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]...
Currently, no effective COVID-19 treatment exists. Vaccines present enormous possibilities, but equally-large hurdles, and require time. Vitamin D biology, is a mature well-researched field, dating back 100 years. Doses, and risks, within clinical parameters, are established and well quantified. Governmental intake guidance exists. Vitamin D deficiency is a medically accepted condition, requiring treatment. Existing blood samples from COVID-19 hospitalized patients could be retrospectively tested for 25(OH)D and linked to outcomes.[25]
We and others (Grant, Lahore)[9, 34] hypothesize vitamin D may have clinical COVID-19 relevance. Vitamin D deficiency may biomark risk of sepsis in all populations; 25(OH)D was significantly lower in patients that died within 30 days.[35, 36] A French clinical RCT recently started, testing effects of a large single vitamin D dose, administered early in infection, compared to a standard dose, on the mortality of older COVID-19 infected adults deficient in vitamin D (Annweiler).[37]
Whilst clinical studies have potential, vitamin D deficiency is an existing, ubiquitous and pressing issue. Deficiency is variable, but widespread globally. BAME people in high latitudes are a group at high risk of deficiency, as observed by NICE[38] and others (Rhein).[39] Surprisingly, vitamin D may be a larger relative COVID-19 causative agent than socioeconomic-factors.[40] Importantly, vitamin D supplementation determinants should include basal level, genetic background, metabolic status and gender.
Albeit vitamin D deficiency most likely accounts for a greater COVID-19 impact on BAME, older, institutionalised and obese persons, COVID-19 severity would undoubtedly be exacerbated by, often socioeconomic related, general micro-nutrient inadequacies.[41, 42]...
Recognition (subject to proof by research), that vitamin D deficiency contributes to COVID-19 infection, progression, severity and mortality would demand policy rethinking on: the seasonality of COVID-19,[43] outdoor access, motivation for physical exercise, food fortification, supplementation, clinical treatment, and provision of free vitamin D supplements to institutions, front-line health and care workers. Sensible (according to latitude and weather) sun exposure is free, available to all and quickly improves vitamin D status, but is inhibited by lock-down...
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]...
Currently, no effective COVID-19 treatment exists. Vaccines present enormous possibilities, but equally-large hurdles, and require time. Vitamin D biology, is a mature well-researched field, dating back 100 years. Doses, and risks, within clinical parameters, are established and well quantified. Governmental intake guidance exists. Vitamin D deficiency is a medically accepted condition, requiring treatment. Existing blood samples from COVID-19 hospitalized patients could be retrospectively tested for 25(OH)D and linked to outcomes.[25]
We and others (Grant, Lahore)[9, 34] hypothesize vitamin D may have clinical COVID-19 relevance. Vitamin D deficiency may biomark risk of sepsis in all populations; 25(OH)D was significantly lower in patients that died within 30 days.[35, 36] A French clinical RCT recently started, testing effects of a large single vitamin D dose, administered early in infection, compared to a standard dose, on the mortality of older COVID-19 infected adults deficient in vitamin D (Annweiler).[37]
Whilst clinical studies have potential, vitamin D deficiency is an existing, ubiquitous and pressing issue. Deficiency is variable, but widespread globally. BAME people in high latitudes are a group at high risk of deficiency, as observed by NICE[38] and others (Rhein).[39] Surprisingly, vitamin D may be a larger relative COVID-19 causative agent than socioeconomic-factors.[40] Importantly, vitamin D supplementation determinants should include basal level, genetic background, metabolic status and gender.
Albeit vitamin D deficiency most likely accounts for a greater COVID-19 impact on BAME, older, institutionalised and obese persons, COVID-19 severity would undoubtedly be exacerbated by, often socioeconomic related, general micro-nutrient inadequacies.[41, 42]...
Recognition (subject to proof by research), that vitamin D deficiency contributes to COVID-19 infection, progression, severity and mortality would demand policy rethinking on: the seasonality of COVID-19,[43] outdoor access, motivation for physical exercise, food fortification, supplementation, clinical treatment, and provision of free vitamin D supplements to institutions, front-line health and care workers. Sensible (according to latitude and weather) sun exposure is free, available to all and quickly improves vitamin D status, but is inhibited by lock-down...
