Dr. Cameron Kyle Sidell says COVID-19 is not the cause of the deaths on ventilators


Dr. Sidell, M. D., is an Emergency-Reponse & Critical Care doctor who has treated COVID-19 infected patients in an intensive care unit at New York City for 9 days and says, what they are dying of is not what we think.

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7 thoughts on “Dr. Cameron Kyle Sidell says COVID-19 is not the cause of the deaths on ventilators”

  1. I support and believe the clinical findings of Dr. Sidell.
    Truth must be uncovered on the true cause of the hidden virulence of Sars-Cov2.
    Likewise, I believe that the drug regimen is just around but surely unseen forces will do their best to discredit or block it.

  2. 5G installed in NY – worth looking at.

    Be with Our Lord and Our Lady this Holy Thursday and Good Friday
    praying for souls and for the Triumph of the Immaculate Heart of Mary!

  3. There is a paper from 2001 which supports Dr Cameron Kyle Sidell’s conclusions
    News | April 10, 2001

    ”Fixed Wireless Communications at 60GHz Unique Oxygen Absorption Properties”

    by Shigeaki (Shey) Hakusui, President, Harmonix Corporation

  4. Wouldn’t it be sensible to assume the new paradigm of autoimmune disease similar to Guillain-Barré syndrome, for explaining the severe stage of Covid-19 ? In this paradigm, pulmonar surfactant would play the role of myelin. Immunity system would be activated during the early benign stage of the disease and then autoimmune antibodies would be delivered and directed against surfactant and relatedly type 2 pneumocytes.
    Several arguments support the hypothesis :
    – Two-step evolution ; suddenness of worsening ; randomness of worsening,
    – Absence of virus in alveoli in several severe cases.
    – Tensio-active properties of both virus coat and surfactant could suggest similarities in their biochemical composition and structure,
    – Recent jump from animal to human species : since human immunity system doesn’ know the virus, it coult react against what is the closest resembling, that is surfactant and relatedly type 2 pneumocytes.

    Thus the altered surfactant would no more play its task and this would produce a decrease in oxygen passage through alveolar membrane without obstruction of respiratory tract. Maybe this could explain your observations of patients with anoxia and no respiratory distress whereas relatedly destroyed type 2 pneumocytes could explain the inflammatory disorders which were observed in other cases.
    If verified, couldn’t such an hypothesis lead to an immunoglobulin-based treatment at severe stage of Covid-19 like in Guillain-Barré disease ?

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