Chronic Fatigue and Dysautonomia following COVID-19 Vaccination Is Distinguished from Normal Vaccination Response by Altered Blood Markers

https://www.mdpi.com/2076-393X/11/11/1642

https://substack.com/home/post/p-207939425

Ich erspare mir jetzt Kommentare. (Hab es Maria versprochen.)

"Figure 3: mRNA vaccines “fly under the radar” of the immune system. Left: the particles of a proper virus are decorated with some of the proteins which are encoded by the viral genome. As a consequence, the virus will efficiently enter cells only when we are first infected with it, whereas on subsequent encounters, the antibodies induced by the first infection will neutralize the virus particles. Right: in contrast, mRNA vaccine particles don’t contain any protein antigen; therefore, antibodies against the encoded protein antigen can’t prevent the particles from entering our body cells and exposing them to immune attack."

Veto

de Puig H, Bosch I, Carré-Camps M, Hamad-Schifferli K. Effect of the Protein Corona on Antibody-Antigen Binding in Nanoparticle Sandwich Immunoassays. Bioconjug Chem. 2017 Jan 18;28(1):230-238. doi: 10.1021/acs.bioconjchem.6b00523. Epub 2016 Dec 8. PMID: 28095684; PMCID: PMC5245486

Kim W, Ly NK, He Y, Li Y, Yuan Z, Yeo Y. Protein corona: Friend or foe? Co-opting serum proteins for nanoparticle delivery. Adv Drug Deliv Rev. 2023 Jan;192:114635. doi: 10.1016/j.addr.2022.114635. Epub 2022 Nov 26. PMID: 36503885; PMCID: PMC9812987.

Park W, Choi J, Hwang J, et al. Apolipoprotein Fusion Enables Spontaneous Functionalization of mRNA Lipid Nanoparticles with Antibody for Targeted Cancer Therapy. ACS Nano. 2025;19(6):6412-6425. doi:10.1021/acsnano.4c16562 (Wie ich einen unerwünschten Effekt als Verkaufsgeschichte verpacke)

Chen, M.Z., Yuen, D., McLeod, V.M. et al. A versatile antibody capture system drives specific in vivo delivery of mRNA-loaded lipid nanoparticles. Nat. Nanotechnol. 20, 1273–1284 (2025). doi: 10.1038/s41565-025-01954-9

Ko, J., Tom, J. & Cheng, M.H.Y. Considerations on antibody-based active targeting strategies for lipid nanoparticle delivery systems. AAPS Open 12, 19 (2026). doi: s41120-026-00159-1

Ich muss über das Park et al. so herzhaft lachen:

Sie präsentieren die LDL-vermittelte Protein-Corona praktisch als den entscheidenden Mechanismus, der die Antikörperbindung reduziert und dadurch die Immuninteraktion verändert. Dabei bleibt für mich die naheliegende Frage offen, ob dieser Effekt überhaupt spezifisch für ihr System ist. Ionisierbare LNPs bilden nach der Injektion ohnehin eine komplexe Protein-Corona aus zahlreichen Plasmaproteinen – darunter ApoE, Albumin, Komplementfaktoren und weitere Lipoprotein-assoziierte Komponenten. Wenn bereits diese natürliche Corona die Oberflächenzugänglichkeit von Epitopen und damit die Antikörperbindung beeinflusst, dann ist die beobachtete Abschirmung möglicherweise gar keine Besonderheit der entwickelten LDL-Strategie, sondern eine generelle Eigenschaft ionisierbarer LNPs.

Ohne einen direkten Vergleich der Protein-Coronas und der Antikörperbindung zwischen konventionellen LNPs und ihrem System lässt sich aus meiner Sicht nicht überzeugend zeigen, dass der Effekt tatsächlich auf der gezielten LDL-Strategie beruht. Andernfalls besteht die Gefahr, einen allgemeinen Protein-Corona-Effekt als neuartigen Mechanismus zu interpretieren.

Dr. med. Klaus Roman Hör (Waldmünchen) - Di., 21. Juli 2026

🔹 Seit 230 Jahren werden Menschen geimpft, und die Infizierung mit Antigenen wird als Gesundheitsvorsorge propagiert.

🔹 Studien zu den Risiken und den sprunghaften Anstiegen von Alzheimer, chronischen Krankheiten, Entwicklungsstörungen, neurologischen Störungen, Krebs etc. sowie zum engen Zusammenhang mit dem Sudden Infant Death Syndrome fallen in den herkömmlichen Medien geflissentlich unter den Tisch.

Wer hätte nur damit rechnen können, dass die Leber nicht nur ein passives detoxifizierendes Organ ist, sondern aktiv in die Endokrine Regulation von Hormonen eingreift? *hust* (Natürlich liegt mein Fokus auch wieder auf die Rolle von MAPKs in der intrazellulären Signalgebung)

Petrescu AD, Kain J, Liere V, Heavener T, DeMorrow S. Hypothalamus-Pituitary-Adrenal Dysfunction in Cholestatic Liver Disease. Front Endocrinol (Lausanne). 2018 Nov 12;9:660. doi: 10.3389/fendo.2018.00660. PMID: 30483216; PMCID: PMC6240761.

Lea S, Li J, Plumb J, et al. P38 MAPK and glucocorticoid receptor crosstalk in bronchial epithelial cells. J Mol Med (Berl). 2020;98(3):361-374. doi:10.1007/s00109-020-01873-3

Westenberger G, Sellers J, Fernando S, Junkins S, Han SM, Min K, Lawan A. Function of Mitogen-Activated Protein Kinases in Hepatic Inflammation. J Cell Signal. 2021;2(3):172-180. PMID: 34557866; PMCID: PMC8457364.

Rhyu J, Yu R. Newly discovered endocrine functions of the liver. World J Hepatol. 2021 Nov 27;13(11):1611-1628. doi: 10.4254/wjh.v13.i11.1611. PMID: 34904032; PMCID: PMC8637678.

Let’s see where the journey of possibile outcomes will end in reality…

Möge der Saft mit euch sein.

https://open.substack.com/pub/myrauk/p/lipid-nanoparticles-lnps-the-delivery

Thank you so much, Dr. Forster-van Hijfte, for this great article. ♥️

Dr Mobean

Hab übrigens noch nen richtig hübschen Witz für euch:

Palmer meinte doch, als ich ihm die unterschiede zwischen LNP-modRNA und AZ demonstrierte, dass ja Beides zu nephrotischem Syndrom führte also gleicher Mechanismus, also egal:

mRNA-LNP cases (Comirnaty):
Case 1: Minimal-change disease (MCD) with nephrotic syndrome, proteinuria 14 g/day, cholesterol 244 mg/dL, LDL 170 mg/dL, triglycerides 159 mg/dL.
Case 3: FSGS-type podocytopathy with nephrotic syndrome, proteinuria UPCR 10.3 g/g, cholesterol 566 mg/dL, LDL 350 mg/dL, triglycerides 302 mg/dL. A detailed lipid profile was reported, including marked LDL and triglyceride elevation in Case 3.
Adenoviral vector case (Janssen):
Case 2: MCD with nephrotic syndrome, proteinuria up to 22.6 g/g, albumin 1,070 mg/dL, cholesterol 589 mg/dL. LDL and triglycerides were not reported. Therefore, the relevant observation is not a simple difference in "presence or absence" of hyperlipidemia.


Dormann H, Knüppel-Ruppert A, Amann K, Erley C. Nephrotic Syndrome After Vaccination Against COVID-19: Three New Cases From Germany. Dtsch Arztebl Int. 2021 Oct 1;118(39):662-663. doi: 10.3238/arztebl.m2021.0330. PMID: 34919048; PMCID: PMC8762589.

"Ashkarran et al.57 reported that the addition of small molecules such as glucose, triglycerides, or phosphatidylcholine to human plasma markedly altered the PC composition on polystyrene NPs. For instance, phosphatidylcholine interacted with albumin via hydrophobic interactions, hydrogen bonding, and water bridges, which consequently reduced the incorporation of albumin into the corona."

https://www.sciencedirect.com/science/article/pii/S2211383526003370

Was sind schon subklinisch relevante Unterschiede in einem Schweizeruhrwerk, wenn man als Kliniker mit nem Vorschlaghammer draufhauen kann, bis es ruhe gibt? Problem gelöst...

Es ist soviel schlimmer: Lest bitte aufmerksam meinen aktuellsten Kommentar:

As long as the biological hazard potential of LNPs is not investigated as an independent scientific question in a rational and mechanistic manner (see our work Lipid nanoparticles as active biointerfaces: From membrane interaction to systemic dysregulation), and downstream effectors such as spike protein or modRNA expression are treated as the only admissible explanatory models, any attempt to establish a complete causal chain will inevitably remain incomplete.

This becomes particularly problematic for pathologies whose development does not necessarily correlate with the local detection of spike protein or modRNA. Examples may include alterations of reproductive organs, cardiac micro-scarring, neurodegenerative processes, or other delayed sequelae whose pathogenesis may be shaped by systemic or early physicochemical and biological processes. Such mechanisms can neither be adequately investigated nor excluded by experimental approaches that focus exclusively on downstream effectors.

This creates a methodological circularity: only mechanisms that are actively investigated can be discovered. If spike protein or modRNA are defined a priori as the only admissible causal mechanisms, LNP-mediated processes become invisible by study design rather than being experimentally excluded. That is not evidence against such mechanisms; it is a consequence of the underlying investigative framework.

“mRNA-LNP cases (Comirnaty):
Case 1: Minimal-change disease (MCD) with nephrotic syndrome, proteinuria 14 g/day, cholesterol 244 mg/dL, LDL 170 mg/dL, triglycerides 159 mg/dL.

Case 3: FSGS-type podocytopathy with nephrotic syndrome, proteinuria UPCR 10.3 g/g, cholesterol 566 mg/dL, LDL 350 mg/dL, triglycerides 302 mg/dL. A detailed lipid profile was reported, including marked LDL and triglyceride elevation in Case 3.

Adenoviral vector case (Janssen):
Case 2: MCD with nephrotic syndrome, proteinuria up to 22.6 g/g, albumin 1,070 mg/dL, cholesterol 589 mg/dL. LDL and triglycerides were not reported. Therefore, the relevant observation is not a simple difference in "presence or absence" of hyperlipidemia.


Dormann H, Knüppel-Ruppert A, Amann K, Erley C. Nephrotic Syndrome After Vaccination Against COVID-19: Three New Cases From Germany. Dtsch Arztebl Int. 2021 Oct 1;118(39):662-663. doi: 10.3238/arztebl.m2021.0330. PMID: 34919048; PMCID: PMC8762589.

"Ashkarran et al.57 reported that the addition of small molecules such as glucose, triglycerides, or phosphatidylcholine to human plasma markedly altered the PC composition on polystyrene NPs. For instance, phosphatidylcholine interacted with albumin via hydrophobic interactions, hydrogen bonding, and water bridges, which consequently reduced the incorporation of albumin into the corona."*

Yu, X., Li, M., Zhou, Y., Shi, J. and Yu, W. (2026) ‘Tuning protein corona on nucleic acid nanodrugs for targeted delivery’, Acta Pharmaceutica Sinica B. doi: 10.1016/j.apsb.2026.06.007.

The demonstrated ability of lipid molecules such as triglycerides to mediate specific protein interactions provides a mechanistic rationale to consider that lipid-based nanoparticles may similarly engage lipid-responsive proteins or lipoprotein-associated factors within biological fluids.

However, Ashkarran et al. themselves highlighted a particularly striking point:

“Metabolites, lipids, vitamins, nutrition, and other types of small biomolecules present in the biological fluid can interact with proteins in these fluids and influence their behavior, including their adsorption onto NPs. For example, it was shown that the addition of glucose and cholesterol to plasma can alter the composition of protein corona on the surface of otherwise identical NPs. Small molecules can alter the protein corona of NPs, after interaction with plasma proteins, due to various mechanisms such as (i) their competition with proteins for binding to the surface of NPs; (ii) altering proteins’ binding affinities to NPs; and (iii) changing protein conformation.”

Ashkarran AA, Gharibi H, Sadeghi SA, Modaresi SM, Wang Q, Lin TJ, Yerima G, Tamadon A, Sayadi M, Jafari M, Lin Z, Ritz D, Kakhniashvili D, Guha A, Mofrad MRK, Sun L, Landry MP, Saei AA, Mahmoudi M. Small molecule modulation of protein corona for deep plasma proteome profiling. Nat Commun. 2024 Nov 7;15(1):9638. doi: 10.1038/s41467-024-53966-z. PMID: 39511193; PMCID: PMC11544298.

https://substack.com/@genervter/note/c-300057777

This consideration suggests that nanoparticle behavior is not exclusively dictated by the nanoparticle formulation itself, but may also depend on the physiological state of the host. Since endogenous metabolites and lipids can influence protein–nanoparticle interactions and reshape the protein corona, interindividual differences in metabolic status, lipid composition, or nutritional state may contribute to variability in the biological identity, biodistribution, and cellular interactions of lipid-based nanoparticles.

*Note: While these observations have thus far been reported for polystyrene nanoparticles and not for LNPs, the general phenomenon of protein corona formation suggests that LNPs may likewise bind triglyceride-rich lipoproteins. This possibility cannot currently be excluded.

Conflating distinct pathogenic mechanisms on the basis of a shared clinical endpoint is not only scientifically unjustified but may also have direct therapeutic implications. Interventions directed at a common downstream phenotype may appear clinically effective while the upstream pathogenic processes remain unaddressed or are even unintentionally exacerbated. Mechanistic understanding is therefore not an academic luxury but a prerequisite for rational, effective, and safe medical practice.