shye wrote:So what did he measure??
My D levels, despite taking 800 IU's for years, was deficient when we finally measured it several years ago. Took mega doses to bring it up to better level. BUT my ca blood levels were always within range.
BUT recently got an ultrasound re: calcification of carotids and arteries, and do have a problem with this.
So, do you, or anyone else, know a bit more about this?? Is taking the excess D to bring it to the higher levels now recommended possibly NOT a good move, in light of calcification??
And yes, Annb57, a link to the Kuwait article would be greatly appreciated.
a Weill Cornell Medical College
b Georgetown University
c Murdoch University
Vitamin D: the alternative hypothesis
Paul J. Alberta, Amy D. Proalb, Trevor G. Marshallc
A B S T R A C T
Early studies on vitamin D showed promise that various forms of the “vitamin” may be protective
against chronic disease, yet systematic reviews and longer-term studies have failed to confirm these
findings. A number of studies have suggested that patients with autoimmune diagnoses are deficient in
25-hydroxyvitamin-D (25-D) and that consuming greater quantities of vitamin D, which further elevates
25-D levels, alleviates autoimmune disease symptoms. Some years ago, molecular biology identified 25-
D as a secosteroid. Secosteroids would typically be expected to depress inflammation, which is in line
with the reports of symptomatic improvement. The simplistic first-order mass-action model used to
guide the early vitamin studies is now giving way to a more complex description of action. When active,
the Vitamin D nuclear receptor (VDR) affects transcription of at least 913 genes and impacts processes
ranging from calcium metabolism to expression of key antimicrobial peptides. Additionally, recent
research on the Human Microbiome shows that bacteria are far more pervasive than previously thought,
increasing the possibility that autoimmune disease is bacterial in origin. Emerging molecular evidence
suggests that symptomatic improvements among those administered vitamin D is the result of 25-D’s
ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in shortterm
palliation, persistent pathogens that may influence disease progression proliferate over the longterm.
linky to full paper
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