I used Gemini Notebook to generate a 50-minute audio overview of this file: https://
See the clot3.
Kevin McCairn has developed a lucrative business where he tricks people into thinking that they have amyloid fibrin microclots in their blood, and then he charges people 60,000 USD to remove the clots.
The structures he typically claims are fibrin microclots are string-like fibers with a diameter around 10-30 µm. In reality they are likely to be fibers from dust, like textile fibers or paper fibers. Cellulose fibers have a diameter around 10-40 µm, including cotton fibers and paper fibers. Nylon fibers similarly have a diameter around 10-50 µm, and polyester fibers have a diameter around 10-15 µm.
Previously fibers in blood samples with a diameter around 10-30 µm have been called graphene oxide ribbons by Philippe van Welbergen, hydrogel filaments by Ana Mihalcea, Morgellons filaments by people in Arne Burkhadt's pathology conference, and fiber optic killer tubes by Shimon Yanowitz.
McCairn used to say that the fibers he saw under a microscope were amyloid fibrils, but he dropped the term fibril because I told him that the term fibril refers to nano-scale structures in biology, and amyloid fibrils have a diameter around 7-13 nm, so they are not even visible with an optical microscope.
The flat ribbon-like shape of McCairn's fibers is also consistent with textile fibers but not with fibrin. Some of his fibers have had sharp corners similar to paper folds, where you can see one part of a flat fiber folded over another part, which is consistent with synthetic textile fibers but not with fibrin.
McCairn does not determine the actual protein composition of his fibers using methods like immunostaining, spectroscopy, or proteomics. But he jumps to the conclusion that if a fiber is fluorescent under a UV light, then the fiber is made of amyloid fibrin, even if the fiber was simply autofluorescent without staining by Thioflavin T. But for example white textiles usually contain optical brightening agents which are fluorescent under UV light. The microclot researcher Resia Pretorius pointed out that white tissue paper fibers are similarly fluorescent, and she indicated that some of the fibers McCairn identified as amyloid clots looked like false positives.
McCairn tells people that when they mail him a sample of blood, they should spread out a drop of blood on a glass slide and let the blood dry overnight in a dust-free environment. But how many people have a perfectly dust-free environment at their home? He specifically tells people to not place a cover slip over the blood, so that the blood remains exposed to open air. And he doesn't tell people to check the next morning that no dust fibers fell on the blood while it was drying.
A fiber with a diameter of 15 or 30 µm couldn't even be circulating freely in human blood, because the fiber would be too big to pass through the capillaries. Capillaries typically have a diameter around 8 µm, which is barely wide enough for a red blood cell to pass through, but the fibers shown in McCairn's microscope images have often been about 2 to 4 times wider than red blood cells.
Even if the fibers with a diameter of 10-30 µm were circulating in blood, the fibers would not be removed by the plasmapheresis ciruit used at Edogawa Hospital. The first filter in the circuit is a plasma separator, which separates the plasma from the red blood cells. The separator has a pore size of 0.3 µm, which is too small for red blood cells to pass through, so the red blood cells get returned to the patient's blood without any filtering. Only components of blood that are small enough to pass through the pores get routed to the immunoadsorption column, which is the filter in the circuit that is meant to provide the therapeutic benefit. However fibers with a diameter of 10-30 µm would be far too big to pass through the pores of the plasma separator, so the fibers would simply be returned back to the patient's blood without any filtering, like what happens to the red blood cells.
The treatment provided by Edogawa Hospital is often incorrectly called double filtration plasmapheresis (DFPP), but in reality the treatment is immunoadsorption (IA), which is also known as plasma adsorption (PA) in Japan. DFPA is a nonstandard designation for IA that seems to have been invented by Edogawa Hospital. The nonstandard terminology makes the treatment provided by the hospital appear somehow unique, even though in reality DFPA refers to regular immunoadsorption treatment that is widely available even outside of Japan.
In a recent German trial of immunoadsorption as a treatment for long COVID, no significant benefit was found compared to a sham treatment, even though the trial employed the same Asahi TR-350 immunoadsorption column that is used by Edogawa Hospital.
McCairn has now started giving expensive treatment to people which supposedly removes the fibers from their blood that he initially called "amyloid fibrils", but that he started calling "fibrillar formations" after I told him he was misusing the word fibril. Now he seems to be calling them "aggregates" instead.
Earlier McCairn gave the impression that the fibers he found in blood samples were circulating freely in the bloodstream, but me and another user on his Discord pointed out that his fibers had a wider diameter than capillaries, so the fibers wouldn't be able to pass through the capillary bed. But then later I figured out that in case the fibers were lodged in the arterioles before the capillaries in the fingertips, the fibers might get released from the arterioles if you do a finger prick sample, because typically a finger prick lancet would reach deep enough to penetrate the arterioles and not only the arterial capillaries. However it's a hypothesis I came up with on my own and that McCairn didn't suggest to me (and I came up with the hypothesis because I was trying to play along with the scenario where the fibers that look like textile fibers would actually be clots made of fibrin, which I was nearly certain was not true): [https://
Earlier I asked McCairn several times if the reason why his supposed clots had a string-like shape was because the clots formed in a small blood vessel and then got dislodged, McCairn came up with explanations like that "there is a coherency in the epistemological grounding of the amyloid PRION formation". [https://
However now when he did a video with one of his first patients, McCairn said himself that the so-called "aggregates" are "lodged into the entrance and exits of capillary beds", where he even used the same verb "lodged" that I had earlier used many times to refer to the hypothetical clots that are stuck before the capillaries. He said: "So, what's the one thing that we can point at right now, which is quantitative in a ways that the aggregations in the plasma disappear? And, are they generated de-novo, or are they a consequence of initial exposure, and then just sort of building up over time? I'm still unsure. But what I can say is between the DFPP - PA session, sorry - you were in the second treatment protocol, in the pre-plasma - there was amyloid-like burden in the pre-plasma that has gone in the post. So my thinking is that there's a bulk movement of the plasma during filtration, and that's gonna drag a whole bunch of these aggregates with them. It's coming back in clean. And then if there's more that are sort of hanging on to the vasculature, they're gonna then be washed off into the plasma again, which is why we're seeing the return of them in the secondary treatment - sorry, in the second treatment. And I would say the fact that you've such a rejuvenating effect - those are the aggregates that were really lodged into the entrance and exits of capillary beds. And so, I think we're moving them, but like I'm saying, in your case it's taking longer than two weeks." [https://
But if the aggregates are lodged before the capillaries but the aggregates are too big to pass through the capillaries, then how could the aggregates be removed by the plasmapheresis treatment? And if the aggregates are lodged after the capillaries, then how do they happen to break loose at the same time when the patient undergoes the plasmapheresis treatment? Does the treatment include some mechanism that induces the aggregates to become embolized?
As of April 2026, McCairn's hardcore fan CoyoteSanctuary was still using the term "amyloid fibril" to refer to the structures McCairn sees in blood samples (or actually he used the word "fibrilla", but it is synonymous with the word "fibril"): [https://
McCairn supposedly found this fiber in the blood of one of his patients, whose username on Twitter is KenCaptn20114: [https://
If the fiber is a fibrin clot that has a string-like shape because it formed inside a blood vessel so it conformed to the shape of the blood vessel, then why is the fiber flat and not cylindrical?
This is what ChatGPT said about the fiber:
What you're seeing is almost certainly a contaminant fiber, not a biological structure from the blood itself.
A few cues from the image:
Uniform thickness along most of its length → biological filaments (like fibrin strands) tend to branch irregularly and form mesh-like networks, not long smooth ribbons.
Sharp bends/kinks → typical of synthetic or textile fibers that have been mechanically deformed.
Flat, ribbon-like morphology → very characteristic of textile fibers (e.g., cotton, rayon, or synthetic microfibers), which often appear twisted or collapsed into ribbon shapes under microscopy.
Strong fluorescence under UV → many fibers (especially synthetic ones or those treated with dyes/brighteners) fluoresce brightly, whereas native blood components usually don't show this kind of linear, high-contrast emission unless specifically stained.
Most likely candidates
Cotton fiber (common lab contaminant; appears as a flattened, twisted ribbon)
Synthetic microfiber (polyester/nylon; often smoother and more uniformly fluorescent)
Lint contamination from clothing, wipes, or lab materials
What it is not likely to be
Fibrin strand → would look more web-like and irregular
Parasite or worm → would show internal structure and biological segmentation
Cellular debris → would be more granular or amorphous
The fiber has one of these "paper fold"-style corners where you can see folded over segments of the flat fiber overlapping each other, like in the case of the fiber in the blood of Jesus4AllAlways, Mihalcea's hydrogel filament, Shimon Yanowitz's killer tube, and Philippe van Welbergen's graphene ribbon:
KenCaptn said that the treatment he got in Japan was very expensive, but he had no choice because he would've died if he didn't get the treatment: [https://
He tweeted: "This clot issue possibly could turn into the biggest problem that humanity has ever faced. Think youre safe because youre unvaxxed? Think again. There are violently ill people here that are unvaxxed in Japan covered in microclots being treated." [https://
KenCaptn also said that stem cell growth factors repair demons: [https://
He said that blood clots are "called fibril or amyloids": [https://
He claims that his life was earlier saved by Mary Talley Bowden who suggested him to double his dose of ivermectin and nattokinase: [https://
Even after he had received the plasmapheresis treatment, he still said that he is afraid to ever get off ivermectin: [https://
Now McCairn seems to have come up with a new explanation for why some of his supposed clots have a flat and not cylindrical cross-section, which is that "veins are flat and non-cylindrical": [https://
So he seems to still be saying that the shape of the clot is explained by the clot being an intravascular cast. ChatGPT said:
Short answer: generally no - a fibrin clot that detaches from a vessel does not reliably preserve the vessel's cross-sectional shape, especially not as a stable, flat "ribbon."
Fibrin networks are viscoelastic and deformable rather than rigid. Once a clot is dislodged and no longer constrained by blood flow and vessel walls, it undergoes stress relaxation, elastic recoil, and internal restructuring. As a result, it can collapse, twist, or fragment, rather than maintaining a fixed molded geometry.
Although veins can be partially collapsed or non-circular in vivo, particularly at low pressure, their lumen remains a three-dimensional, compliant structure rather than a consistently flat channel. After removal from the body, the loss of internal pressure and surrounding tissue support leads to further deformation. Additional handling and fluid forces during extraction can significantly alter the clot's shape.
There are cases where biological material approximates a lumen, such as airway casts or some post-mortem clots, but these typically appear as irregular cylindrical or branching structures. They do not present as long, uniformly flat ribbons.
A persistent flat, ribbon-like morphology is therefore more consistent with ex vivo artifact, mechanical compression, surface-interface effects, or non-fibrin material. It is not well explained by simple intravascular molding of a fibrin clot.
Overall, while a clot may transiently resemble the vessel it formed in, it does not stably retain that geometry, and a consistently flat cross-section is not what would be expected from a true intravascular fibrin clot.
When I asked RexesRule why KenCaptn's fiber was flat and not cylindrical, she didn't answer my question, but she just said that I was a troll, and that McCairn and his patients are heroes who don't deserve trolls in their threads: [https://
McCairn showed me the image below from a paper by Pretorius and Kell, where the bottom right panel appears to show a segment of a string-like clot with a diameter of about 10 µm. But it's not clear how long the structure is or if it has uniform width throughout its length, even though the width of the structure does seem to taper off suddenly towards the right side of the image. The structure doesn't look flat, but it's not clear if other parts of the structure would look more flat. The structure is also not uniformly fluorescent like some of McCairn's fibers have been: [https://
McCairn also found an Indian paper that featured a few images of structures with a string-like shape that the authors described as microclots: [https://
However the images in the Indian paper don't even have scale bars, so it's difficult to tell if the diameter of the string-like structures is consistent with textile fibers or not. And the elongated structures seem to have a more variable diameter than the fibers in McCairn's images, and they have a gel-like appearance, and they don't seem to be flat. The authors didn't describe analyzing the composition of the structures in order to determine if the structures were even clots made of fibrin. And the paper doesn't seem very credible, because it was written in broken English and published in a predatory journal for tropical medicine even though the paper was not about tropical medicine.
McCairn also found a paper from 2025 where the authors described a method for quantifying the number of microclots associated with long COVID in blood samples, which included the figure below where the top left panel shows an elongated structure with a diameter of about 20 µm: [https://
However the elongated structure above looks more cylindrical than flat, and it doesn't have any sharp corners similar to 90 degree paper folds. The structure doesn't seem have the kind of helical twists that are called convolutions in cotton, even though the image has such low quality that it's difficult to discern the shape of the clot. The structure also appears to have a fairly high degree of variability in diameter along its length, so that the diameter is tapered off towards the top of the image. And like in the case of the Indian study, the authors of the study did not describe determining if the structures in the images were actually made of fibrin, or doing any kind of filtering to remove non-fibrin structures from the blood.
Next McCairn found the figure below from a paper published in Nature where the authors quantified the amount of fibrin microclots in 84 children and young adults. Like in the case of the other papers, the authors didn't describe determining the composition of the structures to verify if they were actually clots made of fibrin. But even if the structure on the right is actually a clot made of fibrin, it doesn't look flat, it has quite a bit of variability in diameter along its length, it doesn't have sharp "paper fold"-style corners, and it doesn't have the kind of lengthwise fold running along the middle as the fiber McCairn found from Lyndsey's blood: [https://
Lyndsey House showed that her plasma was more reddish before she got McCairn's DFPP treatment and more yellowish after the treatment: [https://
When I asked what would explain the change in color, ChatGPT said:
What you're seeing actually makes physiologic sense for pre- vs post-DFPP (double filtration plasmapheresis).
A more reddish or orange plasma before DFPP typically reflects a higher concentration of circulating components that affect color and turbidity. Before DFPP, plasma contains higher levels of lipoproteins (especially LDL, VLDL, and possibly chylomicrons), immunoglobulins, and other large plasma proteins. These components can give plasma a darker, more orange or slightly reddish hue due to increased light scattering and overall density. After DFPP, many of these larger molecules are selectively removed, so the plasma appears clearer and shifts toward a more typical yellow or straw color.
Mild hemolysis can also contribute. If the pre-procedure sample has even slight red blood cell breakdown, free hemoglobin in the plasma can create a pink to reddish tint. This effect may be reduced after DFPP due to removal processes and dilutional effects. It's worth considering whether the pre sample had any handling factors that might have introduced minor hemolysis.
Plasma color is also influenced by bilirubin and concentration effects. Normal plasma is straw yellow, deeper yellow or orange can reflect higher bilirubin or increased concentration of solutes, and pink to red suggests hemolysis. After DFPP, the plasma is effectively "cleaned" and somewhat diluted, which tends to lighten its appearance.
Finally, hemoconcentration prior to the procedure can play a role. If the patient was relatively volume-depleted beforehand, plasma components would be more concentrated, contributing to a darker appearance. Fluid shifts during and after DFPP can make the post sample look lighter by comparison.
Overall, the pre-DFPP plasma appears more red or orange primarily because it contains higher levels of lipoproteins and proteins, with possible minor contributions from hemolysis or concentration effects. The post-DFPP plasma looks clearer and more yellow because those larger, color-influencing components have been reduced.
(Edited later: I was incorrectly speaking of DFPP here, even though the treatment provided at Edogawa seems to be immunoadsorption and not DFPP. But McCairn himself used to call the treatment DFPP until January 2026, so I don't know if Edogawa initially provided DFPP treatment but later switched to immunoadsorption.)
Added later: Another patient showed that her plasma was more yellowish before treatment but more reddish after treatment: [https://
Lyndsey and another one of McCairn's patients reported reduced numbness in their toes after getting the DFPP treatment, which might be an outcome of improved perfusion to the toes: [https://
I was wondering that if DFPP doesn't actually induce microclots lodged in the capillaries to break loose, then how could DFPP improve perfusion to the toes? Grok speculated that DFPP might improve perfusion by reducing the viscocity of blood:
Fibrinogen is a key high-molecular-weight plasma protein that dramatically increases viscosity (especially in low-shear microcirculation). DFPP removes 50-88% of fibrinogen per session or cumulatively (along with other contributors like IgM, α2-macroglobulin).
Lower viscosity directly increases capillary flow rate per Poiseuille's law: flow ∝ (pressure × radius⁴) / (viscosity × length). In narrow capillaries, even small viscosity drops yield large perfusion gains. This improves oxygen exchange without needing to dissolve every lodged clot. Studies on plasmapheresis in hyperviscosity syndromes confirm this: reduced plasma viscosity enhances capillary perfusion, shear-dependent vasodilation (via endothelium-derived relaxing factors), and tissue oxygenation.
Result: Better overall microcirculatory flow, even around partial obstructions, leading to the "rejuvenating effect" described in patient reviews.
A paper about HELP apheresis by Beata Jaeger et al. said: "In principle, the decreased fibrinogen concentration causes rheologically significant effects and facilitates oxygen exchange. Plasma viscosity is reduced by an average of 19%, and erythrocyte aggregability is significantly decreased by 60% (33). In addition, the vascular endothelial growth factor (VEGF) and nitric oxide (NO) release are favorably influenced (33). The improvements have also been demonstrated for cerebral blood flow in the cardiac patients, where they profit from a 63% increase in the CO2 reserve capacity (54)." [https://
The reduction in peripheral neuropathy might also be explained by a neurological and not circulatory mechanism. Plasmapheresis is employed as a treatment for chronic inflammatory demyelinating polyneuropathy (CIDP), which is an autoimmune condition that affects the myelin sheath around peripheral nerves. Plasmapheresis removes antibodies in plasma that attack the nerves, even though the effect of the treatment typically lasts for only a few weeks, so the treatment has to be repeated frequently. [https://
A paper from 2011 said: "Based on 2 Class I studies, plasmapheresis is established as effective in the short-term treatment of CIDP; both studies showed the beneficial effect is not sustained, with worsening beginning 1-5 weeks after last plasmapheresis treatment." [https://
When I asked what other explanations there might be for the reduced numbness in the toes after the DFPP treatment, Grok produced this list of 4 possible explanations:
1. Reduction in systemic inflammation and neurotoxic/inflammatory mediators (non-CIDP pathway)
DFPP removes cytokines (e.g., TNF-α), chemokines (e.g., RANTES), oxidized LDL, complement components (C3/C4), and other pro-inflammatory molecules that can directly sensitize or damage peripheral nerves or cause small-fiber neuropathy symptoms.
In patients with metabolic or non-metabolic peripheral neuropathy (including cases with environmental toxin burden), DFPP has been shown to significantly lower serum CRP, TNF-α, eosinophilic cationic protein, and fibrinogen while simultaneously removing heavy metals/pesticides - correlating with clinical sensory improvement.
Similar rapid anti-inflammatory effects are reported in autoimmune encephalitis and other neuroinflammatory states treated with DFPP, where neurological function (including sensory symptoms) improves even without classic demyelinating neuropathy.
This is a neurological (rather than purely circulatory) mechanism: the nerves themselves are less irritated or inflamed, independent of blood flow.
2. Improved rheology beyond simple viscosity (erythrocyte behavior, endothelial function, and microcirculatory dynamics)
Even without physically "breaking loose" lodged microclots, DFPP alters blood flow properties in ways that enhance capillary perfusion and tissue oxygenation:
It reduces erythrocyte aggregability/rouleaux formation (by ~60% in analogous HELP apheresis) and lowers plasma viscosity more broadly than fibrinogen removal alone. This increases shear stress on vessel walls, triggering endothelium-derived relaxing factors (nitric oxide, VEGF) that promote vasodilation.
In conditions like arteriosclerosis obliterans (ASO) or diabetic foot syndrome - where patients classically report toe numbness, coldness, and pins-and-needles - DFPP is an established therapy precisely because it improves lower-limb microcirculation and sensory symptoms via these rheological changes.
Long-COVID apheresis studies (using similar filtration) document disappearance of fibrin fibers and rouleaux on dark-field microscopy alongside symptom relief, showing flow improvement without requiring clot dissolution.
Poiseuille's law still applies, but the effect is amplified by better red-cell deformability and reduced cellular aggregation, allowing plasma to "squeeze" through partially compromised capillaries more effectively.
3. Removal of other hyperviscosity or pro-aggregatory factors (e.g., cryoglobulins, lipids, immune complexes)
DFPP is highly effective for cryoglobulinemic vasculitis or hyperviscosity syndromes, where large proteins cause sluggish flow and neuropathy; sensory symptoms (including distal paresthesias) often resolve rapidly after sessions.
Even in non-cryoglobulinemic cases, it removes oxidized lipids and immune complexes that promote endothelial dysfunction or microvascular sludging - effects documented in long-COVID cohorts and peripheral-artery-disease patients.
Grok said that blood viscosity would typically return close to a normal level in 3-6 days, fibrinogen in 2-5 days, cytokines like TNF-α and IL-6 in about 1-2 days, and oxidized LDL in 1-7 days.
(Edited later: The treatment provided at Edogawa is not actually DFPP but immunoadsorption, but the comments above are also to some extent applicable to immunoadsorption.)
The German anti-vaccine researcher NarfGb posted these comments about McCairn's treatment protocol: [https://
Sorry to say, but this sounds like voodoo without any given evidence! Treating symptoms temporarily is not healthy, offers no better survival chances, and is nothing more than voodoo medicine.
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?)
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 third-rate in vitro experiments that lack any reliable diagnostic or predictive value?
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 used, 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?
How is the absence of time-shifted feedback loops or paradoxical immune responses excluded after application that could lead to long-term exacerbation?
Without addressing dose-dependent toxicity and providing longitudinal omics-data, and a clear tier of evidence this protocol remains a speculative 'Black Box' that fails the most basic requirements of the Helsinki Declaration.
In the comment section NarfGb wrote: "There is not even any animal experiments done. But using it for people with real issues and getting paid for doing human experiments you think is a good thing?! Especially with a therapy that does not really differ from LNPs despite a little bit more biocompatible lipid composition?"
He also wrote: "Sadly: It is not even a scientific argumentation: 'BUT they look and feel great.' I feel also great smoking crack or taking steroids." And he expressed concern how McCairn did not provide numeric data to quantify the effect of his treatment, but he presented evidence like an infomercial-style image where the patient looked happier in the "after" picture than the "before" picture. [https://
NarfGb also wrote: "And in the first line I am more pissed about the fact that he sells this protocol as a mirrage cure than to say it's pure experimental and we don't know by now what we're doing. This is the part really freaks me out." I agree with his concern, and furthermore McCairn has been fearmongering about the clots to the extent that some of his followers now believe that the clots are leading to human extinction. One of his patients said that the clots might be the most important issue humanity is facing, and that everyone is dying from the clots, and that he would have died if he didn't get McCairn's treatment. The patient also speculated that the stem cell growth factors "repair demons", which makes it seem like he didn't understand the purpose of the treatment well enough to have informed consent.
NarfGb next published a second post about the McCairn's protocol. [https://
I'm not saying that abnormal, fibrinolysis-resistant clots don't exist. The fluorescence signal is reproducible. But the term "amyloid" is overinterpreted and unproven.
I replied:
I agree, and the "amyloid" terminology fuels McCairn's fearmongering about how the vaccines are causing a prion zombie apocalypse.
Two years ago Baxter Dmitry from The People's Voice published an article that said: "According to Dr. McCairn, contagious prions released by Covid jabs behind the explosion of disease around the world and explain the mechanism for phenomena including 'silent hypoxia', the formation of white fibrous clots, the sudden deaths of athletes, turbo CJD, turbo cancer, amyloidosis, and the explosion of neurological diseases." [https://
thepeoplesvoice. ]tv/ neuroscientist- contagious- prions- from- covid- jabs- are- transfecting- the- unvaccinated/
Then NarfGb told me:
You knew, that you'll find in almost every protein amyloidogenic peptide sequences?
Tzotzos S, Doig AJ. Amyloidogenic sequences in native protein structures. Protein Sci. 2010 Feb;19(2):327-48. doi: 10.1002/pro.314. PMID: 20027621; PMCID: PMC2865711.
That was the best joke for the panic narrative: using the worst sequences to sell a panic narrative and distract from the injections.
I told him that was a great point, and I hadn't explored that angle before. Grok said:
Amyloidogenic or aggregation-prone sequences (APRs) are very common across proteins. These short segments, typically 5-15 residues long and often hydrophobic with high β-sheet propensity, occur frequently in polypeptide chains. Predictive tools such as TANGO, WALTZ, and AGGRESCAN, along with large-scale proteome analyses, indicate that APRs appear on average at least once every ~50-100 amino acids in typical protein sequences. In globular proteins, roughly 15-20% of residues fall within such predicted aggregation-prone regions, though these are usually buried in the hydrophobic core or stabilized by native folding to prevent uncontrolled aggregation. [https://
www. ]nature. com/ articles/ s41467- 020- 17207- 3 Proteome-wide surveys confirm this high prevalence. In a comprehensive analysis of plant proteomes spanning 75 species and more than 2.9 million protein sequences using the WALTZ algorithm, more than half of all proteins in each proteome contained at least one predicted amyloidogenic region, with a median of around 25% of proteins after applying stricter filters. [https://
www. ] Similar patterns hold in other organisms, including bacteria and eukaryotes. Many proteins - perhaps most - harbor the potential to form amyloid-like structures under permissive conditions such as fragmentation, denaturation, high local concentration, or specific environmental stresses.mdpi. com/ 1422- 0067/ 18/ 10/ 2155
A user that promotes Miles Guo said that the CCP is using a protocol similar to the McCairn protocol but with fresh blood taken from PLA military boys: [https://
Jordan Vaughn in Alabama offers a similar services of testing for microclots as McCairn. One of his patients posted this tweet that showed a report they received from Vaughn, which said: "Micro-clots come in all shapes and sizes. You may also see long, string-like appearing objects in your pictures. These are Endothelial cast and are associated with endothelial damage and inflammation. This is a normal finding for long-COVID patients." The report included three images of elongated clots, even though none of them looked flat, and all had a fairly variable diameter, so they didn't look as much like textile fibers as some of the fibers that McCairn claims are microclots: [https://
Apheresis Center in Cyprus also offers testing for microclots associated with long COVID. The website of the center includes these images of microclots, which all have a globular and not elongated shape: [https://
Beate Jaeger provides HELP apheresis treatment for long COVID in Germany. She posted these photos of microclots, which again have a globular or blob-like shape, and not an elongated shape: [https://
However in a paper by Jaeger from 2023 panel A3 shows a very long string-like structure with roughly uniform diameter: [https://
If the scale bar is correct, then the diameter of the string-like structure is around 20-30 µm, which would be too big to pass through the capillaries. Similarly the structures in panels B1 and B2 (labeled "before treatment") would be too big to pass through the capillaries. So I don't know if the structures are some kind of contaminants and artifacts. Jaeger's group doesn't seem to have verified if the string-like structure was actually made of fibrin, but they just said that it was "hypothesized to contain misfolded fibrinogen and small microclot-like structures".
Peter McCullough scams people by selling a test for spike antibodies, and then he tells people with a high level of antibodies to buy his products in order to "detox" the spike protein, as if a high antibody level would be a sign that people have spike protein left over in their body. However in reality the presence of antibodies for the spike protein is generally a sign that immunity to COVID has been triggered by a vaccine or a natural infection. McCairn replied to a tweet about McCullough's test by saying: "Our patients show significant drops once treatment starts, and extends out for all tested patients. It's an indirect measure of the underlying pathology though." [https://
But how is it a symptom of a "pathology" if someone has antibodies for the spike protein? If McCairn's plasmapheresis treatment actually resulted in the permanent removal of spike antibodies, it might make his patients more susceptible to COVID, which would seem like a downside of the treatment. But of course the immune system will replenish the antibodies soon after the treatment. Antibodies are produced by memory B cells, which mainly reside in the lymph nodes, spleen, tonsils, and bone marrow. And even though a small part of memory B cells are circulating in blood, memory B cells that are removed from the blood still get replenished through a mechanism where the cells make copies of themselves through cell division.
One of McCairn's patients said that he was taking McCullough's Spike Detox supplements in order to reduce his level of spike protein antibodies, as if the antibodies would've somehow been harmful, or as if the anticoagulants in the Spike Detox supplements would've reduced the level of the antibodies. [https://
One of McCairn's patients posted the images below as evidence that her treatment was successful, because her blood looked more "stringy" before the treatment but more "smooth" after the treatment: [https://
Her images were turned into an infomercial-style image by the memetic warrior from naval intelligence: [https://
In June 2025 McCairn did an experiment where he mixed fibrinogen with ThT, heated it up to 42 degrees, and shook the mixture, and as a result he claimed he was able to create the fluorescent fibers below. He said that "using heat and shaking, we've managed to make the fibrinogen aggregate into an amyloidogenic form". [1:39:39] And he said: "In this instance I've been able to make fibrillar forms twisted reactive profile that looks very similar to what we're seeing in the blood. And again, what's the critical factor here? Is it the temperature? Is the Thioflavin intrinsically causing a reaction to the fibrinogen? Is the concentration of fibrinogen too high?" [1:29:43] He was surprised to find fiber-like structures that looked similar to the so-called "amyloid fibrin aggregates" he found in blood samples, even though his experiment was supposed to be the control run where he just looked at regular fibrinogen and he didn't apply any special procedure to form amyloid fibrin, like mixing in LPS or spike protein peptides with the fibrin. But he didn't rule out the possibility that the fibers were not made of fibrin, but they were just contaminants on his slide: [https://
At time 1:18:12 he said "What I've done to try to remove confounders that - fibers, dust, et cetera that could get to our preparation - so every sample that we're using here, has been passed and filtered through a - basically anything larger than a 100 micrometers would not pass the filter". But he didn't mention that dust fibers narrower than 100 µm might still pass through the filter.
He should've also repeated the experiment without the Thioflavin, so he could've seen if he found similar fibers that were autofluorescent without Thioflavin.
When I asked McCairn why the fiber in KenCaptn's blood had a flat shape, McCairn said it was because blood vessels are flat. But the fiber in the second image above also has a flat shape, even though the fiber didn't form inside a blood vessel.
In 2025 when Ian Musgrave said that the fiber in the 3-year-old's blood was cellulose and McCairn got a false positive with ThT, McCairn said that in order to eliminate false positives, "I run antibodies, use SEM/EDX, and Raman on samples". [https://
In 2012 the CDC published a study where they analyzed fibers that were said to be Morgellons filaments, but the fibers were found to be textile fibers or cellulose. For example the IR spectroscopy results of the fiber below were consistent with cellulose, but I have never seen McCairn publish similar spectroscopy results of his supposed fibrin clots: [https://
A Twitter user whose display name is "china Victims of Sinovac COVID-19 Vaccine" was inspired by McCairn to get DFPP treatment in China. But he said "DFPP is completely ineffective; everything rebounded completely after four days. What a tragedy": [https://
He also said "DFPP has left my body weakened, and it delivered zero therapeutic effect". He was confused about whether he should've gotten DFPA or DFPP, but it's likely the results of DFPA wouldn't have been much different: [https://
McCairn seems to have blamed the lack of success on getting DFPP and not DFPA or the baby tooth extracts. The Chinese guy was told by Shoujirou Katou that DFPP should be fine: [https://
Despite what McCairn said in the last tweet above, the Chinese user didn't accuse McCairn of malpractice, but only of not replying to his DM and not making clear enough if his protocol used DFPP or DFPA, and McCairn later admitted he wrong that the Chinese user hadn't sent a DM to him. [https://
Another Chinese user responded that RexesRule and CoyoteSanctuary also spoke about DFPP and not DFPA, and the Chinese user thought they were part of McCairn's marketing team: [https://
McCairn's patient mycityapartment wrote about the treatment that "I have experienced significant improvement that anticoagulants did not/could not provide". [https://
When I asked two of McCairn's patients if they had a rebound in symptoms similar to the Chinese guy, the patient mycityapartment said: "No I'm slowly improving across all symptoms including and especially neuropathy. 6 weeks from when I got home." [https://
But anyway, it was understandable for the Sinovac victims guy to mix up DFPP and DFPA, because even a promotional website about the treatment protocol says: "Edogawa Hospital's program is presented around Dual Filtration Plasmapheresis, also described as DFPP or DFPA in patient materials". [https://
A Japanese guy who did McCairn's blood test said that the elongated fluorescent structure below was in his blood. The structure is fairly short, it has a variable diameter, it doesn't look too flat, and it doesn't have sharp folds, so it might be more likely to be actually made of fibrin than the typical fibers that McCairn finds in blood samples: [https://
But McCairn still doesn't seem to be doing any procedure to determine the composition of the fluorescent structures, like immunostaining for fibrin antibodies or any kind of spectroscopy.
One of McCairn's patients from May 2026 said that he didn't notice any improvement after the plasmapheresis treatment: [https://
A few days later when he was asked about the effect of the baby tooth injections, he said: "It's subtle for me, but I definitely have been just a little bit more functional. I'm able to do a bit more before feeling sore but I still will start to feel symptoms if I push." [https://
I informed Resia Pretorius of the experiment where McCairn mixed fibrinogen with ThT, shook the mixture, and claimed to have manifested a fibrin clot in the mixture (even though the fiber in his mixture looked like a dust fiber). She then quoted my tweet and wrote: "We and others looking for fibrinaloid microclot complexes, always do analysis on fresh blood plasma samples or plasma spun and stored at -80. We do not support dried sample analysis and any shipment at room temp. One must also be careful, as tissue paper fibers can show autofluorescence. However, we cannot comment on this exact photo." [https://
Grok said: "Tissue paper fibers fluoresce under UV light primarily due to optical brighteners (also called fluorescent whitening agents or FWAs) added during manufacturing. These colorless compounds, often stilbene derivatives or distyrylbiphenyl types, absorb invisible ultraviolet radiation (typically 340-370 nm) and re-emit it as visible blue light (around 400-450 nm) through fluorescence." Similar brighteners are also used in white textiles.
Tissue paper fibers look somewhat similar to cotton fibers and other cellulose fibers: [https://
This shows toilet paper fibers: [https://
Resia Pretorius also posted these answers to replies to her tweet:
In June 2026 Mary Talley Bowden interviewed McCairn and his patient Ken Evans, whose username on Twitter is KenCaptn20114. [https://
At time 13:33 Ken Evans said: "We already know that we have spike proteins, we already know we have amyloid. We're just trying to survive. And that's the part of this whole Japan thing. I was not prepared for seeing how ill these people were. If you have a heart and you see these people, it will make you so mad that somebody is in this condition. And we all know that we had amyloids. They were stuck in all our tissues. And in my body, they were opening up in the sores. I was sneezing blood, I was coughing blood, blood in my feces, my stomach, my esophagus, liver, lungs, kidney, fibrosis, my swollen spleen, my heart. Every part of my body was absolutely devastated."
But how did he know he had "amyloids" in other tissues besides his blood? As far as I know, McCairn only tests for the presence of the amyloid fibrin clots in blood, and it wouldn't make sense for the fibrin clots to even exist in other tissues.
Ken Evans also seems to think that because he still has antibodies to the spike protein, it means that his body is full of spike protein coming from the vaccines. At time 16:58 he said that after he got McCairn's treatment, "My spike proteins went down 25%. So the treatment for me not only saved my life, but it pulled a lot of autoantibodies, out misfolding proteins, spike proteins, and all of those blood clots." So he seemed to think the reason why his level of spike protein antibodies was reduced by 25% was because he still had spike protein from the vaccines circulating in his blood which was removed by McCairn's treatment, which doesn't make any sense.
At time 47:49 Bowden asked: "And just to be clear, normally in a normal blood you would not see anything lighting up at all?" Then McCairn showed the image below and said: "I mean you can see something. So look, if you look at that image that's on the screen, you can see smaller - like tiny microdots - that cluster around the image. Every sample will have that - because as the protein dries and desiccates on the slide, and there are some proteins and molecular species that are just fluorescent in and of themselves - but the size differential is what makes them different, okay. The fibrin causes large amyloidogenic twisting structures." Earlier McCairn has given the impression that the smaller fluorescent blobs are also be made of "amyloid fibrin", but now he seemed to suggest that the small blobs are not necessarily made of fibrin, but a characteristic of fibrin aggregates would be a large size or a twisting shape.
At time 1:26:04 Ken said: "People that are taking the vaccine is safe trail are ignoring Pfizer's own statistics. They admitted their vaccine didn't work. They admitted that it killed 82% of the pregnant women in studies."
But he misunderstood a set of preliminary data from the CDC's V-safe study, where at a time when almost no participants had yet completed a full-term pregnancy and only about 4% of pregnancies had completed, 104 out of 127 completed pregnancies had ended in a miscarriage (and not in the death of the pregnant woman). Later after more pregnancies had completed, the ratio of miscarriages divided by completed pregnancies dropped to about 13%. [https://
Now even Jane Ruby seems to think that RexesRule is being paid by McCairn to promote his treatment. Jane Ruby also asked "where are the empirical studies to show the validated instruments measuring the before and after of whatever they are filtering off", which is a very reasonable question. [https://
The plasmapheresis treatment is provided by Shoujirou Katou (加藤正二郎), who is the director of Edogawa Hospital in Tokyo. He also organized a conference at the hospital where the speakers consisted of Japanese anti-vaxxers and alternative medical practicioners: [https://
Katou's pinned tweet says in Japanese that the COVID vaccine is "extremely harmful and useless": [https://
The reason why Katou became the director of the hospital is not necessarily because of medical competency, but because the hospital was founded by his great-great-grandfather. In Japan it's common for the directorship of a hospital to be passed down from father to son. The previous director of the hospital was Katou's older brother.
One of McCairn's patients wrote: "Japan has the highest per capita mRNA vaccination rate in the world! According to Dr. Kato, 3.M Japanese died in the year following the initial rollout." [https://
The estimate of 3.89 million deaths was calculated based on a set of FOI data which included about 4% of the Japanese population, and which had about 150,000 deaths within a year from any vaccine dose, so the number of deaths was then multiplied by 25.8 to estimate the number of deaths in the whole Japan. [https://
In the years 2021-2024, there were likely about 6 million Japanese people who died within a year from eating rice. But that doesn't mean that 6 million people were killed by rice. In the same way the FOI data doesn't show that 3.89 million people were killed by vaccines, but it rather shows that vaccinated people had lower ASMR than unvaccinated people.
Now there's another cat lady who has started to say that McCairn is a hero who deserves a Nobel Prize. She made an AI-generated video where McCairn performs what looks like psychic surgery to "cast out amyloids": [https://
Someone who is going to Japan to get McCairn's treatment posted the image below of a fiber in his blood. If McCairn's scale bar is correct, then the fiber has a diameter of about 10 µm. The fiber has a fairly uniform diameter which doesn't seem like a characteristic of a fibrin clot, but the fiber has the kind of a flat cupped body that is characteristic of cotton: [https://
McCairn now claims that he is finding hydrogel in blood samples: [https://
In 2023 Ana Mihalcea similarly said that she found hydrogel in vaccinated blood, and that the hydrogel was developing into calamari clots: [https://
McCairn is just rehashing old scams by Mihalcea. She also presented spectroscopy results of Hirschman's clots long before McCairn, and in 2022 she already portrayed a dust fiber in a blood sample as a mini version of a calamari clot. McCairn has been making fun of Mihalcea for a long time, and he calls her the "35,000-year-old cacodemon worshipper" because she is a member of a cult whose leader claims to channel a 35,000-year-old Lemurian ascended master. But now McCairn himself is following in Mihalcea's footsteps, and he is trying to make people afraid of scary hydrogel formations in their blood.
The story about the calamari clots was broken by Jane Ruby in January 2022. At the time her show was part of the Stew Peters Network, which about four months earlier broke Carrie Madej's story that vaccines contained hydras. Carrie Madej also said that vaccinated people were growing blood clots that were made up of hydras. In her debut video in July 2020, she said that COVID vaccines were going to contain DARPA hydrogel, which she said was a transhuman technology that would turn humans into cyborgs and hook up the human brain to the cloud. So long before she first presented the narrative about hydras, she was one of the primary people who helped popularize the narrative about DARPA hydrogel. I believe the earliest person in alt media who started to say that COVID vaccines were going to contain DARPA hydrogel was Celeste Solum, who was already doing videos about DARPA hydrogel in March 2020, but she also said that COVID vaccines contained gorilla feces and neanderthal DNA: [https://
In July 2026 McCairn and some of his patients did a video with Mary Talley Bowden. [https://
At time 1:25:55, McCairn's patient Ken Evans said: "If people are listening, and they have symptoms like brain fog, massive headaches, neck aches, fatigue, shortness of breath, your vision - double vision, blurry vision - you get really dizzy, you can't stand up, your heart starts to race, or it starts to plummet, you get skin rashes, or bleeding, weird stomach issues, you're confused, you forget things a lot, you're - 'Oops, where was I?' - 'Oops, I just passed my exit while I'm driving' - severe muscle pain. These are all signs of microclots in your blood." And then he said people who have those symptoms should get their blood tested by McCairn (which will likely lead to McCairn finding microclots in the blood, and then suggesting people to get his 60,000 USD treatment).
Ken might have just as well listed the same litany of symptoms and then said they are a sign that you have Body Thetans, and the way to get rid of the Body Thetans is to pay 60,000 USD in auditing fees to McCairn. The list of symptoms Ken produced was so generic that just about everyone experiences nonzero of those symptoms to some extent. But I think neither McCairn or Ken can know if the symptoms have anything to do with microclots. And even if the plasmapheresis treatment would provide temporary relief to the symptoms, it doesn't necessarily have anything to do with removing microclots from the blood.
Scientologists believe that humans are possessed by disembodied souls of aliens called Body Thetans, and that symptoms of having Body Thetans include physical tightness or pressure in specific parts of the body, negative emotions like unhappiness, fear, or anger, or unexplained ailments, persistent fatigue, or cloudiness of thought. [https://
Ana Mihalcea wrote that the symptoms of Morgellons disease have a lot of overlap with the symptoms of COVID vaccine injury and long COVID. She wrote: "There is a huge overlap between C19 vaccine injury, shedding and long Covid symptoms with the suffering of Morgellon's victims. In particular, chronic fatigue, brain fog, shortness of breath with mucus production, anxiety, blurry vision, ringing in ears, headaches, circulatory problems and palpitations, joint stiffness, digestive problems, strange sensations under the skin and more - all have significant overlap." [https://
Some lady on Twitter posted the image below, posted a link to her GiveSendGo page, and wrote: "The first picture is an amyloid macro clot (next size up from a micro clot) that Dr. McCairn found in my husband's blood sample. Just like my husband, my son and I (second picture) were told we also have severe micro clots. We need to get to Japan for relief and treatment with the McCairn Edogawa protocol - Dual Filtration Plasmapheresis (DFPP) and Stem Cell Growth Factors (SGF). These are some of our symptoms collectively: headaches, fatigue, trouble exercising, stomach cramps, nausea, chronic on/off vomiting, heart pounding, neuropathy, feeling hot/cold, bladder issues, eye and ear inflammation, AFib, sleeping problems, severe depression, brain fog, anxiety, memory issues, mast cell, and cytokine storm. Please share, pray, and give. Thank you!" [https://
Just about anyone experiences the symptoms she listed to some extent, but McCairn seems to have convinced her that she now needs to get his expensive treatment because of the symptoms.
Resia Pretorius said that the image above "does not look like microclot complexes": [https://
She said the image doesn't have a scale bar, but I guess she missed the scale bar in the top left corner (or maybe she was confused by how McCairn used micromolars and not micrometers as the units of his scale bar).
But anyway, I'm not sure if McCairn screwed up his scale bar yet again, because based on the size of both the fibers and the small green blobs, the image looks like it might be taken at around 5 times lower magnification than indicated by the scale bar. Based on the 50 µm scale bar, the small green blobs in the image would be only about 1 µm wide, even though in McCairn's other microscope images, similar green blobs have been about 5 µm wide (even though I'm not sure what the blobs are supposed to be, or if different images feature different types of blobs).
If the scale bar is actually around 250 µm and not 50 µm wide, then the diameter of the spaghetti-like fibers would fall around the typical range of 10-30 µm. But if the scale bar is actually only about 50 µm wide, then the fibers would be much narrower than typically (even though they would match the diameter of microfibers used in cleaning products, which have a diameter around 3-5 µm).
Resia Pretorius also posted these tweets about McCairn's protocol: [https://
Allen Green is an associate medical director of a plasma apheresis center. He posted these tweets about McCairn's treatment protocol: [https://
Allen Green said that "DFPA is not a thing". When I googled for "dual filtration plasma apheresis" in double quotes, there were only 7 pages of results, which all appeared to be about McCairn's protocol.
There's an RCT of therapeutic plasma exchange as a treatment for long COVID, which found no significant difference between the treatment group and placebo group. [https://
In June 2026, The Lancet published a paper about a German RCT of immunoadsorption as a treatment for long COVID. The trial empolyed the same Asahi TR-350 immunoadsorption column that is used by the McCairn-Edogawa protocol. After 5 cycles of treatment given over the course of a single week, no significant benefit was found compared to a sham treatment (even though there were only 20 patients per arm, so the lack of significance may have been due to a small number of patients): [https://
Background
Post-Covid syndrome is a debilitating condition which may be caused and/or aggravated by autoantibodies. The current study aimed to determine whether autoantibody depletion by immunoadsorption is effective to reduce the symptom burden of patients with post-Covid syndrome.
Methods
IAMPOCO was a randomised, patient-blinded, sham-controlled crossover trial of immunoadsorption with tryptophan adsorbers versus sham treatment in patients with post-Covid syndrome at a tertiary academic care centre. The primary outcome was the difference in change in symptom severity before and after the respective therapies. Secondary outcomes included treatment safety, prevalence of autoantibodies against G protein-coupled receptors (adrenergic and muscarinergic receptors), and the influence of treatment on autoantibody levels.
Findings
40 patients with post-Covid syndrome and a symptom severity of at least 2 on the Post-Covid-19 Functional Scale were included and randomised to a treatment sequence. There was no difference in change in symptom severity between immunoadsorption and sham; odds ratio in Post-Covid-19 Functional Scale, OR = 1.17 (95% CI, 0.41-3.36; p = 0.771), mean difference in MFI-20 2.4 (95% CI, -3.7-8.5; p = 0.437), in CFS 0.09 (95% CI, -4.5 to 4.7; p = 0.970), in Bell-Scale -2.6 (95% CI, -6.9 to 1.8; p = 0.246), in MoCA score -0.01 (95% CI, -1.2 to 1.1, p = 0.993) and in Handgrip-strength deviation from individual normal value 1.3 (-0.83 to 3.5, p = 0.234). 34 adverse events occurred, 10 during or after sham treatment and 24 during or after immunoadsorption. Autoantibodies against G protein-coupled receptors were depleted by immunoadsorption but not sham treatment.
Interpretation
Immunoadsorption was not effective in reducing symptom burden in post-Covid syndrome.
Earlier when the Sinovac victims guy got DFPP in China but he said the treatment was ineffective, McCairn blamed it on the treatment being DFPP and not DFPA. It's not clear if DFPA is supposed to mean regular immunoadsorption, or if DFPA means DFPP combined with immunoadsorption. But in either case, the German trial suggests that the TR-350 immunoadsorption column is not necessarily effective in treating long COVID.
A placebo effect was evident in some patients who received a sham treatment in the German study, because the study said: "On the other hand, both of the 2 subjects that left the study after their initial sham treatment reported an improvement and stated that they did not want to risk receiving what they mistakenly thought would be sham treatment in the second cycle (when they would have been treated with true immunoadsorption)."
One of McCairn's patients described the treatment protocol like this: "My blood is drawn out through a catheter in my neck. The plasma is separated from my blood cells and run through a column called the IMMUSORBA TR-350, made by Asahi Kasei Medical in Japan. Inside that column, the pathological antibodies and immune complexes circulating in my blood bind directly to the column material and are captured. My own cleaned plasma is then returned to my body." [https://
She also posted this circuit diagram for IMMUSORBA TR-350, which includes the plasma separator (that is common to both DFPP and immunoadsorption) and an immunoadsorption column, but the diagram is missing the plasma fractionator that acts as the second filter in DFPP: [https://
"Plasma adsorption" seems to be an alternate term for immunoadsorption that is mainly used in Japan. The Japanse manufacturer Asahi's website speaks of plasma adsorption interchangeably with immunoadsorption: [https://
The setup shown in the video by McCairn's patient corresponds to the bottom left immunoadsorption setup here, and not to the DFPP setups on the top row:
I asked Shoujirou Katou on Twitter if what he calls DFPA is some kind of a hybrid between DFPP and IA, or if DFPA is just a nonstandard term for regular IA, but he didn't answer me. [https://
Grok said:
Immunoadsorption (IA) and Plasma Adsorption (PA) are very closely related and often used interchangeably. On Asahi Kasei's official site, they are grouped together as one modality: "Immunoadsorption (IA) / Plasma Adsorption (PA)". The main technique involves separating plasma and then running it through a selective adsorption column (such as the IMMUSORBA TR-350 tryptophan column) that binds specific pathogenic substances like antibodies and immune complexes. The cleaned plasma is then returned to the patient. This is distinct from Double Filtration Plasmapheresis (DFPP), which relies on two membrane filters for size-based separation rather than chemical adsorption. In the context of Edogawa Hospital, the treatment using the TR-350 column is referred to as Plasma Adsorption, and they brand the overall approach as DFPA.
The term "Plasma Adsorption" (PA) is used mainly by Asahi Kasei and in Japanese apheresis literature, though it is not entirely exclusive to them. Asahi Kasei officially lists it alongside immunoadsorption as one of the three main plasmapheresis modalities. In Japan it is a standard clinical term for column-based selective plasma purification. Internationally the term appears in some literature, but Western sources more commonly use "immunoadsorption" or "selective plasma adsorption." When you see "plasma adsorption" mentioned in relation to Edogawa Hospital or the McCairn protocol, it specifically refers to their use of Asahi's IMMUSORBA columns. Overall, it describes essentially the same column-based technique as immunoadsorption, with naming varying by region and manufacturer.
Allen Green pointed out that the term DFPA (dual filtration plasma apheresis) is a misnomer, because it implies the use of a second filter like in DFPP, even though the TR-350 column used at Edogawa is an adsorption column and not a filter: [https://
Asahi's PLASMAFLO plasma separators have a maximum pore size of 0.3 µm, so microclots that are too big to pass through the pores don't pass to the immunoadsorption column, but the clots are rather returned to the patient along with the red blood cells, so that the clots never get filtered. [https://
[Patient Blood] ──> [PLASMAFLO OP Filter (0. 3 µm)] │ │ ▼ (Through Pore) ▼ (Main Path) [Isolated Plasma] [Cell- Rich Blood] (No Microclots) (Contains 10- 30 µm Clots) │ │ ▼ │ [IMMUSORBA TR- 350] │ (Binds Antibodies) │ │ │ ▼ ▼ [Cleaned Plasma] ─────> [Recombined Blood] ──> [Return to Patient]
Asahi's brochure for their PLASMAFLO plasma separators shows that platelets are too big to pass through the pores, but platelets typically have a diameter around 1-4 µm: [https://
McCairn said that the IMMUSORBA column "seems particularly effective at clearing amyloidogenic fibrin". When Allen Green pointed out that the microclots are too big to pass through the pores to the IMMUSORBA column, McCairn said that was why there were two filters. So McCairn doesn't seem to understand that the microclots don't pass through the plasma separator filter, so the clots are never routed to the TR-350 column (which is not even a filter but an adsorption column): [https://
McCairn responded by saying there was a size exclusion mesh after the IA column, because he didn't seem to understand that the microclots don't get passed to the IA column in the first place: [https://
Then McCairn said that after the plasma is combined with the cell-rich-blood, there's a mesh filter before the combined blood is returned to the patient, but he didn't seem to realize that the holes in the mesh were far too large to filter out microclots: [https://
Google AI said this about the "venous line air trap mesh filter" that is located after the spot where the plasma gets combined with the cell-rich blood:
In an Asahi Kasei Medical apheresis circuit, the standard inline venous line blood chamber uses a mesh filter with a hole size typically ranging from 150 µm to 200 µm (micrometers).
The primary purpose of this standard blood mesh filter is to act as a gross macro-aggregate trap right before the blood safely returns to the patient's body.
Purpose of the Mesh Filter Holes
Traps Macro-Clots: It catches any blood clots, fibrin strands, or large particulate matter that may have formed due to blood pooling or surface activation within the extracorporeal tubing.
Catching Persistent Microbubbles: The mesh surface tensions help disrupt and break down macro-air bubbles, assisting the main bubble catcher chamber.
Low Fluid Resistance: Because whole blood cells (red blood cells are roughly 7 to 8 μm) must pass through this stage after recombining with the plasma, a large 150 to 200 μm opening ensures zero resistance, zero clotting of normal blood cells, and stable venous pressures.
So if we assume the microclots have a diameter between 1 and 100 µm, then the clots are too big to pass through the 0.3 µm pores in the plasma separator, so the clots never pass through the "size exclusion return mesh" that is located behind the immunoadsorption column but before the spot where the plasma gets combined with cell-rich blood. The "air trap mesh filter" is located after the spot where the plasma gets combined with cell-rich blood, but the pore size of the filter is around 150-200 µm, which is too large for the microclots to get trapped. So none of the three filters ends up removing the microclots from the patient's blood.
Now after McCairn had been made aware of a fatal flaw in his protocol, he didn't acknowledge the flaw, but he tried to change the topic by claiming that his protocol still reduces clots in the blood, because he showed the photo below and wrote: "And here just for you, pre-treatment hyper-coagulable plasma (LHS), note the large fibrin clot down the side of the tube, and post treatment (RHS)." [https://
But Allen Green pointed out that it's normal for plasma to form clots in a test tube: [https://
McCairn said that the plasma on the right side was taken out of the apheresis circuit, but Allen Green pointed out that anticoagulants are added to blood to prevent clotting in the apheresis circuit: [https://
Allen Green also pointed out that IA treatment is designed to not remove too much fibrinogen, because it would increase bleeding risk, and the level of fibrinogen recovers after about 2-3 days anyway: [https://
There's two studies where IA treatment using TR-350 reduced the fibrinogen level in blood by about 60-70%. [https://
One of McCairn's patients said that while she was undergoing the treatment in Tokyo, a clot formed in the tubes of the plasmapheresis machine, and she said: "This is why the treatment is necessary for me. The clot could have migrated to vital organs like the heart, brain, or lungs, but fortunately, it was caught in time." But Markus and Allen Green pointed out that it's normal for clots to form in the tubes of a plasmapheresis circuit: [https://
One of McCairn's patients now said: "During DFPA #2 on 7/28 a small injury occurred to my right lung leading to a pneumothorax." [https://
Another one of McCairn's patients was asking for donations so the patient with a collapsed lung could undergo a full 4-week treatment instead of only a 2-week treatment: [https://
When the patient whose lung collapsed during the second treatment had undergone a single treatment, she said on GoFundMe: "Many of you have asked if I'm feeling better. The honest answer is...it's still too early to know." So she doesn't seem to have experienced a miracle cure like was reported by some of McCairn's early patients. But she was still enthusiastically asking for donations so she could continue the treatment for the full 4 weeks: [https://
After she had undergone two treatments, she said: "I hoped for some tiny improvement but have had little and a complication. I want to continue care which is usually 4 treatments." [https://
The patient with a collapsed lung said that she was part of a "clinical trial" in Japan, so someone on Twitter was wondering why the patient was raising money if she was part of a clinical trial, because clinical trials should normally be free: [https://
However another one of McCairn's patients responded: "Nobody is hiding the fact that it's an experimental research protocol. If someone casually used the words 'clinical trial' in a social media post, that doesn't suddenly change what it is." [https://
McCairn has had about 50 patients so far, but at least two of them have had a severe adverse event during the treatment, because earlier Lyndsey House experienced a hypovolemic shock during the treatment. So that's a rate of around one severe adverse event per 25 patients, or possibly even more in case other patients have also experienced a severe adverse event that was not publicized.
When the Twitter user Markus told McCairn that the German trial failed to find a significant benefit for immunoadsorption, McCairn said it was because the patients of the trial were not injected with the baby tooth extracts, and because not all patients had the catheter hooked up to the jugular vein.
McCairn has been saying that the reason why his plasmapheresis machine is hooked up to the jugular vein is because it somehow improves the removal of toxins from the brain. His explanation doesn't make sense, because even if some toxins happened to be released from the brain to the jugular vein at the time of the treatment, they would next move to the heart, then to some random artery, and then back from another vein, so the toxins could just as well be removed by hooking up the catheter to some other vein.
Markus also told McCairn that his explanation makes no sense, and a jugular catheter is commonly used in plasmapheresis but not for the purpose of removing toxins from the brain: [https://
Google AI said:
An internal jugular central venous catheter is used in plasmapheresis primarily to provide the exceptionally high blood flow rates and mechanical stability required by apheresis machines.
While peripheral veins (arms) are preferred whenever possible, many patients require a jugular central line due to poor vein quality or the need for multi-day treatments.
The specific reasons a jugular catheter is selected for this procedure include:
High Flow Rates and Pressure Resistance
Prevents vein collapse: Plasmapheresis pumps pull blood out of the body at high velocities, creating intense negative pressure. Small peripheral veins would collapse, whereas the large internal jugular vein can easily handle the vacuum.
Accommodates large-bore tubing: The procedure requires stiff-bodied, dual-lumen, large-bore catheters (often called Shaldon lines or VasCaths) to draw and return blood simultaneously.
Anatomical and Safety Advantages
Straight path to the heart: The right internal jugular vein offers a direct, vertical path straight down into the superior vena cava. This minimizes the risk of the catheter kinking or hitting vessel walls, ensuring smooth blood flow.
Lower risk of stenosis: Compared to a subclavian vein catheter (in the chest), jugular catheters carry a significantly lower risk of causing long-term vein narrowing (stenosis) or thrombosis.
Lower risk of infection: Jugular lines have a lower incidence of infection and lower complication rates compared to femoral vein catheters (placed in the groin).
Patient comfort: A neck catheter allows the patient to keep their arms free and moving during multi-hour, multi-session treatments, which is impossible with large needles in both arm bends.
It's not clear if the majority or minority of patients in the German trial had the catheter connected to the internal jugular vein. In a description of the clinical trial that was written before the trial was conducted, a section about the sham apheresis treatment said: "In some patients, adequate blood flow can be achieved by cannulation of peripheral veins. However, in most patients, placement of a Shaldon catheter into the internal jugular vein is necessary. Shaldon catheter placement carries other potential risks such as injury to the lung resulting in pneumothorax or mispuncture of the carotid artery. However, since the catheter placement is sonography-guided, the risks for such adverse events are minimized." [https://
In a Japanese tweet from August 2026, the plasmapheresis treatment provided by Edogawa Hospital was now described as PA (plasma adsorption) and not DFPA (double filtration plasma adsorption). I don't know if it's because I tagged the director of the hospital in a Twitter thread where we discussed how the nonstandard term DFPA was confusing, or if in Japan the term PA has been used interchangeably with the term DFPA even earlier (even though the term PA is almost never used in English-language discussions of the Edogawa protocol): [https://
On this sheet of paper shown by one of McCairn's patients, the treatment was also called PA and not DFPA: [https://
Allen Green pointed out that unlike IA and DFPP, therapeutic plasma exchange might actually remove microclots from the blood. Then someone posted a photo of plasma in a tube and said: "You can see the amyloid hydrogel from DFPA in this picture. Why would anyone want albumin? It could be tainted with someone else's spike protein and who knows what else if someone got a dangerous shot lot. I'm unvaxxed. No way!" But Green said the albumin would not contain spike protein, and the photo did not show amyloid hydrogel: [https://
In plasmapheresis, the plasma is separated from the cellular fraction either by using a centrifuge or a membrane filter. In the case of both TPE and IA, centrifugation is more common in the United States but a membrane filter is more common in Japan.
The plasma fraction is discarded in TPE, so in TPE the centrifugation would remove the microclots if the clots remain suspended in the plasma fraction, but not if the clots get spun out into the cellular fraction. But it's not clear if the clots would consistently remain suspended in the plasma fraction or not.
ChatGPT said that smaller fibrin microclots might be more likely to end up in the plasma fraction but larger clots in the cellular fraction, and that high-fibrin clots might be more likely to end up in the plasma fraction but low-fibrin clots might be more likely to end up in the cellular fraction:
In centrifugal TPE (e.g. Spectra Optia, COBE Spectra, COM.TEC), red blood cells (density ≈1.09-1.11 g/mL) sediment to the outside of the centrifuge, the buffy coat (white blood cells and platelets) forms the middle layer, and plasma (density ≈1.025 g/mL) remains closest to the center and is collected.
A fibrin microclot is primarily composed of protein (fibrin density around 1.3-1.4 g/mL), but it is also highly hydrated, so its effective density is only modestly greater than plasma. Its behavior during centrifugation depends largely on its size and composition. Small fibrin microclots (tens of micrometers or less) are likely to remain suspended in the plasma layer and be removed with the plasma. Larger fibrin-rich aggregates containing trapped erythrocytes or platelets are more likely to sediment toward the cellular layers and remain with the blood cells.
In membrane filtration TPE, plasma passes through membrane pores while cells are retained. Fibrin microclots that are smaller than the pore size may enter the plasma fraction, whereas larger aggregates may be retained on the membrane or contribute to filter fouling.
Most intravascular fibrin microthrombi are not composed of pure fibrin. They often contain platelets, red blood cells, leukocytes, von Willebrand factor, extracellular DNA, and other plasma proteins. These additional components increase their size and alter their sedimentation behavior.
If the aggregates are sufficiently large or contain many red blood cells, they are more likely to partition with the cellular fraction during centrifugation. Conversely, small fibrin-rich aggregates with little cellular material are more likely to remain in the plasma fraction.
Therefore, if the question is whether TPE removes circulating fibrin microclots, the expectation is that small fibrin-rich aggregates would largely be removed with the discarded plasma, whereas larger or cell-rich thrombi may partition partly into the cellular fraction and be returned to the patient.
To my knowledge, there are very few published studies that have directly measured the partitioning of fibrin microclots during centrifugal TPE, so this conclusion is based primarily on the physical principles of density and particle size rather than direct experimental evidence.
Grok said fibrin-rich microclots would end up in the plasma fraction, and in fact when Pretorius and Kell test for microclots in plasma, they use centrifugation to separate the plasma and microclots from the cellular fraction:
In standard blood centrifugation used for therapeutic plasma exchange (TPE/plasmapheresis) or laboratory preparation of platelet-poor plasma (PPP), fibrin-rich (amyloid/fibrinaloid) microclots remain in the plasma supernatant rather than sedimenting into the cellular pellet (RBCs, WBCs, and platelets).
These microclots are routinely detected and quantified in PPP prepared by centrifugation (commonly ~3,000 x g for ~15 minutes). Researchers such as Pretorius, Kell, and others isolate PPP this way and then visualize the microclots (via thioflavin T or similar stains, fluorescence microscopy, or imaging flow cytometry). Higher-force centrifugation of the plasma itself (e.g., ~20,000 x g) can later pellet them for proteomic analysis, confirming they stay suspended under the milder forces that separate cells from plasma. [https://
pmc. ]ncbi. nlm. nih. gov/ articles/ PMC11131067/ They are typically 1-200 um in size (median often around ~15 um). Although this overlaps with cellular dimensions, their density, structure, and composition mean they do not reliably co-sediment with the cellular fraction under the conditions used for plasma separation in TPE or PPP preparation. [https://
www. ] In TPE, the separated plasma (containing soluble proteins, inflammatory mediators, autoantibodies, fibrinogen-related factors, and these microclots) is removed and replaced with albumin or donor plasma, while the cellular components are returned to the patient. This is one reason TPE has been explored experimentally for conditions associated with circulating microclots (e.g., Long COVID research contexts).frontiersin. org/ journals/ bioengineering- and- biotechnology/ articles/ 10. 3389/ fbioe. 2025. 1604447/ full
Allen Green said: "The median microclot is supposed to be around 20 microns. I'd suspect many at that size would remain in the plasma during centrifugation, but would want to see literature to confirm." [https://
Allen Green wrote: [https://
We know that plasma contains pro-aging, pro-inflammatory factors that accumulate over time and contribute to biological aging. Some of these have been identified: certain inflammatory cytokines, immune complexes, dysfunctional proteins. But the full catalog is unknown. We know these factors exist and that they matter not because we have mapped all of them, but because when we remove plasma broadly and replace it, without knowing exactly what we removed, tissues rejuvenate.
The animal evidence for this is striking. Heterochronic parabiosis experiments, in which the circulatory systems of old and young mice are surgically joined, demonstrated as early as 2005 that old tissue can be rejuvenated by exposure to a younger blood environment. For years the assumption was that young blood contained beneficial factors. But a landmark 2020 study published in Aging (Mehdipour et al.) overturned that interpretation. The researchers performed neutral blood exchanges on old mice, replacing their plasma not with young blood but simply with saline and albumin. A single exchange rejuvenated muscle, brain, and liver, tissues derived from all three embryonic germ layers. Pro-aging protein signatures decreased, pro-regenerative ones increased, and the benefits were comparable to what parabiosis had achieved. The implication was clear: you do not need to add anything from young blood. You need to remove what has accumulated in old blood. This is, in effect, the animal model of therapeutic plasma exchange.
The clinical translation followed. Dr. Kiprov's group demonstrated in the 2022 GeroScience study (Kim et al.) that old plasma dilution reduced measurable biological age in human patients. The 2025 Aging Cell study (Fuentealba et al.), also from Dr. Kiprov's research program, extended this finding using 35 epigenetic clocks, showing that TPE combined with IVIG produced an average reduction in biological age of approximately 2.61 years. These benefits emerged from broad, non-selective removal, not from targeting specific known molecules.
I believe Beate Jaeger was the pioneer of trying to use plasmapheresis to remove the fibrinaloid clots described by Pretorius and Kell. But Jaeger's HELP apheresis treatment seems to use a membrane filter and not a centrifuge.
One of her papers says "During HELP apheresis, blood cells are first separated from plasma in the extracorporeal circuit", and the paper says that she uses B. Braun's HELP system. [https://
B. Braun's H.E.L.P system is Plasmat Futura, which uses Haemoselect plasma filters that have a pore size of either 0.5 µm or 0.7 µm. B. Braun's website says: "The Haemoselect 0.5 / 0.7 plasma filter with a hollow fiber consisting of polyethersulfon is an integral part of the HELP apheresis treatment unit, and is used for plasma separation in HELP apheresis on the Plasmat Futura machine." [https://
Grok said:
Beate Jaeger's HELP apheresis treatments rely on the commercial B. Braun Plasmat Futura system. In this setup, whole blood first passes through the Haemoselect membrane plasma filter, which separates plasma from the cellular components before any further processing occurs. Manufacturer specifications list the pore size of this Haemoselect filter as 0.5 to 0.7 micrometres. The separated plasma is then mixed with high-dose heparin and acetate buffer to lower its pH, causing fibrinogen, LDL, VLDL and related complexes to precipitate; those solid precipitates are subsequently trapped in a downstream precipitation filter, which is the source of the visible white or yellow gel-like material observed after treatment.
Fibrin-rich amyloid microclots reported in Long COVID research typically measure between 1 and 200 micrometres, with a median size often around 15 micrometres. Because these dimensions are substantially larger than the 0.5-0.7 micrometre pores of the Haemoselect membrane, the intact microclots cannot cross into the plasma stream. Instead they remain on the cellular side of the filter and are returned to the patient together with the red cells, white cells and platelets.
Grok said:
No published quantitative before-and-after comparison of microclot burden from the Jaeger / Pretorius collaboration (or closely related group papers) has been identified.
Jaeger's main case series on HELP for Long COVID (the 2023 Gavin Publishers paper and related 2022 theoretical paper) reports:
- Clinical symptom improvement in most patients
- Reductions in fibrinogen and certain coagulation factors measured before and after sessions
However, these publications do not include systematic pre- and post-treatment quantification of microclot load using the methods Pretorius's group typically employs (thioflavin T / fluorescence microscopy, clot scoring/grading, imaging flow cytometry, or similar).
Pretorius's team collaborated with Jaeger starting around late 2021 specifically to evaluate whether HELP could address the microclots they had described, and they developed grading systems for microclots and platelets. Despite this, no peer-reviewed paper from the group presenting paired before-and-after microclot burden data after HELP treatment appears to have been published.
One of Beate Jaeger's papers said: "Additionally, HELP apheresis has been found to remove circulating fibrinolysis-resistant microclots [18,19]." [https://
When I asked if other groups had measured microclot burden before and after apheresis treatment, Grok said:
Here are sources for the later clinic or independent reports that claim reductions in microclot-related measures after apheresis (distinct from the original Jaeger-Pretorius collaborative publications):
1. Dr Yannick Kok / FibriScore presentation (reported by Philip McMillan)
https://
drphilipmcmillan. substack. com/ p/ lessons- from- the- front- line- apheresis This conference summary states that Dr Yannick Kok presented laboratory evidence that microclot complexes, measured by his FibriScore® test, "drop significantly after apheresis."
2. Apheresis Center (Cyprus) claims
https://
apheresiscenter. eu/ blog/ help- apheresis- paper- removes- spike- protein- microclots- more The clinic states that research microscopy shows platelet hyperactivation and microclot-like / amyloid-like structures "dwindle post-treatment" with HELP apheresis.
Both sources Grok linked were somewhat dubious marketing-type materials.
The first source was a presentation by Yannick Kok, who did not actually show that the level of clots would "drop significantly after apheresis", because he only discussed the results of two patients, so the results were not significant in the statistical sense. And compared to the baseline level of the patient before treatment, the level of clots was higher a day after the treatment but lower six days after treatment, so whether the level of clots was higher or lower after the treatment depends on how many days after the treatment you're looking at.
The second source was the website of the Cyprus Apheresis Center, but the website didn't include any numeric data that would've shown that the treatment would reduce the level of microclots. The center in Cyprus provides three forms of apheresis treatment, which are HELP apheresis, DFPP using the German Inuspheresis system, and immunoadsorption. But the center appears to use a membrane filter and not a centrifuge with all three treatments. [https://
Yannick Kok works for Ayus Laboratories, which is the German company that manufactures the Inuspheresis DFPP system. But Inuspheresis would likely not remove microclots, because it employs a membrane filter and not a centrifuge so separate the plasma. [https://
Ayus Laboratories has developed a test called FibriScore to quantify microclot burden. Philip McMillan wrote: [https://
Ayus Laboratories' FibriScore® test uses imaging flow cytometry with fluorescent dyes that bind to amyloid structures, quantifying both the number and size of FMCs in a blood sample. For the first time, clinicians can see what's actually flowing through the pipes rather than inferring from indirect measurements.
The Cytek ImageStream® technology combines the statistical power of flow cytometry with the visual clarity of microscopy. Every particle passing through the machine is photographed, measured, and characterized. The result: patient reports show dramatic differences between healthy individuals (minimal FMCs) and long COVID patients (sometimes three-fold elevations in total microclot area).
FibriScore® is particularly valuable for treatment monitoring, revealing whether interventions are working. Post-apheresis samples show marked reductions, visible proof that the cleaning worked. One patient Kok tracked showed total microclot area dropping from 49.30 mm² to 7.60 mm² six days after treatment. Another showed sustained improvement over five months, from 60.09 mm² to 20.31 mm².
It's weird how McMillan only wrote about the results of two individual patients, and not multiple patients averaged together. The 6-fold variation of the first patient and 3-fold variation of the other patient might be within the normal range of day-to-day variation in clot burden, so the difference was not necessarily because of the treatment.
During an interview with Philip McMillan in 2025, Yannick Kok showed the image below, and he said: "I'm part of the Ayes Medical Group, and the thing of the Ayus Medical Group is that we do apheresis, and specifically we do Inuspheresis. And a big question for us is, is Inuspheresis able to filter out these microclots from a patient? I've used the TKM-58 filter in the Inuspheresis, and the filter - the pore size is in the nanometer range in this filter, and microclots they are in a micrometer range. So from a physical, uh, if you think of the physics, big particle, small hole, doesn't fit. So what [unintelligible] we would expect. We hook up a patient with high microclots, um, and after aphoresis we should not detect these high microclots anymore. Then we got this data. And this was a surprise. So here in gray, you see the initial value before aphoresis. In red, you see the value directly after Inuspheresis, and we see an increase. And we got worried. We were surprised to see this. And we started to think, how can this be? Because if you think of the physics behind it, we should remove it." [https://
Did he really not understand the basic mechanics of his own company's product? The TKM58 filter is the plasma fractionator filter, which is the second filter employed in DFPP. [https://
When Yannick Kok said that the patient had a higher microclot burden a day after treatment than before treatment, he was talking about data for a single patient only, so the increase may have been due to random variation.
But anyway, next Kok showed that when he measured the microclot level 6 days after treatment, the level was about 6 times lower than before treatment. And he said it was consistent with how a patient who has undergone the treatment will not necessarily feel better immediately after the treatment, but only a few days later.
But he again only showed data for a single patient and not multiple patients averaged together, which was really weird. Even the level after 6 days might have been within the normal range of day-to-day variation.
So his sample size is too small to draw conclusions about how the Inuspheresis treatment affects the microclot burden, even though if you understand that the clots are too big to pass through the plasma separator, then it makes sense why the level of the clots was not reduced a day after the treatment.
Added later: I now found a paper by Beate Jaeger from 2023, which included the following measurements of the level of microclot-like structures before and after HELP apheresis. There was no significant reduction in the area of the microclot-like structures (p-value about 0.25) but only in the count of the microclot-like structures (p-value about 0.01): [https://
The so-called microclot-like structures were identified using a method of cytometry called real-time deformability cytometry (RT-DC), so that the authors selected structures with an area at least 100 µm² and a low deformation parameter relative to the area. The deformation parameter indicates how much an object changed in shape as it moved through the measurement channel. The method of identifying microclots may have been prone to false positives, because the authors wrote: "it should be kept in mind that not all events are necessarily clots, as damaged endothelial cells or cellular debris generated by the apheresis process may have been present and therefore recognized in the analysis". The so-called microclot-like structures were not selected based on whether they were fluorescent or stained by Thioflavin. And since only structures with an area above 100 µm² were classified as microclot-like structures, all of the structures would've likely been too big to pass through the pores of Jaeger's plasma separator, which likely has a pore size of 0.5 to 0.7 µm: [https://
McCairn claims that the IA treatment provided at Edogawa is somehow safer than the TPE treatment provided in the United States, because in TPE the patient is given replacement albumin, and he claims the albumin is contaminated with spike protein or microclots. However I have never seen him present evidence that albumin products contain spike protein of SARS-CoV-2.
Here when he claimed that albumin had been found to contain spike protein, Allen Green asked: "Albumin from which manufacturer? Mind sharing the reports?" But McCairn never answered: [https://
One of McCairn's followers said that albumin has been found to bind spike protein in some laboratory studies. But Allen Green pointed out it doesn't mean that the albumin sold by manufacturers would contain spike protein: [https://
Then McCairn's follower said that blood banking protocols don't screen for the presence of spike protein, but Allen Green pointed out that the screening is not necessary because the spike protein is removed by the manufacturing process:
Then McCairn claimed that every batch of blood bank products he had tested had been positive for "cross-seeding amyloidogenic fragments". When Allen Green asked to see the evidence, McCairn didn't show the evidence but he said "I do all the time. You should pay closer attention to my output." However I have paid close attention to McCairn's output, and I don't remember seeing him post the evidence:
Google AI said:
No, the SARS-CoV-2 spike protein does not survive the rigorous manufacturing and purification processes required to produce human serum albumin. The spike protein, like the virus itself, is highly vulnerable to the harsh physical and chemical steps designed specifically to eliminate viral and protein contamination during plasma fractionation.
Human serum albumin is manufactured using the Cohn cold ethanol fractionation method or advanced chromatographic purification, both of which utilize concentrated alcohol and extreme pH adjustments to selectively precipitate and separate proteins. These chemical conditions disrupt the structural integrity of the spike protein, which is a fragile trimeric glycoprotein. Furthermore, the purification process explicitly includes a robust viral inactivation phase called pasteurization, where the albumin solution is heated to exactly 60 °C (333.15 K) for a continuous period of 10 hours.
While native albumin is uniquely heat-stable and survives this thermal stress with the aid of stabilizers like caprylic acid, the SARS-CoV-2 spike protein denatures rapidly at much lower temperatures. This pasteurization step completely unfolds the secondary and tertiary structures of any residual spike protein, rendering it non-functional and completely degraded. As a result, the final therapeutic albumin product has an exceptional safety profile, completely free of intact or active SARS-CoV-2 viral components.
Google AI also said: "No scientific study has ever found the SARS-CoV-2 spike protein in commercially manufactured albumin products. Global regulatory bodies and researchers have continuously monitored plasma-derived therapies throughout the pandemic, and zero instances of spike protein contamination have been reported in finished therapeutic human serum albumin."
Earlier when McCairn has been asked why the catheter is hooked up to the jugular vein in the Edogawa protocol, he has given the implausible-sounding explanation that the jugular catheter somehow helps to capture toxic substances that are released from the brain.
Now he came up another similarly implausible explanation, because McCairn said that the jugular catheter would somehow enhance a mechanical pumping action that causes fibrin deposits to be released from muscle tissue into blood vessels: [https://
When I asked if his explanation was plausible, Grok said:
Fibrinaloid (amyloid-containing) deposits located in the interstitial space of skeletal muscle would not be expected to migrate into blood vessels as a direct result of the mechanical forces of plasmapheresis performed via a jugular catheter.
What the relevant study actually found
In the 2024 Nature Communications paper by Appelman, Wüst and colleagues, amyloid-containing deposits were present at higher levels in the skeletal muscle of long COVID patients than in recovered controls. These deposits sat between muscle fibers (extracellular/interstitial), not inside capillaries, and their density increased after an exercise challenge that induced post-exertional malaise (PEM). The authors explicitly noted they were not located inside capillaries and therefore were not observed to be directly occluding them in the biopsy samples. [https://
www. ]nature. com/ articles/ s41467- 023- 44432- 3 Why the proposed migration mechanism does not hold
Location matters. Interstitial deposits sit outside the vascular compartment, separated from circulating blood by the capillary endothelial barrier and basement membrane. Large, insoluble, amyloid-like fibrin aggregates do not freely diffuse across intact endothelium.
Apheresis mechanics are intravascular. Therapeutic plasma exchange (or double-filtration plasmapheresis) withdraws blood from a vein, separates plasma, removes selected components, and returns the remainder. Whether access is peripheral or central (internal jugular), the flow and shear forces act only on the blood already inside the vascular system. The procedure does not create pressure gradients, "pumping," or mechanical agitation capable of forcing distant interstitial material from muscle tissue into capillaries or larger vessels.
Central (jugular) access is chosen for practical reasons, not tissue mobilization. High-flow central catheters support the blood-processing volumes needed for effective treatment when peripheral veins cannot deliver adequate flow or are otherwise unsuitable. This is a standard technical consideration in apheresis, unrelated to extracting tissue-bound deposits.
Physiological mobilization is a separate issue. Muscle contraction, local inflammation, or changes in vascular permeability could theoretically allow some soluble factors or small particles to enter lymphatics or blood over time. That process, if it occurs at all for these deposits, would be driven by ordinary physiology or pathology - not by the presence or mechanics of a jugular catheter during apheresis.
In short, plasmapheresis can only remove what is already circulating in the blood. Claims that the mechanical action of "deep" (central-access) apheresis specifically mobilizes interstitial muscle fibrinaloid deposits into the vasculature lack support from vascular physiology, apheresis practice, or the muscle-biopsy findings themselves.
In the Twitter thread about the paper, the senior author Wüst referred to the so-called deposits as "microclots", because he wrote: "Blocking of capillaries by amyloid-containing deposits (or microclots) could reduced exercise capacity. We found these deposits in muscle tissue, but surprisingly not inside capillaries." [https://
Grok said:
Wüst and colleagues did not show that the amyloid-containing deposits they observed in muscle were fibrin (or fibrinaloid microclots).
What they actually did
In the 2024 Nature Communications paper (Appelman et al.), the team detected the deposits using Thioflavin T (ThT) staining on skeletal muscle biopsy sections. Thioflavin T is a fluorescent dye that binds to β-sheet-rich structures and is a general marker for amyloid material of various protein origins. They also co-stained some sections with antibodies against CD31 (to mark endothelial cells/capillaries) and LYVE-1 (to mark lymphatic vessels) to determine the location of the deposits.
They consistently described the structures only as "amyloid-containing deposits." They reported that these were more abundant in long COVID patients' muscle (extracellular matrix between fibers, next to but not inside capillaries), and that the amount increased after exercise-induced post-exertional malaise.
What they did not do
No fibrin- or fibrinogen-specific immunohistochemistry, immunofluorescence, or other biochemical identification (e.g., antibodies against fibrin(ogen), mass spectrometry of the deposits, or other fibrin markers).
No claim that the deposits were fibrin, amyloid fibrin, or the "fibrinaloid microclots" described in the Pretorius/Kell literature.
The paper references the circulating microclot hypothesis as background context but concludes that the deposits they saw were not located inside vessels and therefore did not support the idea of capillary blockage by such material. The molecular identity of the muscle deposits was left open; the authors noted that the reason for their intramuscular accumulation remained elusive.
When I asked if Wüst's group had determined in other studies if the deposits were made of fibrin, Grok said:
No. There is no published evidence that Rob Wüst's group (including collaborators such as Appelman or Charlton) has determined that the amyloid-containing deposits observed in skeletal muscle are fibrin (or fibrinaloid microclots).
Original 2024 study
In the Nature Communications paper, the deposits were identified solely by Thioflavin T staining (a general amyloid dye). No fibrin- or fibrinogen-specific antibodies, proteomics, or other compositional analyses were performed. The structures were described only as "amyloid-containing deposits."
Later work by the group
Subsequent papers and preprints from the same team focus on related topics such as: - Muscle fiber-type shifts - Mitochondrial function - Comparisons between long COVID, ME/CFS, and bed-rest deconditioning
These continue to refer to the structures as "amyloid-containing deposits" (or cite the original finding) without new data identifying their protein composition as fibrin.
Wüst has received funding (e.g., from ME Research UK) for projects exploring microclots and microvascular pathology in muscle in the context of long COVID/ME/CFS and PEM. However, no peer-reviewed publications from the group have yet reported specific identification of the muscle deposits as fibrin.
External commentary
Other researchers (particularly in the Pretorius/Kell circle) have noted that the muscle deposits "resemble" or may be related to circulating fibrinaloid microclots, but those interpretations come from outside Wüst's team and are not findings demonstrated by his group.
Some of McCairn's followers seem to think that the deposits described by Wüst had somehow formed in the circulatory system but then migrated to the muscle tissue. But I didn't find that hypothesis actually proposed by Wüst's group anywhere, and his group seems to have not answered the questions of how the deposits are formed or what the deposits are made of.
The authors appeared to assume that the deposits consisted of amyloid protein because the deposits were stained by ThT, but the authors didn't describe doing confirmatory tests like staining with Congo red or an Amytracker dye, or doing electron microscopy to see if the deposits contain amyloid fibrils.
Someone on Twitter told me I was wrong about the Edogawa protocol, because he said there were two studies that showed IA produced an improvement in the symptoms long COVID patients: [https://
But the other study he linked was a trial protocol for a planned study called IA-PACS-CFS, which had no results reported. [https://
The Twitter user Markus posted a video where the authors of the unpublished RCT presented their preliminary results. The primary outcome measured in the study was the change in the Chalder Fatique Scale before treatment and approximately 60 days after treatment, but there was no significant difference in the measure between the treatment and sham groups: [https://
Markus pointed out how the German RCT used a jugular catheter to ensure a high flow rate of blood. McCairn has been making it seem like the reason why his protocol uses a jugular catheter is because it somehow enhances the removal of harmful substances that get released from the brain at the time of the treatment, which doesn't make any sense. So McCairn pretends like the jugular catheter is a secret sauce of his protocol, so if there's some other protocol that doesn't use a jugular catheter, McCairn can say that explains why the protocol is not effective.
But now after Markus pointed out there were two German RCTs that found no significant benefit even though they used a jugular catheter, McCairn pivoted to coming up with a new secret sauce, which was that his protocol targets some specific autoantibodies. But when Markus asked what autoantibodies, McCairn said it was proprietary information, so Markus pointed out the hypocrisy of McCairn's answer, because McCairn had earlier presented himself as a great champion of open source science: [https://
The IA circuit at Edogawa seems to just use the regular TR-350 column, and not any extra column that targets some secret proprietary antibodies. The different components of the IA circuit are visible from the photos and videos posted from the hospital.
Previously McCairn made it seem like the immunoadsorption column used in Japan was some kind of special Japanese technology that was not available outside of Japan, because it was not licensed in the United States. But he failed to mention that the Asahi TR-350 column is licensed in many European and Asian countries, and the column is commonly used in countries like Germany and Italy.
So now after the German IAMPOCO trial showed no significant benefit even though the trial employed both the TR-350 column and a jugular catheter, McCairn has to come up with some new way to convince his customers that his protocol has some proprietary secret sauce, so that his protocol sucks out the amyloid fibrils and hydrogel nanobots better than his competitors.
One of McCairn's patients said that "my medical bills have reached $187,459.72 USD", because "my body is corroded with amyloidogenic hydrogel". She said that she even had to sell her car to get to Japan, and she is now financially devastated: [https://
She also falsely referred to the treatment provided at Edogawa as "double filtration plasmapheresis", and she falsely claimed that the treatment is only available in Japan. McCairn has been marketing his treatment as somehow unique, so McCairn's patients don't seem to realize that similar IA treatment is available at a lower cost in Europe and the United States (and many patients seem to incorrectly think the treatment is DFPP and not IA, because even McCairn himself used to refer to the treatment as DFPP until January 2026).
One of McCairn's patients said she didn't have money for a fourth round of immunoadsorption, but she was shown photos of clots in her plasma that she told contained "amyloidogenic material", so she is now asking for donations to get a fourth round of treatment: [https://
This was the photo of clots in her plasma she showed:
According to the Twitter user Janiesaysyay, the photo was proof that living people are growing calamari clots: [https://
Peter Daszak posted this tweet: [https://
When I explained to Daszak how McCairn's immunoadsorption circuit is unable to even remove the microclots, Daszak retweeted my tweet and told me "I'm glad you're exposing this horrible grift":
Then Daszak blocked me for some unknown reason. Black Tom said that I was in cahoots with Daszak, but when I showed that I had already been blocked by my new friend Pete, Black Tom said we were covering up our tracks: [https://
Jikky said that me and Daszak are affiliated with the same agency: [https://
These were the types of replies Daszak received from McCairn's fans: [https://
One user on Twitter said that McCairn was threatening Peter Daszak's "evil harvest": [https://
Another user suggested that Daszak had organized the attacks against McCairn: [https://
Janiesaysyay said that Daszak had inflicted an extinction-level event on humanity: [https://
In August 2026 McCairn's patient Robert Benson posted a video where he said it had now been about 4 months since he returned from Japan, and he said: "So coming out of Japan, I was 80, 90 percent. I felt my usual self, I was doing real - doing really well, and that carried through, right, you know, into July. I'd say mid-to-late July, all of a sudden I could kind of feel things coming back. It felt like I was had a - you know, wet blanket thrown over my brain again, so I thought things might be coming back. I did go get my spike proteins tested - and my spike protein antibodies tested - I was over 25,000 again. So those numbers come back high." [https://
So mid-July would've been about 3 months after the treatment. Based on how the symptoms of autoimmune conditions rebound within weeks after immunoadsorption treatment, I would've expected the effect of McCairn's treatment to last an even shorter time. The Sinovac victims guy also said that his symptoms had rebounded by four days after the DFPP treatment.
I don't know if McCairn's other patients have experienced a faster or slower rebound than Robert Benson, or no rebound at all.
A few days later Robert Benson posted an update, where he now said he had tried therapeutic plasma exchange in the United States.
He said most of his issues were cognitive and mental, and while the gains from TPE did not last from a mental standpoint, the TPE fixed his gut issues, and it fixed a rash in his foot within days from the treatment. But he said that the catheter was hooked up to his arm in the TPE, and he speculated that perhaps the treatment in Japan had a bigger cognitive benefit because he said that "I think that actually what happens in Japan when they go through the jugular, and use the catherer, that I think it's better allowed to pull the clots out of my brain, that cause me the - just my, numbness in my daily life, every day. So I think that's a big factor." [https://
McCairn should stop falsely advertising his protocol by claiming that the jugular catheter somehow helps to suck out toxins from the brain, or to suck out clots from the brain. He should also inform his patients that his protocol likely does not remove microclots in the first place, but that TPE might actually be able to remove the microclots (even though it's likely that the benefit of TPE has little to do with microclots being removed from the blood).
McCairn's fan Janiesaysyay is now going around Twitter promoting the Edogawa protocol as a treatment for removing calamari clots: [https://
McCairn himself said that he thinks the calamari clots are a post-mortem phenomenon, because he said that if the clots would occur in living people, the clots would be reported by cath labs, and he said he had heard from the staff of a Japanese hospital that they were not seeing calamari clots in living people. [https://
In August 2026, Doug Kell and Resia Pretorius posted a preprint titled "Atherosclerosis as a Localised Amyloid and Proteostasis Disorder". [https://
I had already informed Doug Kell earlier that AmyloGram is meant to be used with peptides and not proteins, and proteins virtually always get an amylogram score above 0.5. I had also showed him how the AmyloGram score is simply the maximum score of 6 aa segments within the input, so the score is not a meaningful measure of the overall amyloidogenicity of a whole protein. But in his paper he didn't mention how the AmyloGram score is calculated, or why full proteins are almost always classified as amyloidogenic by AmyloGram.
The AmyloGram score centers around 0.5 for random 20 aa peptides, because the score is calibrated to be meaningful for peptides but not for proteins. But the average score is about 0.8 for random 500 aa proteins, because random 500 aa proteins virtually always contain nonzero 6 aa segments that are classified as amyloidogenic:
library(AmyloGram); library( biogram); data( AmyloGram_ model) chars=strsplit( " A C D E F G H I K L M N P Q R S T V W Y ", " ")[[ 1]] # average score of 100 random 20 aa sequences l=replicate(100, paste( sample( chars, 20, T)), F) l=setNames( l, 1: length( l)) mean( predict( AmyloGram_ model, l)$ Prob) # 0. #4709998 average score of 100 random 500 aa sequences l=replicate(100, paste( sample( chars, 500, T)), F) l=setNames( l, 1: length( l)) mean( predict( AmyloGram_ model, l)$ Prob) # 0. 8364628
Here when I ran AmyloGram for random amino acid sequences of each length between 6 and 1,000 aa, all sequences longer than 150 aa got a score greater than 0.5, which is the default cutoff AmyloGram employs to determine if an input sequence is likely to be amyloid or not: [clot2.
The paper about AmyloGram said that AmyloGram was trained on a set of peptides with a length between 6 and 25 aa, and a benchmark of AmyloGram relied on input sequences with a length between 6 and 14 aa. [https://
The same problem is much worse for a protein with a length of hundreds of amino acids, so if even one of the hundreds of 6 aa segments gets a score above 0.5, then the entire protein gets classified as amyloidogenic.
In his preprint Kell and Pretorius wrote things like this: "Langley and colleagues (Langley et al. 2017) sought biomarkers of high-risk atherosclerotic plaques, and identified a 4-biomarker signature (matrix metalloproteinase 9, S100A8/S100A9 (calprotectin), cathepsin D, and galectin-3-binding protein). Their AmyloGram scores are respectively 0.9148, 0.7768 (for S100A8), 0.7941, and 0.8661. Clearly, each is highly amyloidogenic ...". But scores of around 0.8 or 0.9 are typical for whole proteins, so the scores are not evidence that the proteins are highly amyloidogenic.
Kell and Pretorius also wrote: "a computational analysis based on AmyloGram showed the strongly amyloidogenic potential of proteins found in various atherosclerotic plaques". But that's wrong, because a high AmyloGram score is not evidence of a protein having a "strongly amyloidogenic potential".
In the new preprint, Kell and Pretorius wrote: "Thus, while 79% of human proteins have an AmyloGram score exceeding 0.7, with a median value of 0.81, typically more than 90% of proteins in plaques have AmyloGram scores exceeding 0.7, with a median score around 0.86. The probability-of-superiority values are around 0.615-0.627 against the human proteome. In addition, a Mann-Whitney test bootstrapped 20,000 times gave a 95% CI 0.0411-0.0497 for the difference in median AmyloGram score in Lewy bodies vs the human proteome."
Even though the p-value is low, the difference in average AmyloGram score was only about 0.05. I thought the difference might have been explained by a different length distribution within the two sets of proteins.
Therefore I downloaded both Kell's set of 1,459 proteins associated with plaques, and I downloaded a reference set of human proteins from UniProt simlar to Kell's reference set. [https://
Then when I calculated average AmyloGram scores by length, the set of proteins associated with plaques got a lower score within the 4 shortest strata, and the set of reviewed human proteins got a higher score within the 6 longest strata:
I don't know what explains the discrepancy between the short and long proteins. But regardless, the results still show that proteins associated with plaques do not consistently get higher AmyloGram scores than the reference proteins.
I showed the length-stratified results to Doug Kell, and I informed him of how AmyloGram is meant to be used for peptides but not proteins. [https://
I had just helped Kell identify a fundamental problem in his recent preprint, so he should've at least thanked me for helping him, so he'll know to correct the preprint before it gets published in a journal. Or he should probably withdraw the preprint entirely, because the primary finding of his preprint was not valid. But instead he just said that I was a "disaffected troublemaker" who was "off on an ego trip".
I understand if Kell and Pretorius don't want to get involved in the debate about McCairn's protocol, because it's such a radioactive topic. But on the other hand their papers serve as a key device McCairn employs to make his patients afraid of the microclots, and to trick his patients into thinking they have to give him their life savings to get rid of the clots. So once McCairn's grift comes crashing down, it might also have an adverse effect on the reputation of Kell and Pretorius (especially since Pretorius has earlier endorsed Beate Jaeger's HELP apheresis as a method to remove the clots, even though Jaeger's HELP protocol seems to have the same pore size problem as McCairn's immunoadsorption protocol).
The website of the apheresis center at Cyprus says: "Please note that we currently no longer utilize traditional Immunoadsorption as part of our routine clinical protocols. Over time, the Apheresis Center has transitioned toward using Inuspheresis® as our preferred and selected form of Immunoapheresis within our broader Combination Therapy Approach." [https://
The website also says:
Despite initial studies showing no effect for Immunoadsorption in Long Covid, clinical experience tells a different story. While not as effective as H.E.L.P. Apheresis, Immunoadsorption has shown a 10-30% success rate in clinical settings, compared to the 80% success rate of H.E.L.P. Apheresis. The results of Immunoadsorption are not always permanent, potentially due to its single mode of action and the high burden of fast application.
Further research, such as this study:(https://
www. ), is needed to improve success rates. New adsorbers, combination treatments, and different application schemes may enhance effectiveness.medrxiv. org/ content/ 10. 1101/ 2024. 06. 18. 24309100v1 All three methods - Immunoadsorption, H.E.L.P. Apheresis, and Inuspheresis® - belong to the wider family of Immunoapheresis and Therapeutic Apheresis when used to target pathogenic autoantibodies and inflammatory mediators.
At our center, we continue to evolve our approach based on patient outcomes, scientific developments, and the complexity of chronic inflammatory conditions. While Immunoadsorption remains a recognized therapy, we increasingly utilize broader therapeutic approaches such as Inuspheresis® and combination therapy protocols to address multiple overlapping disease mechanisms in a more comprehensive way.
The apheresis center at Cyprus might be the only provider of apheresis treatment that has comprehensive experience providing multiple types of apheresis treatment to long COVID patients. For example Edogawa seems to only provide IA treatment, Jaeger provides only HELP apheresis, and some American centers only provide TPE, but the center at Cyprus might be uniquely positioned to compare the efficacy of different forms of apheresis treatment (even though I don't know if the center has compared their efficacy based on any rigorous numeric measurements, and the center didn't explain how they determined that immunoadsorption had a "10-30% success rate" and HELP apheresis had an "80% success rate").
A blog post by the Cyprus center said that HELP apheresis was "by far the most successful type of apheresis we use", and the post said: [https://
Immunoadsorption does one thing only, but at a very high efficiency: Removing autoantibodies. From our clinical experience it is only indicated if the patient has certain very high autoantibody levels. If applied too fast (the often standard 6 sessions in 2 weeks is what we believe (from anecdotes of patients who did immunoadsorption at higher speed as we apply) is too fast for many patients) there is a high risk of 'crashing' or getting worse, sometimes even permanently. Another issue is that most results are only permanent for approximately a third of the patients that undergo the treatment.
In general we have had better results with IVIG treatment so far than with Immunoadsorption - but both are a good combination with H.E.L.P. if applied correctly. More research is needed in this area. H.E.L.P. removes autoantibodies too (at a lower pace without creating issues) and outperforms Immunoadsorption in all other areas, another reason why it is the preferred first line treatment of our medical team.