Remarks: Why is ZINC with HCQ important in treatment for COVID-19 and has Comorbidity of Asthma , Zinc Deficiency is linked to the Comorbidity of Asthma and the hydroxychloroquine, “opens the zinc channel” allowing the zinc to enter the cell, which then “blocks the replication of cellular machinery.” In this instance, chloroquine has no drug action. It is the zinc that is in play. FULL STORY HERE: https://www.4cmitv.com/2020/09/14/2011-dec-07-covid-19-asthma-comorbidity-linked-with-zinc-deficiency-companion-medication-hcq-zinc/
Dr. Anthony Cardillo:
Dr. Anthony Cardillo, added that combining the drug with zinc has been the key to the success. The hydroxychloroquine, he said, “opens the zinc channel” allowing the zinc to enter the cell, which then “blocks the replication of cellular machinery.” In this instance, chloroquine has no drug action. It is the zinc that is in play, and I find it concerning that so many news organizations (and governments) are failing to convey this fact..opting, instead, to portray chloroquine as having the key drug action. It does not…
A new study from the CDC found that 90% of hospitalized patients had one or more underlying condition before contracting COVID-19. Those most susceptible are the elderly and those with underlying health issues such as Diabetes, Obesity, Asthma, COPD, and Hypertension. The symptoms of some include loss of taste and smell and in some diarrhea. As shown below, studies have shown that in all these conditions mentioned, there seems to be a correlation with zinc deficiency.
*Zinc Deficiency and Asthma*
J Inflamm (Lond). 2011; 8: 36.
Published online 2011 Dec 7. doi: 10.1186/1476-9255-8-36
Zinc supplementation alters airway inflammation and airway hyperresponsiveness to a common allergen
Zinc supplementation can modulate immunity through inhibition of NF-κB, a transcription factor that controls many immune response genes. Thus, we sought to examine the mechanism by which zinc supplementation tempers the response to a common allergen and determine its effect on allergic airway inflammation.
Administration of zinc gluconate prior to allergen exposure resulted in significantly decreased neutrophil infiltration and TNFα cytokine release into the airways. This correlated with decreased NF-κB activity in the whole lung.
Treatment with zinc gluconate significantly decreased GC frass-mediated TNFα production from bone-marrow derived neutrophils and HL-60 cells. We confirmed zinc-mediated decreases in NF-κB:DNA binding and IKK activity in HL-60 cells.
A20, a natural inhibitor of NF-κB and a zinc-fingered protein, is a potential target of zinc. Zinc treatment did not alter A20 levels in the short term, but resulted in the degradation of RIP1, an important upstream activator of IKK. TRAF6 protein levels were unaffected.
To determine the application for zinc as a therapeutic for asthma, we administered zinc following the establishment of allergic airway inflammation in a murine model. Zinc supplementation decreased airway hyperresponsiveness and serum IgE levels, but had no effect on Th2 cytokine expression.
This report suggests that the mechanism by which zinc supplementation alters NF-κB activity is via the alteration of A20 activity.
In addition, this study provides evidence that supplementation of zinc to asthmatics may alter airway reactivity and serum IgE levels, suggesting zinc supplementation as a potential treatment for asthmatics.
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