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Vitamin D and COVID-19.
I saw @ChrisMasterjohn post something about how he wasn& #39;t taking vitamin D because it could potentially increase ACE-2 receptors. So, I started checking it on my admitted COVID patients out of curiosity. Invariably, it has been low <=30ng/mL
I saw @ChrisMasterjohn post something about how he wasn& #39;t taking vitamin D because it could potentially increase ACE-2 receptors. So, I started checking it on my admitted COVID patients out of curiosity. Invariably, it has been low <=30ng/mL
There has been a lot of focus on IL-6 inhibiting drugs, and there are reports that these medications have had some success with COVID patients.
Interestingly, researchers have described the exact mechanism for vitamin D& #39;s inhibition of IL-6.
Interestingly, researchers have described the exact mechanism for vitamin D& #39;s inhibition of IL-6.
https://www.jimmunol.org/content/188/5/2127
MKP-1">https://www.jimmunol.org/content/1... is upregulated by vitamin D. MKP-1 is known to inactivate p-38. p-38 phosphorylation, in this case, induced by LPS, increases IL6 and TNF-alpha.
The above study found that adequate vitamin D levels (30ng/ml) suppressed LPS phosphorylation of p-38
MKP-1">https://www.jimmunol.org/content/1... is upregulated by vitamin D. MKP-1 is known to inactivate p-38. p-38 phosphorylation, in this case, induced by LPS, increases IL6 and TNF-alpha.
The above study found that adequate vitamin D levels (30ng/ml) suppressed LPS phosphorylation of p-38
The suppressed phosphorylation of p-38 resulted in lower IL-6 and TNF-alpha levels in the study. Low vitamin D levels did NOT suppress phosphorylation with the LPS challenge, similar to MKP knockout mice, and IL-6 and TNF-alpha levels were significantly higher.
You know what else inhibits p-38? Chloroquine.
https://www.ncbi.nlm.nih.gov/pubmed/18055026?dopt=Abstract
In">https://www.ncbi.nlm.nih.gov/pubmed/18... the above study, infection with HCoV-229E significantly induced phosphorylation of p38, but pretreatment with chloroquine inhibited the phosphorylation of p-38, just like vitamin D did in the first study
https://www.ncbi.nlm.nih.gov/pubmed/18055026?dopt=Abstract
In">https://www.ncbi.nlm.nih.gov/pubmed/18... the above study, infection with HCoV-229E significantly induced phosphorylation of p38, but pretreatment with chloroquine inhibited the phosphorylation of p-38, just like vitamin D did in the first study
This has been observed elsewhere, like in this study of HIV infected patients. Vitamin D deficiency was associated with significantly elevated IL-6, TNF-alpha, d-dimer (something we& #39;re also seeing).
https://www.ncbi.nlm.nih.gov/pubmed/28464004 ">https://www.ncbi.nlm.nih.gov/pubmed/28...
https://www.ncbi.nlm.nih.gov/pubmed/28464004 ">https://www.ncbi.nlm.nih.gov/pubmed/28...
Does an adequate vitamin D level protect against some of the cytokine storm we& #39;re seeing with COVID-19? I don& #39;t know. I just haven& #39;t seen any vitamin D levels in the 40& #39;s or higher yet on ANY patient I& #39;ve admitted with it. I& #39;d be interested to see if others are seeing the same
At the very least, there is a well-defined mechanism for vitamin D& #39;s suppression of p38, like chloroquine, and it would seem very low risk to suggest that people ensure they have an adequate vitamin D level, at the very minimum over 30.
I& #39;m an emergency physician and not a cell biologist, so those people are free to weigh in. @PeterAttiaMD , maybe you have some thoughts or people to run this by?
