Three Facts That Caught My Eye

Teardown of pregnancy test (from BBC)

Three not-quite-random facts that caught my eye recently, two about COVID, one about computers.

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3 Responses to Three Facts That Caught My Eye

  1. Eric says:

    In a previous comment, I began to review the concept of causation and how the field of epidemiology tackles the issue.

    As means of background, I found it rather interesting that the 1918 influenza pandemic was wrongly assumed for many years to have been caused by a bacterium called “Pfeiffer’s bacillus.” As time progressed, further scientific advancement detected the influenza virus and demonstrated that experts can be very wrong in their conclusions. Drastic measures such as the lockdown and suspension of our liberties should always be questioned with a level of scrutiny that has been notoriously absent in the mainstream media and legal circles alike.

    When I read the original article that first identified SARS-CoV-2, I noticed that merely three (3) patients were sampled for identification of a new pathogen. The appendix to the study stated that only twenty-two (22) possible pathogens were ruled-out, of which eighteen (18) were viruses and four (4) were bacteria. Of the virus profiles used to rule-out the cause of the pneumonia cases, only four (4) coronaviruses were examined. Specifically, there were: HCoV-229E, HCoV-NL63, HCoV-OC43 and HCoV-HKU1.

    As a preliminary matter, the study does not indicate whether the hospital patients were treated with any antimicrobial therapy that may have been initiated prior to sample collection. That is important, as it would potentially limit the detection of any other co-infection associated with the illness notwithstanding the presence of a novel coronavirus. Along those same lines, different sampling techniques produce additional evidence of pathogens which can co-exist at the same time. The study in question could not use nasopharyngeal swab specimens because the patients had been experiencing symptoms of respiratory distress for more than three (3) days prior to hospitalization.

    Moreover, it is rather noteworthy that the “RespiFinder Smart22 Kit” profile did not include the SARS-CoV strain of coronavirus which was responsible for the original pandemic of Severe Acute Respiratory Syndrome in 2003. It is strange indeed that no mention was ever made about using a PCR test as a control measure to see if the allegedly novel coronavirus would be detected as the SARS-CoV strain from 2003 or perhaps even the other MERS-CoV strain to prove the reliability of those tests in general.

    Another striking omission in the study involved the “patients in Beijing hospitals with pneumonia of known cause to serve as control samples.” The study utilized “unbiased, high-throughput sequencing . . . to discover microbial sequences not identifiable by [the RespiFinder Smart 22 Kit].” But in order to perform this additional testing, the samples were “centrifuged to remove cellular debris” that would necessarily discard any other classes of pathogen such as bacteria and fungi that were condensed into a “pellet.”

    Considering that this method was referenced under footnote 13 and involved a paper detailing the specific detection of coronaviruses, it makes me wonder if they somehow already knew what they were hoping to find. And since a viral sample requires up to thirty (30) days to fully demonstrate “cytopathic effects,” the collection of samples on December 30, 2019 could not possibly have been fully reviewed by the publication of the study on January 23, 2020. Given that peer review alone takes multiple weeks at an absolute minimum, there is something rather unusual about this paper wholly funded by the government of China.

    At the end of the article, it stated that the newly detected strain of coronavirus is “the likely causative agent of the viral pneumonia in Wuhan” notwithstanding the authors’ admission that the “study does not fulfill Koch’s postulates.” Although I have started to extensively review the literature involving Koch’s postulates with respect to animal models in general and Covid-19 studies in particular, I am still not finished reviewing the issues presented in the foundational paper allegedly discovering SARS-CoV-2 for the first time.

    To be honest, this is much more difficult than I imagined not because the concepts are complex but rather because the field of study is truly immense. I now understand why almost everyone around me has appealed to authority without even attempting to review the logic behind the studies. But with the Internet at my disposal as the last and ultimate bastion of truth, I will continue going into the weeds and keep you posted accordingly.

    It just might take a lot longer than I previously thought.

  2. Eric says:

    Review of the literature regarding Koch’s postulates and SARS-Cov-2 led me to another early article which stated:

    “Traditional identification of a microbe as the causative agent of disease requires fulfillment of Koch’s postulates, modified by Rivers for viral diseases. At the present time, the 2019-nCoV has been isolated from patients, detected by specific assays in patients, and cultured in host cells (one available sequence is identified as a passage isolate), starting to fulfill these criteria. Given the recentness of the 2019-nCoV outbreak, at this point there is no animal model available to fulfill the remaining criteria: 1) testing the capability of 2019-nCoV to cause respiratory disease in a related species, 2) re-isolating the virus from the experimentally infected animal and 3) detection of a specific immune response. These efforts will surely be an area of intense research in the coming months both in China and in CoV research laboratories around the world.”

    Before discussing the animal testing portion of Koch’s postulates in regard to determining causation, it should be noted that I still have many reservations involving the isolation from patients prong as the first step of the analysis. As I mentioned earlier, the original study from China’s CDC did not actually explain how the control patients were properly used as controls in the first place regarding the lack of waiting thirty (30) days to examine cytopathogenic effects involved in their cell lines. Moreover, it seemingly ignored another fundamental aspect of discovery:

    “The process of virus discovery begins with case selection (namely, the identification of a patient or a group of patients with distinctive clinical features that could represent infection by a novel virus in a population with little herd immunity). Such distinctive features may include unusually severe clinical presentations, an increased incidence of the disease syndrome above the baseline, uncommonly seen radiological features, and/or idiosyncratic laboratory test results. . . . While subjecting clinical specimens to tests for novel virus detection, it is important to concomitantly undertake exhaustive specific assays for known bacterial, viral, fungal, and parasitic pathogens that could also account for the clinical scenario.”

    As I continued to explore the issue of selection bias in the original study concerning the focus on a possible viral infection to the exclusion of anything else, I discovered another Chinese study published one week later that raised similar issues concerning the concepts of causation and correlation. With only seven (7) samples and no controls, they assumed coronavirus off the bat (both literally and figuratively):

    “Samples from seven patients with severe pneumonia (six of whom are sellers or deliverymen from the seafood market), who were admitted to the intensive care unit of Wuhan Jin Yin-Tan Hospital at the beginning of the outbreak, were sent to the laboratory at the Wuhan Institute of Virology (WIV) for the diagnosis of the causative pathogen. As a laboratory investigating CoV, we first used pan-CoV PCR primers to test these samples, given that the outbreak occurred in winter and in a market—the same environment as SARS infections. We found five samples to be PCR-positive for CoVs.”

    The laboratory chosen to review the patient samples was already investigating coronavirus strains and essentially demonstrated the inherent bias of Maslow’s hammer. By using “pan-CoV PCR primers” they searched for any strain of coronavirus currently in existence or potentially yet uncovered to get a generalized idea of matching that family of pathogen. Aside from the fact they did not use any other such generic primers to detect potentially new strains of the other types of pathogens associated with pneumonia, two (2) of the samples were not even positive for the coronavirus family of genes. Even more interesting was that none of the stool samples tested positive for the coronavirus per Table 2 which is quite unusual. Finally, the PCR tests never needed to exceed thirty-two (32) cycles which stands in stark contrast to the radically sensitive PCR tests currently used around the world to justify the continued and rapid erosion of our most fundamental liberties.

    As for their stated reason to focus on a novel virus: “The disease was determined to be caused by virus-induced pneumonia by clinicians according to clinical symptoms and other criteria, including a rise in body temperature, decreases in the number of lymphocytes and white blood cells (although levels of the latter were sometimes normal), new pulmonary infiltrates on chest radiography and no obvious improvement after treatment with antibiotics for three days.”

    In other words, they completely ruled out the possibility of any other sort of pathogen because antibiotic treatments did not work after three (3) days. However, the study does not indicate the type of antibiotics used. Moreover, response times can actually take longer depending on the patient’s underlying condition, incorrect choice of medicines and/or antibiotic-resistant bacteria:

    “According to the Infectious Diseases Society of America (IDSA) guidelines, treatment failure in hospitalized patients with [community acquired pneumonia] should only be considered after at least 72?h of initial treatment, which is the standard time required to achieve clinical stability and to reduce bacterial load. This may be problematic because the evaluation of response relies mostly on normalization of the same unspecific clinical and radiological criteria, previously used for CAP diagnosis. Moreover, patient recovery may take longer than bacterial killing itself and the use of cultures to prove bacteria eradication may be misleading and is not recommended. Therefore, nonresponse may easily be mistakenly stated.”

    As another review of the medical literature indicated, response rates to antibiotic treatment can exceed the time limit in the Chinese study of which three (3) days is the absolute minimum time to wait: “Of the 2039 patients included in REACH, 585 (28.7%) had [time to clinical stability] assessed by Halm’s criteria: 332 (56.8%) showed early response (median 3.0 days), and 253 (43.2%) showed later response to treatment (median 7.0 days).”

    As fever and chest congestion are present in all types of pneumonia and decidedly not “distinctive clinical features that could represent infection by a novel virus,” the only other stated factor used by the Chinese study to completely discount bacterial pneumonia was the extremely limited report of blood work without any reference to a complete blood count analysis. Supposedly, the number of lymphocytes was decreased while the total numbers of white blood cells “were sometimes normal.” As these lymphocytes are but one of the many types of white blood cells, their fraction (“ratio” or “differential”) apparently decreased.

    However, the striking result of my research suggests that such a decrease correlates with bacterial pneumonia while a fractional increase correlates with viral pneumonia. That is the exact opposite reasoning employed by the Chinese doctors: “Viral pneumonia was associated with a significantly higher lymphocyte fraction in the white blood cells, and significantly lower serum creatinine levels than non-viral pneumonia (p<0.05, each). However, no significant differences were found in the total white blood cell counts (WBC) and C-reactive protein (CRP).”

    Based on the fact it was submitted on January 20, 2020 and subsequently published on February 3, 2020, I could not fathom how it had been peer-reviewed so quickly. Upon further examination, I discovered that it has not been peer-reviewed at all. Per the publisher’s website: “All peer-reviewed content will carry an anonymous statement of peer reviewer acknowledgement, and for those reviewers who give their consent, we will publish their names alongside the published article.” No such statement exists for this article. I find this to be very odd, considering that this research has more than 2,300 citations and helped lay the foundation for the entire world community to declare an emergency of such remarkably unprecedented proportions.

    Prior to posting the final part of my analysis in this trilogy of trials and tribulations, I wanted to end this second part with an observation made by Thomas Rivers in 1937 when he proposed a modification of the postulates to account for viral disease. As we continue to explore the concept of causation with respect to the rather commonplace symptoms of Covid-19, it should be noted that multiple pathogens can play a part in creating the ultimate expression of symptoms in the progression towards mortality:

    “At the time when they were formulated Koch’s postulates were essential for the progress of knowledge of infectious diseases; but progress having left behind old rules requires new ones which some day without doubt will also be declared obsolete. Thus, in regard to certain diseases, particularly those caused by viruses, the blind adherence to Koch’s postulates may act as a hindrance instead of an aid. For instance, the idea that an infectious malady can be caused only by the action of a single agent is incorrect, and, if Shope had adhered to old ideas, he would never have discovered that swine influenza as it occurs in nature is caused by the combined or synergistic action of two agents, one a virus not cultivable on lifeless media, the other an ordinary hemophilia bacterium.”

    This observation brings me back to the work involving the CDC’s investigation of the 1918 influenza pandemic that originally linked “Pfeiffer’s bacillus” to the outbreak. Even though I remarked in my first part of the analysis that such a mistake implied that the experts can be wrong, I decided to explore why such a connection had been assumed in the first place. To that end, I found a subsequent article published in 2008 that built upon the work of the CDC and prior researchers that had identified the influenza virus and allegedly demonstrated its uniquely virulent properties. The conclusion of that article states:

    “The majority of deaths in the 1918-1919 influenza pandemic likely resulted directly from secondary bacterial pneumonia caused by common upper respiratory-tract bacteria. Less substantial data from the subsequent 1957 and 1968 pandemics are consistent with these findings. If severe pandemic influenza is largely a problem of viral-bacterial copathogenesis, pandemic planning needs to go beyond addressing the viral cause alone (e.g., influenza vaccines and antiviral drugs). Prevention, diagnosis, prophylaxis, and treatment of secondary bacterial pneumonia, as well as stockpiling of antibiotics and bacterial vaccines, should also be high priorities for pandemic planning.”

    So who helped author the study that determined the excess mortality rate of the 1918 pandemic was actually caused by bacterial infections prior to the discovery of antibiotics and not the penultimate influenza virus determined to be so inherently novel?

    Shockingly, it was none other than the Emperor of Epidemiology himself, Dr. Anthony S. Fauci, M.D.:

  3. Eric says:

    Henri Poincaré in his book entitled “Science and Hypothesis” very aptly remarked: “To the superficial observer scientific truth is unassailable, the logic of science is infallible; and if scientific men sometimes make mistakes, it is because they have not understood the rules of the game. . . . But upon more mature reflection the position held by hypothesis was seen; it was recognized that it is as necessary to the experimenter as it is to the mathematician.”

    In this third and final part of my analysis of Covid-19, I am focusing my attention on the hypothesis by the vox populi that SARS-CoV-2 is the causative agent of excess death in the United States. As referenced in the second part of the analysis, a novel pathogen is traditionally associated with a novel disease. But from my understanding, there is no regularly occurring symptom of Covid-19 that is particularly distinct.

    Regarding the cause of pneumonia in general, which is a severe complication of any respiratory infection regardless of the particular pathogen, the medical literature reveals a remarkable inability to detect the known cause in about half the cases. This finding was reinforced by a study that utilized a significantly more rigorous standard of pathogen detection with hundreds of patients in stark contrast to the rushed Chinese studies involving a mere handful of patients with a suspiciously sole focus on possible coronavirus strains:

    “The aetiology of community-acquired pneumonia (CAP) has been studied in various regions and settings. While these studies differ considerably in patient populations, diagnostic methodology, and presence of confounders, one intriguing constant finding is the failure to detect a pathogen in ∼30–60% of cases. Among the factors which may explain this observation, ambulatory antimicrobial pretreatment is the most attractive. Accordingly, there is evidence from the literature that the majority of cases of unknown aetiology may be caused by Streptococcus pneumoniae, a pathogen which is easily missed after one single dose of antimicrobial treatment.”

    As for the claim that Covid-19 is novel because of its high rate of mortality in the elderly, that particular attribute of disease progression is remarkably common regardless of the causative agent: “Pneumonia in the elderly happens fast and the prognosis is poor, and elderly are susceptible to severe Pneumonia. The mortality rate for severe pneumonia is as high as 20%.”

    Even assuming that the SARS-CoV-2 pathogen had been properly isolated by methods of purification from cellular tissue and associated with increased mortality in the elderly, it does not necessarily mean that this particular strain of coronavirus is anything more than correlative. Replication of the severe hallmarks of this disease in animal models has not been demonstrated. If anything, the results merely demonstrate the symptoms of the common cold that one would expect from other strains of coronavirus and similar respiratory pathogens.

    Take for instance one study that convinces me that this particular betacoronavirus in question does indeed cause sickness like any other strain of coronavirus. What it failed to show, however, was any actual mortality from the virus itself even though the study bifurcated between young and old Syrian hamsters alike. While one hamster did indeed die, it should be noted that the experimenters purposefully killed the hamster and therefore invalidated mortality association with SARS-CoV-2. This study also showed a contradiction in the results from another study with hamsters, highlighting the problem with scientific replication:

    “Chan et al. showed that SARS-CoV-2 replicates to higher titers in the nasal turbinates than in the lungs of infected Syrian hamsters. In contrast, we observed that the level of virus replication in the lungs was comparable to that in the nasal turbinates. Chan et al. and we used almost identical experimental designs, with no substantial differences in hamster age, gender, inoculation dose, or volume. Therefore, the reason for this discrepancy is unclear.”

    In another study involving hamsters, there was no mortality either. Of course, there was once again complete recovery without any medical intervention. These mild symptoms reminiscent of a common cold are decidedly not the same symptoms that are causing mass hysteria:

    “Inoculated and naturally infected hamsters showed apparent weight loss on days 6–7 post-inoculation or post-contact; all hamsters returned to their original weight within 14 days and developed neutralizing antibodies. Our results suggest that features associated with SARS-CoV-2 infection in golden hamsters resemble those found in humans with mild SARS-CoV-2 infections.”

    Finally, a third study involving monkeys showed no symptoms at all: “No obvious clinical signs were observed during the study course except that one animal showed reduced appetite. All animals investigated did not show body weight changes from 1 to 6 days post infection (d.p.i.), while 7% and 8% weight loss was observed at 14 d.p.i. in RM1 and RM4, respectively. Body temperatures were monitored from day 1 to day 14 and no obvious changes were found.”

    Back in 2015, a study reviewed the literature involving the original SARS and MERS viruses and the result of animal studies. Other than genetically-engineered mice that were artificially created to be receptive to the virus and therefore not existing in nature, there was no mortality associated with the disease. In fact, just like the studies involving SARS-CoV-2, the results were inconsistent between papers and therefore subject to significant doubt: “The development and evaluation of antiviral drugs and vaccines for SARS and MERS has been challenging, in part because of difficulties in developing animal models that provide consistent and reproducible results.”

    In fact, another paper reviewing the animal studies came to the same general conclusion:

    “In these animal experiments, SARS-CoV was administered intratracheally and intranasally to cynomolgus macaques (intratracheal inoculation was the most effective delivery system to the lower respiratory tract), which resulted in respiratory and constitutional clinical signs (mild cough, sneezing, high body temperature, lethargy, slight decreased activity), viral shedding, and pulmonary lesions. Soon after the monkey experiments, cats, ferrets, mice, pigs, hamsters, guinea pigs, hamsters, chickens, and rats were infected to study various pathogenetic aspects of the disease. All these animals were susceptible to SARS-CoV infection after intrarespiratory inoculation, and most exhibited excretion of the virus in pharyngeal or nasal swabs, histopathologic pulmonary changes, and seroconversion. However, the course of the infection in these animals was shorter than that in humans, and none of these animal models replicated the human disease in all its aspects.”

    These studies from SARS and MERS predictably showed the same inherent problem with the studies of SARS-CoV-2 as summarized very recently with the current situation: “No [non-human primate] model fully reproduces all COVID-19 features observed in humans.”

    Any conclusion in the medical literature that somehow claims the novel coronavirus has satisfied Koch’s postulates is therefore demonstrably wrong. By definition, this means that SARS-CoV-2 has not been proven to be the cause of Covid-19 in the first place.

    That being said, the continued loosening of standards in the field of virology simply reflects a loss of scientific rigor. This in turn most likely has resulted from a sense of frustration in the medical community to understand viral causation that Dr. Thomas Rivers destroyed with his removal of the concept of falsifiability, one of the hallmarks of the scientific method.

    In order to paint a broader picture involving the loss of logic in the evolution of modern virology, it is important to understand how Dr. Robert Koch explained the principles of causation in the first place:

    “If, however, it can be proved: First, that the parasite is met with in each individual case of the particular disease and under conditions which correspond to the pathological changes and the clinical course of the disease; secondly, that in no other disease is it found as an accidental non-pathogenic guest; and, thirdly, that if completely isolated from the body and cultivated in pure cultures with sufficient frequency, it can reproduce the disease-then it can no longer be considered an accidental accompaniment of the disease, but in that case no other relation between the parasite and the disease can be admitted than that the parasite is the cause of the disease.”

    While this framework required the pathogen to be present in every single case of the disease, the previously cited work by Dr. Thomas Rivers modified the correlation as follows: “It is not obligatory to demonstrate the presence of a virus in every case of the disease produced by it.” Unfortunately for the field of virology, this logical failing throws the concept of falsification out the window and creates a foundation built on sand. Perhaps modern medical science needs to further explore the role of environmental pollution in a population such as China that is causing such unusual symptoms in a very small subset of patients with a Covid-19 diagnosis:

    “Since the late 1950s there has been a steady shift of interest from the infectious agent alone to the circumstances of the infection and the response of the host. In other words, it has transpired that the development of illness does not depend on the presence of the infectious agent alone, but also on individual predispositions, i.e. on the physiological state and genetically conditioned susceptibility of the infected individual, as well as on participation of external cofactors that may lower his resistance. This means a definitive departure from the hypothesis of the sufficient cause resting with microbiology.”

    The philosophical underpinnings of causation in the field of medicine show an acceptance of multiple factors in the progression of disease. Even Dr. Fauci recognized the combined role of bacterial infections with viral infections as expressed in the previously cited work about the 1918 influenza pandemic. In the event a person dies of bacterial complications following an initial viral lung infection, it could be argued that the virus was the underlying cause of this death. But for the virus creating a weakened immune system, the bacterial infection would not have developed.

    However, by that exact same line of reasoning, the viral infection could only find expression in light of an underlying health condition. It therefore follows that the underlying cause of death in Covid-19 is neither the coronavirus nor the bacterial complications. As evidenced by the near-complete lack of mortality in the bulk of the population, the underlying cause of death is simply the chronic health condition that plagued these vulnerable individuals in the first place.

    Coupled with the extreme “mutshe-ing” of the elderly population with invasive ventilation and aggressive treatment in March and April, the simplest explanation for the serious complications of Covid-19 is nothing more than the myopic negligence of the doctors treating patients with coronavirus. This in turn has been caused by the profound hysteria surrounding this current variant of the common cold fueled by the highly suspect studies originating from the dystopian hellscape of the Chinese government with a penchant for destabilizing the global economy.

    If science is the art of measuring relationships, then the panic surrounding Covid-19 simply does not add up.

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