Vitamin D Levels Play A Role In Severeness Of Covid19

LLight

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I think these results can be misleading. I'm not convinced by them. But I'm sure other people will disagre with this opinion.

This is observational data and the metabolism between the different forms of Vitamin D is controlled by enzymes in the body. Vitamin D is more a hormone than a vitamin.
FYI, the vitamin D measured is not the "active form" (which is 1,25(OH)2 D3, not 25(OH)D3).

I advise you to elevate your vitamin D levels via sun exposition (instead of supplementing) if you would like to :):
 
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Yes,it is true,what they measure is a reservoir or pool-type of substance,Calcifediol,which gets into tissues and there activated to Calcitriol,which is a necessary Hormone for whatever the immunesystem is.The Author shows a clear hierarchy of D-level and severity of clinical course and outcome.Patients with Calcifediol above 30ng/ml were 85% destined to have only "mild" symptoms,without even radiological signs of the Crown-virus.Only 7% became "ordinary"-level diseased with D above 30ng/ml.





Hormone D sufficiency.JPGHormone D sufficiency.JPG
 

jb116

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I'm not sure why this would be questionable for a Peat forum...???
Vitamin D is one of the main things Peat pushes for and this study aligns perfectly with what we've known before.
 

Motif

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I'm not sure why this would be questionable for a Peat forum...???
Vitamin D is one of the main things Peat pushes for and this study aligns perfectly with what we've known before.



It is? But not over supplements?
 

peateats1

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I think vitamin d can help to lower or suppress an active angiotensin system, and ray has said that angiotensin is responsible for the severe effects especially in the lungs with this covid virus.

Ray was saying that younger people are not getting as sick because they have higher ace2 and ace2 destroys angiotensin.

So anyway, it does make sense that vitamin d is important.
 

LLight

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Cathelicidin preserves intestinal barrier function in polymicrobial sepsis | Critical Care | Full Text

"Our data suggested that 1alpha, 25-dihydroxyvitamin D3 but not cholecalciferol is a potential therapeutic agent for treating sepsis."



"Furthermore, we assessed the therapeutic use of the active form and the inactive form of VD3 in our CLP model. We observed that administration of calcitriol (an active form of VD3) but not cholecalciferol (an inactive form of VD3) after the onset of sepsis led to a better survival outcome in CLP mice. In line with recent publications, high-dose VD3 (cholecalciferol, inactive form of VD3) did not improve the survival outcomes of critically ill patients in terms of 90-day mortality [50]. Since hepatic cytochrome P450 (CYPs) play an essential role in the conversion of VD3 into 25-hydroxyVD3 together with additional evidence showing that hepatic CYPs dysfunctions are linked to sepsis [51,52,53], we further examined the functions of the liver after the onset of sepsis. Our results demonstrated that CLP induced hepatic damage and the associated downregulations of hepatic CYPs at mRNA level, resulting in decreased serum intermediate and active VD3. Fortunately, the administration of calcitriol (an active form of VD3) can bypass hepatic biotransformation of cholecalciferol into 25-hydroxyVD3 mediated by CYP system, directly entering the circulatory system and exerting the beneficial effects. Taken together, we confirmed that the active form of VD3 but not the inactive form of VD3 is a therapeutic drug in our CLP model. Noticeably, the latter worsened 7-day mortality and the associated symptoms in CLP-operated mice, the mechanism of which remains unclear."
 

Motif

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And what Daily Dose when you live in northern countries?
 
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Cathelicidin preserves intestinal barrier function in polymicrobial sepsis | Critical Care | Full Text

"Our data suggested that 1alpha, 25-dihydroxyvitamin D3 but not cholecalciferol is a potential therapeutic agent for treating sepsis."



"Furthermore, we assessed the therapeutic use of the active form and the inactive form of VD3 in our CLP model. We observed that administration of calcitriol (an active form of VD3) but not cholecalciferol (an inactive form of VD3) after the onset of sepsis led to a better survival outcome in CLP mice. In line with recent publications, high-dose VD3 (cholecalciferol, inactive form of VD3) did not improve the survival outcomes of critically ill patients in terms of 90-day mortality [50]. Since hepatic cytochrome P450 (CYPs) play an essential role in the conversion of VD3 into 25-hydroxyVD3 together with additional evidence showing that hepatic CYPs dysfunctions are linked to sepsis [51,52,53], we further examined the functions of the liver after the onset of sepsis. Our results demonstrated that CLP induced hepatic damage and the associated downregulations of hepatic CYPs at mRNA level, resulting in decreased serum intermediate and active VD3. Fortunately, the administration of calcitriol (an active form of VD3) can bypass hepatic biotransformation of cholecalciferol into 25-hydroxyVD3 mediated by CYP system, directly entering the circulatory system and exerting the beneficial effects. Taken together, we confirmed that the active form of VD3 but not the inactive form of VD3 is a therapeutic drug in our CLP model. Noticeably, the latter worsened 7-day mortality and the associated symptoms in CLP-operated mice, the mechanism of which remains unclear."


I looked at that study,and they themselves make the causation clear,acute sepsis disturbs downstream metabolism of D3,which causes a lack of enzyme activity which orderly results in Calcitriol-manifestation.So if you would take D3 7 to 10 days before your sepsis,all D3 would ahve been converted to Calcifediol,they dont seem to claim defective Calcifediol to Calcitriol conversion,but then again,Sepsis is Sepsis,most severe disease,good for them if they intervene with pharmacologic Calcitriol,circumventing the now defective natural Pathing.
 
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