Technical Report

All-cause mortality during COVID-19: No plague and a likely signature of mass homicide by government response

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Abstract

The latest data of all-cause mortality by week does not show a winter-burden mortality that is statistically larger than for past winters. There was no plague. However, a sharp "COVID peak" is present in the data, for several jurisdictions in Europe and the USA. This all-cause-mortality "COVID peak" has unique characteristics: • Its sharpness, with a full-width at half-maximum of only approximately 4 weeks; • Its lateness in the infectious-season cycle, surging after week-11 of 2020, which is unprecedented for any large sharp-peak feature; • The synchronicity of the onset of its surge, across continents, and immediately following the WHO declaration of the pandemic; and • Its USA state-to-state absence or presence for the same viral ecology on the same territory, being correlated with nursing home events and government actions rather than any known viral strain discernment. These "COVID peak" characteristics, and a review of the epidemiological history, and of relevant knowledge about viral respiratory diseases, lead me to postulate that the "COVID peak" results from an accelerated mass homicide of immune-vulnerable individuals, and individuals made more immune-vulnerable, by government and institutional actions, rather than being an epidemiological signature of a novel virus, irrespective of the degree to which the virus is novel from the perspective of viral speciation.

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... e all-cause mortality shows sharp surges in deaths that followed the 11 March 2020 WHO global recommendation for hospital clearing as "pandemic" response, across the world, in those jurisdictions that sent hospitalised infected elderly persons into the community, including locked down care homes.[2] [3][4] [5] e mechanism that made care homes and institutions for sick and elderly persons into killing elds includes the following elements:[2] ...
... The Great VIRAL Debate: Dr Rancourt's Closing Statement -OffGuardian https://off-guardian.org/2020/11/10/the-great-viral-debate-dr-rancourts-closing-statement/ 5/76 [3][4] [5] is was a mass crime. ...
... e post-March-11th "COVID-peaks" that I rst identi ed in the all-cause mortality data for the USA and Europe would not have occurred. [3] In the context of this debate, "herd/community immunity" refers to the business-as-usual natural coping of individuals and society constantly challenged by respiratory disease viruses, as has been the case for thousands of years. In technical terms, the concept of "herd immunity" was introduced by vaccine manufacturers as a pretext for universal vaccination programs, rather than individual personalchoice "protection". ...
Presentation
Welcome to Closing Statements of The Great VIRAL Debate. Track this debate’s progress in our Coronavirus Debate Section. Dr Piers Robinson is our chair. Off-Guardian is your host. -- The mechanism that made care homes and institutions for sick and elderly persons into killing fields includes the following elements: * infection seeding by hospital transfers into the care homes * universal lockdowns of the care homes * denied specialized medical treatment to the residents of the care homes * reduced staffing and staff abandonment in the care homes, and negligence * collateral effects of the universal lockdown of the care homes: extreme social isolation, psychological stress, reduced aerosol-exhaust ventilation, lost oversight of the institutions by family-members
... Your closed-door statement of January 2017 is an indelible part of your professional legacy. 5 But the most graphic representation of your legacy could be the absurdity depicted here: ...
Technical Report
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Alleged "COVID-19 Pandemic" mandated government enforced lockdowns of citizens, leading to massive but ignored K -12 suicide deaths of our children is connectable to Dr. Anthony Fauci.
... Your closed-door statement of January 2017 is an indelible part of your professional legacy. 5 But the most graphic representation of your legacy could be the absurdity depicted here: ...
Preprint
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Technical Report
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• "The 'massacre' of Italy's elderly nursing home residents: Covid-19 patients in Italy's virus epicentre of Lombardy were transferred to nursing homes by an official resolution with catastrophic consequences", by Maria Tavernini and Alessandro Di Rienzo, TRT World, 20 April 2020.
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• "CDC: 80,000 people died of flu last winter in U.S., highest death toll in 40 years", by Associated Press, STAT News, 26 September 2018.
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Alimpiev, Egor (2019) "Rethinking the Virus Species Concept", dated 15 March 2019, posted to stanford.edu http://stanford.edu/~alimpiev/thnk_ppr.pdf
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  • Bendavid
Bendavid et al. (2020) "COVID-19 Antibody Seroprevalence in Santa Clara County, California", medRxiv 2020.04.14.20062463; doi: https://doi.org/10.1101/2020.04.14.20062463
Charter 1a -Epidemiology: Epidemic theory (effective & basic reproduction numbers, epidemic thresholds) & techniques for analysis of infectious disease data (construction & use of epidemic curves, generation numbers, exceptional reporting & identification of significant clusters)
  • Healthknowlege-Uk
HealthKnowlege-UK (2020) "Charter 1a -Epidemiology: Epidemic theory (effective & basic reproduction numbers, epidemic thresholds) & techniques for analysis of infectious disease data (construction & use of epidemic curves, generation numbers, exceptional reporting & identification of significant clusters)", HealthKnowledge.org.uk, accessed on 2020-04-10. https://www.healthknowledge.org.uk/public-health-textbook/research-methods/1a-epidemiology/epidemic-theory
The impact of influenza epidemics on mortality: introducing a severity index
  • L Simonsen
Simonsen, L. et al. (1997) "The impact of influenza epidemics on mortality: introducing a severity index", Am J Public Health. 87(12):1944-1950. doi:10.2105/ajph.87.12.1944 https://pubmed.ncbi.nlm.nih.gov/9431281/
Concentrations and size distributions of airborne influenza A viruses measured indoors at a health centre, a day-care centre and on aeroplanes
  • W Yang
Yang, W. et al. (2011) "Concentrations and size distributions of airborne influenza A viruses measured indoors at a health centre, a day-care centre and on aeroplanes", Journal of the Royal Society, Interface. 2011 Aug;8(61):1176-1184. DOI: 10.1098/rsif.2010.0686. https://royalsocietypublishing.org/doi/10.1098/rsif.2010.0686