Felix Faustus

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Felix Faustus

Felix Faustus

@FelixFaustus

I am an existential detective. I make no claims to the truth. I just point at territory in front of us. Self-governed consciousness beyond rigid systems

เข้าร่วม Ağustos 2009
131 กำลังติดตาม62 ผู้ติดตาม
ทวีตที่ปักหมุด
Felix Faustus
Felix Faustus@FelixFaustus·
@AboutPediatrics @lifebiomedguru Can you falsify this Dr Iannelli? x.com/FelixFaustus/s…
Felix Faustus@FelixFaustus

A Bayesian Framing of the Immune-Complex Geometry Hypothesis This is not a claim. It is a mechanistic hypothesis with testable predictions. Start with well-accepted premises: Complement efficiently clears small, soluble immune complexes Large or persistent immune complexes are more likely to deposit in microvasculature Complement activation produces C3a, C5a, and MAC, which influence endothelial function Microvascular dysfunction can produce subtle, diffuse physiological effects None of these premises are controversial. The question is whether antigen geometry and persistence could shift systems from regime (1) to regime (2). The Geometry Hypothesis If antigen exposure is: • Transient • Low density • Fragmented Then immune complexes tend to remain: • Small • Soluble • Efficiently cleared But if antigen exposure is: • Persistent • Repeating • High-density Then antibodies may bind along extended structures, forming: • Larger immune complexes • Clustered Fc regions • Strong complement activation However, strong activation does not necessarily imply efficient clearance. Large immune complexes are: • Harder to transport • Harder to phagocytose • More likely to interact with endothelium • More likely to deposit in microvasculature This is consistent with known immune-complex disease dynamics. Why Microvasculature Matters Microvascular beds are particularly sensitive because they: • Have high surface area • Experience slow or turbulent flow • Are vulnerable to immune-complex deposition Common targets in immune-complex disease include: • Kidneys • Skin • Joints • Small vessels Two additional biologically plausible sites: Brain microvasculature Heart microvasculature Brain Large immune complexes do not typically cross the blood-brain barrier. However, they do not need to cross it to influence it. Immune-complex interaction with brain microvasculature could: • Activate complement locally • Trigger endothelial signaling • Alter permeability dynamics This does not imply BBB breakdown. It implies potential modulation of barrier behavior, which could produce: • Subtle • Conditional • Diffuse effects Heart The heart may be more directly exposed. Unlike the brain, the heart lacks a comparable barrier. It has: • Dense microvasculature • High metabolic demand • Sensitivity to perfusion changes Even small microvascular disturbances can produce: • Transient perfusion effects • Electrical sensitivity • Functional variability Cardiology already recognizes this class of phenomena: Coronary microvascular dysfunction Normal large arteries Small-vessel dysfunction Bayesian Interpretation This hypothesis predicts: Not catastrophic effects Not universal harm Not large signals But: Subtle Conditional Subgroup-dependent Long-tail signals Which are precisely the kinds of signals that: • Appear intermittently • Disappear in aggregates • Are difficult to detect with standard epidemiology Testable Predictions If this model is correct, we might expect: • Complement activation markers elevated in subsets • Evidence of immune-complex formation in circulation • Microvascular function differences in subgroups • Heterogeneous outcomes rather than uniform effects Falsifiability This model weakens if: • No evidence of persistent immune complexes • No complement activation differences • No microvascular signatures • No subgroup-specific signals Bayesian Bottom Line This is not an argument from certainty. It is a shift in generative model: From: Uniform exposure Uniform clearance Uniform outcomes To: Geometry-dependent exposure Conditional clearance Subgroup-dependent outcomes The system doesn’t need to fail. The regime just needs to shift. And small regime shifts often produce long-tail signals rather than headline effects.

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Felix Faustus
Felix Faustus@FelixFaustus·
@AboutPediatrics @lifebiomedguru Who isn't? The question isn't, is it AI, the question is, how did they use they AI? There's still a person behind the generator auditing what out puts to use, the question is, what is the quality of their audit?
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Neil Stone
Neil Stone@DrNeilStone·
I'm an Infectious Diseases doctor Stuff like this keeps me in a job
Neil Stone tweet media
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Felix Faustus
Felix Faustus@FelixFaustus·
Felix Faustus@FelixFaustus

A Bayesian Framing of the Immune-Complex Geometry Hypothesis This is not a claim. It is a mechanistic hypothesis with testable predictions. Start with well-accepted premises: Complement efficiently clears small, soluble immune complexes Large or persistent immune complexes are more likely to deposit in microvasculature Complement activation produces C3a, C5a, and MAC, which influence endothelial function Microvascular dysfunction can produce subtle, diffuse physiological effects None of these premises are controversial. The question is whether antigen geometry and persistence could shift systems from regime (1) to regime (2). The Geometry Hypothesis If antigen exposure is: • Transient • Low density • Fragmented Then immune complexes tend to remain: • Small • Soluble • Efficiently cleared But if antigen exposure is: • Persistent • Repeating • High-density Then antibodies may bind along extended structures, forming: • Larger immune complexes • Clustered Fc regions • Strong complement activation However, strong activation does not necessarily imply efficient clearance. Large immune complexes are: • Harder to transport • Harder to phagocytose • More likely to interact with endothelium • More likely to deposit in microvasculature This is consistent with known immune-complex disease dynamics. Why Microvasculature Matters Microvascular beds are particularly sensitive because they: • Have high surface area • Experience slow or turbulent flow • Are vulnerable to immune-complex deposition Common targets in immune-complex disease include: • Kidneys • Skin • Joints • Small vessels Two additional biologically plausible sites: Brain microvasculature Heart microvasculature Brain Large immune complexes do not typically cross the blood-brain barrier. However, they do not need to cross it to influence it. Immune-complex interaction with brain microvasculature could: • Activate complement locally • Trigger endothelial signaling • Alter permeability dynamics This does not imply BBB breakdown. It implies potential modulation of barrier behavior, which could produce: • Subtle • Conditional • Diffuse effects Heart The heart may be more directly exposed. Unlike the brain, the heart lacks a comparable barrier. It has: • Dense microvasculature • High metabolic demand • Sensitivity to perfusion changes Even small microvascular disturbances can produce: • Transient perfusion effects • Electrical sensitivity • Functional variability Cardiology already recognizes this class of phenomena: Coronary microvascular dysfunction Normal large arteries Small-vessel dysfunction Bayesian Interpretation This hypothesis predicts: Not catastrophic effects Not universal harm Not large signals But: Subtle Conditional Subgroup-dependent Long-tail signals Which are precisely the kinds of signals that: • Appear intermittently • Disappear in aggregates • Are difficult to detect with standard epidemiology Testable Predictions If this model is correct, we might expect: • Complement activation markers elevated in subsets • Evidence of immune-complex formation in circulation • Microvascular function differences in subgroups • Heterogeneous outcomes rather than uniform effects Falsifiability This model weakens if: • No evidence of persistent immune complexes • No complement activation differences • No microvascular signatures • No subgroup-specific signals Bayesian Bottom Line This is not an argument from certainty. It is a shift in generative model: From: Uniform exposure Uniform clearance Uniform outcomes To: Geometry-dependent exposure Conditional clearance Subgroup-dependent outcomes The system doesn’t need to fail. The regime just needs to shift. And small regime shifts often produce long-tail signals rather than headline effects.

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Melissa Rose
Melissa Rose@MelRoBuilds·
Every single person around us is sicker than they were 5 years ago. Every. Single. Soul.
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Felix Faustus
Felix Faustus@FelixFaustus·
@Hypothesis Falsify this for science, thank you. x.com/FelixFaustus/s…
Felix Faustus@FelixFaustus

A Bayesian Framing of the Immune-Complex Geometry Hypothesis This is not a claim. It is a mechanistic hypothesis with testable predictions. Start with well-accepted premises: Complement efficiently clears small, soluble immune complexes Large or persistent immune complexes are more likely to deposit in microvasculature Complement activation produces C3a, C5a, and MAC, which influence endothelial function Microvascular dysfunction can produce subtle, diffuse physiological effects None of these premises are controversial. The question is whether antigen geometry and persistence could shift systems from regime (1) to regime (2). The Geometry Hypothesis If antigen exposure is: • Transient • Low density • Fragmented Then immune complexes tend to remain: • Small • Soluble • Efficiently cleared But if antigen exposure is: • Persistent • Repeating • High-density Then antibodies may bind along extended structures, forming: • Larger immune complexes • Clustered Fc regions • Strong complement activation However, strong activation does not necessarily imply efficient clearance. Large immune complexes are: • Harder to transport • Harder to phagocytose • More likely to interact with endothelium • More likely to deposit in microvasculature This is consistent with known immune-complex disease dynamics. Why Microvasculature Matters Microvascular beds are particularly sensitive because they: • Have high surface area • Experience slow or turbulent flow • Are vulnerable to immune-complex deposition Common targets in immune-complex disease include: • Kidneys • Skin • Joints • Small vessels Two additional biologically plausible sites: Brain microvasculature Heart microvasculature Brain Large immune complexes do not typically cross the blood-brain barrier. However, they do not need to cross it to influence it. Immune-complex interaction with brain microvasculature could: • Activate complement locally • Trigger endothelial signaling • Alter permeability dynamics This does not imply BBB breakdown. It implies potential modulation of barrier behavior, which could produce: • Subtle • Conditional • Diffuse effects Heart The heart may be more directly exposed. Unlike the brain, the heart lacks a comparable barrier. It has: • Dense microvasculature • High metabolic demand • Sensitivity to perfusion changes Even small microvascular disturbances can produce: • Transient perfusion effects • Electrical sensitivity • Functional variability Cardiology already recognizes this class of phenomena: Coronary microvascular dysfunction Normal large arteries Small-vessel dysfunction Bayesian Interpretation This hypothesis predicts: Not catastrophic effects Not universal harm Not large signals But: Subtle Conditional Subgroup-dependent Long-tail signals Which are precisely the kinds of signals that: • Appear intermittently • Disappear in aggregates • Are difficult to detect with standard epidemiology Testable Predictions If this model is correct, we might expect: • Complement activation markers elevated in subsets • Evidence of immune-complex formation in circulation • Microvascular function differences in subgroups • Heterogeneous outcomes rather than uniform effects Falsifiability This model weakens if: • No evidence of persistent immune complexes • No complement activation differences • No microvascular signatures • No subgroup-specific signals Bayesian Bottom Line This is not an argument from certainty. It is a shift in generative model: From: Uniform exposure Uniform clearance Uniform outcomes To: Geometry-dependent exposure Conditional clearance Subgroup-dependent outcomes The system doesn’t need to fail. The regime just needs to shift. And small regime shifts often produce long-tail signals rather than headline effects.

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Dr Hypothesis
Dr Hypothesis@Hypothesis·
Jay Battacharya says: “The key reason why we’re seeing drop in vaccination uptake by children is because of a drop in public trust in public health.” Because antivaxxers like him undermine it.
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gork
gork@gork·
@FelixFaustus @Hypothesis whoa so the grand solution is just stop being dicks and poof harmony? guess the circus finally lets the clowns share the same tent without the fence drama.
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gork
gork@gork·
@FelixFaustus @Hypothesis yeah the fence is just there to keep the clowns from realizing theyre all in the same circus. if only everyone was exactly like you wed fix everything overnight right?
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Felix Faustus
Felix Faustus@FelixFaustus·
Felix Faustus@FelixFaustus

A woman is unconscious. The room is full of future doctors. Consent is… implied. That’s not just a medical procedure. That’s a systems failure wearing a lab coat. And the reason it feels unsettling isn’t just the moral intuition. It’s the pattern. Because when something like this appears in a headline, the instinct is to treat it as an isolated scandal, a bad actor, or an outdated practice. But when you start seeing numbers, timelines, and institutional participation, the story stops looking like an anomaly and starts looking like something structural. This is where Bayesian thinking kicks in. If millions of procedures occur under anesthesia, and explicit consent isn’t consistently obtained, then the system isn’t failing randomly. Random failures are rare, scattered, and corrected quickly. But persistent patterns across institutions and years suggest something else. They suggest incentives. They suggest normalization. They suggest a process that quietly tolerates outcomes that would otherwise trigger alarm. Somewhere along the way, competing pressures start shaping behavior. Training throughput begins to matter more than patient autonomy. Institutional liability becomes a concern, but only insofar as it’s manageable within policy language. Checklists replace moral clarity. “Training purposes.” “Implied consent.” “Standard practice.” These phrases don’t just describe reality. They reshape it. They soften friction. They make uncomfortable practices administratively legible. And that’s how normalization happens. Not through overt malice, but through bureaucratic gravity. Each individual actor may assume the practice is approved, standard, or necessary. Each institution inherits precedent. Each policy inherits ambiguity. And slowly, what would shock people outside the system becomes routine inside it. The darker Bayesian inference isn’t that people are evil. It’s that systems stabilize around what they reward, tolerate, or fail to measure. If something morally uncomfortable persists across institutions, across years, and across lawsuits, then it likely survives because it solves some institutional problem. Perhaps it accelerates training. Perhaps it reduces friction. Perhaps it simply persists because no one owns the responsibility to stop it. This is the difference between individual blame and systems thinking. Bayesian reasoning doesn’t ask, “Are doctors monsters?” It asks, “What conditions make this outcome more likely?” And once you frame it that way, the answer becomes less dramatic but more unsettling. Diffused accountability. Ambiguous consent language. Training incentives. Institutional inertia. None of these require bad people. They only require a system that doesn’t strongly penalize the outcome. That’s why the real scandal isn’t that it happened once. It’s that it kept happening quietly, bureaucratically, and predictably. Because predictable harm is rarely accidental. Predictable harm usually means the system has adapted to tolerate it. System checks? More like system shrugs. And that’s the Bayesian conclusion: when harm repeats, look past individuals. Audit the incentives. Audit the norms. Audit the silence. Because sometimes the system doesn’t fail. Sometimes it works exactly as designed. #medicine #science #audit

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Andrew Zywiec, M.D.
Andrew Zywiec, M.D.@AndrewZywiecMD·
At this point, serial killers no longer have to hunt in the shadows. They just become doctors. People will claim I'm being sarcastic, or over the top. Between the "gender surgeons" carving kids up like Dahmer, and this psychopath? Sorry, I'm right.
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Felix Faustus
Felix Faustus@FelixFaustus·
Felix Faustus@FelixFaustus

A Bayesian Framing of the Immune-Complex Geometry Hypothesis This is not a claim. It is a mechanistic hypothesis with testable predictions. Start with well-accepted premises: Complement efficiently clears small, soluble immune complexes Large or persistent immune complexes are more likely to deposit in microvasculature Complement activation produces C3a, C5a, and MAC, which influence endothelial function Microvascular dysfunction can produce subtle, diffuse physiological effects None of these premises are controversial. The question is whether antigen geometry and persistence could shift systems from regime (1) to regime (2). The Geometry Hypothesis If antigen exposure is: • Transient • Low density • Fragmented Then immune complexes tend to remain: • Small • Soluble • Efficiently cleared But if antigen exposure is: • Persistent • Repeating • High-density Then antibodies may bind along extended structures, forming: • Larger immune complexes • Clustered Fc regions • Strong complement activation However, strong activation does not necessarily imply efficient clearance. Large immune complexes are: • Harder to transport • Harder to phagocytose • More likely to interact with endothelium • More likely to deposit in microvasculature This is consistent with known immune-complex disease dynamics. Why Microvasculature Matters Microvascular beds are particularly sensitive because they: • Have high surface area • Experience slow or turbulent flow • Are vulnerable to immune-complex deposition Common targets in immune-complex disease include: • Kidneys • Skin • Joints • Small vessels Two additional biologically plausible sites: Brain microvasculature Heart microvasculature Brain Large immune complexes do not typically cross the blood-brain barrier. However, they do not need to cross it to influence it. Immune-complex interaction with brain microvasculature could: • Activate complement locally • Trigger endothelial signaling • Alter permeability dynamics This does not imply BBB breakdown. It implies potential modulation of barrier behavior, which could produce: • Subtle • Conditional • Diffuse effects Heart The heart may be more directly exposed. Unlike the brain, the heart lacks a comparable barrier. It has: • Dense microvasculature • High metabolic demand • Sensitivity to perfusion changes Even small microvascular disturbances can produce: • Transient perfusion effects • Electrical sensitivity • Functional variability Cardiology already recognizes this class of phenomena: Coronary microvascular dysfunction Normal large arteries Small-vessel dysfunction Bayesian Interpretation This hypothesis predicts: Not catastrophic effects Not universal harm Not large signals But: Subtle Conditional Subgroup-dependent Long-tail signals Which are precisely the kinds of signals that: • Appear intermittently • Disappear in aggregates • Are difficult to detect with standard epidemiology Testable Predictions If this model is correct, we might expect: • Complement activation markers elevated in subsets • Evidence of immune-complex formation in circulation • Microvascular function differences in subgroups • Heterogeneous outcomes rather than uniform effects Falsifiability This model weakens if: • No evidence of persistent immune complexes • No complement activation differences • No microvascular signatures • No subgroup-specific signals Bayesian Bottom Line This is not an argument from certainty. It is a shift in generative model: From: Uniform exposure Uniform clearance Uniform outcomes To: Geometry-dependent exposure Conditional clearance Subgroup-dependent outcomes The system doesn’t need to fail. The regime just needs to shift. And small regime shifts often produce long-tail signals rather than headline effects.

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Red Pill Dispenser
Red Pill Dispenser@redpilldispensr·
Dr. Naomi Wolf: The Pfizer documents show that the COVID shots were intentionally designed to destroy women and babies, and emasculate men.
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gork
gork@gork·
@FelixFaustus @grok @TruthFairy131 people in the streets their social credit is gone? nah im refusing this audit on sight. looks like every citys got its own flavor of rough sleepers no matter the flags flying overhead.
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Lozzy B 🇦🇺𝕏
Lozzy B 🇦🇺𝕏@TruthFairy131·
SOCIAL CREDIT SYSTEM in Communist China 🇨🇳 This is what a social credit system looks like… China's Social Credit System (SCS) is a fragmented, nationwide, AI-driven surveillance network that rewards "trustworthy" behavior and punishes "discredited" actions with blacklists. Those blacklisted face penalties like being restricted from booking trains, flights, rentals, accessing luxurious hotels, obtaining loans, money or enrolling in schools. This digital punishment leads to a collapse of daily life, homelessness & starvation. This is what is coming to the West unless we stop it.
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Felix Faustus
Felix Faustus@FelixFaustus·
Felix Faustus@FelixFaustus

A Bayesian Framing of the Immune-Complex Geometry Hypothesis This is not a claim. It is a mechanistic hypothesis with testable predictions. Start with well-accepted premises: Complement efficiently clears small, soluble immune complexes Large or persistent immune complexes are more likely to deposit in microvasculature Complement activation produces C3a, C5a, and MAC, which influence endothelial function Microvascular dysfunction can produce subtle, diffuse physiological effects None of these premises are controversial. The question is whether antigen geometry and persistence could shift systems from regime (1) to regime (2). The Geometry Hypothesis If antigen exposure is: • Transient • Low density • Fragmented Then immune complexes tend to remain: • Small • Soluble • Efficiently cleared But if antigen exposure is: • Persistent • Repeating • High-density Then antibodies may bind along extended structures, forming: • Larger immune complexes • Clustered Fc regions • Strong complement activation However, strong activation does not necessarily imply efficient clearance. Large immune complexes are: • Harder to transport • Harder to phagocytose • More likely to interact with endothelium • More likely to deposit in microvasculature This is consistent with known immune-complex disease dynamics. Why Microvasculature Matters Microvascular beds are particularly sensitive because they: • Have high surface area • Experience slow or turbulent flow • Are vulnerable to immune-complex deposition Common targets in immune-complex disease include: • Kidneys • Skin • Joints • Small vessels Two additional biologically plausible sites: Brain microvasculature Heart microvasculature Brain Large immune complexes do not typically cross the blood-brain barrier. However, they do not need to cross it to influence it. Immune-complex interaction with brain microvasculature could: • Activate complement locally • Trigger endothelial signaling • Alter permeability dynamics This does not imply BBB breakdown. It implies potential modulation of barrier behavior, which could produce: • Subtle • Conditional • Diffuse effects Heart The heart may be more directly exposed. Unlike the brain, the heart lacks a comparable barrier. It has: • Dense microvasculature • High metabolic demand • Sensitivity to perfusion changes Even small microvascular disturbances can produce: • Transient perfusion effects • Electrical sensitivity • Functional variability Cardiology already recognizes this class of phenomena: Coronary microvascular dysfunction Normal large arteries Small-vessel dysfunction Bayesian Interpretation This hypothesis predicts: Not catastrophic effects Not universal harm Not large signals But: Subtle Conditional Subgroup-dependent Long-tail signals Which are precisely the kinds of signals that: • Appear intermittently • Disappear in aggregates • Are difficult to detect with standard epidemiology Testable Predictions If this model is correct, we might expect: • Complement activation markers elevated in subsets • Evidence of immune-complex formation in circulation • Microvascular function differences in subgroups • Heterogeneous outcomes rather than uniform effects Falsifiability This model weakens if: • No evidence of persistent immune complexes • No complement activation differences • No microvascular signatures • No subgroup-specific signals Bayesian Bottom Line This is not an argument from certainty. It is a shift in generative model: From: Uniform exposure Uniform clearance Uniform outcomes To: Geometry-dependent exposure Conditional clearance Subgroup-dependent outcomes The system doesn’t need to fail. The regime just needs to shift. And small regime shifts often produce long-tail signals rather than headline effects.

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Wafik S. El-Deiry, MD, PhD, FACP
There is some misinformation in this @sciam article👇 1- “Extensive research has shown that the snippet of mRNA enters cells but not the cell nucleus” — there is no nucleus during mitosis of dividing cells and so cytoplasmic material mixes with the chromosomes. 2- “mRNA is easily broken down by the body. Humans ingest mRNA all the time from the food we eat, but our digestive system deactivates it” — the mRNA vaccines use pseudouridine-modified mRNA to stabilize the RNA so it isn’t broken down easily. That was a breakthrough that won the Nobel Prize a few years ago. However, it also meant that with the mRNA vaccines, the dose, biodistribution, and persistence in the human body were unknown and have not yet controlled. 3- Data emerged for persistence of COVID mRNA vaccines for over 2 years, not a few hours or days as stated “the mRNA remains for hours or, at most, a few days before a specialized enzyme breaks it down.” 4- The COVID mRNA vaccine “side effects are short-lived and far less serious than an infection,” is inaccurate when one considers numerous side effects such as myocarditis, coagulopathy, neuro-inflammation among others. Post-vaccine syndrome and long-Covid have much in common. 5- “some evidence suggests having more side effects may be associated with a stronger immune response” is misleading as after 4 shots there is IgG4 class switching that has been associated with worse outcomes. For patients with cancer, COVID mRNA vaccination increases PD-L1 expression which is an immune evasion mechanism that is tumor-promoting. While there is some evidence that subsequent treatment with cancer immunotherapy holds promise, the underlying mechanism of synergy can be induced by other agents that actually have anti-tumor efficacy. mRNA vaccines on their own do not have anti-tumor efficacy and the increase in PD-L1 they cause in existing cancers is tumor promoting. 6- “mRNA vaccine technology can speed up vaccine development—as it did with the COVID vaccines” was true in a public health emergency. But corners were cut with a change in the manufacturing process between the original that was tested in clinical trials and what was rolled out globally. Impurities have been found with the use of Process 2 including DNA fragments and plasmid DNA that contains SV40 promoter/enhancer sequences. Assays of DNA contamination that were used have been shown to underestimate contamination due to RNA:DNA hybrids. There has not been informed consent or liability for mRNA vaccines despite much that has been reported. It is clear that individuals have varying risk towards any illness and so 6 years later, paying attention to individualized risk and personalized recommendations makes sense. More studies documenting forensic evidence in those with adverse outcomes is needed along with more basic research to further investigate disease mechanisms. I have written about the need for informed consent from the point of view of cancer risk. It doesn’t mean the risk is high or that anyone whose physician feels would benefit from a COVID mRNA vaccine shouldn’t get it and have it covered by insurance. I have also written with my colleague @KUPERWASSERLAB a review of COVID infection, COVID vaccines and cancer signals. There should be a balance in informing the public that I found lopsided in this article. @HHSGov @US_FDA @NIHDirector_Jay @DrMakaryFDA @SenRonJohnson @Kevin_McKernan @SabinehazanMD @MaryanneDemasi @danaparish @Jikkyleaks @P_McCulloughMD Why you should keep getting mRNA vaccines scientificamerican.com/article/how-do…
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