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No evidence that vitamin D is able to prevent or affect the severity of COVID-19 in individuals with European ancestry: a Mendelian randomisation study of open data

Amin et al., BMJ Nutrition, Prevention & Health, doi:10.1136/bmjnph-2020-000151
Jan 2021  
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COVID-19 severity -32% Improvement Relative Risk Case -8% Vitamin D for COVID-19  Amin et al.  Sufficiency Are vitamin D levels associated with COVID-19 outcomes? Retrospective 175,977 patients in the United Kingdom Higher progression with higher vitamin D levels (not stat. sig., p=0.2) c19early.org Amin et al., BMJ Nutrition, Prevention.., Jan 2021 Favorsvitamin D Favorscontrol 0 0.5 1 1.5 2+
Vitamin D for COVID-19
8th treatment shown to reduce risk in October 2020
 
*, now with p < 0.00000000001 from 122 studies, recognized in 9 countries.
No treatment is 100% effective. Protocols combine treatments. * >10% efficacy, ≥3 studies.
4,300+ studies for 77 treatments. c19early.org
Analysis of vitamin D levels and COVID-19 cases and severity based on genetic predisposition to higher vitamin D levels or lower vitamin D deficiency, finding no significant association.
Mendelian randomization studies compare the estimated effect of SNPs associated with variation in vitamin D levels on the health outcomes in large numbers of patients. For more background on Mendelian randomization studies and their limitations see1.
For reasons why Mendelian randomization may fail in this case, see2. Authors suggest that it may come down to the use of 25(OH)D concentration in serum as a less than ideal proxy for vitamin D status of cells involved in the immune response. For most other purposes, it may not matter much that unbound (free) 25(OH)D is the better predictor of vitamin D deficiency and the resulting unfavourable outcomes. But for the MR analysis, the genetic instrument is strongly dominated by variation in the GC gene which modulates the concentration of vitamin D-binding protein (VDBP) in blood and thereby indirectly the concentrations of 25(OH)D and 1,25-dihydroxy vitamin D. Thus, the common GC alleles rs4588A and rs7041T are both associated with much lower than average vitamin D concentrations. In contrast, directly measured unbound (free) vitamin D concentrations are minimally affected by these alleles, if at all.
3 suggest that the primary reasons for Mendelien randomization failure include that the total SNP-induced variation in 25(OH)D has often been less than assay variance, and that genome-wide association studies of SNP effects have been made on the full range of 25(OH)D levels, while the data is non-linear with a significant percentage in the low and high plateaus of the outcome relationships.
This is the 37th of 198 COVID-19 sufficiency studies for vitamin D, which collectively show higher levels reduce risk with p<0.0000000001 (1 in 361,397 vigintillion).
COVID-19 severity, 32.3% higher, RR 1.32, p = 0.20, high D levels 140,898, low D levels 35,079, inverted to make RR<1 favor high D levels, odds ratio converted to relative risk, >=50nmol/L vs. <25nmol/L, MR Egger, baseline risk approximated with overall risk.
risk of case, 7.6% higher, RR 1.08, p = 0.14, high D levels 140,898, low D levels 35,079, inverted to make RR<1 favor high D levels, odds ratio converted to relative risk, >=50nmol/L vs. <25nmol/L, MR Egger, baseline risk approximated with overall risk.
Effect extraction follows pre-specified rules prioritizing more serious outcomes. Submit updates
Amin et al., 7 Jan 2021, retrospective, population-based cohort, United Kingdom, peer-reviewed, 2 authors.
This PaperVitamin DAll
No evidence that vitamin D is able to prevent or affect the severity of COVID-19 in individuals with European ancestry: a Mendelian randomisation study of open data
Hasnat A Amin, Dr Fotios Drenos
BMJ Nutrition, Prevention & Health, doi:10.1136/bmjnph-2020-000151
Background Upper respiratory tract infections are reportedly more frequent and more severe in individuals with lower vitamin D levels. Based on these findings, it has been suggested that vitamin D can prevent or reduce the severity of COVID-19. Methods We used two-sample Mendelian randomisation (MR) to assess the causal effect of vitamin D levels on SARS-CoV-2 infection risk and COVID-19 severity using publicly available data. We also carried out a genome-wide association analysis (GWA) of vitamin D deficiency in the UK Biobank (UKB) and used these results and two-sample MR to assess the causal effect of vitamin D deficiency on SARS-CoV-2 infection risk and COVID-19 severity. Results We found no evidence that vitamin D levels causally affect the risk of SARS-CoV-2 infection (ln(OR)=0.17 (95% CI −0.22 to 0.57, p=0.39)) nor did we find evidence that vitamin D levels causally affect COVID-19 severity (ln(OR)=0.36 (95% CI −0.89 to 1.61, p=0.57)). Based on our GWA analysis, we found that 17 independent variants are associated with vitamin D deficiency in the UKB. Using these variants as instruments for our two-sample MR analyses, we found no evidence that vitamin D deficiency causally affects the risk of SARS-CoV-2 infection (ln(OR)=−0.04 (95% CI −0.1 to 0.03, p=0.25)) nor did we find evidence that vitamin D deficiency causally affects COVID-19 severity (ln(OR)=−0.24 (95% CI −0.55 to 0.08, p=0.14)). Conclusions In conclusion, we found no evidence that vitamin D is protective against SARS-CoV-2 infection or COVID-19 severity. Our data support the recent statement by the National Institute for Health and Care Excellence that the use of vitamin D supplementation to mitigate COVID-19 is not supported by the available data. What this paper adds ► Uncertainty remains over the use of Vitamin D for the prevention of COVID-19 and the moderation of its symptoms. ► Genetic predisposition for higher levels of vitamin D and for lower chance of vitamin D insufficiency do not have evidence of association with infection from SARS-CoV-2 or severity of COVID-19 following infection. ► Our work supports the current NICE statement that, based on the available evidence, vitamin D should not be considered as protective of infection from SARS-CoV-2 or a way to mitigate its severity.
Competing interests None declared. Patient consent for publication Not required. Provenance and peer review Not commissioned; externally peer reviewed by Dr Emmanuel Baah University of North Carolina System, USA. Data availability statement Data from the COVID-19 Host Genetics Initiative are available in a public, open access repository. UK Biobank data may be obtained from a third party and are not publicly available. The data from the COVID-19 Host Genetics Initiative that were used in this study are available here: https://www. covid19hg. org/ results/. UK Biobank data are available to all bona fide researchers for all types of health-related research which is in the public interest. Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise. Open access This is an open access article distributed in accordance with the Creative..
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