25(OH)D is then transported to the kidneys where it is hydroxylated by another enzyme (CYP27B1, formerly 1a-hydroxylase) to produce 1,25(OH)2D. Vitamin D is transported to the liver where it is hydroxylated by an enzyme (CYP2R1, also known as cytochrome P450 2R1) to produce 25(OH)D.
#Vitamin quest full trainslation skin#
The sequential metabolic processes that convert biologically inactive, parental vitamin D into active metabolites begin when vitamin D 3 is photosynthesized in the skin or when vitamin D 2 or D 3 is ingested. This review ponders the question, “Is low 25(OH)D a cause of, or a consequence of inflammation?” The answer is found in the evidence that adds persistent intracellular infection to the equation. In the clinical setting, a novel immunotherapy is demonstrating the ability to resolve vitamin D metabolism dysfunction, restore immune function, and thus, eliminate infection and reduce inflammation. Analysis of this active metabolite may reveal elevated 1,25(OH)2D) in the presence of low 25(OH)D and lead to a diagnosis of abnormal vitamin D endocrine system function.Īn infectious pathogenesis posits that intracellular bacteria disrupt the vitamin D regulated immune system, resulting in persistent infection and chronic inflammation. Concerns about vitamin D deficiency merit a closer look at the current method of determining vitamin D status because the level of 25(OH)D does not always reflect the level of 1,25-dihydroxyvitamin-D (1,25(OH)2D). The definition of Vitamin D deficiency needs re-evaluation in view of the fact that low 25(OH)D is found in both healthy and sick individuals.
In the absence of definitive studies, authorities are questioning the wisdom of supplementing the general population with vitamin D. Often reiterated causes of vitamin D deficiency can be disputed in the light of more current research. Experts are debating the definition of vitamin D deficiency and the appropriate vitamin D doses, while further research is being done to determine if vitamin D supplementation has the intended effect.Īccording to some current definitions of vitamin D deficiency, even healthy persons, exposed to adequate sunlight, are unable to acquire enough vitamin D without supplementation. This led some authorities to declare a world-wide epidemic of vitamin D deficiency and to recommend vitamin D supplementation. When studies found an association between inflammatory diseases and low serum 25-hydroxyvitamin D (25(OH)D), further research found evidence of low vitamin D in a large segment of the general population. Inflammation is involved in many chronic diseases and concern has been raised about the influence of vitamin D deficiency on inflammatory processes.
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