The hyperbolic manner in which health policymakers and mainstream media pundits talk about it today, flu virus (or COVID-19) is an inexorably lethal force (note: viruses are obligiate parasites, at worst, with no inner motive force to actively “infect” others), against which all citizens, of all ages 6 months or older, need the annual influenza vaccine to protect themselves against, lest they (it is said) face deadly consequences. Worse, those who hold religious or philosophical objections, or who otherwise conscientiously object to vaccinating, are being characterized as doing harm to others by denying them herd immunity (a concept that has been completely debunked by a careful study of the evidence, or lack thereof). For instance, in the interview below Bill Gates tells Sanjay Gupta that he thinks non-vaccinators “kill children”:
But what if I (Sayer Ji, founder of GreenMedInfo) told you that there isn’t even such a thing as “flu virus,” in the sense of a monolithic, disease vector existing outside of us, conceived as it is as the relationship of predator to prey?
First, consider that the highly authoritative Cochrane collaboration acknowledges there are many different flu viruses that are not, in fact, influenza A — against which flu vaccines are targeted — but which nonetheless can contribute to symptoms identical to those attributed to influenza A:
“Over 200 viruses cause influenza and influenza-like illness which produce the same symptoms (fever, headache, aches and pains, cough and runny noses). Without laboratory tests, doctors cannot tell the two illnesses apart. Both last for days and rarely lead to death or serious illness. At best, vaccines might be effective against only Influenza A and B, which represent about 10% of all circulating viruses.” (Source: Cochrane Summaries).” [emphasis added]
This makes for a picture of complexity that powerfully undermines health policies that presuppose vaccination equates to bona fide immunity, and by implication, necessitates the herd collectively participate in the ritual of mass vaccination campaigns as a matter of life-or-death social necessity.
Even the use of the word “immunization” to describe vaccination is highly misleading. The moment the word is used, it already presupposes efficacy, and makes it appear as if non-vaccinators are anti-immunity, instead of what they actually are: pro-immunity (via clean air, food, water, and sunlight), but unwilling to subject themselves or their healthy children to “unavoidably unsafe” medical procedures with only theoretical benefits.
Why Flu Virus Doesn’t Exist (The Way We Were Told)
But the topic gets even more interesting when we consider the findings of a 2015 study entitled “Conserved and host-specific features of influenza virion architecture.” This was the first study ever to plumb the molecular depths of what influenza virus is actually composed of. Amazingly, given the long history of vaccine use and promotion, the full characterization of what proteins it contains, and where they are derived from, was never previously performed. How we invest billions of dollars annually into flu vaccines, and have created a global campaign to countermand a viral enemy, whose basic building blocks were not even known until a few years ago, is hard to understand. But it is true nonetheless.
The study abstract opens with this highly provocative line:
“Viruses use virions to spread between hosts, and virion composition is therefore the primary determinant of viral transmissibility and immunogenicity.” [emphasis added]
Virion are also known as “viral particles,” and they are the means by which viral nucleic acids are able to move and ‘infect’ living organisms. Without the viral particle (taxi) to carry around the virus DNA (passenger), it would be harmless; in fact, viruses are often described as existing somewhere between living and inanimate objects for this reason: they do not produce their own energy, nor are transmissible without a living host. And so, in this first line, the authors are making it clear that virion composition is also the primary determinant in how or whether a virus is infectious (transmits) and what effects it will have in the immune system of the infected host.
This distinction is important because we often think of viruses as simply pathogenic strings of DNA or RNA. The irony, of course, is that the very things we attribute so much lethality to — viral nucleic acids — are not even alive, and can not infect an organism without all the other components (proteins, lipids, extra-viral nucleic acids) which are, technically, not viral in origin, participating in the process. And so, if the components that are non-viral are essential for the virus to cause harm, how can we continue to maintain that we are up against a monolithic disease entity “out there” who “infects” us, a passive victim? It’s fundamentally non-sensical, given these findings. It also clearly undermines the incessant, fear-based rhetoric those beholden to the pro-vaccine stance to coerce the masses into undergoing the largely faith-based rite of vaccination.
Let’s dive deeper into the study’s findings.
The next line of the abstract addresses the fact we opened this article with: namely, that there is great complexity involved at the level of the profound variability in virion composition:
“However, the virions of many viruses are complex and pleomorphic, making them difficult to analyze in detail”
But this problem of the great variability in the virion composition of influenza is exactly why the study was conducted. They explain:
“Here we address this by identifying and quantifying viral proteins with mass spectrometry, producing a complete and quantifiable model of the hundreds of viral and host-encoded proteins that make up the pleomorphic virions of influenza virus. We show that a conserved influenza virion architecture, which includes substantial quantities of host proteins as well as the viral protein NSI, is elaborated with abundant host-dependent features. As a result, influenza virions produced by mammalian and avian hosts have distinct protein compositions.”
How then, do we differentiate influenza virus as fully “other”? Given that it would not exist without “self” proteins, or those of other host animals like birds (avian) or insects, this would be impossible to do with any intellectual honesty intact.
There’s also the significant problem presented by flu vaccine production. Presently, human flu vaccine antigen is produced via insects and chicken eggs. This means that the virus particles extracted from these hosts would contain foreign proteins, and would therefore produce different and/or unpredictable immunological responses in humans than would be expected from human influenza viral particles. One possibility is that the dozens of foreign proteins found within avian influenza could theoretically produce antigens in humans that cross-react with self-structures resulting in autoimmunity. Safety testing, presently, does not test for these cross reactions. Clearly, this discovery opens up a Pandora’s box of potential problems that have never sufficiently been analyzed, since it was never understood until now that “influenza” is so thoroughly dependent upon a host for its transmissibility and immunogenicity.
Are Flu Viruses Really “Hijacked” Exosomes?
Lastly, the study identified something even more amazing:
“Finally, we note that influenza virions share an underlying protein composition with exosomes, suggesting that influenza virions form by subverting micro vesicle” production.”
What these researchers are talking about is the discovery that virion particles share stunning similarities to naturally occurring virus-like particles produced by all living cells called exosomes. Exosomes, like many viruses (i.e. enveloped viruses) are enclosed in a membrane, and are within the 50-100 nanometer size range that viruses are (20-400 nm). They also contain biologically active molecules, such as proteins and lipids, as well as information-containing ones like RNAs — exactly, or very similar, to the types of contents you find in viral particles.
Watch this basic video on exosomes to get a primer:
When we start to look at viruses through the lens of their overlap with exosomes, which as carriers of RNAs are essential for regulating the expression of the vast majority of the human genome, we start to understand how their function could be considered neutral as “information carriers,” if not beneficial. Both exosomes and viruses may actually be responsible for inter-species or cross-kingdom communication and regulation within the biosphere, given the way they are able to facilitate and mediate horizontal information transfer between organisms. Even eating a piece of fruit containing these exosomes can alter the expression of vitally important genes within our body.
In light of this post-Germ Theory perspective, viruses could be described as pieces of information in search of chromosomes; not inherently “bad,” but, in fact, essential for mediating the genotype/phenotype relationship within organisms, who must adapt to ever-shifting environmental conditions in real-time in order to survive; something the glacial pace of genetic changes within the primary nucleotide sequences of our DNA cannot do (for instance, it may take ~ 100,000 years for a protein-coding gene sequence to change versus seconds for a protein-coding gene’s expression to be altered via modulation via viral or exosomal RNAs).
This does not mean they are “all good”, either. Sometimes, given many conditions outside their control, their messages could present challenges or misinformation to the cells to which they are exposed, which could result in a “disease symptom.” These disease symptoms are often if not invariably attempts by the body to self-regulate and ultimately improve and heal itself.
In other words, the virion composition of viruses appears to be the byproduct of the cell’s normal exosome (also known as microvesicle) production machinery and trafficking, albeit being influenced by influenza DNA. And like exosomes, viruses may be a means of extracellular communication between cells, instead of simply a pathological disease entity. This could explain why an accumulating body of research on the role of the virome in human health indicates that so-called infectious agents, including viruses like measles, confer significant health benefits. [see: the Health Benefits of Measles and The Healing Power of Germs?].
Other researchers have come to similar discoveries about the relationship between exosomes and viruses, sometimes describing viral hijacking of exosome pathways as a “Trojan horse” hypothesis. HIV may provide such an example.
The remarkably recent discovery of the host-dependent nature of the influenza virus’ virion composition is really just the tip of an intellectual iceberg that has yet to fully emerge into the light of day, but is already “sinking” ships; paradigm ships, if you will.
This belief, however, is untenable. With the discovery of the indispensable role of the microbiome, and the subpopulation of viruses within it — the virome — we have entered into an entirely new, ecologically-based view of the body and its environs that are fundamentally inseparable. Ironically, the only thing that influenza may be capable of killing is germ theory itself.
For an in-depth exploration of this, watch the lecture below on the virome. I promise, if you do so, you will no longer be able to uphold germ theory as a monolithic truth any longer. You may even start to understand how we might consider some viruses “our friends,” and why we may need viruses far more than they need us.
Flu Death Manipulation
The CDC used to issue the same figure every year for the amount of flu deaths; 36,000. Then they modified that rote estimate, when it was finally challenged. They equivocated: “Flu seasons are unpredictable and can be severe. Over a period of 30 years, between 1976 and 2006, estimates of flu-associated deaths in the United States range from a low of about 3,000 to a high of about 49,000 people.”
In December of 2005, the British Medical Journal (online) published a shocking report by Peter Doshi, which created tremors through the halls of the CDC. Here is a quote from Doshi’s report, “Are US flu death figures more PR than science?” (BMJ 2005; 331:1412):
“[According to CDC statistics], ‘influenza and pneumonia’ took 62,034 lives in 2001—61,777 of which were attributable to pneumonia and 257 to flu, and in only 18 cases was the flu virus positively identified.”
You see, the CDC created one overall category that combines both flu and pneumonia deaths. Why do they do this? Because they disingenuously assume that the pneumonia deaths are complications stemming from the flu. This is an absurd assumption. Pneumonia has a number of causes. But even worse, in all the flu and pneumonia deaths, only 18 revealed the presence of an influenza virus. Therefore, the CDC could not say, with assurance, that more than 18 people died of influenza in 2001. Not 36,000 deaths. 18 deaths.
Doshi continued his assessment of published CDC flu-death statistics: “Between 1979 and 2001, [CDC] data show an average of 1348 [flu] deaths per year (range 257 to 3006).” These figures refer to flu separated out from pneumonia. This death toll is obviously far lower than the parroted 36,000 figure.
However, when you add the sensible condition that lab tests have to actually find the flu virus in patients, the numbers of flu deaths would plummet even further.
In other words, it’s promotion, hype, and uncertainty.
Peter Doshi (associate editor at The BMJ and a MIT graduate) has criticized the CDC’s “aggressive” promotion of flu shots, noting that although the annual public health campaigns deliver a “who-in-their-right-mind-could-possibly-disagree message,” the “rhetoric of science” trotted out each year by public health officials has a “shaky scientific basis.” Viewed within the context of Doshi’s remarks, the CDC’s high-flying flu numbers for 2017-2018 raise a number of questions. If accurate, 80,000 deaths would represent an enormous (and mystifying) one-year jump—tens of thousands more flu deaths compared to the already inflated numbers presented for 2016 (and every prior year). Moreover, assuming a roughly six-month season for peak flu activity, the 80,000 figure would translate to an average of over 13,300 deaths per month—something that no newspaper last year came close to reporting.
The CDC’s statistics are impervious to independent verification because they remain, thus far, unpublished—despite the agency’s pledge on its website to base its public health pronouncements on high-quality data derived openly and objectively. Could the CDC’s disappointment with influenza vaccination coverage—which lags far behind the agency’s target of 80%—have anything to do with the opacity of the flu data being used to peddle the unpopular and ineffective vaccines?
There are a variety of reasons to question the precision with which the CDC likes to imbue its flu statistics. First, although the CDC states that it conducts influenza mortality surveillance with its partner agencies, there is no actual requirement for U.S. states to report adult flu deaths to the CDC. (In public health parlance, adult influenza deaths are not “reportable” or “nationally notifiable.”) In fact, the only “flu-associated deaths” that the CDC requires states and other jurisdictions to report are deaths in children—180 last year.
…when actual death certificates are tallied, influenza deaths on average are little more than 1,000 yearly.
How did the CDC reach its as-yet-unpublished conclusion—widely shared with the media—that 79,820 American adults in addition to 180 children died from the flu in 2017-2018? The agency states that it relies on death certificate data. However, members of the Cochrane research community have observed that “when actual death certificates are tallied, influenza deaths on average are little more than 1,000 yearly.”
Other knowledgeable individuals have also noted that the death records system in the U.S. is subjective, incomplete and politicized, and have suggested that citizens should adopt a “healthy skepticism about even the most accepted, mainstream, nationally reported CDC or other ‘scientific’ statistics.” This skepticism may be especially warranted for the influenza stats, which are so inextricably intertwined with the CDC’s vaccination agenda that the statistical techniques and assumptions that the agency uses focus specifically on “project[ing] the burden of influenza that would have occurred in the absence of vaccination.”
Notwithstanding its incessant use of influenza statistics to justify its flu vaccine policies, the CDC tries to have it both ways, cautioning that because “influenza activity reporting…is voluntary,” influenza surveillance in the U.S. “cannot be used to ascertain how many people have become ill with influenza during the influenza season.” A larger problem is that the vital statistics that form the basis of the CDC’s surveillance data conflate deaths from pneumonia and influenza (P&I). The CDC concedes that this conflation complicates the challenge of specifically estimating flu deaths:
The system “tracks the proportion of death certificates processed that list pneumonia or influenza as the underlying or contributing cause of death. This system…does not provide an exact number of how many people died from flu” [emphasis added].
Curiously, the CDC presented its cause-of-death data slightly differently prior to 2015. Through 2014, the agency’s annual National Vital Statistics Reports included tables showing influenza deaths and pneumonia deaths as separate line items. Those reports made it abundantly clear that pneumonia deaths (at least as transmitted by death certificates) consistently and dramatically outstripped influenza deaths. The table below illustrates this pattern for 2012-2014.
Starting in 2015, the annual vital statistics reports began displaying P&I together and eliminated the distinct line items. At present, only one tool remains to examine mortality associated with influenza as distinct from pneumonia—the CDC’s interactive FluView dashboard—which provides weekly national breakdowns. The dashboard shows the same general pattern as in the annual reports—that is, lower numbers of influenza deaths and much higher numbers of pneumonia deaths. Bearing in mind all the shortcomings and potential biases of death certificate data, dashboard reports for the first week of March (week 9) for the past three years show 257 influenza deaths versus 4,250 pneumonia deaths in 2016, and 534 and 736 flu deaths (versus over 4,000 annual pneumonia deaths) in 2017 and 2018, respectively.
When clinicians in outpatient settings do order testing, relatively few of the “flu” specimens—sometimes as low as 1%—actually test positive for influenza.
Semantics also play a key role in the CDC’s slippery communications about “flu.” For example, CDC’s outpatient surveillance focuses on the broad category of “influenza-like illness” (ILI)—an almost meaningless term describing general symptoms (fever, cough and/or sore throat) that any number of non-influenza viruses are equally capable of triggering. Cochrane lists several problems with the reliance on ILI to make inferences about influenza:
- There is “no reliable system to monitor and quantify the epidemiology and impact of ILI” and no way of knowing what proportion of ILI is caused by influenza.
- There are almost no reliable data on the number of ILI-related physician contacts or hospitalizations—and no one knows what proportion of ILI doctor visits and hospitalizations are due to influenza.
“Pneumonia,” too, is a catch-all diagnosis covering lung infections caused by a variety of different agents: fungi, air pollutants and many others. Interestingly, hospitalization is a common route of exposure to pneumonia-causing pathogens, and mortality from hospital-acquired pneumonia exceeds 60%. In a plausible scenario, an adult hospitalized for suspected (but unconfirmed) “flu” could acquire a lethal pneumonia bug in the hospital, and their death might be chalked up to “flu” regardless of the actual facts, particularly because clinicians do not necessarily order influenza testing. When clinicians in outpatient settings do order testing, relatively few of the “flu” specimens—sometimes as low as 1%—actually test positive for influenza. Over the past couple of decades, the proportion of specimens testing positive has averaged around 15%—meaning that about 85% of suspected “flu” specimens are not, in fact, influenza.
Propaganda with a purpose
It takes little subtlety to recognize that the principal reason for flu hyperbole is to sell more vaccines. However, more and more people—even infectious disease specialists—are realizing that flu shots are fraught with problems. Roughly four-fifths of the vaccine injury and death cases settled through the National Vaccine Injury Compensation Program are flu-vaccine-related. A University of Toronto-based expert recently stated, “We have kind of hyped this vaccine so much for so long we are starting to believe our own hype.”
Pro-flu-vaccination studies—through their skillful placement in prestigious journals—tend to drown out other influenza studies that should be ringing warning bells. Published peer-reviewed studies show that:
- Previous influenza vaccination, particularly in those who get a flu shot every year, diminishes or “blunts” the already low effectiveness of flu shots.
- Getting vaccinated against influenza increases susceptibility to other severe respiratory viruses and also to other strains of influenza.
- Mothers who receive influenza vaccines during pregnancy face an increased risk of miscarriages and their offspring face elevated risks of birth defects and autism.
A systematic review of influenza vaccine trials by Cochrane in 2010 urges the utmost caution. Noting that “studies funded from public sources [have been] significantly less likely [than industry-funded studies] to report conclusions favorable to the vaccines,” and citing evidence of “widespread manipulation of conclusions,” the Cochrane reviewers’ bottom line is that “reliable evidence on influenza vaccines is thin.” We should all keep those words in mind the next time the CDC and the media try to mischaracterize flu facts and science.
History of Influenza
As early as 1799, researchers became puzzled over the cause of influenza, which appeared suddenly, often in diverse places at the same time. The world was not as globalized as it is today and so the contagion theory would not hold much water in this case.
In 1836, influenza specialist Heinrich Schweich noted that all physiological processed produce electricity and theorized that an electrical disturbance of the atmosphere may prevent the body from discharging it. He believed that the over accumulation of electricity can be a cause for influenza symptoms.¹².
With the discovery of the sun’s electrical nature, scientists have made some very interesting observations. The period 1645–1715 is one that astronomers call the “Maunder Minimum” and the sun was very quiet during this time and no sunspot activity was observed.
In 1715, sunspots reappeared again as did the northern lights and activity reached its peak in 1727. In 1728, influenza appeared in waves on every continent. Sunspot activities become more violent until they peaked in 1738, when physicians reported flu in both man and animals.¹³
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