I was surprised to see that even this Rancourt guy disagrees with you, although he commended you on the time yo spent on my "garbage" paper.
Other than that I do not wish to comment on this guy's nonsense that I came to expect of him in the discussions of the D4CE group.
As for you, neither your reply nor this whole Substack "hit-and-run" platform seem respectable enough for this kind of discussion. You are cordially invited to submit a rebuttal letter or paper to the editor of the IJVTPR journal or to any respectable and dignified journal and then we can take this debate to an appropriate academic level.
One word of advice: Dismissing my microscopy findings as "artifacts" is at a level that is not suitable for a dignified debate. This is simply an un uncalled-for blow below the belt. Try to argue to the point and keep it at the point.
For example, I don't hold it against you that you have no background and no understanding neither in Materials Science nor in Electrical Engineering and I do not wish to strike a blow below-the-belt by saying that your comments are artifacts of an ignorant in these fields. Let's keep this scientific and to the point.
Finally, let me remind you that you haven't bothered to look at these injectables through a microscope, have you? Well, I have and my paper contains a detailed account of what I saw. It also contains citations from the most top-tier academic journals. One example is: https://www.nature.com/articles/natrevmats201768
I am not even the only one who came up with such forensic microscopy images. Mine are merely the most detailed and they are woven into a fabric of a unified scientific theory that leans on said top-tier scientific references (and some detailed YouTube presentations of key characters in this whole affair). I hope you have bothered to check my references and citations. They will be a crucial part of this debate.
Hi Shimon. Denis disagreed with me on a point that is not related to the content of your paper. He posited that the LNPs are mainly responsible for vaccine toxicity, whereas I consider the immune response to the spike protein the leading cause. He and I agree that your nanobot hypothesis of vaccine toxicity is not supported by the evidence.
Regarding your invitation to continue the debate at IJVTPR: you are familiar with the reaction I got from the editor when I submitted my criticisms. After that reaction, I no longer take IJVTPR seriously as an academic journal. Unfortunately, I have no epithet for it that is both accurate and usable in polite society.
You try to play the credentials card. While I am indeed not a materials scientist, I am a trained MD and have a specialization in diagnostic bacteriology. I have spent enough hours looking through the microscope at blood smears, cerebrospinal liquor and other patient samples, and at stained bacterial cultures. There was also quite a bit of microscopy involved in the anatomy and pathology classes at medical school. I have seen my share of artifacts in microscopic samples. And anyhow, since we are dealing here primarily with medical questions -- the materials science aspect not having been treated at any level of detail in your paper -- my credentials are clearly more relevant than yours.
Aside from that, I have worked as a practicing experimental scientist for almost 35 years. You might not believe it, but one does learn a thing or two from that sort of experience. One such lesson is that one is more often wrong than right, even if the hypothesis looks good on paper. Therefore, it is no good to go out on a limb and pile assumptions on top of one another, if one does not have the means, or does not take the time, to experimentally test each of these assumptions in their turn.
As I pointed out in my review, you didn't even go to the trouble of formulating a coherent hypothesis, or to propose experiments with which to test that hypothesis. What you have given us might perhaps evolve into actual science someday, somewhere. In its current state, however, it does not qualify as science.
You are very generous with your time and explanations. In my opinion, The IJVTPR paper by Yanowitz and Broudy is utter garbage. It's too bad that this venue IJVTPR sometimes gives an editorially managed platform to truly and obviously-unscientific valueless contributions. On the positive side: It's easy to see that the paper is nonsense.
However, I disagree with the premise of your critique, expressed as: "According to these authors, the harm done by these vaccines is not caused by the production of spike protein in our body cells." In my view it has not been established that spike protein is produced in the bodies of injected persons.
In this regard, I wrote: "A recent study regarding mRNA-vaccine-induced cardiac adverse effects (using an animal model) showed that the vaccine toxicity occurs directly from the bio‑distributed cationic lipid nanoparticles and in particular not from spike protein, and that the adverse effect is stress mediated (Mori et al., 2026). Gutschi (2026) has pointed out the relevance of this study to human health, stress and age."
I have addressed the question of immunological toxicity vs. chemical toxicity in the book "mRNA Vaccine Toxicity." One of the arguments in favour of the immunological mechanism is again the pronounced exacerbation of the damage by repeat injection. With dominant chemical toxicity, each dose should do about the same damage, regardless of sequence.
We cannot entirely rule out a contribution by nanolipid chemical toxicity, and of course the regulatory approval of these dirty chemicals was a scandal, but at this time I see no positive evidence that they are the leading cause of vaccine damage.
You state: "With dominant chemical toxicity, each does should do about the same damage, regardless of sequence." implying in the context that the effect on the organism is additive rather than multiplicative.
In my opinion, your statement is false. The opposite is true for damage that is not repaired, such as in vital organs and tissues in which the cells are replaced slowly or not at all or in which "scarring" is permanent. This is why death rate itself is exponential with age. The impact from additive damage is an exponential effect on reduced survival (increased clinically observable consequences) because the toxicity attacks are breaking links in a complex network. Immune response need not be postulated to explain this.
The second most common finding (~50%) in the Burkhardt series of 101 autopsies after SPED/immune cardio vasculopathy was foreign material in heart, pancreas and spleen that none of the five pathologists (Burkhardt, Lang, Krüger, Mörz, Luck) could identify. The < 50 micron vacuolar blackish-brown birefringent crystalline material appears surrounded by clear material under H&E stain with no inflammatory response or granuloma. This material was present post LNP and vectored vaccines so it could not be LNP but maybe small off-target proteins (spike stain negative) possibly hybridized with host lipids, possibly cholesterol. The material does appear to be immunologically inert but chemically active possibly leading to arthymogenic heart failure (Case 152) and type 1 DM. LNP has its own set of issues but the dose is small in comparison to prolonged protein production from synthetic mRNA.
The brown stuff, in both color and birefringence, looks exactly like heme crystals, found e.g. as "malaria pigment" in that disease. It baffles me that the pathologists have not yet seen this obvious similarity and followed up on it.
In any case, the sheer amount of it found in the tissues makes it clear that this cannot be directly derived from the vaccine but must have originated in the body itself.
Interesting point. I am pulling out all the + cases looking for clues. They did stain for heme. Odd hemazoin does not appear to be part of the histopathology of PNH, mostly parasites. Case 152 caught my attention. Young healthy male, sudden onset, only finding. What happens when whatever this foreign material is deposits in the His-Purkinje system?
You are not wrong in principle, but if you look at the cumulative toxicity for example of cytotoxic anticancer agents, then you will find that it escalates relatively slowly with the number of doses given. The worst example I can think of right now would be adriamycin (aka doxorubicin). Interestingly enough, it prominently affects the heart and the mitochondria, which you will probably consider grist for your mill. But to my knowledge, even with this poison toxicity does not escalate fivefold from the first to the second dose, which is the order of magnitude observed with myocarditis and the first two doses of mRNA vaccine.
It might appear that way in this discussion, but I'm actually relying on the evidence in its entirety. Another argument against a key role of the LNPs is the similarity of the side effects between mRNA vaccines and adenovirus-based vaccines (AstraZeneca and Johnson & Johnson). The latter, as you know, contain no LNP at all.
I think both of your arguments may be based on an overly simplified assumption about the nature of the dose–response relationship. The discussion appears to treat toxicity as if it followed either a relatively linear/additive model or as if a stronger response after repeated exposure necessarily points toward an immunological mechanism. However, for lipid nanoparticles (LNPs), such assumptions may not adequately reflect the underlying biology.
Nanoparticle systems often show highly nonlinear and heterogeneous effects. The relevant factor is not only the administered dose, but also biodistribution, cellular uptake, persistence, degradation pathways, tissue-specific susceptibility, repair mechanisms, and the biological state of the organism at the time of exposure.
Furthermore, LNPs should not be considered a single homogeneous entity. They are stochastic systems in which nanoprecipitation generates a distribution of particle populations, with some compositions and structures occurring more frequently than others. Nevertheless, there can be substantial inter-particle differences in terms of cargo loading, lipid composition, morphology, size, and potentially biological behavior.
This heterogeneity adds another layer of complexity to any dose–response analysis, because the nominal dose does not necessarily represent a uniform biological exposure. Different particle subpopulations may have different biodistribution profiles, cellular uptake patterns, persistence, and biological effects. Therefore, treating LNP exposure as if it were a single, chemically uniform agent may overlook important aspects of nanoparticle pharmacology and toxicology.
Therefore, increased effects after repeated exposure do not by themselves prove an immune-mediated mechanism, but neither do they necessarily demonstrate simple accumulation of chemical damage. Nonlinear threshold effects, altered distribution, changes in cellular responses, or impaired repair capacity could also contribute.
A more appropriate framework may be to consider a dynamic and heterogeneous dose–response relationship driven by the stochastic nature of each formulation and potentially even by each vial, rather than a simple additive model. The important question is which mechanisms are supported by experimental evidence, in which tissues, and under which conditions.
Furthermore, compensatory mechanisms will likely play a major role, and it cannot be ruled out that the effects observed over the past five years represent only the visible part of a larger biological process.
With respect, I think the debate would benefit from moving beyond the dichotomy of "chemical accumulation versus immune amplification" and considering the broader complexity of nanoparticle toxicology.
That is all fine as far as it goes, but I don't think it invalidates the old saying that it is the dose that makes the poison.
There is an RNA/LNP drug called "patisiran" that contains not an mRNA but a siRNA -- it silences the expression of transthyretin protein in the liver. The lipids in the LNPs are not the same as in the COVID vaccines, but their biological effect is similar. The amount of LNP in a single dose is approximately 300 times higher than with a dose of vaccine, and the stuff is given intravenously every couple of weeks. It seems to be at least well enough tolerated to have received approval sometime before the total capture of the regulatory agencies became apparent in the COVID vaccine fiasco.
I don't think we actually disagree that the dose matters. My argument is that, with LNPs, the administered mass alone is not a complete measure of the biologically effective dose. In our paper (see the Elsevier link), we also discuss the effects of patisiran (Onpattro) in detail.
The comparison between patisiran and the COVID-19 vaccines illustrates my key point rather than refuting it. They differ not only in the nominal LNP dose, but also in lipid composition, pKa value, formulation, route of administration (intravenous vs. intramuscular), biodistribution, target cells, immune response, and pharmacokinetics. These variables significantly determine which tissues are exposed and how the particles interact with biological membranes.
This is also supported by comparative experimental studies, as we explain in our paper. Korzun et al. investigated multiple clinically relevant LNP architectures (Onpattro®-like, Pfizer®-like, and Moderna®-like) produced under otherwise comparable conditions and found that changing only the ionizable lipid markedly altered reactogenicity and inflammatory responses in vivo. Likewise, the EMA assessment of the saRNA-LNP platform (Kostaive®) reports tissue persistence of its ionizable lipid that differs substantially from earlier LNP systems, despite being specifically designed for improved degradability. These observations suggest that lipid architecture itself is a major determinant of biological behavior and cannot be reduced to the total amount of lipids administered.
From that perspective, "the dose makes the poison" remains true in principle, but for nanomedicines the biologically relevant dose is a multidimensional parameter. It is not adequately described by milligrams of lipids alone, but by the number and characteristics of the particles themselves, together with their delivery architecture, formulation, biodistribution, individual lipoprotein profile (e.g. ApoE, LDL), protein corona formation, membrane interactions, and ultimately transfection efficiency and gene expression. Importantly, biodistribution is not equivalent to transfection, and transfection is not equivalent to gene expression. These represent distinct biological processes with different determinants. Consequently, one cannot assume that two formulations containing different amounts of LNP will produce comparable biological effects simply because one contains more lipids by mass.
OK, I have read your review. It is well written and a commendable effort, but there is nothing in there that convinces me of the case for LNPs as a major cause of adverse vaccine effects, with the exception of anaphylaxis.
You made much of the difference between the cationic lipids in the COVID vaccines vs. patisiran, but an experimental study you cite -- the one by Korzun et al. -- shows that the differences in the biological effects are rather modest, and they don't come close to making up for the much higher LNP dose given with patisiran.
I discuss some more reasons in my latest post, on the paper by Marks et al. That paper further confirms that the immune response to the foreign antigen is the decisive mechanism of harm, at least with respect to the autoimmune-like inflammation of organs and blood vessels. This was already abundantly clear from the evidence when my co-authors and I published our freely accessible book "mRNA Vaccine Toxicity" in 2023.
That review is an impressive effort -- I will have to spend some time with it.
You are not wrong that the chemical structure of the cationic lipid in question matters. However, I would suggest that it matters less than with drugs or poisons that bind specifically to protein targets. For membrane disruption, the general molecular shape and physicochemical properties seem to be decisive. But I will sit down with that review and see what evidence you have of differences in toxicity or biological effects between the various lipids you discuss.
Histopathological analysis is one of the highest quality sources of truth in medicine as it can define the mechanism of injury. Immunohistochemical analysis performed by Dr. Burkhardt and colleagues differentiates “vaccine” tissue damage from that caused by SARS-CoV-2 viral infection.
I don't condone the use of these compounds that were neither properly purified nor tested for safety. At the same time, I cannot see any evidence in the clinical data that points specifically to a contribution of these compounds to the manifest vacccine damage.
As you say, there is enough BS on the internet. Don't add to it by letting some AI bot doing your thinking and writing for you. Think and write for yourself, and keep the arguments sharp and focused. Nobody wants to read comments that are longer than the entire article they supposedly comment on.
Dear Michael Palmer,
I was surprised to see that even this Rancourt guy disagrees with you, although he commended you on the time yo spent on my "garbage" paper.
Other than that I do not wish to comment on this guy's nonsense that I came to expect of him in the discussions of the D4CE group.
As for you, neither your reply nor this whole Substack "hit-and-run" platform seem respectable enough for this kind of discussion. You are cordially invited to submit a rebuttal letter or paper to the editor of the IJVTPR journal or to any respectable and dignified journal and then we can take this debate to an appropriate academic level.
One word of advice: Dismissing my microscopy findings as "artifacts" is at a level that is not suitable for a dignified debate. This is simply an un uncalled-for blow below the belt. Try to argue to the point and keep it at the point.
For example, I don't hold it against you that you have no background and no understanding neither in Materials Science nor in Electrical Engineering and I do not wish to strike a blow below-the-belt by saying that your comments are artifacts of an ignorant in these fields. Let's keep this scientific and to the point.
Finally, let me remind you that you haven't bothered to look at these injectables through a microscope, have you? Well, I have and my paper contains a detailed account of what I saw. It also contains citations from the most top-tier academic journals. One example is: https://www.nature.com/articles/natrevmats201768
I am not even the only one who came up with such forensic microscopy images. Mine are merely the most detailed and they are woven into a fabric of a unified scientific theory that leans on said top-tier scientific references (and some detailed YouTube presentations of key characters in this whole affair). I hope you have bothered to check my references and citations. They will be a crucial part of this debate.
Hi Shimon. Denis disagreed with me on a point that is not related to the content of your paper. He posited that the LNPs are mainly responsible for vaccine toxicity, whereas I consider the immune response to the spike protein the leading cause. He and I agree that your nanobot hypothesis of vaccine toxicity is not supported by the evidence.
Regarding your invitation to continue the debate at IJVTPR: you are familiar with the reaction I got from the editor when I submitted my criticisms. After that reaction, I no longer take IJVTPR seriously as an academic journal. Unfortunately, I have no epithet for it that is both accurate and usable in polite society.
You try to play the credentials card. While I am indeed not a materials scientist, I am a trained MD and have a specialization in diagnostic bacteriology. I have spent enough hours looking through the microscope at blood smears, cerebrospinal liquor and other patient samples, and at stained bacterial cultures. There was also quite a bit of microscopy involved in the anatomy and pathology classes at medical school. I have seen my share of artifacts in microscopic samples. And anyhow, since we are dealing here primarily with medical questions -- the materials science aspect not having been treated at any level of detail in your paper -- my credentials are clearly more relevant than yours.
Aside from that, I have worked as a practicing experimental scientist for almost 35 years. You might not believe it, but one does learn a thing or two from that sort of experience. One such lesson is that one is more often wrong than right, even if the hypothesis looks good on paper. Therefore, it is no good to go out on a limb and pile assumptions on top of one another, if one does not have the means, or does not take the time, to experimentally test each of these assumptions in their turn.
As I pointed out in my review, you didn't even go to the trouble of formulating a coherent hypothesis, or to propose experiments with which to test that hypothesis. What you have given us might perhaps evolve into actual science someday, somewhere. In its current state, however, it does not qualify as science.
Best wishes,
Michael
You are very generous with your time and explanations. In my opinion, The IJVTPR paper by Yanowitz and Broudy is utter garbage. It's too bad that this venue IJVTPR sometimes gives an editorially managed platform to truly and obviously-unscientific valueless contributions. On the positive side: It's easy to see that the paper is nonsense.
However, I disagree with the premise of your critique, expressed as: "According to these authors, the harm done by these vaccines is not caused by the production of spike protein in our body cells." In my view it has not been established that spike protein is produced in the bodies of injected persons.
In this regard, I wrote: "A recent study regarding mRNA-vaccine-induced cardiac adverse effects (using an animal model) showed that the vaccine toxicity occurs directly from the bio‑distributed cationic lipid nanoparticles and in particular not from spike protein, and that the adverse effect is stress mediated (Mori et al., 2026). Gutschi (2026) has pointed out the relevance of this study to human health, stress and age."
https://denisrancourt.substack.com/p/eight-pivotal-facts-about-covid-period
Hi Denis. Thanks for your comment.
I have addressed the question of immunological toxicity vs. chemical toxicity in the book "mRNA Vaccine Toxicity." One of the arguments in favour of the immunological mechanism is again the pronounced exacerbation of the damage by repeat injection. With dominant chemical toxicity, each dose should do about the same damage, regardless of sequence.
We cannot entirely rule out a contribution by nanolipid chemical toxicity, and of course the regulatory approval of these dirty chemicals was a scandal, but at this time I see no positive evidence that they are the leading cause of vaccine damage.
You state: "With dominant chemical toxicity, each does should do about the same damage, regardless of sequence." implying in the context that the effect on the organism is additive rather than multiplicative.
In my opinion, your statement is false. The opposite is true for damage that is not repaired, such as in vital organs and tissues in which the cells are replaced slowly or not at all or in which "scarring" is permanent. This is why death rate itself is exponential with age. The impact from additive damage is an exponential effect on reduced survival (increased clinically observable consequences) because the toxicity attacks are breaking links in a complex network. Immune response need not be postulated to explain this.
The second most common finding (~50%) in the Burkhardt series of 101 autopsies after SPED/immune cardio vasculopathy was foreign material in heart, pancreas and spleen that none of the five pathologists (Burkhardt, Lang, Krüger, Mörz, Luck) could identify. The < 50 micron vacuolar blackish-brown birefringent crystalline material appears surrounded by clear material under H&E stain with no inflammatory response or granuloma. This material was present post LNP and vectored vaccines so it could not be LNP but maybe small off-target proteins (spike stain negative) possibly hybridized with host lipids, possibly cholesterol. The material does appear to be immunologically inert but chemically active possibly leading to arthymogenic heart failure (Case 152) and type 1 DM. LNP has its own set of issues but the dose is small in comparison to prolonged protein production from synthetic mRNA.
The brown stuff, in both color and birefringence, looks exactly like heme crystals, found e.g. as "malaria pigment" in that disease. It baffles me that the pathologists have not yet seen this obvious similarity and followed up on it.
In any case, the sheer amount of it found in the tissues makes it clear that this cannot be directly derived from the vaccine but must have originated in the body itself.
Interesting point. I am pulling out all the + cases looking for clues. They did stain for heme. Odd hemazoin does not appear to be part of the histopathology of PNH, mostly parasites. Case 152 caught my attention. Young healthy male, sudden onset, only finding. What happens when whatever this foreign material is deposits in the His-Purkinje system?
The vacuoles appear to be filled with lipid.
You are not wrong in principle, but if you look at the cumulative toxicity for example of cytotoxic anticancer agents, then you will find that it escalates relatively slowly with the number of doses given. The worst example I can think of right now would be adriamycin (aka doxorubicin). Interestingly enough, it prominently affects the heart and the mitochondria, which you will probably consider grist for your mill. But to my knowledge, even with this poison toxicity does not escalate fivefold from the first to the second dose, which is the order of magnitude observed with myocarditis and the first two doses of mRNA vaccine.
You are relying heavily on a weak argument, IMO.
It might appear that way in this discussion, but I'm actually relying on the evidence in its entirety. Another argument against a key role of the LNPs is the similarity of the side effects between mRNA vaccines and adenovirus-based vaccines (AstraZeneca and Johnson & Johnson). The latter, as you know, contain no LNP at all.
Dear Denis and Michael,
I think both of your arguments may be based on an overly simplified assumption about the nature of the dose–response relationship. The discussion appears to treat toxicity as if it followed either a relatively linear/additive model or as if a stronger response after repeated exposure necessarily points toward an immunological mechanism. However, for lipid nanoparticles (LNPs), such assumptions may not adequately reflect the underlying biology.
Nanoparticle systems often show highly nonlinear and heterogeneous effects. The relevant factor is not only the administered dose, but also biodistribution, cellular uptake, persistence, degradation pathways, tissue-specific susceptibility, repair mechanisms, and the biological state of the organism at the time of exposure.
Furthermore, LNPs should not be considered a single homogeneous entity. They are stochastic systems in which nanoprecipitation generates a distribution of particle populations, with some compositions and structures occurring more frequently than others. Nevertheless, there can be substantial inter-particle differences in terms of cargo loading, lipid composition, morphology, size, and potentially biological behavior.
This heterogeneity adds another layer of complexity to any dose–response analysis, because the nominal dose does not necessarily represent a uniform biological exposure. Different particle subpopulations may have different biodistribution profiles, cellular uptake patterns, persistence, and biological effects. Therefore, treating LNP exposure as if it were a single, chemically uniform agent may overlook important aspects of nanoparticle pharmacology and toxicology.
Therefore, increased effects after repeated exposure do not by themselves prove an immune-mediated mechanism, but neither do they necessarily demonstrate simple accumulation of chemical damage. Nonlinear threshold effects, altered distribution, changes in cellular responses, or impaired repair capacity could also contribute.
A more appropriate framework may be to consider a dynamic and heterogeneous dose–response relationship driven by the stochastic nature of each formulation and potentially even by each vial, rather than a simple additive model. The important question is which mechanisms are supported by experimental evidence, in which tissues, and under which conditions.
Furthermore, compensatory mechanisms will likely play a major role, and it cannot be ruled out that the effects observed over the past five years represent only the visible part of a larger biological process.
https://www.sciencedirect.com/science/article/pii/S2211383526004235
With respect, I think the debate would benefit from moving beyond the dichotomy of "chemical accumulation versus immune amplification" and considering the broader complexity of nanoparticle toxicology.
With deepest respect for your work,
Falko
That is all fine as far as it goes, but I don't think it invalidates the old saying that it is the dose that makes the poison.
There is an RNA/LNP drug called "patisiran" that contains not an mRNA but a siRNA -- it silences the expression of transthyretin protein in the liver. The lipids in the LNPs are not the same as in the COVID vaccines, but their biological effect is similar. The amount of LNP in a single dose is approximately 300 times higher than with a dose of vaccine, and the stuff is given intravenously every couple of weeks. It seems to be at least well enough tolerated to have received approval sometime before the total capture of the regulatory agencies became apparent in the COVID vaccine fiasco.
I don't think we actually disagree that the dose matters. My argument is that, with LNPs, the administered mass alone is not a complete measure of the biologically effective dose. In our paper (see the Elsevier link), we also discuss the effects of patisiran (Onpattro) in detail.
The comparison between patisiran and the COVID-19 vaccines illustrates my key point rather than refuting it. They differ not only in the nominal LNP dose, but also in lipid composition, pKa value, formulation, route of administration (intravenous vs. intramuscular), biodistribution, target cells, immune response, and pharmacokinetics. These variables significantly determine which tissues are exposed and how the particles interact with biological membranes.
This is also supported by comparative experimental studies, as we explain in our paper. Korzun et al. investigated multiple clinically relevant LNP architectures (Onpattro®-like, Pfizer®-like, and Moderna®-like) produced under otherwise comparable conditions and found that changing only the ionizable lipid markedly altered reactogenicity and inflammatory responses in vivo. Likewise, the EMA assessment of the saRNA-LNP platform (Kostaive®) reports tissue persistence of its ionizable lipid that differs substantially from earlier LNP systems, despite being specifically designed for improved degradability. These observations suggest that lipid architecture itself is a major determinant of biological behavior and cannot be reduced to the total amount of lipids administered.
From that perspective, "the dose makes the poison" remains true in principle, but for nanomedicines the biologically relevant dose is a multidimensional parameter. It is not adequately described by milligrams of lipids alone, but by the number and characteristics of the particles themselves, together with their delivery architecture, formulation, biodistribution, individual lipoprotein profile (e.g. ApoE, LDL), protein corona formation, membrane interactions, and ultimately transfection efficiency and gene expression. Importantly, biodistribution is not equivalent to transfection, and transfection is not equivalent to gene expression. These represent distinct biological processes with different determinants. Consequently, one cannot assume that two formulations containing different amounts of LNP will produce comparable biological effects simply because one contains more lipids by mass.
OK, I have read your review. It is well written and a commendable effort, but there is nothing in there that convinces me of the case for LNPs as a major cause of adverse vaccine effects, with the exception of anaphylaxis.
You made much of the difference between the cationic lipids in the COVID vaccines vs. patisiran, but an experimental study you cite -- the one by Korzun et al. -- shows that the differences in the biological effects are rather modest, and they don't come close to making up for the much higher LNP dose given with patisiran.
I discuss some more reasons in my latest post, on the paper by Marks et al. That paper further confirms that the immune response to the foreign antigen is the decisive mechanism of harm, at least with respect to the autoimmune-like inflammation of organs and blood vessels. This was already abundantly clear from the evidence when my co-authors and I published our freely accessible book "mRNA Vaccine Toxicity" in 2023.
That review is an impressive effort -- I will have to spend some time with it.
You are not wrong that the chemical structure of the cationic lipid in question matters. However, I would suggest that it matters less than with drugs or poisons that bind specifically to protein targets. For membrane disruption, the general molecular shape and physicochemical properties seem to be decisive. But I will sit down with that review and see what evidence you have of differences in toxicity or biological effects between the various lipids you discuss.
And, Prof Rancourt, if Dr Burkhardt's work is inadequate to make you rethink, try this,
https://ijirms.in/index.php/ijirms/article/view/2202
Raman spectroscopic Characterization of Anomalous Intravascular Fibrous Casts: Evidence for Stage-Dependent β-sheet Enriched Protein Maturation
This peer reviewed paper, shows how the spike protein is essential in creating the abnormal polymerised white clots.
The spike protein is really and truly in tissues, and is causing havoc.
Haven't seen that paper -- thanks for pointing it out.
Prof. Rancourt, you constantly disregard medical scientific evidence and promote evidence free theories.
Try looking at this book. It shows conclusively that spike damage is the source of many of the pathologies found in tissues.
https://robertchandler.substack.com/p/burkhardtlangschwarz-the-definitive
Histopathological analysis is one of the highest quality sources of truth in medicine as it can define the mechanism of injury. Immunohistochemical analysis performed by Dr. Burkhardt and colleagues differentiates “vaccine” tissue damage from that caused by SARS-CoV-2 viral infection.
I don't condone the use of these compounds that were neither properly purified nor tested for safety. At the same time, I cannot see any evidence in the clinical data that points specifically to a contribution of these compounds to the manifest vacccine damage.
You persist in posting AI garbage, so I have no choice but to ban you.
As you say, there is enough BS on the internet. Don't add to it by letting some AI bot doing your thinking and writing for you. Think and write for yourself, and keep the arguments sharp and focused. Nobody wants to read comments that are longer than the entire article they supposedly comment on.