New Updates To The COVID 19 Report
People who are G6PD deficient can end up with iron overload and a cytokine storm especially when given ascorbic acid. Many practitioners have discovered throughout the years it is best for G6PD deficient individuals to have food based C which is ascorbate form. As we know with an elevation of serum ferritn that those individuals are in a cytokine flare. So it is best to speak with a medical professional if you are G6PD deficient before taking any ascorbic acid supplements.
C rich foods are always safer for G6PD deficient people than ascorbic acid. Please speak with your doctor who can advise you on what C rich foods to consume during the COVID-19 outbreak. Remember that just because you have a mutation does not mean that it is always problematic.
The World Health Organization (WHO) breaks G6PD into these classifications:
- Class I: Severe deficiency (<10% activity) with chronic (nonspherocytic) hemolytic anemia
- Class II: Severe deficiency (<10% activity), with intermittent hemolysis
- Class III: Mild deficiency (10-60% activity), hemolysis with stressors only
Acute respiratory distress syndrome (ARDS) caused by SARS-CoV-2 is largely the result of a dysregulated host response, followed by damage to alveolar cells and lung fibrosis. Exacerbated proinflammatory cytokines release (cytokine storm) and loss of T lymphocytes (leukopenia) characterize the most aggressive presentation. We propose that a multifaceted anti-inflammatory strategy based on pharmacological activation of nuclear factor erythroid 2 p45-related factor 2 (NRF2) can be deployed against the virus. The strategy provides robust cytoprotection by restoring redox and protein homeostasis, promoting resolution of inflammation, and facilitating repair. NRF2 activators such as sulforaphane and bardoxolone methyl are already in clinical trials. The safety and efficacy information of these modulators in humans, together with their well-documented cytoprotective and anti-inflammatory effects in preclinical models, highlight the potential of this armamentarium for deployment to the battlefield against COVID-19.
What Is NRF2 And Why Is It Important?
NRF2 is a nuclear transcription factor that binds to antioxidant response. It is also called erythroid-related factor 2. It is a powerful protein that is latent in each cell in our bodies.
NRF2 migrates into the cell nucleus and bonds with our DNA. It does this at our antioxidant response element which is the regulator of our antioxidant response system. As we age this system starts to decline.
Among patients with immune-mediated inflammatory diseases (IMIDs) who get COVID-19, the risk for hospitalization and death is lower if they are receiving tumor necrosis factor (TNF) inhibitor monotherapy, compared with receiving most other common drugs for these conditions, with or without TNF inhibitors, according to a study published October 18 in JAMA Network Open. The only combination not associated with an increased risk for hospitalization or death was TNF inhibitor therapy with methotrexate
What Is TNF?
Tumor necrosis factor is produced by cells in your immune system that promote inflammatory responses. It is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It is potent pyrogen-causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia, under certain conditions it can stimulate cell proliferation and induce cell differentiation. Impairs regulatory T-cells (Treg) function in individuals with rheumatoid arthritis via FOXP3 dephosphorylation. Upregulates the expression of protein phosphatase 1 (PP1), which dephosphorylates the key ‘Ser-418’ residue of FOXP3, thereby inactivating FOXP3 and rendering Treg cells functionally defective.
Patients hospitalized with severe COVID-19 infections who have high levels of the blood clotting protein factor V are at elevated risk for serious injury from blood clots such as deep vein thrombosis or pulmonary embolism, investigators at Massachusetts General Hospital (MGH) have found.
What Is FVL/ Factor V Leiden?
FVL is one mutation of a clotting factor in the blood. Protein C, an anticoagulant protein that normally inhibits the pro-clotting activity of factor V, is not able to bind normally to factor V, leading to a hypercoagulable state. People with epigenetic expression of FVL usually end up with DVT (deep vein thrombosis) or pulmonary embolism.
Higher levels of D-dimer, thrombocytopenia and prolonged prothrombin time in COVID-19 patients suggest the occurrence of DIC, yet in DIC the levels of D-dimer is higher than that of COVID-19 and thrombocytopenia is more predominant.
What Is Factor II Prothrombin G20210A?
It is a genetic condition that raises your chances of forming a blood clot and is almost always in 3% of caucasions. People with epigenetic expression of F2 Prothrombin G20210A usually end up with DVT (deep vein thrombosis) or pulmonary embolism.
Chloroquine has infrequently been reported to cause hemolysis in G6PD-deficient patients and caution is advised for its use.11 Hydroxychloroquine, its molecular variant, is generally considered safe. Both antimalarial drugs are being trialed as possible treatments for COVID-19. However, a recent report described an acute hemolytic episode occurring in a COVID-19 patient with G6PD deficiency who was treated with hydroxychloroquine.12 Hydroxychloroquine may increase the oxidative stress in COVID-19 patients with G6PD deficiency, thereby serving as a trigger for hemolytic anemia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7275177/
Back in January of 2020 when I built the COVID-19 report , I had G6PD down as a suspect and contacting scientists and doctors warning them of giving these patients HCQ. I received tons of backlash for this but here it is. Here is an interview I did with My Black Health. https://www.youtube.com/watch?v=Wn5ovUjxVbE