Friday Hope: Vitamin D: Paper from 2021 Definitively Shows How Vitamin D May Completely Negate Severe COVID

My research also shows that Vitamin D may be instrumental in preventing the DNA damage now associated with SARS-CoV-2 and its Spike Protein

Vitamin D continues to astound me in its abilities to mitigate the damage and severity of infection with SARS-CoV-2 and its Spike Protein. A relatively hidden paper from 2021, which is a large systematic review, shows how raising Vitamin D levels to 50 ng/mL could theoretically reduce the risk of Severe COVID to Zero.

The two independent datasets showed a negative Pearson correlation of D3 levels and mortality risk (r(17) = −0.4154, p = 0.0770/r(13) = −0.4886, p = 0.0646). For the combined data, median (IQR) D3 levels were 23.2 ng/mL (17.4–26.8), and a significant Pearson correlation was observed (r(32) = −0.3989, p = 0.0194). Regression suggested a theoretical point of zero mortality at approximately 50 ng/mL D3.

As is well known, the Spike Protein uses ACE2 (among many other) receptors to attach to cells and cause infection. This interaction with ACE2 causes downregulation of the expression of ACE2. ACE2 cleaves Angiotensin II inactivating its deleterious effects when its levels are too high. Vitamin D stimulates ACE2 expression, thereby enabling the cleaving of Angiotensin II.

Interaction of vitamin D3 with the renin-angiotensin system (RAS): The renin-angiotensin system (RAS) is an important regulator of blood volume and systemic vascular resistance for the adjustment of blood pressure. The balance between angiotensin II and angiotensin-(1,7) is a critical factor for the proper functioning of the system. Angiotensin-converting enzyme 2 (ACE2) is responsible for converting angiotensin II to angiotensin-(1,7). Angiotensin II primarily triggers vasoconstriction but can also cause inflammation, fibrosis, and oxidative stress in the absence of its counterpart, angiotensin-(1,7). ACE2 is the primary receptor of SARS-CoV-2, which decreases its activity, leading to an increase in angiotensin II levels and a decrease in angiotensin-(1,7) levels. This effect ultimately triggers SARS-CoV-2-induced “acute respiratory distress syndrome” (ARDS) [85,86]. Calcitriol, the active metabolite of vitamin D3, minimizes this effect by inhibiting renin expression and thus angiotensin II synthesis and by stimulating ACE2 expression, enhancing the conversion of angiotensin II to angiotensin-(1,7). Thus, insufficient vitamin D blood levels lead to the development of severe courses of SARS-CoV-2 disease. In addition, it has been shown that high angiotensin II levels lead to downregulation of the enzyme 1-alpha-hydroxylase, which is required for the formation of calcitriol, thereby exacerbating the negative consequences of vitamin D deficiency.

COVID-19 Mortality Risk Correlates Inversely with Vitamin D3 Status, and a Mortality Rate Close to Zero Could Theoretically Be Achieved at 50 ng/mL 25(OH)D3: Results of a Systematic Review and Meta-Analysis
https://www.mdpi.com/2072-6643/13/10/3596

Yet, there is another significant ability of Vitamin D, which complements the EXTERNAL cell pathologies associated with the Spike Protein and SARS-CoV-2. This is the INTERNAL cell ability of Vitamin D protects DNA and activates tumor suppressing genes and simultaneously inhibits oncogenes (cancer inducing genes).

Vitamin D changes the status of DNA methylation and histone modifications, resulting in the activation of tumor suppressors and inhibition of oncogenes. In addition, vitamin D activates the expression of tumor suppressing miRNAs, which contribute to the tumor suppressive activity. Further understanding of the epigenetic action of vitamin D will help the development of therapeutic strategies targeting the vitamin D signaling pathway without inducing the hypercalcemic side effects.

Vitamin D and the Epigenetic Machinery in Colon Cancer
https://www.eurekaselect.com/article/79788

It is well known that the Spike Protein interacts with tumor suppressors.

Here we performed bioinformatic analysis to investigate the interaction of S2 subunit protein of SARS-nCoV-2 of novel coronavirus with tumor suppressor proteins p53 and BRCA-1/2.

S2 Subunit of SARS-nCoV-2 Interacts with Tumor Suppressor Protein p53 and BRCA: an In Silico Study
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7324311/

Given that Vitamin D appears to be significant in preventing both Acute COVID and mitigating the risk factors for the development of Post-COVID and Spike Protein sequelae, I believe, more than ever, it is vitally important to further understand the optimal dosing of Vitamin D for the general population to achieve these potential results.