbine.substack.com/p/hohere-nebenwirkungsrate-bei-ungenauer
Perhaps sometimes reading more than just selective spike/modRNA literature could solve some already discussed issues?:
What did we describe in the first paper?: Non-heterogeneous, intrinsic entropy in each individual LNP due to the formulation and ratios. We therefore correctly conclude that a colloidal particle system is not predictable.
https://zenodo.org/records/17342544
And what did we write about DSPC recycling and bioavailability?:
"5.5. How Does 1,2-distearoyl-sn-glycero-3-phosphocholine (DSPC) Affect the PI Cycle?
In the context of the recycling processes and membrane organization, another aspect that has received little attention is the phospholipid, 1,2-distearoyl-sn-glycero-3-phosphocholine (DSPC) [255,256], which is used as an auxiliary lipid in LNPs. DSPC (also known as 18:0/18:0) has two saturated stearic acid chains. While structurally similar to the phospholipids naturally found in cell membranes, DSPCs are more tightly packed, more rigid, and more thermally stable [257] than the typical 18:0/18:1 and 18:1/18:1 phospholipids found in eukaryotic membranes [234,258]. It has a high gel-liquid transition temperature (Tm approx. 55°C), which confers it with unusual rigidity [259]. It is a natural phospholipid, primarily found in human pulmonary surfactant [260].
This raises the question of how DSPC affects the PI-cycle, as it is known that PCs are recycled into various phospholipids, including PI. Phospholipase D, which converts PCs into phosphatidic acid (PA), plays an essential role in this process [261,262,263]. PA is converted into CDP-diacylglycerol (CDP-DAG) by CDP-DAG synthase, a key step in channeling PA into the biosynthesis of PI and other phospholipids [264,265]. CDP-DAG subsequently serves as the immediate precursor for phosphatidylinositols, synthesized by PI synthase at the endoplasmic reticulum, forming the core PI scaffold [265,266].
To the best of our knowledge, it remains uncharacterized how DSPC is degraded and whether it can interfere with membrane physiology beyond the process of transfection through recycling. After 24 hours, most DSPC primarily accumulates in the liver, spleen, heart, kidney, and lung, indicating that these organs' plasma membranes take up the lipid [267]. This confirms DSPC's tissue delivery and retention. However, it is known that liposomes composed of phospholipids such as DSPC can strikingly alter membrane structure, as previously discussed in the review by Lonez et al. [223]. The exact cellular mechanism in vivo remains poorly characterized. Studies indicate that DSPC-containing liposomes can undergo hydrolytic and oxidative degradation, producing phospholipid-derived products that may alter membrane structure and stability in unpredictable ways [268,269].
Although not yet demonstrated in vivo, it is conceivable that lipid nanoparticles may interfere with autophagic lysosome reformation (ALR) [270,271], a process essential for sustaining lysosomal homeostasis and autophagic flux [272,273]. Since ALR depends on phosphoinositide transitions [274] and clathrin-mediated membrane remodeling [275], the insertion of ionizable lipids into these organelles could compromise the delicate balance of lysosomal recycling. Such perturbations may not only disturb autophagic flux but could also contribute to organ-specific toxicities observed with LNPs [107]."
https://www.preprints.org/manuscript/202511.0517#sec7-preprints-184611
So the role of DSPC in lipid nanoparticle bioactivity and PI-cycle interactions is not overlooked. It was explicitly analyzed in our work, including potential downstream effects on membrane physiology and organ-specific accumulation. There is a difference between ignoring and dwelling on old ways of thinking and reading attentively and rethinking, because the literature and plausibility have long been discussed.
Will have to read about CARPA. Meanwhile, I wonder if LNP reaction resembles fat embolism reaction which occurs when long bone fractures leak bone marrow into blood stream
Hi Dr Benoit. Thanks for commenting. Happy to see you! Yes, the fat embolism has some overlap (have seen one case and they are SCARY). LNPs and fat embolism are both supramolecular assemblies (so no “mg” amount) and have size dependent vascular effects. Both have non-classical pharmacology or emergent behaviour. But fat embolism are comprised of neutral lipids and cause sheer stress while the LNPs are charged (neutral only at neutral pH) and because they are ionizable amphiphiles cause membrane destabilization, complement activation and down stream effects.
Regarding CARPA. I have a theory there was a LOT of CARPA occuring but was misclassified as immune related stress response. If you’re interested I have a post on this. Was even thinking of writing a paper but I’ve been out of clinical for too long. https://mariagutschi.substack.com/p/carpa-isrr-or-anaphylaxis
LNP is a supramolecular assembly of amphiphilic* molecules that self-organize into nanoscale structures capable of encapsulating nucleic acids (e.g., modRNA or siRNA). They self-assemble AROUND the modRNA.
No. It was supposed to. If it ever was self- organizing or has always been driven by any kind of emf, redlight, bluelight is an ongoing discussion.
Yes, it was supposed to. Based on physical chemistry principles. How else do you make a colloid system? What happens inside the body is now just being worked out. But there are transient increases in cholesterol post jab
Why should I care about any of this? mRNA poisons are never gonna be on my list of things to try. They are useless for anything but destroying the body. I don't do vaccines or drugs or even OTC. Why would I?
The body does not require any of these poisons to live healthy or repair itself. After 6 years, we still don't know much about mRNA poisons other than they are meant to maim and murder. They, like all vaccines and drugs are invented to support the false religion of germ theory.
If you’re genuinely not interested in the topic, the logical question is: why comment at all?
There are documented cases of people with adverse effects, and there are also well-described biological mechanisms (e.g. LNP biodistribution, immune activation, membrane interactions) that warrant discussion regardless of personal lifestyle choices.
You don’t need to take vaccines, drugs, or anything else, but dismissing ongoing scientific questions by calling everything “poison” and rejecting germ theory altogether is not an argument, it’s a belief system.
If a topic doesn’t concern you, scrolling past it is always an option.
Or in terms that even guys hopefully can follow with nothing more than stupid relegious fanatism in the mind:
Commenting on a topic just to declare that you don’t believe in it is like entering a discussion on rocket engineering only to say you don’t believe rockets work.
That may be your personal belief, but it doesn’t add anything to the discussion.
Never considered shedding?
all the time. Shedding is really exosomes and multivescicles acting in a parcrine manner. Other than Bansal et al, we havent had much data on exosomes etc documented. What exactly are inside, how long they are present etc etc, how they are transferred all needs to be worked out. I'm still trying to figure out the beginning, lol.