Friday Hope: Vitamin D Reduces Telomere Attrition
A new 5-year study shows that Vitamin D supplementation preserves telomere length and significantly reduces cancer and autoimmune disease risks, which may prevent/reverse Spike Protein damage.
Of all the stars in the firmament of nutraceuticals we have available to combat SARS-CoV-2 and its Spike Protein, Vitamin D may be the brightest. Once again, we find yet another way that Vitamin D has the potential to prevent, treat and potentially reverse the damage done by the Spike Protein. Additionally, this new finding shows how Vitamin D may be able to reduce the risks of diseases of aging in general.
One of the early observations I made about the Spike Protein was its ability to shorten the length of telomeres. This finding was later supported with evidence, which I present below. Telomeres are the “caps” on our chromosomes that protect our DNA from degradation every time it gets copied. Think of those caps on the ends of shoelaces, if you’d like a visual description.
We recognized the existence of an LIG_TRFH_1 motif (Figure 2A,B) in the SARS-CoV-2 Omicron and Iota variants. In humans, the telomere repeat factor (TRF) homology (TRFH) domain interacts with the conserved TRFH-binding motif (TBM) in the telomere repeat factor 1 (TRF1), telomere repeat factor 2 (TRF2), and TRF1-interacting nuclear protein 2 (TIN2) components of the shelterin complex [10]. Shelterin, a complex of six proteins, TRF1, TRF2, POT1, TPP1, TIN2, and Rap1, protects telomeres from various types of DNA damage and prevents end-to-end chromosomic damage fusions [11]. Figure 2C represents the structural organization and interaction of human TRF1, TRF2, and TIN2. These proteins and other binding partners of shelterin protect telomeric DNA sequences (Figure 2D). The depletion or mutation of any of the components of the shelterin complex triggers telomeric dysfunction and activates DNA damage response (DDR) pathways [12].
Viral infection can also induce DNA damage and evoke the host DDR, and several studies reported that the progression of SARS-CoV-2 severity is associated with decreased telomere length [13,14]. A study on African green monkey kidney cells (Vero E6) showed that SARS-CoV-2 infection could trigger DNA damage response (DDR) and impact telomeric stability [10,15]. We assumed, analogously to cellular TRFH, the identified viral LIG_TRFH_1 could interact with TRF2 and TIN2 proteins. A possible interaction between LIG_TRFH_1, and TRF2 and TIN2 is presented in Figure 2E. TIN2 is the shelterin complex’s central hub that interacts with TRF1, TRF2, and TPP1, and promotes the assembly of an intact shelterin complex that protects the telomeric repeats. TRF2 participates in t-loop formation and protects telomeres from DDR pathways [16].
Computational Analysis of Short Linear Motifs in the Spike Protein of SARS-CoV-2 Variants Provides Possible Clues into the Immune Hijack and Evasion Mechanisms of Omicron Variant
https://pmc.ncbi.nlm.nih.gov/articles/PMC9368778/
Vitamin D has the ability to fight against the attrition that Telomeres naturally experience. It increases the activity of the enzyme Telomerase, which extends Telomeres.
Beside these cross-sectional studies, only one interventional study has been performed in order to clarify the effect of vitamin D supplementation on telomere biology [141]. Zhu et al. treated 37 obese Afro-American subjects in a double-blind randomized fashion with either a monthly oral dose of 60,000 IU of vitamin D3 or placebo for a period of 4 months. At the end of the study the serum 25-OHD concentration in vitamin D treated subjects was markedly increased when compared to baseline. The rise in serum 25-OHD was accompanied by a 19.2% increase of peripheral blood mononuclear cell (PBMC) telomerase activity.
The role of telomeres and vitamin D in cellular aging and age-related diseases
https://www.degruyterbrill.com/document/doi/10.1515/cclm-2014-1184/html
Now, we have evidence that long-term Vitamin D supplementation does, indeed, preserve the length of our Telomeres.
In the VITAL-CTSC subcohort, we found that vitamin D3 supplementation significantly reduced telomere attrition over a 4-y period, preventing 140 bp of LTL loss compared with placebo. Overall trend analysis also showed that vitamin D3 supplementation group had LTLs that were ∼0.035 kb higher per year of follow-up compared with placebo group, which equates to 140 bp over the 4-y period.
Vitamin D3 and marine ω-3 fatty acids supplementation and leukocyte telomere length: 4-year findings from the VITamin D and OmegA-3 TriaL (VITAL) randomized controlled trial
https://www.sciencedirect.com/science/article/abs/pii/S0002916525002552
The same study also found that long-term Vitamin D supplementation significantly reduced the risks of cancer and autoimmune diseases.
The VITamin D and OmegA-3 TriaL (VITAL) is a completed large, randomized, double-blind, placebo-controlled trial with a 2 × 2 factorial design of vitamin D3 (2000 IU/d) and marine n–3 FAs (1 g/d) supplements for 5 y among a representative sample of 25,871 US females aged ≥55 and males aged ≥50 y. Autoimmune diseases, characterized by an inflammatory autoimmune response to self-tissues, and cancer are 2 chronic diseases that increase in prevalence with age. In the VITAL trial, compared with placebo, daily supplementation with 2000 IU/d vitamin D, but not n–3 FAs, reduced the incidence of advanced (metastatic or fatal) cancer by 17% [15]. Moreover, supplementation with vitamin D with or without marine n–3 FAs for 5 y reduced all incident autoimmune diseases by 22%, whereas n–3 FAs supplementation with or without vitamin D reduced the autoimmune disease rate by 15% (not statistically significant) [16].
Vitamin D3 and marine ω-3 fatty acids supplementation and leukocyte telomere length: 4-year findings from the VITamin D and OmegA-3 TriaL (VITAL) randomized controlled trial
https://www.sciencedirect.com/science/article/abs/pii/S0002916525002552
Of course, there is no such thing as magic. However, given the overwhelming evidence of what the correct use of Vitamin D (always consult your Primary Care Provider) can do to improve our lives, it may be the closest thing to it we have.
It has been resplendent here in northern Vermont this week. The aroma of fresh cut grass lingering in the air on a sunny seventy-degree day filled with gentle breezes brings such a deep feeling of joy. I hope all of us experience that in our own fashion this weekend. Thank you, as always, for your readership, dialogue and support.
Thank you for sharing this inexpensive and readily available therapy. I had read that patients who died in the hospital (maybe intensive care unit) had very low vitamin D levels & that those with D levels of 50 ng/ml or above recovered. Forgive my lack of details on the study.
There are tons of vitamin D studies… it’s good for so many things. About 10 years ago I became convinced of its value and have been supplementing plus getting sunshine as much as I can. I experimented and found that my D levels really dropped dramatically without supplementation, despite sunbathing & living in Florida. Most traditional doctors won’t test D levels.
I know a biological dentist that will not work on your mouth if your D levels are below 40ng/ml. She offers D testing in her office with immediate results for $150 which is double the price of an online test but it’s more convenient.
My mother is 89 with cognitive impairment, her doctor finally put her on 2000 IU daily about 5 years ago, which was about 20 years too late. I upped her dose to 5000 IU when I became her caregiver. I haven’t noticed any improvement in her but feel it is probably helping in other ways, possibly with acute illnesses.
Walter, you are a treasure, and are steadfast in your pursuit to bring us information that I get no where else. Thank you!
Love ya, Walt, but it's kinda ironic that in a post about vitamin D, the only mention of SUN is "a sunny seventy-degree day."
Everyone needs to STEP AWAY FROM THE COMPUTER AND GO OUTSIDE AND EAT SOME SALMON. STAT. 😎