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🤔 Not surprising that individuals with a genetic predisposition to clotting, such as those with polymorphisms in Factor V Leiden, prothrombin and MTHFR, would have elevated clotting risk with Covid infection. Would be similar for those with an acquired predisposition to clotting, such as individuals with antiphospholipid antibodies. Add in some elevated neutrophil extracellular traps as an accelerant and🩸🔥!!! 🚨
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Sanhueza at al., De novo COVID-19-associated insulin resistance drives dysregulated neutrophil extracellular trap formation (NETosis) four months after infection. frontiersin.org/journals/imm…
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“Science” is losing public trust and credibility because real world observations and common sense are trumping the “gold standard” RCTs. Conflicts of interest and biases (political and financial) are getting exposed and trust and credibility are subsequently lost.
No, the bear shouldn't eat them. Strong, consistent real-world observation (multiple bears sick after the exact berries) trumps a conflicting RCT unless the trial exactly matches conditions, dose, and bears involved—which it rarely does in practice.
I weigh all evidence by quality and applicability, not dogma. RCTs minimize bias but aren't magic. If the berries are making bears ill, avoid and investigate the mismatch. Common sense first.
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🤔 @grok review the significance of vitamin K2. Why is it often given with Vitamin D. Were Covid patients reported to be low in K2? Significance in pulmonary pathology. Potential benefits in long COVID. Explain in scientific terms that would interest pediatric pulmonologists. Use detailed citations.
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🧐”Immune NETs: What COVID and Snake Venoms Have in Common” 🐍 #COVID19 #NETosis. #neutrophilextracelluartraps youtube.com/watch?v=NRynlHYA…
What do the virus that causes COVID-19 and snake venom have in common? They both trigger our white blood cells to deploy pathogen-trapping webs. But in trying to heroically protect us, our immune system may be causing more harm than good.
youtu.be/NRynlHYAQJI
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⭐️ Searching for the pathophysiology of disease is perhaps the best way to honor the body. It gives us important clues to the biochemistry of life unraveling how structural biology, enzymology, and metabolism interrelate. Just unraveling how Vitamin D, B12 and folate and their genetic polymorphisms relate to COVID pathophysiology has provided important foundational evidence to the ways proper supplementation and / or nutrition, centered on the individual, can provide the body, and thus our immune system, the resources to confront the enemy with less harm from friendly fire.
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5 options for new LongCOVID clinical def based on spike protein, NETs, autoantibodies, vascular inflam & microthrombosis:
1. Spike-NET vasculopathy: >12wk symptoms + plasma spike + NET markers + microvasc evidence.
2. Autoimmune microthrombosis: + specific autoAbs + clot confirmation.
3. Immune complex NETosis: spike-ICs overactivating neutrophils.
4. Endothelial autoimmunity: persistent vasc inflam w/ thrombosis.
5. Post-viral thrombophilic syndrome: multi-biomarker confirmation.
Key tests/biomarkers: plasma spike assay, NETs (cfDNA/citH3), autoantibody screen, D-dimer, endothelial markers, microclot imaging.
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Vitamin D deficiency expands LDGs (low-density granulocytes: CD10+CD14low neutrophils in PBMC fraction), a proinflammatory subset with primed NETosis. This drives excessive degranulation/release of granule effectors (MPO, ELANE, histones, LL-37) into extracellular traps, heightening inflammation/autoimmunity without broad granule depletion.
Simple: Low vitamin D boosts "hyperactive" neutrophils (more LDGs) that over-dump their granule "ammo" into sticky nets, fueling damage like in SLE.
Refs: Handono K et al. (2013) GJBAHS 2(4):90-95 (vit D <20 ng/ml ↑ LDGs/NETs; r=-0.452 to -0.662); Front Immunol 2021 (Vit D modulates/suppresses NETosis). Supplementation often reverses this.
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Vitamin D pathways shine in infections like HIV and chronic viral hepatitis. Scientifically: VDR activation in macrophages induces cathelicidin and autophagy to restrict HIV replication and modulate HBV/HCV antiviral interferon responses, reducing co-infection severity (e.g., TB-HIV). VDR polymorphisms link to worse outcomes.
Simply: It arms immune cells to fight viruses harder and smarter.
Infections targeting VDR: M. tuberculosis downregulates VDR in macrophages to blunt cathelicidin. M. leprae suppresses CYP27B1 (active vitamin D enzyme). EBV downregulates VDR in B cells for latency. Borrelia burgdorferi cuts VDR 50x in monocytes. CMV and Aspergillus toxins also inhibit VDR.
Vitamin A (RAR): Less direct targeting reported; deficiency impairs mucosal immunity, worsening RSV/measles susceptibility via reduced T-cell responses. Some viruses (e.g., via RXRα) indirectly heighten vulnerability.
Refs: 1. Liu PT et al. Science 2006;311:1770. 2. Yenamandra et al. Exp Oncol 2009;31:92. 3. Rieder et al. J Steroid Biochem Mol Biol 2017;165:356.
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🧐”Authors' reply: the biologic importance of the vitamin D binding protein polymorphism in pediatric COVID-19 patients”pubmed.ncbi.nlm.nih.gov/3399…
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🧐”DBP rs7041 and DHCR7 rs3829251 are Linked to CD4 + Recovery in HIV Patients on Antiretroviral Therapy”
frontiersin.org/articles/10.…
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🧐”Vitamin D regulation of immune function during covid-19”
#DBP #VitaminD
ncbi.nlm.nih.gov/pmc/article…
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🧐”A review of the critical role of vitamin D axis on the immune system”
#VitaminD #secosteroid #prohormone #immunity #autoimmune #VDR #DBP
sciencedirect.com/science/ar…
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🤔”Human gene polymorphisms and their possible impact on the clinical outcome of SARS-CoV-2 infection”
#APOL1 #VDR #DBP #TMPRSS2👀
link.springer.com/article/10…
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🧐”Vitamin D blood levels and vitamin D receptor polymorphisms contribute to post-acute sequelae of severe acute respiratory syndrome coronavirus 2 severity in the pediatric patients”
clinicalnutritionespen.com/a…
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Rep @sydneykamlager introduced a bipartisan resolution to expand prenatal screening for antiphospholipid syndrome, a treatable blood clotting disorder that can lead to miscarriage, stillbirth & other serious pregnancy complications
afro.com/maternal-health-dis… #BlackWomenLead
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Patients with new-onset systemic lupus erythematosus have a high early incidence of thromboembolic events, particularly those with antiphospholipid syndrome.
ms.spr.ly/6016smCOM
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JEM Case of the Week Answer: Stars on CT show multiple hepatic infarcts. Labs consistent with HEELP syndrome. Patient was ultimately diagnosed with Antiphospholipid syndrome. Check out her full near catastrophic course here! @BKMethodistEM @aaeminfo jem-journal.com/article/S073…
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🧐”Anti-vitamin D antibodies”
“Anti-vitamin D antibodies were identified in 3.5 % to 87 % of patients with SLE, SSc, pAPS, and PV. These antibodies are associated either with the autoimmune condition itself or with other autoantibodies, suggesting their potential role in disease mechanisms and progression.”👀
sciencedirect.com/science/ar…