Vitamin D deficiency again tied to COVID risk

Rapid Response:

COVID-19 ’ICU’ risk – 20-fold greater in the Vitamin D Deficient. BAME, African Americans, the Older, Institutionalised and Obese, are at greatest risk. Sun and ‘D’-supplementation – Game-changers? Research urgently required.

Dear Editor

COVID-19 (Coronavirus) mortality disproportionately impacts BAME (Black, Asian and Minority Ethnic) UK individuals, African Americans, Swedish Somalis,[1] and the institutionalised; particularly care-home residents. COVID-19 severity and mortality, appear related to vitamin D deficiency, [2 -12] helping explain higher COVID-19 mortality rates in BAME and the obese.[13]

Obesity is a strong COVID-19 risk factor, as are co-morbidities, including diabetes, cardio-vascular disease; and sedentary lifestyle; all are dependent on mitochondrial functionality (Gnaiger).[14] Fat cells accrete vitamin D.[15] The obese consistently have proportionately lower vitamin D status (serum 25-hydroxyvitamin D [25(OH)D]).[16]

Vitamin D is a secosteroid hormone with various skeletal and non-skeletal effects including regulation of innate and adaptive immune responses. Vitamin D, by binding to the vitamin D response element in various gene-promoter-regions, decreases expression of pro-inflammatory-cytokines and increases production of antiviral and antibacterial[17] proteins, suggesting an important role in antiviral innate adaptive immunity.[18] Importantly, vitamin D is also involved in renin–angiotensin system regulation,[19] which is regulated by entry of the SARS-Cov-2 virus into cells via the ACE2 receptor, leading to cytokine storms, with subsequent fatal respiratory distress syndrome.[20]

Pathways, mechanisms, cell-types, proteins and receptors, ‘regulated’ by vitamin D include: airway epithelial cell tight-junction function and integrity; lymphocytes, macrophages T cells, T helper cells, Th1, -17; Tregs[21]; related protein cytokines; IL-1, -2, -4, -5, -6 -10, -12; IFN-beta, TNFalpha, ; defensins and cathelicidin; and receptors HLA-DR, CD4, CD8, CD14, CD38.[2] Vitamin D also regulates mitochondrial respiratory inflammatory, oxidative and wider function. [2, 14] RXR and other receptor crosstalk links steroids, retinoids, vitamin D, thyroid hormone, oxidised lipids and peroxisomal pathways during viral and wider immune response.[22, 23, 24] Tocilizumab and vitamin D both may regulate COVID-19 related cytokine storms, through IL-6.[25]

A remarkable recent preprint (Alipio),[26] entitled, ‘Vitamin D supplementation could possibly improve clinical outcomes of patients infected with Coronavirus-2019 (COVID-19)’, examines vitamin D status, and hospitalization outcomes in 212 COVID-19 patients, using 4 categories: (1) Mild – without pneumonia, (2) Ordinary – confirmed pneumonia with fever, (3) Severe – hypoxia and respiratory distress, (4) Critical – respiratory failure requiring intensive case monitoring. Alipio observes, “Vitamin D status is significantly associated with clinical outcomes (p<0.001). For each standard deviation increase in serum 25(OH)D, the odds of having a mild clinical outcome rather than a severe outcome were increased approximately 7.94 times; the odds of having a mild clinical outcome rather than a critical outcome were increased approximately 19.61 times,” indicating that, in COVID-19 patients, increased serum 25(OH)D level could improve clinical outcomes, and/or mitigate the worst (severe to critical) outcomes. Conversely, decreased serum 25(OH)D levels could worsen clinical outcomes. Normal 25(OH)D levels were classified as >75 nmol/l (30 ng/ml). Deficient were those below 50 nmol/l (20 ng/ml). Deficiency definitions vary: <25 nmol/L, (10 ng/ml) UK; and 50 nmol/L (20 ng/ml) USA.[26]…

https://www.bmj.com/content/369/bmj.m1548/rr-6

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