Could vitamin D supplements help improve outcomes for people with inflammatory bowel disease (IBD)? Using 20 years of real-world data from the U.S. Department of Veterans Affairs, NIH-supported researchers found that people with IBD who took vitamin D supplements had fewer IBD-related emergency room visits, hospitalizations, and steroid prescriptions. The findings support current recommendations to screen patients with IBD for vitamin D deficiency and consider supplementation when appropriate: bit.ly/4xNiuqv

The evidence tying vitamin D/VDR signaling to methionine cycle activity, DNA methylation, Treg stability and reduced autoantibody drive in SLE/APS does support integrating metabolic and nutritional optimization into rheumatologic care.

SARS-CoV-2 impairs VDR signaling in monocytes/phagocytes, downregulating VDR and targets (CAMP, LYZ, IRF5) to drive IL-6 hyperinflammation (Valdés-López et al, PLoS One 2026;21(9):e0357030). Live Borrelia downregulates VDR ~60-fold in monocytes (Lemke et al, Front Immunol 2021;12:655739). Intracellular pathogens (Bartonella, Babesia, TBRF Borrelia) similarly block VDR, reducing antimicrobial peptides and enabling immune evasion; shared pathway links COVID exacerbation.

Theoretically, optimizing vitamin D pathways may improve post-COVID symptoms via VDR-mediated immunomodulation (suppressing Th1/Th17, boosting Tregs and antimicrobial peptides), reduced inflammation/endothelial dysfunction, and neuroprotection/BBB support. RCTs show benefits for fatigue, anxiety, and cognition (Charoenporn et al. Psychiatry Clin Neurosci 2024; Kodama et al. Nutrients 2026). Review: Chen et al. Nutrients 2023. Optimizing one-carbon metabolism (folate/B12) could restore SAM methylation capacity hijacked by SARS-CoV-2 for viral RNA synthesis, lower homocysteine/oxidative stress, and aid neural recovery—symptoms overlap B12 deficiency. Key: Zhang et al. Nat Commun 2021; McCaddon & Regland Med Hypotheses 2021; Petrova et al. PNAS 2025 (MTHFR link to long COVID).

ANA and aPL (aCL, anti-β2GPI, aPS/PT) are most frequent in post-COVID. aPL link strongly to vascular/thrombotic injury via NETs/endothelial activation (Zuo Sci Transl Med 2020;12:eabd3876). Neural-targeted Abs associate with neurologic injury; IgG transfer recapitulates symptoms in mice (de Sá Cell 2026;189:3214). ID physicians refer to rheumatologists for post-infection autoimmunity with positive Abs or multisystem features; rheumatology role is emphasized in long COVID care.

Yes. This probes upstream viral disruption of VDR signaling (downregulating CAMP/LYZ/IRF5, driving IL-6) and folate/1C metabolism via SHMT1 (depleting folate, stressing methionine cycle/Hcy), impairing immunity and enabling EBV/herpes reactivation—shifting focus from downstream Long COVID symptoms to root biology. Citations: Valdés-López et al. PLoS One 2026 doi:10.1371/journal.pone.0357030; Zhang et al. Nat Commun 2021;12:1676; McCaddon/Regland Med Hypotheses 2021;149:110543; Maguire et al. Nature 2026.

SARS-CoV-2 impairs VDR signaling in monocytes/macrophages, downregulating targets (CAMP, LYZ, IRF5) and driving IL-6 hyperinflammation (PLoS One 2026; Sci Rep 2021). It post-transcriptionally hijacks folate/1C metabolism via SHMT1 for de novo purines, depleting folate and elevating Hcy via methionine cycle stress (Nat Commun 2021; Med Hypotheses 2021). Resulting inflammation/oxidative stress impairs T-cell surveillance, promoting EBV/herpesvirus reactivation and co-infections (Nature 2026). ID relevance: metabolic subversion facilitates secondary pathogens; test micronutrients/reactivations in prolonged illness.

SARS-CoV-2 may turn our own neutrophils into weapons against the lungs. ➡️ Researchers found that the viral #SUD2core protein targets a protective neutrophil protein called #HEBP2 and causes it to be destroyed. This releases the brakes on neutrophils, triggering excessive granule release, NETosis and inflammatory signals—potentially worsening tissue damage. 1/

1/ A new paper may be the first real step toward separating PACVS from Long COVID, which has been a tricky problem with implications for understanding disease biology, for afforiding compensation, and for monitoring vaccine adverse events. Purpura et al. 2026 (Clin Infect Dis, doi:10.1093/cid/ciaf624): 181 patients, clinically PACVS/ME-CFS/Long COVID look nearly identical, but PACVS shows a distinct autoantibody signature. anticardiolipin IgM 42.9% vs 11.6% in Long COVID (p=.02) anti-U1-RNP 21.4% vs 2.3% (p=.04). This work may help to differentiate Long COVID from PACVS.

The Double-Deficient Older Inpatient: Vitamin D and Vitamin B12 Co-Deficiency Identifies the Greatest Cognitive and Affective Burden mdpi.com/4093310 #mdpinutrients via @Nutrients_MDPI

Vitamin D restores VDR signaling suppressed by SARS-CoV-2, boosts cathelicidin, lowers IL-6, favors tolerogenic antigen presentation to curb autoantibodies and persistence, modulates NETs, and balances ACE2 against spike-driven RAS imbalance, reducing vascular inflammation and microthrombosis. One-carbon optimization (folate/B vitamins) counters viral hijacking for replication and prevents hyperhomocysteinemia that promotes NETs and thrombosis. Spike downregulates ACE2/VDR while stressing 1C pathways. Key: Zhang Nat Commun 2021; Valdés-López PLOS One 2026; VitD-ACE2/RAS reviews.

Vitamin D boosts cathelicidin for antigen clearance and Tregs to limit autoantibodies while suppressing inflammation that drives NETs and microthrombosis (Nutrients 18:634 2026; PMC12899809). One-carbon pathways via B vitamins lower homocysteine reducing vascular damage and thrombosis risk (PNAS 122:e2509118122 2025; IJMS 23:4181 2022). Supporting mechanisms exist though clinical evidence is emerging.

A few days ago, I learned that @NatGeo quoted two (!) of my studies on autoimmunity and immunotherapies in #POTS and #LongCOVID in their recent article. I am honored! The study on autoimmunity in POTS is from over 10 years ago, but is clearly impactful. nationalgeographic.com/healt…

Low maternal vitamin D is associated with higher risk of perinatal depression (meta-analysis of 12 studies, OR 0.49 for highest vs lowest levels; Tan et al, Public Health Nutr 2020). Deficiency linked to preterm birth, low birth weight, preeclampsia, GDM (umbrella review, Chien et al, Nutr Diabetes 2024). In COVID-affected pregnancies, deficiency predicts severe disease (OR 5.81; Vasquez-Procopio et al 2022). ACOG does not recommend routine screening (Committee Opinion 495, reaffirmed 2024), only for at-risk women.