Vitamin D: Health panacea or false prophet?
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However, this point of view may be excessively optimistic. There also is evidence that despite the current heavy reliance on serum 25-OHD3 concentration for the diagnosis of an individual’s vitamin D status, local tissue vitamin D intoxication may be present in individuals with much lower serum 25-OHD3 concentrations than are currently appreciated. Only rarely are the symptoms of local tissue vitamin D intoxication associated with vitamin D status or intake. An individual’s serum 25-OHD3 concentration may appear to be “low” for reasons totally independent of sunlight exposure or vitamin D intake. Serum 25-OHD3 concentration is only poorly responsive to increases in vitamin D intake, and the prolonged routine consumption of thousands of international units of vitamin D may interfere with the regulation of phosphate homeostasis by fibroblast growth factor-23 (FGF23) and the Klotho gene product, with consequences that are detrimental to human health. In light of these counterbalancing observations, curbing excessive enthusiasm for universally increasing vitamin D intake recommendations may be in order.
In addition, genetic polymorphisms, toxic insults, autoimmune disease, gradually accumulating oxidative damage, or chronic mineral imbalances may result in dysfunctional vitamin D receptors with reduced affinity for 1,25-OH2 D3 and reduced ability of 1,25-OH2 D3 to induce the activity of renal CYP24A1, allowing 1,25-OH2D3 concentration to rise while relieving some of the negative feedback inhibition of the conversion of 25-OHD3 to 1,25-OH2D3 [105,106]. When an excess of dietary vitamin D is present, elevated systemic and local concentrations of 1,25-OH2 D3 can occur. When an excess of 1,25-OH2 D3 is present within a tissue, local hypervitaminosis D can be produced. In the mildly compromised kidney, local hypervitaminosis D can produce hyperphosphatemia, triggering increased FGF23 secretion, whereas elevated 1,25-OH2D3 concentration can inhibit hepatic 25-hydroxylation of ingested vitamin D, resulting in concurrent renal hypervitaminosis D and low serum 25-OHD3 concentration[100]. A desire to establish a higher serum 25-OHD3 concentration may encourage undue clinical reliance on potentially counterproductive dietary supplementation with increasing amounts of vitamin D.
In such a scenario, local vitamin D toxicosis can occur and produce renal atrophy and calcification that may go unrecognized until clinical signs of “idiopathic” renal disease appear [107] Although Queen acknowledges that vitamin D plays important preventive and therapeutic roles in supporting human health, he cautions that renal and cardiovascular toxicity and increased mortality can be caused by covert physiologic vitamin D toxicosis [107]. For example, in the presence of age-associated reduction in Klotho expression, prolonged supplementation with large Klotho-suppressing amounts of vitamin D may produce 1,25-OH2 D3 excess and low serum 25-OHD3 concentration while increasing the risk of the expression of an aberrant FGF23 gene product that fails to regulate renal phosphate reabsorption, resulting in hyperphosphatemic tumoral calcinosis with carotid artery calcification [108,109].
Queen also expresses concerns that the current interpretation of vitamin D requirements and contributions to human health results from an excessive reliance on epidemiologic evidence (the science of association) that has become dissociated from the basic science of vitamin D and mineral homeostasis. He suggests that rather than reflecting inadequate exposure to vitamin D, a low serum 25-OHD3 concentration may reflect, in some individuals, a set of internal homeostatic attempts to correct an excess of free calcium ions and therefore, viewed from a basic science perspective, a strong argument can be made for the conclusion that in some individuals, a low serum 25-OHD3 concentration results from disease rather than produces disease.
In cautioning against excessive enthusiasm for increasing vitamin D intake recommendations, Queen emphasizes the following key points:
• Despite the current heavy reliance on serum 25-OHD3 concentration for the diagnosis of an individual’s vitamin D status, local tissue vitamin D intoxication may be present in individuals with much lower serum 25-OHD3 concentrations than are currently appreciated.
• Only rarely are the symptoms of local tissue vitamin D associated with vitamin D status or intake.
• A serum 25-OHD3 concentration may appear to be “low” for reasons totally independent of sunlight exposure or vitamin D intake. Serum 25-OHD3 concentration is only poorly responsive to increases in vitamin D intake.
• The prolonged routine consumption of megadoses of vitamin D may interfere with Klotho and FGF23 regulation of phosphate homeostasis with consequences that are detrimental to health.
The recent rush to elevate serum 25-OHD3 concentrations universally may benefit from a brief pause to reflect on the actual merits (and potential pitfalls) of doing so. Despite the detailed and persuasive data presented by Holick and his colleagues, reconsideration of the paradigm that a single or even a few biochemical markers can provide meaningful insight into the health status of an individual may be appropriate. This may be an area in which the modern reductionist approach to medical nutrition can benefit from an organismal reassessment.
The Truth About Vitamin D: Fourteen Reasons Why Misunderstanding Endures
http://www.medicinabiomolecular.com.br/ ... b-0439.pdf
Resolution of vitamin D intoxication was associated with a rebound in bone mineral density. In the long run, the best way to reverse the condition is to bring the level of 1,25D in the body back into a range where minerals will no longer be leached from the bones and the level of inflammatory cytokines can return to normal. In the meantime, getting the RDA of calcium from foods and supplements without vitamin D can be helpful.[69] Another misconception among some clinicians is the idea that vitamin D enhances the absorption of calcium. This is not the case. 25-D is a simple steroid which does not affect the genes responsible for calcium absorption. In contrast, the Vitamin D Receptor is a receptor that transcribes thousands of genes,[6] some of which do affect the metabolism of calcium.
Ter aanvulling: twee sluipmoordenaars respectievelijk botontkalking en aderverkalking (het dicht metselen van je bloedvaten) door verhoogde 1,25D gehalten zijn geen acute Vit.D intoxicatie verschijnselen. Wel lange termijn sloop effecten op je gezondheid.
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