The Tainted Blood Scandal to Rule Them All

An update for the aware community

On the Precedent for Ignoring Medical Catastrophes

Jeremy Hunt was UK Health Secretary between 2012 and 2018 and was variously critical of clinicians and NHS managers for institutional cover-ups and evasion. He wrote a book on reducing needless deaths in the NHS, in the wake of the Infected Blood Inquiry (curiously avoided in his book), which examined the scandal of HIV-infected blood products imported, despite warnings, for UK patients between the 1970s and early 1990s. There are various documentaries available, including the Emmy award-winning In Cold Blood.

Hunt described sitting at the top of a “rogue system” and said the Department of Health and NHS were complicit in cover-ups. He described how the corrosive consequences of such thinking led to managers being recycled rather than held accountable. He had testified to the Commission of Inquiry that “institutions and the state close ranks around a lie, sometimes,” and that this was what happened in the contaminated blood scandal. 

We think the ‘covid white clot crisis’ – and its cousins of turbo cancer, immune failure, cardiac damage and neurodegenerative disease – is eclipsing all other medical cover-ups so far. This may seem a giant call, but the WHO’s bare-faced crowing about the 12 billion injections given does set the scene for the scale of damage done and to come. True to form though, the medical and political establishment has been deaf and blind so far, even though evidence so far does suggest the covid spike protein is a likely cause.

Understanding and Answers are Appearing Through the Fog of War

The science on the anomalous white fibrous clots is now moving rapidly and we have been calling attention since 2022. Three independent research streams have converged on a consistent picture. Each team has used different methods and different analytical frameworks. Yet they have arrived at the same fundamental conclusion: these are new, very abnormal, and can only be dangerous.

This post acknowledges the contributions of each team, situates them carefully within the scientific framework (in the way Bruce Rapley has called for in his recent Substack essays) and then asks the question that must not be ignored: how can these structures be compatible with any kind of healthy life?

The Three Streams of Contribution

The Rapley/Shelton trilogy of preprints, currently in peer review as a single paper, was the first comprehensive characterisation of these Anomalous Intravascular Casts (AICs). Using morphology, elemental analysis, and proteomics, they established three critical facts:

• They are morphologically distinct from normal clots
• They are biochemically abnormal
• They are profoundly resistant to breakdown

The Santiago/Harrison Team’s Raman Spectroscopy Paper (July 2026).

This team provided a definitive structural characterisation. Using Raman micro-spectroscopy at the HUN-REN Wigner Research Centre for Physics, they confirmed:

• These casts are beta-sheet enriched: the molecular hallmark of many proteins (including amyloid), with a characteristic Amide I sub-band at approximately 1620 cm⁻¹.
• They seemed to show a stage-dependent maturation process
• They are strongly stabilised by multiple chemical forces

Both these parallel projects were profiled in our write-up here.

Dr Kevin McCairn’s Forensic Investigations (2025–2026)

We have not discussed the insights of Dr Kevin McCairn, a systems neuroscientist with over 25 years of expertise in neurodegenerative disease modelling. Daniel Santiago has profiled his work.  He has conducted a highly detailed forensic analysis of these structures. His contributions are published privately and are substantial:

1. Comprehensive Multi-Modal Characterisation: 
McCairn’s team applied a broad range of techniques: gross morphological inspection, cryosection histology, Thioflavin T (ThT) fluorescence staining, scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDX), real-time PCR, Raman spectroscopy, and Real-Time Quaking-Induced Conversion (RT-QuIC) assays.

2. Near-Definitive Amyloid Confirmation: 
His SEM imaging revealed characteristic ultrastructure of amyloid-like protein pathology: fibrils with a distinct rotational twist, nodular topography, and lateral aggregation features—hallmarks of pathological protein assembly. Thioflavin T staining confirmed beta-sheet rich amyloid domains, and the structures displayed strong intrinsic autofluorescence under UV excitation, consistent with highly ordered molecular architecture.

3. Elemental Characterisation: 
EDX mapping showed high abundance of carbon, nitrogen, oxygen, and sulfur—consistent with proteinaceous material—and notably, no signal for transition or heavy metals (iron, zinc, copper), ruling out metal-driven aggregation. This supports an endogenous (produced by the body) biochemical origin.

4. Preliminary Seeding Evidence: 
RT-QuIC assays, which detect prion-like seeding activity, showed elevated ThT signals consistent with templated misfolding when the clot material was challenged against human plasma. As McCairn notes, the findings are “suggestive but inconclusive for prion-like activity”. This is not a definitive proof of transmissibility, but it is another worrying signal. 

5. Documentation of Pediatric Pathology: 
McCairn has published the first documented case of “amyloidogenic microclots” in a child with in-utero mRNA vaccine exposure. The child was born at 35 weeks, one week after the mother’s second Pfizer dose, without vital signs and requiring resuscitation. At three years of age, the child’s blood showed ThT-positive fibrillar structures, widespread autofluorescence, and dense clotting patterns. This case is deeply concerning and should have triggered immediate formal investigation. 

6. Clinical Diagnostic Work: 
McCairn has developed fluorescence-based amyloid assessment protocols and has been analysing blood samples from living patients, including social activist Elizabeth Glass, who went public to raise awareness. His work with a Japanese hospital has contributed to the McCairn-Edogawa Protocol, a two-phase treatment pathway combining physician assessment, dual filtration plasmapheresis, laboratory analytics, and clinician-directed regenerative support.

A Note on Scientific Language: Dr Rapley’s Caution

Bruce Rapley’s recent Substack essays – When A Hypothesis Gets a Passport and Amyloid or Amyloid-like? – ask an important scientific question: has the evidence truly earned the label “amyloid”?

Bruce argues that the suffix “-like” is not a minor qualifier but a fundamental scientific safeguard. It preserves the distinction between observation and interpretation, between resemblance and identity. He notes that:

“When investigators report that a particular specimen exhibits amyloid-like structural characteristics, they are making a specific scientific observation. They are describing the behaviour observed using a particular analytical technique under particular experimental conditions. Such observations are valuable because they raise important questions worthy of further investigation.”

His concern is valid: the word “amyloid” carries immense weight in biology and medicine, with associations to Alzheimer’s disease, systemic amyloidosis, and specific pathogenic mechanisms. To move from “amyloid-like” to “amyloid” requires more evidence – the specific precursor protein, fibril ultrastructure (cross-beta X-ray diffraction pattern), and a clear pathological consequence.

However, Rapley’s caution should not be mistaken for dismissal. As he states:

“The purpose of this article is not to argue against the possibility that some components of some Anomalous Intravascular Casts may ultimately prove to possess canonical amyloid architecture. That remains an entirely legitimate scientific hypothesis deserving careful investigation.”

Sure, agreeing the distinction is important, but it should not be used to delay investigation. The analytical evidence already accumulated – Raman beta-sheet signatures, Thioflavin T binding, SEM fibrillar morphology, protease resistance, seeding potential – is substantial, quite apart from the first visible data point: embalmers discovering bizarre, ugly large structures filling blood vessels. It is not about whether these structures are concerning but how concerning and what do we do about it.

The Urgent Question: How Can These Structures Be Compatible with Life?

This is the question that governments must answer. Whatever the precise molecular terminology, the physical reality is now well-documented:

• Large, rubbery, white fibrous casts are being found in the vasculature of many deceased individuals, according to large surveys of embalmers.
• Amyloidogenic microclots are being identified in the blood of living patients .
• These structures are resistant to breakdown, deficient in plasminogen, and stabilised by multiple cross-linking mechanisms.
• They exhibit hallmarks of prion-like behavior: self-templating propagation, protease resistance, persistence (and potentially infectious to others).
• They are being found in children with in-utero exposure to mRNA injections.

Two Associated Conditions; One Loud Alarm Bell

Amyloidosis, once established, is a serious condition. Without treatment, the life expectancy of someone suffering from systemic amyloidosis can be as short as six months to four years, after the amyloids have infiltrated tissues and organs. There is no cure.

Similarly concerning is prion disease, which looms large. This is inflammation and degeneration propagating in a falling domino-fashion caused by tiny fragments of mutant proteins interfering with cellular activity. Perhaps the best known prion diseases are Creutzfeldt-Jacob Disease (CJD) and Bovine Spongiform Encephalopathy (BSE), or mad cow disease, both causing fatal dementia.

The possibility of prion disease was raised early on by experts, and here, and famed Nobel prize-winning virologist Luc Montagnier final paper was a case series of recently vaccinated patients who then developed a rapid CJD dementia. 

Swedish Researchers Provide a Molecular Mechanism

Nystrom and Hammarstrom and others have provided one explanation for the formation of these persistent clots which encompasses amyloid and prion concerns. Their work has shown that the SARS-CoV-2 spike protein contains seven sequences with amyloidogenic potential. In their experiments, they focused on a subset of these sequences. When exposed to neutrophil elastase – an enzyme abundant at sites of inflammation, and found by Rapley in his proteomic analysis – the spike protein is broken up by this enzyme, releasing fragments that form amyloid fibrils. ​​​​​​​One specific fragment, designated Spike685, has been shown to induce fibrin clots that are highly resistant to plasmin-mediated breakdown. The same research group has also demonstrated that these spike-amyloid fibrils can cross-seed the misfolding of other amyloidogenic proteins, including the prion protein-associated with CJD and the amyloid-beta peptide associated with Alzheimer’s disease. This provides a plausible mechanism not only for the formation of plasmin-resistant microclots, but also for their potential to propagate pathology through a prion-like seeding mechanism.​​​​​​​

The End Result…

If these types of structures are accumulating in a significant proportion of the population – as McCairn’s findings suggest, with reports of 20-40% of deceased and a high proportion of vaccinated individuals showing these markers – then we are facing a public health crisis of unprecedented scale. Conjecture is inevitable about some aspects still, in order to connect the pieces we have gathered and use them for good, but we must be brave and speak about the discoveries which are reasonably certain.

The denial of this reality must end because the evidence speaks for itself.

What Still Needs to Happen

1. Large-scale population studies to determine the prevalence of amyloidogenic microclotting in the general population—both vaccinated and unvaccinated.
2. Formal investigation of the pediatric cases documented by McCairn and others, with appropriate ethical oversight and transparency.
3. Independent replication of the RT-QuIC seeding findings, with controlled experiments to determine whether these structures are truly self-propagating and possibly even infectious.
4. Development of accessible diagnostic tests for amyloidogenic microclots in living patients, beyond the current specialised fluorescence microscopy methods.
5. Evaluation of treatments, including the McCairn-Edogawa Protocol’s use of dual filtration plasmapheresis, with urgent but properly controlled clinical trials.
6. Immediate withdrawl of all mRNA products in every form – injected, inhaled, self-amplifying etc.

Conclusion

The science is moving forward, making the institutional denial harder to sustain. The issue is no longer whether these structures exist – they do Mr President, Mrs Prime Minister, Director-General, Your Highness, Mr Chairman – but what they mean, and what you are going to do about them.

The three research streams and other efforts profiled here have all contributed essential pieces to the puzzle. Their work is complementary, not contradictory. And Bruce Rapley’s call for scientific precision is not a rejection of the findings, but a direction for the rigor that will ultimately make them unassailable, and treatable.

The path forward is through science, integrity, and persistence.  The awful truth of massive misconduct is becoming harder to ignore, even for the State. And the urgency of the question – how can these structures be compatible with any kind of healthy life? – demands attention that the establishment cannot be allowed to evade.

As we finish writing, St James Infirmary Blues comes on the playlist. For anyone that knows the song, as well as the movie Jaws, the following may resonate:

We’re going to need a bigger mortuary.