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wrote in the abstract: “The attack will cause  that caused the worst disruption was aspartate.   The flu
            less and less hemoglobin that can carry oxygen  Aspartate is a very good model for how glypho-  vaccine has
            and carbon dioxide. The lung cells are toxic and  sate would behave because, like glyphosate, it is
            inflammatory due to the inability to exchange  considerably larger than glycine and negatively  not been
            carbon dioxide and oxygen frequently, which  charged. Turning the molecule into a peroxidase   successful
            eventually results in ground-glass-like lung im-  would result in the release of redox-active fer-  in fighting
            ages. The mechanism also interfered with the  ryl iron (Fe(IV)), a highly oxidized and very
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            normal heme anabolic pathway of the human  dangerous form of iron.                 off flu, and
            body, expecting to result in human disease.”    This predicted effect is borne out in evi-  there is no
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            However, a rebuttal paper appeared shortly  dence from people who have a genetic muta-  reason to
            thereafter, providing a long list of arguments  tion in G139. A paper that is well summarized
            why the theoretical ideas proposed by the first  by its title described a patient who picked up  believe that a

            set of authors did not support their hypothesis  a bad copy of HO-1 from both parents (a ho-  coronavirus
            and claiming that there is no experimental evi-  mozygous change from glycine to valine). The   vaccine
            dence that this can happen.               title is: “Mutating heme oxygenase-1 into a
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               Severe hyperinflammation is perhaps the  peroxidase causes a defect in bilirubin synthesis  would have a
            best descriptor for acute Covid-19. When some  associated with microcytic anemia and severe   high success
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            Covid-19 cases cascade into a hyperinflamma-  hyperinflammation.”  The consequences of   rate either.
            tory state, heme is released from hemoglobin  glyphosate perturbing HO-1 by substituting for
            and then iron is released from heme. The highly  G139 are catastrophic. Normally, HO-1 resolves
            reactive free iron combined with the inflamma-  inflammation, but the opposite happens when
            tory response leads to widespread damage to the  glyphosate disrupts the protein, setting in mo-
            artery walls. This induces an acute thrombotic  tion a dangerous positive feedback loop where
            response, with blood clots appearing throughout  inflammation induces HO-1, which induces
            the vasculature, eventually leading to multiple  more inflammation.
            organ failure and death.                     A final blow comes during the massive
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               If the virus is not causing this inflamma-  thrombotic response triggered by damage to the
            tory cascade, then what is? The answer comes  walls of the blood vessels by the ferryl iron and
            from studies on mutations in the enzyme heme  the oxidizing agents. Thrombin is the enzyme
            oxygenase 1 (HO-1). Normally, this enzyme  that produces fibrin, the main component of
            is able to metabolize heme into biliverdin and  blood clots. Normally, antithrombin suppresses
            subsequently bilirubin, releasing ferrous iron  blood clot formation by binding to thrombin and
            that is then sequestered inside ferritin molecules,  disabling it. Severe Covid-19 disease is charac-
            preventing the iron from damaging the tissues.  terized by elevations in D-dimer, a marker for
            Studies show that HO-1 is usually protective of  thrombin overproduction. Studies have shown
            oxidative stress, and, indeed, inflammation in-  that antithrombin administration is beneficial
            duces increased synthesis of HO-1. Importantly,  to treat sepsis and that it lowers the levels of
            the enzyme contains two critical glycine resi-  D-dimer.  Significantly, antithrombin’s activity
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            dues—G139 and G143—that bind electrostati-  increases over a thousand-fold through binding
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            cally to heme and secure it in place to allow the  to heparan sulfate or heparin.  Heparan sulfate
            reaction to take place. If either of these glycines  synthesis is severely disturbed by glyphosate, as
            is mutated to a different amino acid, the enzyme  I have described together with collaborators in
            can no longer successfully carry out its reaction.  previous papers.
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               The title of a paper published in 2000 clearly   It is plausible that the rapid rollout of 5G
            states the consequences of replacing the first  may work synergistically with glyphosate to
            glycine residue with a different amino acid: “Re-  enhance the effects on iron homeostasis. Several
            placement of the distal glycine 139 transforms  papers have shown evidence that electromag-
            human heme oxygenase-1 into a peroxidase.”   netic fields (EMFs) disrupt iron status through
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            The researchers replaced the first glycine residue  alterations in the iron chelator ferritin, the iron
            with several different amino acids, but the one  regulator hepcidin or iron itself. 52-55

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