McCairn protocoll
More questions than any science. Hopium for the masses?
The temporary relief of symptoms achieved solely through purely experimental approaches offers no guarantee of good health, does not improve the chances of survival, and is nothing more than hybris and quackery if it does not meet recognized standards such as the Bradford-Hill criteria1 and/or for example HAQ2 .
More open questions than anything I’d suggest for treating:
How was it proven that apheresis triggered anything more than a temporal and/or placebo effect? (How was a sham-controlled effect size established to differentiate therapeutic apheresis from a temporal/ placebo response?)3
How was the clearance of modRNA determined following apheresis? (Lack of pharmacokinetic data regarding the removal of synthetic transcripts from systemic circulation.)
In the event of persistence, how were integrative events and/or RNA turnover, driven by cellular homeostatic effects, excluded? (Addressing the risk of genomic integration or compensatory mechanisms masking the treatment’s actual impact.)
How was the clot formation mechanistically attributed to modRNA/Spike persistence without relying on in vitro and/or experiments that lack any reliable diagnostic or predictive value (e.g. using codon optimized SpikeRNA, injecting directly Spikes into organism, using to high dosage values, and other non-clinical relevant exepriments)?
Furthermore, how was the amyloid diagnosis confirmed, and how were amyloid-like fibril structures ruled out given that ThT has a high false positive rate? 4, 5, 6, 7, 8, 9. Furthermore it has limitations in blood samples.
How was the individually dependent dosage determined, particularly concerning the administration of growth factors? (Considering the non-linear dose-response curve and the risk of biological recklessness.)
Which specific exosome formulation was utilized? (Demanding CMC, Chemistry, Manufacturing, and Controls–data: source, purity, and surface markers.)
Which specific growth factors were used10, 11, 12, 13, 14 and what specific cell-line was their recombinant or biological origin? In other terms: what is “SHED”?: It is not clear if it were Mesenchymal stem/stromal cells (Dental Pulp MSCs / SHED-MSCs), Perivascular stem cells / pericyte progenitors, Neural crest–derived stem/progenitor cells, Neural stem or neural progenitor cells, Odontoblastic progenitor cells (dentin-forming precursors)
How was the individual dose-dependency established to avoid over-stimulation of signaling pathways?
By what methodology were the exosomes tracked in vivo to confirm biodistribution and target-tissue engagement?
How were off-target effects and non-specific cellular interactions rigorously excluded?
What is the clearly defined molecular mechanism of action (MoA), including validated in vivo dose–response relationships, that substantiates causality beyond descriptive reports and in vitro experiments employing recombinant spike proteins lacking physiologically relevant dosing?
Where is the supporting multi-omics data (transcriptomics, proteomics, metabolomics, lipidomics (due to using exosomes)) to provide a quantifiable biological basis?
How were all other potential etiologies, other than the “Spike protein”, differentially excluded?
What is the exact N-number and stratification of the cohort regarding previous modRNA-LNP injections?
How was electrostatic membrane interference and receptor shifting excluded, which may lead to disturbed intra-cellular communication, as primary drivers for thrombotic events?15
How is the absence of time-shifted feedback loops or paradoxical immune responses excluded after application that could lead to long-term exacerbation? In other words, this applies to both the safety of exosomes16,17,18,19,20 and that of growth factors.21, 22, 23, 24
Without addressing dose-dependent toxicity, providing longitudinal omics data, and defining a clear hierarchy of evidence, or at least explicitly declaring the protocol as experimental, this approach remains a speculative black box that fails to meet the basic requirements of the Declaration of Helsinki.25
Summary
Assumption a): The spike protein is the driver of the clots. Monocausality. Neglect of LNP colloidal physics. Neglect of multiple confounding factors: not permitted.
Assumption b) based on a): A ThT signal is a “spike clot.”: Unproven and not validated.
Assumption c) based on a) and b): These clots cause all symptoms: unproven.
Assumption d) based on a), b), c): Apheresis permanently removes the cause: unproven.
Assumption e) based on a), b), c), d): Exosomes heal the rest without side effects: speculative.
It is a chain of correlation assumptions whose causality breaks down right from the start.
Fedak KM, Bernal A, Capshaw ZA, Gross S. Applying the Bradford Hill criteria in the 21st century: how data integration has changed causal inference in molecular epidemiology. Emerg Themes Epidemiol. 2015 Sep 30;12:14. doi: 10.1186/s12982-015-0037-4. PMID: 26425136; PMCID: PMC4589117.
Thyberg I, Dahlström Ö, Björk M, Arvidsson P, Thyberg M. Potential of the HAQ score as clinical indicator suggesting comprehensive multidisciplinary assessments: the Swedish TIRA cohort 8 years after diagnosis of RA. Clin Rheumatol. 2012;31(5):775-783. doi:10.1007/s10067-012-1937-0
Balogun RA, Sanchez AP, Klingel R, et al. Update to the ASFA guidelines on the use of therapeutic apheresis in ANCA-associated vasculitis. J Clin Apher. 2020;35(5):493-499. doi:10.1002/jca.21820
Biancalana M, Makabe K, Koide A, Koide S. Molecular mechanism of thioflavin-T binding to the surface of beta-rich peptide self-assemblies. J Mol Biol. 2009;385(4):1052-1063. doi:10.1016/j.jmb.2008.11.006
Girych M, Gorbenko G, Maliyov I, et al. Combined thioflavin T-Congo red fluorescence assay for amyloid fibril detection. Methods Appl Fluoresc. 2016;4(3):034010. Published 2016 Sep 6. doi:10.1088/2050-6120/4/3/034010
Jamali M, Mohajer S, Sheikhlary S, Ara MHM. Z-scan optical method complements the Thioflavin T assay for investigation of anti-Alzheimer’s impact of polyphenols. Photodiagnosis Photodyn Ther. 2022;39:102914. doi:10.1016/j.pdpdt.2022.102914
Hirata Y, Takemori H, Furuta K, Kamatari YO, Sawada M. Ferroptosis induces nucleolar stress as revealed by live-cell imaging using thioflavin T. Curr Res Pharmacol Drug Discov. 2024;7:100196. Published 2024 Jul 8. doi:10.1016/j.crphar.2024.100196
Kalitnik A, Lassota A, Polańska O, et al. Experimental methods for studying amyloid cross-interactions. Protein Sci. 2025;34(6):e70151. doi:10.1002/pro.70151
Burk J, Wein AN, Binkley MM, et al. Trichrome, Congo red, and thioflavin S stains are comparable for the diagnosis of amyloid deposits in endomyocardial biopsies. Cardiovasc Pathol. 2026;82:107815. doi:10.1016/j.carpath.2026.107815
Grimberg A, DiVall SA, Polychronakos C, et al. Guidelines for Growth Hormone and Insulin-Like Growth Factor-I Treatment in Children and Adolescents: Growth Hormone Deficiency, Idiopathic Short Stature, and Primary Insulin-Like Growth Factor-I Deficiency. Horm Res Paediatr. 2016;86(6):361-397. doi:10.1159/000452150
Gyawali B, Bohlke K, Dickter JK, et al. WBC Growth Factors: ASCO Guideline Update. J Clin Oncol. 2026;44(9):812-824. doi:10.1200/JCO-25-02938
Han CM, Cheng B, Wu P; writing group of growth factor guideline on behalf of Chinese Burn Association. Clinical guideline on topical growth factors for skin wounds. Burns Trauma. 2020 Sep 28;8:tkaa035. doi: 10.1093/burnst/tkaa035. PMID: 33015207; PMCID: PMC7520573.
Seger, F.; Gutschi, L. M.; Seneff, S. Lipid Nanoparticles as Active Biointerfaces: From Membrane Interaction to Systemic Dysregulation. Preprints.2025;2025110517:doi:10.20944/preprints202511.0517.v6
Yoon-Jin Kim, Sae Mi Yoo, Hwan Hee Park, Hye Jin Lim, Yu-Lee Kim, Seunghee Lee, Kwang-Won Seo, Kyung-Sun Kang." Exosomes derived from human umbilical cord blood mesenchymal stem cells stimulates rejuvenation of human skin." Biochemical and biophysical research communications. 2017 11 18;493(2);1102-1108. pii: S0006-291X(17)31817-X.
Tzng E, Bayardo N, Yang PC. Current challenges surrounding exosome treatments. Extracell Vesicle. 2023;2:100023. doi:10.1016/j.vesic.2023.100023
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Park KY. Adverse Reactions Following Intradermal Injection of Exosome-Based Formulations: A Case Series. J Cosmet Dermatol. 2025 Oct;24(10):e70520. doi: 10.1111/jocd.70520. PMID: 41097876; PMCID: PMC12528963.
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These are good questions and I'm sure Kevin and the Japanese doctors will have some of the answers already. However the context must be considered. That is, that the vaccine injured have been heinously abandoned by the governments and drug regulators leaving them to seek alternative treatments (even temporary) from other sources, often with very little funds.
The questions should be directed to the governments, regulators and pharma corporations who did this.
You are of course correct that this is treatment not cure. However over time the spikeopathy (assuming that underpins the injury) will likely eventually dissipate and removing as much of the substance as possible is rational, understanding that there are also potential deleterious risks of the procedure.
The victims should never have been put in this position.
when you read the comments under the old post of Dr. Bowden, one would indeed start asking questions, and there were many, McCairn is answering only the positive ones, the rest is silence.... He himself has serious health issue with the clotting, apparently, yet he DOES NOT show everyone that his protocol works on himself. I asked many questions in his weekly presentations, and answers were frequently arrogant, if any. If anyone saw the clots which embalmers pull out, HOW ON EARTH can you filter anything out when their volume is ~ volume of the blood vessels themselves! In terms of the dental pulp stem cells, equally a question how those ever stay healthy AFTER the gene therapy?? Since SO MANY people are dying or a sick, in those 4 months, one could expect a HUGE feedback, including Dr. Bowden. Just do not see anything....
ANyway, when you look at McCairns (british accent) CV things are getting even muddier, from Research Gate:
Okinawa Institute of Science and Technology Graduate University January 2010 - present
Okinawa, Japan
Bar Ilan University January 2007 - present
Ramat Gan, Israel
the latter collaborated with Pfizer for LONG TIME:
https://www.pfizer.com/news/press-release/press-release-detail/bar-ilan-university-work-pfizer-inc-evaluate-drug-delivery and also https://afbiu.org/news/dna-robots