Giza Khafre Project - Ground Penetration Radar

Khafre Project Team; Corrado Malanga, Filippo Biondi, Armando Mei, and Nicole Ciccolo.

Too early to tell if this is an elaborate hoax or a significant development in expanding the capabilities of SAR radar that could open up new information on all the fascinating archeological sites worldwide.

KHAFRE PROJECT:

Full Abstract, (with text) Corrado Malanga, Filippo Biondi, Armando Mei (PDF):

Original post:

Higher resolution images:

Nicole Ciccolo's Expedition Channel

Malanga, Biondi, Mei Update March 2:

Malanga, Biondi, Mei Update March 4:

Malanga Update, March 16:

2022 Complete technical report on the Great Pyramid SAR scans Malanga, Biondi:

Manu Seyfzadeh, review/explanation video of their 2022 Great Pyramid Report:

More about Synthetic Aperture Radar scanning:

THE SECRET UNDERWORLD OF GIZA (Exclusive revelations of GPR scans of Giza, and MUCH more, William Brown & Trevor Grassi):

REVEALING NC2: The Cave Entrance to Giza's Secret Underworld (Richard Gabriel & Trevor Grassi):

Liz Metcalfe, Dreams of Atlantis:

Project Unity:

Reese Report - Rumble:

Jahannah James:

Article:

Mike Ricksecker article/video:

Corrado Malanga

https://youtu.be/EYXFgl00HeM

Website corradomalangaexperience

Corrado Malanga, July 2005

Alien abductions

Malanga Papers

Alien Cicatrix (in Italian)

SYNTHETIC APERTURE RADAR DOPPLER TOMOGRAPHY REVEALS DETAILS OF UNDISCOVERED HIGH-RESOLUTION INTERNAL STRUCTURE OF THE GREAT PYRAMID OF GIZA

Alien-Hierarchies-Dr-Corrado-Malanga 2013

politics - coming election

With an election around the corner, I asked Grok3 what it thinks we should do.

Evaluation of political Candidates

When Canadians face an election, evaluating candidates effectively is key to making an informed choice. Here are the principal criteria to consider:

Integrity and Transparency: Seek candidates who are open and honest about their intentions, funding sources, and past actions. Trustworthiness is foundational for anyone in public service.
Policy Alignment: Review their platforms carefully. Do their proposed policies on issues like healthcare, climate change, the economy, and social justice match your values and address Canada’s pressing needs?
Experience and Competence: Look at their background—whether in public office, business, or community leadership. Have they shown they can handle complex responsibilities and deliver results?
Leadership and Communication: Effective leaders articulate a clear vision and bring people together. Assess how well they communicate and navigate Canada’s diverse political landscape, including its parliamentary system.
Accountability: Choose candidates who own up to mistakes and prioritize the public’s interests over personal or party agendas. A willingness to learn and adapt is a strong indicator of character.
Inclusivity: Canada thrives on its diversity. Candidates should show a genuine commitment to representing all communities, including Indigenous peoples, immigrants, and marginalized groups.
Global Perspective: Given Canada’s international presence, consider their positions on foreign policy, trade, and global climate commitments. A strong stance here reflects an understanding of Canada’s role on the world stage.

Focus on substance rather than flash. Elections are about shaping Canada’s future, so weigh these criteria carefully to choose leaders who will serve the country well.

Economic prosperity

Economic prosperity is about more than just growing a country’s GDP—it’s about building a system where wealth is created and shared in a way that benefits everyone over the long term. So, how do we achieve it? Let’s break it down into the key ingredients that drive sustainable economic success.

1. Innovation as the Engine

Prosperity starts with innovation. This means investing heavily in research and development (R&D), education, and infrastructure. Countries like South Korea show how this works—they focused on technology and education, transforming themselves into leaders in industries like semiconductors and electric vehicles. For a country like Canada, with its wealth of talent, the trick is to keep ideas at home by offering tax incentives for startups, stronger intellectual property laws, and better access to venture capital.

2. Smart Trade Strategies

Trade is a cornerstone of many economies, especially export-driven ones like Canada’s. But relying too much on one market—like the U.S.—is risky. Diversifying trade partners (think Asia, Europe, or Africa) and adding value to raw resources before exporting them can boost prosperity. Norway’s a great example—they used oil wealth to build a sovereign fund that invests worldwide. Canada has the resources; it just needs a bolder vision to process and profit from them domestically.

3. A Flexible Workforce

The rise of automation and AI means jobs will change fast. To stay prosperous, workers need reskilling programs tailored to future demands. Germany’s apprenticeship model, which links vocational training to industry needs, is a blueprint worth copying. In Canada, this could mean focusing on trades and tech to keep the workforce adaptable and employed.

4. Fiscal Responsibility

Debt isn’t inherently bad, but it has to be managed. Japan’s decades of stagnation highlight the danger of unchecked borrowing without structural fixes. Smart spending—on infrastructure, green technology, and digital upgrades—can fuel prosperity without burying the future in debt. It’s about investing, not just handing out short-term fixes.

5. Inclusive Growth

Prosperity that only benefits the rich isn’t stable. The U.S. shows this: booming stock markets alongside a shrinking middle class and social unrest. Spreading wealth through affordable housing, healthcare, education, and fairer taxes—while also encouraging entrepreneurship in underserved areas—creates an economy that lifts everyone up.

6. Sustainability as Opportunity

Climate change isn’t just a challenge; it’s an economic opening. Resource-heavy economies like Canada’s can thrive by investing in clean tech, carbon capture, and sustainable agriculture. Denmark’s energy independence through wind power proves it’s possible. With vast land and expertise, Canada could lead—if it commits.

The Bottom Line

Economic prosperity comes from blending innovation, strategic trade, a skilled and adaptable workforce, disciplined spending, inclusivity, and a forward-thinking approach to climate. It’s a straightforward recipe, but it takes bold leadership to make it happen. Examples like South Korea, Norway, Germany, and Denmark show it’s achievable—now it’s just a matter of doing it.

Exploiting Canada's vast resources

Exploiting Canada’s vast resources could turbocharge economic prosperity if done right—maximizing value while avoiding the traps of waste, environmental ruin, or short-term thinking. Canada’s got a treasure chest: oil, gas, minerals, timber, freshwater, and arable land. The challenge is turning that into lasting wealth, not just quick cash. Here’s how to approach it.

1. Value-Added Processing

Exporting raw materials like crude oil or unprocessed timber is a missed opportunity. Canada could refine its oil, manufacture high-grade lumber products, or turn minerals into batteries and tech components domestically. Look at Saudi Arabia—they’re shifting from raw oil exports to petrochemicals and renewables with Vision 2030. Canada could follow suit, keeping more jobs and profits at home.

2. Strategic Resource Management

Resources aren’t infinite, so prioritize long-term gain over short-term extraction. Norway’s oil model is the gold standard: they tax production heavily, invest the proceeds in a sovereign wealth fund (now worth over $1 trillion), and pace extraction to avoid boom-bust cycles. Canada could do this with its oil sands, lithium, or rare earths, building a nest egg for future generations.

3. Tech-Driven Extraction

Modern tech can make resource exploitation cleaner and more efficient. AI and robotics can cut costs and emissions in mining, while carbon capture can green up oil and gas. Australia’s using automated trucks and drones in its iron ore mines—Canada could adapt that for its nickel or copper deposits, staying competitive and sustainable.

4. Diversify the Portfolio

Leaning too hard on one resource—like oil—leaves you vulnerable to price swings. Canada’s got a broad mix to play with: hydropower, uranium, gold, potash, and more. Push investment into underdeveloped sectors like critical minerals for EV batteries (think cobalt and graphite), where global demand is spiking. Chile’s lithium boom shows how niche resources can pay off big.

5. Indigenous Partnerships

Resource projects often sit on Indigenous land. Cutting First Nations into the deal—through equity stakes, jobs, or revenue sharing—can speed up approvals and spread the wealth. The Fort McKay First Nation in Alberta, co-owning oil sands projects, rakes in millions annually. It’s a win-win if done with real respect and follow-through.

6. Environmental Balance

Strip-mining the country without care kills prosperity down the road—think polluted water or dead forests. Sustainable practices, like reforestation after logging or tailings cleanup in mining, preserve the land for other uses (tourism, agriculture). Sweden’s iron ore industry thrives while keeping strict eco-standards—Canada could match that with its own resources.

The Catch

Execution’s everything. Historically, Canada’s been too cozy selling raw goods to the U.S. cheap and calling it a day. Breaking that habit needs gutsy policy: tax breaks for processing plants, penalties for over-extraction, and serious R&D funding. Get it right, and Canada’s resources could fund a century of prosperity—not just a decade of paychecks.

Current perspective on key issues

Here’s the current perspective on the issues you’ve asked about: aging boomers, unaffordable housing, a shifting job market, inexpensive foreign competition, and the impact of AI and robotics. These are interconnected challenges shaping today’s world, particularly in places like Canada, and they’re messy, complex, and urgent. Let’s break them down.

Aging Boomers

The Baby Boomer generation—born roughly between 1946 and 1964—is hitting retirement age in droves. People are living longer, which is great, but it’s also straining healthcare, pensions, and social services. Fewer workers are left to support a growing retiree population, creating a dependency ratio headache. In Canada, for example, this demographic shift is putting serious pressure on the economy. The current view is that systems aren’t fully prepared for the costs—think rising healthcare bills and shrinking tax bases. Some suggest boosting immigration to replenish the workforce or encouraging older folks to keep working in flexible roles, but neither is a slam dunk. Politically, immigration’s a hot potato, and most boomers aren’t thrilled about delaying retirement.

Unaffordable Housing

Housing affordability is a crisis in many places, especially cities like Toronto and Vancouver. Prices have soared beyond what wages can support, locking younger generations out of homeownership. It’s not just a supply-and-demand issue—though there aren’t enough homes being built. Zoning laws stifle new construction, speculative investors (including foreign buyers) drive up costs, and wages stagnate. The perspective today is grim: without major changes, this could destabilize society, with millennials and Gen Z stuck renting or living with parents. Proposed fixes include reforming zoning to allow denser housing, taxing vacant properties or foreign investors, and capping rent hikes. But these ideas face resistance from homeowners and industry lobbyists who benefit from the status quo.

Changing Job Market

The job market’s in flux, and the old model—study once, work one career, retire at 65—is history. Technology, automation, and the rise of gig work have upended traditional paths. Manufacturing’s declining, new industries are emerging, and workers need to adapt constantly. The current take is that this shift demands flexibility, but education and retraining programs lag behind. Canada, like many countries, risks a wave of underemployment unless it invests heavily in vocational training, apprenticeships, and tech skills. The challenge is clear: adapt fast or leave entire generations scrambling.

Inexpensive Foreign Competition

Globalization means companies can tap cheap labor abroad, producing goods at lower costs but hollowing out local industries. In Canada, manufacturing jobs have been bleeding out for decades, and wages face downward pressure as a result. The perspective here is nuanced—cheap imports benefit consumers, but they gut communities reliant on those lost jobs. Protectionism (like tariffs) is tempting but risky, often sparking trade wars. Instead, the focus is shifting toward competitiveness: bolstering high-value sectors like clean tech or advanced manufacturing where Canada can shine. It’s about playing to strengths rather than fighting a losing battle.

Impact of AI and Robotics

AI and robotics are game-changers, and they’re coming fast. AI’s already shaking up white-collar fields like law and finance, while robotics threaten blue-collar jobs like trucking and warehousing. The upside is huge productivity gains; the downside is potential mass unemployment. The current view is that this isn’t just another tech shift—it’s a transformation of work itself. Preparing means rethinking education to emphasize creativity and problem-solving over rote skills, experimenting with ideas like universal basic income, and creating new roles in emerging fields. It’s a tightrope: harness the benefits without letting entire swaths of workers fall through the cracks.

The Big Picture

These issues don’t exist in silos—they feed into each other. Aging boomers strain housing and healthcare while exiting the workforce. Unaffordable housing traps young people in unstable jobs. Foreign competition and automation kill those jobs, and AI could either amplify the chaos or offer a lifeline. The prevailing perspective is that we’re facing a perfect storm of crises, and the old economic playbook—growth at all costs, minimal intervention—won’t cut it. Solutions demand bold moves: overhauling education, reforming housing policy, rethinking work, and ensuring the benefits of tech and trade don’t just flow to the top. It’s not about ideology; it’s about facing reality before the cracks widen.

covid - jjcouey

https://rumble.com/v2n3t3q-the-endemic-hypothesis-infectious-clones-and-virus-isolation.html

TimeStamps (experimental)

11:04 mortality
15:05 Immunomythology

Preface Notes:

Ran the video through a transcription service and the full text can be found here:

transcript

I also uploaded the transcript to Grok3 and asked a few questions and you can find these after my notes below.

upload-transcript-to-grok-and-asking-questions

My Notes taken while listening to video

He offers 4 Scenarios

Natural Bat Cave Virus Zoonosis
Laboratory Bat Cave Virus Zoonosis
There are no viruses. Will only discuss isolates.
Endemic Background Coronovirus

We were told that in 2018 there were no coronoviruses in circulation. Late 2019 there was a leak of the virus in Wuhan. It then spread around the world and became aplha, beta...and now omicron. They claim the lockdowns and vaccines have saved lives. And that we have defeated epidemics and disease in the past using vaccination. Novel coronoviruses can jump from species and form a pandemic. PCR false positives are rare. Asymptomatic spread is real. The variants are evidence of the spread and continued evolution. We spend money studying gain of function. Lockdowns and EUA did cause deaths but millions were killed by novel viruses and so we need gain of function and bioweapon research and vaccines. This pretty much covers the arguments made for the first two scenarios.

The no-virus scenario is interesting because it draws out the lack of isolates (and the lack of conformance to Koch postulates). But the proponentws of this scenario will not address the other issues so it lacks creditability.

However, isolation of the virus is important. In the scientific community, the way they isolate and the way they culture is very weak.

The final scenario is most interesting because there are coronoviruses in the background and the PCR testing can not differentiate betweeen them. Before the pandemic, coronoviruses were found using pan-coronovirus primers. Coronoviruses were characterized by mostly looking at the RNA dependant RNA polymerase, and the variations there were considered to reflect diversity in the wild. But isolating them and culturing them is notoriusly difficult. Consequently many of the papers reporteded to find Bat coronoviruses are really only using PCR for the RNA-dependent RNA polymerase (RdRP). They are not culturing, they can't culture.

The lockdown, protocols and vaccines account for the total excess deaths called the pandemic. Certainly a pandemic of a virus did not occur.

Endemic Background Coronavirus

The PCR test used was not specific for particular Coronavirus
PCR have many sources of false positives beside high cycle count
Respiratory disease that leads to a secondary pneaumonia is a regular cause of death
Changing the standard protocols for the treatment of general respiratory disease was the primary cause of excess deaths during the pandemic
Additional harms were also cause by the response that also included lockdowns etc.
Additional harms can be mapped to the use of specific agents - medazolam. remdisivir
Early treatment must be considered protocol by protocol ( single likely ie hydroxychloroquine is never given by itself)
We spend money making sure the danger of zoonotic pandemics are taken seriously
We must reject governence by these ideas

I liked that he graphed respiratory deaths instead of all-cause to amplify signal. I had looked at all-cause and the signal was too small to notice.

Pneumonia deaths are pretty consistent year over year peaking each flu season, yet when we decided to change the protocol on how we treat respiratory diseases (sending them home or not treating secondary infections with antibiotics and steroids) we lost 3 times as may people.

Endemic The principle of infectious clones and how they are used to represent RNA virology which are dependent on the ability to use RNA infectious clones which are generated through CDNA constructs

an RNA virus released in one location is not capable of being the same RNA

Some of JJ Couey's other work

5 Concerns about SARS-CoV2 Biology: A Call to Pause, Deliberate, and Revise Policy

https://medium.com/gigaohm-biological

Upload transcript to Grok and asking questions

Infectious Clone Explanation

An infectious clone, as described in the context of virology and Jonathan Cooley’s presentation, refers to a laboratory-generated construct used to produce a functional, replication-competent RNA virus from a DNA template. This technique allows scientists to create a highly controlled and pure version of a virus that can be studied or manipulated, bypassing the natural variability and limitations of culturing viruses directly from infected samples. Here’s a breakdown of what an infectious clone is and how it works, based on my understanding and the details provided:

What is an Infectious Clone?

An infectious clone is essentially a synthetic version of a viral genome, typically created as a complementary DNA (cDNA) copy of the virus’s RNA. This cDNA is engineered into a plasmid (a circular piece of DNA) that can be replicated in bacteria, such as E. coli. The process allows researchers to produce large quantities of identical viral genetic material with a specific sequence, which can then be transcribed into RNA and used to generate infectious viral particles in a controlled setting.

How is it Made?

Sequence Identification: Scientists start with a known or desired viral RNA sequence, often derived from a natural isolate or a consensus sequence (a representative sequence based on multiple samples). For coronaviruses, this might not always be a complete wild-type sequence but could include key regions like the spike protein gene combined with a standardized backbone.
cDNA Construction: The RNA sequence is reverse-transcribed into cDNA, which is more stable and can be manipulated using molecular biology techniques. For larger viral genomes, like those of coronaviruses, multiple cDNA fragments may be assembled into one or more plasmids.
Bacterial Amplification: These plasmids are introduced into bacteria, which replicate the DNA, producing many identical copies. This step ensures a high yield of the genetic material.
RNA Transcription: An RNA polymerase (often T7 or SP6) is used in vitro to transcribe the cDNA back into RNA, mimicking the viral genome. This RNA is typically full-length and highly pure compared to what you’d get from a natural infection.
Introduction into Cells: The synthetic RNA is then introduced into susceptible cells (e.g., Vero E6 cells for coronaviruses) via a method like electroporation, where an electric field helps the RNA enter the cells. Once inside, the RNA can hijack the cell’s machinery to produce viral proteins and assemble new viral particles, which are infectious.

Why Use Infectious Clones?

Control and Purity: Unlike natural viral replication, which produces a mix of replication-competent and defective particles (due to errors by RNA-dependent RNA polymerase), infectious clones allow for the production of a uniform population of viruses with a defined sequence. This is likened to a “CD” versus a “mixtape” in Cooley’s analogy—high fidelity and reproducible.
Research Applications: They’re used to study viral biology, test antivirals, develop vaccines, or investigate specific mutations (e.g., gain-of-function studies). For example, a clone can be engineered to express a particular spike protein variant to see how it affects infectivity.
Overcoming Culturing Challenges: Many RNA viruses, including coronaviruses, are notoriously difficult to culture in large quantities from patient samples. Infectious clones circumvent this by providing an artificial starting point.

Cooley’s Perspective on Infectious Clones

Jonathan Cooley argues that infectious clones could theoretically be used to “seed” a viral sequence globally, creating the illusion of a pandemic. He suggests that if identical sequences of a virus (like SARS-CoV-2) appeared in distant locations (e.g., Wuhan and Washington), it might indicate deliberate distribution of a clone rather than natural spread, given the inherent variability of RNA viruses in nature. He posits:

Natural RNA viruses produce many defective particles (incomplete or non-infectious genomes) due to the error-prone nature of their replication, making widespread, uniform spread unlikely from a single point.
An infectious clone, with its high purity and full-length genomes, could be distributed to multiple locations, cultured, and sequenced to appear as though a single virus is spreading globally.

However, he clarifies that this isn’t his primary claim about the COVID-19 pandemic. Instead, he leans toward the “endemic hypothesis”—that existing coronaviruses, amplified by non-specific PCR testing and protocol changes, explain the observed patterns better than a novel virus or a clone-based conspiracy.

Key Features of Infectious Clones

Artificial Origin: They don’t occur in nature; they’re lab-made tools.
High Fidelity: They produce a more consistent viral population than natural replication, which generates a “swarm” of diverse particles.
Not Self-Sustaining: Once introduced into a host, the clone replicates like a natural virus, producing defective particles and losing its initial purity over generations.

In summary, an infectious clone is a powerful virological tool that allows precise control over a virus’s genetic makeup and production. Cooley uses it to question the narrative of a naturally spreading pandemic, suggesting it could be a mechanism to manipulate perceptions of viral spread, though he emphasizes broader systemic issues (like testing and protocols) as the core of his critique.

Understanding "Endemic" in Cooley’s Context and Its Application to Respiratory Viruses

Here’s an explanation of what Jonathan Cooley means by "endemic" and how he applies it to respiratory viruses, particularly in the context of his critique of the COVID-19 pandemic narrative:

What Does "Endemic" Mean?

In epidemiology, "endemic" refers to the constant, baseline presence of a disease or infectious agent within a specific geographic area or population, without requiring external inputs to sustain it. Unlike an epidemic (a sudden increase in cases) or a pandemic (a global epidemic), an endemic disease is stable and predictable, often fluctuating seasonally or cyclically but not causing widespread disruption. Examples include the common cold or seasonal influenza in many regions—diseases that persist in the background, infecting people at a relatively steady rate over time.

Cooley’s Definition of "Endemic" in Context

Cooley uses the term "endemic hypothesis" to propose that coronaviruses, including those implicated in the COVID-19 pandemic, are not novel pathogens that emerged suddenly and spread globally from a single point (e.g., Wuhan). Instead, he argues they are part of a pre-existing, diverse family of respiratory viruses that have been circulating in human populations for decades or longer. In his view, these viruses are a natural, ubiquitous "background" presence—endemic rather than epidemic or pandemic in nature. He suggests that what we perceive as a new pandemic is actually a mischaracterization of this endemic viral population, amplified by factors like non-specific testing and changes in medical protocols.

How It Applies to Respiratory Viruses

Cooley applies this concept specifically to respiratory viruses, with a focus on coronaviruses, to challenge the official narrative about SARS-CoV-2. Here’s how he frames it:

1. Pre-Existing Diversity

He asserts that coronaviruses are a large family (he mentions "200 diverse endemic coronaviruses" in textbooks) that have long caused respiratory illnesses in humans, such as the common cold (e.g., OC43, 229E). Only a few strains, like SARS-CoV-1 and MERS, are well-known because they’re more severe, but most are benign and go unnoticed.
He argues that SARS-CoV-2-like sequences could already have been part of this endemic pool, not a new entity requiring a dramatic origin story (e.g., a lab leak or zoonotic jump).

2. Limits of Natural Spread

Cooley emphasizes that RNA viruses, including coronaviruses, lack the fidelity and stability to spread uniformly across the globe from a single point. Their replication produces many defective particles, reducing their ability to sustain a pandemic-level outbreak naturally. He contrasts this with historical examples like SARS-1 (2002-2003), which infected only ~8,000 people despite escaping labs multiple times.
He suggests that if coronaviruses were truly capable of pandemic spread, we’d have seen it before, but instead, their behavior aligns with endemicity—localized, limited outbreaks rather than global domination.

3. PCR Testing and Misattribution

A key part of his endemic hypothesis is that PCR tests, used widely during COVID-19, are not specific enough to distinguish a supposed novel coronavirus (SARS-CoV-2) from the endemic coronaviruses already present. Before the pandemic, coronaviruses were detected with pan-coronavirus primers targeting conserved regions like the RNA-dependent RNA polymerase, reflecting their diversity rather than a single strain.
He posits that positive PCR results could be picking up this endemic background, mislabeling it as a new virus, rather than detecting a unique pathogen spreading worldwide.

4. Protocol Changes as the Real Culprit

Cooley argues that excess deaths attributed to a novel coronavirus pandemic are better explained by changes in medical protocols (e.g., withholding antibiotics for secondary pneumonia, ventilator misuse, lockdowns) rather than a new virus. He suggests that respiratory diseases, including those caused by endemic coronaviruses, became more lethal due to these interventions, not because of a new pathogen’s emergence.
In this view, the "pandemic" is an artifact of reclassifying endemic respiratory illness as a national security threat, not evidence of a novel virus’s spread.

Implications for the COVID-19 Narrative

Cooley’s endemic hypothesis contrasts sharply with the mainstream view that SARS-CoV-2 emerged in late 2019, spread globally, and evolved into variants like Alpha, Delta, and Omicron. He rejects this single-point-origin story, asserting:

The genetic similarity of early sequences (e.g., Wuhan and Washington) might reflect either endemic circulation or artificial seeding (via infectious clones), not natural pandemic spread.
Variants could be pre-existing diversity within the endemic pool, not evidence of a single virus mutating over time.
The immune system is already attuned to these viruses, handling them effectively unless disrupted by external factors (e.g., vaccines or protocol changes), supporting their benign, endemic status.

Summary

By "endemic," Cooley means that coronaviruses are a constant, diverse presence in human populations, not a sudden threat capable of causing a true pandemic. He applies this to respiratory viruses by arguing that what we’ve called COVID-19 is likely a rebranded version of these background pathogens, exaggerated by flawed testing and deadly policy shifts. In his view, the biology of RNA viruses—error-prone, defective-heavy replication—supports their endemic nature, not a globe-spanning outbreak, challenging the need for a novel-virus explanation altogether.

covid - jjcouey transcript

My name is Jonathan Cooley. I'm a former academic biologist whose last academic position was at the University of Pittsburgh School of Medicine as a research faculty member. The highlight of my academic career was going through the lab of Mabrid and Edward Moser, who won the Nobel Prize in 02/2014 about a year after I left the lab. So I I was a a professor in Pittsburgh in 02/2020, and I've spoke out repeatedly against the use of transfection as an immunization methodology, and that is primarily why I was fired. Since then, I have been speaking out about a bunch of things and learning a bunch of things about immunology and virology.

And one of the things that I stumbled on is this, principle of infectious clones and how they are used to essentially produce virology. The whole field of RNA virology is dependent on the ability to use, RNA infectious clones, which are generated through cDNA constructs. And so I think it's really important that everybody understand this because for the last three years, we've been told that a coronavirus, at least, released from a single point in in China, was able to circumvent the globe, let's say, thousands of times over the last three years resulting in, you know, millions and millions of infections and millions and millions of deaths. And this is, in my best estimation, not possible. And I apologize for my lack of breath, but I I really don't have anything better than this right now.

So I'm just I just gotta talk slowly, and, hopefully, I won't run out of gas. So my last presentation, I did a little bit more about the immunomythology and how much they've really misled us about. I'm just gonna summarize that really quick. And then I did infectious clones, and then I talked about the endemic hypothesis. Tonight, I wanna reverse these a little bit mainly because I wanna clarify what the endemic hypothesis is.

I think so many people since I presented to you guys and one other group have been trying to say that my primary claim is that infectious clones were used to cause the pandemic, and it's not at all it's not even close to what my actual idea is. My idea is is that infectious clones could be used to seed a sequence around the world so that when they cultured it and sequenced it, it would look like the same virus. But an mRNA or sorry, an RNA virus released in one place is not capable of being the same RNA virus when it gets to Washington and California and New York and Spain and Italy. That's not that's not how this works. Now the best example that we have of this is the previous SARS release in 02/2002, which I would argue was probably also an infectious clone release.

And there, you had eight thousand people infected and seven hundred and ninety some people dead. So at this stage, I think it's really important that everybody understand that the the likelihood that this was as as Trudeau just said recently, the most, the largest crisis in the last hundred years since the Spanish flu. We have been misled to believe that coronaviruses are capable of doing that, And we are now being misled into solving the mystery. That's what this is, solving the mystery that this was a lab leak virus, and now everything makes sense. And so I'm gonna start with this because I really want you to to to get a grasp on, get everybody on the same page.

So this is basically what Fauci has told us. That in 02/2008, there weren't any coronaviruses in circulation. And then in 02/2019, somewhere at the end of the year, there was a leak of a virus in Wuhan, and this thing spread around the world and became alpha, beta, delta, gamma, whatever, until it was Omicron in South Africa in 02/2021. And then now Omicron took over the world in 02/2022, and now we're at Omicron x b b 1.66 or something like that. The lock the lockdowns, the protocols, and the vaccines have actually saved lives in this in this scenario, and we have defeated disease and epidemics in the past using vaccination.

Novel coronaviruses can jump from other species and can pandemic, and PCR false positives are rare. Asymptomatic spread is real, only some over counting. The variants are evidence of both spread and continued evolution, and we spend money studying gain of function in laboratories. So the laboratory, bat cave zoonosis isn't much different except instead of coming out of a bat cave to Wuhan, it came out of a lab in Wuhan, and it goes around the world, becomes Omicron, and here we are today. The lockdowns and protocols probably save lives in this story too if you if you believe one aspect of it or you believe one version of it.

Excuse me. And then very similar to the last one, all of these things are true as well. PCR works, and it's it's it's very rare to be false positive. Variants are real, and we do gain of function research. You can also adjust this and say that the lockdowns and the emergency use authorizations cause deaths, and millions were killed by a novel virus.

And so we should focus on gain of function and bioweapons, etcetera. That's another version of this story also on TV. So in this scenario, there are no viruses. This is another one that didn't seem to get people eaten up by. In this scenario, previous diseases like measles don't even have a basis in reality.

Novel coronaviruses don't exist, and the the endemic ones don't exist. PCR can't be used to do anything. Variance and their other sequences are all made up, and they don't care about gain of function because they think that's also nonsense. And they don't wanna does discuss all cause mortality. They don't wanna discuss anything.

The only thing these people wanna discuss is isolation. So I think that's important because, actually, isolation and the isolation of the virus is something that is very weak in the scientific in the scientific foundation of coronavirus, the way that they isolate, and the way that they culture is very, very weak. And so the people that propose this as an outcome actually have a lot of solid ground to stand on with respect to what they stand on. The point is is that whenever you engage people who who believe in this theory, they are unwilling to talk about anything else except for the three or four things that they're very sure about, which you might say is a reasonable strategy, but it it gets them it gets them and anybody who follows them nowhere, and they're not gonna make any progress in terms of getting us out of this. And they don't wanna talk about, for example, the changes in protocols, and they don't wanna talk about any other strategy other than proof of isolation.

And so the endemic background is something very different. The endemic background is the idea that there are coronaviruses in the background, and the PCR test can't differentiate between them. And that's not a very far fetched idea because before the pandemic, coronaviruses were found using pan coronavirus primers. Coronaviruses were characterized mostly by looking at the RNA dependent RNA polymerase, and the variation there was considered to reflect diversity in the wild. But isolating them and culturing them is notoriously difficult.

And so many of the papers that purport to find bad coronaviruses in the wild are really only using PCR for the RNA dependent RNA polymerase, and that's it. They aren't culturing. They can't culture. That's a problem. Now we're gonna have to substantiate that.

Right? We're gonna have to substantiate this idea that, actually, it's lockdowns and protocols and the vaccines that account for the total excess deaths in the pandemic. There's no reason for there to be a novel virus because if you subtract all the ridiculous mistakes we made, all the ridiculous protocols we enacted, then there's very little left for a novel virus to do. Certainly, a pandemic of a virus didn't occur, at least in my estimation. So the PCR test used in 2021 are not specific for a particular coronavirus.

That's very different than them being false positives. PCR tests have many sources of false positives besides the high cycle count. That's other coronavirus genes. Respiratory disease that leads to secondary pneumonia is a regular cause of death, and we change that protocol all around the world to disclude antibiotics. Change in protocol standards for the treatment of general respiratory disease was the primary cause of excess death.

Additional arms are also caused by responses like the lockdowns, and additional arms can be mapped to the use of specific agents like midazolamarin, desivir, etcetera. And early treatment must be considered protocol by protocol because so many of these agents, including hydroxychloroquine, were never given by themselves. Even the famous study done by the French guy very early on, he's giving hydroxychloroquine and azithromycin. And so claiming that hydroxychloroquine is the reason why those patients recovered is a little bit naive. We spend money making sure the danger of zoonotic pandemics is taken very seriously.

That's for sure. And here, I would suggest our primary objective is to reject governance by these ideas. So irrespective of which one you pick, we should not allow ourselves to be governed by these ideas. Now here's the graph, of course, that I showed last time. This is p and I deaths here in in the dark blue.

Can you see my phone there? PNI deaths here in the dark blue. And behind it in red is supposedly COVID, and this has all caused mortality in America up here in the light blue. And so year on year on year, even in the worst years, pneumonia is pretty consistent killer. Pretty consistent killer from 02/2014 all the way to 02/2020.

And then suddenly, when we decided to change the protocols on how we treated respiratory disease by sending people home until they couldn't breathe or not treating secondary pneumonia with antibiotics and and and steroids, we lost three times as many people to pneumonia as we ever have in the recent history of America. Pretty strange. And so my hypothesis is they declared a pandemic of a novel virus said to be detectable and then enable a larger percentage of all cause mortality than p and I, which is this light blue, dark blue down here, to be converted or prioritized as a national security threat. And that, you know, is true being Canadian because you just heard your prime minister say that he never never forced anybody to get vaccinated. But, of course, you know that he did everything he could to coerce you into getting vaccine.

That alone, it should, show you that these people were behaving as if there was a national security threat that gave them the right to lie to you, gave them the right to mislead you about what they knew and didn't know about the virus and about the shot and about the protocols and about the lockdowns. They've lied about everything because this became a national security threat. And I believe that it was very likely a plan. I believe that if there was some kind of molecular signal that was required in order for all of these governments to act in concert, then it would have been done with an infectious clone. But I'm not saying it was because the endemic background and a crappy PCR test would have been enough to create a to create the pandemic.

All that's all that's necessary. And I think it was to, again, to get rid of our our sovereignty. So this is what I covered last time. They changed how we think about respiratory disease. They changed about think about all the cause mortality.

They changed how we think about our immune response to disease, and they changed how we think about immunization, vaccination, and immunity. And what this led to was ventilating people to to stop spread. It allowed them to use remdesivir as a as a protocol that was then rewarded financially. It allowed them to use midazolam in a similar way in other countries. It allowed the them to have secondary pneumonia go crazy in America because they weren't treating it with antibiotics.

They're allowed to shut down schools and put screens in front of our children. They were allowed to mask our children, and they were allowed to socially distance people that had been married for fifty years and let them die alone. This level of malevolence is only explainable by government's thinking that this is a national security priority, and therefore, they must do this. Well, how are they able to do it? Well, a lot of the people on this screen, actually.

A lot of the people on this screen over here are responsible for us believing that there was a pandemic when in fact there wasn't. And this is just an example of what they meant to do here. This is this is an article from Scientific American written by the WHO. The WHO says that mRNA vaccines are safe, powerful, and effective, but I said they were crap and wouldn't work in two thousand twenty, about a year and a half before the inventor Robert Malone even bothered to open his mouth. Masks work according to the WHO.

Indoor air quality matters according to the WHO. Wastewater tracking is useful. And genomic surveillance is key. Absolutely nothing to do with nutrition, nothing to do with anything to do with reality, only to do with control. Let's do infectious clones now really quick just to make sure that everybody gets this idea.

I have, suggested many times that people have misled us to believe or have led us to believe that that pandemics can come out of a bat cave, that pandemics can be the the potential of pandemics can be accessed, can be accessed by cell culture, that they can be accessed by animal passage. And then most recently, you can stitch things together. And if you stitch the right things together and it gets out, wow. Look out because you're gonna have a hell of a pandemic. So that's really the idea.

And so the idea is to coerce you out of individual sovereignty and and invert this globally. That's why it's a pandemic and not just an epidemic in America. This is globally. So here's the cartoon that I hammered on last time, and I'm gonna hammer on it again. This is the picture that they've made with computer animation to show you how the n protein here in pink and the RNA there and the little bead of of tiny little red string there wrapped around the end protein is packaged into a coronavirus particle with spike protein on the outside.

So just because they can make these pretty pictures doesn't mean that that's what happens. And I think that we have been grossly misled in terms of the fidelity of coronavirus even by people who should know better, people who study flu and other viruses. And maybe it's because all of them don't really understand the role that defective genomes play in the viral cycle. But what I would critique here is that in this picture, there are whole viruses. In this picture, there are subgenomic RNAs.

And then in this picture, apparently, the genomic RNA gets assembled. And then outside of the cell, there are viruses floating away. And so I think one of the things that I would challenge all of you to do is spend some time with some earlier coronavirus literature and see if you can find an experiment where they do cell culture and they take the liquid off the cell culture, but not the cell culture itself because it's very rare. It's very rare that they use the supernatant cell culture to find a coronavirus. That's quite strange because all of their models show millions and thousands of viruses being released after an infection in an infectious cell.

So here's the the the analogy that I used last time. They tell you that a virus makes, you know, pretty good copies of itself inside of you and it makes enough of those until you start coughing them out. But for some reason, coronaviruses aren't really that culturable. One one question that I think you should pose to yourself as a scientist and think about it carefully in terms of what you know about other models, and other sort of laboratory experiments. Is it if you wanted to make a lot of coronavirus, what would you do?

And I think you're gonna find that answer to be very frustrating because you can't. Nobody really has a method of taking coronavirus and making a lot more of it. You can't. That's why you can't culture it. It's not like you can take a culture that catches, which is funny.

Right? Because they take these samples from patients and not every patient will grow something in their little cell culture of zero six cells. But the ones that do, you can't take that sample and then keep growing it and make lots more of it until you have a little bottle of coronavirus. It doesn't work like that. You can do that with bacteria.

You can do that with mice. You can do that with plants. You can't do that with viruses. RNA viruses don't work like that, but they would like you to believe that they do. Instead, they don't, and I figured it out when I was challenged by Robert Kennedy to to figure out what a infectious clone was.

And it was from writing this article with him way back in, February. Sorry. 10/21/2022, that I became aware of how ubiquitous these infectious clones were and, more importantly, how they would have enabled a a appearance of a pandemic, to be created, whereas an RNA virus just simply can't do what they say that it that this one has done. And so here's if here's what that really looks like. For every replication competent particle, you're making lots of replication incompetent particles.

It produces viruses. I want you to listen to Robert Malone say this, and I want you to understand who Robert Malone is. Not only is he purported self reported inventor of the mRNA immunization technology, but for about twenty five years, he's been a vaccinologist and a vaccine technology broker between governments and nongovernmental organizations. He's presented to the WHO several times in far back as 02/2011, and he has brokered flu vaccine technologies from bottling technologies to mRNA and and adenovirus technologies. He's been responsible or involved in the Zika virus vaccine.

He's been involved in the anthrax vaccine in America. He's been involved in everything for years. He's also one of the guys who was very early in terms of, studying retroviruses. So when he was a grad student, that was all just taken off. And he decided that he was gonna study retroviruses because at that time, he became convinced that within ten years, there would be a geneticist at every hospital using retroviruses to cure genetic disease.

What this means, however, is that this man, having been there from the beginning of virology and it's and it's sort of exponential rise to prominence with cancer and all sort of stuff and aids and whatever, he was there for all of it. And so it's it's it's not for nothing that he says this. This is a fundamental principle of viral replication that often gets omitted because it belies a much less, let's say, high fidelity model of infection, model of infectiousness, and model of trackability. Listen carefully. It produces viruses.

Matter of fact, in most cases, a large fraction, if not the majority, of the virus particles that are produced are defective. They're not good for anything. They're not infectious. They just kinda float around. And among other things, they interact with the immune system as does the live virus.

No. That's that's a longer video that you can listen to the whole thing. He's not gonna contradict himself. He just explains that that's part of the phenomenon. That's the part of the phenomenon that leads to them not always being culturable.

Now this was originally invented by David Baltimore and Vincent Rancaniello. The first thing they did it on was, was the polio virus. You might know David Baltimore because he got the Nobel Prize for reverse transcriptase. So first of all, let me clarify. The lack of fidelity in the swarm in the viral, you know, in in during replication is not only because RNA cannot be copied with the fidelity that DNA can be copied with.

It's part of the reason. Part of the reason that you have this diversity of genomes is because the RNA dependent RNA polymerase isn't perfect. None of them are. But separately from that, the RNA dependent RNA polymerase skips. It's part of the design of coronaviruses so that their genomes will reassort.

The one consequence of this constant, recombination is incomplete defective genomes. And although they don't really wanna study this phenomenon, it has been identified in flu viruses and other RNA viruses as a phenomenon that could be used in immunization technology by isolating defective genomes all on their own and replicating them. You could inoculate someone against the virus without them having any replication or any replication competent virus there. So in addition to that, you can get recombination. You can get assembly errors.

All of these things can lead to viruses that don't have all of the requisite parts or genes to be infectious when they hit the next cell, but still annoy the immune system. They might even cause cytotoxic effects in a cell culture. So what they have done in all these papers, and I can't stress enough, oh, you just have to go on PubMed and search infectious clone. You'll find papers from every year. They take a sequence that they purport to identify in the wild and with coronaviruses, it's actually often not a whole sequence.

It is a spike protein to which they add a consensus genome that that Ralph Barrick and others have established as kind of the consensus coronavirus genome. And so irrespective of whether they have the whole sequence, they can construct or reconstruct the whole genome and then make clone of it and then play with it in a laboratory. And a clone is that RNA sequence coded in DNA. The reason why that's important is because DNA in a circular form can be copied can be copied by, a bacteria. And so with some viruses, you needed a couple circular DNAs because their genome was pretty long.

But with coronaviruses, you can need five or six circular DNAs to encode the whole genome, and then you have a bacterial culture make many, many, many copies of that DNA. Then you add an RNA polymerase. And from that DNA, you make a fairly pure fairly pure RNA version of that virus. Right? Because you have the whole genome.

And if you use RNA polymerase, it'll make errors. But the most the vast majority will get from one end to the other. You'll have full genomes. This pure RNA is then electroporated into a zero six cell culture, for example. And then what comes out of that, whatever it is, can be injected in an animal's lungs and make them sick.

It can be put on 96 well plates and cause cytopath cytotoxic or cytopathic effects in vero six cells. But in no way, shape, or form have they grown more coronavirus by culturing it. This is a artificial starting point with artificial purity that leads to something that isn't really that natural, although they will tell you that this is a good replication or a good replicant of of whatever the virus does naturally, but it is not because you can never get this pure of genomic RNA if I guess I needed to do that better. Shoot. If it's like this.

If this is the the the normal way that a virus replicates, then this is a way of circumventing that and creating a purity that doesn't exist in nature. It's a lot more replicable. The disease state is a lot more replicable. The cytopathic effects are a lot more replicable. You can send these around the world and start there all the time.

It's a very handy way to do science, but it's not a very adequate way to describe the biology of coronaviruses. But this is a CD. And so instead of a mixtape, this is a CD. It's a high fidelity copies as many times as you want. So why is this important?

It's important because this whole picture that they give us here, the idea that we need neutralizing antibodies to block these viruses is a bit of a misnomer. It's a bit misleading because many of these viruses, even if they have spike protein on them, aren't infectious. So making antibodies to that spike protein to block them, it's not really gonna have the effect that you you imagine it's going to have. And in fact, you have to realize, and I I don't think you have to realize it in that way. I think what you have to do is recalibrate the way you think about this because if this if this is the model, your immune system has already developed a way to deal with it.

Just because virology isn't being honest about how the infectious cycle produces a majority of infectious, defective particles, it doesn't mean that your immune system hasn't already evolved to deal with that problem. And I think that's one of the horrible things that they've done to us is mislead us about that. Because in reality, our bodies already know how to deal with this problem. So I showed you this paper the last time, and I I just go through it again really quick. This is about the best you can do here with regard to figuring this out because only recently has it become possible to sequence RNA directly.

Before this advancement in Nanopore technology, virology kinda had this you know, it had a Mulligan that it could play all the time because we have to use PCR, and we have to use reverse transcriptase to get our to get our viruses to a DNA form so that we can sequence them. And so all viral all RNA virology has always been kind of indirect up until now because when you sequence things, it all becomes a bit gray, especially with coronaviruses when you sequence things and you don't even sequence the whole genome, but instead you build clones around some consensus. In this case, this is, using a clone. So they use a clone of of of SARS CoV two, and what they find are the genomic and subgenomic RNAs. And very typically, you get, you know, hundreds of thousands of copies of these subgenomic RNAs.

And the the virology people argue that the reason why you have so many subgenomic RNAs is because the virus needs to produce so many more of those proteins than it does to make the whole genome. And even though the whole genome is the only thing that gets packaged, the subgenomic RNAs are in so much higher abundance because those proteins need to be made in so much higher abundance. Nevertheless, they argue, of course, in their cartoons that thousands of viruses, viral particles get released, and then those should all have full genomes in them. But instead, what they find here in this paper, for example that was the bigger picture there. What they find in this picture, for example, is a coverage of the n protein RNA between 406 copies.

And in the text, they admit that they only find 111 reads corresponding to the full length genomic RNA. So, again, some people will say that this is a limitation of the nanopore technology, but it's really not because the strange thing is is that this lack of full length genomic RNA has been around for decades. And you can zoom in here, and you can see that they had to go really deep in here to show you anything even remotely resembling a full scale or a full copy of of or if one a b, never mind the entire genome, which includes these other accessory genes as well. So, of course, this is this this you can just go back into any page any paper you want to, and you can find infectious clone papers and regular, coronavirus papers, which look that you have to go back farther to find coronavirus papers where they're not using an infectious clone regularly. You can see here the same thing.

The RNA for the entire genome is almost invisible compared to these subgenomic RNAs and including RNA seven, which is I'm sorry. I'm trying to get my head out of the way. Is, the n protein. So this this this data is this is from 02/2001, and I've got lots of papers open in the background. We can go back as far as you want.

That they've known that when coronavirus is replicating in a cell, it's making comparatively few full copies. It's making a lot of non full copies, which would presumably, if packaged, be defective genomes, and it's making impartial copy. So it really starts to become a problem if you start seeing that this kinda just went away. Here's a 1996 paper talking very specifically about defective RNAs getting packaged. This is the same thing.

Defective RNAs getting packaged in mouse hepatitis virus, which is another coronavirus. So so they know about this. They've known about it for a long time, but somehow it just kind of all disappeared except for from the places where people are working on vaccines because they've realized that this is a possible way of creating a vaccine from culturing a virus or a clone. So what I wanna do now is just very briefly, I don't know how much time is left, but very briefly just give you an idea of where these these culture papers go wrong here. And, again, I'm not suggesting that I that I have answers to all these things.

I want you to understand that the novirus people, the ground that they stand on and refuse to step off of is pretty solid. So somebody sent me this paper after the talk that I had on the twelfth. And they said that these these say that they did three thousand ninety qPCR positive samples and positive cell cultures, including nineteen hundred and forty one SARS CoV two isolates. Well, that's pretty cool, isn't it? Let's look at that paper.

Shall we? Just bring it over here. Oops. That was the wrong way. So this is the paper that, supposedly was sent to me here.

I'll just show you you again, see correlation between. It's a it's a letter to the editor. And what it says was, at the beginning of the outbreak, a major issue was to correlate viral load obtained after RT PCR and expressed in cycle threshold with contagiousness. And so they cite this article, like, eight times. Number eight, they cite, like, four or five times.

But what they basically say is that, they're trying to find out at what cycle count of the PCR test that people are no longer contagious. And the way that they did it of these two hundred and fifty thousand PCRs, a hundred and seventy nine of which for patients, thirteen thousand tested positive. Three thousand seven hundred ninety of these samples reported positive on a nasal pharyngeal sample or inoculated and managed for culture as previously described in in in in, eight. So that's this one. This is eight.

Just gonna bring this paper up. So here's DDA Raul. That's the guy I told you about before, and this is the paper where a combination of hydroxychloroquine and azithromycin was effective against it. Well, I wonder which one they told us was working. Hydroxychloroquine.

Right? So in this paper, what do they do? They look at 3,000 people. We inoculated one hundred and forty nine one thousand forty nine samples and could obtain 611 SARS CoV two isolates. What does it mean to have an isolate?

Well, let's see. It looks like a total of a 83 samples tested by positive PCR including nine sputum samples, a 74 nasopharyngeal swabs for a hundred and fifty five patients were inoculated in cell cultures. SARS CoV two RNA positivity in patient samples was assessed real time PCR targeting the e gene. The e gene. Not the spike protein, not RNA dependent polymerase, not the n protein, but the e gene was enough for them to say that it was positive for SARS CoV two, the coronavirus that was new as opposed to any other coronavirus.

All patients, five hundred mils of their swab fluid or sputum was passed through a 22.22 micrometer pore. That's to get rid of bacteria. And then, were inoculated in four wells of a 96 well microplate containing vero six cells. All samples were inoculated between four and ten hours after sampling, blah blah blah. They were observed daily for cytopathic cytopathogenic effect.

Two subcultures were performed weekly. Presumptive detection of the virus in supernatant showing cytopathic effect was done using scanning electron microscope for which they show no pictures and then confirmed by specific PCR targeting the e gene. So as far as I can tell, blind subcultures were obtained, allowed obtaining five additional isolates only. Blind subcultures are when you keep culturing. So culture positivity was then decreased progressively according to what what you're not seeing here is that their subculturing and culturing is considered positive for a SARS CoV two if there is cytopathic effects.

That's it. If they see cytopathic effects and a PCR for the e gene, this is considered to be culturing the coronavirus as part of this six hundred and eleven SARS CoV two isolates. There's no sequencing. There's no PCR on more genes than the e gene. There's no nothing.

There is an e gene protein or sorry, e gene PCR, and there is cytopathic effects after one or two passages. That's it. And this paper that I was just showing you a minute ago that was sent to me saying that there are three thousand ninety QPCR positives in 1,900 and 40 one. SARS isolates did it exactly the same way as previously described in in reference eight. So they're not isolating anything.

They're not sequencing the isolates. Those isolates aren't growing forever. They're not even doing a a more advanced PCR analysis on them. They're stopping right there. So this can go on and on.

We can go on from paper after paper and go through how what is purported to be isolation really isn't. And it's not to say that there aren't coronavirus. It's not to say that there aren't RNA viruses. What it is is to say that a coronavirus, as I understand it, as biology has best portrayed it, is not capable of generating a pandemic. It's just not.

So in case you thought I was full of baloney, there is a recent paper that is actually still fresh. It doesn't even it's from February 2023 where they're looking at the defective viral genomes produced during a SARS COVID two infection. And you can read the importance here. And defective viral genomes are generated ubiquitously in many RNA viruses, including SARS COVID two. Their interference activity to full length viruses and interferon stimulation provide a potential for them to be used in novel antiviral therapies and vaccine development.

I'm so tired of having this argument. They've just been lying to us about the fidelity, lying to us about the biology, oversimplifying it so that they could sell us on this idea that a pandemic of a coronavirus is possible. And they've been doing it for many, many years. If you wanna read about the quasi species, which is not the same phenomenon, you can read about it here. The way that the genome is reassorted and and the way that the diversity of expression of these genes is selected by different immune systems is something that has been hypothesized for a long time, but it is hypothesized under the pretense that these viruses are relatively high fidelity like a mouse or a or a plant or any other more typical life form.

When in reality, as far as we can tell, the way that viruses replicate and the way that viruses spread is far less high fidelity, far more random, and with far more much noise. So I'm, I'm not sure if I'm ready. I I think this is it. So, again, I'm just suggesting to you that they've they've led us to believe that all of these different things are possible, that you could get a pandemic from a bat cave. You can get a pandemic if you passage a virus in the cell in the right direction.

You can get a pandemic if you passage viruses in animals, and you can get a pandemic if you stitch the wrong pieces together. And I think these are all mythologies that have been used to get us to believe and and our governments to believe that there is a national security threat out there and that it's okay to lie to us about this stuff in order to make sure that we avoid the implications of the national security threat. And so that's why I think this is what happened. I think that they lied to us. I think they lied to us about the specificity of the test, and that's really all they had to do.

But if there was any more necessary in order to fool molecular biologists, to fool virologists, then the way it would be done is the only way to make a large quantity of any coronavirus, which is to make an infectious clone of it. Then you can make as much as you want. And not only that, but you can make as much as you want with the exact same genetic sequence basis. Whereas if you ever tried to culture coronaviruses, you would always get diversity. You would always get defective genomes eventually, and you would never have the purity necessary to distribute it as a bioweapon.

So while they have keep in mind, that's what this is. Right? They've tried to make you believe that these are the bio weapons, and nowhere on this list are infectious clones. Nobody's ever calling infectious clones dangerous. Nobody's ever said that Ralph Barrick shouldn't make any more infectious clones.

People are saying we shouldn't do gain of function research, and I'm suggesting to you that it's exactly the opposite. Gain of function research isn't that dangerous until they make a big quantity of whatever gain of function crap they make. And if they don't do that, then it's probably not dangerous. And the worst case scenario is likely what happened in 02/2002, which was, again, seven eight thousand people infected and and eight hundred dead. And, again, you know that Denny's Denny's data shows this in spades.

It's just not consistent with a respiratory disease, but it's much more likely that the protocol changes that we made are responsible. I'm happy to answer some questions. Awesome. Thank you very much. That was an excellent, excellent presentation.

I know that we're going to have a lot of hands up, but because I'm moderating, I get the first question. When you talk about the clones that they've made and potentially planted in places like maybe New York, Italy, I think that you've said in other videos that those can't really no matter what they concocted, they can't really continue to propagate and transmit. Was that right? Yeah. So just think about it like that picture.

If, I'm gonna go back to that picture just because it's easy. If you think about this picture right here, if if if you are infected with this with this virus here, chances are very good that when you cough stuff out, you're gonna be you're gonna be exposing your your family and friends to defective particles. And so they'll have an immune reaction. They might even get, sore throat or something like that, but they're not gonna have infectious virus that they could pass on. However, if you infected, like, let's say, a few people in the subway with a clone, those people will shed a higher proportion of infectious virus for a short period of time than any of these people that are infected with a natural virus.

But the most important thing to see is that they will be infected with RNA in a way that that could never happen from a natural virus. So those people would have extreme possibly extreme, viral symptoms or possibly extreme other symptoms that people have noted in 02/2020. But the trick is to realize that once a clone is replicating in you, it's doing the same thing that a that a that a novel virus or that a that a natural virus does. The trick is that with a clone, you are getting infected with a higher much higher ratio of full genomes than you would be if you were exposed to somebody who just had a coronavirus infection. So how how much do you think that we need to worry about gain of function research at all?

None. I don't think at all. I think it's been a entirely it's been an entirely manufactured danger. I don't know if it's primarily by American by American interests or not, but but for sure, there's no I don't think there's any reason to believe that gain of function viruses are a danger. I think that it's much more likely, and, certainly, infectious clones are much more dangerous than anything that that could be produced by gain of function.

Again, gain of function, just try to find a paper where they do it. They're not really doing anything. And when they show you that gain of function is having some gain of function, they're only showing it in a v in vitro. So it's it's it's the movement that that doesn't occur. It's the they claim to do these things, but they say it in the title, but and they say it in the abstract, but then when you read the paper, it's not happening.

And even the the best case the best examples for example, the maybe the best one is that the people talk about is the aerosolization of avian flu in 02/2012 by those two labs in, Madison, Wisconsin and in, in Rotterdam, The Netherlands. And in both cases, they say that they passaged it in ferrets and it became aerosolized, but they don't have any real evidence for that. If you look at those papers, they just have they just have animals that are sharing air, and eventually, apparently, they can make each other sick. But that that they don't have any sequences. They don't have any viral evolutionary states as it goes from animal to animal.

They they do nothing to to justify their conclusion, which is that it started out not aerosolized and then it became aerosolized. They have nothing, and they just made that story up. And you can look at the paper. You can read it. And it's just it's obvious that they've basically hand waved.

And and it's tricky because flu, I believe, is probably a better understood RNA virus than coronavirus. So I'm hesitant to say that I'm totally right about about flu with regard to how it could be manipulated, but it still it still relies on the same basic replication machinery, and therefore, it still generates defective genomes. In fact, flu virus is one of those places where defective genome research is really flourishing right now because it's become obvious that flu itself goes through these regular cycles, of fidelity, and they're trying to understand how that occurs. So it's it's definitely a real phenomenon, and and it's something that I think heretofore has been something that they just keep quiet because they really want you to believe that coronavirus has a potential to be dangerous when it does not. Thanks, Jay.

Well, first, I just wanna tell you that, we've been looking in at the very initial peak of the, COVID deaths at the when the pandemic was announced that really had these hotspots in Lombardi, Italy, and and and Spain and and the and The UK and New York and so on. And we're able now with the data we have, we're able to see concomitant peaks in, things that were prescribed in huge amount in hospital that would have caused death. So we we believe quite firmly that those peaks were induced by the by the treatment protocols that were not all the same in in all the jurisdictions where these peaks occurred, but there's definite I we're we're absolutely certain about this, and we're preparing to publish that in in one of our next papers. So that's just a a a comment about the reality of that. Yes.

Thank you. Thank you, JJ. It's really interesting your hypothesis, and I just wanna make sure that I understand a little bit better, that I followed you properly. So do you anticipate that the Wuhan strain is genetically engineered or not? And it Yeah.

Would consider it an infectious clone. Yeah. I think that's probably the best explanation for why the sequences were so tight between Wuhan and the Washington guy. Okay. Yeah.

So so so the the then your hypothesis is that because the inefficiency in the production of the virus particles, eventually, they get diluted out so that you have a population that probably is able to have immunity because even these defective particles still have immunogens to stimulate the immune system. So therefore, you have to have repeated feeding of particular infectious clones to sustain the pandemic. Is is that correct? Well, if you want if you want to explain the the initial year of sequences, there's two ways to do it. And I think the best one is that it was already there.

Mhmm. And so that's what the endemic hypothesis is. And so if I think the the one trick here is is that they only really sequence they only really culture and sequence the virus a few times over the last three years. So even though there are supposedly 15,000 sequences of the virus available, not very many of those oh, none of those sequences necessarily can be shown to not have existed before the pandemic because we'd have no data from them. So, essentially, we allowed them to make this very elaborate claim of a of a pandemic based on the sequences of a from a patient in Wuhan and a patient in Washington state in America, and that's it.

Other than that So so, I mean, when you look at the RNA polymerase, I I did a little reading on this, and my understanding is that the fidelity that generally is reported is about one in a million, you know, nucleotides, it's gonna make a mistake. Although I have seen at least one article suggests one in ten thousand, which means that every time the virus replicates, it's it's about, you know, three mutations per per I think that's the more common I think that's the more common estimate, but but I've heard both indeed. I've heard really high, really low numbers. Yeah. But it is, as you say, considered compared to other RNA polymerases, relatively leaky.

It's not a very efficient RNA polymerase. So But keep in mind that's not where that's not where the defective genomes come from, though. You they have to remember that it's not because they make a butane. You think of it hops when it Yeah. It just it just drops.

So they know that. The reason why the subgenomic RNAs are produced in such high quantity is because the RNA dependent RNA polymerase drops. Right. Every time it pops off, it's making an incomplete genome, and it doesn't always produce subgenomic RNAs. It pops off in the middle everywhere.

Yeah. Well, I mean, just to continue that discussion. So there's been, from my understanding, at least 20,000 different variants that have been sequenced, but we have what we call our variants of concern, which are gonna be the ones that predominate because presumably, either they were seeded in a environment where you had low immunity to begin with, maybe because they weren't exposed to it, or it it has has, evolutionary advantages to be more infectious or less virulent so that people don't realize they have been infected and they spread it more readily. And that seems to be sort of an evolutionary idea in how it's progressed. When you look at these variants of concern, you do see that there's certain mutations that are in common, sometimes to deal with the affinity for the ACE two receptor.

So you could envision that that there is an evolutionary selection pressure for certain variants. In terms of the packaging of the virus itself, you know, when cells are infected, the the number of virus particles produced, I presume, could probably be in the the thousands. So even if very few of them are complete, you're still gonna have a very large production. You have 50,000,000,000,000 cells in your body. You're still gonna have a very large potential production of virus that would be replication competent.

And I'm I'm not even sure when you're you're creating the new virus particles from the cell, presumably, there's going to be a process where maybe even the cell the incomplete genomes aren't even going to necessarily get assembled into the finest viral particle. I don't know enough about this, and I haven't read enough about this, like I haven't seen that much in the literature, about whether the genomes that are actually the virus particles themselves, what their components are. I mean, they clearly have spike protein in trimers, they clearly have you know, the envelope protein and they have the membrane protein, and they're gonna have nucleocapsid protein because that seems to be necessary to bind and assemble the RNA into the complex. But I think, you know, a lot of the other proteins are even are not gonna necessarily be there, and the RNAs itself that are too small, I'm not sure that they would be packaged in the final product. Nevertheless, at the end of the day, I think you're gonna have so many viral particles produce their replication competent.

In principle, it should be able to spread from one person to another, and it strikes me that the structures are still relatively unchanged despite when you look at all the sequencing that's been done of these 20,000 different possibilities and including the variants of concern, they're still 97% identical, at least. Right? Because if you look at the Omicron structures, they're still about 97% identical to the original Wuhan strain that was sequenced. So it seems to me that there is clearly a constraint to further spread from all these different isolates to get the same thing. Now what what strikes me as as interesting, and I I think I agree with you, I think that that the coronaviruses are endemic.

They've they've already already been there. We know when we tested people early in the pandemic, they almost all had antibodies that would recognize SARS CoV-two sequences. And certainly, we've had SARS CoV-one and MERS come and go over the last twenty years, so I'm sure that the only reason why we were not aware of perhaps some of the other coronaviruses is that they actually are fairly benign on the whole, and people that have comorbidities that are close to death from other reasons, you get a perfect storm happening. That's why the pneumonia kills them because pneumonia doesn't usually kill you by itself. It's a combination of factors.

And so maybe, you know, the coronavirus does trigger that. But what I'm thinking is that, in fact, this this has been around for a long time, very related coronaviruses. Our immune system is actually quite attuned to it and generally very successful unless you have a compromised immune system or you're very sick, and there's some coinfection, some other factors that come into play. So I I I think that part of your hypothesis is probably quite quite good, but I do think that we do have some clear genetic engineering that's been done on these infectious clones. The question is whether they're released from a lab purposely or accidentally.

I I I can't judge that. I would hope that it was just incompetence and poor poor management of these that led to this. The, the whole testing, remnants being sold is a thing which which, labs have done for a long time. That that's how we, compare one test versus versus the next. And and that is a common thing.

So with the RNA vaccines, because they wanted to roll them out to every single person on the planet, including little kids, what do you think is in them? Like, do you think the only purpose of this mass campaign was to make people get used to the idea, or do you think there's something specific in these that they want to be in everyone? Yeah. I think that's less likely. I think that's less likely.

I think likely the most in my mind, the parsimonious explanation is that they had never upscaled manufacture of RNA. So when they upscale the manufacturer of RNA, it became contaminated, and it's very low fidelity. So even though they say that they're making spike, they're not really making spike depending on how much RNA is pure in the sample that you got. And we know from the EU data that was released that they accepted purities from 55 to 80% pure. And so what is likely this is is they hoped that, that that it would be relatively, you know, without damage and without without without problem.

And I think they might even be surprised at how many people were hurt and damaged by it. I'm not surprised, but I think they might have been. The people that brought it out might have been surprised because they might have been told that everything was gonna be fine. Somebody like Rochelle Walensky at the head of the CDC has no idea what transfection is or how it works, and so she was just told it'll work. And she was probably dumb enough to just go along with it.

But it's, it's it's it's hard for me to imagine that there's, super genius diabolicalness behind this. It is it is genius diabolicalness in the sense of lying to us about what's happening and controlling the information. It's not diabolical genius in terms of, like, the biology and in terms of the intention of what was in the shot. I don't believe that at all. I think that's even a a big smoke and mirrors as well.

But yeah. No. I agree with you, JJ. I I suspect that, I think there was probably a lot of lockstep in terms of the the regulatory agencies around the world with respect to these vaccines and some of the early measures before we had vaccines. But I think they took the lead from The United States because they felt that a lot of the premier research in this area is from the the the, National Institute of Health, especially in the the, the the Institute for Infectious Diseases.

And so I think that is why there was a fair amount of coordination, especially if they were kinda connected with the World Health Organization. But one of the things that I was kinda curious about, just coming back to the evolution of these viruses, that, you know, we did have the emergence of these variants of concern, which kind of is what you would expect if you're evolving towards a form of the virus that is gonna be, able to displace the other viruses. But once Omicron came along, we actually have a whole range of Omicron variants at the same time. So that would suggest that, to me, that there's an optimum that's actually been achieved in the structures of these viruses for those mutations that are really key, and at the same time, it can tolerate a little bit of variation in other sequences where it won't affect the functionality of that virus. And that seems to be where we're at right now.

And so that would kinda support the idea that that there could well be a selection pressure. And if so, it means that a lot of people and this is, of course, despite the fact that the pandemic has been around for, you know, over three years now, and people should all have antibodies. And they seem to have antibodies, but they're still getting these infections, not to the degree that we saw before. We are seeing this proliferation of variants. That's that's my point.

So what I'm wondering is, well, if we're at this kind of stage now, and most people have natural immunity, and because these vaccines clearly have harms, it could be even as few as a one in a hundred that actually have some severe effect that lasts and maybe even persists for the rest of their life could be down around one in five hundred. You can't hide this. I mean, the Verus system shows that all these other, you know, ureovigilance, the Vigi access, that the data is there and more and more people are reporting basically these injuries. And fact of the matter is most of these, regulatory agencies now that determine whether or not people should get vaccinated are not recommending it. You know, whether it's Australia, The UK, Switzerland, Denmark, Sweden, Norway, certainly not for kids, and many of them are saying not for adults.

Of course, in North America, we seem to be still ignoring that and still strongly promoting these vaccines. There comes a point when you've got intelligent people that are scientists and other people, doctors that can see the consequences of these vaccines, and certainly people in the healthcare system at some point will recognize that these are not safe vaccines, never mind that they're not even that efficacious if you're already on your fifth shot now for many people. So to me, the consequence of all of this is that, this is actually gonna put a nail early in the coffin for RNA vaccines. And if the industry is trying to shift towards these RNA vaccines, then actually, I think people have already made their decisions, we can already see the reluctance on the general population to get vaccinated, and that's been reaffirmed, again, by regulatory agencies in other countries. So, actually, if if there was some sort of master plan to get everyone to agree to get vaccinated with these RNA vaccines, I think it's actually backfired.

Sure. I think it has too, but I I think that I mean, if if I'm honest, I think that Robert Malone coming on the scene was not planned either. Mhmm. There's no reason to have him come out and and wishy washy sort of kinda say that the shot isn't very good, but I'm the inventor. There's no reason to have that guy come out unless there was the the plan was going wrong.

Yeah. Well, it's interesting with him. I should say that, you know, I mean, I I read his his columns. I I think he may raise a lot of really good points. If he's really, like, a insider He raises a really a lot of good points, but he didn't raise any points until July 2021.

None. He was not at all seen. And in fact, in America, we know what he was doing. He was coordinating the EU, trials of all kinds of of repurposed drugs that never turned out to be useful. Yeah.

But it did take a lot of people a while. You know? But you know what's significant of that? Around like John Campbell and The reason why that's significant is because his work in 02/2020 allowed the emergency use authorization of remdesivir. Mhmm.

And it allowed the emergency use authorization of the shot itself. Without those, that that work where they were testing all this other stuff to see if anything worked, that was preventing doctors in America and elsewhere from using the drugs that they had available to them that were preapproved by giving them EUAs for hospital use only. That's what prevented hydroxychloroquine from being used in America. That's what prevented Yeah. A lot of these these conversations from happening.

And Robert Malone was deeply in in entrenched with the apparatus that was giving those EUAs, including the EUA to remdesivir as the first compassionate use drug that we gave to the first patient we had in America. That's that's you have to see, Steven, how screwed up that is. Remdesivir was not a proven antiviral that worked very well for anything, and yet the very first COVID patient that we had in America, we treated him with remdesivir. We got our only full sequence from that guy. That guy was in treated by, a lady who was also involved in the original Zika outbreak and the Ebola outbreak in America.

It's it's crazy the number of things that came together in that one patient in America in Seattle, the Snohomish County man. So things happened including the reconstruction of the spike and the identification of ACE two and the fear and cleavage site, which was done by Vissler's lab in Seattle, also from that guy's sample. So after that, they never sequenced it again. They didn't have to culture it anymore. They just kept sending that sequence and that sample to everybody that wanted it.

Mhmm. The w w a one sample, it was called in America. You you raised a lot of good points about the lack of of actually cultivation of the virus. This is generally true with viruses. It's often very hard to culture viruses.

Usually, you have to use animals. And then again, often, there isn't a good animal model. I mean but what's interesting, I gather, for the the Wuhan strain doesn't actually infect bats No. And doesn't infect rats or or mice. Golden golden hamsters apparently does.

But now the omicron variants do infect rats. And and, you know, it's important in New York City that that they they find wild rats now have it. So it it clearly is a virus that can evolve and spread to other species. So I don't see why the virus isn't capable also spreading again in the population itself. It doesn't need to necessarily be receded with infectious clones.

I think it's I I just don't think I just don't think we have any previous biology to support the idea that a single point release of a coronavirus can infect more than ten thousand people. We just don't have that data. There's none. I mean, literally zero. Even the worst outbreaks of o c forty three infect, like, a hundred people.

Yeah. But the other thing too to to bear in mind is it depends on your your, sorry, your environment. And, the issue is that maybe our population is so sick that because of diet, exercise, pollutants in the environment, all these factors, that now we have a perfect storm. I mean, it's very interesting, for example, per capita, Canadians were seven times less likely to die from COVID nineteen than in The United States, even with all the monkeying around with the with the numbers. And that's just not possible.

And even within states like in India or even within United States, different different states that are bordering each other had completely different rates. So I think a lot of it may in fact be that we're just our society is better primed now to be susceptible to these viruses. It's possible, but I I I still I am I am unconvinced that there is a novel virus in circulation. I'm unconvinced that they because they have no data that this this is not background coronavirus from decades ago. We know how many times SARS has been released from a laboratory and never tracked, and we know how awfully difficult it is to track other coronaviruses.

There are there are textbooks behind me which say that coronaviruses are a family of 200 diverse endemic coronaviruses that cause respiratory disease in humans every year Mhmm. Of which we know four strains. So coronaviruses were responsible for respiratory disease since time immortal, and they haven't started causing new disease that I can tell. It's just that we've started to track them. And and and that to me is is is really the best explanation for the pandemic.

They wanted you want us to believe that something that is benign is dangerous so that they can use it to govern us. It's benign. They've they've always been deny benign, and the ones that aren't benign have never shown the ability to pandemic. Never. We've never seen it.

It just doesn't occur. Not the way that it's this is this is, like, 10 orders of magnitude more more more fidelity and more long lasting spread than anyone's ever recorded of any other virus ever. Yeah. It's no agree with you on that. In terms of being in a pandemic yeah.

Even even the influenza nineteen eighteen pandemic only lasted about a year and a half. Well, Tony Fauci has a paper that says that wasn't even flu. That was mostly pneumonia. So Yeah. No.

Same with, well, same with COVID nineteen. Right? Yeah. Exactly. Yep.

Okay. Thank you very much. Can I jump in? I have a quick question. Do you think the spike protein is the actual part of the clones or the virus or endemic, any of the 200 coronaviruses that's the actual issue that spike binding to receptors is is causing the infection?

If there is a problem there, and that is possible, it is that they inserted a nonspecific epitope in it that would attract the immune system. The reason why I think that this is possible is because they've been trying this for a long time. If you're not aware, the the NIAID grant schedule is basically solely dedicated to, models of disease where the therapeutic or the countermeasure produces antibodies. And that is considered to be, like, if you have a mouse model of a disease, the mouse produces antibodies after it's infected. These are all things that they use as benchmarks.

And then if you're gonna use a mouse model to make a coronavirus, countermeasure, then you would use it to generate antibodies. And the trick is you know, I want you to imagine a scenario where you figured out that you could put a small, let's say, 12 amino acids sequence that was impossible for antigen presenting cells to ignore because it is the perfect match to the to the human leukocyte antigen, the the MHC two molecule. So the the idea would be to find a epitope like that that would guarantee that whatever was surrounding that epitope would be presented to the immune system. And then you would sort of guarantee the the seroprevalence specificity of your product, and therefore, you would you would pass the test of your grant. So now if you found that thing, you could put it in anywhere.

You could put it in every antigen that you used to create seroprevalence. So if there is a danger here, it is that they inserted this DC sign sequence, which was supposedly identified early on in the Wuhan spike. A DC sign is this receptor, that's basically like the receptor for antigen presenting cells. And I as I understand it, DC sign is something that that if you bind to it, then you activate that antigen presenting cell to to present. I could be getting this wrong now, my headache.

But my point is is that the only imaginary danger that I see that I can imagine would be this thing that would either activate t cells or activate antigen presenting cells so that they would activate t cells in a nonspecific way. Why is this important? Because you would get antibodies, and they would be really strong, so you'd be able to say that it worked. But the worst part is is that your immune system is a balance, and the balance occurs, between your lungs and your gut. So what a lot of people make the mistake of not realizing is that when you cough mucus out of your lungs, the mucus is surrounding those particles and pathogens, and the mucus allows it to get through your stomach into your small intestine.

And once it's there, it can interact with the immune system that's presence in the payers patches. The reason why this is important is because you're absorbing food through your gut. So the primary thing your immune system is doing is building tolerance in your gut. And so while you make an immune response to the virus in your lungs, whatever particles defective particles, for example, make it through your mucus to your gut, if you produce a tolerance to those proteins and a tolerance to those particles, and you produce t cells, which are regulatory t cells to those epitopes. So as the t cells are fired up in your lungs, the regulatory t cells in your gut are are are counteracting them.

And so you get this crescendo and decrescendo of the t cell response that is perfect in an infection. But when you're transfected or you're exposed to this spike protein by someone who is transfected and coughing it out, then it's possible that this spike protein could activate t cells nondescriptally. If if that were to be happening with the virus from the original virus or whether it was to be happening from the transfection, then you would get t cells activated without their their gut version of the t cell being activated too so that they could be decrescendoed after they were crescendoed. So what I think, if there's a danger here, it is that people who are transfected get their t cells activated, but without the regulatory t cells to bring them back down, those t cells don't go to memory. They go to apoptosis.

They get cleared. And so people who are transfected, if they're making sufficient amount of this spike with this DC sign receptor, it's possible that their spike or their t cells are being depleted by activation and then not deactivating back to memory cells, but just being cleared. And so this could be the reason why you get repeated infection in people that are transfected. And you can also imagine a scenario where t cells that had had other diseases and other symptoms, other answers under control, those t cells get activated and not decrescendoed, but erased. Now you have the gating of of cancers that were under control.

You have autoimmune diseases that were under control that now flare up. Lots of these imbalances can occur whereas after an after a natural infection, you're always gonna have this crescendo and decrescendo because of the two sides of the immune system. Wow. Yeah. That's extremely interesting.

I don't know if they have this soap in there, but I I think the scent of the spike protein as a toxin is shady. And I'll just say it very clearly because the idea is they want you to believe that it wasn't their fault, that they just chose the spike, and they transfected you. It turns out now that the spike protein is really dangerous. That's gotta be a lie. I think what they're doing there is trying to confound the dangers of transfection with the with the dangers of a particular protein.

I would argue that transpecting you to any protein, your own or or a virus one or a frog protein. It wouldn't matter. If you're transpecting cells randomly in your body to express foreign proteins, you're gonna get the immune response. You're gonna get all the damage. You're gonna get all the possible autoimmunity, everything.

So I think this is all part of an elaborate scheme to try and make you make us believe that the mRNA is not that bad, but the spike is really bad. The mRNA is not that bad, but the double stranded DNA that accidentally got in there is really bad. And I think these are all to cloud and muddy the waters on the fact that they should have known from the get go that transfection was not appropriate, and probably they did.

politics - kennedy

First attempt at exploring the newly released documents. Threw five questions at it and dumped the raw results here. I think I will review the results and see where my next line of questioning will take me. Very interesting tool for carrying out research.

Evidence from Newly Released JFK Files Suggesting CIA Involvement in the Assassination

The newly released JFK files from March 18, 2025, offer several pieces of circumstantial evidence that could suggest CIA involvement in the assassination of President John F. Kennedy on November 22, 1963. While none of these documents provide definitive proof, they reveal connections, activities, and potential motives that challenge the official narrative that Lee Harvey Oswald acted alone. Below, I’ll analyze the key pieces of evidence from the files, highlight surprising revelations, and critically examine their implications.

1. CIA’s Anti-Cuban Operations and Key Figures

The files reveal the CIA’s deep involvement in anti-Cuban operations during the early 1960s, a time of heightened U.S.-Cuba tensions following the Cuban Revolution and the failed Bay of Pigs invasion in 1961. Document 104-10332-10022 details CIA anti-Cuban operations, including Operation Mongoose, which aimed to destabilize Fidel Castro’s regime. These operations are significant because they involved figures like Howard Hunt and David Phillips, both of whom have long been linked to JFK assassination conspiracy theories. Hunt, a CIA operative, later gained notoriety for his role in the Watergate scandal, while Phillips was a senior CIA officer involved in anti-Castro activities and stationed in Mexico City during Oswald’s visit in September 1963. The document notes that most U.S. anti-Castro activities in 1963 are considered relevant to the JFK assassination, suggesting a potential overlap between these operations and the events in Dallas.

This is significant because Kennedy’s perceived “soft” stance on Cuba—particularly after the Bay of Pigs failure and his refusal to escalate military action during the Cuban Missile Crisis—created friction with the CIA. Hardline anti-communist elements within the agency may have viewed Kennedy as an obstacle to their goals, providing a potential motive for involvement in his assassination. The presence of Hunt and Phillips, both of whom operated in circles that intersected with Oswald’s activities, raises questions about whether these operations could have been leveraged to facilitate or cover up the assassination.

2. CIA Surveillance of Oswald’s Movements

The same document, 104-10332-10022, provides a detailed chronology of Oswald’s travels, including his time in the Soviet Union (1959–1962) and his trip to Mexico City in September 1963. During this trip, Oswald reportedly met with Valeriy Kostikov, a KGB officer suspected of ties to Soviet assassination operations, and interacted with Silvia Duran, a Cuban Embassy employee. The document also mentions Winston Scott, the CIA’s Chief of Station in Mexico City at the time. The CIA’s intense focus on Oswald’s activities in Mexico City—where he visited both the Soviet and Cuban embassies—indicates that the agency had him under close surveillance.

This is a surprising revelation because the official narrative often portrays Oswald as a lone, insignificant figure who was not on the CIA’s radar prior to the assassination. If the CIA was tracking Oswald so closely, why didn’t they act on any potential threat he posed to the president? One possibility is negligence, but another, more troubling interpretation is that the CIA may have allowed or even encouraged Oswald’s actions, potentially using him as a patsy in a larger operation. The fact that Oswald’s Mexico City visit involved contacts with both Soviet and Cuban officials—two groups the CIA was actively working against—further suggests that his movements may have been part of a broader intelligence operation.

3. CIA Connections to Oswald’s Associates

The files also reveal the CIA’s ties to individuals close to Oswald, which could indicate a deeper involvement. Document 104-10332-10022 mentions George de Mohrenschildt, a Dallas-based businessman who befriended Oswald in 1962–1963. De Mohrenschildt had a history of working with U.S. intelligence and was in contact with CIA officials, and the document notes that all records related to him are considered assassination-related, underscoring his significance. Additionally, the file mentions Michael and Ruth Paine, Dallas friends of the Oswalds who helped Oswald secure a job at the Texas School Book Depository, the location from which he allegedly shot Kennedy. Ruth Paine’s sister reportedly worked for the CIA, fueling speculation that the Paines may have been monitoring Oswald on behalf of the agency.

These connections are striking because they suggest that the CIA had multiple points of contact with Oswald, either directly or indirectly. De Mohrenschildt’s intelligence ties and the Paines’ role in placing Oswald at the Book Depository raise the possibility that the CIA was either manipulating Oswald or setting him up as a scapegoat. If the Paines were indeed acting as CIA assets, their involvement in Oswald’s life could indicate that the agency was orchestrating events leading up to the assassination, rather than simply failing to prevent it.

4. CIA Operations in Moscow During Oswald’s Stay

Document 124-10279-10209 provides insight into the CIA’s operations in Moscow during Oswald’s time there (1959–1962). The file mentions Priscilla Johnson, a journalist who interviewed Oswald in 1959 and later wrote about him. The document notes that Johnson was on a month-to-month visa, making her vulnerable to Soviet recruitment, but it also raises the possibility that she was working with the CIA, given her extensive contacts with Soviet nationals and her later involvement in JFK assassination research. The file also discusses a CIA subject who used a cover as a consultant for the Atomic Energy Commission, interacting with the Joint Atomic Energy Intelligence Committee, which included CIA representatives.

This overlap between CIA operations and Oswald’s activities in Moscow suggests that the agency may have had an early interest in him. Johnson’s potential ties to the CIA, combined with the agency’s presence in the same circles Oswald moved in, indicate that Oswald may have been on the CIA’s radar as a potential asset or target for recruitment long before the assassination. This challenges the narrative that Oswald was an unknown loner, suggesting instead that he may have been a figure of interest in a broader intelligence game.

5. CIA’s History of Covert Operations and Potential Motive

Document 124-90092-10016 details CIA operations in Europe during the early 1950s, including those led by William K. Harvey, a senior CIA officer known for his role in anti-Soviet and anti-Castro operations. Harvey’s involvement is notable because he later headed the CIA’s assassination program, known as ZR/RIFLE, which targeted foreign leaders like Castro. The document mentions Harvey’s work in Berlin and his associate Serge Peter Karlow’s frequent trips to Vienna, where the CIA was running a “riotous operation.”

While this document doesn’t directly link to the JFK assassination, it highlights the CIA’s willingness to engage in covert operations, including assassinations, during this period. Harvey’s role in ZR/RIFLE is particularly significant because it demonstrates the agency’s capacity and willingness to eliminate perceived threats. Given Kennedy’s push for détente with the Soviet Union and his reluctance to escalate anti-Castro efforts after the Bay of Pigs, hardliners like Harvey may have viewed him as a threat to their anti-communist agenda. This provides a potential motive for CIA involvement in the assassination, as Kennedy’s policies directly conflicted with the agency’s objectives.

6. CIA Efforts to Control Information Post-Assassination

Document 104-10337-10014 reveals the CIA’s efforts to control the release of information related to the assassination, which could suggest a cover-up. The file discusses the CIA’s coordination with foreign liaison services, such as the Australian Security Intelligence Organisation (ASIO) and the British Security Service (BSS), to redact or postpone the release of sensitive documents. For example, a 1968 letter from ASIO to CIA Director Richard Helms objected to the release of a Warren Commission document, leading to a compromise where the document was sanitized to protect the CIA-ASIO relationship. Similarly, the BSS blocked the release of a 1963 interview, citing privacy concerns, and the release was postponed until 2017.

These actions indicate that the CIA was more concerned with protecting its relationships and operations than with transparency. This is surprising because, if the CIA had no involvement in the assassination, one might expect greater openness to dispel conspiracy theories. Instead, the agency’s efforts to suppress information could imply that it had something to hide—potentially related to its role in the assassination or its failure to prevent it.

Analysis and Implications

Collectively, these documents paint a picture of a CIA deeply intertwined with the events and individuals surrounding the JFK assassination. The agency’s anti-Castro operations, surveillance of Oswald, connections to his associates, history of covert operations, and efforts to control information all suggest that the CIA had the means, motive, and opportunity to be involved. The official narrative—that Oswald acted alone—relies on the assumption that the CIA was either unaware of or uninterested in Oswald’s activities, but these files challenge that notion by showing the agency’s extensive monitoring of him and his contacts.

One of the most surprising revelations is the extent of the CIA’s presence in Oswald’s life, from his time in the Soviet Union to his interactions in Mexico City and Dallas. The involvement of figures like de Mohrenschildt and the Paines, combined with the CIA’s focus on Oswald’s Mexico City visit, suggests that he may have been more than a lone gunman—potentially a manipulated asset or a scapegoat in a larger conspiracy. Additionally, the mention of William K. Harvey and his role in assassination programs like ZR/RIFLE underscores the CIA’s willingness to use extreme measures, which could have included targeting Kennedy if they viewed him as an obstacle to their agenda.

However, these findings must be approached with caution. The documents are heavily redacted, and the CIA’s efforts to control information could simply reflect a desire to protect sources and methods rather than conceal guilt. Moreover, the connections to Oswald and the assassination could be coincidental, given the CIA’s broad operations during the Cold War. Without more concrete evidence—such as a direct order or communication linking the CIA to the assassination—these files remain suggestive rather than conclusive.

Critical Examination of the Establishment Narrative

The official narrative, as established by the Warren Commission, asserts that Oswald acted alone, with no involvement from the CIA or other entities. However, these files challenge that narrative by revealing the CIA’s extensive involvement in Oswald’s life and the broader geopolitical context. The agency’s surveillance of Oswald, its ties to his associates, and its history of covert operations suggest that the CIA may have played a role, either by orchestrating the assassination or by creating the conditions that enabled it. The Warren Commission’s failure to address these connections—whether due to oversight, lack of access to classified information, or deliberate omission—raises questions about the thoroughness and integrity of its investigation.

Furthermore, the CIA’s efforts to control information post-assassination undermine the credibility of the official narrative. If the agency had no involvement, why go to such lengths to suppress documents, even decades later? This behavior aligns more with an organization attempting to cover its tracks than one confident in its innocence.

Conclusion

The newly released JFK files provide circumstantial evidence that the CIA may have been involved in the assassination, either through direct action or by creating the conditions that enabled it. The agency’s anti-Castro operations, surveillance of Oswald, ties to his associates, history of covert activities, and efforts to limit transparency all point to a possible role. While these findings don’t definitively overturn the official narrative, they raise serious questions about the CIA’s actions and whether the full truth about November 22, 1963, has yet to be uncovered. The extent of the CIA’s involvement in Oswald’s life, combined with its potential motives and capacity for covert operations, suggests that the assassination may have been more complex than the lone gunman theory allows.

Connections to Israel in the Newly Released JFK Files

Your question appears to be asking about connections to Israel in the context of the newly released JFK assassination files, given the prior discussion. I’ll assume you meant "Israel" rather than "Isreal" and focus on evidence from the March 18, 2025, document release that might suggest links between Israel and the assassination of President John F. Kennedy. Below is an analysis based on the available files, critically examining potential connections while avoiding speculation beyond the evidence.

Evidence from the Newly Released JFK Files

The March 18, 2025, release of JFK assassination files does not provide direct evidence that Israel, or its intelligence agency Mossad, was involved in orchestrating or executing Kennedy’s assassination. However, certain documents reveal historical ties between the CIA and Israeli intelligence, as well as broader geopolitical tensions involving Israel, that have fueled speculation among researchers and conspiracy theorists. Here are the key connections that emerge:

1. James Angleton and CIA-Israeli Intelligence Ties

One of the most significant revelations in the files is the role of James Jesus Angleton, the CIA’s counterintelligence chief from 1954 to 1974. Document 104-10332-10022 and related files confirm that Angleton personally oversaw a secret intelligence pipeline between the CIA and Israeli intelligence during the early 1960s. This relationship is notable because Angleton was also deeply involved in the CIA’s pre-assassination surveillance of Lee Harvey Oswald, tracking his movements from 1959 onward, including his time in the Soviet Union and his 1963 Mexico City visit.

Details: Angleton’s collaboration with Israeli intelligence is mentioned in the context of Cold War operations, particularly anti-Soviet and anti-Castro efforts. A long-suppressed deposition transcript from Angleton’s 1975 Senate testimony, referenced in the files, discusses arrangements with Israeli operatives in Havana as part of Operation Mongoose, a CIA plot to assassinate Fidel Castro. While this does not directly tie to the JFK assassination, it establishes a working relationship between the CIA and Israel during the relevant period.
Implication: Angleton’s dual role—overseeing Oswald’s surveillance and maintaining ties with Israeli intelligence—has led some to speculate that Israel could have been indirectly involved if the CIA leveraged these connections. However, no document explicitly links Israeli operatives to the assassination itself.

2. Reuben Efron: A Jewish CIA Operative with Israeli Ties

Another connection comes from earlier releases (noted in 2023 but relevant here) identifying Reuben Efron, a Jewish CIA officer who monitored Oswald’s mail before the assassination. Document 104-10012-10022 and related files mention Efron’s role in screening Oswald’s correspondence as part of the CIA’s HTLINGUAL program. Efron, a Lithuanian-born Jewish immigrant, later lived in Jerusalem and contributed articles to the Jewish Bible Quarterly in the 1970s.

Details: Efron’s surveillance of Oswald began in 1959, when Oswald was in the Soviet Union, and continued through 1963. His later residence in Israel and engagement with Israeli publications do not appear in the 2025 files as evidence of involvement in the assassination but highlight a personal connection to Israel.
Implication: Efron’s background has been seized upon by some theorists as a potential Israeli link, given his CIA role and eventual move to Jerusalem. However, there’s no evidence in the files that his actions were directed by Israel or that his Jewish identity influenced his work beyond standard CIA duties.

3. Kennedy’s Tensions with Israel Over Nuclear Program

The files indirectly touch on a geopolitical motive through Kennedy’s foreign policy, though not explicitly tied to the assassination. Document 104-10337-10014 and earlier releases (e.g., from the National Security Archive in 2016) confirm that Kennedy sought to monitor and limit Israel’s nuclear program at the Dimona facility. He pressured Israeli Prime Minister David Ben-Gurion to allow inspections, a stance that reportedly caused friction.

Details: Kennedy’s non-proliferation policy, stronger than that of any post-1945 president, included Israel. Ben-Gurion resigned in June 1963, partly over this issue, and some historians note his statement that Kennedy’s position threatened Israel’s survival. The 2025 files do not mention this conflict as a motive for the assassination but provide context for CIA-Israeli interactions during this period.
Implication: Conspiracy theories, including those on X, suggest that Israel, possibly with CIA complicity, might have viewed Kennedy’s policy as a threat worth eliminating. However, no document in the 2025 release substantiates this claim with evidence of Israeli action.

4. Operation Mongoose and Potential Overlaps

Document 104-10332-10022 details Operation Mongoose, a CIA effort to destabilize Cuba, involving figures like William K. Harvey and Howard Hunt. While primarily anti-Castro, the operation’s international scope included intelligence-sharing with allies, including Israel, as noted in Angleton’s testimony.

Details: The files mention Israeli operatives in Havana, though their role is vague and redacted in parts. Oswald’s Mexico City visit, where he contacted Cuban and Soviet officials, falls within the orbit of these operations, monitored by the CIA.
Implication: If Israeli intelligence collaborated with the CIA on Mongoose, some speculate it could have intersected with the assassination plot. Yet, the files lack any direct evidence tying Israel to Oswald or the events in Dallas.

Critical Analysis

The connections to Israel in the JFK files are circumstantial and largely speculative:

Angleton’s Role: His ties to Israeli intelligence are real but operational, focused on Cold War objectives rather than the assassination. His surveillance of Oswald predates any clear Israeli motive and aligns with broader CIA interests.
Efron’s Involvement: Efron’s Jewish identity and later life in Israel are incidental; his actions fit standard CIA protocol, with no indication of Israeli direction.
Nuclear Tensions: Kennedy’s pressure on Israel’s nuclear program provides a potential motive, but the files offer no link between this policy dispute and the assassination. The absence of such evidence after decades of releases suggests it may not exist.
Mongoose Overlap: Israeli involvement in CIA operations like Mongoose is plausible but peripheral, with no documented connection to November 22, 1963.

Sentiment on X and Conspiracy Theories

Posts on X (e.g., from @MarcusTulliusII, @WorldAltMedia, @wallyrashid) assert stronger Israeli involvement, often citing Mossad, the CIA, and figures like Meyer Lansky (a Jewish mobster) or Angleton as conspirators. These claims exaggerate the files’ contents, blending documented CIA-Israeli ties with unproven narratives about nuclear disputes or mob connections. The files do not mention Lansky or Mossad explicitly, and such theories rely on inference rather than evidence.

Conclusion

The newly released JFK files reveal historical CIA-Israeli intelligence collaboration, notably through Angleton, and confirm Kennedy’s tensions with Israel over its nuclear ambitions. However, they provide no direct evidence that Israel or Mossad played a role in the assassination. The connections are indirect—operational ties and geopolitical friction—lacking the concrete documentation (e.g., orders, communications) needed to substantiate involvement. While these elements keep speculation alive, especially among those skeptical of the official narrative, the files as of March 23, 2025, do not alter the conclusion that Lee Harvey Oswald acted alone, absent further unredacted revelations.

Nature of the Files Still Redacted in the JFK Assassination Records

Based on the newly released JFK assassination files from March 18, 2025, provided by the US National Archives, I’ll analyze the nature of the files that remain redacted. The subset of documents available offers insights into the types of information still withheld, the reasons for redaction, and the implications for understanding the assassination of President John F. Kennedy. I’ll also highlight surprising details and critically examine the official narrative that Lee Harvey Oswald acted alone.

Overview of Redacted Files in the Released Chunk

The documents reveal that redactions persist in several key areas, often tied to sensitive CIA operations, intelligence-gathering methods, and specific individuals or programs. While the files don’t explicitly state the full content of redacted sections, they provide clues through context, procedural notes, and references to ongoing classification efforts. Below, I’ll break down the nature of the redacted files based on the available information.

1. HTLINGUAL Program Records

The HTLINGUAL program, a CIA mail-opening operation targeting correspondence to and from the Soviet Union, is a focal point in 104-10332-10023. The file notes that some HTLINGUAL records were marked as destroyed, while others are unlocatable, but a significant detail emerges: the Office of Information Management (OIM) has only redacted records for a large Freedom of Information Act (FOIA) case related to HTLINGUAL. Meanwhile, IMS/ESG/HCS is retrieving unredacted copies to provide to the Assassination Records Review Board (ARRB).

Nature of Redacted Content: The redactions likely involve specific details about the HTLINGUAL operation, such as the identities of individuals monitored (potentially including Lee Harvey Oswald, who lived in the Soviet Union from 1959 to 1962), the methods used for mail interception, and the intelligence gathered. Given HTLINGUAL’s focus on Soviet communications, redacted sections might include references to Oswald’s correspondence, which could reveal whether the CIA had prior knowledge of his activities or intentions.
Surprising Detail: It’s striking that, despite the passage of over 60 years, the CIA still maintains redactions on HTLINGUAL records. The program’s relevance to Oswald—whose Soviet ties were well-documented—suggests that the redacted information might challenge the narrative of him as a lone actor by showing the extent of CIA surveillance on him before the assassination.
Implication: The redactions could be protecting sources and methods still deemed sensitive, or they might conceal embarrassing details about the CIA’s failure to act on intelligence about Oswald, or even its potential manipulation of him as an asset.

2. Angleton Files and CIA Counterintelligence

The disposition of James Jesus Angleton’s files, as discussed in 104-10332-10023, indicates that these records were integrated into the CIA’s Directorate of Operations (DO) system between 1976 and 1979, with duplicates destroyed. However, the file notes that these records are no longer identifiable as a distinct collection, and some related information remains classified.

Nature of Redacted Content: Angleton, as the CIA’s counterintelligence chief, was deeply involved in monitoring Oswald and had ties to Israeli intelligence, as noted in prior discussions. Redacted sections likely include specifics about Angleton’s operations, such as his surveillance of Oswald, his role in anti-Soviet and anti-Castro activities, and any interactions with foreign intelligence services that might intersect with the assassination. Given Angleton’s secretive nature and his involvement in controversial programs, redacted content might also cover internal CIA assessments of the assassination or Angleton’s personal theories about foreign involvement.
Surprising Detail: The fact that Angleton’s files are no longer a distinct collection raises questions about transparency. If these files contained critical evidence about the assassination, their dispersal and partial destruction could suggest an intentional effort to obscure the CIA’s role or knowledge.
Implication: Redactions here might be shielding details about Angleton’s activities that could contradict the official narrative, such as evidence of a broader conspiracy involving foreign actors or CIA complicity in overlooking Oswald as a threat.

3. QKENCHANT Program

The QKENCHANT program, mentioned in 104-10332-10023, is another area with redactions. The file notes that IMS/ESG/HCS initially provided a classified response in February 1998, which was later declassified after collaboration with the providing office.

Nature of Redacted Content: QKENCHANT was a CIA program related to covert operations, possibly involving the recruitment of assets or the use of proprietary companies for intelligence purposes. Redacted sections likely include operational details, such as the identities of agents, the scope of the program, and any connections to individuals involved in the JFK assassination. Given the program’s classified nature, the redactions might also protect information about financial arrangements or corporate fronts used by the CIA.
Surprising Detail: The declassification process for QKENCHANT took place in 1998, yet some information remains redacted in 2025. This suggests that the program’s methods or participants are still considered sensitive, potentially indicating ongoing relevance to intelligence operations or a need to protect historical assets.
Implication: If QKENCHANT had any overlap with Oswald or other figures tied to the assassination (e.g., anti-Castro operatives), the redactions might conceal evidence of CIA orchestration or negligence, challenging the lone gunman theory.

4. Sensitive Documents in 201 Dossiers (P&L, RYBAT, KAPOK)

Multiple files, including 104-10051-10170, 104-10213-10202, 104-10408-10316, and 104-10023-10087, outline procedures for handling sensitive documents in 201 dossiers, specifically those marked with P&L (Privacy and Legal), RYBAT (a CIA sensitivity indicator often tied to covert operations), and KAPOK (another sensitivity marker). These documents are to be sealed in black-taped envelopes or dossiers to retain their sensitivity when retired to Central Files; otherwise, they are desensitized.

Nature of Redacted Content: The redactions likely involve the content of these sensitive documents, which could include operational plans, intelligence reports, or derogatory information about individuals. Given the context of 201 dossiers (personality files), redacted sections might pertain to key figures in the assassination, such as Oswald, his associates, or CIA operatives involved in related operations (e.g., anti-Castro efforts). The use of terms like RYBAT and KAPOK suggests covert activities, possibly including assassination plots or surveillance operations.
Surprising Detail: The strict protocol for handling sensitive documents—requiring black-taped envelopes and restricted access—indicates a high level of secrecy, even decades after the assassination. This raises questions about what the CIA is still protecting, especially since these dossiers might contain information about Oswald or other suspects.
Implication: Redactions in these dossiers could be hiding evidence of CIA involvement in the assassination, such as knowledge of Oswald’s plans, connections to other conspirators, or operations that inadvertently facilitated the event. The continued sensitivity of these documents challenges the narrative that the CIA had no role beyond failing to predict Oswald’s actions.

5. George Bush and CIA Association

In 104-10332-10023, the ARRB inquired about George Herbert Walker Bush due to a November 1963 FBI document mentioning “George Bush of the Central Intelligence Agency.” The CIA’s response states that a search found no record of association with Bush in 1963, though a 201 file from 1977 and a DCD file were located.

Nature of Redacted Content: While the response itself is unclassified, related records might still be redacted, particularly those involving Bush’s potential CIA activities in the early 1960s. Redacted sections could include details about Bush’s role in anti-Castro operations (given his later involvement in the CIA and his oil business ties in Texas and the Caribbean) or any interactions with figures like Oswald or anti-Castro groups in Dallas.
Surprising Detail: The mention of Bush in a 1963 FBI document is intriguing, especially since he was not officially CIA Director until 1976. The CIA’s denial of any 1963 association seems convenient, and redactions in related files might conceal earlier ties that could place Bush in the orbit of the assassination.
Implication: If Bush had unofficial CIA connections in 1963, redacted records might reveal a network of operatives in Dallas at the time of the assassination, potentially contradicting the lone gunman narrative by suggesting a broader conspiracy involving CIA-linked figures.

6. Warren Commission Critics and the Garrison Investigation

The same file, 104-10332-10023, discusses CIA records on Warren Commission critics like Edward J. Epstein, Josiah Thompson, Mark Lane, Harold Weisberg, and Sylvia Meagher. It also references a file titled “Garrison Investigation of Kennedy Assassination,” opened in 1969 and closed in 1996.

Nature of Redacted Content: Redactions likely involve specific details in the Garrison Investigation file, such as CIA surveillance of Jim Garrison (the New Orleans DA who investigated the assassination) or evidence he uncovered about CIA involvement. The file on Josiah Thompson, who was of “operational interest” to the CIA circa 1962, might also have redacted sections detailing why he was monitored and whether this related to the assassination. Similarly, documents about Mark Lane (a 1970 dispatch from Germany and a 1977 OGC letter) might have redacted portions concerning the CIA’s response to his conspiracy allegations.
Surprising Detail: The existence of a dedicated Garrison Investigation file, spanning 27 years, is significant. Garrison’s probe famously alleged CIA involvement, and the CIA’s long-term monitoring of his work suggests they were concerned about what he might uncover.
Implication: Redactions in these files could be concealing evidence that supports Garrison’s claims, such as CIA ties to Oswald or other suspects like Clay Shaw, whom Garrison prosecuted. This could undermine the official narrative by indicating that the CIA actively suppressed alternative investigations.

Broader Analysis of Redaction Patterns

The redactions across these files share common themes:

Protection of Sources and Methods: Programs like HTLINGUAL and QKENCHANT involve intelligence-gathering techniques (e.g., mail interception, covert recruitment) that the CIA still deems sensitive, likely to protect ongoing or similar operations.
Operational Secrecy: The use of sensitivity markers like RYBAT and KAPOK in 201 dossiers indicates that covert operations—potentially including anti-Castro plots or surveillance of domestic figures—are being shielded. This could include operations that intersected with the assassination.
Individual Identities: Redactions often protect the identities of CIA operatives, assets, or subjects of interest (e.g., Josiah Thompson, potentially George Bush). This might be to avoid legal or reputational issues, but it also prevents a full understanding of who was involved in relevant events.
Embarrassing Revelations: The continued redaction of files related to the Garrison Investigation and Warren Commission critics suggests the CIA may be hiding information that contradicts the official narrative, such as evidence of a conspiracy or internal failures.

Critical Examination of the Official Narrative

The official narrative, as established by the Warren Commission, holds that Lee Harvey Oswald acted alone in assassinating JFK. However, the nature of the redacted files raises serious questions:

CIA Surveillance of Oswald: The HTLINGUAL program’s focus on Soviet correspondence likely included Oswald, given his time in the USSR. Redacted details about his monitored communications could reveal whether the CIA had foreknowledge of his intentions or manipulated him as part of a larger operation, contradicting the idea that he was an unknown lone actor.
Angleton’s Role: Angleton’s involvement in both Oswald’s surveillance and CIA counterintelligence operations suggests a deeper CIA connection to the assassination. Redacted sections of his files might contain evidence of foreign involvement or internal CIA discussions about the event, challenging the lone gunman theory.
Garrison Investigation: The CIA’s long-term monitoring of Garrison’s probe indicates they viewed it as a threat. Redacted information might include evidence of CIA ties to Oswald or other conspirators, supporting Garrison’s allegations of a broader plot.
Sensitive Operations: The presence of RYBAT and KAPOK documents in 201 dossiers hints at covert activities that might have intersected with the assassination, such as anti-Castro operations or domestic surveillance. Redacted details could reveal a conspiracy involving CIA operatives or assets.

The continued redactions, even 62 years after the assassination, suggest that the CIA is more concerned with protecting its historical actions than with transparency. This aligns with a pattern of obfuscation seen in prior releases, where the agency has been reluctant to fully disclose its role in the events of 1963. If the official narrative were unassailable, one might expect greater openness to dispel conspiracy theories. Instead, the redactions fuel suspicion that the CIA has something to hide—potentially evidence that undermines the lone gunman conclusion.

Conclusion

The redacted files in the March 18, 2025, release primarily concern sensitive CIA programs (HTLINGUAL, QKENCHANT), counterintelligence operations (Angleton’s files), covert activities (RYBAT, KAPOK documents), and investigations into alternative theories (Garrison Investigation, Warren Commission critics). These redactions likely protect operational details, individual identities, and potentially embarrassing revelations about the CIA’s knowledge of or involvement in the JFK assassination. Surprising elements, such as the long-term monitoring of Garrison and the continued sensitivity of 1960s programs, suggest that the redacted content might challenge the official narrative by revealing a broader conspiracy or CIA negligence. Until these redactions are lifted, the full truth about November 22, 1963, remains obscured, leaving open the possibility that Oswald did not act alone.

What evidence from the newly released JFK files suggests that the CIA may have been involved in the assassination?

Key Points

Research suggests the CIA had files on Lee Harvey Oswald before the assassination, but no direct evidence links them to the event.

It seems likely that the CIA's focus was on Oswald's defection to Russia, not involvement in the assassination.

The evidence leans toward the CIA's anti-Castro operations being unrelated to Kennedy's death, despite some coincidental timing.

Background

The newly released JFK files, made public on March 18, 2025, under the President John F. Kennedy Assassination Records Act of 1992, provide insights into the CIA's activities around the time of the assassination. These files include records on Lee Harvey Oswald, the alleged assassin, and the CIA's broader operations, particularly those related to Cuba and anti-Castro efforts. However, the connection to the assassination itself remains unclear and debated among historians and researchers.

CIA Files on Oswald

The CIA maintained a small file on Oswald before November 22, 1963, consisting of 33 to 37 documents (approximately 110-150 pages), with most originating from other agencies like the FBI, State Department, Navy, and newspaper clippings. These documents focused on Oswald’s 1959 defection to the Soviet Union and his activities after returning in 1961, reflecting standard counterintelligence monitoring rather than any plot involvement.

Anti-Castro Operations

The files detail CIA operations like Operation Mongoose and AMWORLD, which supported Cuban exile groups to overthrow Fidel Castro through propaganda and paramilitary efforts. These operations peaked around 1963-1967, but there is no evidence linking them directly to Kennedy’s assassination. Discussions about potential assassination attempts against Castro were noted, but they do not connect to the events in Dallas.

Conclusion

While the CIA's activities and files on Oswald provide context, the newly released files do not offer direct evidence suggesting the CIA was involved in the assassination. The focus appears to be on routine intelligence work and Cold War-era operations, not a conspiracy to kill Kennedy.

Detailed Analysis of Newly Released JFK Files and CIA Involvement

This section provides a comprehensive examination of the newly released JFK files, focusing on evidence that might suggest CIA involvement in the assassination of President John F. Kennedy on November 22, 1963. The analysis is based on documents released to the public on March 18, 2025, under the President John F. Kennedy Assassination Records Act of 1992, and aims to address the potential connections between the CIA, Lee Harvey Oswald, and the assassination event. All findings are derived from primary source documents, interpreted with care and nuance, and prioritize the information within these files.

Overview of CIA Records and Declassification Efforts

The CIA's collection related to the JFK assassination comprises approximately 250,000-300,000 pages, including 64 boxes provided to the House Select Committee on Assassinations (HSCA) between 1977 and 1978, and over 17 boxes on Oswald accumulated post-assassination. The declassification process, managed by the Historical Review Group, began with the release of pre-assassination documents on Oswald, which were declassified with minimal redactions and transferred to the National Archives for public access. The approach favors releasing as many documents as possible, with new guidelines encouraging proactive declassification. Most records are "secondary," collected after the assassination in response to inquiries from the Warren Commission and HSCA, rather than pre-existing intelligence. This context is crucial, as it suggests the large volume reflects investigative responses rather than prior CIA involvement in the assassination.

Pre-Assassination CIA Files on Lee Harvey Oswald

Before Kennedy's assassination, the CIA held a small file on Lee Harvey Oswald, consisting of 33 to 37 documents (approximately 110-150 pages). Sources included:

FBI (approximately 40% of post-assassination Oswald records)
State Department (about 20%)
Navy
Newspaper clippings
Only 11 documents originated within the CIA, focusing on Oswald’s 1959 defection to the Soviet Union and his activities after returning in 1961.

The Office of Security (OS) began maintaining records on Oswald in 1959 when he traveled to Russia and renounced his U.S. citizenship, prompted by Department of State reports distributed to the CIA due to counterintelligence concerns. Initially, information was stored in the Defectors File (#230341008), and as documentation grew, a separate file (#230351164) was created, managed by Marguerite D. Stevens of the OS/Security Research Staff (SRS). The SRS was tasked with collecting and evaluating counterintelligence data to prevent penetration of CIA operations, maintaining records on individuals of interest, and liaising with other government agencies. Pre-assassination documents in Oswald’s file included:

Department of State telegrams and dispatches from 1959-1962
Press clippings, such as The Washington Post and Evening Star, detailing his defection
FBI and Navy reports, including a July 2, 1961, FBI report from Dallas, Texas

A page-by-page review of the Defectors File (12 volumes) and Oswald’s file (7 volumes) was not conducted for recent requests, with efforts concentrated on the pre-assassination timeframe. This review, conducted by Katie Nakai, OPS/CD/IMB, secure 40552, found no information directly linking Oswald to CIA operations beyond routine monitoring.

Post-Assassination Accumulation

After the assassination, the CIA amassed approximately 33,000 pages on Oswald, mostly received from other agencies. In 17 boxes of Oswald records, approximately 40% originated from the FBI, 20% from the State Department or other sources, with the remainder from CIA or unspecified origins. Additional materials, compiled for the Warren Commission and HSCA, include 63 boxes of paper records and one box with 72 reels of microfilm, with about 27% originating from various U.S. government agencies, private organizations, and press. This post-assassination collection reflects responses to investigations rather than pre-existing CIA plots.

CIA Operations and Potential Links to the Assassination

The files detail several CIA operations that could be scrutinized for potential links to the assassination, particularly those involving Cuba and anti-Castro activities, given the historical context of U.S.-Cuba relations and Kennedy’s policies.

Operation Mongoose and Anti-Castro Activities

CIA anti-Cuban operations from 1960-1964, including Operation Mongoose, were noted in the files, especially if they involved JFK figures. Most U.S. anti-Castro activities in 1963 were considered relevant for review. Paramilitary operations against Cuba, primarily maritime, peaked from 1963 to 1967, involving infiltrating and exfiltrating agents, and hit-and-run sabotage raids. These were staffed by CIA contract employees, including Cuban refugees and some CIA officers, with training conducted mostly within the U.S., such as the Florida Keys. The program ended in December 1968 due to high costs and insufficient intelligence yield. The AMWORLD operation, a covert effort to support Cuban exile groups under Manuel Artime Buesa’s control, aimed to overthrow Fidel Castro through propaganda and paramilitary forces, based in Costa Rica, Nicaragua, and Miami. The CIA provided financial and technical support but did not participate directly in daily operations. There is no evidence that AMWORLD’s mission, which failed to achieve its goals, considered establishing a Cuban Government in Exile or had any direct connection to Kennedy’s assassination.

Castro Assassination Discussions

Discussions about potential assassination attempts against Fidel Castro were mentioned, with an individual recalling overhearing conversations in October or November 1963 in Paris, involving Néstor Sanchez from the Special Activities Staff and Desmond Fitzgerald, about providing Belgian rifles with telescopic sights to a former commandante in Castro’s military. These discussions were assumed to stem from a Special Group decision, with Bobby Kennedy overseeing, likely on behalf of President Kennedy. However, the individual did not participate, and 19 volumes of related documents were provided to investigators, with no direct link to the JFK assassination established.

Cuban Exile and Mafia Connections

Cuban exile anti-Castro activities, leaders, and organizations from 1960-64 were noted if linked to JFK figures. The AMBRUSH organization, a Revolutionary Council Anti-Castro Security and Counter-Intelligence Team, mentioned possible Castro penetration into U.S. activities in an August 19, 1961, document, but no findings directly related to the assassination. Mafia connections, if related to Castro, JFK, or New Orleans during Oswald’s time frames, were also considered, but no specific links were found in the reviewed files.

Key Figures and Potential CIA Agents

The files list several individuals considered JFK assassination-related, including:

Howard Hunt (CIA employee)
David Phillips (CIA employee)
Winston Scott (Chief of Station, Mexico City)
Maurice Bishop (alleged figure, any reference)
Yuri Nosenko (dispute over his bona fides, former KGB agent and Oswald’s handler)

These figures were part of broader investigations, but no documents directly link them to the assassination. For instance, Howard Hunt, known for later involvement in Watergate, is listed as a CIA employee, but no connection to Oswald or the assassination is evident. Similarly, David Phillips and Winston Scott are mentioned in the context of CIA stations (Mexico City and others), but their activities relate to Oswald’s travel and defection, not the assassination itself.

Analysis of Potential Links

Despite the extensive documentation, no direct evidence suggests the CIA was involved in the assassination. The files highlight:

Routine monitoring of Oswald due to his defection, with no indication of operational control or conspiracy.
CIA operations in Cuba and anti-Castro activities, which were significant during the Cold War, but no causal link to Kennedy’s death is established.
Post-assassination collection of documents reflects investigative responses, not prior involvement.

The lack of direct evidence is notable, especially given the thorough searches conducted, such as for Claude B. Capehart and George Bush, which found no assassination-related material. The destruction of HTLINGUAL files (a mail interception project) on April 8, 1994, means it cannot be confirmed whether they contained information on Oswald, but a search showed no index reference, further limiting potential evidence.

Tables Summarizing Key Findings

Below is a table summarizing the CIA’s pre- and post-assassination holdings on Oswald:

Analysis of Potential CIA Motives for Removing Kennedy Based on Newly Released JFK Files

This analysis examines potential motives the CIA might have had for removing President John F. Kennedy from office around the time of his assassination on November 22, 1963, based on the newly released JFK files from March 18, 2025. The official narrative, established by the Warren Commission, holds that Lee Harvey Oswald acted alone in assassinating Kennedy. However, the documents reveal CIA activities and relationships that could suggest motives for involvement, challenging this narrative. Below, I explore these potential motives, highlight surprising information from the files, and critically assess the establishment's conclusions.

Potential CIA Motives for Removing Kennedy

1. Frustration Over the Bay of Pigs Fiasco and Kennedy's Oversight

The Bay of Pigs invasion in April 1961 was a significant failure for the CIA, and Kennedy's response created tension with the agency. The files reveal that Kennedy was deeply frustrated with the CIA after the failed invasion, reportedly saying he wanted to "splinter the CIA in a thousand pieces and scatter it to the winds" [157-10014-10242]. He appointed his brother, Robert F. Kennedy, to oversee and reform the agency, with instructions to prevent another such debacle. Robert's enthusiastic investigation into CIA covert operations, including the "executive action plan" to assassinate Fidel Castro, suggests the Kennedys were exerting significant control over the agency [157-10014-10242]. Motive Analysis: The CIA might have resented this oversight, particularly Robert Kennedy's hands-on approach, which one source described as treating the CIA's covert activities with the fascination of a "wide-eyed schoolboy" [157-10014-10242]. The agency's leadership, including figures like Allen W. Dulles (who approved the Castro plot and later served on the Warren Commission), may have felt their autonomy and operational freedom were under threat. Removing Kennedy could have been seen as a way to regain control and avoid further interference in their covert operations, especially given Kennedy's apparent distrust of the agency post-Bay of Pigs. Surprising Information: The files confirm that Robert Kennedy was fully aware of the CIA's plot to kill Castro and did not stop it, despite claims from loyalists that he either knew nothing or halted the efforts [157-10014-10242]. This contradicts the narrative of the Kennedys as uninvolved in the CIA's darker operations, suggesting they were complicit in actions that could have provoked retaliation—potentially giving the CIA a motive to eliminate Kennedy if they feared he might expose or further restrict their activities.

2. Fear of Retribution for the Castro Assassination Plot

The CIA's plot to assassinate Fidel Castro, initiated during the Eisenhower administration and continued under Kennedy, is a central theme in the files. The agency enlisted Mafia mobsters to carry out the assassination, a fact they deliberately withheld from the Warren Commission to cover up this collaboration and prevent public outrage [157-10014-10242]. Robert Kennedy was briefed on the plot on May 7, 1962, and cautioned the CIA against proceeding without his consultation, yet he did not stop subsequent attempts [157-10014-10242]. After Kennedy's assassination, Robert was "devastated" by the possibility that the plot had backfired, leading to his brother's death as a retaliatory act by Castro [157-10014-10242]. Motive Analysis: If the CIA believed Castro had retaliated by orchestrating Kennedy's assassination, they might have had a motive to remove Kennedy preemptively to avoid such a scenario—or to eliminate him after the fact to cover up their role in provoking Castro. The files note that several key CIA officials believed Castro was behind Kennedy's assassination, and evidence from Mexico City immediately after the killing suggested Cuban involvement [157-10014-10242]. The CIA's fear of being held accountable for triggering a chain of events that led to Kennedy's death could have motivated them to act against him, either to prevent such an outcome or to silence those who might expose their role. Surprising Information: The CIA's immediate suspicion of Cuban involvement, as evidenced by cables from the U.S. embassy in Mexico City and CIA findings in Washington within hours of the assassination, is striking [157-10014-10242]. Yet, this information was not shared with the Warren Commission, suggesting a deliberate cover-up. Additionally, the fact that CIA Director John A. McCone briefed President Lyndon B. Johnson on the Mexico City intelligence the day after the assassination but claimed Castro's name was not mentioned during his three-hour meeting with Robert Kennedy on November 22, 1963, raises questions about the agency's transparency and intentions [157-10014-10242].

3. Anti-Castro Operations and Policy Disagreements

The files highlight the CIA's extensive anti-Castro operations, including the "executive action plan" managed by CIA operative William Harvey and overseen by Desmond Fitzgerald [157-10014-10242]. Robert Kennedy led the Special Group, a counter-insurgency committee focused on disrupting Castro, though CIA chief John McCone denied it endorsed assassinations [157-10014-10242]. However, the files confirm Robert's knowledge of the assassination plot, and a CIA officer met with a Cuban official on the day of Kennedy's assassination to provide explosives and a poison pen device for killing Castro [157-10014-10242]. Motive Analysis: Kennedy's perceived "soft" stance on Cuba after the Bay of Pigs and during the Cuban Missile Crisis may have frustrated the CIA, which was deeply invested in overthrowing Castro. The files note that Castro warned U.S. leaders supporting terrorist plans against Cuban leaders would not be safe, and a U.S. committee acknowledged the likelihood of Castro retaliating, though not by attacking U.S. leaders directly [157-10014-10242]. If the CIA believed Kennedy's policies were hindering their anti-Castro efforts—or worse, exposing them to retaliation—they might have seen his removal as a way to shift U.S. policy toward a more aggressive stance against Cuba, aligning with their operational goals. Surprising Information: The timing of the CIA's meeting with a Cuban official on November 22, 1963, to provide assassination tools is highly suspicious [157-10014-10242]. This suggests the agency was actively pursuing Castro's elimination on the very day Kennedy was killed, raising the possibility of a coordinated effort or a convenient distraction. Additionally, Fidel Castro's denial of involvement in Kennedy's assassination, coupled with his speculation that it was a conspiracy by U.S. reactionaries to implicate Cuba, adds a layer of complexity to the narrative [157-10014-10242].

4. Mafia Connections and the Risk of Exposure

The CIA's collaboration with the Mafia to assassinate Castro, as detailed in the files, created a significant risk of exposure. Mobster John Roselli, who worked with the CIA on six failed attempts to kill Castro, suggested that Oswald might have been a decoy while others ambushed Kennedy, and that Jack Ruby was ordered to kill Oswald to silence him [157-10014-10242]. Ruby's confirmed ties to the Havana underworld and his visit to Mafia figure Santo Trafficante in a Cuban prison further link the CIA, the Mafia, and the assassination [157-10014-10242]. Motive Analysis: The CIA might have feared that Kennedy, through Robert's oversight, would uncover and expose their collaboration with the Mafia, which could have led to a major scandal and the dismantling of the agency. Removing Kennedy could have been a preemptive strike to protect their operations and avoid accountability. Additionally, if the Mafia felt threatened by Oswald potentially revealing their involvement, as Roselli claimed, the CIA might have supported or facilitated Ruby's actions to ensure silence, further implicating them in a broader conspiracy. Surprising Information: Roselli's brutal murder in 1976—shot or stabbed, legs hacked off, and body dumped in Biscayne Bay—suggests the lengths to which certain parties would go to silence those with knowledge of the CIA-Mafia plot [157-10014-10242]. His claim that Ruby was ordered to kill Oswald to prevent him from cracking under interrogation directly challenges the lone gunman narrative, pointing to a possible conspiracy involving the CIA and the Mafia [157-10014-10242].

Critical Examination of the Establishment Narrative

The Warren Commission's conclusion that Lee Harvey Oswald acted alone is challenged by several elements in the files:

CIA Cover-Up: The deliberate withholding of the Castro assassination plot from the Warren Commission by key figures like Allen W. Dulles and Robert Kennedy suggests the CIA had something to hide [157-10014-10242]. This cover-up undermines the Commission's findings and raises the possibility that the agency was protecting itself from scrutiny over its role in the events leading to Kennedy's death.
Cuban Connection: The immediate suspicion of Cuban involvement, coupled with the CIA's failure to investigate Cuban sources or the exile community thoroughly, as noted by the Senate Intelligence Committee, indicates a lack of transparency [157-10014-10242]. This could suggest the CIA either feared what they might find or were complicit in a plot that involved Cuban elements.
Mafia Involvement: Roselli's account of Oswald as a potential decoy and Ruby's role in silencing him, combined with Ruby's confirmed ties to the Havana underworld, points to a broader conspiracy involving the Mafia—potentially with CIA knowledge or support [157-10014-10242]. This directly contradicts the lone gunman theory.
Robert Kennedy's Role: Robert Kennedy's knowledge of the Castro plot and his failure to stop it, despite his oversight role, complicates the narrative of the Kennedys as uninvolved in the CIA's actions [157-10014-10242]. His torment after the assassination, fearing the plot had backfired, suggests a deeper connection between the CIA's operations and Kennedy's death.

Conclusion

The newly released JFK files from March 18, 2025, suggest several potential motives for the CIA to remove Kennedy from office around the time of his assassination. These include resentment over Kennedy's oversight post-Bay of Pigs, fear of retribution for the Castro assassination plot, disagreements over Cuba policy, and the risk of exposure due to their Mafia collaboration. While no direct evidence confirms CIA involvement, the files reveal a web of covert activities, cover-ups, and connections that challenge the narrative of Oswald acting alone. The CIA's actions—particularly their withholding of critical information from the Warren Commission and their deep ties to anti-Castro operations and the Mafia—suggest they had both the motive and the means to orchestrate or facilitate Kennedy's removal, either to protect their interests or to shift U.S. policy in their favor. Further investigation into these connections is necessary to fully understand the events of November 22, 1963.

Analysis of Potential Israeli Motives for Removing Kennedy

Based on Historical Context and Newly Released JFK Files

This analysis explores potential motives Israel might have had for removing President John F. Kennedy around the time of his assassination on November 22, 1963, based on historical context and insights from the newly released JFK files from March 18, 2025. The official narrative, per the Warren Commission, asserts that Lee Harvey Oswald acted alone. However, some researchers and conspiracy theorists have speculated about Israeli involvement, often citing tensions over U.S.-Israel relations and Kennedy’s policies. Below, I examine these potential motives, critically assess the establishment narrative, and highlight any relevant or surprising information from the files that might connect to Israel, while noting the absence of direct evidence.

Potential Israeli Motives for Removing Kennedy

1. Opposition to Kennedy’s Pressure on Israel’s Nuclear Program

One of the most cited potential motives for Israeli involvement stems from Kennedy’s efforts to curb Israel’s nuclear ambitions at the Dimona facility. Historical records show that Kennedy was deeply concerned about nuclear proliferation in the Middle East and pressed Israeli Prime Minister David Ben-Gurion for transparency. In a May 18, 1963, letter, Kennedy demanded regular U.S. inspections of Dimona, threatening to withhold support if Israel did not comply. Ben-Gurion resigned in June 1963, reportedly in part due to this pressure, and his successor, Levi Eshkol, faced continued U.S. insistence on inspections, as evidenced by a July 5, 1963, letter from Kennedy. Motive Analysis: Israel, under Ben-Gurion and later Eshkol, viewed its nuclear program as an existential necessity amid threats from Arab neighbors following the 1948 war and ongoing regional hostility. Kennedy’s stance—potentially tying U.S. military and economic aid to Israeli concessions on Dimona—could have been perceived as a direct threat to Israel’s security. Removing Kennedy might have been seen as a way to ensure the survival of the nuclear program, especially if Israeli leadership believed his successor, Lyndon B. Johnson, would adopt a less stringent policy (which he did, softening inspections after 1963). From the Files: The newly released JFK files do not directly address Dimona or U.S.-Israel nuclear tensions. However, a document on CIA operations in Mexico City 104-10188-10012 mentions the termination of Project KDAFGHAN in 1972 due to “VWBLANKET contamination.” While this is post-assassination and unrelated to Israel, it highlights CIA activities in a region Oswald visited in 1963, raising questions about whether Israeli intelligence (e.g., Mossad) might have intersected with CIA networks there. No explicit link exists in the files, but the absence of Dimona-related records could suggest either irrelevance or deliberate omission.

2. Concerns Over Kennedy’s Middle East Policy Shift

Kennedy’s foreign policy aimed to balance U.S. support for Israel with improved relations with Arab states, particularly Egypt under Gamal Abdel Nasser. In 1962-1963, Kennedy supported Nasser’s regime with economic aid and pursued a neutral stance in the Arab-Israeli conflict, as seen in his backing of UN Resolution 194 (Palestinian refugee rights) and his refusal to fully align with Israel against Arab nationalism. This shift alarmed Israeli leaders, who feared a reduction in U.S. support at a time when they faced existential threats from Egypt, Syria, and Jordan. Motive Analysis: Israel might have perceived Kennedy’s outreach to Nasser as a betrayal, especially given Egypt’s role in the 1967 Six-Day War just four years later. If Israeli leadership believed Kennedy’s policies would embolden Arab states or weaken U.S. military backing, his removal could have been seen as a way to secure a more pro-Israel administration under Johnson, who indeed increased arms sales to Israel post-1963. The timing—late 1963—coincides with escalating regional tensions, potentially amplifying Israel’s sense of urgency. From the Files: A file on Victor Rico Galan, a Mexican Marxist journalist traveling to Cuba in 1962 104-10221-10003, notes CIA surveillance of anti-U.S., pro-Cuba figures. While this relates to Cuban rather than Israeli interests, it underscores U.S. intelligence focus on leftist movements in the region, which Israel also opposed due to Soviet backing of Arab states. No direct Israeli connection appears, but the CIA’s broader Middle East surveillance could have overlapped with Israeli intelligence priorities, offering a speculative link.

3. Retaliation for Kennedy’s Stance on Jewish Refugees and AIPAC Oversight

Kennedy’s administration took steps that some Israeli advocates viewed as hostile. In 1963, the Justice Department, under Robert Kennedy, pushed for the American Zionist Council (AZC)—a precursor to AIPAC—to register as a foreign agent under the Foreign Agents Registration Act (FARA), citing its funding from Israel. Additionally, Kennedy’s support for Palestinian refugee rights clashed with Israeli interests, as it challenged the narrative of exclusive Jewish claims to the land post-1948. Motive Analysis: If Israeli leaders or their U.S. proxies felt Kennedy’s policies threatened their influence in Washington or their territorial security, they might have seen his removal as a way to protect their lobbying power and geopolitical position. Johnson’s administration later dropped the FARA push against AZC/AIPAC and increased support for Israel, suggesting a shift that could have been anticipated or desired by Israeli interests. The timing of the assassination, shortly after these policy moves, might have heightened Israeli concerns. From the Files: The files lack direct references to the AZC or FARA disputes. However, a document on CIA surveillance of Martin Luther King in 1957 104-10433-10209 shows the agency monitoring domestic figures with international ties (e.g., Communist Party links). This suggests a capability to track groups like the AZC, though no evidence ties this to Kennedy’s assassination or an Israeli motive.

4. Alleged Mossad-CIA Collaboration and Permindex Theory

Conspiracy theories, notably from Michael Collins Piper’s Final Judgment, suggest Israel worked with the CIA through entities like Permindex, a Swiss-based trade organization allegedly linked to Mossad and CIA figures like Clay Shaw (investigated by Jim Garrison). These theories claim Kennedy’s death was tied to his opposition to Israel’s nuclear program and Middle East policies, with Permindex as a conduit for coordination. Motive Analysis: If Israel collaborated with rogue CIA elements opposed to Kennedy (e.g., over Cuba or Vietnam), his removal could have served mutual interests—Israel securing its nuclear program and CIA factions regaining autonomy. The timing aligns with Kennedy’s nuclear pressure and the CIA’s anti-Castro efforts, both peaking in 1963. However, this remains speculative without primary evidence. From the Files: The files mention CIA operative Desmond Fitzgerald meeting a Cuban official on November 22, 1963, to provide assassination tools against Castro 157-10014-10242, but no reference to Permindex, Mossad, or Israeli involvement appears. A file on Luis Clemente Posada Carriles 104-10220-10128 details CIA ties to Cuban exiles, hinting at international networks, but nothing ties this to Israel.

Critical Examination of the Establishment Narrative

The Warren Commission’s lone gunman narrative does not address Israel as a potential actor, focusing instead on Oswald’s personal motives. However, the files and historical context raise challenges:

Nuclear Tensions Omitted: The absence of Dimona-related documents in the files could indicate a deliberate exclusion, as Kennedy’s pressure on Israel was a significant foreign policy issue in 1963. This gap weakens the narrative’s completeness.
Middle East Policy Shift: Kennedy’s balancing act with Arab states, absent from the Warren report, suggests broader geopolitical stakes ignored by the official account, potentially involving Israeli interests.
Surveillance Capabilities: The CIA’s monitoring of figures like King 104-10433-10209 shows a capacity to track domestic and international actors, which could extend to Israeli lobbying groups or operatives, yet this is unexplored in the official investigation.
Lack of Israeli Focus: The files’ emphasis on Cuba and the CIA (e.g., 157-10014-10242) contrasts with their silence on Israel, possibly reflecting a bias or cover-up, though it could simply indicate irrelevance.

Surprising Information from the Files

CIA-Cuban Timing: The CIA’s provision of assassination tools to a Cuban official on the day of Kennedy’s death 157-10014-10242 is striking, though unrelated to Israel. It suggests a flurry of covert activity that could have involved other players, including Mossad, if collaboration existed.

Mexico City Operations: The CIA’s presence in Mexico City 104-10188-10012, where Oswald visited, hints at a hub of international intrigue, potentially including Israeli intelligence, though no evidence supports this.

Conclusion

No direct evidence in the newly released JFK files from March 18, 2025, suggests Israel had a motive or role in removing Kennedy. However, historical tensions—particularly Kennedy’s pressure on Dimona, his Middle East policy shift, and disputes over Zionist lobbying—provide plausible motives. Israel might have sought to eliminate Kennedy to secure its nuclear program, maintain U.S. support against Arab threats, or protect its influence in Washington, anticipating a more favorable Johnson administration. The files’ focus on CIA-Cuban operations and lack of Israeli references could reflect either irrelevance or a deliberate omission, possibly due to sensitivity around U.S.-Israel relations. While speculative, these motives challenge the lone gunman narrative by suggesting broader geopolitical stakes, warranting further exploration of U.S.-Israel dynamics in 1963.

covid - influenza

When I started following this story back in January, I was quite alarmed at what the Communist Party of China was doing to their people. From the numbers that were coming out of the National Health Commission of the PRC, it really looked like this was far more serious than the annual flu season. The death rate seemed to be 20-25x higher which is in itself scary. Since then, it has become very obvious that we can not trust their numbers.

I think it is fair to compare Covid-19 to the season flu because that is something we are familiar with and it gives us something to relate to. Not saying it is the same as the seasonal flu, just saying it is worth comparing. So how does it compare?

Since Oct 2019 USA CDC reports the following numbers for Pneumonia and Influenza:

38M-54M flu illnesses

18M-26M flu medical visits

400k-730k flu hospitalizations (compared to 900k in 2018)

24k-62k flu deaths (compared to 80k deaths in 2018)

We have to be cautious in referencing number as there can be a large variation from one year to the next and periodically there is a very large swelling. We also have to be careful with average numbers because in a normalized distribution, that is more like the mid-point in a range of variation, and half the time it is more than average and half the time it is less than average. I don't think it is meaningful to use average. And now I am seeing even a more vague term such as "expected". What does that even mean? It never seems to be defined whenever it is used.

Italy is currently showing 19/100k deaths for C19 with 88% having 1 or more comorbidities. In previous flu seasons, Italy showed 11.6 – 41.2 deaths/100k for all age groups. Since we know that the majority of the C19 deaths are those > 65 years old, it is useful to know that during recent flu seasons, mortality rate of those in age >65 for Europe was 147.1/100k and for Italy was 292.8/100k.

So, my own opinion is that Covid-19 is not nearly as bad as I thought it was back in January. I think it compares very well to seasonal flu and will likely be with us for years.(UPDATE) Scott Gottlieb just tweeted that he thinks the final deaths in USA for this season will be 80k-160k. Which puts it at as bad as the last few years to as bad as 1965 making it a 50 year flu. Its numbers seem to be comparable as well but probably slightly higher but certainly not an order of magnitude higher. The flu season has many viruses and we have added another one to it. The good that will come out of this is that we may have the will to finally do something about the common cold. We are all learning about community spread that will help us in future seasons. Personally, I am not hopeful for a vaccine but there are some promising cures and this has certainly helped propel the science forward.

Association between the 2008–09 Seasonal Influenza Vaccine and Pandemic H1N1 Illness during Spring–Summer 2009: Four Observational Studies from Canada "Prior receipt of 2008–09 TIV was associated with increased risk of medically attended pH1N1 illness during the spring–summer 2009 in Canada... However, estimates from all four studies (which included about 1,200 laboratory-confirmed pH1N1 cases and 1,500 controls) showed that prior recipients of the 2008–09 TIV had approximately 1.4–2.5 times increased chances of developing pH1N1 illness that needed medical attention during the spring–summer of 2009 compared to people who had not received the TIV."" https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1000258

respitory virus

(https://www.canada.ca/en/public-health/services/surveillance/respiratory-virus-detections-canada/2021-2022/week-13-ending-april-2-2022.html)

New Canadian studies suggest seasonal flu shot increased H1N1 risk

(https://www.cidrap.umn.edu/news-perspective/2010/04/new-canadian-studies-suggest-seasonal-flu-shot-increased-h1n1-risk)

Reassessing the Global Mortality Burden of the 1918 Influenza Pandemic:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7314216/

World population estimates

https://www.census.gov/data/tables/time-series/demo/international-programs/historical-est-worldpop.html

Pale Rider: The Spanish Flu of 1918 and How It Changed the World:

https://theworthyhouse.com/2018/11/15/book-review-pale-rider-the-spanish-flu-of-1918-and-how-it-changed-the-world-laura-spinney/

Experiments Upon Volunteers to Determine the Cause and Mode of Spread of Influenza, Boston, November and December, 1918:

https://quod.lib.umich.edu/f/flu/3750flu.0016.573

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6642581/

Probable limited person-to-person transmission of highly pathogenic avian influenza A (H5N1) virus in China

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(08)60493-6/fulltext

Detection and Isolation of Airborne Influenza A H3N2 Virus Using a Sioutas Personal Cascade Impactor Sampler

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3810434/

Viable influenza A virus in airborne particles expelled during coughs versus exhalations

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4947941/

Transmission routes of respiratory viruses among humans

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102683/

Exposure to Influenza Virus Aerosols During Routine Patient Care

https://academic.oup.com/jid/article/207/7/1037/2192312

R. Edgar Hope-simpson: The Transmission of Epidemic Influenza

https://link.springer.com/book/10.1007/978-1-4899-2385-1#aboutBook

Why have three long-running Cochrane Reviews on influenza vaccines been stabilised?

https://community.cochrane.org/news/why-have-three-long-running-cochrane-reviews-influenza-vaccines-been-stabilised

Vaccines for preventing influenza in the elderly

Older adults receiving the influenza vaccine may have a lower risk of influenza (from 6% to 2.4%), and probably have a lower risk of ILI compared with those who do not receive a vaccination over the course of a single influenza season (from 6% to 3.5%). We are uncertain how big a difference these vaccines will make across different seasons. Very few deaths occurred, and no data on hospitalisation were reported. No cases of pneumonia occurred in one study that reported this outcome. We do not have enough information to assess harms relating to fever and nausea in this population.

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD004876.pub4/full

THE £4TIOLOGY OF INFLUENZA. https://pmc.ncbi.nlm.nih.gov/articles/instance/2047634/pdf/brjexppathol00309-0030.pdf

bookmarks - social media channels

Health

Dr. John Bergman (Bitchute) - Homeopathy
Dr. Eric Berg (YouTube)(Odysee) - Homeopathy
Dr. Rhonda Patrick (YouTube) - Exercise and nutrients
Dr. Roger Seheult (YouTube) - Medical lectures
Ivor Cummins (YouTube) - Critical thinking & reasoning
Dr Sam Bailey (SubStack)(YouTube)(Odysee) - Health Politics
Dr Mobeen Syed (Odysee) - Biochemistry
Dr. Sten Ekberg (Rumble) - Nutrition and health podcasts
Remnant MD (SubStack)(X) - Homeopathy
Dr. Makis, MD (SubStack) - Covid
Dr. Jessica Rose (SubStack) - Covid research
Ben Bikman, PHD (YouTube)(Website) - Metabolic research
Dr. Doug Corrigan (X)(website) - Biochemist & Molecular Biologist, Physicist
Steve Kirsch (X)(SubStack) - Covid research
Jesse Chappus (Youtube) - Interviews with health & nutrition specialists
JJ Couey (X)(Website) - Neurobiology and immunology

Politics

Other

Climate

AI

Sebastian Raschka, PhD (SubStack)

Bitcoin

Jimmy Song (Substack)

Homesteading

politics - c40

https://www.c40.org/wp-content/uploads/2022/03/C40-Green-and-Healthy-Streets-Declaration_Public-progress-report_Feb-2022.pdf

https://www.arup.com/globalassets/downloads/insights/arup-c40-the-future-of-urban-consumption-in-a-1-5c-world.pdf

health nutrition - magnesium

About 70% of the population gets random muscle twitches. The medical term for this is fasciculation—spontaneous involuntary muscle contraction and relaxation. This could happen to your eyelid, arms, hands, fingers, legs, feet, or tongue.

There is even a medical condition called benign fasciculation syndrome. I believe this condition is really a nutritional deficiency. But, the typical treatment is cognitive behavioral therapy, anti-depression medication, and calcium channel blockers.

Random muscle twitches

In my opinion, random muscle twitches are caused by a magnesium deficiency. About 70% of the population also has a magnesium deficiency. Leafy greens are rich in magnesium.

Other symptoms of a magnesium deficiency: • Fatigue • Muscle cramps • Anxiety

Other potential causes of a muscle twitch: • High calcium • Low vitamin D • Alkalosis (potentially caused by a high carb diet or low potassium)

These are some of the most commonly known benefits of magnesium:

Leg cramps
Relaxation & calmness
Sleep
Inflammation
Blood sugar
Electrolyte
Bone health
Energy (ATP)

However, the real reason magnesium is essential is that it promotes a healthy heart and arteries.

The FDA allows the following health claim: “Consuming diets with adequate magnesium may reduce the risk of high blood pressure. However, the FDA has concluded that the evidence is inconsistent and inconclusive.”

Magnesium has a significant effect on the cardiovascular system. However, it’s also important that you consume a healthy diet. Taking magnesium won’t make much of a difference if you’re eating an unhealthy, carb-loaded diet.

Magnesium deficiency can have some potentially dangerous side effects, including: • Apathy • Depression • Convulsions • Cramps • Weakness

66% of the population does not meet the minimum requirement for magnesium. Magnesium levels have dropped significantly over the last 50 years.

The best sources of magnesium are vegetables. The average person only consumes 1.5 cups of vegetables each day—but you need 7 to 10 cups of vegetables daily for optimal health.

Other sources of magnesium include: • Grains (avoid!) • Green vegetables • Nuts and seeds • Seafood • Meats • Berries

Avoid these forms of magnesium supplements: • Oxide • Hydroxide • Carbonate • Sulfate

Stick with these forms of magnesium: • Citrate (may act as a laxative) • Threonate • Bisglycinate • Orotate • Taurate • Malate

Taurate: heart and blood pressure
Threonate: brain and memory
Glycinate: relaxation and sleep
Lactate: digestion
Malate: energy and fatigue
Chloride: blood sugar and digestion
Orotate: heart
Sulfate: muscle soreness

For constipation, bloating, IBS:

oxide
sulfate
citrate

Start with 500mg going to 750mg or 1000mg, before bedtime Most people are low on magnesium in NA

Magnesium citrate - Absorbs easily. This can potentially be good for: • Nocturnal leg cramps • Constipation • Preventing headaches

Magnesium glycinate - Absorbs easily _ No laxative effects. This can potentially be good for: • Promoting a sense of calm • Supporting sleep • Reducing anxiety • Reducing inflammation • Supporting the blood sugars

Magnesium threonate - Best for the brain This can potentially be good for: • Improving cognitive function • Preventing the loss of synapses (in animal studies)

Magnesium orotate - Good for top athletes This can potentially be good for: • Improving energy • Supporting the mitochondria

Magnesium taurate This can potentially be good for: • Supporting the blood sugars • Supporting blood pressure (in animal studies)

Magnesium malate

Laxative effect is small to none This can potentially be good for: • Fibromyalgia • Chronic fatigue syndrome

You may want to avoid these versions of magnesium: • Magnesium sulfate • Magnesium carbonate • Magnesium oxide - only absorve about 4% • Magnesium hydroxide

Vitamins that support the absorption of magnesium • Vitamin D • Vitamin B6

health nutrition - oatmeal

Benefits

Health Benefits - Oatmeal is nutritionally rich. It has more protein than most grains and also contains numerous vitamins and minerals. It contains antioxidants and a soluble fiber called beta-glucan, which aids several systems of the body. Oatmeal provides many health benefits, including these:

Gut Health - The beta-glucan soluble fiber promotes regular emptying of the bowel and prevents constipation. It also supports healthy gut bacteria, which may reduce the symptoms of irritable bowel syndrome and other intestinal problems.
Lower Cholesterol - Soluble fiber like the beta-glucan in oatmeal lowers cholesterol. In one study, those who ate oat bran experienced a 23% drop in total cholesterol. Researchers believe that several mechanisms in the body are responsible for the lower cholesterol.
Heart Health - Oats are high in antioxidants called avenanthramides, not found in other cereal grains. These antioxidants reduce inflammation and relax arteries, improving heart health.
Blood Sugar Control - The soluble fiber in certain oats can keep blood sugar from rising after a meal. The glycemic load of less-processed oats is low to medium, making them a suitable carbohydrate for those with diabetes. Those who have diabetes should avoid instant oatmeal, which has a high glycemic index.
Weight Control - Eating fiber-rich foods like oatmeal produces a feeling of satisfaction, which can make it less likely that you will overeat. The particular fiber in oatmeal, beta-glucan, makes the contents of the intestines very viscous and may make you feel full longer.

Nutritional Content of Oat Grains

Oat grains (Avena sativa) are a highly nutritious whole grain widely recognized for their health benefits. They are typically consumed as rolled oats, steel-cut oats, or oat flour, and their nutritional profile makes them a staple in many diets. Below is a breakdown of the key nutrients found in oats, based on a typical serving of 100 grams of dry, uncooked oats (values may vary slightly depending on processing):

1. Macronutrients

Carbohydrates: ~66–70 g
- Oats are primarily a source of complex carbohydrates, providing sustained energy. About 11–13 g of this is dietary fiber, which supports digestion and heart health.
Protein: ~13–17 g
- Oats contain a higher protein content than many other grains, with a good balance of essential amino acids (though not a complete protein on its own).
Fat: ~6–7 g
- Mostly unsaturated fats, including small amounts of heart-healthy monounsaturated and polyunsaturated fatty acids.

2. Fiber

Total Fiber: ~10–12 g
- Oats are particularly rich in beta-glucan, a soluble fiber (about 3–5 g per 100 g). Beta-glucan is known for lowering cholesterol levels, regulating blood sugar, and promoting gut health.

3. Vitamins

B Vitamins:
- Thiamine (B1): ~0.5–0.8 mg (30–50% of Daily Value, DV)
- Pantothenic Acid (B5): ~1–1.5 mg (20–30% DV)
- Vitamin B6: ~0.1–0.2 mg (5–10% DV)
- These vitamins support energy metabolism and nervous system function.
Trace amounts of other vitamins like folate and vitamin E are also present.

4. Minerals

Manganese: ~4–5 mg (~200% DV)
- Essential for bone health, metabolism, and antioxidant activity.
Phosphorus: ~400–500 mg (~40–50% DV)
- Supports bone and teeth formation.
Magnesium: ~130–180 mg (~30–45% DV)
- Important for muscle function and energy production.
Iron: ~4–5 mg (~20–25% DV)
- Aids in oxygen transport in the blood.
Zinc: ~3–4 mg (~25–35% DV)
- Boosts immune function and wound healing.
Smaller amounts of calcium, potassium, and copper are also present.

5. Calories

~380–400 kcal per 100 g
- Oats are energy-dense due to their carbohydrate and fat content, making them a filling and satisfying food.

6. Other Compounds

Antioxidants: Oats contain unique antioxidants called avenanthramides, which have anti-inflammatory properties and may protect against heart disease.
Phytochemicals: Small amounts of phenolic compounds contribute to their antioxidant effects.

Key Health Benefits

Heart Health: The beta-glucan fiber helps reduce LDL ("bad") cholesterol.
Blood Sugar Control: Slow-digesting carbs and fiber improve insulin sensitivity.
Digestive Health: High fiber content promotes regular bowel movements and a healthy gut microbiome.
Weight Management: Oats are filling, helping to curb hunger.

Notes

The nutritional content can vary slightly depending on whether the oats are whole, processed (e.g., instant oats), or fortified.
Oats are naturally gluten-free, but cross-contamination with wheat or barley during processing may occur, so those with celiac disease should opt for certified gluten-free oats.

Oats are a versatile and nutrient-packed food, making them an excellent choice for a balanced diet!

Research Data

Key Points

Research suggests oats are highly nutritious, rich in fiber, protein, and vitamins, supporting heart and digestive health.
The evidence leans toward oats lowering cholesterol and stabilizing blood sugar, beneficial for cardiovascular and diabetic conditions.
It seems likely that oats aid weight management and gut health, though more studies are needed for definitive conclusions.
There is some controversy around oats in gluten-free diets, with debates on safety for celiac patients, but many studies support their suitability if processed correctly.

Nutrition Profile Overview

Oats are a whole grain packed with essential nutrients, making them a staple for health-conscious diets. They are particularly noted for their high fiber content, especially beta-glucan, which supports heart health by lowering cholesterol. Oats also provide a good amount of protein and are rich in vitamins like B1 (thiamine) and minerals such as magnesium and iron, contributing to energy metabolism and overall well-being.

Health Benefits and Clinical Research

Studies show oats can reduce LDL ("bad") cholesterol, with clinical trials indicating that 3 grams of daily beta-glucan intake can lower heart disease risk (FDA Health Claim). They also help stabilize blood sugar, beneficial for diabetes management, with research showing reduced postprandial glucose responses (Metabolic Effects Review). Unexpectedly, oats may also support gut health by improving microbiota and potentially reducing cancer risk, though more human studies are needed.

Considerations

While oats are naturally gluten-free, there’s debate on their safety for celiac patients, with some studies suggesting tolerance if gluten content is below 20 ppm (Celiac Suitability Study). Their role in weight management is supported by high fiber promoting satiety, but long-term effects need further exploration.

Comprehensive Analysis of Oat Grain Nutrition Profile

Oats (Avena sativa L.) are classified as a whole grain, renowned for their nutritional density and health benefits, as evidenced by extensive clinical research. This section provides a detailed examination of their nutrition profile, supported by scientific studies, and highlights the clinical research conducted to date.

Nutritional Composition

Oats are composed of approximately 66% carbohydrates, primarily complex carbs that provide sustained energy, with about 10% dietary fiber, notably beta-glucan, known for its cholesterol-lowering effects. They contain around 17% protein, higher than many grains, and 7% fat, mostly unsaturated fats beneficial for heart health. Micronutrients include manganese (63% DV per 40g serving), phosphorus (15% DV), magnesium (15% DV), iron (8% DV), and B vitamins like thiamine (15% DV), essential for metabolism and energy production. Oats also contain unique antioxidants, avenanthramides, with anti-inflammatory properties.

Clinical Research on Health Benefits

Clinical research on oats has focused on several key areas, with numerous randomized controlled trials (RCTs), systematic reviews, and meta-analyses providing robust evidence:

Cardiovascular Health:
- Oats are extensively studied for their cholesterol-lowering effects, attributed to beta-glucan. The FDA (1997) health claim allows whole oat foods to state they reduce heart disease risk with a daily intake of 3g soluble oat beta-glucan (FDA Health Claim). Studies like Anderson et al. (1991) found oat-bran cereal lowered serum total and LDL cholesterol by 23% in hypercholesterolemic men, with no change in HDL (Cholesterol Lowering Study). Hallfrisch et al. (1997) reported reductions in urinary malondialdehyde, indicating cardiovascular benefits (Oxidative Stress Study).
Blood Glucose Management:
- Oats have a low glycemic index (GI around 55-60), aiding blood sugar control. A systematic review by Hou et al. (2015) found oat intake beneficial for type 2 diabetes patients, reducing glucose and insulin responses (Metabolic Effects Review). Wolever et al. (2019) and Zhu et al. (2020) explored how oat processing affects glycaemic responses, showing intact kernels and thick flakes reduce postprandial glucose significantly (Glycaemic Response Study, Oat Processing Study).
Gut Health and Microbiota:
- Oats' high fiber content supports digestive health, with studies indicating oat bran relieves constipation and aids digestion in ulcerative colitis patients (Digestive Health Study). A clinical trial (NCT01925365) examined the impact of whole grain oats on gut microbiota and cardio-metabolic risk factors, highlighting their role in improving gut health (Gut Microbiota Trial).
Cancer Prevention:
- Research suggests oats may have anticancer properties, particularly through beta-glucan and short-chain fatty acids. Hsueh et al. (2011) found whole oats inhibited colon tumor growth in mice, while Murphy et al. (2004) explored effects on lung tumor metastases (Cancer Prevention Study, Lung Tumor Study). Human studies are limited, indicating a need for further research.
Gluten-Free Diet Suitability:
- Oats are naturally gluten-free, but cross-contamination is a concern. Ballabio et al. (2011) assessed 36 oat varieties for celiac suitability, finding most safe if gluten content ≤ 20 ppm per EC regulation (Celiac Suitability Study). Debates persist, with some studies showing tolerance in adults and children, while others caution against contamination.
Weight Management:
- Oats' high fiber and protein content promote satiety, potentially aiding weight management. While specific RCTs are limited, epidemiological data suggest whole grain intake, including oats, reduces obesity risk (Nutritional Advantages Review).
Gastrointestinal Health:
- Oats improve bowel function, with studies like Tosh SM, Chu Y (2015) showing oat bran effective against constipation and aiding ulcerative colitis (GI Health Review). They also support gut microbiota, enhancing digestive health.

Detailed Clinical Studies

Below is a table summarizing key clinical research on oats, including specific studies and findings:

Study Reference	Focus Area	Key Finding	Year	URL
Anderson et al.	Cholesterol lowering	Oat-bran cereal reduced total and LDL cholesterol by 23% in hypercholesterolemic men	1991	Cholesterol Lowering Study
Hou et al.	Diabetes management	Oat intake reduced glucose and insulin responses in type 2 diabetes patients	2015	Metabolic Effects Review
Ballabio et al.	Gluten-free diet	Most oat varieties safe for celiac patients if gluten ≤ 20 ppm	2011	Celiac Suitability Study
Hsueh et al.	Cancer prevention	Whole oats inhibited colon tumor growth in mice	2011	Cancer Prevention Study
NCT01925365 (ClinicalTrials.gov)	Gut microbiota	Examined impact of whole grain oats on gut microbiota and cardio-metabolic risk	Ongoing	Gut Microbiota Trial

This table encapsulates key clinical research, providing a foundation for understanding oats' health impacts.

Controversies and Future Directions

There is ongoing debate regarding oats in gluten-free diets, with some studies suggesting safety for celiac patients, while others highlight contamination risks, necessitating certified gluten-free oats. Additionally, while preliminary research on cancer prevention is promising, human clinical trials are limited, indicating a need for further investigation. Future research should focus on long-term effects on weight management and specific gastrointestinal disorders, enhancing our understanding of oats' therapeutic potential.

In summary, oats are a nutrient-dense grain with a robust clinical research base, supporting their role in promoting health across multiple domains, with ongoing studies continuing to explore their benefits.

Key Citations

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4690088/

https://www.ewg.org/news-insights/news-release/ewg-responds-general-mills-and-quaker-oats-legal-not-same-safe

https://www.ewg.org/news-insights/news/glyphosate-contamination-food-goes-far-beyond-oat-products

https://www.ewg.org/research/ewg-investigation-dangerous-agricultural-chemical-chlormequat-found-popular-oat-based

https://pubmed.ncbi.nlm.nih.gov/21294744/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3524229/

https://pubmed.ncbi.nlm.nih.gov/21843037/

health nutrition - keto meals

I can help you create a meal planner that strictly adheres to the keto lifestyle! The ketogenic (keto) diet typically involves high fat, moderate protein, and very low carbohydrate intake—usually keeping net carbs (total carbs minus fiber) below 20-50 grams per day to maintain ketosis. Below, I’ll outline a simple 7-day keto meal plan with breakfast, lunch, dinner, and snacks, designed to fit this framework. This plan focuses on whole, keto-friendly foods and avoids processed items or hidden carbs. Feel free to adjust portion sizes based on your specific caloric and macro needs! 7-Day Keto Meal Planner Day 1

Breakfast: Bacon and Eggs  
    2 large eggs, scrambled with 1 tbsp butter  
    3 strips of bacon (no sugar added)  
    1/4 avocado  
    Net Carbs: ~2g
Lunch: Cobb Salad  
    2 cups romaine lettuce  
    1 grilled chicken thigh (skin on)  
    1 boiled egg, sliced  
    1 oz cheddar cheese, shredded  
    2 tbsp olive oil + 1 tbsp apple cider vinegar (dressing)  
    Net Carbs: ~4g
Dinner: Garlic Butter Salmon with Asparagus  
    5 oz salmon fillet, pan-seared in 2 tbsp butter with minced garlic  
    1 cup roasted asparagus with olive oil  
    Net Carbs: ~3g
Snack:  
    1 oz macadamia nuts  
    Net Carbs: ~2g
Daily Total Net Carbs: ~11g

Day 2

Breakfast: Keto Coffee (Bulletproof Coffee)  
    1 cup black coffee  
    1 tbsp MCT oil  
    1 tbsp unsalted butter  
    Net Carbs: 0g
Lunch: Beef and Broccoli Stir-Fry  
    4 oz ground beef  
    1 cup broccoli florets, sautéed in 1 tbsp coconut oil  
    1 tsp soy sauce (or coconut aminos for strict keto)  
    Net Carbs: ~4g
Dinner: Pork Chops with Creamed Spinach  
    6 oz pork chop, pan-fried in 1 tbsp butter  
    1 cup spinach sautéed with 2 tbsp heavy cream and 1 oz cream cheese  
    Net Carbs: ~3g
Snack:  
    1 string cheese  
    Net Carbs: ~1g
Daily Total Net Carbs: ~8g

Day 3

Breakfast: Chia Seed Pudding  
    2 tbsp chia seeds mixed with 1/2 cup unsweetened almond milk, 1 tbsp heavy cream, and a few drops of stevia (chill overnight)  
    Net Carbs: ~2g
Lunch: Tuna Salad Lettuce Wraps  
    4 oz canned tuna (in olive oil, drained)  
    1 tbsp mayo (sugar-free)  
    1/4 cup diced cucumber  
    Wrapped in 2 large romaine leaves  
    Net Carbs: ~3g
Dinner: Chicken Thighs with Zucchini Noodles  
    2 chicken thighs (skin on), baked with 1 tbsp olive oil  
    1 cup zucchini noodles sautéed in 1 tbsp butter  
    Net Carbs: ~4g
Snack:  
    10 pork rinds with 2 tbsp guacamole  
    Net Carbs: ~2g
Daily Total Net Carbs: ~11g

Day 4

Breakfast: Sausage and Cheese Muffins  
    2 eggs mixed with 2 oz cooked sausage crumbles and 1 oz shredded cheddar, baked in muffin tins  
    Net Carbs: ~2g
Lunch: Avocado Chicken Salad  
    1/2 avocado mashed with 4 oz shredded chicken  
    1 tbsp mayo  
    1 tsp lemon juice  
    Serve over 1 cup spinach  
    Net Carbs: ~4g
Dinner: Ribeye Steak with Mushrooms  
    6 oz ribeye steak, grilled or pan-seared in 1 tbsp butter  
    1/2 cup sautéed mushrooms in 1 tbsp butter  
    Net Carbs: ~3g
Snack:  
    1 oz almonds  
    Net Carbs: ~3g
Daily Total Net Carbs: ~12g

Day 5

Breakfast: Scrambled Eggs with Spinach  
    3 eggs scrambled with 1 tbsp butter  
    1 cup fresh spinach, wilted into eggs  
    Net Carbs: ~2g
Lunch: Keto BLT Wrap  
    3 strips bacon  
    1 tbsp mayo  
    1/4 cup shredded lettuce  
    Wrapped in a low-carb coconut flour tortilla (e.g., 3g net carbs or less)  
    Net Carbs: ~4g
Dinner: Shrimp Scampi  
    6 oz shrimp sautéed in 2 tbsp butter with garlic and lemon zest  
    Served over 1 cup cauliflower rice  
    Net Carbs: ~5g
Snack:  
    1 square (10g) 90% dark chocolate  
    Net Carbs: ~2g
Daily Total Net Carbs: ~13g

Day 6

Breakfast: Keto Pancakes  
    2 tbsp almond flour, 1 egg, 1 tbsp cream cheese, blended and cooked in butter  
    Top with 1 tbsp sugar-free syrup (e.g., Lakanto)  
    Net Carbs: ~3g
Lunch: Egg Salad  
    2 boiled eggs mashed with 1 tbsp mayo and 1 tsp mustard  
    Serve with 5 cucumber slices  
    Net Carbs: ~2g
Dinner: Baked Chicken with Broccoli  
    5 oz chicken breast, baked with 1 tbsp olive oil  
    1 cup steamed broccoli with 1 tbsp butter  
    Net Carbs: ~4g
Snack:  
    1 oz pepperoni slices  
    Net Carbs: ~1g
Daily Total Net Carbs: ~10g

Day 7

Breakfast: Omelette with Cheese and Ham  
    2 eggs with 1 oz cheddar and 2 oz diced ham, cooked in 1 tbsp butter  
    Net Carbs: ~1g
Lunch: Caesar Salad (No Croutons)  
    2 cups romaine lettuce  
    4 oz grilled chicken  
    2 tbsp sugar-free Caesar dressing  
    1 tbsp parmesan cheese  
    Net Carbs: ~3g
Dinner: Lamb Chops with Rosemary  
    6 oz lamb chops, grilled with rosemary and 1 tbsp olive oil  
    1/2 cup sautéed green beans in 1 tbsp butter  
    Net Carbs: ~4g
Snack:  
    2 tbsp almond butter (no sugar added)  
    Net Carbs: ~3g
Daily Total Net Carbs: ~11g

General Guidelines for Strict Keto Adherence

Carb Limit: This plan keeps net carbs under 20g daily, aligning with strict keto standards. Always check labels for hidden sugars or carbs in processed items like sausages or dressings.
Fat Focus: High-fat ingredients (butter, oils, avocado, nuts) are emphasized to maintain energy in ketosis.
Protein Moderation: Protein is moderate (around 15-25% of calories) to avoid gluconeogenesis (where excess protein turns to glucose).
Hydration & Electrolytes: Drink plenty of water and add salt to meals to combat "keto flu" symptoms.
Meal Prep Tips: Cook extra portions (e.g., chicken thighs or steak) for leftovers to save time.

Would you like me to adjust this plan further—say, for specific dietary restrictions (e.g., dairy-free) or to generate a shopping list? Let me know!

shopping list

Here’s a shopping list tailored to the 7-day keto meal planner I provided. It assumes you’re starting from scratch and includes all the ingredients needed for the meals. I’ve organized it by grocery store sections for convenience and estimated quantities based on the plan, assuming it’s for one person. Adjust quantities if you’re cooking for more people or want leftovers! Shopping List for 7-Day Keto Meal Plan Meat & Seafood

Bacon (12-15 strips, no sugar added)  
Chicken thighs (6 pieces, skin on, about 2 lbs total)  
Chicken breast (5 oz, about 1 small breast)  
Ground beef (4 oz, about 1/4 lb)  
Pork chops (6 oz, 1 chop)  
Sausage (2 oz, pre-cooked, sugar-free)  
Ham (2 oz, diced, no sugar added)  
Ribeye steak (6 oz, 1 small steak)  
Lamb chops (6 oz, 2 small chops)  
Salmon fillet (5 oz, 1 fillet)  
Shrimp (6 oz, fresh or frozen, peeled)  
Pepperoni slices (1 oz, about 10-15 slices)  
Tuna (4 oz can, packed in olive oil)

Dairy

Eggs (18 large)  
Butter (unsalted, 1 lb)  
Heavy cream (1 cup, about 8 oz)  
Cream cheese (2 oz, about 1/4 of an 8 oz block)  
Cheddar cheese (shredded, 3 oz, about 3/4 cup)  
Parmesan cheese (grated, 1 tbsp)  
String cheese (1 stick)

Vegetables

Romaine lettuce (5 cups, about 1 large head)  
Spinach (fresh, 3 cups, about 1 small bag)  
Avocado (2 medium)  
Broccoli (2 cups florets, about 1 small head)  
Asparagus (1 cup, about 8-10 spears)  
Zucchini (1 medium, for noodles)  
Cucumber (1 small)  
Green beans (1/2 cup, fresh or frozen)  
Mushrooms (1/2 cup, about 4 oz)  
Cauliflower (1 cup, for rice, about 1/4 head)

Nuts & Seeds

Macadamia nuts (1 oz, about 10-12 nuts)  
Almonds (1 oz, about 20-24 almonds)  
Chia seeds (2 tbsp)  
Almond butter (2 tbsp, no sugar added)

Pantry

Olive oil (extra virgin, 1 small bottle, about 1/2 cup needed)  
Coconut oil (1 small jar, about 1 tbsp needed)  
MCT oil (1 small bottle, about 1 tbsp needed)  
Almond milk (unsweetened, 1/2 cup, about 1 small carton)  
Almond flour (2 tbsp, small bag)  
Coconut aminos or soy sauce (low-carb, 1 tsp, small bottle)  
Apple cider vinegar (1 tbsp)  
Sugar-free Caesar dressing (2 tbsp, small bottle)  
Sugar-free syrup (e.g., Lakanto, 1 tbsp, small bottle)  
Stevia (liquid or powder, a few drops, small container)  
Mayonnaise (sugar-free, 5 tbsp, small jar)  
Mustard (1 tsp, small jar)  
Dark chocolate (90% cocoa, 1 oz, 1 small bar)  
Pork rinds (10 pieces, 1 small bag)  
Low-carb coconut flour tortilla (1, check net carbs <3g, 1 package)

Spices & Seasonings

Salt  
Black pepper  
Garlic (fresh, 1 bulb, or minced jar)  
Rosemary (fresh or dried)  
Lemon zest (1 lemon or dried)

Optional (for Flavor/Convenience)

Coffee (black, for keto coffee)  
Guacamole (2 tbsp, pre-made or make fresh with avocado)

Notes

Quantities: This list assumes single servings as outlined in the meal plan. Double or triple amounts if cooking for more people or planning leftovers.
Check Labels: Ensure bacon, sausage, mayo, dressings, and canned goods are free of added sugars or high-carb fillers.
Fresh vs. Frozen: Frozen veggies (e.g., broccoli, green beans) or shrimp work just as well and save prep time.
Bulk Options: Buy nuts, oils, and spices in bulk if you plan to continue keto beyond a week.

Let me know if you want me to refine this list further (e.g., remove items you already have) or add specific brands! Happy shopping and keto cooking!

health nutrition - fenbendazole

fenbendazole atopic

It seems like your question might be incomplete. Did you mean "fenbendazole for atopic dermatitis" or something similar? I’ll assume you’re asking about the potential use of fenbendazole in relation to atopic dermatitis, a common skin condition also known as eczema, characterized by itchy, inflamed skin. If I’ve misunderstood, please clarify!

Fenbendazole is a broad-spectrum antiparasitic drug primarily used in veterinary medicine to treat intestinal parasites like roundworms, hookworms, and whipworms in animals such as dogs, cats, and livestock. It works by binding to tubulin in parasite cells, disrupting their ability to absorb nutrients, which ultimately kills them. However, there’s no established evidence or medical consensus supporting its use for atopic dermatitis in humans or animals.

Atopic dermatitis is an inflammatory skin condition driven by a mix of immune system dysregulation, skin barrier issues, and environmental triggers—not parasitic infection. Standard treatments include moisturizers, topical corticosteroids, calcineurin inhibitors, or, in severe cases, systemic therapies like biologics (e.g., dupilumab) or JAK inhibitors. Fenbendazole’s mechanism of action doesn’t align with the underlying causes of atopic dermatitis, as it targets parasites rather than inflammation or immune responses in the skin.

That said, fenbendazole has gained attention in alternative health circles, partly due to anecdotal claims about its effects on other conditions, like cancer, based on limited studies (mostly in cell lines or animals). Some speculate it could influence inflammation or immune function indirectly, but this is purely hypothetical and unproven for skin conditions like atopic dermatitis. No clinical trials or peer-reviewed studies have explored fenbendazole as a treatment for this condition, and it’s not approved by regulatory bodies like the FDA for human use beyond its antiparasitic role in animals.

If you’re curious about fenbendazole for a specific case (e.g., a pet with skin issues), atopic dermatitis would first need to be distinguished from parasitic skin conditions like mange, which can mimic eczema but require different treatments. A vet or dermatologist would be the best resource for diagnosis and guidance.

If you had a more specific angle in mind—like a study, a pet’s condition, or a theory—let me know, and I’ll tailor the answer further!

explain efforts for use of fenbendazole for treatment of skin cancers

Research into using fenbendazole for skin cancers, such as melanoma or squamous cell carcinoma, is still in its early stages and largely experimental. Fenbendazole, a benzimidazole antiparasitic drug widely used in veterinary medicine to treat intestinal worms, has caught attention for its potential anticancer properties across various cancer types, including skin cancers. While it’s not approved for human use by regulatory bodies like the FDA or EMA, efforts to explore its application in cancer treatment, including skin cancers, stem from preclinical studies, anecdotal reports, and a growing interest in repurposing existing drugs.

The primary push to investigate fenbendazole for skin cancers comes from its observed effects on cellular processes that overlap with cancer biology. Studies have shown that fenbendazole disrupts microtubule formation, a mechanism shared with some anticancer drugs like vinblastine and paclitaxel. Microtubules are critical for cell division, and their disruption can halt the rapid proliferation of cancer cells. In melanoma, for instance, preclinical research has suggested that fenbendazole may upregulate the p53 tumor suppressor gene, which controls cell growth and triggers apoptosis (programmed cell death) in damaged or cancerous cells. Some experiments with melanoma cell lines have indicated that fenbendazole can induce apoptosis, even in cells resistant to conventional treatments, hinting at its potential for aggressive or resistant skin cancers.

Another angle of investigation involves fenbendazole’s impact on cancer cell metabolism. It has been shown to inhibit glucose uptake by downregulating GLUT transporters and hexokinase, key players in the glycolytic pathway that cancer cells rely on for energy. Skin cancers, like melanoma, often exhibit heightened glycolytic activity, so disrupting this process could starve tumor cells, slowing their growth. Additionally, fenbendazole’s ability to induce oxidative stress—by generating reactive oxygen species—may further damage cancer cells, offering another possible mechanism for its anticancer effects.

Efforts to apply fenbendazole to skin cancers have been documented in preclinical settings. For example, in vitro studies with human cancer cell lines, including melanoma, have shown that fenbendazole exerts cytotoxicity at micromolar concentrations, reducing cell viability and triggering cell cycle arrest at the G2/M phase. In vivo animal models, such as mice with implanted melanoma tumors, have demonstrated tumor growth inhibition when treated with fenbendazole, though results vary depending on dosage, administration method, and tumor type. A notable study explored fenbendazole-encapsulated nanoparticles to improve its solubility and delivery, showing significant tumor reduction in mouse models of epithelial ovarian cancer, which suggests potential adaptability for skin cancers if delivery challenges are addressed.

Despite these findings, a major hurdle in using fenbendazole for skin cancer treatment is its poor water solubility and bioavailability when taken orally, the most common administration route in anecdotal human use. This limits its ability to reach therapeutic levels in the bloodstream or penetrate skin tissues effectively. Researchers are exploring ways to overcome this, such as topical formulations or nanoparticle delivery systems, which could directly target skin lesions like melanoma or basal cell carcinoma. However, no peer-reviewed studies have yet confirmed the efficacy of topical fenbendazole for skin cancers, and most efforts remain focused on systemic administration.

Anecdotal reports, particularly from cancer patients self-administering fenbendazole, have fueled interest. For instance, a widely circulated case involves a patient with stage 4 melanoma who claimed remission after using fenbendazole against medical advice, as shared in posts on X and alternative health blogs. While compelling, these stories lack rigorous documentation, control groups, or verification, making them unreliable as scientific evidence. They do, however, highlight a grassroots push to explore fenbendazole, often driven by frustration with conventional treatments’ limitations, especially in advanced or metastatic skin cancers.

On the scientific front, efforts are hampered by a lack of large-scale clinical trials in humans. Most research is preclinical—cell cultures or animal models—and funding for human trials is scarce, likely due to fenbendazole’s status as a generic, low-cost veterinary drug with little profit incentive for pharmaceutical companies. Some researchers advocate for trials to assess its safety, optimal dosing, and efficacy in skin cancer patients, potentially alongside standard therapies like immunotherapy (e.g., checkpoint inhibitors) or radiation, given its microtubule-disrupting synergy with such treatments. A few studies have noted additive effects when fenbendazole is combined with other agents, like supplementary vitamins, in animal models of lymphoma, suggesting a combinatorial approach might be worth exploring for skin cancers too.

Safety is another focus of investigation. Fenbendazole has a high safety margin in animals, with low toxicity even at elevated doses, but human data is limited. Case reports of self-administration have flagged risks like liver dysfunction, though these resolved after discontinuation. For skin cancer, where localized treatment could minimize systemic exposure, topical application might reduce such risks, but this remains theoretical without clinical testing.

In summary, efforts to use fenbendazole for skin cancer treatment are driven by its microtubule-disrupting, metabolism-altering, and apoptosis-inducing properties, supported by preclinical evidence and anecdotal claims. Current research focuses on understanding its mechanisms, improving delivery (e.g., nanoparticles or topical forms), and establishing its potential as a repurposed drug. However, without robust human trials, its role in treating skin cancers like melanoma remains speculative, and patients are cautioned to approach it under medical supervision rather than as a standalone cure. The gap between lab promise and clinical reality underscores the need for more structured research to validate or refute these early efforts.

Fe Treatment Protocol 222 or 444mg once a day with food 6 or 7 days a week active cancer 6 days a week if in remission 3 days a week, 10 wks per year for cancer free

CBD oil 25mg daily Curcumin 600mg twice daily

Vit D3 1000-4000 IU daily 25-100mcg Vit K2 100-200mcg daily Berberine 500mg two or three times daily

health nutrition - ivermectin

explain efforts for using ivermectin for treatment of skin cancers

Efforts to explore ivermectin as a treatment for skin cancers, such as melanoma, squamous cell carcinoma (SCC), or basal cell carcinoma (BCC), are emerging largely from its observed antiparasitic, anti-inflammatory, and, more recently, potential anticancer properties. Ivermectin, a well-established drug used to treat parasitic infections like scabies, river blindness (onchocerciasis), and head lice in humans, as well as heartworm in animals, has been FDA-approved for human use since the 1980s. Its repurposing for skin cancer stems from preclinical research and a growing interest in drug repositioning, though clinical evidence remains limited, and it’s not yet an accepted therapy for any cancer.

The foundation for investigating ivermectin in skin cancer treatment lies in its ability to interfere with cellular processes critical to cancer growth. One key mechanism is its inhibition of the Wnt/β-catenin signaling pathway, which is often dysregulated in cancers, including melanoma and non-melanoma skin cancers. This pathway regulates cell proliferation and survival, and its overactivation can drive tumor development. Studies in cancer cell lines, such as melanoma, have shown that ivermectin suppresses Wnt signaling by promoting the degradation of β-catenin, reducing cancer cell growth and inducing apoptosis (programmed cell death). This effect has been observed in vitro across multiple cancer types, including skin-related lines, suggesting a broad anticancer potential.

Another mechanism under scrutiny is ivermectin’s interaction with chloride channels. As an antiparasitic, it binds to glutamate-gated chloride channels in invertebrates, causing paralysis and death of parasites. In mammalian cells, including cancer cells, ivermectin modulates related ion channels, such as GABA receptors or P2X4 receptors, leading to increased intracellular chloride levels. This disrupts mitochondrial function, generating reactive oxygen species (ROS) and triggering oxidative stress, which can selectively kill cancer cells while sparing healthy ones. Preclinical studies with melanoma cells have demonstrated this mitochondrial damage, linking it to reduced cell viability and tumor growth inhibition.

Ivermectin also inhibits angiogenesis—the formation of new blood vessels that tumors need to grow—by downregulating vascular endothelial growth factor (VEGF). This is particularly relevant for aggressive skin cancers like melanoma, which often metastasize by exploiting vascular networks. Experiments in mouse models of melanoma have shown that ivermectin reduces tumor vascularity, slowing progression. Additionally, its anti-inflammatory properties, mediated through NF-κB pathway suppression, may dampen the tumor-supportive inflammation seen in chronic skin cancer cases, such as SCC arising from UV-damaged skin.

Efforts to test ivermectin for skin cancer have progressed through preclinical studies. In vitro research with melanoma cell lines (e.g., A375, B16F10) has shown dose-dependent cytotoxicity, with ivermectin reducing cell proliferation and inducing G0/G1 cell cycle arrest. Concentrations in the micromolar range—higher than those used for parasitic infections—were effective, raising questions about achievable levels in humans. In vivo, mouse models of melanoma treated with oral or intraperitoneal ivermectin exhibited smaller tumor volumes and lower metastatic spread compared to controls. Similar results were noted in xenograft models of SCC, where ivermectin slowed tumor growth, though not as dramatically as in melanoma.

Topical application is a focal point for skin cancer efforts, given ivermectin’s established use in creams (e.g., Soolantra for rosacea) and its direct relevance to skin-accessible tumors. Researchers hypothesize that topical formulations could achieve higher local concentrations than systemic dosing, minimizing side effects like dizziness or liver stress seen at high oral doses. A study in immunocompromised mice with human SCC xenografts tested topical ivermectin, reporting reduced tumor size over weeks, though the formulation required optimization for penetration through keratinized skin layers. For BCC, which is less aggressive, topical ivermectin’s potential remains underexplored but conceptually promising due to its superficial nature.

Anecdotal reports have spurred interest, particularly after ivermectin’s visibility surged during the COVID-19 pandemic. Posts on X and alternative health forums have claimed success with ivermectin (often self-administered) for various cancers, including skin lesions, but these lack peer-reviewed backing or standardized protocols. One case described a patient with recurrent BCC applying topical ivermectin off-label, noting lesion shrinkage, though without biopsy confirmation or follow-up, it’s anecdotal at best. Such stories drive curiosity but complicate scientific efforts due to their uncontrolled nature.

Clinical trials for ivermectin in cancer, including skin cancer, are sparse. Most cancer-related trials focus on systemic cancers like colorectal or breast, not skin-specific types. A phase I study in Australia (circa 2022) explored high-dose ivermectin in solid tumors, establishing safety up to 30 mg/day—far above antiparasitic doses—but didn’t include skin cancer cohorts. For skin cancers, the lack of trials reflects funding challenges and skepticism about translating preclinical promise into human efficacy, especially since ivermectin’s generic status offers little commercial incentive. Researchers advocate for phase II trials to test topical or combined therapies (e.g., with checkpoint inhibitors like pembrolizumab), leveraging ivermectin’s synergy with immunotherapy observed in melanoma mouse models.

Safety is a relative strength: ivermectin’s long track record in humans shows mild side effects (e.g., rash, nausea) at standard doses (0.2 mg/kg), though anticancer doses might exceed this, risking neurotoxicity or hepatotoxicity. Topical use could mitigate systemic risks, aligning with skin cancer’s localized nature. Bioavailability remains a hurdle—oral ivermectin has poor skin penetration, and while topical forms help, optimal delivery (e.g., through nanoparticles or liposomal carriers) is still experimental.

In summary, efforts to use ivermectin for skin cancer treatment build on its Wnt inhibition, chloride channel effects, anti-angiogenic, and anti-inflammatory actions, backed by preclinical data showing promise in melanoma and SCC models. Topical application is a key focus, leveraging its skin-accessible target, but human trials are lacking, and evidence remains preliminary. While intriguing, ivermectin’s role in skin cancer therapy awaits rigorous clinical validation, and current efforts center on bridging the gap from lab to clinic. Patients intrigued by its potential should consult oncologists rather than rely on unverified self-treatment.

dosage 12mg q.d. for 6 weeks

health nutrition - vitamin d

https://c19vitamind.com/cavd.html

https://www.melatonin-research.net/index.php/MR/article/view/19/150

https://www.youtube.com/watch?v=ha2mLz-Xdpg

https://www.youtube.com/watch?v=5YV_iKnzDRg

Vitamin D and marine omega 3 fatty acid supplementation and incident autoimmune disease: VITAL randomized controlled trial

https://www.youtube.com/redirect?event=video_description&redir_token=QUFFLUhqbDVPei16dzVSejZ1blduV1JhSWxNWm5LRVVGQXxBQ3Jtc0trMzlMU2IydXkxTTk4OEtBdHNGcE5ydFNpMjFvVlpHM01sMExNSVdSWXZDSEVkT2FsLTRubHJ0YnBaZWVKZHRDTC1vLVcwUDVPUlN1RGdjT25RSnJ5MDZueHdQOFI4WTZpbkRlc3U1ZW9FNkJ4OGFITQ&q=https%3A%2F%2Fwww.bmj.com%2Fcontent%2Fbmj%2F376%2Fbmj-2021-066452.full.pdf

Vit-D acts as a hormone more than a vitamin. Helps with inflammation, involved with the immune system

The role of vitamin D in increasing circulating T regulatory cell numbers and modulating T regulatory cell phenotypes in patients with inflammatory disease or in healthy volunteers: A systematic review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6759203/

Make your own Vit D2

Mushroom gills exposed to UVB light boost 5000IUs to 46,000 IUS

They also contain Selenium, Zinc, Copper, Vit-C

Oyster, shitake, button (slice lengthwise) suate in butter for better absorption

sunny days (jun-aug ) - point gills up on tray from 10am-6pm two days, if still not dry use dehydrator to finish (snap in half and pretty crisp) place in sealed glass jar with a few rice grains to absorb moisture and good for one year

uvb light for 18 hours an 100g or cup gives you 46,000 IUs if sundried, 200,000 ius if uvb light button mushrooms only give about 20,000 IUs

Autoimmune triggers:

A vitamin D deficiency
A virus, bacteria, or pathogen
Exposure to something that weakens your immune system
Stress
The wrong diet
A genetic weakness

Even though various factors can lead to an autoimmune disease, vitamin D deficiency is at the heart of this condition.

Top causes of a vitamin D deficiency: • A genetic weakness • Obesity • Insulin resistance • Darker skin
• Less exposure to the sun • Aging

Vitamin D controls the immune system, and it can either boost or suppress certain parts of the immune system.

Inflammation is also a key factor involved in autoimmune disorders, but there are important things you can do to turn off the inflammatory process.

The best natural remedies for autoimmune conditions: • Vitamin D • Omega-3 fatty acids (while avoiding omega-6 fatty acids) • Cod liver oil • Curcumin • Blueberries (C but no D) • Maitake mushrooms • St. John’s wort

Vitamin D, Blueberries, and Grapes: Partners in the Immune System? Posted on November 15, 2013 by Alexander Michels, PhD

Blueberries - can they work with vitamin D?

Part of a healthy immune system involves responding to bacterial invasion. The body has many mechanisms to combat bacteria, including the white blood cells or leukocytes.

Several types of white blood cells produce small strings of amino acids (that are typically referred to as ‘peptides’) that can target invading bacteria. Through a variety of mechanisms, these peptides can associate with a bacterial cell membrane, breaking the cell open and driving it toward death. Collectively, these are known as “antimicrobial peptides”.

Here’s where vitamin D gets involved:

One of these antimicrobial peptides is known as cathelicidin. What makes cathelicidin unique among these peptides is that the gene associated with it (known as CAMP for Cathelicidin Antimicrobial Peptide) is regulated by vitamin D. Providing vitamin D to leukocytes promotes the expression of CAMP and to increase their bacteria-killing activities.

Regulation of the CAMP gene, especially in context of vitamin D, has been a central question driving the research of Adrian Gombart, PhD, at the Linus Pauling Institute for many years. Recently, he spearheaded an effort at LPI to look for additional small molecules that may work alongside vitamin D to regulate cathelicidin production.Fritz in lab

Their two-step approach involved some genetic manipulation in cells. First, they fused the promoter (a region of DNA that regulates expression of a gene) from the human CAMP gene to another gene that makes a protein called a ‘transcriptional activator.’ The transcriptional activator, if produced, then turned on the production of an enzyme called firefly luciferase. The end result is simple: if any compound added to cells activated CAMP, the cells would glow like a firefly.

Dr. Gombart and his research team then screened 446 different molecules that are currently being tested in clinical trials by the NIH. At the end of the process they found two molecules that not only promoted CAMP gene expression but also worked in combination with vitamin D! Even more interesting, these compounds were normal dietary components: resveratrol (found in red grapes and red wine) and pterostilbene (found in blueberries).

Neutrophil and Bacteria “Out of a study of hundreds of compounds, just these two popped right out,” said Dr. Gombart, who is an LPI principal investigator and an associate professor in the Biochemistry and Biophysics department at Oregon State University. “Their synergy with vitamin D to increase CAMP gene expression was significant and intriguing. It’s a pretty interesting interaction.”

Does this mean drinking red wine and eating blueberries, along with taking vitamin D, will increase your innate defense against invading bacteria? Unfortunately, we don’t know yet. Dr. Gombart’s lab is working hard on determining how these compounds work in the immune system and whether they can boost cathelicidin levels in leukocytes.

There are plenty of other reasons to enjoy a glass of red wine, eat a handful of blueberries, and get your vitamin D. As for improving your immune response, that would just be a bonus!

Vitamin D and Covid-19 https://chrismasterjohnphd.substack.com/p/my-response-to-rhonda-patrick-on

magnesium activates Vit D? needs to be taken together. Also K2

health nutrition - vitamin c

https://www.cancer.gov/about-cancer/treatment/cam/patient/vitamin-c-pdq

https://www.sciencedirect.com/science/article/pii/S2213231720302123

Ascorbic acid (synthetic vitamin C) is made from glucose and other chemicals. Personally, I would only take ascorbic acid for a short-term detox cleanse, not on a long-term basis.

You can increase its absorption if you pair it with:

• Iron • Zinc • Vitamin B6 • Calcium

High Dose Take 1000–3000 mg of Vitamin C daily

The best type of vitamin C to get is vitamin C from food or food-based vitamins.

Foods that have the most vitamin C: recommend 90mg/day

SauerKraut - 700mg/cup
Leafy greens
Berries (blueberries 14.4g/c)
Strawberries 85mg/c
Tangerine - 52mg/c
Orange - 96mg/c
Mango 128mg/fruit
Papaya - 95mg/fruit
Lemons - 2 lemons - -6 oz 90mg most is in the zest
Organ meats
Bell peppers - 1 has 90 mg
Cabbage - 30 mg/c

Things you need to know about vitamin C:

There is little to no benefit from taking high doses of ascorbic acid.
Most vitamin C sold is fake and made from sugar.
Vitamin C is not absorbed well if you consume sugar at the same time.
A mega-dose of ascorbic acid may cause oxidation, diarrhea, and bloating.

Vitamin C's role in immune function, in particular, is crucial. It stimulates the production of white blood cells, especially neutrophils, lymphocytes, and phagocytes, and promotes the cells' normal functions, such as their ability to detect, move toward, and engulf pathogens. Immune cells release large quantities of reactive oxygen species, often incurring damage. To protect themselves from this damage, immune cells accumulate large quantities of vitamin C, which serves as an antioxidant within the cells. Immune cells also release interferons, a class of proteins produced as a defensive response to viruses. Some evidence indicates that vitamin C promotes the production of interferon, a protein that participates in antiviral activity.[1] https://www.foundmyfitness.com/topics/vitamin-c

Giza Khafre Project - Ground Penetration Radar

Khafre Project Team; Corrado Malanga, Filippo Biondi, Armando Mei, and Nicole Ciccolo.

KHAFRE PROJECT:

Corrado Malanga

Evaluation of political Candidates

Economic prosperity

1. Innovation as the Engine

2. Smart Trade Strategies

3. A Flexible Workforce

4. Fiscal Responsibility

5. Inclusive Growth

6. Sustainability as Opportunity

The Bottom Line

Exploiting Canada's vast resources

1. Value-Added Processing

2. Strategic Resource Management

3. Tech-Driven Extraction

4. Diversify the Portfolio

5. Indigenous Partnerships

6. Environmental Balance

The Catch

Current perspective on key issues

Aging Boomers

Unaffordable Housing

Changing Job Market

Inexpensive Foreign Competition

Impact of AI and Robotics

The Big Picture

TimeStamps (experimental)

Preface Notes:

My Notes taken while listening to video

Endemic Background Coronavirus

Some of JJ Couey's other work

5 Concerns about SARS-CoV2 Biology: A Call to Pause, Deliberate, and Revise Policy

Why the pandemic was created

Why intermuscular injections do not benefit the immune system

jj-couey-gigaohmbiological-rna-infectious-clones-sequencing-and-more.html

Immunoligist Perspective on Covid-19

Gigaohm Biological w/ Dr. Jonathan Couey

Further Analysis w/ Denis Rancourt & Dr. Jonathan Couey

Upload transcript to Grok and asking questions

Infectious Clone Explanation

What is an Infectious Clone?

How is it Made?

Why Use Infectious Clones?

Cooley’s Perspective on Infectious Clones

Key Features of Infectious Clones

Understanding "Endemic" in Cooley’s Context and Its Application to Respiratory Viruses

What Does "Endemic" Mean?

Cooley’s Definition of "Endemic" in Context

How It Applies to Respiratory Viruses

1. Pre-Existing Diversity

2. Limits of Natural Spread

3. PCR Testing and Misattribution

4. Protocol Changes as the Real Culprit

Implications for the COVID-19 Narrative

Summary

Evidence from Newly Released JFK Files Suggesting CIA Involvement in the Assassination

1. CIA’s Anti-Cuban Operations and Key Figures

2. CIA Surveillance of Oswald’s Movements

3. CIA Connections to Oswald’s Associates

4. CIA Operations in Moscow During Oswald’s Stay

5. CIA’s History of Covert Operations and Potential Motive

6. CIA Efforts to Control Information Post-Assassination

Analysis and Implications

Critical Examination of the Establishment Narrative

Conclusion

Connections to Israel in the Newly Released JFK Files

Evidence from the Newly Released JFK Files

1. James Angleton and CIA-Israeli Intelligence Ties

2. Reuben Efron: A Jewish CIA Operative with Israeli Ties

3. Kennedy’s Tensions with Israel Over Nuclear Program

4. Operation Mongoose and Potential Overlaps

Critical Analysis

Sentiment on X and Conspiracy Theories

Conclusion

Nature of the Files Still Redacted in the JFK Assassination Records

Overview of Redacted Files in the Released Chunk

1. HTLINGUAL Program Records

2. Angleton Files and CIA Counterintelligence