January 24, 2022

The entire Spike Protein binding saga of ACE2, though critical for viral entry and respiratory symptoms, is not the most dangerous target of the Protein. HEMOGLOBIN IS. And we have been deceived yet again.

Liu, et al. (2020) suggest that the key pathogenic molecular step of COVID-19 is to attack hemoglobin causing dissociation of the porphyrins from iron and releasing iron into the circulation. Thus, hemoglobin loses its capacity to bind with oxygen and hinders its delivery to major organs, which is coupled with rapid multi-organ failures. Moreover, the free iron released into the circulation may result in iron overload causing oxidative damage to the lungs and other organs. Iron overload may also result in inflammation and immune dysfunction. These dictate increased uptake and storage of iron in iron-binding proteins. Indeed, this notion is supported by the increased ferritin (the iron storage molecule in the body) concentrations in the circulation of COVID-19 patients. Amplified iron load leads to increased blood viscosity with recurrent and diffuse macro and micro circulatory thrombosis; this may explain the cause of unexpected deterioration and death in some cases.


Iron-induced oxidative stress modifies the genome, epigenome, and proteome, giving rise to tumor heterogeneity and evolving metastatic potential. In a rodent model, rats were repeatedly administered ferric nitrilotriacetate which induced widespread genomic alterations that led to the development of tumors. Iron treatment of colonocytes caused widespread hypomethylation, especially to oncogenes belonging to Akt, MAPK, and EGFR pathways and subsequently their expression increased. Iron overload as a result of hemochromatosis, causes aberrant hypermethylation of genes characteristic of HCC, suggesting iron-induced epigenetic modification could be an early event in malignant transformation.


Iron overload is a hallmark of many neurodegenerative processes such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. Unbound iron accumulated as a consequence of brain aging is highly reactive with water and oxygen and produces reactive oxygen species (ROS) or free radicals. Vast evidence has demonstrated that iron is a clear generator of oxidative stress. Both iron and oxidative stress have been linked to Aβ aggregation. However, the exact order in the molecular events that lead to the onset of AD still remains elusive. Exploring the brain’s own iron homeostatic mechanisms and the signaling events involved in response to metal overload may shed light on several unclear aspects of the disease and may therefore lead straightaway to the development of a definite therapeutic tool.


The poor ability of lymphocytes to sequester excess iron in ferritin may help to explain the immune system abnormalities in iron-overloaded patients. Iron overload as seen in hereditary hemochromatosis patients enhances suppressor T-cell (CD8) numbers and activity, decreases the proliferative capacity (which we are observing as it has been established an in vitro model using a cocktail of proteins from SARS-CoV-2 and blood cells from healthy volunteers. S glycoprotein, a transmembrane protein localized in the outer portion of the virus that facilitates binding to the host cells through angiotensin-converting enzyme 2 (ACE2); N protein, a structural component bound to the RNA of the virus; and the Papain-like protease (P), which is required to process the viral polyprotein into functional subunits; were used to mimic the presence of the virus. Our data demonstrated the induction of a specific monocyte profile (HLA-DRlowPD-L1high) due to the presence of the cocktail of proteins from SARS-CoV-2, which in turn caused a patent T-cells exhaustion.), numbers, and activity of helper T cells (CD4) with increases in CD8/CD4 ratios, impairs the generation of cytotoxic T cells, and alters immunoglobulin secretion when compared to treated hereditary hemochromatosis patients or controls.


Coagulopathy is a hallmark of severe ferrous sulfate poisoning in humans and laboratory animals. Although nontransferrin-bound Fe3+ is thought to initiate the disorder, little is known about how it interferes with blood coagulation. At iron concentrations comparable to those of previous animal investigations, we reproduced the coagulopathy, in other words, the dose-related prolongation of the prothrombin, thrombin, and partial thromboplastin time, in human plasma in vitro. Studies of the mechanism by which iron prevents a normal plasma coagulation revealed that the proenzymes of the coagulation cascade and fibrinogen were not damaged by iron. Fibrinogen coagulability and fibrin monomer aggregation were unaffected by very high iron concentrations. Instead, thrombin was markedly inhibited by iron in its clotting effect on fibrinogen and, specifically, in its fibrinopeptide A-generating capacity, the inhibitory effect being reversible upon iron removal by EDTA chelation and gel filtration. Thrombin generation in the presence of iron was reduced as well, indicating an inhibition of one or several other enzymes of the intrinsic coagulation cascade. Because the amidolytic activity of human thrombin as well as factor Xa, kallikrein, and bovine trypsin was also reversibly suppressed by ferrous sulfate as well as ferric citrate, we consider it likely that the coagulopathy occurring in iron poisoning is the consequence of a general, physiologically important phenomenon: the susceptibility of serine proteases to nontransferrin-bound Fe3+.


Findings demonstrate that iron overload is associated with increased levels of oxidative stress and shorter relative telomere length. Also, moderately to markedly increased ferritin concentrations represent a biological biomarker predictive of early death in a dose-dependent linear manner in the general population.

The strong signal for haem metabolism, in combination with the MR results, suggests the evidence for the involvement of this pathway in human ageing is reasonably robust. Haem synthesis declines with age and its deficiency leads to iron accumulation, oxidative stress, and mitochondrial dysfunction. In turn, iron accumulation helps pathogens to sustain an infection, which is in line with the known increase in infection susceptibility with age. In the brain, abnormal iron homeostasis is commonly seen in neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease and multiple sclerosis. Plasma ferritin concentration, a proxy for iron accumulation when unadjusted for plasma iron levels, has been associated with premature mortality in observational studies, and has been linked to liver disease, osteoarthritis, and systemic inflammation in MR studies.

Once again, I believe we have been led very far and disastrously astray while the foxes have routed our anesthetized chicken coops.

Referenced/Related Papers

Impact of Oxidative Stress in Premature Aging and Iron Overload in Hemodialysis Patients

Multivariate genomic scan implicates novel loci and haem metabolism in human ageing

Total and Cause-Specific Mortality by Moderately and Markedly Increased Ferritin Concentrations: General Population Study and Metaanalysis

Blood coagulation and acute iron toxicity. Reversible iron-induced inactivation of serine proteases in vitro

Proteins from SARS-CoV-2 reduce T cell proliferation: A mirror image of sepsis

Effects of iron overload on the immune system

The Aging of Iron Man

The role of iron in the pathogenesis of COVID-19 and possible treatment with lactoferrin and other iron chelators

SARS-CoV-2 Proteins Bind to Hemoglobin and Its Metabolites